Fatty acid-binding protein-4 as a biomarker predicting acromegaly-associated diabetes mellitus

Background/aimThe known pathogenesis of diabetes mellitus (DM) in acromegaly is mainly based on growth hormone (GH) and insulin-like growth factor-1 (IGF-1) excess. Fatty acid-binding protein 4 (FABP-4), a novel adipokine, is found to induce insulin resistance and type 2 DM. We aimed to investigate the possible effect of FABP-4 on glucose metabolism in patients with acromegaly.Materials and methodsThis case-control study included 28 patients newly diagnosed with acromegaly and 57 healthy volunteers. The patients with acromegaly were classified according to their glycemic status as with DM, prediabetes, and normal glucose tolerance. Anthropometric measurements, laboratory test results, and FABP-4 levels of the subjects were evaluated.ResultsAlthough no difference was observed in FABP-4 levels between acromegaly and control groups, the FABP-4 level was higher in the patients with acromegaly having DM compared to the patients with acromegaly having prediabetes and NGT, and the control group (p = 0.004, p = 0.001, p = 0.004, respectively). Logistic regression analysis suggested that the FABP-4 is an independent predictor of DM in acromegaly (β = 7.382, OR = 38.96, 95% CI: 1.52-5.76, p = 0.018).Conclusion The FABP-4 may be a helpful predictor of acromegaly-associated DM.     

肾脏占位性病变的超声造影特点

目的探讨不同类型肾脏占位病变的超声造影特点。方法对照病理诊断结果分析76例肾脏占位病变Sono Vue超声造影特征。结果肾恶性肿瘤62例,良性肿瘤14例。肾恶性肿瘤超声造影剂的充盈和消退呈多样性,以同步增强和快增强多见,造影剂的快速消退和缓慢消退之间无明显差别,差异无统计学意义(P>0.05)。恶性肿瘤典型的表现是整个病灶弥漫增强,轮廓边界清晰,呈"亮球"征(95.2%),并多有假包膜(87.1%)。肾错构瘤表现为无假包膜的不均匀增强,而肾囊肿始终无增强。结论超声造影有助于肾占位病变的鉴别诊断和预后判断。     

A systematic review of the evidence for Canada's Physical Activity Guidelines for Adults

This systematic review examines critically the scientific basis for Canada's Physical Activity Guide for Healthy Active Living for adults. Particular reference is given to the dose-response relationship between physical activity and premature all-cause mortality and seven chronic diseases (cardiovascular disease, stroke, hypertension, colon cancer, breast cancer, type 2 diabetes (diabetes mellitus) and osteoporosis). The strength of the relationship between physical activity and specific health outcomes is evaluated critically. Literature was obtained through searching electronic databases (e.g., MEDLINE, EMBASE), cross-referencing, and through the authors' knowledge of the area. For inclusion in our systematic review articles must have at least 3 levels of physical activity and the concomitant risk for each chronic disease. The quality of included studies was appraised using a modified Downs and Black tool. Through this search we identified a total of 254 articles that met the eligibility criteria related to premature all-cause mortality (N = 70), cardiovascular disease (N = 49), stroke (N = 25), hypertension (N = 12), colon cancer (N = 33), breast cancer (N = 43), type 2 diabetes (N = 20), and osteoporosis (N = 2). Overall, the current literature supports clearly the dose-response relationship between physical activity and the seven chronic conditions identified. Moreover, higher levels of physical activity reduce the risk for premature all-cause mortality. The current Canadian guidelines appear to be appropriate to reduce the risk for the seven chronic conditions identified above and all-cause mortality.     

新疆维吾尔族成人支气管哮喘的影响因素研究

摘要:目的　探讨新疆乌鲁木齐市维吾尔族人群成人支气管哮喘的影响因素。方法　本研究采用成组匹配病例对照研究方法,病例组为新疆医科大学第一附属医院呼吸内科在2014年1-12月确诊的维吾尔族支气管哮喘成人患者（n＝120例）,对照组为同期体检中心健康维吾尔族体检者（n＝126例）,两组在年龄、性别相匹配。采用问卷调查的方法收集相关暴露资料,并采用单因素分析及多因素非条件Logistic回归模型分析成人支气管哮喘影响因素。结果　多因素Logistic回归分析显示,吸烟（OR＝1.88,95% CI:1.28～2.96）、家族支气管哮喘史（OR＝6.20,95% CI:2.10～18.31）、家中铺有纯毛地毯数量多（OR＝1.87,95% CI:1.18～2.95）,睡眠质量（OR＝1.46,95% CI:1.22～1.75）,患慢性支气管炎（OR＝13.43,95% CI:6.65～25.34）及过敏性鼻炎（OR＝6.27,95% CI:3.63～10.81）是维吾尔族成人支气管哮喘的主要影响因素。结论　维吾尔族成人支气管哮喘是生活方式、环境及遗传等多种因素共同作用的结果,应加强对相关影响因素的预防及治疗,减少哮喘的发生,改善哮喘患者生活质量。     

Human epidermal growth factor receptor 2 oncoprotein expression in breast cancer patients from central Anatolia, Turkey

Aim:   Human epidermal growth factor receptor 2 (HER2) overexpression is associated with poor prognosis and the frequency of HER2 positivity in breast cancer patients varies among different regions of the world. We studied HER2 expression in Turkish breast cancer patients.
Methods:   HER 2 expression was evaluated immunohistochemically in 107 breast cancer patients. HER2 expression was reported as negative or positive (3+) according to cellular membrane staining characteristics. The frequency of HER2 overexpression, distribution according to clinical characteristics, effect on survival and effect of chemotherapy on survival in relation to HER2 overexpression was evaluated.
Results:   The median age of patients was 49 years (range 27–76). HER2 was 3+ in 34 patients (31.8%). There was no significant difference in age, menopausal status, histopathology, lymph node involvement, stage and estrogen and/or progesterone receptor positivity in relation to HER2 expression. Forty-three patients (40.2%) relapsed and 21 patients (19.6%) died during the follow-up period. There was no significant difference in the relapse rate, distribution of relapse sites and death rate in relation to HER2 expression. The 3- and 5-year disease free survival rates were 67.1 and 40.5%, and the overall survival rates were 87.5 and 66.1%, respectively. Survival rate and calculated survival time were relatively shorter in HER2 3+ patients than in non-HER2 3+ patients, but these differences were not statistically significant. HER2 status did not affect survival period according to chemotherapy group.
Conclusion:   Immunohistochemistry findings of HER2 expression in Turkish breast cancer patients were similar to those found in the published reports. A shorter survival period was observed in HER2 3+ patients, but the difference was not statistically significant.     

Mutation spectrum and genotype-phenotype analyses in Cowden disease and Bannayan-Zonana syndrome, two hamartoma syndromes with germline PTEN mutation

The tumour suppressor gene PTEN , which maps to 10q23.3 and encodes a 403 amino acid dual specificity phosphatase (protein tyrosine phosphatase; PTPase), was shown recently to play a broad role in human malignancy. Somatic PTEN deletions and mutations were observed in sporadic breast, brain, prostate and kidney cancer cell lines and in several primary tumours such as endometrial carcinomas, malignant melanoma and thyroid tumours. In addition, PTEN was identified as the susceptibility gene for two hamartoma syndromes: Cowden disease (CD; MIM 158350) and Bannayan-Zonana (BZS) or Ruvalcaba-Riley-Smith syndrome (MIM 153480). Constitutive DNA from 37 CD families and seven BZS families was screened for germline PTEN mutations. PTEN mutations were identified in 30 of 37 (81%) CD families, including missense and nonsense point mutations, deletions, insertions, a deletion/insertion and splice site mutations. These mutations were scattered over the entire length of PTEN , with the exception of the first, fourth and last exons. A 'hot spot' for PTEN mutation in CD was identified in exon 5 that contains the PTPase core motif, with 13 of 30 (43%) CD mutations identified in this exon. Seven of 30 (23%) were within the core motif, the majority (five of seven) of which were missense mutations, possibly pointing to the functional significance of this region. Germline PTEN mutations were identified in four of seven (57%) BZS families studied. Interestingly, none of these mutations was observed in the PTPase core motif. It is also worthy of note that a single nonsense point mutation, R233X, was observed in the germline DNA from two unrelated CD families and one BZS family. Genotype-phenotype studies were not performed on this small group of BZS families. However, genotype-phenotype analysis inthe group of CD families revealed two possible associations worthy of follow-up in independent analyses. The first was an association noted in the group of CD families with breast disease. A correlation was observed between the presence/absence of a PTEN mutation and the type of breast involvement (unaffected versus benign versus malignant). Specifically and more directly, an association was also observed between the presence of a PTEN mutation and malignant breast disease. Secondly, there appeared to be an interdependent association between mutations upstream and within the PTPase core motif, the core motif containing the majority of missense mutations, and the involvement of all major organ systems (central nervous system, thyroid, breast, skin and gastrointestinal tract). However, these observations would need to be confirmed by studying a larger number of CD families.      

Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group

Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system. While its etiology is not well understood, genetic factors are clearly involved. Until recently, most genetic studies in MS have been association studies using the case-control design testing specific candidate genes and studying only sporadic cases. The only consistently replicated finding has been an association with the HLA-DR2 allele within the major histocompatibility complex (MHC) on chromosome 6. Using the genetic linkage design, however, evidence for and against linkage of the MHC to MS has been found, fostering suggestions that sporadic and familial MS have different etiologies. Most recently, two of four genomic screens demonstrated linkage to the MHC, although specific allelic associations were not tested. Here, a dataset of 98 multiplex families was studied to test for an association to the HLA-DR2 allele in familial MS and to determine if genetic linkage to the MHC was due solely to such an association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta) in the MHC demonstrated strong genetic linkage (parametric lod scores of 4.60, 2.20 and 1.24, respectively) and a specific association with the HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results by HLA-DR2 status showed that the linkage results were limited to families segregating HLA-DR2 alleles. These results demonstrate that genetic linkage to the MHC can be explained by the HLA-DR2 allelic association. They also indicate that sporadic and familial MS share a common genetic susceptibility. In addition, preliminary calculations suggest that the MHC explains between 17 and 62% of the genetic etiology of MS. This heterogeneity is also supported by the minority of families showing no linkage or association with loci within the MHC.