发刊词

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凝心聚力谱华章 与时俱进启新程

回眸《中华消化杂志》创刊40年来的办刊历程、报道主题和所取得的主要成绩,面对新形势,将始终恪守为读者和作者服务的办刊初心,与时俱进启新程,服务中国消化事业,创办精品期刊。     

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努力提高《中华消化杂志》的编辑质量

努力提高《中华消化杂志》的编辑质量中华消化杂志编辑部：《中华消化杂志》创刊已进入第十六个年头。她凝聚了无数医界前辈的心血，推动了我国消化专业的进步，功在千秋。只有在成绩中发现缺点、在前进中找出不足，才能永远立于不败之地，勇攀科学高峰。在《中华消化杂志...     

本期导读

春华秋实三十载, 岁月如歌谱华章。2023年, 《中华肝脏病杂志》创刊30周年, 其英文姊妹刊Journal of Clinical and Translational Hepatology(JCTH)创刊10周年。值此新年伊始, 任红教授、贾继东教授、徐小元教授代表《中华肝脏病杂志》和JCTH编辑委员会, 向关心、支持《中华肝脏病杂志》和JCTH的各位编审者、作者、读者致以诚挚的感谢与衷心的祝福(第1～2页)!     

团结协作 提高质量──谈《中华消化杂志》质量的再提高

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《中华消化杂志》回顾与展望

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承前启后再创佳绩

值此《内镜》杂志更名为《中华消化内镜杂志》 10周年及2005年新年到来之际,我谨代表中华消 化内镜杂志编委会向全国消化内镜的同道们致以节 日的祝贺和问候。 过去的10年来,中华消化内镜杂志在全国广大 消化内镜工作者的大力支持下,通过编委会及编辑 部同仁们的辛勤劳动和努力,杂志的期刊特色、学术 水平、栏目种类、文章编排、印刷质量等各方面都取 得了长足的进步;在此基础上逐年获得了由中华医     

努力办刊 再创佳绩──祝贺中华消化杂志荣获中国科协优秀科技期刊奖

努力办刊再创佳绩──祝贺中华消化杂志荣获中国科协优秀科技期刊奖中华消化杂志第四届编委会《中华消化杂志》是中华医学会消化系病学会的专业学术期刊。属中华医学会的系列杂志之一，由中华医学会主办，中华医学会上海分会委办。自１９８１年２月创刊以来，经历届编委会...     

中华医学会消化病分会网站开通

中华医学会消化病学分会网站(http://www.csge.org)已于2001年5月1日起正式开通,网页包括学会简介、科研动态、学术会议、继续教育及共识意见等内容,以及《中华消化杂志》1998年至今的文献目录与摘要和《中华消化病杂志》(英文版)2000年创刊至今的目录与摘要。欢迎广大     

Golgi inheritance in small buds of Saccharomyces cerevisiae is linked to endoplasmic reticulum inheritance

According to the cisternal maturation hypothesis, endoplasmic reticulum (ER)-derived membranes nucleate new Golgi cisternae. The yeast Saccharomyces cerevisiae offers a unique opportunity to test this idea because small buds contain both ER and Golgi structures early in the cell cycle. We previously predicted that mutants defective in ER inheritance also would show defects in Golgi inheritance. Surprisingly, studies of S. cerevisiae have not revealed the expected link between ER and Golgi inheritance. Here, we revisit this issue by generating mutant strains in which many of the small buds are devoid of detectable ER. These strains also show defects in the inheritance of both early and late Golgi cisternae. Strikingly, virtually all of the buds that lack ER also lack early Golgi cisternae. Our results fit with the idea that membranes exported from the ER coalesce with vesicles derived from existing Golgi compartments to generate new Golgi cisternae. This basic mechanism of Golgi inheritance may be conserved from yeast to vertebrate cells.     

Recessive autosomal inheritance in Marfan syndrome]

Three brothers 9, 12, and 14 years of age were studied. The three of them fulfilled the diagnostic criteria of Marfan Syndrome that was made based on physical and ophthalmologic examination, these criteria included musculoskeletal abnormalities, subluxation of lens, myopia and aortic aneurysm. The three siblings died due to complications of the aortic aneurysm, which had an early onset as well as the other clinical manifestations of the disease. They were 2 brothers and one sister. There was neither mental or psychomotor retardation, nor metabolic disease in any of the patients. Family history did not show any clinical manifestation of the disease in parents or grandparents. We propose that the hereditary pattern is recessive autosomic instead of dominant autosomic given the features of these cases and their history.     

The inheritance of hand osteoarthritis in Iceland

OBJECTIVE: To assess the contribution of genetics to hand osteoarthritis (HOA) and its subsets in the Icelandic population. METHODS: A list of 2,919 HOA patients, constituting 1% of the Icelandic population, was compiled through nationwide sources. This patient list was cross-referenced with a comprehensive Icelandic genealogy database, enabling the use of algorithms to assess familiality of HOA. Two methods were used: the average pairwise kinship coefficient (KC) of the patients, and the relative risk (RR) of HOA in relatives of patients. In each case, the results were compared with 1,000 control sets of similar composition with regard to number, age, and sex, generated from the genealogy database. RESULTS: The KC for patients was significantly higher than for the control sets and was proportional to the degree of both interphalangeal (IP) and thumb base (first carpometacarpal [CMC] joint) involvement. The RR of HOA in sisters of women in the study was 2.0 (P < 0.001), while the RR in spouses was not significantly different from that in controls. The RR increased with the severity of the disease. Thus, sisters of women with severe IP HOA had an RR of 5.0 and sisters of those with severe first CMC involvement had an RR of 6.9. The increased risk also extended beyond the nuclear family, with significantly increased risk in cousins. CONCLUSION: Patients seeking medical services for HOA are more related to each other than matched controls, supporting the role of a genetic component in the disease. The genetic influence in both IP and first CMC HOA appears to be similar and increases with increasing severity of the disease.     

The inheritance of hip osteoarthritis in Iceland

OBJECTIVE: To assess, in a population-wide study in Iceland, the genetic contribution to hip osteoarthritis (OA) leading to total hip replacement (THR). METHODS: Information from 2 population-based databases in Iceland was combined: a national registry of all THRs performed between 1972 and 1996, and a genealogy database of all available Icelandic genealogy records for the last 11 centuries. A genetic contribution to THR for OA was assessed by 1) identifying familial clusters of OA patients with THR, 2) applying the minimum founder test (MFT) to estimate the minimum number of ancestors ("founders") that would account for the genealogy of all 2,713 patients with THR for OA, compared with the average number of founders for control lists, 3) calculating an average pairwise kinship coefficient (KC) for the patient list and control lists, and 4) estimating the relative risk (RR) for THR among relatives of OA patients who have undergone the procedure. One thousand matched control lists, each the same size as the patient list, were created using the genealogy database. RESULTS: A large number of familial clusters of patients with THR for OA were identified. The MFT showed that OA patients descended from fewer founders than did subjects in the control groups (P < 0.001). The average pairwise KC among patients with OA was greater than in the control population (P < 0.001). The RR for THR among siblings of OA patients was 3.05 (95% confidence interval 2.52-3.10). CONCLUSION: This population-based study shows that Icelandic patients with hip replacement for OA are significantly more related to each other than are matched controls drawn from the Icelandic population. These findings support a significant genetic contribution to a common form of OA and encourage the search for genes conferring an increased susceptibility to OA.     

The inheritance of rheumatoid arthritis in Iceland

OBJECTIVE: Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis. Although there is a large body of evidence suggesting that RA is immune mediated, the etiology remains unresolved. Twin studies have shown disease concordance rates of approximately 15% in monozygotic twins and 4% in dizygotic twins, while the estimated risk ratio for siblings of RA patients ranges from 5 to 8. Our goal was to use genealogic data from Iceland to further investigate the genetic component of RA. METHODS: Data were obtained from a population-based, computerized genealogy database that was developed to examine multigenerational relationships among individuals in the relatively homogeneous population of Iceland. Using an algorithm, the minimum founder test, we calculated the least number of founders required to account for a list of RA patients, and compared it with 1,000 sets of same-sized matched control groups. In addition, we estimated the kinship coefficient and risk ratios for relatives of the RA patients. RESULTS: Several familial clustering tests demonstrated that the RA patients were more related to each other than were the average control set of Icelanders. A significantly fewer number of founders was necessary to account for our patient list than for the random sets of matched controls (P < 0.001), and the average pairwise identity-by-descent sharing was greater among the patients than among the control sets (P < 0.001). In addition, there was an increased risk of RA in first- and second-degree relatives of the patients; e.g., for siblings, the risk ratio was 4.38 (95% confidence interval 3.26-5.67), and for uncles/aunts, the risk ratio was 1.95 (95% confidence interval 1.52-2.43). CONCLUSION: The familial component of RA is shown to extend beyond the nuclear family, thus providing stronger evidence for a significant genetic component to RA.     

The inheritance of familial hypercholesterolemia

Several forms of familial hypercholesterolemia are now recognized. The most common is characterized by elevated serum cholesterol levels with normal or only modestly elevated serum triglyceride levels, currently classified as type II hyperlipoproteinemia. It is the current consensus that this form of familial hypercholesterolemia is transmitted by a single dominant gene, although polygenic inheritance has been proposed by McKusick as an alternate hypothesis. Decision as to the most probable mode of inheritance of familial hypercholesterolemia must be based upon family studies which enumerate a recognizable characteristic of hypercholesterolemia and compare the observed incidence with models for Mendelian inheritance. Several characteristics have been used over the years. Serum total cholesterol level is now most widely accepted, although attempts at use of the beta lipoprotein level are now in progress, and in the future use of other attributes can be anticipated. When the serum total cholesterol level is used the available evidence indicates that polygenic inheritance is more probable than transmission by a single dominant gene. The practical implications of this conclusion are (1) In family studies of hypercholesterolemia, the serum cholesterol level of both parents must be tested. (2) Genetic counseling should take into account the probability that children will have serum cholesterol levels more nearly resembling a midparent than either normal parent or hypercholesterolemic parent. (3) It is not possible to select any single cholesterol level as a valid characteristic for familial hypercholesterolemia. (4) Children who have borderline cholesterol values cannot be classified as having or not having the hypercholesterolemic trait. (5) The effect of any single medication or therapeutic procedure predictably will vary in different families.