Charcot-Marie-Tooth disease (CMT) is a clinically and genetically heterogenous group of disorders. Useful classifi cation is still clinical and electrophysiological classifi cation that divides CMT into CMT type 1 - demyelinating form and CMT type 2 - axonal form. An intermediate type is also increasingly being determined. Inheritance can be autosomal dominant, X-linked and autosomal recessive (AR). In this review, we will focus on the clinical and/or electrophysiological findings and molecular genetics of ARCMT1 (CMT4). Ten genes, GDAP1, MTMR2, MTMR13, SH3TC2, NDRG1, EGR2, PRX, CTDP1, FGD4 and SAC3 have been identifi ed in the CMT4A, CMT4B1, CMT4B2, CMT4C, CMT4D, CMT4E, CMT4F, CCFDN, CMT4H and CMT4J types, respectively. In addition, susceptibility locus on chromosome 10q23 has been found for CMT4G disease. Molecular genetics of demyelinating ARCMT are large disabilities of proteins in Schwann cells and their functions (transcriptional factor, protein transport, protein sorting, intra/extra cellular compartments, signal transduction, cell division, and cell differentiation). It has been rising necessary requirements to defi ne clinical and genetic subtypes of the ARCMT1, prevent from disease, give reproductive and genetic counselling, and develop methods for reducing and clear disease risk factor.

Introduction : In the last years other country scientists told about not only determine infant weights, need to interest correlation between maternal weight, height and infant weight. In our country few research articles posted about anthropometry of obstetrics and gynecology. Our study aim is determine maternal weight, infant weight, placenta weight and assess factors affecting roles on maternal story of “Amgalan” Maternity Hospital in 2014-2015. Goal: The current study aimed at assessing maternal weight, infant weight, placenta weight and evaluating the effect of factors leading to it. Materials and Methods: The data was already collected from “Amgalan” Maternity Hospital using maternal history and record and it was collected measuring general physical characteristics such as body weight and height, infant weight, placenta weight and body circumferences. We used retrospective method and collected statistical data was analyzed using SPSS 21.0 software. Results: Of total 964 study participants aged 18-45. The average age of participants was 29.6 ± 5.8 years old and 49.7% (n=479) was working during pregnancy, 45.7% (n=441) hadn’t works, 4.6% (n=44) was student. The average weight of mothers was 75.4±11.5, weight of infants was 3439.5±456, weight of placenta was 685±129. The following factors affected maternal and infant weights: lower education, working, early and late pregnancy complication. Maternal weight had a low direct correlation with infant weight (r=0.267, p<0.01) and placenta weight (r=0.208, p<0.01). In our study maternal height had a low direct correlation with infant weight(r=0.173, p<0.01) and infant weight had a moderate direct correlation with placenta weight (r=0.376, p<0.01). Conclusions
1. The average maternal weight was 75.4±11.5, infant weight was 3539.5±456, placenta weight was 685±129.
2. The following factors affected maternal and infant weights: lower education, working status, early and late pregnancy complications.
3. Maternal weight had a little direct correlation with infant weight (r=0.267, p<0.01) and placenta weight (r=0.208, p<0.01).

Background: The effect of lipopolysaccharide (LPS) on valproic acid (VPA)-induced cell death was examined by using mouse RAW 264.7 macrophage cells. Materials and methods, results: LPS inhibited the activation of caspase 3 and poly (ADP-ribose) polymerase (PARP) and prevented VPA-induced apoptosis. LPS inhibited VPA-induced p53 activation and pifithrin-α as a p53 inhibitor as well as LPS prevented VPA-induced apoptosis. LPS abolished the increase of Bax/Bcl-2 ratio, which is a critical indicator of p53-mediated mitochondrial damage, in response to VPA. The nuclear factor (NF)-κB inhibitors, Bay 11-7082 and parthenolide, abolished the preventive action of LPS on VPA-induced apoptosis. A series of toll-like receptor (TLR) ligands, Pam3CSK4, poly I:C, and CpG DNA as well as LPS prevented VPA-induced apoptosis. Conclusion Taken together, LPS was suggested to prevent VPA-induced apoptosis via activation of anti-apoptotic NF-κB and inhibition of pro-apoptotic p53 activation.