Lifeboat Foundation

Directed with clinical precision by Academy Award winner Robert Wise, this compelling account of the earth’s first biological crisis is perhaps the most chillingly realistic science fiction thriller ever made. After an errant satellite crashes on Earth near a remote New Mexico village, the recovery team discovers that almost everyone in the town are victims of a horrible death, with the mysterious exception of an infant and an old homeless man. The survivors are brought to a state-of-the-art laboratory descending five stories beneath the ground where the puzzled scientists race against time to determine the nature of the deadly microbe before it wreaks worldwide havoc. A trailblazer in the areas of special effects and inventive sets, The Andromeda Strain is based on Michael Crichton’s best-selling novel that created national paranoia for its topical relevance to the first moon landing.

It’s estimated that almost half of the world’s population — about 3.7 billion people under the age of 50 — are infected with (HSV-1), which can cause oral herpes. About half a billion people between the ages of 15 and 49 are infected with herpes simplex virus-2 (HSV-2), the cause of genital herpes. There are therapeutics that can eliminate some symptoms of herpes, like blisters, but there is no cure for the infection, and those who are infected can spread the virus to others. Studies have suggested that HSV-1 may increase the risk of dementia, and HSV-2 raises the risk of HIV infection.

Scientists have now developed a gene therapy that can eliminate as much as 90 percent of oral herpes and 97 percent of genital herpes infections in pre-clinical mouse models. The gene therapy also reduced the level of virus that was released from an individual in a mouse model of the infection. These reductions took about one month to be completed, and more of the virus seemed to be eliminated over time. The work has been reported in Nature Communications.

Scaling back treatment for three kinds of cancer can make life easier for patients without compromising outcomes, doctors reported at the world’s largest cancer conference.

It’s part of a long-term trend toward studying whether doing less — less surgery, less chemotherapy or less radiation — can help patients live longer and feel better. The latest studies involved ovarian and esophageal cancer and Hodgkin lymphoma.

Thirty years ago, cancer research was about doing more, not less. In one sobering example, women with advanced breast cancer were pushed to the brink of death with massive doses of chemotherapy and bone marrow transplants. The approach didn’t work any better than chemotherapy and patients suffered.

All patients in pembrolizumab trial were found to be cancer-free after combination of drug and surgery.

Researchers based at the Dept of Biology and School of Physics, Engineering and Technology have developed a remarkable new technology which is able to study single biological molecules using intrinsic twist properties to bring about essential functions in cells.

“Nano twists” that drive life

There are myriad so-called “chiral” molecules in biology, which have a fascinating property of not appearing to have the same structure were you to look at their image in a mirror — one of the best known examples being DNA, the “molecule of life”, whose chirality comes from its amazing double helix structure. This chirality, which looks in the case of extended DNA molecules like “nano twists”, results in a property which physicists describe as “symmetry breaking” which in turn can drive molecules into a range of different states. With input from sources of energy, these molecules can then jump between different states as part of their normal function, and it is this state jumping which essentially drives all processes in living cells — so chirality is an enormously fundamental feature which in effect effect steers key cellular processes.

Though one in two people will develop some form of cancer in their lifetime, there’s still much we don’t know about this disease. But thanks to continued research efforts, we keep learning more about the biology of cancer. One of these recent discoveries could even transform our understanding of how cancers develop.

But before we talk about the new discovery, let’s first discuss the classical theory that attempts to explain why normal cells become cancer cells. This theory posits that DNA mutations are the primary cause of cancers.

It’s well known that ageing, as well as some lifestyle and environmental factors (such as smoking and UV radiation) cause random DNA mutations (also known as genetic alterations) in our cells. Most genetic alterations trigger cell death or have no consequence.

Move over, graphene. There’s a new, improved two-dimensional material in the lab. Borophene, the atomically thin version of boron first synthesized in 2015, is more conductive, thinner, lighter, stronger, and more flexible than graphene, the 2D version of carbon. Now, researchers at Penn State have made the material potentially more useful by imparting chirality — or handedness — on it, which could make for advanced sensors and implantable medical devices. The chirality, induced via a method never before used on borophene, enables the material to interact in unique ways with different biological units such as cells and protein precursors.

The team, led by Dipanjan Pan, Dorothy Foehr Huck & J. Lloyd Huck Chair Professor in Nanomedicine and professor of materials science and engineering and of nuclear engineering, published their work — the first of its kind, they said — in ACS Nano.

“Borophene is a very interesting material, as it resembles carbon very closely including its atomic weight and electron structure but with more remarkable properties. Researchers are only starting to explore its applications,” Pan said. “To the best of our knowledge, this is the first study to understand the biological interactions of borophene and the first report of imparting chirality on borophene structures.”

With over 37,000 views, this special issue discusses the relationship between phytochemicals and chronic disease prevention, aiming to promote the development of this field.

The special issue focuses on phytochemicals’ isolation, identification, structure–activity relationships, bioactivities, and…

This Special Issue, entitled Phytochemicals and Prevention of Chronic Diseases, features a series of high-quality research articles that explore the isolation, identification, and bioactivities of phytochemicals, as well as the underlying molecular mechanisms implicated in chronic diseases via antioxidation, neuroprotection, and the modulation of the gut microbiota.

Advanced glycation end products (AGEs) accumulate in the brain, leading to neurodegenerative conditions such as Alzheimer’s disease (AD). The pathophysiology of AD is influenced by receptors for AGEs and toll-like receptor 4 (TLR4). Protein glycation results in irreversible AGEs through a complicated series of reactions involving the formation of Schiff’s base, the Amadori reaction, followed by the Maillard reaction, which causes abnormal brain glucose metabolism, oxidative stress, malfunctioning mitochondria, plaque deposition, and neuronal death. Amyloid plaque and other stimuli activate macrophages, which are crucial immune cells in AD development, triggering the production of inflammatory molecules and contributing to the disease’s pathogenesis. The risk of AD is doubled by risk factors for atherosclerosis, dementia, advanced age, and type 2 diabetic mellitus (DM). As individuals age, the prevalence of neurological illnesses such as AD increases due to a decrease in glyoxalase levels and an increase in AGE accumulation. Insulin’s role in proteostasis influences hallmarks of AD-like tau phosphorylation and amyloid β peptide clearance, affecting lipid metabolism, inflammation, vasoreactivity, and vascular function. The high-mobility group box 1 (HMGB1) protein, a key initiator and activator of a neuroinflammatory response, has been linked to the development of neurodegenerative diseases such as AD. The TLR4 inhibitor was found to improve memory and learning impairment and decrease Aβ build-up. Therapeutic research into anti-glycation agents, receptor for advanced glycation end products (RAGE) inhibitors, and AGE breakers offers hope for intervention strategies. Dietary and lifestyle modifications can also slow AD progression. Newer therapeutic approaches targeting AGE-related pathways are needed.