University of Texas Medical Branch

About: University of Texas Medical Branch is a education organization based out in Galveston, Texas, United States. It is known for research contribution in the topics: Population & Virus. The organization has 22033 authors who have published 38268 publications receiving 1517502 citations. The organization is also known as: The University of Texas Medical Branch at Galveston & UTMB.

The COVID-19 Pandemic and Physical Activity

Abstract: The SARS-CoV-2-caused COVID-19 pandemic has resulted in a devastating threat to human society in terms of health, economy, and lifestyle. Although the virus usually first invades and infects the lung and respiratory track tissue, in extreme cases, almost all major organs in the body are now known to be negatively impacted often leading to severe systemic failure in some people. Unfortunately, there is currently no effective treatment for this disease. Pre-existing pathological conditions or comorbidities such as age are a major reason for premature death and increased morbidity and mortality. The immobilization due to hospitalization and bed rest and the physical inactivity due to sustained quarantine and social distancing can downregulate the ability of organs systems to resist to viral infection and increase the risk of damage to the immune, respiratory, cardiovascular, musculoskeletal systems and the brain. The cellular mechanisms and danger of this “second wave” effect of COVID-19 to the human body, along with the effects of aging, proper nutrition, and regular physical activity, are reviewed in this article.

Regulation of protein-ligand binding affinity by hydrogen bond pairing.

Abstract: Hydrogen (H)-bonds potentiate diverse cellular functions by facilitating molecular interactions. The mechanism and the extent to which H-bonds regulate molecular interactions are a largely unresolved problem in biology because the H-bonding process continuously competes with bulk water. This interference may significantly alter our understanding of molecular function, for example, in the elucidation of the origin of enzymatic catalytic power. We advance this concept by showing that H-bonds regulate molecular interactions via a hitherto unappreciated donor-acceptor pairing mechanism that minimizes competition with water. On the basis of theoretical and experimental correlations between H-bond pairings and their effects on ligand binding affinity, we demonstrate that H-bonds enhance receptor-ligand interactions when both the donor and acceptor have either significantly stronger or significantly weaker H-bonding capabilities than the hydrogen and oxygen atoms in water. By contrast, mixed strong-weak H-bond pairings decrease ligand binding affinity due to interference with bulk water, offering mechanistic insight into why indiscriminate strengthening of receptor-ligand H-bonds correlates poorly with experimental binding affinity. Further support for the H-bond pairing principle is provided by the discovery and optimization of lead compounds targeting dietary melamine and Clostridium difficile toxins, which are not realized by traditional drug design methods. Synergistic H-bond pairings have therefore evolved in the natural design of high-affinity binding and provide a new conceptual framework to evaluate the H-bonding process in biological systems. Our findings may also guide wider applications of competing H-bond pairings in lead compound design and in determining the origin of enzymatic catalytic power.

Light-induced reduction of cytoplasmic free calcium in retinal rod outer segment

Abstract: The response of retinal rod photoreceptors to light consists of a membrane hyperpolarization resulting from the decrease of a light-sensitive conductance in the outer segment1. According to the calcium hypothesis, this conductance is blocked by a rise in intracellular free Ca triggered by light2, a notion supported by the findings that an induced rise in internal Ca leads to blockage of the light-sensitive conductance3–9 and that light triggers a net Ca efflux from the outer segment via a Na–Ca exchanger, suggesting a rise in internal free Ca in the light10–13. We have now measured both Ca influx and efflux through the outer segment plasma membrane and find that, contrary to the calcium hypothesis, light seems to decrease rather than increase the free Ca concentration in the rod outer segment. This result implies that Ca does not mediate visual excitation but it probably has a role in light adaptation.

Effects of unilateral cardiac sympathetic denervation on the ventricular fibrillation threshold.

Abstract: A train of gated stimuli scanning the entire vulnerable period was delivered to the right anterior or left posterior ventricular surface to study the ventricular fibrillation threshold in anesthetized and vagotomized dogs. Heart rate was held constant by atrial pacing. Measurements were obtained in control conditions and after surgical removal of one stellate ganglion. To avoid the shortcomings associated with an irreversible procedure like stellectomy, control fibrillation threshold measurements were also alternated with determinations during reversible blockade by cooling of one stellate ganglion. The results were similar with both techniques. In nine animals, ablation or cooling of the left stellate ganglion increased ventricular fibrillation threshold by 72 ± 35 (mean ± standard deviation) percent compared with control values (P These results suggest that right and left cardiac sympathetic nerves may have different and specific effects on cardiac excitability. They also contribute to the understanding of the pathogenesis of the long Q-T syndrome (characterized by episodes of ventricular fibrillation associated with increased sympathetic activity) and increase the rationale for left stellectomy as the specific treatment for this illness. Left stellectomy, by raising the ventricular fibrillation threshold, may also represent an alternative measure in patients at high risk of sudden death from ventricular arrhythmias resistant to medical therapy.