[Impact of the summer 2003 heat wave on the activity of two psychiatric emergency departments]. / Impacto de la ola de calor del verano 2003 en la actividad de dos servicios de urgencias psiquiátricas.

INTRODUCTION: Heat waves have been related with lethal effects, especially in Europe during the intensely hot summer of 2003. However, besides increased deaths and ailments, there are no specific data on the psychiatric effects of heat waves. METHODS: We have compared psychiatric emergencies in Barcelona during a 15-day heat waves period with the rest of the 2003 summer days. The main variables of the study were total emergencies, admissions, diagnoses, Severity of Psychiatric Illness scale (SPI), psychosocial variables, treatment rendered (including use of restraints), and referrals. RESULTS: No differences were found in the number of emergencies and admissions. During the heat wave, there were more patients with psychiatric backgrounds, more diagnoses of alcohol and drug abuse, but fewer anxiety disorders. The proportion of patients with mechanical restraint increased, but this only occurred in half of the cases in patients with drug or alcohol abuse. The item "dangerousness toward others" (part of the SPI scale) scored significantly higher during the heat waves. CONCLUSIONS: There were no significant increases or decreases in psychiatric emergencies or admissions. However, the heat wave was related to more violent behavior and higher drug and alcohol abuse. It should be noted that anxiety conditions and benzodiazepine prescriptions were lower during this period. These findings may be useful to implement medical-psychiatric preventive measures against the heat wave phenomenon.

Impacto de la ola de calor del verano 2003 en la actividad de dos servicios de urgencias psiquiátricas / Impact of the summer 2003 heat wave on the activity of two psychiatric emergency departments

Introducción. La ola de calor se ha relacionado con efectos letales, especialmente en Europa durante el caluroso verano de 2003. Pero aparte del incremento de muertes y enfermedades, no existen datos específicos de los efectos psiquiátricos de la ola de calor. Metodología. Se compararon las urgencias psiquiátricas de dos hospitales de Barcelona durante los 15 días de la ola de calor con el resto del verano de 2003. Las principales variables del estudio fueron: urgencias totales, ingresos, diagnósticos, gravedad, variables psicosociales, tratamientos aplicados (incluyendo contención mecánica), y derivaciones. Resultados. No se encontraron diferencias en el número de urgencias ni de ingresos. Durante la ola de calor, hubo más pacientes con antecedentes psiquiátricos, más diagnóstico de abuso de alcohol y drogas, pero menos trastornos de ansiedad. También aumentó la proporción de pacientes con sujeción mecánica, pero sólo en la mitad de casos, esto ocurrió en pacientes con abuso de alcohol o drogas. El ítem «peligro hacia los demás» de la escala de gravedad se puntuó significativamente más alto en la ola de calor. Conclusiones. No hubo incrementos o disminuciones significativos en urgencias o los ingresos psiquiátricos, aunque los que acudieron tenían más antecedentes psiquiátricos. Durante la ola de calor hubo un cierto incremento significativo de violencia y de abuso de alcohol y drogas, pero menor porcentaje de trastornos de ansiedad y menos prescripciones de benzodiazepinas durante este período. Estos datos exploratorios indican el interés de considerar medidas preventivas médico psiquiátricas frente al fenómeno de la ola de calor (AU)

Introduction. Heat waves have been related with lethal effects, especially in Europe during the intensely hot summer of 2003. However, besides increased deaths and ailments, there are no specific data on the psychiatric effects of heat waves. Methods. We have compared psychiatric emergencies in Barcelona during a 15-day heat waves period with the rest of the 2003 summer days. The main variables of the study were total emergencies, admissions, diagnoses, Severity of Psychiatric Illness scale (SPI), psychosocial variables, treatment rendered (including use of restraints), and referrals. Results. No differences were found in the number of emergencies and admissions. During the heat wave, there were more patients with psychiatric backgrounds, more diagnoses of alcohol and drug abuse, but fewer anxiety disorders. The proportion of patients with mechanical restraint increased, but this only occurred in half of the cases in patients with drug or alcohol abuse. The item «dangerousness toward others» (part of the SPI scale) scored significantly higher during the heat waves. Conclusions. There were no significant increases or decreases in psychiatric emergencies or admissions. However, the heat wave was related to more violent behavior and higher drug and alcohol abuse. It should be noted that anxiety conditions and benzodiazepine prescriptions were lower during this period. These findings may be useful to implement medical-psychiatric preventive measures against the heat wave phenomenon (AU)

Construction and biological properties of yellow fever 17D/dengue type 1 recombinant virus.

Dengue virus, a mosquito-borne flavivirus, is one of the most formidable public health threats in tropical and subtropical regions. As yet, there is no licensed vaccine to protect against the disease. A chimeric yellow fever (YF) 17D/dengue (DEN) type 1 virus was constructed by replacing the pre-membrane and envelope genes of YF 17D virus with those from DEN 1 VeMir95 virus, a Venezuelan isolate. The chimeric YF 17D/DEN 1 VeMir95 virus was regenerated from full-length infectious clones stably propagated in Escherichia coli by transfection of Vero cells with in vitro transcribed RNA. The chimeric virus proliferated efficiently in Vero cells ( approximately 6.6 log(10) plaque-forming units/ml). The chimeric virus was not neurovirulent to 3-week-old Swiss Webster mice inoculated by the intracerebral route, in contrast to the YF 17DD vaccine strain that was lethal for 90% of the mice. The YF 17D/DEN 1 virus at Passage 6 was more attenuated for rhesus monkeys than the YF 17DD commercial vaccine after intracerebral inoculation according to the standard neurovirulence test. This virus is a potential candidate to be included in a tetravalent DEN vaccine formulation. The availability of the cloned cDNA allows further structure/function studies on the viral envelope.

Intrinsic resistance of Mycobacterium smegmatis to fluoroquinolones may be influenced by new pentapeptide protein MfpA.

The fluoroquinolones (FQ) are used in the treatment of Mycobacterium tuberculosis, but the development of resistance could limit their effectiveness. FQ resistance (FQ(R)) is a multistep process involving alterations in the type II topoisomerases and perhaps in the regulation of efflux pumps, but several of the steps remain unidentified. Recombinant plasmid pGADIV was selected from a genomic library of wild-type (WT), FQ-sensitive M. smegmatis by its ability to confer low-level resistance to sparfloxacin (SPX). In WT M. smegmatis, pGADIV increased the MICs of ciprofloxacin (CIP) by fourfold and of SPX by eightfold, and in M. bovis BCG it increased the MICs of both CIP and SPX by fourfold. It had no effect on the accumulation of (14)C-labeled CIP or SPX. The open reading frame responsible for the increase in FQ(R), mfpA, encodes a putative protein belonging to the family of pentapeptides, in which almost every fifth amino acid is either leucine or phenylalanine. Very similar proteins are also present in M. tuberculosis and M. avium. The MICs of CIP and SPX were lower for an M. smegmatis mutant strain lacking an intact mfpA gene than for the WT strain, suggesting that, by some unknown mechanism, the gene product plays a role in determining the innate level of FQ(R) in M. smegmatis.

Modulation of glutamate neurotoxicity on mesencephalic dopaminergic neurons in primary cultures by the presence of striatal target cells.

Glutamate toxicity was compared in substantia nigra (SN)/striatum (STR) and SN/cerebellum (CRB) co-cultures on both the entire neuronal population (neuron specific enolase (NSE) immunopositive cells) and dopaminergic neurons (tyrosine hydroxylase (TH) immunopositive cells). In SN/CRB co-cultures NSE- and TH-positive cells were more sensitive to glutamate-induced toxicity than in SN/STR co-cultures. Moreover, in SN/STR co-cultures as compared to SN/CRB and SN cultures, glutamate toxicity was prevented to a larger extent by TCP, a non-competitive NMDA antagonist. These results suggest that target cells induce a differential expression of the different glutamate receptor subtypes in mesencephalic dopaminergic cells. Alternatively, the presence of target cells may induce the selective development of a subpopulation of dopaminergic neurons expressing predominantly NMDA receptors.

Comparison of glutamate and N-methyl-D-aspartate toxicities on rat mesencephalic primary cell cultures.

Excitotoxicities of glutamate and NMDA were studied on primary cultures of rat embryonic substantia nigra. The toxicity of the general neuronal population (identified with neuron specific enolase-NSE) was compared with that of dopaminergic neurons (identified with TH antibodies). We have shown that there exists a time-dependent toxicity to glutamate in 9 d old cultures in vitro and exposures as short as 5 min are significantly toxic. By comparing the effects of long time exposures (24 h) to NMDA and glutamate, we can show dose-dependent toxicity; however NMDA shows a less marked effect, especially at high doses (> 500-1000 microM) as opposed to less potent lower doses (< 500 microM). In comparison to the general population of NSE-positive mesencephalic neurons, TH-positive neurons seem to exhibit a similar vulnerability to EAA. The fact that TH-positive neurons are only partially protected against glutamate toxicity by the non-competitive NMDA antagonist TCP indicates that they are more susceptible to non-NMDA mediated neurotoxicity than the general neuronal population.

Blockade of potassium or calcium channels provokes modifications in TRH-induced TSH release from rat perifused pituitaries.

The aim of the present study was to determine the functional relationship between blockade of potassium or calcium channel activity and the initial burst of TSH secretion in response to TRH. Perifused rat pituitary fragments were stimulated by a 6-min pulse of physiological concentration of TRH (10 nM) in the presence or absence of pharmacological blockers of K+ or Ca2+ channels. Blockade of Ca(2+)-activated K+ channels with TEA (10 mM and 30 mM), apamin (200 nM), or charybdotoxin (50 nM) completely or partially blunted TRH-induced TSH release. By contrast, blockade of voltage-dependent K+ channels with 4-aminopyridine (4-AP) (500 microM) or with dendrotoxin (DTX) (350 nM) significantly increased TSH response. Moreover, blockade of T-type voltage-sensitive Ca2+ channels (VSCC) with NiCl (3 mM) or with diphenylhydantoin (100 microM) significantly (P < 0.01) reduced TSH response to TRH, whereas blockade of L-type Ca2+ channels with verapamil (50 microM) was ineffective. Our results suggest that secretion of TSH in response to nanomolar concentrations of TRH is correlated with stimulation of Ca(2+)-activated K+ channels, and inhibition of 4-AP-and DTX-sensitive voltage-dependent K+ channels; furthermore TSH response seems to depend on the activation of T-type VSCC.