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1.
Trop Med Int Health ; 20(5): 589-606, 2015 May.
Artículo en Inglés | MEDLINE | ID: mdl-25641212

RESUMEN

OBJECTIVE: The Demographic and Health Surveys (DHS) are a vital data resource for cross-country comparative analyses. This study is part of a set of analyses assessing the types of providers being used for reproductive and maternal health care across 57 countries. Here, we examine some of the challenges encountered using DHS data for this purpose, present the provider classification we used, and provide recommendations to enable more detailed and accurate cross-country comparisons of healthcare provision. METHODS: We used the most recent DHS surveys between 2000 and 2012; 57 countries had data on family planning and delivery care providers and 47 countries had data on antenatal care. Every possible response option across the 57 countries was listed and categorised. We then developed a classification to group provider response options according to two key dimensions: clinical nature and profit motive. RESULTS: We classified the different types of maternal and reproductive healthcare providers, and the individuals providing care. Documented challenges encountered during this process were limitations inherent in household survey data based on respondents' self-report; conflation of response options in the questionnaire or at the data processing stage; category errors of the place vs. professional for delivery; inability to determine whether care received at home is from the public or private sector; a large number of negligible response options; inconsistencies in coding and analysis of data sets; and the use of inconsistent headings. CONCLUSIONS: To improve clarity, we recommend addressing issues such as conflation of response options, data on public vs. private provider, inconsistent coding and obtaining metadata. More systematic and standardised collection of data would aid international comparisons of progress towards improved financial protection, and allow us to better characterise the incentives and commercial nature of different providers.

2.
Nat Genet ; 24(2): 171-4, 2000 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-10655064

RESUMEN

Smad proteins are intracellular mediators of signalling initiated by Tgf-betasuperfamily ligands (Tgf-betas, activins and bone morphogenetic proteins (Bmps)). Smads 1, 2, 3, 5 and 8 are activated upon phosphorylation by specific type I receptors, and associate with the common partner Smad4 to trigger transcriptional responses. The inhibitory Smads (6 and 7) are transcriptionally induced in cultured cells treated with Tgf-beta superfamily ligands, and downregulate signalling in in vitro assays. Gene disruption in mice has begun to reveal specific developmental and physiological functions of the signal-transducing Smads. Here we explore the role of an inhibitory Smad in vivo by targeted mutation of Madh6 (which encodes the Smad6 protein). Targeted insertion of a LacZ reporter demonstrated that Smad6 expression is largely restricted to the heart and blood vessels, and that Madh6 mutants have multiple cardiovascular abnormalities. Hyperplasia of the cardiac valves and outflow tract septation defects indicate a function for Smad6 in the regulation of endocardial cushion transformation. The role of Smad6 in the homeostasis of the adult cardiovascular system is indicated by the development of aortic ossification and elevated blood pressure in viable mutants. These defects highlight the importance of Smad6 in the tissue-specific modulation of Tgf-beta superfamily signalling pathways in vivo.


Asunto(s)
Anomalías Cardiovasculares/genética , Sistema Cardiovascular/embriología , Sistema Cardiovascular/crecimiento & desarrollo , Proteínas de Unión al ADN/genética , Proteínas de Unión al ADN/metabolismo , Músculo Liso Vascular/fisiología , Transducción de Señal/fisiología , Transactivadores/genética , Transactivadores/metabolismo , Animales , Proteínas de Unión al ADN/deficiencia , Femenino , Biblioteca Genómica , Homeostasis , Homocigoto , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Endogámicos , Ratones Noqueados , Ratones Transgénicos , Músculo Liso Vascular/patología , Mutagénesis Insercional , Proteínas Recombinantes de Fusión/metabolismo , Mapeo Restrictivo , Proteína smad6 , Transactivadores/deficiencia
3.
Mol Cell Biol ; 20(3): 878-82, 2000 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-10629044

RESUMEN

The mouse tubby phenotype is characterized by maturity-onset obesity accompanied by retinal and cochlear degeneration. A positional cloning effort to find the gene responsible for this phenotype led to the identification of tub, a member of a novel gene family of unknown function. A splice defect mutation in the 3' end of the tub gene, predicted to disrupt the C terminus of the Tub protein, has been implicated in the genesis of the tubby phenotype. It is not clear, however, whether the Tub mutant protein retains any biological activity, or perhaps has some dominant function, nor is it established that the tubby mutation is itself responsible for all of the observed tubby phenotypes. To address these questions, we generated tub-deficient mice and compared their phenotype to that of tubby mice. Our results demonstrate that tubby is a loss-of-function mutation of the tub gene and that loss of the tub gene is sufficient to give rise to the full spectrum of tubby phenotypes. We also demonstrate that loss of photoreceptors in the retina of tubby and tub-deficient mice occurs by apoptosis. In addition, we show that Tub protein expression is not significantly altered in the ob, db, or melanocortin 4 receptor-deficient mouse model of obesity.


Asunto(s)
Obesidad/genética , Proteínas/genética , Proteínas/fisiología , Proteínas Adaptadoras Transductoras de Señales , Envejecimiento/genética , Animales , Cóclea/patología , Exones , Femenino , Homocigoto , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Obesidad/patología , Fenotipo , Empalme del ARN/genética , Mapeo Restrictivo , Retina/patología , Degeneración Retiniana/genética , Degeneración Retiniana/patología , Eliminación de Secuencia , Caracteres Sexuales , Aumento de Peso
4.
Sleep Med ; 6(4): 347-52, 2005 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-15978517

RESUMEN

BACKGROUND AND PURPOSE: To determine the prevalence of sleep disturbance in a memory clinic population of Alzheimer's disease (AD) patients and identify its clinical correlates. PATIENTS AND METHODS: Data from 215 attendees at a memory clinic, who were diagnosed with Alzheimer's disease, were examined. This included data from cognitive, functional and neuropsychological assessments. Sleep disturbance was determined using the question about diurnal rhythm disturbance on the BEHAVE-AD questionnaire. Two groups, with and without sleep disturbance, were compared. Group differences were analysed using univariate analysis and stepwise logistic regression analysis. RESULTS: The prevalence of sleep disturbance in this sample was 24.5%. The BEHAVE-AD 'aggressiveness' (P=0.009) and 'global rating' (P=0.029) (a measure of global impact of behavioural disturbance) were found to be significant predictors of sleep disturbance in AD. CONCLUSIONS: Sleep disturbance in AD is associated with other behavioural symptoms, notably aggressiveness. Sleep disturbance in AD has significant impact on the patient and/or caregiver. Consideration of co-morbid behavioural symptoms may aid the clinician in choosing a suitable treatment for sleep disturbance in AD.


Asunto(s)
Enfermedad de Alzheimer/epidemiología , Trastornos del Sueño-Vigilia/epidemiología , Anciano , Enfermedad de Alzheimer/diagnóstico , Cuidadores , Trastornos del Conocimiento/diagnóstico , Costo de Enfermedad , Femenino , Humanos , Masculino , Pruebas Neuropsicológicas , Prevalencia , Índice de Severidad de la Enfermedad , Trastornos del Sueño-Vigilia/diagnóstico
6.
Mol Endocrinol ; 11(5): 630-7, 1997 May.
Artículo en Inglés | MEDLINE | ID: mdl-9139806

RESUMEN

Dominant mutations at the agouti locus induce several phenotypic changes in the mouse including yellow pigmentation (phaeomelanization) of the coat and adult-onset obesity. Nonpigmentary phenotypic changes associated with the agouti locus are due to ectopic expression of the agouti-signaling protein (ASP), and the pheomelanizing effects on coat color are due to ASP antagonism of alpha-MSH binding to the melanocyte MC1 receptor. Recently it has been demonstrated that pharmacological antagonism of hypothalamic melanocortin receptors or genetic deletion of the melanocortin 4 receptor (MC4-R) recapitulates aspects of the agouti obesity syndrome, thus establishing that chronic disruption of central melanocortinergic signaling is the cause of agouti-induced obesity. To learn more about potential downstream effectors involved in these melanocortinergic obesity syndromes, we have examined expression of the orexigenic peptides galanin and neuropeptide Y (NPY), as well as the anorexigenic POMC in lethal yellow (A(y)), MC4-R knockout (MC4-RKO), and leptin-deficient (ob/ob) mice. No significant changes in galanin or POMC gene expression were seen in any of the obese models. In situ hybridizations using an antisense NPY probe demonstrated that in obese A(y) mice, arcuate nucleus NPY mRNA levels were equivalent to that of their C57BL/6J littermates. However, NPY was expressed at high levels in a new site, the dorsal medial hypothalamic nucleus (DMH). Expression of NPY in the DMH was also seen in obese MC4-RKO homozygous (-/-) mice, but not in lean heterozygous (+/-) or wild type (+/+) control mice. This identifies the DMH as a brain region that is functionally altered by the disruption of melanocortinergic signaling and suggests that this nucleus, possibly via elevated NPY expression, may have an etiological role in the melanocortinergic obesity syndrome.


Asunto(s)
Galanina/genética , Hipotálamo/metabolismo , Péptidos y Proteínas de Señalización Intercelular , Neuropéptido Y/genética , Obesidad/genética , Proopiomelanocortina/genética , Proteínas/genética , Proteína de Señalización Agouti , Animales , Galanina/biosíntesis , Regulación de la Expresión Génica , Ratones , Ratones Endogámicos C57BL , Ratones Obesos , Mutación , Neuropéptido Y/biosíntesis , Obesidad/metabolismo , Proopiomelanocortina/biosíntesis
7.
Gene ; 121(2): 365-9, 1992 Nov 16.
Artículo en Inglés | MEDLINE | ID: mdl-1446834

RESUMEN

The cDNA (DHFR) encoding the wild-type (wt) dihydrofolate reductase (DHFR) was used as a dominant selectable marker in the transfection of murine hybridoma Sp2/0-Ag14 cells by protoplast fusion. The initial clones contained 100-400 copies of integrated plasmid DNA, and the high level of wt DHFR protein produced enabled the cells to survive the drug selection at 100 nM methotrexate (MTX). The expression of the gene of interest was several fold higher than when the mutant DHFR with decreased MTX binding was used as the selection marker, presumably because the clones were more sensitive to the stress induced by MTX. When the clones were propagated at higher concentrations of MTX, expression of both DHFR and the gene of interest increased. This induction is freely reversible, and we have shown that it is controlled at the transcriptional level, by nuclear run-off transcription assays.


Asunto(s)
Vectores Genéticos , Metotrexato/farmacología , Tetrahidrofolato Deshidrogenasa/genética , Transfección , Secuencia de Bases , ADN/genética , Expresión Génica/efectos de los fármacos , Datos de Secuencia Molecular , Oligodesoxirribonucleótidos/química , ARN Mensajero/genética , Selección Genética , Transcripción Genética
8.
Am J Med Sci ; 310(3): 111-4, 1995 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-7668306

RESUMEN

Two male patients with mild gastrointestinal bleeding had peculiar dark pigmentation of their duodenum on upper endoscopy. These pigmented lesions were still present 3 months after the original endoscopy and after resolution of all other mucosal lesions. Both patients had other medical problems, including hypertension. They have been on multiple antihypertensive medications for many years. Biopsies of these duodenal lesions showed the pigment to be present inside the macrophages found in the lamina propria and in between the epithelial cells. Electron microscopy revealed a lysosomal localization of this pigment. This melanin-like pigment proved to contain varying amounts of iron, sulfur, and calcium. This pigmentation is closely associated with systemic hypertension, even in the pediatric population.


Asunto(s)
Enfermedades Duodenales/complicaciones , Duodeno/patología , Hipertensión/complicaciones , Mucosa Intestinal/patología , Melanosis/complicaciones , Anciano , Calcio/análisis , Enfermedades Duodenales/metabolismo , Enfermedades Duodenales/patología , Duodenoscopía , Duodeno/química , Microanálisis por Sonda Electrónica , Humanos , Mucosa Intestinal/química , Hierro/análisis , Lisosomas/química , Macrófagos/química , Macrófagos/ultraestructura , Masculino , Melanosis/metabolismo , Melanosis/patología , Microscopía Electrónica , Microvellosidades/química , Persona de Mediana Edad , Pigmentación , Azufre/análisis
9.
Otolaryngol Head Neck Surg ; 107(3): 370-3, 1992 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-1408220

RESUMEN

At present, electrocochleography is the only proven investigation that can demonstrate objectively the presence of endolymphatic hydrops. The electrophysiologic recordings in response to sound stimuli show an enhancement of the negative summating potential in these cases. It is well established that patients with unilateral Meniere's disease have a high likelihood of development of the disease bilaterally in the fullness of time. Using transtympanic electrocochleography in 40 patients who manifested unilateral clinical Meniere's disease, we have recorded bilateral abnormalities indicative of endolymphatic hydrops in 35% of cases. The early recognition of incipient Meniere's disease in the asymptomatic contralateral ear of a patient with known unilateral disease has obvious profound implications for patient management.


Asunto(s)
Audiometría de Respuesta Evocada , Enfermedad de Meniere/fisiopatología , Potenciales de Acción/fisiología , Adulto , Anciano , Audiometría de Respuesta Evocada/métodos , Audiometría de Tonos Puros , Potenciales Microfónicos de la Cóclea/fisiología , Femenino , Humanos , Masculino , Persona de Mediana Edad
10.
J Laryngol Otol ; 107(7): 620-2, 1993 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-15125282

RESUMEN

An unusual case of a patient with bilateral Ménière's disease is described whose disease presented in the second ear as a sensorineural hearing loss which fluctuated with the patient's level of blood glucose. The literature concerning the role of abnormal glucose metabolism in Ménière's disease is reviewed and the investigation and management of this patient's condition is discussed.


Asunto(s)
Glucemia/metabolismo , Pérdida Auditiva Sensorineural/sangre , Enfermedad de Meniere/sangre , Adulto , Audiometría de Tonos Puros , Glucemia/análisis , Femenino , Pérdida Auditiva Sensorineural/diagnóstico , Pérdida Auditiva Sensorineural/etiología , Humanos , Enfermedad de Meniere/complicaciones , Enfermedad de Meniere/cirugía , Periodo Posprandial
12.
Ir J Med Sci ; 177(1): 29-33, 2008 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-18057979

RESUMEN

BACKGROUND: Alzheimer's Disease (AD) is a progressive neurodegenerative disorder with as yet poorly understood aetiology. Both environmental and genetic factors have been implicated as predisposing factors. The APOE e4 allele is an established genetic susceptibility factor for AD for several populations including the Irish. Polymorphisms (-491A/T and -427T/C) at the promoter region of the APOE gene are postulated to affect the expression of the gene through differential binding of transcription factors. AIMS: Two APOE promoter polymorphisms (-491A/T and -427T/C) are examined for possible association with AD. METHODS: Using a case-control study design, a sample of 112 Irish late onset Alzheimer's (LOAD) patients and 107 ethnically matched controls were investigated for association with the above polymorphisms. CONCLUSIONS: No evidence of association between any of the examined markers and AD was observed. Haplotype analysis using markers -491A/T and -427T/C in conjunction with the APOE (Hha I) polymorphism revealed significant associations of three haplotypes with AD. However, this association was mainly due to the highly significant association of the APOE e4 allele with AD and not of the promoter variants.


Asunto(s)
Enfermedad de Alzheimer/genética , Apolipoproteínas E/genética , Polimorfismo Genético , Regiones Promotoras Genéticas/genética , Anciano , Estudios de Casos y Controles , Marcadores Genéticos , Predisposición Genética a la Enfermedad , Haplotipos , Humanos , Desequilibrio de Ligamiento , Reacción en Cadena de la Polimerasa
13.
Glob Public Health ; 1(2): 157-72, 2006.
Artículo en Inglés | MEDLINE | ID: mdl-19153904

RESUMEN

The role of cost-sharing in health care is a crucial, yet contentious issue. In conflict situations, cost-sharing becomes even more controversial as health and other institutions are failing. In such situations, NGOs manage health programmes which aim to aid populations in crisis and improve or at least sustain a deteriorating health system. This study looks at the issue of cost-sharing in the wider context of utilization rates and management approaches of three NGOs in the chronic, high-mortality crisis of the eastern DRC. Approaches to increase access to health care were found to exist, yet cost-recovery, even on the basis of maximum utilization rates, would only partially sustain the health system in the eastern DRC. Factors external to the direct management of NGO health programs, such as the wider economic and security situation, local management structures, and international donor policies, need to be taken into account for establishing more integrated management and financing approaches.


Asunto(s)
Seguro de Costos Compartidos , Atención a la Salud/organización & administración , Sector Privado/economía , Sector Público/economía , República Democrática del Congo , Países en Desarrollo , Urgencias Médicas , Costos de la Atención en Salud , Servicios de Salud/estadística & datos numéricos , Humanos , Entrevistas como Asunto , Agencias Voluntarias de Salud
14.
Dement Geriatr Cogn Disord ; 21(1): 40-3, 2006.
Artículo en Inglés | MEDLINE | ID: mdl-16254429

RESUMEN

BACKGROUND: Making an early diagnosis of dementia is becoming increasingly important, but is difficult in practice. The Clinical Dementia Rating (CDR) scale is a widely used dementia staging instrument, yielding a global score and a summated score (sum of box score). This study examines the utility of the CDR sum of box score, rather than the CDR global score, in making a diagnosis of early dementia. OBJECTIVE: To determine whether the CDR sum of box score is predictive of an ICD-10 diagnosis of dementia in cases with mild cognitive deficits. METHODS: Clinical data recorded on our Memory Clinic database were examined for all patients seen over a 6-year period. Data were extracted from 276 first visits in which patients had scored 0.5 using the CDR global score. We examined the relationship between CDR sum of box score and consensus diagnosis of dementia using logistic regression. RESULTS: We found that increased CDR sum of box score was significantly associated with a higher probability of being assigned an ICD-10 diagnosis of dementia (p < 0.001). The odds ratio for the coefficient of CDR sum of box was 2.3 (95% CI 1.7-3.1), indicating that the likelihood of being diagnosed as having dementia increased by a factor of 2.3 for every point increase on the CDR sum of box score. CONCLUSION: These findings indicate that the CDR sum of box score provides additional information to the CDR global score in mild cases. The CDR sum of box score is a helpful indicator in making/excluding a diagnosis of dementia in people with mild cognitive deficits.


Asunto(s)
Enfermedad de Alzheimer/diagnóstico , Pruebas Neuropsicológicas/estadística & datos numéricos , Enfermedad de Alzheimer/clasificación , Enfermedad de Alzheimer/psicología , Humanos , Clasificación Internacional de Enfermedades , Psicometría/estadística & datos numéricos , Reproducibilidad de los Resultados
15.
J Clin Gastroenterol ; 22(1): 66-70, 1996 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-8776101

RESUMEN

A 74-year-old man had an isolated colonic ganglioneuroma presenting endoscopically as filiform polyposis coli. Extensive workup failed to show either von Recklinghausen's neurofibromatosis or multiple endocrine neoplasia (MEN) 2b. We discuss the clinical implications of this and review the literature.


Asunto(s)
Poliposis Adenomatosa del Colon/diagnóstico , Neoplasias del Colon/diagnóstico , Ganglioneuroma/diagnóstico , Poliposis Adenomatosa del Colon/patología , Anciano , Neoplasias del Colon/patología , Ganglioneuroma/patología , Humanos , Masculino
16.
Cell ; 88(1): 131-41, 1997 Jan 10.
Artículo en Inglés | MEDLINE | ID: mdl-9019399

RESUMEN

The melanocortin-4 receptor (MC4-R) is a G protein-coupled, seven-transmembrane receptor expressed in the brain. Inactivation of this receptor by gene targeting results in mice that develop a maturity onset obesity syndrome associated with hyperphagia, hyperinsulinemia, and hyperglycemia. This syndrome recapitulates several of the characteristic features of the agouti obesity syndrome, which results from ectopic expression of agouti protein, a pigmentation factor normally expressed in the skin. Our data identify a novel signaling pathway in the mouse for body weight regulation and support a model in which the primary mechanism by which agouti induces obesity is chronic antagonism of the MC4-R.


Asunto(s)
Marcación de Gen/métodos , Obesidad/genética , Receptores de Péptidos/fisiología , Animales , Glucemia/análisis , Química Encefálica , Modelos Animales de Enfermedad , Ingestión de Alimentos , Femenino , Expresión Génica , Heterocigoto , Homocigoto , Insulina/sangre , Leptina , Masculino , Ratones , Ratones Noqueados , Ratones Obesos , Obesidad/sangre , Proopiomelanocortina/genética , Proteínas/análisis , ARN Mensajero/análisis , Receptor de Melanocortina Tipo 4 , Receptores de Péptidos/genética , Transducción de Señal , Aumento de Peso/genética
18.
Sch Health Rev ; 5(6): 42-5, 1974.
Artículo en Inglés | MEDLINE | ID: mdl-4497646
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