藁杆双脐螺在中国内陆的分布现状与传病风险

藁杆双脐螺可作为曼氏血吸虫中间宿主,1981年证实在深圳市局部地区有该螺孳生;2013年再次调查发现,该螺已在深圳市、以及周边的东莞市和惠州市等地大范围蔓延扩散,并已在当地形成较优势种群,有进一步扩散的趋势。由于深圳市及周边地区与国际交流密切,劳务输出等人口流动性大,且目前我国由境外输入的曼氏血吸虫病病例报道亦逐渐增多,因此曼氏血吸虫病在我国传播或流行的潜在风险因素正在逐步增加,必须引起高度重视,及早采取相应的防控措施,加强监测,降低该病在我国传播或流行的风险。本文就藁杆双脐螺在中国内陆的发现、分布、扩散蔓延及传病风险等进行了综述,并提出相关的防控建议。

Pancreatic cancer: A review of clinical diagnosis, epidemiology, treatment and outcomes

This review aims to outline the most up-to-date knowledge of pancreatic adenocarcinoma risk, diagnostics, treatment and outcomes, while identifying gaps that aim to stimulate further research in this understudied malignancy. Pancreatic adenocarcinoma is a lethal condition with a rising incidence, predicted to become the second leading cause of cancer death in some regions. It often presents at an advanced stage, which contributes to poor five-year survival rates of 2%-9%, ranking firmly last amongst all cancer sites in terms of prognostic outcomes for patients. Better understanding of the risk factors and symptoms associated with this disease is essential to inform both health professionals and the general population of potential preventive and/or early detection measures. The identification of high-risk patients who could benefit from screening to detect pre-malignant conditions such as pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasms and mucinous cystic neoplasms is urgently required, however an acceptable screening test has yet to be identified. The management of pancreatic adenocarcinoma is evolving, with the introduction of new surgical techniques and medical therapies such as laparoscopic techniques and neo-adjuvant chemoradiotherapy, however this has only led to modest improvements in outcomes. The identification of novel biomarkers is desirable to move towards a precision medicine era, where pancreatic cancer therapy can be tailored to the individual patient, while unnecessary treatments that have negative consequences on quality of life could be prevented for others. Research efforts must also focus on the development of new agents and delivery systems. Overall, considerable progress is required to reduce the burden associated with pancreatic cancer. Recent, renewed efforts to fund large consortia and research into pancreatic adenocarcinoma are welcomed, but further streams will be necessary to facilitate the momentum needed to bring breakthroughs seen for other cancer sites.

Promoting genetics in non-alcoholic fatty liver disease: Combined risk score through polymorphisms and clinical variables

Non-alcoholic fatty liver disease(NAFLD) has a prevalence of approximately 30% in western countries, and is emerging as the first cause of liver cirrhosis and hepatocellular carcinoma(HCC). Therefore, risk stratification emerges as fundamental in order to optimize human and economic resources, and genetics displays intrinsic characteristics suitable to fulfill this task. According to the available data, heritability estimates for hepatic fat content range from 20% to 70%, and an almost 80% of shared heritability has been found between hepatic fat content and fibrosis. The rs738409 single nucleotide polymorphism(SNP) in patatin-like phospholipase domain-containing protein 3 gene and the rs58542926 SNP in transmembrane 6 superfamily member 2 gene have been robustly associated with NAFLD and with its progression, but promising results have been obtained with many other SNPs. Moreover, there has been proof of the additive role of the different SNPs in determining liver damage, and there have been preliminary experiences in which risk scores created through a few genetic variants, alone or in combination with clinical variables, were associated with a strongly potentiated risk of NAFLD, non-alcoholic steatohepatitis(NASH), NASH fibrosis or NAFLD-HCC. However, to date, clinical translation of genetics in the field of NAFLD has been poor or absent. Fortunately, the research we have done seems to have placed us on the right path: We should rely on longitudinal rather than on cross-sectional studies; we should focus on relevant outcomes rather than on simple liver fat accumulation; and we should put together the genetic and clinical information. The hope is that combined genetic/clinical scores, derived from longitudinal studies and built on a few strong genetic variants and relevant clinical variables, will reach a significant predictive power, such as to have clinical utility for risk stratification at the single patient level and even to esteem the impact of intervention on the risk of disease-related outcomes. Well-structured future studies would demonstrate if this vision can become a reality.

Genetic characteristics and pathogenicity of human hepatitis E virus in Nanjing,China

AIM： To investigate the genetic characteristics and pathogenicity of hepatitis E virus （HEV） and assess the potential risk factors for sporadic hepatitis E.

Colorectal cancer in inflammatory bowel disease:What is the real magnitude of the risk?

The association between inflammatory bowel disease(IBD) and colorectal cancer(CRC) has been recognised since 1925 and still accounts for 10%-15% of deaths in IBD.IBD-associated CRC(IBD-CRC) affects patients at a younger age than sporadic CRC.The prognosis for sporadic CRC and IBD-CRC is similar,with a 5-year survival of approximately 50%.Identifying at risk patients and implementing appropriate surveillance for these patients is central to managing the CRC risk in IBD.The increased risk of colorectal cancer in association with IBD is thought to be due to genetic and acquired factors.The link between inflammation and cancer is well recognised but the molecular biology,immune pathobiology and genetics of IBD-CRC are areas of much ongoing research.This review examines the literature relating to IBD-CRC,focusing on the incidence of IBD-CRC and examining potential risk factors including age at diagnosis,gender,duration and extent of colitis,severity of inflammation,family history of sporadic CRC and co-existent primary sclerosing cholangitis(PSC).Confirmed risk factors for IBD-CRC are duration,severity and extent of colitis,the presence of co-existent PSC and a family history of CRC.There is insufficient evidence currently to support an increased frequency of surveillance for patients diagnosed with IBD at a younger age.Evidence-based guidelines advise surveillance colonoscopy for patients with colitis 8 to 10 years after diagnosis,with the interval for further surveillance guided by risk factors(extent of disease,family history of CRC,post-inflammatory polyps,concomitant PSC,personal history of colonic dysplasia,colonic strictures).There is a move away from using random colonic biopsies towards targeted biopsies aimed at abnormal areas identified by newer colonoscopic techniques(narrow band imaging,chromoendoscopy,confocal microendoscopy).

Characteristics of distribution of Mycobacterium tuberculosis lineages in China

The genotyping methods of Mycobacterium tuberculosis would dramatically improve our understanding of the molecular epidemiology of tuberculosis. 3,929 isolates, from a National Survey of Drug-Resistant Tuberculosis in 2007 in China, were successfully genotyped by large sequence polymorphisms and 15 loci variable number tandem repeats. We found that 2,905(2,905/3,929, 73.9%) cases belonged to Lineage 2, dominated in the east and central regions, 975 cases(975/3,929, 24.8%) were Lineage 4, highly prevailed in the west regions, and 36 and 13 cases were Lineage 3 and Lineage 1, respectively. We also explored the associations between lineages(Lineage 2 vs. Lineage 4) and clinical characteristics by logistic regression. For Lineage 2, the risk factors were Han-ethnicity population and fever. However, for Lineage 4, they were occupation(farmer), and degree of education(non-literate). Fully understanding of the distribution of Mycobacterium tuberculosis lineage and its risk factors would play a critical role in tuberculosis prevention, control, and treatment.

Schizophrenia:a classic battle ground of nature versus nurture debate

Much has been learned about the etiology and pathogenesis of schizophrenia since the term was first used by Eugene Bleuler over a century ago to describe one of the most important forms of major mental illness to affect mankind.Both nature and nurture feature prominently in our understanding of the genesis of the overall risk of developing schizophrenia.We now have a firm grasp of the broad structure of the genetic architecture and several key environmental risk factors have been identified and delineated.However,much of the heritability of schizophrenia remains unexplained and the reported environmental risk factors do not explain all the variances not attributable to genetic risk factors.The biggest problem at present is that our understanding of the causal mechanisms involved is still in its infancy.In this review,we describe the extent and limits of our knowledge of the specific genetic/constitutional and non-genetic/environmental factors that contribute to the overall risk of schizophrenia.We suggest novel methods may be required to understand the almost certainly immensely complex multi-level causal mechanisms that contribute to the generation of the schizophrenia phenotype.

Epidemic transition of environmental health risk during China's urbanization

China has experienced rapid urbanization in recent decades along with dramatic economic growth. Previous studies have shown that urbanization has both positive and negative effects on health. However, there is a lack of research on the overall effects of urbanization on the epidemic transition of environmental health risks considering various pathways in China. In the present study, we studied the contributions of different aspects of urbanization in China to epidemic transitions using provincial and multi-year （1995, 2000, 2005, and 2010） panel data. Statistical models with fixed and random effects were developed to explore the impacts of different urbanization indicators on the overall epidemic tran- sition of environmental health （general model） and the changes in cause-specific mortality rates of typ- ical diseases （cause-specific models）. The results show that the impacts of non-communicable diseases continue to grow during the urbanization process in China. The ratio of communicable disease-related mortality to non-communicable disease-related mortality continues to decrease over time. The general model shows that the improved medical conditions （coefficient =-0.0011, P= 0.037）, the improved urban infrastructure （e.g., tap water supply） （coefficient = -0.00065, P 〈 0,001）, and the rise in income （coefficient = -0.00027, P = 0.047） during the urbanization process are important factors that promote this overall epidemic transition. The cause-specific models show that the mechanisms behind the general model are complicated. More attention should be paid to non-communicable diseases in urban health management. Specific health policies for different diseases should incorporate the considerations of dif- ferent impact pathwavs of urbanization,