The trend of burn mortality in Iran — A study of fire,heat and hot substance-related fatal injuries from 1990 to 2015

Introduction

Burn injuries are a major cause of preventable mortality worldwide. To implement preventive strategies, a detailed understanding of the rate and trend of fatal burn injuries is needed. The aim of this study was to determine the rate and trend of burn mortality at national and province level in Iran from 1990 to 2015.

Diagnostic utility of low-affinity nerve growth factor receptor (P 75) immunostaining in atypical fibroxanthoma

Background: Atypical fibroxanthoma (AFX) is a locally destructive, dermal‐based, fibrohistiocytic, mesenchymal tumor. Immunohistochemistry helps to differentiate AFX from squamous cell carcinoma and spindle cell melanoma. Immunomarkers against p75 yield positive stains in spindled cell melanomas and negative stains in AFX, suggesting that these may be useful in differentiating these two entities. However, a recent study concluded that p75 is not a specific marker of neuroectodermal tumors; furthermore, p75 staining in AFX has only been evaluated in a few cases. Methods: We stained 20 AFXs for p75 and various other markers. Results: Reactivity was noted for vimentin (20 of 20 cases), CD10 (17/20), CD68 (14/20), CD99 (13/20), D2‐40 (10/20) and p75 (1/20). Conclusions: We confirmed that CD99 and CD10 are frequently expressed in AFX (65 and 85%, respectively) and that CD31 rarely stains positive (5%). The 50% positivity rate of D2‐40, in contrast with published evidence for its absence in melanoma, suggests that D2‐40 may be useful for distinguishing AFX from melanoma. Furthermore, because only one sample was positive for p75, we confirm that p75 is useful in differentiating AFX from spindle cell melanoma. We advocate adding p75 and D2‐40 to assist in differentiating AFX from melanoma. Bull C, Mirzabeigi M, Laskin W, Dubina M, Traczyc T, Guitart J, Gerami P. Diagnostic utility of low‐affinity nerve growth factor receptor (P 75) immunostaining in atypical fibroxanthoma.     

Evaluation of bone mineral density in Iranian HIV/AIDS patients

Bone disorders have emerged as a worrisome complication in HIV-infected patients in recent years. It is not clear that HIV infection itself or antiretroviral treatment or both are causes of bone loss. However, most studies have found a high prevalence of osteopenia and osteoporosis in HIV/AIDS patients. The objectives of this study were to determine the prevalence of osteopenia and osteoporosis in HIV-infected patients either untreated or receiving Highly Active Antiretroviral Therapy as compared with HIV negative persons. We also assessed the factors associated with these conditions. Bone Mineral Density was assessed by Dual Energy X-Ray Absorptiometry scans at the hip and lumbar spine in 36 AIDS patients receiving antiretroviral therapy and 44 HIV infected patients not receiving antiretroviral therapy (na?ve patients) and 40 HIV negative individuals as control. Factors that affect BMD were also determined. Prevalence of osteopenia or osteoporosis in different regions was significantly higher in HIV/AIDS patients compared with HIV negative subjects (77.3% in HIV positive na?ve patients, 86.1% in HAART-treated patients and 60% in the control group, P=0.002). Mean serum alkaline phosphatase was higher in HIV/AIDS patients than the control group (P=0.003). Osteopenia and osteoporosis in HIV-infected patients were associated with duration of HIV infection (P<0.0001) and antiretroviral treatment (P=0.012). Prevalence of osteopenia and osteoporosis in HIV/AIDS patients was higher than HIV negative individuals. Osteopenia and osteoporosis in HIV/AIDS patients was associated with duration of HIV infection and antiretroviral treatment.     

Assessing the prevalence of HIV among Afghan immigrants in Iran through rapid HIV testing in the field

Throughout the world, many migrant and mobile populations are at elevated risk for HIV. Iran has a large immigrant population from neighboring Afghanistan; however, few data exist on the prevalence of HIV in this community. In 2008, we conducted a study to assess the presence of HIV infection among 477 immigrants in a town to the northeast of Tehran using a rapid test in the field. HIV prevalence was 0.2% (95% CI 0.005-1.2) with one person HIV-positive. We recommend periodic HIV sero-surveillance with detailed behavioral measures for this population in the future.     

Vacuoles of Candida yeast as a specialized niche for Helicobacter pylori

Helicobacter pylori(H.pylori)are resistant to hostile gastric environments and antibiotic therapy,reflecting the possibility that they are protected by an ecological niche,such as inside the vacuoles of human epithelial and immune cells.Candida yeast may also provide such an alternative niche,as fluorescently labeled H.pylori were observed as fast-moving and viable bacterium-like bodies inside the vacuoles of gastric,oral,vaginal and foodborne Candida yeasts.In addition,H.pylori-specific genes and proteins were detected in samples extracted from these yeasts.The H.pylori present within these yeasts produce peroxiredoxin and thiol peroxidase,providing the ability to detoxify oxygen metabolites formed in immune cells.Furthermore,these bacteria produce urease and VacA,two virulence determinants of H.pylori that influence phago-lysosome fusion and bacterial survival in macrophages.Microscopic observations of H.pylori cells in new generations of yeasts along with amplification of H.pylori-specific genes from consecutive generations indicate that new yeasts can inherit the intracellular H.pylori as part of their vacuolar content.Accordingly,it is proposed that yeast vacuoles serve as a sophisticated niche that protects H.pylori against the environmental stresses and provides essential nutrients,including ergosterol,for its growth and multiplication.This intracellular establishment inside the yeast vacuole likely occurred long ago,leading to the adaptation of H.pylori to persist in phagocytic cells.The presence of these bacteria within yeasts,including foodborne yeasts,along with the vertical transmission of yeasts from mother to neonate,provide explanations for the persistence and propagation of H.pylori in the human population.This Topic Highlight reviews and discusses recent evidence regarding the evolutionary adaptation of H.pylori to thrive in host cell vacuoles.     

Matrix metalloproteinase-2 is involved in myelination of dorsal root ganglia neurons

Matrix metalloproteinases (MMPs) comprise a large family of endopeptidases that are capable of degrading all extracellular matrix components. There is increasing evidence that MMPs are not only involved in tissue destruction but may also exert beneficial effects during axonal regeneration and nerve remyelination. Here, we provide evidence that MMP-2 (gelatinase A) is associated with the physiological process of myelination in the peripheral nervous system (PNS). In a myelinating co-culture model of Schwann cells and dorsal root ganglia neurons, MMP-2 expression correlated with the degree of myelination as determined by immunocytochemistry, zymography, and immunosorbent assay. Modulation of MMP-2 activity by chemical inhibitors led to incomplete and aberrant myelin formation. In vivo MMP-2 expression was detected in the cerebrospinal fluid (CSF) of patients with Guillain-Barré syndrome as well as in CSF and sural nerve biopsies of patients with chronic inflammatory demyelinating polyneuropathy. Our findings suggest an important, previously unrecognized role for MMP-2 during myelination in the PNS. Endogenous or exogenous modulation of MMP-2 activity may be a relevant target to enhance regeneration in demyelinating diseases of the PNS.     

Prevalence and Correlates of Hepatitis C Infection among Male Injection Drug Users in Detention,Tehran, Iran

For the benefit of planning for the future care and treatment of people infected with hepatitis C virus (HCV) and to help guide prevention and control programs, data are needed on HCV seroprevalence and associated risk factors. We conducted a cross-sectional sero-behavioral survey of injection drug users (IDU) detained for mandatory rehabilitation during a police sweep of Tehran, Iran, in early 2006. During the study period, a consecutive sample comprising 454 of 499 (91.0%) men arrested and determined to be IDU by urine test and physical examination consented to a face-to-face interview and blood collection for HCV antibody testing. Overall, HCV prevalence was 80.0% (95% confidence interval (CI) 76.2–83.6). Factors independently associated with HCV infection included history of incarceration (adjusted OR 4.35, 95% CI 1.88–10.08), age of first injection ≤25 years (OR 2.72, 95% CI 1.09–6.82), and history of tattooing (OR 2.33, 95% CI 1.05–5.17). HCV prevalence in this population of IDU upon intake to jail was extremely high and possibly approaching saturation. Findings support that incarceration is contributing to the increased spread of HCV infection in Iran and calls for urgent increased availability of HCV treatment, long-term preparation for the care of complications of chronic infection, and rapid scale-up of programs for the primary prevention of parenterally transmitted infections among drug users.     

Familial early onset frontotemporal dementia caused by a novel S356T MAPT mutation,initially diagnosed as schizophrenia

Autosomal dominant frontotemporal dementia (FTD) due to mutations in the MAPT gene is referred to as FTD with parkinsonism linked to chromosome 17 with tau pathology (FTDP-17T). Typically the disease begins in the sixth decade of life. We report a novel exon 12 mutation in MAPT (S356T), in a family with an exceptionally early age at onset (27 and 29 years), causing familial behavioural variant frontotemporal dementia. Both the proband and the proband's father were initially diagnosed as having schizophrenia. Pathological examination showed frontotemporal lobar degeneration with extensive neuronal and glial tau deposition. This mutation is one of a small group of MAPT mutations (including P301S, G335V and S352L) that cause very early onset FTDP-17T. It is likely that the early age at onset reflects a marked pathogenic effect of the mutation involving a disturbance of microtubule binding, tau phosphorylation or a major acceleration of tau aggregation.     

Sequence analysis of all identified open reading frames on the frontal temporal dementia haplotype on chromosome 3 fails to identify unique coding variants except in CHMP2B

A segregating splice site mutation in the CHMP2B gene has been shown in the single Danish family which has been reported to show linkage between dementia and chromosome 3 markers. Despite extensive analysis, no other segregating mutations have been found in other kindreds, although some point variants have been found both in sporadic cases and in controls. We recently found a premature stop codon in a person without dementia and this led us to investigate whether the splice site mutation in the Danish kindred did not explain the disease, but rather was hitchhiking on the segregating disease haplotype. We determined to test this possibility by sequencing every other gene on the haplotype in a case from the kindred. We did not find any other unique variants. The implications of these findings for the likely mode of pathogenesis of frontal temporal dementia are discussed.     

Characteristics of frontotemporal dementia patients with a Progranulin mutation

OBJECTIVE: Mutations in the Progranulin gene (PGRN) recently have been discovered to be associated with frontotemporal dementia (FTD) linked to 17q21 without identified MAPT mutations. The range of mutations of PGRN that can result in the FTD phenotype and the clinical presentation of patients with PGRN mutations have yet to be determined. METHODS: In this study, we examined 84 FTD patients from families not known previously to have illness linked to chromosome 17 for identified PGRN and MAPT mutations and sequenced the coding exons and the flanking intronic regions of PGRN. We compared the prevalence, clinical characteristics, magnetic resonance imaging and 18-fluoro-deoxyglucose positron emission tomography results, and neuropsychological testing of patients with the PGRN R493X mutation with those patients without identified PGRN mutations. RESULTS: We discovered a new PGRN mutation (R493X) resulting in a stop codon in two patients. This was the only PGRN mutation identified in our sample. The patients with the PGRN R493X mutation had a rapid illness course and had predominant right-sided atrophy and hypometabolism on magnetic resonance imaging and 18-fluoro-deoxyglucose positron emission tomography. The affected father of one of the patients with the PGRN R493X mutation showed frontal and temporal atrophy without neurofibrillary tangles on neuropathological examination. INTERPRETATION: Known PGRN and MAPT mutations were rare and of similar prevalence in our sample (2 compared with 1/84). The patients with the PGRN R493X mutation had a clinical presentation comparable with other behavior-predominant FTD patients. The neuropathology of an affected family member of a patient with the PGRN R493X mutation appears not to be Alzheimer's disease.