[Hearing aids at the International Center of Auditory rehabilitation in Abidjan: Prosthetics gains and satisfaction in patients].

Subject: To evaluate patients wearing hearing aid at the International Center of Auditory Correction in Abidjan.

Method And Material: It is a descriptif and transversal study from 07/01/99 to 06/30/10. We have included the files of patients completely filled.

Role of angiotensin II type 2 receptor during regression of cardiac hypertrophy in spontaneously hypertensive rats.

We previously reported that the AT1 receptor antagonist valsartan and the angiotensin converting enzyme (ACE) inhibitor enalapril decrease DNA synthesis and stimulate apoptosis in interstitial fibroblasts and epicardial mesothelial cells during regression of ventricular hypertrophy in spontaneously hypertensive rats (SHR). To examine the role of the AT2 receptor in this model, we studied hearts from SHR treated with valsartan or enalapril either alone or combined with the AT2 antagonist PD123319 for 1 or 2 weeks. Apoptosis was evaluated by quantification of DNA fragmentation or by TUNEL labeling.

[Removal of an intratracheobronchial foreign body opaque to X-rays in a child within a context of inadequate medical technical equipment].

Intratracheobronchial foreign bodies are common accidents in children. In developed countries, the removal of these intratracheobronchial foreign bodies is performed with flexible or rigid fiberoptic bronchoscopy. Resorting to surgery is rare.

Cervical cellulitis and mediastinitis following esophageal perforation: a case report.

Unlabelled: Chicken bone is one of the most frequent foreign bodies (FB) associated with upper esophageal perforation. Upper digestive tract penetrating FB may lead to life threatening complications and requires prompt management. We present the case of a 52-year-old man who sustained an upper esophageal perforation associated with cervical cellulitis and mediastinitis.

[Therapeutic management of glottic tumours: about a series of 41 cases of subtotal laryngectomy with cricohyoidoepiglottopexy (CHEP)].

Objectives: 1) To analyse the oncological and early functional results of partial supra-cricoid laryngectomy with crico-hyoido-pexy performed as a primary treatment modality on patients diagnosed with glottic squamous cell carcinoma involving the anterior commissure; 2) To propose a therapeutic management.

Patients And Methods: This is a retrospective study conducted over a period of 10 years (1995-2005). Inclusion criteria included: 1) Squamous cell carcinoma of the vocal cords reaching the anterior commissure; 2) Absence of previous treatment for the glottic lesion; 3) Minimum follow-up period of 24 months.

Regulation of therapeutic apoptosis: a potential target in controlling hypertensive organ damage.

Cell growth and survival are potential therapeutic targets for the control of complications associated with hypertension. In most cardiovascular disorders, cardiac fibroblasts and large-vessel smooth muscle cells can replicate and thus contribute to the disease. We propose that cardiovascular hyperplasia may be reversed via therapeutic apoptosis induction with drugs that are safe and already used in the clinic.

Regression of neointimal lesions in the carotid artery of nifedipine-treated SHR and WKY rats: possible role of apoptosis.

We previously observed that nifedipine reduces aortic hypertrophy in spontaneously hypertensive rats (SHR) partly by inducing smooth muscle cell (SMC) apoptosis. The present study examined nifedipine regulation of SMC apoptosis in carotids with or without a neointima. A neointima was produced by endothelial denudation of the left carotid of SHR and WKY rats.

Workshop: excess growth and apoptosis: is hypertension a case of accelerated aging of cardiovascular cells?

Several groups including ours have demonstrated cardiac hyperplasia in neonates from genetically hypertensive rat strains. We have shown that similar problems exist in the kidney as well. More recently, we found that excessive heart and kidney weight is neonatally related to inhibition of apoptosis.

Proapoptotic and growth-inhibitory role of angiotensin II type 2 receptor in vascular smooth muscle cells of spontaneously hypertensive rats in vivo.

Angiotensin type 2 (AT(2)) receptors for angiotensin II suppress cell growth and induce apoptosis in vitro, but their role is poorly defined in vivo. We reported that transient induction of smooth muscle cell (SMC) apoptosis precedes DNA synthesis inhibition and aortic hypertrophy regression in spontaneously hypertensive rats treated with the AT(1) antagonist losartan or the converting-enzyme inhibitor enalapril. Although both drugs are equipotent in reducing SMC number, apoptosis occurs significantly earlier with losartan than enalapril.

Apoptosis during regression of cardiac hypertrophy in spontaneously hypertensive rats. Temporal regulation and spatial heterogeneity.

We previously reported that increased apoptosis participates in the regression of aortic hypertrophy in spontaneously hypertensive rats. To further document the potential role of apoptosis in cardiovascular therapy, we examined apoptosis during regression of hypertrophy in the heart of spontaneously hypertensive rats receiving the antihypertensive drug enalapril (30 mg. kg(-1).

Altered balance between cell replication and apoptosis in hearts and kidneys of newborn SHR.

Apoptosis is involved in neonatal remodeling of organs of the cardiovascular system. Since we previously reported hyperplasia of these organs at birth in several forms of genetic hypertension, the aim of this study was to determine whether alterations of the apoptotic process could explain our findings. The heart, aorta, and kidneys of newborn Wistar-Kyoto and spontaneously hypertensive rats were harvested 24 hours after an injection of [3H]thymidine.

Smooth muscle apoptosis during vascular regression in spontaneously hypertensive rats.

We previously reported that apoptosis is increased in smooth muscle cells cultured from the aorta of spontaneously hypertensive rats versus normotensive controls. As an initial in vivo exploration, we now examined smooth muscle cell apoptosis regulation during the regression of vascular hypertrophy in the thoracic aorta media of spontaneously hypertensive rats receiving the antihypertensive drug enalapril (30 mg.kg-1.

The time window of apoptosis: a new component in the therapeutic strategy for cardiovascular remodeling.

APOPTOSIS AND EXPERIMENTAL HYPERTROPHY: Apoptosis (programmed cell death) is a physiological counterpart of cell replication with shared as well as specific pathways. Our initial studies have demonstrated increased apoptosis in the heart, kidney and brain of spontaneously hypertensive rats (SHR) and mice, persisting in cultured vascular smooth muscle cells. In these target organs of hypertension, programmed cell death paralleled the well known hypertrophy/hyperplasia.

Apoptosis and vascular wall remodeling in hypertension.

Vascular structure plays a key role in the pathogenesis of hypertension. Because it is less readily reversible than protein accumulation, DNA accumulation in the arterial wall may be considered as a record of past episodes of vascular growth, contributing to the persistence of the vascular disease. Apoptosis, a ubiquitous and highly regulated form of programmed cell death that is involved in tissue morphogenesis and homeostasis as the essential counterpart of cell replication, is potentially involved in the regulation of vascular structure, via the deletion of cells in the vessel wall.

Apoptosis in pressure overload-induced heart hypertrophy in the rat.

Pressure overload induces cardiac growth in the rat, which implies the hypertrophy of cardiac muscle cells and proliferation of nonmuscle cells. The cardiac cell loss observed in parallel has generally been attributed to necrosis. Using an in situ assay, we demonstrated a phase of apoptosis or programmed cell death during the first 7 d after pressure overload with a peak at day 4 while cardiac growth continued for over 30 d.