Sickle cell disease (SCD) is an autosomal recessive inheritance disorder that affects the beta-globin gene and results in the replacement of the amino acid glutamic acid by valine in the β chain of the hemoglobin molecule, producing erythrocytes with defective forms and functions. A range of pathological conditions is associated with SCD, however, one in particular stands out by gravity. Acute thoracic syndrome (STA), characterized by the presence of pulmonary infiltrates associated with a clinical symptom such as chest pain, cough, wheezing, tachypnea and fever, is considered a leading cause of death in patients with sickle cell disease. Early diagnosis and introduction of an effective approach to complication are needed to improve outcomes and minimize associated morbidity and mortality. Risk factors associated with STA in the SCDAbdominal surgery for splenectomy and cholecystectomy [19] Hypersensitivity [20,21] Smoking [20,21] Asthma [22] Infections [9,[23][24][25] Post-Surgical Hypoventilation [9,[23][24][25] Fatty Embolism [9,[23][24][25]
Obesity is characterized as a health problem of high prevalence worldwide, and to date, about two thirds of the US population is affected, generating a high financial cost for health management systems. Traditionally, the model for the study of obesity has been rodents, mainly rats and mice, and although the obesity field has progressed a lot, there has been a clear need for a cheaper and more efficient model. C. elegans is a small worm with a life expectancy of about 21 days that possesses rapid growth and feeds on non-pathogenic strains of Escherichia coli. This small nematode has about 60 to 80 percent of its genes related to human diseases, and it is now known to the scientific community that manipulating its genome can provide valuable information to define the pathophysiological aspects of obesity. C. elegans has been successfully reported as an animal model in research related to nutritional physiology, in addition to the characterization of several metabolic pathways, storage mechanisms and lipid release. In recent years, due to the advances of C. elegans in the physiological characterization of lipid metabolism, it is now possible with its use as an animal model to offer the possibility of in vivo identification of compounds that modulate fat storage.
As of late the relationship between oxidative stress and maturing has been brought into question. It has recommended that while oxidative occasions may assume a part in the movement of age-related pathologies, it is not pertinent to maturing forms not including particular infections related with senescence. The confirmation in support of this idea is to a great extentgivenstudies with Caenorhabditis elegans (C. elegans) that has been broadly utilized as a model framework to study maturing. This critique assesses information got from got from C. elegans and reports that the prevalence of proof from this species bolsters the part of expert oxidant occasions just like a critical supporter to typical maturing. Conceivable explanations behind some bizarre discoveries are clashing with this ideatalked
The nematode Caenorhabditis elegans has risen as a critical creature show in different fields including neurobiology, formative science, and hereditary qualities. Qualities of this creature demonstrate that have added to its prosperity incorporate its hereditary manipulability, invariant and completely depicted formative program, all around portrayed genome, simplicity of support, short and productive life cycle, and little body estimate. These same elements have prompted to an expanding utilization of C. elegans in toxicology, both for robotic reviews and highthroughput screening approaches. We depict a portion of the exploration that has been completed in the territories of neurotoxicology, hereditary toxicology, and ecological toxicology, and additionally high-throughput tries different things with C. elegans including all inclusive screening for sub-atomic focuses of harmfulness and fast danger evaluation for new chemicals. We contend for an expanded part for C. elegans in supplementing other model frameworks in toxicological research.
Acute Myocardial Infarction (AMI) is one of the leading causes of morbidity and mortality worldwide. The greatest risk of fatality occurs within the first hours of initiation of AMI. Thus, the early diagnosis of cardiac ischemia is fundamental for the effective management of AMI patients. Inadequate diagnosis of patients with chest pain often leads to inadequate admission of patients without AMI and vice versa. In addition to the clinical history, physical examination, accurate electrocardiogram findings, and evaluation of cardiac biomarkers play an important role in the early diagnosis of acute ischemia. The present review discusses in detail the various cardiac biomarkers released during the event of an AMI.
Before examining the assessment of renal capacity, it is valuable to quickly audit typical renal physiology. The kidney plays out various basic procedures. It takes part in the support of the consistent extracellular environment that is required for sufficient working of the cells. This is accomplished by discharge of a portion of the waste results of digestion system, (for example, urea, creatinine, and uric acid) and by particularly modifying the urinary discharge of water and electrolytes to match net admission and endogenous generation. The kidney can control separately the discharge of water and solutes, for example, sodium, potassium, and hydrogen, to a great extent by changes in tubular reabsorption or emission. It secretes hormones that take an interest in the control of systemic and renal hemodynamics (renin, prostaglandins, and bradykinin), red platelet creation (erythropoietin), and calcium, phosphorus, and bone digestion system (1,25-dihydroxyvitamin D3 or calcitriol).
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