Treatment of mandibular angle fracture: Revision of the basic principles / 中华创伤杂志(英文版)

Biodynamics of mandibular angle fractures has been extensively discussed in the literature in search for the best way to fixate and expedite recovery of trauma patients. Pioneers like Michelet and Champy had the greatest impact on evolving of osteosynthesis in maxillofacial traumatology; they introduced their basic principles frequently used to describe the biomechanics of mandibular fixation. Their concept states when a physiologic load is applied on mandibular teeth a negative tension will be created at superior border and a positive pressure will appear at inferior border. These simple definitions are the basis for the advent of fixation modalities in mandibular angle fracture. This article sought to reassess these principals based on load location via finite elements method.

Immunomodulatory effects of bee venom in human synovial fibroblast cell line

As in Iranian traditional medicine, bee venom [BV] is a promising treatment for the rheumatoid arthritis [RA] which is considered as a problematic human chronic inflammatory disease in the present time. Smoking is considered to be a major risk factor in RA onset and severity. The main aim of this study is to investigate the effects of BV on cigarette smoke-induced inflammatory response in fibroblast-like synoviocytes [FLS]. Cytotoxicity of cigarette smoke condensate [CSC] and bee venom were determined by the tetrazolium [MTT] method in cultured synovial fibroblastes. The expression of interleukin-1 beta and sirtuin1 mRNA were analyzed by SYBR green real-time quantitative PCR. Differences between the mean values of treated and untreated groups were assessed by student t-test. Based on MTT assay, CSC and BV did not exert any significant cytotoxic effects up to 40 micro g/mL and 10 micro g/mL, respectively. Our results showed that interleukin-1 beta mRNA level was significantly up-regulated by CSC treatments in LPS-stimulated synoviocytes in a dose-dependent manner. Conversely, the expressions of IL-1 beta and Sirt1 were up-regulated even in lower concentrations of BV and attenuated at higher concentrations. Also, BV attenuated the CSC-induced and LPS-induced inflammatory responses in synovial fibroblasts. Our results support the epidemiological studies indicating pro-inflammatory effects of CSC and anti-inflammatory effects of BV on FLS cell line

Edaravone decreases paraquat toxicity in a549 cells and lung isolated mitochondria

Edaravone, an antioxidant and radical scavenger, showed protective effects against oxidative stress-like condition. Paraquat [PQ] is toxic herbicide considerable evidence suggests that oxidative stress and mitochondrial dysfunction contribute to PQ toxicity. In this study, protective effect of edaravone against PQ induced toxicity and reactive oxygen species [ROS] generation in A549 cells and lung isolated mitochondria were evaluated. A549 cells and lung isolated mitochondria were divided into control group, PQ group, edaravone group and PQ plus edaravone-pretreated group. Cellular and mitochondrial viability assayed using MTT test and ROS generations in both cellular and mitochondrial fraction were determined by fluorometry using DCFH-DA as indicator. Our results showed that edaravone [5-100 microM] prevented PQ [500 microM] induced cytotoxicity in A549 celIs that the best protective effect was observed at concentration of 50 microM of edaravone. In addition, PQ-induced ROS generation in A549 cells significantly inhibited by edaravone. Moreover, PQ decreased mitochondria viability and also increased ROS generation in lung isolated mitochondria that edaravone [25-400 microM] markedly inhibited these toxic effects. In overall, the results of this study suggest that lung mitochondria maintenance is essential for maintaining PQt cytotoxicity and Edaravone is a protective drug against PQ toxicity in-vitro

Perform gene analaysis in an Iranian family with familial hemophagocytic lytnphohistiocytosis

Perform gene [PRF1] mutations have been reported in 20-30% of patients with familial hemophagocytic lymphohistiocytosis [FHL], an immune disorder of infancy and early childhood. Cytotoxic T and natural killer [NK] cell activities are remarkably reduced or absent in FHL patients. We report the first cases of familial hemophagocytic lymphohistiocytosis in an Iranian family with two siblings. Exons 2 and 3 of the PRF1 gene were analyzed by polymerase chain reaction [PCR] amplification and direct sequencing. Perform gene mutation[s] were detected in none of the cases. The result of our study indicates that not much evidence is present concerning a correlation between perforin gene defects and familial hemophagocytic lymphohistiocytosis etiology in these cases