Clin Lab
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The diversity of primary and secondary traumatic injuries specific for the critically ill polytrauma patient is complicating the therapeutic management in the absence of a strict assessment of the biological changes. Inflammation, redox imbalance, and immunosuppression can be quantified by various biochemical parameters; however, they do not fully respond to the current requirements. Another phenomenon responsible for worsening the clinical status and for the development of complications in such patients is oxidative stress. Its aggressiveness combined with biochemical and physiological imbalances leads to increased morbidity and mortality. To minimize the effects induced by free radicals, various substances are administered with high antioxidant capacity. However, the dosage optimization for each patient is difficult without strict monitoring of oxidative stress. In this paper we will summarize and present the pathophysiology of oxidative stress, as well as the specificity of miRNAs for a series of molecular changes at the cellular level. ⋯ Introducing miRNAs can revolutionize both monitoring and therapy modulation in these patients, adapting to the organic damage.
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Diagnosis of neonatal sepsis is difficult because of the nonspecific nature of the clinical presentation. Inflammation and coagulation can activate each other. Coagulation activation can occur in the early phase of sepsis. The main purposes of this study were to investigate the value of platelet parameters and coagulation parameters in predicting neonatal sepsis. ⋯ PT has a potential to be an additional indicator for neonatal sepsis, the combined use of PT and other markers such as CRP should be considered in the early diagnosis of neonatal sepsis.
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The aim of the study was to investigate oxidant/antioxidant status by determining serum ischemia-modified albumin (IMA) levels with oxidative/antioxidant parameters in patients with ankylosing spondylitis (AS) compared to the controls. ⋯ Depletion in antioxidant systems and overproduction of free radicals leading to formation of the oxidative stress may play a role in the development of AS. Increased levels of IMA might provide important contributions to the underlying oxidative stress in AS.
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Hypertrophic cardiomyopathy (HCM) is the leading cause of sudden cardiac death (SCD) in children and young adults and is the most frequent genetically determined cardiovascular disease following autosomal dominant pattern of inheritance. A number of genes have been shown to be responsible for HCM including MYBPC3. Cmybc, the protein encoded by MYBPC3 is a sarcomeric thick filament protein that interacts with titin, myosin, and actin to control sarcomeric gathering. Mutations in the MYBPC3 gene have been found to be associated with a history of sudden cardiac death in HCM patients. The main objective of the present study was to investigate the type and frequency of mutations in the MYBPC3 gene in HCM patients from the North-West of Iran. ⋯ The results obtained from the present study indicate a significant role of MYBPC3 gene mutations in HCM disease and can be used for pre-symptomatic diagnosis of at risk family members of affected individuals.
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Recently, autoimmune mechanisms and pulmonary epithelial cells have attracted attention in chronic obstructive pulmonary disease (COPD). Circulating antibodies against human bronchial epithelial cells (anti-HBEC) bind to bronchial epithelial antigens and induce bronchial epithelial cell damage. This study aimed to detect the expression of IgG, IgM, and IgA anti-HBEC in patients with COPD. ⋯ Our results suggest that an autoimmune component associated with bronchial epithelial cell damage is possibly involved in COPD and the presence of IgG and IgA anti-HBEC correlated with the GOLD stage of COPD. Therefore, our studies indicate that IgG and IgA anti-HBEC may associate with the disease severity of COPD.