Notes

Arginine promotes testicular development in boars by way of n . o . and putrescine.
BACKGROUND Endothelial-to-mesenchymal transition (EndMT) has been implicated in initiation and progression of pulmonary arterial hypertension (PAH). Gremlin-1 promotes vascular remodeling of PAH and mediates epithelial-mesenchymal transition, which is similar to EndMT. In the present study we investigated the potential role of gremlin-1 plays in EndMT of pulmonary artery endothelial cells (PAECs). METHODS Immunofluorescence staining was performed to detect the expression of alpha smooth muscle actin (α-SMA) and von Willebrand factor (VWF). Migration and angiogenic responses of PAECs were determined by transwell assay and tube formation assay, respectively. Protein expression levels were determined by western blotting. RESULTS Gremlin-1 induced EndMT of PAECs in a phospho-smad2/3-dependent manner. This was characterized by the loss of platelet endothelial cell adhesion molecule 1 and an increase in protein levels of a-SMA, nerve-cadherin, and matrix metalloproteinase 2. It was also determined that gremlin-1 facilitated the migration and angiogenic responses of PAECs in a dose-dependent manner. Bone morphogenetic protein 7 (BMP-7) was found to attenuate gremlin-1-mediated EndMT, migration and angiogenesis of PAECs by inducing phosphorylation of Smad1/5/8 and suppressing phosphorylation of Smad2/3. CONCLUSION Gremlin-1 mediates EndMT in PAECs, and BMP-7 reverses gremlin-1-induced EndMT by an induction of p-Smad1/5/8 and suppression of p-Smad2/3. Individuals with tetraplegia, typically attributed to spinal cord injuries (SCI) at the cervical level, experience significant health care costs and loss of independence due to their limited reaching and grasping capabilities. Neuromuscular electrical stimulation (NMES) is a promising intervention to restore arm and hand function because it activates a person's own paralyzed muscles; however, NMES sometimes lacks the accuracy and repeatability necessary to position the limb for functional tasks, and repeated muscle stimulation can lead to fatigue. Robotic devices have the potential to restore function when used as assistive devices to supplement or replace limited or lost function of the upper limb following SCI. Unfortunately, most robotic solutions are bulky or require significant power to operate, limiting their applicability to restore functional independence in a home environment. Combining NMES and robotic support systems into a single hybrid neuroprosthesis is compelling, since the robotic device can srther, increased integration of the control action between NMES and robotic subsystems to reanimate the limb should be pursued. Standardized reporting of system performance and expanded clinical assessments of these systems are also needed. All of these advancements are critical to facilitate translation from lab to home. Chondroitin sulfate proteoglycans (CSPGs), extracellular matrix molecules that increase dramatically following a variety of CNS injuries or diseases, have long been known for their potent capacity to curtail cell migrations as well as axon regeneration and sprouting. The inhibition can be conferred through binding to their major cognate receptor, Protein Tyrosine Phosphatase Sigma (PTPσ). However, the precise mechanisms downstream of receptor binding that mediate growth inhibition have remained elusive. Recently, CSPGs/PTPσ interactions were found to regulate autophagic flux at the axon growth cone by dampening the autophagosome-lysosomal fusion step. Because of the intense interest in autophagic phenomena in the regulation of a wide variety of critical cellular functions, we summarize here what is currently known about dysregulation of autophagy following spinal cord injury, and highlight this critical new mechanism underlying axon regeneration failure. Furthermore, we review how CSPGs/PTPσ interactions influence plasticity through autophagic regulation and how PTPσ serves as a switch to execute either axon outgrowth or synaptogenesis. This has exciting implications for the role CSPGs play not only in axon regeneration failure after spinal cord injury, but also in neurodegenerative diseases where, again, inhibitory CSPGs are upregulated. BACKGROUND Meningioma is the most common primary intracranial tumor, representing 13-36.6% of all primary central nervous system tumors. Meningiomas are benign in about 90% of cases. World Health Organization (WHO) grade II meningioma is associated with a high rate of recurrence and poorer survival than in grade I. The reference treatment is surgery, which should be as complete as possible. Currently, in grade II, there are no recommendations for systematic adjuvant treatment such as radiotherapy. We studied a homogeneous series of grade II meningiomas treated by surgery in two university hospital centers to analyze use of radiotherapy and its efficacy. METHODS We retrospectively analyzed patients in our database with WHO grade II meningioma, operated on between 2007 and 2010 in the university hospitals of Montpellier and Bordeaux, France. https://www.selleckchem.com/ Clinical and radiological data, treatments and survival were analyzed. RESULTS Eighty-eight patients were included. Five-year overall survival was 89.7%. Nineteen patients received radiotherapy during follow-up, without significant impact on survival (p=0.27). CONCLUSION In WHO grade II meningioma, it is currently difficult to establish clear recommendations for radiotherapy. The present study is in accordance with the literature that early postoperative radiotherapy is not mandatory in grade II meningioma with macroscopically total resection. Intrinsically disordered proteins do not adopt well-defined structures, yet they still play functional roles in many different aspects of biology. Their lack of stable conformations poses new challenges to the quantitative description and understanding of their processes, since they cannot be formulated within the classical terms of structural biology. Polymer physics is emerging as a powerful language to identify, describe, and quantify the molecular determinants of the disordered conformational ensemble. Here, I will review the application of key-concepts of polymer theories to intrinsically disordered proteins, with a particular focus on the role played by residue-residue and residue-solvent interactions in modulating conformational transitions in the disordered structural ensemble.
Website: https://www.selleckchem.com/