Researchers from the Max Planck Institute for Polymer Research have developed a drug that disrupts the adaptability of cancer cells!
Abstract: in situ assembly of platinum(ii)-metallopeptide nanostructures disrupts energy homeostasis and cellular metabolism.
A team of scientists is using the tools offered by the HBP’s digital research infrastructure EBRAINS to address one of the oldest enigmas in neuroscience: the dichotomy of brain structure and function.
Every human brain is different. But even with structural differences, individual brains function in a similar way. In other words, there are functional brains based on completely different configurations. At the same time, a structural change may cause loss of function in one brain, but have no consequences in another individual. Or a drug cocktail may be efficient for one patient, and have no effects for another.
Cancer is one of the major global public health problems and is caused by abnormal cell proliferation. A plant immune protein has recently been found to enable widespread anti-tumor responses by alleviating micro-RNA
Ribonucleic acid (RNA) is a polymeric molecule similar to DNA that is essential in various biological roles in coding, decoding, regulation and expression of genes. Both are nucleic acids, but unlike DNA, RNA is single-stranded. An RNA strand has a backbone made of alternating sugar (ribose) and phosphate groups. Attached to each sugar is one of four bases—adenine (A), uracil (U), cytosine ©, or guanine (G). Different types of RNA exist in the cell: messenger RNA (mRNA), ribosomal RNA (rRNA), and transfer RNA (tRNA).
The study population comprised 6,245,282 older adults (age ≥65 years) who had medical encounters with healthcare organizations between 2/2/2020–5/30/2021 and had no prior diagnosis of Alzheimer’s disease. The population was divided into two cohorts: 1) COVID-19 cohort (n = 410,748)— contracted COVID-19 between 2/2/2020–5/30/2021; 2) non-COVID-19 cohort (n = 5,834,534)— had no documented COVID-19 but had medical encounters with healthcare organizations between 2/2/2020–5/30/2021. The status of Alzheimer’s disease and COVID-19 were based on the International Classification of Diseases (ICD-10) diagnosis codes and laboratory tests (details in the Supplementary Material).
We examined risks for new diagnosis of Alzheimer’s disease in COVID-19 and non-COVID-19 cohorts in all older adults, three age groups (65–74, 75–84, ≥85), and three racial/ethnic groups (Black, White, and Hispanic). Cohorts were propensity-score matched (1:1 using a nearest neighbor greedy matching) for demographics, adverse socioeconomical determinants of health including problems with education, occupational exposure, physical, social and psychosocial environment, and known risk factors for Alzheimer’s disease [13] (details in the Supplementary Material). Kaplan-Meier analysis was used to estimate the probability of new diagnosis of Alzheimer’s disease within 360 days after the COVID-19 diagnosis. Cox’s proportional hazards model was used to compare matched cohorts using hazard ratios and 95% confidence intervals. All statistical tests were conducted within the TriNetX Advanced Analytics Platform at significance set at p < 0.05 (2-sided).
U.S. regulators have approved a new purple tomato, genetically engineered to be packed with antioxidants and anthocyanins. The fruit will go on sale in 2023.
Tumor cells are notoriously good at evading the human immune system; they put up physical walls, wear disguises and handcuff the immune system with molecular tricks. Now, UC San Francisco researchers have developed a drug that overcomes some of these barriers, marking cancer cells for destruction by the immune system.
The new therapy, described in Cancer Cell, pulls a mutated version of the protein KRAS to the surface of cancer cells, where the drug-KRAS complex acts as an “eat me” flag. Then, an immunotherapy can coax the immune system to effectively eliminate all cells bearing this flag.
“The immune system already has the potential to recognize mutated KRAS, but it usually can’t find it very well. When we put this marker on the protein, it becomes much easier for the immune system,” said UCSF chemist and Howard Hughes Medical Institute Investigator Kevan Shokat, Ph.D., who also helped lead the new work.
Being able to decode brainwaves could help patients who have lost the ability to speak to communicate again, and could ultimately provide novel ways for humans to interact with computers. Now Meta researchers have shown they can tell what words someone is hearing using recordings from non-invasive brain scans.
Our ability to probe human brain activity has improved significantly in recent decades as scientists have developed a variety of brain-computer interface (BCI) technologies that can provide a window into our thoughts and intentions.
The most impressive results have come from invasive recording devices, which implant electrodes directly into the brain’s gray matter, combined with AI that can learn to interpret brain signals. In recent years, this has made it possible to decode complete sentences from someone’s neural activity with 97 percent accuracy, and translate attempted handwriting movements directly into text at speeds comparable to texting.
(Medical Xpress)—A team of researchers at the Max Planck Institute has found what they believe is the DNA mutation that led to a change in function of a gene in humans that sparked the growth of a larger neocortex. In their paper published in the journal Science Advances, the team describes how they engineered a gene found only in humans, Denisovans and Neanderthals to look like a precursor to reveal its neuroproliferative effect.
A year ago, another team of researchers found the human gene that most in the field believe was a major factor in allowing the human brain to grow bigger, allowing for more complex processing. In this new effort, the researchers have found what they believe was the DNA change that arose in that gene.
To pinpoint that change, the researchers engineered the unique ARHGAP11B gene to make it more similar to the ARHGAP11A gene, which researchers believe was a predecessor gene—they swapped a single nucleotide (out of 55 possibilities) for another and in so doing, found the ARHGAP11B gene lost its neuroproliferative abilities. This, the team claims, shows that it was a single mutation that allowed humans to grow bigger brains. Such a mutation, they note, was not likely due to natural selection, but was more likely a simple mistake that occurred as a brain cell was splitting. Because it conferred an advantage (the ability to grow higher than normal amounts of brain cells) the mutation was retained through subsequent generations. They also point out that such a mutation would have resulted specifically in a larger neocortex—a portion of the cortex that has been associated with hearing and sight.
When the right gene is expressed in the right manner in the right population of stem cells, the developing mouse brain can exhibit primate-like features. In a paper publishing August 7th in the Open Access journal PLOS Biology, researchers at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) succeeded in mimicking the sustained expression of the transcription factor Pax6 as seen in the developing human brain, in mouse cortical progenitor cells. This altered the behavior of these cells to one that is akin to that of progenitors in the developing primate neocortex. Consequently, the mouse progenitors generated more neurons — a prerequisite for a bigger brain.
The neocortex consists of different types of progenitors, but one particular class, the basal progenitors, behave differently in small-brained animals such as mice than in large-brained animals such as humans. In humans, basal progenitors can undergo multiple rounds of cell division, thereby substantially increasing neuron number and ultimately the size of the neocortex. In mice, these progenitors typically undergo only one round of cell division, thus limiting the number of neurons produced. A potential cause underlying this difference in the proliferative capacity of basal progenitors could be the differential expression of Pax6 between species. Mouse basal progenitors, in contrast to human, do not express Pax6. “We were very curious to see what would happen if we were to change the expression pattern of Pax6 in developing mouse brain to mimic that observed in large-brained animals”, says Fong Kuan Wong, a PhD student in the lab of Wieland Huttner and first author of the study.
To this end, another PhD student in the lab, Ji-Feng Fei, generated a novel transgenic mouse line. This line provided the basis for altering the expression of Pax6 in the cortical stem cell lineage such that it would be sustained in basal progenitors. The researchers then introduced the Pax6 gene into the stem cells of these mice. Strikingly, sustaining Pax6 expression in mouse basal progenitors increased their capacity to undergo multiple rounds of cell division, as typically observed in primates. This not only expanded the size of the basal progenitor population in a way somewhat reminiscent to what is seen in large-brained animals. It also resulted in an increase in cortical neurons, notably those in the top layer, another characteristic feature of an expanded neocortex.
