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Biomedical subjects

G Rodier

Publications and source records attributed to G Rodier.

At least 19 recordsLinked to original sources
PubMed2006

Two clusters of human infection with influenza A/H5N1 virus in the Republic of Azerbaijan, February-March 2006.

Following the appearance of influenza A/H5 virus infection in several wild and domestic bird species in the Republic of Azerbaijan in February 2006, two clusters of potential human avian influenza due to A/H5N1 (HAI) cases were detected and reported by the Ministry of Health (MoH) to the World Health Organization (WHO) Regional Office for Europe during the first two weeks of March 2006. On 15 March 2006, WHO led an international team, including infection control, clinical management, epidemiology, laboratory, and communications experts, to support the MoH in investigation and response activities. As a result of active surveillance, 22 individuals, including six deaths, were evaluated for HAI and associated risk infections in six districts. The investigations revealed eight cases with influenza A/H5N1 virus infection confirmed by a WHO Collaborating Centre for Influenza and one probable case for which samples were not available. The cases were in two unrelated clusters in Salyan (seven laboratory confirmed cases, including four deaths) and Tarter districts (one confirmed case and one probable case, both fatal). Close contact with and de-feathering of infected wild swans was considered to be the most plausible source of exposure to influenza A/H5N1 virus in the Salyan cluster, although difficulties in eliciting information were encountered during the investigation, because of the illegality of some of the activities that might have led to the exposures (hunting and trading in wild birds and their products). These cases constitute the first outbreak worldwide where wild birds were the most likely source of influenza A/H5N1 virus infection in humans. The rapid mobilisation of resources to contain the spread of influenza A/H5 in the two districts was achieved through collaboration between the MoH, WHO and its international partners. Control activities were supported by the establishment of a field laboratory with real-time polymerase chain reaction (RT-PCR) capacity to detect influenza A/H5 virus. Daily door-to-door surveillance undertaken in the two affected districts made it unlikely that human cases of influenza A/H5N1 virus infection remained undetected.

Azerbaijan↗
PubMed2005

[Emergent pathogens, international surveillance and international health regulations (2005)].

In order to address the vitality of the microbial world, to detect emerging infectious diseases, to determine their potential threat to public health, and to establish effective interventions, the World Health Organization (WHO) has developed and coordinates the Global Outbreak Alert and Response Network (GOARN) which connects several surveillance networks. Some of these networks are specific to epidemic-prone diseases, such as influenza, dengue, yellow fever or meningitis. Others were especially designed to track unusual events--such as the emergence of SARS--that are naturally-occurring, accidental, or deliberately created (biological weapons, bio-terrorism). Lastly, a special effort is being made at the international level to modernize the International Health Regulations, now obsolete, and to support all the countries in the reinforcement of their outbreak alert and response capacity.

Communicable Diseases, Emerging↗
PubMed2003

[Progression of cerebral venous thromboses. A retrospective study].

OBJECTIVES: The management of patients with presumed cerebral venous thrombosis has been recently modified by magnetic resonance imaging and evidence that the early use of heparin decreases mortality and morbidity. Long term outcome of patients with cerebral venous thrombosis (CVT) has rarely been described. We present the results of a follow-up study. METHODS: Twenty patients admitted between 1987 and 1999 for CVT were retrospectively studied. Outcome and follow-up were obtained from direct observation or telephone interviews. RESULTS: There were 16 women and 4 men aged a mean of 39 years (range: 19 to 72). The population was followed-up for a mean of 34 months (range: 12-96). All the patients were initially treated with full-dose heparin. Thirteen of the 20 patients (65%) exhibited no after effects. Seven patients (35%) remained neurologically impaired. The outcome of clinical forms with intracranial hypertension appeared better, but the existence of an initial neurological deficit is of poor prognosis. The small cohort in our series did not permit us to identify other poor prognostic factors. One patient (5%) exhibited subsequent epilepsy. Only one patient (5%) suffered for a second CVT. One patient died from an ovarian neoplasm. No systemic venous thromboembolic relapse was reported. Three patients had non complicated pregnancies. CONCLUSION: Recurrent CVT and systemic venous thrombo-embolic episodes are rare although heparin treatment was suspended early in more than half of the patients. This would question the indication of long-term antivitamin K, which is clearly indicated in auto-immune diseases but is debatable in cases of thrombophilia.

Adult↗
PubMed2002

[Thrombophilias associated with cerebral venous thrombosis].

Many coagulation disorders have been associated with cerebral venous thrombosis. These disorders may be primary like protein C and S deficiency, antithrombine III deficiency and activated protein C resistance. Antiphospholipid antibodies represent an acquired disorders of coagulation. A prothrombotic state induced by more common factor including oral contraceptive, pregnancy and puerperium increases the venous thrombosis risk.

3' Untranslated Regions↗
PubMed2001

p27 cytoplasmic localization is regulated by phosphorylation on Ser10 and is not a prerequisite for its proteolysis.

The activity of the cyclin-dependent kinase inhibitor p27 is controlled by its concentration and subcellular localization. However, the mechanisms that regulate its intracellular transport are poorly understood. Here we show that p27 is phosphorylated on Ser10 in vivo and that mutation of Ser10 to Ala inhibits p27 cytoplasmic relocalization in response to mitogenic stimulation. In contrast, a fraction of wild-type p27 and a p27(S10D)-phospho-mimetic mutant translocates to the cytoplasm in the presence of mitogens. G1 nuclear export of p27 and its Ser10 phosphorylation precede cyclin-dependent kinase 2 (Cdk2) activation and degradation of the bulk of p27. Interestingly, leptomycin B-mediated nuclear accumulation accelerates the turnover of endogenous p27; the p27(S10A) mutant, which is trapped in the nucleus, has a shorter half-life than wild-type p27 and the p27(S10D) mutant. In summary, p27 is efficiently degraded in the nucleus and phosphorylation of Ser10 is necessary for the nuclear to cytoplasmic redistribution of a fraction of p27 in response to mitogenic stimulation. This cytoplasmic localization may serve to decrease the abundance of p27 in the nucleus below a certain threshold required for activation of cyclin-Cdk2 complexes.

Alanine↗
PubMed2000

[Atypical phenotype of Fabry disease. Evidence of a new mutation].

BACKGROUND: Fabry disease is a lysosomal disease resulting from deficient alpha galactosidase A activity. The enzyme's gene is situated on Xq22-1. Cardiac and cerebrovascular complications are usually observed late in the disease course. CASE REPORT: A 54-year-old patient was admitted for ischemic stroke subsequent to thrombosis of the right sylvian artery. The only significant event in the patient's history was hypertrophic cardiomyopathy that had progressed for 9 years. Search for an etiology identified alpha galacosidase A deficiency. Gene sequencing identified a new mutation. DISCUSSION: Two clinical forms of Fabry disease are described. The classical form has an early onset and is associated with systemic manifestations. The less common atypical form is associated with late-onset cardiomyopathy with no other systemic manifestations. Several mutations of the alpha galactosidase A gene have been recognized but to date no correlation has been established between the genotype and the phenotype. Our patient had an "intermediary" form of the disease associating a late onset, predominant cardiac manifestations, and limited systemic manifestations. The mutation observed in this case has not been described previously. Its relationship with the observed clinical phenotype remains to be demonstrated.

Age of Onset↗
PubMed2000

[Ciguatera and peripheral neuropathy: a case report].

Ciguatera is the most frequently observed form of tropical fish poisoning. It appears as a syndrome associating general signs, gastrointestinal, cardiac and neurological problems. Peripheral and central nervous system signs may be observed. We report a case of a 60-year-old man who developed Ciguatera poisoning with diarrhea, facial paresthesia, myalgia, cramps and weakness. Physical examination revealed a motor distal deficit of the four limbs, myokymia and ataxia. EMG testing was in favor of an axonal neuropathy. Neurologic symptoms persisted for two months. This case illustrates a new pathophysiological mechanism of neuropathy: "axonal channelopathy. Abnormalities of peripheral nerve sodium and potassium channels result in clinical and electrophysiological manifestations unrelated to axonal degeneration or demyelinization. The ciguatoxin mainly acts on sodium channels. Prolonged sodium channel activation results in repetitive axon firing. Recently ciguatoxin was recently demonstrated to have a novel action, blocking the sodium channel leading to slowed nerve conduction and decreased motor and sensory action potential amplitudes.

Animals↗
PubMed2000

[Lysosome enzyme pseudodeficiency].

Inherited deficiency of lysosomal hydrolase often displays different clinical features. However, a greatly reduced enzyme activity may be observed in healthy individuals. This pseudo-deficiency concerns at least nine lysosomal hydrolases. When a deficiency has been proved, the presence of mutations known to cause pseudodeficiencies must be searched, above all in Tay-Sachs disease and metachromatic leukodystrophy.

Cerebroside-Sulfatase↗
PubMed1999

[Eales disease with neurologic manifestation: differential diagnosis of multiple sclerosis. Report of two cases].

BACKGROUND: Eales disease is a condition associating recurrent vitreous and retinal hemorrhage related to retinal periphlebitis. This ophthalmological disease is sometimes associated with central nervous system manifestations. CASE REPORT: Two patients with Eales disease of the retina developed a progressively worsening neurological deficit several years later. DISCUSSION: Evidence of multifocal anomalies of the white matter initially suggested a possible association of Earles disease with multiple sclerosis. Pathology findings enable formal differentiation of these two entities. Earles disease with neurological manifestations remains an uncommon condition and constitutes a differential diagnosis of multiple sclerosis.

Adult↗
PubMed1999

Ebola hemorrhagic fever: lessons from Kikwit, Democratic Republic of the Congo.

The outbreak of Ebola hemorrhagic fever in Kikwit, Democratic Republic of the Congo, clearly signaled an end to the days when physicians and researchers could work in relative obscurity on problems of international importance, and it provided many lessons to the international public health and scientific communities. In particular, the outbreak signaled a need for stronger infectious disease surveillance and control worldwide, for improved international preparedness to provide support when similar outbreaks occur, and for accommodating the needs of the press in providing valid information. A need for more broad-based international health regulations and electronic information systems within the World Health Organization also became evident, as did the realization that there are new and more diverse partners able to rapidly respond to international outbreaks. Finally, a need for continued and coordinated Ebola research was identified, especially as concerns development of simple and valid diagnostic tests, better patient management procedures, and identification of the natural reservoir.

Democratic Republic of the Congo↗
PubMed1999

Glicentin and oxyntomodulin modulate both the phosphoinositide and cyclic adenosine monophosphate signaling pathways in gastric myocytes.

We have investigated the transduction pathways mediating the contractile effect of two glucagon-containing peptides, glicentin (GLIC) and oxyntomodulin (OXM), on smooth muscle cells isolated from rabbit antrum. Low concentrations of GLIC induced a biphasic and rapid (first phase at 5-8 sec) Ins(1,4,5)P3 production. By comparison, higher concentrations of OXM or OXM(19-37) were required to obtain biphasic time-courses of Ins(1,4,5)P3 production. In a Ca2+ free medium, the first phase of Ins(1,4,5)P3 production induced by GLIC or OXM was maintained, while the second phase disappeared. In saponin-permeabilized cells, all three peptides induced cell contraction with similar efficacies and potencies. Exogenous Ins(1,4,5)P3 mimicked the contractile effect of the peptides and heparin, which inhibits the Ins(1,4,5)P3 binding to its receptor, prevented contraction stimulated by each effector. We conclude that a Ca2+ mobilization from the intracellular stores is essential in the contractile effects of GLIC and OXM. Using the fluo-3 probe, a [Ca2+]i increase was observed in the presence of GLIC, OXM, or OXM(19-37). The three peptides reduced by 30-40% the cAMP content of cells stimulated by forskolin. This effect was pertussis toxin sensitive as demonstrated with OXM(19-37). Our data constitute important clues for the existence in smooth muscle cells of receptor(s) specific for the GLIC/OXM hormones, coupled via G protein(s) to both Ca2+ and cAMP pathways.

Animals↗
PubMed1998

Oxyntomodulin reduces hydromineral transport through rat small intestine.

Glicentin (GLIC) and oxyntomodulin (OXM) are released from the ileum and colon during digestion. Both hormones reduce fluid and proton secretion in the stomach. The luminal concentration of sodium and chloride underlying the nutrient absorption, the effect of OXM on electrolyte transport through the small intestine, was assessed in vivo using ligated loops and in vitro using Ussing chambers. In vivo, a zero transport state, estimated by the net water, chloride, and sodium fluxes, was observed when an 80 mM NaCl normoosmolar solution (274 mosm) was administered intraluminally. Active secretion was observed with hyperosmotic challenge (474 mosm). The amplitude of this active secretion increased 2.5- to 3-fold when an electrogenic challenge (NaCl 40 mM) was substituted to the hyperosmotic one. OXM (800 fmol/ml plasma) did not modify the basal transport in the duodenum or in the jejunum (t = 45 min). When active secretion was induced by the hyperosmotic challenge, OXM (200 fmol/ml plasma) had no effect on duodenal or jejunal transport (t = 50 min). When active secretion was induced by an electrogenic challenge, OXM (300 fmol/ml plasma) preferentially reduced the hydromineral transport in jejunum. In vitro, OXM also induced a reduction in the ion transport towards the jejunal lumen (EC50 = 20 pM), the amplitude of which depended upon the integrity of the tetrodotoxin-sensitive neurons. In conclusion, OXM was able to reduce the large secretion induced in rat jejunum in vivo by an electrogenic gradient. In vitro, the antisecretory effect of OXM was partly mediated by the neurons present in the intrajejunal wall.

Animals↗