Shahid Beheshti University of Medical Sciences and Health Services

About: Shahid Beheshti University of Medical Sciences and Health Services is a education organization based out in Tehran, Iran. It is known for research contribution in the topics: Population & Cancer. The organization has 19456 authors who have published 33659 publications receiving 365676 citations.

The impact of dietary habits and metabolic risk factors on cardiovascular and diabetes mortality in countries of the Middle East and North Africa in 2010: a comparative risk assessment analysis

Abstract: Objective/design We conducted a comparative risk assessment analysis to estimate the cardiometabolic disease (CMD) mortality attributable to 11 dietary and 4 metabolic risk factors in 20 countries of the Middle East by age, sex and time. The national exposure distributions were obtained from a systematic search of multiple databases. Missing exposure data were estimated using a multilevel Bayesian hierarchical model. The aetiological effect of each risk factor on disease-specific mortality was obtained from clinical trials and observational studies. The number of disease-specific deaths was obtained from the 2010 Global Burden of Disease mortality database. Mortality due to each risk factor was determined using the population attributable fraction and total number of disease-specific deaths. Setting/population Adult population in the Middle East by age, sex, country and time. Results Suboptimal diet was the leading risk factor for CMD mortality in 11 countries accounting for 48% (in Morocco) to 72% (in the United Arab Emirates) of CMD deaths. Non-optimal systolic blood pressure was the leading risk factor for CMD deaths in eight countries causing 45% (in Bahrain) to 68% (in Libya) of CMD deaths. Non-optimal body mass index and fasting plasma glucose were the third and fourth leading risk factors for CMD mortality in most countries. Among individual dietary factors, low intake of fruits accounted for 8% (in Jordan) to 21% (in Palestine) of CMD deaths and low intake of whole grains was responsible for 7% (in Palestine) to 22% (in the United Arab Emirates) of CMD deaths. Between 1990 and 2010, the CMD mortality attributable to most risk factors had decreased except for body mass index and trans-fatty acids. Conclusions Our findings highlight key similarities and differences in the impact of the dietary and metabolic risk factors on CMD mortality in the countries of the Middle East and inform priorities for policy measures to prevent CMD.

Breast-feeding and childhood-onset type 1 diabetes: A pooled analysis of individual participant data from 43 observational studies

Abstract: OBJECTIVE To investigate if there is a reduced risk of type 1 diabetes in children breastfed or exclusively breastfed by performing a pooled analysis with adjustment for recognized confounders. RESEARCH DESIGN AND METHODS Relevant studies were identified from literature searches using MEDLINE, Web of Science, and EMBASE. Authors of relevant studies were asked to provide individual participant data or conduct prespecified analyses. Meta-analysis techniques were used to combine odds ratios (ORs) and investigate heterogeneity between studies. RESULTS Data were available from 43 studies including 9,874 patients with type 1 diabetes. Overall, there was a reduction in the risk of diabetes after exclusive breast-feeding for >2 weeks (20 studies; OR = 0.75, 95% CI 0.64–0.88), the association after exclusive breast-feeding for >3 months was weaker (30 studies; OR = 0.87, 95% CI 0.75–1.00), and no association was observed after (nonexclusive) breast-feeding for >2 weeks (28 studies; OR = 0.93, 95% CI 0.81–1.07) or >3 months (29 studies; OR = 0.88, 95% CI 0.78–1.00). These associations were all subject to marked heterogeneity (I 2 = 58, 76, 54, and 68%, respectively). In studies with lower risk of bias, the reduced risk after exclusive breast-feeding for >2 weeks remained (12 studies; OR = 0.86, 95% CI 0.75–0.99), and heterogeneity was reduced (I 2 = 0%). Adjustments for potential confounders altered these estimates very little. CONCLUSION The pooled analysis suggests weak protective associations between exclusive breast-feeding and type 1 diabetes risk. However, these findings are difficult to interpret because of the marked variation in effect and possible biases (particularly recall bias) inherent in the included studies.

Thioredoxin-Interacting Protein (TXNIP) in Cerebrovascular and Neurodegenerative Diseases: Regulation and Implication

Abstract: Neurological diseases, including acute attacks (e.g., ischemic stroke) and chronic neurodegenerative diseases (e.g., Alzheimer's disease), have always been one of the leading cause of morbidity and mortality worldwide. These debilitating diseases represent an enormous disease burden, not only in terms of health suffering but also in economic costs. Although the clinical presentations differ for these diseases, a growing body of evidence suggests that oxidative stress and inflammatory responses in brain tissue significantly contribute to their pathology. However, therapies attempting to prevent oxidative damage or inhibiting inflammation have shown little success. Identification and targeting endogenous "upstream" mediators that normalize such processes will lead to improve therapeutic strategy of these diseases. Thioredoxin-interacting protein (TXNIP) is an endogenous inhibitor of the thioredoxin (TRX) system, a major cellular thiol-reducing and antioxidant system. TXNIP regulating redox/glucose-induced stress and inflammation, now is known to get upregulated in stroke and other brain diseases, and represents a promising therapeutic target. In particular, there is growing evidence that glucose strongly induces TXNIP in multiple cell types, suggesting possible physiological roles of TXNIP in glucose metabolism. Recently, a significant body of literature has supported an essential role of TXNIP in the activation of the NOD-like receptor protein (NLRP3)-inflammasome, a well-established multi-molecular protein complex and a pivotal mediator of sterile inflammation. Accordingly, TXNIP has been postulated to reside centrally in detecting cellular damage and mediating inflammatory responses to tissue injury. The majority of recent studies have shown that pharmacological inhibition or genetic deletion of TXNIP is neuroprotective and able to reduce detrimental aspects of pathology following cerebrovascular and neurodegenerative diseases. Conspicuously, the mainstream of the emerging evidences is highlighting TXNIP link to damaging signals in endothelial cells. Thereby, here, we keep the trend to present the accumulative data on CNS diseases dealing with vascular integrity. This review aims to summarize evidence supporting the significant contribution of regulatory mechanisms of TXNIP with the development of brain diseases, explore pharmacological strategies of targeting TXNIP, and outline obstacles to be considered for efficient clinical translation.