Hiva Saffar

Esophageal squamous cell carcinoma (ESCC) shows remarkable variation in incidence that is not fully explained by known lifestyle and environmental risk factors. It has been speculated that an unknown exogenous exposure(s) could be responsible. Here we combine the fields of mutational signature analysis with cancer epidemiology to study 552 ESCC genomes from eight countries with varying incidence rates. Mutational profiles were similar across all countries studied. Associations between specific mutational signatures and ESCC risk factors were identified for tobacco, alcohol, opium and germline variants, with modest impacts on mutation burden. We find no evidence of a mutational signature indicative of an exogenous exposure capable of explaining differences in ESCC incidence. Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC)-associated mutational signatures single-base substitution (SBS)2 and SBS13 were present in 88% and 91% of cases, respectively, and accounted for 25% of the mutation burden on average, indicating that APOBEC activation is a crucial step in ESCC tumor development. The incidence of esophageal squamous cell carcinoma varies significantly across different geographical regions. Mutational signature analysis of tumors sampled from high- and low-incidence areas suggests that these variations may not be explained by mutagenic exposures.

BACKGROUND: According to official data, 60-70% of clinical decisions about hospitalization and discharge are based on laboratory results. AIMS: The objective of this study is to examine the frequency of errors before, during, and after analysis in a major medical laboratory. MATERIALS AND METHODS: This descriptive, cross-sectional study was conducted throughout 2012 (January-December 2012). Errors are recorded by the Quality Control Committee in a specially designed record. RESULTS: A total of 303,866 samples, 2,430,928 tests were received for analysis. The total number of errors was 153,148 (6.3%) (116,392 for inpatients and 36,756 for outpatients). Analysis of the results revealed that about 65.09% of the errors occur across preanalytical phase, whereas 23.2% and 11.68% are related to analytical and postanalytical phase, respectively. CONCLUSION: More than half of the laboratory errors are related to preanalytical phase; therefore, proper training and knowledge of intervening factors are essential for reducing errors and optimizing the quality.

BACKGROUND & OBJECTIVE: Angiogenesis is an essential component of tumor growth. Expression of PSMA on the neo-vasculature of many solid tumors, including glioblastoma multi-form, has been determined. The pattern of expression suggests that PSMA may play a functional role in angiogenesis. METHODS: expression of PSMA in different grades of brain glioma was evaluated by the immunohistochemistry method to determine the probable usefulness of anti-PSMA antibody as complementary target therapy in different grades of glioma. RESULTS: Overall, 72 cases of low (grade I and II) and high (grade III and IV) grade gliomas were evaluated for expression of PSMA. Positive PSMA staining was observed in 12 (33.3%) of high grade and 3 (8.3%) of low grade gliomas. Although, high grade tumors more commonly had positive result for PSMA (P value=0.009), the intensity of staining was significantly stronger in low-grade tumors (P value=0.009). CONCLUSION: Expression of PSMA in different grades of glioma might provide a basis for further investigations focusing on selective target therapy in combination with the current standard care in all glioma grades, to improve treatment efficacy.

Acute bowel ischemia (ABI) can be life threatening with high mortality rate. In spite of the advances made in diagnosis and treatment of ABI, no significant change has occurred in the mortality over the past decade. ABI is potentially reversible with prompt diagnosis. The radiologist plays a central role in the initial diagnosis and preventing progression to irreversible intestinal ischemic injury or bowel necrosis. The most single imaging findings described in the literature are either non-specific or only present in the late stages of ABI, urging the use of a constellation of features to reach a more confident diagnosis. While ABI has been traditionally categorized based on the etiology with a wide spectrum of imaging findings overlapped with each other, the final decision for patient's management is usually made on the stage of the ABI with respect to the underlying pathophysiology. In this review, we first discuss the pathologic stages of ischemia and then summarize the various imaging signs and causes of ABI. We also emphasize on the correlation of imaging findings and pathological staging of the disease. Finally, a management approach is proposed using combined clinical and radiological findings to determine whether the patient may benefit from surgery or not.

BACKGROUND: The long-term duration of cell-mediated immunity induced by neonatal hepatitis B virus (HBV) vaccination is unknown. OBJECTIVES: Study was designed to determine the cellular immunity memory status among young adults twenty years after infantile HB immunization. PATIENTS AND METHODS: Study subjects were party selected from a recent seroepidemiologic study in young adults, who had been vaccinated against HBV twenty years earlier. Just before and ten to 14 days after one dose of HBV vaccine booster injection, blood samples were obtained and sera concentration of cytokines (interleukin 2 and interferon) was measured. More than twofold increase after boosting was considered positive immune response. With regard to the serum level of antibody against HBV surface antigen (HBsAb) before boosting, the subjects were divided into four groups as follow: GI, HBsAb titer < 2; GII, titer 2 to 9.9; GIII, titer 10 to 99; and GIV, titers ≥ 100 IU/L. Mean concentration level (MCL) of each cytokines for each group at preboosting and postboosting and the proportion of responders in each groups were determined. Paired descriptive statistical analysis method (t test) was used to compare the MCL of each cytokines in each and between groups and the frequency of responders in each group. RESULTS: Before boosting, among 176 boosted individuals, 75 (42.6%) had HBsAb 10 IU/L and were considered seroprotected. Among 101 serosusceptible persons, more than 80% of boosted individuals showed more than twofold increase in cytokines concentration, which meant positive HBsAg-specific cell-mediated immunity. MCL of both cytokines after boosting in GIV were decreased more than twofold, possibly because of recent natural boosting. CONCLUSIONS: Findings showed that neonatal HBV immunization was efficacious in inducing long-term immunity and cell-mediated immune memory for up to two decades, and booster vaccination are not required. Further monitoring of vaccinated subjects for HBV infections are recommended.