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Recombinant Coronavirus Vaccines Delivered via Microneedle Array

Curator: Irina Robu, PhD

Coronavirus is an evolving pathogen with exponentially increasing significance due to the high case fatality rate, the large distribution of reservoir, and the lack of medical countermeasures. The public health emergencies triggered by coronaviruses, including SARS-CoV and SARS-CoV-2, obviously validate the urgency to assess candidate vaccines to fight these outbreaks. Continuous research contributes to the efforts of scientists to quickly progress safe vaccines against these developing infections. The recent COVID-19 pandemic indicates a vital need for the rapid design, production, testing, and clinical translation of candidate vaccines.

Coronavirus virus particles contain four main structural proteins. These are the spike, membrane, envelope, and nucleocapsid proteins, all of which are encoded within the 3′ end of the viral genome. Coronaviruses contain a non-segmented, positive-sense RNA genome, which contains a 5′ cap structure along with a 3′ poly (A) tail, allowing it to act as a mRNA for translation of the replicase polyproteins. The replicase gene encoding the nonstructural proteins inhabits two-thirds of the genome, which make up only about 10 kb of the viral genome. The 5′ end of the genome contains a leader sequence and untranslated region that encompasses multiple stem loop structures required for RNA replication and transcription. Furthermore, at the start of each structural gene are the transcriptional regulatory sequences that are essential for expression of each of these genes.

Researchers at U of Pittsburg generated codon optimized MERS-S1 subunit vaccines fused with a foldon trimerization domain to mimic the native viral structure. They engineered immune stimulants (RS09 or flagellin, as TLR4 or TLR5 agonists) into this trimeric design and tested the pre-clinical immunogenicity of MERS-CoV vaccines in mice, distributed subcutaneously by needle injection or intracutaneously by dissolving microneedle arrays by assessing virus specific IgG antibodies in the serum of vaccinated mice by ELISA and using virus neutralization assays.

Microneedle array mediated immunization has several mechanistic differences from traditional intramuscular needle injections, which could clarify the variations in the magnitude and kinetics of the ensuing responses. Due to the urgent need for COVID-19 vaccines, they used this approach to quickly advance MNA SARS-CoV-2 subunit vaccines and tested their pre-clinical immunogenicity in-vivo by manipulating the previous research on MNA MERS-CoV vaccines.

Even though it is still premature to predict whether humans immunized with these vaccine candidates will have similar responses and be protected from SARS-CoV-2 infections, their previous research show that development, production, and initial animal testing of clinically translatable MNA vaccine candidates against SARS-CoV-2. Incidentally it will be vital to determine whether antibodies from MNA-SARS-CoV-2 immunized animals will neutralize virus infectivity.

Finally, we note that the immunogenicity differences between MNA coronavirus vaccines and coronavirus vaccines delivered by traditional needle injection that we observe will need to be evaluated in clinical trials to establish the clinical advantages of MNA delivery.

SOURCE

E. Kim et al., Microneedle array delivered recombinant coronavirus vaccines: Immunogenicity and rapid translational development, EBioMedicine (2020).

Fehr, Anthony R, and Stanley Perlman. Coronaviruses: an overview of their replication and pathogenesis. Methods in molecular biology, vol. 1282 (2015): 1-23.

Susan R. Weiss, Sonia Navas-Martin. Coronavirus Pathogenesis and the Emerging Pathogen Severe Acute Respiratory Syndrome Coronavirus. Microbiology and Molecular Biology Reviews Dec 2005, 69 (4) 635-664.

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Economic Implications Of The Coronavirus

“From: Washington Post (March 19, 2020), The Atlantic (March 19, 2020), American Progress (3/6/2020), Morningstar (March 10, 2020)

1. THE CONCEPT OF A PANDEMIC

Pandemics are particularly dangerous because the general population does not have immunity to the disease. Interestingly, flu pandemics have decreased in severity with time, perhaps partly due to viral preference for diseases that are very transmissible but not lethal. Despite some similarities between seasonal and pandemic flu, there are also key differences. While seasonal flu is every year, pandemics can have multiple waves; Spanish flu came in three waves, and the 2009 swine flu had two waves.

Past pandemics have varied substantially in their lethality. For example, the 1957 Asian flu, considered a moderate pandemic, emerged in China in February 1957, reached the U.S. by June, and spread very rapidly in the fall in the U.S. and Europe, with the return to school seen as a significant driver for starting new community epidemics during that pandemic. The corresponding vaccine was developed too late and was not more than 60% effective. Most schools remained open and no travel restrictions or restrictions on social gatherings were undertaken; 25% of the U.S. population was infected. The 1968 Hong Kong flu was milder but more widespread (estimated at almost 40% of the U.S. population infected). The death rate may have been significantly lower than Asian flu because patients had some pre-existing immunity.

Coronavirus 101: A New Virus Related to SARS and MERS

On Jan. 7, a new coronavirus was identified as the cause of several cases of pneumonia in Wuhan, China. COVID-19 is the disease caused by SARS-CoV-2, one of a family of coronaviruses, and this particular strain was new to humans. Most coronaviruses spread between animals, although the common cold is often caused by a coronavirus. Like more serious coronaviruses SARS and MERS, SARS-CoV-2 is believed to have jumped to humans by first moving from one species known to carry these diseases to another species capable of transmitting the disease to humans. Like SARS-CoV and MERS, it is believed to be mostly spread through respiratory droplets, often from a patient’s cough.

A comparison with other outbreaks is one of the easiest ways to think about the potential spread of coronavirus, although every disease has slightly different characteristics that limit the accuracy of this analysis. The intersection of the fatality rate (the percentage of infected patients who succumb to the disease) and how contagious it is, if left unchecked, is a simple way to begin to outline the potential impact versus past pandemics. Epidemiologists measure how contagious a disease is using a reproduction number, termed R0, reflecting how many people an infected person can typically infect. Generally speaking, an R0 of greater than 1 is a threshold for a disease being able to expand into an epidemic, and a virus with an R0 above 1.9 is considered highly transmissible. In addition, a higher R0 means a sharper rise and fall of infection rates with a shorter duration of the outbreak. An R0 of 1.9 could imply an outbreak of months, with a two-month peak in infections, as seen with the 1957 and 1968 pandemics.

Diseases are generally the most dangerous if they are both very deadly and very contagious (high R0), but most diseases tend to be more one than the other, as the self-interest of viruses would favor evolution toward diseases that don’t kill their victims. For example, Ebola and rabies have very high fatality rates but are tougher to transmit. At the opposite end of the spectrum is the common cold, which is fairly easy to transmit but almost never fatal. Smallpox was one of the most destructive diseases, as it was both very contagious and very deadly. Also, the Spanish flu of 1918-19 caused more than 50 million deaths worldwide and killed nearly 3% of the population. However, the spread of a disease is more than these numbers–significant efforts to contain SARS have eradicated the disease, even though it is more easily transmissible than the standard flu (which is very widespread every year).

Even though death rates have been falling gradually for flu pandemics since the 1918 pandemic, coronavirus pandemics are a newer phenomenon and don’t have an established trend. Fatality rates are already being estimated, but this is very difficult to do accurately at the start of any pandemic.

One interesting observation on the lethality of the 1918 flu pandemic is that the high mortality rate of soldiers on the front lines of Western Europe exerted an evolutionary pressure on the flu virus. From the virus’ viewpoint, it makes no sense to preserve the life of your victim if the victim is going to die anyway from non-flu causes. Therefore, natural selection favored the emergence of flu mutation that both infected and killed rapidly.

2. WHAT IS TO BE DONE?

International Monetary Fund says the outbreak is the world’s “most pressing uncertainty.” The economic disruptions caused by the virus and the increased uncertainty are being reflected in lower valuations and increased volatility in the financial markets. While the exact effect of the coronavirus on the U.S. economy is unknown and unknowable, it is clear that it poses tremendous risks.

Policymakers should therefore immediately undertake a number of steps to address any economic fallout from the virus. The burden of meeting this challenge falls squarely on Congress and the Trump administration. The guiding principles need to be:

• Do no harm
• Put more, not fewer, resources in public health efforts
• Assure businesses that things will be fine if the virus hits their sector and remediate harm when necessary
• Calm financial markets
• Ease the risks for households and vulnerable populations

3. THE CHINA SYNDROME – 2020 VERSION

Economists have been using the SARS epidemic to put the coronavirus outbreak in context. The 2003 SARS epidemic is estimated to have shaved 0.5 percent to 1 percent off of China’s growth that year and cost the global economy about $40 billion (or 0.1 percent of global GDP).The coronavirus epidemic, which like SARS originated in China, differs in a few key ways.

China’s economy accounted for roughly 4 percent of the world’s GDP in 2003; it now commands 16.3 percent. If the coronavirus has a similar effect on China as SARS, the impact on global growth will be worse. Moreover, China’s growth is weaker than it was in 2003—after years of rapid economic development, China’s growth stands at 6 percent, the lowest it’s been since 1990. The dual effects of general economic deceleration and the U.S.-China trade war escalation has shaken its confidence. Even before the epidemic, China’s Purchasing Managers’ Index was already showing signs of contraction. The February reading slowed from 50 to 35.7, a level in line with that of November 2008 during the global financial crisis. The economic fallout from the coronavirus could rattle China’s economy further and dampen global growth.

Outside China, the outbreak has also affected global supply chains, as other governments have also taken immediate steps to slow the spread of the virus. The Harvard Business Review predicts that the peak of the impact will occur in late-March, “forcing thousands of companies to throttle down or temporarily shut assembly and manufacturing plants in the U.S. and Europe.” This again will disrupt global supply chains as well as demand for goods and services in the affected economies. These disruptions make it more difficult for companies in the U.S. and elsewhere to bring their goods to customers, and these companies will reduce exports from the U.S. to the rest of the world in the coming months.

Furthermore, households, companies, and governments alike are deeper in debt now than they were when SARS hit. For example, the U.S. nonfinancial corporate debt of large companies is currently around $10 trillion, up from around $4.8 trillion in 2003. Deutsche Bank released analysis showing the world’s major economies harboring the highest debt levels of the past 150 years, with World War II as an exception. They all still need to continue repaying that debt, even if jobs, customers, and tax revenues decline in a weakening economy. These fixed costs then will leave less money to spend on other things. Large amounts of debt often exacerbate an economic slowdown, especially if central banks can do little to ease that burden by cutting interest rates.

The world looks different from the last global virus outbreak in 2003. Global growth is already slow, and financial markets already have very low interest rates, which means that central banks in almost every major country have little ammunition with which to mitigate any potential economic fallout. This puts greater pressure on governments to use the power of their purse to counter the economic fallout from the coronavirus. While the fallout from the coronavirus will disrupt supply chains and global demand that could also affect the U.S. economy, the current situation also creates a lot of uncertainty over the longer term. Congress and the Trump administration can do a lot to counter the risks associated with the spread of the virus by engaging in fiscal policies (deficit spending) that will provide relief to affected populations and mitigate disruptions to U.S firms.

4. OUR FRAGILE SUPPLY CHAIN….CHEAP, BUT AT A PRICE

When Trump invoked the Defense Production Act, it was telling in two respects. First, it showed that the full force of the federal government will be brought to bear in the manufacturing of vital medical supplies. Second, it underlined what has already become clear: The way our modern supply chain is built is incredibly fragile.

We’ve built a global supply chain that runs on outsourcing and thin margins, and the coronavirus has exposed just how delicate it is.

We need to realize that there’s almost no industry sector—manufacturing and non-manufacturing—that isn’t reliant on China in the United States.
Chinese materials and manufacturing are so pervasive that the average customer has no idea how many of their everyday products contain Chinese components, or how reliant on Chinese components most companies have become. If you don’t have a first-tier supplier who’s sourcing from China, then your supplier’s supplier is.

To understand why the modern supply chain is uniquely vulnerable to a threat like the coronavirus, you have to realize how quickly it has changed. China joined the World Trade Organization in 2001, and surpassed the U.S. as an industrial powerhouse in 2010. During the SARS epidemic of 2002 and 2003, China represented 4.31 percent of worldwide GDP – today, it’s 16 percent.

Western companies find it cheaper to manufacture goods in China, and elsewhere in Asia, than to do so closer to home. Car parts, technology, fashion, medical gear, and drug components are particularly vulnerable to disruptions in Asian markets. In 2012, after the Japanese tsunami, you couldn’t buy a red Toyota for months, because the one factory that made red pigment for Toyota was offline. Apple, Fiat Chrysler, and Hyundai have already warned investors of potential supply constraints due to the coronavirus pandemic.

In addition to offshoring, companies have emphasized “just in time” delivery, keeping only 15 to 30 days of products on hand. That has made global companies more profitable but has also “significantly increased supply-chain risk.”


The worst of the supply-chain disruptions would begin now. Fewer Chinese ships are on the water, and major ports around the world, such as Rotterdam and Le Havre, are already feeling the effects. Those 15 to 30 days of inventory (even if a company stocked up prior to the Chinese Lunar New Year holiday) are likely running low now. We are going to see a slowdown, disruption, less variety, less options to the customers.

As the COVID-19 pandemic ripples throughout the world economy, it’s possible that it may begin to change the way global supply chains work. Companies will come under pressure to diversify where they make their products, which will prove easier for some than for others. While the blood thinner heparin may still be made in China, it’s not as difficult to move the infrastructure for, say, the kind of fashion sold at H&M and Zara to other Asian countries. “You can still emphasize low labor costs by moving into Vietnam, Malaysia, and Cambodia,” he said. More electronic and car-part production could shift to factories in Mexico and Brazil.

5. THE NEW NORMAL

Taking the above into account (plus numerous other factors): how bad will this all be?

We have essentially made a collective decision to have ourselves a recession. We’ve shut down a significant portion of our economy, knowing that the result will be businesses going bankrupt, huge job losses and people losing their homes.

How bad it gets depends on decisions the federal government makes in coming days.

JP Morgan forecast that the second quarter contraction would be a stunning 14 percent — worse than the depth of the Great Recession. If they’re right, this would translate to 7.5 million jobs lost by the summer. In the Great Recession, about 8 million jobs disappeared. Now some are predicting that the drop in payrolls for April alone could be as high as 5 million.

Recessions are often set off by some kind of shock, but it’s usually preceded by a period of slowdown or uncertainty. Now we’ve gone from 60 to zero in days. You can now go to restaurants that are shuttered that were doing a booming business a few weeks ago.

We’re already seeing a dramatic jump in unemployment claims, but current data almost certainly underestimate how bad the situation has already gotten. Those who have filed so far were people who were laid off last week, and also got their act together to file unemployment claims.

If we know that we’re plunging off a cliff, the next question is how quickly we might begin to recover. Forecasts from Goldman Sachs, JPMorgan and Bank of America all assume the economy will bounce back in the third and fourth quarters of this year, but that might not be the case even if we get the virus under control: there are a lot of people losing their livelihoods.

As part of the federal solution, we have to make it possible for businesses not to lay people off even if they aren’t working, through some combination of grants and low-interest loans, to get a “quick bounce-back” by keeping people connected to their employers.

All these economists said we must do everything: Give support to state governments that are particularly vulnerable because they’re required by law to balance budgets; help employers not go out of business; shore up the safety net, including unemployment insurance, Medicaid and food stamps; and give support directly to people.

During the Great Recession, we turned to austerity way too fast and lengthened the pain way longer than we should have. The danger is not in building up debt that eventually will have to be repaid, but in holding back because the numbers look too large. The risk is not in doing too much, but in doing too little. All this is pretty frightening — and it doesn’t even take into account how long it might take to control the coronavirus.

Sources: Washington Post (March 19, 2020) , The Atlantic (March 19, 2020), American Progress (3/6/2020), Morningstar (March 10, 2020)

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Reporter: Gail S. Thornton, M.A.

The following article is reprinted from the Anchorage Daily News.

https://www.adn.com/alaska-news/2020/03/18/one-of-alaskas-first-confirmed-coronavirus-patients-tells-his-story/

One of Alaska’s first confirmed coronavirus patients tells his story

March 19, 2020

A Ketchikan man who contracted the illness caused by the new coronavirus is speaking out about his experience.

In a social media post and an interview with the Ketchikan Daily News, he described his symptoms, how he was tested and his experience communicating with Alaska public health officials.

As of Wednesday morning, Glenn Brown, the attorney for the Ketchikan Gateway Borough, is one of nine people statewide who have confirmed cases of the virus. Officials have not said any of the people with confirmed cases have been hospitalized.

Brown said in a Facebook post that he was feeling better and was notified by public health officials that he’d tested positive for COVID-19 on Tuesday afternoon.

“I became sick Saturday morning with fever, headache, general achiness and chills,” Brown wrote.

Brown said he has “no idea” how he contracted the illness.

“I interacted with no one in recent weeks who was exhibiting obvious symptoms,” he wrote.

According to a statement Tuesday from the Ketchikan Emergency Operations Center saying one of its employees tested positive for the virus, the employee had a history of travel to the Lower 48. The Ketchikan Emergency Operations Center on Wednesday confirmed Brown is the employee.

The Ketchikan Daily News reported that Brown had recently traveled to Oregon and Juneau before returning to Ketchikan on March 9.

After public health officials told Brown his diagnosis, he said that he went through more than an hour of questions with them, he told the Ketchikan Daily News.

“I used everything from cellphone records to work calendars to debit card bills, to recall everybody that I may have had contact with,” Brown told the Ketchikan Daily News. “I wanted to provide that information to public health, (so) that they could alert those people and really hope to kind of arrest this thing.”

Brown told the paper that public health officials focused on two days before he developed symptoms of the illness. Brown had been “working closely with borough staff and upper management” in those days as part of his job, the paper reported.

“I apologize for causing undue concern for anyone, especially my co-workers at the Borough,” Brown said in the Facebook post.

Ketchikan Gateway Borough employees in direct contact with Brown were instructed to self-quarantine for two weeks, according to the Ketchikan Emergency Operations Center statement.

The statement also said that the borough had hired a service to disinfect the now-closed White Cliff Building, which houses the Ketchikan Borough offices.

According to the Ketchikan Daily News, the last time Brown was at the borough’s White Cliff Building was Friday.

The paper reported that as of Tuesday night, there were no plans to test people who had been in direct contact with Brown.

A public information officer for Ketchikan’s Emergency Operations Center told the Ketchikan Daily News that she understood that to be tested, people would need to have “several” symptoms of the virus.

“I would also ask that you join me and all of Ketchikan to actively minimize community transmission so that we can protect our seniors or other medically vulnerable folks in Ketchikan,” Brown wrote. “I pray that we all make it through this largely unharmed, and together.”

The first person in Alaska to test positive for COVID-19 was an air cargo pilot who arrived at Ted Stevens Anchorage International Airport on March 11, officials announced last week. He went through the airport’s North Terminal, which is separate from the domestic terminal.

Alaska’s chief medical officer, Dr. Anne Zink, said last week the man had self-isolated and was “stable.”

On Monday, officials said two older men in Fairbanks were diagnosed with the illness. Both had recently traveled to the Lower 48, Zink said, but were not traveling together.

In addition to the Anchorage case, the case in Ketchikan and the two in Fairbanks, officials on Tuesday announced that two more people had become sick with the virus — one in Fairbanks and one in Anchorage — bringing the total number of confirmed cases as of Wednesday morning to six.

Zink said that both of those cases were also travel-related. None of the three people who tested positive for COVID-19 on Tuesday were hospitalized, Zink said.

Fairbanks Memorial Hospital released a statement Tuesday saying a woman with a history of recent travel had tested positive for COVID-19.

“She self-isolated prior to testing,” the statement said. “This patient has been notified and is in stable condition and does not require hospitalization.”

A University of Alaska Fairbanks employee was one of the people who had recently tested positive for the virus in Alaska, university officials said Tuesday.

An internal email advised anyone who had used the O’Neill Building, which houses the College of Fisheries and Ocean Sciences, to stay home and monitor themselves for two weeks.

State and local officials have taken a series of steps to stem the spread of COVID-19 in Alaska, including closing schools, calling on hospitals to halt elective surgeries and shutting down dine-in service at all restaurants, bars, breweries, cafes and similar businesses.

About this Author

Morgan Krakow

Morgan Krakow is a general assignment reporter for the Anchorage Daily News. She is a 2019 graduate of the University of Oregon and spent the past summer as a reporting intern on the general assignment desk of The Washington Post. Contact her at mkrakow@adn.com.

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Ethics Behind Genetic Testing in Breast Cancer: A Webinar by Laura Carfang of survivingbreastcancer.org

Reporter: Stephen J. Williams, PhD

The following are Notes from a Webinar sponsored by survivingbreastcancer.org  on March 12,2020.

The webinar started with a brief introduction of attendees , most who are breast cancer survivors.  Survivingbreastcancer.org is an organization committed to supplying women affected with breast cancer up to date information, including podcasts, webinars, and information for treatment, care, and finding support and support groups.

Some of the comments of survivors:

  • being strong
  • making sure to not feel overwhelmed on initial diagnosis
  • get good information
  • sometimes patients have to know to ask for genetic testing as physicians may not offer it

Laura Carfang discussed her study results presented at  a bioethics conference in Clearwater, FL   on issues driving breast cancer patient’s  as well as at-risk women’s decision making process for genetic testing.  The study was a phenomenological study in order to determine, through personal lived experiences, what are pivotal choices to make genetic testing decisions in order to improve clinical practice.

The research involved in depth interviews with 6 breast cancer patients (all women) who had undergone breast cancer genetic testing.

Main themes coming from the interviews

  • information informing decisions before diagnosis:  they did not have an in depth knowledge of cancer or genetics or their inherent risk before the diagnosis.
  • these are my genes and I should own it: another common theme among women who were just diagnosed and contemplating whether or not to have genetic testing
  • information contributing to decision making after diagnosis: women wanted the option, and they wanted to know if they carry certain genetic mutations and how it would guide their own personal decision to choose the therapy they are most comfortable with and gives them the best chance to treat their cancer (the decision and choice is very personal)
  • communicating to family members and children was difficult for the individual affected;  women found that there were so many ramifications about talking with family members (how do I tell children, do family members really empathize with what I am going through).  Once women were tested they felt a great strain because they now were more concerned with who in their family (daughters) were at risk versus when they first get the diagnosis the bigger concern was obtaining information.
  • Decision making to undergo genetic testing not always linear but a nonlinear process where women went from wanting to get tested for the information to not wanting to get tested for reasons surrounding negative concerns surrounding knowing results (discrimination based on results, fear of telling family members)
  • Complex decision making involves a shift or alteration in emotion
  • The Mayo Clinic has come out with full support of genetic testing and offer to any patient.

Additional resources discussed was a book by Leslie Ferris Yerger “Probably Benign” which discusses misdiagnoses especially when a test comes back as “probably benign” and how she found it was not.

 

for more information on further Podcasts and to sign up for newsletters please go to https://www.survivingbreastcancer.org/

and @SBC_org

More articles on this Online Open Access Journal on Cancer and Bioethics Include:

Ethical Concerns in Personalized Medicine: BRCA1/2 Testing in Minors and Communication of Breast Cancer Risk

Tweets and Re-Tweets by @Pharma_BI ‏and @AVIVA1950 at 2019 Petrie-Flom Center Annual Conference: Consuming Genetics: Ethical and Legal Considerations of New Technologies, Friday, May 17, 2019 from 8:00 AM to 5:00 PM EDT @Harvard_Law

Genomics & Ethics: DNA Fragments are Products of Nature or Patentable Genes?

Study Finds that Both Women and their Primary Care Physicians Confusion over Ovarian Cancer Symptoms May Lead to Misdiagnosis

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Early menopause, defined as the cessation of ovarian function before the age of 45 years, affects approximately 10% of women in Western populations. Current research suggests that women who experience early menopause are at increased risk of premature mortality, cognitive decline, osteoporosis, and cardiovascular disease.

 

The reproductive aging process is characterized by the gradual decrease in both quantity and quality of oocytes within ovarian follicles. The number of oocytes a woman is born with, the rate of loss of those oocytes during the life span because of the process of atresia, and the threshold number of oocytes needed to produce sufficient hormones to maintain menstrual cyclicity have been identified as determinants of age at menopause.

 

Women who breastfed their infants exclusively for seven to 12 months may have a significantly lower risk of early menopause than their peers who breastfed their infants for less than a month, according to an analysis funded by the National Institutes of Health. The study was conducted at University of Massachusetts provide the strongest evidence to date that exclusive breastfeeding may reduce the risk of early menopause. The study also suggests that pregnancy can reduce the risk of early menopause.

 

Previous studies have suggested that menopause before age 45 (early menopause) increases the risk of early death, cognitive decline, osteoporosis and cardiovascular disease. Smaller studies have found evidence linking pregnancy and breastfeeding with later menopause, but because of their size and other limitations, the results are inconclusive. Moreover, the earlier studies focused on timing of menopause and not on the risk of early menopause.

 

In the present study, researchers analyzed data from more than 100,000 women ages 25 to 42 years. Every two years, from 1989 to 2015, the participants responded to detailed questionnaires, providing health information and medical history, including pregnancy history. Compared to women who had never been pregnant or who had been pregnant for less than six months, women who had one full-term pregnancy had an 8% lower risk of early menopause. Those who had two pregnancies had a 16% lower risk, and those who had three pregnancies had a 22% lower risk.

 

Women who breastfed had an even smaller risk for early menopause. Those who breastfed for a total of 25 months or more during their premenopausal years had a 26% lower risk than women who breastfed for less than a month. Similarly, women who breastfed exclusively seven to 12 months had a 28% lower risk of early menopause, compared to those who breastfed for less than a month.

 

It is yet to be determined why pregnancy and breastfeeding lower the risk of early menopause. However, researchers theorize that because pregnancy and breastfeeding halt ovulation, the slowing of the egg loss may delay menopause. This study population is fairly homogeneous with respect to race and ethnicity, but it is expected that the physiological association between the reproductive factors of parity, breastfeeding, and early menopause would not differ substantially by race/ethnicity. Additional evaluation of these associations in more diverse populations as well as further study of the association with anti-Müllerian hormone levels are important.

 

References:

 

https://www.nih.gov/news-events/news-releases/pregnancy-breastfeeding-may-lower-risk-early-menopause-nih-study-suggests

 

https://www.ncbi.nlm.nih.gov/pubmed/31968114

 

https://www.ncbi.nlm.nih.gov/pubmed/19733988

 

https://www.ncbi.nlm.nih.gov/pubmed/18192670

 

https://www.ncbi.nlm.nih.gov/pubmed/7856687

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2615483/

 

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What's The Big Data?

Terence Parr: “I am a computer scientist retooling as a machine learning droid and have found the nomenclature used by statisticians to be peculiar to say the least, so I thought I’d put this document together. It’s meant as good-natured teasing of my friends who are statisticians, but it might actually be useful to other computer scientists. I look forward to a corresponding document written by the statisticians about computer science terms!” (Statisticians say the darndest things)

I know of at least one corresponding document, published in 1994 with the rise of Neural Networks or what I have called Statistics on Steroids (SOS), which are responsible, to a large extent, to the success of today’s “AI” or Deep Learning, an advanced version of machine learning.

In Neural Networks and Statistical Models (1994), Warren Sarle explained to his worried and confused fellow statisticians that the ominous-sounding artificial neural…

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Healing traumatic brain injuries with self-assembling peptide hydrogels

Reporter : Irina Robu, PhD

In 2014, TBIs resulted in about 2.53 million emergency department visits in the U.S., according to the Centers for Disease Control and Prevention. A traumatic brain injury (TBI) can range from a mild concussion to a severe head injury. It is caused by a blow to the head or body, a wound that breaks through the skull or another injury that jars or shakes the brain. Individuals with traumatic brain injuries can develop secondary disorders after the initial blow. Researchers, Biplab Sarkar and Vivek Kumar from New Jersey Institute of Technology are hoping to prevent secondary disorders by injecting a self-assembling peptide hydrogel into the brains of rats with traumatic brain injury and see what happens. They observed that the hydrogel helped blood vessels regrow in addition to neuronal survival.

The researchers explained that after traumatic brain injury, the brain can amass glutamate which kills some neurons which is marked by overactive oxygen-containing molecules (oxidative stress), inflammation and disruption of the blood-brain barrier. Furthermore, TBI survivors can experience impaired motor control and depression. Within the experiment, the researchers showed that a week after injecting the gel in rats, the neurons have twice as many neurons at the injury site than the control animals did.

The NJIT researchers distinguished that they needed to inject the hydrogel directly in a rat’s brain just seconds after a TBI, which is not ideal, because it would be impossible to give a patient the treatment within that short period of time. The next step in showing that the self-assembling peptide hydrogel works is to combine their previous blood vessel-growing peptide and the new version to see whether it could enhance recovery. And the researchers plan to inspect whether the hydrogels work for more diffuse brain injuries such as concussions.

SOURCE

https://www.fiercebiotech.com/research/healing-traumatic-brain-injuries-self-assembling-peptide-hydrogels

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