The Moral Atrocity of 'Top Surgery'

 Beverly* from Oregon emails me: “Urgent need help with ROGD daughter please answer ASAP.” Her daughter announced out of the blue that she’s a boy (this is called Rapid Onset Gender Dysphoria, or ROGD). I’m a child and adolescent psychiatrist, and I receive messages like this almost daily. That’s because unlike most of my colleagues, I won’t automatically affirm a child’s new identity, or refer her to a clinic where she’ll be put on experimental hormone therapy.

Beverly has reason to panic. She learned not only that her daughter, a 15-year-old, has declared herself to be a boy, but that her daughter’s best friend and main influence, Mia, just had her breasts removed as part of her own male identification process. Beverly is beside herself. “Do doctors really do that to a 16-year-old?” she asks incredulously. “They sure do,” I reply.

Increasingly, confused girls with mental-health issues are lining up to have their breasts removed, erroneously believing my colleagues who tell them the operation will alleviate their emotional pain and allow them to emerge as their authentic selves. Girls as young as 13 are having “top surgery,” a euphemism for a bilateral mastectomy—the removal of both breasts—in order to create, as gender surgeons put it, a “masculinized” chest. “Bilateral mastectomy” sounds jarring and clinical; it’s a treatment for cancer, after all—one that women agonize over. 

Mind you, these are the same people who insist that five-year-olds use anatomically accurate terms, not childish nicknames, for their genitals. They soberly instruct us to teach the words “scrotum” and “vulva” to kindergarteners. But the vague, trivial-sounding terms “top” and “bottom” surgeries—that language is fine. As if the consequences of those major operations—infertility, sexual dysfunction, infection, and chronic pelvic pain, to name a few—aren’t permanent and debilitating.

As an intern in pediatrics, when one of my patients needed a medical procedure, I was required to obtain informed consent from the parents or guardian of the minor. I was obligated to explain, accurately and comprehensively, the risks—both immediate and long-term—of the procedure. I wonder how accurate and comprehensive are the consents obtained by surgeons who perform double mastectomies on minors. Mia’s mother was almost certainly told that mastectomies for minors with gender dysphoria are evidence-based treatment, supported by well-documented standards of care. But did the surgeon mention that this deceptive reassurance is being challenged in court, with the help of an amicus brief by the Society for Evidence-Based Gender Medicine?  

SEGM’s arguments against mastectomies for girls like Mia are compelling. They point out that long-term outcomes are highly uncertain and that many girls have untreated mental-health issues. They explain why the evidence supporting mastectomies in minors is low-quality and unreliable. According to SEGM, mastectomies on minors are an “experimental procedure on vulnerable youth” whose brains and identities are still developing. Leading gender clinics and psychiatric associations worldwide are rejecting these procedures. They’re saying that girls who want their breasts removed need in-depth psychotherapy, not a surgeon’s scalpel.

I know many girls like Mia, and I’m well aware that she can’t tolerate talking about her periods, let alone pregnancy, because she’s fleeing womanhood. But her identity is still evolving; if she’s like other gender-confused girls, she wore lace push-up bras less than a year ago. In the next decade, she will go through many more changes—and one of them, I hope, will be re-acceptance of her female biology. She may follow the same path as Daisy Chadra, a young woman who lived as a man for five years and had her breasts “amputated” (her word). What she lost is irreplaceable, but Daisy’s back at peace with her female biology. There appear to be thousands like her, who regret the medical and surgical interventions they believed would solve their emotional problems. Transgender activists claim regret is rare, but this de-transitioners’ site alone has 26,000 members. If Mia someday joins their growing ranks, she may experience her flat, scarred chest as a loss.

And what if she decides to have a child? The surgeon was obligated to discuss with the mother the consequences of Mia’s breast removal—not only to her daughter but also to her grandchildren. Because in this case, organ removal may have negative consequences for two generations. 

Nursing is a cornerstone of mother-infant bonding, and when she signed on the dotted line, Mia’s mother agreed to deprive her daughter and grandchildren of the opportunity to nurse. At the moment, it may have seemed irrelevant, but for consent to be informed, the surgeon was obligated to consider long-term consequences. No bottle, pacifier, plush toy, bouncer, swing, rocker, sound machine, mobile, light show, or vibrating mat will soothe an unhappy baby like nursing. Breast milk is considered the gold standard by pediatricians and the World Health Organization. It provides lasting health benefits for both mother and child.

Mia cannot fathom the magic of mother-child bonding, or the many other wonders of her female biology. If she’s like most kids, her sex education, instead of inspiring a sense of awe for her female physiology, taught that the differences between herself and a guy are due to socialization, not biology—and that it’s normal for her to reject reality and identify as a boy. But her surgeon, and her mother, should have known better. Is it really necessary to point out that adults have more wisdom than children, and that they must resist their impulses to give in to a child’s demands just because she is distressed and feels certain?

The surgeons and “gender specialists” who support or perform these procedures on children must be held accountable. Take, for example, Johanna Olson–Kennedy from Children’s Hospital L.A., a pediatrician who believes that there should be no minimum age for a double mastectomy. What if a girl regrets it? Olson–Kennedy says: “If you want breasts at a later point in your life, you can go and get them.” 

Children are being victimized on the altar of an ideology that seeks to obliterate a fundamental truth of civilization—the reality of male and female.  

Finally, the investigations are starting. Let the truth come out: the radical social agendas that animate sexuality education; the capture of the medical, mental health, social work, and educational professions; the undermining and silencing of parents. Let’s hear expert witnesses explain the denial of biological truths, the false and dangerous promises made to vulnerable kids, and the informed consents for irreversible medical interventions that were hardly informed.

Give a public platform to the victims—those who’ve been sterilized and scarred, and their families, who’ve been traumatized and betrayed. When enough people learn the truth and stand up, when the dogma is successfully challenged, and when schools, doctors, and therapists promoting the dogma are exposed, we can start to write an end to this medical calamity.

* This and other names have been changed for this article.

Miriam Grossman, M.D., is a child, adolescent, and adult psychiatrist and author of the 2009 book You’re Teaching My Child WHAT? A Physician Exposes the Lies of Sex Education and How They Harm Your Child.

https://www.city-journal.org/moral-atrocity-top-surgery

Why exercise gets harder the less you do

 Doing less exercise could deactivate a vital protein in the body, causing further inactivity and making exercise more difficult, new research suggests.

University of Leeds scientists have discovered that deactivating the Piezo1 protein, a blood flow sensor, reduces the density of capillaries carrying blood to the muscles.

This restricted blood flow means activity becomes more difficult and can lead to a reduction in how much exercise is possible, the team found.

They say the results help to explain the biology of why exercise becomes harder the less you do.

The paper, Endothelial Piezo1 sustains muscle capillary density and contributes to physical activity, is published today in Journal of Clinical Investigation.

The experiments were carried out in mice, but the Piezo1 protein is found in humans, suggesting the same results could occur.

Lead author Fiona Bartoli, a Postdoctoral Researcher in the University of Leeds' School of Medicine, said: "Exercise protects against cardiovascular disease, diabetes, depression and cancer. Unfortunately, many people fail to exercise enough, for reasons such as injury and computer usage. This puts people at more risk of disease. The less people exercise, the less fit they become, often leading to a downward spiral.

"Although many responses to exercise are known, how the benefits of exercise are initially triggered at a molecular level is mysterious. Our study highlights the crucial link between physical activity and physical performance made at this level by Piezo1. Keeping our Piezo1s active by exercising may be crucial in our physical performance and health."

During the experiment, scientists compared two groups of mice -- a control group, and a group whose Piezo1 levels had been disrupted for 10 weeks. Walking, climbing and running wheel activity was observed, with the Piezo1 mice showing a striking reduction in activity levels. This suggests an important role for Piezo1 in sustaining normal physical activity.

The researchers considered whether the Piezo1 mice were less interested in exercise, but they found no differences in the amount or duration of activity between the two groups. Instead, there were fewer running wheel revolutions per exercise session, and slower running speed, suggesting a lowered ability to exercise, without a lesser desire.

Supervising author Professor David Beech, in the University of Leeds' School of Medicine, said: "Our work sheds new light on how Piezo1's role in blood vessels is connected to physical activity. A lot was already known about its role in blood vessel development, but far less was known about its contribution to vessel maintenance in adults.

"Our discovery also provides an opportunity to think about how loss of muscle function could be treated in new ways: if we activate Piezo1, it might help to maintain exercise capability."

The study is funded by the British Heart Foundation.

Story Source:

Materials provided by University of Leeds. Note: Content may be edited for style and length.

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Journal Reference:

1. Fiona Bartoli, Marjolaine Debant, Eulashini Chuntharpursat-Bon, Elizabeth L. Evans, Katie E. Musialowski, Gregory Parsonage, Lara C. Morley, T. Simon Futers, Piruthivi Sukumar, T. Scott Bowen, Mark T. Kearney, Laeticia Lichtenstein, Lee D. Roberts, David J. Beech. Endothelial Piezo1 sustains muscle capillary density and contributes to physical activity. Journal of Clinical Investigation, 2022; 132 (5) DOI: 10.1172/JCI141775

https://www.sciencedaily.com/releases/2022/02/220228191000.htm

Harmless or deadly? New study examines evolution of E. coli bacteria

 Genetic material from E. coli bacteria in farm animals could be contributing to the evolution of deadly pandemic strains of E. coli in humans, new research shows.

E. coli usually live as harmless bacteria in the gastrointestinal tracts of birds and mammals, including humans. They also reside, independent of a host, in environments such as water and soil, and in food products including chicken and turkey meat, raw milk, beef, pork and mixed salad.

These bacteria can cause disease if they possess or acquire factors that allow them survive in areas of the human body outside the gut.

E. coli is the primary source of urinary tract infections, a common reason for hospital admissions. It can also lead to sepsis, which kills 11 million people globally each year, and meningitis, an infection that affects the brain and spinal cord.

Dr Cameron Reid, from the University of Technology Sydney, said the aim of the study, recently published in Nature Communications, was to better understand the evolution and genomic characteristics of an emerging strain of E. coli known as ST58.

ST58 has been isolated from bloodstream infections in patients around the world, including France, where the number of infections with this strain was shown to have doubled over a 12 year period. ST58 is also more drug resistant than other strains.

"Our team analysed E. coli ST58 genomes from more than 700 human, animal and environmental sources around the world, to look for clues as to why it is an emerging cause of sepsis and urinary tract infections," said Dr Reid.

"We found that E. coli ST58 from pigs, cattle and chickens contain pieces of genetic material, called ColV plasmids, which are characteristic of this strain of disease causing E. coli," he said.

Plasmids are tiny double-stranded DNA molecules, separate from the bacterial chromosome, that can replicate independently and transfer across different E. coli strains, aiding the evolution of virulence.

Acquisition of ColV plasmids may prime E. coli strains to cause extra-intestinal infections in humans, and also increase the likelihood of antimicrobial resistance, the research suggests.

"Zoonosis, particularly in relation to E. coli, should not be viewed simply as the transfer of a pathogen from an animal to a human," said research co-author Professor Steven Djordjevic.

"Rather, it should be understood as a complex phenomenon arising from a vast network of interactions between groups of E. coli (and other bacteria), and the selective pressures they encounter in both humans and animals," he said.

The findings suggest all three major sectors of food animal production (cattle, chickens and pigs), have acted as backgrounds for the evolution and emergence of this pathogen.

"The contribution of non-human sources to infectious disease in humans is typically poorly understood and its potential importance under-appreciated, as the debate regarding the ecological origins of the SARS-CoV2 virus attest," said Dr Reid.

"In a globalised world, eminently susceptible to rapid dissemination of pathogens, the importance of pro-active management of microbial threats to public health cannot be understated."

The study has broad implications for public health policy that spans across food industry, veterinary and clinical settings.

"To date, infectious disease public health has been a reactive discipline, where action can only be taken after a pathogen has emerged and done some damage," said Dr Reid.

"Ideally, with the advent and widespread uptake of genome sequencing technology, future infectious disease public health can transition to a primarily pro-active discipline, where genomic surveillance systems are able to predict pathogen emergence and inform effective interventions."

Dr Reid said for such a system to work, it requires ongoing research and collaboration with government, public health bodies, food producers and clinicians, and it would involve surveillance of a variety of non-human sources of microbes.

"This would include domestic and wild animals -- particularly birds -- food products, sewerage and waterways, in what is referred to as a 'One Health' approach. Some microbes, like ST58 E. coli, know very few barriers between these increasingly interconnected hosts and environments.

"A One Health genomic pathogen surveillance system would be a revolution within public health and do much to break down historically human-centric approaches devoid of connection with the world around us."

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Story Source:

Materials provided by University of Technology Sydney. Note: Content may be edited for style and length.

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Journal Reference:

1. Cameron J. Reid, Max L. Cummins, Stefan Börjesson, Michael S. M. Brouwer, Henrik Hasman, Anette M. Hammerum, Louise Roer, Stefanie Hess, Thomas Berendonk, Kristina Nešporová, Marisa Haenni, Jean-Yves Madec, Astrid Bethe, Geovana B. Michael, Anne-Kathrin Schink, Stefan Schwarz, Monika Dolejska, Steven P. Djordjevic. A role for ColV plasmids in the evolution of pathogenic Escherichia coli ST58. Nature Communications, 2022; 13 (1) DOI: 10.1038/s41467-022-28342-4

https://www.sciencedaily.com/releases/2022/03/220301093707.htm

Why multiple myeloma returns

 Multiple myeloma is a cancer which affects 'plasma cells', a type of immune cell found in the bone marrow. This cancer can weaken the immune system, cause kidney damage, and weaken bones, which may lead to fractures. Average survival rates have improved considerably thanks to new treatment options. These include lenalidomide and pomalidomide, drugs which are often successful in forcing the cancer into remission. In nearly all cases, however, the cancer will become increasingly less susceptible to these drugs, meaning it develops drug resistance. When cancer growth eventually resumes despite treatment, the patient's prognosis is poor.

Using latest improvements for a method known as proteomics, an interdisciplinary team of researchers in Berlin was able to decode a previously unknown mechanism which can cause this type of relapse. "We were able to show that production of CDK6, a cell division-promoting cell cycle regulator, is particularly high once the cancer has become resistant to treatment," explains one of the study's two co-leads, Prof. Dr. Jan Krönke of the Department of Hematology, Oncology and Cancer Immunology on Campus Benjamin Franklin. "Based on our data, we believe that CDK6 inhibition could represent a new treatment approach in relapsed multiple myeloma."

Despite extensive DNA sequencing studies, treatment resistance in multiple myeloma has only rarely been linked to changes at the genetic level, such as gene mutations or gene deletions. "This suggests that the changes taking place within the cancer cell which would explain this relapse must take place at a different level," says the study's second co-lead, Dr. Philipp Mertins, an MDC researcher who heads the Proteomics Platform at both the MDC and the BIH. He continues: "The cancer cells' growth potential may also be subject to various means of control at the protein level. Here, we observed this type of effect in relation to the protein CDK6." The researchers employed cutting-edge mass spectrometry technology in order to establish whether changes at the protein level are responsible for the cancer becoming resistant to treatment. Using both pre- and post-relapse samples from patients with multiple myeloma, the researchers were able to quantify more than 6,000 different proteins.

Comparing cancer cells collected before and after relapse, the researchers found that a range of proteins were present at either higher or lower concentrations post-relapse. Using statistical and bioninformatics analyses, the researchers were able to trace the majority of these effects back to a single protein: cyclin-dependent kinase 6, or CDK6, an enzyme which controls the cell's entry into the cell division phase of the cell cycle.

As a first step, the researchers used cell cultures to demonstrate that CDK6 plays a key role in the development of treatment resistance in multiple myeloma. "When we artificially increased the amount of CDK6 present inside cultured myeloma cells, they lost their susceptibility to the drugs lenalidomide and pomalidomide," explains the study's first author, Dora Ng, a researcher at the Department of Hematology, Oncology and Cancer Immunology on Campus Benjamin Franklin. She adds: "However, when we also added a CDK6 inhibitor, the drugs became effective again and the cancer cells died. This shows that CDK6 inhibition enables at least a partial reversal of the myeloma cells' treatment resistance."

The researchers were then able to confirm this effect in an animal model, where the combination of pomalidomide with a CDK6 inhibitor significantly improved the odds of survival. "These data suggest that patients with treatment-resistant multiple myeloma may also benefit from the addition of CDK6 inhibitors," says Prof. Krönke, a researcher at the German Cancer Consortium's (DKTK) translational research center in Berlin, who is being funded via the DFG's Emmy Noether Program. "Further studies will be needed in order to test this hypothesis. One advantage is that some CDK6 inhibitors have already been authorized for use in the treatment of breast cancer."

The study's second first author, Dr. Evelyn Ramberger, was responsible for performing the project's protein analyses. A postdoc at Charité and the MDC/BIH Proteomics Platform, she is convinced that the technology holds enormous benefits for the field of cancer research: "We want to continue pursuing this new approach of using modern, comprehensive protein analyses to study cancer tissues -- both in multiple myeloma and other cancers. We hope this will unveil further treatment targets and biomarkers for use in personalized cancer medicine," she says.

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Story Source:

Materials provided by Charité - Universitätsmedizin Berlin. Note: Content may be edited for style and length.

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Journal Reference:

1. Yuen Lam Dora Ng, Evelyn Ramberger, Stephan R. Bohl, Anna Dolnik, Christian Steinebach, Theresia Conrad, Sina Müller, Oliver Popp, Miriam Kull, Mohamed Haji, Michael Gütschow, Hartmut Döhner, Wolfgang Walther, Ulrich Keller, Lars Bullinger, Philipp Mertins, Jan Krönke. Proteomic profiling reveals CDK6 upregulation as a targetable resistance mechanism for lenalidomide in multiple myeloma. Nature Communications, 2022; 13 (1) DOI: 10.1038/s41467-022-28515-1

https://www.sciencedaily.com/releases/2022/03/220301131117.htm

Role of lipids in the development of Alzheimer’s disease

 Neurons in the brain coexist with and rely on many other cell types to function properly. Astrocytes, which take their name from their star shape, ensure the survival of neurons by feeding and detoxifying them with the help of a multifunctional protein, APOE. One of three forms of this protein, APOE4, significantly increases the risk of developing Alzheimer's disease, but the mechanisms at play are unknown. A collaboration between the University of Geneva (UNIGE), the European Molecular Biology Laboratory (EMBL), the University of Zurich and the pharmaceutical company AbbVie has discovered a potential mechanism: far from ceasing to function, APOE4 is on the contrary more efficient. By triggering astrocytic lipid secretion, it causes the accumulation of potentially toxic lipids that are harmful to neurons, and thus might contribute to the development of Alzheimer's disease. These results published in the journal Cell Reports, shed new light on the neurodegenerative mechanisms of a disease that affects nearly 50 million people worldwide.

Astrocytes, present in very large numbers in the brain, have a major protective function. These cells secrete apolipoprotein E (or APOE), a small protein that forms particles containing lipids and vitamins to feed the neurons. It also detoxifies the neurons by getting them rid of "lipid waste" that could become harmful if not removed. As the neurons are unable to eliminate this waste on their own, APOE comes into play to collect it and bring it back to the astrocytes where it is destroyed.

The gene coding for APOE exists in three frequent variants in humans: APOE2, present in 8% of the population, APOE3, the most common, and APOE4, which is found in nearly 15% of people and increases the risk of developing Alzheimer's disease by a factor of ten. "The reasons why APOE4 increases the risk of Alzheimer's disease so significantly are not well understood," explains Anne-Claude Gavin, a professor in the Department of Cell Physiology and Metabolism at the UNIGE Faculty of Medicine and holder of a Louis-Jeantet Foundation Chair, who directed this research together with Viktor Lakics, a Research fellow and Biology Area Leader in Neuroscience discovery at AbbVie. What are the mechanisms behind the dysfunction of APOE4? And above all, could they serve as a basis for prevention or therapy? To answer these questions, Anne-Claude Gavin and her team joined forces with scientists from the European Molecular Biology Laboratory (EMBL), the University of Zurich and AbbVie.

A protein that is too effective

Working on these questions, the research team identified novel molecular mechanisms that explain how APOE binds to astrocyte membranes to detect and extract the lipids it needs. Employing human cell lines with different APOE variants, in vitro experiments demonstrated that APOE is very efficient at transporting potentially harmful lipids produced in neurons. "And to our great surprise, the APOE4 variant proved to be even more efficient than the other forms," reveals Katharina Beckenbauer, a former post-doc in Anne-Claude Gavin's group, senior scientist at AbbVie, and one of the first authors of the work. "So, contrary to what we thought until now, the problem is not that APOE4 stops working, but, in fact, the opposite. And the mechanism goes haywire."

A hijacked function

As astrocytes age, they become less efficient and start to accumulate lipids rather than destroy them. "We modelled this process experimentally and observed the molecules secreted by the astrocytes," explains Karina Lindner, a PhD student in Anne-Claude Gavin's laboratory and one of the first authors of this work. "We observed that cellular ageing diverts APOE from its primary function -- transporting lipids to neurons and also recovering lipid waste from them -- towards the secretion of triglycerides, particular lipid species that could become harmful if not removed." And this phenomenon is exacerbated with APOE4: it stimulates the secretion of triglycerides, leading to their uncontrolled accumulation. This deleterious accumulation of potentially harmful lipids could very well be an important contributor to the neuronal death, a hallmark of Alzheimer's disease. "APOE4 would thus have the capacity to accelerate the pathological process in the disease through the mechanism we have discovered."

In order to better understand the details of the action of APOE and especially of the E4 variant, the scientists at UNIGE want now to determine how secretion of these potentially harmful lipids is regulated and whether this secretion can be detected in people suffering from Alzheimer's disease.

Story Source:

Materials provided by Université de Genève. Note: Content may be edited for style and length.

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Journal Reference:

1. Karina Lindner, Katharina Beckenbauer, Larissa C. van Ek, Kevin Titeca, Sherida M. de Leeuw, Khader Awwad, Franziska Hanke, Alla V. Korepanova, Vladimir Rybin, Elizabeth Louise van der Kam, Eric G. Mohler, Christian Tackenberg, Viktor Lakics, Anne-Claude Gavin. Isoform- and cell-state-specific lipidation of ApoE in astrocytes. Cell Reports, 2022; 38 (9): 110435 DOI: 10.1016/j.celrep.2022.110435

https://www.sciencedaily.com/releases/2022/03/220301131037.htm

U.S. Supreme Court Mulls 'Pill Mill' Doctors' Opioid Convictions

 The U.S. Supreme Court on Tuesday wrestled with the circumstances under which doctors can be convicted of operating as drug dealers under the cover of their medical practices to illegally distribute opioid painkillers and other dangerous narcotics.

The justices heard arguments in an appeal by two doctors, Xiulu Ruan and Shakeel Kahn, of lower court rulings upholding their convictions on narcotics violations and related crimes stemming from what prosecutors called the misuse of medical licenses to engage in drug trafficking.

Lawyers for Ruan, who practiced in Alabama, and Kahn, who practiced in Arizona and then Wyoming, complained to the justices that jurors convicted the doctors of unlawfully dispensing massive amounts of opioids through "pill mill" clinics without having to weigh whether they had a "good faith" reason to believe their prescriptions were medically valid.

Some of the justices questioned why jurors should be instructed to consider the doctors' beliefs at all about the medical validity of their prescriptions when determining if they violated a federal law called the Controlled Substances Act.

Chief Justice John Roberts asked "how is that different" than if police pulled over a driver on a highway for going over a 50-mile-per-hour (80 km) speed limit who then argued that the speed limit should be higher. The driver would still get ticketed, Roberts said.

There has been an increase in U.S. criminal prosecutions of doctors who have prescribed addictive pain pills amid a law enforcement push to combat an opioid abuse epidemic that has caused hundreds of thousands of overdose deaths over the past two decades.

The Supreme Court took up the doctors' appeals amid divisions in lower courts about the standard under which doctors could be convicted of violating the Controlled Substances Act for writing prescriptions outside the bounds of professional practice.

Eric Feigin, a U.S. deputy solicitor general arguing for the government, said accepting the doctors' arguments would upend the purposes of licenses issued by the U.S. Drug Enforcement Administration for doctors to prescribe dangerous drugs.

"They want to be free of any obligation even to undertake any minimal effort to act like doctors when they prescribe dangerous, highly addictive and, in one case, lethal dosages of drugs to trusting and vulnerable patients," Feigin said.

Ruan was sentenced to 21 years in prison and Kahn to 25 years in separate criminal prosecutions.

Prosecutors said Ruan, through a clinic in Mobile, issued nearly 300,000 controlled-substance prescriptions from 2011 to 2015 and accepted kickbacks from drugmaker Insys Therapeutics Inc to prescribe a fentanyl spray to patients.

Prosecutors said Kahn regularly sold prescriptions for cash and unlawfully prescribed large amounts of opioid pills, resulting in at least one patient dying of an overdose.

Lawrence Robbins, Ruan's lawyer, said that while jurors are free to disbelieve that a doctor had a good faith belief in the medical validity of their drug prescriptions, they should be instructed by courts to consider that defense before reaching a verdict.

Justice Samuel Alito said the Controlled Substance Act by his reading had no mention of such a requirement.

"As for 'good faith,' I don't know where that word comes from at all," Alito said.

Justice Brett Kavanaugh said the statute's requirement of a "legitimate medical purpose" to prescribe controlled substances was vague and something "on which reasonable people can disagree."

Kavanaugh appeared open to instructing jurors to hear good faith defenses from doctors, saying jurors would almost certainly disbelieve them if they came in with "some outlandish theory."

https://www.usnews.com/news/top-news/articles/2022-03-01/u-s-supreme-court-mulls-pill-mill-doctors-opioid-convictions

Hong Kong leader calls for calm, after supermarkets emptied ahead of mass COVID testing

 Hong Kong's leader Carrie Lam called for calm on Tuesday after residents emptied supermarkets, stocking up on produce ahead of reports of compulsory mass COVID-19 testing and rumours of a city-wide lockdown.

Local media reported compulsory COVID testing would start after March 17, sparking concerns many people will be forced to isolate and families with members testing positive would be separated.

Lam appealed to the public "not to fall prey to rumours to avoid unnecessary fears being stirred," with the supply of food and goods remaining normal, according to a statement on Tuesday.

"There is no need for members of the public to worry, they should stay vigilant and pay attention to the information disseminated by the government so as to avoid being misled by rumours."

Officials are planning to test the city's 7.4 million people three times over nine days, with the government recommending that people stay home during the period, Sing Tao newspaper reported, citing unidentified sources.

Exemptions would be made for those who buy food, seek medical treatment and maintain societal operations. Hong Kong's stock market would continue to operate, the paper said.

Lam had previously said she was not considering a city-wide lockdown.

The Chinese ruled city has seen coronavirus infections surge some 34 times to over 34,000 on Monday from just over 100 at the start of February. Deaths are also climbing, with facilities for storing dead bodies at hospitals and public mortuaries at maximum capacity. read more

Hong Kong continues to stick to a COVID policy of "dynamic zero", the same as mainland China, which seeks to curb all outbreaks at any cost. The Chinese ruled territory has implemented its most draconian measures since the start of the pandemic in 2020.

The rules have exacerbated separation fears among many families, with many fleeing ahead of the mass testing scheme and the build out of tens of thousands of isolation centres. read more

Lam, who inspected a mainland Chinese built isolation centre on Monday, said the team had raced against the clock to "create a miracle" in the city's construction industry.

The Tsing Yi facility, located in the northwest of the city, would provide around 3,900 rooms for infected people with mild or no symptoms and others who need to isolate, she said.

https://www.reuters.com/world/asia-pacific/hong-kong-leader-calls-calm-after-supermarkets-emptied-ahead-mass-covid-testing-2022-03-01/