A Clonal NG2-Glia Cell Response in a Mouse Model of Multiple Sclerosis.

NG2-glia, also known as oligodendrocyte precursor cells (OPCs), have the potential to generate new mature oligodendrocytes and thus, to contribute to tissue repair in demyelinating diseases like multiple sclerosis (MS). Once activated in response to brain damage, NG2-glial cells proliferate, and they acquire a reactive phenotype and a heterogeneous appearance. Here, we set out to investigate the distribution and phenotypic diversity of NG2-glia relative to their ontogenic origin, and whether there is a clonal NG2-glial response to lesion in an experimental autoimmune encephalomyelitis (EAE) murine model of MS.

Clonal Glial Response in a Multiple Sclerosis Mouse Model.

Multiple sclerosis (MS) is an autoimmune disease causing central nervous system (CNS) demyelination and axonal injury. In the last years the importance of astrocytes in MS is rapidly increasing, recognizing astrocytes as highly active players in MS pathogenesis. Usually the role assigned to astrocytes in MS lesions has been the formation of the glial scar, but now their implication during lesion formation and the immune response increasingly recognized.

Inhibition of Casein Kinase 2 Protects Oligodendrocytes From Excitotoxicity by Attenuating JNK/p53 Signaling Cascade.

Oligodendrocytes are highly vulnerable to glutamate excitotoxicity, a central mechanism involved in tissue damage in Multiple Sclerosis (MS). Sustained activation of AMPA receptors in rat oligodendrocytes induces cytosolic calcium overload, mitochondrial depolarization, increase of reactive oxygen species, and activation of intracelular pathways resulting in apoptotic cell death. Although many signals driven by excitotoxicity have been identified, some of the key players are still under investigation.

Deregulation of the endocannabinoid system and therapeutic potential of ABHD6 blockade in the cuprizone model of demyelination.

Multiple sclerosis (MS) is a chronic demyelinating disease of unknown etiology in which tissue pathology suggests both immune-dependent attacks to oligodendroglia and primary oligodendrocyte demise. The endocannabinoid system has been crucially involved in the control of autoimmune demyelination and cannabinoid-based therapies exhibit therapeutic potential, but also limitations, in MS patients. In this context, growing evidence suggests that targeting the hydrolysis of the main endocannabinoid 2-arachidonoylglycerol (2-AG) may offer a more favorable benefit-to-risk balance in MS than existing cannabinoid medicines.

Isolation, Expansion, and Maturation of Oligodendrocyte Lineage Cells Obtained from Rat Neonatal Brain and Optic Nerve.

Oligodendrocytes are the myelin-forming cells in the central nervous system (CNS) and their loss or dysfunction is a hallmark of CNS demyelinating diseases, such as multiple sclerosis (MS), hypoxic-ischemic demyelination, or spinal cord injury. In the rodent CNS, oligodendrocyte progenitor cells (OPCs) arise in multiple ventral and dorsal locations of the forebrain during late embryogenesis and early postnatal periods. OPCs migrate out from these germinal zones and disperse throughout the CNS, to populate the developing white and gray matter.

Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism.

Oligodendrocytes make myelin and support axons metabolically with lactate. However, it is unknown how glucose utilization and glycolysis are adapted to the different axonal energy demands. Spiking axons release glutamate and oligodendrocytes express NMDA receptors of unknown function.

Pío del Río Hortega and the discovery of the oligodendrocytes.

Pío del Río Hortega (1882-1945) discovered microglia and oligodendrocytes (OLGs), and after Ramón y Cajal, was the most prominent figure of the Spanish school of neurology. He began his scientific career with Nicolás Achúcarro from whom he learned the use of metallic impregnation techniques suitable to study non-neuronal cells. Later on, he joined Cajal's laboratory.

Recurrent polymyositis-associated lung disease after lung transplantation.

The association between interstitial lung disease and polymyositis/dermatomyositis is well known. It severely affects patients' quality of life, worsens prognosis and represents a major risk factor for premature death. Current treatment is unclear and therapeutic options are based on case series.

Mortality risk factors in critical post-surgical patients treated using continuous renal replacement techniques.

Objective: To determine the influence of demographics, medical, and surgical variables on 30-day mortality in patients who need continuous renal replacement therapy (CRRT).

Materials And Methods: A retrospective-following study was conducted using the data of 112 patients admitted to the postoperative intensive care unit who required CRRT, between August 2006 and August 2011, and followed-up for 30 days. The following information was collected: age, gender, history of HBP, DM, cardiovascular disease, and CKD, urgent surgery, surgical speciality, organic dysfunction according to the SOFA scale, the number of organs with dysfunction, use of mechanical ventilation, diagnostic and origin of sepsis, type of CRRT, and 30-day mortality.

Analysis of patients referred to a lung transplantation unit.

This cross-sectional, concurrent and descriptive study presents the decisions regarding patients referred to our Lung Transplantation Unit (LTxU). Each patient is discussed in a multidisciplinary clinical session (phase I), rejecting some and accepting others for assessment in our LTxU (phase II) according to criteria of the National and International Guidelines for Transplantation. A protocol assessment in phase II, leads to a decision to reject, accept, or follow-up the candidate for LTx.

[Spanish Society of Anaesthesia (SEDAR) guidelines for pre-anaesthesia checking procedures].

We present this document as a guide to preparing a specific institutional pre-anaesthesia checklist, as recommended in the Helsinki declaration on patient safety in anaesthesiology. Also, the recently recommended WHO "safe surgery check-list" includes a check-list for anaesthesia. A working group was established in accordance with the charter of the Spanish Society of Anaesthesiology and Resuscitation (Sociedad Española de Anestesiología y Reanimación [SEDAR]).

Increased expression of glutamate transporters in subcortical white matter after transient focal cerebral ischemia.

Transient focal cerebral ischemia leads to extensive excitotoxic glial damage in the subcortical white matter. Efficient reuptake of released glutamate is essential for preventing glutamate receptor overstimulation and neuronal and glial death. The present study evaluates the expression of the main glutamate transporters (EAAT1, EAAT2, and EAAT3) in subcortical white matter of the rat after transient middle cerebral artery occlusion.

Functional glutamate transport in rodent optic nerve axons and glia.

Recent findings suggest that synaptic-type glutamate signaling operates between axons and their supporting glial cells. Glutamate reuptake will be a necessary component of such a system. Evidence for glutamate-mediated damage of oligodendroglia somata and processes in white matter suggests that glutamate regulation in white matter structures is also of clinical importance.

Anesthetic management of a combined heart and liver transplantation in an amyloidotic patient: a case report.

Few cases of combined heart and liver transplantation (CHLT) have been reported for familial amyloidosis. Our first CHLT was performed on a female patient with familial amyloidosis due to a genetic defect in transthyretin, characterized by deposition of amyloid in various organs and tissues. This disease produced autonomic heart dysfunction that preceded the development of clinical manifestations and may be an important factor in determining the optimal timing for liver transplantation.

P2X(7) receptor blockade prevents ATP excitotoxicity in oligodendrocytes and ameliorates experimental autoimmune encephalomyelitis.

Oligodendrocyte death and demyelination are hallmarks of multiple sclerosis (MS). Here we show that ATP signaling can trigger oligodendrocyte excitotoxicity via activation of calcium-permeable P2X(7) purinergic receptors expressed by these cells. Sustained activation of P2X(7) receptors in vivo causes lesions that are reminiscent of the major features of MS plaques, i.

Excitotoxic damage to white matter.

Glutamate kills neurons by excitotoxicity, which is caused by sustained activation of glutamate receptors. In recent years, it has been shown that glutamate can also be toxic to white matter oligodendrocytes and to myelin by this mechanism. In particular, glutamate receptor-mediated injury to these cells can be triggered by activation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, kainate and N-methyl-D-aspartate glutamate receptor types.

First Spanish series of intestinal transplantation in adult recipients.

Background: short-bowel transplantation has experienced a substantial growth worldwide following improved results from the late 1990's on, and its coverage by Medicare. According to the International Registry (1985-2005), a total of 1,292 intestinal transplants for 1,210 patients in 65 hospitals across 20 countries have been carried out thus far.

Objective: to know short-term (6 months) results regarding patient and graft survival from the first Spanish series of intestinal transplants in adult recipients.

High-frequency jet ventilation in interventional bronchoscopy: factors with predictive value on high-frequency jet ventilation complications.

Study Objective: To evaluate the incidence and impact on clinical outcome of complications observed during high-frequency jet ventilation (HFJV) at interventional bronchoscopy and to identify the perioperative factors that may be associated to an increased incidence of such complications.

Design: Observational retrospective, study with an observational prospective validation of the statistically significant associations.

Setting: University hospital.

Activation of kainate receptors sensitizes oligodendrocytes to complement attack.

Glutamate excitotoxicity and complement attack have both been implicated separately in the generation of tissue damage in multiple sclerosis and in its animal model, experimental autoimmune encephalomyelitis. Here, we investigated whether glutamate receptor activation sensitizes oligodendrocytes to complement attack. We found that a brief incubation with glutamate followed by exposure to complement was lethal to oligodendrocytes in vitro and in freshly isolated optic nerves.

[Patient with right ventricular arrhythmogenic dysplasia, ascites and ulcerative colitis: anesthetic management during major abdominal surgery].

A 43-year-old man with ulcerative colitis was scheduled for pancolectomy owing to adenomatous transformation of polyps. The patient had right ventricular arrhythmogenic dysplasia, with deteriorating ventricular function, and carried an automatic implantable defibrillator. We discuss the general features of arrhythmogenic right ventricular dysplasia and its implications for management and monitoring during major abdominal surgery.

Increased expression and function of glutamate transporters in multiple sclerosis.

Recent studies have shown that glutamate excitotoxicity may be a component in the etiology of multiple sclerosis (MS). Glutamate transporters determine the levels of extracellular glutamate and are essential to prevent excitotoxicity. We have analyzed here the expression of the glutamate transporters EAAT1, EAAT2 and EAAT3 in control and in MS optic nerve samples.

Multiple sclerosis: novel perspectives on newly forming lesions.

The mechanisms underlying lesion formation in multiple sclerosis are unknown. The prevailing view is that macrophages are primary mediators of myelin destruction in the relapsing and remitting forms of this disease. However, recent findings have revealed widespread oligodendrocyte apoptosis in the absence of a clear cellular immune response.

Simultaneous liver-kidney transplantation for adult recipients with irreversible end-stage renal disease.

Hypothesis: Combined liver-kidney transplantation is safe (low morbidity and acceptable mortality) and effective in patients with end-stage liver disease. Although refinements in surgical technique have resulted in better patient and allograft outcomes, the negative impact of renal insufficiency on survival in patients undergoing liver transplantation has been widely reported, although some aspects are controversial.

Design: Analysis of the clinical characteristics and outcome in the management of patients undergoing combined liver-kidney transplantation.

Simultaneous liver-kidney transplant for combined renal and hepatic end-stage disease.

Introduction: After the first combined liver-kidney transplantation (CLKT) reported by Margreiter in 1984, it became clear that renal failure was no longer an absolute contraindication.

Objective: Our goal was to assess our results with combined liver-kidney transplant. Among 875 liver transplants performed between May 1986 and October 2002, there were 17 cases (1.