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Background: Melanoma, originated from melanocytes located on the basal membrane of the epithelial tissue, is the most aggressive form of skin cancer that accounts for 75% of skin cancer-related death. Although it is believed that BRAF mutation and the mitogen-activated protein kinase (MAPK) pathway play critical roles in the pathogenesis of melanoma, how the MAPK signaling is regulated in melanoma carcinogenesis is still not fully understood. Methods: We characterized JMJD6 expression in melanoma tissue array by immunohistochemistry analysis. We used human melanoma A375, 451Lu and SK-MEL-1 cell lines for in vitro proliferation and invasion experiments, and xenograft transplanted mice using murine melanoma B16F10 cells by bioluminescence imaging for in vivo tumor growth and pulmonary metastasis assessments. Endothelial tube formation assay, chicken yolk sac membrane assay and matrigel plug assay were performed to test the effect of JMJD6 on the angiogenic potential in vitro and in vivo. Results: Here we report that the jumonji C domain-containing demethylase/hydroxylase JMJD6 is markedly up-regulated in melanoma. We found that high expression of JMJD6 is closely correlated with advanced clinicopathologic stage, aggressiveness, and poor prognosis of melanoma. RNA-seq showed that knockdown of JMJD6 affects the alternative splicing of a panel of transcripts including that encoding for PAK1, a key component in MAPK signaling pathway. We demonstrated that JMJD6 enhances the MAPK signaling and promotes multiple cellular processes including melanogenesis, proliferation, invasion, and angiogenesis in melanoma cells. Interestingly, JMJD6 is transcriptionally activated by c-Jun, generating a feedforward loop to drive the development and progression of melanoma. Conclusions: Our results indicate that JMJD6 is critically involved in melanoma carcinogenesis, supporting the pursuit of JMJD6 as a potential biomarker for melanoma aggressiveness and a target for melanoma intervention. [ABSTRACT FROM AUTHOR]

Background: Schizophrenia (SCZ) is a common mental disorder with high heritability, and genetic factors play a major role in the pathogenesis. Recent researches indicated that the CACNAH involved in calcium channels probably affect the potential pathogenesis of SCZ. Results: In this study, we attempted to investigate whether the CACNAH gene contributes the risk to SCZ in the Uighur Chinese population, and performed a case-control study involving 985 patient samples and 1218 normal controls to analyze nine SNPs within the CACNAH gene. Among these sites, six SNPs were significantly associated with SCZ in the allele distribution: rs132575 (adjusted Pallele = 0.039, OR = 1.159), rs713860 (adjusted Pallele = 0.039, OR = 0.792), rs738168 (adjusted Pallele = 0.039, OR = 0.785), rs136805 (adjusted Pallele = 0.014, OR = 1.212), rs5757760 (adjusted Pallele = 0.042, OR = 0.873) and rs5750871 (adjusted Pallele = 0.039, OR = 0.859). In addition, two SNPs turned to be risk factors for SCZ not only in the allele distribution, but also in the genotype distribution: rs132575 (adjusted Pgenotype = 0.037) and rs136805 (adjusted Pgenotype = 0.037). Conclusions: Overall, the present study provided evidence that significant association exists between the CACNA1I gene and SCZ in the Uighur Chinese population, subsequent validation of functional analysis and genetic association studies are needed to further extend this study. [ABSTRACT FROM AUTHOR]

Studies have implied that the circadian oscillation of mitogen-activated protein kinase (MAPK) signal pathways is crucial for hippocampus-dependent memory. NF1 mouse models (Nf1 heterozygous null mutants; Nf1+/-) displayed enhanced MAPK activity in the hippocampus and resulted in memory deficits. We assumed a link between MAPK pathways and hippocampal rhythmic oscillations, which have never been explored in Nf1+/- mice. We demonstrated that the level of extracellular signal-regulated kinases 1 and 2 (ERK1/2) phosphorylation in Nf1+/- mice were significantly higher at nighttime than at daytime. Moreover, the in vivo recording revealed that for the Nf1+/- group, the power spectral density of theta rhythm significantly decreased and the firing rates of pyramidal neurons increased. Our results indicated that the hippocampal MAPK oscillation and theta rhythmic oscillations in Nf1+/- mice were disturbed and hinted about a possible mechanism for the brain dysfunction in Nf1+/- mice. [ABSTRACT FROM AUTHOR]

Background: Prostaglandin E2 (PGE2)-involved neuroinflammatory processes are prevalent in several neurological conditions and diseases. Amyloid burden is correlated with the activation of E-prostanoid (EP) 2 receptors by PGE2 in Alzheimer's disease. We previously demonstrated that electromagnetic field (EMF) exposure can induce pro-inflammatory responses and the depression of phagocytosis in microglial cells, but the signaling pathways involved in phagocytosis of fibrillar β-amyloid (fAβ) in microglial cells exposed to EMF are poorly understood. Given the important role of PGE2 in neural physiopathological processes, we investigated the PGE2-related signaling mechanism in the immunomodulatory phagocytosis of EMF-stimulated N9 microglial cells (N9 cells). Methods: N9 cells were exposed to EMF with or without pretreatment with the selective inhibitors of cyclooxygenase-2 (COX-2), Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), and mitogen-activated protein kinases (MAPKs) and antagonists of PG receptors EP1-4. The production of endogenous PGE2 was quantified by enzyme immunoassays. The phagocytic ability of N9 cells was evaluated based on the fluorescence intensity of the engulfed fluorescent-labeled fibrillar β-amyloid peptide (1-42) (fAβ42) measured using a flow cytometer and a fluorescence microscope. The effects of pharmacological agents on EMF-activated microglia were investigated based on the expressions of JAK2, STAT3, p38/ERK/JNK MAPKs, COX-2, microsomal prostaglandin E synthase-1 (mPGES-1), and EP2 using real-time PCR and/or western blotting. Results: EMF exposure significantly increased the production of PGE2 and decreased the phagocytosis of fluorescent-labeled fAβ42 by N9 cells. The selective inhibitors of COX-2, JAK2, STAT3, and MAPKs clearly depressed PGE2 release and ameliorated microglial phagocytosis after EMF exposure. Pharmacological agents suppressed the phosphorylation of JAK2-STAT3 and MAPKs, leading to the amelioration of the phagocytic ability of EMF-stimulated N9 cells. Antagonist studies of EP1-4 receptors showed that EMF depressed the phagocytosis of fAβ42 through the PGE2 system, which is linked to EP2 receptors. Conclusions: This study indicates that EMF exposure could induce phagocytic depression via JAK2-STAT3- and MAPK-dependent PGE2-EP2 receptor signaling pathways in microglia. Therefore, pharmacological inhibition of PGE2 synthesis and EP2 receptors may be a potential therapeutic strategy to combat the neurobiological deterioration that follows EMF exposure. [ABSTRACT FROM AUTHOR]

Background: Studies have indicated that depressive disorders are observed frequently in dentists. It's suggested that dentists encounter numerous sources of stress in their professional career. We noticed that the noises in dental environments are very unpleasant. The animal modeling studies suggested that stressful noise could produce depressive-like phenotypes in rodent animals. We hypothesize that the dental noise may be one of the primary stressors causing depressive disorders in dentists. Results: We treated C57BL/6 mice with programmatically played wide-spectrum dental noise for 8 h/day at 75 ± 10 dB SPL level for 30 days, and then tested the behaviors. After exposure to dental noise, animals displayed the depressive-like phenotypes, accompanied by inhibition of neurogenesis in hippocampus. These deficits were ameliorated by orally administered with antidepressant fluoxetine. Conclusions: Our results suggested that dental noise could be one of the primary stressors for the pathogenesis of depressive disorders and the dental noise mouse model could be used in further depression studies. [ABSTRACT FROM AUTHOR]

Background: The high and continually increasing prevalence of human immunodeficiency virus (HIV) and other sexually transmitted diseases among men who have sex with men (MSM) in China underscores the critical importance of examining the exact sexual networks that result in HIV transmission, as well as HIV infection, using powerful sampling methods, such as respondent-driven sampling (RDS), to improve the sexual health of this population.Methods: Using RDS, a cross-sectional study was conducted among MSM in Wenzhou, Zhejiang province, China from December 2013 to June 2014. The type of sex, numbers of anal sex partners, male oral sex partners and vaginal sex partners, condom use during each type of sex over the previous 6 months, prevention behaviors, risk perception, and the burdens of HIV and syphilis were investigated and analyzed.Results: Of 424 MSM, a great number of them did anal sex, male oral sex, and vaginal sex during the previous 6 months, and weighted estimates for the prevalence that MSM did not conduct these sexual behaviors were 11.2 % (95 % confidence interval [CI] =6.7-16.50 %), 20.3 % (95 % CI = 15.2-27.1 %), and 58.9 % (95 % CI = 52.1-65.8 %), respectively. Multiple sexual partners, engaging in regular, casual and commercial sex, and lack of condom use during all types of sex were common among MSM. The estimated HIV and syphilis prevalences were 22.8 % (95 % CI = 16.9-28.5 %) and 9.7 % (95 % CI = 6.4-13.6 %), respectively. Of the participants, 53.5 % (95 % CI = 45.3-60.2 %) received HIV-related interventions during the previous year, 48.1 % (95 % CI = 39.7-55.1 %) had never been tested for HIV, and only 14.1 % (95 % CI =10.1-19.2 %) perceived a risk of contracting HIV. Multiple logistic regression analysis revealed that age over 44 years (adjusted odds ratio [AOR] = 3.60, 95 % CI = 1.34-9.64), a monthly income of 3001-4000 yuan (approximately 470-630 US$) (AOR = 1.96, 95 % CI = 1.67-3.60), multiple anal sex partners (AOR = 1.93, 95 % CI = 1.15-3.24), awareness of the possibility of contracting HIV (AOR = 3.18, 95 % CI = 1.56-6.48), and current syphilis infection (AOR = 3.01, 95 % CI = 1.44-6.29) were predictors of HIV infection.Conclusions: HIV transmission has become highly prevalent and will likely become more prevalent among MSM and their female partners if these risky sexual networks persist. Our findings call for urgent and effective interventions to prevent the rapid transmission of HIV among MSM in Wenzhou. [ABSTRACT FROM AUTHOR]

Objectives: The objective of this study was to determine the rate of acquired immune deficiency syndrome (AIDS) in Zhejiang province and to identify specific factors associated with progression of this disease. Methods: This study utilized a retrospective cohort to identify the specific factors involved in the progression of human immunodeficiency virus (HIV) to AIDS. We collected data of patients existing in care between 2008 and 2012 from the national surveillance system databases. We performed our analyses using a multivariate Cox proportional hazards model. Results: This study included 9216 HIV-positive patients (75.6 % male), which yielded 12,452 person-years (py) of follow-up-data. The AIDS progression rates were 33.9 % (2008), 33.6 % (2009), 38.1 % (2010), 30.6 % (2011) and 25.9 % (2012). We observed a significant reduction in the rate of progression Of HIV to AIDS post-2010 (Pearson χ2= 4341.9, P < 0.001). The cumulative AIDS progression incidence rates were 33.4, 35.4, 36.4, 37.0 and 37.04 per 100 py in 1 each of the 5 years of follow-up. This study found that age was an independent risk factor for the progression of HIV to AIDS. Compared with patients infected with HIV by homosexual transmission, patients infected with HIV by heterosexuals transmission or blood transfusion had a reduced hazard ratio (HR) for progression to AIDS (heterosexual transmission: HR = 0.695, 0.524, P = 0.007; blood transfusion: HR = 0.524, P = 0.015). Diagnosed with HIV from 2011 to 2012 and having a higher CD4+ cell count (350-500 cells/mm3; or >500 cells/mm3) at baseline were independently associated with lower rates of HIV progression to AIDS [HR = 0.382, 0.380, 0.187, P < 0.001]. Patients with a CD+ T-cell count of 200-350 cells/mm3 or greater than 350 cells/mm3 were less likely to develop AIDS following HIV diagnosis than were those patients without HAART treatment. Conclusion: This study found a high progression rate from HIV to AIDS in HIV patients residing within Zhejiang province from 2008 to 2010. This rate decreased after 2010, which coincided with the new criteria for HAART treatment, which likely contributed to the observed reduction in the rate of progression. Initiation of HAART with higher CD4+ T-cell count may reduce rate of AIDS progression. Based on our results, we conclude that efficient strategies for HIV screening, as well as early diagnosis and treatment are necessary to reduce the progression of HIV to AIDS. [ABSTRACT FROM AUTHOR]

Background: Many species of the genus Prevotella are pathogens that cause oral diseases. Prevotella intermedia is known to cause various oral disorders e.g. periodontal disease, periapical periodontitis and noma as well as colonize in the respiratory tract and be associated with cystic fibrosis and chronic bronchitis. It is of clinical significance to identify the main drive of its various adaptation and pathogenicity. In order to explore the intra-species genetic differences among strains of Prevotella intermedia of different niches, we isolated a strain Prevotella intermedia ZT from the infected root canal of a Chinese patient with periapical periodontitis and gained a draft genome sequence. We annotated the genome and compared it with the genomes of other taxa in the genus Prevotella. Results: The raw data set, consisting of approximately 65X-coverage reads, was trimmed and assembled into contigs from which 2165 ORFs were predicted. The comparison of the Prevotella intermedia ZT genome sequence with the published genome sequence of Prevotella intermedia 17 and Prevotella intermedia ATCC25611 revealed that ~14% of the genes were strain-specific. The Preveotella intermedia strains share a set of conserved genes contributing to its adaptation and pathogenic and possess strain-specific genes especially those involved in adhesion and secreting bacteriocin. The Prevotella intermedia ZT shares similar gene content with other taxa of genus Prevotella. The genomes of the genus Prevotella is highly dynamic with relative conserved parts: on average, about half of the genes in one Prevotella genome were not included in another genome of the different Prevotella species. The degree of conservation varied with different pathways: the ability of amino acid biosynthesis varied greatly with species but the pathway of cell wall components biosynthesis were nearly constant. Phylogenetic tree shows that the taxa from different niches are scarcely distributed among clades. Conclusions: Prevotella intermedia ZT belongs to a genus marked with highly dynamic genomes. The specific genes of Prevotella intermedia indicate that adhesion, competing with surrounding microbes and horizontal gene transfer are the main drive of the evolution of Prevotella intermedia. [ABSTRACT FROM AUTHOR]

Background The relationship between genetic factors and the development of cerebral palsy (CP) has recently attracted much attention. Polymorphisms in the genes encoding proinflammatory cytokines have been shown to be associated with susceptibility to perinatal brain injury and development of CP. Interleukin-6 (IL-6) is a proinflammatory cytokine that plays a pivotal role in neonatal brain injury, but conflicting results have been reported regarding the association between IL-6 single nucleotide polymorphisms (SNPs) and CP. The purpose of this study was to analyze IL-6 gene polymorphisms and protein expression and to explore the role of IL-6 in the Chinese CP population. Methods A total of 753 healthy controls and 713 CP patients were studied to detect the presence of five SNPs (rs1800796, rs2069837, rs2066992, rs2069840, and rs10242595) in the IL-6 locus. Of these, 77 healthy controls and 87 CP patients were selected for measurement of plasma IL-6 by Luminex assay. The SHEsis program was used to analyze the genotyping data. For all comparisons; multiple testing on each individual SNP was corrected by the SNPSpD program. Results There were no differences in allele or genotype frequencies between the overall CP patients and controls among the five genetic polymorphisms. However, subgroup analysis found significant sex-related differences in allele and genotype frequencies. Differences were found between spastic CP and controls in males for rs2069837; between CP with periventricular leukomalacia and controls in males for rs1800796 and rs2066992; and between term CP and controls in males for rs2069837. Plasma IL-6 levels were higher in CP patients than in the controls, and this difference was more robust in full-term male spastic CP patients. Furthermore, the genotype has an effect on IL-6 synthesis. Conclusions The influence of IL-6 gene polymorphisms on IL-6 synthesis and the susceptibility to CP is related to sex and gestational age. [ABSTRACT FROM AUTHOR]

Background Much of the data resolution of the haploid non-recombining Y chromosome (NRY) haplogroup O in East Asia are still rudimentary and could be an explanatory factor for current debates on the settlement history of Island Southeast Asia (ISEA). Here, 81 slowly evolving markers (mostly SNPs) and 17 Y-chromosomal short tandem repeats were used to achieve higher level molecular resolution. Our aim is to investigate if the distribution of NRY DNA variation in Taiwan and ISEA is consistent with a single pre-Neolithic expansion scenario from Southeast China to all ISEA, or if it better fits an expansion model from Taiwan (the OOT model), or whether a more complex history of settlement and dispersals throughout ISEA should be envisioned. Results We examined DNA samples from 1658 individuals from Vietnam, Thailand, Fujian, Taiwan (Han, plain tribes and 14 indigenous groups), the Philippines and Indonesia. While haplogroups O1a*-M119, O1a1*-P203, O1a2-M50 and O3a2-P201 follow a decreasing cline from Taiwan towards Western Indonesia, O2a1-M95/M88, O3a*-M324, O3a1c-IMSJST002611 and O3a2c1a-M133 decline northward from Western Indonesia towards Taiwan. Compared to the Taiwan plain tribe minority groups the Taiwanese Austronesian speaking groups show little genetic paternal contribution from Han. They are also characterized by low Y-chromosome diversity, thus testifying for fast drift in these populations. However, in contrast to data provided from other regions of the genome, Y-chromosome gene diversity in Taiwan mountain tribes significantly increases from North to South. Conclusion The geographic distribution and the diversity accumulated in the O1a*-M119, O1a1*-P203, O1a2-M50 and O3a2-P201 haplogroups on one hand, and in the O2a1-M95/M88, O3a*- M324, O3a1c-IMS-JST002611 and O3a2c1a-M133 haplogroups on the other, support a pincer model of dispersals and gene flow from the mainland to the islands which likely started during the late upper Paleolithic, 18,000 to 15,000 years ago. The branches of the pincer contributed separately to the paternal gene pool of the Philippines and conjointly to the gene pools of Madagascar and the Solomon Islands. The North to South increase in diversity found for Taiwanese Austronesian speaking groups contrasts with observations based on mitochondrial DNA, thus hinting to a differentiated demographic history of men and women in these populations. [ABSTRACT FROM AUTHOR]

Background DNA methylation has been viewed as the most highly characterized epigenetic mark for genome regulation and development. Postnatal brains appear to exhibit stimulus-induced methylation changes because of factors such as environment, lifestyle, and diet (nutrition). The purpose of this study was to examine how extensively the brain DNA methylome is regulated by nutrition in early life. Results By quantifying the total amount of 5-methylcytosine (5mC) in the thalamus and the hippocampus of postnatal malnourished mice and normal mice, we found the two regions showed differences in global DNA methylation status. The methylation level in the thalamus was much higher than that in the hippocampus. Then, we used a next-generation sequencing (NGS)-based method (MSCC) to detect the whole genome methylation of the two regions in malnourished mice and normal mice. Notably, we found that in the thalamus, 500 discriminable variations existed and that approximately 60% were related to neuronal development or psychiatric diseases. Pathway analyses of the corresponding genes highlighted changes for 9 genes related to long-term potentiation (5.3-fold enrichment, P = 0.033). Conclusions Our findings may help to indicate the genome-wide DNA methylation status of different brain regions and the effects of malnutrition on brain DNA methylation. The results also indicate that postnatal malnutrition may increase the risk of psychiatric disorders. [ABSTRACT FROM AUTHOR]

Abstract A recent genome-wide association study has reported three newly identified susceptible loci (rs2842992 near the gene SOD2, rs1789110 near the gene MBP and rs722782 near the gene C8orf42) to be associated with the geographic atrophy subtype of age-related macular degeneration in European-descent population. We investigated the correlation between these variants and advanced age-related macular degeneration for the first time in a Han Chinese cohort; however, no evidence supports these previously identified loci contribute to advanced age-related macular degeneration susceptibility in Chinese population. [ABSTRACT FROM AUTHOR]

Background: Metastatic lung cancer is one of the leading causes of cancer death. In recent years, epithelialto- mesenchymal transition (EMT) has been found to contribute to metastasis, as it enables migratory and invasive properties in cancer cells. Previous genome-wide studies found that DNA methylation was unchanged during EMT induced by TGF-β in AML12 cells. In this study, we aimed to discover EMT-related changes in DNA methylation in cancer cells, which are poorly understood. Methods: We employed a next-generation sequencing-based method, MSCC (methyl-sensitive cut counting), to investigate DNA methylation during EMT in the A549 lung cancer cell line. Results: We found that methylation levels were highly correlated to gene expression, histone modifications and small RNA expression. However, no differentially methylated regions (DMRs) were found in A549 cells treated with TGF-β for 4 h, 12 h, 24 h and 96 h. Additionally, CpG islands (CGIs) showed no overall change in methylation levels, and at the single-base level, almost all of the CpGs showed conservation of DNA methylation levels. Furthermore, we found that the expression of DNA methyltransferase 1, 3a, 3b (DNMT1, DNMT3a, DNMT3b) and ten-eleven translocation 1 (TET1) was altered after EMT. The level of several histone methylations was also changed. Conclusions: DNA methylation-related enzymes and histone methylation might have a role in TGF-β-induced EMT without affecting the whole DNA methylome in cancer cells. Our data provide new insights into the global methylation signature of lung cancer cells and the role of DNA methylation in EMT. [ABSTRACT FROM AUTHOR]

Background: Brain tumor remains the leading cause of disease-related death in children. Many studies have focused on the complex biological process involved in pediatric brain tumors but little is know about the possible role of microRNAs in the genesis of these tumors. Methods: In this study, we used a microRNA microarray assay to study the expression pattern of microRNAs in pediatric gliomas and matched normal tissues. Results: We found 40 differentially expressed microRNAs, among which miR-1321, miR-513b, miR-769-3p were found be related to cancer genesis for the first time. The expression of selected microRNAs were then confirmed by qRT-PCR. Furthermore, GO and pathway analysis showed that the target genes of the 40 differentially expressed microRNAs were significantly enriched in nervous system-related and tumor-related biological processes and signaling pathways. Additionally, an apoptosis-related network of microRNA–mRNA interaction, representing the critical microRNAs and their targets, was constructed based on microRNA status. Conclusions: In the present study we identified the changed expression pattern of microRNAs in pediatric gliamas. Our study also provides a better understanding of pediatric brain tumor biology and may assist in the development of less toxic therapies and in the search for better markers for disease stratification. [ABSTRACT FROM AUTHOR]

Background: Non-ischemic dilated cardiomyopathy (DCM) is the most common cardiomyopathy worldwide, with significant mortality. Correct evaluation of the patient's myocardial function has important clinical significance in the diagnosis, therapeutic effect assessment and prognosis in non-ischemic DCM patients. This study evaluated the feasibility of three-dimensional speckle tracking imaging (3D-STE) for assessment of the left ventricular myocardial strain in patients with non-ischemic dilated cardiomyopathy (DCM). Methods: Apical full-volume images were acquired from 65 patients with non-ischemic DCM (DCM group) and 59 age-matched normal controls (NC group), respectively. The following parameters were measured by 3D-STE: the peak systolic radial strain (RS), circumferential strain (CS), longitudinal strain (LS) of each segment. Then all the parameters were compared between the two groups. Results: The peak systolic strain in different planes had certain regularities in normal groups, radial strain (RS) was the largest in the mid region, the smallest in the apical region, while circumferential strain (CS) and longitudinal strain (LS) increased from the basal to the apical region. In contrast, the regularity could not be applied to the DCM group. RS, CS, LS were significantly decreased in DCM group as compared with NC group (P < 0.001 for all). The interobserver, intraobserver and test-retest reliability were acceptable. Conclusions: 3D-STE is a reliable tool for evaluation of left ventricular myocardial strain in patients with nonischemic DCM, with huge advantage in clinical application. [ABSTRACT FROM AUTHOR]

Background: CYP2E1 encodes a member of the cytochrome P450 superfamily of enzymes which play a central role in activating and detoxifying many carcinogens and endogenous compounds thought to be involved in the development of cancer. The PstI/RsaI and DraI polymorphism are two of the most commonly studied polymorphisms of the gene for their association with risk of head and neck cancer, but the results are conflicting. Methods: We performed a meta-analysis using 21 eligible case-control studies with a total of 4,951 patients and 6,071 controls to summarize the data on the association between the CYP2E1 PstI/RsaI and DraI polymorphism and head and neck cancer risk, especially by interacting with smoking or alcohol. Results: Compared with the wild genotype, the OR was 1.96 (95% CI: 1.33-2.90) for PstI/RsaI and 1.56 (95% CI: 1.06-2.27) for DraI polymorphism respectively. When stratified according to ethnicity, the OR increased in the Asians for both polymorphisms (OR = 2.04, 95% CI: 1.32-3.15 for PstI/RsaI; OR = 2.04, 95% CI: 1.27-3.29 for DraI), suggesting that the risk is more pronounced in Asians. Conclusion: Our meta-analysis suggests that individuals with the homozygote genotypes of PstI/RsaI or DraI polymorphism might be associated with an increased risk of head and neck cancer, especially in Asians. [ABSTRACT FROM AUTHOR]

Background: Genetic factors related to the regulation of apoptosis in schizophrenia patients may be involved in a reduced vulnerability to cancer. XRCC4 is one of the potential candidate genes associated with schizophrenia which might induce colorectal cancer resistance. Methods: To examine the genetic association between colorectal cancer and schizophrenia, we analyzed five SNPs (rs6452526, rs2662238, rs963248, rs35268, rs2386275) covering ~205.7 kb in the region of XRCC4. Results: We observed that two of the five genetic polymorphisms showed statistically significant differences between 312 colorectal cancer subjects without schizophrenia and 270 schizophrenia subjects (rs6452536, p = 0.004, OR 0.61, 95% CI 0.44-0.86; rs35268, p = 0.028, OR 1.54, 95% CI 1.05-2.26). Moreover, the haplotype which combined all five markers was the most significant, giving a global p = 0.0005. Conclusions: Our data firstly indicate that XRCC4 may be a potential protective gene towards schizophrenia, conferring reduced susceptibility to colorectal cancer in the Han Chinese population. [ABSTRACT FROM AUTHOR]

Background: Vitamin A and its derivatives (retinoids) are crucial for the development, maintenance and morphogenesis of the central nervous system (CNS). Although motor impairment has been reported in postnatal vitamin A depletion rodents, the effect of vitamin A depletion on homeostasis maintaining capability in response to external interference is not clear. Methods: In the current study, we measured the effect of vitamin A depletion on motor ability and pain sensitivity under two different conditions: 1. prior to any injection and 2. after the injection of an N-methyl-D-aspartate (NMDA) receptor antagonist (MK-801). Results: Vitamin A depletion mice showed decreased body weight, enhanced locomotor activity, increased rearing and less tail flick latency. Vitamin A depletion also induced hypersensitivity of stereotypy, ataxia, rearing, and tail flick latency to MK-801, but hyposensitivity of locomotion to MK-801. Conclusions: These findings suggest that vitamin A depletion affect broad basal behavior and disrupt homeostasis maintaining capability in response to glutamate perturbation. We provide a useful animal model for assessing the role of vitamin A depletion in regulating animal behavior, and for detecting how neurotransmitter pathways might be involved in vitamin A depletion related behavioral abnormalities. [ABSTRACT FROM AUTHOR]

Background: Fatty acid-binding proteins (FABPs), small cytosolic proteins that function in the uptake and utilization of fatty acids, have been extensively studied in higher vertebrates while invertebrates have received little attention despite similar nutritional requirements during periods of reproductive activity. Results: Therefore, a cDNA encoding Eriocheir sinensis FABP (Es-FABP) was cloned based upon EST analysis of a hepatopancreas cDNA library. The full length cDNA was 750 bp and encoded a 131 aa polypeptide that was highly homologous to related genes reported in shrimp. The 9108 bp Es-FABP gene contained four exons that were interrupted by three introns, a genomic organization common among FABP multigene family members in vertebrates. Gene expression analysis, as determined by RT-PCR, revealed the presence of Es-FABP transcripts in hepatopancreas, hemocytes, ovary, gills, muscle, thoracic ganglia, heart, and intestine, but not stomach or eyestalk. Real-time quantitative RT-PCR analysis revealed that Es-FABP expression in ovary, hemocytes, and hepatopancreas was dependent on the status of ovarian development, with peak expression observed in January. Conclusions: Evidence provided in the present report supports a role of Es-FABP in lipid transport during the period of rapid ovarian growth in E. sinensis, and indirectly confirms the participation of the hepatopancreas, ovary, and hemocytes in lipid nutrient absorption and utilization processes. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes is becoming an epidemic in China. To evaluate the prevalence, clustering of metabolic risk factors and their impact on type 2 diabetes, we conducted a population-based study in Shanghai, China's largest metropolitan area. Methods: From 2006 to 2007, 2,113 type 2 diabetes cases and 2,458 comparable controls of adults aged 40 to 79 years were enrolled. Demographic, lifestyle, and dietary factors were assessed via standardized questionnaires. Plasma, red and white blood cells were collected and stored for future studies. Anthropometric indices and biochemical intermediates (including blood pressure, fasting glucose, glycosylated hemoglobin, and blood lipids) were measured. The prevalence of metabolic syndrome were also compared following two criteria recommended by the Chinese Diabetes Society (CDS, 2004) and the National Cholesterol Education Program's Adult Treatment Panel III (ATP III, 2002). Results: Prevalence of metabolic syndrome (62% vs. 15% using CDS criteria) and its individual components, including obesity (51% vs. 42%), hypertension (54% vs. 41%), hypertriglyceridemia (42% vs. 32%), and low high-density lipoprotein-cholesterol (HDL) levels (36% vs. 25%) were higher in diabetes cases than controls. Regardless of criteria used, those with impaired fasting glucose (IFG) had similarly high prevalence of metabolic syndrome as did diabetes cases. In a multiple logistic regression model adjusted for demographics and lifestyle risk factors, the odds ratios of diabetes (95% CI) were 1.23 (1.04-1.45) for overweight (28 >= BMI >= 24), 1.81 (1.45-2.25) for obesity (BMI > 28), 1.53 (1.30-1.80) for central obesity (waist circumference > 80 cm for woman or waist circumference > 85 cm for man), 1.36 (1.17-1.59) for hypertension (sbp/dbp >= 140/90 mmHg), 1.55 (1.32-1.82) for high triglycerides (triglycerides > 1.70 mmol/l) and 1.52 (1.23-1.79) for low HDL-C (HDL-C < 1.04 mmol/L). Conclusions: These data indicate that multiple metabolic risk factors-individually or jointly-were more prevalent in diabetes patients than in controls. Further research will examine hypotheses concerning the high prevalence of IFG, family history, and central obesity, aiding development of multifaceted preventive strategies specific to this population. [ABSTRACT FROM AUTHOR]

Background: 2',3'-Cyclic nucleotide 3'-phosphodiesterase (CNP), one of the promising candidate genes for schizophrenia, plays a key part in the oligodendrocyte function and in myelination. The present study aims to investigate the relationship between CNP and schizophrenia in the Chinese population and the effect of different factors on the expression level of CNP in schizophrenia. Methods: Five CNP single nucleotide polymorphisms (SNPs) were investigated in a Chinese Han schizophrenia case-control sample set (n = 180) using direct sequencing. The results were included in the following meta-analysis. Quantitative real-time polymerase chain reaction (PCR) was conducted to examine CNP expression levels in peripheral blood lymphocytes. Results: Factors including gender, genotype, sub-diagnosis and antipsychotics-treatment were found not to contribute to the expression regulation of the CNP gene in schizophrenia. Our meta-analysis produced similar negative results. Conclusion: The results suggest that the CNP gene may not be involved in the etiology and pathology of schizophrenia in the Chinese population. [ABSTRACT FROM AUTHOR]

Background: The occurrence of liver cancer is higher in males than in females, and the incidence increases during aging. Signaling pathways regulated by retinoid x receptor α (RXRα) are involved in hepatocellular carcinogenesis. The phenotype of hepatocyte RXRα deficient mice is different between genders. To explore the impact of hepatocyte RXRα deficiency on gender-dependent hepatic gene expression, we compared the expression profiles of cancer-related genes in 6 and 24 month old male and female mice. Results: In 6 month old mice, male mutant mice showed more cancer-related genes with alteration in mRNA levels than females did (195 vs. 60). In aged mice (24 month), female mutant mice showed greater deviation in mRNA expression levels of cancer-related genes than their male counterparts (149 vs. 82). The genes were classified into five categories according to their role in carcinogenesis: apoptosis, metastasis, cell growth, stress, and immune respnse. In each category, dependent upon age and gender, the genes as well as the number of genes with altered mRNA levels due to RXRα deficiency varies. Conclusion: The change in hepatic cancer-related gene expression profiles due to RXRα deficiency was gender- and age-dependent. The alteration of mRNA levels of cancer-related genes implied that aberrant RXRα signaling could potentially increase the risk of liver cancer and that retinoid signaling might contribute to gender- and age-associated liver cancer incidence. [ABSTRACT FROM AUTHOR]

Background and Aim: The traditional method of taking Chinese Medicine involves creating a decoction by cooking medicinal Chinese herbs. However, this method has become less popular, being replaced by the more convenient method of consuming concentrated Chinese herbal extracts, which creates challenges related to the complexity of stacking multiple formulas., Methods: We developed the Chinese Intelligence Prescription System (CIPS) to simplify the prescription process. In this study, we used data from our institutions pharmacy to calculate the number of reductions, average dispensing time, and resulting cost savings., Results: The mean number of prescriptions was reduced from 8.19 ± 3.65 to 7.37 ± 3.34 ([Formula: see text]). The reduction in the number of prescriptions directly resulted in decreased dispensing time, reducing it from 1.79 ± 0.25 to 1.63 ± 0.66 min ([Formula: see text]). The reduced dispensing time totaled 3.75 h per month per pharmacist, equivalent to an annual labor cost savings of $15,488 NTD per pharmacist. In addition, drug loss was reduced during the prescription process, with a mean savings of $4,517 NTD per year. The combined savings adds up to a not insignificant $20,005 NTD per year per pharmacist. When taking all TCM clinics/hospitals in Taiwan into account, the total annual savings would be $77 million NTD., Conclusion: CIPS assists clinicians and pharmacists to formulate precise prescriptions in a clinical setting to simplify the dispensing process while reducing medical resource waste and labor costs., (© 2023. The Author(s).)

The Editor-in-Chief has retracted this article [1] because of an error in the meta analysis. Re-examination of the data has showed that there is only one published randomized controlled trial comparing Superion with XStop. Due to a misunderstanding of the published clinical data, the conclusions drawn in the article are incorrect. Author Xing Yu approved this retraction, none of the other authors replied to correspondence from the publisher about this retraction.

Background: Decompressive laminectomy (DI) is a standard operation for lumbar spinal stenosis (LSS) patient with severe claudication symptoms for many years. However, patients whose symptom severity does not meet undergoing invasive surgery make therapeutic options into dilemma. Interspinous spacers (ISP) bridge the gap between surgical interventions and CC in management of LSS. In our study, we aim to systematically assess the two FDA-approved interspinous spacers for treatment of lumbar spinal stenosis: Superion versus X-STOP., Methods: Electronic databases, including PubMed, Embase, MEDLINE, Cochrane Library were searched to retrieve clinical trials concerning the comparison between Superion and X-STOP in treatment for lumbar spinal stenosis before April 2017. The following outcome measures were extracted: (1) Zurich Claudication Questionnaire (ZCQ) patient satisfaction score, (2) axial pain severity, (3) extremity pain severity, (4) back-specific functional impairment, (5) reoperation, and (6) complication. The data analysis was conducted with Review Manager 5.3., Results: Five randomized controlled trials (RCTs) with 1118 patients were included in this meta-analysis. The pooled analysis indicated that the Superion group is superior to X-STOP in axial pain severity (SMD: 0.03; 95% CI 0.15, 0.45; p < 0.0001, I 2  = 41%, p = 0.16), ZCQ patient satisfaction score (SMD: 0.23; 95% CI 0.08, 0.38; p = 0.002, I 2  = 0%, p = 0.61). However, Superion group showed similarity outcome in extremity pain severity (SMD: 0.18; 95% CI - 0.06, 0.43; p = 0.14, I 2  = 62%, p = 0.05), back-specific functional impairment (SMD: 0.04; 95% CI - 0.10, 0.19; p = 0.56, I 2  = 0%, p = 0.77), reoperation rate (RR: 1.10; 95% CI 0.82, 1.48; p = 0.51, I 2  = 19%, p = 0.30), and complication (RR: 0.98; 95% CI 0.63, 1.53; p = 0.92, I 2  = 0%, p = 0.83)., Conclusion: Both the Superion and X-STOP interspinous spacers can relieve symptoms of LSS. In addition, the Superion spacer may represent a promising spacer for patient with LSS. As we know, the effectiveness and safety of ISP is still considered investigational and unfavor clinical results in the medical literature may continue to limit the appeal of IPS to many surgeons in the future. However, because of the advantage of IPS technique, it will win a wide place in the future degenerative lumbar microsurgery.

Background: Many osteoarthritis (OA) susceptibility genes have been identified in recent years. Given the overlap in the phenotype of joint inflammation between OA and Kashin-Beck disease (KBD), the aim of this study is to explore whether the reported OA susceptibility genes and two genes that may link to OA pathophysiology are associated with KBD in the Tibetan population., Method: Fifteen single-nucleotide polymorphisms (SNPs) in 12 candidate genes previously reported as OA susceptibility loci were selected for investigation. Genotyping was performed using the SNaPshot method for these SNPs in a Tibetan population composed of 849 KBD patients and 565 normal controls. Meanwhile, the coding regions of two genes, COL10A1 and HABP2, which may involve in the pathological mechanism of OA/KBD, were sequenced by Sanger sequencing to identify susceptibility coding variants for KBD in the Tibetan population., Results: The two arthritis-susceptible candidate SNPs, rs7775 (p.Arg324Gly) in the FRZB gene and rs7033979 in the ASPN gene, showed associations with KBD (OR = 1.568, P = 4 × 10 -3 and OR = 0.744, P = 8 × 10 -3 , respectively). The coding variants rs142463796 (p.Asp128Asn) and rs2228547 (p.Gly545Arg) in the COL10A1 gene (OR = 9.832 and P = 6 × 10 -3 and OR = 1.242, P = 0.043, respectively) and rs548354451 (p.Asp272Glu) in the HABP2 gene (OR = 2.813, P = 0.010) were associated with KBD patients., Conclusion: These finding suggested that rs7775 in the FRZB gene may increase susceptibility to KBD, while rs7033979 in the ASPN gene may play a protective role in susceptibility to KBD in Tibetans. Moreover, genetic variants in chondrogenesis-related genes COL10A1 and HABP2 may play a role in the risk of developing KBD in the Tibetan population.