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The efficacy of a brief intervention to reduce alcohol misuse in patients with HIV in South Africa: study protocol for a randomized controlled trial
Huis in ’t Veld Diana,Skaal Linda,Peltzer Karl,Colebunders Robert
Trials , 2012, DOI: 10.1186/1745-6215-13-190
Abstract: Background Alcohol abuse comes with risks for increased morbidity and mortality among patients with HIV. This study aims to determine the prevalence of alcohol use and other risk factors in a sample of primary care patients with HIV in South Africa and to assess a brief intervention to reduce the use of alcohol in this group. Methods/Design A single-blinded randomized controlled trial is designed to determine the efficacy of a brief intervention to reduce hazardous alcohol use in patients with HIV. The study will be carried out on out-patients with HIV in two primary healthcare HIV clinics near Pretoria, South Africa. Alcohol use will be assessed with the Alcohol Use Disorder Identification Test questionnaire. Other data that will be collected relate to health-related quality of life, depression, sexual behavior, internalized AIDS stigma, HIV-related information and adherence to antiretroviral therapy (self-reported 7-day recall of missed doses, Visual Analog Scale and pill count). The intervention consists of a brief counseling session to reduce alcohol risk; the control group receives a health education leaflet. Discussion The findings will be important in the public health setting. If the intervention proves to be efficient, it could potentially be incorporated into the HIV care policy of the Ministry of Health. Trial registration Pan African Clinical trial Registry: PACTR201202000355384
Effects of Prenatal Alcohol Exposure on the Developing Kidneys
Farahnak Assadi
Iranian Journal of Pediatrics , 2008,
Abstract: Objective: Clinical and experimental studies strongly suggest that prenatal alcohol exposure is associated with zinc deficiency and impaired renal tubular function. Whether maternal alcohol consumption during pregnancy causes renal tubular cell injury is unknown.Material & Methods: Renal function was studied in 8 infants with fetal alcohol syndrome (FAS) and 8 healthy age-matched infants. Renal function and structure were also examined in 11 offspring of rats exposed to alcohol during gestation.Findings: Infants with FAS had limited ability to concentrate urine after water restriction (P<0.001) and impaired acidification after acute acid loading (P<0.001) compared to control group. Plasma zinc levels were lower (P<0.001) and urinary zinc excretion was higher (P<0.001) in infants with FAS compared to control infants. Scanning electron microscopic studies revealed cytoplasmic mitochondrial hypertrophy and vacuolar structures of the epithelial cells of the cortical collecting ducts in the rat kidney following fetal exposure to alcohol.Conclusion: These findings suggest that offspring of rats exposed to alcohol during fetal life have renal functional and structural abnormalities that may be responsible in the genesis of renal functional abnormalities as described in infants with FAS.
The DYD-RCT protocol: an on-line randomised controlled trial of an interactive computer-based intervention compared with a standard information website to reduce alcohol consumption among hazardous drinkers
Elizabeth Murray, Jim McCambridge, Zarnie Khadjesari, Ian R White, Simon G Thompson, Christine Godfrey, Stuart Linke, Paul Wallace
BMC Public Health , 2007, DOI: 10.1186/1471-2458-7-306
Abstract: In a two-arm randomised controlled trial, an on-line psychologically enhanced interactive computer-based intervention is compared with a flat, text-based information web-site. Recruitment, consent, randomisation and data collection are all on-line. The primary outcome is total past-week alcohol consumption; secondary outcomes include hazardous or harmful drinking, dependence, harm caused by alcohol, and mental health. A health economic analysis is included.This trial will provide information on the effectiveness and cost-effectiveness of an on-line intervention to help heavy drinkers drink less.International Standard Randomised Controlled Trial Number Register ISRCTN31070347Excessive alcohol consumption is a significant public health problem throughout the world. Regular heavy alcohol consumption and binge drinking are associated with physical problems, mental health problems, antisocial behaviour, violence, accidents, suicides, injuries, road traffic accidents, unsafe sexual behaviour, underperformance at work or school, and crime. People who drink too much can be described as hazardous or harmful drinkers, although there is considerable overlap between these two categories. Hazardous drinkers are those whose alcohol consumption puts them at risk of physical, mental or social harm, while harmful drinkers are those who are already experiencing harm as a result of alcohol consumption. It has been estimated that 26% of the population of England (38% of men and 16% of women aged 16 – 64) drink hazardously or harmfully, equating to approximately 7.1 million people in England alone [1], and costing the NHS £1.7bn p.a. [2]. Alcohol misuse is a problem throughout Europe and comes third after smoking and high blood pressure as the most significant risk factor for ill health in the European Union [3]. In the US in 2002 – 03, 23% of the population reported binge drinking in the past month [4]. The health care costs of alcohol misuse in the US have been estimated at $26.3 bill
The Contribution of Childhood Parental Rejection and Early Androgen Exposure to Impairments in Socio-Cognitive Skills in Intimate Partner Violence Perpetrators with High Alcohol Consumption  [PDF]
ángel Romero-Martínez,Marisol Lila,Alba Catalá-Mi?ana,Ryan K. Williams,Luis Moya-Albiol
International Journal of Environmental Research and Public Health , 2013, DOI: 10.3390/ijerph10083753
Abstract: Alcohol consumption, a larger history of childhood parental rejection, and high prenatal androgen exposure have been linked with facilitation and high risk of recidivism in intimate partner violence (IPV) perpetrators. Participants were distributed into two groups according to their alcohol consumption scores as high (HA) and low (LA). HA presented a higher history of childhood parental rejection, prenatal masculinization (smaller 2D:4D ratio), and violence-related scores than LA IPV perpetrators. Nonetheless, the former showed poor socio-cognitive skills performance (cognitive flexibility, emotional recognition and cognitive empathy). Particularly in HA IPV perpetrators, the history of childhood parental rejection was associated with high hostile sexism and low cognitive empathy. Moreover, a masculinized 2D:4D ratio was associated with high anger expression and low cognitive empathy. Parental rejection during childhood and early androgen exposure are relevant factors for the development of violence and the lack of adequate empathy in adulthood. Furthermore, alcohol abuse plays a key role in the development of socio-cognitive impairments and in the proneness to violence and its recidivism. These findings contribute to new coadjutant violence intervention programs, focused on the rehabilitation of basic executive functions and emotional decoding processes and on the treatment of alcohol dependence.
Prenatal intervention for urinary obstruction and myelomeningocele
Swana, Hubert S.;Sutherland, Ronald S.;Baskin, Laurence;
International braz j urol , 2004, DOI: 10.1590/S1677-55382004000100010
Abstract: widespread use of ultrasonography has resulted in an increase in the recognition of fetal hydronephrosis. the enthusiasm that accompanied early interventions has been tempered by the experience and results obtained over the past 2 decades. the goal has remained the same: to identify patients with serious prenatal obstruction and to identify those which may benefit from intervention. myelomeningocele remains a devastating congenital anomaly. fetal and experimental studies suggested that patients with myelomeningocele could benefit from prenatal intervention. advances in technology and perinatal management have made intervention for more complex malformations such as myelomeningocele possible. this article will review current knowledge and will detail rational management for the management of prenatal hydronephrosis. the current state of antenatal myelomeningocele repair and the urologic implications will be described as well.
Prenatal intervention for urinary obstruction and myelomeningocele  [cached]
Swana Hubert S.,Sutherland Ronald S.,Baskin Laurence
International braz j urol , 2004,
Abstract: Widespread use of ultrasonography has resulted in an increase in the recognition of fetal hydronephrosis. The enthusiasm that accompanied early interventions has been tempered by the experience and results obtained over the past 2 decades. The goal has remained the same: to identify patients with serious prenatal obstruction and to identify those which may benefit from intervention. Myelomeningocele remains a devastating congenital anomaly. Fetal and experimental studies suggested that patients with myelomeningocele could benefit from prenatal intervention. Advances in technology and perinatal management have made intervention for more complex malformations such as myelomeningocele possible. This article will review current knowledge and will detail rational management for the management of prenatal hydronephrosis. The current state of antenatal myelomeningocele repair and the urologic implications will be described as well.
Social Behavior of Offspring Following Prenatal Cocaine Exposure in Rodents: A Comparison with Prenatal Alcohol  [PDF]
Sonya K. Sobrian,R. R. Holson
Frontiers in Psychiatry , 2011, DOI: 10.3389/fpsyt.2011.00066
Abstract: Clinical and experimental reports suggest that prenatal cocaine exposure (PCE) alters the offsprings’ social interactions with caregivers and conspecifics. Children exposed to prenatal cocaine show deficits in caregiver attachment and play behavior. In animal models, a developmental pattern of effects that range from deficits in play and social interaction during adolescence, to aggressive reactions during competition in adulthood is seen. This review will focus primarily on the effects of PCE on social behaviors involving conspecifics in animal models. Social relationships are critical to the developing organism; maternally directed interactions are necessary for initial survival. Juvenile rats deprived of play behavior, one of the earliest forms of non-mother directed social behaviors in rodents, show deficits in learning tasks and sexual competence. Social behavior is inherently complex. Because the emergence of appropriate social skills involves the interplay between various conceptual and biological facets of behavior and social information, it may be a particularly sensitive measure of prenatal insult. The social behavior surveyed include social interactions, play behavior/fighting, scent marking, and aggressive behavior in the offspring, as well as aspects of maternal behavior. The goal is to determine if there is a consensus of results in the literature with respect to PCE and social behaviors, and to discuss discrepant findings in terms of exposure models, the paradigms, and dependent variables, as well as housing conditions, and the sex and age of the offspring at testing. As there is increasing evidence that deficits in social behavior may be sequelae of developmental exposure alcohol, we compare changes in social behaviors reported for prenatal alcohol with those reported for prenatal cocaine. Shortcomings in the both literatures are identified and addressed in an effort to improve the translational value of future experimentation.
Prenatal exposure to alcohol does not affect radial maze learning and hippocampal mossy fiber sizes in three inbred strains of mouse
Frans Sluyter, Laure Jamot, Jean-Yves Bertholet, Wim E Crusio
Behavioral and Brain Functions , 2005, DOI: 10.1186/1744-9081-1-5
Abstract: Although we anticipated a modification of both learning and IIPMF sizes, no such effects were detected. Prenatal alcohol exposure did, however, interfere with reproduction in C57BL/6J animals and decrease body and brain weight (in interaction with the genotype) at adult age.Prenatal alcohol exposure influenced neither radial maze performance nor the sizes of the IIPMF terminal fields. We believe that future research should be pointed either at different targets when using mouse models for Fetal Alcohol Syndrome (e.g. more complicated behavioral paradigms, different hippocampal substructures, or other brain structures) or involve different animal models.It has long been known that prenatal exposure to alcohol can have devastating effects. In 1968, Lemoine et al. published a paper, in French, that described "des anomalies dans les infants de parents alcooliques" [1]. Five years later Jones and Smith [2] followed with their now classic paper on Fetal Alcohol Syndrome (FAS), which is the name given to a group of physical and mental birth defects that are the direct result of a woman's drinking alcohol during pregnancy. These defects may include mental retardation, growth deficiencies, central nervous system dysfunction, craniofacial abnormalities, and behavioral maladjustments (for an enumeration, see, among others, [3], and http://www.acbr.com/fas/index.htm webcite).Since then literally thousands of studies have been done and substantial advances in the understanding of FAS have been made, not in the least because of animal models, among them the mouse [4,5]. These models strongly parallel the physiological responses to alcohol in human development and have led to valuable insights into the susceptibility to alcohol of specific parts of the developing embryo. One of the more vulnerable brain regions, for instance, is the hippocampus, which is believed to be a primary target of prenatal alcohol and therefore responsible for many neurobehavioral abnormalities [6]. Thus,
Fetal Alcohol Spectrum Disorder (FASD) Associated Neural Defects: Complex Mechanisms and Potential Therapeutic Targets  [PDF]
Pooja Muralidharan,Swapnalee Sarmah,Feng C. Zhou,James A. Marrs
Brain Sciences , 2013, DOI: 10.3390/brainsci3020964
Abstract: Fetal alcohol spectrum disorder (FASD), caused by prenatal alcohol exposure, can result in craniofacial dysmorphism, cognitive impairment, sensory and motor disabilities among other defects. FASD incidences are as high as 2% to 5 % children born in the US, and prevalence is higher in low socioeconomic populations. Despite various mechanisms being proposed to explain the etiology of FASD, the molecular targets of ethanol toxicity during development are unknown. Proposed mechanisms include cell death, cell signaling defects and gene expression changes. More recently, the involvement of several other molecular pathways was explored, including non-coding RNA, epigenetic changes and specific vitamin deficiencies. These various pathways may interact, producing a wide spectrum of consequences. Detailed understanding of these various pathways and their interactions will facilitate the therapeutic target identification, leading to new clinical intervention, which may reduce the incidence and severity of these highly prevalent preventable birth defects. This review discusses manifestations of alcohol exposure on the developing central nervous system, including the neural crest cells and sensory neural placodes, focusing on molecular neurodevelopmental pathways as possible therapeutic targets for prevention or protection.
Acetaldehyde reinforcement and motor reactivity in newborns with or without a prenatal history of alcohol exposure  [PDF]
Samanta M. March,Paula Abate,José I. Hernández
Frontiers in Behavioral Neuroscience , 2013, DOI: 10.3389/fnbeh.2013.00069
Abstract: Animal models have shown that early ontogeny seems to be a period of enhanced affinity to ethanol. Interestingly, the catalase system that transforms ethanol (EtOH) into acetaldehyde (ACD) in the brain, is more active in the perinatal rat compared to adults. ACD has been found to share EtOH's behavioral effects. The general purpose of the present study was to assess ACD motivational and motor effects in newborn rats as a function of prenatal exposure to EtOH. Experiment 1 evaluated if ACD (0.35 μmol) or EtOH (0.02 μmol) supported appetitive conditioning in newborn pups prenatally exposed to EtOH. Experiment 2 tested if prenatal alcohol exposure modulated neonatal susceptibility to ACD's motor effects (ACD dose: 0, 0.35 and 0.52 μmol). Experiment 1 showed that EtOH and ACD supported appetitive conditioning independently of prenatal treatments. In Experiment 2, latency to display motor activity was altered only in neonates prenatally treated with water and challenged with the highest ACD dose. Prenatal EtOH experience results in tolerance to ACD's motor activity effects. These results show early susceptibility to ACD's appetitive effects and attenuation of motor effects as a function of prenatal history with EtOH, within a stage in development where brain ACD production seems higher than later in life.
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