Translocation of viable bacteria from gut to bloodstream and other sterile body sites during shock has been demonstrated in several experimental and clinical studies. The factors causing translocation and its incidence at different stages of shock are not known. The aim of the study was to evaluate the importance of several factors causing translocation of indigenous micro¯ora in an experimental model of septic shock based on intraperitoneal Escherichia coli sepsis in rats. Counts of inoculated E. coli and translocated bacteria in different locations, gut morphology and haematological values were evaluated at different stages of sepsis. Sepsis developed in all animals and E. coli achieved the highest counts in blood 6 h after inoculation. Translocation was commonest at 6 and 12 h after inoculation. Frequently translocating bacteria were lactobacilli, bi®dobacteria, bacteroides and peptostreptococci. In early sepsis, translocation was associated with high E. coli counts in blood, yet in late sepsis the opposite correlation was present. Low in®ltration by neutrophils in the ileum and decreased mitotic activity in the colon were associated with a high translocation rate. In early sepsis, translocation was associated with low lymphocyte counts, but in late sepsis, with low neutrophil counts. Translocation of bacteria (including anaerobes) that colonise the gut in high counts takes place during sepsis. Putative in¯uencing factors such as activity of the primary disease (bacterial counts in blood), gut morphology or haematological values seem to have different impacts on translocation, depending on the stage of the disease.

Insulin receptor substrates (IRS) mediate the biological actions of insulin, growth factors and cytokines. This action is via receptor-mediated tyrosine phosphorylation of IRS proteins. The aim of present study was to demonstrate the distribution of IRS-1-3, the glucose transporter class I subfamily (GLUT-1-4), signal regulatory protein 1alpha (SIRP1alpha), protein kinase B (PKB) and phosphatidylinositol kinase (PI3-K) in the human testis to determine whether signal transduction mediated by these proteins is active in testicular cells. In the present study, the expression of IRS-1-3, GLUT-1-4, SIRP1alpha, P13-K and PKB was studied in the human testis at the protein level using immunohistochemistry and western blotting. A positive immunoreaction for IRS-1 was found in the human testis in peritubular myoid cells and macrophage-like interstitial cells. A positive immunoreaction for GLUT-3 was found in the human testis in Sertoli cells, peritubular myoid cells, early spermatocytes, macrophage-like interstitial cells and cells in the small vessels walls. Western blotting demonstrated IRS-1, IRS-2 and GLUT-3 proteins in the human testis. Expression of IRS-3, GLUT-1, GLUT-2, GLUT-4, SIRP1alpha, P13-K and PKB was not detected in the human testis. The results of the present study suggest that proteins like insulin and certain cytokines using IRS-1, IRS-2 and GLUT-3 in their signal transduction pathways can have effects on different cell types of the testis in humans.

Insulin receptor substrate (IRS) proteins are key mediators in insulin signaling from the insulin receptor. It takes place through receptor-mediated tyrosine phosphorylation of IRS proteins. The aim of the present article is to demonstrate the distribution of IRS 1-3, glucose transporters 1-4 (GLUT 1-4), signal regulatory protein 1alpha (SIRP1alpha), PKB, and PI 3-kinase in the rat testis to see if signal transduction mediated by these proteins is active in testicular cells. Wistar rats were used as donors of testis tissue. Expression of these genes was studied at the protein level by using immunohistochemistry and Western blotting. IRS-1, IRS-2, GLUT 1, GLUT 2, GLUT 3, and SIRP1alpha were strongly expressed in the Sertoli cells (except GLUT 1), early spermatocytes, peritubular myoid cells, macrophage-like interstitial cells, and testicular endothelial cells in all the testes investigated by immunohistochemistry. IRS-2 was also expressed in the Leydig cells. Immunoblotting experiments demonstrated the presence of about 26-67 kDa reactive with anti- IRS-1, IRS-2, GLUT 1, GLUT 2, GLUT 3, PKB, and SIRP1alpha. The present results suggest that proteins like insulin and certain cytokines using IRS-1, IRS-2, GLUT 1, GLUT 2, GLUT 3, PKB, and SIRP1alpha in their signal transduction can have effects on the different types of testicular cells in the rat.

Massive penetration of bacteria into all tissues without significant polymorphonuclear infiltration may take place in severe septic shock.

The aim of this study was to determine whether blood cultures reflect real bacterial dissemination into the tissues of patients who die of septic shock. A total of 20 patients were divided into two groups with surgical (nine) and nonsurgical (11) sepsis. Blood cultures were taken and the adequacy of antibacterial therapy was assessed. Postmortem tissue samples of different organs were studied using light microscopy for the presence of bacteria. A semiquantitative measure, the contamination index, was applied. Despite negative blood cultures from 14 patients, bacteria were found in almost all of the organs examined from all of the patients. There was no difference in contamination index between patients who received adequate antibacterial therapy and those who did not. We conclude that septic shock is the manifestation of bacterial dissemination into the organs, and that blood cultures are of limited value in the diagnosis of sepsis, especially when they are taken during adequate antibacterial therapy.