BiTherapca Health

Failure of the folding protein response will lead to inability to fold proteins that are necessary for proper mitochondrial function and cell survival.  Calcium overload and ensuing reactive oxygen signaling will lead to apoptosis. This is characteristic of Alzheimer's, Parkinson's and Huntington's diseases. Psychological stress, which could stem from nutritional deprivation, that results in unfolded proteins, prompts the unfolded protein stress response(UPR). In addition to folding the unfolded protein, there is the breakdown, of misfolded protein yielding amyloid peptides, and of sphingomyelin to yield ceramide. The exosomes containing amyloid peptides and ceramide are themselves problematic outside the nerve cells as they form plaque that prevents the transmission of nerve signals. During the endoplasmic reticulum(ER) stress, serotonin is released in the brain, in response, to counter the stress--and there...

Too much of unfolded proteins that overwhelms the Endoplasmic reticulum(ER)-coping mechanisms, through over-activity of the Endoplasmic reticulum, or otherwise, will switch the cell from its anti-oxidation pathways over to the unfolded protein stress response(UPR), by putting a halt to protein translation, engaging the degradation of misfolded  proteins and activation of the heat shock protein(hsp)--the chaperone--that folds unfolded proteins. When UPR is prolonged and overwhelmed, apoptosis takes place as ROS, in turn, overwhelm any anti-oxidation-induction. This is characteristic of Alzheimer's, Parkinson's disease and Huntington's disease. In the trained athlete, the switch to slow-oxidative, fast, fatigue-resistant fibers, lowers ROS levels, which still remain at an anti-oxidation-inducing levels that at the same time promote UPR. This is an adaptation that prepares the muscles for eventual stress. In the oute...

When the biological system encounters some sort of stress, compensation recovery systems kick in to protect the body. Once damage is done, damage recovery response is engaged. While many compensatory mechanisms are immediate and comprise mainly reflexes involving the nervous system and pre-formed hormones(neurotransmitters) and mediators, prolonged stress and damage response will involve growth factor or nucleus-acting hormone release, priming, and genetic involvement in the synthesis of effector proteins for long-term adaptation. Increased cyclic AMP fuels metabolism, needed for stress, until exhaustion of nutrients sets in. Gene regulation involves epigenetic modification, and feed-back(end-product) inhibition. There is up-regulation of heat-shock protein to fold proteins(in endoplasmic stress), anti-oxidants (in oxidative[phosphorylation] stress), immune response in infections, autophagy, repairs and apoptosis. Hence, small or ...

It is often said and acknowledged that physicians are trained in the Sciences to practice the art of healing. This underlines the importance of social and practical skills in medicine. In all fairness, Doctors are taught interpersonal skills in addition to the growing knowledge in the biomedical Sciences. Procedural skills which are acquired later on in the medical training are more of an art--due to the motor component of and personalized touch to it--though there is a scientific basis, to all of them, which is founded on the Sciences learnt in the earlier phase. Without doubt, in the absence of scientific knowledge, medical judgement would be hollow, action to take conjectural and prediction of outcomes speculative; eventual complications would be misconstrued and mismanaged. Most medical treatment is medication-based and there is lot of Science involved in drug discovery,  manufacture, action, use and complications ther...

The G1 phase of the cell cycle determines if a cell is to differentiate or not. During this phase, the cell develops protuberances(cilia) which sense the environment, effect movement and  in turn stimulate autophagy(nerve and muscle cells are much elongated from these protuberances). Levels of Nrf2, which lower levels of free radicals, fall in this pro-differentiation state. The longer the G1 the more likely the switch to differentiation from cell cycling. When there is transient fall in energy resources or growth factors, there will be less proliferation and more pro-differentiation, and when those resources later become available, more pronounced differentiation will take place. Transient spike in psychological, physical or nutritional stress will cause the engagement of the 5-phosphate pentose pathway that yields the anti-oxidant NADPH, and as well produces intermediates for protein synthesis. This promotes cellular prolif...

Senescence is the hallmark of cellular aging. The senescent cells have stopped dividing. Cells accumulate mutations and structural damage with age. The damage is sensed and the cells are then taken out of the cell cycle by the tumor suppressor, p53, for autophagy and repairs or to undergo programmed cell death. In either case there is rejuvenation. There is, however, an intermediate scenario where, due to lack of the necessary resources, these cells become stuck in limbo. A brake is pulled on them and the cells shrivel due low growth or activity and fail to perform the normal biological function. They still occupy space and prevent the capable cells--stem or induced-stem--from dividing. They, however, begin to secrete inflammatory factors, instead. Coupled to the renegade shriveled state, inflammation causes further structural damage in tissues and organs of the body, leading to degeneration. The common obvious...

Phagocytic degradation of microbes and apoptotic microbe-infested cell is a much safer and effective way of combatting infections. This is the ultimate goal of acquired, specific immunity. Otherwise, necroptosis and necrosis result in non-specific events outside the controlled and protective environment of the phagolysome inside the phagocyte. The extent of degradation is dependent on the opsonization of the usually toxic antigens. Toxic antigenic material will damage the phagolysosomal  membrane, the plasma membrane and cause the premature dumping of microbes out of the cell. Hence, even cytokines, which are intrinsically toxic, like TNF, and aid in inflammation, and by extension, in the influx of leucocytes, will prevent effective phagocytosis. Normally, opsonizing antibodies promote safe and effective phagocytosis, and cytotoxic T-cells, that promote apoptosis of infected host cells, help in enclosing t...