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The insect apocalypse: ‘Our world will grind to a halt without them’

Few people seem to realise how devastating this is, not only for human wellbeing – we need insects to pollinate our crops, recycle dung, leaves and corpses, keep the soil healthy, control pests, and much more – but for larger animals, such as birds, fish and frogs, which rely on insects for food. Wildflowers rely on them for pollination. As insects become more scarce, our world will slowly grind to a halt, for it cannot function without them.


A strong argument can be made that humans ought to farm more insects as an alternative to pigs, cows or chickens. Farming insects is more energy efficient and requires less space and water. They are a healthier source of protein, being high in essential amino acids and lower in saturated fats than beef, and we are much less likely to catch a disease from eating insects (think bird flu or Covid-19). So if we wish to feed the 10–12 billion people who are projected to be living on our planet by 2050, then we should be taking the farming of insects seriously as a healthier source of protein and a more sustainable option to conventional livestock.

While western societies may not eat insects, we do regularly consume them at one step removed in the food chain. Freshwater fish such as trout and salmon feed heavily on insects, as do game birds like partridge, pheasant and turkey.

Aside from their role as food, insects perform a plethora of other vital services in ecosystems. For example, 87% of all plant species require animal pollination, most of it delivered by insects. The colourful petals, scent and nectar of flowers evolved to attract pollinators. Without pollination, wild flowers would not set seed, and most would eventually disappear. There would be no cornflowers or poppies, foxgloves or forget-me-nots. But an absence of pollinators would have a far more devastating ecological impact than just the loss of wild flowers. Approximately three-quarters of the crop types we grow also require pollination by insects, and if the bulk of plant species could no longer set seed and died out, then every community on land would be profoundly altered and impoverished, given that plants are the basis of every food chain.

Centenarians have unique gut bacteria that enables them to live longer

TOKYO — Centenarians have unique gut bacteria that enables them to live to a ripe old age, according to new research. Scientists in Japan say this unique gut makeup fuels bile acids that protect against disease.

The discovery could lead to yogurts and other probiotic foods that increase longevity.

“In people over the age of 100, an enrichment in a distinct set of gut microbes generate unique bile acids,” says lead author Professor Kenya Honda of Keio University in a statement per South West News Service. “They might inhibit the growth of pathogens.”

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DeepMind says it can predict the shape of every protein in the human body

The predicted shapes still need to be confirmed in the lab, Ellis told Technology Review. If the results hold up, they will rapidly push forward the study of the proteome, or the proteins in a given organism. DeepMind researchers published their open-source code and laid out the method in two peer-reviewed papers published in Nature last week.


And in 20 other animals often studied by science, too.

Deep learning on computational biology and bioinformatics tutorial: from DNA to protein folding and alphafold2

AlphaFold 2 paper and code is finally released. This post aims to inspire new generations of Machine Learning (ML) engineers to focus on foundational biological problems.

This post is a collection of core concepts to finally grasp AlphaFold2-like stuff. Our goal is to make this blog post as self-complete as possible in terms of biology. Thus in this article, you will learn about:

Researchers identify a cellular defect common to familial and sporadic forms of ALS

This study builds on an earlier paper by the Rothstein lab that looked at the most common genetic cause of ALS, a mutation in the C9orf72 gene (also referred to as the “C9 mutation”). There, they showed that the C9 mutation produced defects in a structure called the nuclear pore that is responsible for moving proteins and other molecules in and out of the nucleus of cells.


Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and fatal degenerative disease affecting the nerve cells in the brain and spinal cord responsible for controlling voluntary muscle movement. “Sporadic” or non-inherited ALS, accounts for roughly 90% percent of cases, and 10% of cases are due to known genetic mutations. By studying lab-grown neurons derived from skin or blood cells from 10 normal controls, eight with an ALS causing mutation, and 17 with non-inherited ALS, researchers have found a possible starting point for the dysfunction that causes the disease. The study, which was published in Science Translational Medicine, was funded in part by the National Institute for Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.

Using a library of ALS patient-derived , the research team led by Jeffrey Rothstein, M.D., Ph.D., at Johns Hopkins University School of Medicine, Baltimore, developed induced (iPSC)-derived neurons from the patients’ cultured cells to discover a common defect regardless of whether the cell came from persons with inherited or non-inherited ALS. They report that in ALS nerve cells, there is an accumulation of a protein called CHMP7 in the nucleus of cultured nerve cells as well as in ALS samples from the brain region that controls movement. Treatments that decrease the amount of CHMP7 in the cultured cells prevented a series of abnormalities that are characteristic of ALS.

“There is considerable interest in identifying new therapeutic targets for ALS, particularly for the sporadic form of the disorder,” said Amelie Gubitz, Ph.D., program director, NINDS. “Gene-targeting strategies like the one shown here now allow us to move from biological discovery straight to therapy development.”

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