[Epidemiology of out-of-hospital sudden cardiac arrest in « Basse-Normandie ¼ according to RéAC registry]. / Épidémiologie des arrêts cardiaques extrahospitaliers recensés en Basse-Normandie par le registre RéAC.

OBJECTIVE: Identify from the RéAC registry, out-of-hospital sudden cardiac arrest in Caen and it's suburbs, to study epidemiology and assess our medical practices. STUDY DESIGN: Observational, prospective and monocentric study. PATIENTS AND METHODS: From March 2012 to March 2013, we identified 151 patients. Demographic parameters, delays until treatment, drugs given and patient outcomes were analyzed from the RéAC data registry. Depending on the variable studied, the statistical analysis used Mann-Whitney or the Chi(2) tests. RESULTS: Twenty-two patients were excluded (no resuscitation attempt and patients who were transported to hospital with chest compressions only, in the absence of spontaneous circulation). One hundred and twenty-nine sudden cardiac arrests were analyzed: 107 (83%) with medical origin and 22 (17%) with traumatic origin. Direct witnesses were present for 94 (73%) of them. Basic life support actions were begun for 59 (46%) patients and a telephone advice was issued by the medical response team for 47 (36%) of them. After an advanced life support, 74 (57%) patients died on the spot. Of the 55 patients reaching the hospital alive, 39 (71%) died in the intensive care unit and 16 (29%) were discharged alive from hospital, of whom 14 (88%) with a favorable neurological outcome. CONCLUSION: RéAC national registry has allowed us to analyze epidemiological data on out-of-hospital sudden cardiac arrests in our center. This register has also allowed us to highlight areas for improvement. They should be taken into account to improve our medical practices.

Is Vacuum Assisted Closure a valid technique for debriding chronic leg ulcers?

OBJECTIVE: Between May 2001 and October 2002 a prospective controlled open non-comparative study was performed to assess the effectiveness of topical negative pressure in the fibrinous debridement of chronic leg ulcers. METHOD: Fifteen leg ulcers that had not responded to several other treatment modalities were treated with the Vacuum Assisted Closure system (KCI) for six days. RESULTS: The median percentage reduction in fibrinous tissue was 28% on day three and 40% on day six. Between days one and three the percentage change was > or = 50% in four patients and > or = 25% in six patients. Between days three and six percentages of fibrin in the wound were lower in all patients, except for two who had higher percentages and two who had the same percentage. CONCLUSION: VAC therapy was rapidly efficacious, promoting angiogenesis and the formation of healthy tissue.

Towards an odor communication system.

We propose a setup for an odor communication system. Its different parts are described, and ways to realize them are outlined. Our scheme enables an output device-the whiffer-to release an imitation of an odorant read in by an input device-the sniffer-upon command. The heart of the system is the novel algorithmic scheme that makes the scheme feasible. We are currently at work researching and developing some of the components that constitute the algorithm, and we hope that the description of the overall scheme in this paper will help to get other groups to join in this effort.

Lactic dehydrogenase isoenzyme in cerebrospinal fluid of children with febrile convulsions.

AIM: To study the lactic dehydrogenase isoenzyme values in children with simple and complex febrile convulsions. METHODS: Cerebrospinal fluid samples were collected from 115 children, 57 with simple febrile convulsions, 27 with complex febrile convulsions and 31 with no neurological or intracranial pathology (controls). Lactic dehydrogenase activity and isoenzyme levels were measured on a Hitachi analyser. RESULTS: Mean total lactic dehydrogenase activity was similar in the three groups. In the control group, lactic dehydrogenase-1 was the main fraction, followed by lactic dehydrogenase-2 and lactic dehydrogenase-3; only small percentages of lactic dehydrogenase-4 and lactic dehydrogenase-5 were detected. In the febrile convulsion group, the lactic dehydrogenase-1 fraction percentage was lower and lactic dehydrogenase-2, lactic dehydrogenase-3 percentages were higher than those in the control group; and the differences were statistically significant between the control and study groups (p < 0.01). Values of lactic dehydrogenase-4 and lactic dehydrogenase-5 were similar in all three groups. CONCLUSION: This is the first report on the lactic dehydrogenase isoenzyme pattern in the cerebrospinal fluid of patients with simple and complex febrile convulsions. The important finding that focal and general febrile convulsions are not associated with cell damage and changes in aerobic and anaerobic metabolism as lactic dehydrogenase remained unchanged. Analysis of cerebrospinal fluid lactic dehydrogenase isoenzyme levels can assist clinicians in differentiating febrile convulsions from clinical situations that might mimic them.

Lactic dehydrogenase isoenzymes in cerebrospinal fluid of children with Guillain-Barré syndrome.

BACKGROUND: Increased levels of lactic dehydrogenase (LDH) in the cerebrospinal fluid (CSF) have been reported in association with several intracranial pathologies. No studies have been performed on patients with Guillain-Barré syndrome (GBS). AIMS: To study LDH isoenzymes in CSF of children with GBS. METHODS: CSF samples collected from nine patients with GBS were analysed for total LDH isoenzymes activity, and compared to samples from 15 patients with normal results. RESULTS: Mean total LDH activity was 33.33 (6.63) U/l. All patients had significantly increased LDH-3 isoenzyme compared to controls. LDH-3 was the predominant fraction, accounting for more than 50% of total LDH activity and present in more than twice the percentage of LDH-1 or LDH-2. By contrast, in the control group, there were high percentages of mainly LDH-1 and LDH-2. CONCLUSIONS: GBS is apparently associated with a distinct LDH isoenzyme pattern in the CSF. More studies are needed to confirm the rise in LDH-3, as serial CSF analyses are unavailable, and to determine the optimum time of analysis when this finding first becomes detectable.

Estimating the size of the olfactory repertoire.

The concept of shape space, which has been successfully implemented in immunology, is used here to construct a model for the discrimination power of the olfactory system. Using reasonable assumptions on the behaviour of the biological system, we are able to estimate the number of distinct olfactory receptor types. Our estimated value of around 1000 receptor types is in good agreement with experimental data.

Changes in vesicular monoamine transporter (VMAT2) and synaptophysin in rat Substantia nigra and prefrontal cortex induced by psychotropic drugs.

We investigated the regulatory effect of the dopaminergic agent L-dopa, the mood stabilizer lithium and the nonselective monoamine oxidase inhibitor phenelzine on brain vesicular monoamine transporter (VMAT2) expression. Rats were treated chronically (21 days) with the three psychoactive drugs. VMAT2 gene expression at the protein level was assessed in the prefrontal cortex and striatum by autoradiography with high-affinity [(3)H]dihydrotetrabenazine ([(3)H]TBZOH) binding and at the mRNA level in the substantia nigra pars compacta by in situ hybridization. In addition, the effect of various treatments on the synaptophysin mRNA level was determined in the substantia nigra by in situ hybridization. Chronic administration of L-dopa resulted in a significant decrease (28%, p < 0.05) in the density of [(3)H]TBZOH binding in the prefrontal cortex but had no effect on VMAT2 and synaptophysin mRNA levels in the substantia nigra. Lithium treatment increased [(3)H]TBZOH-specific binding in the prefrontal cortex (23%, p < 0.05) but had no effect on VMAT2 and synaptophysin mRNA levels. Phenelzine did not modulate VMAT2 gene expression but reduced the synaptophysin mRNA level (19%, p < 0.05). The modulatory activities of these drugs, although relatively weak, may be relevant to the drug-induced synaptic and neuronal plasticity as well as to the molecular and cellular pathophysiology of monoamine-related neuropsychiatric disorders.

Lactic dehydrogenase isoenzymes in cerebrospinal fluid associated with hydrocephalus.

UNLABELLED: Various neurological disorders are associated with specific changes in the level of total lactic dehydrogenase and concentrations of its isoenzymes in the cerebrospinal fluid. We describe the lactic dehydrogenase isoenzyme values in children with hydrocephalus. Cerebrospinal fluid samples collected from 10 patients (2 to 16 mo) with hydrocephalus were analysed for total lactic dehydrogenase activity and lactic dehydrogenase isoenzymes. Findings were compared with those in samples from 15 paediatric patients, with normal results. Mean total lactic dehydrogenase activity in the cerebrospinal fluid was significantly higher in the patients with hydrocephalus (101 +/- 23.11 U/L) than in the controls (33.53 +/- 5.75 U/L) (p <0.001). In the control samples, lactic dehydrogenase-1 was the main fraction, followed by lactic dehydrogenase-2 and 3; only small concentrations of lactic dehydrogenase-4 and lactic dehydrogenase-5 were detected. By contrast, patients with hydrocephalus had lower concentrations of the lactic dehydrogenase-1 fraction and higher lactic dehydrogenase-2 and lactic dehydrogenase-3 concentrations, the differences between these results and those in the control group being statistically significant (p < 0.001). The values for lactic dehydrogenase-4 and lactic dehydrogenase-5 were similar in both groups. CONCLUSION: Findings should be considered together with computed tomography/magnetic resonance imaging and ultrasound scans. The cerebrospinal fluid lactic dehydrogenase profile may prove to be an important predictor of cerebral injury, obstructive hydrocephalus and long-term neurodevelopmental problems.

The effect of estrogen replacement therapy on plasma serotonin and catecholamines of postmenopausal women.

We examined the effect of estrogen replacement therapy (ERT) on plasma serotonin (5HT) and norepinephrine (NE) and their correlation with serum estradiol, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in 12 postmenopausal women. Plasma 5HT and NE, estrogen, progesterone, LH and FSH were examined every 4 days for 2 consecutive months (before and during ERT). Serotonin values were low (32.29 +/- 38.36 nmol/l) and showed an intrinsic spontaneous cyclicity with a nadir every 10-11 days. Plasma NE was similar to that observed during the follicular phase of the ovulatory cycle (1,216.8 +/- 503.4 pmol/l) and showed no cyclicity. ERT significantly increased mean (+/- SD) serum estrogen values (from 95.40 +/- 73.31 to 390.72 +/- 347.17 pmol/l, P = 0.0001), significantly decreased serum FSH (from 84.04 +/- 14.97 to 52.97 +/- 20.74 mIU/ml, P = 0.0001) and LH (from 35.35 +/- 13.82 mIU/ml to 29.69 +/- 16.46 mIU/ml, P = 0.03). Plasma 5HT levels showed a tendency to rise under the influence of ERT, but this increase was not statistically significant. Plasma NE decreased significantly from 1,216.8 +/- 503.4 to 994.1 +/- 353.89 pmol/l, P <0.05. In conclusion, plasma serotonin in postmenopausal women has a 10-11 day cycle and is significantly lower than in the follicular phase of ovulating women. Plasma NE shows no cyclicity and is significantly decreased by ERT.

Mutations in the SLC3A1 transporter gene in cystinuria.

Cystinuria is an autosomal recessive disease characterized by the development of kidney stones. Guided by the identification of the SLC3A1 amino acid-transport gene on chromosome 2, we recently established genetic linkage of cystinuria to chromosome 2p in 17 families, without evidence for locus heterogeneity. Other authors have independently identified missense mutations in SLC3A1 in cystinuria patients. In this report we describe four additional cystinuria-associated mutations in this gene: a frameshift, a deletion, a transversion inducing a critical amino acid change, and a nonsense mutation. The latter stop codon was found in all of eight Ashkenazi Jewish carrier chromosomes examined. This report brings the number of disease-associated mutations in this gene to 10. We also assess the frequency of these mutations in our 17 cystinuria families.

Localization of a gene causing cystinuria to chromosome 2p.

Cystinuria is an autosomal recessive disorder of amino acid transport. It is a common hereditary cause of kidney stones worldwide, and is associated with significant morbidity. In 17 affected families, we found linkage between cystinuria and three chromosome 2p markers. Maximal two-point lod scores between cystinuria and D2S119, D2S391 and D2S288 were 8.23 (theta = 0.07), 3.73 (theta = 0.15) and 3.03 (theta = 0.12), respectively. Analysis of recombinants and multipoint linkage data indicated that the most likely order is cen-D2S391-D2S119-cystinuria-D2S177-tel. We also observed high rates of homozygosity for markers in this chromosomal region among 11 affected offspring of consanguineous marriages. Based on its map position and function, the recently cloned SLC3A1 amino acid transporter gene is a primary candidate gene for this disease.

The effect of vigabatrin on central nervous system oxygen toxicity in rats.

The toxicity of hyperbaric oxygen in the central nervous system is expressed by clinical and electroencephalographic (EEG) manifestations resembling those of generalized tonic-clonic seizures. In the search for drugs effective against these seizures, we tested vigabatrin, an irreversible inhibitor of GABA (gamma-aminobutyric acid) transaminase. Five different doses of vigabatrin (ranging from 50 to 500 mg/kg) or vehicle were injected i.p. in rats implanted with cortical electrodes, 4 h prior to exposure to 5 ATA (0.5 MPa) oxygen. EEG and spectral analysis of the background EEG activity were monitored for the different dosages of the drug. The duration of the latent period before the appearance of electrical discharges in the EEG was used as an index of oxygen toxicity. The protective effect of vigabatrin was dose-related, and complete protection against hyperoxic-induced discharges was at 180 mg/kg. The protective effect lasted 24 h and decreased gradually disappearing completely on the third day. An increase in the low frequency bands of the EEG and a decrease in the faster activity were correlated with the vigabatrin dosage injected. Our results suggest that vigabatrin has the potential of being a useful drug in the treatment and prevention of oxygen-induced seizures during hyperbaric oxygen therapy.

Myelopathy as a complication of diabetes mellitus.

Clinical signs of spinal cord involvement in diabetes mellitus have gained very little attention in the past four decades. On the other hand many pathological studies have shown spinal cord lesions in diabetic patients. We report 12 diabetic patients with clinical signs of myelopathy which, per exclusion, could be explained only as related to diabetes mellitus. Posterior column lesions were more common than corticospinal tract involvement. All our patients had combined peripheral sensory polyneuropathy with myelopathic signs. The combination of peripheral neuropathy, disturbed sense of position and/or vibration with pyramidal signs is highly suggestive of diabetic myelopathy with polyneuropathy. Even though myelopathy is not common in diabetic patients, it is one of the most debilitating neurological complications of diabetes mellitus. We believe that there is enough pathological and clinical evidence to accept the concept of diabetic myelopathy, especially with its prognostic and rehabilitative implications.

Cimetidine as an immunomodulator in the treatment of herpes zoster.

As there is evidence of a possible immunoregulatory role for H2-histamine receptor antagonists, we carried out a prospective randomized trial to evaluate the in vivo and in vitro effect of cimetidine, an H2-blocker, in the treatment of herpes zoster infection. Cimetidine treatment shortened the median interval until the first decrease in pain, the median interval until the complete resolution of pain and promoted faster complete healing of skin lesions than symptomatic treatment. The immunological trends observed in vitro support an important role for histamine in the induction of immunosuppression, as measured by the response to the mitogen phytohemagglutinin. This effect of histamine was antagonized by cimetidine.

Changes in creatine kinase activity in the course of acute myocardial infarction.

Peak activity of creatine kinase (CK; EC 2.7.3.2) and its decline were determined in 380 patients with acute myocardial infarction (AMI) whose CK values had peaked after admission to the hospital. During hospitalization, 26 patients either died (14 patients) or experienced nonfatal re-infarction (12 patients). In 22 of these 26 patients CK activity decreased by less than 50% within 48 h after the peak value was measured. In all patients who did not die or develop re-infarction, CK activity decreased by greater than 50% during the 48 h after the peak. Evidently the rate of decline of CK (i.e., whether more than or less than 50%) from its peak value during the 48 h after AMI may be helpful in assessing which patients are at high risk for developing re-infarction or dying.

A 3D building blocks approach to analyzing and predicting structure of proteins.

A new approach is introduced for analyzing and ultimately predicting protein structures, defined at the level of C alpha coordinates. We analyze hexamers (oligopeptides of six amino acid residues) and show that their structure tends to concentrate in specific clusters rather than vary continuously. Thus, we can use a limited set of standard structural building blocks taken from these clusters as representatives of the repertoire of observed hexamers. We demonstrate that protein structures can be approximated by concatenating such building blocks. We have identified about 100 building blocks by applying clustering algorithms, and have shown that they can "replace" about 76% of all hexamers in well-refined known proteins with an error of less than 1 A, and can be joined together to cover 99% of the residues. After replacing each hexamer by a standard building block with similar conformation, we can approximately reconstruct the actual structure by smoothly joining the overlapping building blocks into a full protein. The reconstructed structures show, in most cases, high resemblance to the original structure, although using a limited number of building blocks and local criteria of concatenating them is not likely to produce a very precise global match. Since these building blocks reflect, in many cases, some sequence dependency, it may be possible to use the results of this study as a basis for a protein structure prediction procedure.