RESUMEN

BACKGROUND: Early risk stratification is important in the management of patients with acute coronary syndromes (ACS). OBJECTIVE: To develop a rapidly available risk stratification tool for use in all ACS. DESIGN AND METHODS: Application of modern data mining and machine learning algorithms to a derivation cohort of 7520 ACS patients included in the AMIS (Acute Myocardial Infarction in Switzerland)-Plus registry between 2001 and 2005; prospective model testing in two validation cohorts. RESULTS: The most accurate prediction of in-hospital mortality was achieved with the "Averaged One-Dependence Estimators" (AODE) algorithm, with input of seven variables available at first patient contact: age, Killip class, systolic blood pressure, heart rate, pre-hospital cardiopulmonary resuscitation, history of heart failure, history of cerebrovascular disease. The c-statistic for the derivation cohort (0.875) was essentially maintained in important subgroups, and calibration over five risk categories, ranging from <1% to >30% predicted mortality, was accurate. Results were validated prospectively against an independent AMIS-Plus cohort (n = 2854, c-statistic 0.868) and the Krakow-Region ACS Registry (n = 2635, c-statistic 0.842). The AMIS model significantly outperformed established "point-of-care" risk-prediction tools in both validation cohorts. In comparison to a logistic regression-based model, the AODE-based model proved to be more robust when tested on the Krakow validation cohort (c-statistic 0.842 vs 0.746). Accuracy of the AMIS model prediction was maintained at 12-month follow-up in an independent cohort (n = 1972, c-statistic 0.877). CONCLUSIONS: The AMIS model is a reproducibly accurate point-of-care risk stratification tool for the complete range of ACS, based on variables available at first patient contact.

Asunto(s)

Síndrome Coronario Agudo/diagnóstico , Técnicas de Apoyo para la Decisión , Sistemas de Atención de Punto , Síndrome Coronario Agudo/fisiopatología , Anciano , Anciano de 80 o más Años , Algoritmos , Inteligencia Artificial , Diagnóstico por Computador/métodos , Métodos Epidemiológicos , Reacciones Falso Positivas , Femenino , Humanos , Masculino , Persona de Mediana Edad , Pronóstico , Medición de Riesgo/métodos

RESUMEN

We report on a 46-year-old man with vasospastic angina. The differential diagnosis, the eventful course of the patient and in particular the clinical image with diagnostic approach, therapy and prognosis of vasospastic angina are discussed.

Asunto(s)

Angina Pectoris Variable/diagnóstico , Dolor en el Pecho/etiología , Vasoespasmo Coronario/diagnóstico , Síndrome Coronario Agudo/diagnóstico , Angiografía Coronaria , Estenosis Coronaria/diagnóstico , Diagnóstico Diferencial , Electrocardiografía , Humanos , Masculino , Persona de Mediana Edad , Troponina/sangre , Fibrilación Ventricular/diagnóstico

RESUMEN

The publisher regrets that this was an accidental duplication of an article that has already been published in Eur. J. Echocardiogr., 4 (2003) 223-225, . The duplicate article has therefore been withdrawn.

RESUMEN

The wear and tear processes that are thought to contribute to human ageing may play an important role in the development of vascular diseases. One such process is cellular senescence. In endothelial cells the senescent phenotype can be induced by a number of factors, including telomere damage, oxidative stress and sustained mitogenic stimulation. Several lines of evidence indicate that endothelial cell senescence maybe relevant to vascular disease. In this chapter we examine the causes, mechanisms and regulation of endothelial cell senescence as they emerge from studies in cell culture. We also describe the senescent phenotype and discuss its pathophysiological implications. We review the evidence for the occurrence of endothelial cell senescence in vivo and examine findings in animal models of ageing and human genetic disorders that argue for and against a role of endothelial cell senescence in age-related vascular pathology. Finally, we address the particular case of endothelial progenitor cell senescence and discuss the relevance of this phenomenon for angiogenesis and vascular repair.

Asunto(s)

Envejecimiento/fisiología , Senescencia Celular , Células Endoteliales/fisiología , Células Madre Mesenquimatosas/fisiología , Animales , Apoptosis , Enfermedades Cardiovasculares/genética , Enfermedades Cardiovasculares/fisiopatología , Proliferación Celular , Humanos , Modelos Animales , Fenotipo , Transducción de Señal , Telomerasa/metabolismo , Telómero/genética , Telómero/metabolismo , Síndrome de Werner/genética , Síndrome de Werner/fisiopatología

RESUMEN

OBJECTIVE: To evaluate the long term outcome of familial idiopathic enlargement of the right atrium (IERA) and the risk of developing this disorder among unaffected offspring. DESIGN: 23 year follow up study. PATIENTS: 14 members (eight men, mean age 54 years, range 40-78) of a pedigree with familial IERA. METHODS: All patients were examined clinically and echocardiographically in 1979 and 2002. Normal cross sectional dimensions of the right atrium were derived from echocardiographic evaluation of 100 people (47% men) with no structural or haemodynamic signs of heart disease. The 90th centile was chosen as the upper normal limit. IERA was defined as an increased right atrial long axis indexed to body surface area (RALAX(i), men > 2.6 cm/m2, women > 2.8 cm/m2) in the absence of other cardiac abnormalities. Severe IERA was defined arbitrarily as RALAX(i) > or = 4 cm/m2. RESULTS: The course of the two index patients with severe IERA diagnosed in 1979 was complicated by atrial fibrillation, systemic embolism, and symptoms of heart failure without systolic dysfunction, resulting in the death of one man (77 years old). One of two patients with initially mild forms progressed to severe IERA. All of the initially unaffected offspring (n = 9) remained asymptomatic, although four of them had developed mild IERA. CONCLUSIONS: During 23 years' follow up, severe IERA induced atrial fibrillation, systemic embolism, and symptoms of heart failure without systolic dysfunction in all cases in this family. Mild IERA seems to become manifest during middle age and may be followed by gradual progression to clinically relevant disease.

Asunto(s)

Cardiomegalia/genética , Adulto , Anciano , Cardiomegalia/diagnóstico por imagen , Ecocardiografía Doppler , Femenino , Estudios de Seguimiento , Atrios Cardíacos , Humanos , Masculino , Persona de Mediana Edad , Linaje , Radiografía

RESUMEN

OBJECTIVE: To define the entity of tricuspid regurgitation caused by tethering of the tricuspid valve leaflets by aberrant tendinous chords. DESIGN: Retrospective study. SETTING: Tertiary care centre (university teaching hospital). PATIENTS: 10 patients with unexplained severe tricuspid regurgitation. METHODS: The last 13 500 echocardiographic studies from our facility were reviewed to identify patients with severe unexplained tricuspid regurgitation. Tethering was defined by the presence of aberrant tendinous chords to the tricuspid valve leaflets limiting the mobility of the tricuspid leaflet and resulting in incomplete coaptation and apical displacement of the regurgitant jet origin. Aberrant tendinous chords were defined as those inserting at the clear zone of the tricuspid leaflet and not originating from the papillary muscle. Patients fulfilling the diagnostic criteria for Ebstein's anomaly were excluded. RESULTS: 10 patients with aberrant tendinous chords tethering one or more tricuspid valve leaflets were identified. There were short non-aberrant tendinous chords in seven patients, five of whom also had right ventricular or tricuspid annulus dilatation. CONCLUSIONS: Tethering of the tricuspid valve leaflets by aberrant tendinous chords can be the sole mechanism of congenital tricuspid regurgitation. It is often associated with short non-aberrant tendinous chords, which may develop secondary to right ventricular or tricuspid annulus dilatation. Awareness of tethering as a cause of tricuspid regurgitation may be important in planning reconstructive surgery.

Asunto(s)

Cuerdas Tendinosas/anomalías , Insuficiencia de la Válvula Tricúspide/congénito , Válvula Tricúspide/anomalías , Adolescente , Adulto , Niño , Ecocardiografía Doppler en Color , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Insuficiencia de la Válvula Tricúspide/diagnóstico por imagen

RESUMEN

Diverticula and aneurysms are rare congenital anomalies of the right atrium. Here, we report a case of a giant congenital diverticulum of the right atrium in a 27-year-old female and discuss the morphological characteristics distinguishing diverticula and aneurysms.

Asunto(s)

Divertículo/diagnóstico , Aneurisma Cardíaco/diagnóstico , Atrios Cardíacos/patología , Adulto , Aleteo Atrial/diagnóstico , Diagnóstico Diferencial , Ecocardiografía , Femenino , Atrios Cardíacos/diagnóstico por imagen , Sistema de Conducción Cardíaco/diagnóstico por imagen , Sistema de Conducción Cardíaco/patología , Ventrículos Cardíacos/diagnóstico por imagen , Ventrículos Cardíacos/patología , Humanos

RESUMEN

The fundamental disturbance of the parkinsonian gait is the reduction in walking velocity. This is mainly due to reduction in stride length, while cadence (steps/min) is slightly enhanced. Treatment with L-dopa increases stride length while cadence is unchanged. Chronic stimulation of the thalamus has no effect on Parkinsonian gait. The efficacy of electrical stimulation of the subthalamic nucleus (STN) on gait in advanced Parkinson's disease has been clearly demonstrated clinically. The aim of the present study was to quantify the changes in gait measures induced by STN stimulation and L-dopa and to assess possible differential or additive effects. Eight Parkinson's disease patients (mean +/- SD age 48.1 +/- 7.3 years) with chronic bilateral STN stimulation (mean duration of disease 13.3 +/- 2.4 years, mean stimulation time 15.4 +/- 10.6 months) and 12 age-matched controls were investigated. Subjects walked on a special treadmill with a closed-loop ultrasound control system that used the subject's position to adjust treadmill speed continuously for the actual walking velocity. In an appropriate crossover design, spatiotemporal gait measures and leg joint angle movements were assessed for at least 120 stride cycles in four treatment conditions: with and without stimulation and with and without a suprathreshold dose of L-dopa. With STN stimulation, there were increases of almost threefold in mean walking velocity (from 0.35 to 0.96 m/s) and stride length (from 0.34 to 0.99 m). Cadence remained constant. The range of motion of the major leg joints also increased. L-Dopa alone had a slightly weaker effect, with an increase in walking velocity to 0.94 m/s and in stride length to 0.92 m at a similar cadence. These increased values were in the range of those for healthy age-matched subjects performing the same task. The combination of both treatments further increased the mean walking velocity to 1.19 m/s and stride length to 1.20 m at an unchanged cadence. However, not all patients receiving STN stimulation improved further when they also received L-dopa. These results demonstrate that chronic bilateral STN stimulation, like treatment with L-dopa, improves walking velocity by increasing stride length without changing cadence. STN stimulation almost exclusively affects mechanisms involved in the control of spatial gait measures rather than rhythmicity. The gait measures obtained with STN stimulation alone are in the range of control subjects.

Asunto(s)

Antiparkinsonianos/farmacología , Trastornos Neurológicos de la Marcha/terapia , Levodopa/farmacología , Enfermedad de Parkinson/terapia , Núcleo Subtalámico/fisiología , Adulto , Estimulación Eléctrica , Femenino , Humanos , Masculino , Persona de Mediana Edad , Enfermedad de Parkinson/complicaciones , Resultado del Tratamiento

RESUMEN

The hypothesis that increased cellular proliferation in the vasculature may lead to replicative senescence has been tested in a model of neointima formation. We have used a biomarker of replicative senescence, senescence-associated beta-galactosidase (SA-beta-gal), to detect senescence in rabbit carotid arteries subjected to single and double balloon denudations. We found an accumulation of senescent cells in the neointima and media of all injured vessels, in contrast to the near absence of such cells in control vessels. The relative area occupied by SA-beta-gal-positive cells was higher in vessels subjected to double denudation than in those subjected to single denudation, both in the neointima (0.99% versus 0.06%, respectively; P:<0.001) and in the media (0.11% versus 0.01%, respectively; P:<0.02). The majority of SA-beta-gal-positive cells were vascular smooth muscle cells, and a minority were endothelial cells. SA-beta-gal-positive cells showed no evidence of apoptosis by use of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling. Our results indicate that the proliferative response that follows intraluminal injury to the artery leads to the emergence of senescent endothelial and smooth muscle cells. The demonstration that vascular cell senescence can occur in vivo suggests that this process may be involved in cardiovascular pathologies that have a proliferative component.

Asunto(s)

Angioplastia de Balón/efectos adversos , Arterias Carótidas/patología , Traumatismos de las Arterias Carótidas/patología , Senescencia Celular/fisiología , Endotelio Vascular/citología , Músculo Liso Vascular/citología , Animales , Biomarcadores , Traumatismos de las Arterias Carótidas/etiología , Senescencia Celular/genética , Endotelio Vascular/lesiones , Masculino , Músculo Liso Vascular/lesiones , Conejos , beta-Galactosidasa/metabolismo

RESUMEN

Senescence-associated (beta)-galactosidase is widely used as a biomarker of replicative senescence. However, it remains unknown whether this is a distinct enzyme active at pH 6, and differentially expressed in senescence, or a manifestation of an increase in the classic acid lysosomal (beta)-galactosidase. Here we have investigated the origin of senescence-associated-(beta)-galactosidase activity by modifying the intracellular and lysosomal pH of young and senescent human umbilical vein endothelial cells and examining the effect of these manipulations on the levels of activity, using a flow cytometric assay. Lysosomal alkalinisation with chloroquine or bafilomycin A(1), as well as equilibration of the intracellular milieu to pH 6 with nigericin, caused a profound (92-99%) inhibition of the total intracellular (beta)-galactosidase activity. However, independent of pH alterations, senescent cells showed levels of (beta)-galactosidase activity three- to sixfold higher than young cells. This increase in activity occurred in parallel to an increase in (beta)-galactosidase protein levels. Acridine Orange staining revealed an increase in lysosomal content with replicative age, which correlated with the increase in (beta)-galactosidase. These findings demonstrate that senescence-associated (beta)-galactosidase is a manifestation of residual lysosomal activity at a suboptimal pH, which becomes detectable due to the increased lysosomal content in senescent cells.

Asunto(s)

Senescencia Celular , Endotelio Vascular/citología , Endotelio Vascular/enzimología , Lisosomas/enzimología , Lisosomas/ultraestructura , Macrólidos , beta-Galactosidasa/metabolismo , Naranja de Acridina , Antibacterianos/farmacología , Cloroquina/farmacología , Citoplasma/metabolismo , Endotelio Vascular/ultraestructura , Inhibidores Enzimáticos/farmacología , Fibroblastos/enzimología , Fibroblastos/ultraestructura , Citometría de Flujo , Colorantes Fluorescentes , Histocitoquímica , Humanos , Concentración de Iones de Hidrógeno , Nigericina/farmacología , beta-Galactosidasa/antagonistas & inhibidores

RESUMEN

A large coronary aneurysm, originating from a side branch of the right coronary artery, caused recurrent ischemia resulting in myocardial infarction. Successful surgical excision, without concomitant coronary artery bypass grafting, is described.

Asunto(s)

Aneurisma Coronario/complicaciones , Infarto del Miocardio/etiología , Adulto , Aneurisma Coronario/cirugía , Humanos , Masculino

RESUMEN

BACKGROUND: Anginal chest pain without creatine kinase (CK) elevation is frequently observed in the first hours after coronary stenting. Possible causes of ischemic episodes are microembolism, side branch occlusion, coronary vasospasm, and disturbances of microvascular circulation. In a prospective, double-blind, randomized trial, we tested the effect of intravenous nitroglycerin on the incidence of angina and minor myocardial necrosis (MMN), as detected by cardiac troponin I increase, after elective coronary stenting. METHODS AND RESULTS: One hundred patients were randomly assigned to intravenous nitroglycerin (group A: n = 50, goal dose 100 microgram/min) or placebo (group B: n = 50, NaCl 0.9%) during 12 hours after stenting. Patients with acute myocardial infarction, known intolerance to nitrates, and hemodynamic instability during angioplasty were excluded. The 2 groups were comparable in respect to baseline and interventional variables, except for age (group A: 60 +/- 9 years, group B: 56 +/- 10 years; P =.04). The incidence of chest pain was not influenced by nitroglycerin (group A: 18%, group B: 22%; P = not significant). However, the occurrence of MMN was significantly reduced by nitroglycerin (group A: 5%, group B: 19%, P =.036). A rise in CK with significant CK-MB fraction was observed in only 2 patients in group B (both less than twice upper limit). Only 4 of the 10 patients with MMN also had chest pain. CONCLUSIONS: Routine use of intravenous nitroglycerin after coronary stenting significantly reduced the occurrence of minor myocardial necrosis. However, the incidence of postprocedural chest pain remained unchanged.

Asunto(s)

Angina de Pecho/prevención & control , Oclusión de Injerto Vascular/tratamiento farmacológico , Corazón/efectos de los fármacos , Infarto del Miocardio/tratamiento farmacológico , Miocardio/patología , Nitroglicerina/administración & dosificación , Dolor Postoperatorio/prevención & control , Stents , Vasodilatadores/administración & dosificación , Angina de Pecho/sangre , Angina de Pecho/diagnóstico por imagen , Angioplastia Coronaria con Balón , Biomarcadores/sangre , Angiografía Coronaria , Enfermedad Coronaria/diagnóstico por imagen , Enfermedad Coronaria/terapia , Método Doble Ciego , Femenino , Oclusión de Injerto Vascular/complicaciones , Oclusión de Injerto Vascular/diagnóstico por imagen , Humanos , Incidencia , Inyecciones Intravenosas , Masculino , Persona de Mediana Edad , Infarto del Miocardio/diagnóstico por imagen , Infarto del Miocardio/etiología , Necrosis , Dolor Postoperatorio/sangre , Dolor Postoperatorio/diagnóstico por imagen , Estudios Prospectivos , Troponina I/sangre

Asunto(s)

Estimulación Cardíaca Artificial , Electrodos Implantados/normas , Impedancia Eléctrica , Seguridad de Equipos/normas , Humanos

RESUMEN

About 30% of patients develop AF after open heart surgery. Biatrial synchronous pacing (BSP) has been shown to promote sinus rhythm in patients with paroxysmal AF refractory to drug therapy. We conducted a prospective, randomized study to test the effect of BSP via epicardial electrodes on the incidence of AF after heart surgery, as compared to conventional therapy. To apply BSP, we attached two epicardial electrodes to the right and one to the left atrium. Immediately following surgery, BSP was initiated in the AAI-Mode at a rate of 10 beats/min above the underlying rhythm (maximum 110 beats/min) and continued for 3 days, during which the rhythm was continually monitored. After 21 (age 63 +/- 9 years) of the planned 200 patients, the study was prematurely aborted because of the proarrhythmic effect of BSP: 6 of the 12 patients treated with BSP developed sensing failure (P amplitude < 1 mV), which provoked AF in 5 of these 6 patients. BSP was discontinued due to diaphragmal stimulation in two patients and due to ventricular stimulation by a dislocated left atrial electrode in one patient. Two patients in the control group (n = 9) developed AF. Using the available standard technology, BSP via epicardial electrodes is not suitable to suppress AF after heart surgery, primarily due to postoperative deterioration of atrial sensing and its profibrillatory effect. In patients requiring atrial pacing after heart surgery, sensing thresholds must be closely monitored to prevent induction of AF.

Asunto(s)

Fibrilación Atrial/prevención & control , Estimulación Cardíaca Artificial/métodos , Procedimientos Quirúrgicos Cardíacos/efectos adversos , Fibrilación Atrial/etiología , Puente Cardiopulmonar/efectos adversos , Femenino , Estudios de Seguimiento , Frecuencia Cardíaca , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Resultado del Tratamiento

RESUMEN

PURPOSE: Patients with fundus albipunctatus uniformly experience difficulty with vision at night. Their retinas are spotted with characteristic light yellow flecks of unknown composition that typically spare the macula. A defect in the transport or utilization of visual cycle retinoids is thought to underlie this recessive disorder with variable clinical expression. To elucidate the molecular defect we considered the genes for interphotoreceptor retinoid-binding protein (RBP3) and 11-cis retinol dehydrogenase (RDH5) as candidates for this disease. METHODS: We examined two unrelated families with fundus albipunctatus. The diagnosis was determined clinically and RBP3 and RDH5 were analyzed by molecular screening methods and direct genomic sequencing. RESULTS: Each family had two affected members with typical fundus albipunctatus. The affected members were siblings born to unaffected parents who were seventh cousins in the first family and unrelated in the second family. The probands from both families were clinically similar except for the fundus dots that were more extensive in the second family to the point of involving the parafoveal region. In the initial phase of genetic screening RBP3 defects were ruled-out as the cause of the disease in both families. In contrast, RDH5 mutations were found in the affected siblings in both families. The proband in one had a homozygotic Gly238Trp missense mutation (GGG -> TGG) involving exon 4 and in the other carried compound heterozygotic changes Arg280His (CGC -> CAC) and Ala294Pro (GCC -> CCC) in exon 5. The disease phenotype was only manifested in family members with two abnormal RDH5 alleles consistent with autosomal recessive inheritance in both pedigrees. CONCLUSIONS: These findings strongly implicate defects of RDH5 as the cause of fundus albipunctatus and point to a heterogeneity of RDH5 mutations in this form of congenital stationary night blindness with variable expressivity.

Asunto(s)

Oxidorreductasas de Alcohol/genética , Enfermedades Hereditarias del Ojo/genética , Proteínas del Ojo , Ceguera Nocturna/genética , Enfermedades de la Retina/genética , Proteínas de Unión al Retinol/genética , Adulto , Secuencia de Bases , ADN/química , Femenino , Humanos , Masculino , Mutación , Ceguera Nocturna/congénito , Linaje , Reacción en Cadena de la Polimerasa , Polimorfismo Conformacional Retorcido-Simple , Enfermedades de la Retina/congénito

RESUMEN

A 46-year-old white female was admitted for decompensated cor pulmonale (CP). It had not interfered with her daily activities and she had not experienced shortness of breath, fatigue or muscle weakness prior to the onset of right heart failure. A thorough investigation revealed severe generalized muscle weakness with restrictive chest bellows disease and secondary CP (mean pressure in the pulmonary artery 60 mm Hg). After having refused respiratory support the patient died a few days after admission. The muscle biopsy was consistent with adult-onset acid-maltase deficiency. This is a rare case of metabolic myopathy presenting as decompensated CP without previous symptoms of muscle weakness. This condition can easily be treated with nocturnal ventilatory support, improving the quality and length of life.

Asunto(s)

Glucano 1,4-alfa-Glucosidasa/deficiencia , Enfermedad del Almacenamiento de Glucógeno Tipo II/diagnóstico , Insuficiencia Cardíaca/etiología , Enfermedad Cardiopulmonar/etiología , Diagnóstico Diferencial , Resultado Fatal , Femenino , Enfermedad del Almacenamiento de Glucógeno Tipo II/complicaciones , Enfermedad del Almacenamiento de Glucógeno Tipo II/patología , Humanos , Persona de Mediana Edad , alfa-Glucosidasas

RESUMEN

The variable prognosis after myocardial infarction necessitates an individual tailoring of follow-up treatment. Therapeutic decisions must be based on a complete risk stratification including assessment of persisting ischemia, left ventricular function, rhythmic instability and cardiovascular risk factor profile. High risk patients (prognostic indication) as well as symptomatic patients (symptomatic indication) should be referred for coronary angiography to assess the need for revascularisation procedures (PTCA, CABG). The individual risk profile also defines drug therapy for secondary prevention (not more than 3-4 drugs): anti-platelet agents or anticoagulation in every patient; beta blockers in all but the lowest risk group; ACE-inhibitors in heart failure or asymptomatic, substantial left ventricular dysfunction; liberal use of cholesterol-reducing drugs. Life style alterations should be encouraged in almost every patient. Information about the necessary measures to be taken upon occurrence of angina at rest or other cardiac symptoms must be repeatedly given to all patients.

Asunto(s)

Cuidados Posteriores/métodos , Infarto del Miocardio/rehabilitación , Terapia Combinada , Angiografía Coronaria , Humanos , Infarto del Miocardio/diagnóstico por imagen , Pronóstico , Recurrencia , Factores de Riesgo

RESUMEN

PIP: This study of domestic violence uses data gathered from interviews in 1987-88 from a random sample of 129 women with children who were divorced in Philadelphia, Pennsylvania, courts in 1986 to demonstrate that violence is a significant determinant of divorce and that violence plays an important role during asset negotiations after marital separation. The study revealed that many of the women experienced violence during their marriages and stated that it was a factor in their leaving their husbands (19% left because of the violence). Women left their husbands after particularly serious violent incidents or when they believed that witnessing the violence was harming their children. This sample was not asked to specify if they experienced violence during or after marriage, but 4% of the women reported experiencing violence for the first time during the separation, 11 women volunteered that violence extended from their marriages into their separation, and 6 women faced immediate threats of violence during separation. Reports in the literature indicate that marital separation increases women's risk of injury and of death. The current study indicates that experiences of violence impeded women's ability to negotiate for marital assets and child support during separation or for visitation rights after the divorce. Several women were also afraid to try to obtain increases in child support or to force their husbands to pay ordered amounts. Policy implications include the necessity of providing women with guaranteed child support and of exercising caution when recommending divorce mediation.^ieng

Asunto(s)

Divorcio , Violencia Doméstica , Recursos en Salud , Mujeres , Américas , Crimen , Países Desarrollados , Matrimonio , América del Norte , Organización y Administración , Pennsylvania , Problemas Sociales , Estados Unidos

RESUMEN

Soil erosion is a major environmental threat to the sustainability and productive capacity of agriculture. During the last 40 years, nearly one-third of the world's arable land has been lost by erosion and continues to be lost at a rate of more than 10 million hectares per year. With the addition of a quarter of a million people each day, the world population's food demand is increasing at a time when per capita food productivity is beginning to decline.