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Biomedical subjects

A Mebazaa

Publications and source records attributed to A Mebazaa.

At least 19 recordsLinked to original sources
PubMed2006

[Feasibility and technical problems of sentinel node analysis in melanoma].

BACKGROUND: Development of the sentinel lymph node (SLN) biopsy the last 10 years has changed surgical approach of solid tumor treatment and particularly of melanoma. The aim of our study was to analyze in our hospital, the feasibility of the SLN biopsy technique in order to define a better prognostic classification of melanomas. PATIENTS AND METHODS: Between July 1999 and October 2003, 97 patients were included in this study in our center. Criteria for inclusion were cutaneo-mucosal melanoma of Breslow >or=1,5 mm, and/or Clarck >or=IV, and/or ulceration, and/or signs of regression, before any surgical margins. RESULTS: Lymphoscintigraphy (LS) identified at least 1 SLN in 94 cases/97 (97%), thus permitting intraoperative SLN mapping and sentinel node biopsy of at least 1 lymph node in 88 cases/94 (94%). Failure of the SLN procedure was noted in 9 cases: in 3 cases, no lymph node was individualized by LS, in 1 patient, intraoperative SLN mapping failed to find the previously identified SLN and in 5 cases, a SLN was identified by LS and intraoperative mapping but could not be removed because of its deep location and difficulty of dissection. In 17 patients, removal of one or two "non sentinel lymph node(s)" was (were) made by the surgeon because of its (their) suspected aspect (black or large). Among the 88 patients who had dissection of at least 1 SLN, a micrometastasis was detected by standard histological evaluation and/or immunohistochemical stains in 14 cases (16%) and into a "non SLN" in 2 cases (2,3%). The median follow up of patients was 16 months (1- 48 months). Among the 14 patients with positive SLN, 6 (43%) relapsed. The other eight were in complete remission of their melanoma with a mean follow up of 11,44 months . Among the 74 patients with negative SLN, 7 (9,5%) developed a recurrence. Among the 9 patients in whom any sentinel lymph node have been removed, 3 had a relapse (one in transit than on lymph nodes, and two on lymph nodes). CONCLUSION: Our results are in accordance with the literature, and confirm the feasibility of SLN mapping and of SLN histological analysis in our center. We described in this study technical problems we encountered. Our study also show the prognostic value of this technique. However, advantage in global survey of sentinel node dissection and regional lymph node dissection in cases of micrometastases has still to be demonstrated.

Adolescent↗
PubMed2006

Chondroid syringoma of the arm: an unusual localization.

Chondroid syringoma (CS) is an uncommon, benign, sweat-gland tumor. The usual presentation is of an asymptomatic, slowly growing mass, typically located on the head and neck region. We present a case of a CS located in the right arm of a 43-year-old woman. This tumor developed slowly over 8 years. The diagnosis of CS was made by histopathological examination; it showed an abundant chondroid stroma intermingled with a fibro-adipoid tissue. There was no recurrence after total excision of the tumor with a 2-year followup. The unusual localization of chondroid syringoma made an accurate preoperative diagnosis difficult and diagnosis was achieved only by microscopy. Surgical tumor excision remains the best therapeutic option to avoid relapses of this tumor. Close followup is recommended because malignant transformation, although rare, is possible.

Adenoma, Pleomorphic↗
PubMed2006

[Homocysteinemia and coronary artery disease: a case-control study in a Tunisian population].

We have determined the prevalence of hyperhomocysteinemia and tested its relationship with coronary heart disease in Tunisian patients. The study included 70 angiogrphically proven coronary patients and 140 age- and sex-matched healthy subjects. Plasma homocysteine folate and vitamin B12 were analyzed by immunoenzymatic methods. Hyperhomocysteinemia was considered for plasma homocysteine concentration >17 micromol/L. Mean plasma homocysteine concentration and hyperhomocysteinemia prevalence were significantly (p<0.001) higher in patients (16.3 +/- 7.9 micromol/L and 29%) than controls (12.6 +/- 4.0 micromol/L and 10%). The association between hyperhomocysteinemia and coronary heart disease persisted after adjusting on main cardiovascular risk factors (multi adjusted odds ratio, 2.99; 95% CI, 1.18-7.59; p=0.02). No association was observed between hyperhomocysteinemia and coronary disease severity and extent. This study showed an independent association between hyperhomocysteinemia and coronary heart disease, suggesting a role of hyperhomocysteinemia in atherothrombogenesis. However, causal relationship is not yet established. Until results of homocysteine-lowering therapy trials become available, hyperhomocysteinemia should be researched and treated in coronary heart disease patients.

Case-Control Studies↗
PubMed2004

[Distribution of cardiovascular risk factors in a Tunisian cohort of 6901 coronary patients].

The Tunisian epidemiological data on cardiovascular disease in the hospital environment are scarce. The aim of this study was to evaluate the frequency of cardiovascular risk factors and their association in patients hospitalised for coronary disease in coronary care units at Rabta, Charles Nicolle, Habib Thameur and Military hospitals, Tunis, over the period 1994-1998. The clinical features of 6901 patients (75.7% men, 3760 myocardial infarction, 3141 unstable angina) on hospital admission were analysed. The prevalence of smoking, dyslipidemia, hypertension, diabetes and obesity was 86; 49.8; 33.9; 40.7 and 15.2% respectively in the men and 12.9; 52.4; 64.6; 53.4 and 29.8% respectively in women. With this risk factor profile Tunisia has to implement a national strategy of primary prevention and heart health promotion in addition to the efforts recently made in secondary prevention of some chronic disease such as hypertension, diabetes and smoking.

Adult↗
PubMed2003

Levosimendan: a new dual-action drug in the treatment of acute heart failure.

Levosimendan is a new agent for the treatment of acute heart failure. Levosimendan acts via complementary mechanisms; it enhances contractility by sensitising cardiac myofilaments to calcium and dilates blood vessels by opening ATP-dependent potassium channels. In contrast to traditional inotropes (beta-agonists or phosphodiesterase inhibitors), levosimendan does not raise myocyte calcium levels and is therefore less likely to elicit arrhythmias or to impair diastolic relaxation. The clinical efficacy of levosimendan is supported by four key clinical studies, including more than 900 patients hospitalised for cardiac decompensation due to acutely worsened chronic heart failure or to heart failure following myocardial infarction. When given as short-term therapy, levosimendan enhances cardiac output, reduces systemic vascular resistance and lowers pulmonary capillary wedge pressure. At 31 days post-treatment, mortality rates were halved in decompensated chronic heart failure patients who received levosimendan, compared with those on dobutamine--an advantage sustained at 180 days. Similar survival gains were observed among acute failure patients treated with levosimendan following myocardial infarction. With its substantial haemodynamic and survival benefits, levosimendan is well suited to be part of routine management for patients with acutely decompensated heart failure.

Acute Disease↗
PubMed2002

[Multiple keratoacanthoma centrifugum marginatum].

INTRODUCTION: Keratoacanthoma centrifugum marginatum is a rare variety of commonly isolated keratoacanthoma. The size of the lesions and prolonged evolution often raise therapeutic problems. CASE REPORT: A 63-year-old man presented with multiple keratoacanthoma centrifugum marginatum evolving for 6 months and predominating on the lower limbs. Because of the multiplicity and size of the lesions, the patient was treated at acitretine at the dose of 1 mg/kg/day for five months, leading to the regression of all the lesions. DISCUSSION: Keratoacanthoma centrifugum marginatum has rarely been reported in the literature. Our observation remains exceptional in the multiplicity and size of the lesions. The efficacy of retinoids, previously reported in the treatment of solitary giant keratoacanthoma, multiple keratoacanthoma and keratoacanthoma centrifugum marginatum, was demonstrated even in this handicapping form of keratoacanthoma.

Humans↗
PubMed2001

Activation of cardiac endothelium as a compensatory component in endotoxin-induced cardiomyopathy: role of endothelin, prostaglandins, and nitric oxide.

BACKGROUND: In view of growing evidence of an important endothelial paracrine regulation of cardiac function, the present study investigated the role of cardiac endothelium-derived endothelin-1 (ET-1), prostaglandins, and nitric oxide (NO) during endotoxin-induced cardiomyopathy in rabbits. METHODS AND RESULTS: Immunohistochemical studies showed a marked transient coinduction of the inducible isoforms of NO synthase (NOS-2) and cyclooxygenase (COX-2) in endocardial endothelium and coronary arteriolar endothelium of hearts 12 hours after intravenous administration of lipopolysaccharide (LPS+12h); staining for both isoforms was much weaker 24 hours later (LPS+36h). Nitrotyrosine localization was similar to that of NOS-2, suggesting a NOS-2-related endothelial formation of peroxynitrite in septic hearts. Contractile performance of papillary muscles was depressed in both LPS-treated groups. In the LPS+12h group, however, isometric twitches were significantly prolonged (482+/-14 versus 420+/-14 ms in the saline-treated group, P<0.005). This twitch prolongation was completely reversed by simultaneous administration of BQ-123 and indomethacin to block endogenous ET-1 and prostaglandins, respectively. In addition, in the LPS+12h group, myocardial inotropic responsiveness to exogenous ET-1 was enhanced (P<0.01). CONCLUSIONS: Cardiac endothelial activation and myocardial sensitization to endothelium-derived mediators may be part of an adaptive response in the early (12 hours) stages of septic cardiomyopathy.

Animals↗
PubMed2001

[Successful endovascular embolization in the vertebral artery after failed surgery in a patient with severe hemorrhagic shock].

Injury of the vertebral artery following penetrating trauma is rare and treatment is usually a surgical double ligation. We report a case of a 19-year old man, suffering from potentially fatal haemorrhage related to a penetrating trauma of the left vertebral artery. After failure of surgery, bleeding has been successfully stopped by endovascular embolization. The patient did not suffer any ischaemic cerebral complication and was discharged from intensive care unit 24 hours later.

Adult↗
PubMed2001

Sepsis is associated with reciprocal expressional modifications of constitutive nitric oxide synthase (NOS) in human skeletal muscle: down-regulation of NOS1 and up-regulation of NOS3.

OBJECTIVE: To study the expression (mRNA and protein) and activity of the constitutive isoforms of nitric oxide synthase (NOS1 and NOS3) in a skeletal muscle of septic patients. DESIGN: Prospective study. SETTING: An adult trauma/surgical intensive care unit in an urban teaching hospital. PATIENTS: Sixteen septic patients and 21 controls. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Samples of the rectus abdominis muscle were obtained during surgical procedure. NOS mRNA, protein, and activity were detected by reverse-transcriptase polymerase chain reaction, Western blot, and the conversion of [3H]L-arginine to [3H]L-citrulline, respectively. The main results of this study are as follows: a) Levels of NOS1 mRNA and protein were significantly higher than those of NOS3 in the rectus abdominis muscle of control patients; b) NOS1 expression was down-regulated in septic patients, whereas NOS3 was up-regulated; c) these modulations were associated with a reduction in constitutive NOS activity; and d) modifications of NOS1 and NOS3 protein expression were correlated significantly with the severity of sepsis, assessed by the Simplified Acute Physiology Score II. CONCLUSIONS: Sepsis induces reciprocal expressional modifications of NOS1 and NOS3 in human skeletal muscle, which decreases muscular constitutive NOS activity. These modifications may have implications for muscle impairment in septic patients.

Caenorhabditis elegans Proteins↗
PubMed2001

Phosphorylation-dependent alteration in myofilament ca2+ sensitivity but normal mitochondrial function in septic heart.

The subcellular mechanisms responsible for myocardial depression during sepsis remain unclear. Recent data suggest a role for impaired energy generation and utilization, resulting in altered contractile function. Here, we studied the energetic and mechanical properties of skinned fibers isolated from rabbit ventricle in a nonlethal but hypotensive model of endotoxemia. Thirty-six hours after lipopolysaccharide (LPS) injection (in the presence of altered myocardial contractility), mitochondrial respiration, coupling between oxidation and phosphorylation, and creatine kinase function were similar in preparations from endotoxemic (LPS) and control animals. The maximal Ca2+-activated force was similar in LPS and control preparations. However, the Ca2+ concentration corresponding to half-maximal force (pCa50, where pCa = -log10[Ca2+]) was 5.55 +/- 0.01 (n = 11) in LPS fibers versus 5.61 +/- 0.01 (n = 10) in control fibers (p < 0.01). Both protein kinase A (PKA) and alkaline phosphatase treatment led to the disappearance in the difference between control and LPS pCa50 values. Incubation of control fibers with the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) did not change the Ca2+ sensitivity after subsequent skinning, whereas isoproterenol decreased pCa50 from 5.62 +/- 0.01 to 5.55 +/- 0.01 (p < 0.01). These data suggest that during sepsis, cardiac mitochondrial and creatine kinase systems remain unaltered, whereas protein phosphorylation decreases myofibrillar Ca2+ sensitivity and may contribute to the depression of cardiac contractility.

Actin Cytoskeleton↗
PubMed2001

Prolactin levels in Behçet's disease: no correlation with disease manifestations and activity.

OBJECTIVE: To assess prolactin level and its possible role in the pathogenesis and disease expression of patients with Behçet's disease (BD). MATERIALS AND METHODS: Twenty-eight patients with the diagnosis of Behçet's disease were selected. They all fulfilled the international criteria for BD. The control group consisted of 17 males and 6 females. Patients are divided into subgroups according to the clinical and paraclinical characteristics such as disease duration, ocular, articular and neurological involvement. Serum prolactin was measured by ELISA using Merck Kits on a Maggia 7000 Analyser. The normal range in males was<17ng/ml in males and<18ng/ml in females. The mean PRL level in each group and subgroup was calculated and compared with Student's t test. RESULTS: The mean prolactin level in the BD group (mean=13.76, SD=6.82), was higher than in the control group (mean=10.13, SD=5.46) with no statistically significant difference. The mean prolactin levels in all subgroups of patients with BD were higher than normal, but no statistically significant difference was shown between these subgroups. CONCLUSION: Hyperprolactinemia occurred in a small number of patients with BD and its significance remained unclear. Serum PRL level did not correlate with disease manifestations and activity.

Adolescent↗
PubMed2001

[Vitamin E: structure, metabolism, and functions].

Vitamin E is a generic term denoting eight different isomers among which alpha-tocopherol is the most important and most active. Vitamin E metabolism is closely linked to lipids during intestinal absorption, plasma secretion and transport, and tissue uptake. It is a key compound involved in many physiological processes, such as neurological and immune functions. The most common role of vitamin E is its antioxidant effect, protecting molecules and tissues against the deleterious effect of free radicals. Vitamin E also contributes to the stabilization of biological membranes. In addition, it intervenes in the regulation of several enzymes and probably has impact on gene expression. Advancing knowledge about vitamin E has been achieved with high performance liquid chromatography, making assay accessible to many laboratories, and the use of deuterated derivatives to better apprehend its metabolism. Certain issues remain unresolved concerning the molecular basis of vitamin E's mechanism of action and the exact nature of metabolic dysfunction leading to the clinical manifestations of severe vitamin E deficiency.

Humans↗
PubMed2001

[Vitamin E deficiency. Etiopathogenesis, clinical, histopathologic, and electrical features, and main etiologies].

Vitamin E deficiency is frequently observed in human pathology. In most cases, deficiency is moderate and asymptomatic. Severe deficiency is rare and presents as a progressive neurological syndrome including cerebellar ataxia and posterior cord injury. Neuropathological and electrophysiological features confirm spinocerebellar degeneration. The pathophysiology of vitamin E deficiency nervous dysfunction is still unknown. Oxidative alterations due to the lack of the main lipid-soluble antioxidant could be involved. A few causes of vitamin E deficiency are recognized (malnutrition, impaired lipid absorption, specific anomaly of hepatic or intestinal secretion of vitamin E, excessive endogenous consumption), but diseases associated with vitamin E deficiency are numerous and divers. Symptomatic severe deficiency is constantly observed in ataxia with vitamin E deficiency and abetalipoproteinemia. Intestinal, hepatobiliary, and pancreatic diseases are often associated with more or less marked deficiency. Other pathological circumstances such as malnutrition, alcoholism, hemolytic anemia, renal failure and hemodialysis could be associated with moderated and asymptomatic vitamin E deficiency. Oral or regular administration of high-dose vitamin E is required for patients with symptomatic severe deficiency. An adapted supplementation is recommended for patients with a marginal vitamin E status.

Electrophysiology↗
PubMed2001

[Vitamin E deficiency: risk factor in human disease?].

Oxidative stress is suspected to intervene in certain chronic diseases. Much research has been devoted to the relationship between vitamin E, a major lipid-soluble antioxidant, and certain widespread diseases. Experimental and epidemiological proof supports a protective effect of vitamin E in a number of pathological processes such as coronary heart disease, cancer, cataract, diabetes mellitus, and Alzheimer disease. Randomized clinical trials have not confirmed a beneficial effect of vitamin E supplementation on the progression of these diseases. Certain methodological biases could however have affected these studies, explaining conflicting results. These biases include inaccuracy of vitamin E intake estimates and changes in eating habits during the course of the survey. An insufficient supplementation period using an insufficient dose and inclusion of aged and high-risk patients are the main limitations of the reported clinical trials. Large scale randomized clinical trials including healthy and low-risk subjects, along with prolonged administration of high-dose natural vitamin E, associated with synergetic compounds, and testing on morphological or biological features, will allow a better understanding of the relationship between vitamin E and chronic diseases.

Cardiovascular Diseases↗
PubMed2000

Cardiac contractile impairment associated with increased phosphorylation of troponin I in endotoxemic rats.

The subcellular mechanisms underlying intrinsic myocardial depression during sepsis remain poorly defined, in particular the relative roles of altered intracellular Ca2+ transients versus changes in myofilament properties. We studied contractile function of cardiac myocytes isolated 12 h after induction of endotoxemia (5 mg/kg intravenous E. coli lipopolysaccharide [LPS]) in conscious rats. Cardiomyocytes from LPS-injected rats had depressed twitch shortening compared with control cells (4.10.2% versus 7.80.3%; P2+ transients (peak indo-1 ratio 1.130.02 versus 1.120.02; P = NS). Contractile depression was unaffected by inhibitors of nitric oxide synthase. Steady-state myofilament response to Ca2+, assessed by tetanization of intact cells over a range of [Ca2+], was reduced significantly in the LPS group (P2+ was unaffected by isoproterenol (3 nmol/L) in endotoxemic cells, whereas there was a rightward shift in control cells. A reduction in myofilament response to Ca2+ is the major determinant of intrinsic cardiac depression in systemic endotoxemia. This condition appears to be related to an increase in myocardial troponin I phosphorylation.

Actin Cytoskeleton↗