DNA sequences from tumor cells can be used to direct the immune system to attack cancer, according to scientists. The immune system relies on an intricate network of alarm bells, targets and safety brakes to determine when and what to attack.
linked atypical gene activity to excessive growth in the autistic brain
autistic brain sprouts an excess of neurons and continues to balloon during the first five years of life, as all those extra neurons grow larger and form connections.
start to lose neural connections, faster than typical brains
67 percent more neurons in their prefrontal cortex (PFC) than typical children
executive functions"—high-level thinking, such as planning ahead, inhibiting impulses and directing attention.
In brain tissue from both autistic children and autistic adults, genes coding for proteins that identify and repair mistakes in DNA were expressed at unusually low levels. Additionally, all autistic brains demonstrated unusual activity levels for genes that determine when neurons grow and die and how newborn neurons migrate during early development
Some genes involved in immune responses, cell-to-cell communication and tissue repair, however, were expressed at unusual levels in adult autistic brains, but not in autistic children's brains
Errors accumulate.
autistic child develops in the womb, something—an inherited mutation or an environmental factor like a virus, toxin or hormone—muffles the expression of genes coding for proteins that usually fix mistakes in sequences of DNA
The genetic systems controlling the growth of new neurons go haywire, and brain cells divide much more frequently than usual, accounting for the excess neurons found in the PFC of autistic children.
autistic brain grow physically larger and form more connections than in a typical child's brain.
immune system reacts against the brain's overzealous growth,
Not all researchers, however, accept
If scientists definitively link autism to a characteristic sequence of changes in gene expression and unusual neural growth, then it becomes possible to target and reverse any one of the thousands of steps in that sequence.
human stem cells can be genetically engineered into HIV-fighting cells
surrogate model
CD8 cytotoxic T lymphocytes -- the "killer" T cells that help fight infection -- from an HIV-infected individual and identified the molecule known as the T cell receptor, which guides the T cell in recognizing and killing HIV-infected cells.
Using mice as lab rats, researchers are able to produce a large amount of T cells that can fight off HIV more effectively.
Expanding on previous research providing proof-of-principle that human stem cells can be genetically engineered into HIV-fighting cells
The engineered stem cells developed into a large population of mature, multi-functional HIV-specific CD8 cells that could specifically target cells containing HIV proteins. The researchers also discovered that HIV-specific T cell receptors have to be matched to an individual in much the same way an organ is matched to a transplant patient.
In this current study, the researchers similarly engineered human blood stem cells and found that they can form mature T cells that can attack HIV in tissues where the virus resides and replicates. They did so by using a surrogate model, the humanized mouse, in which HIV infection closely resembles the disease and its progression in humans.
increased, while levels of HIV in the blood decreased. CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections. These results indicated that the engineered cells were capable of developing and migrating to the organs to fight infection there.
Social stress is known to have adverse health effects on both humans and primates. Now, researchers report that it also affects the immune system of female rhesus macaques at the genetic level.
Physical activities can change the DNA sequence which can be passed on to later generations. However this has only been tested on frogs and may not apply to mammals like us.
athletic frogs tended to have faster-changing genomes.
During exercise, the circulatory system provides blood and oxygen to the tissues that are needed most
When physical activity has stopped, the rush of blood and oxygen when circulation is restored to those tissues produces a burst of free radicals that can cause wear and tear on DNA, eventually causing genetic changes that -- if they affect the DNA of cells that make eggs or sperm -- can be passed to future generations.
epigenetics, the study of how people’s experience and environment affect the function of their genes.
Studies suggest that such add-on, or epigenetic, markers develop as an animal adapts to its environment, whether in the womb or out in the world — and the markers can profoundly affect behavior.
In studies of rats, researchers have shown that affectionate mothering alters the expression of genes, allowing them to dampen their physiological response to stress. These biological buffers are then passed on to the next generation: rodents and nonhuman primates biologically primed to handle stress tend to be more nurturing to their own offspring, and the system is thought to work similarly in humans.
the offspring of parents who experience famine are at heightened risk for developing schizophrenia, some research suggests — perhaps because of the chemical signatures on the genes that parents pass on.
in some people with autism, epigenetic markers had silenced the gene which makes the receptor for the hormone oxytocin. Oxytocin oils the brain’s social circuits, and is critical in cementing relationships; a brain short on receptors for it would most likely struggle in social situations.
In one large study of people with schizophrenia, researchers at Johns Hopkins are analyzing blood and other data to see whether the degree of epigenetic variation is related to the inherited risk of developing the disorder. In another, researchers at Tufts are studying the genes of animals dependent on opiates to see how epigenetic alterations caused by drug exposure affect the opiate sensitivity of the animals’ offspring.
Drugs that alter some chemical tags on DNA make cancer cells behave more like normal cells
And the drugs seem to make cancer cells more susceptible to chemotherapy and attacks from the immune system.
drugs called azacitidine and decitabine, when used in low doses, change gene activity in leukemia and breast cancer cells in the lab. If DNA is a cell’s hard drive, then chemical tags attached to the DNA or DNA-packaging proteins called histones serve as software packages to tell the hard drive how to function. This type of chemical programming is called epigenetics.
The genetic code in DNA provides the template to manufacture protein into all the cells of an organism.
Proteins are made by stringing together amino acids. For general purposes there are twenty amino acids in protein and they can be put together in endless combinations, some in short chains (yeast averages 466 amino acids), some long chains (titins have nearly 27,000 amino acids) and everything in-between. The pattern of amino acids determines much of the functionality of the protein.
Proteins are three-dimensional puzzle pieces. They are generally very complicated in shape. Even a small protein of only 100 amino acids can theoretically have 10^100 (ten to the hundredth power) different configurations.
most protein reconfigurations occur in nanoseconds
In research on proteins, it was assumed (given their chemical composition) proteins would uniformly fold as they cool down and unfold as they heat up. (Think of a balloon expanding and shrinking with the temperature of the air inside.) The experiments didn’t bear this out; the rate of folding or unfolding according to temperature change was unequal (asymmetric) and uneven (nonlinear).
In recent biochemistry a great deal of work is done with ‘tagging’ or ‘marking’ molecules with fluorescent and phosphorescent materials. It’s well known that fluorescence and phosphorescence are phenomena closely related to protein folding and they can only be understood in terms of quantum transition between molecules.
With a quantum transition, the protein could change configuration by ‘jumping’ – skipping all the transition steps – to the final configuration. They call this quantum folding and they developed a mathematical model that shows how the folding, which is virtually instantaneous, would react to change in temperature.
Their quantum transition model matched the folding curves for 15 different proteins and also provides an explanation for the different rates of folding and unfolding among these proteins.
Luo and Lu’s paper is short, a mere 16 pdf pages, and the model is unpretentious mathematically. (Luo has several other related papers on arXiv.) It comes from unknown researchers in an unknown corner of the academic world, and it’s published on the open-source arXiv system. The lack of pedigree means that it will take more time than usual for scientists around the world to learn of it, examine it, and possibly test it.
It is developing therapeutics to prove the validity of ddRNAi in treating cancer, infectious diseases, and disorders of the central nervous system.
The ddRNAi platform focuses on the long-term downregulation of genes, making it suitable for targeting chronic life-threatening diseases. “We are silencing genes instead of introducing new genes, which separates us from traditional gene therapy companies,” Dr. French asserts.
“This targeted treatment markedly enhanced the benefits of radiation therapy in both cellular and tumor models,” the researchers concluded. Other radiotherapy-resistant tumors may benefit from the shRNAs created for the prostate cancer study.
The applied insect genetics laboratory in the Entomology Department at the University of Georgia has focused on invasive subterranean term
Thus we continue to track and monitor through genetics the Formosan termite movements into and around Georgia. The knowledge of how they are coming into the state as well as how they are moving about the state can be invaluable for managing this traffic.
A new method to detect proteins associated with longevity which helps further our understanding into why some animals live longer than others.
The study, led by Dr. Joao Pedro Magalhaes and postgraduate student, Yang Li, is the first to show evolutionary patterns in biological repair systems in long-lived animals and could, in the future, be used to help develop anti-ageing interventions by identifying proteins in long-lived species that better respond to, for example, DNA damage
these species have optimised pathways that repair molecular damage, compared to shorter-lived animals, such as mice
found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins
Proteins associated with the degradation of damaged proteins, a process that has been connected to ageing, were also linked with the evolution of longevity in mammals.
If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the ageing process.
“We developed a method to detect proteins whose molecular evolution correlates with longevity of a species. The proteins we detected changed in a particular pattern, suggesting that evolution of these proteins was not by accident, but rather by design to cope with the biological processes impacted by ageing, such as DNA damage. The results suggest that long-lived animals were able to optimise bodily repair which will help them fend off the ageing process.”