[Analysis of pharmaceutical interventions related to outpatient treatment of chronic heart failure].

Objective: Our aim was to analyze pharmaceutical interventions related to heart failure (HF) outpatient treatment.

Methods: An observationnal study was carried out over 6 months at the Abidjan Institute of Cardiology (ICA). Data were collected using a survey form that focused on therapeutic adherence, drugs related-problems (DRP) and pharmaceutical interventions (PI).

Small Molecule Myeloperoxidase (MPO) Inhibition Prevents Delayed Cerebral Injury (DCI) After Subarachnoid Hemorrhage (SAH) in a Murine Model.

Background: Delayed cerebral injury (DCI) after aneurysmal subarachnoid hemorrhage (SAH) is a preventable injury that would improve patient outcomes if an effective treatment can be developed. The most common long-term disability in patients with SAH is cognitive dysfunction. Contrary to the common theory that damage from DCI originates solely from ischemia caused by cerebral vasospasm, inflammation has been shown to be an important independent mediator of DCI.

A potential therapeutic target: The role of neutrophils in the central nervous system.

Neutrophils play a critical role in immune defense as the first recruited and most abundant leukocytes in the innate immune system. As such, regulation of neutrophil effector functions have strong implications on immunity. These cells display a wide heterogeneity of function, including both inflammatory and immunomodulatory roles.

Neutrophil modulation of behavior and cognition in health and disease: The unexplored role of an innate immune cell.

Behavior and cognition are multifaceted processes influenced by genetics, synaptic plasticity, and neuronal connectivity. Recent reports have demonstrated that peripheral inflammation and peripheral immune cells play important roles in the preservation and deterioration of behavior/cognition under various conditions. Indeed, several studies show that the activity of peripheral immune cells can be critical for normal cognitive function.

AAV vectors accumulate in the pineal gland after injections into the brain or spinal cord.

AAV vectors are being used extensively for gene-modifying therapies for neurological disorders. Here, we report the surprising discovery that injections of different AAVs into the brain, spinal cord, or cerebrospinal fluid (CSF) lead to robust transduction of cells in the pineal gland. We document transduction of cells in the pineal gland following focal injections of AAV2/9-shPTEN-zsGreen into the sensorimotor or hippocampus of rats and injections of AAV2/Cre into the spinal cord of transgenic mice with a stop-flox tdT reporter.

Neutrophil Enzyme Myeloperoxidase Modulates Neuronal Response in a Model of Subarachnoid Hemorrhage by Venous Injury.

Background And Purpose: Aneurysmal subarachnoid hemorrhage (SAH) is associated with the development of delayed cognitive deficits. Neutrophil infiltration into the central nervous system is linked to the development of these deficits after SAH. It is however unclear how neutrophil activity influences central nervous system function in SAH.

Microbiological and Physicochemical Characteristics of Three Types of "Soumbara" from Seeds of African Locust Bean in Korhogo Markets, Côte d'Ivoire.

"Soumbara" is a fermented product sold in the markets of several West African countries. In the markets, it is sold in several formats (granulated, powder, and paste). The objective of this study was to evaluate the microbiological and physicochemical characteristics of these three types of "Soumbara" sold in the Korhogo markets.

Activated Microglia in the Rat Spinal Cord Following Peripheral Axon Injury Promote Glial and Neuronal Plasticity Which is Necessary for Long-Term Neuronal Survival.

Following the transection of peripheral sympathetic preganglionic axons comprising the cervical sympathetic trunk (CST), we observe robust glial and neuronal plasticity at 1 week post-injury in the rat spinal cord intermediolateral cell column (IML), which houses the injured parent neuronal cell bodies. This plasticity contributes to neuroprotection, as no neuronal loss in the IML is present at 16 weeks post-injury. Here, we administered the antibiotic minocycline or vehicle (VEH) daily for 1 week after CST transection to investigate the role of activated microglia in IML glial and neuronal plasticity and subsequent neuronal survival.

AAVshRNA-mediated PTEN knockdown in adult neurons attenuates activity-dependent immediate early gene induction.

Genetic deletion or knockdown of PTEN enables regeneration of CNS axons, enhances sprouting of intact axons after injury, and induces de novo growth of uninjured adult neurons. It is unknown, however how PTEN deletion in mature neurons alters neuronal physiology. As a first step to address this question, we used immunocytochemistry for activity-dependent markers to assess consequences of PTEN knockdown in cortical neurons and granule cells of the dentate gyrus.

Late mortality after cardiac interventions over 10-year period in two Cameroonian government-owned hospitals.

Background: Cardiac surgery is a growing activity in Sub-Saharan Africa, however, data related to long-term mortality are scarce. We aimed to analyze outcome data of cardiac interventions in two hospitals in Cameroon over 10 years' period.

Methods: we conducted a retrospective analytical and descriptive study at the Douala General Hospital and Yaoundé General Hospital.

Retrograde influences of SCG axotomy on uninjured preganglionic neurons.

There is evidence that neuronal injury can affect uninjured neurons in the same neural circuit. The overall goal of this study was to understand the effects of peripheral nerve injury on uninjured neurons located in the central nervous system (CNS). As a model, we examined whether axotomy (transection of postganglionic axons) of the superior cervical ganglion (SCG) affected the uninjured, preganglionic neurons that innervate the SCG.

Incidence, characteristics and prognosis of acute kidney injury in Cameroon: a prospective study at the Douala General Hospital.

Objective: There are limited data on AKI in sub-Saharan Africa. We aim to determine the incidence, characteristics and prognosis of AKI in Cameroon.

Patients And Methods: A prospective study including all consenting acute admissions in the internal medicine and the ICU of a tertiary referral hospital in Cameroon from January 2015 to June 2016.

Outcome of permanent vascular access for haemodialysis in patients with end-stage renal disease in Cameroon: results from the pilot experience of the Douala general hospital.

Background Chronic Kidney disease is a major health problem in the world. Native arteriovenous Fistula (AVF) is well established as the best vascular access for haemodialysis. Little is known about the outcome of AVF in sub-Saharan Africa.

Increased Cx32 expression in spinal cord TrkB oligodendrocytes following peripheral axon injury.

Following injury to motor axons in the periphery, retrograde influences from the injury site lead to glial cell plasticity in the vicinity of the injured neurons. Following the transection of peripherally located preganglionic axons of the cervical sympathetic trunk (CST), a population of oligodendrocyte (OL) lineage cells expressing full length TrkB, the cognate receptor for brain derived neurotrophic factor (BDNF), is significantly increased in number in the spinal cord. Such robust plasticity in OL lineage cells in the spinal cord following peripheral axon transection led to the hypothesis that the gap junction communication protein connexin 32 (Cx32), which is specific to OL lineage cells, was influenced by the injury.

Distribution and phenotype of TrkB oligodendrocyte lineage cells in the adult rat spinal cord.

The distribution and phenotype of a previously undescribed population of nonneuronal cells in the intact spinal cord that expresses TrkB, the cognate receptor for brain derived neurotrophic factor (BDNF) and neurotrophin 4 (NT-4), were characterized by examining the extent of co-localization of TrkB with NG2, which identifies oligodendrocyte progenitors (OPCs) or CC1, a marker for mature oligodendrocytes (OLs). All TrkB nonneuronal cells expressed Olig2, confirming their role in the OL lineage. Similar to OPCs and OLs, TrkB cells resided in gray and white matter of the spinal cord in similar abundance.

Transection of preganglionic axons leads to CNS neuronal plasticity followed by survival and target reinnervation.

The goals of the present study were to investigate the changes in sympathetic preganglionic neurons following transection of distal axons in the cervical sympathetic trunk (CST) that innervate the superior cervical ganglion (SCG) and to assess changes in the protein expression of brain derived neurotrophic factor (BDNF) and its receptor TrkB in the thoracic spinal cord. At 1 week, a significant decrease in soma volume and reduced soma expression of choline acetyltransferase (ChAT) in the intermediolateral cell column (IML) of T1 spinal cord were observed, with both ChAT-ir and non-immunoreactive neurons expressing the injury marker activating transcription factor 3. These changes were transient, and at later time points, ChAT expression and soma volume returned to control values and the number of ATF3 neurons declined.

Transient changes in spinal cord glial cells following transection of preganglionic sympathetic axons.

Following peripheral nerve injury, retrograde signals originating from the injury site may activate intrinsic factors in the injured neurons, possibly leading to regenerative growth. Retrograde influences from peripheral injury sites may lead to the activation of glial cells in the vicinity of the centrally located cell bodies of the injured neurons. Few studies have examined changes in the spinal cord intermediolateral cell column (IML), which houses sympathetic preganglionic cell bodies, following injury to distal axons in the cervical sympathetic trunk (CST).

Ischemia-induced increase in RGS7 mRNA expression in gerbil hippocampus.

The present study investigated the changes in the expression of regulators of G-protein-coupled signaling proteins RGS2, 7 and 8 in gerbil hippocampus to better understand alterations of G-protein-coupled receptors signaling after cerebral ischemia. In situ hybridization revealed a transient, robust early increase in RGS7 mRNA levels in the dentate gyrus after ischemia. RGS8 mRNA expression started to increase at a later time point in the CA3 region but no changes were found for RGS2.