header logo image


Page 12«..11121314..2030..»

Archive for April, 2020

Seattle Genetics (NASDAQ:SGEN) Is In A Strong Position To Grow Its Business – Yahoo Finance

Thursday, April 23rd, 2020

We can readily understand why investors are attracted to unprofitable companies. For example, biotech and mining exploration companies often lose money for years before finding success with a new treatment or mineral discovery. But the harsh reality is that very many loss making companies burn through all their cash and go bankrupt.

So, the natural question for Seattle Genetics (NASDAQ:SGEN) shareholders is whether they should be concerned by its rate of cash burn. In this report, we will consider the company's annual negative free cash flow, henceforth referring to it as the 'cash burn'. We'll start by comparing its cash burn with its cash reserves in order to calculate its cash runway.

View our latest analysis for Seattle Genetics

A company's cash runway is calculated by dividing its cash hoard by its cash burn. When Seattle Genetics last reported its balance sheet in December 2019, it had zero debt and cash worth US$811m. In the last year, its cash burn was US$234m. That means it had a cash runway of about 3.5 years as of December 2019. Notably, however, analysts think that Seattle Genetics will break even (at a free cash flow level) before then. In that case, it may never reach the end of its cash runway. The image below shows how its cash balance has been changing over the last few years.

NasdaqGS:SGEN Historical Debt April 22nd 2020

Some investors might find it troubling that Seattle Genetics is actually increasing its cash burn, which is up 4.3% in the last year. The silver lining is that revenue was up 40%, showing the business is growing at the top line. On balance, we'd say the company is improving over time. While the past is always worth studying, it is the future that matters most of all. For that reason, it makes a lot of sense to take a look at our analyst forecasts for the company.

There's no doubt Seattle Genetics seems to be in a fairly good position, when it comes to managing its cash burn, but even if it's only hypothetical, it's always worth asking how easily it could raise more money to fund growth. Issuing new shares, or taking on debt, are the most common ways for a listed company to raise more money for its business. One of the main advantages held by publicly listed companies is that they can sell shares to investors to raise cash to fund growth. We can compare a company's cash burn to its market capitalisation to get a sense for how many new shares a company would have to issue to fund one year's operations.

Since it has a market capitalisation of US$24b, Seattle Genetics's US$234m in cash burn equates to about 1.0% of its market value. That means it could easily issue a few shares to fund more growth, and might well be in a position to borrow cheaply.

It may already be apparent to you that we're relatively comfortable with the way Seattle Genetics is burning through its cash. In particular, we think its cash runway stands out as evidence that the company is well on top of its spending. While its increasing cash burn wasn't great, the other factors mentioned in this article more than make up for weakness on that measure. Shareholders can take heart from the fact that analysts are forecasting it will reach breakeven. After considering a range of factors in this article, we're pretty relaxed about its cash burn, since the company seems to be in a good position to continue to fund its growth. Taking an in-depth view of risks, we've identified 2 warning signs for Seattle Genetics that you should be aware of before investing.

Story continues

Of course, you might find a fantastic investment by looking elsewhere. So take a peek at this free list of companies insiders are buying, and this list of stocks growth stocks (according to analyst forecasts)

If you spot an error that warrants correction, please contact the editor at editorial-team@simplywallst.com. This article by Simply Wall St is general in nature. It does not constitute a recommendation to buy or sell any stock, and does not take account of your objectives, or your financial situation. Simply Wall St has no position in the stocks mentioned.

We aim to bring you long-term focused research analysis driven by fundamental data. Note that our analysis may not factor in the latest price-sensitive company announcements or qualitative material. Thank you for reading.

Excerpt from:
Seattle Genetics (NASDAQ:SGEN) Is In A Strong Position To Grow Its Business - Yahoo Finance

Read More...

Rapidly Revealing COVID-19s Journey and Evolution With Genetic Tracing Barcode – SciTechDaily

Thursday, April 23rd, 2020

Researchers have reported a method to quickly identify mutated versions of SARS-CoV-2, the virus that causes COVID-19. Credit: Drexel University

Drexel University researchers have reported a method to quickly identify and label mutated versions of the virus that causes COVID-19. Their preliminary analysis, using information from a global database of genetic information gleaned from coronavirus testing, suggests that there are at least six to 10 slightly different versions of the virus infecting people in America, some of which are either the same as, or have subsequently evolved from, strains directly from Asia, while others are the same as those found in Europe.

First developed as a way of parsing genetic samples to get a snapshot of the mix of bacteria, the genetic analysis tool teases out patterns from volumes of genetic information and can identify whether a virus has genetically changed. They can then use the pattern to categorize viruses with small genetic differences using tags called Informative Subtype Markers (ISM).

Major SARS-CoV-2 genetic subtypes in countries/regions with the most sequences (indicating date subtype was firstsequenced in that country/region). Subtypes with less than 5% abundance are plotted as OTHER. Credit: Drexel University

Applying the same method to process viral genetic data can quickly detect and categorize slight genetic variations in the SARS-CoV-2, the novel coronavirus that causes COVID-19, the group reported in a paper recently posted on the preliminary research archive, bioRxiv. The genetic analysis tool that generates these labels is publicly available for COVID-19 researchers on GitHub.

The types of SARS-CoV-2 viruses that we see in tests from Asia and Europe is different than the types were seeing in America, said Gail Rosen, PhD, a professor in Drexels College of Engineering, who led the development of the tool. Identifying the variations allows us to see how the virus has changed as it has traveled from population to population. It can also show us the areas where social distancing has been successful at isolating COVID-19.

Relative abundance of ISMs in DNA sequences from Canada as sampled over time. Credit: Drexel University

The ISM tool, developed by Rosen and a focused team including doctoral studentZhengqiao Zhao and Bahrad A. Sokhansani, PhD, an independent researcher and intellectual property attorney, is particularly useful because it does not require analysis of the full genetic sequence of the virus to identify its mutations. In the case of SARS-CoV-2, this means reducing the 30,000-base-long genetic code of the virus to a subtype label 17 bases long.

Its the equivalent of scanning a barcode instead of typing in the full product code number, Rosen said. And right now, were all trying to get through the grocery store a bit faster. For scientists this means being able to move to higher-level analysis much faster. For example, it can be a faster process in studying which virus versions could be affecting health outcomes. Or, public health officials can track whether new cases are the result of local transmission or coming from other regions of the United States or parts of the world.

While these genetic differences might not be enough to delineate a new strain of virus, Rosens group suggests understanding these genetically significant subtypes, where theyre being found and how prevalent they are in these areas is data granular enough to be useful.

Stacked plot of the number of sequences of the reference sequence ISM subtype (CCCCGCCCACAGGTGGG). Credit: Drexel University

This allows us to see the very specific fingerprint of COVID-19 from each region around the world, and to look closely at smaller regions to see how it is different, Rosen said. Our preliminary analysis, using publicly available data from across the world, is showing that the combination of subtypes of virus found in New York is most similar to those found in Austria, France and Central Europe, but not Italy. And the subtype from Asia, that was detected here early in the pandemic has not spread very much, instead we are seeing a new subtype that only exists in America as the one most prevalent in Washington state and on the west coast.

In addition to helping scientists understand how the virus is changing and spreading, this method can also reveal the portion of its genetic code that appears to remain resistant to mutations a discovery that could be exploited by treatments to combat the virus.

Were seeing that the two parts of the virus that seem not to be mutating are the ones responsible for its entry into healthy cells and packaging its RNA, Rosen said. Both of these are important targets for understanding the bodys immune response, identifying antiviral therapeutics and designing vaccines.

Rosens Ecological and Evolutionary Signal-Processing and Informatics Laboratory will continue to analyze COIVD-19 data as it is collected and to support public health researchers using the ISM process.

Reference: Characterizing geographical and temporal dynamics of novel coronavirus SARS-CoV-2 using informative subtype markers by Zhengqiao Zhao, Bahrad A. Sokhansanj and Gail Rosen, 10 April 2020, bioRxiv.DOI: 10.1101/2020.04.07.030759

This research is supported in part by the National Science Foundation.

Original post:
Rapidly Revealing COVID-19s Journey and Evolution With Genetic Tracing Barcode - SciTechDaily

Read More...

A coronavirus strain from Washington state was one of the earliest and most potent found and it’s in Utah – Salt Lake Tribune

Thursday, April 23rd, 2020

Seattle As the coronavirus outbreak consumed the city of Wuhan in China, new cases of the virus began to spread out like sparks flung from a fire.

Some landed thousands of miles away. By the middle of January, one had popped up in Chicago, another one near Phoenix. Two others came down in the Los Angeles area. Thanks to a little luck and a lot of containment, those flashes of the virus appear to have been snuffed out before they had a chance to take hold.

But on Jan. 15, at the international airport south of Seattle, a 35-year-old man returned from a visit to his family in the Wuhan region. He grabbed his luggage and booked a ride-share to his home north of the city.

The next day, as he went back to his tech job east of Seattle, he felt the first signs of a cough not a bad one, not enough to send him home. He attended a group lunch with colleagues that week at a seafood restaurant near his office. As his symptoms got worse, he went grocery shopping near his home.

Days later, after the man became the first person in the United States to test positive for the coronavirus, teams from federal, state and local agencies descended to contain the case. Sixty-eight people the ride-share driver at the airport, the lunchmates at the seafood restaurant, the other patients at the clinic where the man was first seen were monitored for weeks. To everyones relief, none ever tested positive for the virus.

But if the story ended there, the arc of the coronaviruss sweep through the United States would look much different.

As it turned out, the genetic building block of the virus detected in the man who had been to Wuhan would become a crucial clue for scientists who were trying to understand how the pathogen gained its first, crucial foothold.

Working out of laboratories along Seattles Lake Union, researchers from the University of Washington and the Fred Hutchinson Cancer Research Center rushed to identify the RNA sequence of the cases from Washington state and around the country, comparing them with data coming in from around the world.

Using advanced technology that allows them to rapidly identify the tiny mutations that the virus makes in its virulent path through human hosts, the scientists working in Washington and several other states made two disconcerting discoveries.

The first was that the virus brought in by the man from Wuhan or perhaps, as new data has suggested, by someone else who arrived carrying a nearly identical strain had managed to settle into the population undetected.

Then they began to realize how far it had spread. A small outbreak that had established itself somewhere north of Seattle, they realized as they added new cases to their database, was now responsible for all known cases of community transmission they examined in Washington state in the month of February.

A genetically similar version of the virus directly linked to that first case in Washington was identified across 14 other states, as far away as Connecticut and Maryland. It settled in other parts of the world, in Australia, Mexico, Iceland, Canada, Britain and Uruguay. It landed in the Pacific, on the Grand Princess cruise ship.

The unique signature of the virus that reached U.S. shores in Seattle now accounts for a quarter of all U.S. cases made public by genomic sequencers in the United States.

With no widespread testing available, the high-tech detective work of the researchers in Seattle and their partners elsewhere would open the first clear window into how and where the virus was spreading and how difficult it would be to contain.

Even as the path of the Washington state version of the virus was coursing eastward, new sparks from other strains were landing in New York, in the Midwest and in the South. And then they all began to intermingle.

The researchers in Seattle included some of the worlds most renowned experts on genomic sequencing, the process of analyzing the letters of a viruss genetic code to track its mutations. Before the outbreak, one of the labs had done more sequencing of human coronaviruses than anywhere else in the world 58 of them.

When a virus takes hold in a person, it can replicate billions of times, some of those with tiny mutations, each new version competing for supremacy. Over the span of a month, scientists have learned, the version of the novel coronavirus moving through a community will mutate about twice each one a one-letter change in an RNA strand of 29,903 nucleotides.

The alterations provide each new form of the virus with a small but distinctive variation to its predecessor, like a recipe passed down through a family. The mutations are so small, however, that it is unlikely that one version of the virus would affect patients differently than another one.

The virus originated with one pattern in Wuhan; by the time it reached Germany, three positions in the RNA strand had changed. Early cases in Italy had two entirely different variations.

For each case, the Seattle researchers compile millions of fragments of the genome into a complete strand that can help identify it based on whatever tiny mutations it has undergone.

What were essentially doing is reading these small fragments of viral material and trying to jigsaw puzzle the genome together, said Pavitra Roychoudhury, a researcher for the two institutions working on the sequencing in Seattle.

With some viruses, the puzzles are more challenging to assemble. The virus that causes COVID-19, she said, was relatively well behaved.

Researchers looked closely at the man who had flown in from Wuhan, who has not been publicly identified and did not respond to a request to speak to The New York Times.

They confirmed he had brought a strain of the virus that was already extending broad tentacles from the Wuhan area to Guangdong on Chinas Pacific coast to Yunnan in the mountainous west. Along the way, its signature varied significantly from the version of the virus that spread in Europe and elsewhere: Its mutations were at positions 8,782, 18,060 and 28,144 on the RNA strand.

That gave Roychoudhury and the scientists around the country she has been working with the unique ability to see what the contact tracers in Seattle had been unable to: the invisible footprints of the pathogen as it moved.

On the hunt for the viruss path through the United States, one of the first signposts came on Feb. 24, when a teenager came into a clinic with what looked like the flu. The clinic was in Snohomish County, Washington, where the man who had traveled to China lived. Doctors gave the teenager a nasal swab as part of a tracking study that was already being done on influenza in the region.

Only later did they learn that the teenager had not had the flu, but the coronavirus. After the diagnosis, researchers in Seattle ran the sample through a sequencing machine. Trevor Bedford, a scientist at the Fred Hutchinson Cancer Research Institute who studies the spread and evolution of viruses, said he and a colleague sipped on beers as they waited for the results to emerge on a laptop.

It confirmed what they had feared: The case was consistent with being a direct descendant of the first U.S. case, from Wuhan.

The teenager had not been in contact with the man who had traveled to Wuhan, so far as anyone knew. He had fallen ill long after that man was no longer contagious.

Additional sequencing in the days afterward helped confirm that other cases emerging were all part of the same group. This could only mean one thing: The virus had not been contained to the traveler from Wuhan and had been spreading for weeks. Either he had somehow spread it to others, or someone else had brought in a genetically identical version of the virus.

That latter possibility has become more likely in recent days, after new cases entered into the researchers database showed an interesting pattern. A virus with a fingerprint nearly identical to the Wuhan travelers had shown up in cases in British Columbia, just across the border from Washington state, suggesting to Bedford that it might not have been the first Wuhan traveler who had unleashed the outbreak.

Either way, the number of cases emerging around the time the teenagers illness was identified indicated that the virus had been circulating for weeks.

Exposing a lot of people

On its path through Washington state, one of the viruss early stops appears to have been at a square dance on Feb. 16 in the city of Lynnwood, midway between Seattle and Everett.

It was a full month since the Wuhan travelers arrival. A couple dozen square dancers had gathered for a pie and ice cream social, capping off a series of practices and events from all over the region over the course of a three-day weekend.

Three groups of square dancers swung through promenades and allemandes huffing and sweating to Free Ride and Bad Case of Loving You.

Stephen Cole, who was the dance caller that night, said he did not recall anyone showing signs of illness. But over the next few days, he and a woman who had been cuing the dance fell ill.

Another dancer, Suzanne Jones, had attended a class with Cole the day before. By the next weekend, Jones said, she started to feel symptoms she dismissed as allergies, since she had noticed the scotch broom starting to bloom.

After resting for a couple of days, Jones felt better and drove from her home in Skagit County more than 100 miles south to visit her mother in Enumclaw, helping pack some belongings for storage. On the way back, she visited the strip malls in Renton, then a store in Everett, then a laundromat in Arlington. She stopped to apply for a job with the Census Bureau.

I probably exposed a lot of people that day, she said.

Jones only realized it could be something more than allergies after getting a notification on March 2 that one of her square-dancing friends had died of the coronavirus as the outbreak began to emerge. She too tested positive.

There was minimal coronavirus testing in the United States during February, leaving researchers largely blind to the specific locations and mutations of the spread that month. The man who had traveled from Wuhan was not at the dance, nor was anyone else known to have traveled into the country with the coronavirus. But researchers learned that the virus by then was already spreading well beyond its point of origin and all the cases of community transmission that month were part of that same genetic branch.

There was another spreading event. On the Saturday after the dance, a group of friends packed the living room of a one-bedroom apartment in Seattle, sharing homemade food and tropical-themed drinks.

Over the following days, several people began coming down with coronavirus symptoms. Among people who attended, 4 out of every 10 got sick, said Hanna Oltean, an epidemiologist with the Washington State Department of Health.

Several people passed on the virus to others. By late March, the state health department had documented at least three generations of transmission occurring before anyone was symptomatic, Oltean said.

By then, it was becoming clear that there were probably hundreds of cases already linked to the first point of infection that had been spreading undetected. It left a lingering question: If the virus had this much of a head start, how far had it gone?

As cases of the virus spread, scientists in other states were sequencing as many as they could. In a lab at the University of California, San Francisco, Dr. Charles Chiu looked at a range of cases in the Bay Area, including nine passengers from the Grand Princess cruise ship, which had recently returned from a pair of ill-fated sailings to Mexico and Hawaii that left dozens of passengers infected with the coronavirus.

Chiu was stunned by his results: Five cases in the San Francisco area whose origins were unknown were linked back to the Washington state cluster. And all nine of the Grand Princess cases had a similar genetic link, with the same trademark mutations plus a few new ones. The massive outbreak on the ship, Chiu believed, could probably be traced to a single person who had developed an infection linked to the Washington state cluster.

But it did not stop with the Grand Princess. David Shaffer, who had been on the first leg of the cruise with members of his family, said passengers on that leg did not discover until after they disembarked that the coronavirus had been aboard when they learned that a fellow passenger had died.

He and his family felt fine when they returned to their home in Sacramento, California, he said, and when he started feeling sick the next day, on Feb. 22, he at first assumed it was a sinus infection.

Days later, he was tested and learned he had the coronavirus. His wife later tested positive, too, as did one of his sons and one of his grandsons, who had not been on the cruise.

Chiu remembers going over the implications in his head. If its in California and its in Washington state, its very likely in other states.

The same day Shaffer got sick, another person landed at Raleigh-Durham International Airport in North Carolina, having just visited the Life Care Center nursing home in Kirkland, which would become a center of infection. At the time, there were growing signs of a respiratory illness at the facility, but no indication of the coronavirus.

A few days later, the traveler began feeling ill, but with no sign that it might be anything serious, he went out for dinner at a restaurant in Raleigh. Just then, officials in Washington state began to report a coronavirus outbreak at Life Care Center. The person in North Carolina tested positive a few days later the first case in the state.

By the middle of March, a team at Yale gathered nine coronavirus samples from the Connecticut region and put them through a portable sequencing machine. Seven came back with connections to Washington state.

I was pretty surprised, said Joseph Fauver, one of the researchers at the lab. At the time, he said, it suggested that the virus had been spreading more than people had initially believed.

In sequencing more recent cases, the researchers have found cases emanating from a larger cluster, with its own distinct genetic signature, originating in the New York area.

A group of cases throughout the Midwest, first surfacing in early March, appears to have roots in Europe. A group of cases in the South, which emerged around the same time, on March 3, appears like a more direct descendant from China.

But of all the branches that researchers have found, the strain from Washington state remains the earliest and one of the most potent.

It has surfaced in Arizona, California, Connecticut, the District of Columbia, Florida, Illinois, Michigan, Minnesota, New York, North Carolina, Oregon, Utah, Virginia, Wisconsin and Wyoming, and in six countries.

And new cases are still surfacing.

One of the enduring mysteries has been just how the virus managed to gain its first, fatal foothold in Washington.

Did the contact tracers who followed the steps of the man who had traveled from Wuhan miss something? Did he expose someone at the grocery store, or touch a door handle when he went to the restaurant near his office?

In recent days, the sequencing of new cases has revealed a surprising new possibility. A series of cases in British Columbia carried a genetic footprint very similar to the case of the Wuhan traveler. That opened up the possibility that someone could have carried that same branch of the virus from Wuhan to British Columbia or somewhere else in the region at nearly the same time. Perhaps it was that person whose illness had sparked the fateful outbreak.

But who? And how? That would probably never be known.

Read more from the original source:
A coronavirus strain from Washington state was one of the earliest and most potent found and it's in Utah - Salt Lake Tribune

Read More...

Childhood Psychopathology Linked to Higher Levels of Genetic Vulnerability of Adult Depression – Clinical OMICs News

Thursday, April 23rd, 2020

Emotional, social, and psychiatric problems in children and adolescents have been linked to higher levels of genetic vulnerability for adult depression, according to University of Queensland scientists. They made the finding Genetic Associations Between Childhood Psychopathology and Adult Depression and Associated Traits in 42998 Individuals: A Meta-Analysis, which appears inJAMA Psychiatry, while analyzing the genetic data of more than 42,000 children and adolescents from seven cohorts across five European countries.

Christel Middeldorp, MD, PhD, a child and adolescent psychiatrist at the Child Health Research Centre at the University of Queensland, said that researchers have also found a link with a higher genetic vulnerability for insomnia, neuroticism, and body mass index.

By contrast, study participants with higher genetic scores for educational attainment and emotional wellbeing were found to have reduced childhood problems, she pointed out.

We calculated a persons level of genetic vulnerability by adding up the number of risk genes they had for a specific disorder or trait, and then made adjustments based on the level of importance of each gene. We found the relationship was mostly similar across ages.

Adult mood disorders are often preceded by behavioral and emotional problems in childhood. It is yet unclear what explains the associations between childhood psychopathology and adult traits. To investigate whether genetic risk for adult mood disorders and associated traits is associated with childhood disorders, write the investigators.

This meta-analysis examined data from 7 ongoing longitudinal birth and childhood cohorts from the U.K., the Netherlands, Sweden, Norway, and Finland. Starting points of data collection ranged from July 1985 to April 2002. Participants were repeatedly assessed for childhood psychopathology from ages 6 to 17 years. Data analysis occurred from September 2017 to May 2019.

Individual polygenic scores (PGS) were constructed in children based on genome-wide association studies of adult major depression, bipolar disorder, subjective well-being, neuroticism, insomnia, educational attainment, and body mass index (BMI).

Results from this study suggest the existence of a set of genetic factors influencing a range of traits across the life span with stable associations present throughout childhood. Knowledge of underlying mechanisms may affect treatment and long-term outcomes of individuals with psychopathology.

The results indicate there are shared genetic factors that affect a range of psychiatric and related traits across a persons lifespan. Around 50 percent of children and adolescents with psychiatric problems, such as attention deficit hyper-activity disorder (ADHD), continue to experience mental disorders as adults, and are at risk of disengaging with their school community among other social and emotional problems, added Middeldorp.

Our findings are important as they suggest this continuity between childhood and adult traits is partly explained by genetic risk, she continued. Individuals at risk of being affected should be the focus of attention and targeted treatment. Although genetic vulnerability is not accurate enough at this stage to make individual predictions about how a persons symptoms will develop over time, it may become so in the future, in combination with other risk factors.

Middeldorp believes that this study and others may support precision medicine by providing targeted treatments to children at the highest risk of persistent emotional and social problems.

See the original post here:
Childhood Psychopathology Linked to Higher Levels of Genetic Vulnerability of Adult Depression - Clinical OMICs News

Read More...

Lozier praises promising, and ethical, blindness study – OneNewsNow

Thursday, April 23rd, 2020

New research results show promise in treating people who are blind.

The National Eye Institute funded the study, which is research considered to be ethical.

Dr. David Prentice of the Charlotte Lozier Institute says there have been discussions over using adult stem cells to restore sight, which he calls a different tack for advancing science and medicine.

It's still an ethical way to go about this, he observes. There's no embryonic stem cells, no fetal tissue, none of this unethical type of research direction.

What the scientists did was turn a skin cell directly into a photoreceptor for vision then transplanted it.

Prenticeadvises the testing is very preliminary after the experiment on mice.

But what they find was when they transplanted this newly formed type of vision cell into the eyes of these blind mice, he says, they restored their vision.

The researchers applied chemicals that transformed one cell type into another needed for vision, and there is now potential to help people with all forms of vision blindness or vision correction, which would include macular degeneration and other retinal disorders.

Editor's note: Original posting attribute comments to wrong person.

Continue reading here:
Lozier praises promising, and ethical, blindness study - OneNewsNow

Read More...

Very low-dose Avastin effective for preventing blindness in preterm infants – National Institutes of Health

Thursday, April 23rd, 2020

News Release

Thursday, April 23, 2020

Babies born prematurely who require treatment to prevent blindness from retinopathy of prematurity (ROP) could be treated with a dose of Avastin (bevacizumab) that is a fraction of the dose commonly used for ROP currently. Results from the dose-finding study were published April 23 in JAMA Ophthalmology. The study was conducted by the Pediatric Eye Disease Investigator Group (PEDIG) and supported by the National Eye Institute (NEI), part of the National Institutes of Health.

Preterm babies are at high risk of abnormal blood vessel growth in the retina, the light-sensitive tissue in the back of the eye. These abnormal blood vessels are fragile and prone to leaking. If left untreated, vessel growth can lead to scarring and retinal detachment, the main cause of ROP-related vision loss. ROP is one of the leading causes of blindness in children.

Established ROP treatments include laser therapy and cryotherapy. Both interventions work by causing the abnormal blood vessels to stop growing before they can cause scarring and retinal detachment.

Avastin is one of several available drugs that inhibit abnormal blood vessel growth by suppressing the overproduction of a signal protein called vascular endothelial growth factor (VEGF).

The U.S. Food and Drug Administration approved Avastin in 2004 as a cancer therapy. Since then, ophthalmologists have used it off-label to inhibit abnormal blood vessel growth in ROP, as well as in other ocular disorders. Results from a clinical trial published in 2011 confirmed the benefit of using Avastin over laser therapy for treating the most severe cases of ROP, which occur in a region of the retina known as posterior zone 1.

As a faster and easier treatment option, anti-VEGF eye injections were a welcomed alternative to laser therapy for treating severe ROP, said the new studys protocol chair, David Wallace, M.D., MPH, chair of ophthalmology at the Indiana University School of Medicine. Laser therapy requires sedating the baby for as long as 90 minutes; an Avastin injection takes much less time and is generally less stressful to the infant.

But we know that anti-VEGF agents injected into the eye also get into the bloodstream, and doctors worry that inhibiting VEGF systemically could interfere with normal development of brain, lung, bone, and kidney tissues, he said. Evidence suggests that injections of anti-VEGF in the eye reduce levels of VEGF in the bloodstream.

In this study, Wallace and colleagues in the NEI-funded PEDIG hoped to pinpoint the lowest possible therapeutic dose of Avastin by testing progressively lower doses in 10-14 infants per dose. We didnt want to start by testing an ineffective dose and risk a child going blind, so we started with 40% of the dose commonly used for ROP. When a dose was successful, we halved it and then tested that dose. Eventually we cut the dose in half seven times, he said.

In the current study, we found that 0.004 mg of Avastin a dose thats merely 0.6% of the dose used in the 2011 study of Avastin for ROP may be the lower limit to be effective for most infants with ROP, said Wallace. The findings set the stage for a randomized controlled trial comparing long-term effects of low-dose Avastin with laser therapy for treating ROP, he said.

They plan to follow children over time to compare the long-term effects of each strategy on vision and organ development. Previous studies suggest that babies treated with Avastin versus laser may be less likely to become myopic and require glasses for nearsightedness as they grow older.

The study involved 59 preterm infants with type 1 ROP, the most severe form. Each infant had one eye treated by a single injection containing 0.016 mg, 0.008 mg, 0.004 mg, or 0.002 mg of Avastin. If the other eye required treatment, it received twice the concentration (one dose level higher). By comparison, currently used doses of Avastin for ROP range from 0.25 mg to 0.625 mg.

Treatment was considered a short-term success if ROP improved by day four after therapy, and if there was no recurrence or need for additional treatment within four weeks. Such success was achieved in all eyes treated with the 0.016 mg and 0.008 mg doses, and in 9 of 10 eyes receiving 0.004 mg, but only in 17 of 23 eyes receiving 0.002 mg, resulting in the conclusion that 0.004 mg may be the lowest effective dose.

The study was supported by NEI grants EY011751, EY023198, and EY018810. The clinicaltrials.gov record is NCT02390531.

NEI leads the federal governments research on the visual system and eye diseases. NEI supports basic and clinical science programs to develop sight-saving treatments and address special needs of people with vision loss. For more information, visit https://www.nei.nih.gov.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

Wallace DK, Kraker RT, Freedman SF, Crouch ER, Bhatt AR, Hartnett ME, Yang MB, Rogers DL, Hutchinson AK, VanderVeen DK, Haider KM, Siatkowski RM, Dean TW, Beck RW, Repka MX, Smith LE, Good WV, Kong L, Cotter SA, Holmes JM for the Pediatric Eye Disease Investigator Group (PEDIG). Short-term Outcomes After Very Low-Dose Intravitreous Bevacizumab for Retinopathy of Prematurity. Published April 23, 2020 in JAMA Ophthalmology.

###

Continue reading here:
Very low-dose Avastin effective for preventing blindness in preterm infants - National Institutes of Health

Read More...

Clear vision, many smiles: How a non-profit is helping children in India see better – YourStory

Thursday, April 23rd, 2020

India is home to 472 million children. According to a study published by the National Centre for Biotechnology Information, out of 668 hospitals, only 192 (28.7 percent) reported that they provided pediatric eye care services a handful in a country as vast as India.

Primary and quality eye care is a necessity, and to make it accessible, Orbis International, a non-profit non-governmental organisation, started its saving initiative in India with its flagship Flying Eye Hospital. Orbis International was founded in 1982 in the United States. After running multiple Flying Eye Hospital programmes in Hyderabad and New Delhi, Orbis India established an office in New Delhi in 2000.

Orbis India launched India Childhood Blindness Initiative (ICBI) flagship programme in 2002. Its aims to ensure that Indias children across geographies have access to quality eye care for generations to come.

Dr Rishi Raj Borah has been an integral part of the Orbis journey for the last 12 years and has developed innovative, impactful, and sustainable home-grown eye care initiatives for millions of children in Indian and Nepalese communities. He is the Country Director of Orbis India.

Before working in the field of eye care, Dr Rishi worked with UNICEF, CORDAID and Don Bosco Institute. He is also a Board Member of VISION 2020: The Right to Sight India.

As part of Orbis Comprehensive Childhood Blindness Project, their partner, Akhand Jyoti Eye Hospital (AJEH) conducts school screenings in some of Bihars districts. Several children with vision problems were identified and prescribed spectacles during the school screening in the village of Dariyapur.

In one of Dariyapurs schools where the screening was conducted, a girl named Rinky was identified to have poor vision. The AJEH team discovered that the 13-year-old had been suffering for the last two years.

Rinky

Her poor vision would also hinder her daily activities and despite being scolded in class for being unable to read, Rinky was largely unaware of her problems. Due to uncorrected refractive error, which was blurring her vision, Rinky would be uncomfortable while watching the television and identifying objects in low light conditions. She even had difficulties in seeing under bright light.

Rinky and her friends

The Orbis-AJEH team came to Rinkys rescue. They identify cases like Rinkys, while generating awareness for teachers in these schools. The team also actively engages with the parents of children who go on to get treatments done via the screenings.

Rinky was identified with myopia, which is the inability to see objects at a distance, and was prescribed with a pair of spectacles by the team.

Rinky in her classroom

Rinky was glad about wearing spectacles and soon realised that, like her friends, she was also able to see things clearly.

As of today, Orbis India has presence in Delhi, Punjab, Uttar Pradesh, Uttarakhand, Chhattisgarh, West Bengal, Odisha, Bihar, Maharashtra, Rajasthan, Gujarat, Madhya Pradesh, Kerala, Karnataka, Andhra Pradesh, Arunachal Pradesh, and Assam.

Millions of childrens lives have been positively affected by programs similar to the one in Rinkys school. 33 Childrens Eye Centers (CEC) have been established across the country, which are supported and equipped with quality partners and teams.

How has the coronavirus outbreak disrupted your life? And how are you dealing with it? Write to us or send us a video with subject line 'Coronavirus Disruption' to editorial@yourstory.com

Read more from the original source:
Clear vision, many smiles: How a non-profit is helping children in India see better - YourStory

Read More...

Why Julia’s Eyes Is Better Than Bird Box (& Is Overlooked) – Screen Rant

Thursday, April 23rd, 2020

While the film description, a horror movie where the protagonist wears a blindfold, would conjure 2018 sci-fi horror Bird Box in most peoples minds, it also serves to describe the 2010 Spanish movie,Julias Eyes.

Released on Netflix, Bird Box depicts a post-apocalyptic world where humans are forced to wear blindfolds to avoid seeing madness-causing monsters. Starring Sandra Bullock as Malorie, the movie leans heavily into its star power. It came out the same year A Quiet Place hit theaters, and many were quick to point out the similarities between the two. WhileA Quiet Placewas the higher-rated movie,Bird Boxbecame something of a viral, meme-worthy hit, garnering significant acclaim and attention. Despite all eyes being on the Sandra Bullock-led thriller, which was based off a novel by Josh Malerman, a lesser-known foreign horror is the more direct choice for comparisons, notA Quiet Place.

Related: Why Bird Box 2 Shouldn't Happen

Julias Eyes was directed by Spanish director Guillem Morales and produced by two-time Oscar-winner Guillermo del Toro. A horror thriller, it follows the story Julia, a woman who is slowly losing her sight. Played by the extremely talented Beln Rueda, Julia investigates her sisters suicide while also undergoing an eye surgery that temporarily blinds her.

In both movies, the blindfold serves both a mechanical and symbolic purpose. In Bird Box, supernatural monsters take the shape of ones worst fear, leading those who see them to either madness or suicide; blindfolds are a protective measure. The audience never sees the monsters outright, only their effect. It represents a fear of the unknown.

In Julias Eyes, the blindfold is a necessary measure to ensure her eye operation takes. Here, the blindfold represents sacrifice, a running theme through the movie: a moment of darkness for a brighter future. Much of the tension comes not just from knowing that something sinister is happening around Julia, but that if she peeks to look at it, it condemns her to permanent blindness. It exchanges one kind of blindness for another.

In terms of reception, Julias Eyes has Bird Box beat. Its 90% score on Rotten Tomatoes is leagues ahead of Bird Boxs 63%. The blindfold mechanic in Julias Eyes is much more organic as well. In eschewing any sci-fi elements, Julias Eyes grounds its horror in humanity. It is a story that weaves its concept with its horror, developing multiple levels of tension. The film leans into dramatic irony; from the first scene, the audience knows something is amiss, while Julia is left to grope in the dark.

Related: Every Sci-Fi Horror Movie Releasing In 2020

It is also an extremely beautiful movie. Its high caliber cinematography and acting put it in the realm of horror like Silence Of The Lambs and Psycho. Julia's Eyes alsoincludes one of the most arguably tense scenes in horror history, combining open eyes and a knifes edge to capture many of humanitys innate fears, while developing character-specific tension.

Spanish-language cinema has had a lot to offer horror. The Orphanage balances a terrifying atmosphere with supernatural dread. [REC] uses high stakes zombie horror to make one of the most tense found footage films. The acting is one of the strongest points of Julias Eyes, something that would be lost in an adaptation.

Julias Eyes rarely makes it onto top ten horror lists. It released at a time when horror and foreign language horror were generally still treated as separate. There is a bias in the film world towards English language movies; instead of distributing East Asian horror globally as is, it is usually adapted and translated in the West, often to the detriment of the story. Limiting horror to a single language limits the scope of imagination and possibility.

Fortunately, this trend is slowly disappearing, as exemplified by Korean thriller Parasite becoming the first non-English film to win the Oscar for Best Picture. The future holds hope for movies like Julias Eyes, which have the merit but still deserve to one day reach the scope of films like Bird Box.

Next: Netflix Is Adding So Much Foreign Horror (& What That Means For Streaming)

Jennifer's Body: Every Similarity To 2000's Ginger Snaps

Shannon Lewis is a features and news writer on Screen Rant. She has experience in editorial working as the deputy editor for Specialty Food, an online and print magazine, curating its news section and social media. She has worked as a freelance writer since 2017, writing articles, features, and profiles in a wide range of topics, from business and tech to pop culture and media. Previously, she has also worked as a ghost writer for a fiction manuscript, and co-founded arts-and-literature magazine, Octarine.Hailing from Queretaro, Mexico, she is a graduate of the University of East Anglia's English Literature with Creative Writing program. An avid reader and fan of writing, she leverages her love of literature to dissect movies in her favorite genres, including horror, rom-coms, and superhero movies. Her focus is on the cross-section between story, cultural background, and character development. When she isn't busy reading everything ever published under the mantle of Image Comics, you might find her writing fiction, rock climbing, or putting together a horror anthology with friends.

Read the rest here:
Why Julia's Eyes Is Better Than Bird Box (& Is Overlooked) - Screen Rant

Read More...

Glaucoma can be successfully treated with gene therapy – Daijiworld.com

Thursday, April 23rd, 2020

London, Apr 22 (IANS): A common eye condition, glaucoma, could be successfully treated with a single injection using gene therapy, which would improve treatment options, effectiveness and quality of life for many patients, say researchers.

Glaucoma affects over 64 million people worldwide and is a leading cause of irreversible blindness. It is usually caused by fluid building up in the front part of the eye, which increases pressure inside the eye and progressively damages the nerves responsible for sight.

Current treatments include either eye drops, laser or surgery, all of which have limitations and disadvantages.

"At present, there is no cure for glaucoma, which can lead to loss of vision if the disease is not diagnosed and treated early," said study researcher Dr Colin Chu from the University of Bristol in the UK.

For the findings, published in the journal Molecular Therapy, the research team tested a new approach that could provide additional treatment options and benefits.

The researchers designed a gene therapy and demonstrated proof of concept using experimental mouse models of glaucoma and human donor tissue.

The treatment targeted part of the eye called the ciliary body, which produces the fluid that maintains pressure within the eye.

Using the latest gene-editing technology called CRISPR, a gene called Aquaporin 1 in the ciliary body was inactivated leading to reduced eye pressure.

"We hope to advance towards clinical trials for this new treatment in the near future. If it's successful it could allow a long-term treatment of glaucoma with a single eye injection, which would improve the quality of life for many patients whilst saving the NHS time and money," Chu said

The researchers are currently in discussion with industry partners to support further laboratory work and rapidly progress this new treatment option towards clinical trials.

Excerpt from:
Glaucoma can be successfully treated with gene therapy - Daijiworld.com

Read More...

Ivermectin emerges as possible treatment option for Covid-19 – The Irish Times

Thursday, April 23rd, 2020

Could a drug discovered in the 1970s help to tackle the Covid-19 pandemic? New evidence from research in Australia shows that the anti-parasitic drug ivermectin can inhibit the virus that causes Covid-19 from replicating in cells in the lab.

While findings show promise, the news should be greeted with caveats, according to Donegal scientist Professor William C. Campbell, who shared a Nobel Prize for his role in the discovery of ivermectin.

The report is, in itself, of great importance, says Prof Campbell of the study, which was carried out by scientists at Monash University in Melbourne. But perspective is needed, even though perspective can be boring when the results are exciting.

The researchers in Melbourne grew mammalian cells in the lab and infected them with the Sars-CoV-2 virus that causes Covid-19. Then they exposed the cells and viruses in the lab to ivermectin, a drug that has been widely used for decades to control parasitic worms and insects in livestock, pets and humans.

One of the best known uses of ivermectin in humans is against the worm that causes river blindness - the pharmaceutical company Merck donated the drug for that use for millions of people in affected areas.

Prof Campbell, a graduate of Trinity College Dublin, shared the Nobel Prize in Physiology or Medicine in 2015 for his part in the discovery and development of ivermectin and its use in treating river blindness.

While he was working at Merck Research Laboratories in New Jersey, he was part of an extensive team that identified a substance called avermectin, which was produced by bacteria and could stop parasitic worm infections.

The compound was enhanced and developed as ivermectin, becoming a treatment for parasitic diseases such as heart worm in dogs and river blindness in humans. The Royal Irish Academy will publish Campbells memoir this June.

While ivermectin has not been approved as a drug against viruses, it is known to be effective in the lab against a broad range of viruses including HIV, Dengue and Influenza.

The Australian research showed that ivermectin resulted in a 5,000-fold reduction of Sars-CoV-2 RNA within 48 hours. Ivermectin therefore warrants further investigation for possible benefits in humans, explains the study authors in the journal Antiviral Reports.

The experiments used high concentrations of ivermectin, notes Proff Campbell: the concentration of drug needed to kill the virus in the lab was many times higher than the concentration of ivermectin found in the blood of people in the normal use of ivermectin to control parasitic disease.

So the probability of ivermectin being used safely to kill the virus in people must be considered low, he says.

On the other hand, there is, as the authors of the report point out, the possibility that a safe dosage of ivermectin might reduce the rate of viral replication in the mammalian body, or affect the virus in other ways that might be revealed by further research. That is a more positive prospect.

Commenting on the study, lead researcher Dr Kylie Wagstaff from the Biomedicine Discovery Institute at Monash University says: Ivermectin is very widely used and seen as a safe drug. We need to figure out now whether the dosage you can use it at in humans will be effective - thats the next step.

See more here:
Ivermectin emerges as possible treatment option for Covid-19 - The Irish Times

Read More...

Glaucoma Could Be Successfully Treated With Gene Therapy – Technology Networks

Thursday, April 23rd, 2020

A new study led by the University of Bristol has shown a common eye condition, glaucoma, could be successfully treated with a single injection using gene therapy, which would improve treatment options, effectiveness and quality of life for many patients.

Glaucoma affects over 64 million people worldwide and is a leading cause of irreversible blindness. It is usually caused by fluid building up in the front part of the eye, which increases pressure inside the eye and progressively damages the nerves responsible for sight. Current treatments include either eye drops, laser or surgery, all of which have limitations and disadvantages.

The research team led by academics at the Bristol Medical School: Translational Health Sciences tested a new approach that could provide additional treatment options and benefits. Their findings are published in the journalMolecular Therapy.

The researchers designed a gene therapy and demonstrated proof of concept using experimental mouse models of glaucoma and human donor tissue.

The treatment targeted part of the eye called the ciliary body, which produces the fluid that maintains pressure within the eye. Using the latest gene editing technology called CRISPR, a gene called Aquaporin 1 in the ciliary body was inactivated leading to reduced eye pressure.

Dr Colin Chu, Visiting Senior Research Fellow in theBristol Medical School: Translational Health Sciencesand corresponding author, said: "Currently there is no cure for glaucoma, which can lead to loss of vision if the disease is not diagnosed and treated early.

"We hope to advance towards clinical trials for this new treatment in the near future. If it's successful it could allow a long-term treatment of glaucoma with a single eye injection, which would improve the quality of life for many patients whilst saving the NHS time and money."

The academics are currently in discussion with industry partners to support further laboratory work and rapidly progress this new treatment option towards clinical trials.

Reference: Wu et al. (2020). Gene Therapy for Glaucoma by Ciliary Body Aquaporin 1 Disruption Using CRISPR-Cas9. Molecular Therapy.DOI: 10.1016/j.ymthe.2019.12.012.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

Read the original post:
Glaucoma Could Be Successfully Treated With Gene Therapy - Technology Networks

Read More...

New campaign could save lives of Bradford babies during lockdown – Bradford Telegraph and Argus

Thursday, April 23rd, 2020

A CAMPAIGN has been launched that could help save the lives of babies during the coronavirus pandemic.

The Bradford Partnership, which works to safeguard children in the district, says the Covid-19 lockdown can make it especially difficult for anyone coping with the challenge of caring for a new born infant.

Often new parents would be able to call on the support of other family members, such as grandparents, or take time out with support from others and get out and about with the baby.

Self-isolation, social distancing restrictions on activities which might lessen stress, like sports, social engagements and entertainment, and restrictions on parent and baby groups and classes, and baby clinics, might all add pressure.

The Partnership understands that mums and dads who cant calm their baby can feel helpless, or think they are a poor parent. When this happens some people feel they are going to tip over the edge. They can become so angry and frustrated they act on impulse and shake their baby.

Shaking or losing your temper with a baby is very dangerous and can cause blindness, learning disabilities, physical disabilities or even death, the Partnership says.

Using the message Babies Cry, You Can Cope, a four step approach using the word ICON is designed to give parents a strategy for managing a crying infant.

Jane Booth, Independent Chair of the Partnership, said: A babys cry is designed to get our attention. Unfortunately, when a parent is very stressed or anxious it can cause an over-reaction that can sometimes lead to physical abuse.

The ICON approach sets out clear steps parents can take that will relieve pressure so that they dont find themselves in a position where they shake or strike an infant. Its about providing support at a time when people cant always get help in their community because of social distancing.

Cllr Adrian Farley, Bradford Council's Executive Member for Children and Families, said: Bringing up young children can be stressful, and we know that coronavirus (Covid-19) is putting families under additional strain.

This initiative helps to provide parents with helpful ways to try and stop a baby crying and advice on what to do if they cant.

The Partnership says babies can cry for no particular reasons or because they are hungry, tired, wet/dirty or unwell.

Dont get angry with your baby or yourself. Put the baby in a safe place and walk away so that you can calm yourself down by doing something that takes your mind off the crying. After a few minutes when you are calm, go back and check on the baby.

Parents can visit Bradford Council's Early Year's advice website for more information.

See the article here:
New campaign could save lives of Bradford babies during lockdown - Bradford Telegraph and Argus

Read More...

University of North Texas Professor Fired For Mocking ‘Microaggression’ Fliers on Campus – i95rock.com

Thursday, April 23rd, 2020

Nathaniel Hiers is no longer a professor at the University of North Texas. He was let go after the administration said he mocked "microaggression" fliers passed out on campus. According to the College Fix, Hiers found a stack of fliers referring to microaggression issues on campus in the faculty lounge and decided to make what he called a "joke." Hiers leaned one of the fliers on the bottom of the chalkboard and wrote above it, "Please don't leave garbage lying around."

Microaggression:

is a term used for brief and commonplace daily verbal, behavioral, or environmental indignities, whether intentional or unintentional, that communicate hostile, derogatory, or negative prejudicial slights and insults toward any group, particularly culturally marginalized groups.

The fliers reportedly came from the University of New Hampshire's ADVANCE PROGRAM and partially focus onphrases like; "America is a melting pot," claiming a term like this canpropagate the myth of meritocracy and promote color blindness. The fliers also claim that being "forced" to choose male or female when completing basic forms issexist/heterosexist.

In the wake of his firing, Nathaniel Hier filed a First Amendment lawsuit last Thursday (4/16/20) and is being represented byAlliance Defending Freedom. The suit claims Hier was retaliated against and this isviewpoint-based discrimination.

I will now recuse myself from any and all national social discussions of any kind. If this is even a bullet point on the greater agenda in this county, I'll just take the check please. Another day, another "words hurt" topic.

Here's an idea, instead of focusing any energy on language, language use, intent or perceived intent make the life you want and surround yourself with people whose opinions you can tolerate. The reality is no one wants to do that, instead we will all continue to fire hot air at one another about our opinions and feelings while the world melts around us.

Have a ball y'all, I'm out!

See the original post:
University of North Texas Professor Fired For Mocking 'Microaggression' Fliers on Campus - i95rock.com

Read More...

Restaurant’s licence revoked after illegal immigrants found working in kitchen – Clacton and Frinton Gazette

Thursday, April 23rd, 2020

A RESTAURANT has lost its licence after three Bangladeshi men were found illegally working in the kitchen during an immigration raid.

The Home Offices Immigration Compliance and Enforcement (ICE) team executed a search warrant alongside Essex Police at the Great Gurkha in Old Road, Clacton, earlier this year.

Police and immigration officers found five men in the restaurant, three of whom were working illegally.

All three had overstayed their visas and were arrested before being released on immigration bail.

The restaurant was previously raided in February last year and two men were arrested for immigration offences.

It was decided at that time to issue a formal warning rather than to apply for a review.

But following the latest raid on January 10, Essex Police called on Tendring Council to revoke the restaurants licence, which gives it permission to sell alcohol on and off the premises, play recorded music and offer late night refreshment.

A report by Essex Police said: Whether by negligence or wilful blindness one or more illegal workers were engaged in activity on the premises, yet it is a simple process for an employer to ascertain what documents they should check before a person is allowed to work.

Essex Police asks that the premises licence is revoked. Merely remedying the existing situation - for instance by the imposition of additional conditions or a suspension - is insufficient to act as a deterrent to the licence holder and other premises licence holders from engaging in criminal activity by employing illegal workers and facilitating disqualified immigrants to work illegally.

A firm response to this criminal behaviour is required to ensure that the licence holder and its agents are not allowed to repeat the exercise and in particular, in the interests of the wider community to support responsible businesses and the jobs of both UK citizens and lawful migrants.

Tendring Councils licensing sub-committee met online on Wednesday to considered the reports and evidence presented by the licensing team, Essex Police and immigration officials, and decided to revoke the premises licence.

This sanction, the most severe the panel could impose, was issued in line with the council's policy which states that even in the case of a first immigration offence revocation could be considered.

In their reasoning councillors stated that the fact it was a second breach within 12 months meant that a warning, tightening or suspension of the licence would not be severe enough to reflect the seriousness of the offence..

Val Guglielmi, sub-committee chairman, said: There is a wide range of fabulous restaurants and takeaways across Tendring, not only providing delicious food but also creating jobs.

However, it is important that businesses operate legally, and as per our policy we will not hesitate to take action against those who do not follow the law.

Restaurant owner Aishwarya Enterprise and designated premises supervisor Mithula Varatharasa were permitted to take part, but did not attend the online meeting.

But in a statement to the police the supervisor said she had been taking a break due to health issues and that another person was looking after the businesses at the time of the raid The statement said she admitted to having lost control of business and that the chef must have brought his friends in to work independently.

The restaurant could not be contacted for comment, but a notice in the shop window stated it was temporarily closed due to Covid-19 restrictions.

The licence holder has 21 days within which to lodge an appeal at magistrates court against the decision.

Read this article:
Restaurant's licence revoked after illegal immigrants found working in kitchen - Clacton and Frinton Gazette

Read More...

Wolverhampton optician saves eyesight of city boxing coach – expressandstar.com

Thursday, April 23rd, 2020

Specialist opticians, Flint and Partners Optometrists, is remaining on hand to help people with acute emergency eye problems amid coronavirus.

The opticians, which has sites in Codsall, Wednesfield and Wolverhampton, has made the decision to remain open and doing so has saved the eyesight of Richie Carter, head coach at Wolverhampton Amateur Boxing Club.

The company's decision aims to ease the burden on GPs and hospitals, treating patients with infections, injuries and other sight threatening conditions.

Richie had been sparring in the garden with his son and sustained a blow to the right side of his head.

A few days later, knowing something wasn't quite right, Mr Carter called Flint and Partners to explain his symptoms and an appointment was arranged for him to attend for a consultation at the Tettenhall Road practice.

Using specialist tests, a tear was found in his retina that could have lead to blindness if left untreated - an appointment was arranged with a surgeon at New Cross within the hour, and his eye was operated on the following morning.

Mr Carter said: "I can't thank Flints enough, Mr Lyons - the fella who dealt with me - got me sorted straight away, diagnosed my problem and got me into the hospital - he saved the sight in my right eye".

Anyone with concerns about their eyesight can contact Flints on 01902 422096.

Link:
Wolverhampton optician saves eyesight of city boxing coach - expressandstar.com

Read More...

‘Stem cell therapy more effective on Covid-19’ – Korea Biomedical Review – Korea Biomedical Review

Thursday, April 23rd, 2020

I dont know why people pay attention only to vaccines and treatments against the new coronavirus. Stem cell therapies are more useful to treat Covid-19.

So claimed Lee Hee-young, president of the Korean Association of Stemcell Therapy, at a news conference in Seoul, Monday. He called for active use of stem cell therapies to treat Covid-19 patients.

Several studies have proved the effects of autologous stem cells in treating acute respiratory distress syndrome (ARDS), which is the leading cause of death in Covid-19 patients, Lee said. The concept of stem cell therapy is the same as that of blood transfusion or bone marrow transplantation. Decades of cell therapies have proved that stem cell therapy is safe.

While the development of a treatment or a vaccine against Covid-19 takes a long time and it may not be able to treat patients immediately because of virus mutation possibilities, stem cell therapies can restore damaged lungs directly, Lee claimed.

It is more important to restore damaged lungs than to fight the virus. Stem cell therapy restores the lungs, giving patients time to beat the virus, he went on to say. However, people are paying attention to vaccine or treatment candidates only. This is why I am holding a news conference.

Lee pointed out that the local environment makes it difficult to use stem cell therapies. Thus, the government should ease regulations on the management and use of cell culture facilities so that doctors can perform stem cell therapies with simple cell culture, he said.

As long as physicians have a positive pressure facility and a culture kit, they can separate and culture cells with simple training, he said. If the authorities allow doctors to perform stem cell therapies with a disposable mobile culture autonomously, the cost of stem cell therapies will go down significantly.

Lee added that he asked related officials to include such rules in the Act on Safety and Support for Advanced Regenerative Medicine and Advanced Biopharmaceuticals, which is to take effect in the second half of the year.

same@docdocdoc.co.kr

< Korea Biomedical Review, All rights reserved.>

Read more here:
'Stem cell therapy more effective on Covid-19' - Korea Biomedical Review - Korea Biomedical Review

Read More...

Diabetes Reversed in Mice With CRISPR-Edited Stem Cells From Patients – Technology Networks

Thursday, April 23rd, 2020

Using induced pluripotent stem cells produced from the skin of a patient with a rare, genetic form of insulin-dependent diabetes calledWolfram syndrome, researchers transformed the human stem cells into insulin-producing cells and used the gene-editing tool CRISPR-Cas9 to correct a genetic defect that had caused the syndrome. They then implanted the cells into lab mice and cured the unrelenting diabetes in those mice.

The findings, from researchers at Washington University School of Medicine in St. Louis, suggest the CRISPR-Cas9 technique may hold promise as a treatment for diabetes, particularly the forms caused by a single gene mutation, and it also may be useful one day in some patients with the more common forms of diabetes, such as type 1 and type 2.

The study is published online April 22 in the journal Science Translational Medicine.

Patients with Wolfram syndrome develop diabetes during childhood or adolescence and quickly require insulin-replacement therapy, requiring insulin injections multiple times each day. Most go on to develop problems with vision and balance, as well as other issues, and in many patients, the syndrome contributes to an early death.

This is the first time CRISPR has been used to fix a patients diabetes-causing genetic defect and successfully reverse diabetes, said co-senior investigatorJeffrey R. Millman, PhD, an assistant professor of medicine and of biomedical engineering at Washington University. For this study, we used cells from a patient with Wolfram syndrome because, conceptually, we knew it would be easier to correct a defect caused by a single gene. But we see this as a stepping stone toward applying gene therapy to a broader population of patients with diabetes.

Wolfram syndrome is caused by mutations to a single gene, providing the researchers an opportunity to determine whether combining stem cell technology with CRISPR to correct the genetic error also might correct the diabetes caused by the mutation.

A few years ago, Millman and his colleagues discovered how to convert human stem cells into pancreatic beta cells. When such cells encounter blood sugar, they secrete insulin. Recently, those same researchers developed a new technique to more efficiently convert human stem cells into beta cells that are considerably better at controlling blood sugar.

In this study, they took the additional steps of deriving these cells from patients and using the CRISPR-Cas9 gene-editing tool on those cells to correct a mutation to the gene that causes Wolfram syndrome (WFS1). Then, the researchers compared the gene-edited cells to insulin-secreting beta cells from the same batch of stem cells that had not undergone editing with CRISPR.

In the test tube and in mice with a severe form of diabetes, the newly grown beta cells that were edited with CRISPR more efficiently secreted insulin in response to glucose. Diabetes disappeared quickly in mice with the CRISPR-edited cells implanted beneath the skin, and the animals blood sugar levels remained in normal range for the entire six months they were monitored. Animals receiving unedited beta cells remained diabetic. Their newly implanted beta cells could produce insulin, just not enough to reverse their diabetes.

We basically were able to use these cells to cure the problem, making normal beta cells by correcting this mutation, said co-senior investigatorFumihiko Urano, MD, PhD, the Samuel E. Schechter Professor of Medicine and a professor of pathology and immunology. Its a proof of concept demonstrating that correcting gene defects that cause or contribute to diabetes in this case, in the Wolfram syndrome gene we can make beta cells that more effectively control blood sugar. Its also possible that by correcting the genetic defects in these cells, we may correct other problems Wolfram syndrome patients experience, such as visual impairment and neurodegeneration.

In the future, using CRISPR to correct certain mutations in beta cells may help patients whose diabetes is the result of multiple genetic and environmental factors, such as type 1, caused by an autoimmune process that destroys beta cells, and type 2, which is closely linked to obesity and a systemic process called insulin resistance.

Were excited about the fact that we were able to combine these two technologies growing beta cells from induced pluripotent stem cells and using CRISPR to correct genetic defects, Millman said. In fact, we found that corrected beta cells were indistinguishable from beta cells made from the stem cells of healthy people without diabetes.

Moving forward, the process of making beta cells from stem cells should get easier, the researchers said. For example, the scientists have developed less intrusive methods, making induced pluripotent stem cells from blood and they are working on developing stem cells from urine samples.

In the future, Urano said, we may be able to take a few milliliters of urine from a patient, make stem cells that we then can grow into beta cells, correct mutations in those cells with CRISPR, transplant them back into the patient, and cure their diabetes in our clinic. Genetic testing in patients with diabetes will guide us to identify genes that should be corrected, which will lead to a personalized regenerative gene therapy.

Reference:

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

View original post here:
Diabetes Reversed in Mice With CRISPR-Edited Stem Cells From Patients - Technology Networks

Read More...

Stem Cells and Silk Make a New Way to Study the Brain – Tufts Now

Thursday, April 23rd, 2020

More than five million Americans, mostly sixty-five or older, suffer from Alzheimers disease (AD), and that number is expected to triple by 2060, as todays twenty-somethings become seniors. No treatments exist for this devastating disease, and its root causes remain as tangled as the curious brain deformities that German physician Alois Alzheimer first described in 1906.

Now a team of Tufts researchers from the School of Medicine and the School of Engineering has received a five-year, $5 million grant from the National Institute on Aging, part of the National Institutes of Health, to study the role of different cell types and mutations in AD. They will use a unique bioengineered mini brain that realistically simulates the human brain environment for years.

The work, which builds on years of collaboration among the researchers, will overcome two traditional stumbling blocks to such studies: the limited relevance of animal models and the inability of cell culture systems to reproduce the physiology of the human brain. While age is the biggest risk factor for AD, genetics also plays a role. Scientists have uncovered twenty gene variants that increase the risk of AD, said Giuseppina Tesco, professor of neuroscience and lead investigator on the research, who has devoted her career to studying the disease.

Recent studies show that most of the genes that carry these variants are expressed in glial cells, particularly astrocytes and microglial cells. Once dismissed as onlookers in the brain, glia are now front and center in Alzheimers research said glia expert Philip Haydon, a principal investigator on the project. Haydon, the Annetta and Gustav Grisard Professor of Neuroscience, likens these cells to the pit crew for the flashy race-car-like neurons, supporting top performance by, for example, preventing buildup of protein plaques.

But unlike neurons, human glial cells behave very differently from those of other mammals. What we can learn from mouse models is very limited. It is very important to study these genes in human cells, said Tesco. And we need to do this over time. It may take months to see the effect of genetic variation.

The Tufts team will use cells derived from patients with AD as well as healthy subjects, drawing on advanced stem cell technology that makes it possible to reverse engineer human primary cells into induced pluripotent stem cells, which can then differentiate into neurons, astrocytes, and microglia.

These glia and other brain cells will grow on a unique three-dimensional doughnut-shaped scaffold made of porous silk and collagenwhat the researchers have dubbed a mini brain. Bioengineer David Kaplan, Stern Family Professor and a principal investigator on the grant, and his team have spent six years perfecting the mini brain for research on AD, traumatic brain injury, and brain cancer.

This model allows us to put cells where we want, determine ratios of different cells to use in the system, and control interactions, so we can study electrophysiology, synaptic activity, and other functions as the tissue ages, said Kaplan. That control over the long term supports exploration of age-related questions about disease progression and contributes to reproducibility, a scientific pillar. Past experiments using these mini brains have mimicked structural and functional features and neural activity for up to two years.

In contrast, a two-dimensional culture systemlike the proverbial petri dishwont replicate the complexities of multiple cell types and physiologies. And organoidssimplified organs in miniature now in vogueare subject to cellular death after a few weeks or months.

To complement the in vitro studies with the scaffolds, scientists in Haydons lab will transplant some of the human cells, both mutated and normal, into mice. As they grow, the human glia cells will replace the mouse cells, giving researchers an opportunity to study human brain function. This is the first step towards translational studies, said Haydon.

The grant complements donations from Tufts alumni, parents, friends, and other private individuals who have experienced the pain of Alzheimers disease in their own lives. Donor dollars really got some of our early, exploratory work up and running, said Haydon. Now we are building on that.

The NIH support is a bright spot at a time when COVID-19 has forced Tufts scientists, like their peers around the world, to halt laboratory research, sometimes losing years of work.

Tesco said that while it is difficult to be away from her lab, safety is more important than anything else. Im from Italy, where we have more than 22,000 deaths, she said. Being healthy and having the possibility to continue to do some work, I feel lucky. Well be in the best position possible when were ready to start because well be able to start something completely new and very exciting.

Kim Thurler can be reached at kimberly.thurler@tufts.edu.

Follow this link:
Stem Cells and Silk Make a New Way to Study the Brain - Tufts Now

Read More...

Normal human uterus is colonised by clones with cancer-driving mutations that arise early in life, study finds – Cambridge Network

Thursday, April 23rd, 2020

The work, just published in Nature, provides insights into the earliest stages of uterine cancer development.

The endometrium is the inner part of the uterus, more commonly known as the womb lining. It is regulated by hormones such as oestrogen and progesterone and enters different states during childhood, reproductive years, pregnancy and after menopause.

Uterine cancer is the fourth most common cancer in women in the UK, accounting for five per cent of all new female cancer cases. Around 9,400 new cases are diagnosed every year, leading to the death of 2,300 women. Most cases occur in the seventh and eighth decades. Since the early 1990s, the incidence of uterine cancer has risen by 55 per cent in the UK*.

All cancers occur due to changes in DNA, known as somatic mutations, which continuously occur in all of our cells throughout life. A tiny fraction of these somatic mutations can contribute to a normal cell turning into a cancer cell and are known as driver mutations, which occur within a subset of cancer genes.

This study used whole-genome sequencing to better understand the genetic changes in healthy endometrial tissue. The team developed technology to sequence the genomes of small numbers of cells from individual glands in the endometrial epithelium, the tissue layer that sheds and regenerates during a womans menstrual cycle.

Laser-capture microscopy was used to isolate 292 endometrial glands from womb tissue samples donated by 28 women aged 19 to 81 years**, before DNA from each gland was whole-genome sequenced. The team then searched for somatic mutations in each gland by comparing them with whole genome sequences from other tissues from the same individuals.

The researchers found that a high proportion of cells carried driver mutations, even though they appeared completely normal under the microscope. Many of these driver mutations appear to have arisen early in life, in many cases during childhood.

Dr Luiza Moore, the lead researcher based at the Wellcome Sanger Institute, said: Human endometrium is a highly dynamic tissue that undergoes numerous cycles of remodelling during female reproductive years. We identified frequent cancer driver mutations in normal endometrium and showed that many such events had occurred early in life, in some cases even before adolescence. Over time, these mutant stem cells accumulate further driver mutations.

Despite the early occurrence of the first cancer-driver mutations, it takes several decades for a cell to accumulate the remaining drivers that will lead to invasive cancer. Typically, three to six driver mutations in the same cell are required for cancer to develop. As such, the vast majority of normal cells with driver mutations never convert into invasive cancers. When an invasive cancer develops, it may have been silently evolving within us for most of our lifetime.

Dr Kourosh Saeb-Parsy, University of Cambridge and Director of the Cambridge Biorepository for Translational Medicine (CBTM), said: Incidence of uterine cancers have been steadily rising in the UK for several decades, so knowing when and why genetic changes linked to cancer occur will be vital in helping to reverse this trend. This research is an important step and wouldnt have been possible without the individuals who gifted precious samples for this study, including transplant donors and their families.

Professor Sir Mike Stratton, Director of the Wellcome Sanger Institute, added: New technologies and approaches to investigating DNA mutations in normal tissues are providing profound insights into the procession of genetic changes that convert a normal cell into a cancer cell. The results indicate that, although most cancers occur at relatively advanced ages, the genetic changes that underlie them may have started early in life and we may have been incubating the developing cancer for most of our lifetime.

*Information and statistics about uterine cancers are available from the Cancer Research UK website: https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/uterine-cancer

**The Cambridge Biorepository for Translational Medicine (CBTM) supports research requiring human tissue that aims to improve healthcare for patients. Tissue samples used in this study were from post-mortem or transplant donors, with samples also coming from biopsies for non-endometrial diseases. The authors would like to acknowledge all those who provided tissue used in this study, one third of whom were post-mortem or transplant donors. Their generous contribution is incredibly important for facilitating research that will help to improve the quality of healthcare for patients. https://www.cbtm.group.cam.ac.uk/aboutus

Luiza Moore, Daniel Leongamornlert and Tim H. H. Coorens et al. (2020). The mutational landscape of normal human endometrial epithelium. Nature. DOI: 10.1038/s41586-020-2214-z

Image: Endometrial_glands_Luiza Moore_ Wellcome Sanger Institute

Follow this link:
Normal human uterus is colonised by clones with cancer-driving mutations that arise early in life, study finds - Cambridge Network

Read More...

Photos of the fight to save the world’s last two northern white rhinos – i-D

Thursday, April 23rd, 2020

This story appeared as part of the Atmoss Stewards of The Wild portfolio. Buy the print copy here.

Professor Thomas Hildebrandt, head of the reproduction management department at Leibniz Institute for Zoo and Wildlife Research, leads the team of scientists who announced in September of last year that they had successfully created two viable northern white rhino embryos using in vitro technology and sperm from long-dead males. Following decades of poaching for their horns, there are just two northern white rhinos left in existence, mother and daughter pair Najin and Fatu, who live under 24-hour guard at the Ol Pejeta Conservancy in Kenyas central highlands. Both are infertile. The two embryos will now be inserted into a surrogate southern white rhino, the closest subspecies. If a calf is born, it would herald a new era for conservation -- and for one of the worlds most important critically endangered animals.

Jennifer OMahony: When did you start working with the concept that in vitro technology could be an asset for biodiversity and conservation?Thomas Hildebrandt: For the northern white rhino project, there are two really important developments. Firstly, the in vitro technology that was already used for other species in the past. What is new since 2012 was pairing that with stem cell technology, because for the northern white rhino, assisted reproduction would be not sufficient to actually create a self-sustaining population. If you dont get together enough genetic diversity in the population, then it makes no sense to speak about future reintroduction plans. By pairing these two approaches, that gave us a totally new horizon on saving critically endangered species, and it also changed the way we evaluate the status of species which are on the brink of extinction. While in the past, that was based on the number of fertile individuals in the population, that is no longer necessaryor at least in the future it will no longer be unnecessary, because every infertile or even dead animal can contribute to the population by utilizing this kind of technique.

And how have you shifted your approach as the technology has evolved? We were quite disappointed, because we worked with the northern white rhinos in the early 2000s, and all our efforts got less and less successful because of a very small population. We went to San Diego Zoo, we scanned all the individuals there, we collected semen from the last bull, which had a poor semen quality. We did that, but we were not hopeful that it had any implication for saving the species. At that time, there was the existing population of 30 individuals in Garamba. And actually, we were invited to go there to harvest more semen from the wild ones, when they were supposed to get a transponder put into their horns. But the trip was cancelled, due to the civil war. So, we never went and shortly after, all of those individuals were gone. And there is still a rumor that there are some remaining individuals left in Sudan, but nobody can prove that. The stem cell technique is only proven in a mouse, not in a rhinoceros, but its available to us. These samples we have for the northern white rhino are of equal or even higher genetic diversity than those of the southern white rhino (there are more than 17,000 southern white rhinos left in existence and just two northern white rhinos).

The last male northern white rhino, Sudan, died in 2018 leaving behind a daughter and granddaughter. Before his death, nine years had gone by with no northern white rhino births. Why is it so hard for rhinos to reproduce?Infertility comes quite early. In the wild, the female would have one ovarian cycle every five years, because she finds a suitable breeding partner, and then she gets pregnant for 16 months. After she gives birth, then shes lactating and is raising the calf, and during that entire time, we have an ovarian dormancy (she cannot get pregnant). If the suitable breeding partner is missing, then the female is ovulating every month, and estrogen is a carcinogenic substance. If you have about two years of cycle activity in a female rhino, then the likelihood that you develop severe pathologies is very high.

So, it is dangerous for them not to get pregnant?The pregnancy is actually a curing element, and ovulation is a very rare event. A rhino ovulates every four years.

What is the best way to tackle the biggest threat to rhinos: poaching?There are different organizations which are quite good at stopping smugglers and enforcing a military presence in natural reserves or national parks. But theres one aspect, which I think should be a little bit more explored: the option to breed or to produce rhino horn in vitro. Nobody is doing that. If there is such demand on the Asian market for this kind of product, it could be easilywell, not easily, but at least it is thinkable that you could produce it like you do silk from spiders. Then, most likely is the argument that these people want the real horn. But I think that would be an option, but on every side, its very hard. And it is really a kind of war. Its a very sad point, and as a reflection of that, we always get the argument, You are now spending so much effort and so much resources to create the northern white rhino population to a level that you can reintroduce them, and then they will all be shot again. My answer to that is that we see a lot of examples, and the best one is in Australia. In the 1930s, Australia paid a bounty for killing Tasmanian tigers, and they erased all the Tasmanian tiger population. And now they invested millions of Australian dollars to create an institute exploring the option to recreate the Tasmanian tiger to reintroduce it to Tasmania. I think if the African nations get the option to utilize the northern white rhino as a magnet for ecotourism, there will be sufficient protection from the government and from the younger generation, which will allow them to propagate in the right way and will protect them in the future.

Species have died out throughout history. Why do you think its important to focus research and money on these larger mammals like rhinos? What is it about them for you that makes them so important to save?The rhino didnt die out because of a failure in evolution. It died out because its not bulletproof. Its an absolutely human-made effect. And its a key species, which is an umbrella species for hundreds of other species. It distributes plants on a large scale; it produces feces for insects; it makes avenues for small antelopes and other small animals; its a landscape architect, one of the most important ones. It lives in swampy areas, so you cant actually bring southern white rhinos to Central Africa. So, it is a very important element, and you may remember what happens when you disturb a fragile ecosystem. It didnt fail in evolution, it didnt fade out slowly, but it was shot. So, by messing with this fragile ecosystem, by taking out such an important element, I think we will pay badly for this mistake, and therefore, I think its our responsibility to fix it.

Do you think in your lifetime, you will see a rhino being born from the embryos that you have developed?It is not the scale of my lifetime, it is a scale of the lifetime of Najin and Fatu. So, we have to be successful as soon as possible, because we have the genetic code, which makes up species, but we also have tradition, we have the behavior aspect (any future calf would be born from a surrogate, but raised with the last remaining northern white rhinos who are both infertile). And we really want that new northern white rhino calf. These embryos have the potential to develop into such a calf, and they can learn from the last two remaining northern white rhinos. That is our goal right now. I hope I dont fail in this kind of hope.

Credits

All images courtesy Atmos

i-D is committed to ongoing coverage of the global climate crisis. Read all of our Earth Day 2020 coverage here, and more of our climate change coverage here.

Read more here:
Photos of the fight to save the world's last two northern white rhinos - i-D

Read More...

Page 12«..11121314..2030..»


2025 © StemCell Therapy is proudly powered by WordPress
Entries (RSS) Comments (RSS) | Violinesth by Patrick