Tag: 28/10/21

Categories : COVIDTags :

Mask-wearing Protects Wearers Too

On By ModernMedia
Source: Visuals on Unsplash

People who adhered to masking outside of the home, but were more exposed to infection due to their circumstances, still had “significantly” lower COVID infection rates, according to research published in BMJ Open.

Although it has been widely asserted that face coverings serve to protect others, rather than the wearer, this large-scale study established a clear link between wearing a face covering outside the home and infection.

The Oxford-led study links individuals’ and households’ ability to follow non-pharmaceutical interventions (NPIs) often known as COVID behavioural interventions, using the largest and most representative dataset to date in the UK, including people from different ethnic and age groups.

Using the COVID Infection Study (CIS), study participants were asked to complete a short questionnaire, as well as taking regular COVID tests. Respondents were asked to share how often they worked outside the home, how easy it was to keep social distance in their workplace, whether they took public transport and whether they had direct contact with others on a day-to-day basis.

According to the study, “Wearing a face covering outside was a significant predictor of a lower chance of infection before mid-December 2020 in the UK, when a stricter second lockdown was implemented.”

There was a higher rate of infections among those who lacked autonomy to follow COVID behavioural measures and did not comply with masking.

Author Professor Melinda Mills said, “Lack  of  compliance  to  COVID behavioural measures  has  often been  positioned  as  an  attitude  or  choice. Yet there are large groups of people who, due to their household or employment circumstances, cannot follow measures to work from home, engage in physical distancing at the workplace or avoid public transportation. This, in turn, means that they have a higher exposure to becoming infected.

“The inability for some groups of people to follow behavioural interventions exacerbates existing health inequalities and we showed that face coverings are one measure that can mitigate this unequal exposure.”

The team found, “The  level  of  autonomy  to  adhere  to  behavioural interventions does not  predict  COVID infection  alone,  but  rather the risk of infection is diminished when individuals wear face  covering/masks.”

The study concluded that masking reduces the effects of unequal COVID exposure.
Professor Mills added, “Using a very large individual and household sample and COVID swab tests, we showed that the inability for certain groups such as women in large households or those working in occupations where it is hard to maintain physical distancing were protected from infection during key periods in 2020 in the UK”.

Source: Oxford University

Categories : CancerTags :

Foiling Cancer With its Own Sweet Tooth

On By ModernMedia
Photo by Louis Reed on Unsplash

Cold Spring Harbor Laboratory Professor Christopher Vakoc and his lab have found that acute myeloid leukaemia (AML), an aggressive cancer that originates in the bone marrow, depends on a transporter to bring in the nutrient inositol, and the researchers believe they can find a way to cut off the cells’ food supply and kill them.

Cancers may streamline certain cell processes and rely on just one method to survive; for example, some remove backup pathways for DNA repair, “putting all their eggs in one basket” and depending only on a single pathway for survival. Prof Vakoc’s lab could then develop treatments to knock out that remaining pathway, killing the cancer cells.

In a study published in Cancer Discovery, Prof Vakoc and his lab reported that AML depends on inositol, an abundant sugar that is made in many human body tissues. It is also found in a wide variety of foods like fruits, beans, grains, and nuts, so cells can obtain it from outside the body, via the bloodstream.

Prof Vakoc discovered that the AML cells had streamlined and boosted their growth by disabling their own inositol production, instead relying on external inositol, bringing it in with a transporter on the cell surface. If a simple treatment could turn off or block this transporter, the cancer cells would starve. As Prof Vakoc explained, “An antibody approach would be very attractive. You could make an antibody that just sticks to this transporter. It doesn’t need to get into the cell, and it could shut off the transport function. The other possibility, from a drug development point of view, is inositol. You could build a molecular medicine that sort of looks like inositol, but maybe it has a few chemical differences that can clog the transport function.”

Not only could this method kill the cancer cells, but it would also leave normal cells unharmed since they can make their own inositol. 

Source: Cold Spring Harbor Laboratory

Categories : General Interest GeneticsTags :

Chief Sitting Bull’s DNA Matched to Living Descendant

On By ModernMedia
By Orlando Scott Goff – Heritage Auctions, Public Domain, https://commons.wikimedia.org/w/index.php?curid=27530348

A team of researchers led by the University of Cambridge has proven a man’s claim to be the great-grandson of legendary Native American leader Sitting Bull has been confirmed using DNA extracted from Sitting Bull’s scalp lock. This is the first time ancient DNA has been used to confirm a familial relationship between living and historical individuals.

The researchers used a new method to analyse family lineages using ancient DNA fragments, which searches for ‘autosomal DNA’ in the genetic fragments extracted from a body sample. Since half of our autosomal DNA is inherited from the father and half from the mother, this means genetic matches can be checked regardless of whether an ancestor is on the father or mother’s side of the family.

Autosomal DNA from Lakota Sioux leader Sitting Bull’s scalp lock was compared to DNA samples from Ernie Lapointe and other Lakota Sioux. The resulting match confirms that Lapointe is Sitting Bull’s great-grandson, and his closest living descendant.

“Autosomal DNA is our non-gender-specific DNA. We managed to locate sufficient amounts of autosomal DNA in Sitting Bull’s hair sample, and compare it to the DNA sample from Ernie Lapointe and other Lakota Sioux – and were delighted to find that it matched,” said senior author of the study, Professor Eske Willerslev in the University of Cambridge’s Department of Zoology and Lundbeck Foundation GeoGenetics Centre, who also developed the new DNA analysis technique.

Lapointe said: “over the years, many people have tried to question the relationship that I and my sisters have to Sitting Bull.”

Lapointe believes that Sitting Bull’s bones currently lie at a site in Mobridge, South Dakota, in a place that has no significant connection to Sitting Bull and the culture he represented. He also has concerns about the care of the gravesite. There are two official burial sites for Sitting Bull – at Fort Yates, North Dakota and Mobridge – and both receive visitors.

Lapointe, with the help of the DNA evidence confirming his heritage, now hopes to rebury the great Native American leader’s bones in a more appropriate location.

The new technique can be used when very limited genetic data are available, as was the case in this study. This could be used to match up long-dead historical figures and their living descendants.

The technique could also be used on old human DNA that might previously have been considered too degraded to analyse – for example in forensic investigations.

“In principle, you could investigate whoever you want – from outlaws like Jesse James to the Russian tsar’s family, the Romanovs. If there is access to old DNA – typically extracted from bones, hair or teeth, they can be examined in the same way,” said Willerslev, who is a Fellow of St John’s College, Cambridge.

It took the scientists 14 years to find a way of extracting useable DNA from the 5-6cm piece of Sitting Bull’s hair, which was extremely degraded, having been stored for over a century at room temperature in a museum before it was returned to Lapointe and his sisters in 2007.

In traditional DNA analysis, which searches for a genetic match between specific DNA in the Y chromosome passed down the male line, or, in females, specific DNA in the mitochondria passed from a mother to her offspring. Neither are particularly reliable, and in this case neither could be used as Lapointe claimed to be related to Sitting Bull on his mother’s side.

Tatanka-Iyotanka, better known as the Native American leader and military leader Sitting Bull (1831–1890), led 1,500 Lakota warriors at the Battle of the Little Bighorn in 1876 and wiped out US General Custer and five companies of soldiers.

“Sitting Bull has always been my hero, ever since I was a boy. I admire his courage and his drive. That’s why I almost choked on my coffee when I read in a magazine in 2007 that the Smithsonian Museum had decided to return Sitting Bull’s hair to Ernie Lapointe and his three sisters, in accordance with new US legislation on the repatriation of museum objects,” said Willerslev.

He added: “I wrote to Lapointe and explained that I specialised in the analysis of ancient DNA, and that I was an admirer of Sitting Bull, and I would consider it a great honour if I could be allowed to compare the DNA of Ernie and his sisters with the DNA of the Native American leader’s hair when it was returned to them.”

Until this study, the familial relationship between LaPointe and Sitting Bull was based on birth and death certificates, a family tree, and a review of historical records. This new genetic analysis lends further credence to his claims. Before the remain can be reburied, they will have to be analysed in the same to ensure a genetic match to Sitting Bull.

Before the remains from the Mobridge burial site can be reburied elsewhere, they will have to be analysed in a similar way to the hair sample to ensure a genetic match to Sitting Bull. 

Source: Cambridge University

Categories : COVIDTags :

US Health Body Admits Funding Coronavirus Enhancement Study

On By ModernMedia
SARS-CoV-2 virus. Source: Fusion Medical Animation on Unsplash

In an unexpected turn of events, the US National Institutes of Health (NIH) has acknowledged that it funded research into enhancing coronavirus infectivity, Vanity Fair reported.

The agency had last week sent a letter to the US House Committee on Energy and Commerce stating that its grant recipient, EcoHealth Alliance, enhanced a bat coronavirus to become potentially more infectious to humans. This was an “unexpected result” of the research, done in collaboration with Wuhan Institute of Virology.

The NIH letter also noted that EcoHealth Alliance violated terms of its grant conditions, which had stipulated that it was supposed to report to the agency if its work boosted viral growth by a factor of 10.

EcoHealth Alliance was supposed to submit a progress report at the end of the grant period in 2019 but it didn’t arrive at the NIH until August 2021, according to Vanity Fair. However, in a statement to Vanity Fair, EcoHealth Alliance said that it had reported the relevant information “as soon as we were made aware, in our four year report in April 2018.”

In that missing progress report (dated August 2021), lab mice infected with the enhanced virus became more ill than those infected with a wild one, reported Vanity Fair.

The Vanity Fair report also reveals a rather concerning detail contained in a leaked EcoHealth Alliance grant proposal submitted to the Defense Advanced Research Projects Agency in 2018. EcoHealth Alliance and the Wuhan Institute of virology proposed to engineer a furin cleavage site for the coronavirus to more easily enter humans cells. This matches a distinctive segment of SARS-CoV-2’s genetic code.

“If I applied for funding to paint Central Park purple and was denied, but then a year later we woke up to find Central Park painted purple, I’d be a prime suspect,” Jamie Metzl, a member of the WHO advisory committee on human genome editing, told Vanity Fair.

In its letter to US Congress, the NIH emphasised that the virus EcoHealth Alliance was studying could not have sparked the pandemic, as there was a vast genetic difference between it and SARS-CoV-2. NIH Director Francis Collins, MD, PhD, also issued a statement addressing the concerns raised by the letter, noting that such claims were “demonstrably false.”

“The scientific evidence to date indicates that the virus is likely the result of viral evolution in nature, potentially jumping directly to humans or through an unidentified intermediary animal host,” Dr Collins said in the statement.

Gilles Demaneuf, a data scientist in New Zealand, told Vanity Fair, “I cannot be sure that [COVID originated from] a research-related accident or infection from a sampling trip. But I am 100% sure there was a massive cover-up.”

In response to these criticisms of poor oversight and bad scientific judgment, the NIH has “circled its wagons”, Vanity Fair observed.

Source: Vanity Fair

Categories : Diseases, Syndromes and ConditionsTags :

Tamoxifen Found to be Ineffective in Fungal Meningitis Trial

On By ModernMedia
Photomicrograph of a sample extracted from a lesion that revealed the presence of Cryptococcus neoformans. Credit: CDC

In a disappointing outcome, a clinical trial has shown that tamoxifen, a promising candidate to improve survival for a deadly form of fungal meningitis, is ineffective. The trial was conducted by University of Oxford researchers and published in eLife.

The study finds that adding tamoxifen, a breast cancer drug, to standard antifungal treatment was no faster in clearing fungal infection from the spinal fluid of people with meningitis. More patients who received tamoxifen had evidence of heart conduction disturbances, rates of severe side effects were similar.

Cryptococcal meningitis is a leading cause of death in people with HIV, but also affects those without HIV, regardless of whether they are immunocompromised. Most infections are caused by a fungus called Cryptococcus neoformans (C. neoformans) and occur in low-income tropical settings. The gold-standard treatment is a combination of three drugs: flucytosine and amphotericin B initially, followed by fluconazole. Yet, even on this gold-standard therapy, a third of patients die within 10 weeks of being diagnosed. Moreover, the drug flucytosine is severely restricted by availability and cost, meaning it is rarely used where the disease burden is highest.

Co-first author Nguyen Thi Thuy Ngan, Clinician at the Oxford University Clinical Research Unit (OUCRU): ‘Tamoxifen has shown antifungal activity against various yeasts in the lab; we subsequently showed that it acts synergistically with amphotericin against two-thirds of clinical Cryptococcus isolates from our archive. As a well-understood, off-patent, cheap and widely available medicine, it was a promising candidate for treating cryptococcal meningitis.’

Co-first author Nhat Thanh Hoang Le, Biostatistician at OUCRU, added: ‘We designed a randomised trial to determine whether using these drugs in combination could improve the speed of clearance of Cryptococcus from patients with meningitis with and without HIV.’

The trial involved 50 patients, 40 with HIV. Of the patients, 24 were assigned to receive a standard anti-fungal treatment of amphotericin B and fluconazole plus tamoxifen, and 26 received the standard anti-fungal treatment only. Researchers measured the Early Fungicidal Activity (EFA) for both groups – how quickly C. neoformans amounts declined in a patient’s spinal fluid in the two weeks following treatment.

Based on their prior work, the team were hoping for better EFA for patients receiving tamoxifen, but there was no detectable difference in EFA.

The only observed difference was increased heart toxicity in the tamoxifen group. Lab studies had shown that a tamoxifen dose five to 10 times higher than that used routinely in breast cancer would be needed to have an antifungal effect. However, high doses of tamoxifen cause QT prolongation, which can cause cardiac arrest. While there was one sudden death in the tamoxifen group in this study, this occurred after the period of tamoxifen administration and it was not associated with an abnormal heart rhythm.

Senior author Professor Jeremy Day, Professor of Infectious Diseases, Oxford University, said: “Despite its apparent anti-cryptococcal effect and synergy with other drugs, tamoxifen does not increase the rate of clearance of yeast from spinal fluid in people with meningitis and is unlikely to result in clinical benefit.

“Our results show the importance of small-scale trials such as this for rapidly evaluating repurposable drugs and preventing the time and cost of a larger clinical study that is likely to fail. However, sadly this does mean that we urgently still need new, specific anti-cryptococcal drugs to be developed, and we also need to ensure that existing, available treatments are made accessible and affordable.”

Source: Oxford University

Categories : Neurodegenerative DiseasesTags :

Deaths from Parkinson’s on the Rise

On By ModernMedia
Photo by Kindel Media on Pexels

Over the last two decades, the death rate from Parkinson’s disease has risen about 63% in the US, and the death rate was twice as high in men as in women, with a higher death rate in White people than other racial/ethnic groups.

“We know that people are living longer and the general population is getting older, but that doesn’t fully explain the increase we saw in the death rate in people with Parkinson’s,” study author Wei Bao, MD, PhD, who conducted the research at the University of Iowa in Iowa City. “Understanding why more people are dying from this disease is critical if we are going to reverse the trend.”

The study, published in Neurology, looked at a national death registry that included 479 059 people who died of Parkinson’s from 1999–2019.

After adjusting for age, researchers found that the number of people who died from the disease increased from 5.4 per 100,000 people in 1999 to 8.8 per 100 000 people in 2019. The average annual increase was 2.4%.

Mortality increased significantly across all age groups, both sexes, various racial and ethnic groups and different urban-rural classifications. However, death rates were twice as high in men as in women. According to Dr Bao, a possible explanation for this sex difference is that oestrogen, which leads to higher dopamine levels in parts of the brain that control motor responses, may protect women from developing Parkinson’s.

White people were more likely to die from Parkinson’s than other racial and ethnic groups. In 2019, the death rate for White people was 9.7 per 100 000, followed by Hispanic people, at 6.5 per 100 000, and non-Hispanic Black people, at 4.7 per 100 000. In previous studies, compared to White people, Black and Hispanic people are less likely to see an outpatient neurologist, due to socioeconomic barriers, suggesting that White people may have a higher chance of receiving a Parkinson’s diagnosis.

“It’s important to continue to evaluate long-term trends in Parkinson’s death rates,” Dr Bao said. “This can inform future research that may help pinpoint why more people are dying of the disease. Also, updating vital statistics about Parkinson’s death rates may be used for priority setting and financing of health care and policy.”

A limitation of the study is that only one underlying cause of death was recorded on each death certificate, so only people who were recorded as having died of Parkinson’s were included in the study. This may not accurately reflect the prevalence of the disease as a cause of death.

Source: American Academy of Neurology