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Find video protocols related to scientific articles indexed in Pubmed.
An Overview of Hedgehog Signaling in Fibrosis.
Mol. Pharmacol.
PUBLISHED: 11-13-2014
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The Hedgehog (Hh) signaling plays an important role during embryogenesis and tissue regeneration. Recently, studies revealed that over-activated Hh signaling leads to fibrogenesis in many types of tissues. The activation of Hh signaling is involved in epithelial-mesenchymal transition (EMT) and excessive extracellular matrix deposition. Blockade of Hh signaling abolishes the induction of EMT and ameliorates tissue fibrosis. Therefore, new therapeutic targets to alleviate fibrosis based on the Hh signaling have attracted a great deal of attention. This is a new strategy for treating fibrosis and other related diseases. In this review, we will discuss the crucial role of Hh signaling in fibrogenesis to provide a better understanding of their relationship and to encourage the study of novel targeted therapies.
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Hepatic stellate cell is activated by microRNA-181b via PTEN/Akt pathway.
Mol. Cell. Biochem.
PUBLISHED: 08-23-2014
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Activation of hepatic stellate cells (HSCs) is an essential event in the initiation and progression of liver fibrosis. MicroRNAs have been shown to play a pivotal role in regulating HSC functions such as cell proliferation, differentiation, and apoptosis. Recently, miR-181b has been reported to promote HSCs proliferation by targeting p27. But whether alpha-smooth muscle actin (?-SMA) or collagens could be promoted by miR-181b in activated HSCs is still not clear. Therefore, the understanding of the role of miR-181b in liver fibrosis remains limited. Our results showed that miR-181b expression was increased much higher than miR-181a expression in vitro in transforming growth factor-?1-induced HSC activation as well as in vivo in carbon tetrachloride-induced rat liver fibrosis. Of note, overexpression of miR-181b significantly increased the expressions level of ?-SMA and type I collagen, and further promoted HSCs proliferation. Furthermore, phosphatase and tensin homologs deleted on chromosome 10 (PTEN), a negative regulator of PI3K/Akt pathway, were confirmed as a direct target of miR-181b. We demonstrated that miR-181b could suppress PTEN expression and increase Akt phosphorylation in HSCs. Interestingly, the effects of miR-181b on the activation of HSCs were blocked down by Akt inhibitor LY294002. Our results revealed a profibrotic role of miR-181b in HSC activation and demonstrated that miR-181b could activate HSCs, at least in part, via PTEN/Akt pathway.
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Resveratrol inhibits epithelial-mesenchymal transition and renal fibrosis by antagonizing the hedgehog signaling pathway.
Biochem. Pharmacol.
PUBLISHED: 07-03-2014
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Epithelial-to-mesenchymal transition (EMT), a biologic process in which tubular cells lose their epithelial phenotypes and acquire new characteristic features of mesenchymal properties, is increasingly recognized as an integral part of renal tissue fibrogenesis. Recent studies indicate that resveratrol, a botanical compound derived mainly from the skins of red grapes, may have anti-fibrotic effects in many tissues, but the potential molecular mechanism remains unknown. In the present study, we identified that resveratrol inhibits the induction of EMT and deposition of extracellular matrix (ECM) through antagonizing the hedgehog pathway in vitro and in vivo. In rats with unilateral ureteral obstruction (UUO), administration of resveratrol (20mg/kg/day) significantly reduced serum creatinine. Resveratrol also decreased expression of TGF-?1, and inhibited the phenotypic transition from epithelial cells to mesenchymal cells, and the deposition of ECM in UUO rats. In cultured renal tubular epithelial cells (NRK-52E), TGF-?1-induced EMT and ECM synthesis was abolished with the treatment of resveratrol. The induction of EMT was associated with the activation of the hedgehog pathway. Resveratrol treatment markedly inhibited the over-activity of the hedgehog pathway in the obstructed kidney and in TGF-?1-treated NRK-52E cells, resulted in reduction of cellular proliferation, EMT and ECM accumulation. Thus, these results suggest that resveratrol is able to inhibit EMT and fibrosis in vivo and in vitro through antagonizing the hedgehog pathway, and resveratrol may have therapeutic potential for patients with fibrotic kidney diseases.
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Reversion of trichostatin A resistance via inhibition of the Wnt signaling pathway in human pancreatic cancer cells.
Oncol. Rep.
PUBLISHED: 06-16-2014
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Drug resistance is a major impediment to successful chemotherapy in pancreatic cancer (PC) patients. We investigated the effect of Wnt/?-catenin signaling inhibition by wnt-c59 on chemoresistance in a trichostatin A-resistant Panc-1 cell line (Panc-1/TSA). Panc-1/TSA cells were treated with the Wnt/??catenin signaling inhibitor wnt-c59 (10 µmol?·?l-1) and/or trichostatin A (TSA; 10 µmol?·?l-1) for 24 h. CCK-8 assay was utilized to analyze the interactive effect of TSA and wnt-c59 on induction of apoptosis of the Panc-1/TSA cells. Cell apoptosis was measured by flow cytometry. Real-time PCR and western blotting were used to assess Wnt/?-catenin signaling, epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). Real-time cell analysis (RTCA) was used to detect the cell migration ability. After wnt-c59 treatment for 24 h, relative genes and transcriptional targets of Wnt/?-catenin signaling were downregulated (P<0.05). CCK-8 assay indicated that the combination of TSA and wnt-c59 had a synergistic effect on induction of Panc-1/TSA cell apoptosis. As detected by FACS, cell apoptosis rates increased significantly (P<0.05). The results of RTCA showed that the cell indices of the control group, wnt-c59 group, TSA group and TSA+wnt-c59 combination group were 1.2842±0.0257, 1.2155±0.0282, 1.2533±0.0194 and 0.8541±0.0250, respectively. In accordance, MMP-9 protein in the wnt-c59 treatment groups was decreased compared to the non-wnt-c59 treatment groups. Meanwhile, E-cadherin protein was upregulated and vimentin protein was downregulated, both of which are characteristic markers of EMT. Chemoresistant gene MDR1 and P-glycoprotein (P-gp) in the wnt-c59 treatment groups had a reduced expression compared to the non-wnt-c59 treatment groups. This study revealed that TSA sensitivity, migration ability, and the EMT phenotype in Panc-1/TSA cells were reversed following Wnt/?-catenin signaling inhibition.
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Investigation of the epidermal growth factor receptor mutation rate in non-small cell lung cancer patients and the analysis of associated risk factors using logistic regression.
Oncol Lett
PUBLISHED: 04-30-2014
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The aim of the present study was to investigate the mutation rate of the epidermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC) patients and to apply logistic regression analysis to investigate the factors associated with EGFR gene mutation to provide data for the treatment of NSCLC. Paraffin tissue, bronchoscopy or pleural effusion specimens were collected from 176 NSCLC patients following pathological diagnosis. The EGFR gene exon 19 delL747-S75linss and delL747-S752ins deletion mutations, and the exon 20 T790M and exon 21 L858R mutations were identified using amplification refractory mutation system analysis. The clinical data and laboratory results of the patients were collected, and the total mutation rate of the EGFR gene in exons 19, 20 and 21 in the 176 NSCLC patients was found to be 48.3% (85/176). In addition, the EGFR gene mutation rate in adenocarcinoma was found to be significantly higher than that in squamous cell and large cell carcinoma (?(2)=12.454; P=0.002). Furthermore, the mutation rate was found to be significantly higher in females than in males (?(2)=13.78; P=0.001). The rate of exon 19 mutation was 21.0% (37/176), whereas the rate of exon 20 T90M mutation was 1.7% (3/176) and that of exon 21 L858R mutation was 29.0% (51/176). The logistic regression analysis revealed that the female gender, adenocarcinoma, distant metastasis and chemotherapy are factors associated with EGFR gene mutation (P<0.05). The female gender resulted in an increased incidence (2.438 times that of males) of EGFR mutation. Similarly, adenocarcinoma, distant metastasis and chemotherapy exhibited an increase in EGFR mutation risk (by 2.571, 2.810 and 0.367 times, respectively). The rate of EGFR mutation was high in the NSCLC patients, predominantly in exons 21 and 19. Therefore, these factors (female gender, adenocarcinoma, distant metastasis and chemotherapy) may increase the probability of EGFR gene mutations.
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Effect of Sedum sarmentosum BUNGE extract on aristolochic acid-induced renal tubular epithelial cell injury.
J. Pharmacol. Sci.
PUBLISHED: 03-27-2014
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Aristolochic acid (AA) is known as a potent mutagen that induces significant cytotoxic and mutagenic effects on renal tubular epithelial cells. Clinically, the persistent injury of AA results in the infiltration of inflammatory cells, epithelial-to-mesenchymal transition (EMT), and renal tubulointerstitial fibrosis. There are no truly effective pharmaceuticals. In this study, we investigated the potential role of the extract of Sedum sarmentosum Bunge (SSB), a traditional Chinese herbal medicine, on rat tubuloepithelial (NRK-52E) cells after AA injury in vitro. Evidence revealed that AA induced mitochondrial-pathway-mediated cellular apoptosis, accompanied by cell proliferation in a feedback mechanism. Treatment with SSB also induced cells to enter early apoptosis, but inhibited cell proliferation. In cultured NRK-52E cells, AA induced the imbalance of MMP-2/TIMP-2 and promoted EMT and ECM accumulation. SSB treatment significantly alleviated AA-induced NRK-52E cells fibrosis-like appearance, inhibited the induction of EMT, and deposition of ECM. SSB also decreased the activity of the NF-?B signaling pathway, resulting in down-regulated expression of NF-?B-controlled chemokines and pro-inflammatory cytokines, including MCP-1, MIF, and M-CSF, which may regulate the macrophage-mediated inflammatory reaction during renal fibrosis in vivo. Therefore, these findings suggest that SSB exerts protective effects against AA-induced tubular epithelial cells injury through suppressing the synthesis of inflammatory factors, EMT, and ECM production.
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Elevated dopamine induces minimal hepatic encephalopathy by activation of astrocytic NADPH oxidase and astrocytic protein tyrosine nitration.
Int. J. Biochem. Cell Biol.
PUBLISHED: 01-20-2014
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We previously demonstrated that dopamine (DA) overload may be a key mechanism behind development of minimal hepatic encephalopathy (MHE) in rats. It has been shown that low-grade cerebral oedema and oxidative stress play important roles in the pathogenesis of MHE. In the current study, DA-triggered oxidative injury in cerebral cortex was studied.
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Sedum sarmentosum Bunge extract exerts renal anti-fibrotic effects in vivo and in vitro.
Life Sci.
PUBLISHED: 01-03-2014
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Sedum sarmentosum Bunge, a traditional Chinese herbal medicine, has a wide range of clinical effects, including anti-oxidation, anti-inflammation, and anti-cancer properties. In this study, we determined whether S. sarmentosum Bunge Extract (SSBE) has anti-fibrotic effects on renal tissues.
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Regional arterial infusion with lipoxin A4 attenuates experimental severe acute pancreatitis.
PLoS ONE
PUBLISHED: 01-01-2014
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Investigate the therapeutic effect of regional arterial infusion (RAI) with Aspirin-Triggered Lipoxin A4 (ATL) in experimental severe acute pancreatitis (SAP) in rats.
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Antitumor efficacy of ?-solanine against pancreatic cancer in vitro and in vivo.
PLoS ONE
PUBLISHED: 01-01-2014
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?-solanine, a steroidal glycoalkaloid in potato, was found to have proliferation-inhibiting and apoptosis-promoting effect on multiple cancer cells, such as clone, liver, melanoma cancer cells. However, the antitumor efficacy of ?-solanine on pancreatic cancer has not been fully evaluated. In this study, we inquired into the anti-carcinogenic effect of ?-solanine against human pancreatic cancer cells. In the present study, we investigated the anti-carcinogenic effect of ?-solanine against human pancreatic cancer cells. In vitro, ?-solanine inhibited proliferation of PANC-1, sw1990, MIA PaCa-2 cells in a dose-dependent manner, as well as cell migration and invasion with atoxic doses. The expression of MMP-2/9, extracellular inducer of matrix metalloproteinase (EMMPRIN), CD44, eNOS and E-cadherin were suppressed by ?-solanine in PANC-1 cells. Moreover, significantly decreased vascular endothelial growth factor (VEGF) expression and tube formation of endothelial cells were discerned following ?-solanine treatment. Suppressed phosphorylation of Akt, mTOR, and Stat3, and strengthen phosphorylation of ?-catenin was found, along with markedly decreased tran-nuclear of NF-?B, ?-catenin and TCF-1. Following the administration of ?-solanine (6 µg/g for 2 weeks) in xenograft model, tumor volume and weight were decreased by 61% and 43% (p<0.05) respectively, showing decreased MMP-2/9, PCNA and VEGF expression. In conclusion, ?-solanine showed beneficial effects on pancreatic cancer in vitro and in vivo, which may via suppressing the pathway proliferation, angiogenesis and metastasis.
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Lipoxin A4 attenuation of endothelial inflammation response mimicking pancreatitis-induced lung injury.
Exp. Biol. Med. (Maywood)
PUBLISHED: 09-02-2013
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Lipoxins (LXs) and their analogues are known to display potent anti-inflammatory actions. Previously, we reported that lipoxin A4 (LXA4) possessed powerful anti-inflammatory properties in acute pancreatitis in rats and that it may ameliorate the concomitant acute lung injury by reducing cytokine generation and inhibiting neutrophil activation. Considering that the vascular endothelium plays an important role during adherence, migration and activation of leukocytes, the present study was designed to investigate the effects of LXA4 on the inflammatory response induced by tumor necrosis factor ? (TNF-?) in human pulmonary microvascular endothelial cells (HPMECs) and explore the potential mechanisms involved in these processes. We found that LXA4 markedly down-regulated the expression of monocyte chemotactic protein-1 (MCP-1), E-selectin, and interleukin-6 (IL-6) mRNA, as well as intercellular adhesion molecule-1 (ICAM-1) in TNF-?-exposed HPMECs. Moreover, LXA4 inhibited the phosphorylation and nuclear translocation of nuclear factor-?B/p65 (NF-?B/p65) and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) in HPMECs following TNF-? stimulation. Heme oxygenase-1 (HO-1), a cytoprotective enzyme, was up-regulated by LXA4 in both non- and TNF-?-stimulated HPMECs. In conclusion, the protective effects of LXA4 to ALI may be executed through inhibition inflammation pathways of NF-?B and p38 MAPK and up-regulation of cytoprotective HO-1.
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Anti-fatigue effect of ginsenoside Rb1 on postoperative fatigue syndrome induced by major small intestinal resection in rat.
Biol. Pharm. Bull.
PUBLISHED: 08-06-2013
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Ginsenoside Rb1 (GRb1), one of the principle active ingredients of Panax ginseng, exerts multiple pharmacological activities to fight fatigue. In the present study, we investigate the anti-fatigue effect of GRb1 on postoperative fatigue syndrome (POFS) in a rat model induced by major small intestinal resection. GRb1 (10 mg/kg) was administrated intraperitoneally once daily for 1, 3, 7, and 10 d from the operation day. Anti-fatigue effect was assessed by grasping test and biochemical parameters in blood or skeletal muscle were determined by autoanalyzer or commercially available kits. Transmission electron microscope was applied to observe the ultra microstructure of skeletal muscles. The results revealed that GRb1 significantly enhanced rat maximum grip strength with POFS. Similarly, negative alterations in biochemical parameters (lactic acid, hepatic glycogen, muscle glycogen and malondialdehyde) of POFS rats were improved by GRb1. In addition, GRb1 also increased the activity of lactate dehydrogenase and superoxide dismutase in POFS. No significant differences of levels of blood urea nitrogen and ultra microstructure of skeletal muscles were found between the POFS and GRb1 treatment rats. The potent anti-fatigue effect of GRb1 on POFS might be achieved through improvement of energy metabolism and suppression of skeletal muscle oxidative stress.
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Curcumin up-regulates phosphatase and tensin homologue deleted on chromosome 10 through microRNA-mediated control of DNA methylation - a novel mechanism suppressing liver fibrosis.
FEBS J.
PUBLISHED: 07-24-2013
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Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) has been reported to play a role in the suppression of activated hepatic stellate cells (HSCs). Moreover, it has been demonstrated that hypermethylation of the PTEN promoter is responsible for the loss of PTEN expression during HSC activation. Methylation is now established as a fundamental regulator of gene transcription. MicroRNAs (miRNAs), which can control gene expression by binding to their target genes for degradation and/or translational repression, were found to be involved in liver fibrosis. However, the mechanism responsible for miRNA-mediated epigenetic regulation in liver fibrosis still remained unclear. In the present study, curcumin treatment significantly resulted in the inhibition of cell proliferation and an increase in the apoptosis rate through the up-regulation of PTEN associated with a decreased DNA methylation level. Only DNA methyltransferase 3b (DNMT3b) was reduced in vivo and in vitro after curcumin treatment. Further studies were performed aiming to confirm that the knockdown of DNMT3b enhanced the loss of PTEN methylation by curcumin. In addition, miR-29b was involved in the hypomethylation of PTEN by curcumin. MiR-29b not only was increased by curcumin in activated HSCs, but also was confirmed to target DNMT3b by luciferase activity assays. Curcumin-mediated PTEN up-regulation, DNMT3b down-regulation and PTEN hypomethylation were all attenuated by miR-29b inhibitor. Collectively, it is demonstrated that curcumin can up-regulate miR-29b expression, resulting in DNMT3b down-regulation in HSCs and epigenetically-regulated PTEN involved in the suppression of activated HSCs. These results indicate that miRNA-mediated epigenetic regulation may be a novel mechanism suppressing liver fibrosis.
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Association study of OPRM1 polymorphisms with Schizophrenia in Han Chinese population.
BMC Psychiatry
PUBLISHED: 03-12-2013
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The expression of ?-opioid receptor has important role in cognitive dysfunction in Schizophrenia (SZ). The results of studies about the association of polymorphisms of ?-opioid receptor gene (OPRM1) with SZ were inconsistent.
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The efficiency of continuous regional intra-arterial infusion in the treatment of infected pancreatic necrosis.
Pancreatology
PUBLISHED: 02-15-2013
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Our aim was to investigate the efficiency of continuous regional intra-arterial infusion (CRAI) with antisecretory agents and antibiotics in the treatment of infected pancreatic necrosis.
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Sirolimus damages podocytes in rats with protein overload nephropathy.
J. Nephrol.
PUBLISHED: 09-23-2011
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Conversion from calcineurin inhibitors (CNIs) to sirolimus could significantly improve long-term graft survival after kidney transplantation. Proteinuria was found in some recipients after the switch, which could be alleviated by an angiotensin II receptor blocker (ARB). But the mechanisms for this have remained unclear. In this study, we utilized a rat model with protein overload nephropathy to explore the mechanisms of sirolimus-related proteinuria.
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Glutathione S-transferases T1 null genotype is associated with susceptibility to aristolochic acid nephropathy.
Int Urol Nephrol
PUBLISHED: 04-07-2011
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This study aims to determine whether six polymorphisms of the genes involved in drug metabolism are associated with susceptibility to the development and progression of aristolochic acid nephropathy (AAN).
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Cordyceps sinensis extracts attenuate aortic transplant arteriosclerosis in rats.
J. Surg. Res.
PUBLISHED: 02-14-2011
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Transplant arteriosclerosis is a hallmark of chronic rejection and is still the major limiting factor affecting the success of long-term organ transplants. Development of transplant arteriosclerosis is refractory to conventional immunosuppressive drugs, and adequate therapy is not yet available. The aim of this study was to determine the role of Cordyceps sinensis extracts in reducing the formation of transplant arteriosclerosis in a rat aortic transplant model.
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Statistical phase-shifting step estimation algorithm based on the continuous wavelet transform for high-resolution interferometry metrology.
Appl Opt
PUBLISHED: 02-02-2011
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We propose a statistical phase-shifting estimation algorithm for temporal phase-shifting interferometry (PSI) based on the continuous wavelet transform (CWT). The proposed algorithm explores spatial information redundancy in the intraframe interferogram dataset using the phase recovery property on the power ridge of the CWT. Despite the errors introduced by the noise of the interferogram, the statistical part of the algorithm is utilized to give a sound estimation of the phase-shifting step. It also introduces the usage of directional statistics as the statistical model, which was validated, so as to offer a better estimation compared with other statistical models. The algorithm is implemented in computer codes, and the validations of the algorithm were performed on numerical simulated signals and actual phase-shifted moiré interferograms. The major advantage of the proposed algorithm is that it imposes weaker conditions on the presumptions in the temporal PSI, which, under most circumstances, requires uniform and precalibrated phase-shifting steps. Compared with other existing deterministic estimation algorithms, the proposed algorithm estimates the phase-shifting step statistically. The proposed algorithm allows the temporal PSI to operate under dynamic loading conditions and arbitrary phase steps and also without precalibration of the phase shifter. The proposed method can serve as a benchmark method for comparing the accuracy of the different phase-step estimation methods.
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The protective effects of Lipoxin A4 during the early phase of severe acute pancreatitis in rats.
Scand. J. Gastroenterol.
PUBLISHED: 10-18-2010
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Our aim was to investigate the protective effects of a Lipoxin A(4) analogue (LXA4) in the early phase of acute pancreatitis in rats.
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A canine portal hypertension model induced by intra-portal administration of Sephadex microsphere.
J. Gastroenterol. Hepatol.
PUBLISHED: 05-25-2010
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Big animal models of portal hypertension are important for the research into this disease. The aim of this study was to establish a canine portal hypertension model by intra-portal administration of microspheres.
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Blockade of gammac signals in combination with donor-specific transfusion induces cardiac allograft acceptance in murine models.
J. Huazhong Univ. Sci. Technol. Med. Sci.
PUBLISHED: 04-23-2010
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The gammac cytokines play an important role in proliferation and survival of T cells. Blocking the gammac signals can cause the activated donor-reactive T cells losing the ability to proliferate, and getting into apoptosis pathway, which contributes to induction of the peripheral tolerance. In this study, we induced the transplant tolerance through blocking the gammac in combination with donor-specific transfusion (DST) in the cardiac transplantation. Following DST, on the day 2, 4 and 6, C57BL/6 recipients received anti-gammac monoclonal antibodies (mAbs) injection, and those in control group were not given anti-gammac mAbs. On the day 7, Balb/c cardiac allografts were transplanted. All recipients in experimental group accepted cardiac allografts over 30 days, and two of them accepted allografts without rejection until sacrifice on the 120 day. Animals only receiving DST rejected grafts within 5 days, and the mice receiving cardiac transplantation alone rejected grafts within 9 days. Our study showed that blockade of gammac signaling combined with DST significantly prolonged allograft survival, which was probably associated with inhibition of antigen-specific T-cell proliferation and induction of apoptosis.
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The meta-analysis of the association of PPARG P12A, C161T polymorphism and coronary heart disease.
Wien. Klin. Wochenschr.
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Two common variations of peroxisome proliferator-activated receptor ? (PPARG), P12A (Pro12Ala, rs1801282), and C161T (His447His, rs3856806), are thought to have an effect on susceptibility to coronary heart disease (CHD), but the results are inconsistent. Therefore, a meta-analysis of published studies was performed.
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The clinical diagnostic significance of cerebrospinal fluid D-lactate for bacterial meningitis.
Clin. Chim. Acta
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To study the clinical and laboratory significance of D?lactate in the diagnosis of bacterial meningitis (BM).
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Pathogenesis of hepatic fibrosis analyzed at the proteome level.
Saudi Med J
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Proteomic technologies have provided effective approaches to the analysis of the pathogenesis of hepatic fibrosis. A large number of proteins that have been revealed by this technology play a critical role in various aspects of pathological liver fibrosis. Comprehensive evaluations of these proteins have led to the understanding that the mechanisms of hepatic fibrosis can be stratified into several broad classifications. Here, we describe the mechanisms of action that are defined as being related to 1) oxidative stress and mitochondrial damage, 2) inflammatory response and immune injury, 3) abnormal cell proliferation and apoptosis, 4) abnormal metabolism, 5) abnormal cellular signal transduction, and 6) abnormal extracellular matrix metabolism.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.