Dietary risk factors for inflammatory bowel disease in Shanghai: A case-control study.

BACKGROUND AND OBJECTIVES: Inflammatory bowel disease (IBD) is a multifactorial condition involving the complex interplay of genomics, microbiota, immunology, environment, and personal behaviors, particularly diet. METHODS AND STUDY DESIGN: A case-control study in a tertiary referral hospital. Fifty patients with IBD and 50 controls without gastrointestinal diseases were enrolled consecutively from October 1, 2016, to December 31, 2017. Sociodemographic and Food Frequency Questionnaires (FFQs) were completed, and dietary risk factors for IBD were identified. RESULTS: Six major foods were associated with the recurrent incidence of IBD (p<0.05): chili, fish, milk, nuts, eggs, and fruit. Logistic regression analysis revealed that eating chili and drinking milk more than three times weekly increased the risk of relapse, as did eating fish and nuts one or two times weekly. Eating fruit more than once weekly reduced the risk of IBD. Fish, seafood, vegetables, nuts, beef, and fruit, along with a history of food allergy, were associated with a high risk of clinically recurrent IBD. Dietary patterns featuring seafood and nuts also increased the risk of relapse. CONCLUSIONS: The consumption of chili, milk, fish, and nuts beyond moderate weekly frequencies increased the risk of IBD, whereas fruit consumption was consistently protective against IBD development. Relapse susceptibility was also associated with a history of food allergy. Thus, IBD risk management can involve more personalized and less restrictive dietary patterns, as well as the enforcement of weekly dose thresholds. Uncertainty remains regarding association differentials between ulcerative colitis (UC) and Crohn's disease (CD).

Pterostilbene pre-treatment reduces LPS-induced acute lung injury through activating NR4A1.

CONTEXT: Pterostilbene (PTE), a common polyphenol compound, exerts an anti-inflammatory effect in many diseases, including acute lung injury (ALI). OBJECTIVE: This study explores the potential mechanism of PTE pre-treatment against lipopolysaccharide (LPS)-induced ALI. MATERIALS AND METHODS: Sixty Sprague-Dawley rats were divided into control, ALI, 10 mg/kg PTE + LPS, 20 mg/kg PTE + LPS, and 40 mg/kg PTE + LPS groups. At 24 h before LPS instillation, PTE was administered orally. At 2 h before LPS instillation, PTE was again administered orally. After 24 h of LPS treatment, the rats were euthanized. The levels of inflammatory cells and inflammatory factors in the bronchoalveolar lavage fluid (BALF), the expression of nuclear receptor subfamily 4 group A member 1 (NR4A1), and the nuclear factor (NF)-κB pathway-related protein levels were detected. NR4A1 agonist was used to further investigate the mechanism of PTE pre-treatment. RESULTS: After PTE pre-treatment, the LPS induced inflammation was controlled and the survival rate was increased to 100% from 70% after LPS treatment 24 h. For lung injury score, it decreased to 1.5 from 3.5 after treating 40 mg/kg PTE. Compared with the control group, the expression of NR4A1 in the ALI group was decreased by 20-40%. However, the 40 mg/kg PTE pre-treatment increased the NR4A1 expression by 20-40% in the lung tissue. The results obtained with pre-treatment NR4A1 agonist were similar to those obtained by pre-treatment 40 mg/kg PTE. CONCLUSIONS: PTE pre-treatment might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS.

Design, synthesis and mechanistic studies of a TICT based fluorogenic probe for lighting up protein HSA.

Human serum albumin (HSA) in blood serves as an important biomarker for clinical diagnosis, and fluorescence sensing method has attracted extensive attention. In this work, a small organic molecule probe, YS8, involving twisted intramolecular charge transfer (TICT) characteristic, was designed and investigated to detect HSA. YS8 kept silent state in fluorescence under physiological conditions, but the encapsulation of YS8 in the hydrophobic subdomain IB region of HSA inhibited the TICT state and produced a clear light-up fluorescent signal. Especially, YS8 was demonstrated to be an efficient fluorogenic probe to discriminate HSA from other proteins including the bovine serum albumin (BSA). Moreover, YS8/HSA complex could be applied in fluorescence imaging in living cells and is also useful in the study of artificial fluorescent protein (AFP).

20(S)-Protopanaxadiol-Induced Apoptosis in MCF-7 Breast Cancer Cell Line through the Inhibition of PI3K/AKT/mTOR Signaling Pathway.

20(S)-Protopanaxadiol (PPD) is one of the major active metabolites of ginseng. It has been reported that 20(S)-PPD shows a broad spectrum of antitumor effects. Our research study aims were to investigate whether apoptosis of human breast cancer MCF-7 cells could be induced by 20(S)-PPD by targeting the Phosphatidylinositol 3-kinase/Protein kinase B/Mammalian target of rapamycin (PI3K/AKT/mTOR) signal pathway in vitro and in vivo. Cell cycle analysis was performed by Propidium Iodide (PI) staining. To overexpress and knock down the expression of mTOR, pcDNA3.1-mTOR and mTOR small interfering RNA (siRNA) transient transfection assays were used, respectively. Cell viability and apoptosis were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)-test and Annexin V /PI double-staining after transfection. The antitumor effect in vivo was determined by the nude mice xenograft assay. After 24 h of incubation, treatment with 20(S)-PPD could upregulate phosphorylated-Phosphatase and tensin homologue deleted on chromosome 10 (p-PTEN) expression and downregulate PI3K/AKT/mTOR-pathway protein expression. Moreover, G0/G1 cell cycle arrest in MCF-7 cells could be induced by 20(S)-PPD treatment at high concentrations. Furthermore, overexpression or knockdown of mTOR could inhibit or promote the apoptotic effects of 20(S)-PPD. In addition, tumor volumes were partially reduced by 20(S)-PPD at 100 mg/kg in a MCF-7 xenograft model. Immunohistochemical staining indicated a close relationship between the inhibition of tumor growth and the PI3K/AKT/mTOR signal pathway. PI3K/AKT/mTOR pathway-mediated apoptosis may be one of the potential mechanisms of 20(S)-PPD treatment.

[Effect of PEG-6000 Simulation Drought Stress on Physiological Characteristics of Guangfeng Medicinal Yam Plantlets].

Objective: In order to provide the theoretical basis for the Guangfeng medicinal yam( Dioscorea opposita) in field transplanting, the effect of PEG-6000 simulation drought stress on physiological characteristics of Guangfeng medicinal yam plantlets was studied. Methods: Using the method of spectrophotometer,the content of total chlorophyll,soluble total sugar, soluble protein and praline,as well as the activities of SOD,CAT and POD of Guangfeng medicinal yam plantlets were tested under PEG-6000 treatment. Results: Under PEG-6000 simulated drought stress, with the increasing of drought stress and the extension of stress time, the total chlorophyll content of Guangfeng medicinal yam plantlets continued to decline, the content of total soluble sugar, proline and MDA of Guangfeng medicinal yam plantlets significantly increased, the content of soluble protein and the activities of CAT,POD and SOD of Guangfeng medicinal yam plantlets increased at first and then decreased. Conclusion: This study reveals the changes of physiological indices of Guangfeng medicinal yam plantlets under PEG-6000 simulation drought stress, which indicated that Guangfeng medicinal yam plantlets have certain drought tolerance.

Triptolide induces apoptosis and inhibits the growth and angiogenesis of human pancreatic cancer cells by downregulating COX-2 and VEGF.

Triptolide (TPL) inhibits the growth and proliferation of a wide range of human cancer cells, but the underlying mechanism is largely unknown. Here, we report that TPL induces apoptosis and inhibits proliferation of PANC-1 pancreatic cancer cells by downregulating cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF). Cell viability and apoptosis were measured by MTT assay and flow cytometry. Real-time PCR and Western blot were used to examine the expression of COX-2 and VEGF. The Matrigel angiogenesis and Transwell migration were employed to assess tube formation and cell migration. Pancreatic cancer mouse xenografts were established to investigate the in vivo antitumor effects of TPL. TUNEL staining and immunohistochemistry were used to detect the apoptosis rate and protein expression in tumor tissues. TPL inhibited the proliferation of pancreatic cancer cells in a time and concentration-dependent manner and decreased the expression of COX-2 and VEGF in vitro. Furthermore, medium from TPL-treated PANC-1 cells inhibited the proliferation, migration, and tube formation of HUVECs. TPL significantly reduced the growth of pancreatic cancer mouse xenografts, accompanied by an induction of apoptosis, inhibition of angiogenesis, and reduction of COX-2 and VEGF. Our data indicate that suppressing the expression of COX-2 and VEGF may be one of the molecular mechanisms by which TPL induces apoptosis and inhibits the growth and angiogenesis of human pancreatic cancer cells.

Safety and feasibility of modified duct-to-mucosa pancreaticojejunostomy during pancreatoduodenectomy: A retrospective cohort study.

BACKGROUND: Pancreatoduodenectomy (PD) is the most effective surgical procedure to remove a pancreatic tumor, but the prevalent postoperative complications, including postoperative pancreatic fistula (POPF), can be life-threatening. Thus far, there is no consensus about the prevention of POPF. AIM: To determine possible prognostic factors and investigate the clinical effects of modified duct-to-mucosa pancreaticojejunostomy (PJ) on POPF development. METHODS: We retrospectively collected and analyzed the data of 215 patients who underwent PD between January 2017 and February 2022 in our surgery center. The risk factors for POPF were analyzed by univariate analysis and multivariate logistic regression analysis. Then, we stratified patients by anastomotic technique (end-to-side invagination PJ vs modified duct-to-mucosa PJ) to conduct a comparative study. RESULTS: A total of 108 patients received traditional end-to-side invagination PJ, and 107 received modified duct-to-mucosa PJ. Overall, 58.6% of patients had various complications, and 0.9% of patients died after PD. Univariate and multivariate logistic regression analyses showed that anastomotic approaches, main pancreatic duct (MPD) diameter and pancreatic texture were significantly associated with the incidence of POPF. Additionally, the POPF incidence and operation time in patients receiving modified duct-to-mucosa PJ were 11.2% and 283.4 min, respectively, which were significantly lower than those in patients receiving traditional end-to-side invagination PJ (27.8% and 333.2 minutes). CONCLUSION: Anastomotic approach, MPD diameter and pancreatic texture are major risk factors for POPF development. Compared with traditional end-to-side invagination PJ, modified duct-to-mucosa PJ is a simpler and more efficient technique that results in a lower incidence of POPF. Further studies are needed to validate our findings and explore the clinical applicability of our technique for laparoscopic and robotic PD.

A novel pathogenic splicing mutation of RPGR in a Chinese family with X-linked retinitis pigmentosa verified by minigene splicing assay.

AIM: To report a novel splicing mutation in the RPGR gene (encoding retinitis pigmentosa GTPase regulator) in a three-generation Chinese family with X-linked retinitis pigmentosa (XLRP). METHODS: Comprehensive ophthalmic examinations including best corrected visual acuity, fundus photography, vision field, and pattern-visual evoked potential were performed to identify the disease phenotype of a six-year-old boy from the family (proband). Genomic DNA was extracted from peripheral blood of five available members of the pedigree. Whole-exome sequencing (WES), Sanger sequencing, and pSPL3-based exon trapping were used to investigate the aberrant splicing of RPGR. Human Splice Finder v3.1 and NNSPLICE v0.9 were used for in silico prediction of splice site variants. RESULTS: The proband was diagnosed as having retinitis pigmentosa (RP). He had severe symptoms with early onset. A novel splicing mutation, c.619+1G>C in RPGR was identified in the proband by WES and in four family members by Sanger sequencing. Minigene splicing assays verified that c.619+1G>C in RPGR would result in the formation of a damaging alternative transcript in which the last 91 bp of exon 6 were skipped, leading to the subsequent deletion of 623 correct amino acids (c.529_619del p.Val177Glnfs*16). CONCLUSION: We identify a novel splice donor site mutation causing aberrant splicing of RPGR. Our findings add to the catalog of pathological mutations of RPGR and further emphasize the functional importance of RPGR in RP pathogenesis and its complex clinical phenotypes.

2-Chloro-4-(3,3-dichloro-all-yloxy)-1-nitro-benzene.

In the crystal structure of the title compound, C(9)H(6)Cl(3)NO(3), mol-ecules are connected by C-H⋯O hydrogen bonds, forming chains along the b axis. The dihedral angle between the benzene ring and the plane of the nitro group is 16.2 (1)° and that between the benzene ring and the plane of the dichloro-allyl group is 10.2 (1)°.

[Clinical and medication characteristics of senior hospitalized patients with chronic constipation].

OBJECTIVE: To analyze the clinical features, risk factors and drug uses of senior hospitalized patients with chronic constipation. METHODS: A total of 162 hospitalized patients aged 85 years and over at our hospital during the period of January-March 2012 conducted a questionnaire survey. There were 137 males and 25 females. And 112 cases of chronic constipation were diagnosed in accordance with the Rome III criteria. The survey included general condition, risk factors of constipation, spectrum of symptoms, associated symptoms, previous medication and medication for constipation after admission. The results were statistically analyzed by Logistic regression. RESULTS: Their average age was (90 ± 4) years old. And the total prevalence of chronic constipation was 69.1% (112/162). Logistic regression analysis showed that less activity (OR = 10.873) and diet (OR = 4.752) were the important risk factors. Defecation effort was the most common symptom (n = 85, 75.9%). A total of 88 cases (78.6%) took lactulose alone or lactulose plus other laxatives. The reasons of using lactulose were as follows: dietary restrictions (n = 31, 35.2%), aspiration prevention (n = 21, 23.9%) and poor efficacy of other laxatives (n = 36, 40.9%). CONCLUSIONS: Prevalence of constipation is high among senior hospitalized patients. Less activity and diet are the main risk factors. And lactulose should be a first-line therapy.

Hyperlipidemic versus healthy pancreases: a proteomic analysis using an animal model.

Hyperlipidemia is associated with a variety of pancreatic diseases; however, the underlying pathophysiology and molecular mechanisms remain undefined. Here, we performed a comparative proteomic analysis of pancreatic tissue obtained from hyperlipidemic rats to identify proteins that may be involved in mediating hyperlipidemia-associated pancreatic injury. Rats were fed a high-fat diet to induce hyperlipidemia. Control rats were fed a diet with normal fat content. Pancreatic tissue samples were obtained after 6 or 12 weeks and comparative proteomic analysis, using gel electrophoresis and mass spectrometry, was conducted to identify proteins, the expression of which were altered in pancreases from hyperlipidemic compared with control rat pancreases. The expression levels of 3 of 13 proteins were significantly altered in pancreatic samples from hyperlipidemic rats. Alpha-amylase and arginase II were dysregulated by more than twofold. These modulations persisted in pancreatic tissue obtained from late-stage hyperlipidemic rats. The levels of alpha-amylase and arginase II were significantly altered in pancreases obtained from rats with hyperlipidemia. These enzymes may be putative biomarkers of hyperlipidemia-mediated pancreatic injury.

Meta-analysis: the effect of supplementation with lactoferrin on eradication rates and adverse events during Helicobacter pylori eradication therapy.

BACKGROUND: Recent evidence shown that lactoferrin could exert an antimicrobial effect against Helicobacter pylori both in vitro and in vivo models. To systematically evaluate whether adding lactoferrin to H. pylori eradication regimens could improve eradication rates and reduce side-effects during anti-H. pylori treatment. MATERIALS AND METHODS: Eligible articles were identified by searches of electronic databases. We included all randomized trials comparing lactoferrin supplementation to placebo or no treatment during anti-H. pylori regimens. Statistical analysis was performed with Review Manager 5.0.10. Subanalysis/Sensitivity analysis was also performed. RESULTS: We identified nine randomized trials (n = 1343). Pooled H. pylori eradication rates were 86.57% (95% confidence interval (CI) = 83.99-89.15%) and 74.44% (95% CI = 71.14-77.74%) for patients with or without lactoferrin by intention-to-treat analysis, respectively, the odds ratio (OR) was 2.26 (95% CI = 1.70-3.00); the occurrence of total side-effects was 9.05% (95% CI = 6.83-11.27%) and 16.28% (95% CI = 13.43%-19.13%) for groups with or without lactoferrin, especially for nausea, the summary OR was 0.15 (95% CI = 0.04-0.54). CONCLUSIONS: Our review suggests that supplementation with lactoferrin could be effective in increasing eradication rates of anti-H. pylori therapy, and could be considered helpful for patients with eradication failure. Furthermore, lactoferrin shows a positive impact on H. pylori therapy-related side-effects.

Design, synthesis, and in-vivo evaluation of 4,5-diaryloxazole as novel nonsteroidal anti-inflammatory drug.

A series of 4,5-diaryloxazole analogs were designed and the interaction between oxaprozin and cyclooxygenase-2 studied by the docking method to improve the biological activity and reduce the gastrointestinal side effects of oxaprozin. Finally, 3-(4-(4-fluorophenyl)-5-(4-aminosulfonyl-3-fluorophenyl)-oxazole-2-yl) propanoic acid (NC-2142), the best candidate, was selected for synthesis and bioassay based on the screening result. NC-2142 could lower the tumefaction rates of back metatarsus in rats, as well as reduce the writhing times in mice. NC-2142 produced fewer gastric lesions than oxaprozin. After the aminosulfonyl group was introduced into the benzene ring of oxaprozin, its analgesic and anti-inflammatory activities remained unchanged, and it reduced the number of gastric lesions. This provided a feasible method for further structure modification and optimization of oxaprozin.

Associations of Bone Mineral Density and Bone Metabolism Indices with Urine Albumin to Creatinine Ratio in Chinese Patients with Type 2 Diabetes.

OBJECTIVE: To identify correlations of bone mineral density (BMD) and bone metabolism indices with the urine albumin to creatinine ratio (ACR) as an indicator of nephropathy in Chinese patients with type 2 diabetes (T2D). METHODS: In this retrospective analysis, 297 patients with T2D were divided into 3 groups according to the urine ACR. Patients' data were analyzed to identify associations of general conditions, blood glucose level, lipid levels, and uric acid level with BMD and bone metabolism indices. RESULTS: BMD at every location tested (femoral neck, trochanter, inside hip, Ward's triangle, total hip, and lumbar vertebrae) was negatively correlated with the urine ACR (all p<0.05). Osteocalcin, beta-C-terminal telopeptide (ß-CTX), and procollagen type 1 N- peptide (P1NP) were positively correlated with urine ACR (all p<0.05). Finally, 25-hydroxyvitamin D [25(OH)D] was negatively correlated with urine ACR (p<0.05). Multiple regression analysis with adjustment for age, body mass index, disease duration, and other clinical measurements revealed no significant correlation between urine ACR and BMD measurements or ß-CTX (p>0.05). However, significant correlations remained between urine ACR and osteocalcin, P1NP, and 25(OH)D (p<0.05). The same results were obtained for postmenopausal women specifically, with the exception of a significant correlation between the ACR and ß-CTX (p<0.05). CONCLUSION: In the early stage of diabetic nephropathy, BMD changes and bone transformation acceleration may occur, and the acceleration of bone transformation may occur before the change in BMD. Therefore, it is important to monitor bone metabolism indices in the early stage of diabetic nephropathy in T2D patients.

Triptolide enhances the sensitivity of pancreatic cancer PANC-1 cells to gemcitabine by inhibiting TLR4/NF-κB signaling.

BACKGROUND: This study aimed to investigate roles of Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signaling in triptolide (TPL)-induced sensitivity of pancreatic cancer cells to gemcitabine (GEM). METHODS: In vitro, pancreatic cancer PANC-1 cells were treated with lipopolysaccharide (LPS) to activate TLR4, TLR4-siRNA, GEM alone, or GEM plus TPL. In vivo, nude mice bearing PANC-1 cell xenografts were treated with GEM, TPL, or both. Cell proliferation was detected by MTT assay and Ki-67 staining. Apoptosis was assessed by flow cytometry and TUNEL assay. A double luciferase reporter gene was used to detect NF-κB activity. RESULTS: The sensitivity of PANC-1 cells to GEM was reduced by LPS but enhanced by TLR4-siRNA. TPL inhibited expression of TLR4/NF-κB signaling components, which was reversed by LPS. The TPL+GEM group showed more apoptosis than the LPS+TPL+GEM group. Moreover, the activity of NF-κB and the expression of TLR4, p-p65 Survivin, CyclinD1 and Bcl-2 in the TPL+GEM group were lower than in the LPS+TPL+GEM group, whereas Bax expression was higher. The volume of transplanted tumors in the TPL+GEM group was lower than that in the TPL or GEM group. Phospho-p65, Survivin, CyclinD1 and Bcl-2 expression in transplanted tumors was lower in TPL+GEM group than in either single drug group. The Ki-67 staining score of the TPL+GEM group was lower and tumor cells apoptosis rate was increased when compared with TPL or GEM alone. CONCLUSIONS: TPL enhances the sensitivity of pancreatic cancer PANC-1 cells to GEM by inhibiting TLR4/NF-κB signaling.

Ginsenoside Re Improves Isoproterenol-Induced Myocardial Fibrosis and Heart Failure in Rats.

Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng. We aimed to investigate the protective effect of ginsenoside Re on isoproterenol-induced myocardial fibrosis and heart failure in rats. Methods. A model of myocardial fibrosis and heart failure was established by once-daily subcutaneous injection of isoproterenol (5 mg/kg/day) to rats for 7 days. Simultaneously, rats were orally administrated ginsenoside Re (5 or 20 mg/kg) or vehicle daily for 4 weeks. Results. Isoproterenol enhanced the heart weight, myocardial fibrosis, and hydroxyproline content in rat hearts. Ginsenoside Re inhibited (at least in part) the isoproterenol-induced increase in heart weight, myocardial fibrosis, and hydroxyproline content. Compared with the isoproterenol group, treatment with ginsenoside Re ameliorated changes in left ventricular systolic pressure, left ventricular end diastolic pressure, and the positive and negative maximal values of the first derivative of left ventricular pressure. Ginsenoside Re administration also resulted in decreased expression of transforming growth factor (TGF)-ß1 in serum and decreased expression of Smad3 and collagen I in heart tissue. Conclusion. Ginsenoside Re can improve isoproterenol-induced myocardial fibrosis and heart failure by regulation of the TGF-ß1/Smad3 pathway.

Validation in China of a non-invasive salivary pepsin biomarker containing two unique human pepsin monoclonal antibodies to diagnose gastroesophageal reflux disease.

OBJECTIVES: Peptest is a new non-invasive reflux diagnostic test based on lateral flow technology that containing two highly specific human pepsin monoclonal antibodies for detecting pepsin, a biomarker for reflux disease. The primary aim of this multicenter clinical study was to validate the efficacy of Peptest in patients diagnosed with gastroesophageal reflux and healthy controls in China. METHODS: Patients with suspected gastroesophageal reflux underwent an endoscopy and were classified into non-erosive reflux disease and erosive esophagitis subgroups. A healthy control group was also recruited. All participants were given a reflux disease questionnaire-patients scoring greater than 12 and controls scoring zero. All participants provided a postprandial saliva sample and most patients gave an additional post-symptom sample for pepsin analysis. RESULTS: Altogether 1032 participants aged between 19 and 78 years were recruited. They consisted of 488 patients with non-erosive reflux disease, 221 with erosive esophagitis and 323 healthy controls. The number of postprandial and post-symptom samples analyzed totaled 1031 and 692, respectively. The results across all centers showed an overall pepsin-positive sensitivity of 85%, a specificity of 60%, a positive predictive value of 82%, a negative predictive value of 65% and a positive likelihood ratio of 2.12. CONCLUSION: The sensitivity of Peptest was high, but the specificity achieved in some centers was low, resulting overall in only a moderate specificity. Further diagnostic investigative studies are warranted.

The Emerging Role of Circular RNAs in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) ranks the third leading cause of cancer death in the world and has a notably low survival rate. Circular RNAs (circRNAs) are newly classed non-coding RNA (ncRNA) members that are capable of regulating gene expression at transcription or post-transcription levels. Recent studies demonstrate that some circRNAs are differentially expressed in HCC, and the deregulation of these circRNAs is associated with the clinical pathological and prognostic significance. They also play essential roles in HCC progression, and contribute to cell proliferation, migration, invasion and metastasis by targeting different microRNAs (miRNAs) and protein-coding genes. In this review, we concentrate on recent progress of some important circRNAs in HCC, with an emphasis on their deregulation, functions and regulatory mechanisms, and discuss their potential utility as diagnostic and/or prognostic biomarkers or therapeutic targets for HCC.

Ginsenoside Re Attenuates Isoproterenol-Induced Myocardial Injury in Rats.

Objective. Panax ginseng is widely used for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of Panax ginseng. This study aimed to investigate the protective effect of Ginsenoside Re on isoproterenol-induced myocardial injury in rats. Methods. Male Wistar rats were orally given Ginsenoside Re (5, 20 mg/kg) daily for 7 days. Isoproterenol was subcutaneously injected into the rats for two consecutive days at a dosage of 20 mg/kg/day (on 6th and 7th day). Six hours after the last isoproterenol injection, troponin T level and creatine kinase-MB (CK-MB) activity were assayed. Histopathological examination of heart tissues was performed. The levels of malondialdehyde (MDA) and glutathione (GSH) in heart tissues were measured. The nuclear factor erythroid 2-related factor 2 (Nrf2) content in nucleus and the proteins of glutathione cysteine ligase catalytic subunit (GCLC) and glutathione cysteine ligase modulatory subunit (GCLM) in heart tissues were assayed by western blotting method. Results. Treatment with Ginsenoside Re at dose of 5, 20 mg/kg reduced troponin T level and CK-MB activity of rats subjected to isoproterenol. The cardioprotective effect of Ginsenoside Re was further confirmed by histopathological examination which showed that Ginsenoside Re attenuated the necrosis and inflammatory cells infiltration. Ginsenoside Re inhibited the increase of MDA content and the decrease of GSH in heart tissues. Moreover, the Nrf2 content in nucleus and the expressions of GCLC and GCLM were significantly increased in the animals treated with Ginsenoside Re. Conclusion. These findings suggested that Ginsenoside Re possesses the property to attenuate isoproterenol-induced myocardial ischemic injury by regulating the antioxidation function in cardiomyocytes.

Assessment of health-related quality of life in Chinese patients with minimal hepatic encephalopathy.

AIM: To evaluate the health-related quality of life (HRQOL) based on the Chinese version of SF-36 and Chronic Liver Disease Questionnaire (CLDQ) in subjects with chronic hepatitis B, liver cirrhosis, including patients with minimal hepatic encephalopathy (MHE). METHODS: The SF-36 and CLDQ were administered to 160 healthy volunteers, 20 subjects with chronic hepatitis B and 106 patients with cirrhosis (33 cases exhibited MHE). HRQOL scores were compared among the different study groups. The SF-36 includes eight health concepts: physical functioning, role-physical, body pain, general health, vitality, social functioning, role-emotion, and mental health. Six domains of CLDQ were assessed: abdominal symptoms, fatigue, systemic symptoms, activity, emotional function and worry. RESULTS: Compared with healthy controls (96.9 +/- 4.5, 86.6 +/- 18.4, 90.1 +/- 12.5, 89.0 +/- 5.7, 87.5 +/- 4.3, 95.8 +/- 7.1, 88.5 +/- 15.9, 88.7 +/- 5.2 in SF-36 and 6.7 +/- 0.5, 6.1 +/- 0.6, 6.3 +/- 0.6, 6.5 +/- 0.5, 6.3 +/- 0.5, 6.8 +/- 0.4 in CLDQ), patients with chronic hepatitis B (86.3 +/- 11.0, 68.8 +/- 21.3, 78.9 +/- 14.4, 60.8 +/- 10.5, 70.8 +/- 8.6, 76.1 +/- 12.6, 50.0 +/- 22.9, 72.2 +/- 10.6 and 5.5 +/- 1.0, 4.5 +/- 1.0, 5.2 +/- 1.1, 5.3 +/- 0.9, 4.8 +/- 0.9, 4.9 +/- 1.0) and cirrhosis (52.8 +/- 17.4, 32.8 +/- 27.9, 61.6 +/- 18.9, 30.2 +/- 18.3, 47.9 +/- 20.1, 54.0 +/- 19.2, 28.9 +/- 26.1, 51.1 +/- 17.8 and 4.7 +/- 1.2, 3.9 +/- 1.2, 4.7 +/- 1.2, 4.7 +/- 1.3, 4.7 +/- 1.0, 4.4 +/- 1.1) had lower HRQOL on all scales of the SF-36 and CLDQ (P < 0.01 for all). Increasing severity of liver cirrhosis (based on the Child-Pugh score/presence or absence of MHE) was associated with a decrease in most components of SF-36 and CLDQ, especially SF-36. CONCLUSION: The Chinese version of SF-36 along with CLDQ is a valid and reliable method for testing MHE in patients with liver cirrhosis. Cirrhosis and MHE are associated with decreased HRQOL.