The definition of recurrent shoulder dislocation in tramadol induced seizure patients

Background: Prevalence of recurrent shoulder dislocation in patients taking tramadol has not been studied yet; so, this study aims to study the recurrent shoulder dislocation following tramadol induced seizure. Methods: In this cross-sectional study, 205 patients with recurrent shoulder dislocation complaints (2 or more) referred to Shafa Orthopedic and Iranmehr hospitals Tehran, Iran, from October 2012 to October 2014 were studied. Data on patient history and physical examination, patient demographic information such as age, sex, age at first dislocation, total number of dislocation, cause of the first dislocation, history of tramadol use, number of dislocation following tramadol induced seizure, history of other drugs use, the dominant hand, involved side, direction of dislocations and greater tuberosity fracture was recorded using a pre-designed questionnaire. Categorical variables were compared by chi-square test and the means were compared with student T-test. Results: In this study, 50 patients (24.4) suffered from tramadol induced seizures and recurrent shoulder dislocation. Results showed that there was a significant relationship between the number of dislocation and tramadol use (P = 0.02). Recurrent shoulder dislocation following tramadol induced seizure was significantly associated with greater tuberosity fracture of humerus (P = 0.04); in 49 out of 50 patients (98) dislocation was of anterior type. Conclusion: The findings of this study suggest that tramadol induced seizure may increase the risk of recurrent shoulder dislocation. Furthermore, the prevalence of greater tuberosity fracture in shoulder dislocation increases following tramadol induced seizure; and anterior shoulder dislocation is the most common type of dislocation following tramadol induced seizure

The study on fishing and resource management of bony fisheries within southern Caspian Sea

The project of the Study on fishing and resource management of fisheries within Southern Caspian Sea was conducted on the base of an agreement made between fisheries organization (Shilat) and the Iranian fishery research organization (IFRO) signed in 2010. In this library-based study the current situation of bony fish fisheries and biology of these species has been surveyed in Iranian waters of the Caspian Sea . In this survey internal and external environmental factors of bony fishes activities were considered. Using SWOT analysis method, current situation of fisheries was investigated..One of the most important strategies for conserving anadromous species such as Caspian kutum , common carp, roach, bream and …. is rehabilitation of the natural spawning ground in rivers, coastal lagoon specially Anzali lagoon .By conducting this strategy not only restocks of bony fishes is done ,but also reduced the cost of artificial restocking programs and releasing fingerlings .In short term , it is nessesary to enhance the stocks of the species that have low catch is done by huge releasing of the fingerlings and study the qualification of the program

Allele-Specific Deletions in Mouse Tumors Identify Fbxw7 as Germline Modifier of Tumor Susceptibility

Genome-wide association studies (GWAS) have been successful in finding associations between specific genetic variants and cancer susceptibility in human populations. These studies have identified a range of highly statistically significant associations between single nucleotide polymorphisms (SNPs) and susceptibility to development of a range of human tumors. However, the effect of each SNP in isolation is very small, and all of the SNPs combined only account for a relatively minor proportion of the total genetic risk (5–10%). There is therefore a major requirement for alternative routes to the discovery of genetic risk factors for cancer. We have previously shown using mouse models that chromosomal regions harboring susceptibility genes identified by linkage analysis frequently exhibit allele-specific genetic alterations in tumors. We demonstrate here that the Fbxw7 gene, a commonly mutated gene in a wide range of mouse and human cancers, shows allele-specific deletions in mouse lymphomas and skin tumors. Lymphomas from three different F1 hybrids show 100% allele-specificity in the patterns of allelic loss. Parental alleles from 129/Sv or Spretus/Gla mice are lost in tumors from F1 hybrids with C57BL/6 animals, due to the presence of a specific non-synonymous coding sequence polymorphism at the N-terminal portion of the gene. A specific genetic test of association between this SNP and lymphoma susceptibility in interspecific backcross mice showed a significant linkage (p = 0.001), but only in animals with a functional p53 gene. These data therefore identify Fbxw7 as a p53-dependent tumor susceptibility gene. Increased p53-dependent tumor susceptibility and allele-specific losses were also seen in a mouse skin model of skin tumor development. We propose that analysis of preferential allelic imbalances in tumors may provide an efficient means of uncovering genetic variants that affect mouse and human tumor susceptibility

New national and regional bryophyte records, 49

Peer reviewe

RNAi screen reveals synthetic lethality between cyclin G-associated kinase and FBXW7 by inducing aberrant mitoses

Background: F-box and WD40 repeat domain-containing 7 (FBXW7) is an E3 ubiquitin ligase involved in the ubiquitination and degradation of multiple oncogenic substrates. The tumour suppressor function is frequently lost in multiple cancers through genetic deletion and mutations in a broad range of tumours. Loss of FBXW7 functionality results in the stabilisation of multiple major oncoproteins, culminating in increased cellular proliferation and pro-survival pathways, cell cycle deregulation, chromosomal instability and altered metabolism. Currently, there is no therapy to specifically target FBXW7-deficient tumours. Methods: We performed a siRNA kinome screen to identify synthetically lethal hits to FBXW7 deficiency. Results: We identified and validated cyclin G-associated kinase (GAK) as a potential new therapeutic target. Combined loss of FBXW7 and GAK caused cell cycle defects, formation of multipolar mitoses and the induction of apoptosis. The synthetic lethal mechanism appears to be independent of clathrin-mediated receptor endocytosis function of GAK. Conclusions: These data suggest a putative therapeutic strategy for a large number of different types of human cancers with FBXW7 loss, many of which have a paucity of molecular abnormalities and treatment options