UGT201H1 overexpression confers cyflumetofen resistance in Tetranychus cinnabarinus (Boisduval).

BACKGROUND: Tetranychus cinnabarinus is one of the most common polyphagous arthropod herbivores, and is primarily controlled by the application of acaricides. The heavy use of acaricides has led to high levels of resistance to acaricides such as cyflumetofen, which poses a threat to global resistance management programs. Cyflumetofen resistance is caused by an increase in metabolic detoxification; however, the role of uridine diphosphate (UDP)-glycosyltransferase (UGT) genes in cyflumetofen resistance remains to be determined. RESULTS: Synergist 5-nitrouracil (5-Nul) significantly enhanced cyflumetofen toxicity in T. cinnabarinus, which indicated that UGTs are involved in the development of cyflumetofen resistance. Transcriptomic analysis and quantitative (q)PCR assays demonstrated that the UGT genes, especially UGT201H1, were highly expressed in the YN-CyR strain, compared to those of the YN-S strain. The RNA interference (RNAi)-mediated knockdown of UGT201H1 expression diminished the levels of cyflumetofen resistance in YN-CyR mites. The findings additionally revealed that the recombinant UGT201H1 protein plays a role in metabolizing cyflumetofen. Our results also suggested that the aromatic hydrocarbon receptor (AhR) probably regulates the overexpression of the UGT201H1 detoxification gene. CONCLUSION: UGT201H1 is involved in cyflumetofen resistance, and AhR may regulates the overexpression of UGT201H1. These findings provide deeper insights into the molecular mechanisms underlying UGT-mediated metabolic resistance to chemical insecticides. © 2024 Society of Chemical Industry.

The mixed biofilm formed by Listeria monocytogenes and other bacteria: Formation, interaction and control strategies.

Listeria monocytogenes is an important foodborne pathogen. It can adhere to food or food contact surface for a long time and form biofilm, which will lead to equipment damage, food deterioration, and even human diseases. As the main form of bacteria to survive, the mixed biofilms often exhibit higher resistance to disinfectants and antibiotics, including the mixed biofilms formed by L. monocytogenes and other bacteria. However, the structure and interspecific interaction of the mixed biofilms are very complex. It remains to be explored what role the mixed biofilm could play in the food industry. In this review, we summarized the formation and influence factors of the mixed biofilm developed by L. monocytogenes and other bacteria, as well as the interspecific interactions and the novel control measures in recent years. Moreover, the future control strategies are prospected, in order to provide theoretical basis and reference for the research of the mixed biofilms and the targeted control measures.

Antibiofilm and Antiquorum Sensing Potential of Lactiplantibacillus plantarum Z057 against Vibrio parahaemolyticus.

Vibrio parahaemolyticus is a widespread foodborne pathogen that causes serious seafood-borne gastrointestinal infections. Biofilm and quorum sensing (QS) are critical in regulating these infections. In this study, first, the ability of Lactiplantibacillus plantarum Z057 to compete, exclude, and displace V. parahaemolyticus biofilm was evaluated. Then, the inhibitory effects of L. plantarum Z057 extract (Z057-E) on V. parahaemolyticus biofilm and QS were explored from the aspects of biofilm biomass, metabolic activity, physicochemical properties, extracellular polymer matrix content, QS signal AI-2 activity, biofilm microstructure, and the expression levels of biofilm and QS-related genes. Results showed that L. plantarum Z057 effectively inhibited biofilm formation of V. parahaemolyticus and interfered with the adhesion of V. parahaemolyticus on the carrier surface. In addition, the Z057-E could significantly reduce the biofilm biomass, metabolic activity, hydrophobicity, auto-aggregation ability, swimming and swarming migration diameter, AI-2 activity, extracellular polysaccharide (EPS), and extracellular protein content of V. parahaemolyticus. Fluorescence microscope and scanning electron microscope (SEM) images demonstrated that the Z057-E could efficiently inactivate the living cells, destroy the dense and complete biofilm architectures, and reduce the essential component of the extracellular polymer matrix. Real-time fluorescence quantitative PCR revealed that the Z057-E treatment down-regulated the expression of flagellum synthesis-related genes (flaA, flgM), EPS, and extracellular protein synthesis-related genes (cpsA, cpsQ, cpsR, ompW), QS-related genes (luxS, aphA, opaR), and hemolysin secretion-related genes (toxS, toxR) of V. parahaemolyticus. Thus, our results suggested that L. plantarum Z057 could represent an alternative biocontrol strategy against foodborne pathogens with anti-adhesive, antibiofilm, and antiquorum sensing activities.

Complete genome sequence of camellia virus A, a tentative new member of the genus Waikavirus.

A new positive-strand RNA virus genome was discovered in Camellia japonica plants. The complete genome of the virus is 12,570 nt in size, excluding the poly(A) tail, and contains one large open reading frame (ORF1) and two small open reading frames (ORF2, ORF3). ORF1 and ORF2 are homologous to sequences of waikaviruses, while ORF3 has no relatives in the databases. ORF1 encodes a putative polyprotein precursor that is putatively processed into eight smaller proteins, as in typical waikaviruses. Comprehensive analysis, including BLAST searches, genome organization and pairwise sequence comparisons, and phylogeny reconstructions, invariably placed the virus with the waikaviruses. Furthermore, due to lower amino acid sequence identity to known waikaviruses than the threshold species demarcation cutoff, this virus may represent a new species in the genus Waikavirus, family Secoviridae, and we have tentatively named it "camellia virus A" (CamVA). Finally, a field survey was conducted to assess the occurrence of CamVA in camellias and its associated symptoms.

Recombinant fusion protein by lysozyme and antibacterial peptide enhances ischemic wound healing via angiogenesis and reduction of inflammation in diabetic db/db mice.

BACKGROUND & AIMS: Lysozyme and antibacterial peptides have been reported to broad-spectrum antibacterial activity and can further improve wound healing. The aim of this study was to assess the effectiveness of a recombinant fusion protein created by combining lysozyme and an antibacterial peptide in forming new vessels and wound healing in an ischemic hind limb. METHODS: An ischemic hind limb model was established by isolation and ligation of the femoral artery in diabetic db/db mice. Cutaneous wounds were created with or without ischemia. Adductor muscles and wounds were treated with or without the fusion protein. RESULTS: The fusion protein accelerated ischemic diabetic wound healing and attenuated impairment of ischemic adductor muscle . Further, the fusion protein elevated expression of platelet derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) protein and mRNA in ischemic adductor muscle, reduced levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in serum and expression of phosphorylated nuclear factor κB (p-NF-κB) and p-IKB α in ischemic adductor. The fusion protein also enhanced levels of phosphorylated VEGF and PDGF receptors in the ischemic adductor muscles from diabetic db/db mice. CONCLUSION: The data showed that the beneficial effects of the fusion protein on ischemic wound healing may be associated with angiogenesis and reduction of inflammatory response in the ischemic adductor muscles of diabetic db/db mice.

Lysozyme-Antimicrobial Peptide Fusion Protein Promotes the Diabetic Wound Size Reduction in Streptozotocin (STZ)-Induced Diabetic Rats.

BACKGROUND Lysozymes and antibacterial peptides have been confirmed to protect humans against viral and bacterial infection, and accelerate wound healing. The study aimed to evaluate the effect of lysozyme-antimicrobial peptide fusion protein on the diabetic wound size reduction in streptozotocin (STZ)-induced diabetic rats. MATERIAL AND METHODS Diabetic rats were prepared via intraperitoneal injection of STZ, 70 mg/kg. A 2-cm circular incision with full thickness was made on the dorsum skin of the rats for preparation of diabetic wound model. The wounds were treated with the fusion protein or phosphate buffer saline. RESULTS The fusion protein markedly accelerated wound healing, decreased levels of proinflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α, lipid peroxide (LPO) content, and expression of cyclooxygenase-2 (COX-2), and increased activities of antioxidant enzyme including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in serum, levels of pro-angiogenic cytokines such as vascular endothelial growth factor (VEGF) and intercellular adhesion molecule (ICAM-1), and expression of VEGF, FGF-2, p-ERK, and p-Akt protein in granulation. CONCLUSIONS The results of the present study suggested that the fusion protein accelerated wound healing by improving anti-inflammation and antioxidant, and increasing angiogenesis in granulation tissues of diabetic rats.

Image quality and spectral performance evaluations of a polarization imaging spectrometer based on a Savart polariscope.

The modulation transfer function (MTF) and signal-to-noise ratio (SNR) are the key parameters to evaluate quantitatively the image quality and spectral performance in a polarization imaging spectrometer based on a Savart polariscope. In order to evaluate the image quality and reflect the detecting ability of the imaging spectrometer, calibration experiments on the MTF, SNR, and spectral resolution were carried out and some important conclusions were obtained. For incident radiance values 4.464, 3.119, and 0.523 w/m2·sr, the average SNRs of the interferogram were 500, 400, and 200 dB, respectively, and the MTF is 0.24. During the spectral resolution calibration, the maximum optical path difference was set as 57.08 µm, and the measured value is greater than the theoretical value, which is mainly caused by the structural design of the polarization imaging spectrometer. For the wavelength range of [500 nm, 600 nm], the SNR of the spectrum is lower and about 50 dB, while the SNR is obviously higher in a range of λ∈[600 nm, 960 nm]. This study provides a theoretical and practical guidance for improving the image quality and judging the spectral performance of the polarization imaging spectrometer.

Synergetic effects of ciliary neurotrophic factor and olfactory ensheathing cells on optic nerve reparation (complete translation).

At present, there is no effective treatment for the repair of the optic nerve after injury, or improvement of its microenvironment for regeneration. Intravitreally injected ciliary neurotrophic factor (CNTF) and olfactory ensheathing cells (OECs) promote the long-distance regrowth of severed optic nerve fibers after intracranial injury. Here, we examined the efficacy of these techniques alone and in combination, in a rat model of optic nerve injury. We injected condensed OEC suspension at the site of injury, or CNTF into the vitreous body, or both simultaneously. Retrograde tracing techniques showed that 4 weeks postoperatively, the number of surviving retinal ganglion cells and their axonal density in the optic nerve were greater in rats subjected to OEC injection only than in those receiving CNTF injection only. Furthermore, combined OEC + CNTF injection achieved better results than either monotherapy. These findings confirm that OECs are better than CNTF at protecting injured neurons in the eye, but that combined OEC and CNTF therapy is notably more effective than either treatment alone.

Heme Oxygenase-1 Promotes Delayed Wound Healing in Diabetic Rats.

Diabetic ulcers are one of the most serious and costly chronic complications for diabetic patients. Hyperglycemia-induced oxidative stress may play an important role in diabetes and its complications. The aim of the study was to explore the effect of heme oxygenase-1 on wound closure in diabetic rats. Diabetic wound model was prepared by making an incision with full thickness in STZ-induced diabetic rats. Wounds from diabetic rats were treated with 10% hemin ointment for 21 days. Increase of HO-1 protein expression enhanced anti-inflammation and antioxidant in diabetic rats. Furthermore, HO-1 increased the levels of VEGF and ICAM-1 and expressions of CBS and CSE protein. In summary, HO-1 promoted the wound closure by augmenting anti-inflammation, antioxidant, and angiogenesis in diabetic rats.

CXCL1 Triggers Caspase-3 Dependent Tau Cleavage in Long-Term Neuronal Cultures and in the Hippocampus of Aged Mice: Implications in Alzheimer's Disease.

Truncation of tau protein is considered an early event in Alzheimer's disease (AD) and is believed to play a major pathogenic role in sporadic AD. However, causative factors that trigger tau truncation in AD remain poorly understood. In the present study, we demonstrate that CXCL1 (C-X-C motif ligand 1), a specific ligand for the chemokine receptor CXCR2, induced cleavage of tau at ASP421 in a caspase-3-dependent manner in long-term but not short-term cultured neurons. The cleaved tau formed varicosities or bead-like structures along the neurites, an abnormal distribution of tau induced by CXCL1 that has not been observed previously. CXCL1-induced activation of GSK3ß and the subsequent phosphorylation of tau preceded and were required for caspase-3 activation and tau cleavage. Moreover, intrahippocampal microinjection of lentiviral CXCL1 induced tau cleavage in hippocampal neurons in aged (15-18 months of age) but not adult mice (5-10 months of age). Our data highlight a new role of CXCR2 in tau cleavage and suggest that targeting CXCR2 may offer therapeutic benefits to patients with AD and potentially other tauopathies.

Hydrogen sulfide accelerates wound healing in diabetic rats.

AIM: The aim of this study was to explore the role of hydrogen sulfide on wound healing in diabetic rats. METHODS: Experimental diabetes in rats was induced by intraperitoneal injection of streptozotocin (STZ) (in 0.1 mol/L citrate buffer, Ph 4.5) at dose of 70 mg/kg. Diabetic and age-matched non-diabetic rats were randomly assigned to three groups: untreated diabetic controls (UDC), treated diabetic administrations (TDA), and non-diabetic controls (NDC). Wound Healing Model was prepared by making a round incision (2.0 cm in diameter) in full thickness. Rats from TDA receive 2% sodium bisulfide ointment on wound, and animals from UDC and NDC receive control cream. After treatment of 21 days with sodium bisulfide, blood samples were collected for determination of vascular endothelial growth factor (VEGF), intercellular cell adhesion molecule-1 (ICAM-1), antioxidant effects. Granulation tissues from the wound were processed for histological examination and analysis of western blot. RESULTS: The study indicated a significant increase in levels of VEGF and ICAM-1 and a decline in activity of coagulation in diabetic rats treated with sodium bisulfide. Sodium bisulfide treatment raised the activity of superoxide dismutase (SOD) and heme oxygenase-1 (HO-1) protein expression, and decreased tumor necrosis factor α (TNF-α) protein expression in diabetic rats. CONCLUSIONS: The findings in present study suggested that hydrogen sulfide accelerates the wound healing in rats with diabetes. The beneficial effect of H2S may be associated with formation of granulation, anti-inflammation, antioxidant, and the increased level of vascular endothelial growth factor (VEGF).

Ginkgolide B increases hydrogen sulfide and protects against endothelial dysfunction in diabetic rats.

AIM: To evaluate the effect of ginkgolide B treatment on vascular endothelial function in diabetic rats. METHODS: The study included four groups with 15 male Sprague-Dawley rats: control group; control group treated with ginkgolide B; diabetic group; and diabetic treated with ginkgolide B. The activity of superoxide dismutase (SOD), malondialdehyde content, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, and glutathione peroxidase 1 (GPX1) protein expression were determined in aortic tissues. Vasoconstriction to phenylephrine (PHE) and vasorelaxation to acetylcholine (Ach) and sodium nitroprusside (SNP) were assessed in aortic rings. Nitric oxide (NO) and hydrogen sulfide (H2S) were measured, as well as cystathionine γ lyase (CSE) and cystathionine ß synthetase (CBS) protein expression, and endothelial nitric oxide synthase (eNOS) activity. RESULTS: Diabetes significantly impaired PHE-induced vasoconstriction and Ach-induced vasorelaxation (P<0.001), reduced NO bioavailability and H2S production (P<0.001), SOD activity, and GPX1 protein expression (P<0.001), and increased malondialdehyde content and NADPH oxidase subunits, and CSE and CBS protein expression (P<0.001). Ginkgolide B treatment improved PHE vasoconstriction and Ach vasorelaxation (P<0.001), restored SOD (P=0.005) and eNOS (P<0.001) activities, H2S production (P=0.044) and decreased malondialdehyde content (P=0.014). Vasorelaxation to SNP was not significantly different in control and diabetic rats with or without ginkgolide B treatment. Besides, ginkgolide B increased GPX1 protein expression and reduced NADPH oxidase subunits, CBS and CSE protein expression. CONCLUSION: Ginkgolide B alleviates endothelial dysfunction by reducing oxidative stress and elevating NO bioavailability and H2S production in diabetic rats.

Achromatic Savart polariscope: choice of materials.

This paper presents the achromatization of Savart Polariscope to decrease the lateral-shear dispersion in the lateral displacement. The achromatic Savart Polariscope can be made from two different birefringent crystal materials. The achromatic model for the choices of material is presented. The achievements and performances of different achromatic Savart Polariscopes are demonstrated with numerical simulations and ray tracing program. The chromatic variation in lateral displacement can be reduced by an order of magnitude across the spectral range 0.4µm to 0.9µm.

[Detecting Down syndrome with a novel dual-color competitive quantitative fluorescent polymerase chain reaction method].

OBJECTIVE: To develop a rapid method for the detection of Down syndrome (DS) using dual-color competitive quantitative fluorescent polymerase chain reaction (DCC-QF-PCR), and to assess its feasibility for the prenatal diagnosis of Down syndrome. METHODS: DNA was extracted from peripheral blood of 30 DS patients and 60 normal men, common primers for DSCR and USC2 genes and respective TaqMan probes were designed and synthesized. The results of DCC-QF-PCR were compared with those of QF-PCR which measured the ratio between DSCR and GAPDH. Forty-six amniotic fluid samples were assayed with DCC-QF-PCR. The results were compared with that of karyotyping. Monoclone fragments for DSCR and USC2 genes were obtained from direct cloning of PCR products. DCC-QF-PCR was carried out using different DNA ratios of DSCR and USC2 as the template. The dosage ratio between DSCR and USC2 was calculated. RESULTS: The gene dosage ratio of the DS patients was 1.41-1.74, which was significantly higher than that of normal men (0.93-1.15). The dosage ratio range of DSCR and GAPDH by QF-PCR was comparatively greater than that of DSCR and USC2. Three samples were diagnosed as DS, which was in good agreement with that of karyotyping analysis. There was no significant difference between the gene dosage ratio from DCC-QF-PCR and that of predetermined (P>0.05). CONCLUSION: DCC-QF-PCR is an accurate, rapid, and low cost method, which only requires tiny amount of sample and therefore has broad application in the genetic and prenatal diagnosis.

Perceptual variation in umami taste and polymorphisms in TAS1R taste receptor genes.

BACKGROUND: The TAS1R1 and TAS1R3 G protein-coupled receptors are believed to function in combination as a heteromeric glutamate taste receptor in humans. OBJECTIVE: We hypothesized that variations in the umami perception of glutamate would correlate with variations in the sequence of these 2 genes, if they contribute directly to umami taste. DESIGN: In this study, we first characterized the general sensitivity to glutamate in a sample population of 242 subjects. We performed these experiments by sequencing the coding regions of the genomic TAS1R1 and TAS1R3 genes in a separate set of 87 individuals who were tested repeatedly with monopotassium glutamate (MPG) solutions. Last, we tested the role of the candidate umami taste receptor hTAS1R1-hTAS1R3 in a functional expression assay. RESULTS: A subset of subjects displays extremes of sensitivity, and a battery of different psychophysical tests validated this observation. Statistical analysis showed that the rare T allele of single nucleotide polymorphism (SNP) R757C in TAS1R3 led to a doubling of umami ratings of 25 mmol MPG/L. Other suggestive SNPs of TAS1R3 include the A allele of A5T and the A allele of R247H, which both resulted in an approximate doubling of umami ratings of 200 mmol MPG/L. We confirmed the potential role of the human TAS1R1-TAS1R3 heteromer receptor in umami taste by recording responses, specifically to l-glutamate and inosine 5'-monophosphate (IMP) mixtures in a heterologous expression assay in HEK (human embryonic kidney) T cells. CONCLUSIONS: There is a reliable and valid variation in human umami taste of l-glutamate. Variations in perception of umami taste correlated with variations in the human TAS1R3 gene. The putative human taste receptor TAS1R1-TAS1R3 responds specifically to l-glutamate mixed with the ribonucleotide IMP. Thus, this receptor likely contributes to human umami taste perception.

[Effect of ligand pioglitazone activating PPAR-gamma on the invasiveness of cholangiocarcinoma cell in vitro and the expression regulation of related genes].

OBJECTIVE: To explore the effect and mechanism of ligand pioglitazone (PGZ) activating PPAR-gamma on the invasiveness of cholangiocarcinoma cell in vitro. METHODS: Human hilar cholangiocarcinoma cell line QBC939 was selected and cultured in vitro for this research. The rate of QBC939 cell growth inhibition was detected by MTT, and the influence of PGZ on the expression of MMP-7 mRNA and TIMP-1 mRNA was measured by using FQ-PCR. The in vitro invasiveness and mobility of QBC939 were quantified by Matrigel invasion assay and crossing-river test. RESULTS: Among the low concentration (5 micromol/L-40 micromol/L) groups at the point of 12-hours, PGZ did not show to inhibit significantly the growth of QBC939 cells (P>0. 05). However, the PGZ could down-regulate the expression of MMP-7 mRNA in QBC939 cells (P<0. 01), and up-regulate the TIMP-1 mRNA expression to be without obvious statistics significance (P>0. 05). At last, PGZ could reduce the number of QBC939 cell breaking through the matrigel and prolonging the time of crossing-river significantly (P< 0. 01) in a dose-dependent manner. CONCLUSION: For ligand PGZ to activate PPAR-gamma can inhibit the invasiveness of QBC939 cells in vitro via regulating the expression of MMP-7 and the mobility of QBC939 cells probably.

Case-control association study of Disrupted-in-Schizophrenia-1 (DISC1) gene and schizophrenia in the Chinese population.

Disrupted-in-Schizophrenia-1 (DISC1) has first been identified as a candidate gene for schizophrenia through study of a Scottish family with a balanced (1; 11) (q42.1; q14.3) translocation. Lots of linkage and association studies supported DISC1 as a risk factor for schizophrenia. In this study, we genotyped three SNPs in DISC1 using a set of Han Chinese samples of 560 schizophrenics and 576 controls. No positive association was detected in the whole samples but analysis of allele frequencies in female samples showed weak association between SNP rs2295959 and the disease (chi(2)=6.188, P=0.0135, OR=0.728, 95% CI=0.567-0.935). Our results provide further evidence for sex difference for the effect of the gene on the aetiology of schizophrenia. Our findings also would encourage further studies, particularly family-based association studies with larger samples, to analyze the association between DISC1 and schizophrenia.

Analysis of the association between Apolipoprotein D and schizophrenia.

Schizophrenia is a severe, chronic and common complex debilitating mental illness with a large genetic component. Evidence to date suggests that apolipoprotein D protein may be closely related to schizophrenia. To investigate the role of the APOD gene in the etiology of schizophrenia, we genotyped three genetic polymorphisms (rs7659, rs2280520 and rs4677695) in a case-control study using subjects from the Chinese population, and altogether 425 cases and 473 controls were analyzed in the study. However, we found no significant discrepancies in allele and genotype frequencies of the three polymorphisms nor in the haplotype distribution between the cases and the controls. Our data indicate no direct evidence of association between schizophrenia and the APOD gene, and the results suggest that the three genetic polymorphisms within the APOD gene are unlikely to confer increased susceptibility to the illness in the Chinese population.

[Gene mutation analysis of coagulation factor VIII from a female patient with hemophilia A].

Hemophilia A affects male, whereas females are carriers and generally spared from this disease. However, we here reported a 65-year-old female with Hemophilia A while screening the gene mutation of coagulation factor VIII. The female went to hospital because of tripping to lead her right chest to be injured with subcutaneous hematoma. She had historically a hemorrhagic diathesis. The physical examination discovered her hip limited to bend and move, but no discrepancy length between her two legs. The initial laboratory tests showed that the activated partial thromboplastin time (APTT) was 61. 3 seconds (20-40 seconds), and the APTT corrected by mixing with normal plasma was 41.3 s, but the levels of PT, FIB and TT were normal. The plain radiographs revealed the hip joints to suffer from the acetabular dysplasia and osteoarthritis. The level of FVIII:C was 2%, F IX:C 200%, vWF:Ag 120%, vWF:Rcof 100%, vWF:CBA 128%, and the F VIII binding assay to vWF was normal. The primers for exon 14 of F VIII gene were designed according to the NM - 000132 gene sequence. DNA was abstracted from the patient blood. PCR were carried out and the DNA sequence was followed. A new mutation of 4111A-->C was discovered, which caused the amino acid sequence changed (T 1314 P). The mutation of T 1314 P may be the cause of this female patient to get the hemophilia A. This mutation was a novel one which has never been reported before.

Association between the brain-derived neurotrophic factor (BDNF) gene and schizophrenia in the Chinese population.

Brain-derived neurotrophic factor (BDNF) belongs to a family of the neurotrophin which plays important roles in the development of the brain. BDNF has been suggested as a factor that increases the risk of schizophrenia. In this study, we genotyped three single nucleotide polymorphisms (SNPs) in the BDNF gene using a set sample of Han Chinese subjects consisting of 560 schizophrenes and 576 controls. No significant differences were found for either the genotype or allele distribution of analyzed polymorphisms, nor was any gender-specific association found. Thus, our data suggest that the BDNF gene may not be an important factor in susceptibility to schizophrenia.