US News is a recognized leader in college, grad school, hospital, mutual fund, and car rankings. Track elected officials, research health conditions, and find news you can use in politics, business, health, and education.
Lagos, Nigeria is officially part of the Wuhan Coronavirus Pandemic.
“Coronavirus in Africa: The first confirmed novel coronavirus case in Nigeria is an Italian citizen who traveled to Lagos. Nigeria is the third African nation to report the virus, and the first in sub-Saharan Africa. The others are Egypt and Algeria, which both have one case each.”
The first confirmed novel coronavirus case in Nigeria is an Italian citizen who traveled to Lagos. Follow here for the latest.
A new technique to convert human stem cells into insulin-producing cells could hold huge promise for future diabetic treatments, if results seen in an experiment with mice can be successfully replicated in humans.
In a study, researchers figured out a new way to coax human pluripotent stem cells (hPSCs) into pancreatic beta cells that make insulin. When these insulin-producing cells were transplanted into mice induced to have an acute form of diabetes, their condition was rapidly cured.
“These mice had very severe diabetes with blood sugar readings of more than 500 milligrams per decilitre of blood – levels that could be fatal for a person,” explains biomedical engineer Jeffrey R. Millman from Washington University.
The company’s called Adriano Di Marti and they’ve formulated a new technique to create a fabric using cactus leaves called Desserto. Cactus, known for its rugged nature is quite hard and thick and pointy, however, when fully processed, it not only feels like actual leather, but since it is made from cactus — a plant that can grow in the desert with minimum moisture — it doesn’t consume as much water.
Don’t Miss
Incredible Ai
A new wearable sensor could save the lives of heart-failure patients.
The artificially intelligent technology helps doctors remotely detect critical changes days before a crisis occurs.
Continue reading “AI-Powered Wearable Predicts Heart Failure Before It Happens” »
If you want to reduce levels of inflammation throughout your body, delay the onset of age-related diseases, and live longer—eat less food. That’s the conclusion of a new study by scientists from the US and China that provides the most detailed report to date of the cellular effects of a calorie-restricted diet in rats. While the benefits of caloric restriction have long been known, the new results show how this restriction can protect against aging in cellular pathways, as detailed in Cell on February 27, 2020.
“We already knew that calorie restriction increases life span, but now we’ve shown all the changes that occur at a single-cell level to cause that,” says Juan Carlos Izpisua Belmonte, a senior author of the new paper, professor in Salk’s Gene Expression Laboratory and holder of the Roger Guillemin Chair. “This gives us targets that we may eventually be able to act on with drugs to treat aging in humans.”
Aging is the highest risk factor for many human diseases, including cancer, dementia, diabetes and metabolic syndrome. Caloric restriction has been shown in animal models to be one of the most effective interventions against these age-related diseases. And although researchers know that individual cells undergo many changes as an organism ages, they have not known how caloric restriction might influence these changes.
The serendipitous disruption of the klotho gene promoter in 1997 by a cardiologist in Japan begot a phenotype of early multiorgan failure mimicking premature aging [1]. The gene was aptly named after the Greek Goddess who spins the threads of life. In 2005, the same investigator did the opposite experiment and showed that transgenic overexpression of klotho in mice extends life, placing Klotho once again in the spotlight and generated volumes of antiaging research [2]. Several findings that followed changed the landscape. Klotho is a single-pass transmembrane protein, primarily expressed in the kidney, but its extracellular domain is secreted into circulation as a soluble protein after being cleaved by proteases [3]; thus, the kidney supplies the body with soluble Klotho [3]. In multiple preclinical studies with diverse models, both acute and chronic kidney diseases are states of renal and systemic klotho deficiency [3], including human CKD. The relationship between Klotho and kidney disease is more than just a biomarker because restoration of Klotho ameliorated renal dysfunction and extrarenal complications in both acute [4] and chronic settings bringing Klotho supplementation into the therapeutic realm. However, how should Klotho be given?
In rodents, several methods have been used successfully to raise systemic Klotho levels (Fig. 1). The transgenic insertion of klotho into the genome of a mouse was the first attempt [2]. While this has been enormously useful as proof-of-concept in experimental animals, this technique is not applicable to patients currently. Recombinant Klotho protein was used successfully in the laboratory in both acute and chronic [5] settings that prevented AKI, accelerated AKI recovery, presented and retarded AKI-to-CKD transition, and ameliorated extrarenal complications [4]. Recombinant Klotho protein administration is a method where translation to human therapeutics is much more practical and proximal.
