(searched for: doi:10.46610/japp.2020.v02i02.005)
Published: 26 August 2021
Journal of Cardiology and Cardiovascular Medicine, Volume 6, pp 048-054; https://doi.org/10.29328/journal.jccm.1001118
Protein phosphorylation regulates several dimensions of cell fate and is substantially dysregulated in pathophysiological instances as evident spatiotemporally via intracellular localizations or compartmentalizations with discrete control by specific kinases and phosphatases. Cardiovascular disease manifests as an intricately complex entity presenting as a derangement of the cardiovascular system. Cardiac or heart failure connotes the pathophysiological state in which deficient cardiac output compromises the body burden and requirements. Protein kinases regulate several pathophysiological processes and are emerging targets for drug lead or discovery. The protein kinases are family members of the serine/threonine phosphatases. Protein kinases covalently modify proteins by attaching phosphate groups from ATP to residues of serine, threonine and/or tyrosine. Protein kinases and phosphatases are pivotal in the regulatory mechanisms in the reversible phosphorylation of diverse effectors whereby discrete signaling molecules regulate cardiac excitation and contraction. Protein phosphorylation is critical for the sustenance of cardiac functionalities. The two major contributory ingredients to progressive myocardium derangement are dysregulation of Ca2+ processes and contemporaneous elevated concentrations of reactive oxygen species, ROS. Certain cardiac abnormalities include cardiac myopathy or hypertrophy due to response in untoward haemodynamic demand with concomitant progressive heart failure. The homeostasis or equilibrium between protein kinases and phosphatases influence cardiac morphology and excitability during pathological and physiological processes of the cardiovascular system. Inasmuch as protein kinases regulate numerous dimensions of normal cellular functions, the pathophysiological dysfunctionality of protein kinase signaling pathways undergirds the molecular aspects of several cardiovascular diseases or disorders as related in this study. These have presented protein kinases as essential and potential targets for drug discovery and heart disease therapy.
Published: 20 January 2021
International Journal of Clinical Microbiology and Biochemical Technology, Volume 4, pp 001-004; https://doi.org/10.29328/journal.ijcmbt.1001018
Cystoisosporiasis (formerly isosporiasis) is caused by Cystoisospora belli (erstwhile named Isospora belli) is encountered globally, particularly in tropical and subtropical regions. Cystoisosporiasis is a human intestinal disease whose etiology is the parasite Cystoisospora belli with infection frequent in immunocompromised subjects, principally HIV-infected and AIDS patients. This coccidium parasite infects the epithelial cells and lining of the villi of the small and large intestines. C. belli is the least frequent of the three intestinal coccidia, viz: Cryptosporidium, microsporidium and C. belli which perturb humans. The clinical presentation of cystoisosporiasis gives a semblance of inflammatory bowel disease and irritable bowel syndrome, as well as other gastrointestinal symptoms, nausea, vomiting and diarhoea found in COVID-19, AIDS and HIV-infected patients. Research has not presented comorbid features of COVID-19 and cystoisosporiasis. The oocytes of C. belli are visualizable microscopically on wet mounts via bright-field, differential interference contrast (DIC) and epifluorescence. Trimethoprin sulfamethoxazole constitute the normal treatment of choice. C. belli,HIV-infected/AIDS and COVID-19 patients have clinicopathological correlates necessary to elucidate comorbidities and mechanisms of the diseases.