Paederus dermatitis in Egypt: a clinicopathological and ultrastructural study.

BACKGROUND: Outbreaks of paederus dermatitis (PD) have been observed in different parts of the world, yet the histopathological and ultrastructural changes and their relationship to pederin toxin have not been described. OBJECTIVE: To describe the clinical presentations of PD in Egypt and to study the effects of pederin toxin on the skin by evaluating the histopathological and ultrastructural changes of some representative cases. METHODS: One hundred and thirteen patients with PD were studied clinically and epidemiologically. Skin biopsies were taken from 40 patients for histopathological examination and from 20 patients for electron microscopic (EM) examination. RESULTS: Clinically, the most common presentation comprised erythematous plaques with micropustules. Blisters exhibited a linear configuration in 40% of the patients and kissing lesions were observed in 13%. Multiple lesions occurred in 78% of the patients and the face was the most commonly involved site (48%). The insect was identified as Paederus alfierii. Histopathological examination revealed features of acute irritant dermatitis in the upper epidermis. Mitotic figures and apoptotic changes such as chromatin condensation and DNA fragmentation were identified in the basal and suprabasal layers. These features were confirmed by EM. CONCLUSIONS: Clinical, histopathological and, for the first time, ultrastructural characteristics of paederus dermatitis are described. The pathological abnormalities of the upper epidermis are caused by the irritant effect of pederin toxin. The presence of apoptosis within the lower epidermis can be related to this toxin, a point that needs further research, hoping for its future implications in the management of hyperproliferative disorders.

Gains on 9p are common genomic aberrations in idiopathic myelofibrosis: a comparative genomic hybridization study.

Ideopathic myelofibrosis (IMF) is a chronic myeloproliferative disorder resulting in bone marrow fibrosis as a consequence of growth factor release from clonal haematopoiesis. Conventional cytogenetic analysis identifies abnormalities in approximately a third of cases at diagnosis, although rarely uncovers unique, primary genetic events. We have used comparative genomic hybridization (CGH) to study 25 IMF cases and have compared the results with conventional cytogenetics. Metaphase cells were available for analysis in 13 cases, of which seven showed an abnormal karyotype. CGH chromosomal profiles showed imbalances in 21 of 25 cases. The most frequent aberrations were gains of 9p (12 cases), 2q (seven cases), 3p (seven cases), chromosome 4 (seven cases), 12q (seven cases), 13q (eight cases). The main losses were at 17q and occurred in six cases. The results for CGH and cytogenetics were matched for one case only. Investigation of IMF by CGH suggests that genomic aberrations are much more common than has been previously indicated by conventional cytogenetic analysis and occur in the majority of cases. Gains of 9p were the most frequent finding, occurring in 50% of patients and suggests that genes on 9p may play a crucial role in the pathogenesis of IMF.

Incidence of important hemobilia following transhepatic biliary drainage: left-sided versus right-sided approaches.

Our purpose here is to describe our experience with important hemobilia following PTBD and to determine whether left-sided percutaneous transhepatic biliary drainage (PTBD) is associated with an increased incidence of important hemobilia compared to right-sided drainages. We reviewed 346 transhepatic biliary drainages over a four-year period and identified eight patients (2.3%) with important hemobilia requiring transcatheter embolization. The charts and radiographic files of these patients were reviewed. The side of the PTBD (left versus right), and the order of the biliary ductal branch entered (first, second, or third) were recorded. Of the 346 PTBDs, 269 were right-sided and 77 were left-sided. Of the eight cases of important hemobilia requiring transcatheter embolization, four followed right-sided and four followed left-sided PTBD, corresponding to a bleeding incidence of 1.5% (4/269) for right PTBD and 5.2% (4/77) for left PTBD. The higher incidence of hemobilia associated with left-sided PTBD approached, but did not reach the threshold of statistical significance (p = 0.077). In six of the eight patients requiring transcatheter embolization, first or second order biliary branches were accessed by catheter for PTBD. All patients with left-sided bleeding had first or proximal second order branches accessed by biliary drainage catheters. In conclusion, a higher incidence of hemobilia followed left-versus right-sided PTBD in this study, but the increased incidence did not reach statistical significance.

Regulation of FOS by different compartmental stresses induced by low levels of ionizing radiation.

We irradiated different cellular compartments and measured changes in expression of the FOS gene at the mRNA and protein levels. [(3)H]Thymidine and tritiated water were used to irradiate the nucleus and the whole cell, respectively. (125)I-Concanavalin A binding was used to irradiate the cell membrane differentially. Changes in FOS mRNA and protein levels were measured using semi-quantitative RT-PCR and SDS-PAGE Western blotting, respectively. Irradiation of the nucleus or the whole cell at a dose rate of 0.075 Gy/h caused no change in the level of FOS mRNA expression, but modestly (1.5-fold) induced FOS protein after 0.5 h. Irradiation of the nucleus at a dose rate of 0.43 Gy/h induced FOS mRNA by 1.5-fold after 0.5 h, but there was no significant effect after whole-cell irradiation. FOS protein was transiently induced 2.5-fold above control levels 0.5 h after a 0. 43-Gy/h exposure of the nucleus or the whole cell. Irradiation of the cell membrane at a dose rate of 1.8 Gy/h for up to 2 h caused no change in the levels of expression of FOS mRNA or protein, but a dose rate of 6.8 Gy/h transiently increased the level of FOS mRNA 3-fold after 0.5 h. These data demonstrate the complexity of the cellular response to radiation-induced damage at low doses. The lack of quantitative agreement between the transcript and protein levels for FOS suggests a role for post-transcriptional regulation.

Retinal pericytes control expression of nitric oxide synthase and endothelin-1 in microvascular endothelial cells.

Pericytes are known to communicate with endothelial cells by direct contact and by releasing cytokines such as TGF-beta. There is also strong evidence that pericytes act as regulators of endothelial cell proliferation and differentiation. We have investigated the effect of pericyte-conditioned medium (PCM) on proliferation of human microvascular endothelial cells in vitro, together with the expression of the vasoregulatory molecules, constitutive and inducible nitric oxide synthases (ecNOS and iNOS), and endothelin-1 (ET-1). Expression was measured at the mRNA level using semiquantitative RT-PCR for all three genes and at the protein level for ecNOS and iNOS using Western blotting. Growth curves for HMECs showed that PCM inhibits proliferation, eventually leading to cell death. Exposure to PCM repressed iNOS mRNA expression fivefold after 6 h. A similar, though delayed, reduction in protein levels was observed. ecNOS mRNA was slightly induced at 6 h, though there was no significant change in ecNOS protein. By contrast, ET-1 mRNA was induced 2.3-fold after 6 h exposure to PCM. We conclude that pericytes release a soluble factor or factors that are potent inhibitors of endothelial cell growth and promote vasoconstriction by up-regulating endothelin-1 and down-regulating iNOS.