Glia maturation factor beta stimulates axon regeneration in transected rat sciatic nerve.

Rat sciatic nerves were bilaterally transected and repaired with an entubulation technique. The nerve interstump gap was filled with either collagen gel or collagen gel mixed with a putative neurotrophic factor (leupeptin, 4-aminopyridine, lipid angiogenic factor or glia maturation factor beta (GMF-beta]. Six weeks after nerve transection, the myelinated distal stump axons were quantified for each nerve. Only the nerves treated with GMF-beta had significantly more axons than the control side.     

Luteal phase support with estradiol and progesterone versus progesterone alone in GnRH antagonist ICSI cycles: a randomized controlled study

In vitro fertilization (IVF) cycles are associated with a defective luteal phase. Although progesterone supplementation to treat this problem is standard practice, estrogen addition is debatable. Our aim was to compare pregnancy outcomes in 220 patients undergoing antagonist intracytoplasmic sperm injection (ICSI) cycles protocol. The patients were randomly assigned into two equal groups to receive either vaginal progesterone alone (90?mg once daily) starting on the day of oocyte retrieval for up to 12 weeks if pregnancy occurred or estradiol addition (2?mg twice daily) starting on the same day and continuing up to seven weeks (foetal viability scan). Primary outcomes were pregnancy and ongoing pregnancy rates per embryo transfer. Secondary outcomes were implantation and early pregnancy loss rates. Pregnancy rates showed no significant difference between group 1 (39.09%) and 2 (43.63%) (p value?=?0.3). Similarly, both groups were comparable regarding ongoing pregnancy rate (32.7% group 1 and 36.3% group 2, p value?=?0.1). Implantation rates showed no difference between group 1 (19.25%) and group 2 (23.44%) (p value?=?0.2). Early pregnancy loss rates were comparable, with 6.3% and 7.2% in groups 1 and 2, respectively, (p value?=?0.4). In conclusion, the addition of 4?mg estrogen daily to progesterone for luteal support in antagonist ICSI cycles is not beneficial for pregnancy outcome.     

Genetic overview of postaxial polydactyly: Updated classification

Polydactyly or polydactylism, also known as a hyperdactyly, is a congenital limb defect with various morphologic phenotypes. Apart from physical and functional impairments, the presence of polydactyly is an indication of an underlying syndrome in the newborn. Usually, it follows as an autosomal dominant/recessive inheritance pattern with defects in the limb development's anteroposterior patterning. Although mutations in several genes have been associated with polydactyly; however, the exact underlying cause, pathways, and disease mechanisms are still unexplored, thus making it of multi-factorial origin. Polydactyly is divided into three subtypes; radial, ulnar, and central polydactyly. So far, 11 loci (PAPA1-PAPA11) and seven human genes have been reported to cause non-syndromic postaxial polydactyly in humans, including the ZNF141, GLI3, IQCE, GLI1, FAM92A1, KIAA0825, and DACH1. In this review, we discuss emerging evidences of clinical and molecular characterization of polydactyly types in term of the involvement of newly associated genes and loci for non-syndromic postaxial polydactyly, and how these might impact our understanding of the genetic mechanisms and molecular etiology involved in the cause of polydactyly.