TGF-β1 gene polymorphism in renal transplant patients with and without gingival overgrowth

Oral Diseases (2011) 17 , 414–419 Background: The incidence of gingival overgrowth among renal transplant patients treated with cyclosporine A ranges from 13% to 84.6%, and the overgrowth is not only esthetic but also a medical problem. We studied the determination of association between TGF‐β1 (TGFB1) gene polymorphism and gingival overgrowth in kidney transplant patients medicated with cyclosporin A. Methods: Eighty‐four kidney transplant patients with gingival overgrowth and 140 control transplant patients without overgrowth were enrolled into the case control study. TGFB1 polymorphism was determined using the PCR‐RFLP assay for +869T>C in codon 10 and +915G>C in codon 25 as well as TaqMan real‐time PCR assays for promoter ?800G>A and ?509C>T SNPs. Results: In kidney transplant patients suffering from gingival overgrowth, mean score of gingival overgrowth was 1.38 ± 0.60, whereas in control subjects it was 0.0. The patients with gingival overgrowth were characterized by similar distribution of TGFB1 genotypes and allele in comparison to subjects without gingival overgrowth. Among 16 potentially possible haplotypes of TGFB1 gene, only four were observed in the studied sample of kidney transplant patients: G_C_T_G, G_T_C_G, G_C_C_C, and A_C_T_G, with similar frequency in patients with and without gingival overgrowth. Conclusion: No association between the TGFB1 gene polymorphism and gingival overgrowth was revealed in kidney transplant patients administered cyclosporine A.     

Analysis of the association of polymorphism in the osteoprotegerin gene with susceptibility to chronic kidney disease and periodontitis

Background and Objective:  Chronic kidney disease (CKD) is a complex disorder, which results in several complications involving disturbance of mineral metabolism. Periodontal disease is an infectious disease that appears to be an important cause of systemic inflammation in CKD patients. Periodontal disease is characterized by clinical attachment loss (CAL) caused by alveolar bone resorption around teeth, which may lead to tooth loss. Osteoprotegerin (OPG) is a key regulator of osteoclastogenesis. Polymorphisms are the main source of genetic variation, and single nucleotide polymorphisms (SNPs) have been reported as major modulators of disease susceptibility. The aim of this study was to investigate the association of a polymorphism located at position –223 in the untranslated region of the OPG gene, previously known as –950, with susceptibility to CKD and periodontal disease.
Material and Methods:  A sample of 224 subjects without and with CKD (in hemodialysis) was divided into groups with and without periodontal disease. The OPG polymorphism was analyzed by polymerase chain reaction and restriction fragment length polymorphism.
Results:  No association was found between the studied OPG polymorphism and susceptibility to CKD or periodontal disease.
Conclusion:  It was concluded that polymorphism OPG –223 (C/T) was not associated with CKD and periodontal disease in a Brazilian population. Studies on other polymorphisms in this and other genes of the host response could help to clarify the involvement of bone metabolism mediators in the susceptibility to CKD and periodontal disease.     

白细胞介素-1单核苷酸多态性与甘肃回族、东乡族人群慢性牙周炎的相关性研究

目的 通过检测并分析白细胞介素(IL)-1B+3954位点的单核苷酸多态性(SNP),探索其与甘肃回族与东乡族人群慢性牙周炎的关系.方法 收集215例回族、东乡族慢性牙周炎患者及219例正常对照组健康者的静脉血,提取外周静脉血白细胞DNA,采用聚合酶链式反应-限制性片段长度多态性技术(PCR-RFLP)方法检测IL-1...     

Investigation of IL4 gene polymorphism in individuals with different levels of chronic periodontitis in a Brazilian population

BACKGROUND: Cytokines are key factors that mediate the inflammatory process during periodontal disease. Recent works have shown that the levels of cytokine expression are regulated by genetic polymorphisms, and that these variations can interfere with the progression of disease. The-590 (C-->T) polymorphism of the IL4 gene is associated with high levels of IgE in asthmatic families, and the frequency of the T allele was increased in asthmatic children. The concentration of IgE in gingival tissue was found to be elevated in patients with periodontitis. OBJECTIVE: In this study the relationship between the-590 (C-->T) polymorphism in the IL4 gene and different levels of chronic periodontal disease was investigated. MATERIAL AND METHODS: DNA was extracted from buccal epithelial cells of 113 unrelated adult individuals with different levels of periodontitis. The PCR-RFLP technique was used to investigate the polymorphism in the promoter of IL4 gene. RESULTS: No significant differences in the allele and genotype frequencies of the polymorphism were found between control and groups with periodontal disease. CONCLUSION: : We conclude that the-590 (C-->T) polymorphism in the IL4 gene is not associated with the susceptibility to chronic periodontal disease.     

HTR2C polymorphisms,olanzapine-induced weight gain and antipsychotic-induced metabolic syndrome in schizophrenia patients: A meta-analysis

Objective. To conduct meta-analyses of all published association studies on the HTR2C -759C/T (rs3813829) polymorphism and olanzapine-induced weight gain in schizophrenia patients and on the HTR2C -759C/T, -697G/C (rs518147) and rs1414334:C> G polymorphisms and olanzapine/clozapine/risperidone-induced metabolic syndrome in schizophrenia patients. Methods. Eligible studies were identified by searching PubMed and Web of Science databases. Meta-analyses were performed using Cochrane Review Manager (RevMan, version 5.2) to calculate the pooled odds ratio (OR) and its corresponding 95% confidence interval (CI). Results. Our meta-analyses revealed both a significant positive association between the rs1414334 C allele and olanzapine/clozapine/risperidone-induced metabolic syndrome and a marginally significant positive association between the -697C allele and the induced metabolic syndrome in schizophrenia patients, but no significant association between the -759C/T polymorphism and the induced metabolic syndrome in schizophrenia patients. Our analysis further revealed a pronounced trend toward a significant negative association between the -759T allele and high olanzapine-induced weight gain and a trend toward a significant positive association between the -759C allele and high olanzapine-induced weight gain in Caucasian schizophrenia patients. Conclusions. Our results support that HTR2C polymorphisms play a role in antipsychotic-induced metabolic disturbance. More association studies are needed to further elucidate association of different HTR2C polymorphisms and antipsychotic-induced metabolic disturbance.     

5DF血球分析仪检测白细胞分类计数与瑞氏染色镜检结果对比研究

目的　探讨5DF血球分析仪白细胞分类计数与传统的瑞氏染色镜检计数结果之间的差异。方法　用5分类血球分析仪和瑞氏染色法同时对10 0份血样进行分类计数,并用统计学分析研究。结果　中性粒细胞、嗜酸、嗜碱性细胞和淋巴细胞分类计数两法无明显差异(P均>0 .0 5 ) ,但单核细胞分类计数仪器法比镜检法结果偏高(P <0 .0 0 1)。结论　对于一般血液常规检查可选用仪器法筛查,而血液系统疾病或某种原因引起的细胞结构改变应选用镜检法。     

Novel mGluR5 Positive Allosteric Modulator Improves Functional Recovery,Attenuates Neurodegeneration,and Alters Microglial Polarization after Experimental Traumatic Brain Injury

Traumatic brain injury (TBI) causes microglial activation and related neurotoxicity that contributes to chronic neurodegeneration and loss of neurological function. Selective activation of metabotropic glutamate receptor 5 (mGluR5) by the orthosteric agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), is neuroprotective in experimental models of TBI, and has potent anti-inflammatory effects in vitro. However, the therapeutic potential of CHPG is limited due to its relatively weak potency and brain permeability. Highly potent, selective and brain penetrant mGluR5 positive allosteric modulators (PAMs) have been developed and show promise as therapeutic agents. We evaluated the therapeutic potential of a novel mGluR5 PAM, VU0360172, after controlled cortical impact (CCI) in mice. Vehicle, VU0360172, or VU0360172 plus mGluR5 antagonist (MTEP), were administered systemically to CCI mice at 3 h post-injury; lesion volume, hippocampal neurodegeneration, microglial activation, and functional recovery were assessed through 28 days post-injury. Anti-inflammatory effects of VU0360172 were also examined in vitro using BV2 and primary microglia. VU0360172 treatment significantly reduced the lesion, attenuated hippocampal neurodegeneration, and improved motor function recovery after CCI. Effects were mediated by mGluR5 as co-administration of MTEP blocked the protective effects of VU0360172. VU0360172 significantly reduced CD68 and NOX2 expression in activated microglia in the cortex at 28 days post-injury, and also suppressed pro-inflammatory signaling pathways in BV2 and primary microglia. In addition, VU0360172 treatment shifted the balance between M1/M2 microglial activation states towards an M2 pro-repair phenotype. This study demonstrates that VU0360172 confers neuroprotection after experimental TBI, and suggests that mGluR5 PAMs may be promising therapeutic agents for head injury.

Electronic supplementary material

The online version of this article (doi:10.1007/s13311-014-0298-6) contains supplementary material, which is available to authorized users.     

Microscopic Visualization of Metabotropic Glutamate Receptors on the Surface of Living Cells Using Bifunctional Magnetic Resonance Imaging Probes

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