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Acute superior mesenteric venous thrombosis (ASMVT) is an abdominal vascular condition. Early recanalization is essential to successful treatment. The aim of the study was to establish rabbit models of ASMVT and assess the time course of intestinal epithelial barrier disruption.


After surgical exposure of superior mesenteric vein (Sham group), large-vessel (L-group) and small-vessel (S-group) models were established by endothelium damage, stenosis creation, and thrombin injection. At baseline, 6, 9, and 12 h, hemodynamic and serum parameters were tested. Serum from ASMVT patients diagnosed at 24, 36, 48, and 60 h from symptom onset was collected. Intestinal barrier disruption was assessed by tight junction (TJ) protein expression, morphology changes, and bacterial translocation. Mesenteric arteriospasm was measured by flow velocity and intestinal wet/dry weight ratio. The serum level of intestinal fatty acid–binding protein and endotoxin in patients was also measured as an indicator for intestinal barrier function.


Severe acidosis and lacticemia were observed in both the groups. The L-group experienced greater hemodynamic alteration than the S-group. Intestinal barrier disruption was detected by significantly decreased TJ protein expression, histology and ultrastructure injury of TJ, increased permeability, and bacterial translocation, at 9 h in the S-group and 12 h in the L-group. Secondary mesenteric arteriospasm occurred at the same time of complete intestinal barrier disruption and could be a significant cause of bowel necrosis. Significant increased level of intestinal fatty acid–binding protein and endotoxin was found in patients at 48 h in the S-group type and 60 h in the L-group type.


The ASMVT animal models of both the types were first established. The loss of intestinal barrier function occurred at 6 h in the S-group model and 9 h in the L-group model. For clinical patients, the time window extended to 36 h in the S-group type and 48 h in the L-group type.


Mesenteric venous thrombosis; Intestinal epithelial barrier; Acute ischemic injury; Therapeutic time window

Coagonist of GLP-1 and glucagon decreases liver inflammation and atherosclerosis in dyslipidemic condition

Posted by V Patel, A Joharapurkar, S Kshirsagar, et al. on 2018-01-14 18:49:27


Dyslipidemia enhances progression of atherosclerosis. Coagonist of GLP-1 and glucagon are under clinical investigation for the treatment of obesity and diabetes. Earlier, we have observed that coagonist reduced circulating and hepatic lipids, independent of its anorexic effects. Here, we investigated the role of coagonist of GLP-1 and glucagon receptors in complications of diet-induced dyslipidemia in hamsters and humanized double transgenic mice. Hamsters fed on high fat high cholesterol diet were treated for 8 weeks with coagonist of GLP-1 and glucagon receptors (75 and 150?ug/kg). Pair-fed control was maintained. Cholesterol fed transgenic mice overexpressing hApoB100 and hCETP with coagonist (300 ug/kg) for 4 weeks. After the completion of treatment, biochemical estimations were done. Coagonist treatment reduced triglycerides in plasma, liver and aorta, plasma cholesterol and hepatic triglyceride secretion rate. Expressions of HMG-CoA reductase and SBREBP-1C were reduced and expressions of LDLR, CYP7A1, ABCA1 and ABCB11 were increased in liver, due to coagonist treatment. Coagonist treatment increased bile flow rate and biliary cholesterol excretion. IL-6 and TNF-beta were reduced in plasma and expression of TNF-beta, MCP-1, MMP-9 and TIMP-1 decreased in liver. Treatment with coagonist reduced oxidative stress in liver and aorta. Energy expenditure was increased and respiratory quotient was reduced by coagonist treatment. These changes were correlated with reduced hepatic inflammation and lipids in liver and aorta in coagonist treated hamsters. Coagonist treatment also reduced lipids in cholesterol-fed transgenic mice. These changes were independent of glycaemia and anorexia observed after coagonist treatment. Long term treatment with coagonist of GLP-1 and glucagon receptor ameliorated diet-induced dyslipidemia and atherosclerosis by regulating bile homeostasis, liver inflammation and energy expenditure.


A Chinese perfluorooctane sulfonate (PFOS) substitute frequently detected in the environment, 6:2 chlorinated polyfluorinated ether sulfonate (F-53B), has a similar structure to PFOS and it is proposed to cause thyroid dysfunction. To further confirm this hypothesis, the effects of F-53B on the thyroid endocrine system and underlying mechanisms were investigated in vitro and in vivo using rat pituitary GH3 cells and developing zebrafish, respectively. In GH3 cells, F-53B enhanced cell proliferation in a dose-dependent manner, indicative of thyroid receptor agonistic activity. In zebrafish larvae, F-53B exposure induced significant developmental inhibition and increased thyroxine (T4) but not 3,5,3-triiodothyronine (T3) levels accompanied by a decrease in thyroglobulin (TG) protein and transcript levels of most genes involved in the hypothalamic-pituitary-thyroid (HPT) axis. Interestingly, T4 levels remained significantly increased while TG protein and gene transcription levels were markedly upregulated after depuration. Molecular docking studies revealed that F-53B binds to transthyretin (TTR) by forming hydrogen bonds with Lys123 and Lys115, thereby interfering with thyroid hormone homeostasis. Our collective in vitro, in vivo and in silico studies provide novel evidence that F-53B disrupts the thyroid endocrine system at environmentally relevant concentrations, which cannot be recovered after depuration. Given the persistence of F-53B in the environment, the long-term consequences of thyroid hormone disruption by this chemical warrant further investigation.


The purpose of the present study was to investigate the possible therapeutic effects of the human Wharton-Jelly mesenchymal stromal cells derived micro-vesicles (hWJMSCs-MVs) on renal ischemia-reperfusion injury (IRI) after cardiac death (CD) renal transplantation in rats. MVs were injected intravenously in rats immediately after renal transplantation. The animals were sacrificed at 24h, 48h, 1 and 2 weeks post-transplantation. ELISA was used to determine the von Willebrand Factor (vWF), tumor necrosis factor (TNF)-alpha, and interleukin (IL)-10 levels in the serum. Tubular cell proliferation and apoptosis were identified by Ki67 immunostaining and TUNEL assay. Renal fibrosis was assessed by Masson s tri-chrome straining and alpha-smooth muscle actin (alpha-SMA) staining. The infiltration of inflammatory cells was detected by CD68+ staining. The transforming growth factor (TGF)-beta, hepatocyte growth factor (HGF), and alpha-SMA expression in the kidney was measured by Western blot. After renal transplantation, the rats treated with hWJMSCs-MVs improved survival rate and renal function. Moreover, MVs mitigated renal cell apoptosis, enhanced proliferation, and alleviated inflammation at the first 48h. In the late period, abrogation of renal fibrosis was observed in the MVs group. MVs also could decrease the number of CD68+ macrophages in the kidney. Furthermore, MVs decreased the protein expression levels of alpha-SMA and TGF-beta1 and increased the protein expression level of HGF at any point (24 h, 48 h, 1 or 2 weeks). The administration of MVs immediately after renal transplantation could ameliorate IRI in both the acute and chronic stage.

Maternal hypertrophy and diastolic disfunction and brain natriuretic peptide concentration in early and late Pre-Eclampsia

Posted by V.T.M.Borges, S.G.Zanati MD, J.R.Poiati MS, et al. on 2017-12-18 00:25:37


Objective: Pre-eclampsia is associated with maternal cardiac remodelling and diastolic dysfunction. The aim of this study was to assess and compare maternal left ventricular structure and diastolic function and Brain Natriuretic Peptide (BNP) levels in women with early-onset pre-eclampsia (<34 weeks of gestation) and late-onset pre-eclampsia (≥34weeks of gestation).

Methods: A prospective, cross-sectional observational study was performed in 30 women with early-onset pre-eclampsia, 32 with late-onset pre-eclampsia and 23 normotensive controls. Maternal cardiac structure and diastolic function as assessed by echocardiography and plasma levels of BNP were measured by enzyme immunoassay.

Results: Pre-eclampsia was associated with an increased left ventricular mass index and relative wall thickness in early-onset pre-eclampsia compared with late-onset pre-eclampsia and normotensive controls. The prevalence of concentric hypertrophy (40%) and diastolic dysfunction (23%) was also significantly higher in early-onset pre-eclampsia than in late-onset pre-eclampsia (16% for both, all p<0.05). Maternal serum BNP values were also significantly higher in early-onset pre-eclampsia (p<0.05) and correlated with relative wall thickness and left ventricular mass index.

Conclusions: Early-onset pre-eclampsia has more severe cardiac impairment than late-onset pre-eclampsia as evidenced by increased prevalence of concentric hypertrophy, diastolic dysfunction and high concentrations BNP. These findings suggest that early-onset pre-eclampsia causes greater myocardial damage increasing the risk of both peripartum and postpartum cardiovascular morbidity. Although these cardiovascular effects are easily identified by echocardiographic parameters and measuring BNP, further studies are needed to assess their clinical utility.

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