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Substance use disorder (SUD) is an extremely difficult disorder to overcome, and many individuals with SUD return to regular use after repeated attempts to quit.
A return to regular drug use can be caused by the body’s physical dependence on the drug as well as experiences associated with prior drug use. Exactly how these drug associations are formed in the brain and how they trigger a return to drug use remain unclear.
“Individuals make long-lasting associations between the euphoric experience of the drug and the people, places and things associated with drug use,” said Christopher Cowan, Ph.D. professor in the Department of Neuroscience at the Medical University of South Carolina (MUSC) and member of the Brain and Behavior Research Foundation Scientific Council.
Talking about E5.
Rats are also useful for aging research and for cooking ratatouille. But in all seriousness, take a look at this recent headline article — “We have the oldest living female Sprague Dawley rat,” said Dr Harold Katcher, a former biology professor at the University of Maryland, now chief scientific officer at Yuvan Research, a California-based startup.
So, Rejuvenation & rats. That’s what we’re talking about today, and how this rat has apparently become the longest living rat for its species following concentrated plasma injections from young blood plasma, and what this could mean for human therapeutics, along my perspectives. But, before we get there we must go back, back to the late 1950s and early 1960…to a time when The Sheekey Science Show did not exist, but when researchers, such as Clive McKay did, and these researchers were conducting a procedure called heterochronic parabiosis.
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Cancer is not a uniform disease. Rather, cancer is a disease of phenotypic plasticity, meaning tumor cells can change from one form or function to another. This includes reverting to less mature states and losing their normal function, which can result in treatment resistance, or changing their cell type altogether, which facilitates metastasis.
In addition to direct changes in your DNA in cancer, a key driver of cancer progression is where and when your DNA is activated. If your DNA contains the “words” that spell out individual genes, then epigenetics is the “grammar” of your genome, telling those genes whether they should be turned on or off in a given tissue. Even though all tissues in the body have almost exactly the same DNA sequence, they can all carry out different functions because of chemical and structural modifications that change which genes are activated and how. This “epigenome” can be influenced by environmental exposures such as diet, adding a dimension to how researchers understand drivers of health beyond the DNA code inherited from your parents.
I’m a cancer researcher, and my laboratory at Johns Hopkins University studies how the differences among normal tissues are controlled by an epigenetic code, and how this code is disrupted in cancer. In our recently published review, colleague Andre Levchenko at Yale University and I describe a new approach to understanding cancer plasticity by combining epigenetics with mathematics. Specifically, we propose how the concept of stochasticity can shed light on why cancers metastasize and become resistant to treatments.
By combining combine genetic and electrical engineering, scientists have developed a new technique for wiring electronics into living matter.
ATP, the compound essential for the functioning of photosynthetic organisms such as plants, algae, and cyanobacteria, is produced by an enzyme called “chloroplast ATP synthase” (CFoCF1). To control ATP production under varying light conditions, the enzyme uses a redox regulatory mechanism that modifies the ATP synthesis activity in response to changes in the redox state of cysteine (Cys) residues, which exist as dithiols under reducing (light) conditions, but forms a disulfide bond under oxidizing (dark) conditions. However, this mechanism has not yet been fully understood.
Now, in a study published in the Proceedings of the National Academy of Sciences, a team of researchers from Japan led by Prof. Toru Hisabori from Tokyo Institute of Technology (Tokyo Tech) has uncovered the role of the amino acid sequences present in CFoCF1, revealing how the enzyme regulates ATP production in photosynthetic organisms.
To understand how the conformation of the amino acids present in CFoCF1 contributes to the redox regulation mechanism, the researchers used the unicellular green alga, Chlamydomonas reinhardtii, to produce the enzyme. “By leveraging the powerful genetics of Chlamydomonas reinhardtii as a model organism for photosynthesis, we conducted a comprehensive biochemical analysis of the CFoCF1 molecule,” explains Prof. Hisabori.
In a recent study published in Cell, researchers presented eight hallmarks of neurodegenerative diseases (NDDs), their in vivo biomarkers, and interactions to help categorize NDDs and specify patients within a specific NDD.
Despite being linked to rare genetic forms, all eight NDD hallmarks (cellular/molecular processes) also contribute to sporadic NDDs. In addition, they contribute to neuronal loss in preclinical (animal) models and NDD patients, manifesting as an altered molecular (hallmark) biomarker.
An NDD patient could have defects in multiple NDD hallmarks. However, the primary NDD hallmark depends on the NDD insult and the neuronal susceptibility and resilience, i.e., one’s ability to handle insults in the affected brain region.