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Low levels of vitamin D may put people at risk for developing COVID-19, a new study by לאומית שירותי בריאות and the Azrieli Faculty of Medicine of Bar-Ilan University.


Vitamin D has long been understood to impact immune response. According to Dr. Milana Frenkel-Morgenstern, leader of the Azrieli Faculty of Medicine research group, as much as 70% of the adult population worldwide is vitamin D insufficient or deficient.

The Leumit and Bar-Ilan scientists analyzed if the risk of developing COVID-19 or becoming hospitalized because of it increases for people who have a low level of vitamin D.

They studied 782 Israeli COVID-19-positive patients and 7,825 negative patients and determined that a low plasma vitamin D level appears to be an independent risk factor for COVID-19 infection and hospitalization.

“We don’t know the mechanism,” Frenkel-Morgenstern said. “What we do know is that people who develop severe COVID and were hospitalized – these people have significantly low vitamin D levels.”

North Korea declared a state of emergency on Sunday after one person in the country was suspected of being positive for COVID-19.

On Sunday, local time, state news agency KCNA reported North Korean leader Kim Jong Un Kim Jong UnNorth Korea declares state of emergency due to a suspected COVID-19 case Pompeo downplays chance of summit with North Korea this year Juan Williams: Trump’s silence on Russian bounties betrays America MORE convened an emergency politburo meeting after a person who defected to South Korea three years ago was “suspected to have been infected with the vicious virus.” The person is reported have returned to the North Korean border city of Kaesong, Reuters reported.

Kim declared a state of emergency and imposed a lockdown in Kaesong, reportedly calling it a “critical situation in which the vicious virus could be said to have entered the country.”

The clues have been mounting for a while. First, scientists discovered patients who had recovered from infection with Covid-19, but mysteriously didn’t have any antibodies against it. Next it emerged that this might be the case for a significant number of people. Then came the finding that many of those who do develop antibodies seem to lose them again after just a few months.

In short, though antibodies have proved invaluable for tracking the spread of the pandemic, they might not have the leading role in immunity that we once thought. If we are going to acquire long-term protection, it looks increasingly like it might have to come from somewhere else.

But while the world has been preoccupied with antibodies, researchers have started to realise that there might be another form of immunity – one which, in some cases, has been lurking undetected in the body for years. An enigmatic type of white blood cell is gaining prominence. And though it hasn’t previously featured heavily in the public consciousness, it may well prove to be crucial in our fight against Covid-19. This could be the T cell’s big moment.


While the latest research suggests that antibodies against Covid-19 could be lost in just three months, a new hope has appeared on the horizon: the enigmatic T cell.

CORPUS CHRISTI, Texas (AP) — Hurricane Hanna roared ashore onto the Texas Gulf Coast on Saturday, bringing winds that lashed the shoreline with rain and storm surge, and even threatening to bring possible tornadoes to a part of the country trying to cope with a spike in coronavirus cases.

The first hurricane of the 2020 Atlantic hurricane season made landfall twice as a Category 1 storm on Saturday afternoon within the span of little over an hour. The first landfall happened at around 5 p.m. about 15 miles (24 kilometers) north of Port Mansfield, which is about 130 miles (209 km) south of Corpus Christi. The second landfall took place nearby in eastern Kenedy County. Hanna had come ashore with maximum sustained winds of 90 mph (145 kph). As of Saturday night, those winds had weakened to 75 mph (120 kph).

Many parts of Texas, including areas near where Hanna came ashore, have been dealing with a surge in coronavirus cases in recent weeks, but local officials said they were prepared for whatever the storm might bring.

University of Rochester researchers are setting a new standard when it comes to producing ultrafast laser pulses over a broader range of wavelengths than traditional laser sources.

In work published in Physical Review Letters, William Renninger, an assistant professor of optics, along with members of his lab, describe a new device, called the “stretched-pulse soliton Kerr resonator,” that enhances the performance of ultrafast laser pulses. The work has important implications for a range of engineering and biomedical applications, including spectroscopy, frequency synthesis, distance ranging, pulse generation, and others.

The device creates an ultrafast laser pulse—on the order of femtoseconds, or one quadrillionth of a second—that’s freed from the physical limits endemic to sources of laser light—what laser scientists call laser gain—and the limits of the sources’ wavelengths.

Cholangiocarcinoma may not be a household word unless, of course, you happen to be a pathologist studying hepatic cancers. Still, it does affect a fair number of individuals, typically over the age of 50. Cholangiocarcinoma is a group of cancers that begin in the bile ducts, which carry digestive fluid to the small intestine. Cholangiocarcinomas are classified by their location in relation to the liver and typically grouped in with other types of liver cancer. Now, a team of investigators at the Spanish National Cardiovascular Research Centre (CNIC) believe they have uncovered a mechanism that controls the development of intrahepatic cholangiocarcinoma.

Findings from the new study—published recently in PNAS through an article entitled “JNK-mediated disruption of bile acid homeostasis promotes intrahepatic cholangiocarcinoma”—identified a protein that, when blocked, dramatically reduces the impact and progression of the cancer.


Spanish scientists have designed an animal model to study the development of liver cancer caused by bile acids, whcih could speed drug discovery.

What changed things for Germany? A handful of prominent scientists communicating regularly and openly with the public. (via CNBC)…and a leader who is a scientist.

Germany, like many other countries, had a contingent of people who fought lockdowns and argued that Covid-19 was a hoax. But it also had a handful of prominent scientists communicating regularly and openly with the public. That played a huge role in drowning out rumors and misinformation, locals tell CNBC.

“We have a great educational system and everyone has access to it,” said Dennis Traub, a tech worker in Hamburg, Germany. “So I believe that many people and the majority listened to both sides and one of those sides sounded much more reasonable.”


Germany stood out for its strong science communication. For months, its top podcast was ‘Der Coronavirus,’ which provided an update on the disease from a top virologist.

Utilizing neurotransmitters as a passport into the brain:


Safe and efficient delivery of blood-brain barrier (BBB)–impermeable cargos into the brain through intravenous injection remains a challenge. Here, we developed a previously unknown class of neurotransmitter–derived lipidoids (NT-lipidoids) as simple and effective carriers for enhanced brain delivery of several BBB-impermeable cargos. Doping the NT-lipidoids into BBB-impermeable lipid nanoparticles (LNPs) gave the LNPs the ability to cross the BBB. Using this brain delivery platform, we successfully delivered amphotericin B (AmB), antisense oligonucleotides (ASOs) against tau, and genome-editing fusion protein (−27)GFP-Cre recombinase into the mouse brain via systemic intravenous administration. We demonstrated that the NT-lipidoid formulation not only facilitates cargo crossing of the BBB, but also delivery of the cargo into neuronal cells for functional gene silencing or gene recombination. This class of brain delivery lipid formulations holds great potential in the treatment of central nervous system diseases or as a tool to study the brain function.

We’re going back to Mars, and we’d like you to be our virtual guest on the trip. On July 30, NASA will launch the Mars 2020 Perseverance rover on a seven-month journey to the Red Planet. After landing in Jezero Crater, the robotic astrobiologist and scientist will search for signs that microbes might have lived on Mars long ago, collect soil samples to be returned to Earth on a future mission and pave the way for human exploration beyond the Moon. Perseverance will be accompanied by a helicopter called Ingenuity, the first attempt at powered flight on another world.

Because of the coronavirus pandemic and in the interest of health and safety, NASA can’t invite you to Florida to watch the launch personally. However, there are many ways you can participate virtually:

In mammals, the acquisition of the germline from the soma provides the germline with an essential challenge, the necessity to erase and reset genomic methylation1. In the male germline, RNA-directed DNA methylation silences young active transposable elements (TEs)2–4. The PIWI protein MIWI2 (PIWIL4) and its associated PIWI-interacting RNAs (piRNAs) instruct TE DNA methylation3,5. piRNAs are proposed to tether MIWI2 to nascent TE transcripts; however, the mechanism by which MIWI2 directs de novo TE methylation is poorly understood but central to the immortality of the germline. Here we define the interactome of MIWI2 in foetal gonocytes that are undergoing de novo genome methylation and identify a novel MIWI2-associated factor, SPOCD1, that is essential for young TE methylation and silencing. The loss of Spocd1 in mice results in male-specific infertility but impacts neither piRNA biogenesis nor localization of MIWI2 to the nucleus. SPOCD1 is a nuclear protein and its expression is restricted to the period of de novo genome methylation. We found SPOCD1 co-purified in vivo with DNMT3L and DNMT3A, components of the de novo methylation machinery as well as constituents of the NURD and BAF chromatin remodelling complexes. We propose a model whereby tethering of MIWI2 to a nascent TE transcript recruits repressive chromatin remodelling activities and the de novo methylation apparatus through SPOCD1. In summary, we have identified a novel and essential executor of mammalian piRNA-directed DNA methylation.