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41.
Palmiero Monteleone Alfonso Tortorella Vassilis Martiadis Ismene Serino Carmela Di Filippo Mario Maj 《Neuroscience letters》2007
Genes involved in serotonin transmission are likely involved in the biological predisposition to bulimia nervosa. We investigated whether the A218C polymorphism of the tryptophan-hydroxylase-1 gene was associated to bulimia nervosa and/or to some phenotypic aspects of the disorder. One hundred eighty Caucasian women (91 patients with bulimia nervosa and 89 healthy controls) were enrolled into the study. They underwent a blood sample collection for A218C polymorphism of the tryptophan-hydroxylase-1 genotyping and a clinical evaluation assessing comorbidity for Axis I and II psychiatric disorders, harm avoidance personality dimension and bulimic symptoms. The distribution of both tryptophan-hydroxylase-1 A218C genotypes and alleles did not significantly differ between patients and controls. Bulimic women with the AA genotype exhibited a more severe binge eating behavior and higher harm avoidance scores than those with CC genotype. These findings support the idea that tryptophan-hydroxylase-1 A218C polymorphism does not play a part in the genetic susceptibility to bulimia nervosa, but it seems to be involved in predisposing bulimic patients to a more disturbed eating behavior and higher harm avoidance. 相似文献
42.
F Hecht A Grix B K Hecht C Berger H Bixenman S Szucs D O'Keeffe H J Finberg 《Cancer Genetics and Cytogenetics》1984,11(1):107-111
A fetal tumor was suspected at 31 weeks of gestation. The occurrence of polyhydramnios led to an ultrasound examination, which revealed deformation of the fetal head, face, eye, and neck. This was confirmed by computerized tomography. Amniocentesis yielded cells with an inverted duplication of chromosome #1. This abnormality of chromosome #1 marked the malignant teratoma cells in the amniotic fluid. Cytogenetic analysis of tumor tissue and of normal tissue obtained postnatally confirmed that the abnormality of chromosome #1 observed in amniotic fluid cells was confined to the tumor. The constitutional karyotype was normal. To our knowledge, this is the first report of the direct chromosomal detection of malignancy before birth. 相似文献
43.
BackgroundThe non-inferiority of combined breast conservation surgery (BCS) and radiotherapy (breast conservation therapy or BCT) compared to mastectomy in sporadic breast cancer cases is well recognised. Uncertainty remains regarding optimal surgical practice in BRCA mutation carriers.AimsTo evaluate the oncological safety of combined BCT versus mastectomy in BRCA mutation carriers following breast cancer diagnosis.MethodsA systematic review was performed as per PRISMA and MOOSE guidelines. Observational studies comparing BCS and mastectomy in BRCA carriers were identified. Dichotomous variables were pooled as odds ratios (OR) using the Mantel–Haenszel method. Log hazard ratios (lnHR) for locoregional recurrence (LRR), contralateral breast cancer, disease-free and overall survival and their standard errors were calculated from Kaplan-Meier or cox-regression analyses and pooled using the inverse variance method.ResultsTwenty three studies of 3807 patients met inclusion criteria; 2200 (57.7%) were BRCA1 and 1212 (31.8%) were BRCA2 carriers. Median age at diagnosis was 41 years with 96 months follow up. BCS was performed on 2157 (56.7%) while 1408 (41.5%) underwent mastectomy. An increased risk of LRR was observed in patients treated with BCS (HR:4.54, 95% Confidence Interval: 2.77–7.42, P < 0.001, heterogeneity (I2) = 0%). However, the risks of contralateral breast cancer (HR:1.51, 95%CI: 0.44–5.11, P = 0.510, I2 = 80%), disease recurrence (HR:1.16, 95%CI: 0.78–1.72, P = 0.470, I2 = 44%), disease-specific recurrence (HR:1.58, 95%CI: 0.79–3.15, P = 0.200, I2 = 38%) and death (HR:1.10, 95%CI: 0.72–1.69, P = 0.660, I2 = 38%) were equivalent for combined BCT and mastectomy.ConclusionsSurvival outcomes following combined BCT is comparable to mastectomy in BRCA carriers. However, the risk of LRR is increased. Patient counselling should be tailored to incorporate these findings. 相似文献
44.
45.
Apolipoprotein genes and atherosclerosis 总被引:1,自引:0,他引:1
J. L. Breslow 《Journal of molecular medicine (Berlin, Germany)》1992,70(5):377-384
Summary In order to elucidate the genetic abnormalities underlying lipoprotein disorders associated with coronary heart disease susceptibility, researchers have looked for candidate genes. The studies have focused particularly on the lipoprotein transport genes. Relatively common as well as rare mutations have already been identified in several of these genes. In addition, further metabolic and genetic studies indicate that some of these loci harbor significant, but as yet undefined, genetic variation. In the next few years, it is not unreasonable to expect that all or most of the significant mutations at these loci will be catalogued. It is too early to know whether this will be sufficient to explain the genetic basis of altered lipoprotein levels or whether new loci will need to be investigated. Additional candidate gene loci might be those coding for genes involved in intracellular cholesterol metabolism, cholesterol absorption, or insulin resistance. New loci may also be revealed by the technique of reverse genetics. A more complete understanding of the genetics of atherosclerosis susceptibility will probably also entail the identification of variants at genetic loci that control both the reaction of the blood vessel wall to atherogenic lipoproteins and the thrombosis system. Investigation of the genetic basis of coronary heart disease susceptibility remains a worthwhile and lively field, with important clinical and public health ramifications.Abbreviations LPL
lipoprotein lipase
- HL
hepatic lipase
- LCAT
ecithin cholesteryl acyltransferase
- CETP
cholesteryl ester transfer protein
- RFLP
restriction fragment length polymorphism
- FCR
fractional catabolic rate
- HDL, LDL, VLDL, SDL
high, low, very low, intermediate density lipoproteins 相似文献
46.
47.
Summary The clinical and genetic features of 80 patients with Friedreich's disease from 64 families are described. Diagnostic criteria were: no evidence of dominant inheritance, onset by the age of 20 years, progressive unremitting ataxia of limbs and gait, and absence of knee and ankle jerks. Furthermore, at least one of the following accessory signs was present: dysarthria, extensor plantar response and echocardiographic evidence of hypertrophic cardiomyopathy. Two peaks of onset age were evident at 6–9 and 12–15 years. Analysis of intrafamily variation of onset age and absence of clustering of cardiomyopathy and diabetes did not suggest genetic heterogeneity. Peripheral nerve impairment was an early finding and showed slight further progression, whereas involvement of the cerebellar and corticospinal pathways appeared later and mainly accounted for the progressive worsening of the disease. 相似文献
48.
J. F. Knight 《Pediatric nephrology (Berlin, Germany)》1990,4(5):533-541
Laboratory studies of the pathophysiology of Henoch-Schönlein purpura (HSP) have become more numerous in recent years with the recognition of the disease's links with the mucosal immune system in general and IgA nephropathy in particular. There are weak genetic associations with C4 null phenotypes and with HLA B35 and DR4. Studies of plasma proteins in HSP patients show an increased IgA concentration, activation of the alternative pathway of complement and consumption of factor XIII. High molecular weight (polymeric) IgA has been detected in affected individuals, which some investigators have called immune complexes. Many patients synthesise an IgA rheumatoid factor in the acute phase, but other autoantibodies are largely absent. In vitro studies of lymphocytes from HSP patients have demonstrated an increased number of IgA-bearing and secreting B-cells, with altered T-cell regulation of antibody synthesis. While these observations point to immune dysregulation — primarily of IgA production — as a consistent feature of acute HSP, there is as yet insufficient information available to allow a consistent theory of pathogenesis to be formulated. 相似文献
49.
50.
甲胎蛋白启动子调控表达p53基因的肝癌细胞靶向性基因治疗?… 总被引:7,自引:1,他引:6
目的 利用含有人甲胎蛋白启动子的腺相关病毒载体,构建能在人肝癌细胞株中特异表达目的的基因的质粒。方法 通过设计含有特定酶切点位点的引物,选择性地从人基因组中扩增出人甲胎蛋启动子(AFP promoter)主列并克琶含有绿色荧光蛋白(GFP报基因的质粒,pRT-UF5上,构建成含报告基因的重组腺相关病毒质粒rAAV-AFP-GFP转染表达AFP的Hep G2细胞株和不表达AFP的293因的质粒rAA 相似文献