Surgical repair of incisional ventral hernias: tension-free technique using prosthetic materials (expanded polytetrafluoroethylene Gore-Tex Dual Mesh).

Repairing an incisional ventral hernia is a major challenge for a surgeon. The high recurrence rates observed during hernia repair by tissue approximation led to development of tension-free procedures by using prosthetic materials. The purpose of this study is to report the results of a tension-free repair technique using expanded polytetrafluoroethylene Gore-Tex Dual Mesh (Gore-Tex Soft Tissue Patch, W.L. Gore and Associates Inc, Flagstaff, AZ) in patients with primary or recurrent incisional ventral hernias. Over 3 years, 52 patients with incisional hernias have undergone this procedure in our clinic. Fourteen of them had recurrent hernias which had been primarily repaired by Mayo hernioplasty. Six of our patients had irreducible hernias preoperatively. Twenty-five patients had hernias on midline incisions, and the rest of them had hernias on transverse abdominal incisions. The median patient age was 65 years, and all were operated on under general anesthesia. The majority of the patients had 4 to 6 days of hospitalization. A subcutaneous seroma developed in eight patients. They all were treated by multiple paracentesis. Four of our patients experienced wound infection and were treated by mesh removal. None of the patients presented with cardiovascular or pulmonary complications. During the follow-up period, no other hernia recurrence, except the cases with mesh removal, has been noticed. The tension-free incisional hernia repair using expanded polytetrafluoroethylene mesh is, to our experience, a safe and easy procedure with no major morbidity or recurrence.

Massive infiltration of basophilic cells in inflamed tissue after injection of RANTES.

Regulated upon activation normal T expressed and secreted (RANTES) is a new inducible protein member of the human C-C branch of chemokines. RANTES is a potent monocyte and lymphocyte chemoattractant and is a mediator of inflammatory responses. In these studies we found that RANTES 10 ng/50 microl chemoattracts basophilic cells in a dose-dependent manner 4 h after an intradermal injection in rat skin sites, as revealed by optic microscopy. Moreover, in biopsy specimens from rat skin injection sites histamine release was significantly higher (P < 0.05) than in controls (PBS 50 microl) after 4 h from RANTES treatment. The presence of basophilic cells in rat skin injection sites after RANTES-treatment was also confirmed by electron microscopy studies. In addition, histidine decarboxylase (HDC) mRNA was increased in rat skin sites injected with RANTES compared to sites injected with PBS (controls). Our report describes additional biological activities for RANTES, suggesting that this human chemoattractant protein may play a fundamental role in histamine and HDC generation, along with basophilic cell recruitment.

Human recombinant interleukin-1 beta induces thromboxane A2 release in polymorphonuclear leukocytes, macrophages and platelets: effect of IL-1 receptor antagonist.

Prostaglandins and thromboxanes (Txs) are produced by polymorphonuclears (PMNs) and macrophages (Mphis) in response to various stimuli. PMNs were separated from other human blood cells and Mphis were separated from rat peritoneal lavage. In this paper we show that human recombinant interleukin-1 (hrIL-1) can stimulate the release of thromboxane B2 (TxB2) by PMNs and Mphis. In addition, we have shown that aggregation of PMNs may occur when calcium ions (7 mM) and hrIL-1 (100 ng/ml) are added to the cell preparation, but not when Ca2+ alone, hrIL-1 alone, or first hrIL-1 then calcium are added to the cell preparation. The treatment of human platelets with hrIL-1 shows that after 15 min incubation TxB2 is released. In addition, we compared the aggregation of platelets caused by ADP with that caused by hrIL-1. Human recombinant IL-1 at a concentration of 100 ng/ml also causes little aggregation of platelets, in this case the aggregation is reversible. In conclusion, hrIL-1 beta stimulates TxB2 release in PMNs, Mphis and platelets and this effect increases with addition of Ca2+ ions. The mixture of hrIL-1 and Ca2+ causes little aggregation of PMNs. In monocyte suspensions, pretreated with human recombinant IL-1 receptor antagonist (IL-1ra) 500 ng/ml for 10 min and then treated with LPS or hrIL-1 beta 10 micrograms/ml, the release of TxB2 was partially inhibited. IL-1ra may play a significant role in the control of IL-1 and LPS induction in the release of TxB2.