Lifeboat Foundation

Primates given an experimental jab against the virus are less susceptible to illness after only a few days.

Yellow fever epidemics are happening across Nigeria spreading state by state. The yellow fever is another haemorgic disease like ebola.

Over 160 million people, more than half of Nigeria’s current estimated population, are at risk of yellow fever in the country, reports by the World Health Organisation Africa Region have recently highlighted. Lately, the yellow fever virus has become of serious global health concern more because the wakes of its historic outbreaks are trailed by devastating outcomes.

The WHO says the virus is spreading rapidly across Africa, warning that the rising trend could cause an epidemic in Nigeria particularly, mainly because of its large population. Consequently, it issued an advisory for travellers to and out of Nigeria to consult their healthcare provider on precautionary measures required against the virus if need be.

Continue reading “Nigeria’s rising Yellow fever epidemic” »

A team of researchers in the United States has discovered a novel mechanism in which a key protein drives the inflammatory damage associated with rheumatoid arthritis. The foundational finding is hoped to direct research toward entirely new pathways to treat this autoimmune disease affecting millions.

One of the most impactful rheumatoid arthritis discoveries over the past few decades was finding an immune cytokine called tumor necrosis factor‑alpha (TNF-alpha) plays a crucial role in joint tissue inflammation. Following this discovery the development of monoclonal antibody TNF inhibitors offered rheumatoid arthritis patients a completely new type of medicine to treat their condition.

But, as senior author on the new research Salah‑Uddin Ahmed explained, TNF inhibitors aren’t effective in all patients. And even then, they are not ideal long-term medicines dues to a variety of side effects.

Senescent macrophages are in fact also found to express senescence-related markers p16(Ink4a) and β-galactosidase (β-gal), and promote inflammation in diseased tissues [25, 26]. Our previous work has indicated increased cellular senescence in dystrophic muscles of mdx/utr(−/−) mice [3], however, whether or not macrophages in particular develop cellular senescence and promote senescence associated phenotypes was still unknown. To this end, here we further examined mdx/utr(−/−) mice and solved these puzzles.

Immune cells in the skeletal muscle are activated during muscle injury and promote the process of muscle regeneration by coordinating with muscle stem cells. However, studies with severely diseased muscles further demonstrate that immune cells can become dominantly activated and is inductive of increased fatty infiltration and fibrosis formation, while at the same time potently repress the proliferation and function of muscle stem cells [27]. Our current results in severely dystrophic muscle reveal a similar situation of interaction between macrophages and MPCs, showing that the function of MPCs is repressed by the senescent macrophages. As senescent cells accumulate in the aged or diseased tissues, it can exert profound effects on the growth and function of normal cells by releasing SASPs [9, 10].

Today, an international team of researchers led by Séamus Davis, Professor of Physics at the University of Oxford and University College Cork, has announced results that reveal the atomic mechanism behind high-temperature superconductors. The findings are published in PNAS.

Superconductors are materials that can conduct electricity with zero resistance, so that an electric current can persist indefinitely. These are already used in various applications, including MRI scanners and high-speed maglev trains, however superconductivity typically requires extremely low temperatures, limiting their widespread use. A major goal within physics research is to develop super conductors that work at ambient temperatures, which could revolutionize energy transport and storage.

Certain copper oxide materials demonstrate superconductivity at higher temperatures than conventional superconductors, however the mechanism behind this has remained unknown since their discovery in 1987.

The technology at the heart of this research takes aim at one of the key metabolic functions of cells in all living things called ATP, or adenosine triphosphate. This molecule is the primary energy carrier in cells, capturing chemical energy from the breakdown of food molecules and distributing it to power other cellular processes.

Among those cellular processes is the proliferation of cancerous cells, and because of this we have seen ATP implicated in previous anti-cancer breakthroughs. The authors of the new study sought to cut off the supply of ATP, which is generated as mitochondria soak up oxygen and convert it into the molecule.

Circa 2015 face_with_colon_three

The disease is linked to genetic changes on the evolutionary road from ape to human.

Once-esoteric physics will underlie sensor revolutions in medicine, tech, and engineering.

Circa 2005 Bacteria that is resistant to radiation could lead to better radiation resistance in humans.

Relatively little is known about the biochemical basis of the capacity of Deinococcus radiodurans to endure the genetic insult that results from exposure to ionizing radiation and can include hundreds of DNA double-strand breaks. However, recent reports indicate that this species compensates for extensive DNA damage through adaptations that allow cells to avoid the potentially detrimental effects of DNA strand breaks. It seems that D. radiodurans uses mechanisms that limit DNA degradation and that restrict the diffusion of DNA fragments that are produced following irradiation, to preserve genetic integrity. These mechanisms also increase the efficiency of the DNA-repair proteins.