Infection within 2 weeks before liver transplantation closely related to prognosis of posttransplant infection: A single-center retrospective observational study in China.

BACKGROUND: Infections still represent the main factors influencing morbidity and mortality following liver transplantation. This study aimed to evaluate the incidence and risk factors for infection and survival after liver transplantation. METHODS: We retrospectively examined medical records in 210 liver recipients who underwent liver transplantation between April 2015 and October 2017 in our hospital. Clinical manifestations and results of pathogen detection test were used to define infection. We analyzed the prevalence, risk factors and prognosis of patients with infection. RESULTS: The median follow-up was 214 days; the incidence of infection after liver transplantation was 46.7% (n = 98) which included pneumonia (43.4%), biliary tract infection (21.9%), peritonitis (21.4%) and bloodstream infection (7.6%). Among the pathogens in pneumonia, the most frequently isolated was Acinetobacter baumanii (23.5%) and Klebsiella pneumoniae (21.2%). Model for end-stage liver disease (MELD) score (OR = 1.083, 95% CI: 1.045-1.123; P < 0.001), biliary complication (OR = 4.725, 95% CI: 1.119-19.947; P = 0.035) and duration of drainage tube (OR = 1.040, 95% CI: 1.007-1.074; P = 0.017) were independent risk factors for posttransplant infection. All-cause mortality was 11.0% (n = 23). The prognostic factors for postoperative infection in liver recipients were prior-transplant infection, especially pneumonia within 2 weeks before transplantation. Kaplan-Meier curves of survival showed that recipients within 2 weeks prior infection had a significantly lower cumulative survival rate compared with those without infection (65.2% vs. 90.0%; hazard ratio: 4.480; P < 0.001). CONCLUSIONS: Infection, especially pneumonia within 2 weeks before transplantation, complication with impaired renal function and MELD score after 7 days of transplantation was an independent prognostic factor for postoperative infection in liver transplant recipients.

Rapid Detection of Nocardia by Next-Generation Sequencing.

In this original study, we retrospectively reviewed the cases of nocardiosis diagnosed through culture and next-generation sequencing (NGS) methods between 2014 and 2018 in Huashan Hospital and found out that the latter way can not only improve the detection rate of Nocardia spp. but also greatly reduce the turnaround time. In addition, by comparing nocardiosis and non-nocardiosis patients both of whose samples had Nocardia spp. detected by NGS, we found that Nocardia's specific reads ranking among top two might be a satisfactory cutoff value for clinical diagnosis of the disease. Our study introduced the promising value of the NGS method in the rapid diagnosis of nocardiosis.

Correlation of postoperative splenic volume increase with prognosis of hepatocellular carcinoma after curative hepatectomy

Background: Previous studies have reported a close connection between the spleen and hepatic tumours. We investigated the prognostic value of postoperative splenic volume increase (PSVI) in patients with hepatocellular carcinoma after curative hepatectomy. Methods: This was a retrospective study of adult patients with hepatocellular carcinoma who underwent hepatectomy between January 2007 and May 2013. We categorized patients into 2 groups according to the cut-off value of the receiver operating characteristic curve: group A (PSVI < 19.0%) and group B (PSVI ≥ 19.0%). We compared the clinicopathological data, overall survival and disease-free survival between the 2 groups. We performed univariate and multivariate analyses to identify factors associated with disease-free and overall survival. Results: There were 275 patients in group A and 196 patients in group B. The 1-, 3- and 5-year overall survival rates were 98.9%, 74.9% and 63.6%, respectively, for patients in group A, and 97.4%, 65.3% and 49.8%, respectively, for patients in group B (p = 0.004). The corresponding disease-free survival rates were 69.5%, 48.0% and 40.3%, and 58.1%, 36.5%, and 29.8% (p = 0.01). On multivariate analysis, PSVI was an independent predictor of overall (p = 0.01) and disease-free (p = 0.03) survival. Conclusion: Postoperative splenic volume increase correlates with poor prognosis of patients with hepatocellular carcinoma after curative hepatectomy.

Contexte: Des études antérieures faisaient état d'un lien étroit entre la rate et les tumeurs hépatiques. Nous avons étudié la valeur pronostique de l'augmentation postopératoire du volume de la rate (APVR) chez les patients ayant subi une hépatectomie curative en raison d'un carcinome hépatocellulaire. Méthodes: Il s'agit d'une étude rétrospective portant sur des adultes qui ont subi une hépatectomie entre janvier 2007 et mai 2013 pour cause de carcinome hépatocellulaire. Nous avons classé les patients en 2 groupes, selon un seuil sur la courbe ROC : le groupe A (APVR : < 19,0 %) et le groupe B (APVR : ≥ 19,0 %). Nous avons ensuite comparé les données clinicopathologiques, le taux de survie globale et le taux de survie sans récidive des 2 groupes, et avons effectué des analyses univariées et multivariées pour repérer les facteurs associés à la survie sans récidive et à la survie globale. Résultats: Le groupe A comptait 275 patients, tandis que le groupe B en comptait 196. Les taux de survie globale à 1 an, à 3 ans et à 5 ans étaient de 98,9 %, de 74,9 % et de 63,6 %, respectivement, dans le groupe A, et de 97,4 %, de 65,3 % et de 49,8 %, respectivement, dans le groupe B (p = 0,004). Les taux de survie sans récidive à 1 an, à 3 ans et à 5 ans étaient de 69,5 %, de 48,0 % et de 40,3 %, respectivement, dans le groupe A, et de 58,1 %, de 36,5 % et de 29,8 %, respectivement, dans le groupe B (p = 0,01). Selon l'analyse multivariée, l'APVR était un prédicteur indépendant de survie globale (p = 0,01) et de survie sans récidive (p = 0,03). Conclusion: L'augmentation postopératoire du volume de la rate est corrélée à un mauvais pronostic chez les patients ayant subi une hépatectomie curative en raison d'un carcinome hépatocellulaire.

Mechanism of CO2-formation promotion by Au in plasma-catalytic oxidation of CH4 over Au/γ-Al2O3 at room temperature.

The plasma-catalytic oxidation of methane (CH4) is a potential reaction for controlling CH4 emissions at low temperatures. However, the mechanism of the CH4 plasma-catalytic oxidation is still unknown, which inhibits the further optimization of the oxidation process. Herein, a CH4 oxidation mechanism over an Au/γ-Al2O3 catalyst was proposed based on our experimental findings. CH4 is first decomposed to CH3 and H by the discharge, and a fraction of the CH3 is adsorbed on γ-Al2O3 surface for deep oxidation. The oxygen atoms produced by the discharge react with H2O to yield surface reactive OH groups that contribute to the CH3 oxidation. Oxygen atoms also promote the release of H2O from the surfaces of the γ-Al2O3 and Au/γ-Al2O3 and especially promote CO2 desorption from the surface of the Au/γ-Al2O3. When γ-Al2O3 was used as the catalyst, the CO2 selectivity was only 15 vol.%, and the CH4 conversion decreased after 7 h of plasma-catalytic oxidation. In contrast, when Au/γ-Al2O3 was used, the CO2 selectivity was 80 vol.%, long-term CH4 conversion was obtained. Experimental results revealed that Au was beneficial for the decomposition of surface carbonate species into gaseous CO2, whereas the carbonate species accumulated on γ-Al2O3 when Au was absent.

Up-regulation of microRNA-497 inhibits the proliferation, migration and invasion but increases the apoptosis of multiple myeloma cells through the MAPK/ERK signaling pathway by targeting Raf-1.

Multiple myeloma (MM) is a cancer that occurs in plasma cells, which fall under the category of white blood cells that are in charge of antibody production. According to previous studies, microRNA-497 (miR-497) functions as a tumor suppressor in several types of cancer, including gastric cancer and colorectal cancer. Therefore, the present study aims to investigate the effects of miR-497 on cellular function of human MM cells through the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway by targeting Raf-1. The differentially expressed genes and miRs in MM, and the relationship between the miR and gene were verified. It was found that Raf-1 was a target gene of miR-497. The data obtained from MM tissues showed increased Raf-1 level and decreased miR-497 level. MM cells were treated with mimic, inhibitor and siRNA in order to evaluate the role of miR-497, Raf-1 and MAPK/ERK in MM. The expression pattern of miR-497, Raf-1, ERK1/2, survivin, B-cell lymphoma-2 (Bcl-2) and BCL2-Associated X (Bax) as well as the extent of ERK1/2 phosphorylation were determined. Retored miR-497 and si-Raf-1 resulted in increases in the Bax expression and cell apoptosis and decreases in the expressions of Raf-1, MEK-2, survivin, Bcl-2, along with the extent of ERK1/2 phosphorylation. In addition, the biological function evaluations of MM cells revealed that miR-497 mimic or si-Raf-1 led to suppression in cell proliferation, invasion and migration. In conclusion, our results have demonstrated that miR-497 targets Raf-1 in order to inhibit the progression of MM by blocking the MAPK/ERK signaling pathway.

THR1 mediates GCN4 and CDC4 to link morphogenesis with nutrient sensing and the stress response in Candida albicans.

Candida albicans (C. albicans) CDC4 (CaCDC4), encoding the F­box protein for the substrate specificity of the Skp1­cullin­F­box E3 ubiquitin ligase complex, suppresses the yeast­to­filament transition in C. albicans. In our previous study, Thr1 was identified as a CaCdc4­associated protein using affinity purification. THR1 encodes a homoserine kinase, which is involved in the threonine biosynthesis pathway. The present study generated a strain with repressible CaCDC4 expression and continuous THR1 expression. Colony and cell morphology analyses, as well as immunoblotting, revealed that the Thr1 protein was detectable under conditions in which the expression of CaCDC4 was repressed and that the filaments resulting from the repressed expression of CaCDC4 were suppressed by the constitutive expression of THR1 in C. albicans. Additionally, by using the CaSAT1­flipper method, the present study produced null mutants of THR1, GCN4, and CaCDC4. The phenotypic consequences were evaluated by growth curves, spotting assays, microscopic analysis, reverse transcription­polymerase chain reaction and XTT­based biofilm formation ability. The results revealed that fewer cells lacking THR1 entered the stationary phase but had no apparent morphological alteration. It was observed that the expression of THR1 was upregulated concurrently with GCN4 during nutrient depletion and that cells lacking GCN4 rescued the lethality of cells in the absence of THR1 in conditions accumulating homoserine in the threonine biosynthesis pathway. Of note, it was found that cells with either CaCDC4 or THR1 loss were sensitive to oxidative stress and osmotic stress, with those with THR1 loss being more sensitive. In addition, it was observed that cells with loss of either CaCDC4 or THR1 exhibited the ability to increase biofilm formation, with those lacking CaCDC4 exhibiting a greater extent of enhancement. It was concluded that CaCDC4 is important in the coordination of morphogenesis, nutrient sensing, and the stress response through THR1 in C. albicans.

First human infection by a novel avian influenza A(H7N4) virus.

Multiple reassortant strains of novel, highly pathogenic avian influenza A have recently emerged and spread over the world. Here we report on a 68-year-old woman in Jiangsu, China, with influenza A(H7N4) infection and associated illness, which strongly demonstrating the ability of the virus to spread from animals to humans and thus emphasizing the importance of continuous surveillance of the emerging viruses.

Human Endophthalmitis Caused By Pseudorabies Virus Infection, China, 2017.

We report human endophthalmitis caused by pseudorabies virus infection after exposure to sewage on a hog farm in China. High-throughput sequencing and real-time PCR of vitreous humor showed pseudorabies virus sequences. This case showed that pseudorabies virus might infect humans after direct contact with contaminants.

Epidemiological features of lung giant cell carcinoma and therapy for patients with EGFR mutations based on case reports and the surveillance, epidemiology, and end results (SEER) database.

Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are the standard first line treatment for advanced non-small cell lung cancer (NSCLC) with sensitive EGFR mutations. Among NSCLC, giant cell carcinoma of the lung (GCCL) is a rare pathological subtype with poor prognosis, with no confirmed evidence about its epidemiological features or therapeutic efficiency of EGFR-TKIs. We present two advanced GCCLs with sensitive EGFR mutations, also collected the cases of GCCL from our hospital and the Surveillance, Epidemiology, and End Results (SEER) program. Kaplan-Meier methods and Cox proportional hazards modeling were used to perform the survival analyses. Both two cases of advanced GCCL with sensitive EGFR mutations benefited from EGFR-TKIs. Twelve GCCLs were recorded in our hospital from May 2006 to July 2015. GCCL is associated with males (83.3%) and smoking status (63.6%). The EGFR mutation rate was 40.0%. In SEER database, the total number of GCCLs was 184, 0.11% for all NSCLCs. In Kaplan-Meier analysis, the 5-year overall survival of GCCL patients was significantly lower than that of non-GCC NSCLC (16% and 19%; P<0.001), and it was confirmed in multivariate analysis. Further survival analyses indicated that male were more susceptible to GCCL and GCCL was prone to metastasize. Only age and M stage were independent prognostic factors for GCCL in the multivariate analysis. In conclusion, GCCL was an unfavorable prognostic factor and associated with males and metastasis. GCCL patients with sensitive EGFR mutations may also benefit from EGFR-TKI, we therefore recommend the evaluation of EGFR in the treatment of advanced GCCL.

Effects of Duodenal-Jejunal Exclusion and New Bilio-Pancreatic Diversion on Blood Glucose in Rats with Type 2 Diabetes Mellitus.

OBJECTIVE: The current study aimed to investigate the effects of duodenal-jejunal bypass (DJB), new bilio-pancreatic diversion (NBPD), and duodenal-jejunal exclusion (DJE) on blood glucose in rats with type 2 diabetes mellitus (T2DM). METHODS: Male Sprague Dawley rats were fed with high glucose, high fat food, and intraperitoneally injected with streptozotocin to establish a T2DM animal model. T2DM rats were randomly assigned into 4 groups: a sham group (n = 8), DJB group (n = 9), NBPD group (n = 10), and DJE group (n = 10). Body weight, 2-h postprandial glucose, oral glucose tolerance, fasting serum bile acid, 2-h postprandial serum bile acid, fasting insulin, 2-h postprandial insulin (INS), fasting glucagon-like peptide-1 (GLP-1), and 2-h postprandial GLP-1 were measured before and after surgery. RESULTS: Six weeks after surgery, the 2-h postprandial glucose in the DJB (16.1 ± 6.7 mmol/L) and NBPD (19.5 ± 5.7 mmol/L) groups decreased significantly compared to the sham group (25.8 ± 4.9 mmol/L) (P < 0.05). There was no significant difference between the DJE (25.0 ± 5.0 mmol/L) and sham groups (P > 0.05). Four weeks after surgery, fasting serum bile acid in the DJB group (60.6 ± 11.4 µmol/L) and NBPD group (54.4 ± 7.64 µmol/L) was significantly higher than that in the sham group (34.3 ± 6.98 µmol/L; P < 0.05). However, fasting GLP-1, 2-h postprandial GLP-1, and insulin remained unchanged at different time points after surgery (P > 0.05). Body weight remained stable after surgery in all 4 groups (P > 0.05). CONCLUSION: NBPD plays a major role in the therapy of T2DM with DJB. NBPD may significantly increase fasting serum bile acid in T2DM rats, an action that may be one of the mechanisms underlying the therapeutic effects of DJB on T2DM.

Bisphenol A Increases the Migration and Invasion of Triple-Negative Breast Cancer Cells via Oestrogen-related Receptor Gamma.

Triple-negative breast cancer (TNBC) is characterized by great metastasis and invasion capability. Our study revealed that nanomolar bisphenol A (BPA), one of the most ubiquitous endocrine disruptors, can increase wound closure and invasion of both MDA-MB-231 and BT-549 cells. BPA treatment can increase protein and mRNA expression of matrix metalloproteinase-2 (MMP-2) and MMP-9, while had no effect on the expression of vimentin (Vim) and fibronectin (FN) in TNBC cells. The expression of G-protein-coupled receptor (GPER), which has been suggested to mediate rapid oestrogenic signals, was not varied in BPA-treated MDA-MB-231 and BT-549 cells. Its inhibitor G15 also had no effect on BPA-induced MMPs expression and cell invasion. Interestingly, BPA treatment can significantly increase the mRNA and protein expressions of oestrogen-related receptor γ (ERRγ), but not ERRα or ERRß, in both MDA-MB-231 and BT-549 cells. The knock-down of ERRγ can markedly attenuate BPA-induced expression of MMP-2 and MMP-9 in TNBC cells. BPA treatment can activate both ERK1/2 and Akt in TNBC cells. Both inhibitors of ERK1/2 (PD98059) and Akt (LY294002) can attenuate BPA-induced ERRγ expression and cell invasion of MDA-MB-231 cells. Collectively, our data revealed that BPA can increase the expression of MMPs and in vitro motility of TNBC cells via ERRγ. Both activation of ERK1/2 and Akt participated in this process. Our study suggests that more attention should be paid to the roles of xenoestrogens such as BPA in the development and progression of TNBC.

Metachronous Primary Adenocarcinoma of Lung During Adjuvant Imatinib Mesylate Therapy for Gastrointestinal Stromal Tumor of Stomach: A Case Report.

Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor in gastrointestinal tracts; however, the synchronous or metachronous coexistence of GIST with additional primary malignancy is not common.Here, we present an unusual case of gastric GIST with metachronous primary lung adenocarcinoma diagnosed during his adjuvant treatment with oral receptor tyrosine kinase inhibitor imatinib mesylate (400 mg daily). After 6-month use of imatinib, the patient suffered from dry cough and dyspnea. Subsequent lung biopsy demonstrated adenocarcinoma with diffuse interstitial changes.Our research emphasizes the possibility of an additional primary tumor with GIST, and reminds the clinicians to strengthen the surveillance of the additional cancer during the follow-up of GIST patients.

[Heavy metal pollution characteristics and ecological risk analysis for soil around Haining electroplating industrial park].

The pollution status and potential ecological risks of heavy metal in soils around Haining electroplating industrial park were studied. Hakanson index approach was used to assess the ecological hazards of heavy metals in soils. Results showed that average concentrations of six heavy metals (Cu, Ni, Pb, Zn, Cd and Cr) in the soils were lower than the secondary criteria of environmental quality standard for soils, indicating limited harmful effects on the plants and the environment in general. Though the average soil concentrations were low, heavy metal concentrations in six sampling points located at the side of road still exceeded the criteria, with excessive rate of 13%. Statistic analysis showed that concentrations of Cu and Cd in roadside soils were significantly higher than those in non-roadside soils, indicating that the excessive heavy metal accumulations in the soil closely related with traffic transport. The average potential ecological hazard index of soils around Haining electroplating industrial park was 46.6, suggesting a slightly ecological harm. However, the potential ecological hazard index of soils with excessive heavy metals was 220-278, suggesting the medium ecological hazards. Cd was the most seriously ecological hazard factor.

Critical appraisal of the role of gefitinib in the management of locally advanced or metastatic non-small cell lung cancer.

Past studies have demonstrated that epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors can significantly improve clinical outcomes in patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) and sensitive EGFR gene mutations. Gefitinib (Iressa(®)), the first oral EGFR tyrosine kinase inhibitor, has been shown to be more effective and better tolerated than chemotherapy either in first-line or second-line treatment for patients with advanced NSCLC harboring sensitive EGFR mutations. Conversely, among patients with wild-type EGFR, gefitinib is inferior to standard chemotherapy in both the first-line and second-line settings. Further, gefitinib is effective in patients with brain metastases because of its low molecular weight and excellent penetration of the blood-brain barrier. In this review, we summarize the current data from clinical trials with gefitinib and appraise its role in the management of locally advanced or metastatic NSCLC.

Effects of modified biliopancreatic diversion on glucose tolerance of GK rats.

BACKGROUND: The purpose of this study was to investigate the hypoglycemic effect of new biliopancreatic diversion and duodenal-jejunal bypass in Goto-Kakizaki rats and observe effects of the new surgical procedure on the glucose tolerance of GK rats. METHODS: Twenty-four 10-week-old rats (SPF grade) were randomly divided into groups A, B, and C, each with eight rats. Group A underwent duodenal-jejunal bypass, group B underwent modified biliopancreatic diversion, and group C underwent a sham operation. Median rat body weight, fasting blood glucose, OGTT, and blood lipids were measured in fasting 1 week before surgery and 1, 2, 4, and 8 weeks after surgery. Changes in gastric inhibitory polypeptide, glucagon P-like peptide-1, and insulin levels were measured by ELISA 1 week before surgery and 8 weeks after surgery. RESULTS: Rats' mean body weight in groups A and B decreased significantly from 368.025 ± 11.726 and 373.100 ± 9.859 g preoperatively to 345.750 ± 11.403 and 343.260 ± 12.399 g at the early postoperative stage (P < 0.05), and with statistically significant differences compared to the weight of rats in group C (P < 0.05). Comparisons between fasting blood glucose before surgery and 8 weeks after surgery revealed no significant differences between all three groups (P > 0.05). Glucose tolerance in groups A and B decreased from preoperative 21.175 ± 3.684 and 20.820 ± 1.671 mmol/L to postoperative 8.950 ± 0.580 and 10.500 ± 1.509 mmol/L, and both were better than that of group C (P < 0.001). CONCLUSIONS: Both new biliopancreatic diversion and duodenal-jejunal bypass improve glucose tolerance of Goto-Kakizaki rats.

[Effect of Aloe emodin on invasion and metastasis of high metastatic breast cancer MDA-MB-231 cells].

OBJECTIVE: To investigate the effect of Aloe emodin (AE) on the invasive and metastatic abilities of human high metastatic breast cancer MDA-MB-231 cells. METHODS: MTT assay was used to evaluate the viability of MDA-MB-231 cells after treated with AE for 6 h and 24 h. The adhesive potential of MDA-MB-231 cells to FN and LN was tested by cell-matrix adhesion assay. The effect of AE on invasion of MDA-MB-231 cells was measured by Transwell chamber assay. Scratch wound healing assay was applied to determine the effect on migration of MDA-MB-231 cells. The effect of AE on MDA-MB-231 lung metastasis was determined on an experimental metastatic model. RESULTS: 80 micromol/L AE significantly inhibited the invasion, adhesion to FN, LN of MDA-MB-231 cells in vitro, the inhibitory rates were (52.98 +/- 5.46)%, (34.99 +/- 2.63)%, (28.73 +/- 7.00)%, respectively. After 24 h treatment, AE significantly inhibited the migration of MDA-MB-231 cells. The number and volume of lung metastatic nodules formed by MDA-MB-231 cells after 80 micromol/L AE 24 h treatment were decreased compared with control group. CONCLUSION: AE can suppress the metastasis of MDA-MB-231 cells. Their mechanisms may be related to the inhibition of the capabilities of invasion and migration of MDA-MB-231 cells.

Reactive oxygen species are the cause of the enhanced cardiorespiratory response induced by intermittent hypoxia in conscious rats.

This study was carried out to investigate the role of reactive oxygen species (ROS) in the elevation of cardiorespiratory responses during the development of intermittent hypoxia (IH)-induced hypertension. Rats were exposed to either 30 days of IH [(30s N2)+(45 s room air (RA)] or RA for 6 h/day. After 5 days of exposure, stable mean arterial pressure, normalized low-frequency power of pulses interval spectrogram (a marker of cardiac sympathetic outflow), and minute ventilation (an index for arterial chemoreflex activation) were significantly increased throughout the observation period in IH-exposed rats, but not in RA-exposed rats. FosB expression in rostral ventrolateral medulla was elevated after IH exposure for 5 days. Intraperitoneal injection of MnTMPyP (a superoxide scavenger) or N-acetylcysteine (an antioxidant) prevented IH-induced elevation of the cardiorespiratory responses and lipid peroxidation of lung tissues. These results suggest that ROS are essential for IH-induced elevation of arterial chemoreflex activation and sympathetic outflow, which may, in turn, contribute to IH-induced hypertension.

Effects of 5-hydroxytamine and its antagonists on hepatic stellate cells.

BACKGROUND: Hepatic stellate cell (HSC) plays a key role in hepatic fibrosis. This study was undertaken to investigate the expression of 5-hydroxytamine receptors in HSC and the effect of 5-hydroxytamine on biological characteristics of HSC. METHODS: Liver ex vivo perfusion of collagenase and density gradient centrifugation were used to isolate HSCs. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of 5-hydroxytamine receptor subtypes 1A, 2A, 2B and 3. Western blot hybridization was used to elucidate the effect of 5-hydroxytamine and its 2A receptor antagonist ketanserin and 3 receptor antagonist ondanosetron on the expression of transforming growth factor-beta1 (TGF-beta1) and Smad4 in HSC. RESULTS: HSC expressed 5-hydroxytamine receptor subtypes 1A, 2A and 2B. 5-hydroxytamine significantly increased the expression of TGF-beta1 and Smad4 in HSC (P<0.05). This action can be antagonized by ketanserin, not by ondanosetron. CONCLUSIONS: HSC expresses 5-hydroxytamine receptors. 5-Hydroxytamine could effect the biological characteristics of HSC through its receptor mediation, and may play a role in the pathogenesis of liver cirrhosis and portal hypertension.