Genetic Diversity of Hepatic/Non-Hepatic Cystic Echinococcosis in Baqiyatallah Hospital, Tehran, Iran.

BACKGROUND: Cystic echinococcosis (CE) is a worldwide zoonotic helminthic disease caused by the larval stage of Echinococcus granulosus. The infection is particularly important in terms of economic and medico-veterinary aspects in endemic areas including Iran. Considering the possibility of organ-tropism in E. granulosus strains, the present study was aimed to identify the genotypes of E. granulosus in different organs involved in patients, undergone surgery in Baqiyatallah Hospital, Tehran, Iran from 2005-2015. METHODS: Overall, 29 formalin-fixed paraffin-embedded tissues (FFPT) from patients with histologically confirmed CE including liver (N: 14) lungs (N: 6) abdomen (N: 2), pancreas (N: 2) and each of spleen, gallbladder and, muscles (N: 1) plus unknown organs (N: 2) were used and genetically characterized using polymerase chain reaction, followed by partial sequencing of mitochondrial cytochrome c oxidase gene subunit 1(cox1) and analyzed. RESULTS: Nineteen out of 29 isolates including liver (N: 6) lungs (N: 4) abdomen (N: 2), pancreas (N: 2) and each of spleen, gallbladder, and muscle (N: 1), unknown organs (N: 2) obtained from paraffin-embedded blocks of human CE created an acceptable sequence in two directions. All 19 isolates regardless of the organ involved were recognized as E. granulosus sensu stricto (G1). CONCLUSION: The sequence alignments of the isolates displayed two profiles. All sequenced samples showed E. granulosus sensu stricto (G1) with no organ-related genotype.

Characterization of Lung Fibroblasts More than Two Decades after Mustard Gas Exposure.

PURPOSE: In patients with short-term exposure to the sulfur mustard gas, the delayed cellular effects on lungs have not been well understood yet. The lung pathology shows a dominant feature consistent with obliterative bronchiolitis, in which fibroblasts play a central role. This study aims to characterize alterations to lung fibroblasts, at the cellular level, in patients with delayed respiratory complications after short-term exposure to the sulfur mustard gas. METHODS: Fibroblasts were isolated from the transbronchial biopsies of patients with documented history of exposure to single high-dose sulfur mustard during 1985-7 and compared with the fibroblasts of control subjects. RESULTS: Compared with controls, patients' fibroblasts were thinner and shorter, and showed a higher population doubling level, migration capacity and number of filopodia. Sulfur mustard decreased the in vitro viability of fibroblasts and increased their sensitivity to induction of apoptosis, but did not change the rate of spontaneous apoptosis. In addition, higher expression of alpha smooth muscle actin showed that the lung's microenvironment in these patients is permissive for myofibroblastic differentiation. CONCLUSIONS: These findings suggest that in patients under the study, the delayed pulmonary complications of sulfur mustard should be considered as a unique pathology, which might need a specific management by manipulation of cellular components.