RESUMEN
The integration of the folk affect concept of "contempt" into the analysis of the complex institution known generally as charivari is mutually beneficial for both ethno-anthropology (which may thus access inner causes for disputed social and collective behaviors) and evolutionary psychology (which may thus study the length of tradition together with the width of the institution spread, serving the same social functions).
Asunto(s)
Asco , Emociones , Actitud , Relaciones InterpersonalesRESUMEN
As cultural anthropologists, we noticed an unexpected and interesting convergence of the therapeutic practices suggested in the target article and the rites of passage occurring across multiple societies, as individuals make the transition from one significant age or status to another.
Asunto(s)
Memoria Episódica , Procesos Psicoterapéuticos , Etnología , Humanos , SemánticaRESUMEN
The comorbidity between epilepsy and sleep disorders is well documented. However, the mechanisms underlining this comorbidity are not fully understood. The putative role of anti epileptic drugs in sleep architecture disturbances in epileptic children needs to be explored. In this study, we analysed sleep architecture of 75 epileptic children (30 females and 45 males), aged from 4 to 15 years (mean-age: 8.3 years). They were divided in three groups according to their antiepileptic treatments: NT group: no antiepileptic treatment (n = 20), MT group: monotherapy (n = 29) and PT group: polytherapy (n = 26). All underwent video-polysomnographic recordings to assess main sleep parameters: stages of light sleep and slow waves sleep, REM sleep, total sleep time and awakenings. Percentages of paroxystic activity duration (PA) on TST were also calculated and classified in three subgroups: (<5%, 5% ≤ PA ≤ 20% and >20%). As result, significant decreases of REM sleep and of the sleep efficiency as well as significant increased awakenings were observed in PT group comparing to the NT group. No significative difference was found concerning the light sleep and slow waves sleep. A correlation was also observed between awakenings and PA. First, our data confirm that sleep disorders remain a hidden companion of childhood epilepsy. Second, we demonstrate that anti epileptic drugs may have some causal contribution. Diagnosing sleep disturbances should be part of the management of childhood epilepsy and should be taken into account in the choice of therapeutic strategy.
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Anticonvulsivantes/efectos adversos , Epilepsia/complicaciones , Fases del Sueño/fisiología , Trastornos del Sueño-Vigilia/inducido químicamente , Adolescente , Análisis de Varianza , Anticonvulsivantes/uso terapéutico , Niño , Preescolar , Epilepsia/tratamiento farmacológico , Femenino , Humanos , Masculino , Polisomnografía , Trastornos del Sueño-Vigilia/epidemiología , Sueño REM/fisiologíaRESUMEN
The aim of this article is to describe the roles of water channel proteins (WCPs) in some neurological diseases in which the implications of these proteins became obvious in the decades after the discovery of WCPs of their presence in the CNS. The diseases which were selected for this review include: epilepsies, muscular dystrophies, amyotrophic lateral sclerosis, neuromyelitis optica, Parkinson's disease, and spongiform encephalopathies. The priorities of Benga group from Cluj-Napoca, Romania, are mentioned, such as the idea of a generalized membrane defect affecting water permeability in epilepsy and in Duchenne muscular dystrophy. Some of these neurological disorders discussed in this article appeared to be water channelopathies. A typical example is neuromyelitis optica (NMO), in which the identification of the specific marker autoantibody against aquaporin 4 in the sera of patients was a milestone in the diagnosis. This has aided understanding of the pathogenesis of NMO and led to better control of its treatment. However, further studies are needed to characterize the function and regulation of WCPs in other neurological diseases, in particular to determine if modulation of WCP function may provide a novel approach to therapy in such diseases.
Asunto(s)
Esclerosis Amiotrófica Lateral/metabolismo , Acuaporinas/metabolismo , Epilepsia/metabolismo , Distrofia Muscular de Duchenne/metabolismo , Neuromielitis Óptica/metabolismo , Enfermedad de Parkinson/metabolismo , Enfermedades por Prión/metabolismo , Agua/metabolismo , Esclerosis Amiotrófica Lateral/patología , Acuaporinas/antagonistas & inhibidores , Autoanticuerpos/biosíntesis , Autoanticuerpos/inmunología , Biomarcadores/metabolismo , Membrana Celular/metabolismo , Permeabilidad de la Membrana Celular , Epilepsia/patología , Humanos , Inmunoglobulina G/biosíntesis , Inmunoglobulina G/inmunología , Distrofia Muscular de Duchenne/patología , Neuromielitis Óptica/patología , Enfermedad de Parkinson/patología , Enfermedades por Prión/patología , Equilibrio Hidroelectrolítico/fisiologíaRESUMEN
The aim of this study is to evaluate the bioelectrical and structural-functional changes in frontal cortex after the bee venom (BV) experimental treatments simulating both an acute envenomation and a subchronic BV therapy. Wistar rats were subcutaneously injected once with three different BV doses: 700 µg/kg (T(1) group), 2100 µg/kg (T(3) group), and 62 mg/kg (sublethal dose-in T(SL) group), and repeated for 30 days with the lowest dose (700 µg/kg-in T(S) group). BV effects were assessed by electrophysiological, histological, histochemical, and ultrastructural methods. Single BV doses produced discharges of negative and biphasic sharp waves, and epileptiform spike-wave complexes. The increasing frequency of these elements suggested a dose-dependent neuronal hyperexcitation or irritation. As compared to the lower doses, the sublethal dose was responsible for a pronounced toxic effect, confirmed by ultrastructural data in both neurons and glial cells that underwent extensive, irreversible changes, triggering the cellular death. Subchronic BV treatment in T(S) group resulted in a slower frequency and increased amplitude of cortical activity suggesting neuronal loss. However, neurons were still stimulated by the last BV dose. Structural-functional data showed a reduced cellular density in frontal cortex of animals in this group, while the remaining neurons displayed both specific (stimulation of neuronal activity) and unspecific modifications (moderate alterations to necrotic phenomena). Molecular mechanisms involved in BV interactions with the nervous tissue are also discussed. We consider all these data very important for clinicians who manage patients with multiple bee stings, or who intend to set an appropriate BV therapy.
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Venenos de Abeja/toxicidad , Fenómenos Electrofisiológicos/efectos de los fármacos , Lóbulo Frontal/patología , Lóbulo Frontal/ultraestructura , Animales , Electroencefalografía , Lóbulo Frontal/efectos de los fármacos , Lóbulo Frontal/fisiopatología , Inmunohistoquímica , Masculino , Ratas , Ratas WistarRESUMEN
BACKGROUND: micro-Opiate receptor agonism has been associated with weight gain, whereas micro-antagonists have been associated with weight neutrality, or even weight loss. AIM: This study examined the course of weight changes in opiate-dependent patients over the first 6 months of treatment in methadone (agonist) versus naltrexone (antagonist) maintenance. DESIGN: A retrospective chart review was conducted on 36 opiate-dependent patients maintained on methadone (n=16) or naltrexone (n=20). OUTCOME MEASURES AND ANALYSES: The primary outcome measure was change in body weight from baseline to 3 months and 6 months into treatment. Analysis of variance was used to compare mean weights between the methadone- and naltrexone-maintained patients. Secondarily, mean percent weight changes from baseline to 3 months and from baseline to 6 months into treatment were compared using Student's t-test. RESULTS: There was no difference between weight at baseline, 3 months, or 6 months into treatment between the two treatment groups. Furthermore, there was also no difference between the two groups regarding percent weight change from baseline to 3 months or baseline to 6 months. At 3 months, n=16 methadone patients had a mean weight increase of 1.86 percent (standard deviation [SD] = 7.22 percent) when compared with n=20 Behavioral Naltrexone Therapy (BNT) patients with an increase of 4.63 percent (SD = 6.49 percent). At 6 months, n=16 methadone patients had a mean weight increase relative to baseline of 3.67 percent (SD = 9.52percent) when compared with n=20 BNT patients, who demonstrated a mean increase of 6.69 percent (SD = 7.56 percent). No association was found between baseline weight, defined as "low" or "high" relative to group medians, and percent gain within and between treatment groups. CONCLUSIONS: This study did not detect a statistically different course of weight gain between methadone and naltrexone maintenance treatment for opiate-dependent patients.
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Metadona/efectos adversos , Naltrexona/efectos adversos , Antagonistas de Narcóticos/efectos adversos , Tratamiento de Sustitución de Opiáceos/métodos , Trastornos Relacionados con Opioides/rehabilitación , Aumento de Peso/efectos de los fármacos , Adulto , Femenino , Humanos , Masculino , Metadona/administración & dosificación , Metadona/uso terapéutico , Naltrexona/administración & dosificación , Naltrexona/uso terapéutico , Antagonistas de Narcóticos/administración & dosificación , Antagonistas de Narcóticos/uso terapéutico , Trastornos Relacionados con Opioides/tratamiento farmacológico , Estudios Retrospectivos , Factores de TiempoRESUMEN
Autism spectrum disorders (ASD) comprise a complex and heterogeneous group of conditions of unknown aetiology, characterized by significant disturbances in social, communicative and behavioural functioning. Recent studies suggested a possible implication of the high-density lipoprotein associated esterase/lactonase paraoxonase 1 (PON1) in ASD. In the present study, we aimed at investigating the PON1 status in a group of 50 children with ASD as compared to healthy age and sex matched control participants. We evaluated PON1 bioavailability (i.e. arylesterase activity) and catalytic activity (i.e. paraoxonase activity) in plasma using spectrophotometric methods and the two common polymorphisms in the PON1 coding region (Q192R, L55M) by employing Light Cycler real-time PCR. We found that both PON1 arylesterase and PON1 paraoxonase activities were decreased in autistic patients (respectively, P < 0.001, P < 0.05), but no association with less active variants of the PON1 gene was found. The PON1 phenotype, inferred from the two-dimensional enzyme analysis, had a similar distribution in the ASD group and the control group. In conclusion, both the bioavailability and the catalytic activity of PON1 are impaired in ASD, despite no association with the Q192R and L55M polymorphisms in the PON1 gene and a normal distribution of the PON1 phenotype.
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Arildialquilfosfatasa/genética , Arildialquilfosfatasa/metabolismo , Trastorno Autístico/enzimología , Polimorfismo Genético , Arildialquilfosfatasa/sangre , Trastorno Autístico/genética , Niño , Pruebas de Enzimas , Femenino , Frecuencia de los Genes , Genotipo , Humanos , Desequilibrio de Ligamiento , MasculinoRESUMEN
Numerous studies have assessed the acute efficacy of antidepressants, including selective serotonin reuptake inhibitors, in treating dysthymic disorder; however, escitalopram, the S-enantiomer of citalopram, has not been studied. Thirty-six outpatients with Structured Clinical Interview for DSM-III-R-diagnosed dysthymic disorder, aged 23-65 years (mean±SD=44.7±11 years), were randomly assigned to double-blind escitalopram (maximum dose 20 mg/day) versus placebo for 12 weeks. Inclusion criteria included age 18-65 years and Hamilton Depression Rating Scale (HDRS) score≥12. We hypothesized that escitalopram would be superior to placebo in the HDRS-24 item total score at week 12. We also hypothesized the superiority of escitalopram over placebo for secondary measures, including the percentage of participants classified as responders and remitters, as well as social functioning (Social Adjustment Scale), clinical global impression-improvement, Global Assessment of Functioning Scale. Participants' baseline HDRS-24 averaged 23.4±5.9. Final HDRS-24 scores at last observation carried forward did not differ significantly between escitalopram-treated (mean±SD=10.88±5.83) and placebo-treated individuals (mean±SD=16.4±6.34) (F=2.82, degrees of freedom=1,32, P=0.10). Significant differences favoring active medication were found on the Social Adjustment Scale and the Clinical Global Impression Severity and Global Assessment of Functioning Scale, but not in the percentages of responders or remitters. A larger study sample or higher escitalopram dose may show more significant placebo-medication differences.
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Antidepresivos de Segunda Generación/uso terapéutico , Citalopram/uso terapéutico , Trastorno Distímico/tratamiento farmacológico , Adulto , Antidepresivos de Segunda Generación/administración & dosificación , Antidepresivos de Segunda Generación/efectos adversos , Citalopram/administración & dosificación , Citalopram/efectos adversos , Relación Dosis-Respuesta a Droga , Método Doble Ciego , Esquema de Medicación , Femenino , Humanos , Masculino , Persona de Mediana Edad , Placebos , Escalas de Valoración Psiquiátrica , Estereoisomerismo , Resultado del Tratamiento , Adulto JovenRESUMEN
Autism spectrum disorders (ASDs), which include the prototypic autistic disorder (AD), Asperger's syndrome (AS) and pervasive developmental disorders not otherwise specified (PDD-NOS), are complex neurodevelopmental conditions of unknown aetiology. The current study investigated the metabolites in the methionine cycle, the transsulphuration pathway, folate, vitamin B(12) and the C677T polymorphism of the MTHFR gene in three groups of children diagnosed with AD (n= 15), AS (n= 5) and PDD-NOS (n= 19) and their age- and sex-matched controls (n= 25). No metabolic disturbances were seen in the AS patients, while in the AD and PDD-NOS groups, lower plasma levels of methionine (P= 0.01 and P= 0.03, respectively) and alpha-aminobutyrate were observed (P= 0.01 and P= 0.001, respectively). Only in the AD group, plasma cysteine (P= 0.02) and total blood glutathione (P= 0.02) were found to be reduced. Although there was a trend towards lower levels of serine, glycine, N, N-dimethylglycine in AD patients, the plasma levels of these metabolites as well as the levels of homocysteine and cystathionine were not statistically different in any of the ASDs groups. The serum levels of vitamin B(12) and folate were in the normal range. The results of the MTHFR gene analysis showed a normal distribution of the C677T polymorphism in children with ASDs, but the frequency of the 677T allele was slightly more prevalent in AD patients. Our study indicates a possible role for the alterations in one carbon metabolism in the pathophysiology of ASDs and provides, for the first time, preliminary evidence for metabolic and genetic differences between clinical subtypes of ASDs.