The effectiveness of artificial reefs for rehabilitation and production of fisheries in Iran

An artificial Reef is a fabricated, underwater structure, typically built for promoting marine life in areas of generally featureless bottom. Creating artificial reefs began from 2000 in southern provinces in Iran. This study has surveyed about the Bushehr and Khozestan states. The objective is to determine the effectiveness of artificial reefs in attracting and enhancing the production different aquatics through increasing of fish assemblage and fishery. The performance of artificial reefs deployed off the coast of the Persian Gulf in 10 to 15m, was evaluated. The reefs comprised of seven artificial and one control (natural) statistical tests plan in three replicates. Three types of artificial reefs were used in this study. That two were designed reefs and one was not designed or used material. The experimental plan consisted (i) Reef ball (R), designed hemispherical shaped; (ii) Laneh Mahi (L), designed pyramid shaped; (iii) Used material (U); (iv) mixed (RL); (v) mixed (RU); (vi) mixed (LU); (vii) mixed (RLU); and (viii) control site (CS). Trap nets and under-water visual census surveys were adopted for seasonal sampling of fish aggregation. Results of statistical analysis using ANOVA and T-test of the mean Catch per Unit Effort (CPUE) showed significant difference (p<0.05) in term of computing number of fish for aggregation of fishes. The study has concluded that reef deployments have influenced favorably the fish communities and fish harvests. Therefore, the artificial reefs, especially the mixed RLU, are appropriate tools for future fishing enhancement in the Persian Gulf of Iran

National and sub-national trend and burden of injuries in Iran, 1990-2013: A study protocol

Background: Worldwide, injuries are a major public health concern and make a considerable contribution to the disease burden. The present study is a component of the National and Subnational Burden of Diseases, Injuries, and Risk Factors from 1990 to 2013 (NASBOD) study in Iran, which was designed to investigate the burden of most important injuries (road traffic injuries, falls, burns, poisonings and drownings) at the national and sub-national levels in Iran. In this paper we explain definitions, organization, injuries selection process, data sources, data gathering methods, and data analyses of the national and sub-national burden of injuries study in Iran. Methods: The burden of most important injuries in current metric of DALYs at the national and sub-national levels in Iran over 1990-2013 will be estimated through comprehensive reviews of either published or national data sources. Statistical modeling will be used to impute the missing data on the burden of selected important injuries for each district-year. Conclusion: The results of present study can help health policy makers to plan more comprehensive and cost-effective strategies at national and sub-national level for prevention and control of burden caused by injuries

Phosphodiesterase 3A and arterial hypertension

BACKGROUND: High blood pressure is the primary risk factor for cardiovascular death worldwide. Autosomal-dominant hypertension with brachydactyly (HTNB) clinically resembles salt-resistant essential hypertension and causes death by stroke before age 50 years. Recently, we implicated the gene encoding phosphodiesterase 3A (PDE3A); however, in vivo modeling of the genetic defect and thus showing an involvement of mutant PDE3A is lacking. METHODS: We used genetic mapping, sequencing, transgenic technology, CRISPR-Cas9 gene editing, immunoblotting, and fluorescence resonance energy transfer (FRET). We identified new patients, performed extensive animal phenotyping, and explored new signaling pathways. RESULTS: We describe a novel mutation within a 15 bp region of the PDE3A gene and define this segment as mutational hotspot in HTNB. The mutations cause an increase in enzyme activity. A CRISPR/Cas9-generated rat model, with a 9 bp deletion within the hotspot analogous to a human deletion, recapitulates HTNB. In mice, mutant transgenic PDE3A overexpression in smooth muscle cells confirmed that mutant PDE3A causes hypertension. The mutant PDE3A enzymes display consistent changes in their phosphorylation and an increased interaction with the 14-3-3θ adaptor protein. This aberrant signaling is associated with an increase in vascular smooth muscle cell proliferation and changes in vessel morphology and function. CONCLUSIONS: The mutated PDE3A gene drives mechanisms that increase peripheral vascular resistance causing hypertension. We present two new animal models that will serve to elucidate the underlying mechanisms further. Our findings could facilitate the search for new antihypertensive treatments