Archive for October, 2022

Many people whove recently received a diagnosis of type 1 diabetes (T1D) immediately think, When will there be a cure?

While the potential for a cure has been dangling in front of people with T1D for what seems like forever, more researchers currently believe that gene therapy could finally one day soon, even be the so-called cure thats been so elusive.

This article will explain what gene therapy is, how its similar to gene editing, and how gene therapy could potentially be the cure for T1D, helping millions of people around the world.

Gene therapy is a medical field of study that focuses on the genetic modification of human cells to treat or sometimes even cure a particular disease. This happens by reconstructing or repairing defective or damaged genetic material in your body.

This advanced technology is only in the early research phases of clinical trials for treating diabetes in the United States. Yet, it has the potential to treat and cure a wide range of other conditions beyond just T1D, including AIDS, cancer, cystic fibrosis (a disorder that damages your lungs, digestive tract, and other organs), heart disease, and hemophilia (a disorder in which your blood has trouble clotting).

For T1D, gene therapy could look like the reprogramming of alternative cells, making those reprogrammed cells perform the functions your original insulin-producing beta cells would otherwise perform. If you have with diabetes, that includes producing insulin.

But the reprogrammed cells would be different enough from beta cells so that your own immune system wouldnt recognize them as new cells and attack them, which is what happens in the development of T1D.

While gene therapy is still in its infancy and available only in clinical trials, the evidence so far is becoming clearer about the potential benefits of this treatment.

In a 2018 study, researchers engineered alpha cells to function just like beta cells. They created an adeno-associated viral (AAV) vector to deliver two proteins, pancreatic and duodenal homeobox 1 and MAF basic leucine zipper transcription factor A, to a mouses pancreas. These two proteins help with beta cell proliferation, maturation, and function.

Alpha cells are the ideal type of cell to transform into beta-like cells because not only are they also located within the pancreas, but theyre abundant in your body and similar enough to beta cells that the transformation is possible. Beta cells produce insulin to lower your blood sugar levels while alpha cells produce glucagon, which increases your blood sugar levels.

In the study, mouse blood sugar levels were normal for 4 months with gene therapy, all without immunosuppressant drugs, which inhibit or prevent the activity of your immune system. The newly created alpha cells, performing just like beta cells, were resistant to the bodys immune attacks.

But the normal glucose levels observed in the mice werent permanent. This could potentially translate into several years of normal glucose levels in humans rather than a longtime cure.

In this Wisconsin study from 2013 (updated as of 2017), researchers found that when a small sequence of DNA was injected into the veins of rats with diabetes, it created insulin-producing cells that normalized blood glucose levels for up to 6 weeks. That was all from a single injection.

This is a landmark clinical trial, as it was the first research study to validate a DNA-based insulin gene therapy that could potentially one day treat T1D in humans.

This was how the study worked:

The researchers are now working on increasing the time interval between therapy DNA injections from 6 weeks to 6 months to provide more relief for people with T1D in the future.

While this is all very exciting, more research is needed to determine how practical the therapy is for people. Eventually, the hope is that the AAV vectors could eventually be delivered to the pancreas through a nonsurgical, endoscopic procedure, in which a doctor uses a medical device with a light attached to look inside your body.

These kinds of gene therapy wouldnt be a one-and-done cure. But it would provide a lot of relief to people with diabetes to perhaps enjoy several years of nondiabetes glucose numbers without taking insulin.

If subsequent trials in other nonhuman primates are successful, human trials may soon begin for the T1D treatment.

Does that count as a cure?

It all depends on who you ask because the definition of a cure for T1D varies.

Some people believe that a cure is a one-and-done endeavor. They see a cure as meaning youd never have to think about taking insulin, checking blood sugars, or the highs and lows of diabetes ever again. This even means you wouldnt have to ever go back to a hospital for a gene therapy follow-up treatment.

Other people think that a once-in-a-few-years treatment of gene editing may be enough of a therapy plan to count as a cure.

Many others believe that you need to fix the underlying autoimmune response to truly be cured, and some people dont really care one way or another, as long as their blood sugars are normal, and the mental tax of diabetes is relieved.

One potential one-and-done therapy could be gene editing, which is slightly different from gene therapy.

The idea behind gene editing is to reprogram your bodys DNA, and if you have type 1 diabetes, the idea is to get at the underlying cause of the autoimmune attack that destroyed your beta cells and caused T1D to begin with.

Two well-known companies, CRISPR Therapeutics and regenerative med-tech company ViaCyte, have been collaborating for a few years to use gene editing to create islet cells, encapsulate them, and then implant them into your body. These protected, transplanted islet cells would be safe from an immune system attack, which would otherwise be the typical response if you have T1D.

The focus of gene editing is to simply cut out the bad parts of our DNA in order to avoid conditions such as diabetes altogether and to stop the continuous immune response (beta cell attack) that people who already have diabetes experience daily (without their conscious awareness).

The gene editing done by CRISPR in their partnership with ViaCyte is creating insulin-producing islet cells that can evade an autoimmune response. These technology and research are ever evolving and hold a lot of promise.

Additionally, a 2017 study shows that a T1Dcure may one day be possible by using gene-editing technology.

Both gene therapy and gene editing hold a lot of promise for people living with T1D who are hoping for an eventual future without needing to take insulin or immunosuppressant therapy.

Gene therapy research continues, looking at how certain cells in the body could be reprogrammed to start making insulin and not experience an immune system response, such as those who develop T1D.

While gene therapy and gene-editing therapy are still in their early stages (and much has been held up by the coronavirus disease 19 [COVID-19] pandemic), theres a lot of hope for a T1D cure in our near future.

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Gene therapy: The Potential for Treating Type 1 Diabetes - Healthline

Two years ago, a mother received a phone call with a devastating diagnosis. That mother shares her son's experience with spinal muscular atrophy (SMA), a rare genetic disease, and how early diagnosis and treatment transformed his life.

BANNOCKBURN, Ill., Oct.12, 2022 /PRNewswire/ --

BACKGROUND:

Hannah Weaver did not think much about her son Payne's newborn screening test until she received a phone call five days after bringing him home from the hospital. The results showed Payne tested positive for spinal muscular atrophy (SMA), a rare, progressive neuromuscular disease and a leading genetic cause of infant death when left untreated that affects one in every 11,000 babies born in the U.S.1,2 SMA causes irreversible loss of motor neurons, which can rob infants of their ability to walk, swallow and even breathe.1,2 If left untreated in its most severe forms, 90% of children require permanent feeding and breathing support or pass away by their second birthday.3,4 SMA can progress quickly, making early diagnosis and treatment crucial.

Experience the full interactive Multichannel News Release here: https://www.multivu.com/players/English/9064751-novartis-spinal-muscular-atrophy-health-alert/

Knowing it was imperative to act fast, the Weaver family worked quickly to schedule appointments with specialists to discuss treatment options. Payne's care team went over the available treatment options for SMA, discussing the route of administration and available efficacy and safety data of each. Together, they decided to treat Payne when he was just a few weeks old with a gene therapy called ZOLGENSMA (onasemnogene abeparvovec-xioi), the only SMA treatment designed to directly address the genetic root cause of the disease by replacing the function of the missing or non-working SMN1 gene with a single, one-time dose.

Zolgensma has a boxed warning for acute serious liver injury and acute liver failure. In clinical trials, the most common side effects were elevated liver enzymes and vomiting. Please keep reading for additional important safety information and please see accompanying Full Prescribing Information.

Payne's parents are now able to plan for his future something that would not be possible without early intervention and treatment. They look forward to what he will accomplish next and celebrate every milestone along the way. On the heels of SMA Awareness Month, we kick off Newborn Screening Awareness Month this September, and Hannah is advocating for parents and physicians to recognize the early signs of SMA to avoid a delayed diagnosis.

Dr. Sandra Reyna (Vice President of Global Medical Affairs at Novartis Gene Therapies) and Hannah Weaver (SMA parent advocate) shared information on the signs of SMA, the importance of an early diagnosis, and how Zolgensma has the potential to transform the lives of babies born with this disease.

Results and outcomes vary among children based on several factors, including how far their SMA symptoms progressed prior to receiving treatment.

Please continue reading for Indication and Important Safety Information, and please see accompanying Full Prescribing Information including Boxed Warning.

For more information, please visit: http://www.Zolgensma.com

Interview opportunities are courtesy of Novartis Gene Therapies.

About Spinal Muscular Atrophy

Spinal muscular atrophy (SMA) is a rare, genetic neuromuscular disease and a leading genetic cause of infant death.3,5Caused by the lack of a functional SMN1 gene, the most severe forms of SMA result in the rapid and irreversible loss of motor neurons, affecting muscle functions including breathing, swallowing and basic movement.1Severity varies across a spectrum of types corresponding to the number of copies of the back-up SMN2 gene.6The majority of patients with two copies of SMN2 develop Type 1, the most common form accounting for 60 percent of cases.4,7,8Type 1 is severe and, left untreated, leads to death or the need for permanent ventilation by the age of two in more than 90 percent of cases.3,5Most patients with three copies of SMN2 develop Type 2, accounting for about 30 percent of cases.4,8 Loss of motor neurons cannot be reversed, so it is imperative to diagnose SMA and begin treatment, including proactive supportive care, as early as possible to halt irreversible motor neuron loss and disease progression.9,10

IndicationandImportant Safety InformationforZOLGENSMA(onasemnogeneabeparvovec-xioi)

Whatis ZOLGENSMA?

ZOLGENSMA is a prescription gene therapy used to treat children less than 2 years old with spinal muscular atrophy (SMA). ZOLGENSMA is given as a one-time infusion into a vein. ZOLGENSMA was not evaluated in patients with advanced SMA.

WhatisthemostimportantinformationIshouldknowaboutZOLGENSMA?

Whatshould Iwatchforbeforeandafterinfusion withZOLGENSMA?

WhatdoIneedtoknowaboutvaccinationsandZOLGENSMA?

DoIneedtotakeprecautionswiththepatient'sbodilywaste?

Temporarily, small amounts of ZOLGENSMA may be found in the patient's stool. Use good hand hygiene when coming into direct contact with bodily waste for 1 month after infusion with ZOLGENSMA. Disposable diapers should be sealed in disposable trash bags and thrown out with regular trash.

Whatarethepossible orlikelysideeffectsof ZOLGENSMA?

The most common side effects that occurred in patients treated with ZOLGENSMA were elevated liverenzymesandvomiting.

The safety information provided here is not comprehensive. Talk to the patient's doctor about anysideeffects thatbotherthepatientorthatdon'tgoaway.

You are encouraged to report suspected side effects by contacting the FDA at 1-800-FDA-1088 orwww.fda.gov/medwatch,orNovartis GeneTherapiesat833-828-3947.

Please see the Full Prescribing Information.

2022 Novartis Gene Therapies, Inc.

US-ZOL-22-0136

References

MEDIA CONTACT: Katie Lesch, [emailprotected]

SOURCE Novartis Gene Therapies

Originally posted here:
Health Alert for Parents: How one boy is thriving following treatment with a gene therapy after receiving an early diagnosis - PR Newswire

Its October and for the past few years thats meant masks and wait on your vaccine shot. Its also meant hesitancy, political division and limitation on what you can and cannot do with your day. This October seems to be different. Theres been no mask mandate, nor have there been any closures, and thats mostly to do with the gradual weakening of the variants of the COVID-19 virus. But that doesnt mean were through the woods and out the other side. The variant strains may be weaker, but there are still dangers attached. Its good for us that there are medical tech and biotechnology companies out there in the space looking for cures and treatments better than those presently on the market.

Thats also not to disregard the host of other health related issues we face as a society every winter.

Here are five biotechnology and medical tech companies pooling their resources to make our lives easier.

Novavax (NASDAQ:NVAX) presented data from its phase 3 PREVENT-19 trial and study 307 at the World Vaccine congress Europe 2022.

The data from adults and adolescents aged 12 to 17 showed the companys prototype COVID-19 vaccine (NVX-COV2373) met its immunologic endpoint. Also, study 307 met its objective, showing that three lots of the vaccine tested as a successful booster for immune responses in previously vaccinated adults.

These data further demonstrate the consistent immunogenicity and safety profile of the Novavax COVID-19 vaccine as a booster, regardless of previous vaccine history. These data are an early indication that our vaccine may be effective against variants such as Omicron. We have ongoing trials further exploring the Novavax COVID-19 vaccines potential as an effective booster against these variants, including BA.4/5, and look forward to sharing these data, said Gregory M. Glenn, M.D., president of research and development for Novavax.

Novavax wants the world to be a healthier place and its working towards that end. It does this through the discovery, development and commercialization of vaccines for serious infectious diseases. The company uses a recombinant technology platform to produce drugs that boost the immune system in response to global health needs.

The Novavax COVID-19 vaccine is a protein-based vaccine engineered from the genes of the first SARS-CoV-2 strain. The company put the vaccine together using its recombinant nanoparticle technology to generate antigen from the original coronavirus spike protein. The company reformulates the antigen to enhance the immune response and help with developing high levels of neutralizing antibodies.

Multiple regulatory bodies across the world, including the FDA, the WHO and the European Commission, have given the sign off on the companys COVID-19 vaccine. Its presently under review by more.

Also, Novavax is working on a COVID-19-Influenza combination vaccine. Its presently in a Phase 1/2 clinical trial.

The PREVENT-19 trial involved an adult receiving a booster dose approximately eight or 11 months after the primary dose. The anti-spike immunoglobulin G, which is a type of antibody, levels increased relative to pre-boost levels.

They rose significantly, with neutralizing antibodies increasing by 34 to 27 fold compared to pre-boost levels when boosted at eight or 11 months.

The booster evaluations were the same in the version of the PREVENT-19 expansion given to adolescents between 12 and 17. The tests showed a significant antibody boost against Omicron BA.1, BA.2, and BA.5.

The Vitamin Shoppe, a subsidiary of Franchise Group (NASDAQ:FRG), is offering a free protein bar or healthy snack to anyone who can prove they have gotten their flu vaccine.

The name of the campaign is Snax for Vax and it supports healthy communities during the flu season. It isnt quite as catchy as vax and scratch or shot and a beer, which were a free scratch lotto card or a free beer for getting the COVID-19 vaccine, but if it gets people out, then its probably doing its job.

The Vitamin Shoppe is dedicated to the lifelong wellness of our customers and the communities we serve. Public health experts have advised that the current flu season may be severe, so we want to encourage Americans to engage in healthy habits, such as getting an annual flu vaccine and supporting their immune systems with a healthy diet, regular exercise, and proper sleep routines. Our Health Enthusiast store teams look forward to our Snax for Vax weekend and giving away some of our most popular, protein-packed snacks as a tasty and healthy reward for supporting your wellness with a flu vaccine, said Sharon Leite, CEO of The Vitamin Shoppe.

The Vitamin Shoppe is a omnichannel specialty retailer and wellness lifestyle company. Its based in Secaucus, New Jersey, and offers an assortment of nutritional offerings, including vitamins and minerals, supplements and herbs, sports nutrition and homeopathy remedies. It also carries products from approximately 700 national brands. It also has its own brands, including The Vitamin Shoppe, Vthrive The Vitamin Shoppe, BodyTech, BodyTech Elite, fitfactor, fitfactor KETO, plnt, ProBioCare, True Athlete, and TrueYou.

The campaign kicks off on October 22-23 wherein anyone who gets a recent flu vaccine complete with proof from a doctor, pharmacist or other healthcare provider, can pick a protein bar or snack from any of the 700 The Vitamin Shoppe and Super Supplements stores in the U.S. and Puerto Rico. No purchase required.

Some of the options include:

Read more: The Mugglehead technology roundup: alternative medicine options edition

Read more: Transforming System licenses platforms for greater operational efficiency: NHS

Excellence Canada awarded Scotiabank (TSX:BNS) (NYSE:BNS) with the Gold Standard Award for its role in creating a psychologically safe environment.

Depression causes an estimated 200 million lost workdays, and costs $17 billion to $44 billion to employers, according to the Center for Disease Control (CDC). Half of employees suffering from depression go untreated. The disease effects the absentee rate, causes loss of productivity, and effects the overall climate in the workplace. Thats why this is important.

World Mental Health Day provides an opportunity for us to listen and reflect on the importance of the mental health and well being for all of our employees. The recognition from Excellence Canada is a proud moment for us as an employer, recognizing the culture we strive to create for employees, said Barb Mason, group head and chief human resources officer for Scotiabank. By supporting and empowering employees to take care of their mental health and wellbeing, and speak up about how theyre feeling, were creating a workplace where everyone can thrive.

Scotiabank has made a number of different contributions to maintaining sustained mental health, including:

Bioproduction tool and service provider for cell and gene therapy (CGT), BioLife solutions (NASDAQ:BLFS), and temperature control shipping solution provider Csafe inked a partnership to provide a global service net in support of CGT products.

The overall goal of the partnership is to increase reliability, enhance security and improve quality. Csafe is joining BioLifes global network of cold chain solution providers in the CGT market. The numbers bear out to 10,000-12,000 shipments of CGT materials and manufactured doses over a year. Specifically, the new partnership provides expanded supply chain options for any CGT product at any stage of development.

CSafe is honored to partner with the team at BioLife Solutions, whose range of CGT bioproduction tools and services is peerless in the market. We are excited to merge these exceptional tools and services with our expertise in global, reliable scaled delivery. CGT is hitting its stride and needs global support. We know how important these therapies are to patients everywhere, and its our mission at CSafe to protect every shipment, said Patrick Schafer, CSafe CEO.

BioLife Solutions is a supplier of bioproduction tools and services for CGT and other biopharma markets. Its tools include the CryoStor and HypoThermosol biopresevation media for shipping and storage. Additionally, the ThawSTAR family of automated, water-free thawing products, and the evo cold chain management system.

In contrast, Csafe offers thermal shipping solutions for pharma cold chain shipping needs. Csafe deliveries use active and passive bulk air cargo, parcel, cell and gene and specialty last-minute use cases that can meet the complete range of pharma cold-chain shipping requirements with quality and reliability.

Additionally, Csafe operates from over fifty service centers worldwide. The company has built a reputation as a proven partner for biopharmaceutical manufacturers looking to simplify supply chain woes. This includes a track record for finding shipping solutions for six billion doses of a COVID-19 vaccine.

Were excited to work with a global partner with a strong history of reliability and performance and a deep dedication to innovative therapies, said BioLife Solutions CEO Mike Rice. We have the best LN2 technology and cGMP storage facilities in the market, in addition to our other world-class CGT solutions, and we are confident our collaboration with CSafe will extend our reach and result in even more reliability and real-time service for CGT partners.

The cold chain CGT market was worth USD$1.3 billion in 2021. The market is anticipated to reach USD$2.8 billion at a compound annual growth rate of 14.29 per cent until 2027.

IceCure Medical (NASDAQ:ICCM) is a company with a curious bit of technology. It uses something called cryoablation technology, which it has called the ProSense System. It destroys tumours by freezing as an alternative to surgical removal.

IceCure announced that its ProSense cryoprobes and introducers have received regulatory approval from Agncia Nacional de Vigilncia Sanitria (ANVISA), the Brazilian health regulatory agency, to operate in said country. The company originally submitted the application in June 2022 through KTRFIOS IMPORTACAO E EXPORTACAO LTDA, IceCures distributor in Brazil

We are very pleased to achieve this first step in the path to receiving full regulatory approval in Brazil. Working with KTRFIOS has been highly productive, and we anticipate strong demand in Brazil upon the additional pending approval of the ProSense Cryoablation System,said Eyal Shamir, IceCures CEO.

The ProSense cryoprobes and introducers are disposal Class II devices as per ANVISA. Doctors insert cryoprobes into the body to freeze tumours, after which, introducers go to work on the tumour tissue. However, the system is considered a Class III medical device and the application is presently waiting for approval.

IceCures distribution agreement with its Brazilian partner includes the guarantee of at least USD$6.6 million sales in five years.

Previously, the company sought regulatory approval to operate in Vietnam. It submitted a filing for its ProSense System and accessories with the Department of Medical Equipment and Construction (DMEC) of Vietnams Ministry of Health.

The application included benign and malignant tumours in the breasts, lungs, liver, kidneys, and musculoskeletal tumours.

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The Mugglehead technology roundup: medical tech and biotechnology edition - Mugglehead

Commentary

I am being somewhat ironic. But really, not that ironic.

How many people in the land of the free lost their ability to care for their families for refusing to go along with the COVID-19 jab mandates?

For saying no to injecting themselves with an experimental gene therapy vaccine, even thoughmost of them were not at severe risk from the virus?

When Pfizer executive Janine Small admitted to the European Parliament on Oct. 10 that the vaccine had never been tested to stop the viruss transmission, many may have subsequently felt vindicated.

Conservative Member of the European Parliament from the Netherlands Rob Roos asked Small point-blank whether the claim that we were all fed from day one of the vaccines release had any grounding in fact.

Those who refused the shot on principle endured the vitriolic attack by their government and peers. They were labeled as antisocial and denied access to society in many cases.

Roos may have made his statement in Brussels, but it also resonated with those of us in the United States and Canada. The latter endured particularly draconian lockdown orders and vaccination requirements.

When Dr. Anthony Fauci told us that the vaccine turns you into a dead end for the virus, we were told to trust the science. Now, Small tells us that the speed of science was moving too fast to be able to test that claim.

In other words, she reaffirmed what many of us already knewmuch of the COVID fiasco has been unrelated to any actual science but rather a pretext for the government to increase its power.

Conform, or else become an untouchable. That was their goal all along. Divide and conquer. Remember when nearly 50 percent of Democratic voters said they would potentially be okay with forcibly interning the unvaccinated in isolated locationsyou know, as in camps? Forty-eight percent wanted the government to fine or imprison anyone who merely questioned the efficacy of vaccines.

Its not just livelihoods. How many families were torn apart by the governments nonsensical tyranny? Many of us had holidays canceled, gatherings unattended, and relatives who just outright stopped talking to us because we werent vaccinated.

They bought into the narrative that was pushed on us from every direction. No vaccine, no life.

What about going to nursing homes or hospitals to see our loved ones in their most vulnerable moments when they most needed the warmth and comfort of friends and family gathered around? Even when we said, Fine, Ill get tested if I need to. Nope. Not good enough.

Were there vaccine requirements in place when George Floyd died, and the entire country was allowed to go on an anti-racist blood-letting, parading in the streets and burning down cities?

No? Oh, right, that was when over 1,000 medical health professionals signed a letter saying that the protests were more important than any worries related to COVID.

What about when all those young professionals celebrated in front of the White House gates when Joe Biden was declared the winner of the presidential race, attacking an effigy of then-President Donald Trump?

Well, of course, you cant let COVID get in the way of thatTrump posed the greatest threat to this country since the Cuban Missile Crisis. Remember all those mean tweets!

This is nothing new to most of us here. Anyone who could see beyond the faade of the established science knew that the media and government, as well as the medical and pharmaceutical industries, were propagating falsehoods and exaggerations to cow us into going along with their agenda.

The COVID response is a social trauma that will likely take at least a generation to recover from. As we learn morenot only about the vaccines ineffectiveness in stopping the virus, but the potentially harmful side-effects accompanying itthe wound will only grow deeper.

This all says nothing of the largely pointless lockdowns, the repercussions of which have yet to be fully understood. Skyrocketing drug use and overdose, stunted mental development for children and impaired learning, increased depression, and missed doctor appointments. All of these considerations were buried under the government demand to trust the science.

Still, many of these considerations were out of our control. Whether or not we got the vaccine was one of the few areas where we had an actual choice. In the United States, at least, they still did everything they could to make that choice as difficult as possible.

Sure, youre free not to get the vaccinebut youre a bad person, and we will do everything in our power to ostracize you from society.

So hearing Small (the Pfizer executive) plainly state that they had no scientifically tested basis for claiming that the virus stopped transmission might seem like a victory.

But its only a moral victory.

Im not kidding when I say that I believe reparations are justified. Maybe not in a cash hand-out, but an easy place to start would be the various businesses that were forced to fire employees offering to hire back the unvaccinated with back pay for the income lost. The government should support this.

Then again, those employees might not want to be rehired by the employers who betrayed them. The government should still pay the difference in lost income for those who lost their jobs.

Washington can send endless billions to Ukraine because of democracy. So why not take care of the citizens in our own country? You know, the citizens that it turned its back on.

That is likely too much to expect, at least from this administration. We all know that. Most of the individuals who refused the jab on principle probably dont want Washingtons money anyways. Thats fine.

But there is one other thing that the people of this country undoubtedly deserveeven more than reparations. It is something that they will almost definitely never get.

How about an apology?

Views expressed in this article are the opinions of the author and do not necessarily reflect the views of The Epoch Times.

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Dominick Sansone is a PhD student at the Hillsdale College Van Andel Graduate School of Statesmanship. He is a regular contributor to The Epoch Times, and has additionally been published at The American Conservative, The Federalist, and the Washington Examiner.

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The Unvaccinated Deserve Reparations - The Epoch Times

Jeanne Smith of Ferndale, Michigan, was diagnosed with invasive ductal carcinoma, the most common form of breast cancer, in May 2014 at the age of 44.

The cancer was caught very early, and after a lumpectomy and six weeks of radiation, I was on my way, she says.

For the next three years, Smith had follow-up appointments every six months to ensure she remained cancer-free. By February 2017, she was cleared to drop down to yearly follow-ups. But in July 2017, while swimming in her sisters pool, Smith noticed a small purple bruise on her right breast, the same side where she had cancer.

She figured she had bumped it when she jumped onto a pool float. A month later, however, at her annual gynecology appointment, the bruise was still there, so she pointed it out to her doctor. He said bruises were not uncommon on previously radiated breasts but that if it was still there in two weeks to call him.

Two weeks later, the bruise seemed to be growing, which was odd. Bruises shouldnt grow. It was also odd that the bruise was painless, Smith says.

Her gynecologist referred her back to her breast specialist, but the breast specialist commented that shed never seen anything like that and referred her back to her radiation oncologist. Smith wasnt able to see the oncologist right away, so the nurse took a picture of the bruise and sent it to the doctor.

That night, my radiation oncologist called me and said, I need to get you in here. I think you have angiosarcoma, she recalls.

Smith had secondary breast angiosarcoma, also called radiation-induced breast angiosarcoma. This type of cancer develops in people who have previously been treated for breast cancer. Most often, it happens in women who have had radiation to the breast. But it can also arise in women whove had long-term lymphedema (swelling) in the breast or arm.

Breast angiosarcoma starts in the blood or lymphatic vessels of the breast, and the first signs can appear on the skin of the breast or the arms. It can grow and sometimes spread quickly to other parts of the body.

Smith didnt know what angiosarcoma was, and its no wonder. Its extremely rare. Far fewer than 1% 0.05% to 0.3% of breast cancer survivors who have breast-conserving surgery followed by radiation later develop secondary breast angiosarcoma, according to study findings published in the journal Clinical Sarcoma Research in 2017.

Smith didnt recall learning about the risk for secondary cancers before she started radiation, but even if she had, it wouldnt have changed her care.

The benefits of radiation far outweigh the risk of ever getting angiosarcoma, she says.

Angelia Carpenter of New London, Missouri, developed angiosarcoma of the breast five years after completing treatment for breast cancer, which included a lumpectomy, chemotherapy and radiation. Only then did she go back and look at some of the patient information she received prior to starting radiation.

At the bottom of the page, it says that less than 1% of patients that receive radiation may have some of these other problems, Carpenter recalls.

When doctors dont go into great detail about the extremely low risk of angiosarcoma after breast radiation, its not necessarily an oversight. They may underemphasize this risk by design. Like any medical decision, the benefits must be weighed against the risks and in most situations, the reduction in the risk of recurrence or death due to breast cancer by far outweighs the risk of developing or dying of angiosarcoma. However, this points out the need to provide these numbers as best estimates of the patients specific situation.

We can educate as long as we dont alarm people, says Dr. David Euhus, a breast surgeon and professor of surgery at Johns Hopkins Medicine in Baltimore. Angiosarcoma is a terrible thing, but if anyone ever decided not to have radiation because they didnt want to get angiosarcoma, then we would have done them a huge disservice.

When women do learn about this risk, they typically hear about it from their radiation oncologist before undergoing treatment.

At our institution and I would imagine at other tertiary care centers patients are informed of the risk of developing a secondary angiosarcoma post-radiation, typically showing up six to 10 years after theyve had radiation, but we emphasize that the risk is less than 1%, explains Dr. Yara Abdou, a breast medical oncologist at UNC Lineberger Comprehensive Cancer Center in Chapel Hill, North Carolina.

Because secondary breast angiosarcoma is so rare, its a challenge to study large groups of women who have had this cancer and identify any potential risk factors they may have in common. As a result, there is limited research in this area.

The typical patient who will get this is someone whos had breast-conserving therapy, which includes lumpectomy followed by radiation, for their generally early-stage breast cancer. Many years after thats completed, a small subset of these people will develop secondary angiosarcoma, advises Dr. Michael Wagner, a medical oncologist who treats sarcomas at Fred Hutchinson Cancer Center in Seattle and assistant professor at the University of Washington School of Medicine.

Besides radiation exposure, chronic lymphedema after breast cancer treatment is also a risk factor. Outside these known risks, there isnt a consensus on other risk factors.

A study published in the Annals of Surgical Oncology in 2021 of nearly 600 women who had secondary breast angiosarcoma found that the following factors may also put patients at higher risk:

White race.

Older age.

Having had an invasive tumor.

Lymph node removal (a cause of lymphedema).

Having had a lumpectomy.

Having had a tumor in the left breast.

Identifying the risk factors for this late complication is one of the main challenges, notes Dr. Suzanne George, a medical oncologist and director of clinical research at the Dana-Farber Cancer Institute Sarcoma Center and associate professor of medicine at Harvard Medical School in Boston. What puts someone at risk, and is there anything we can do to modify those risk factors early on? Thats a super important question.

Although risk for this secondary cancer is extremely low, its important to know the signs to catch it early, especially because angiosarcoma of the breast can spread quickly.

As with many cancers, management when its (diagnosed) early likely improves longer-term outcomes, George says.

The most common signs of secondary breast angiosarcoma are:

Swelling in the breast or arm.

A painful lump in the breast.

A discoloration on the skin of the breast or arm that looks like a bruise or rash.

Women can get bruises on their breasts, Euhus mentions. Thats far more common than angiosarcoma. But a bruise should start to fade in a couple of days. A bruise thats not fading needs a skin punch biopsy a two-minute procedure in the office.

Women can also develop other types of radiation-related discolorations on their breasts that arent cancerous.

They can get little vascular lesions, but theyre not growing, which can be confused with angiosarcoma, Wagner notes. Or an angiosarcoma can be confused with just an abnormal growth of blood vessels. Thats why its very important that a pathologist trained and experienced in sarcoma review the biopsy sample.

A skin biopsy is the key tool in diagnosis of secondary breast angiosarcoma and is ideally done in the context of an evaluation by a dermatologist. Diagnosis might also involve a mammogram, breast MRI, PET scan or ultrasound.

Another challenge of extremely rare cancers is identifying the most effective treatment. Theres no standard, go-to treatment for secondary breast angiosarcoma, so doctor recommendations may vary by hospital.

Since its a very rare tumor, theres a limited number of published studies, so treatment guidelines are based on expert opinion rather than published data, Abdou mentions. We usually extrapolate data or experience from other soft tissue sarcomas.

Surgery, however, is the key component of treatment. Surgical options include complete mastectomy of the radiated breast or removal of only the affected, discolored area, much like removal of a cancerous mole.

We think of it as a malignancy of the skin, George advises. It can extend deeper into the breast tissue itself, but we think of it as originating in the skin.

Research has begun to show that the more radical surgery option gets far better results. A 2017 study in Annals of Surgery looked at the percentage of women who had not died from breast angiosarcoma (that is, disease-specific survival) within five years of either radical or conservative surgery. The five-year disease-specific survival rate among women whod had the most aggressive surgery was 86% compared with 46% of women whod had the more conservative surgery.

Surgery is the mainstay of treatment for secondary breast angiosarcoma. Whether doctors recommend additional adjuvant chemotherapy or radiation treatments varies from one health care facility to the next. When they do recommend it, doctors tend to use a taxane-based chemotherapy regimen. But it may not be beneficial for everyone.

The vast majority (of patients) are not terribly chemotherapy sensitive, but there is a small subset of patients who are exquisitely sensitive to Taxol (paclitaxel), the common chemotherapy drug we use in the breasts, Euhus notes.

In some cases, though it may seem counterintuitive, people get radiation for this type of cancer, too.

Its the tissue damage and inflammation (from previous radiation) thats causing the breast angiosarcoma in the first place, but the radiation therapy post surgery is cleaning up whatever cancer cells may be left in the breast, Abdou says.

Smith had surgery to remove the radiated breast and chemotherapy to treat the breast angiosarcoma. She has been cancer-free since she completed treatment in 2018.

Carpenter had surgery in 2016, and nine months later, that familiar purple bruise reappeared near her mastectomy scar.

Recurrence rates for this type of cancer are high around 50% according to some estimates. Carpenter, now 62, has learned to live with that risk.

Some tell me my risk for another recurrence goes down as I get older, but others say its not if but when, she notes. Ive learned I also have to live my life. Im just diligent about it. If anything comes up around my scar, we watch it.

After her recurrence, Carpenter had another surgery, which she describes as having left a hole in her chest, to remove as much tissue as possible from the radiated side of her chest and additional tissue from under her arm. After surgery, she underwent chemotherapy.

When we get a localized recurrence, if its possible to do another surgery, we would treat it in the same way with surgery and chemotherapy, Wagner advises. If a repeat surgery isnt possible, we would use systemic medicines, such as chemotherapy or targeted drugs.

Recurrences can be harder to get under control than first occurrences. Research is underway to identify other medications that may be more effective than the current options. The Alliance for Clinical Trials in Oncology has an ongoing trial examining the efficacy of immunotherapy in the treatment of angiosarcomas.

Trial participants who have never been treated with taxane-based chemotherapy will receive Taxol with or without Opdivo (nivolumab). Those who have already had taxane will receive Opdivo and Cabometyx (cabozantinib).

Opdivo, already in use in numerous metastatic cancers, is whats known as a checkpoint inhibitor, the most common class of immunotherapy used in cancer. It blocks proteins on the surface of cancer cells that protect them from an immune system attack. Cabometyx, also used in the treatment of several other metastatic cancers, is whats known as a kinase inhibitor and targets certain gene mutations in cancer cells that help the cancer grow and spread.

Novel approaches to immunotherapy, targeted therapy and combinations with standard chemotherapy are all areas of current research interest, George says. This disease can be very challenging when it recurs, so we need to continue to work toward improving systemic therapies through ongoing international trials and collaboration across the community of patients and physicians. Thats whats going to help us improve outcomes.

For more news on cancer updates, research and education, dont forget tosubscribe to CUREs newsletters here.

To learn more about Angelia Carpenter's experience with secondary angiosarcoma after undergoing breast cancer treatment and what it was like to be left with a hole in her chest, listen to this episode of the "Cancer Horizons" podcast.

Read the rest here:
New Approaches Have Emerged that May Better Treat Secondary Breast Cancer Years After an Initial Diagnosis - Curetoday.com

Diagnosis

Many infertile couples have more than one cause of infertility, so it's likely you will both need to see a doctor. It might take a number of tests to determine the cause of infertility. In some cases, a cause is never identified.

Infertility tests can be expensive and might not be covered by insurance find out what your medical plan covers ahead of time.

Diagnosing male infertility problems usually involves:

Your semen is then sent to a laboratory to measure the number of sperm present and look for any abnormalities in the shape (morphology) and movement (motility) of the sperm. The lab will also check your semen for signs of problems such as infections.

Often sperm counts fluctuate significantly from one specimen to the next. In most cases, several semen analysis tests are done over a period of time to ensure accurate results. If your sperm analysis is normal, your doctor will likely recommend thorough testing of your female partner before conducting any more male infertility tests.

Your doctor might recommend additional tests to help identify the cause of your infertility. These can include:

Often, an exact cause of infertility can't be found. Even if an exact cause isn't clear, your doctor might be able to recommend treatments or procedures that will lead to conception.

In cases of infertility, it's recommended that the female partner also be checked. There may be specific treatments recommended for your partner. Or, you may learn that proceeding with assisted reproductive techniques is appropriate in your situation.

Treatments for male infertility include:

In rare cases, male fertility problems can't be treated, and it's impossible for a man to father a child. Your doctor might suggest that you and your partner consider using sperm from a donor or adopting a child.

Our caring team of Mayo Clinic experts can help you with your health concerns. Visit Mayo Clinic Men's Health to get started.

There are a few steps you can take at home to increase your chances of achieving pregnancy:

Evidence is limited on whether or how much herbs or supplements might help increase male fertility. None of these supplements treats a specific underlying cause of infertility, such as a sperm duct defect or chromosomal disorder.

Supplements with studies showing possible benefits for improving sperm count or quality include:

Talk with your doctor before taking dietary supplements for male infertility. There is no clear evidence that they work, and some supplements may cause side effects or interact adversely with medications you take.

Coping with infertility can be difficult. It's an issue of the unknown you can't predict how long it will last or what the outcome will be. Infertility isn't necessarily solved with hard work. The emotional burden on a couple is considerable, and plans for coping can help.

If you have never been evaluated by a doctor, you might begin by seeing your family doctor. If, however, you have a known condition resulting in infertility or have any abnormalities on your testing by your primary care doctor, then you may be referred to a specialist.

Here's some information to help you get ready for your appointment, and what to expect from your doctor.

Examples of questions to ask include:

Don't hesitate to ask additional questions at any time during your appointment.

Be ready to answer questions your doctor is likely to ask, including:

Our caring team of Mayo Clinic experts can help you with your health concerns. Visit Mayo Clinic Men's Health to get started.

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Male infertility - Diagnosis and treatment - Mayo Clinic

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Sexual male enhancement, as the euphemism goes, is big business. Last year, Viagra, the pharmaceutical market leader, raked in about $2 billion.

That success has spawned a shadow industry of largely unregulated "natural male enhancement," or sex pill, products. But according to the FDA, some of these products aren't natural, aren't tested and some might even be dangerous.

Here's a list of 10 sex pill products the FDA issued health warnings about this year or told manufacturers to get them off the shelves.

The issue, says the agency, is the product uses "sulfoaildenafil, a chemical similar to sildenafil, the active ingredient in Viagra."

Like Viagra, sulfoaildenafil can have dangerous interactions with other prescription drugs such as nitrates, and can cause dangerously low blood pressure. But because consumers think they are taking a "natural" product they are usually not under a doctor's care.

Also, sulfoaildenafil has not undergone the same clinical trials as sildenafil, so all its effects are not known.

FDA Warning

It's not clear if "Stiff Nights" is a "dietary supplement" as its maker claims, or a bad b-movie title, but in either case the FDA says men looking to "regain the thunder" should stay clear because the pill really contains sulfoaildenafil, an untested chemical similar to the active ingredient in Viagra, which can interact badly with nitrates and cause low blood pressure.

FDA Warning.

The marketing geniuses behind "Stiff Nights" also sell "Rock Hard Weekend." Same unregulated chemical, says the FDA, different laugh out loud brand.

FDA Warning.

It's not clear who Don Wands is or how he became so magical, but the FDA didn't seem to care.

In August 2010, they told the manufacturer of this supplement to drop the magic act and take it off the shelves because the product's two main ingredients, hydroxyhomosildenafil and sulfoaildenafil, aren't listed on the box, aren't "supplements" and aren't really tested.

FDA Warning.

Magic Power Coffee's website says the extra mojo comes from honey goat weed and goji berries.

FDA Warning.

If you wind up with Duro Extend in your stocking this year, you might want to send it back to Santa.

The FDA recalled the product in early December 2010 because the "dietary supplement" is secretly supplemented with sulfoaidenafil, a drug similar to Viagra, but not tested.

FDA Warning.

"This product is dangerous to consumers because it claims to contain only natural ingredients when it actually contains a prescription drug ingredient," says the FDA's warning letter.

Dangerous interactions with nitrates and low blood pressure are possible.

FDA Warning.

FDA Warning.

The FDA doesn't recommend hitting up Luong for pills, however. They say Vitalex's "all natural" and "herbal" concoction is really acetildenafil, another chemical similar to the drug in Viagra, but not tested.

FDA Warning.

Eager men trying to get their hands on a box of Xiadafil VIP, might have to wait in line. In July 2010, U.S. Marshals seized almost $75,000 worth of it after the manufacturer refused an FDA request to recall it.

The problem? The FDA says the product's VIP power comes from hydroxyhomosildenafil, a drug similar to Viagra, but untested.

FDA Warning.

Read more:
Dangerous Male Sex Pills - CBS News

Male honey bee

A drone is a male honey bee. Unlike the female worker bee, drones do not have stingers. They gather neither nectar nor pollen and are unable to feed without assistance from worker bees. A drone's only role is to mate with an unfertilized queen.

Drones carry only one type of allele at each chromosomal position, because they are haploid (containing only one set of chromosomes from the mother). During the development of eggs within a queen, a diploid cell with 32 chromosomes divides to generate haploid cells called gametes with 16 chromosomes. The result is a haploid egg, with chromosomes having a new combination of alleles at the various loci. This process is called arrhenotokous parthenogenesis or simply arrhenotoky.

Because the male bee technically has only a mother, and no father, its genealogical tree is unusual. The first generation has one member (the male). One generation back also has one member (the mother). Two generations back are two members (the mother and father of the mother). Three generations back are three members. Four back are five members. This sequence 1, 1, 2, 3, 5, 8, and so on is known as the Fibonacci sequence.[1]

Much debate and controversy exists in scientific literature about the dynamics and apparent benefit of the combined forms of reproduction in honey bees and other social insects, known as the haplodiploid sex-determination system. The drones have two reproductive functions: each drone grows from the queen's unfertilized haploid egg and produces some 10 million male sperm cells, each genetically identical to the egg. Drones also serve as a vehicle to mate with a new queen to fertilize her eggs. Female worker bees develop from fertilized eggs and are diploid in origin, which means that the sperm from a father provides a second set of 16 chromosomes for a total of 32: one set from each parent. Since all the sperm cells produced by a particular drone are genetically identical, full sisters are more closely related than full sisters of other animals where the sperm is not genetically identical.

A laying worker bee exclusively produces totally unfertilized eggs, which develop into drones. As an exception to this rule, laying worker bees in some subspecies of honey bees may also produce diploid (and therefore female) fertile offspring in a process called thelytoky, in which the second set of chromosomes comes not from sperm, but from one of the three polar bodies during anaphase II of meiosis.

In honey bees, the genetics of offspring can best be controlled by artificially inseminating (referred to in beekeeping as 'instrumental insemination') a queen with drones collected from a single hive, where the drones' mother is known. In the natural mating process, a queen mates with multiple drones,[2] which may not come from the same hive. Therefore, batches of female offspring have fathers of a completely different genetic origin.

A drone is characterized by eyes that are twice the size of those of worker bees and queens, and a body size greater than that of worker bees, though usually smaller than the queen bee. His abdomen is stouter than the abdomen of workers or queen. Although heavy bodied, the drone must be able to fly fast enough to accompany the queen in flight. The average flight time for a drone is about 20 minutes.

An Apis cerana colony has about 200 drones during high summer peak time.Drones depend on worker bees to feed them.

Drones die off or are ejected from the hive by the worker bees in late autumn, dying from exposure and the inability to protect or feed themselves, and do not reappear in the bee hive until late spring. The worker bees evict them as the drones would deplete the hive's resources too quickly if they were allowed to stay.[3]

The drones' main function is to be ready to fertilize a receptive queen. Drones in a hive do not usually mate with a virgin queen of the same hive because the queen flies further to a drone congregation area than the drones do. Mating generally takes place in or near drone congregation areas. How these areas are selected is not understood, but they do exist. When a drone mates with a queen of the same hive, the resultant queen will have a spotty brood pattern (numerous empty cells on a brood frame) due to the removal of diploid drone larvae by nurse bees (i.e., a fertilized egg with two identical sex genes will develop into a drone instead of a worker). The worker bees remove the inbred brood and consume it to recycle the protein.

Mating occurs in flight, which accounts for drones needing better vision, which is provided by their large eyes. Should a drone succeed in mating, the first thing that happens is all of the drone's blood in his body rushes to his endophallus which causes him to lose control over his entire body. His body falls away, leaving a portion of his endophallus attached to the queen which helps guide the next drone in the queen.

Honey bee queen breeders may breed drones to be used for instrumental insemination[4] or open mating. A queen mating yard must have many drones to be successful.

In areas with severe winters, all drones are driven out of the hive in the autumn. A colony begins to rear drones in spring and drone population reaches its peak coinciding with the swarm season in late spring and early summer. The life expectancy of a drone is about 90 days.

Although the drone is highly specialized to perform one function, mating and continuing the propagation of the hive, they may have other purposes. All bees, when they sense the hive's temperature deviating from proper limits, either generate heat by shivering, or exhaust heat by moving air with their wingsbehaviours which drones share with worker bees.

Drones do not exhibit typical worker bee behaviors such as nectar and pollen gathering, nursing, or hive construction. While drones are unable to sting, if picked up, they may swing their tails in an attempt to frighten the disturber.[5] In some species, drones buzz around intruders in an attempt to disorient them if the nest is disturbed.

Drones fly in abundance in the early afternoon and are known to congregate in drone congregation areas a good distance away from the hive.

The everted endophallus, with the cornua in focus, resembling hooks.

The extended bulbus of the endophallus, containing sperm, is in focus.

The drone endophallus is designed to disperse a large quantity of seminal fluid and spermatozoa with great speed and force. The endophallus is held internally in the drone. During mating, the organ is everted (turned inside out), into the queen. The eversion of the endophallus is achieved by contracting abdominal muscles, which increases hemolymph pressure, effectively "inflating" the endophallus. Cornua claspers at the base of the endophallus help to grip the queen.

Mating between a single drone and the queen lasts less than 5 seconds, and it is often completed within 12 seconds. Mating occurs mid-flight, and 1040m (33131ft) above ground. Since the queen mates with 519 drones, and drones die after mating, each drone must make the most of his single shot. The drone makes first contact from above the queen, his thorax above her abdomen, straddling her. He then grasps her with all six legs, and everts the endophallus into her opened sting chamber. If the queen's sting chamber is not fully opened, mating is unsuccessful, so some males that mount the queen do not transfer semen. Once the endophallus has been everted, the drone is paralyzed, flipping backwards as he ejaculates. The process of ejaculation is explosivesemen is blasted through the queen's sting chamber and into the oviduct. The process is sometimes audible to the human ear, akin to a "popping" sound. The ejaculation is so powerful that it ruptures the endophallus, disconnecting the drone from the queen. The bulb of the endophallus is broken off inside of the queen during matingso drones mate only once, and die shortly after. The leftover endophallus remaining in the queen's vagina is referred to as the "mating sign". The plug will not prevent the next drone from mating with the same queen, but may prevent semen from flowing out of the vagina.[6]

Mating between the drones and a virgin queen takes place away from the colony, in mid-air mating sites. These mating sites, called 'congregation areas', are specific locations, where drones wait for the arrival of virgin queens. A congregation area is typically 1040m (33131ft) above ground, and can have a diameter of 30200m (98656ft). The boundaries of a congregation area are distinct; queens flying a few meters outside the boundaries are mostly ignored by the drones. Congregation areas are typically used year after year, with some spots showing little change over 12 years. Since drones are expelled from a colony during the winter, and new drones are raised each spring, inexperienced drones must find these congregation areas anew. This suggests some environmental cues define a congregation area, although the actual cues are unknown.

Congregation areas are typically located above open ground, away from trees or hills, where flight is somewhat protected from the wind (calm winds may be helpful during mating flight). At the same time, many congregation areas do not show such characteristics, such as those located above water or the forest canopy. Some studies have suggested that magnetic orientation could play a role, since drones older than 6 days contain cells in the abdomen that are rich in magnetite.

Congregation areas can be located by attaching a virgin queen (in a cage) to a balloon floating above ground. The person then moves around, taking note of where drones are attracted to the caged queen. Congregation areas are not found closer than 90m (300ft) from an apiary, and congregation areas located farther away from apiaries receive more drones. In a congregation area, drones accumulate from as many as 200 colonies, with estimates of up to 25,000 individual drones. This broad mixing of drones is how a virgin queen can ensure she will receive the genetic diversity needed for her colony. By flying to congregation areas further away from her colony, she further increases the probability of out-breeding.

A single drone visits multiple congregation areas during his lifetime, often taking multiple trips per afternoon. A drone's mating flight averages 2025 minutes, before he must return to the colony to refuel with honey. While at the site, the drones fly around passively, waiting for the arrival of a virgin. When the virgin queen arrives to the congregation area, the drones locate her by visual and olfactory cues. At this point, it is a race to mate with the virgin queen, to be genetically represented in the newly founded colony. The swarming drones, as they actively follow the queen, reportedly resemble a "drone comet", dissolving and reforming as the drones chase the virgin queen. Drones greatly outnumber the quantity of virgin queens produced per season, so even with multiple mating by the queen, very few drones mate successfully (estimated at less than one in 1,000). If needed, a virgin queen can embark on multiple 'nuptial flights', to be sure to receive enough semen from enough drones.

Varroa destructor, a parasitic mite, propagates within the brood cell of bees. The Varroa mite prefers drone brood as it guarantees a longer development period, which is important for its own propagation success. The number of Varroa mites can be kept in check by removing the capped drone brood and either freezing the brood comb or heating it.

Read more here:
Drone (bee) - Wikipedia

Jamie Lo, M.D., M.C.R.,associate professor of obstetrics and gynecology (perinatology and maternal-fetal medicine), OHSU School of Medicine, and Division of Reproductive & Developmental Sciences, Oregon National Primate Research Center at OHSU. (OHSU/Christine Torres Hicks)

A physician-scientist at Oregon Health & Science University is one of just six researchers across the country to receive an Avenir Award in Genetics and Epigenetics of Substance Abuse from the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health.

Jamie Lo, M.D., M.C.R., will use the award to develop and execute creative and transformative research to explore how parents behavior and environment affects their offspring before birth in some cases, even before conception.

The award is expected to provide $1.5 million over five years. NIDAs DP1 Avenir Awards support early-career investigators proposing new areas of research for the genetics or epigenetics of addiction.

Lo is an associate professor of obstetrics and gynecology (maternal-fetal medicine) in the OHSU School of Medicine and the Division of Reproductive and Developmental Sciences at the Oregon National Primate Research Center (ONPRC) at OHSU.

Being a scientist at ONPRC has allowed for leading-edge scientific pursuits across scientific and clinical disciplines with researchers at OHSU and at other institutions, and has allowed me to leverage the translational strength of nonhuman primate models that drive scientific discovery, she said. Im grateful and really looking forward to new discoveries we can achieve next.

In her clinical practice, Lo focuses on caring for people with high-risk pregnancies. She frequently encounters patients asking about the safety of cannabis use and other substances while theyre trying to conceive, while pregnant and during breastfeeding..

Most recently, Lo published two widely publicized studies suggesting that chronic use of cannabis may greatly affect male fertilityand reproductive outcomes, and female reproductive health, including increased menstrual cycle length. The male fertility study, in nonhuman primates, used edible cannabis similar to human dosages and found significant decreases in male reproductive hormones, including testosterone, and greater than 50% shrinkage of the testicles.

In earning the elite Avenir Award, Lo credits the support shes received from her clinical and academic departments, along with collaborations forged with other scientists at OHSU, including those in the departments of urology and biomedical engineering, and researchers at other top academic institutions.

Lo plans to use the new funding to delve into how the active ingredient in cannabis, THC, affects the expression of genes in the brains of offspring. The research will set out to determine how a fathers or mothers consumption of cannabis may affect their offspring both in early childhood and later in life or even their childrens offspring.

Were going to look at whether or not those changes that happen to the sperm, egg, fetus or infant are then inherited and how they impact offspring development, she said.

Generally, due to the lack of safety data and the preliminary findings of her work, she advises expectant parents to refrain from cannabis use while pregnant and for those who cannot quit to limit use.

Lo said she feels privileged to be part of ONPRCs team of scientists making discoveries that she can bring back to patients in the clinic.

We do know that cannabis use seems likely to impact reproductive health and fertility in both males and females, and that prenatal cannabis exposure can adversely affect the placenta and fetus, Lo said. But its very hard to study cannabis in humans, especially in pregnancy, because people are often using other substances, affected by their socioeconomic conditions, limited by the inaccuracies of self-reporting, and the quantity and dose of THC used is often difficult to determine.

Using a nonhuman primate model, scientists can control background variables, including diet and exercise, that would not be possible to achieve in people. The award number is 1DP1DA056493-01, through the National Institute on Drug Abuse of the NIH.

OHSU IACUC

All research involving animal subjects at OHSU must be reviewed and approved by the universitysInstitutional Animal Care and Use Committee(IACUC). The IACUCs priority is to ensure the health and safety of animal research subjects. The IACUC also reviews procedures to ensure the health and safety of the people who work with the animals. The IACUC conducts a rigorous review of all animal research proposals to ensure they demonstrate scientific value and justify the use of live animals.

Excerpt from:
Prestigious award advances OHSU research on impact of drug use over generations - OHSU News

While looking towards the excitement of candy and costumes this Halloween, October is also a time to pull out the pink for Breast Cancer Awareness Month. While women who are 40 years old have the option to begin an annual breast cancer screening with mammograms, familiarizing oneself with their lemonsregardless of agecan assist with early detection if breast cancer occurs.

Breast cancer is fairly common. About 1 in 8 women are going to be diagnosed with breast cancer at some point in their lives, said Marianne Vivien, a genetic counselor at Overlake Clinics & Medical Center.

According to Vivien about 5-10% of cancer cases are due to genetic mutations or hereditary conditions, while over 90% of cancer cases are random, sporadic, and are usually due to age, and environmental and lifestyle factors.

We all have cancer genes and their job is to protect us from cancer generally, but if someone is born with a mutation or inherits that mutation from a parent, all that really means is theres a change in the DNA, said Vivien.

The change in the DNA causes the gene to no longer function properly, and when this happens to a cancer gene, tumors develop more easily and at earlier ages. BRCA 1 and BRCA 2 are the most common breast cancer genes that are also associated with ovarian cancer, pancreatic cancer, melanoma and prostate cancer, said Vivien.

The general population risk for female breast cancer over a lifetime is 12%, according to Vivien, which increases to greater than 60% with BRCA mutations.

Male breast cancer is pretty rare in the general population. I believe its roughly a half a percent chance over a lifetime for someone who was born male to develop breast cancer, said Vivien, who said that risk increases to about 7% over a lifetime with BRCA mutations.

Vivien expressed that if an individual has any breast tissue, regardless of gender, its important to screen for breast cancer.

We definitely have that conversation with our patients who are Trans[gender], said Vivien. Depending on what surgeries they may or may not have had already, we would discuss essentially what screening or management would be recommended based on the particular gene that were concerned with and what other cancers are associated with that gene.

A breakdown of breast cancer rates on the Eastside

The Washington State Cancer Registry collects incidence data for numerous types of cancer across the state, including female breast cancer. Incidence rates are per 100,000 and the registry data for female breast cancer from 2014-2018 include:

Further data from the National Cancer Institutes state cancer profiles shows that the age-adjusted incidence rate cases per 100,000 for females in King County who are under 50 years old is 50.7; the average annual count is 372 cases and that the recent trends of rates for this demographic are rising.

The lens of a genetic counselor

Part of Viviens work as a genetic counselor includes talking to patients who have received a cancer diagnosis from their primary care physician, or those who received a referral to see if genetic testing would be beneficial.

Im starting to see a lot younger peoplewomen in their twentiescoming in and having that conservation, said Vivien. It doesnt necessarily mean were doing testing right now or were starting screening right now, but were having a conversation so that we can determine when testing or when screening should start and what that might look like for them.

In addition to seeing younger women, Vivien has also been seeing patients who want to know their risks because they were adopted and have no information on their family history.

During the counseling sessions, Viven conducts a thorough family history and medical history to decide if genetic testing is appropriate and to assist with developing a personalized management care plan moving forward. Red flags with genetics include individuals diagnosed at 50 years of age or younger and multiple generations having been affected by breast and other types of cancer, said Vivien.

Ideally, if were getting this information ahead of time, or even if somebody is already diagnosed with breast cancer, were able to make better decisions in terms of treatment, surgical decisions and then management moving forward, said Vivien.

Vivien mentioned how genetic testing and breast cancer screenings are generally covered by health insurance if an individual meets specific criteria. If the criteria is not met and health insurance wont cover, the majority of labs offer genetic testing for approximately $250, said Vivien. For those who are uninsured or underinsured, Vivien feels like breast cancer screenings can be moreso a barrier when compared to genetic testing.

Testing can only get you so far. If youre not going to follow through with the management then testing is a little bit pointless, said Vivien.

You can call them lemons, or you can call them limes

While Vivien believes that Breast Cancer Awareness Month shouldnt be merely one month, she said a good way to celebrate the month is by learning how to conduct a self breast exam.

Know Your Lemons, a nonprofit organization focused on improving early detection of breast cancer through education, provides signs and symptoms of breast cancer, which include:

While theres never a bad time to conduct a self breast exam, Know Your Lemons suggests conducting the exam after ones period, which is when the breast is the least tender and swollen.

A self breast exam can be conducted while standing, sitting or lying down. One should flatten their breast by stretching their arm behind their head. Then, the individual should feel the area (using any pattern such as circles, side to side, and up-down/all around) from their armpit to their collarbone, and then to the bottom of their ribs where lymph nodes live. According to Know Your Lemons, sometimes the areas where lymph nodes are located swell when cancer is present.

Milk lobes and lymph nodes are normal lumps in breasts that feel like soft peas or beans. To be more specific, the soft feeling peas are milk lobes while the soft feeling beans are lymph nodes. Cancerous lumps feel hard like a lemon seed, are usually immovable and can be any shape or size. On the other hand, those hard feeling lemon seeds could potentially be cysts.

See the rest here:
Breast Cancer Awareness Month: The importance of getting to know your lemons - Bothell-Kenmore Reporter

Identification of DEGs after weight loss

After standardizing gene sets (Fig.1), 1011 DEGs (|logFC|>1, p<0.05) were screened out from GSE103766, GSE35411, GSE112307, GSE43471, and GSE35710 based on the above method. The results included 513 downregulated and 498 upregulated genes, as shown in the volcano plot (Fig.2 and Supplementary Table S1). The abscissa in the volcano plot is log2 (fold change) value, and the ordinate is log10 (p-value).

Box-plots of the expression profiles after consolidation and standardization. The x-axis label represents the sample symbol and the y-axis label represents gene expression values. The black line in the box-plot represents the median value of gene expression. (a) Standardization of GSE43471, (b) Standardization of GSE35411, (c) Standardization of GSE103766, (d) Standardization of GSE35710, (e) Standardization of GSE112307.

Volcano plot to identify differentially expressed genes (DEGs). (a) GSE43471, (b) GSE35710, (c) GSE35411, (d) GSE103766, (e) GSE112307. The x-axis label represents fold changes and the y-axis label represents the p-values. Red dots represent the 498 upregulated genes and green dots represent the 513 downregulated genes.

As shown in Supplementary Fig. S1, the PPI network of DEGs, based on the Search Tool for the Retrieval of Interacting Genes (STRING) database, includes 584 nodes and 1417 edges. Using the MCODE plugin in Cytoscape software, the most significant modules (score=6.667) were recognized from the PPI network as comprising 27 hub genes, including ACP5, CETP, COL1A1, COL1A2, CSF1, DNMT3B, EED, HIST1H2AI, HIST1H2BB, HIST1H2BD, HIST1H4B, HIST1H4H, HIST2H3C, HP, LCN2, LIPC, LPA, MMP2, MMP7, MMP9, MSR1, MUC1, PLA2G7, SPP1, THBS1, THBS2, and VLDLR (Table 1 and Fig.3).

Subnetwork of 27 hub genes from the proteinprotein interaction (PPI) network. Node size and temperature color reflect the degree of connectivity (bigger node represents a higher degree and smaller node represents a lower degree; red node represents a higher degree and yellow node represents a lower degree).

An enrichment analysis bubble chart was drawn under GO level 2 classifications using Omicshare tools (Fig.4 and Supplementary Table S2). As shown in the figure, hub genes were significantly enriched in regulating plasma lipoprotein particle levels, lipid transport, extracellular matrix (ECM) organization, response to reactive oxygen species, and the oxygen-containing compound for biological process (BP). The hub genes were significantly enriched for cell composition (CC) in lipoprotein particles, extracellular regions, ECM, extracellular exosomes, and secretory granules. For molecular function (MF), the hub genes were significantly elevated in lipoprotein particle binding, glycosaminoglycan binding, ECM structural constituents, and peptidase activity.

Biological functions based on Gene Ontology (GO) analysis of obesity-related hub genes. Advanced bubble chart shows significance in GO enrichment items of hub genes in three functional groups: biological process (BP), cell composition (CC), and molecular function (MF). The x-axis label represents the gene ratio (Rich Factor) and the y-axis label represents GO terms.

KEGG pathway enrichment analysis showed that the hub genes were primarily enriched in ECMreceptor interaction, cholesterol metabolism, PI3K-Akt, IL-17, and TNF signaling pathways, endocrine resistance, and leukocyte transendothelial migration (Fig.5 and Supplementary Table S3).

Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of hub genes. The x-axis label represents the gene ratio (Rich factor) and the y-axis label represents the pathway.

We converted 27 gene names of the hub genes into protein names that could be recognized through the TCMSP database using the Universal Protein Resource (Uniprot). Moreover, the hub genes can be input in the required format to identify potential herbs with anti-obesity effects from the TCMSP database. After excluding the genes that were not present in the databases or those that had no related ingredients, nine were screened for further research, namely, COL1A1, MMP2, MMP9, SPP1, DNMT3B, MMP7, CETP, COL1A2, and MUC1. These genes corresponded to 16 ingredients [(-)-epigallocatechin-3-gallate (EGCG), arachidonic acid, arctiin, baicalein, beta-carotene, capillarisin, deoxypodophyllotoxin, ellagic acid, fisetin, irisolidone, luteolin, matrine, nobiletin, quercetin, rutaecarpine, tanshinone IIa] showing adequate OB and DL values (OB30%, DL0.18) (Supplementary Table S4).

There were 254 herbs with active ingredients in the databases. The top 10 herbs were Aloe, Portulacae Herba, Mori Follum, Silybum Marianum, Phyllanthi Fructus, Pollen Typhae, Ginkgo Semen, Leonuri Herba, Eriobotryae Folium, and Litseae Fructus. These were associated with more DEGs (related genes=6) and were, therefore, selected as crucial herbs in our study and annotated using Chinese pharmaceutical properties (CMPs), including characters, tastes, and meridian tropisms (Table 2).

We screened the key ingredients in treating obesity using an Ingredients-Targets network containing 25 nodes and 27 edges (Fig.6). The nine orange nodes represent the target genes and 16 green nodes represent the active ingredients. As most genes could be linked (degree=4), quercetin and EGCG were considered the most critical components in the treatment of obesity.

Ingredients-Targets network. Nine orange nodes represent the target genes, whereas the 16 green nodes represent the active compounds. The edges represent the interaction between the compounds and targets.

As shown in Fig.7a, the Herbs-Ingredients-Targets network containing 24 nodes and 43 edges was constructed to demonstrate the relationship between them: the 10 green nodes represent the key herbs and the six yellow nodes represent the active ingredients in them; the eight blue nodes depict the target genes. By analyzing the network, Phyllanthi Fructus and Portulacae Herba were associated with the most ingredients (degree=4). Moreover, quercetin was the most frequent active ingredient (degree=23) found in all herbs. Regarding gene targets, MMP2 was targeted by most ingredients (degree=5) followed by MMP9 (degree=4). Other genes were only acted upon by one component (degree=1).

Herbs-Ingredients-Targets network (a) and Herbs-Taste-Meridian tropism (b) network. (a) Yellow nodes represent the active ingredients and the blue nodes represent the target genes. (b) Yellow nodes represent tastes and purple nodes represent meridian tropisms. In all networks, the light green nodes represent cold-cool herbs, medium green nodes represent calm herbs, and dark green nodes represent warm herbs.

We also established the Herbs-Taste-Meridian tropism network containing 24 nodes and 40 edges to clarify the distribution of CMPs (Fig.7b). Five yellow nodes represent tastes and eight purple nodes represent meridian tropisms. To indicate different characters, we presented 10 nodes of herbs having different greens (light green, medium green, and dark green). Regarding characters, cold-cool herbs like Mori Follum were the most frequent (nodes=7), followed by herbs having calm (nodes=2) and warm (nodes=1) characters. In terms of taste, herbs were mostly bitter (edges=6), followed by sweet (edges=4), acid (edges=2), symplectic (edges=2), and astringent (edges=2). Regarding meridian tropism, most herbs belonged to the liver meridian (edges=6), followed by the stomach and lung (edges=4), large intestine (edges=2), bladder (edges=2), kidney (edges=2), pericardium (edges=2), spleen (edges=1), and gallbladder (edges=1) meridians.

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Identification of hub genes and candidate herbal treatment in obesity through integrated bioinformatic analysis and reverse network pharmacology |...

The Neanderthals have won a Nobel prize. Well, almost. Even if most people havent heard of Svante Pbo, the Swedish geneticist whose work on ancient genomes and human evolution has landed him with 2022s award for physiology or medicine, or the exact science behind palaeogenomics and ancient DNA, they certainly have heard of Neanderthals.

Honouring his contribution to building this incredibly vibrant field of palaeogenomics, the award is much deserved: you need vision, persistence and pioneering methods to recover and sequence immensely old, fragile genetic material. But its also a recognition of the astonishing revelations about our deep history that have come from palaeogenomics, which holds many untapped secrets about who we are today, including settling the long-debated question of whether Neanderthals and Homo sapiens ever encountered each other and, lets say, warmed up those icy tundra nights (the answer is yes, many times).

For research communities, the prize also feels like a recognition of the relevance of work on palaeogenomics, human origin and archaeology more broadly and its continuing importance. Research in the 21st century on our hominin relations, including Neanderthals, is an entirely interdisciplinary, collaborative endeavour. All kinds of material analyses take place, in all sorts of ways. We use photogrammetry or lasers to record entire caves in 3D; trace how stone tools were moved across the land; examine microlayers within ancient hearths; even pick out the starches preserved in grot between ancient teeth. And the advent of the ability to retrieve palaeogenomics from extraordinarily old contexts was nothing short of revolutionary. Today, DNA can be extracted not only from bones, but even from cave sediments: the dust of long vanished lives, waiting for millennia to be found. It has made it possible to assess individual Neanderthals genetic profiles, and has opened windows into previously invisible population histories and interactions.

More than a decade on from the first big findings, today there is a huge community of palaeogenomics researchers, in large part thanks to Pbo, with many having trained with him. Among the younger generations at the front end of the sampling, processing and analytical work who may be the first to make and recognise key new discoveries many are women. They include Mateja Hajdinjak of the Crick Institute whose work has identified complex patterns of interbreeding among Neanderthals and the earliest Homo sapiens in Europe, and Samantha Brown from the University of Tbingen, whose meticulous work on unidentifiable bone scraps found the only known first-generation hybrid, a girl whose mother was Neanderthal and father Denisovan (closely related hominins from eastern Eurasia). Alongside wielding scientific clout, they are overturning outdated ideas that the hard sciences of statistics and white coats (or, in palaeogenomics, full-body protection) are male domains.

As an incredibly fast-moving field, palaeogenomics has achieved an enormous amount in a relatively short space of time. Innovative approaches are constantly being developed, and it must be admitted, even for those of us working in human origins, that keeping up with new methods and jargon can be challenging. The rapidity of advances, especially in competitive academic contexts, has also led to a number of ethical issues. While many are being tackled, the direction of some research may soon force the field to lay out official standards and draw ethical red lines when, for example, reconstructing the brains of Neanderthals using genetic engineering.

Ultimately, while decoding ancient hominin genomes has allowed us to identify which inherited genes we have today hence the physiology or medicine element of the Nobel prize the recognition of Pbos work seems more about much deeper themes, resonating with something of a Neanderthal zeitgeist. Since the discovery of their fossils more than 165 years ago, science has been engaged in dethroning Homo sapiens, demoting us from special creations to something still marvellous but not entirely unique.

Palaeogenomics bolstered this vision of an Earth that hosted many sorts of human, at least five of which were still walking around just 40,000 years ago; translate that figure to a generational scale, and youd see a chain of just 2,000 people linking hands. Ancient DNA has confirmed that we are both embedded within a rich history of hominin diversity, and that we still embody that history ourselves. Alongside the genetic material we acquired sideways through interbreeding with Neanderthals and other species, a recent study found that less than 10% of our genome is distinctive to Homo sapiens, evolved uniquely in us.

Most strikingly, popular understanding has shifted too. While some still drag out Neanderthal as a slur, it now seems somewhat abstracted from general public views. The archaeological evidence for Neanderthals complex, sophisticated minds, with genetic revelations of how close we really are to them, has transformed opinion on who they were, and what that means for us. The knowledge that the very stuff of Neanderthals is still present today in each human heart, thumping with fear or joy has forged a new emotional connection not just to them, but to all our other hominin relations. It also underlines the fact that they, and we, have always been part of a planetary web of life.

The most profound legacy of Pbos establishment of palaeogenomics is, or should be, humility. Because it turns out that many of the earliest Homo sapiens populations entering Eurasia eventually shared the same fate as the Neanderthals they met and mingled with. Their lineages vanished, culturally but also genetically, leaving behind no descendants among living humans. Perhaps the greatest inheritance they left us is understanding that our story is not one of predestined, exceptional success, but a blend of serendipity and coincidence; and that being the last hominin standing is not necessarily something to be proud of.

Excerpt from:
Behind this Nobel prize is a very human story: theres a bit of Neanderthal in all of us - The Guardian

Zainabu was in good health in the days before she gave birth to her fourth baby, despite the fact that her blood pressure was likely somewhere around 280/220.

For a human, such a reading would be catastrophic. Spiking blood pressure in a pregnant or recently postpartum woman is a sign of preeclampsia, a common but potentially fatal condition that can affect the heart, lungs, liver and kidneys.

Zainabu, fortunately, is a Masai giraffe at the Los Angeles Zoo. Giraffes have the highest known blood pressure in the animal kingdom, but this has no apparent effect on fetal or maternal health.

Zainabu, a Masai giraffe, with her fourth baby at the Los Angeles Zoo.

(Los Angeles Zoo)

For Dr. Barbara Natterson-Horowitz, a UCLA cardiologist with a long-standing interest in cross-species health, this raises some compelling questions.

What adaptations have evolved in female giraffes that protect their cardiovascular systems from the damage high blood pressure can cause?

And why dont we know enough about the physiology of human females to prevent a common complication like preeclampsia?

Natterson-Horowitzs side gig treating animals at the L.A. Zoo has led her to explore health connections across species. She and collaborator Kathryn Bowers wrote the 2012 bestseller Zoobiquity about the intersection of human medicine, veterinary medicine and evolutionary biology, followed by 2019s Wildhood, which examined adolescence across the animal kingdom.

Her latest focus is on cross-species similarities in female health, a field that has long been underfunded, understudied and misunderstood. Diseases that primarily affect women get a disproportionately small amount of research money relative to the years of healthy life they steal. (The reverse is true for diseases that primarily affect men.) In addition, women have historically been a minority of clinical trial participants, and for several years those of childbearing age were barred as research subjects in the U.S., a policy the National Institutes of Health reversed in 1986.

We cant go back in time, Natterson-Horowitz says. But we can fill some of the gaps by looking to the animal world.

Many of the species that share our planet are exposed to similar stressors and environmental contaminants. Some endure the same chronic diseases that humans do, while others appear to be naturally resistant. Solutions to some of medicines most vexing questions could be walking on four feet beside us.

Theres a pretty vast landscape of unexamined assumptions about human uniqueness, Natterson-Horowitz said. Failing to recognize our place in the animal kingdom, she added, can prevent us from recognizing connections that, were we to see and understand them, could allow us to better understand the cause of disease and to be better at innovating effective solutions.

Natterson-Horowitz grew up in Los Angeles as the daughter of two psychotherapists. She made occasional trips to the zoo as a child, with no inkling that some of the animals she was looking at would later become her patients.

She studied evolutionary biology at Harvard under famed biologists E.O. Wilson and Stephen Jay Gould. She returned to California for medical school at UC San Francisco and a residency and fellowship at UCLA.

Shed been on the faculty at UCLA for a decade when, in 2005, she got a call from the zoo asking for assistance with a transesophageal echocardiogram, a type of ultrasound exam she specialized in. This one would be for a chimpanzee, her first nonhuman patient.

It was a procedure shed performed countless times before. But probing the internal biology of a fellow primate, albeit one that wasnt human, was like that gleam of light you see when you crack open a door, she recalled: In this case, the door happened to be separating my world of modern human medicine and the natural worlds endless health insights.

Physicians tend to be human-centric in their approach. But veterinarians investigating perplexing problems often look to the medical histories of other species including Homo sapiens.

Natterson-Horowitz feeds a giraffe at the Los Angeles Zoo. Giraffes have the highest known blood pressure in the animal kingdom, but this has no apparent effect on fetal or maternal health.

(Robert Gauthier / Los Angeles Times)

Weve always done that, because we know that theres a lot more research that goes on in many of these diseases in humans, said Jane Sykes, a professor of small animal internal medicine at the UC Davis School of Veterinary Medicine. Were always looking for parallels. ... Is there anything in humans that can help this dog in front of us?

Now Natterson-Horowitz wanted to do the same thing, just in the other direction. The more she consulted with the L.A. Zoo, the more she came to admire that inclusive approach and to question its absence in human medicine.

Anthropocentrism is a blindfold, she said of humans fixation on our own species. If we can move beyond that, we could see connections that are meaningful and powerful.

One of the first patients to spark her interest in female health was a lioness with pericardial effusion, or fluid in the sac around her heart. The condition affects at least 20% of cancer patients, both feline and human, and breast cancer is common in lions. Those two facts made veterinarians worry the lioness had an advanced case of the disease.

Natterson-Horowitz started researching. She knew that breast cancers in some women were connected to BRCA1, a gene on the 17th chromosome. People born with certain versions of the gene are more likely to develop breast cancer when exposed to an environmental or hormonal trigger.

Natterson-Horowitz visits the flamingo enclosure at the zoo. Theres a pretty vast landscape of unexamined assumptions about human uniqueness, she said.

(Robert Gauthier / Los Angeles Times)

What she had not realized was how many non-primate species shared this vulnerability. English springer spaniels with certain BRCA1 variants were four times more likely to develop breast cancer than dogs with the most common version of the gene, Natterson-Horowitz noted in Zoobiquity. Another study found that zoo jaguars taking a particular type of hormonal birth control developed breast cancer in rates similar to human women with high-risk BRCA1 variants, and that the cancer was common in lions and other big cats.

Many factors influence breast cancer rates in females across the animal kingdom: age, genetics, the frequency and duration of lactation, environmental factors and hormonal changes.

Column One

A showcase for compelling storytelling from the Los Angeles Times.

Taken together, the range of mammals vulnerable to breast cancers could offer a trove of valuable comparative data, Natterson-Horowitz realized. But virtually no one was looking for it even for a disease that claims the lives of more than 42,000 women in the U.S. alone each year.

So she started researching these evolutionary links herself. As she dug in, she said she noticed something else: Not only is human medicine anthropocentric, its androcentric that is, focused on cisgender men.

Until the 1993 passage of the NIH Revitalization Act, women and people of color were not required to be part of research studies or clinical trials funded by the NIH, and as a result they usually werent. The same preference for males is even seen in research on mice. In 2016, NIH set a new policy requiring researchers to at least consider biological sex as a variable in the design of human cell and animal studies, though they can study one only sex if they can show strong justification for it.

The good news is that today, over half of the participants in NIH clinical trials are women, said Dr. Janine Austin Clayton, director of the NIH Office of Research on Womens Health. But, she noted, women are still underrepresented in studies of several major diseases, including cardiovascular disease, kidney disease, hepatitis and HIV/AIDS.

Until we have representation across every disease category that affects women and men, she said, we still have work to do.

A male-centered research approach manifests in many ways. It isnt just the dearth of funding for conditions primarily affecting women, like endometriosis and rheumatoid arthritis. Its that data on female bodies are often absent from medical research altogether, resulting in skewed results that can shortchange all genders.

The result is that researchers often havent even realized when their results apply only to men.

Take heart attacks. When the Physicians Health Study, whose sample consisted of 22,071 men and zero women, found in 1989 that a low regular dose of aspirin led to a 44% decrease in heart attacks, many physicians recommended the treatment to men and women alike.

But the 39,876 participants in the Womens Health Study allowed researchers to report in 2005 that for women younger than 65, aspirin didnt help at all. And for those 65 and older, aspirin prevented not only heart attacks but strokes a benefit that was not apparent in the all-male study and would have remained unseen without studying women.

Excluding women from research studies forces doctors to treat them as guinea pigs, generation after generation after generation, said Chloe Bird, a sociologist who heads the Center for Health Equity Research at Tufts Medical Center in Boston.

For the record:

1:22 p.m. Oct. 14, 2022An earlier version of this article reported that the Center for Health Equity Research was at Tufts University. It is based at Tufts Medical Center, which is not part of the university.

Bird has not been involved in Natterson-Horowitzs efforts to take a broader look at the female population of the animal kingdom, which she called fantastic, and so needed.

There is a tremendous opportunity to look across species, and begin to understand ... what happens with what systems and why, and how we could improve healthcare, Bird said.

Natterson-Horowitz is now leading a team of obstetrician/gynecologists, wildlife veterinarians and veterinary pathologists to study giraffe pregnancy to understand why animals like Zainabu who delivered a healthy, 172-pound calf in April are not vulnerable to the cardiovascular crises that strike pregnant humans. Shes also working with dairy veterinarians to better understand mastitis, a common but painful inflammation of breast tissue, to come up with improved treatments and design a better breast pump for women.

But Natterson-Horowitz knows unlocking the secrets of the animal world is not a one-person job. Since 2011 she has organized Zoobiquity conferences that have brought together thousands of physicians, veterinarians and evolutionary biologists to examine health issues from multispecies perspectives. The most recent, titled Female Health Across the Tree of Life, took place in July in Lisbon, Portugal.

She also teaches the relevance of the animal world to undergraduates and medical students at UCLA and Harvard, and is heartened to see the eagerness of a new generation of physicians to look across species for answers.

Climate change and urbanization have blurred the boundaries between the human and nonhuman animal worlds, Natterson-Horowitz pointed out. Zoonotic diseases like COVID-19 and influenza have shown us how closely were tied to fellow members of the animal kingdom.

When she first got into medicine, she pledged to do no harm. Today, she believes, If we can move from an androcentric, anthropocentric view to a sex-, gender-, and species-spanning perspective, then we can do good.

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Column One: Why this UCLA professor is studying female animals to gain insights into women's health - Los Angeles Times

Simone Kaho.

Tulia Thompson talks to Simone Kaho about writing, surviving PTSD and the silencing of survivors

When you study poetry at university you are told you can write a poem about anything as long as it is well-crafted, but then you also learn that poetry in Aotearoa actually means restrained, lyric poems about nature. There's an invisible forcefield around what "counts" as a good poem.

Poets like Hera Lindsay Bird and Chris Tse push past the forcefield. Tongan-Pkeh writer Simone Kaho's stunning collection of poetry, Heal!, about being attacked, fighting back and experiencing PTSD, is a vital challenge to the poetry canon.

Kaho is a documentary-maker who works as a reporter/director for Tagata Pasifika. In Heal! the sexual assault acts as a refracting prism for her interactions with men, who are revealed to be rape-complicit by expressing "common-sense" views that support rape. There's the British guy she swims naked with who says, "Perhaps it's because you are so beautiful." When she is stalked, there is a drunk boss: "You're a sexy beast / he said / you / should / expect / stalkers."

When she posts a poem about the stalker, a male in the poetry community says, "What if he'd committed suicide?" It is the ordinary, banal comments from men that convey to women that they see us as sexually available, able to be objectified, and given less empathy. It's a profoundly uncomfortable read, in part because these views are so familiar.

It reminds me a lot of Claudia Rankine's award-winning Citizen: An American Lyric, about white privilege, in which short prose poems about things white people said to her create a sustained, multilayered impression of racism. In both poetry collections, the repeated incidents reveal their force.

While not being strictly narrative, Heal! maintains narrative tension, and a sense of movement. Assault has given Kaho a different lens on past events. In one poem, set during her childhood, she remembers her Tongan dad taking a machete to the bus stop, trying to find a man who sexually assaulted her.

She writes, "The machete is evidence of love and she enjoys the moment quietly." Kaho asked me when we met if anything surprised me about the collection. I said, "No, nothing really surprised me." But it was a lie. What actually surprised me was that another girl had felt about her dad's machete the way I felt about my dad's machete that it was an ordinary, protective and appropriate weapon.

Tulia Thompson: It's a very brave book. What made you decide to tell this story?

Simone Kaho: Can I just ask you why you think it's brave?

TT: I think it's brave because it's explicitly talking about rape and PTSD. Within New Zealand poetry, it feels like you're discouraged from writing about experiences like this, not necessarily explicitly, but just through the atmosphere.

SK: Yeah, I haven't heard anybody say to me, "You shouldn't write about that." But it feels like there's just a vibe about it. Like it's sharp or the wrong colour or too pungent or visceral or too political. This is not something that fits in.

But I didn't think about that writing this. I'd done the South Seas Film and Television course in 2017, when a lot of my PTSD symptoms were really becoming noticeable. I was really struggling.

I tried to make an action film about a female vigilante. And there was pushback. Pushback can be quite subtle. I was discouraged from making a film about a female protagonist responding violently to male violence. When I was pitching it to industry professionals in front of the whole school, it was questioned whether it was morally right, what the protagonist wanted to do. The horror film pitched straight after me featured a guy eating his mother's face, and got the feedback, "That was a delicious moment!"

So the pushback I got led to an understanding that I was being hushed. And at some point, I just really was like "Nah, f*** this s***." I need to use the most powerful way I have to express myself, which is poetry.

TT: If you're a woman, you are used to men making excuses for male violence. It's just so pervasive.

SK: It's co-opted into politeness. Boys will be boys. That's a blind spot that we all have to agree on. If you respond aggressively or even just assertively to predatory male behaviour, you're being rude. You're the problem. That is definitely something I felt all the time. I was enraged all the time. It was so tiring. And because I'd been in that moment, physically fighting a man during the assault, when I knew there was nothing between us that could protect me, all of those "boys will be boys" behaviours happening afterwards triggered the same sort of horror I'd felt in that moment. Like the only difference between them and the attacker was that he'd made a decision to commit and deal with the consequences.

TT: There's a rigour to your poetry. Is that because of your time at the International Institute of Modern Letters?

SK: I became the poet I am at the IIML, because you're absorbed in it. I had Hinemoana Baker as my supervisor. She said, "Do you care about line breaks? I want you to have no punctuation." And this guttural voice appeared. It's not blaming, even, it's just like brutal truth.

TT: There are men in the book who say sorry that happened, but they don't change their own misogyny. It seems very difficult to create change without men taking more responsibility for talking about sexual violence. What do you think needs to happen?

SK: My concern is with people who've been through sexual violence. My first concern is around our ability to talk about it it's not a crime that we have done. I don't mean with no regard for context or incessantly but in the same way that if somebody robbed your house and beat you up [you'd talk about it]. It's been really hard, working and going back to life, and trying to find a safe place. It's a lot to navigate. I really want to smash the hushing and shaming that makes survivors of sexual violence have to be brave just to talk about it.

Heal! by Simone Kaho (Saufo'i Press, $30) is out now.

Aroha, by Dr Hinemoana Elder, was Aotearoa's biggest-selling non-fiction title of last year. The acclaimed psychiatrist is following up with Wawata: Moon Dreaming (Penguin, $30), a book of wisdom centred around the cycle of the moon which offers 30 lessons based on the 30 faces of Hina, the Maori moon goddess.

Black Ferns star Ruby Tui's new biography, Straight Up (Allen & Unwin, $37), lays it all out there. Her tough childhood, her drive to overcome personal tragedy, her love of rugby and her incredible rise to international fame.

The fifth short story collection from a master of the form, George Saunders, Liberation Day (Bloomsbury, $33) is out on Tuesday. Saunders won the Man Booker Prize for his only novel, Lincoln in the Bardo, in 2017 but is best known for his short stories and essays.

1. You deliver an ecological message in the guise of a coffee table book. Is the artwork a lure?

It was too good an opportunity to miss. Collectively our early painters and photographers produced a rich and unique record of a relatively pristine New Zealand, at the time when settlement from Europe was just beginning. For example, the book includes two paintings, from 1839 and 1840, by Charles Heaphy of the kauri forests on the Wairoa River, Kaipara.

Such images were used as propaganda by the New Zealand Company, to encourage immigration, with the result that vast areas of kauri were felled and destroyed in the process to provide timber for the new settlers' homes. Then there's Alfred Sharpe's 1876 subtly elevated panorama of the Waikato plains, which provides a stark contrast with a photograph of a similar view 140 years later, of the Taupiri interchange on the Waikato Expressway.

2. If a reader takes away one nugget from this book, what do you hope it will be?

My aim in compiling the book was to record the various changes that a thousand or so years of human settlement have inflicted on the New Zealand landscape. With those in mind, I hope it will encourage us to question where we go from here. As we become increasingly aware of the effects of climate change, we must wonder how, and to what extent, we can keep on modifying our natural environment. This is, of course, not just a New Zealand problem. It's worldwide, and at its heart is the ability of the Earth's resources to sustain a growing population in the manner to which it has grown accustomed. As for New Zealanders, this poses such challenges as the degree to which our towns and cities can continue to sprawl, destroying remaining areas of bush and gobbling up good agricultural land.

3. Do you have a favourite image in the book?

There are many "landmark" images, such as the well-known and starkly symbolic Frozen Flames, painted in 1931 by Christopher Perkins, which depicts the aftermath of a bush burn-off. Another of my favourites is Kennett Watkins' 1885 painting, The Haunt of the Moa: A Scene in a Puriri Forest, also in the collection of the Auckland Art Gallery Toi o Tmaki. Deep withIn a dark forest of nkaupalms and gnarled puriri trunks, a hapless moa emerges from behind a tree and is about to reveal itself to a pair of Mori stalkers. The big bird appears to be at the crossroads, for if the hunt is successful it might mark the extinction of the species.

4. You are that rare thing in New Zealand, a full-time writer. How do you make that work?

I had never planned to be a full-time writer. Back in 1997, along with two dozen other staff members, I was made redundant (as Curator of Display) at the Auckland War Memorial Museum. That unexpected change of direction gave me the opportunity to spend more time on what had previously been just an after-hours activity. A quarter of a century and some 40 books later, I'm still at it. I enjoy coming up with ideas for books, and am grateful to publishers who have given me opportunities to realise them. I also enjoy the challenge of dreaming up and researching articles for our leading art quarterly, Art New Zealand.

5. What book have you read this year that you are recommending to others?

I have recently read and enjoyed A Brief History of Everyone Who Ever Lived: The Stories in Our Genes, by English science writer and genetics expert Adam Rutherford (no relation to Sir Ernest). He divulges the startling fact that anyone of European extraction is descended from Charlemagne, the first emperor of the Holy Roman Empire, who lived from 747 to 814AD. The point is that the further we go back up our family trees, the more interconnected and related all of us are. Perhaps if humanity at large was more aware of this fact, the world would be a much happier place.

Footprints on the Land, by Richard Wolfe (Oratia Books, $45), is out now.

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Books wrap: Simone Kaho on her new poetry collection and PTSD; a conversation with Richard Wolfe; and more - New Zealand Herald

Overview

Masculinizing hormone therapy is used to induce the physical changes in your body caused by male hormones during puberty (secondary sex characteristics) to promote the matching of your gender identity and body (gender congruence). If masculinizing hormone therapy is started before the changes of female puberty begins, female secondary sex characteristics, such as the development of breasts, can be avoided. Masculinizing hormone therapy is also known as gender-affirming hormone therapy.

During masculinizing hormone therapy, you'll be given the male hormone testosterone, which suppresses your menstrual cycles and decreases the production of estrogen from your ovaries. Changes caused by these medications can be temporary or permanent. Masculinizing hormone therapy can be done alone or in combination with masculinizing surgery.

Masculinizing hormone therapy isn't for all transgender men, however. Masculinizing hormone therapy can affect your fertility and sexual function and cause other health problems. Your doctor can help you weigh the risks and benefits.

Masculinizing hormone therapy is used to alter your hormone levels to match your gender identity.

Typically, people who seek masculinizing hormone therapy experience discomfort or distress because their gender identity differs from their sex assigned at birth or from their sex-related physical characteristics (gender dysphoria). To avoid excess risk, the goal is to maintain hormone levels in the reference range for the target gender.

Masculinizing hormone therapy can:

Research suggests that masculinizing hormone therapy can be safe and effective.

If used in an adolescent, hormone therapy typically begins at age 16. Ideally, treatment starts before the development of secondary sex characteristics so that teens can go through puberty astheir identified gender. Gender affirming hormone therapy is not typically used in children.

Masculinizing hormone therapy isn't for everyone, however. Your doctor might discourage masculinizing hormone therapy if you:

Talk to your doctor about the changes in your body and any concerns you might have. Complications of masculinizing hormone therapy include:

Evidence suggests that transgender men have no increased risk of breast cancer or cardiovascular disease when compared to women whose gender identity and expression matches the stereotypical societal characteristics related to their sex assigned at birth (cisgender women).

Conclusions cant be drawn about whether masculinizing hormone therapy increases the risk of ovarian and uterine cancer. Further research is needed.

Because masculinizing hormone therapy might reduce your fertility, you'll need to make decisions about your fertility before starting treatment. The risk of permanent infertility increases with long-term use of hormones, especially when hormone therapy is initiated before puberty. Even after stopping hormone therapy, ovarian and uterine function might not recover well enough to ensure that you can become pregnant without reproductive technology assistance.

If you want to have biological children, talk to your doctor about egg freezing (mature oocyte cryopreservation) or embryo freezing (embryo cryopreservation). Another option involves having ovarian tissue surgically removed, frozen and later thawed and reimplanted (ovarian tissue cryopreservation). Keep in mind that egg freezing has multiple steps ovulation induction, egg retrieval and freezing. If you want to freeze embryos, you'll need to go through the additional step of having your eggs fertilized before they are frozen.

At the same time, while testosterone might limit your fertility, you're still at risk of pregnancy if you have your uterus and ovaries. If you want to avoid becoming pregnant, use an intrauterine device, a barrier form of contraception or a continuous progestin form of birth control.

Before starting masculinizing hormone therapy, your doctor will evaluate your health to rule out or address any medical conditions that might affect or contraindicate treatment. The evaluation might include:

You might also need a behavioral health evaluation by a provider with expertise in transgender health. The evaluation might assess:

Adolescents younger than age 18, accompanied by their custodial parents or guardians, also should see doctors and behavioral health providers with expertise in pediatric transgender health to discuss the risks of hormone therapy, as well as the impact and possible complications of gender transition in that age group.

You'll begin masculinizing hormone therapy by taking testosterone. Typically, your doctor will prescribe a low dose and slowly increase the dosage over a period of months. Testosterone is given either by injection or a gel applied to the skin. Other testosterone preparations can be used, such as a patch or pellets placed under the skin. In the U.S., testosterone also can be given as a long lasting injection or as twice daily pills (testosterone undecanoate). Oral methyltestosterone or synthetic male sex hormone (androgen) medication shouldn't be used because of potential harmful effects on your liver and lipids.

If you have persistent menstrual flow, your doctor might recommend taking progesterone to control it.

Masculinizing hormone therapy will begin producing changes in your body within weeks to months. Your timeline might look as follows:

While on masculinizing hormone therapy, you'll meet regularly with your doctor. He or she will:

You will also need routine preventive care if you havent had certain surgical interventions, including:

The rest is here:
Masculinizing hormone therapy - Mayo Clinic

What is human growth hormone (hGH)?

Human growth hormone, also known as hGH and somatotropin, is a natural hormone your pituitary gland makes and releases that acts on many parts of the body to promote growth in children. Once the growth plates in your bones (epiphyses) have fused, hGH no longer increases height, but your body still needs hGH. After youve finished growing, hGH helps to maintain normal body structure and metabolism, including helping to keep your blood sugar (glucose) levels within a healthy range.

Hormones are chemicals that coordinate different functions in your body by carrying messages through your blood to your organs, muscles and other tissues. These signals tell your body what to do and when to do it. Your body makes over 50 hormones, and many of them interact with each other, creating a complex web of processes.

Your pituitary gland is a small, pea-sized endocrine gland located at the base of your brain below your hypothalamus. Its made of two lobes: the anterior (front) lobe and posterior (back) lobe. Your anterior lobe makes hGH.

Your pituitary gland is connected to your hypothalamus through a stalk of blood vessels and nerves. This is called the pituitary stalk. Your hypothalamus is the part of your brain that controls functions like blood pressure, heart rate, body temperature and digestion. Through the stalk, your hypothalamus communicates with your pituitary gland and tells it to release certain hormones. In this case, your hypothalamus releases growth hormone-releasing hormone (GHRH), which stimulates your pituitary gland to release hGH, and somatostatin, which prevents (inhibits) that release.

Healthcare providers use a synthetic form of hGH (sometimes called recombinant hGH) to treat certain health conditions, including growth hormone deficiency. You should never take synthetic hGH without a prescription from your provider.

Your pituitary gland normally releases hGH in short bursts (pulses) throughout the day. The release of hGH is mainly controlled by two hormones your hypothalamus releases: growth hormone-releasing hormone (GHRH), which stimulates hGH release, and somatostatin, which prevents (inhibits) hGH release.

Several other endocrine hormones also regulate hGH, including insulin-like growth factor 1 (IGF-1). IGF-1 is a major suppressor of GH production, whereas thyroxine, glucocorticoids and ghrelin stimulate hGH release.

IGF-1 thats released by your liver is one of the best-characterized effects of hGH activity. IGF-1 plays a critical role in preventing (inhibiting) the release of the hGH through a negative feedback loop by stimulating somatostatin and inhibiting GHRH release. However, hGH and IGF-1 secretion are regulated by each other, where hGH triggers IGF-1 release and the IGF-1 inhibits hGH release in a feedback loop. In healthy people, hGH release is inhibited by hyperglycemia (high blood sugar) and stimulated by sleep, stress, exercise, hypoglycemia (low blood sugar) and amino acids.

Human growth hormone has two main functions: stimulating growth (mainly in children) and impacting metabolism (how your body turns the food you eat into energy).

Human growth hormone triggers growth in nearly every tissue and organ in your body. However, its most well-known for its growth-promoting effect on cartilage and bone, especially in the adolescent years during puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts receive signals from hGH to increase replication and thus allow for growth in size.

Once the growth plates in a childs bones have fused, hGH no longer increases height. Instead, hGH helps to maintain normal body structure throughout the rest of your life.

Metabolism consists of the chemical reactions in your body that change the food you eat into energy. All of the cells in your body need energy to function properly. Several different complex processes are involved in metabolism.

hGH impacts metabolism primarily by increasing the production of insulin-like growth factor-1 (IGF-1) and its effect on cells in your body. IGF-1 is a hormone similar in structure to insulin that manages the effects of hGH in your body. Insulin is an essential hormone your pancreas makes that helps regulate your blood sugar (glucose) levels by decreasing them. Like insulin, IGF-1 has glucose-lowering effects.

Your body normally carefully regulates your blood glucose levels. Blood glucose, or sugar, is the main sugar found in your blood. You get glucose from carbohydrates in the food you eat. This sugar is an important source of energy and provides nutrients to your body's organs, muscles and nervous system.

Insulin is the main hormone your pancreas makes to lower blood glucose levels when they get too high, and glucagon is the main hormone your pancreas makes to raise glucose levels when they get too low. Other hormones can counteract the effects of insulin, such as epinephrine (adrenaline) and cortisol.

While hGH normally increases blood glucose levels when they get too low, if you have excess amounts of hGH in your body, it can counteract the effects of insulin, causing elevated blood glucose levels.

Human growth hormone increases vertical growth in children. However, once your growth plates have fused, hGH cannot make you taller. Instead, after youve reached your final height, hGH helps maintain your bodys structure and has other important effects on your metabolism.

Your pituitary gland releases hGH in pulses. The size and duration of the pulses vary with time of day and your age and sex. Because of this, random hGH measurements are rarely useful to healthcare providers in confirming or ruling out a diagnosis. Instead, hGH measurement tests are most useful when measured as part of a stimulation or suppression test.

In general, the normal range for hGh levels include:

Normal value ranges may vary from lab to lab. Be sure to reference your labs normal range on your lab report when analyzing your results. If you have any questions about your results, talk to your healthcare provider.

Having lower-than-normal levels of hGH is called growth hormone deficiency. Its usually due to an issue with or damage to your pituitary gland that results in hypopituitarism when one, several or all of the hormones your pituitary gland makes are deficient. Human growth hormone could be one of the affected hormones.

Growth hormone deficiency affects adults and children differently.

When adults have a lack of hGH, it causes the following issues:

In adults, hypopituitarism that results in hGH deficiency may develop due to a benign pituitary adenoma (a noncancerous tumor) or damage to your pituitary gland or hypothalamus.

A lack of hGH in children results in poor growth. The main sign of hGH deficiency in children is slow height growth each year after a child's third birthday. This means they grow less than about 1.4 inches in height a year. A child with hGH deficiency may also have:

In children, hypopituitarism that results in hGH deficiency may be present from birth where the cause can be unknown (idiopathic), genetic or due to injury to their pituitary gland (during fetal development or at birth).

Children can also develop hypopituitarism due to damage to their pituitary gland or hypothalamus later in life.

The main condition associated with higher-than-normal hGH levels is a condition called acromegaly, though it affects adults and children differently. Its a rare condition.

Adults with acromegaly usually have enlarged or swollen hands and feet and altered facial features.

Adults with acromegaly can also have thickened bones and enlarged organs and are more likely to have conditions such as high blood pressure (hypertension), Type 2 diabetes and heart disease. Over 99% of acromegaly cases are due to pituitary adenomas, noncancerous (benign) tumors on your pituitary gland. These tumors can produce excess amounts of hGH. Acromegaly is more common after middle-age when growth is complete. Because of this, adults with acromegaly dont get any taller. Instead, their bones can become thicker.

Very rarely, children can experience elevated growth hormone levels before they reach their final height, which can lead to excessive growth of long bones and very tall height. This condition is called pediatric acromegaly, but its sometimes called gigantism. If left untreated, children with acromegaly usually grow to be seven feet tall or taller. Children with acromegaly may also have general weakness, delayed puberty and headaches.

Pituitary adenomas are usually the cause of pediatric acromegaly.

Your healthcare provider can order a series of blood tests to check your hGH levels if youre experiencing symptoms related to hGH issues.

Your pituitary gland normally releases hGH into your bloodstream in pulses throughout the day and night, with peaks that occur mostly during the night. Because of this, a single blood test to measure hGH measurement is difficult to interpret and is not usually medically useful.

Providers most often use procedures called growth hormone stimulation and suppression tests to diagnose conditions caused by hGH deficiency or excess.

They may also order a blood test that measures the amount of insulin-like growth factor 1 (IGF-1) in your blood.

The U.S. Food and Drug Administration (FDA) has approved the synthetic form of hGH for treatment for certain conditions. The synthetic form of hGH is available only by prescription and is injected.

In children, healthcare providers prescribe hGH to treat:

In adults, providers prescribe hGH to treat:

Its important to only take synthetic hGH if your provider has prescribed it for you.

The use of synthetic hGH for medical treatment can cause certain side effects including:

Researchers dont have enough information about the long-term effects of hGH treatment.

If you or your child are experiencing symptoms related to hGH deficiency or excess, contact your healthcare provider.

If youre receiving treatment for abnormal hGH levels, its important to see your provider regularly to make sure your treatment is working.

A note from Cleveland Clinic

Human growth hormone (hGH) is a powerful hormone thats necessary for several important bodily processes. Sometimes, your pituitary gland can make too much or too little of it. If you or your child are experiencing symptoms related to hGH deficiency or excess, its important to talk to your healthcare provider. Theyre there to help.

More here:
Human Growth Hormone (hGH) - Cleveland Clinic

Chronic stress puts your health at risk

Chronic stress can wreak havoc on your mind and body. Take steps to control your stress.

Your body is hard-wired to react to stress in ways meant to protect you against threats from predators and other aggressors. Such threats are rare today, but that doesn't mean that life is free of stress.

On the contrary, you likely face many demands each day, such as taking on a huge workload, paying the bills and taking care of your family. Your body treats these so-called minor hassles as threats. As a result, you may feel as if you're constantly under attack. But you can fight back. You don't have to let stress control your life.

When you encounter a perceived threat such as a large dog barking at you during your morning walk your hypothalamus, a tiny region at your brain's base, sets off an alarm system in your body. Through a combination of nerve and hormonal signals, this system prompts your adrenal glands, located atop your kidneys, to release a surge of hormones, including adrenaline and cortisol.

Adrenaline increases your heart rate, elevates your blood pressure and boosts energy supplies. Cortisol, the primary stress hormone, increases sugars (glucose) in the bloodstream, enhances your brain's use of glucose and increases the availability of substances that repair tissues.

Cortisol also curbs functions that would be nonessential or harmful in a fight-or-flight situation. It alters immune system responses and suppresses the digestive system, the reproductive system and growth processes. This complex natural alarm system also communicates with the brain regions that control mood, motivation and fear.

The body's stress response system is usually self-limiting. Once a perceived threat has passed, hormone levels return to normal. As adrenaline and cortisol levels drop, your heart rate and blood pressure return to baseline levels, and other systems resume their regular activities.

But when stressors are always present and you constantly feel under attack, that fight-or-flight reaction stays turned on.

The long-term activation of the stress response system and the overexposure to cortisol and other stress hormones that follows can disrupt almost all your body's processes. This puts you at increased risk of many health problems, including:

That's why it's so important to learn healthy ways to cope with your life stressors.

Your reaction to a potentially stressful event is different from anyone else's. How you react to your life stressors is affected by such factors as:

You may have some friends who seem relaxed about almost everything and others who react strongly to the slightest stress. Most people react to life stressors somewhere between those extremes.

Stressful events are facts of life. And you may not be able to change your current situation. But you can take steps to manage the impact these events have on you.

You can learn to identify what causes you stress and how to take care of yourself physically and emotionally in the face of stressful situations.

Stress management strategies include:

Avoid unhealthy ways of managing your stress, such as using alcohol, tobacco, drugs or excess food. If you're concerned that your use of these products has increased or changed due to stress, talk to your doctor.

The rewards for learning to manage stress can include peace of mind, less stress and anxiety, a better quality of life, improvement in conditions such as high blood pressure, better self-control and focus, and better relationships. And it might even lead to a longer, healthier life.

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Chronic stress puts your health at risk - Mayo Clinic

OverviewWhats a migraine? What does it feel like?

A migraine is more than a bad headache. Its a neurologic disease with a series of symptoms that might include debilitating pain on one side of your head that you may describe as pulsing or throbbing. Menstrual migraines, also known as hormone headaches, happen right before or during a womans period (up to two days before through three days during) and may get worse with movement, light, smells, or sound. Your symptoms may last for a few hours, but theyll likely last days.

Its estimated that 70% of people who experience migraines are women. Of these women, 60% to 70% report a connection between their menstruation (periods) and their migraine attacks. Women experience migraine attacks three times more frequently than men.

A menstrual migraine is one of several types of migraine headaches. Examples of other migraines include migraine with aura, migraine without aura and chronic migraine.

Hormones are often called your bodys chemical messengers. Theyre in your organs, tissues and bloodstream and theyre made by the endocrine glands. Examples of endocrine glands include your thyroid gland, adrenal glands and pituitary gland. If you have too little of a certain hormone, or too much, that can throw your entire system off balance.

Estrogen and progesterone are the two main sex hormones in women. Estrogen causes female physical features, sets off puberty and aids with reproduction. It also affects your cholesterol, controls your menstrual cycle, protects bone health and affects your heart, skin, bones, brain and other tissues. Its mostly produced by your ovaries.

Your levels of estrogen change. Theyre at the highest amount in the middle of your cycle and the lowest amount when youre on your period. When youre in menopause, they drop very low.

Headaches in women, especially migraines, are related to changes in the levels of estrogen. Levels of estrogen drop immediately before the start of your menstrual flow (menses).

Premenstrual migraines regularly occur during or after the time when the female hormones, estrogen and progesterone, drop to their lowest levels.

Migraine attacks usually improve during pregnancy. However, some women have reported that their migraines started during the first trimester of pregnancy, and then went away.

Menstrual migraines are triggered by a drop in estrogen. Other migraines may be triggered by stress, missing a meal, caffeine, or many other reasons.

About 12% of Americans experience migraines. The majority are women, at least 60% of those women have observed a correlation between their menstrual cycle and their migraines. In other words, theyve noticed that they get a migraine right before or during their period.

Menstrual migraines can start up to three days before your period.

While migraines can start when youre a child, menstrual migraines dont until your periods begin. Women who have periods are the ones who get menstrual migraines.

Changes in estrogen levels, which happen right before your period begins.

In addition to a drop in estrogen, birth control pills and hormone replacement therapy for menopause can change the frequency or severity of migraines. If you notice your migraine headache getting worse after starting one of these medications, it may be worthwhile to ask your healthcare provider for a medication that contains a lower dose of estrogen, or ask for a change from an interrupted dosing regimen to a continuous one.

The symptoms of a menstrual migraine are the same as the symptoms for other types of migraines:

Your healthcare provider will want to establish a history of your migraine-related symptoms, likely asking you to:

Your healthcare provider may also order blood tests and imaging tests (such as a CT scan or MRI) to make sure there are no other causes for your headache. An electroencephalogram (EEG) may be ordered to rule out seizures.

Its helpful to both you and your healthcare provider if you keep a migraine journal. Take note of what symptoms you get, how long your symptoms last, and what makes your menstrual migraine better or worse. You and your healthcare provider may be able to use that information to help you heal, and possibly prevent or anticipate your migraine.

A menstrual migraine is usually treated with nonsteroidal anti-inflammatory medications (NSAIDs). The NSAIDs most often used for menstrual migraine include:

Treatment with the NSAID should begin two to three days before your period starts, and continue through your menstrual flow. Because the medication is taken for a short time only, the risk of gastrointestinal side effects is limited.

Triptans selective serotonin receptor agonists are medicines used for acute migraines. They stop your menstrual migraine after it begins. In the United States there are seven triptan medications approved for use:

Other medications that might be prescribed include:

These drugs should also be started two to three days before your period starts. Continue taking them throughout your menstrual flow.

Because fluid retention (retaining water) often occurs at the same time as your menses, diuretics have been used to prevent menstrual migraines. Some healthcare providers may recommend that you follow a low-salt diet immediately before the start of your menses.

Leuprolide (Lupron) is a medication that affects your hormone levels. Its used only when all other treatment methods have been tried and havent worked.

Talk with your healthcare provider and pharmacist about the side effects of each medication prescribed. The most common side effects of medications prescribed to fight migraines include:

Ask your primary healthcare provider to refer you to a headache specialist.

If you need to continue estrogen supplements after menopause, you should start on the lowest dose of these agents, on an uninterrupted basis. Instead of seven days off the drug, you may be told to take it every day. By maintaining a steady dose of estrogen, the headaches may be prevented. An estrogen patch (such as Estraderm) may be effective in stabilizing the levels of estrogen.

Because most medications taken for migraines can affect your baby, you should avoid them. However, your healthcare provider may give you permission to take a mild pain reliever like acetaminophen. Talk to your healthcare provider before you take any medicine.

Do your best to figure out what makes your hormone headaches better or worse. For example, if light causes pain and you feel overheated, stay in a cool, dark room. Additional tips include:

Your healthcare provider may prescribe preventative medications that you take daily, then increase the dose when youre near your period. Possibilities include:

No type of migraine causes brain damage.

You may have menstrual migraines until youre in menopause.

Schedule a visit with your healthcare provider if:

Call 911 or go immediately to an Emergency Room if:

A note from Cleveland Clinic

A migraine is more than a bad headache. Not only can menstrual migraines get severe, but women have reported that they can be even worse than a migraine that occurs when theyre not on their period. Talk to your healthcare provider about your symptoms. There are preventative measures and treatment options. A menstrual migraine might not be something you just have to live with every month.

Read more from the original source:
Menstrual Migraines (Hormone Headaches) - Cleveland Clinic

OverviewWhat is acromegaly?

Acromegaly (pronounced a-krow-meh-guh-lee) is a rare but serious medical condition that happens when you have high levels of growth hormone (GH) in your body. Your pituitary gland normally produces GH, but tumors on your pituitary or in other parts of your body produce excess GH in acromegaly.

Your pituitary gland is a small, pea-sized endocrine gland located at the base of your brain below your hypothalamus. Your pituitary gland releases eight important hormones, including GH.

Growth hormone, also known as human growth hormone (hGH) and somatotropin, is a natural hormone that acts on many parts of the body to promote growth in children. Once the growth plates (epiphyses) in your bones have fused, GH no longer increases height, but your body still needs GH. After youve finished growing, GH helps to maintain normal bone, cartilage and organ structure and metabolism, including helping to keep your blood glucose (sugar) levels within a healthy range.

If you have too much GH in your body as an adult, it can result in irregularly-shaped bones, increased organ size, elevated blood sugar levels (hyperglycemia) and other symptoms.

Acromegaly and gigantism are both conditions that result from excess growth hormone (GH). The difference is in who the conditions affect adults develop acromegaly, whereas children develop gigantism.

In children, gigantism occurs when they experience excess GH before the growth plates in their bones fuse (before the end of puberty). This causes them to grow very tall. Gigantism is more rare than acromegaly. Some healthcare providers refer to gigantism as pediatric acromegaly.

Once your growth plates have fused, excess GH causes acromegaly. In this case, you dont grow in height, but the excess GH affects your bones shape and your organ size as well as other health factors.

Acromegaly can develop at any age after puberty, but healthcare providers most often diagnose it during the fourth and fifth decades of life (middle age).

Acromegaly is rare. Approximately 3 to 14 of every 100,000 people have been diagnosed with acromegaly.

In adults, acromegaly (excess growth hormone) causes bones, cartilage, body organs and other tissues to increase in size. Characteristic changes in appearance include larger hands, feet, ears, lips and nose and a more prominent jaw and forehead.

Growth hormone (GH) signals your liver to produce another hormone called insulin-like growth factor 1 (IGF-1). IGF-1 is the hormone that actually causes your bones and body tissue to grow and also affects how your body processes blood glucose (sugar) and lipids (fats). High levels of GH result in high levels of IFG-1, which can lead to Type 2 diabetes, high blood pressure (hypertension) and heart disease.

The most common cause of acromegaly is a tumor in your pituitary gland called a pituitary adenoma that causes your pituitary gland to release excess growth hormone (GH).

Pituitary adenomas (tumors) are almost always benign (noncancerous). Most adenomas that cause acromegaly grow slowly, and you may not notice symptoms of excess GH for many years.

Depending on its size and location, the adenoma may press against other pituitary tissue and affect other hormones your pituitary gland makes. If the adenoma is large, it may also press against nearby parts of your brain, causing headaches and vision problems.

In adults, acromegaly affects your bodys bones and tissues and causes them to grow in irregular ways.

Adults with acromegaly may experience the following symptoms:

Other symptoms include:

Acromegaly symptoms often start slowly and may be difficult to notice at first. Some people only notice their hands have grown in size when rings they regularly wear feel tight or their shoe size changes, especially the width.

If youre experiencing these symptoms, its important to talk to your healthcare provider.

Symptoms of acromegaly often show up very slowly over many years. This makes it hard to diagnose.

Your healthcare provider may recommend you see an endocrinologist, a healthcare provider who specializes in hormone-related conditions. They'll make a diagnosis based on your medical history, a thorough clinical evaluation and specialized tests like blood tests and imaging tests.

If youve been diagnosed with acromegaly, your provider may order additional tests to see if the condition has affected other parts of your body. These tests may include:

There are several treatment options for acromegaly. Your healthcare provider will consider your symptoms and circumstances before offering treatment options that are right for you.

The most common treatments for acromegaly are surgery, medication and radiation therapy.

In many cases, surgery greatly improves acromegaly symptoms or corrects the condition entirely. Surgeons most often use a type of surgery called transsphenoidal surgery, which involves going through your nose and sphenoid sinus, a hollow space in your skull behind the nasal passages and below your brain, to perform surgery.

The specifics of the surgery will depend on the size and location of the tumor. The goal of surgery is to remove all of a tumor that is causing excess growth hormone production. If your surgeon removes enough of the tumor, you may not need further treatment. If your surgeon can remove only a part of a tumor, you may need medication or radiation therapy to manage your symptoms and reduce the production of growth hormone.

Your healthcare provider may prescribe one medication or a combination of medications. Medications work in different ways to normalize your bodys growth hormone levels and improve your symptoms. In some cases, a person may take medication until the tumor has shrunk. This can allow a surgeon to then safely remove it. Other people may need to take medication long-term to effectively manage growth hormone levels and symptoms.

Acromegaly is curable in some situations but not all. The cure rate for surgical removal of a pituitary tumor thats causing acromegaly is about 85% for small tumors and 40% to 50% percent for large tumors.

Medication cant cure acromegaly but offers long-term, safe treatment.

Unfortunately, theres nothing you can do to prevent acromegaly. Scientists arent sure what causes pituitary tumors that cause acromegaly to develop, though they think certain genetic factors may play a role.

The prognosis (outlook) for acromegaly depends on how severe it is and how effectively therapies treat the symptoms. Many people with acromegaly see a significant improvement in symptoms after treatment.

If its not treated, acromegaly can significantly change your appearance and the shape of your bones. These symptoms can greatly affect your self-image and quality of life. Support groups help some people cope with the challenges they face because of acromegaly.

Health complications of acromegaly such as heart disease or Type 2 diabetes can also decrease quality of life and even shorten your lifespan. Because of this, its important to contact your healthcare provider if youre experiencing symptoms and to adhere to your treatment plan if youve been diagnosed.

If left untreated, acromegaly can cause the following complications:

Life expectancy for someone with acromegaly depends on the severity of the condition and if they have other health conditions, usually due to untreated acromegaly.

If your growth hormone levels arent properly managed and you have other conditions like heart disease and Type 2 diabetes, your life expectancy may reduce by approximately 10 years.

If you have acromegaly thats properly treated and have normal growth hormone and insulin-like growth factor 1 (IGF-1) levels, youll likely have a normal life expectancy.

If youre experiencing symptoms of acromegaly, its important to talk to your healthcare provider.

If youve been diagnosed with acromegaly, youll need to see your provider regularly to make sure your treatment is working well.

A note from Cleveland Clinic

Acromegaly is a rare but serious condition. The good news is that its treatable with surgery, medication and/or radiation therapy. If youve noticed an increase in size in your hands, feet and/or facial features, its important to talk to your healthcare provider. They can order some simple tests to see if your growth hormone levels are the cause of your symptoms.

See original here:
Acromegaly: What It Is, Causes, Symptoms & Treatment - Cleveland Clinic

It is sometimes called frozen shoulder, even menopause shoulder.

Doctors say the condition, known as adhesive capsulitis, causes stiffness and pain in the shoulder joint. Little is definitively known about the cause.

The ailment more commonly occurs in women over the age of 40. Having diabetes, thyroid disease, heart disease, or Parkinsons disease can also put you at higher risk.

In a new study, researchers decided to hone in on the demographic most affected by adhesive capsulitis menopausal women.

The Duke University team conducted the first known study evaluating whether hormone therapy might reduce the risk of adhesive capsulitis in menopausal women.

The team evaluated medical records from a single institution for nearly 2,000 menopausal women ages 45 to 60. In the group, 152 of the women were receiving hormone replacement therapy (HRT).

While acknowledging the small sample size, the researchers concluded that those not receiving hormone replacement therapy had 99% greater odds of adhesive capsulitis compared to those receiving HRT.

The findings are being presented this week at the North American Menopause Society annual meeting in Atlanta, Georgia. The results have not been published yet in a peer-reviewed journal.

Dr. Anne Cunanan Ford, NCMP, an associate professor of obstetrics and gynecology at the Duke University Medical Center in North Carolina, is the studys lead author.

Our study draws attention to estrogens potential benefit apart from the FDA (Food and Drug Administration) approved indications vasomotor symptoms, bone protection, and vulvovaginal atrophy, she told Healthline.

We know that estrogen plays an important role in the musculoskeletal system, stimulating new bone formation, promoting muscle growth and repair, maintaining connective tissue integrity, and reducing inflammation Ford explained.

If borne out by future prospective studies, the use of systemic hormone therapy may be protective in minimizing adhesive capsulitis she added. Its a condition that causes significant pain, reduction in range of motion, and decreased quality of life in peri and post-menopausal women.

Experts who spoke to Healthline agreed that there needs to be more research.

This pilot study provides preliminary data that will guide future studies further investigating a potential link between menopause and hormone therapy use or non-use, and risk of adhesive capsulitis, said Dr. Stephanie Faubion, the director of the Mayo Clinics Center for Womens Health in Minnesota and Medical Director of the North American Menopause Society.

No conclusions can be made based on these data, she told Healthline.

Its a small study so something like this has to be looked at in bigger numbers, added Dr. G. Thomas Ruiz, the lead OB-GYN at MemorialCare Orange Coast Medical Center in California.

I think its an interesting study in that we know that estrogen receptors are found throughout a womans body, he told Healthline. So its not surprising that there would also be an interaction between joint function ligaments and tendons with estrogen.

So the menopausal state in the absence of estrogen is probably going to change he added. We know with bone, for example, in the absence of estrogen, women will start to lose calcium at a more rapid rate. That puts them at risk of osteoporosis and osteopenia, at an increased risk for hip fractures. So looking at this study I dont necessarily find it too surprising but its also too small a number to make a definitive statement.

Going forward, Ford said: Our data is preliminary and due to the small sample size, this association did not reach statistical significance. Larger prospective studies are needed to evaluate and confirm our findings.

Would hormone therapy work to treat adhesive capsulitis?

We have no idea. There is no data. Hormone therapy does appear to be associated with less joint pain. But the mechanism behind this effect is unknown Faubion said.

Hormone therapy is effective for management of hot flashes, night sweats, sleep disturbance associated with menopause, prevention of osteoporosis, fractures and the treatment of genitourinary syndrome of menopause she explained. It also appears to help with depressive symptoms in the menopause transition.

The benefits of hormone therapy typically outweigh the risks for symptomatic women who are under the age of 60 and within 10 years of the onset of menopause, she added.

Still, many women have questions about the safety of hormone treatment because of previous studies linking some forms of hormone treatment to an increased breast cancer risk.

The American Cancer Society states that estrogen-only HRT is not linked to a higher risk of breast cancer. The Womens Health Initiative studies also found no increase in breast cancer risk in women using systemic estrogen-only HRT.

But organization officials note that in women who have a uterus, using systemic estrogen-only HRT has been shown to increase the risk of endometrial cancer.

Other studies have found a link between systemic estrogen-only HRT and a higher risk of ovarian cancer.

Ruiz says theres an increase in the use of bioidentical hormones that replicate those your body produces and methods of delivering the hormones that bypass the liver.

Keep in mind the medications that were used Premarin and Provera were taken orally and metabolized through the liver, he said. Physiologically that causes a lot of activity in the breast tissue.

Bioidentical hormones are more like your ovaries made thats the definition he added. Then the estrogen can even be given in cream or patch thats absorbed directly So these medications are not metabolized in the liver to make them active.

Ruiz says hormone replacement doses are much lower now and that perhaps new studies need to be done.

Read more from the original source:
Hormone Therapy and Shoulder Pain During Menopause - Healthline

October is recognized as Breast Cancer Awareness Month. During this time, health care systems and organizations aim to provide education, resources, support and prevention information regarding the disease.

The American Cancer Society (ACS), offers these statistics about breast cancer:

Early detection is important because there are more treatment options available and a better chance of survival when breast cancer is caught early, said Charissa Williams, APN, a ThedaCare Hematology & Oncology Specialist. Studies show theres a more than 90% survival rate, if the tumor is caught early.

Regular self-breast exams are one way to detect a cancerous tumor. A breast cancer screening is another way. Mammograms can spot tiny tumors, making it more likely to catch the disease at an earlier stage.

For most women, screening mammography is a safe and effective way to detect breast cancer early, Williams added.

Medical organizations vary on the best age to start screening mammograms (some say as early as age 40) and how often to repeat them. The Centers for Disease Control and Prevention (CDC) has a comparative chart, Breast Cancer Screening Guidelines for Women, to better sort out the timing and frequency of mammogram screening based on your particular situation.

It is important to discuss your individual screening guidelines with your primary care provider, said Williams. For example, those who have a strong family history or certain genetic mutations (BRCA1 or BRCA2) often have earlier screening guidelines than the general population.

Women might also help minimize their chances of developing the disease by modifying their lifestyle. However, Williams notes there are some risks factors that cannot be changed: your age, family history, genetics, race, and being a woman.

There are several modifiable factors that can increase your breast cancer risk, including obesity, poor diet, lack of physical activity, alcohol and tobacco use, and certain types of hormone replacement therapy, she said.

To reduce your risk of breast cancer, Williams suggests you form these habits:

There are more than 3.8 million breast cancer survivors in the United States.

For more information on breast cancer prevention tips, screenings and treatments, visit thedacare.org/breast-cancer.

About ThedaCare

For more than 110 years, ThedaCare has been committed to improving the health and well-being of the communities it serves in Northeast and Central Wisconsin. The organization delivers care to more than 600,000 residents in 17 counties and employs approximately 7,000 health care professionals. ThedaCare has 180 points of care, including eight hospitals. As an organization committed to being a leader in Population Health, team members are dedicated to empowering people to live their unique, best lives. ThedaCare also partners with communities to understand needs, finding solutions together, and encouraging health awareness and action. ThedaCare is the first in Wisconsin to be a Mayo Clinic Care Network Member, giving specialists the ability to consult with Mayo Clinic experts on a patients care. ThedaCare is a not-for-profit health system with a level II trauma center, comprehensive cancer treatment, stroke and cardiac programs, as well as primary care.

For more information, visit thedacare.org or follow ThedaCare on social media. Members of the media should call Cassandra Wallace, Public and Media Relations Consultant at 920.442.0328 or the ThedaCare Regional Medical Center-Neenah switchboard at 920.729.3100and ask for the marketing person on call.

Related

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Helping Reduce Your Risk of Breast Cancer ThedaCare - ThedaCare

CARBONDALE (WSIL) -- A reproductive health clinic that will also provide abortion serves has opened in Carbondale.

TheCHOICES: Memphis Center for Reproductive Health announced they would open a clinic in southern Illinois after learning the Supreme Court would overrule Roe v. Wade. Tennessee has now banned abortion services.

The CHOICES clinic is located on Giant City Road and is now accepting appointments for medication abortions. They started seeing their first patients Tuesday.

The clinic will be the southernmost abortion clinic for most people across the southeast, according to a release.

Eventually, the clinic will also offer gender-affirming hormone therapy, procedural abortions, birth control, sexual wellness and more.

The Memphis location is still open, they just will no longer provide abortion services. They will still provide reproductive and sexual health care.

More coverage:

Read the original:
CHOICES Reproductive Health clinic now open in Carbondale - WSIL TV

Its not all bad news for the province, however, as it received the fewest reports of stock-outs by public healthcare users. Photo: Reuters

NEWS

Every three months, Vuyo* has to travel for about four hours from Matatiele in the Eastern Cape to Durban in KwaZulu-Natal to get her antiretroviral (ARV) treatment.

She has been featured in the second edition of the Eastern Cape State of Health report by Ritshidze, a community-led monitoring system developed by organisations representing people living with HIV.

The organisations include the Treatment Action Campaign, the National Association of People Living with HIV, the Positive Action Campaign, the Positive Womens Network, and the SA Network of Religious Leaders Living with and affected by HIV/Aids.

The Ritshidze data, which was launched on Thursday, reveal improvements at Eastern Cape clinics, but patients still complained about poor treatment at healthcare facilities, which saw them missing their appointments and even stopping their clinic visits.

READ: Intimate partner violence impedes ARV treatment adherence among adolescents - study

Vuyo tested positive for HIV two years ago and was getting her treatment from Matatiele Community Clinic.

On this day, I was in pain and decided to go to the clinic. I told the nurse my problem and she started shouting that I was being careless with my life for not using a condom. She called other nurses and they started talking about me as if I was not there. That day was so embarrassing, and I was hating myself so much. I even thought of dying, and thats when I decided to quit the clinic, she said.

For some time after that incident, Vuyo defaulted on her medication because, when she went to other clinics, she was referred back to Matatiele.

She said:

I then decided to go and get my medication in Durban, as my sister works there. It is working better for me like that, and they give me medication for three months. I dont have problems with the medication and I dont default.

No privacy

Ritshidze data show that 55% of the people interviewed thought that clinic staff were always friendly and professional in the Eastern Cape. This is down from 63% last year.

This poor treatment is off-putting enough for people to miss appointments or even stop going to the clinic altogether. Some report being terrified at what awaits them, read the report.

Some people complained that clinic staff members disclose the status of patients living with HIV in waiting areas.

There were also reports of two or more patients consulted with or counselled in the same room, and people living with HIV separated from other chronic patients.

According to the report for key populations, clinic visits can be traumatic, and staff can be unfriendly and even openly hostile.

Many people we spoke to had given up on healthcare altogether, including 47% of gay and bisexual people, and men who have sex with men; 41% of people who use drugs; 39% of sex workers; and 47% of transgender people.

Despite commitments by Pepfar [The US Presidents Emergency Plan for Aids Relief] and the national health department to roll out a robust key population sensitisation toolkit as part of standard in-service training for all facility staff, disrespect, ill-treatment and dehumanisation of key populations remain a widespread challenge that should be urgently fixed, with consequences for clinic staff who commit privacy violations.

READ: Study finds SA street sex workers have a high chance of being infected with HIV

The report states that, for those key populations still getting healthcare, most go to public healthcare facilities, yet specific services remain extremely limited.

Lubricants were only available in 41% of sites during this reporting period. While, notably, PrEP [pre-exposure prophylaxis] was reported as available at all 45 facilities monitored, the number of facilities that reported offering PrEP to key populations was far lower. Drug dependence and overdose treatments are not available at our clinics, neither is hormone therapy, yet 36% of people who use drugs wanted access to methadone and 35% wanted access to naloxone, and 29% of transgender people wanted access to hormone treatments at their facilities, reads the report.

Slight improvement

Its not all bad news for the province, however, as it received the fewest reports of stock-outs by public healthcare users in the current reporting period, with only 7% of patients who had left, or knew someone who had left, a facility without the medication they needed.

The report said:

Of the sites that reported a stock-out, 15% were forced to send people away empty-handed. The issues outlined in the second edition of the state of health report identify reasons people do not want to go to the clinic to access HIV and tuberculosis prevention and treatment services, and why some people interrupt treatment or disengage from care altogether.

According to the report, understaffed clinics meant that healthcare workers were overburdened, which led to longer waiting times, limited time to attend to public healthcare users and bad attitudes.

These factors directly and negatively impact people living with HIV from starting and staying on treatment. By June next year, the Eastern Cape health department should fill 70% of vacancies in the province, including the 322 vacancies reported at Ritshidze sites, and fill the remaining 30% by the end of the 2023/24 financial year.

The provincial health department should produce annual reports on the number of healthcare workers employed in each district and the number of people and size of areas covered by these healthcare workers. These reports should also include year-on-year comparisons (from at least 2020) of the number of filled posts in all districts and the cost of these posts to the government, the report recommends.

*Not her real name

Read more here:
HIV patients abused and humiliated - News24

Diabetes is characterized by insufficient production of insulin due to the loss or dysfunction of pancreatic beta cells.

A new study published in Cell Metabolism shows that a protein called beta cell expansion factor A (BefA) secreted by gut bacteria could induce the replication of insulin-producing beta cells in neonatal mice.

Understanding the mechanisms underlying the actions of BefA protein could help develop therapies to stimulate beta cell proliferation in individuals with diabetes.

The study also provides a potential explanation of how the gut microbiome could play a role in the development of diabetes.

Study author Dr. Karen Guillemin, a professor at the University of Oregon in Eugene, told Medical News Today:

[Our findings imply] that the activities of gut bacteria in young animals including possibly humans can shape the development of the pancreas in early life. This is important because early life corresponding to about the first 2 years of life in a human is when insulin-producing beta cells are most proliferative, after which they become more quiescent. If this population of beta cells does not proliferate enough during early life, it means that the individual with a small beta cell pool is more vulnerable to developing type 1 diabetes if beta cells are depleted by autoimmune attack.

Dr. Martin Blaser, a professor in the Departments of Medicine and Pathology and Laboratory Medicine at Rutgers University, NJ, commented that this study is exciting because it represents a novel way that we might be able to regrow beta cells in situations with injury like type 1 diabetes.

This is a great example of how basic research on the microbiome of zebrafish can lead to new approaches to treating important human diseases, he added.

Individuals with type 1 diabetes are unable to regulate blood sugar levels due to the loss of insulin-producing beta cells in the pancreas. The loss of beta cells in type 1 diabetes is caused by an autoimmune response against these cells.

In contrast, in type 2 diabetes the body is initially able to produce insulin but the cells in the body do not respond to insulin. In response to the consequent increase in blood glucose levels, beta cells produce more insulin to compensate for the resistance of cells to the hormone. This leads to the exhaustion of beta cells and their dysfunction, resulting in lower insulin levels.

The replication rate of beta cells is high immediately after birth but rapidly declines thereafter. Thus, therapies that stimulate the replication or regeneration of beta cells in adults could help treat diabetes.

The studys authors had previously identified such a protein, called BefA, secreted by gut microbes that could stimulate the proliferation of beta cells in zebrafish.

Moreover, the authors had also identified a version of the BefA protein synthesized by gut bacteria in humans that could stimulate the proliferation of beta cells in zebrafish. In other words, the BefA proteins secreted by gut microbes in humans and zebrafish share a similar structure and function.

In the present study, the researchers further examined the mechanism through which BefA could facilitate the proliferation of pancreatic beta cells in young mice and zebrafish.

Previous studies have shown that the gut microbiome could potentially play a role in the development of diabetes. In their previous work, the study authors had shown that germ-free zebrafish larvae, which show a complete absence of gut microbes, show lower levels of pancreatic beta cell proliferation during development.

In addition, exposure to BefA prevented this decline in beta cell proliferation in germ-free zebrafish larvae.

In the current study, the researchers examined whether the BefA protein performed a similar function in mice. Specifically, they examined the impact of BefA in germ-free and specific pathogen-free (SPF) mice.

SPF mice are reared so that they are not exposed to disease-causing microorganisms that may interfere with the goals of the study.

Similar to germ-free zebrafish larvae, germ-free neonatal mice and SPF mice treated with antibodies at birth showed lower levels of beta cells than untreated SPF.

Notably, the BefA protein was able to rescue beta cell development in germ-free and antibody-treated SPF neonatal mice. Moreover, mice treated with BefA also showed lower blood glucose levels than untreated animals.

The researchers then examined whether the BefA protein could directly interact with beta cells to stimulate their expansion instead of exerting these effects by interacting with other tissues. They cultured pancreatic tissue dissected from germ-free zebrafish larvae and mice pups in the laboratory and exposed the cells to the BefA protein.

The researchers found that the BefA protein was able to directly interact with and stimulate the proliferation of pancreatic beta cells.

In subsequent studies using zebrafish larvae, the researchers examined how BefA protein synthesized by gut microbes could reach the beta cells in the pancreas. The BefA protein could be transmitted to the pancreas via the bloodstream or the hepatopancreatic duct, which connects the pancreas to the gut.

Using zebrafish models with a compromised hepatopancreatic duct or lacking blood vessels, the researchers found that pancreatic beta cell proliferation was reduced in both models.

These results show that BefA protein produced by intestinal microbiota could indeed travel from the intestine via the hepatopancreatic duct or blood vessels to reach the pancreas.

To better understand the function of the BefA protein, the researchers examined the structure of the protein. They found that BefA proteins derived from the bacterial species Klebsiella aerogenes in the human gut, and Aeromonas veronii in zebrafish showed considerable structural differences but shared an identical domain or region of the protein called SYLF.

The researchers found that the SYLF domain could rescue the loss of pancreatic beta cells in germ-free zebrafish larvae. These results suggest that this region could underlie the ability of the BefA protein to induce the proliferation of pancreatic cells.

Evidence from previous studies examining other proteins containing the SYLF domain from a wide range of organisms suggested that the ability of the BefA protein to stimulate beta cell proliferation may be mediated by its interaction with lipid membranes that surround cells.

Consistent with this, the researchers found that the BefA protein was able to permeabilize or disrupt synthetic membranes as well as membranes surrounding the cells of bacteria.

The secretion of BefA protein by certain gut bacteria could damage the cell membrane of other gut bacteria and confer a competitive advantage over these microbes. Moreover, this ability to disrupt cell membranes could also potentially explain the BefA proteins ability to enhance beta cell proliferation.

To test this hypothesis, the researchers exposed cultured pancreatic beta cells to a mutated form of BefA protein with a reduced ability to permeabilize membranes. The mutated BefA protein had a reduced ability to induce the proliferation of cultured pancreatic beta cells from neonatal mice.

These results suggest that the membrane permeabilizing activity of BefA was responsible for mediating its effects on beta cell proliferation. Proteins such as BefA may be secreted by gut microbes to gain a competitive advantage over other bacteria, but could also confer incidental benefits to the human host by facilitating normal pancreatic development.

However, Dr. Guillemin noted: We dont know yet whether BefA can stimulate proliferation of beta cells in older animals, in animals that have experienced beta cell autoimmune attack, or in people, but these are questions we are currently pursuing. We also dont know yet how membrane permeabilization stimulates beta cells to proliferate, but we are also pursuing this question.

In addition to the BefA protein synthesized by a subset of gut microbes, other proteins produced by human cells also possess membrane permeabilizing properties. This includes antimicrobial proteins that form pores in the membrane of bacterial cells and protect the body from harmful bacteria.

The researchers found that the Reg3 protein, a member of the antimicrobial protein family, was also able to increase the proliferation of mice and zebrafish pancreatic cells.

Proteins such as BefA that are produced during microbial competition are known to activate antimicrobial proteins. The study authors think that proteins secreted by gut microbes such as BefA and the antimicrobial proteins that are produced in response to these proteins could play an important role in the development of pancreatic beta cells.

These findings could facilitate the development of strategies for the prevention or treatment of diabetes. The diversification of the microbial communities in the gut occurs at the same time as the proliferation of beta cells after birth.

A lack of microbial diversity during early childhood, especially lower levels of microbes that secrete proteins such as BefA, could thus increase the risk of type 1 diabetes.

Dr. Guillemin explained:

There are several potential future therapeutic applications of our findings. One area is in prevention. It may be possible to perform microbiome profiling combined with other genetic and environmental data analysis to predict whether infants are at high risk for developing type 1 diabetes and if they may benefit from prophylactic administration of BefA-producing gut bacteria or BefA protein formulations to stimulate the development of their beta cell population in the first 2 years of life, which is when beta cells are most proliferative and when the lifelong pool of beta cells is established.

The second area is in the treatment of [type 1 diabetes], she added. It is possible that BefA will prove useful for stimulating the proliferation of beta cells in older individuals and in pancreases following the autoimmune destruction of beta cells, which is the process that causes [type 1 diabetes].

Even if BefA itself is not able to stimulate beta cell proliferation in these circumstances, our studies of the BefA mechanism may uncover new strategies to stimulate beta cell proliferation through membrane manipulations, said Dr. Guillemin.

Read the rest here:
Diabetes and the gut: How a bacterial protein may impact insulin - Medical News Today

During a Targeted Oncology case-based roundtable event, Jennifer M. Matro, MD, discussed the data supporting systemic therapies for treatment of early-stage HER2-positive breast cancer including trastuzumab and pertuzumab.

Targeted OncologyTM: What are the recommended approaches to treating early-stage HER2-positive breast cancer?

MATRO: [What I will discuss] is by no means meant to be a dogmatic approach, but more an adaptive algorithm for early-stage HER2-positive breast cancer. There are patients for whom neoadjuvant treatment is appropriate and patients for whom adjuvant treatment would be appropriate. Starting in the neoadjuvant population, which is now most of our patients: Generally, these are patients who have either positive lymph nodes or T2 tumors, and IV chemotherapy along with dual HER2-targeted therapies [is] appropriate.

After their up-front chemotherapy, they go to surgery. If they have a pCR, like our patient did here, then they proceed to HER2-directed therapy to complete 1 year. [When looking at] trastuzumab plus or minus pertuzumab there is some thought, extrapolating from the APHINITY trial [NCT01358877], that for patients who presented initially with a node-negative diseasemaybe they were T2N0and had a pCR, that you do not necessarily need the pertuzumab; but for patients who are node positive at presentation, include the pertuzumab.1,2

For patients who did not have a pCR, based on the KATHERINE trial [NCT01772472], we have the adjuvant T-DM1 [trastuzumab emtansine (Kadcyla)] for 14 cycles.3 Patients who do not have preoperative therapy and have surgery first are going to be patients who are mostly earlier stage with imaging, T1N0, or if there is a question of the extent of disease.

[In the patient in this case] there are 6 cm of nonmass enhancement and biopsy of the nonmass enhancement shows DCIS. It is unclear what the extent of disease is, and you go ahead with surgery first. If the patient comes out of surgery with negative lymph nodes and smaller tumors, then paclitaxel/trastuzumab for 12 weeks is recommended, as it has been shown in the APT trial [NCT00542451] and a subsequent larger study that the outcomes for those patients are excellent.4

For patients who have larger node-negative cancers, maybe 2 or 3 cm, or are younger and you are worried more about their risk, TCH [docetaxel, carboplatin, and trastuzumab] would also be appropriate. For node-positive patients, we are going to include the dual HER2 therapy. Neratinib [Nerlynx] in the ExteNET trial [NCT00878709] was shown to provide some benefit, particularly for patients with hormone receptorpositive disease and multiple positive lymph nodes.5 That is also part of the consideration in the algorithm for higher-risk patients.

I want to highlight that the trastuzumab biosimilars can be used interchangeably with the brand-name Herceptin, and the subcutaneous formulations of trastuzumab and trastuzumab/pertuzumab can also be used in place of the IV formulations.

Can you discuss APHINITY?

APHINITY is the study that led to the use of dual HER2 therapy in the adjuvant setting.1 The patients, who already had surgery, were randomized to chemotherapy with trastuzumab plus pertuzumab or placebo. The primary end point was invasive-diseasefree survival. They did not restrict the type of chemotherapy; it could be anthracycline or nonanthracycline based. Patients who had hormone-positive disease also got endocrine therapy.

[In the] updated analyses, with invasive-diseasefree survival by subgroup, in the intention-to-treat population, there was just under 3% improvement with the use of pertuzumab. It did not seem to matter whether they were hormone positive or hormone negative, but where the difference was really seen was in the patients who were node positive. The patients who were node positive were driving the benefit seen, and patients who were node negative did not see [much] difference with the addition of pertuzumab. So far, we do not have any overall survival benefit, but it is early and we are waiting for those results.

What is the role of the subcutaneous formulation of trastuzumab and pertuzumab?

The combination of trastuzumab, pertuzumab, and hyaluronidase [Phesgo] for subcutaneous injection has an FDA-approved indication for both early-stage and metastatic disease.6 It can be used in the neoadjuvant or adjuvant setting in combination with chemotherapy, and in the metastatic setting in combination with taxane therapy, predominantly in the first line. I believe it is preconcentrated. I know with the loading dose it is a slightly higher volumeI think it is 15 mL as opposed to 10 mLbut it is [like] a fixed dose.

The FeDeriCa study [NCT03493854] showed that the pharmacokinetics are essentially the same between the subcutaneous formulation and the IV formulation.7 In other studies that have used combination trastuzumab and pertuzumab in those settings, the thought is that the fixed-dose combination can be used for those indications as well.

FeDeriCa was a phase 3 study that was looking primarily at the pharmacokinetics. Patients who were getting preoperative chemotherapy, which was predominantly anthracycline based, were randomly assigned to IV formulation or subcutaneous formulation, and then they had surgery, and then afterward they were continued either on the IV formulation or the subcutaneous formulation. The primary end point was noninferiority of the cycle 7 trough concentration of the pertuzumab, with the fixed dose compared with the IV formulation.

One of the advantages of doing neoadjuvant studies is that we have an immediate end point of response rate. The rate of pCR was the same for both [Figure7]. It was well tolerated; no major differences in risks associated with the IV vs the subcutaneous formulation. A few more patients had a little bit of irritation at the injection site vs infusion reactions.

If you want to discontinue pertuzumab in a low-risk patient as adjuvant therapy, do you have to change back to IV?

There is a trastuzumab-[plus hyaluronidase] subcutaneous injection. The brand name is Hylecta. So, it is the same idea: If you can get access to Phesgo or the dual HER2 injection, you should be able to get access to the trastuzumab-based injection. The trastuzumab-based injection also has extensive pharmacokinetics studies showing that it is similar in efficacy to IV trastuzumab.8,9

Can you discuss the difference in timing between IV and subcutaneous administration?

With standard IV, in the first loading dose, the pertuzumab is supposed to be given over [30 to 60] minutes, and the trastuzumab is given over 30 to 90 minutes, and you have this observation period in between [of 30 to 60 minutes]. It can take hours.

Once you are on and tolerating the trastuzumab and pertuzumab IV, they can be given over 30 minutes each. There is a much shorter observation window, but nonetheless it is going to be at least 1 hour, potentially up to 2 hours. Whereas with the fixed-dose subcutaneous administration, the injection itself takes a couple of minutes. You watch them for another 15 to 30 minutes, so the total time is generally 20 to 40 minutes, so it takes at least half the time. This opens chair time for other patients who need IV infusions, and saves patients from having an IV placed, and it allows them to potentially get their port removed earlier. Generally, it can provide benefits to patients and providers. One thing that remains to be seen is whether this is something that eventually could be given at home.

I was working in Philadelphia at the beginning of the [COVID-19] pandemic, and the University of Pennsylvania at that time took most of the patients who were on leuprolide [Lupron] for ovarian suppression and transitioned them to home nursing. All of those patients were getting injections at home with their leuprolide. They did not have to come in. If you have skilled nursing in the community, is this something that patients may even be able to get at their home or their office? I think that is something that has potential for opening that up as an option, which would be even better for patients.

What is known about which option patients prefer?

We see, based on the PHranceSCa study [NCT03674112], that patients do prefer the subcutaneous formulation.10 PHranceSCa looked at patient preference. Patients who had completed their chemotherapy and surgery and were going to be completing a year of HER2-directed therapy were randomized. Half of the patients got the IV formulation, half got subcutaneous administration for the first 3 cycles, and then they crossed over and switched to whichever one they had not received before, and then they were allowed to choose which one they wanted to finish the rest of the year of HER2 therapy with. The primary objective was patient preference.

What we saw was that 85% of patients preferred the subcutaneous formulation over the IV and 87% chose to use that subcutaneous formulation to finish their treatment after experiencing it. The main reasons were less time in clinic and administration being more comfortable.

REFERENCES

1. Piccart M, Procter M, Fumagalli D, et al; APHINITY Steering Committee and Investigators. Adjuvant pertuzumab and trastuzumab in early HER2-positive breast cancer in the APHINITY trial: 6 years follow-up. J Clin Oncol. 2021;39(13):1448-1457. doi:10.1200/JCO.20.01204

2. von Minckwitz G, Procter M, de Azambuja E, et al; APHINITY Steering Committee and Investigators. Adjuvant pertuzumab and trastuzumab in early HER2-positive breast cancer. N Engl J Med. 2017;377(2):122-131. Published correction in N Engl J Med. 2017;377(7):702

3. von Minckwitz G, Huang CS, Mano MS, et al; KATHERINE Investigators. Trastuzumab emtansine for residual invasive HER2-positive breast cancer. N Engl J Med. 2019;380(7):617-628. doi:10.1056/NEJMoa1814017

4. Tolaney SM, Barry WT, Dang CT, et al. Adjuvant paclitaxel and trastuzumab for node-negative, HER2-positive breast cancer. N Engl J Med. 2015;372(2):134-141. doi:10.1056/NEJMoa1406281

5. Chan A, Delaloge S, Holmes FA, et al; ExteNET Study Group. Neratinib after trastuzumab-based adjuvant therapy in patients with HER2-positive breast cancer (ExteNET): a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncol. 2016;17(3):367-377. doi:10.1016/S1470-2045(15)00551-3

6. Phesgo. Prescribing information. Genentech; 2020. Accessed May 5, 2022. https:// bit.ly/3RFnCsv

7. Tan AR, Im SA, Mattar A, et al; FeDeriCa study group. Fixed-dose combination of pertuzumab and trastuzumab for subcutaneous injection plus chemotherapy in HER2-positive early breast cancer (FeDeriCa): a randomised, open-label, multicentre, non-inferiority, phase 3 study. Lancet Oncol. 2021;22(1):85-97. Published correction in Lancet Oncol. 2021;22(2):e42

8. Pivot X, Verma S, Fallowfield L, et al. Efficacy and safety of subcutaneous trastuzumab and intravenous trastuzumab as part of adjuvant therapy for HER2-positive early breast cancer: Final analysis of the randomised, two-cohort PrefHer study. Eur J Cancer. 2017;86:82-90. doi:10.1016/j.ejca.2017.08.019

9. Jackisch C, Stroyakovskiy D, Pivot X, et al. Subcutaneous vs intravenous trastuzumab for patients with ERBB2-positive early breast cancer: final analysis of the HannaH phase 3 randomized clinical trial. JAMA Oncol. 2019;5(5):e190339. doi:10.1001/ jamaoncol.2019.0339

10. OShaughnessy J, Sousa S, Cruz J, et al; PHranceSCa study group. Preference for the fixed-dose combination of pertuzumab and trastuzumab for subcutaneous injection in patients with HER2-positive early breast cancer (PHranceSCa): a randomised, open-label phase II study. Eur J Cancer. 2021;152:223-232. doi:10.1016/j.ejca.2021.03.047

Originally posted here:
Recommended Approaches to Treatment for Early-Stage HER2+ Breast Cancer - Targeted Oncology