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#28752213   2017/07/28 Save this To Up

Changes of haemogram and serum biochemistry in neonatal piglet diarrhoea associated with porcine rotavirus type A.

Porcine rotavirus type A (RVA) is a major cause of neonatal piglet mortality in India. The effect of the disease on haemogram and serum biochemical profile is not well established in piglets. Accordingly, we assessed the haemogram and serum biochemical profile in the neonatal piglet diarrhoea with RVA infection (n = 17). The diagnosis of RVA was confirmed using RNA-polyacrylamide gel electrophoresis (RNA-PAGE), commercially available enzyme-linked immunosorbent assay (ELISA) kit and reverse transcription-polymerase chain reaction (RT-PCR). Non-infected healthy piglets (n = 6) served as control. The concentrations of total protein, albumin, alanine amino transaminase (ALT), aspartate amino transaminase (AST), blood urea nitrogen (BUN) and creatinine in serum were measured by spectrophotometric method. Haemogram was done in the blood using sodium ethylenediaminetetraacetic acid (Na2 EDTA) as anticoagulant. The mean values of total protein, albumin and globulin concentrations were significantly (P < 0.001) decreased and concentrations of ALT, AST, BUN and creatinine were significantly increased (P < 0.001) in the RVA-infected piglets. Haemogram showed marked haemoconcentration (P < 0.001), leukopenia (P < 0.01) and neutropenia (P < 0.01) in the presence of RVA infection than healthy piglets. The results indicated a possible extra-intestinal spread of RVA in piglets during neonatal diarrhoea. The finding might be helpful to clinicians and while treating such type of clinical cases, incorporation of organ protective drugs will be helpful for better response in the treatment schedule.

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Bovine Androstenedione,AS Human interleukin 2(IL-2) Bovine prolactin-induced Sterile filtered goat se Sterile filtered goat se Sterile filtered mouse s Sterile filtered rat ser MOUSE ANTI BOVINE ROTAVIR ELISA grade porcine type ELPI ELISA grade porcine ELPI ELISA grade porcine ELMGPI Mouse IgG anti por

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#28741343   2017/07/25 Save this To Up

Relationships between certain metabolic diseases and selected serum biochemical parameters in seropositive dairy cows against Neospora caninum infection in different stages of lactation

Neospora caninum is an important cause of abortion in dairy cattle. The general health of affected cows has not been investigated before. Therefore, the main objective of this study was to identify possible relationships between certain metabolic diseases and selected serum biochemical parameters in seropositive dairy cows against N. caninum antibodies in different stages of lactation. The study was carried out using 72 N. caninum seropositive cows and 61 seronegative dairy cows (control). Serum from all cows was tested to determine their N. caninum status (seropositive vs seronegative) using commercially available indirect enzyme-linked immunosorbent assay test kit (iELISA). In addition, serum biochemical parameters including beta-hydroxybutyrate (BHB), glucose, creatinine, blood urea nitrogen, total protein, albumin, alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH) and gamma-glutamyltranspeptidase (GGT) were determined using routine laboratory methods. The stage of lactation was obtained at the time of sampling from farm records. Student independent t-test showed that there was a significant difference in the serum concentrations of BHB, AST, ALT, and LDH between seropositive and seronegative cows. There was no significant association between seropositivity and the stage of lactation. However, multivariable logistic regression analysis showed that there was a strong association between seropositivity and BHB concentrations. Results of this study indicate a possible relationship between N. caninum seropositivity and certain metabolic diseases such as ketosis and fatty liver syndrome in dairy cows.

2021 related Products with: Relationships between certain metabolic diseases and selected serum biochemical parameters in seropositive dairy cows against Neospora caninum infection in different stages of lactation

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#27891207   2016/11/28 Save this To Up

The Antiapoptosis Effect of Glycyrrhizate on HepG2 Cells Induced by Hydrogen Peroxide.

This study demonstrated that glycyrrhizate (GAS) could protect HEPG2 cells against damage and apoptosis induced by H2O2 (1600 μM, 4 h). Cell viability assay revealed that GAS was noncytotoxity at concentration 125 µg/mL, and GAS (5 μg/mL, 25 μg/mL, and 125 μg/mL) protected HepG2 cells against H2O2-induced cytotoxicity. H2O2 induced the HepG2 cells apoptosis, obvious morphologic changes were observed after Hochest 33258 staining, and more apoptotic cells were counted in flow cytometry assay compared to that of the natural group. Pretreatment GAS (5 μg/mL, 25 μg/mL, and 125 μg/mL) prior to H2O2 reverses the morphologic changes and reduced the apoptotic cells in HepG2 cells. GAS reduced the release of MDA, increased the activities of superoxide dismutase, and diminished the release of ALT and AST during oxidative stress in HepG2 cells. After Elisa kit detecting, GAS inhibited the caspase activity induced by H2O2, GAS decreased the level of caspase-3 and caspase-9 from mitochondria in dose-dependent manner. Western blot results showed that pretreatment GAS upregulated the expression of Bcl-2 and decreased the expression of Bax. These results reveal that GAS has the cytoprotection in HepG2 cells during ROS exposure by inhibiting the caspase activity in the mitochondria and influencing apoptogenic factors of the expression of Bax and Bcl-2.

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#27788708   2016/10/28 Save this To Up

[Role of neutrophils in treatment of rats with D-galactosamine-induced acute liver failure with bone marrow mesenchymal stem cells].

Objective: To investigate the therapeutic effect of bone marrow mesenchymal stromal cell (BMSC) transplantation on D-galactosamine-induced acute liver failure in Sprague-Dawley (SD) rats, as well as the mechanism of neutrophils in this process. Methods: A total of 39 male SD rats were divided into control group (8 rats, intraperitoneal injection of isotonic saline), model group (10 rats, intraperitoneal injection of D-galactosamine), solvent group (9 rats, tail vein injection of isotonic saline at 2 hours after intraperitoneal injection of D-galactosamine), and treatment group (12 rats, tail vein injection of MSCs at 2 hours after intraperitoneal injection of D-galactosamine). The rats were sacrificed at 24 hours after the model of D-galactosamine-induced acute liver failure was established, and the blood and liver tissue were harvested. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and total bilirubin (TBil) were measured, and blood analysis was performed to measure the number and percentage of neutrophils in peripheral blood. Immunofluorescence assay was used to measure the expression of the neutrophil marker Ly6g in the liver, the myeloperoxidase (MPO) kit was used to measure the activity of MPO in liver, and RT-PCR was used to measure the mRNA expression of inflammatory cytokines and chemokines in the liver, i.e., tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), interferon-γ(IFN-γ), interleukin-10 (IL-10), CXC chemokine ligand 1 (CXCL1), and CXC chemokine ligand 2 (CXCL2). Another 64 male SD rats were randomly divided into groups, and the survival rates of rats in each group were observed for 7 days. The independent samples t-test was used for comparison between any two groups (Levene homogeneity test of variance, and the corrected t-test was used for a P value of < 0.05), and the log-rank test was used for comparison of survival rates between any two groups. Results: At 24 hours after acute liver failure was induced by D-galactosamine in the SD rats, there were significant increases in the liver function parameters (ALT: 2884.1±541.0 U/L vs 45.4±11.0 U/L,P< 0.001; AST: 3634.9±755.9 U/L vs 143.9±23.7 U/L,P< 0.001; TBil: 44.4±8.4μmmol/L vs 0.9±0.2μmmol/L,P< 0.001) and the number and percentage of peripheral blood neutrophils [number: (4.7±1.1)×109 vs (1.4±0.4)×109,P< 0.001; percentage: 44.9%±8.0% vs 18.3%±4.4%,P< 0.001]. A large number of neutrophils aggregated in the liver tissue, and there were significant increases in the MPO activity (4.72±1.09 U/g vs 1.13±0.24 U/g,P< 0.001), inflammatory cytokines, and chemokines. Compared with the model group, the treatment group showed significant improvements in liver function (ALT: 1 823.9±389.2 U/L vs 2 884.1±541.0 U/L,P< 0.001; AST: 2173.0±567.3 U/L vs 3634.9±755.9 U/L,P< 0.001; TBil: 30.9±6.5μmmol/L vs 44.4±8.4μmmol/L,P< 0.001) and survival rate (50% vs 12.5%,P= 0.023). Meanwhile, the treatment group also showed significant reductions in the number and percentage of peripheral blood neutrophils [number: (3.5±1.0)×109 vs (4.7±1.1)×109,P= 0.012; percentage: 35.9%±8.9% vs 44.9%±8.0%,P= 0.021], number of neutrophils in the liver, and MPO activity (3.52±1.03 U/g vs 4.72±1.09 U/g,P= 0.040), as well as significantly inhibited expression of inflammatory cytokines and chemokines (TNF-α: 2.458±0.762 vs 3.778±1.046, P = 0.005; IL-1β: 2.498±0.547 vs 4.065 ± 0.953,P= 0.002; IFN-γ: 3.977±1.039 vs 5.418±1.255, P = 0.025; IL-10: 6.056±1.542 vs 3.368±0.952,P= 0.001; CXCL1: 7.988±1.911 vs 10.366±1.239,P= 0.010; CXCL2: 3.441±1.005 vs 4.847±1.113,P= 0.019). Conclusion: BMSC transplantation has a therapeutic effect on D-galactosamine-induced acute liver failure in rats, and this process is accompanied by reduced aggregation and activity of neutrophils in peripheral blood and liver. Inflammatory cytokines and chemokines may be involved in the mechanism of regulation of these two aspects.

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#27667108   2016/09/26 Save this To Up

[Role of endoplasmic reticulum stress-mediated glycogen synthase kinase 3β activity in pathogenesis of acute liver failure in mice].

Objective: To study the role of endoplasmic reticulum (ER) stress-mediated glycogen synthase kinase 3β (GSK3β) activity in the pathological process of liver injury in acute liver failure (ALF) mice. Methods: ALF model was established by intraperitoneal injection of D-galactosamine/lipopolysaccharide (D-GalN/LPS) in C57BL/6 mice. The mice were divided into control group (n=10), ALF model group (n=18), 4-phenylbutyrate (4-PBA, an ER stress inhibitor) group (n=18) and SB216763 (a specific inhibitor of GSK3β) group (n=16). The serum alanine transaminase (ALT) and aspartate transaminase (AST) levels were measured to reflect the liver function, liver injury was assessed by observing pathological changes of liver tissue, the levels of proteins in liver tissue were analyzed by Western blotting, the activity of GSK3β in liver tissue was detected using GSK3β activity assay kit, and the survival rate of hepatocyte was measured by methyl thiazolyl tetrazolium (MTT) assay. Results: In in vivo experiment, the expression levels of ER stress markers, glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP), were upregulated during the progression of D-GalN/LPS-induced ALF, indicating activation of severe ER stress and increased activity of GSK3β. Compared with the model group, inhibition of ER stress by 4-PBA improved liver function[ALT: (365.4±58.6) U/L vs (1 094.5±201.5) U/L, P<0.05; AST: (555.1±60.8) U/L vs (1 444.3±533.7) U/L, P<0.05)and pathological injury, also decreased the activity of GSK3β (2.6±0.3 vs 4.6±1.3, P<0.05). Inhibition of GSK3β activity was shown to alleviate liver injury in ALF by reducing the expression levels of GRP78 and CHOP. The in vitro experiment of tunicamycin-induced hepatocyte apoptosis showed that inhibition of GSK3β activity increased the cell survival rate. Conclusion: In ALF induced by D-GalN/LPS, severe ER stress may accelerate the development and progress of ALF by upregulating the activity of GSK3β.

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#27346966   2016/06/27 Save this To Up

A reference interval study for common biochemical analytes in Eastern Turkey: a comparison of a reference population with laboratory data mining.

The aim of this study was to define the reference intervals (RIs) in a Turkish population living in Northeast Turkey (Erzurum) for 34 analytes using direct and indirect methods. In the present study, the regional RIs obtained were compared with other RI studies, primarily the nationwide study performed in Turkey.

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#27158210   2016/05/09 Save this To Up

Serum Mac-2 binding protein is a novel biomarker for chronic pancreatitis.

To determine the efficacy of Mac-2 binding protein (Mac-2bp) for diagnosis of chronic pancreatitis.

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#26330104   2015/09/02 Save this To Up

Effect of miR-34a in regulating steatosis by targeting PPARα expression in nonalcoholic fatty liver disease.

MicroRNA-34a (miR-34a) is thought to be involved in nonalcoholic fatty liver disease (NAFLD). However, the association between altered expression of miR-34a and the pathophysiological features of NAFLD remains unclear. Here, we investigated the mechanisms by which miR-34a influences NAFLD through the PPARα-related pathway. Real-time quantitative PCR, western blotting and other assays kit were used to investigate the expression and function of miR-34a in an NAFLD model. Cultured cells transfected with miR-34a inhibitor and C57BL/6 mice injected with the miR-34a inhibitor through vein tail were conducted for the effects of miR-34a on its target. MiR-34a levels were significantly upregulated in steatosis-induced hepatocytes and in liver tissues of high-fat diet-fed mice. The upregulation of miR-34a resulted in the downregulation of hepatic PPARα and SIRT1 that are the direct targets of miR-34a. Silencing miR-34a led to an initially increased expression of PPARα, SIRT1 and PPARα's downstream genes. Activation of the central metabolic sensor AMPK was also increased. The miR-34a inhibitor suppressed lipid accumulation and improved the degree of steatosis. Taken together, our data indicated that decreased expression of miR-34a potentially contributes to altered lipid metabolism in NAFLD. Downregulation of miR-34a may be a therapeutic strategy against NAFLD by regulating its target PPARα and SIRT1.

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#26004721   2015/05/25 Save this To Up

Serum haematological and biochemical indices of oxidative stress and their relationship with DNA damage and homocysteine in Pakistani type II diabetic patients.

Diabetes mellitus (DM) is a heterogeneous metabolic disorder characterized by chronic hyperglycaemia, higher glycated hemoglobin (HbA1C) as well as protein. Oxidative stress can cause damage to leukocytic DNA and enhancement of homocysteine (Hcy) level in sera of type 2 diabetic patients. Haematological and biochemical parameters are severely affected by oxidative stress, which results in damages to DNA and Hcy in these patients. Eighty DM patients and 80 normal subjects, after having their consent, were selected for the present study. Leukocytes were characterized for DNA damage by comet assay kit while, blood plasma was taken into account for biochemical indices using commercial test kits. Results indicated that DNA damage was strongly linked with erythrocyte sedimentation rate (ESR) (P<0.01), glycated hemoglobin (HbA1C) (P<0.0001), glycated serum protein (P<0.005), cholesterol (P<0.011), triglycerides (P<0.001), albumin (P<0.001), creatinine (P<0.006), urea (P<0.007) and ALT (P<0.02), and negatively associated with packed cell volume (PCV) (P<0.002) and hemoglobin (P<0.001). Homocysteine was strongly linked with ESR, HbA1C, glycated protein (P<0.002), cholesterol (P<0.016), triglycerides (P<0.0001), albumin, creatinine, urea, ALT and AST in diabetic patients. Hyc and DNA damages both were negatively linked with total hemoglobin and PCV. Both of these even in their normal range may have a role in the endothelium damage. Nutritional intervention to lower down Hyc and DNA damages in the Pakistani population may mitigate their effect and guarantee in maintenance of a healthy nation.

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#25177034   2014/09/01 Save this To Up

Chloroquine improved carbon tetrachloride-induced liver fibrosis through its inhibition of the activation of hepatic stellate cells: role of autophagy.

Autophagy is involved in the activation of hepatic stellate cells (HSCs), which is the key process of liver fibrosis. We reasoned that chloroquine, based on its ability to inhibit autophagy, might exert beneficial effects in liver fibrosis. Liver fibrosis in rats was induced by carbon tetrachloride (CCl4). Rats were divided into three groups, a normal control group (N group), model group (M group), and chloroquine group (CQ group). Liver fibrosis in the rats was evaluated by hematoxyline-eosin (H&E) and Masson staining. The activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TB) were determined using an automated biochemistry analyzer. Total hepatic hydroxyproline levels were determined with a kit. The expressions of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) were detected by immunofluorescence staining, and the expressions of LC3-II and p62 were determined by Western blotting. Compared with N group, M group showed impaired liver function, liver fibrosis, increased hydroxyproline content, up-regulated expressions of α-SMA and TGF-β1, which have been reported to be pro-fibrogenic genes in vivo, and increased autophagy flux as indicated by the accumulation of LC3-II and degradation of p62. These changes were attenuated by chloroquine treatment. Chloroquine exerts beneficial effects in CCl4-induced liver fibrosis. The mechanism of action includes inhibition of autophagy pathways and inhibition of activation of HSCs.

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