MiR-29c-3p inhibits proliferation and migration in rat primary cardiac fibroblasts via interacting with STAT3.

BACKGROUND: The aim of this study was to elucidate the influence and molecular mechanism of microRNA-29c-3p (miR-29c-3p) on cell functions of cardiac fibroblasts. METHODS: Rat primary cardiac fibroblasts were induced with high-level glucose (HG), followed by determination of miR-29c-3p and signal transducer and activator of transcription 3 (STAT3) levels. The regulatory effects of miR-29c-3p and STAT3 (AG490) on proliferative and migratory potentials in HG-induced cardiac fibroblasts were examined by cell counting kit-8 (CCK-8) and Transwell assay, respectively. The interaction between miR-29c-3p and STAT3 was assessed by bioinformatics analysis and dual-luciferase reporter assay. RESULTS: MiR-29c-3p was downregulated, and STAT3 was upregulated in HG-induced cardiac fibroblasts. HG induction stimulated proliferative and migratory potentials in cardiac fibroblasts, which were attenuated by overexpression of miR-29c-3p. STAT3 was the target gene binding miR-29c-3p. Application of AG490, the STAT3 inhibitor, was able to reverse the promoted proliferative and migratory potentials in HG-induced cardiac fibroblasts with miR-29c-3p knockdown. CONCLUSIONS: MiR-29c-3p weakens the over-proliferative and over-migratory potentials in HG-induced cardiac fibroblasts via inactivating the STAT3 signaling.

Trends of Tourette Syndrome in children from 2011 to 2021: A bibliometric analysis.

Objective: Analyze the research status of Tourette Syndrome (TS) in children by CiteSpace and determine the current research hotspots and frontiers. Materials and methods: We chose publications indexed in the Web of Science Core Collection (WoSCC) database for studies related to TS in children from 2011 to 2021. We built online cooperation maps of countries/regions, institutions, authors, journals, references, and keywords by CiteSpace, and identified hotspots and frontiers of study for children's TS. Results: A total of 1,232 publications about TS in children were downloaded from the WoSCC. The USA (414) was the country with the highest rate of production, and University College London (87) was the institution that had the highest publication rate. Andrea Eugenio Cavanna was the most prolific author (39 papers). There was inactive cooperation between institutions, countries/regions, and authors. The Journal of European Child & Adolescent Psychiatry was the most active journal. Hot topics focused on epidemiology, comorbidities, deep brain stimulation, behavioral therapy, basal ganglia, pharmacological treatment, and risk factors of TS in children. Conclusion: According to the CiteSpace results, this study found that authors, countries/regions, and institutions were not actively working together. Current research hotspots mainly consist of epidemiology, comorbidities, deep brain stimulation, behavior therapy, and basal ganglia. The main research trends include comorbidities, pharmacological treatment, and risk factors. Therefore, international cooperation should be strengthened in the future, and it should be mindful of the psychiatric comorbidities of TS, the choice of intervention measures, and early warning of risk factors.

Circ_0050908 up-regulates TRAF3 by sponging miR-324-5p to aggravate myocardial ischemia-reperfusion injury.

BACKGROUND: Aberrant circular RNAs (circRNAs) expression is closely associated with cardiovascular diseases. However, the regulatory functions of circRNAs in myocardial ischemia-reperfusion (I/R) injury remain largely undefined. METHODS: We established myocardial I/R model in vitro by oxygen and glucose deprivation and reperfusion in cardiomyocytes. The expression of circ_0050908, microRNA (miR)-324-5p, and TNF receptor-associated factor (TRAF3) was detected using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The apoptosis was assayed by flow cytometry and Western blot. The activity of interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF-α), lactate dehydrogenase (LDH), creatine kinase myocardial band (CK-MB), CK, and superoxide dismutase (SOD) was evaluated using the relative commercial kits. Reactive oxygen species (ROS) detection was conducted using Dihydroethidium (DHE) staining. The interactions between miR-324-5p and circ_0050908 or TRAF3 were determined by dual-luciferase activity, RNA immunoprecipitation (RIP), and pull-down assays. RESULTS: I/R stimulation up-regulated circ_0050908 expression in cardiomyocytes. Functional experiments suggested that circ_0050908 knockdown led to the rescue of apoptosis enhancement, inflammation, and oxidative stress induced by I/R in cardiomyocytes. Mechanistically, circ_0050908 directly targeted miR-324-5p, and miR-324-5p inhibition reversed the inhibitory action of circ_0050908 knockdown on myocardial I/R injury. TRAF3 was verified to be a target of miR-324-5p, and miR-324-5p suppressed I/R-induced apoptosis, inflammatory response, and oxidative stress in cardiomyocytes through TRAF3. Besides that, circ_0050908 could regulate TRAF3 expression by miR-324-5p. CONCLUSION: Circ_0050908 knockdown protects cardiomyocytes against I/R injury by reducing apoptosis, inflammatory response, and oxidative stress through miR-324-5p/TRAF3 axis, revealing a novel therapeutic strategy for preventing myocardial I/R injury.

Identification of WRKY transcription factors responding to abiotic stresses in Brassica napus L.

MAIN CONCLUSION: A total of 278 BnWRKYs were identified and analyzed. Ectopic expression of BnWRKY149 and BnWRKY217 suggests that they function in the ABA signaling pathway. WRKY transcription factors play an important role in plant development, however, their function in Brassica napus L. abiotic stress response is still unclear. In this study, a total of 278 BnWRKY transcription factors were identified from the B. napus genome data, and they were subsequently distributed in three main groups. The protein motifs and classification of BnWRKY transcription factors were analyzed, and the locations of their corresponding encoding genes were mapped on the chromosomes of B. napus. Transcriptome analysis of rapeseed seedlings exposed to drought, salt, heat, cold and abscisic acid treatment revealed that 99 BnWRKYs responded to at least one of these stresses. The expression profiles of 12 BnWRKYs were examined with qPCR and the result coincided with RNA-seq analysis. Two genes of interest, BnWRKY149 and BnWRKY217 (homologs of AtWRKY40), were overexpressed in Arabidopsis, and the corresponding proteins were located to the nucleus. Transgene plants of BnWRKY149 and BnWRKY217 were less sensitive to ABA than Arabidopsis Col-0 plants, suggesting they might play important roles in the responses of rapeseed to abiotic stress.

Up-regulation of CTRP12 ameliorates hypoxia/re-oxygenation-induced cardiomyocyte injury by inhibiting apoptosis, oxidative stress, and inflammation via the enhancement of Nrf2 signaling.

C1q/TNF-related protein 12 (CTRP12) has been reported to play a key role in coronary artery disease. However, whether CTRP12 plays a role in the regulation of myocardial ischemia-reperfusion injury is not fully understood. The goals of this work were to assess the possible relationship between CTRP12 and myocardial ischemia-reperfusion injury. Here, we exposed cardiomyocytes to hypoxia/re-oxygenation (H/R) to establish an in vitro cardiomyocyte injury model of myocardial ischemia-reperfusion injury. Our results showed that H/R treatment resulted in a decrease in CTRP12 expression in cardiomyocytes. The up-regulation of CTRP12 ameliorated H/R-induced cardiomyocyte injury via the down-regulation of apoptosis, oxidative stress, and inflammation. In contrast, the knockdown of CTRP12 enhanced cardiomyocyte sensitivity to H/R-induced cardiomyocyte injury. Further investigation showed that CTRP12 enhanced the levels of nuclear Nrf2 and increased the expression of Nrf2 target genes in cardiomyocytes exposed to H/R. However, the inhibition of Nrf2 markedly diminished CTRP12-overexpression-mediated cardioprotective effects against H/R injury. Overall, these data indicate that CTRP12 protects against H/R-induced cardiomyocyte injury by inhibiting apoptosis, oxidative stress, and inflammation via the enhancement of Nrf2 signaling. This work suggests a potential role of CTRP12 in myocardial ischemia-reperfusion injury and proposes it as an attractive target for cardioprotection.

Curcumin Reduces Cognitive Deficits by Inhibiting Neuroinflammation through the Endoplasmic Reticulum Stress Pathway in Apolipoprotein E4 Transgenic Mice.

Apolipoprotein E4 (ApoE4) is the main genetic risk factor for Alzheimer's disease (AD), but the exact way in which it causes AD remains unclear. Curcumin is considered to have good therapeutic potential for AD, but its mechanism has not been clarified. This study aims to observe the effect of curcumin on ApoE4 transgenic mice and explore its possible molecular mechanism. Eight-month-old ApoE4 transgenic mice were intraperitoneally injected with curcumin for 3 weeks, and the Morris water maze test was used to evaluate the cognitive ability of the mice. Immunofluorescence staining, immunohistochemistry, western blotting, and enzyme-linked immunosorbent assay (ELISA) were used to examine the brain tissues of the mice. Curcumin reduced the high expression of ApoE4 and the excessive release of inflammatory factors in ApoE4 mice. In particular, the expression of marker proteins of endoplasmic reticulum (ER) stress was significantly increased in ApoE4 mice, while curcumin significantly reduced the increase in the expression of these proteins. Collectively, curcumin alleviates neuroinflammation in the brains of ApoE4 mice by inhibiting ER stress, thus improving the learning and cognitive ability of transgenic mice.

Inhibition of sphingomyelin synthase 2 relieves hypoxia-induced cardiomyocyte injury by reinforcing Nrf2/ARE activation via modulation of GSK-3ß.

Sphingomyelin synthase 2 (SMS2) is a vital contributor to tissue injury and affects various pathological processes. However, whether SMS2 participates in the modulation of cardiac injury in myocardial infarction has not been determined. This study aimed to evaluate the potential role of SMS2 in the regulation of cardiomyocyte injury induced by hypoxia, an in vitro model for studying myocardial infarction. Our data revealed that SMS2 expression was significantly upregulated in cardiomyocytes in response to hypoxia. Loss-of-function experiments revealed that knockdown of SMS2 markedly restored the viability of cardiomyocytes impaired by hypoxia, and attenuated hypoxia-evoked apoptosis and reactive oxygen species (ROS) generation. In contrast, cardiomyocytes that highly expressed SMS2 were more sensitive to hypoxia-induced injury. Moreover, SMS2 deficiency enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling through inactivation of glycogen synthase kinase-3ß. Notably, suppression of Nrf2 markedly abrogated SMS2 knockdown-mediated cardioprotective effects on hypoxia-exposed cardiomyocytes. Our results illustrate that downregulation of SMS2 exerts a cardioprotective function by protecting cardiomyocytes from hypoxia-induced apoptosis and oxidative stress through enhancement of Nrf2 activation. Our study indicates a potential role of SMS2 in the modulation of cardiac injury, which may contribute to the progression of myocardial infarction.

Tumor microenvironment triggered biodegradation of inorganic nanoparticles for enhanced tumor theranostics.

Inorganic nanoparticles (NPs)-mediated tumor theranostics have attracted widespread attention due to their unique physicochemical properties, such as optical, electrical, magnetic, and thermal properties. In the past decade, great advancements have been made in inorganic NPs-associated drug delivery, multimodal tumor imaging, and tumor therapy. However, the potential toxicity of inorganic NPs due to their low biodegradability, background signals interference and treatment side effects limit their clinical application. Therefore, developing biodegradable and intelligent NPs is beneficial to avoid excessive metal ions deposition, specific tumor imaging and treatment. In this review, we summarize the recent advances in tumor microenvironment (TME)-triggered biodegradation of inorganic NPs accompanied by imaging signal amplification and the released ions-mediated tumor therapy. First, the feature characteristics of the TME are introduced, including mild acidity, hypoxia, overexpressed reactive oxygen species (ROS), glutathione (GSH), and enzymes et al.; then, the biodegradation of NPs in a TME-induced activation of imaging signals, such as magnetic resonance (MR) imaging and fluorescence imaging is described; furthermore, tumor therapies through "Fenton", "Fenton-like" reactions, and interference of biological effects in cells is presented. Finally, the challenges and outlook for improving the degradation efficiency, imaging, specificity and efficiency of tumor imaging and treatment are discussed.

Screening of abiotic stress-responsive cotton genes using a cotton full-length cDNA overexpressing Arabidopsis library.

Cotton (Gossypium hirsutum L.) is a major crop and the main source of natural fiber worldwide. Because various abiotic and biotic stresses strongly influence cotton fiber yield and quality, improved stress resistance of this crop plant is urgently needed. In this study, we used Gateway technology to construct a normalized full-length cDNA overexpressing (FOX) library from upland cotton cultivar ZM12 under various stress conditions. The library was transformed into Arabidopsis to produce a cotton-FOX-Arabidopsis library. Screening of this library yielded 6,830 transgenic Arabidopsis lines, of which 757 were selected for sequencing to ultimately obtain 659 cotton ESTs. GO and KEGG analyses mapped most of the cotton ESTs to plant biological process, cellular component, and molecular function categories. Next, 156 potential stress-responsive cotton genes were identified from the cotton-FOX-Arabidopsis library under drought, salt, ABA, and other stress conditions. Four stress-related genes identified from the library, designated as GhCAS, GhAPX, GhSDH, and GhPOD, were cloned from cotton complementary DNA, and their expression patterns under stress were analyzed. Phenotypic experiments indicated that overexpression of these cotton genes in Arabidopsis affected the response to abiotic stress. The method developed in this study lays a foundation for high-throughput cloning and rapid identification of cotton functional genes.

Exploring transcription factors reveals crucial members and regulatory networks involved in different abiotic stresses in Brassica napus L.

BACKGROUND: Brassica napus (B. napus) encompasses diverse transcription factors (TFs), but thorough identification and characterization of TF families, as well as their transcriptional responsiveness to multifarious stresses are still not clear. RESULTS: Totally 2167 TFs belonging to five families were genome-widely identified in B. napus, including 518 BnAP2/EREBPs, 252 BnbZIPs, 721 BnMYBs, 398 BnNACs and 278 BnWRKYs, which contained some novel members in comparison with existing results. Sub-genome distributions of BnAP2/EREBPs and BnMYBs indicated that the two families might have suffered from duplication and divergence during evolution. Synteny analysis revealed strong co-linearity between B. napus and its two ancestors, although chromosomal rearrangements have occurred and 85 TFs were lost. About 7.6% and 9.4% TFs of the five families in B. napus were novel genes and conserved genes, which both showed preference on the C sub-genome. RNA-Seq revealed that more than 80% TFs were abiotic stress inducible and 315 crucial differentially expressed genes (DEGs) were screened out. Network analysis revealed that the 315 DEGs are highly co-expressed. The homologous gene network in A. thaliana revealed that a considerable amount of TFs could trigger the differential expression of targeted genes, resulting in a complex clustered network with clusters of genes responsible for targeted stress responsiveness. CONCLUSIONS: We identified and characterized five TF families in B. napus. Some crucial members and regulatory networks involved in different abiotic stresses have been explored. The investigations deepen our understanding of TFs for stress tolerance in B. napus.

Multi-gene co-expression can improve comprehensive resistance to multiple abiotic stresses in Brassica napus L.

Rapeseed (Brassica napus L.) is an important oil crop worldwide. For current B. napus production, it is urgent to develop new varieties with higher seed productivity and increased stress tolerance for better adaptation to the abiotic stresses as a result of global climate change. Genetic engineering, to some extent, can overcome the limitations of genetic exchange in conventional breeding. Consequently, it considered as an effective method for improving modern crop breeding for B. napus. Since crop stress resistance is a polygenic complex trait, only by multi-gene synergistic effects can effectively achieve the comprehensive stress resistance of crops. Hence, in the present study, five stress resistance genes, NCED3, ABAR, CBF3, LOS5, and ICE1 were transferred into B. napus. Compared with wildtype (WT) plants, the multi-gene transformants K15 exhibited pronounced growth advantage under both normal growth and stress conditions. Additionally, K15 plants also showed significantly higher resistance response to multiple stresses at seed germination and seedling stages than WT plants. Furthermore, K15 plants had significantly higher leaf temperature and significantly lower stomatal aperture and water loss rate than WT plants, which indicated that the water-holding capacity of K15 plants was significantly superior to that of WT plants after stress treatment. In addition, K15 plants had significantly higher abscisic acid (ABA) content and significantly lower malondialdehyde (MDA) content than WT plants. In conclusion, the above results suggested that multi-gene co-expression could rapidly trigger plant stress resistance, reduce the stress injury on plants and synergistically improve the comprehensive resistance of B. napus.

Association of genetic variation in B-cell activating factor with chronic hepatitis B virus infection.

The outcome of hepatitis B virus (HBV) infection is considered to be related to the host immunogenetic susceptibility. B cell activating factor (BAFF) is involved in both B cell and T cell mediated immunity and its circulating levels were shown to be significantly elevated in HBV-related liver diseases. This study examined BAFF rs9514828 and rs12583006 polymorphisms in 386 patients with various liver diseases related to chronic HBV infection, 69 HBV infection resolvers, and 191 healthy controls. Both rs9514828 and rs12583006 polymorphisms and serum BAFF levels were determined in 232 patients with chronic HBV infection, and 61 healthy controls. The results showed that patients with chronic hepatitis had higher frequencies of rs9514828 genotype TT (19.75% vs. 11.86%, OR=2.397, 95% CI=1.121-5.125, P=0.023), genotypes CT+TT (74.69% vs. 63.55%, OR=1.478, 95% CI=1.050-2.080, P=0.045), and allele T (47.22% vs. 37.72%, OR=1.478, 95% CI=1.050-2.080, P=0.025) compared with patients with cirrhosis. Patients with chronic HBV infection and HBV infection resolvers had higher frequency of rs9514828 and rs12583006 haplotype TA compared with healthy controls (21.6% vs. 15.0%, OR=1.672, 95% CI=1.138-2.456, P=0.009 and 27.3% vs. 15.0%, OR=2.258, 95%CI=1.272-4.007, P=0.005, respectively). The rs9514828 and rs12583006 genotypes had no significant association with serum BAFF levels. These results suggest that the rs9514828 allele T may predispose to the liver inflammation in chronic HBV infection, and the rs9514828 and rs12583006 polymorphisms may combinatorially confer susceptibility to chronic HBV infection and resolution of the infection, possibly not through direct effect on serum BAFF levels.

Transcriptomic basis for drought-resistance in Brassica napus L.

Based on transcriptomic data from four experimental settings with drought-resistant and drought-sensitive cultivars under drought and well-watered conditions, statistical analysis revealed three categories encompassing 169 highly differentially expressed genes (DEGs) in response to drought in Brassica napus L., including 37 drought-resistant cultivar-related genes, 35 drought-sensitive cultivar-related genes and 97 cultivar non-specific ones. We provide evidence that the identified DEGs were fairly uniformly distributed on different chromosomes and their expression patterns are variety specific. Except commonly enriched in response to various stimuli or stresses, different categories of DEGs show specific enrichment in certain biological processes or pathways, which indicated the possibility of functional differences among the three categories. Network analysis revealed relationships among the 169 DEGs, annotated biological processes and pathways. The 169 DEGs can be classified into different functional categories via preferred pathways or biological processes. Some pathways might simultaneously involve a large number of shared DEGs, and these pathways are likely to cross-talk and have overlapping biological functions. Several members of the identified DEGs fit to drought stress signal transduction pathway in Arabidopsis thaliana. Finally, quantitative real-time PCR validations confirmed the reproducibility of the RNA-seq data. These investigations are profitable for the improvement of crop varieties through transgenic engineering.

Elevated serum soluble CD14 levels in chronic HBV infection are significantly associated with HBV-related hepatocellular carcinoma.

Hepatitis B virus (HBV) infection is a major cause of chronic liver diseases including hepatocellular carcinoma (HCC). CD14 and its soluble form sCD14 play important roles in immunity and are involved in the translocation of bacteria and their products which is related to the pathogenesis in chronic HBV infection. This study investigated serum sCD14 levels in HBV chronically infected patients with various clinical diseases. Serum sCD14 levels in HBV patients were significantly elevated compared with those of healthy controls. HCC patients had significantly highest levels of serum sCD14 across all the HBV-related diseases. Serum sCD14 levels significantly discriminated HCC from other HBV-related non-HCC diseases. The area under the receiver operating characteristic curve (AUC) of sCD14 levels for HCC was significantly higher in comparison with other HBV-related non-HCC diseases. The AUC of sCD14 for HCC (0.868, 95 % CI 0.791-0.946, P < 0.001) was higher than that of alpha-fetoprotein (0.660, 95 % CI 0.508-0.811, P = 0.039). Serum level of sCD14 was associated with the overall survival (OS) of HCC patients, with sCD14 levels >20 ng/mL being significantly related to poorer OS (P = 0.017). Multivariate regression showed that serum sCD14 level was an independent factor associated with the OS rates of HBV-related HCC patients (HR 2.544, 95 % CI 1.169-5.538, P = 0.019). HCC resection resulted in a significant decrease of sCD14 levels (P < 0.001). These findings suggest the potential role of sCD14 in the pathogenesis of chronic HBV infection, especially the development of HCC, and the potential usefulness of sCD14 as a biomarker for discriminating clinical diseases and predicting survival of HCC patients in chronic HBV infection.

Association of PTPN22 gene polymorphisms with chronic hepatitis B virus infection in Chinese Han population.

Lymphoid protein tyrosine phosphatase encoded by protein tyrosine phosphatase non-receptor 22 (PTPN22) gene plays an important regulatory role in T- and B-cell activation. This study investigated PTPN22 -1123G/C and intron 16 T/C polymorphisms in 372 patients with chronic hepatitis B virus (HBV) infection, 72 HBV infection resolvers and 273 healthy controls. Genotypic association tests between groups assuming codominant, dominant or log-additive genetic models were performed. In recessive model, PTPN22 -1123G/C genotype GG in healthy controls was more frequent than infection resolvers (P=0.037, OR=3.606, 95%CI=1.079-12.053) and this genotype in HBV patients was more frequent than resolvers although the difference was not significant (P=0.059). The PTPN22 intron 16 T/C genotype TC in cirrhosis patients was significantly higher than asymptomatic carriers (ASC) in codominant (P=0.028, OR=9.792, 95%CI=1.281-74.832) and overdominant (P=0.025, OR=10.142, 95%CI=1.332-77.214) models. This genotype in hepatocellular carcinoma (HCC) patients was significantly higher than ASC in codominant (P=0.034, OR=9.200, 95%CI=1.176-71.990) and overdominant (P=0.030, OR=9.677, 95%CI=1.241-75.442) models. These findings suggest that PTPN22 polymorphisms may predispose the chronicity or the development of cirrhosis and HCC in HBV infection.

microRNA-4717 differentially interacts with its polymorphic target in the PD1 3' untranslated region: A mechanism for regulating PD-1 expression and function in HBV-associated liver diseases.

Programmed cell death-1 (PD-1) is involved in hepatitis B virus (HBV) infection, the leading cause of hepatocellular carcinoma (HCC) worldwide. Single-nucleotide polymorphism, rs10204525, located in the PD1 3' untranslated regions (UTR), is associated with chronic HBV infection. MicroRNAs (miRNAs) regulate gene expression via specific binding to the target 3'UTR of mRNA. In this study, three miRNAs were predicted to putatively interact with PD1 rs10204525 polymorphic site of allele G. One of them, miRNA-4717, was demonstrated to allele-specifically affect luciferase activity in a dose-dependent manner in cells transfected with vectors containing different rs10204525 alleles. In lymphocytes from chronic HBV patients withrs10204525 genotype GG, miR-4717 mimics significantly decreased PD-1 expression and increased (TNF)-α and interferon (IFN)-γ production. miR-4717 inhibitor significantly increased PD-1 expression and decreased TNF-α and IFN-γ production although not significantly. In lymphocytes from chronic HBV patients with rs10204525 genotype AA, no similar effects were observed. miR-4717 levels in peripheral lymphocytes from patients with HBV-related chronic hepatitis, cirrhosis and HCC were significantly decreased. In conclusion, miR-4717 may allele-specifically regulate PD-1 expression through interaction with the 3' UTR of PD1 mRNA, leading to the alteration of immune regulation and affecting the susceptibility and disease course of chronic HBV infection.

Association between TNFAIP3 nonsynonymous single-nucleotide polymorphism rs2230926 and chronic hepatitis B virus infection in a Chinese Han population.

BACKGROUND: Single-nucleotide polymorphisms (SNPs) in tumor necrosis factor alpha-inducible protein 3 (TNFAIP3) gene have been linked to inflammatory, immunological and malignant diseases. Hepatitis B virus (HBV) infection is characterized by immunopathogenesis. This study investigated the association of rs2230926, a nonsynonymous SNP in TNFAIP3 gene, with chronic HBV infection. METHODS: Four hundred and fifty-five patients with chronic HBV infection with clinical diseases of chronic hepatitis (n = 183), liver cirrhosis (n = 167) and hepatocellular carcinoma (n = 105), 92 HBV infection resolvers and 171 healthy controls were included. All subjects were of Chinese Han ethnicity. Genotyping of rs2230926 was carried out by polymerase chain reaction-restriction fragment length polymorphism method. RESULTS: The gender and age between HBV patients, HBV infection resolvers and healthy controls had no statistical difference. The genotypes of rs2230926 in HBV patients, HBV infection resolvers and healthy controls are in Hardy-Weinberg equilibrium. The genotype and allele frequencies of TNFAIP3 rs2230926 polymorphism between HBV patients, HBV infection resolvers and healthy controls had no significant difference. The genotype and allele frequencies of TNFAIP3 rs2230926 polymorphism between HBV patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma also showed no significant difference. CONCLUSIONS: The TNFAIP3 rs2230926 polymorphism is not suggested to be associated with the susceptibility of chronic HBV infection or the progression of HBV-related diseases in this study. Replicative studies and studies in large control and HBV patient populations of different ethnicity by genotyping more polymorphisms in TNFAIP3 gene are needed.

Hepatocellular carcinoma in a large medical center of China over a 10-year period: evolving therapeutic option and improving survival.

BACKGROUND: Hepatocellular carcinoma (HCC) is among the most common and lethal cancers worldwide, especially in China. METHODS: We retrospectively analyzed data from patients who were diagnosed and treated HCC between 2002 and 2011 in a large hospital in northwest China and compared the data between periods 2002-2006 (P1) and 2007-2011 (P2). RESULTS: 2045 patients were included in analysis. The HCC stages at diagnosis according to the Barcelona clinic liver cancer staging system had no significant change. Treatment options of liver transplantation, transcatheter arterial chemoembolization and other therapy decreased while percutaneous local ablation and supportive care increased from P1 to P2. Options of surgical resection and systematic therapy had no significant change. Patient survival rates at 1, 3 and 5 years significantly improved from P1 to P2. The treatments with increasing option trend had a higher magnitude of survival increase and vise versa. CONCLUSION: Over the last 10 years, the patient survival had a significant increase which was mainly a result of the optimal therapeutic selections according to disease stages in this center. However, the proportion of patients diagnosed at early stages of HCC remained low and did not increase, a result calling for implementing surveillance system for at risk patients.

Gels based on anion recognition between triurea receptor and phosphate anion.

Anion recognition between the triurea receptor and phosphate anion is demonstrated as the cross-linkage to build supramolecular polymer gels for the first time. A novel multi-block copolymer (3) is designed to have functional triurea groups as cross-linking units along the polymer main chain. By virtue of anion coordination between the triurea receptor and phosphate anion with a binding mode of 2:1, supramolecular polymer gels are then prepared based on anion recognition using 3 as the building block.

Mean platelet volume on admission improves risk prediction in patients with acute coronary syndromes.

Our aim was to evaluate the incremental predictive value of adding mean platelet volume (MPV) to the Global Registry of Acute Coronary Events (GRACE) risk score. The MPV and GRACE score were determined on admission in 509 consecutive patients with acute coronary syndrome (ACS). Six-month mortality or nonfatal myocardial infarction (MI) was the study end point. Overall, 61 (12%) patients reached the combined end point. Cox multivariate analysis showed that an elevated MPV was an independent predictor of 6-month mortality or MI in patients with ACS. The addition of MPV to the GRACE model improved its global fit and discriminatory capacity. The new model including MPV allowed adequate reclassification of 16% of the patients. In conclusion, the inclusion of MPV into the GRACE risk score could allow improved risk classification, thereby refining risk stratification of patients with ACS.