俄罗斯养禽业的疾病态势

俄罗斯农业部兽医局雅科夫列夫撰文报道,在当前俄罗斯境内养禽业中,因疾病所造成的损失态势是:传染性疾病由于采取有力预防措施。发病所占比例不高,其中,传染性法氏囊病和禽痘占5％,白痢病-伤寒占4％,大肠杆菌病占55％,球虫病占10％。马立克氏病占3％,其它传染病占23％;而普通病所占比重却是很高的,其中主要是胃肠道病、肝病、卵形成器官病和物质代谢障碍。这些疾病的发生,在颇大程度上均同家禽的饲养、培育和管理以及执行兽医卫生规章有关。

新诊断2型糖尿病患者疾病态度对短期胰岛素泵强化治疗后长期无药缓解的影响

目的新诊断T2DM患者短期使用胰岛素泵强化治疗(CSII)可修复受损β细胞,改善胰岛素敏感性,并获得仅靠饮食、运动治疗的"无药缓解期"。本研究使用密西根糖尿病管理评定量表(DCP)评估患者对糖尿病的态度,并探讨其对获得长期临床缓解的影响。方法对符合入选标准的新诊断T2DM患者进行为期2～3周的CSII强化治疗,并接受统一的自我管理教育(按照《中国2型糖尿病防治指南》制定的自我管理内容)。同时,入选对象在CSII治疗前、治疗后3、6个月、1年完成DCP,评价患者对糖尿病的态度(包括积极态度、消极态度、自我护理能力、自我管理重要性认识、自我管理坚持性认识)。结果经短期CSII治疗后,118例患者血糖水平达到接近正常,65例患者无药缓解期>1年,其中文化学历水平较高的患者比例明显高于无药缓解期<1年的患者,短期CSII治疗后获得更好的血糖控制,以及胰岛素分泌第一时相(AIR)获得显著改善。同时,无药缓解期>1年的患者从CSII治疗开始时表现出对疾病的积极态度、自我护理能力、自我管理重要性认识和坚持性认识得分较高,消极态度得分较低。1年随访期内,这些患者对疾病的积极态度、自我护理能力、自我管理重要性认识和坚持性认识得分高于同时期的无药缓解期<1年的患者;消极态度得分低于同时期的1年内治疗失效的患者。Cox回归分析结果显示,对疾病自我管理坚持性认识(HR0.184,P<0.001),以及反映CSII治疗前IR的HOMA-IR值(0.854,P=0.053)均是短期CSII后维持长期临床无药缓解的独立预测因素,然而患者CSII后餐后2h血糖(1.156,P=0.015)是引起临床无药失效的危险因素。结论经过短期胰岛素泵强化治疗后,新诊断T2DM患者对疾病的态度影响临床无药缓解期的长短。

缺氧诱导因子与骨稳态失衡类疾病的相关性

背景:缺氧诱导因子是骨缺氧微环境中关键的基因表达调节因子,了解缺氧诱导因子在骨形成、骨重塑中的作用机制及其对骨稳态失衡类疾病的影响,对探索骨稳态失衡类疾病的防治新途径具有重要意义。目的:查阅国内外相关医学文献,对缺氧诱导因子在骨形成、骨重塑过程中的作用机制,以及对缺氧诱导因子与骨稳态失衡类疾病相关性的研究进展进行综述分析。方法:在2021年4月检索中国知网、万方、维普、NCBI和PubMed数据库2000-2021年所发表的文献,中文关键词:"缺氧诱导因子、骨形成、骨重塑、骨稳态失衡类疾病、调控机制";英文关键词:"Hypoxia inducible factor,bone formation,bone remodeling,bone homeostasis disorders,regulatory mechanism";通过对相关资料的整理与分析,综述缺氧诱导因子对骨形成、骨重塑的作用机制,并分析缺氧诱导因子在骨稳态失衡类疾病中的作用。结果与结论:①缺氧应激条件下成骨细胞过度表达的缺氧诱导因子1α能够促进骨形成,增加长骨体积,而破骨细胞中缺氧诱导因子2α表达的显著上调能促进破骨细胞的成熟与分化,引起进行性骨丢失。②抑制破骨细胞中缺氧诱导因子1α表达可削弱破骨细胞活性,降低骨吸收,提高骨重塑,缺氧诱导因子2α则通过介导成骨细胞与破骨细胞间的调节来实现骨重塑。③关于缺氧诱导因子3在骨形成、骨重塑中的作用机制目前尚未有研究涉及。④在骨质疏松症中,成骨细胞数量、成骨功能及血管形成能力下降,抑制部分缺氧诱导因子α表达,引起骨量减少、骨密度下降,增加了骨折发生风险。⑤在骨关节炎中,缺氧诱导因子2α呈明显高表达,其通过调控炎性因子、基质分解酶类等分解代谢基因的表达,刺激所介导的软骨细胞凋亡,并加速软骨成分破坏。⑥在软骨肉瘤中,新血管的生成与缺氧诱导因子1α过表达相关,缺氧诱导因子1α可作为软骨肉瘤中与肿瘤新血管生成相关的恶性标志物,缺氧诱导因子1抑制治疗可干预软骨肉瘤中的血管生成。⑦缺氧诱导因子对骨稳态失衡类疾病的血管生成过程及成骨细胞、破骨细胞、软骨细胞组织的增殖与活性具有重要调控作用,因此研发缺氧诱导因子相关激活类或抑制类药物,对修复骨缺损、加快骨折愈合、改善骨关节炎症等骨稳态失衡类病变有十分积极的意义。

证是疾病功能态

证是机体在疾病发生发展过程中某一阶段的病理概括,这一思想是在2000年的证的研究中逐步形成的。从系统科学来看,人的发生功能产生和维持人的形态结构及其官能,功能异常是疾病更深一层的本质。中医以证为核心的功能病理学包含着极其深刻的科学原理:疾病在本质上是功能性的,证在本质上是功能性的。人体科学的人体功能态学说认为,人体功能态是人的整体功能状态中一些各具特征的状态,从医学角度可以将它们分为两类:健康功能态和疾病功能态。疾病功能态是人在疾病功能状态下的各种特殊状态,它是疾病的不同性质、不同进程等内容在人体功能上的具体体现。中医的证是功能性的,不同的证是不同内容的功能异常。从人体科学来看,证是疾病功能态,辨证论治是辨识和调理疾病功能态。发扬中医的这一特色,对于人体功能态学说乃至整个人体科学的研究具有重要意义。

论体质与证的相关性及其临床意义

体质分型除正常质外 ,其他各型体质如气虚质、血虚质、痰湿质等均有潜病未病态及疾病态二种状态 ,与证既有区别又有联系 ,表现为对特定疾病的易患性。这方面的研究可用于指导养生、疾病的群体预防及疾病的治疗。

基于DKI的步态障碍型帕金森病患者脑结构网络的拓扑属性改变研究

目的 探讨步态障碍型帕金森患者(PIGD)脑结构网络的拓扑属性特点.方法 对扬州大学附属苏北人民医院自2019年9月-2023年9月收治的32例PIGD患者及30例年龄、性别相匹配的健康志愿者进行DKI扫描,采用图论分析方法计算脑拓扑网络属性参数,使用独立样本t检验对两组脑结构网络的总体参数及节点属性参数进行对比分析.运用Spearman相关分析统计差异脑区的网络特性参数与临床认知评分的相关性.结果 PIGD组较对照组脑网络全局效率明显减小,包括Eglob明显低于对照组(P=0.004,FDR校正).PIGD组Lp值明显高于对照组(P=0.012,FDR校正),而Cp比较,差异无统计学意义(P>0.05,FDR校正).与对照组比较,PIGD组脑结构网络节点效率在右额中回、右中央前回、右颞下回、右顶上回、右枕叶外侧皮层、右杏仁核、左顶下叶、左中央后回明显降低,差异均有统计学意义(P<0.05,FDR校正).PIGD组左侧顶下叶及右侧枕叶外侧皮层节点效率与MMSE评分呈正相关(r=0.504,P=0.003;r=0.374,P=0.035),并且左侧顶下叶节点效率与MOCA评分呈正相关(r=0.437,P=0.012).结论 PIGD患者脑结构网络存在连接异常.

论“证”的功能性及特定性

钱学森曾强调：“中医的证也是功能态。”越来越多的专家学者认识到证的功能性特点，如“证是多系统功能的变化”，“中医的证亦是研究在致病因素作用下人体病理功能态的改变”。特别是祝世讷教授在他的文章中提出：证“是人的功能异常的特定疾病态”。下面就证的功能性（...

柴胡剂群药物不同剂量及煎法探讨

《伤寒论》中小柴胡汤及其加减方中主药的剂量有所不同,大致可分为大、中、小三种剂量,而且针对不同的剂量,仲景采取的煎药方法也不尽相同,究其实质是由疾病的本态所决定的。少阳证变化多端、症状复杂,临证时我们只有抓住疾病本态,并全面理解柴胡剂群的各个方证,灵活遣方用药,方能取得满意的疗效。

走出亚健康的良方

亚健康是二十世纪末出现的概念。亚健康是处于健康与疾病之间的不稳定的中间状态。亚健康态容易变化，具有双向性．若采取养生调理措施则向健康态转化．若不采取措施则向疾病态转化。

走出亚健康的良方

亚健康是二十世纪末出现的概念.亚健康是处于健康与疾病之间的不稳定的中间状态.亚健康态容易变化,具有双向性,若采取养生调理措施则向健康态转化,若不采取措施则向疾病态转化.最近中华医学会调查指出,健康和疾病的人群各占15%,而亚健康的人群占70%.另据中国保健科技学会对16个百万人口以上的城市调查,今年4月份公布的结果:北京人处于亚健康状态的占75.3%,上海人占73.49%,高于其它地区.

Relationship between Crohn’s disease, infection with Mycobacterium avium subspecies paratuberculosis and SLC11A1 gene polymorphisms in Sardinian patients

AIM： To study the association between Crohn＇s disease （CD）, Mycobacterium avium subspecies paratubercuolsis （MAP）, and genetic factors by examining the role of natural resistance-associated macrophage protein 1 （NRAMP1） gene polymorphisms （now SLCllA1） in Sardinian patients with CD and controls. METHODS： Thirty-seven CD patients and 34 controls with no inflammatory bowel disease （IBD） were recruited at the University of Sassari after giving written consent. Six SCL11A1 polymorphisms previously reported to be the most significantly associated with IBD were searched. M, pafatubefculosis was identified by IS900 PCR and sequencing. Logistic regression was used to calculate odds ratios （OR） for the associations among CD, presence of MAP, and 6 loci described above.＇ RESULTS： For the first time, a strong association was observed between polymorphisms at NRAMP1 locus 823C/T and CD. While CD was strongly associated with both NRAMP1 and MAP, NRAMP1 polymorphisms and MAP themselves were not correlated. CONCLUSION： Combined with previous work on the NOD2/CARD15 gene, it is clear that the interplay of genetic, infectious, and immunologic factors in the etiology of CD is complex.

Clinical application of hepatic CT perfusion

Complicated changes occur in hemodynamics of hepatic artery and vein, and portal vein under various kinds of pathologic status hepatic blood supply. This because of distinct double article reviews the clinical application of hepatic computed tomography perfusion in some liver diseases.

Intestinal mucosal adaptation

Intestinal failure is a condition characterized by malnutrition and/or dehydration as a result of the inadequate digestion and absorption of nutrients. The most common cause of intestinal failure is short bowel syndrome, which occurs when the functional gut mass is reduced below the level necessary for adequate nutrient and water absorption. This condition may be congenital, or may be acquired as a result of a massive resection of the small bowel. Following resection, the intestine is capable of adaptation in response to enteral nutrients as well as other trophic stimuli. Identifying factors that may enhance the process of intestinal adaptation is an exciting area of research with important potential clinical applications.

Drug-induced liver injury:Is it somehow foreseeable?

The classic view on the pathogenesis of drug-induced liver injury is that the so-called parent compounds are made hepatotoxic by metabolism (formation of neosubstances that react abnormally), mainly by cytochromes P-450 (CYP), with further pathways, such as mitochondrial dysfunction and apoptosis, also playing a role. Risk factors for drug-induced liver injury include concomitant hepatic diseases, age and genetic polymorphisms of CYP. However, some susceptibility can today be predicted before drug administration, working on the common substrate, by phenotyping and genotyping studies and by taking in consideration patients' health status. Physicians should always think of this adverse effect in the absence of other clear hepatic disease. Ethical and legal problems towards operators in the health care system are always matters to consider.

Relevance of MUC1 mucin variable number of tandem repeats polymorphism in H pylori adhesion to gastric epithelial cells

AIM:To evaluate the influence of MUC1 mucin variable number of tandem repeats (VNTR) variability on H pylori adhesion to gastric cells. METHODS: Enzyme linked immunosorbent assay (ELISA)-based adhesion assays were performed to measure the adhesion of different H pylori strains (HP26695 and HPTx30a) to gastric carcinoma cell lines (GP202 and MKN45) and GP202 clones expressing recombinant MUC1 with different VNTR lengths. RESULTS: Evaluation of adhesion results shows that H pylori pathogenic strain HP26695 has a significantly higher (P < 0.05) adhesion to all the cell lines and clones tested, when compared to the non-pathogenic strain HPTx30a. Bacteria showed a significantly higher (P < 0.05) adhesion to the GP202 cell line, when compared to the MKN45 cell line. Furthermore, both strains showed a significantly higher (P < 0.05) adhesion to GP202 clones with larger MUC1 VNTR domains. CONCLUSION: This work shows that MUC1 mucin variability conditions H pylori binding to gastric cells. The extent of bacterial adhesion depends on the size of theMUC1 VNTR domain. The adhesion is further dependent on bacterial pathogenicity and the gastric cell line. MUC1 mucin variability may contribute to determine H pylori colonization of the gastric mucosa.

Psychosocial stress and liver disease status

"Psychosocial stress" is an increasingly common concept in the challenging and highly-demanding modern society of today. Organic response to stress implicates two major components of the stress system, namely the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Stress is anamnestically reported by patients during the course of disease, usually accompanied by a decline in their overall health status. As the mechanisms involving glucocorticoids and catecholamines have been deciphered, and their actions on immune cell function deeper understood, it has become clear that stress has an impact on hepatic inflam-matory response. An increasing number of articles have approached the link between psychosocial stress and the negative evolution of hepatic diseases. This article reviews a number of studies on both human populations and animal models performed in recent years, all linking stress, mainly of psychosocial nature, and the evolution of three important liver-related pathological entities: viral hepatitis, cirrhosis and hepatocellular carcinoma.

Characteristic features of ghrelin cells in the gastrointestinal tract and the regulation of stomach ghrelin expression and production

Ghrelin was isolated as an endogenous ligand for the GH secretagogue receptor from the rat stomach. Although physiological effects of ghrelin have been revealed by numerous studies, the regulation of stomach ghrelin remains obscure, and the factor that directly regulates ghrelin expression and production has not been identified. Here, we show some data regarding the characteristic features of ghrelin cells and the regulation of stomach ghrelin. In the gastrointestinal tract, ghrelin cells were identified as opened- and closed-type cells, and it was found that the number of ghrelin cells decreased from the stomach to the colon. The postnatal change in number of ghrelin cells in the stomach showed a sexually dimorphic pattern, indicating a role of estrogen in the regulation of stomach ghrelin. In vitro studies revealed that estrogen stimulated both ghrelin expression and production and that treatment with formestane, an aromatase (estrogen synthetase) inhibitor, decreased ghrelin expression level. On the other hand, leptin was found to inhibit both basal and estrogen-stimulated ghrelin expression. Moreover, both aromatase mRNA- expressing cells and leptin cells were found to be located close to ghrelin cells in the gastric mucosa. Furthermore, we found an inverse relationship between gastric ghrelin and leptin levels in a fasting state, and we revealed relative changes in expression of gastric ghrelin, estrogen and leptin in the postnatal rats. We propose that gastric estrogen and leptin directly regulate stomach ghrelin and that the balance control through gastric estrogen and leptin contributes to the altered ghrelin expression level in some physiological states.

Technique for Controlling Spread of Limnotic Oncomelania

Schistosomiasis is a parasitic disease mostly found in areas along the Changjiang River of China. The disease is spread solely through an intermediary named oncomelania, so its spread of schistosomiasis can be controlled by properly designing water intakes which prevent oncomelania from entering farming land or residential areas. This paper reports a successful design process and a new oncomelania free intake device. The design of the new intake is based on a sound research program in which extensive experimental studies were carried out to gain knowledge of oncomelania eco hydraulic behavior and detailed flow field information through CFD simulation.

New method for long-term monitoring of intragastric pH

AIM: Consecutive monitoring of intragastric pH using the Bravo? capsule. METHODS: We put threads through a Bravo? capsule and then affixed it to the gastric wall by endoscopic hemoclipping in seven subjects. Study data were uploaded to a computer via Datalink every 48 h. In this way,repeated monitoring of intragastric pH was undertaken. RESULTS: All subjects were able to monitor gastric pH over a 1-wk period,and five for > 2 wk. No complications were encountered during the monitoring. After pH monitoring,we safely retrieved the capsule endoscopically. CONCLUSION: Clipping a Bravo? capsule onto the gastric wall enabled long-term intragastric pH monitoring. This is a methodological report of pH monitoring over a period of > 2 wk.

Single nucleotide polymorphism in the tumor necrosis factor-alpha gene affects inflammatory bowel diseases risk

AIM: To investigate the role that single nucleotide polymorphisms (SNPs) in the promoter of the tumour necrosis factor-alpha (TNF-α) gene play in the risk of inflammatory bowel diseases (IBDs) in a New Zealand population, in the context of international studies. METHODS: DNA samples from 388 patients with Crohn's disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis (IC) and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common polymorphisms in the TNF-α receptor: -238 G→A, -308 G→A and -857C→T, using a TaqmanR assay. A meta-analysis was performed on the data obtained on these polymorphisms combined with that from other published studies. RESULTS: Individuals carrying the -308 G/A allele had a significantly (OR = 1.91, χ2 = 17.36, P < 0.0001) increased risk of pancolitis, and a 1.57-fold increased risk (OR = 1.57, χ2 = 4.34, P = 0.037) of requiring a bowel resection in UC. Carrying the -857 C/T variant decreased the risk of ileocolonic CD (OR = 0.56, χ2 =4.32, P = 0.037), and the need for a bowel resection (OR = 0.59, χ2 = 4.85, P = 0.028). The risk of UC was reduced in individuals who were smokers at diagnosis, (OR = 0.48, χ2 = 4.86, P = 0.028). CONCLUSION: TNF-α is a key cytokine known to play a role in inflammatory response, and the locus for the gene is found in the IBD3 region on chromosome 6p21, known to be associated with an increased risk for IBD. The -308 G/A SNP in the TNF-α promoter is functional, and may account in part for the increased UC risk associated with the IBD3 genomic region. The -857 C/T SNP may decrease IBD risk in certain groups. Pharmaco- or nutrigenomic approaches may be desir- able for individuals with such affected genotypes.