Long-term results of suture rectopexy in patients with fecal incontinence associated with incomplete rectal prolapse

Suture rectopexy is the recommended therapy for complete rectal prolapse that is associated with fecal incontinence. It has been suggested that correction of an incomplete rectal prolapse is also worthwhile for patients with fecal incontinence. PURPOSE: Aims of this study were 1) to evaluate the clinical outcome of suture rectopexy in a consecutive series of patients with incomplete rectal prolapse associated with fecal incontinence, and 2) to compare these results with those obtained from patients with complete rectal prolapse. METHODS: Between 1979 and 1994, suture rectopexy was performed in 13 incontinent patients (3 males; median age, 65 (range, 45–77) years) with incomplete rectal prolapse (Group I) and in 24 incontinent patients (21 females; median age, 71 (range, 24–86) years) with complete rectal prolapse (Group II). RESULTS: After a median follow-up of 67 months, continence was restored in 5 of 13 (38 percent) patients with incomplete rectal prolapse and in 16 of 24 (67 percent) patients with complete rectal prolapse. In both groups, all male patients became continent. CONCLUSIONS: For the majority of incontinent patients with incomplete rectal prolapse, a suture rectopexy is not beneficial. The clinical outcome of this procedure is only good in incontinent patients with complete rectal prolapse. Based on these data, it is questionable whether incomplete rectal prolapse plays a causative role in fecal incontinence.Read at the meeting of the International Society of University Colon and Rectal Surgeons, Lisboa, Portugal, April 14 to 18, 1996.No reprints are available.     

2010年欧洲神经病学联盟阿尔茨海默病诊疗指南

一、概述 (一)目的 2008年成立工作组的目的是修改前一版欧洲神经病学联盟(EFNS)的阿尔茨海默病(AD)诊疗指南.前一版指南采用了第4版诊断和统计手册(DSM Ⅳ)及美国国立神经病学、语言障碍和脑卒中研究所-阿尔茨海默病及相关疾病学会(NINCDS-ADRDA)对痴呆综合征和AD的诊断标准.     

A genetic polymorphism in connexin 37 as a prognostic marker for atherosclerotic plaque development

BACKGROUND AND OBJECTIVES: Atherosclerosis is a multifactorial disease, in part characterized by chronic inflammatory changes in the vessel wall and loss of normal physical and biochemical interactions between endothelial cells and smooth muscle cells. Previous studies [Hu J., Cotgreave IA. J Clin Invest; 99: 1-5] have provided molecular links between inflammation and myoendothelial communication via gap junctions, suggesting that these structures may be important in the development of the atherosclerotic vessel phenotype. In order to strengthen this premise, the aim of the present work was to probe for structural polymorphisms in connexin 37, a gap junctional protein uniquely expressed in endothelial cells, and to assess for potential genotypic segregation in individuals displaying atherosclerotic plaque. METHODS AND RESULTS: Computer-based comparisons of Expressed Sequence Tags (ESTs) predicted a polymorphism in the human gap junctional protein connexin 37 (cx37). The C1019-T mutation results in a proline to serine shift at codon 319 (cx37*1-cx37*2). A Restriction Fragment Length Polymorphism (RFLP) assay, involving the insertion of a novel Drd I cleavage site in the proline variant revealed a statistically significant over-representation of the cx37*1 allele in association with atherosclerotic plaque-bearing individuals (Odds-ratio for the homozygote = 2.38, Chi2 = 7.693, P = 0.006), in comparison to individuals lacking plaque, irrespective of a history of hypertension. CONCLUSIONS: These data suggest that the C1019-T polymorphism in cx37 may provide 'single gene marker', which could be useful in assessing atherosclerotic plaque development, particularly in cardiovascular risk groups such as those with borderline hypertension.     

Specificity of autoantibodies in autoimmune thrombocytopenia

In 42 patients with autoimmune thrombocytopenia (AITP) and a positive direct platelet suspension immunofluorescence test (PSIFT), the antigenic specificity of the autoantibodies was studied. Because the autoantibodies were often not detectable in the serum and additional HLA antibodies may disturb the reaction pattern with the platelet panel, we used eluates prepared from the patients' platelets for this study. Thirty-five patients had antibodies equally reactive with normal platelets, irrespective of their antigenic make-up, but not with the platelets from two Glanzmann's disease patients. Absorption and elution experiments in two patients showed that his was probably not due to the presence of a combination of anti-Zwa and anti-Zwb antibodies. Thus, the majority of autoantibodies against platelets seems to be directed against antigenic determinants not present on Glanzmann's disease platelets, but perhaps located on the platelet-membrane glycoproteins IIb and/or IIIa. In ten patients, antibodies of no, or still unknown, specificity were detected. Three of these had additional antibodies not reactive with the platelets of the two Glanzmann patients.     

Variation in serum cholesterol level in the same person: what is the true value and when is it called a significant change?]

The blood cholesterol level is not constant over time. Changing values may be found when rechecking high values, especially in patients on a diet or receiving medication. Repeated measurements are necessary. It will then be possible to estimate the 'true mean value'. This is the theoretical average of a large number of measurements taken from one person. The study concentrated on the intra-individual variation of the serum cholesterol and the consequences for screening and follow-up. For this purpose, during a period of four weeks, cholesterol levels were measured 12 times in 33 men aged 25-40. The mean coefficient of variation was 5.7%, with wide differences between participants, ranging from 2.9% to 9.8%. The position of the 'true mean value' was estimated (with 90% confidence), after I resp. 3 determinations. These findings have consequences for the classification of subjects in the different risk categories as defined in the Dutch Cholesterol Consensus. It is also possible to determine if, after a period of intervention, there is a significant decline in the cholesterol level. Roughly, a decline of 10-12% indicates a significant difference.     

Markers of oxidative stress and antioxidant activity in plasma and erythrocytes in neonatal respiratory distress syndrome

Markers of oxidative stress and antioxidant activity in plasma and erythrocytes were studied for 14 d after birth in infants with neonatal respiratory distress syndrome ( n = 9) and controls ( n = 36). In plasma, the total radical trapping antioxidant capacity and the chain-breaking antioxidants vitamin C, sulfhydryl groups and bilirubin were similar. The differences in uric acid levels were not consistent, but vitamin E levels and vitamin E/total-lipid ratio were lower in the neonatal respiratory distress group ( p < 0.01). In erythrocytes, the antioxidant enzymes glutathione peroxidase, glutathione reductase and superoxide dismutase did not differ postnatally. Indicators of oxidative damage in plasma (sulfhydryl/protein ratio and thiobarbituric acid reactive substances) showed the same postnatal course in both groups and were not influenced by oxygen therapy. In erythrocytes the reduced/oxidized glutathione ratio showed no consistent differences. In conclusion, this study, using erythrocytes and plasma, does not provide convincing evidence of oxidative damage and diminished antioxidant defenses in preterm infants with neonatal respiratory distress syndrome.     

Cloning, functional activities and in vivo tissue distribution of rat NKR-P1+ TCR alpha beta + cells

We have successfully cloned nine NKR-P1+ TCR alpha beta + cells from PVG rat spleens, utilizing murine macrophage inflammatory protein-1 alpha (MIP-1 alpha) and IL-2. These clones are either double negative (DN, CD4-CD8-), which included clones 3.31, 3.71, 4.19, 4.59 and 4.65, or single positive (SP, CD4+CD8-), which included clones 1.64, 3.8, 3.76 and 3.78. No CD8+ clone was recovered. All nine clones are restricted in terms of their expression of the V beta antigens, since they express V beta 8.2 but not V beta 8.5, V beta 10 or V beta 16. These clones are agranular and they fall to generate NK or LAK activity upon incubation with IL-2, IL-12 or their combination. On the basis of their production of intracellular cytokines they can be divided into three categories: (I) SP clones (1.64, 3.8, 3.76 and 3.78) do not produce IL-2 or IL-4, but produce IFN-gamma and IL-12, and they vary in their production of IL-1, RANTES or tumor necrosis factor (TNF)-alpha; (II) DN clones 4.59 and 4.65 produce IL-1 alpha and IFN-gamma only, and fall to produce other cytokines; and (III) DN clones 3.31, 3.71 and 4.19 produce IL-1 alpha, IL-1 beta, IL-2, IL-12, IFN-gamma, RANTES and TNF-alpha. From all the clones examined only DN clones 3.31 and to a lesser degree 4.19 produce IL-4. In vivo tissue localization of clones 3.8, 3.31 and 4.59 shows that these cells distribute into the liver and bone marrow 24 h post i.v. administration. Their accumulation in the liver and bone marrow along with their ability to secrete various cytokines suggest that these cells may influence the generation, differentiation or apoptosis of immune or hematopoietic cells.