62 research outputs found

    Effect of Diclofenac on Hematological Parameters and Inflammatory Markers in Rat after Injection of Escherichia coli Lipopolysaccharide

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    Background: FBacterial lipopolysaccharide (LPS) is a large pathogen-associated molecule that affects both animals and humans. Objective: The aim of this study was to assess the effect of diclofenac sodium on hematological parameters and inflammatory markers after intraperitoneal injection of LPS in rats. Materials and Methods: Ninety-six male Wistar rats were divided randomly into 8 equal groups. Groups I, II, and III were only injected intraperitoneally (IP) with 100, 200, and 300 ÎĽg/kg LPS, respectively. Groups IV, V, and VI were injected with LPS at doses similar to the above groups plus diclofenac 2.5 mg/kg (IM). Group VII was injected only with diclofenac at the same dose and group VIII (control group) was injected with normal saline. Blood samples were collected from the rats in different times (0, 1, 6, and 24 hours) after injection. Results: The results showed that white blood cell (WBC), neutrophil, and lymphocyte counts significantly decreased in all groups at 1 and 6 hours after injection of LPS (P<0.05). The total leukocyte count, neutrophils, and lymphocytes increased at 24 hours after injection of LPS, in groups I, II, III, and VI (P<0.05). The C-reactive protein (CRP) levels at 6 and 24 hours after injection of LPS, in groups I, II, III, and VI, showed significant changes (P<0.05). The CRP level decreased in groups IV, V and VI (LPS + diclofenac) compared with the groups that were not injected with diclofenac (P<0.05). A significant increase was seen in fibrinogen level in all challenged groups (with or without diclofenac) at 24 hours after injection of LPS (P<0.05). Conclusion: Injection of diclofenac together with LPS did not affect the leukocyte changes (total and different count) and plasma fibrinogen level in rats. Diclofenac was effective in preventing high CRP changes induced by injection of LPS

    Effects of total protein and cholesterol on spermatology traits of common carp (Cyprinus carpio)

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    Seminal plasma has contained organics factors same as proteins and cholesterol. The information about role and variety of fish seminal plasma and relationship with other factors especially in common carp is rare. The aim of this study was evaluation of effects of total protein and cholesterol on physical and biochemical factors of cultural common carp milt in Khouzestan province. For this study 40 fish have been bought (20 in March and 20 in April) and examinations of physical and biochemical were tested. Base on the results, total protein in March and April was 0.29±0.14 and 0.37±0.35 g/dl respectively, cholesterol in March and April was 9/95±8.83 and 14/12±12.73 mg/dl respectively. The total protein and cholesterol in April compared to March increased non significantly. The ions of calcium, chloride, sodium and potassium in April compared to March increased. Based on the results there was significant and positive correlation between total protein and Albumin, cholesterol and K in march and significant and negative correlation with Cl but total protein in April had significant and positive with Cl, P, spermatocrite, cholesterol and Albumin and negative and significant correlation with weight of fish. Cholesterol in March had significant and positive with albumin and negative significant correlation with Cl and P but cholesterol in April had positive significant correlation with spermatocrite, Albumin, P and Cl. According to the data of this study, total protein, cholesterol, calcium, chloride, sodium, potassium of the Common carp seminal plasma increased in April compared to March. So because of these factors have effects on fertility, quality and quantity of common carp sperm so it is possible to adjust the parameters of protein, cholesterol and minerals of dietary in spawning season increase the quality of common carp sperm

    CRISPLD1: a novel conserved target in the transition to human heart failure

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    Heart failure is a major health problem worldwide with a significant morbidity and mortality rate. Although studied extensively in animal models, data from patients at the compensated disease stage are lacking. We sampled myocardium biopsies from aortic stenosis patients with compensated hypertrophy and moderate heart failure and used transcriptomics to study the transition to failure. Sequencing and comparative analysis of analogous samples of mice with transverse aortic constriction identified 25 candidate genes with similar regulation in response to pressure overload, reflecting highly conserved molecular processes. The gene cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) is upregulated in the transition to failure in human and mouse and its function is unknown. Homology to ion channel regulatory toxins suggests a role in Ca(2+) cycling. CRISPR/Cas9-mediated loss-of-function leads to dysregulated Ca(2+) handling in human-induced pluripotent stem cell-derived cardiomyocytes. The downregulation of prohypertrophic, proapoptotic and Ca(2+)-signaling pathways upon CRISPLD1-KO and its upregulation in the transition to failure implicates a contribution to adverse remodeling. These findings provide new pathophysiological data on Ca(2+) regulation in the transition to failure and novel candidate genes with promising potential for therapeutic interventions

    Homeosis in a scorpion supports a telopodal origin of pectines and components of the book lungs

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    This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated
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