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Secretary of Labor Scalia on the August Jobs Report – “Today’s jobs report is encouraging where to get antabuse news for American workers heading into Labor Day. The report significantly beat expectations, with the unemployment rate dropping to 8.4 percent even as more Americans entered the labor force. Unemployment fell across all demographics, and the 1.4 million jobs added showed increases across most industry sectors. This follows a where to get antabuse string of other reports showing a strong recovery underway.

The Administration remains focused on returning millions more Americans to work, and providing additional support to the unemployed through the Lost Wages Assistance Program authorized by the President when Congress failed to act on enhanced unemployment benefits.” Secretary Scalia also joined Fox News, Fox Business and CNN to discuss the report. Defending Workers’ Rights to where to get antabuse Paid Leave and Wages Earned. U.S. Department of Labor Offers Webinar for Ohio Employers – The Wage and Hour Division and the Occupational Safety and Health Administration presented a webinar for Ohio area employers and human resources where to get antabuse professionals on the paid leave requirements of the Families First alcoholism Response Act and safety guidance for returning to work and maintaining a safe and healthy working environment.During the alcoholism antabuse, the Department of Labor is focused on protecting the safety and health of American workers, assisting our state partners as they deliver traditional unemployment and expanded unemployment benefits, ensuring Americans know their rights to new paid sick leave and expanded family and medical leave, providing guidance and assistance to employers, and carrying out the mission of the Department.

The mission of the Department of Labor is to foster, promote and develop the welfare of the wage earners, job seekers and retirees of the United States. Improve working conditions. Advance opportunities for where to get antabuse profitable employment. And assure work-related benefits and rights.WASHINGTON, DC – U.S.

Secretary of Labor Eugene Scalia issued the following statement on the August 2020 Employment Situation Report:“Today’s jobs report is encouraging news for American workers heading into Labor where to get antabuse Day. The report significantly beat expectations, with the unemployment rate dropping to 8.4 percent even as more Americans entered the labor force. Unemployment fell across all demographics, and the 1.4 million jobs added showed increases across where to get antabuse most industry sectors. This follows a string of other reports showing a strong recovery underway.

The Administration remains focused on returning millions more Americans to work, and providing additional support to the unemployed through the Lost Wages Assistance Program authorized by the President when Congress failed to act on enhanced unemployment benefits.”.

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alcoholism treatment impact on cisgender gay men and other men who have sex with men (MSM) on a global scaleThe alcoholism treatment antabuse is thought to disproportionately buy antabuse online with free samples threaten antabuse weight loss the health of underserved and underinvestigated populations. To investigate the impact of alcoholism treatment transmission mitigation measures on MSM, an international team did a cross-sectional study that included 2732 MSM from 103 antabuse weight loss countries who responded to a questionnaire distributed through a gay social networking app. Findings suggest that the spread of alcoholism treatment, and the global response to contain it, has variably disrupted economic, mental health, general health and clinical services among MSM populations, with a greater impact on those living with HIV, racial/ethnic minorities, immigrants, sex workers and socioeconomically disadvantaged groups. As alcoholism treatment may deepen health disparities and social inequalities, continued monitoring and creative strategies are needed to mitigate reduction in access to services for MSM with intersecting vulnerabilities.Santos GM, antabuse weight loss Ackerman B, Rao A, et al.

Economic, mental health, HIV prevention and HIV treatment impacts of alcoholism treatment and the alcoholism treatment response on a global sample of cisgender gay men and other men who have sex with men. AIDS Beha 2020 antabuse weight loss. 11:1–11.https://doi.org/10.1007/s10461-020-02969-0Influence of antabuse weight loss sexual positioning on syphilis acquisition and its stage at diagnosisIn a retrospective study of MSM in Melbourne, Australia, researchers examined the association between sexual positioning and a diagnosis of primary (n=338) or secondary (n=221) syphilis. Of 247 penile chancres, 244 (98.7%) occurred in MSM who reported versatile or exclusive top sexual positioning.

Of 77 anal chancres, 75 (97.4%) occurred in MSM who antabuse weight loss reported versatile or exclusive bottom sexual positioning. MSM who practised receptive anal sex were more likely to present with secondary rather than primary syphilis (OR 3.90. P<0.001, adjusted antabuse weight loss for age, HIV status and condom use). This suggests that because anorectal chancres are less noticeable, they are less likely to prompt evaluation.

Findings highlight the need for improved screening of MSM who report receptive anal sex to ensure early antabuse weight loss syphilis detection and treatment.Cornelisse VJ, Chow EPF, Latimer RL, et al. Getting to antabuse weight loss the bottom of it. Sexual positioning and stage of syphilis at diagnosis, and implications for syphilis screening. Clin Infect Dis 2020;71(2):318–322 antabuse weight loss.

Https://doi.org/10.1093/cid/ciz802A novel rapid, point-of-care test (POCT) for confirmatory testing of active syphilis The re-emergence of syphilis is a global public health concern especially in resource-limited settings. Current POCTs detect Treponema pallidum (TP) total antibodies but do not distinguish between active and past/treated syphilis, resulting in potential overtreatment antabuse weight loss and contributing to shortages of penicillin. A new, investigational POCT based on the detection of TP-IgA was evaluated against standard laboratory-based serological tests in 458 stored plasma samples from China and 503 venous blood samples from South Africa. Sensitivity and specificity of TP-IgA POCT for identifying active syphilis were 96.1% (95% antabuse weight loss CI.

91.7% to 98.5%) and 84.7% antabuse weight loss (95% CI. 80.1% to 88.6%) in Chinese samples, and 100% (95% CI. 59% to 100%) and 99.4% (95% antabuse weight loss CI. 98.2% to 99.9%) in South African samples, respectively.

These preliminary findings suggest that this TP-IgA-based POCT meets the WHO target product profile antabuse weight loss for confirmatory diagnosis of active syphilis.Pham MD, Wise A, Garcia ML, et al. Improving the coverage and accuracy of syphilis testing. The development antabuse weight loss of a novel rapid, point-of-care test for confirmatory testing of active syphilis and its early evaluation in China and South Africa. EClinicalMedicine 2020;24:100440 antabuse weight loss.

Https://doi.org/10.1016/j.eclinm.2020.100440Early antiretroviral therapy (ART) initiation and wide coverage reduces population-level HIV s in FranceIn 2013, France implemented the early initiation of ART irrespective of CD4 counts to fast-track progress toward UNAIDS (Joint United Nations Programme on HIV/AIDS) 90-90-90 goals (90% of people with HIV diagnosed, 90% on ART, 90% virologically suppressed).1 An analysis of 61 822 HIV-diagnosed people within the national Dat’AIDS prospective cohort study shows that 91.9% of HIV-diagnosed people were receiving ART by 2014 and 90.5% were virologically suppressed by 2013. This was accompanied by a 36% and 25% decrease in the number of primary (diagnosed with symptoms of acute HIV) and recent HIV (diagnosed with CD4 cell count ≥500/mm3), respectively, between 2013 and antabuse weight loss 2017. These findings on two of three goals support the effectiveness of ‘Treatment as Prevention’ in dramatically reducing HIV incidence at the population level.Le Guillou A, Pugliese P, Raffi F, Cabie A, Cuzin L, Katlama C, et al. Reaching the second and third joint United Nations Programme on Human Immunodeficiency antabuse (HIV)/AIDS 90-90-90 targets is accompanied by a dramatic reduction in primary HIV and in recent antabuse weight loss HIV s in a large French nationwide HIV cohort.

Clinical Infectious Diseases 2019;71(2):293–300. Https://doi.org/10.1093/cid/ciz800No evidence of an association between human papillomaantabuse (HPV) vaccination and infertilityDespite well-established evidence of effectiveness antabuse weight loss and safety, HPV treatment uptake remains below target in many countries, often due to safety concerns. To evaluate claims antabuse weight loss that HPV vaccination increases female infertility, researchers analysed 2013–2016 National Health and Nutrition Examination Survey data from 1114 US women aged 20 to 33 years—those young enough to have been offered HPV treatments and old enough to have been asked about infertility. The 8.1% of women who self-reported infertility were neither more nor less likely to have received an HPV treatment.

Vaccinated women who had antabuse weight loss ever been married were less likely to report infertility. Findings should engender confidence among healthcare providers, whose recommendation is a key factor in patients’ acceptance of HPV vaccination.Schmuhl N, Mooney KE, Zhang X, Cooney LG, Conway JH, and LoCont NK. No association between HPV vaccination and infertility in antabuse weight loss U.S. Females 18–33 years old.

treatment 2020;38(24):4038–4043 antabuse weight loss. Https://doi.org/10.1016/j.treatment.2020.03.035A pay-it-forward antabuse weight loss approach to improve uptake of gonorrhoea and chlamydia testingDespite WHO recommendations that MSM receive gonorrhoea and chlamydia testing, affordability remains a barrier in many countries. In a randomised trial, researchers tested three incentivising strategies, randomising 301 MSM in MSM-run community-based organisations in Guangzhou and Beijing, China. Gonorrhoea and chlamydia test uptake was antabuse weight loss 56% in the pay-it-forward arm (free testing and an invitation to donate to a future person’s test), 46% in a pay-what-you-want arm and 18% in the standard-cost arm (¥150, €1.2).

The estimated difference in test uptake between pay-it-forward and standard cost was 38.4% (95% CI lower bound 28.4%). Almost 95% of MSM in the pay-it-forward arm donated to antabuse weight loss testing for future participants. The pay-it-forward strategy significantly increased gonorrhoea and chlamydia testing uptake in China and has potential to drive testing in other settings.Yang F, Zhang TP, Tang W, Ong JJ, Alexander M, Forastiere L, Kumar N, Li KT, Zou F, Yang L, Mi G, Wang Y, Huang W, Lee A, Zhu W, Luo D, Vickerman P, Wu D, Yang B, Christakis NA, Tucker JD. Pay-it-forward gonorrhoea and chlamydia testing among men who have sex with antabuse weight loss men in China.

A randomised controlled trial antabuse weight loss. Lancet Infect Dis 2020;20(8)976-982. Https://doi.org/10.1016/S1473-3099(20)30172-9The Shape of Training review1 and the Future Hospital Commission2 identified the need for a reform of postgraduate medical training antabuse weight loss in the UK for doctors to adapt to changing population and service needs. The focus of postgraduate training needed to move from a ‘time-served’ approach to a competency-based one with doctors developing high-level learning outcomes, capabilities in practice (CiPs).

The General Medical Council (GMC) also recommended that all revised curricula from 2020 should include generic professional capabilities (GPCs), including communication, leadership, multidisciplinary teamwork and patient safety, antabuse weight loss which are crucial to safe and effective patient care.Genitourinary medicine (GUM), along with many other physicianly specialities, will adopt a dual training model from August 2022, leading to accreditation in both GUM and general internal medicine (GIM). The GUM curriculum will continue to offer training in the diagnosis, investigation and management of sexually transmitted s and related conditions, contraception, HIV inpatient and outpatient care, management of ….

alcoholism treatment impact on cisgender gay men and other men who have sex with men (MSM) on a global how to get antabuse tablets scaleThe alcoholism treatment antabuse is thought where to get antabuse to disproportionately threaten the health of underserved and underinvestigated populations. To investigate the impact of alcoholism treatment transmission mitigation measures on MSM, an international team did a cross-sectional study where to get antabuse that included 2732 MSM from 103 countries who responded to a questionnaire distributed through a gay social networking app. Findings suggest that the spread of alcoholism treatment, and the global response to contain it, has variably disrupted economic, mental health, general health and clinical services among MSM populations, with a greater impact on those living with HIV, racial/ethnic minorities, immigrants, sex workers and socioeconomically disadvantaged groups. As alcoholism treatment may deepen health disparities where to get antabuse and social inequalities, continued monitoring and creative strategies are needed to mitigate reduction in access to services for MSM with intersecting vulnerabilities.Santos GM, Ackerman B, Rao A, et al.

Economic, mental health, HIV prevention and HIV treatment impacts of alcoholism treatment and the alcoholism treatment response on a global sample of cisgender gay men and other men who have sex with men. AIDS Beha where to get antabuse 2020. 11:1–11.https://doi.org/10.1007/s10461-020-02969-0Influence of sexual positioning on syphilis acquisition and its stage at diagnosisIn a retrospective study of where to get antabuse MSM in Melbourne, Australia, researchers examined the association between sexual positioning and a diagnosis of primary (n=338) or secondary (n=221) syphilis. Of 247 penile chancres, 244 (98.7%) occurred in MSM who reported versatile or exclusive top sexual positioning.

Of 77 anal chancres, 75 (97.4%) occurred in MSM where to get antabuse who reported versatile or exclusive bottom sexual positioning. MSM who practised receptive anal sex were more likely to present with secondary rather than primary syphilis (OR 3.90. P<0.001, adjusted for age, where to get antabuse HIV status and condom use). This suggests that because anorectal chancres are less noticeable, they are less likely to prompt evaluation.

Findings highlight the need for improved screening where to get antabuse of MSM who report receptive anal sex to ensure early syphilis detection and treatment.Cornelisse VJ, Chow EPF, Latimer RL, et al. Getting to the bottom of it where to get antabuse. Sexual positioning and stage of syphilis at diagnosis, and implications for syphilis screening. Clin Infect where to get antabuse Dis 2020;71(2):318–322.

Https://doi.org/10.1093/cid/ciz802A novel rapid, point-of-care test (POCT) for confirmatory testing of active syphilis The re-emergence of syphilis is a global public health concern especially in resource-limited settings. Current POCTs detect Treponema pallidum (TP) total antibodies but do not distinguish between active and past/treated syphilis, resulting in potential overtreatment and contributing to shortages of where to get antabuse penicillin. A new, investigational POCT based on the detection of TP-IgA was evaluated against standard laboratory-based serological tests in 458 stored plasma samples from China and 503 venous blood samples from South Africa. Sensitivity and specificity of TP-IgA POCT for identifying active syphilis were 96.1% where to get antabuse (95% CI.

91.7% to 98.5%) and 84.7% (95% CI where to get antabuse. 80.1% to 88.6%) in Chinese samples, and 100% (95% CI. 59% to where to get antabuse 100%) and 99.4% (95% CI. 98.2% to 99.9%) in South African samples, respectively.

These preliminary findings suggest that where to get antabuse this TP-IgA-based POCT meets the WHO target product profile for confirmatory diagnosis of active syphilis.Pham MD, Wise A, Garcia ML, et al. Improving the coverage and accuracy of syphilis testing. The development of a novel rapid, point-of-care test for confirmatory testing of active syphilis where to get antabuse and its early evaluation in China and South Africa. EClinicalMedicine 2020;24:100440 where to get antabuse.

Https://doi.org/10.1016/j.eclinm.2020.100440Early antiretroviral therapy (ART) initiation and wide coverage reduces population-level HIV s in FranceIn 2013, France implemented the early initiation of ART irrespective of CD4 counts to fast-track progress toward UNAIDS (Joint United Nations Programme on HIV/AIDS) 90-90-90 goals (90% of people with HIV diagnosed, 90% on ART, 90% virologically suppressed).1 An analysis of 61 822 HIV-diagnosed people within the national Dat’AIDS prospective cohort study shows that 91.9% of HIV-diagnosed people were receiving ART by 2014 and 90.5% were virologically suppressed by 2013. This was accompanied by a 36% and 25% decrease in the number of primary (diagnosed with symptoms of acute HIV) and recent HIV (diagnosed with CD4 cell count ≥500/mm3), where to get antabuse respectively, between 2013 and 2017. These findings on two of three goals support the effectiveness of ‘Treatment as Prevention’ in dramatically reducing HIV incidence at the population level.Le Guillou A, Pugliese P, Raffi F, Cabie A, Cuzin L, Katlama C, et al. Reaching the second and third joint United Nations Programme on Human Immunodeficiency antabuse (HIV)/AIDS 90-90-90 targets is accompanied by a dramatic reduction in primary HIV and in recent HIV s in a where to get antabuse large French nationwide HIV cohort.

Clinical Infectious Diseases 2019;71(2):293–300. Https://doi.org/10.1093/cid/ciz800No evidence of an association between human papillomaantabuse (HPV) vaccination and infertilityDespite well-established evidence of effectiveness and safety, HPV treatment where to get antabuse uptake remains below target in many countries, often due to safety concerns. To evaluate claims that HPV vaccination increases female infertility, researchers analysed 2013–2016 National Health and where to get antabuse Nutrition Examination Survey data from 1114 US women aged 20 to 33 years—those young enough to have been offered HPV treatments and old enough to have been asked about infertility. The 8.1% of women who self-reported infertility were neither more nor less likely to have received an HPV treatment.

Vaccinated women where to get antabuse who had ever been married were less likely to report infertility. Findings should engender confidence among healthcare providers, whose recommendation is a key factor in patients’ acceptance of HPV vaccination.Schmuhl N, Mooney KE, Zhang X, Cooney LG, Conway JH, and LoCont NK. No association between HPV where to get antabuse vaccination and infertility in U.S. Females 18–33 years old.

treatment 2020;38(24):4038–4043 where to get antabuse. Https://doi.org/10.1016/j.treatment.2020.03.035A pay-it-forward approach to improve uptake of gonorrhoea and chlamydia testingDespite WHO recommendations that MSM receive gonorrhoea and where to get antabuse chlamydia testing, affordability remains a barrier in many countries. In a randomised trial, researchers tested three incentivising strategies, randomising 301 MSM in MSM-run community-based organisations in Guangzhou and Beijing, China. Gonorrhoea and chlamydia test uptake was 56% in the pay-it-forward arm (free testing and an invitation to donate to a where to get antabuse future person’s test), 46% in a pay-what-you-want arm and 18% in the standard-cost arm (¥150, €1.2).

The estimated difference in test uptake between pay-it-forward and standard cost was 38.4% (95% CI lower bound 28.4%). Almost 95% of MSM in the pay-it-forward arm donated to where to get antabuse testing for future participants. The pay-it-forward strategy significantly increased gonorrhoea and chlamydia testing uptake in China and has potential to drive testing in other settings.Yang F, Zhang TP, Tang W, Ong JJ, Alexander M, Forastiere L, Kumar N, Li KT, Zou F, Yang L, Mi G, Wang Y, Huang W, Lee A, Zhu W, Luo D, Vickerman P, Wu D, Yang B, Christakis NA, Tucker JD. Pay-it-forward gonorrhoea where to get antabuse and chlamydia testing among men who have sex with men in China.

A randomised where to get antabuse controlled trial. Lancet Infect Dis 2020;20(8)976-982. Https://doi.org/10.1016/S1473-3099(20)30172-9The Shape of Training review1 and the Future Hospital Commission2 identified the where to get antabuse need for a reform of postgraduate medical training in the UK for doctors to adapt to changing population and service needs. The focus of postgraduate training needed to move from a ‘time-served’ approach to a competency-based one with doctors developing high-level learning outcomes, capabilities in practice (CiPs).

The General Medical Council (GMC) also recommended that all revised curricula from 2020 should include generic professional capabilities (GPCs), including communication, leadership, multidisciplinary teamwork and patient safety, which are crucial to where to get antabuse safe and effective patient care.Genitourinary medicine (GUM), along with many other physicianly specialities, will adopt a dual training model from August 2022, leading to accreditation in both GUM and general internal medicine (GIM). The GUM curriculum will continue to offer training in the diagnosis, investigation and management of sexually transmitted s and related conditions, contraception, HIV inpatient and outpatient care, management of ….

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Credit. IStock Share Fast Facts New @HopkinsMedicine study finds African-American women with common form of hair loss at increased risk of uterine fibroids - Click to Tweet New study in @JAMADerm shows most common form of alopecia (hair loss) in African-American women associated with higher risks of uterine fibroids - Click to Tweet In a study of medical records gathered on hundreds of thousands of African-American women, Johns Hopkins researchers say they have evidence that women with a common form of hair loss have an increased chance of developing uterine leiomyomas, or fibroids.In a report on the research, published in the December 27 issue of JAMA Dermatology, the researchers call on physicians who treat women with central centrifugal cicatricial alopecia (CCCA) to make patients aware that they may be at increased risk for fibroids and should be screened for the condition, particularly if they have symptoms such as heavy bleeding and pain. CCCA predominantly affects black women and is the most common form of permanent alopecia in this population. The excess scar tissue that forms as a result of this type of hair loss may also explain the higher risk for uterine fibroids, which are characterized by fibrous growths in the lining of the womb.

Crystal Aguh, M.D., assistant professor of dermatology at the Johns Hopkins University School of Medicine, says the scarring associated with CCCA is similar to the scarring associated with excess fibrous tissue elsewhere in the body, a situation that may explain why women with this type of hair loss are at a higher risk for fibroids.People of African descent, she notes, are more prone to develop other disorders of abnormal scarring, termed fibroproliferative disorders, such as keloids (a type of raised scar after trauma), scleroderma (an autoimmune disorder marked by thickening of the skin as well as internal organs), some types of lupus and clogged arteries. During a four-year period from 2013-2017, the researchers analyzed patient data from the Johns Hopkins electronic medical record system (Epic) of 487,104 black women ages 18 and over. The prevalence of those with fibroids was compared in patients with and without CCCA. Overall, the researchers found that 13.9 percent of women with CCCA also had a history of uterine fibroids compared to only 3.3 percent of black women without the condition.

In absolute numbers, out of the 486,000 women who were reviewed, 16,212 had fibroids.Within that population, 447 had CCCA, of which 62 had fibroids. The findings translate to a fivefold increased risk of uterine fibroids in women with CCCA, compared to age, sex and race matched controls. Aguh cautions that their study does not suggest any cause and effect relationship, or prove a common cause for both conditions. €œThe cause of the link between the two conditions remains unclear,” she says.

However, the association was strong enough, she adds, to recommend that physicians and patients be made aware of it. Women with this type of scarring alopecia should be screened not only for fibroids, but also for other disorders associated with excess fibrous tissue, Aguh says. An estimated 70 percent of white women and between 80 and 90 percent of African-American women will develop fibroids by age 50, according to the NIH, and while CCCA is likely underdiagnosed, some estimates report a prevalence of rates as high as 17 percent of black women having this condition. The other authors on this paper were Ginette A.

Okoye, M.D. Of Johns Hopkins and Yemisi Dina of Meharry Medical College.Credit. The New England Journal of Medicine Share Fast Facts This study clears up how big an effect the mutational burden has on outcomes to immune checkpoint inhibitors across many different cancer types. - Click to Tweet The number of mutations in a tumor’s DNA is a good predictor of whether it will respond to a class of cancer immunotherapy drugs known as checkpoint inhibitors.

- Click to Tweet The “mutational burden,” or the number of mutations present in a tumor’s DNA, is a good predictor of whether that cancer type will respond to a class of cancer immunotherapy drugs known as checkpoint inhibitors, a new study led by Johns Hopkins Kimmel Cancer Center researchers shows. The finding, published in the Dec. 21 New England Journal of Medicine, could be used to guide future clinical trials for these drugs. Checkpoint inhibitors are a relatively new class of drug that helps the immune system recognize cancer by interfering with mechanisms cancer cells use to hide from immune cells.

As a result, the drugs cause the immune system to fight cancer in the same way that it would fight an . These medicines have had remarkable success in treating some types of cancers that historically have had poor prognoses, such as advanced melanoma and lung cancer. However, these therapies have had little effect on other deadly cancer types, such as pancreatic cancer and glioblastoma. The mutational burden of certain tumor types has previously been proposed as an explanation for why certain cancers respond better than others to immune checkpoint inhibitors says study leader Mark Yarchoan, M.D., chief medical oncology fellow.

Work by Dung Le, M.D., associate professor of oncology, and other researchers at the Johns Hopkins Kimmel Cancer Center and its Bloomberg~Kimmel Cancer Institute for Cancer Immunotherapy showed that colon cancers that carry a high number of mutations are more likely to respond to checkpoint inhibitors than those that have fewer mutations. However, exactly how big an effect the mutational burden has on outcomes to immune checkpoint inhibitors across many different cancer types was unclear. To investigate this question, Yarchoan and colleagues Alexander Hopkins, Ph.D., research fellow, and Elizabeth Jaffee, M.D., co-director of the Skip Viragh Center for Pancreas Cancer Clinical Research and Patient Care and associate director of the Bloomberg~Kimmel Institute, combed the medical literature for the results of clinical trials using checkpoint inhibitors on various different types of cancer. They combined these findings with data on the mutational burden of thousands of tumor samples from patients with different tumor types.

Analyzing 27 different cancer types for which both pieces of information were available, the researchers found a strong correlation. The higher a cancer type’s mutational burden tends to be, the more likely it is to respond to checkpoint inhibitors. More than half of the differences in how well cancers responded to immune checkpoint inhibitors could be explained by the mutational burden of that cancer. €œThe idea that a tumor type with more mutations might be easier to treat than one with fewer sounds a little counterintuitive.

It’s one of those things that doesn’t sound right when you hear it,” says Hopkins. €œBut with immunotherapy, the more mutations you have, the more chances the immune system has to recognize the tumor.” Although this finding held true for the vast majority of cancer types they studied, there were some outliers in their analysis, says Yarchoan. For example, Merkel cell cancer, a rare and highly aggressive skin cancer, tends to have a moderate number of mutations yet responds extremely well to checkpoint inhibitors. However, he explains, this cancer type is often caused by a antabuse, which seems to encourage a strong immune response despite the cancer’s lower mutational burden.

In contrast, the most common type of colorectal cancer has moderate mutational burden, yet responds poorly to checkpoint inhibitors for reasons that are still unclear. Yarchoan notes that these findings could help guide clinical trials to test checkpoint inhibitors on cancer types for which these drugs haven’t yet been tried. Future studies might also focus on finding ways to prompt cancers with low mutational burdens to behave like those with higher mutational burdens so that they will respond better to these therapies. He and his colleagues plan to extend this line of research by investigating whether mutational burden might be a good predictor of whether cancers in individual patients might respond well to this class of immunotherapy drugs.

€œThe end goal is precision medicine—moving beyond what’s true for big groups of patients to see whether we can use this information to help any given patient,” he says. Yarchoan receives funding from the Norman &. Ruth Rales Foundation and the Conquer Cancer Foundation. Through a licensing agreement with Aduro Biotech, Jaffee has the potential to receive royalties in the future..

Credit. IStock Share Fast Facts New @HopkinsMedicine study finds African-American women with common form of hair loss at increased risk of uterine fibroids - Click to Tweet New study in @JAMADerm shows most common form of alopecia (hair loss) in African-American women associated with higher risks of uterine fibroids - Click to Tweet In a study of medical records gathered on hundreds of thousands of African-American women, Johns Hopkins researchers say they have evidence that women with a common form of hair loss have an increased chance of developing uterine leiomyomas, or fibroids.In a report on the research, published in the December 27 issue of JAMA Dermatology, the researchers call on physicians who treat women with central centrifugal cicatricial alopecia (CCCA) to make patients aware that they may be at increased risk for fibroids and should be screened for the condition, particularly if they have symptoms such as heavy bleeding and pain. CCCA predominantly affects black women and is the most common form of permanent alopecia in this population. The excess scar tissue that forms as a result of this type of hair loss may also explain the higher risk for uterine fibroids, which are characterized by fibrous growths in the lining of the womb.

Crystal Aguh, M.D., assistant professor of dermatology at the Johns Hopkins University School of Medicine, says the scarring associated with CCCA is similar to the scarring associated with excess fibrous tissue elsewhere in the body, a situation that may explain why women with this type of hair loss are at a higher risk for fibroids.People of African descent, she notes, are more prone to develop other disorders of abnormal scarring, termed fibroproliferative disorders, such as keloids (a type of raised scar after trauma), scleroderma (an autoimmune disorder marked by thickening of the skin as well as internal organs), some types of lupus and clogged arteries. During a four-year period from 2013-2017, the researchers analyzed patient data from the Johns Hopkins electronic medical record system (Epic) of 487,104 black women ages 18 and over. The prevalence of those with fibroids was compared in patients with and without CCCA. Overall, the researchers found that 13.9 percent of women with CCCA also had a history of uterine fibroids compared to only 3.3 percent of black women without the condition.

In absolute numbers, out of the 486,000 women who were reviewed, 16,212 had fibroids.Within that population, 447 had CCCA, of which 62 had fibroids. The findings translate to a fivefold increased risk of uterine fibroids in women with CCCA, compared to age, sex and race matched controls. Aguh cautions that their study does not suggest any cause and effect relationship, or prove a common cause for both conditions. €œThe cause of the link between the two conditions remains unclear,” she says.

However, the association was strong enough, she adds, to recommend that physicians and patients be made aware of it. Women with this type of scarring alopecia should be screened not only for fibroids, but also for other disorders associated with excess fibrous tissue, Aguh says. An estimated 70 percent of white women and between 80 and 90 percent of African-American women will develop fibroids by age 50, according to the NIH, and while CCCA is likely underdiagnosed, some estimates report a prevalence of rates as high as 17 percent of black women having this condition. The other authors on this paper were Ginette A.

Okoye, M.D. Of Johns Hopkins and Yemisi Dina of Meharry Medical College.Credit. The New England Journal of Medicine Share Fast Facts This study clears up how big an effect the mutational burden has on outcomes to immune checkpoint inhibitors across many different cancer types. - Click to Tweet The number of mutations in a tumor’s DNA is a good predictor of whether it will respond to a class of cancer immunotherapy drugs known as checkpoint inhibitors.

- Click to Tweet The “mutational burden,” or the number of mutations present in a tumor’s DNA, is a good predictor of whether that cancer type will respond to a class of cancer immunotherapy drugs known as checkpoint inhibitors, a new study led by Johns Hopkins Kimmel Cancer Center researchers shows. The finding, published in the Dec. 21 New England Journal of Medicine, could be used to guide future clinical trials for these drugs. Checkpoint inhibitors are a relatively new class of drug that helps the immune system recognize cancer by interfering with mechanisms cancer cells use to hide from immune cells.

As a result, the drugs cause the immune system to fight cancer in the same way that it would fight an . These medicines have had remarkable success in treating some types of cancers that historically have had poor prognoses, such as advanced melanoma and lung cancer. However, these therapies have had little effect on other deadly cancer types, such as pancreatic cancer and glioblastoma. The mutational burden of certain tumor types has previously been proposed as an explanation for why certain cancers respond better than others to immune checkpoint inhibitors says study leader Mark Yarchoan, M.D., chief medical oncology fellow.

Work by Dung Le, M.D., associate professor of oncology, and other researchers at the Johns Hopkins Kimmel Cancer Center and its Bloomberg~Kimmel Cancer Institute for Cancer Immunotherapy showed that colon cancers that carry a high number of mutations are more likely to respond to checkpoint inhibitors than those that have fewer mutations. However, exactly how big an effect the mutational burden has on outcomes to immune checkpoint inhibitors across many different cancer types was unclear. To investigate this question, Yarchoan and colleagues Alexander Hopkins, Ph.D., research fellow, and Elizabeth Jaffee, M.D., co-director of the Skip Viragh Center for Pancreas Cancer Clinical Research and Patient Care and associate director of the Bloomberg~Kimmel Institute, combed the medical literature for the results of clinical trials using checkpoint inhibitors on various different types of cancer. They combined these findings with data on the mutational burden of thousands of tumor samples from patients with different tumor types.

Analyzing 27 different cancer types for which both pieces of information were available, the researchers found a strong correlation. The higher a cancer type’s mutational burden tends to be, the more likely it is to respond to checkpoint inhibitors. More than half of the differences in how well cancers responded to immune checkpoint inhibitors could be explained by the mutational burden of that cancer. €œThe idea that a tumor type with more mutations might be easier to treat than one with fewer sounds a little counterintuitive.

It’s one of those things that doesn’t sound right when you hear it,” says Hopkins. €œBut with immunotherapy, the more mutations you have, the more chances the immune system has to recognize the tumor.” Although this finding held true for the vast majority of cancer types they studied, there were some outliers in their analysis, says Yarchoan. For example, Merkel cell cancer, a rare and highly aggressive skin cancer, tends to have a moderate number of mutations yet responds extremely well to checkpoint inhibitors. However, he explains, this cancer type is often caused by a antabuse, which seems to encourage a strong immune response despite the cancer’s lower mutational burden.

In contrast, the most common type of colorectal cancer has moderate mutational burden, yet responds poorly to checkpoint inhibitors for reasons that are still unclear. Yarchoan notes that these findings could help guide clinical trials to test checkpoint inhibitors on cancer types for which these drugs haven’t yet been tried. Future studies might also focus on finding ways to prompt cancers with low mutational burdens to behave like those with higher mutational burdens so that they will respond better to these therapies. He and his colleagues plan to extend this line of research by investigating whether mutational burden might be a good predictor of whether cancers in individual patients might respond well to this class of immunotherapy drugs.

€œThe end goal is precision medicine—moving beyond what’s true for big groups of patients to see whether we can use this information to help any given patient,” he says. Yarchoan receives funding from the Norman &. Ruth Rales Foundation and the Conquer Cancer Foundation. Through a licensing agreement with Aduro Biotech, Jaffee has the potential to receive royalties in the future..

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Los Angeles antabuse and naltrexone https://bugeysud-tourisme.fr/where-to-buy-ventolin-pills. New Orleans. And Seattle were among those signing the declaration released by the C40 Cities Climate Leadership Group, a consortium of nearly 100 global cities committed to climate change action. C40 was launched in 2005 and, antabuse and naltrexone along with the U.S.

Climate Mayors conference, has led urban climate policy initiatives, particularly during the Trump administration. The declaration calls on C40 cities to meet urban green space goals through one of two pathways. One is ensuring that 30% to 40% of total built-up surface antabuse and naltrexone area is green space or permeable surface by 2030. Secondly, cities can meet a “fit-for-purpose green or blue space” standard by ensuring that 70% of residents can walk or bike to a park or water feature within 15 minutes.

Such spaces “must be equitably prioritized to maximize accessibility and connectivity to nature for the most vulnerable,” according to the declaration. €œThese pathways antabuse and naltrexone will allow us to establish ambitious nature targets to achieve climate resilience and create an agenda for people and nature to support one another,” C40 leaders said in a statement. €œAction is vital now as globally currently, over 800 million people are vulnerable to sea-level rise, over 650 million people are vulnerable to water security, and 1.6 billion city residents will face extreme heat by 2050.” Los Angeles, the nation’s second-largest city with nearly 4 million residents, is among the largest to sign on. Mayor Eric Garcetti, who’s the current chairman of C40 and President Biden’s choice for ambassador to India, said in a statement that the declaration “is a reminder of the obligation we have to restore the natural world around us and an example of how mayors are leading with climate solutions that strengthen communities hit hardest by the climate emergency.” Emailed questions about how Los Angeles would meet one or both of the C40 pathways by 2030 were not answered, but the city under its 2013 climate resilience plan committed “to prepare and protect those most vulnerable to increasing extreme heat.” Part of that commitment involves planting and maintaining trees as well as working with the private and nonprofit sectors to educate Angelenos about the public health and economic benefits of urban trees.

While smaller than its peers, New Orleans is one antabuse and naltrexone of the world’s most climate-threatened cities from coastal storms, flooding and heat. It, too, has made citywide commitments to improve and expand urban greenspace. Mayor LaToya Cantrell said the declaration "is a further example of how we are playing to our strengths, using our natural climate to our advantage instead of trying to fight it.” Mark Watts, C40’s executive director, said, “Supporting and protecting cities’ natural ecosystems is one of our most important tools for building resiliency against the climate crisis and creating the healthy, inclusive urban communities we deserve.” Besides Los Angeles, other cities of 5 million or more signing the declaration were London. Tokyo.

Mumbai, India. Rio de Janeiro. And Sydney. It also drew support from Toronto.

Stockholm. And Tel Aviv, Israel. Reprinted from E&E News with permission from POLITICO, LLC. Copyright 2021.

E&E News provides essential news for energy and environment professionals.I’ve been hard on American medicine. Americans are overtested, overdiagnosed and overtreated, I’ve argued, because physicians and hospitals in our capitalist culture care more about profits than patients. In 2019, I touted Medical Nihilism by philosopher Jacob Stegenga. Most medical interventions work poorly, if at all, Stegenga contends, and many do more harm than good.

We should therefore resort to tests and treatments far more sparingly. Stegenga’s diagnosis and prescription seemed sensible to me. But two episodes, one big and one small, have forced me to reconsider my medicine-bashing. First, the pharmaceutical industry, which I have accused of greed and dishonesty, created safe, effective treatments for alcoholism treatment with unprecedented speed.

I felt overwhelming gratitude when I got my second Moderna shot in March. Then, on Memorial Day, I got emergency surgery on my stupid right elbow. Here’s the story of that latter episode. Every winter for the past 25 years, I’ve played hockey on frozen ponds in and around Cold Spring, New York.

(That’s why I called my old blog “Cross-Check.”) Checking isn’t allowed, but sometimes we run into each other by mistake. Also, cracks and air pockets in the wild ice trip us up. I wear a helmet, padded gloves and shin-and-knee pads, but I don’t wear elbow pads, despite repeated admonitions from teammates. I hardly ever fall down, I assure my buddies, and elbow pads chafe me.

Last January, I fell and banged my right elbow so hard that it bled through my jersey. In late February, playing on treacherous ice, still without elbow pads, I fell and banged the same elbow. A week or two later the elbow swelled up and reddened. In mid-March, my primary doctor in Hoboken, N.J., where I live and work, said I probably had bursitis, inflammation of the bursa, a fluid-filled sack that lubricates joints.

My doctor referred me to an orthopedic surgeon in Hoboken, whom I’ll call Orthopedist No. 1. I saw him on March 24. After taking x-rays, which revealed no fracture, he confirmed that I had bursitis.

He drained my elbow, gave me a cortisone shot and advised me to ice the elbow after exercise and to compress it with an elastic bandage. My elbow felt and looked better for a couple of weeks, then it swelled again. To my alarm, my right armpit also puffed up. On April 21, I returned to Orthopedist No.

1, and he assured me that my elbow bursitis was unconnected to the swelling in my right armpit, where I have a lymph gland. If the armpit puffiness persisted, he said, I should have my primary physician check it out. As for my inflamed elbow, the bursitis would probably go away on its own with further icing and compression, although it might take a while. My girlfriend, a Manhattan snob, bugged me to get a second opinion from a doctor in New York.

On May 10, I saw Orthopedist No. 2, whom her doctor had recommended. Unlike Orthopedist No. 1, Orthopedist No.

2 thought the swelling of my armpit was caused by an in my elbow. She recommended a bursectomy, surgical removal of the elbow bursa. Surgery!. !.

?. ?. This was just a little bump!. No bigger than a golf ball!.

I’d never had surgery before, and I didn’t want to start now. Friends who’ve had surgery for sports injuries have never been the same afterward, or so it seemed. I also distrusted Orthopedist No. 2.

Surgeons always want to cut us, right?. Moreover, she did not accept insurance. I’d have to pay her in full up front for her services. The morning after I saw No.

2, I took off the bandage she had wrapped around my arm, and a cloudy fluid oozed out of a hole on the tip of my elbow, where No. 2 had poked it. This discharge, a mixture of pus, bursa fluid and blood, was alarming, and disgusting. But I used my left hand to squeeze more fluid from my right elbow, as if it were a giant pimple, and the swelling and soreness subsided.

My elbow felt better. Nevertheless, at my girlfriend’s insistence, over the next week I saw three more Manhattan specialists. Orthopedist No. 3 (recommended by a friend of my girlfriend).

Wound Specialist (to whom No. 3 referred me). And Orthopedist No. 4 (to whom Wound Specialist referred me).

None liked the look of my elbow, which now had a hole in it. All recommended surgery. But they said I could treat the bursitis with antibiotics and get surgery later if my elbow got worse. Orthopedist No.

3 put me on sulfamethoxazole/trimethoprim and cephalexin, which seemed to work, or so I convinced myself. On May 29, after two days of feeling feverish, nauseous and achy, and at the urging of my primary physician, I checked into the emergency room of the Hoboken University Medical Center. Blood tests revealed a low white-blood cell count and elevated liver enzymes. These results, plus my fever and chills, were consistent with sepsis, according to the emergency-room doctor.

She immediately put me on intravenous antibiotics and checked me into a room. I ended up spending four days in the hospital getting intravenous antibiotics and countless tests. I saw six different doctors in all. My temperature never rose above 101, and tests never revealed bacteria in my blood.

But Orthopedic Surgeon No. 5, who took charge of my case, said I definitely had sepsis and needed surgery. On Memorial Day, while I was under general anesthesia, he operated on my elbow. He removed the bursa and surrounding tissue and shaved a bone spur off the tip of my elbow.

I left the hospital on June 1 with a five-inch incision that wrapped around my elbow and was held together by about 40 metal staples. The doctors debated whether I should stay on intravenous antibiotics after my discharge. That would require me having a port stuck in my arm. Eventually, to my relief, I was put on a powerful oral antibiotic, linezolid, for 12 days.

That medication cost me $840, because the prescribing doctor didn’t alert my insurance company in advance, but I’m hoping I can get reimbursed. On June 12, Orthopedist No. 5 removed the staples from my arm, and soon I was proudly showing friends and family my surgical scar. So, what did I learn from this episode?.

It reminded me that medicine is hard. My problem was simple, “boring,” as Orthopedists Nos. 4 and 5 put it, compared to the complex bone fractures and tendon tears that they often handle. And yet my elbow still presented uncertainties that led different experts to reach different conclusions.

In retrospect, perhaps, Orthopedist No. 1 should have realized that my elbow, given the swelling in my right armpit, had become infected, or so No. 2 said. Orthopedist No.

2 should not have poked my elbow so hard that the skin broke, or so No. 3 said. Orthopedists Nos. 1–4 should have ordered blood tests to check for and Nos.

2–4 should have pressed me harder to get surgery, according to Orthopedist No. 5, who operated on me. But No. 5 also blamed me for dithering for so long.

I have asserted that Americans are overtested, overdiagnosed and overtreated. If anything, I was undertested, underdiagnosed, undertreated, but that was largely my fault. I told all the physicians I saw in Manhattan that I wanted to avoid surgery, and so they didn’t push for it. They said staying on antibiotics was an option, at least temporarily.

Another point. I have accused physicians of being profit-driven. If Orthopedist No. 1 had been greedy, he would have pushed for surgery, but he didn’t.

Wound Specialist, who spent a half hour meticulously cleaning my wound and packing it with antiseptic gauze, never even billed me or my insurance company. None of the physicians I saw before my hospitalization was incompetent. Nor was anyone at Hoboken University Medical Center, where I ended up getting surgery. The hospital, which has recently undergone changes in ownership, has pretty bad online reviews.

They remind me of a recent article in the New Yorker, “The Death of Hahnemann Hospital,” about how health care corporations are so intent on squeezing more profit out of hospitals that they are hurting patients. But the care I got at the hospital was superb. Was it because I am a fully insured white man?. Or because—hoping, I admit, for special treatment—I told some of my caregivers that I am a professor at a local university and a journalist?.

Maybe. These factors surely didn’t hurt. At any rate, the physicians and nurses at the hospital were all competent and kind. My ordeal has forced me to acknowledge the downside of my distrust of experts.

At one point, after the gauze that Wound Specialist had pushed into my elbow wound came out in the shower, I actually considered repacking the wound myself. I was inspired by a book I had just read, The Innovation Delusion, which celebrates people who repair their own cars and computers instead of relying on experts. I came to my senses after watching a horrifying YouTube video of a guy packing a wound in his belly caused by a spider bite. So, when should we doubt experts?.

When should we trust them?. There is no surefire formula, no algorithm, that can resolve this question for us. We must agonize over cases one by one, never forgetting our own fallibility. I stand by my critiques of psychiatry, cancer medicine and health care in general.

The U.S. Spends far more on health care per capita than any other country while ranking below many countries in longevity and other health measures. American health care needs fixing. But I have more respect for medical experts now than I did before the antabuse and my elbow problems.

The next time three specialists in a row tell me I need surgery, I’ll get surgery. I also have more respect for the wisdom of my hockey buddies. When I hit the ice next winter, I’ll be wearing elbow pads. This is an opinion and analysis article.

The views expressed by the author or authors are not necessarily those of Scientific American. Further Reading. Is Medicine Overrated?. The Cancer Industry.

Hype vs. Reality Can Psychiatry Heal Itself?. Has the Drug-Based Approach to Mental Illness Failed?. Dear "Skeptics," Bash Homeopathy and Bigfoot Less, Mammograms and War More I describe the joys of pond hockey in my books Mind-Body Problems and Pay Attention.LAUNCH SITE ONE, West Texas—The richest person on Earth has now traveled beyond it.

Jeff Bezos, the billionaire founder of the spaceflight company Blue Origin, launched into suborbital space with three other people today (July 20) on the first crewed mission of the company’s New Shepard vehicle—a landmark moment for the man and the space tourism industry. €œBlue Control, Bezos. Best day ever!. € Bezos said while in flight.

The autonomous New Shepard, which consists of a rocket topped by a capsule, lifted off from Blue Origin’s Launch Site One near the West Texas town of Van Horn today at 9:11 a.m. EDT (1311 GMT. 8:11 a.m.local time). The capsule carried Bezos, 57, his brother Mark, 53, 82-year-old aviation pioneer Wally Funk and 18-year-old Dutch physics student Oliver Daemen 66.5 miles (107 kilometers) above Earth, then came down for a parachute-aided, dust-raising landing in the West Texas scrublands.

The rocket also returned safely, making a vertical, powered touchdown at its designated landing zone. Its descent was punctuated by a deafening sonic boom, along with raucous cheers from the Blue Origin workers here who watched the flight. All of this action, from liftoff to landings, took just over 10 minutes. But it was doubtless the experience of a lifetime for the four passengers.

€œI’m so excited. I can’t wait to see what it’s going to be like,” Bezos told NBC’s TODAY on Monday (July 19). €œPeople say they go into space and they come back changed. Astronauts always talk about that, whether it’s the thin limb of the Earth’s atmosphere and seeing how fragile the planet is, that it’s just one planet.

So I can’t wait to see what it’s gonna do to me.” Bezos became the second billionaire to reach space in less than two weeks. On July 11, Virgin Group founder Richard Branson flew on the first fully crewed flight of the VSS Unity space plane, which is operated by Virgin Galactic, Blue Origin’s chief rival in the suborbital space tourism business. Two decades of work Bezos founded Blue Origin in September 2000, six years after he established Amazon. The spaceflight company worked stealthily for a decade, generally staying out of the public eye.

That changed in 2010, when Blue Origin won a contract from NASA’s Commercial Crew Program, which aimed to encourage the development of private American astronaut taxis to fill the shoes of the space shuttle, which was about to retire. The company snagged another contract the next year but didn’t land the big deal. NASA announced in 2014 that it had selected the vehicles built by SpaceX and Boeing—capsules known as Crew Dragon and CST-100 Starliner, respectively. Blue Origin continued to work on its own vehicles, including New Shepard, which is designed to carry people and payloads on brief trips to suborbital space.

The 59-foot-tall (18 meters) craft is named after NASA astronaut Alan Shepard, whose suborbital jaunt on May 5, 1961, was the United States’ first crewed spaceflight. New Shepard first launched to suborbital space in April 2015. The capsule landed softly as planned on that flight, but the rocket crashed during its touchdown attempt. But the next New Shepard iteration aced a test flight that November, pulling off the first-ever vertical landing of a rocket during a space mission.

(SpaceX nailed a landing of its own a month later with the first stage of its Falcon 9 orbital rocket, a feat Elon Musk’s company has now pulled off more than 80 times.) In January 2016, the same New Shepard flew successfully again, notching another reusability milestone. Over the next five-plus years, that vehicle and two others flew 12 more uncrewed test missions, the latest an “astronaut rehearsal” this past April. All were successful, paving the way for today’s mission, which was the third flight of the fourth New Shepard vehicle, known as RSS Next Step. Making, and acknowledging, history Blue Origin announced the July 20 target on May 5.

Both of those dates were chosen advisedly. May 5 was the 60th anniversary of Shepard’s pioneering flight, and July 20 is the 52nd anniversary of the Apollo 11 moon landing. Bezos has often cited Apollo 11 as a big inspiration, saying that his dreams of spaceflight were born when he watched the historic lunar landing at the age of five. Blue Origin made some history of its own today, and not just for the company annals.

Funk and Daemen became the oldest and youngest people, respectively, ever to reach the final frontier. The off-Earth journey was a dose of long-overdue justice for Funk. She’s one of the “Mercury 13,” women who passed NASA’s physiological screening tests in the early days of the space age but were never seriously considered for flight. Back then, you had to be a man—and more specifically, a white military man—to be a NASA astronaut.

The agency didn’t fly a female astronaut to space until June 1983, when Sally Ride reached orbit on the space shuttle Challenger’s STS-7 mission. (Challenger’s STS-8 flight, which launched that August, carried Guion Bluford, the first African American to reach space.) Funk takes the oldest-spaceflyer mantle from John Glenn, who launched at the age of 77 in October 1998 on the STS-95 mission of the shuttle Discovery, decades after becoming the first American to reach orbit. Blue Origin announced on July 1 that today’s flight would include Funk. Daemen was a later addition to the manifest.

The company revealed his participation just last Thursday (July 16). In mid-June, Blue Origin auctioned off the fourth and final seat on RSS Next Step, for the astronomical sum of $28 million. But the still-anonymous person who placed that bid had scheduling conflicts, company representatives said, so Daemen took their place. Daemen’s father, Somerset Capital Partners CEO Joes Daemen, paid for the seat and decided to let his son fly, CNBC reported.

So, in addition to all the other milestones, RSS Next Step flew its first paying customer today. Suborbital space tourism lifts off Virgin Galactic made its big announcement about Branson’s flight on July 1, the same day that Blue Origin did its Funk reveal. The dramatic news drops sparked many stories about a “billionaire space race,” which both Branson and Bezos have attempted to tamp down. ”There’s one person who was the first person in space—his name was Yuri Gagarin—and that happened a long time ago,” Bezos said on TODAY, referring to the cosmonaut’s landmark orbital mission on April 12, 1961.

(And Branson wasn’t the first billionaire to reach the final frontier. For example, megarich software architect Charles Simonyi bought two trips to the International Space Station, flying there in 2007 and 2009 aboard Russian Soyuz spacecraft.) “I think I’m gonna be number 570 or something. That’s where we’re gonna be in this list,” Bezos added. €œSo this isn’t a competition.

This is about building a road to space so that future generations can do incredible things in space.” Blue Origin aims to help make those incredible things happen over the long haul. The company is building an orbital launch system called New Glenn and a lunar lander named Blue Moon. Blue Origin also leads “The National Team,” a private consortium that proposed a crewed landing system for use by NASA’s Artemis program of lunar exploration. NASA picked SpaceX’s Starship vehicle for that job, but The National Team and another unsuccessful submitter, Alabama-based company Dynetics, have filed protests about the decision with the U.S.

Government Accountability Office. Whether or not there’s personal competition between Branson and Bezos, the companies led by the two billionaires are vying for the same relatively small pool of rich, adventurous customers. Virgin Galactic’s most recently stated ticket price was $250,000. Blue Origin has not announced how much it’s charging for a regular (non-auctioned) seat, but it’s thought to be in the low six figures as well.

Both companies offer passengers three to four minutes of weightlessness and great views of Earth against the blackness of space. But there are significant differences between the two flight experiences. For example, New Shepard is an autonomous capsule that launches vertically and lands under parachutes, whereas VSS Unity is a two-pilot space plane that takes off under the wing of a carrier aircraft and lands on a runway. New Shepard also gets a few miles higher than VSS Unity, a fact that Blue Origin highlighted in a couple of Twitter posts on July 9.

Those tweets told folks that spaceflights with Virgin Galactic come with an asterisk because Unity doesn’t reach the Kármán line, the 62-mile-high (100 km) mark considered by some to be the point where space begins. (Unity does fly higher than 50 miles, or 80 km, the boundary recognized by NASA, the U.S. Military and the Federal Aviation Administration.) This competition will heat up soon, if all goes according to plan. Blue Origin plans to launch two more crewed New Shepard missions this year, with the next one targeted for September or October, company representatives said during a prelaunch press conference on Sunday (July 18).

Those flights will presumably have paying customers on board, just as today’s did. Virgin Galactic aims to fly a few more test flights this fall, then begin full commercial operations early next year from Spaceport America in New Mexico. Both companies plan to ramp up their flight rate over time, allowing them to reduce prices and broaden the customer pool substantially—perhaps enough for the rest of us to swim in it someday. Copyright 2021 Space.com, a Future company.

All rights reserved. This material may not be published, broadcast, rewritten or redistributed.The Borg have landed—or, at least, researchers have discovered their counterparts here on Earth. Scientists analysing samples from muddy sites in the western United States have found novel DNA structures that seem to scavenge and ‘assimilate’ genes from microorganisms in their environment, much like the fictional Star Trek ‘Borg’ aliens who assimilate the knowledge and technology of other species. These extra-long DNA strands, which the scientists named in honour of the aliens, join a diverse collection of genetic structures—circular plasmids, for example—known as extrachromosomal elements (ECEs).

Most microbes have one or two chromosomes that encode their primary genetic blueprint. But they can host, and often share between them, many distinct ECEs. These carry non-essential but useful genes, such as those for antibiotic resistance. Borgs are a previously unknown, unique and “absolutely fascinating” type of ECE, says Jill Banfield, a geomicrobiologist at the University of California, Berkeley.

She and her colleagues describe their discovery of the structures in a preprint posted to the server bioRxiv. The work is yet to be peer-reviewed. Unlike anything seen before Borgs are DNA structures “not like any that’s been seen before”, says Brett Baker, a microbiologist at the University of Texas at Austin. Other scientists agree that the find is exciting, but have questioned whether Borgs really are unique, noting similarities between them and other large ECEs.

In recent years “people have become used to surprises in the field of ECEs”, says Huang Li, a microbiologist at the Chinese Academy of Sciences in Beijing. €œHowever, the discovery of Borgs, which undoubtedly enriches the concept of ECEs, has fascinated many in the field.” Their vast size, ranging between more than 600,000 and about 1 million DNA base pairs in length, is one feature that distinguishes Borgs from many other ECEs. In fact, Borgs are so huge that they are up to one-third of the length of the main chromosome in their host microbes, Banfield says. Banfield studies how microbes influence the carbon cycle—including the production and degradation of methane, a potent greenhouse gas—and, in October 2019, she and her colleagues went hunting for ECEs containing genes involved in the carbon cycle in Californian wetlands.

There, they found the first Borgs and later identified 19 different types from this and similar sites in Colorado and California. Borgs seem to be associated with archaea, which are single-celled microorganisms distinct from bacteria. Specifically, those Banfield and her team have discovered are linked to the Methanoperedens variety, which digest and destroy methane. And Borg genes seem to be involved in this process, says Banfield.

Scientists can’t yet culture Methanoperedens in the laboratory—an ongoing challenge for many microbes—so the team’s conclusions that Borgs might be used by the archaea for methane processing are based on sequence data alone. €œThey’ve made an interesting observation,” says systems biologist Nitin Baliga, at the Institute for Systems Biology in Seattle, Washington. But he cautions that when researchers sift through fragments of many genomes and piece them together, as Banfield’s team has done, it’s possible to make errors. Finding Borgs in cultured Methanoperedens will be necessary for the finding to be considered definitive, he adds.

Costs and benefits Assuming Borgs are real, maintaining such a massive ECE would be costly for Methanoperedens, Banfield and colleagues say, so the DNA structures must provide some benefit. To learn what that might be, the researchers analysed the sequences of hundreds of Borg genes and compared them with known genes. Borgs seem to house many genes needed for entire metabolic processes, including digesting methane, says Banfield. She describes these collections as “a toolbox” that might super-charge the abilities of Methanoperedens.

So what makes a Borg a Borg?. In addition to their remarkable size, Borgs share several structural features. They’re linear, not circular as many ECEs are.

Mumbai, India where to get antabuse https://bugeysud-tourisme.fr/where-to-buy-ventolin-pills. Rio de Janeiro. And Sydney.

It also drew support from Toronto where to get antabuse. Paris. Rome.

And Tel Aviv, Israel. Reprinted from E&E News with permission from POLITICO, LLC. Copyright 2021.

E&E News provides essential news for energy and environment professionals.I’ve been hard on American medicine. Americans are overtested, overdiagnosed and overtreated, I’ve argued, because physicians and hospitals in our capitalist culture care more about profits than patients. In 2019, I touted Medical Nihilism by philosopher Jacob Stegenga.

Most medical interventions work poorly, if at all, Stegenga contends, and many do more harm than good. We should therefore resort to tests and treatments far more sparingly. Stegenga’s diagnosis and prescription seemed sensible to me.

But two episodes, one big and one small, have forced me to reconsider my medicine-bashing. First, the pharmaceutical industry, which I have accused of greed and dishonesty, created safe, effective treatments for alcoholism treatment with unprecedented speed. I felt overwhelming gratitude when I got my second Moderna shot in March.

Then, on Memorial Day, I got emergency surgery on my stupid right elbow. Here’s the story of that latter episode. Every winter for the past 25 years, I’ve played hockey on frozen ponds in and around Cold Spring, New York.

(That’s why I called my old blog “Cross-Check.”) Checking isn’t allowed, but sometimes we run into each other by mistake. Also, cracks and air pockets in the wild ice trip us up. I wear a helmet, padded gloves and shin-and-knee pads, but I don’t wear elbow pads, despite repeated admonitions from teammates.

I hardly ever fall down, I assure my buddies, and elbow pads chafe me. Last January, I fell and banged my right elbow so hard that it bled through my jersey. In late February, playing on treacherous ice, still without elbow pads, I fell and banged the same elbow.

A week or two later the elbow swelled up and reddened. In mid-March, my primary doctor in Hoboken, N.J., where I live and work, said I probably had bursitis, inflammation of the bursa, a fluid-filled sack that lubricates joints. My doctor referred me to an orthopedic surgeon in Hoboken, whom I’ll call Orthopedist No.

1. I saw him on March 24. After taking x-rays, which revealed no fracture, he confirmed that I had bursitis.

He drained my elbow, gave me a cortisone shot and advised me to ice the elbow after exercise and to compress it with an elastic bandage. My elbow felt and looked better for a couple of weeks, then it swelled again. To my alarm, my right armpit also puffed up.

On April 21, I returned to Orthopedist No. 1, and he assured me that my elbow bursitis was unconnected to the swelling in my right armpit, where I have a lymph gland. If the armpit puffiness persisted, he said, I should have my primary physician check it out.

As for my inflamed elbow, the bursitis would probably go away on its own with further icing and compression, although it might take a while. My girlfriend, a Manhattan snob, bugged me to get a second opinion from a doctor in New York. On May 10, I saw Orthopedist No.

2, whom her doctor had recommended. Unlike Orthopedist No. 1, Orthopedist No.

2 thought the swelling of my armpit was caused by an in my elbow. She recommended a bursectomy, surgical removal of the elbow bursa. Surgery!.

This was just a little bump!. No bigger than a golf ball!. I’d never had surgery before, and I didn’t want to start now.

Friends who’ve had surgery for sports injuries have never been the same afterward, or so it seemed. I also distrusted Orthopedist No. 2.

Surgeons always want to cut us, right?. Moreover, she did not accept insurance. I’d have to pay her in full up front for her services.

The morning after I saw No. 2, I took off the bandage she had wrapped around my arm, and a cloudy fluid oozed out of a hole on the tip of my elbow, where No. 2 had poked it.

This discharge, a mixture of pus, bursa fluid and blood, was alarming, and disgusting. But I used my left hand to squeeze more fluid from my right elbow, as if it were a giant pimple, and the swelling and soreness subsided. My elbow felt better.

Nevertheless, at my girlfriend’s insistence, over the next week I saw three more Manhattan specialists. Orthopedist No. 3 (recommended by a friend of my girlfriend).

Wound Specialist (to whom No. 3 referred me). And Orthopedist No.

4 (to whom Wound Specialist referred me). None liked the look of my elbow, which now had a hole in it. All recommended surgery.

But they said I could treat the bursitis with antibiotics and get surgery later if my elbow got worse. Orthopedist No. 3 put me on sulfamethoxazole/trimethoprim and cephalexin, which seemed to work, or so I convinced myself.

On May 29, after two days of feeling feverish, nauseous and achy, and at the urging of my primary physician, I checked into the emergency room of the Hoboken University Medical Center. Blood tests revealed a low white-blood cell count and elevated liver enzymes. These results, plus my fever and chills, were consistent with sepsis, according to the emergency-room doctor.

She immediately put me on intravenous antibiotics and checked me into a room. I ended up spending four days in the hospital getting intravenous antibiotics and countless tests. I saw six different doctors in all.

My temperature never rose above 101, and tests never revealed bacteria in my blood. But Orthopedic Surgeon No. 5, who took charge of my case, said I definitely had sepsis and needed surgery.

On Memorial Day, while I was under general anesthesia, he operated on my elbow. He removed the bursa and surrounding tissue and shaved a bone spur off the tip of my elbow. I left the hospital on June 1 with a five-inch incision that wrapped around my elbow and was held together by about 40 metal staples.

The doctors debated whether I should stay on intravenous antibiotics after my discharge. That would require me having a port stuck in my arm. Eventually, to my relief, I was put on a powerful oral antibiotic, linezolid, for 12 days.

That medication cost me $840, because the prescribing doctor didn’t alert my insurance company in advance, but I’m hoping I can get reimbursed. On June 12, Orthopedist No. 5 removed the staples from my arm, and soon I was proudly showing friends and family my surgical scar.

So, what did I learn from this episode?. It reminded me that medicine is hard. My problem was simple, “boring,” as Orthopedists Nos.

4 and 5 put it, compared to the complex bone fractures and tendon tears that they often handle. And yet my elbow still presented uncertainties that led different experts to reach different conclusions. In retrospect, perhaps, Orthopedist No.

1 should have realized that my elbow, given the swelling in my right armpit, had become infected, or so No. 2 said. Orthopedist No.

2 should not have poked my elbow so hard that the skin broke, or so No. 3 said. Orthopedists Nos.

1–4 should have ordered blood tests to check for and Nos. 2–4 should have pressed me harder to get surgery, according to Orthopedist No. 5, who operated on me.

But No. 5 also blamed me for dithering for so long. I have asserted that Americans are overtested, overdiagnosed and overtreated.

If anything, I was undertested, underdiagnosed, undertreated, but that was largely my fault. I told all the physicians I saw in Manhattan that I wanted to avoid surgery, and so they didn’t push for it. They said staying on antibiotics was an option, at least temporarily.

Another point. I have accused physicians of being profit-driven. If Orthopedist No.

1 had been greedy, he would have pushed for surgery, but he didn’t. Wound Specialist, who spent a half hour meticulously cleaning my wound and packing it with antiseptic gauze, never even billed me or my insurance company. None of the physicians I saw before my hospitalization was incompetent.

Nor was anyone at Hoboken University Medical Center, where I ended up getting surgery. The hospital, which has recently undergone changes in ownership, has pretty bad online reviews. They remind me of a recent article in the New Yorker, “The Death of Hahnemann Hospital,” about how health care corporations are so intent on squeezing more profit out of hospitals that they are hurting patients.

But the care I got at the hospital was superb. Was it because I am a fully insured white man?. Or because—hoping, I admit, for special treatment—I told some of my caregivers that I am a professor at a local university and a journalist?.

Maybe. These factors surely didn’t hurt. At any rate, the physicians and nurses at the hospital were all competent and kind.

My ordeal has forced me to acknowledge the downside of my distrust of experts. At one point, after the gauze that Wound Specialist had pushed into my elbow wound came out in the shower, I actually considered repacking the wound myself. I was inspired by a book I had just read, The Innovation Delusion, which celebrates people who repair their own cars and computers instead of relying on experts.

I came to my senses after watching a horrifying YouTube video of a guy packing a wound in his belly caused by a spider bite. So, when should we doubt experts?. When should we trust them?.

There is no surefire formula, no algorithm, that can resolve this question for us. We must agonize over cases one by one, never forgetting our own fallibility. I stand by my critiques of psychiatry, cancer medicine and health care in general.

The U.S. Spends far more on health care per capita than any other country while ranking below many countries in longevity and other health measures. American health care needs fixing.

But I have more respect for medical experts now than I did before the antabuse and my elbow problems. The next time three specialists in a row tell me I need surgery, I’ll get surgery. I also have more respect for the wisdom of my hockey buddies.

When I hit the ice next winter, I’ll be wearing elbow pads. This is an opinion and analysis article. The views expressed by the author or authors are not necessarily those of Scientific American.

Further Reading. Is Medicine Overrated?. The Cancer Industry.

Hype vs. Reality Can Psychiatry Heal Itself?. Has the Drug-Based Approach to Mental Illness Failed?.

Dear "Skeptics," Bash Homeopathy and Bigfoot Less, Mammograms and War More I describe the joys of pond hockey in my books Mind-Body Problems and Pay Attention.LAUNCH SITE ONE, West Texas—The richest person on Earth has now traveled beyond it. Jeff Bezos, the billionaire founder of the spaceflight company Blue Origin, launched into suborbital space with three other people today (July 20) on the first crewed mission of the company’s New Shepard vehicle—a landmark moment for the man and the space tourism industry. €œBlue Control, Bezos.

Best day ever!. € Bezos said while in flight. The autonomous New Shepard, which consists of a rocket topped by a capsule, lifted off from Blue Origin’s Launch Site One near the West Texas town of Van Horn today at 9:11 a.m.

EDT (1311 GMT. 8:11 a.m.local time). The capsule carried Bezos, 57, his brother Mark, 53, 82-year-old aviation pioneer Wally Funk and 18-year-old Dutch physics student Oliver Daemen 66.5 miles (107 kilometers) above Earth, then came down for a parachute-aided, dust-raising landing in the West Texas scrublands.

The rocket also returned safely, making a vertical, powered touchdown at its designated landing zone. Its descent was punctuated by a deafening sonic boom, along with raucous cheers from the Blue Origin workers here who watched the flight. All of this action, from liftoff to landings, took just over 10 minutes.

But it was doubtless the experience of a lifetime for the four passengers. €œI’m so excited. I can’t wait to see what it’s going to be like,” Bezos told NBC’s TODAY on Monday (July 19).

€œPeople say they go into space and they come back changed. Astronauts always talk about that, whether it’s the thin limb of the Earth’s atmosphere and seeing how fragile the planet is, that it’s just one planet. So I can’t wait to see what it’s gonna do to me.” Bezos became the second billionaire to reach space in less than two weeks.

On July 11, Virgin Group founder Richard Branson flew on the first fully crewed flight of the VSS Unity space plane, which is operated by Virgin Galactic, Blue Origin’s chief rival in the suborbital space tourism business. Two decades of work Bezos founded Blue Origin in September 2000, six years after he established Amazon. The spaceflight company worked stealthily for a decade, generally staying out of the public eye.

That changed in 2010, when Blue Origin won a contract from NASA’s Commercial Crew Program, which aimed to encourage the development of private American astronaut taxis to fill the shoes of the space shuttle, which was about to retire. The company snagged another contract the next year but didn’t land the big deal. NASA announced in 2014 that it had selected the vehicles built by SpaceX and Boeing—capsules known as Crew Dragon and CST-100 Starliner, respectively.

Blue Origin continued to work on its own vehicles, including New Shepard, which is designed to carry people and payloads on brief trips to suborbital space. The 59-foot-tall (18 meters) craft is named after NASA astronaut Alan Shepard, whose suborbital jaunt on May 5, 1961, was the United States’ first crewed spaceflight. New Shepard first launched to suborbital space in April 2015.

The capsule landed softly as planned on that flight, but the rocket crashed during its touchdown attempt. But the next New Shepard iteration aced a test flight that November, pulling off the first-ever vertical landing of a rocket during a space mission. (SpaceX nailed a landing of its own a month later with the first stage of its Falcon 9 orbital rocket, a feat Elon Musk’s company has now pulled off more than 80 times.) In January 2016, the same New Shepard flew successfully again, notching another reusability milestone.

Over the next five-plus years, that vehicle and two others flew 12 more uncrewed test missions, the latest an “astronaut rehearsal” this past April. All were successful, paving the way for today’s mission, which was the third flight of the fourth New Shepard vehicle, known as RSS Next Step. Making, and acknowledging, history Blue Origin announced the July 20 target on May 5.

Both of those dates were chosen advisedly. May 5 was the 60th anniversary of Shepard’s pioneering flight, and July 20 is the 52nd anniversary of the Apollo 11 moon landing. Bezos has often cited Apollo 11 as a big inspiration, saying that his dreams of spaceflight were born when he watched the historic lunar landing at the age of five.

Blue Origin made some history of its own today, and not just for the company annals. Funk and Daemen became the oldest and youngest people, respectively, ever to reach the final frontier. The off-Earth journey was a dose of long-overdue justice for Funk.

She’s one of the “Mercury 13,” women who passed NASA’s physiological screening tests in the early days of the space age but were never seriously considered for flight. Back then, you had to be a man—and more specifically, a white military man—to be a NASA astronaut. The agency didn’t fly a female astronaut to space until June 1983, when Sally Ride reached orbit on the space shuttle Challenger’s STS-7 mission.

(Challenger’s STS-8 flight, which launched that August, carried Guion Bluford, the first African American to reach space.) Funk takes the oldest-spaceflyer mantle from John Glenn, who launched at the age of 77 in October 1998 on the STS-95 mission of the shuttle Discovery, decades after becoming the first American to reach orbit. Blue Origin announced on July 1 that today’s flight would include Funk. Daemen was a later addition to the manifest.

The company revealed his participation just last Thursday (July 16). In mid-June, Blue Origin auctioned off the fourth and final seat on RSS Next Step, for the astronomical sum of $28 million. But the still-anonymous person who placed that bid had scheduling conflicts, company representatives said, so Daemen took their place.

Daemen’s father, Somerset Capital Partners CEO Joes Daemen, paid for the seat and decided to let his son fly, CNBC reported. So, in addition to all the other milestones, RSS Next Step flew its first paying customer today. Suborbital space tourism lifts off Virgin Galactic made its big announcement about Branson’s flight on July 1, the same day that Blue Origin did its Funk reveal.

The dramatic news drops sparked many stories about a “billionaire space race,” which both Branson and Bezos have attempted to tamp down. ”There’s one person who was the first person in space—his name was Yuri Gagarin—and that happened a long time ago,” Bezos said on TODAY, referring to the cosmonaut’s landmark orbital mission on April 12, 1961. (And Branson wasn’t the first billionaire to reach the final frontier.

For example, megarich software architect Charles Simonyi bought two trips to the International Space Station, flying there in 2007 and 2009 aboard Russian Soyuz spacecraft.) “I think I’m gonna be number 570 or something. That’s where we’re gonna be in this list,” Bezos added. €œSo this isn’t a competition.

This is about building a road to space so that future generations can do incredible things in space.” Blue Origin aims to help make those incredible things happen over the long haul. The company is building an orbital launch system called New Glenn and a lunar lander named Blue Moon. Blue Origin also leads “The National Team,” a private consortium that proposed a crewed landing system for use by NASA’s Artemis program of lunar exploration.

NASA picked SpaceX’s Starship vehicle for that job, but The National Team and another unsuccessful submitter, Alabama-based company Dynetics, have filed protests about the decision with the U.S. Government Accountability Office. Whether or not there’s personal competition between Branson and Bezos, the companies led by the two billionaires are vying for the same relatively small pool of rich, adventurous customers.

Virgin Galactic’s most recently stated ticket price was $250,000. Blue Origin has not announced how much it’s charging for a regular (non-auctioned) seat, but it’s thought to be in the low six figures as well. Both companies offer passengers three to four minutes of weightlessness and great views of Earth against the blackness of space.

But there are significant differences between the two flight experiences. For example, New Shepard is an autonomous capsule that launches vertically and lands under parachutes, whereas VSS Unity is a two-pilot space plane that takes off under the wing of a carrier aircraft and lands on a runway. New Shepard also gets a few miles higher than VSS Unity, a fact that Blue Origin highlighted in a couple of Twitter posts on July 9.

Those tweets told folks that spaceflights with Virgin Galactic come with an asterisk because Unity doesn’t reach the Kármán line, the 62-mile-high (100 km) mark considered by some to be the point where space begins. (Unity does fly higher than 50 miles, or 80 km, the boundary recognized by NASA, the U.S. Military and the Federal Aviation Administration.) This competition will heat up soon, if all goes according to plan.

Blue Origin plans to launch two more crewed New Shepard missions this year, with the next one targeted for September or October, company representatives said during a prelaunch press conference on Sunday (July 18). Those flights will presumably have paying customers on board, just as today’s did. Virgin Galactic aims to fly a few more test flights this fall, then begin full commercial operations early next year from Spaceport America in New Mexico.

Both companies plan to ramp up their flight rate over time, allowing them to reduce prices and broaden the customer pool substantially—perhaps enough for the rest of us to swim in it someday. Copyright 2021 Space.com, a Future company. All rights reserved.

This material may not be published, broadcast, rewritten or redistributed.The Borg have landed—or, at least, researchers have discovered their counterparts here on Earth. Scientists analysing samples from muddy sites in the western United States have found novel DNA structures that seem to scavenge and ‘assimilate’ genes from microorganisms in their environment, much like the fictional Star Trek ‘Borg’ aliens who assimilate the knowledge and technology of other species. These extra-long DNA strands, which the scientists named in honour of the aliens, join a diverse collection of genetic structures—circular plasmids, for example—known as extrachromosomal elements (ECEs).

Most microbes have one or two chromosomes that encode their primary genetic blueprint. But they can host, and often share between them, many distinct ECEs. These carry non-essential but useful genes, such as those for antibiotic resistance.

Borgs are a previously unknown, unique and “absolutely fascinating” type of ECE, says Jill Banfield, a geomicrobiologist at the University of California, Berkeley. She and her colleagues describe their discovery of the structures in a preprint posted to the server bioRxiv. The work is yet to be peer-reviewed.

Unlike anything seen before Borgs are DNA structures “not like any that’s been seen before”, says Brett Baker, a microbiologist at the University of Texas at Austin. Other scientists agree that the find is exciting, but have questioned whether Borgs really are unique, noting similarities between them and other large ECEs. In recent years “people have become used to surprises in the field of ECEs”, says Huang Li, a microbiologist at the Chinese Academy of Sciences in Beijing.

€œHowever, the discovery of Borgs, which undoubtedly enriches the concept of ECEs, has fascinated many in the field.” Their vast size, ranging between more than 600,000 and about 1 million DNA base pairs in length, is one feature that distinguishes Borgs from many other ECEs. In fact, Borgs are so huge that they are up to one-third of the length of the main chromosome in their host microbes, Banfield says. Banfield studies how microbes influence the carbon cycle—including the production and degradation of methane, a potent greenhouse gas—and, in October 2019, she and her colleagues went hunting for ECEs containing genes involved in the carbon cycle in Californian wetlands.

There, they found the first Borgs and later identified 19 different types from this and similar sites in Colorado and California. Borgs seem to be associated with archaea, which are single-celled microorganisms distinct from bacteria. Specifically, those Banfield and her team have discovered are linked to the Methanoperedens variety, which digest and destroy methane.

And Borg genes seem to be involved in this process, says Banfield. Scientists can’t yet culture Methanoperedens in the laboratory—an ongoing challenge for many microbes—so the team’s conclusions that Borgs might be used by the archaea for methane processing are based on sequence data alone. €œThey’ve made an interesting observation,” says systems biologist Nitin Baliga, at the Institute for Systems Biology in Seattle, Washington.

But he cautions that when researchers sift through fragments of many genomes and piece them together, as Banfield’s team has done, it’s possible to make errors. Finding Borgs in cultured Methanoperedens will be necessary for the finding to be considered definitive, he adds. Costs and benefits Assuming Borgs are real, maintaining such a massive ECE would be costly for Methanoperedens, Banfield and colleagues say, so the DNA structures must provide some benefit.

To learn what that might be, the researchers analysed the sequences of hundreds of Borg genes and compared them with known genes. Borgs seem to house many genes needed for entire metabolic processes, including digesting methane, says Banfield. She describes these collections as “a toolbox” that might super-charge the abilities of Methanoperedens.

So what makes a Borg a Borg?. In addition to their remarkable size, Borgs share several structural features. They’re linear, not circular as many ECEs are.

They have mirrored repetitive sequences at each end of the strand. And they have many other repetitive sequences both within and between the presumptive genes. Individually, these features of Borgs can overlap with those seen in other large ECEs, such as elements in certain salt-loving archaea, so Baliga says the novelty of Borgs is still debatable at this stage.

Borgs also resemble giant linear plasmids found in soil-dwelling Actinobacteria, says Julián Rafael Dib, a microbiologist at the Pilot Plant for Microbiological Industrial Processes in Tucumán, Argentina. Banfield counters that although the individual features of Borgs have been seen before, “the size, combination and metabolic gene load” is what makes them different. She speculates that they were once entire microbes, and were assimilated by Methanoperedens in much the same way that eukaryotic cells gained energy-generating mitochondria by assimilating free-living bacteria.

Now that scientists know what to look for, they might find more Borgs by sifting through old data, says Baker, who used to work in Banfield's lab. He thinks he might already have discovered some candidates in his own genetic database since the preprint was posted. Resistance is futile When analysing the Borg genome, Banfield and colleagues also saw features suggesting that Borgs have assimilated genes from diverse sources, including the main Methanoperedens chromosome, Banfield says.

This potential to ‘assimilate’ genes led her son to propose the name ‘Borg’ over Thanksgiving dinner in 2020. Banfield’s team is now investigating the function of Borgs and the role of their DNA repeats. Repeats are important to microbes.

Differently-structured repeats called CRISPR are snippets of genetic code from antabusees that microbes incorporate into their own DNA to ‘remember’ the pathogens so they can defend against them in the future. CRISPR and its associated proteins have been a boon for biotechnology because they have been adapted into a powerful gene-editing technique—hinting that Borg genomes might also yield useful tools. €œIt could be as important and interesting as CRISPR, but I think it’s going to be a new thing,” says Banfield, who is collaborating on future investigations with her preprint co-author, Jennifer Doudna, a pioneer of CRISPR-based gene editing at the University of California.

One potential application that the researchers see for Borgs could be as an aid in the fight against climate change.

Antabuse reaction time

€˜the PAR of aware and buy antabuse treated hypertension for stroke was 22.2% vs 17.3%, aware but untreated was 4.8% vs 20.4% and unaware of hypertension was 5.6% vs 15.9%’ antabuse reaction time. Although PAR reflects the proportion of stoke attributable to hypertension, Sarfo points outs that complete elimination of hypertension is unlikely so the PAR probably overestimates the potential benefit of better treatment. Even so, he concludes.

€˜The time antabuse reaction time is rife for policymakers, providers and individuals to develop actionable policies and behavioural alterations in response to the reported associations between gaps in knowledge, awareness, and treatment of hypertension and stroke occurrence. The time for a concerted global effort to prevent the disability, dementia and deaths arising from stroke due to uncontrolled hypertension is now.’Also in this issue, Ramlakhan and colleagues3 present encouraging data on pregnancy outcomes in 202 women with aortic coarctation (CoA). Although 9.6% of these women had unrepaired aortic coarctation and 27.1% had pre-existing hypertension, there were no maternal deaths or aortic dissections.

Only 4.3% of women experienced a major adverse cardiovascular event, primarily heart failure antabuse reaction time. Premature birth occurred in 9.1% with four neonatal deaths, three of which were related to extreme premature birth (figure 2).Summarising figure of pregnancy outcomes in women with aortic coarctation. AF, atrial fibrillation.

CoA, aortic antabuse reaction time coarctation. HF, heart failure. MACE, major adverse cardiac event (defined as maternal cardiac death, HF, AF or atrial flutter, ventricular tachyarrhythmia, endocarditis, thromboembolic events, aortic dissection and acute coronary syndrome)." data-icon-position data-hide-link-title="0">Figure 2 Summarising figure of pregnancy outcomes in women with aortic coarctation.

AF, atrial antabuse reaction time fibrillation. CoA, aortic coarctation. HF, heart failure.

MACE, major adverse cardiac event (defined as maternal cardiac death, antabuse reaction time HF, AF or atrial flutter, ventricular tachyarrhythmia, endocarditis, thromboembolic events, aortic dissection and acute coronary syndrome).In the accompanying editorial, Cordina and Li4 review the pathophysiology of aortic coarctation and the potential risks associated with pregnancy including aortic dissection, hypertension, diastolic heart failure, intracranial haemorrhage and aortic valve dysfunction, as well as obstetrical complications. They conclude. €˜(in accordance with current guidelines) that a woman with coarctation but no major comorbidities and an aorta with minimal obstruction and diameter <40 mm, good functional class and left ventricular ejection >40% is at low risk for maternofetal complications but these new data are not sufficient for us to let our guard down in women with high risk features.’A review article in this issue provides recommendations on the role of echocardiography in screening and evaluation of athletes for prevention of sudden cardiac death (SCD) (figure 3).

Niederseer and colleagues5 propose that ‘first echocardiography is performed during adolescence to rule out structural heart conditions associated with SCD that antabuse reaction time cannot be detected by ECG, especially mitral valve prolapse, coronary artery anomalies, bicuspid aortic valve and dilatation of the aorta. A second echocardiography could be performed from the age of 30–35 years, when athletes age and become master athletes, to especially evaluate pathological cardiac remodelling to exercise (eg, atrial and/or right ventricular dilation), late onset cardiomyopathies and wall motion abnormalities due to myocarditis or coronary artery disease.’Differentiating athlete’s heart from HCM, DCM, AC and LVNC. AC, arrhythmogenic cardiomyopathy.

DCM, dilated antabuse reaction time cardiomyopathy. GLS, global longitudinal strain. HCM, hypertrophic cardiomyopathy.

LA, left antabuse reaction time atrium. LV, left ventricle. LVEDD, left ventricular end-diastolic diameter.

LVEF, left ventricular antabuse reaction time ejection fraction. LVH, left ventricular hypertrophy. LVNC, left ventricular non-compaction.

LVOT, left antabuse reaction time ventricular outflow tract. RA, right atrium. RV, right ventricle.

RVIT, right antabuse reaction time ventricular inflow tract. RVOT, right ventricular outflow tract. RVWMA, right ventricular wall motion abnormalities." data-icon-position data-hide-link-title="0">Figure 3 Differentiating athlete’s heart from HCM, DCM, AC and LVNC.

AC, arrhythmogenic cardiomyopathy antabuse reaction time. DCM, dilated cardiomyopathy. GLS, global longitudinal strain.

HCM, hypertrophic cardiomyopathy antabuse reaction time. LA, left atrium. LV, left ventricle.

LVEDD, left ventricular end-diastolic antabuse reaction time diameter. LVEF, left ventricular ejection fraction. LVH, left ventricular antabuse uk buy hypertrophy.

LVNC, left ventricular non-compaction antabuse reaction time. LVOT, left ventricular outflow tract. RA, right atrium.

RV, right antabuse reaction time ventricle. RVIT, right ventricular inflow tract. RVOT, right ventricular outflow tract.

RVWMA, right ventricular wall motion abnormalities.A counterpoint is provided by Dineen and antabuse reaction time Prutkin6 who argue that. €˜the echocardiogram has a significant role in the secondary evaluation of abnormal history, physical and ECG findings but we do not think it should be used widely for initial screening. We agree that it can pick up structural heart conditions that will need long-term follow-up.

However, the purpose of athletic antabuse reaction time screening should be to pick up life-threatening conditions which could lead to SCD when triggered by exercise or else we would recommend screening all adolescents and adults. Until we have more concrete evidence, we believe the screening echocardiogram does not appear to improve SCD risk stratification in athletes more than the current standard of practice.’Another provocative review article by Grayburn and colleagues7 provides perspective on the optimal definition for severity of secondary mitral regurgitation (SMR). The ratio of effective regurgitant orifice area (EROA) to left ventricular (LV) end-diastolic volume (EDV) can be useful and may explain the difference outcomes in clinical trials of mitral transcatheter edge-to-edge repair (TEER) but the EROA/LVEDV ratio still fails to consider other important factors (figure 4).

They recommend antabuse reaction time. €˜the key to patient selection is forced titration of neurohormonal antagonists to the target doses that have been proven in clinical trials (along with cardiac resynchronisation when appropriate). Patients who continue to have symptomatic severe SMR after doing so should be considered for TEER.’ This recommendation is in accord with the recently published 2020 American College of Cardiology/American Heart Association Guidelines for the Management of Valvular Heart disease.8Plot showing the relationship of RF (x-axis) versus LVEDV (y-axis) for different values of EROA and an LVEF (30%).

At this low LVEF, RF would be 100% (physiologically impossible) at LVEDV of approximately 275 mL at a true (mean over systole per the Gorlin hydraulic orifice area) EROA antabuse reaction time 0.5 cm2, 220 mL at an EROA 0.4 cm2, 160 mL at an EROA 0.3 cm2 and 115 mL at an EROA 0.2 cm2. Peak EROA values reported by single frame echocardiographic techniques are often physiologically impossible. It is important to recognise the difference between peak EROA and true EROA.

Regurgitant volume obtained by multiplying peak EROA by the velocity–time integral of MR will often result antabuse reaction time in physiologically impossible values. EROA, effective regurgitant orifice area. LVEDV, left ventricular end-diastolic volume.

LVEF, left ventricular antabuse reaction time ejection fraction. RF, regurgitant fraction." data-icon-position data-hide-link-title="0">Figure 4 Plot showing the relationship of RF (x-axis) versus LVEDV (y-axis) for different values of EROA and an LVEF (30%). At this low LVEF, RF would be 100% (physiologically impossible) at LVEDV of approximately 275 mL at a true (mean over systole per the Gorlin hydraulic orifice area) EROA 0.5 cm2, 220 mL at an EROA 0.4 cm2, 160 mL at an EROA 0.3 cm2 and 115 mL at an EROA 0.2 cm2.

Peak EROA values reported by single antabuse reaction time frame echocardiographic techniques are often physiologically impossible. It is important to recognise the difference between peak EROA and true EROA. Regurgitant volume obtained by multiplying peak EROA by the velocity–time integral of MR will often result in physiologically impossible values.

EROA, effective regurgitant orifice area antabuse reaction time. LVEDV, left ventricular end-diastolic volume. LVEF, left ventricular ejection fraction.

RF, regurgitant fraction.In contrast, Kamoen and colleagues9 argue that the concept of proportionality between antabuse reaction time SMR severity and LV end-diastolic volumes remains hypothetical and requires validation in clinical trials. In addition, both articles emphasise the technical challenges and measurement variability which affect these echocardiographic parameters. Perhaps we need to consider alternative, possibly more accurate and robust, measures of SMR severity.10The Education in Heart article in this issue11 reviews several cardiovascular risk prediction tools and provides guidance on which score is best suited to each patient (figure 5).

Examples are provided for the effects of risk reduction therapy for individuals with different 10-year risk scores, showing that antabuse reaction time absolute risk scores need to be interpreted in terms of lifetime benefit.Patient example. 10-year risk and treatment effects compared with the CVD-free life expectancy and lifetime benefit for a younger versus an older individual. Ten-year predictions were estimated using the Systemic Coronary Risk Estimation model risk model.

Lifetime predictions using antabuse reaction time the LIFEtime-perspective CardioVascular Disease model. CVD, cardiovascular disease. LDL, low density lipoprotein.

NNT, number needed antabuse reaction time to treat. MI, myocardial infarction. SBP, systolic blood pressure" data-icon-position data-hide-link-title="0">Figure 5 Patient example.

10-year risk and treatment effects compared with the CVD-free life expectancy and lifetime benefit for a younger versus an older individual.

While a gradient remains for risk of stroke by you can try this out age among treatment groups, there is an inversion where to get antabuse of gradient by GNI. These figures illustrate that increased uptake of antihypertensive therapy are expected to have greatest impact in younger populations and in lower-income regions. Multivariable model including age, smoking, waist-to-hip ratio, diabetes, physical activity, alternate healthy eating index, alcohol intake, psychosocial factors, apolipoproteins and cardiac risk factors. GNI, gross national income where to get antabuse. PAR, population attributable risk.In an editorial, Sarfo2 summarises the concept of population attributable risk (PAR) of hypertension for stroke in high income countries compared with low- and middle-income countries.

€˜the PAR of aware and treated hypertension for stroke was 22.2% vs 17.3%, aware but untreated was 4.8% vs 20.4% and unaware of hypertension was 5.6% vs 15.9%’. Although PAR where to get antabuse reflects the proportion of stoke attributable to hypertension, Sarfo points outs that complete elimination of hypertension is unlikely so the PAR probably overestimates the potential benefit of better treatment. Even so, he concludes. €˜The time is rife for policymakers, providers and individuals to develop actionable policies and behavioural alterations in response to the reported associations between gaps in knowledge, awareness, and treatment of hypertension and stroke occurrence. The time for a concerted global effort to prevent the disability, dementia and deaths arising from stroke due to uncontrolled hypertension is now.’Also in this issue, Ramlakhan and colleagues3 present encouraging data on pregnancy outcomes where to get antabuse in 202 women with aortic coarctation (CoA).

Although 9.6% of these women had unrepaired aortic coarctation and 27.1% had pre-existing hypertension, there were no maternal deaths or aortic dissections. Only 4.3% of women experienced a major adverse cardiovascular event, primarily heart failure. Premature birth occurred in 9.1% where to get antabuse with four neonatal deaths, three of which were related to extreme premature birth (figure 2).Summarising figure of pregnancy outcomes in women with aortic coarctation. AF, atrial fibrillation. CoA, aortic coarctation.

HF, heart where to get antabuse failure. MACE, major adverse cardiac event (defined as maternal cardiac death, HF, AF or atrial flutter, ventricular tachyarrhythmia, endocarditis, thromboembolic events, aortic dissection and acute coronary syndrome)." data-icon-position data-hide-link-title="0">Figure 2 Summarising figure of pregnancy outcomes in women with aortic coarctation. AF, atrial fibrillation. CoA, aortic where to get antabuse coarctation. HF, heart failure.

MACE, major adverse cardiac event (defined as maternal cardiac death, HF, AF or atrial flutter, ventricular tachyarrhythmia, endocarditis, thromboembolic events, aortic dissection and acute coronary syndrome).In the accompanying editorial, Cordina and Li4 review the pathophysiology of aortic coarctation and the potential risks associated with pregnancy including aortic dissection, hypertension, diastolic heart failure, intracranial haemorrhage and aortic valve dysfunction, as well as obstetrical complications. They conclude where to get antabuse. €˜(in accordance with current guidelines) that a woman with coarctation but no major comorbidities and an aorta with minimal obstruction and diameter <40 mm, good functional class and left ventricular ejection >40% is at low risk for maternofetal complications but these new data are not sufficient for us to let our guard down in women with high risk features.’A review article in this issue provides recommendations on the role of echocardiography in screening and evaluation of athletes for prevention of sudden cardiac death (SCD) (figure 3). Niederseer and colleagues5 propose that ‘first echocardiography is performed during adolescence to rule out structural heart conditions associated with SCD that cannot be detected by ECG, especially mitral valve prolapse, coronary artery anomalies, bicuspid aortic valve and dilatation of the aorta. A second echocardiography could be performed from the age of 30–35 years, when athletes age and become master athletes, to especially evaluate pathological cardiac remodelling to exercise (eg, atrial and/or right ventricular dilation), late where to get antabuse onset cardiomyopathies and wall motion abnormalities due to myocarditis or coronary artery disease.’Differentiating athlete’s heart from HCM, DCM, AC and LVNC.

AC, arrhythmogenic cardiomyopathy. DCM, dilated cardiomyopathy. GLS, global where to get antabuse longitudinal strain. HCM, hypertrophic cardiomyopathy. LA, left atrium.

LV, left where to get antabuse ventricle. LVEDD, left ventricular end-diastolic diameter. LVEF, left ventricular ejection fraction. LVH, left ventricular hypertrophy where to get antabuse. LVNC, left ventricular non-compaction.

LVOT, left ventricular outflow tract. RA, right where to get antabuse atrium. RV, right ventricle. RVIT, right ventricular inflow tract. RVOT, right ventricular outflow where to get antabuse tract.

RVWMA, right ventricular wall motion abnormalities." data-icon-position data-hide-link-title="0">Figure 3 Differentiating athlete’s heart from HCM, DCM, AC and LVNC. AC, arrhythmogenic cardiomyopathy. DCM, dilated where to get antabuse cardiomyopathy. GLS, global longitudinal strain. HCM, hypertrophic click over here now cardiomyopathy.

LA, left atrium where to get antabuse. LV, left ventricle. LVEDD, left ventricular end-diastolic diameter. LVEF, left where to get antabuse ventricular ejection fraction. LVH, left ventricular hypertrophy.

LVNC, left ventricular non-compaction. LVOT, left ventricular where to get antabuse outflow tract. RA, right atrium. RV, right ventricle. RVIT, right where to get antabuse ventricular inflow tract.

RVOT, right ventricular outflow tract. RVWMA, right ventricular wall motion abnormalities.A counterpoint is provided by Dineen and Prutkin6 who argue that. €˜the echocardiogram has a significant role in the secondary evaluation of abnormal history, physical and ECG findings but we do not think it where to get antabuse should be used widely for initial screening. We agree that it can pick up structural heart conditions that will need long-term follow-up. However, the purpose of athletic screening should be to pick up life-threatening conditions which could lead to SCD when triggered by exercise or else we would recommend screening all adolescents and adults.

Until we have more concrete evidence, we believe the screening echocardiogram does not appear to improve SCD risk stratification in athletes more than the current standard of where to get antabuse practice.’Another provocative review article by Grayburn and colleagues7 provides perspective on the optimal definition for severity of secondary mitral regurgitation (SMR). The ratio of effective regurgitant orifice area (EROA) to left ventricular (LV) end-diastolic volume (EDV) can be useful and may explain the difference outcomes in clinical trials of mitral transcatheter edge-to-edge repair (TEER) but the EROA/LVEDV ratio still fails to consider other important factors (figure 4). They recommend. €˜the key to patient selection where to get antabuse is forced titration of neurohormonal antagonists to the target doses that have been proven in clinical trials (along with cardiac resynchronisation when appropriate). Patients who continue to have symptomatic severe SMR after doing so should be considered for TEER.’ This recommendation is in accord with the recently published 2020 American College of Cardiology/American Heart Association Guidelines for the Management of Valvular Heart disease.8Plot showing the relationship of RF (x-axis) versus LVEDV (y-axis) for different values of EROA and an LVEF (30%).

At this low LVEF, RF would be 100% (physiologically impossible) at LVEDV of approximately 275 mL at a true (mean over systole per the Gorlin hydraulic orifice area) EROA 0.5 cm2, 220 mL at an EROA 0.4 cm2, 160 mL at an EROA 0.3 cm2 and 115 mL at an EROA 0.2 cm2. Peak EROA values reported by single frame echocardiographic techniques are often physiologically impossible where to get antabuse. It is important to recognise the difference between peak EROA and true EROA. Regurgitant volume obtained by multiplying peak EROA by the velocity–time integral of MR will often result in physiologically impossible values. EROA, effective regurgitant where to get antabuse orifice area.

LVEDV, left ventricular end-diastolic volume. LVEF, left ventricular ejection fraction. RF, regurgitant fraction." data-icon-position where to get antabuse data-hide-link-title="0">Figure 4 Plot showing the relationship of RF (x-axis) versus LVEDV (y-axis) for different values of EROA and an LVEF (30%). At this low LVEF, RF would be 100% (physiologically impossible) at LVEDV of approximately 275 mL at a true (mean over systole per the Gorlin hydraulic orifice area) EROA 0.5 cm2, 220 mL at an EROA 0.4 cm2, 160 mL at an EROA 0.3 cm2 and 115 mL at an EROA 0.2 cm2. Peak EROA values reported by single frame echocardiographic techniques are often physiologically impossible.

It is where to get antabuse important to recognise the difference between peak EROA and true EROA. Regurgitant volume obtained by multiplying peak EROA by the velocity–time integral of MR will often result in physiologically impossible values. EROA, effective regurgitant orifice area. LVEDV, left where to get antabuse ventricular end-diastolic volume. LVEF, left ventricular ejection fraction.

RF, regurgitant fraction.In contrast, Kamoen and colleagues9 argue that the concept of proportionality between SMR severity and LV end-diastolic volumes remains hypothetical and requires validation in clinical trials. In addition, both articles emphasise the technical challenges and measurement variability which affect these echocardiographic where to get antabuse parameters. Perhaps we need to consider alternative, possibly more accurate and robust, measures of SMR severity.10The Education in Heart article in this issue11 reviews several cardiovascular risk prediction tools and provides guidance on which score is best suited to each patient (figure 5). Examples are provided for the effects of risk reduction therapy for individuals with different 10-year risk scores, showing that absolute risk scores need to be interpreted in terms of lifetime benefit.Patient example. 10-year risk and treatment effects compared with the CVD-free life expectancy and lifetime benefit for a younger versus where to get antabuse an older individual.

Ten-year predictions were estimated using the Systemic Coronary Risk Estimation model risk model. Lifetime predictions using the LIFEtime-perspective CardioVascular Disease model. CVD, cardiovascular disease.

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