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While a large body of research has investigated cultural differences in behavior, this typical study assesses a single behavioral outcome, in a single context, compared across two countries. The current study compared a broad array of behaviors across 21 countries (N = 5,522). Participants described their behavior at 7:00 p.m. the previous evening using the 68 items of the Riverside Behavioral Q-sort (RBQ). Correlations between average patterns of behavior in each country ranged from r =.69 to r =.97 and, in general, described a positive and relaxed activity. The most similar patterns were United States/Canada and least similar were Japan/United Arab Emirates (UAE). Similarities in behavior within countries were largest in Spain and smallest in the UAE. Further analyses correlated average RBQ item placements in each country with, among others, country-level value dimensions, personality traits, self-esteem levels, economic output, and population. Extroversion, openness, neuroticism, conscientiousness, self-esteem, happiness, and tolerant attitudes yielded more significant correlations than expected by chance.

Glioblastoma (GBM) continues to show a poor prognosis despite advances in diagnostic and therapeutic approaches. The discovery of reliable prognostic indicators may significantly improve treatment outcome of GBM. In this study, we aimed to explore the function of verbascoside (VB) in GBM and its effects on GBM cell biological processes via let-7g-5p and HMGA2. Differentially expressed GBM-related microRNAs (miRNAs) were initially screened. Different concentrations of VB were applied to U87 and U251 GBM cells, and 50 µmol/L of VB was selected for subsequent experiments. Cells were transfected with let-7g-5p inhibitor or mimic, and overexpression of HMGA2 or siRNA against HMGA2 was induced, followed by treatment with VB. The regulatory relationships between VB, let-7g-5p, HMGA2 and Wnt/β-catenin signalling pathway were determined. The results showed that HMGA2 was a direct target gene of let-7g-5p. VB treatment or let-7g-5p overexpression inhibited HMGA2 expression and the activation of Wnt/β-catenin signalling pathway, which further inhibited cell viability, invasion, migration, tumour growth and promoted GBM cell apoptosis and autophagy. On the contrary, HMGA2 overexpression promoted cell viability, invasion, migration, tumour growth while inhibiting GBM cell apoptosis and autophagy. We demonstrated that VB inhibits cell viability and promotes cell autophagy in GBM cells by up-regulating let-7g-5p and down-regulating HMGA2 via Wnt/β-catenin signalling blockade., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)

A Gram-negative, aerobic, non-motile, rod-shaped bacterial strain, designated 25-1(T), was isolated from the air inside giant panda enclosures at the Chengdu Research Base of Giant Panda Breeding, China. Strain 25-1(T) grew optimally at pH 7.0-8.0, at 28-30 °C and in the presence of NaCl concentrations from 0.0% to 0.5 %. 16S rRNA gene sequence analysis indicated that strain 25-1(T) belongs to the genus Chryseobacterium within the family Flavobacteriaceae and is related most closely to C. carnis G81(T) (96.4% similarity), C. lathyri RBA2-6(T) (95.8% similarity), and C. zeae JM1085(T) (95.8% similarity). Its genomic DNA G+C molar composition was 36.2%. The major cellular fatty acids were iso-C15:0 (44.0%), iso-C17:0 3OH (19.8%) and C16:1 ω7c/16:1 ω6c (12.7%). The only isoprenoid quinone was menaquinone 6 (MK-6). The major polar lipids were phosphatidylethanolamine, two unidentified amino lipids and two unidentified lipids. The DNA-DNA relatedness between strain 25-1(T) and C. lathyri RBA2-6(T) was 38%. Phenotypic, genotypic, and phylogenetic characteristics indicated that strain 25-1(T) is a novel member of the genus Chryseobacterium, for which the name C. chengduensis sp. nov. is proposed. The type strain is 25-1(T) (CCTCC AB2015133(T)=DSM 100396(T)).

Aim: To evaluate the efficacy of ursodeoxycholic acid (UDCA) as a chemotherapeutic agent for the treatment of hepatocellular carcinoma (HCC)., Methods: BALB/c nude mice were randomized into four groups 24 h before subcutaneous injection of hepatocarcinoma BEL7402 cells suspended in phosphate buffered saline (PBS) into the right flank. The control group (n = 10) was fed a standard diet while treatment groups (n = 10 each) were fed a standard daily diet supplemented with different concentrations of UDCA (30, 50 and 70 mg/kg per day) for 21 d. Tumor growth was measured once each week, and tumor volume (V) was calculated with the following equation: V = (L × W(2)) × 0.52, where L is the length and W is the width of the xenograft. After 21 d, mice were killed under ether anesthesia, and tumors were excised and weighed. Apoptosis was evaluated through detection of DNA fragmentation with gel electrophoresis and the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay. Western blot analysis was performed to determine the expression of apoptosis-related proteins BAX, BCL2, APAF1, cleaved caspase-9, and cleaved caspase-3., Results: UDCA suppressed tumor growth relative to controls. The mean tumor volumes were the following: control, 1090 ± 89 mm(3); 30 mg/kg per day, 612 ± 46 mm(3); 50 mg/kg per day, 563 ± 38 mm(3); and 70 mg/kg per day, 221 ± 26 mm(3). Decreased tumor volumes reached statistical significance relative to control xenografts (30 mg/kg per day, P < 0.05; 50 mg/kg per day, P < 0.05; 70 mg/kg per day, P < 0.01). Increasing concentrations of UDCA led to increased DNA fragmentation observed on gel electrophoresis and in the TUNEL assay (control, 1.6% ± 0.3%; 30 mg/kg per day, 2.9% ± 0.5%; 50 mg/kg per day, 3.15% ± 0.7%, and 70 mg/kg per day, 4.86% ± 0.9%). Western blot analysis revealed increased expression of BAX, APAF1, cleaved-caspase-9 and cleaved-caspase-3 proteins, which induce apoptosis, but decreased expression of BCL2 protein, which is an inhibitor of apoptosis, following administration of UDCA., Conclusion: UDCA suppresses growth of BEL7402 hepatocellular carcinoma cells in vivo, in part through apoptosis induction, and is thus a candidate for therapeutic treatment of HCC.

The aim of this study was to assess the role of the VEGF -2578C/A, +936C/T, and -460T/C gene polymorphisms in the development of osteosarcoma. A total of 182 patients with osteosarcoma and 182 age- and gender-matched healthy controls were enrolled into our study during January 2011 and December 2013. Genotype frequencies of the VEGF -2578C/A and -460T/C alleles in controls were found to be within the parameters of Hardy-Weinberg equilibrium, but the genotype frequencies of +936C/T alleles were not. By conditional regression analysis, we detected a statistically significantly increased risk of osteosarcoma in patients with the AA genotype (OR = 1.97; 95%CI = 1.02-3.83) and the CA+AA genotype (OR = 1.57; 95%CI = 1.01-2.44) of -2578C/A when compared with CC genotype. Therefore, our study showed that the AA and CA+AA genotypes of the VEGF -2578C/A polymorphism might modify the risk of osteosarcoma in a Chinese population.

Programmed cell death factor 4 (PDCD4) is one of the genes that has been found to be up-regulated during apoptosis and loss of PDCD4 expression has been found in many kinds of progressive carcinomas. The objective of this study was to investigate the interactions between PDCD4 and smoking status in hepatocellular carcinoma. This case-controlled study included 68 Chinese male patients with hepatocellular carcinoma who were classified as smokers or non-smokers according to their pack-years of smoking status. Samples were obtained from carcinoma and normal tissues and examined using Western blotting. The results indicated that levels of PDCD4 were significantly lower in hepatocellular carcinoma tissues compared with normal tissues and that, in normal tissue, PDCD4 levels in smokers were significantly lower than in non-smokers.

Background: Hepatic fibrosis is the key stage of the pathological progress from hepatic injury to cirrhosis. Ursodeoxycholic acid (UDCA) has been known as having significant clinical therapeutic effects on chronic liver diseases. Our research aimed to study the effect of UDCA on the signaling pathway of transforming growth factor beta1 (TGFbeta1)/Smad and discuss its possible molecular mechanisms of inhibiting hepatic fibrosis., Methods: Rat hepatic stellate cells were cultured in vitro and randomly assigned to 4 groups. Group A was control group, with only DMEM culture medium applied, and groups B, C, D were experimental groups, with different doses of UDCA (1.0 mmol/L, 0.5 mmol/L and 0.25 mmol/L respectively) added into their DMEM culture medium for further culture of 24 hours and 48 hours. The protein expressions of TGFbeta1, TGF type I receptor, Smad3, Smad4 and Smad7 were measured by Western blotting, as well as the expressions of TGFbeta1, Smad3, Smad7 and cAMP response element (CREB) binding protein (CBP) mRNA by real-time PCR. SPSS 11.5 statistical package was adopted for data analyses., Results: Compared with control group, the mRNA expressions of TGFbeta1 in the high and middle UDCA dose groups for 24 hours and 48 hours significantly decreased (P < 0.05), the protein expressions of TGFbeta1 in the two above groups for 48 hours and in the high dose group for 24 hours significantly decreased (P < 0.05). The protein and mRNA expressions of Smad3 in each UDCA dose group for 24 hours and 48 hours significantly decreased, with significant difference among different UDCA dose groups and between that of 24 hours and 48 hours observed (P < 0.05). The protein and mRNA expressions of Smad7 in the high and middle UDCA dose groups for 24 hours and 48 hours significantly increased. The CBP mRNA expression in each UDCA dose group for 24 hours and 48 hours significantly decreased (P < 0.05), with significant difference among different UDCA dose groups observed (P < 0.05)., Conclusion: UDCA could curb the development of hepatic fibrosis through affecting the signaling pathway of TGFbeta1/Smad by inhibiting the expressions of TGFbeta1, Smad3 and CBP and increasing the expression of Smad7.

Aim: To investigate the effects of ursodeoxycholic acid (UDCA) on apoptosis and proliferation of hepatoma cell lines., Methods: Human hepatoma cell lines HepG2 and BEL 7402 were cultured in medium supplemented with different concentrations of UDCA, normal human hepatic line L-02 was used as control. Cell proliferation, apoptosis and gene expression were detected using methyl thiazolyl tetrazolium (MTT) assay, flow cytometry, Western blot, DNA ladder assay, electron microscopy, and immunocytochemistry., Results: Ursodeoxycholic acid inhibited the proliferation of HepG2 and BEL7402 cell lines in a dose-dependent manner. Ursodeoxycholic acid can change cell cycle distribution of HepG2 and BEL7402, the proportion of cells in G0-G1 phase increased whereas the proportion of S phase cells and G2-M phase cells decreased. Ursodeoxycholic acid arrested the cell cycle in G0-G1 phase by down-regulating the cell cycle related proteins cyclin D1, D3 and retinoblastoma protein (p(Rb)). The apoptotic rates of HepG2 and BEL7402 treated with UDCA (1.0 mmol/L) were significantly higher than those of control. In the HepG2 and BEL7402 treated with UDCA, expression of bcl-2 decreased whereas expression of Bax increased, the nuclear fragmentation and chromosomal condensed, cells shrank and lost attachment, apoptotic bodies and DNA ladders appeared. UDCA had no effect in inducing apoptosis on L-02 cell lines., Conclusion: UDCA can selectively inhibit proliferation and induce apoptosis of HepG2 and BEL7402 cell lines by blocking cell cycle and regulating the expression of Bax/bcl-2 genes.

Aim: To probe the value of gamma-glutamyl transpeptidase (GGT) messenger RNA in monitoring canceration of liver cells and for early diagnosis of hepatocellular carcinoma (HCC), by researching the types of GGT messenger RNA (GGTmRNA) in liver tissues and peripheral blood of different hepatopathy., Methods: The three types of GGTmRNA (A, B, C) in liver tissues and peripheral blood from the patients with HCC, noncancerous hepatopathy, hepatic benign tumor, secondary carcinoma of liver, and healthy persons were detected by reverse-transcription polymerase chain reaction (RT-PCR)., Results: (1) In normal liver tissues, type A was predominantly found (100.00 %), type B was not found, type C was found occasionally (25.00 %). (2) The distribution of types of GGTmRNA in liver tissues with acute hepatitis, chronic hepatitis, cirrhosis, alcoholic hepatopathy was similar as in normal liver tissues (P>0.05), but type B was found in 3 of 18 patients with chronic hepatitis (16.67 %), and also in 3 of 11 patients with cirrhosis (27.27 %). (3) There was no significant difference of types of GGTmRNA between liver tissues with hepatic benign tumor, secondary carcinoma of liver and normal liver tissues (P>0.05). (4) Type B was predominant in cancerous tissues with HCC (87.5 %), the prevalence of type B in cancerous tissues was significantly higher than that in normal liver tissues (0/12) (P<0.05), but the prevalence of type A in cancerous tissues (46.88 %) was significantly lower than that in normal liver tissues (100.00 %) (P<0.05), and the prevalence of type C (6.25 %) in cancerous was the same as that in normal liver tissues (25.00 %) (P>0.05). In noncancerous tissues of livers with HCC, the main types were type A and type B, the prevalence of type A (85.71 %, 90.48 %) and type C (14.29 %, 9.52 %) in noncancerous tissues of liver with HCC was similar as that in normal liver tissues (A: 100.00 %; C: 25.00 %) (P>0.05), but the prevalence of type B (80.95 %, 76.19 %) in noncancerous tissues of livers with HCC was significantly higher than that in normal liver tissues (0/12) (P<0.05). (5) The prevalence of type B (37.5 %) in peripheral blood with HCC was higher than that in normal person (0/12) (P<0.05). In peripheral blood, type B was found in 4 of 11 cases of HCC with serum AFP negative., Conclusion: The shift of types of GGTmRNA from A to B in liver tissues may be closely related to the development of HCC, and the analysis of GGT gene may provide a useful tool for early diagnosis of HCC.

Objective: To observe and measure the inside diameter of basicranial arteries, the angulation of main arteries, the three dimensional image characteristic of internal carotid arteries and the anatomical variation of Willis circle., Methods: The arteries of 30 formalin-fixed adult heads were injected with latex after which the caliber and characteristic of cerebral arteries were observed and measured. The three dimensional image characteristic of internal carotid arteries and its branches were measured using 3D-DSA., Results: (1) Main artery caliber: origin of internal carotid artery (Left 5.12 +/- 1.48 mm; Right 5.11 +/- 1.42 mm); origin of middle cerebral artery (Left 2.93 +/- 1.44 mm; Right 2.92 +/- 1.46 mm); origin of anterior cerebral artery (Left 2.63 +/- 1.33 mm; Right 2.61 +/- 1.32 mm); origin of vertebral artery (Left 4.37 +/- 1.21 mm; Right 3.22 +/- 1.64 mm); origin of basilar artery (4.45 +/- 1.28 mm); origin of posterior cerebral artery (Left 2.62 +/- 1.36 mm; Right 2.61 +/- 1.22 mm). (2) The angulation of main arteries: C1, 2 of ICA and C4, 5 of ICA (Left 32 +/- 22 degrees; Right 36 +/- 28 degrees ); ICA and ACA (Left 43 +/- 26 degrees; Right 46 +/- 28 degrees). (3) The results show that anatomical and three dimensional image characteristic of internal carotid arteries have no difference (P > 0.05). (4) The anatomical variation of Willis circle: Type O (56.7%); Type A (16.7%); Type P (20.0%); Type AP (6.7%)., Conclusions: It is helpful to measure the inside diameter of basicranial arteries for the selection of various catheter in interventional neuroradiology, to observe the angulation of main arteries and the three dimensional image characteristic of internal carotid arteries for the moulding of various catheter in endovascular therapy and to master the anatomical variation of Willis circle for decreasing complications of endovascular treatment and judging prognosis of cerebrovascular diseases.

Tetrandrine, a bis-benzylisoquinoline alkaloid derived from the Chinese medicinal herb Stephania tetrandra, is a putative Ca2+ entry blocker whose mechanism of action is unknown. To investigate this mechanism, the effects of tetrandrine were characterized on binding of three chemical classes of Ca2+ entry blockers in cardiac sarcolemmal membrane vesicles. In the range 25-37 degrees C, tetrandrine completely blocks diltiazem binding, partially inhibits D-600 binding, and markedly stimulates nitrendipine binding, with greatest enhancement occurring at 37 degrees C. The potency of tetrandrine is increased 10-fold as temperature is raised from 25 to 37 degrees C. Scatchard analyses indicate that inhibition of diltiazem binding and stimulation of nitrendipine binding result from changes in ligand affinities while inhibition of D-600 binding is due to both an increase in KD and decrease in Bmax of aralkylamine receptors. Ligand dissociation studies reveal that tetrandrine increases D-600 off-rates, decreases nitrendipine off-rates, but has no effect on diltiazem dissociation kinetics. In addition, tetrandrine reversibly blocks inward Ca2+ currents through L-type Ca2+ channels in GH3 anterior pituitary cells. These results indicate that tetrandrine interacts directly at the benzothiazepine-binding site of the Ca2+ entry blocker receptor complex and allosterically modulates ligand binding at other receptors in this complex. These findings suggest that tetrandrine is a structurally unique natural product Ca2+ entry blocker and provide a rationale explanation for the therapeutic effectiveness of this agent.

Platelet-activating factor (PAF) is a potent lipid mediator of inflammation and asthma. Using a receptor preparation of rabbit platelet membranes, we identified a novel antagonist of PAF in the methylene chloride extract of a Chinese herbal plant, haifenteng (Piper futokadsura). The active antagonist, kadsurenone, was isolated and characterized in several in vitro and in vivo assays. It is a specific and competitive inhibitor of PAF binding to its receptor with a Ki of 5.8 X 10(-8) M vs. a Ki of 6.3 X 10(-9) M for PAF itself. It inhibits PAF-induced aggregation of rabbit platelets and human neutrophils at 2.4-24 microM, without showing any PAF agonistic activity. It potently inhibits PAF-induced degranulation of human neutrophils at 2.5-50 microM, also without any agonist activity. Kadsurenone is active orally at 25-50 mg/kg of body weight in blocking PAF-induced cutaneous permeability in the guinea pig. It also inhibits PAF-induced increases of hematocrit and circulating N-acetylglucosaminidase in the rat at greater than 10 mg/kg i.p. in a dose-dependent manner. Kadsurenone does not interfere with the function of several pharmacological mediators and receptors tested. Its structural specificity is evidenced by the poor PAF-antagonistic activities of three related structures isolated from the same haifenteng extract.