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COVID-19 is the most devastating pandemic situation we have experienced in our age, affecting all systems. Although it affects all systems, it shows its most important effect through thrombophilia. Therefore, the possible cause of sudden death due to COVID-19 may be embolism caused by thrombophilia. D-dimer amounts increase due to COVID-19. The thrombosis is associated with sudden death in COVID-19 disease in populations. Since individuals with thrombophilia will be more prone to death due to COVID-19, it may be appropriate to administer low doses of Clexane (Enoxaparin sodium) or low-weight heparin for prophylactic purposes in order to consider these individuals at high risk and to prevent deaths. Moreover, in order not to risk the lives of healthcare professionals with thrombophilia, it would be appropriate to keep them away from individuals with COVID-19 disease and to employ them in different healthcare services according to their fields of expertise. It should also not be forgotten that different symptoms related to COVID-19 appear day by day, these different symptoms probably show that the virus has undergone mutations in order to survive, but no matter what, its effect on thrombophilia has not been eliminated yet. This compilation aims to present the reasons and causes of death due to COVID-19, possible treatment options, and thrombophilia panel tests and new parameters that may have a place in the meticulous interpretation of these tests and possible etiopathology in the light of current information. Therefore, presenting this information in a rational manner and keeping the parameters of the thrombophilia panel under strict control predict that the deaths due to the virus will be partially reduced.

Metabolic syndrome (MetS) is a prevalent public health problem. Uric acid (UA) is increased by MetS. We investigated whether administration of UA and 10% fructose (F) would accelerate MetS formation and we also determined the effects of irisin and exercise. We used seven groups of rats. Group 1 (control); group 2 (sham); group 3 (10% F); group 4 (1% UA); group 5 (2% UA); group 6 (10% F + 1% UA); and Group 7, (10% F + 2% UA). After induction of MetS (groups 3 -7), Group 3 was divided into three subgroups: 3A, no further treatment; 3B, irisin treatment; 3C, irisin treatment + exercise. Group 4, 1% UA, which was divided into three subgroups: 4A, no further treatment; 4B, irisin treatment; 4C, Irisin treatment + exercise. Group 5, 2% UA, which was divided into three subgroups: 5A, no further treatment; 5B, irisin treatment; 5C, irisin treatment + exercise. Group 6, 10% F + 1% UA, which was divided into three subgroups: 6A, no further treatment; 6B, irisin treatment; 6C, irisin treatment + exercise. Group 7, 10% F + 2% UA, which was divided into three subgroups: 7A, no further treatment; 7B, irisin treatment; 7C, irisin treatment + exercise., İrisin was administered 10 ng/kg irisin intraperitoneally on Monday, Wednesday, Friday, Sunday each week for 1 month. The exercise animals (in addition to irisin treatment) also were run on a treadmill for 45 min on Monday, Wednesday, Friday, Sunday each week for 1 month. The rats were sacrificed and samples of liver, heart, kidney, pancreas, skeletal muscles and blood were obtained. The amounts of adropin (ADR) and betatrophin in the tissue supernatant and blood were measured using an ELISA method. Immunohistochemistry was used to detect ADR and betatrophin expression in situ in tissue samples. The duration of these experiments varied from 3 and 10 weeks. The order of development of MetS was: group 7, 3 weeks; group 6, 4 weeks; group 5, 6 weeks; group 4, 7 weeks; group 3, 10 weeks. Kidney, liver, heart, pancreas and skeletal muscle tissues are sources of adropin and betatrophin. In these tissues and in the circulation, adropin was decreased significantly, while betatrophin was increased significantly due to MetS; irisin + exercise reversed this situation. We found that the best method for creating a MetS model was F + UA2 supplementation. Our method is rapid and simple. Irisin + exercise was best for preventing MetS. [ABSTRACT FROM AUTHOR]

Copyright of Firat Universitesi Sağlik Bilimleri Tip Dergisi is the property of Firat Universitesiu, Saglik Bilimleri Enstitusu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Although paraoxonase is synthesized in many tissues including the heart, colon, kidneys, lungs, small intestines and brain, its major locus of synthesis is the liver. PON1 is in close association with apolipoproteins and protects LDL against oxidation. It was reported that PON1 quantities dropped to 40 times lower than normal in cardiovascular diseases and diseases like diabetes, ulcerative colitis, Crohn's disease, chronic renal failure, SLE, Behcet's disease, cancer, hepatitis B, obesity, metabolic syndrome, Alzheimer's and dementia. It is speculated that the concerning decline in serum PON1 amount results from single nucleotide polymorphism in the coding (Q192R, L55M) and promoter (T-108C) sites of the PON1 gene. Additionally, circulating amounts of PON1 are affected by vitamins, antioxidants, fatty acids, dietary factors, drugs, age and lifestyle. This collection attempts to review and examine the past and present studies of paraoxonase and its relation with the cardiovascular system and some relevant diseases.

Occupational cement dust exposure has been associated with an increased risk of liver abnormalities, pulmonary disorders, and carcinogenesis. Decreased anti oxidant capacity and increased plasma lipid peroxidation have been posed as possible causal mechanisms of disease. Accordingly, this study examined the serum paraoxonase (PON1) arylesterase (AE), ghrelin, HDL-C, LDL-C and serum nitrite (NOx) levels in cement dust exposed workers. Twenty-eight volunteer male cement plant workers and 30 volunteer control male workers, aged 29-54 years, participated. The concentrations of serum PON1, AE, NOx, ghrelin, and HDL-cholesterol and LDL-cholesterol were mea sured in both groups. PON-1, AE, ghrelin and HDL-cholesterol were lower in the cement plant workers than in controls. Serum nitrite (NOx), and LDL-C levels in cement plant workers were higher (p

Exercise training increases fibronectin type III domain-containing protein 5 (FNDC5/irisin) via the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α)-pathway. The PGC1α pathway induced FNDC5/irisin changes in response to exercise training and ischemic stroke are not entirely understood. We investigated the relation of the PGC-1α/FNDC5/irisin pathway to exercise training and to the pathophysiology of ischemic stroke in paretic muscles of stroke-induced rat models. We induced cerebral ischemia following completion of high-intensity interval training (HIIT) to evaluate PGC1α-pathway biofactors in paretic muscles. To define the underlying molecular mechanisms for improvement in paretic muscles following cerebral ischemia, we evaluated PCG-1α-pathway factors using immunofluorescence tracking and enzyme-linked immunosorbent assay (ELISA) immunoassay. We found that HIIT for 3 weeks produced increased expression and release of PGC-1α-pathway biomarkers in both the serum and paretic muscle of stroke-induced rats. We also found a close relation between the expression of PCG-1α-pathway factors in skeletal muscle and their concentration in blood. We found that PGC-1α-pathway biomarkers cause irisin up-regulation following induction of cerebral ischemia. The reduction in neurofunctional deficits following increased PGC-1α-pathway biomarkers suggests that these factors may act as markers of improvement in paretic muscle healing following cerebral ischemia. [ABSTRACT FROM AUTHOR]

COVID-19 is the most devastating pandemic situation we have experienced in our age, affecting all systems. Although it affects all systems, it shows its most important effect through thrombophilia. Therefore, the possible cause of sudden death due to COVID-19 may be embolism caused by thrombophilia. D-dimer amounts increase due to COVID-19. The thrombosis is associated with sudden death in COVID-19 disease in populations. Since individuals with thrombophilia will be more prone to death due to COVID-19, it may be appropriate to administer low doses of Clexane (Enoxaparin sodium) or low-weight heparin for prophylactic purposes in order to consider these individuals at high risk and to prevent deaths. Moreover, in order not to risk the lives of healthcare professionals with thrombophilia, it would be appropriate to keep them away from individuals with COVID-19 disease and to employ them in different healthcare services according to their fields of expertise. It should also not be forgotten that different symptoms related to COVID-19 appear day by day, these different symptoms probably show that the virus has undergone mutations in order to survive, but no matter what, its effect on thrombophilia has not been eliminated yet. This compilation aims to present the reasons and causes of death due to COVID-19, possible treatment options, and thrombophilia panel tests and new parameters that may have a place in the meticulous interpretation of these tests and possible etiopathology in the light of current information. Therefore, presenting this information in a rational manner and keeping the parameters of the thrombophilia panel under strict control predict that the deaths due to the virus will be partially reduced. [ABSTRACT FROM AUTHOR]

The aims of the study were to assess the levels of serum TMAO, S-equol, and indoxyl sulfate in subjects with ocular active Behçet’s disease (OABD) and ocular inactive Behçet’s disease (OIBD).The study involved 22 patients with OABD, 22 patients with OIBD, and thwentythree control participants. 5 mL venous blood was taken from the participants. The TMAO, S-equol, and indoxyl sulfate in the serum were measured using the ELISA method.When compared to the TMAO levels of the control group, the TMAO levels of the participants with OABD and OIBD were considerably greater (p<0.05). Similarly, when compared to the S-equol levels of the control group, the S-equol levels of the participants with OABD and OIBD were significantly higher (p<0.05). Additionally, when compared to the indoxyl sulfate of the control group, the indoxyl sulfate amounts of the participants OABD and OIBD were significantly higher (p<0.05).It was first time shown that microbiota molecules could have an impact on Behçet’s disease (BD) pathogenesis. Additionally, measuring these molecules in addition to the BD Ocular Attack Score 24 (BOS24) might offer advice to medical professionals regarding the diagnosis and treatment of the illness. [ABSTRACT FROM AUTHOR]

Copyright of Firat Tip Dergisi is the property of Firat University, Faculty of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)