Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective series of 106 inguinal hernias in 91 patients is studied, comparing two methods of laparoscopic hernia repair: a transperitoneal technique with preperitoneal stapled mesh fixation (TransAbdominal PrePeritoneal or TAPP-technique) performed in 33 patients, and a totally extraperitoneal placement of non stapled mesh (Totally ExtraPeritoneal Approach or TEPA-technique) performed in 58 patients. Conversions to open repair were equally frequent (5% vs. 7% respectively) and were due to adhesions, haemorrhage, irreducible intestinal loop in the hernial sac or important subcutaneous emphysema. Minor postoperative complications included regional seroma or haematoma, testicular pain and meralgia paraesthetica. There was no mortality nor long lasting complication. Recurrence rates in both groups amounted 2.7% (TAPP) and 2.8% (TEPA) respectively after a mean follow-up of 15.8 months (TAPP) and 17.6 months (TEPA). In both groups early recovery of normal activities was noted, after a mean of respectively 13.6 days (TAPP) and 12.9 days (TEPA). It is concluded that the transabdominal route and the totally extraperitoneal approach for laparoscopic herniorrhaphy are both adequate techniques for inguinal hernia repair with similar complication and short-term recurrence rates.
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PMID:Laparoscopic transperitoneal versus extraperitoneal inguinal hernia repair: a prospective clinical trial. 968 74

Previously, it had been shown that T-lymphocytes are the predominant inflammatory cells found in the alveolar wall of smokers and their numbers correlated with the extent of emphysema. However, the phenotype of these cells was not defined. The aim of this study was to describe the different T-cell phenotypes and investigate the possible presence of apoptosis in the lung parenchyma of smokers. Samples from lungs were obtained at surgery from 15 patients who smoked and six who had never smoked. Samples were frozen and prepared for histological and immunocytochemical examination. Slides were stained for CD3+, CD4+, CD8+, gammadelta T-cells, CD56 natural killers ((NK) cells), and elastase (neutrophils). Anti-CD95 monoclonal antibodies and in situ end-labelling techniques were used to detect Fas expression and apoptosis. Positive staining cells were expressed as cells-mm alveolar wall-, percentage of total cells, and Fas/APO and apoptosis index. Emphysema was identified macroscopically, microscopically and reported as present or absent. All subjects had pulmonary function tests before surgery. Neutrophils were the predominant cell in the lung parenchyma of nonsmokers and smokers without emphysema. In smokers with emphysema, the CD3+ and CD8+ were the predominant cells (p<0.05) in the alveolar wall. gammadelta cells were increased in all smokers and no increased numbers of NK cells was found. The T-cell numbers x mm alveolar wall(-1) showed a bilinear relationship with the amount smoked increasing at an inflection point of 30 packs yr(-1) (R2= 0.345; p < 0.01). Apoptosis in smokers showed a bilinear relationship with the amount smoked increasing sharply in smokers with emphysema (R2=0.3613; p < 0.009). It is concluded that the pathogenesis of emphysema might be mediated by T-lymphocytes, mainly CD8+ cytolytic T-cells, and that apoptosis might be one of the mechanisms of lung destruction leading to the development of emphysema. If this is the case, it could be speculated that T-cell inflammation is a response to antigenic stimuli originating in the lung and induced by cigarette smoking.
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PMID:Lymphocyte population and apoptosis in the lungs of smokers and their relation to emphysema. 1148 31