Saturday, March 24, 2018

Toshiba Unveiled a New Lithium-Ion Battery that can be Fully Charged in Six Minutes! Its called An SCiB Lithium-ion Battery. Basically, The Anode Material is Different

Toshiba Unveils New Super Fast Charging Lithium Battery Upping the Stakes for Li-on Market - Oil & Gas 360

The electric vehicle market seems poised for another wave of expansion as battery technology improves to efficiency levels never seen before, thanks to innovations being unveiled by the likes of Toshiba. The EV market has sent lithium companies soaring as projected demand has gone over the top in the last quarter


From article, (Toshiba recently unveiled a li-ion battery which they claim charges fully in just six minutes, delivering a 200-mile range on a full charge.
This is a big leap from Tesla’s current configuration which takes up to an hour to charge fully.
Toshiba’s next generation SCiB lithium ion battery replaces the conventional lithium titanium oxide anode with a titanium niobium oxide anode. The new battery maintains the longevity of the previous older configuration, promising a life cycle of 14 years, assuming a full charge and discharge cycle per day.
The new technology will be feeding an already accelerating EV market that is led by Tesla and a host of European and Asian carmakers.
Tesla has taken the EV industry by the scruff of its neck, multiplying not only car production, but also interest in EVs, a wave that other electric car manufacturers have been keen to ride. In the next few years it is expected that Tesla will have put over a million EVs on the road, while European giants Volvo and Volkswagen have made commitments to turn to electric vehicles as their main products in the near future.
In China, the world’s largest car market, the EV revolution has well and truly hit top gear, with nearly 500,000 EVs being sold last year alone.
Governments around the world have also been pushing for the EV revolution, with bans on petroleum and diesel cars coming into effect as part of the Paris Climate Agreement to cut emissions.
According to Global X research, global revenue from lithium-ion battery sales is anticipated to post a compound annual growth rate of 43.1% in reaching a projected $36.5 billion by 2020.)



Why Losing Seagrass Due to Warming Oceans is a Bad Thing. The Good News is Seagrass Can be Replanted, Although Difficulty. Advice: Maybe, it Should Be Done in More Temperate Waters? So, As Not to Have a Repeat, Die Off.

The Ocean Has Released an Insane Amount of CO2, And No One Even Noticed

Our planet's climate is built on a whole host of interlinked chemical reactions and counter-reactions, and we just learned about another: an underwater heatwave has triggered a worryingly huge release of CO2 from Amphibolis antarctica seagrass off north-western Australia.
From article, (Our planet's climate is built on a whole host of interlinked chemical reactions and counter-reactions, and we just learned about another: an underwater heatwave has triggered a worryingly huge release of CO2 from Amphibolis antarcticaseagrass off north-western Australia.

Vast tracts of these flowering marine plants were killed by the stress of living in waters that were 2-4 degrees Celsius (3.6-7.2 degrees Fahrenheit) warmer than normal back in the summer of 2010-2011, researchers have found.
More than a third of the seagrass meadows were potentially affected. And no one really noticed.
And the findings have very real implications for the kind of self-perpetuating heat rises we could be in for, say the international team of researchers, as too much carbon dioxide in the atmosphere warms the planet and leads to the release of even more greenhouse gases.
 Losing seagrass is a double whammy for our environment's health – not only do we lose the plant's ability to capture and store CO2, all the CO2 that's already being stored gets released back out into the ecosystem.
"This is significant, as seagrass meadows are CO2 sinks, known as Blue Carbonecosystems," says one of the team, Pere Masqué from the Universitat Autònoma de Barcelona (ICTA-UAB) in Spain.
"They take up and store carbon dioxide in their soils and biomass through biosequestration. The carbon that is locked in the soils is potentially there for millennia if seagrass ecosystems remain intact."
The Shark Bay region we're talking about is one of the largest remaining seagrass ecosystems on Earth – about 1.3 percent of all the CO2 stored by seagrass across the world is stored here.
Plans are now underway to work out how to help the area recover, perhaps by removing dead seagrass (which can hamper regrowth) and planting new seedlings.
Even so, it's important to emphasis the urgency in reducing greenhouse gas emissions and stopping adverse feedback loops like this from happening, say the researchers – otherwise dying seagrass will be giving up more CO2 than healthy seagrass can take back.)

If you Get Pregnant? It Might be a Good Idea to Take Your Vitamins. Vitamin D Deficiency May Cause Autism in Developing Fetus

Low vitamin D levels linked to autism, study says

Getting a dose of vitamin D is often as simple as basking in the rays of the sun. But as Scientific American noted, the lack of this crucial nutrient, often called the sunshine vitamin, may be related to autism, which has seen an alarming spike in cases in recent years.
From article, (Getting a dose of vitamin D is often as simple as basking in the rays of the sun. But as Scientific American noted, the lack of this crucial nutrient, often called the sunshine vitamin, may be related to autism, which has seen an alarming spike in cases in recent years.
Low levels of vitamin D during pregnancy and breastfeeding may be connected to autism later in life, according to a study published in the Journal of Endocrinology by Caitlin Wyrwoll at the University of Western Australia, as Cosmos Magazine noted.
Earlier studies in Scotland and the Netherlands also found that lower levels of maternal Vitamin D during the first trimester of pregnancy may be linked with a heightened risk of autism in children but this latest study involved rats. Scientists examined changes in brain function and social behaviors of adult rats, who had been born to mothers lacking vitamin D. Rats with deficient mothers displayed abnormal social behaviors, altered brain chemistry and impaired learning and memory, all of which are consistent with Autism Spectrum Disorder.
 “Our work reinforces that vitamin D levels in early life influence brain development and can impact on how the brain functions in later life,” Wyrwoll told Cosmos. “We know that early life environment can be a powerful determinant of health outcomes in offspring and, although this is a rat study, these data indicate that vitamin D levels during pregnancy are important for brain development, and may point to a contributing factor in the development of neurodevelopmental conditions, such as ASD.”)

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Understanding the Regulation and Limitation of Telomerase Enzyme May Hold the Secret of the Fountain of Youth.

Immortality Protein Reveals Anti-Aging Secrets

Research from the laboratory of Professor Julian Chen in the School of Molecular Sciences at Arizona State University recently uncovered a crucial step in the telomerase enzyme catalytic cycle. This catalytic cycle determines the ability of the human telomerase enzyme to synthesize DNA "repeats" (specific DNA segments of six nucleotides) onto chromosome ends, and so afford immortality in cells.

From article, (Understanding the regulation and limitation of the telomerase enzyme holds the promise of reversing telomere shortening and cellular aging with the potential to extend human lifespan and improve the health and wellness of elderly individuals. Research from Cheb’s laboratory recently uncovered a crucial step in the telomerase catalytic cycle that limits the ability of telomerase to synthesize telomeric DNA repeats onto chromosome ends.

"Telomerase has a built-in braking system to ensure precise synthesis of correct telomeric DNA repeats. This safe-guarding brake, however, also limits the overall activity of the telomerase enzyme," said Professor Chen. "Finding a way to properly release the brakes on the telomerase enzyme has the potential to restore the lost telomere length of adult stem cells and to even reverse cellular aging itself."

This intrinsic brake of telomerase refers to a pause signal, encoded within the RNA template of telomerase itself, for the enzyme to stop DNA synthesis at the end of the sequence ‘GGTTAG’. When telomerase restarts DNA synthesis for the next DNA repeat, this pause signal is still active and limits DNA synthesis. Moreover, the revelation of the braking system finally solves the decades-old mystery of why a single, specific nucleotide stimulates telomerase activity. By specifically targeting the pause signal that prevents restarting DNA repeat synthesis, telomerase enzymatic function can be supercharged to better stave off telomere length reduction, with the potential to rejuvenate aging human adult stem cells.

Human diseases that include dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis have been genetically linked to mutations that negatively affect telomerase activity and/or accelerate the loss of telomere length. This accelerated telomere shortening closely resembles premature aging with increased organ deterioration and a shortened patient lifespan from critically insufficient cell populations. Increasing telomerase activity is the seemingly most promising means of treating these diseases.

While increased telomerase activity could bring youth to aging cells and cure premature aging-like diseases, too much of a good thing can be damaging for the individual. Just as youthful stem cells use telomerase to offset telomere length loss, cancer cells employ telomerase to maintain their aberrant and destructive growth. Augmenting and regulating telomerase function will have to be performed with precision, walking a narrow line between cell rejuvenation and a heightened risk for cancer development.

Distinct from human stem cells, somatic cells constitute the vast majority of the cells in the human body and lack telomerase activity. The telomerase deficiency of human somatic cells reduces the risk of cancer development, as telomerase fuels uncontrolled cancer cell growth. Therefore, drugs that increase telomerase activity indiscriminately in all cell types are not desired. Toward the goal of precisely augmenting telomerase activity selectively within adult stem cells, this discovery reveals the crucial step in telomerase catalytic cycle as an important new drug target. Small molecule drugs can be screened or designed to increase telomerase activity exclusively within stem cells for disease treatment as well as anti-aging therapies without increasing the risk of cancer.)

Immunotheraputics Could Target and Neutralize HIV-1 Virus Particles. Does this Mean AIDS is Cured?

A Cure for AIDS - Live Trading News

A team of researchers at IBBR, led by Dr. Yuxing Li, Associate Professor at the University of Maryland School of Medicine, Baltimore, and Principal Investigator at the Institute for Bioscience and Biotechnology Research (IBBR), Rockville, is showing how engineered multi-specific antibodies appear to be highly effective at preventing infection across a broad range of HIV-1 ...


From article, (A team of researchers at IBBR, led by Dr. Yuxing Li, Associate Professor at the University of Maryland School of Medicine, Baltimore, and Principal Investigator at the Institute for Bioscience and Biotechnology Research (IBBR), Rockville, is showing how engineered multi-specific antibodies appear to be highly effective at preventing infection across a broad range of HIV-1 virus strains.

Over 36 million people worldwide are currently infected with HIV and the disease has claimed another 35 million lives since the start of the epidemic (www.hiv.gov). Effective treatment of HIV infection currently involves using combinations of antiretroviral drugs (ARV). While ARV treatment can improve the overall quality of life of HIV-positive individuals, better alternative treatments are needed since they can cause undesirable side effects and patients can become resistant to ARV therapy.
Immunotherapeutics, molecules derived from the immune system, can be used to specifically target and neutralize HIV-1 virus particles. Several of these broadly neutralizing antibodies (bNAbs) are being developed and preliminary trials indicate that these individual bNAbs are safe, well-tolerated, and can reduce HIV-1 infection early on. However, treatment is not associated with long-term reductions in virus levels and, due to HIV’s ability to rapidly mutate, resistant strains can emerge. Additionally, the risk of transmission still exists.
Dr. Li’s laboratory successfully created a bispecific antibody (bi-NAb) combining two bNAbs and tested it on a panel of 208 strains of HIV virus that are prevalent in humans. “The bi-NAb neutralized 95% of the circulating HIV-1 viruses, which is superior to any single agent,” said Dr. Li. “We further improved antiviral potency by engineering a tri-NAb and found that it can inhibit 99.5% of circulating HIV-1 viruses.” This technology could lead to development of the broadest-spectrum anti-HIV-1 immunotherapeutic and preventive treatment that exist worldwide.)

Discovery of What Causes Leukemia Means: New Treatments Can Be Created To Stop the Disease.

Two genes cooperate to trigger leukemia development

Researchers have made a breakthrough in understanding the development of acute lymphoblastic leukemia, an aggressive cancer of the blood. While scientists were already familiar with many cancer-causing genes and their separate functions, the VIB team has now illustrated how two of these cancer genes work together to trigger leukemia.

From article, ( Acute lymphoblastic leukemia (ALL) is the most commonly occurring cancer in children, with 100 new cases reported in Belgium every year. Despite the efficacy of chemotherapy in treating this disease, its long and short-term side effects are considerable.

ALL is caused by the accumulation of genetic changes (mutations) that alter the behavior of developing immune cells that transform them into aggressive leukemia cells. Recent studies have found that ALL cases are often characterized by mutations in a certain gene pathway, called JAK3/STAT5.

Prof. Jan Cools (VIB-KU Leuven): "JAK3/STAT5 mutations are important in ALL, since they stimulate the growth of the cells. However, leukemia patients have additional gene mutations, and we found that JAK3/STAT5 mutations, frequently occur together with HOXA9 mutations."

In this study, Jan Cools and his team created a mouse model with cancer-associated JAK3/STAT5 and HOXA9 mutations to determine if they cooperate to drive the development of ALL. HOXA9 mutations have a well-established role in leukemia development.


Dr. Charles de Bock (VIB-KU Leuven): "We examined the cooperation between JAK3/STAT5 mutation and HOXA9. We observed that HOXA9 boosts the effects of other genes, leading to tumor development. As a result, when JAK3/STAT5 mutations and HOXA9 are both present, leukemia develops more rapidly and aggressively."

The team's identification of a direct cooperation between these two cancer genes paves the way for targeted treatments -- not only in ALL, but also in other leukemias where JAK3/STAT5 could cooperate with HOXA9.)