干细胞治疗糖尿病的研究现状及未来

目的:综述干细胞治疗糖尿病的研究现状及未来发展。资料来源:应用计算机检索Pubmed2000-01/2006-11有关干细胞治疗糖尿病方面文献,检索词“diabetes mellitus and stem cell not review”,限定文章语言种类为English。资料选择:对检索到的干细胞治疗糖尿病相关文献进行整理,选取针对性强文章。同一领域文献则选择近期发表或权威杂志文章。资料提炼:共检索到359篇相关文献,有关胚胎干细胞、胰腺干细胞、造血干细胞、神经干细胞、骨髓基质干细胞在糖尿病方面研究文章50篇,其中29篇符合要求。资料综合:干细胞极强的自我更新能力和多向分化潜能为糖尿病的细胞治疗开辟了新途径,按其发育阶段不同可以将干细胞分为胚胎干细胞和胰腺干细胞、造血干细胞、神经干细胞、骨髓基质干细胞等成体干细胞。干细胞移植是治疗糖尿病的一条新途径。干细胞生成胰岛素分泌细胞前需要经过诱导分化、细胞选择和细胞成熟3个阶段。干细胞治疗糖尿病研究已取得一定进展,部分实验已纠正糖尿病动物的高血糖状态。结论:干细胞定向分化为胰岛β细胞研究为糖尿病患者点燃了新希望,其勿庸置疑的成为治疗糖尿病的最佳种子细胞。     

“双重束缚”解析

目的:介绍了Bateson提出双重束缚概念的过程,阐述双重束缚概念的特征,并且论述了这一概念对心理治疗起到的积极作用以及概念本身存在的问题。资料来源:应用计算机在ProQuest数据库、EBSCOhost数据库中搜索1980-01/2006-05相关文章,检索的关键词为“doublebind”,“paradox”;在西南大学图书馆手工查找有关“双重束缚”资料。资料选择:对查找的资料进行筛选,纳入阐述双重束缚提出的历史、概念以及应用的文献。排除:①非实证研究和综述。②管理、文化和道德中双重束缚的研究。③重复性的研究。资料提炼:共收集49篇文章,选择与本文相关的28篇进行综述。另外还参考《理解人性》,《家庭治疗基础》两本书籍。资料综合:“双重束缚”是Bateson结合“再学习”和“Russellian矛盾”两个概念提出的。对“双重束缚”的各种定义均体现了这一概念的如下特征:矛盾性、命令性、不平等性、不可逃避性和长期性。“双重束缚”在心理治疗中有广泛的应用,但是各种对“双重束缚”的研究都存在着不足。结论:“双重束缚”的提出有其特定的历史背景,它对精神分裂、精神错乱的形成有一定的解释力。     

Validation of a modified Rotterdam Symptom Checklist for use with cancer patients in the United States

The Rotterdam Symptom Checklist (RSCL) is a well-known instrument for the assessment of symptom-related distress among cancer patients. Despite its broad application, the utility of the RSCL with patients of some cancers is hindered by the omission of several important physical symptoms and methodological limitations of previous validation studies. The aims of the present study were to modify the RSCL through the addition of several physical symptoms and to subsequently validate the modified version of the Rotterdam Symptom Checklist (RSCL-M) with a heterogeneous sample of cancer patients from the United States. A total of 1,005 male and female cancer patients from two midwestern states completed the RSCL-M and several other self-report instruments. Results indicated that the RSCL-M is a reliable and valid instrument for use with cancer patients in the United States and is sensitive to differences in physical distress across groups expected to have distinct symptom-related distress profiles.     

ASURA (PHB2) Is Required for Kinetochore Assembly and Subsequent Chromosome Congression

ASURA (PHB2) knockdown has been known to cause premature loss of sister chromatid cohesion, and disrupt the localization of several outer plate proteins to the kinetochore. As a result, cells are arrested at mitotic phase and chromosomes fail to congress to the metaphase plate. In this study, we further clarified the mechanism underlying ASURA function on chromosome congression. Interestingly, ASURA is not specifically localized at the kinetochore during mitotic phase, unlike other kinetochore proteins which construct the kinetochore. Electron microscopy (EM) observation showed that ASURA is required for proper kinetochore formation. By the partial depletion of ASURA, kinetochore maturation is impaired, and kinetochores showing fibrillar balls without a well-defined outer plates are often observed. Moreover, even when the outer plates of kinetochores are constructed, most showed structures stretched and/or distended from the centromere, which resembled premature kinetochores at prometaphase, indicating that the constructed kinetochore plates are less rigid against tension derived from kinetochore microtubule pulling forces. We concluded that ASURA is an essential protein for complete kinetochore development, although ASURA is not being integrated to the kinetochore. These results highlight the uniqueness of ASURA as a kinetochore protein.     

Hepatocellular carcinoma with indeterminate or false-negative findings at initial MR imaging: effect on eligibility for curative treatment initial observations

PURPOSE: To retrospectively evaluate the effect of indeterminate or false-negative findings at magnetic resonance (MR) imaging on eligibility for curative treatment of hepatocellular carcinoma (HCC). MATERIALS AND METHODS: This HIPAA-compliant retrospective study was approved by the institutional review board; the need for informed consent was waived. Of 166 patients with cirrhosis in whom HCC was detected with MR imaging, 21 (13 men, eight women; mean age, 60 years) had 33 proved HCCs that were not detected on previous MR images obtained 6-24 months earlier. MR imaging included T1-weighted, T2-weighted, and dynamic contrast material-enhanced T1-weighted imaging. Serial MR images and treatment records were reviewed to evaluate nodule growth and the effect of delayed diagnosis on treatment eligibility. RESULTS: Of 33 HCCs in 21 patients, 24 corresponding nodules (73%) were described on previous MR images as benign or indeterminate. Five additional nodules were visible at retrospective evaluation, but only on arterial phase images. The diameters of these 29 visible but indeterminate nodules were initially 0.6-1.9 cm (mean, 1.1 cm) and increased to 0.9-4.5 cm (mean, 1.9 cm) at HCC diagnosis (mean follow-up, 378 days). The mean doubling time was 856 days for diameter and 285 days for volume. All nine HCCs with a delayed diagnosis of less than 1 year were smaller than 3 cm at diagnosis, and the patients had undergone liver transplantation (n=3) or technically successful ablation or embolization (n=6). All 10 subcentimeter indeterminate nodules were smaller than 2 cm at HCC diagnosis, and none progressed to untreatable HCC. CONCLUSION: Indeterminate nodules smaller than 2 cm did not become untreatable HCC with delayed HCC diagnosis of 6-12 months.     

Proven germline mosaicism in a father of two children with CHARGE syndrome

CHARGE syndrome is an autosomal dominant malformation syndrome caused by mutations in the CHD7 gene. The majority of cases are sporadic and only few familial cases have been reported. In these families, mosaicism in one parent, as well as parent- to-child transmission of a CHD7 mutation, has been described. In some further cases, germline mosaicism has been suggested. Here, we report the first case in which germline mosaicism could be demonstrated in a father of two affected children with CHARGE syndrome. The truncating mutation c.7302dupA in exon 34 of the CHD7 gene was found in both affected children but was not detected in parental lymphocytes. However, in DNA extracted from the father's spermatozoa, the c.7302dupA mutation could be identified. Furthermore, mutation analysis of DNA isolated from 59 single spermatozoa revealed that the c.7302dupA mutation occurs in 16 spermatozoa, confirming germline mosaicism in the father of the affected children. This result has a high impact for genetic counselling of the family and for their recurrence risk in further pregnancies.     

The genetics of vitiligo in Korean patients

Background Vitiligo is a common disorder whose exact cause is unknown, but genetic factors are thought to be involved. We analyzed 120 Korean proband families to clarify which genetic factors are involved in the pathogenesis of vitiligo in Korean patients. Methods The genetics of vitiligo were analyzed in 120 Korean proband families out of 1030 vitiligo patients. Each family was analyzed through a proband afflicted with vitiligo. Results In 51 (42.5%) of 120 proband families, at least one first-degree relative of the proband had vitiligo. The incidence of those affected among 1755 relatives (first-, second-, and third-degree) was found to be 8.0 ± 0.6%. There was a statistically significant departure for segregation analysis which was inconsistent with inheritance as an autosomal or X-linked locus model. On the basis of our results, the inheritance pattern of vitiligo is more likely to tend toward the model of multifactorial inheritance. The threshold trait among first-degree relatives (7.2%) appeared to tend more toward the square root of the frequency in the general population (10%) than towards those of dominant (50%) or recessive (25%) models. Conclusions These results indicate that there are certain genetic factors involved in the etiology of vitiligo, and that vitiligo seems to have a polygenic nature.