牙龈卟啉单胞菌外膜囊泡与阿尔茨海默病的相关性研究进展

牙龈卟啉单胞菌(Porphyromonas gingivalis)是牙周炎的主要致病菌,在其生长过程中可产生大量毒力因子。P. gingivalis及其毒力因子不仅可引发牙周组织的破坏,还可扩散至全身并影响包括阿尔茨海默病(Alzheimer’s disease, AD)在内的多种系统疾病的发生、发展。P. gingivalis外膜囊泡包含亲本细菌的大量毒力因子且体积小,更易扩散至远处组织和器官。近期研究发现,P.gingivalis外膜囊泡可能在诱发神经炎症和促进AD的发生、发展中起重要作用,但具体机制尚不清楚。本文就P. gingivalis外膜囊泡的发生与调控、所含主要毒力因子及其与AD的关系进行综述,以阐明牙周炎与AD相关的生物学机制。     

新型冠状病毒肺炎与牙周炎的潜在关联

新型冠状病毒肺炎(COVID-19)是目前全球面临的最紧迫的公共卫生问题之一。牙周炎是一种高发病率的慢性疾病,同时也是多种全身性疾病的诱因。最新研究表明COVID-19与心血管疾病、高血压、糖尿病、肥胖和慢性肾病等其他慢性疾病存在相关性。旨在基于严重急性呼吸综合征冠状病毒2(SARS-CoV-2)的感染与牙周炎发生的主要致病机制探讨两者之间是否存在潜在关联。总结发现牙周炎与COVID-19发病率的上升没有直接关联,但是牙周炎能间接影响COVID-19预后。对两者关系的进一步了解,不仅可以预防牙周炎,还可以降低COVID-19不良预后的发生。本文为COVID-19合并牙周炎患者的治疗提供新型研究思路及理论参考。     

人类巨细胞病毒、EB病毒和单纯疱疹病毒1型与慢性牙周炎的相关性研究

目的　研究人类巨细胞病毒( HCMV)、Epstein- Barr病毒( EBV)和单纯疱疹病毒1型( HSV- 1)与慢性牙周炎的相关性。方法　收集6 2例慢性牙周炎患者(男性2 7例,女性35例;平均年龄5 3岁)的牙周炎部位,轻度龈炎部位的龈下菌斑,提取DNA后使用巢式PCR检测HCMV、EBV和HSV- 1,比较分析它们在同一患者不同部位的检出率。结果　牙周炎部位的HCMV检出率为38.7% ,EBV的检出率为5 8.0 % ,HSV- 1的检出率为30 .6 % ,2种以上病毒合并感染的检出率为4 0 .3% ;轻度龈炎部位的HCMV检出率为12 .9% ,EBV为19.4 % ,HSV- 1为9.7% ,2种以上病毒合并感染的检出率为8.0 %。这3种病毒及其合并感染在牙周炎部位的检出率均高于轻度龈炎部位,差异有统计学意义( P<0 .0 5 )。结论　提示HCMV、EBV、HSV- 1与慢性牙周炎有相关性。     

体外牙周微生态模型构建方法及应用研究进展

牙周炎的病因学研究经历了从非特异性菌斑学说、特异性菌斑学说到生态菌斑学说的转变,但其具体的发病机制仍有待进一步研究.近年来,有学者提出了多微生物协同和生态失调模型,病原体组作为疾病病因学中的新概念也逐渐引起重视,这些都提示牙周感染中牙菌斑生物膜与宿主之间存在复杂的相互作用.因此,构建牙周微生态模型对牙周炎病因及防治的研...     

人DNAJB6蛋白与人巨细胞病毒皮层蛋白pUL23相互作用的鉴定

pUL23是人巨细胞病毒（HCMV）UL23基因编码的皮层蛋白. HCMV皮层蛋白与病毒颗粒的形成、病毒转移、免疫调控等病毒生活过程相关.利用GAL4 酵母双杂交系统筛选人胚肾cDNA文库,获得与人巨细胞病毒皮层蛋白pUL23相互作用的宿主蛋白分子DNAJB6 ［DnaJ (Hsp40) homolog, subfamily B, member 6］.回复酵母双杂交、体外GST-Pull down和免疫共沉淀试验再次确认两者之间的相互作用.该结果为进一步研究pUL23蛋白在HCMV生活周期中的作用机制提供依据.     

利用酵母双杂交系统筛选与人巨细胞病毒皮层蛋白pUL23相互作用的病毒编码蛋白

人巨细胞病毒(HCMV) UL23基因编码病毒皮层蛋白,该基因缺失时,病毒在人包皮成纤维细胞(HFF)中的繁殖速度加快.为进一步阐述HCMV UL23基因编码产物 pUL23的功能及调控机制,采用鸟枪法构建了融合于GAL4活性区域的HCMV Towne株 基因组随机表达文库.利用酵母双杂交技术,以pGBKT7 -UL23为诱饵质粒,从构建 的HCMV基因组表达文库中筛选到与pUL23相互作用的病毒编码蛋白pUL24. GST-pull down实验和免疫共沉淀实验进一步确认两种病毒蛋白之间的相互作用.结果 表明,构建的HCMV基因组表达文库能够用于GAL4酵母双杂交系统筛选与诱饵蛋白相互作用的病毒自身编码蛋白.病毒蛋白pUL23和pUL24之间具有相互作用,这为进一 步阐述pUL23在HCMV感染过程中的功能提供依据.该研究为揭示HCMV病毒感染机制奠定了基础.     

带状疱疹后遗神经痛的动物模型及病理机制研究

带状疱疹后遗神经痛(postherpetic neuralgia,PHN)是带状疱疹最常见的并发症,其发生率随年龄的增加而增加,并且严重影响患者的生活质量。目前PHN的治疗多采用复合用药,但效果不佳。阻碍其治疗发展的关键是对PHN的发病机制不甚清楚,究其根本原因是缺乏与临床符合的动物模型。目的:综述带状疱疹病毒感染模型的改良和进展,使PHN的病理机制得到进一步揭示。内容:介绍与PHN相关的水痘-带状疱疹病毒潜伏感染模型、体外模型及慢性感染模型,综述与PHN发生发展有关的潜伏机制、与其他神经病理性痛相似的机制及近年来较为关注的中枢与外周损伤机制。趋向:进一步研究与人类水痘带状疱疹病毒感染更为相似的动物模型,并随其改良和进展,使发生PHN的机制得到进一步的阐释。     

高原低氧环境下牙周炎的发病机制

牙周炎的病理过程受全身和局部因素的综合调控,一些调查研究显示高原牙周炎患病率高于平原地区,显然高原特殊环境在牙周炎的发生和发展过程中起到一定的作用,因此本文就高原低氧环境下牙周病变组织的变化、可能的发病机制作一综述。     

高原低氧环境下牙周炎的发病机制

牙周炎的病理过程受全身和局部因素的综合调控,一些调查研究显示高原牙周炎患病率高于平原地区,显然高原特殊环境在牙周炎的发生和发展过程中起到一定的作用,因此本文就高原低氧环境下牙周病变组织的变化、可能的发病机制作一综述。     

GBV-C与艾滋病毒的相互作用及其机制

GBV-C（GB Virus C)是20世纪90年代中期发现的一种单股正链RNA病毒,属黄病毒科Pegivirus属,全基因组长约9.4 kb,编码约2 900个氨基酸序列.早期认为,该病毒与肝炎有关,但随后的研究发现,该病毒对人类无致病作用.最近的研究表明,GBV-C与艾滋病毒（人类免疫缺陷病毒,human immunodeficiency virus,HIV）共感染情况下可抑制HIV的增殖、提高机体免疫、延缓HIV 患者疾病进程.进一步研究GBV-C与HIV的相互作用及其机制可能会为艾滋病（acquired immune deficiency syndrome,AIDS）治疗提供新思路. 本文就GBV-C与HIV-1相互作用的两种主要类型--间接和直接的作用以及其机制进行了综述.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.