The effects of breathing patterns and massage on the pain and perception of labor in primiparous women

زمینه و هدف: زایمان یک تجربه مهم در زندگی زن محسوب می شود وکیفیت این تجربه اثرات کوتاه مدت و دراز مدتی بر جای می گذارد. تجارب منفی آن سبب بروز مشکلات روحی- روانی و اختلالات جنسی در دوره بعد از زایمان شده و بر رابطه عاطفی بین مادر و نوزاد تأثیر شگرف می گذارد. از طرفی ترس و اضطراب از درد زایمان منجر به افزایش روزافزون مداخلات جراحی می شود. لذا این مطالعه با هدف بررسی اثرات الگوهای تنفسی و ماساﮊ بر نگرش و شدت درد زایمان انجام گرفت. روش بررسی: در این بررسی که به روش کارآزمایی بالینی صورت گرفته است، 50 زائوی نخست زا که جهت زایمان واژینال به بیمارستان ارجمند شهر کرمان مراجعه کرده بودند به صورت تصادفی به دو گروه مساوی آزمون و کنترل تقسیم شدند. برای گروه آزمون از ابتدا تا پایان مرحله دوم زایمان ماساژ و تکنیک های تنفسی مختلفی اجرا گردید در صورتی که برای گروه کنترل این مداخلات صورت نگرفت. شدت درد زایمان به کمک پرسشنامه Visual Analogue Scale (VAS) توسط زائوها در دیلاتاسیون های 2، 4، 6، 8 و 10 سانتی متر مشخص گردید. داده ها از طریق VAS، فرم مشاهده رفتاری و فرم مصاحبه بعد از زایمان جمع آوری و با استفاده از آزمون های آماری تی تست، کای دو، ضریب همبستگی پیرسون و ANOVA توسط نرم افزار SPSS مورد تجزیه و تحلیل قرار گرفت. یافته ها: نتایج پژوهش نشان داد که میانگین شدت درد در مرحله اول زایمان در گروه آزمون و کنترل به ترتیب 67/0±22/5 و 72/0±23/6 بدست آمد (05/0>p). نگرش مادران نسبت به پروسه زایمان در گروه آزمون مثبت تر بود (05/0>p) و تغییرات رفتاری در طول مرحله فعال زایمان مثل گریه بلند، جیغ زدن، بیان ترس، و غیره در مادران گروه کنترل بیشتر از گروه آزمون بود (05/0>p). نتیجه گیری: با توجه به یافته های فوق، بکارگیری الگوهای تنفسی و ماساﮊ روشهای مداخله گر مقرون به صرفه ای بوده که می تواند بطور مؤثری در کاهش شدت درد زایمان و ایجاد نگرش مثبت به آن مفید باشد

The genetics of dementia

Over the past decade, there has been a dramatic evolution of genetic methodologies that can be used to identify genes contributing to disease. Initially, the focus was primarily on classical linkage analysis; more recently, genomewide association studies, and high-throughput whole genome and whole exome sequencing have provided efficient approaches to detect common and rare variation contributing to disease risk. Application of these methodologies to dementias has led to the nomination of dozens of causative and susceptibility genes, solidifying the recognition that genetic factors are important contributors to the disease processes. In this review, the authors focus on current knowledge of the genetics of Alzheimer's disease and frontotemporal lobar degeneration. A working understanding of the genes relevant to common dementias will become increasingly critical, as options for genetic testing and eventually gene-specific therapeutics are developed

A multivariate finite mixture latent trajectory model with application to dementia studies

Dementia patients exhibit considerable heterogeneity in individual trajectories of cognitive decline, with some patients showing rapid decline following diagnoses while others exhibiting slower decline or remaining stable for several years. Dementia studies often collect longitudinal measures of multiple neuropsychological tests aimed to measure patients’ decline across a number of cognitive domains. We propose a multivariate finite mixture latent trajectory model to identify distinct longitudinal patterns of cognitive decline simultaneously in multiple cognitive domains, each of which is measured by multiple neuropsychological tests. EM algorithm is used for parameter estimation and posterior probabilities are used to predict latent class membership. We present results of a simulation study demonstrating adequate performance of our proposed approach and apply our model to the Uniform Data Set from the National Alzheimer's Coordinating Center to identify cognitive decline patterns among dementia patients

Expression profiling and QTL analysis: a powerful complementary strategy in drug abuse research

Alcoholism is a complex disease exhibiting a multifactorial mode of transmission. To simplify the genetic and phenotypic complexity of the alcoholic phenotype, alcohol-preferring (P) and -non-preferring (NP) rats were developed on the basis of alcohol preference and consumption as an animal model of alcoholism. Total gene expression analysis (TOGA) and quantitative trait loci (QTL) analysis were applied to selectively bred, inbred P and NP rats as complementary studies to identify genetic factors that contribute to alcohol preference and consumption. TOGA analysis was utilized to screen for differential expression in several brain regions involved in the mesocorticolimbic dopamine (DA) system. Genes exhibiting differences in expression were then screened for an association to the alcohol preference phenotype, the quantitative trait of a previously identified QTL. By evaluating differences in gene expression for linkage to a quantitative trait, this combined approach was implemented to identify alpha-synuclein, a candidate gene for alcohol preference

From QTL to candidate gene: a genetic approach to alcoholism research

A major focus of research in alcohol-related disorders is to identify the genes and pathways that modulate alcohol-seeking behavior. In light of this, animal models have been established to study various aspects of alcohol dependence. The selectively bred alcohol-preferring (P) and -nonpreferring (NP) lines were developed from Wistar rats to model high and low voluntary alcohol consumption, respectively. Using inbred P and NP strains, a strong QTL (LOD-9.2) for alcohol consumption was identified on rat chromosome 4. To search for candidate genes that underlie this chromosomal region, complementary molecular-based strategies were implemented to identify genetic targets that likely contribute to the linkage signal. In an attempt to validate these genetic targets, corroborative studies have been utilized including pharmacological studies, knock-out/transgenic models as well as human association studies. Thus far, three candidate genes, neuropeptide Y (Npy), alpha-synuclein (Snca), and corticotrophin-releasing factor receptor 2 (Crhr2), have been identified that may account for the linkage signal. With the recent advancements in bioinformatics and molecular biology, QTL analysis combined with molecular-based strategies provides a systematic approach to identify candidate genes that contribute to various aspects of addictive behavior

Genetic and neurophysiological correlates of the age of onset of alcohol use disorders in adolescents and young adults.

Discrete time survival analysis was used to assess the age-specific association of event-related oscillations (EROs) and CHRM2 gene variants on the onset of regular alcohol use and alcohol dependence. The subjects were 2,938 adolescents and young adults ages 12-25. Results showed that the CHRM2 gene variants and ERO risk factors had hazards which varied considerably with age. The bulk of the significant age-specific associations occurred in those whose age of onset was under 16. These associations were concentrated in those subjects who at some time took an illicit drug. These results are consistent with studies which associate greater rates of alcohol dependence among those who begin drinking at an early age. The age specificity of the genetic and neurophysiological factors is consistent with recent studies of adolescent brain development, which locate an interval of heightened vulnerability to substance use disorders in the early to mid teens

Genome-wide association studies of the self-rating of effects of ethanol (SRE).

The level of response (LR) to alcohol as measured with the Self-Report of the Effects of Alcohol Retrospective Questionnaire (SRE) evaluates the number of standard drinks usually required for up to four effects. The need for a higher number of drinks for effects is genetically influenced and predicts higher risks for heavy drinking and alcohol problems. We conducted genome-wide association study (GWAS) in the African-American (COGA-AA, N = 1527 from 309 families) and European-American (COGA-EA, N = 4723 from 956 families) subsamples of the Collaborative Studies on the Genetics of Alcoholism (COGA) for two SRE scores: SRE-T (average of first five times of drinking, the period of heaviest drinking, and the most recent 3 months of consumption) and SRE-5 (the first five times of drinking). We then meta-analyzed the two COGA subsamples (COGA-AA + EA). Both SRE-T and SRE-5 were modestly heritable (h2 : 21%-31%) and genetically correlated with alcohol dependence (AD) and DSM-IV AD criterion count (rg : 0.35-0.76). Genome-wide significant associations were observed (SRE-T: chromosomes 6, rs140154945, COGA-EA P = 3.30E-08 and 11, rs10647170, COGA-AA+EA P = 3.53E-09; SRE-5: chromosome13, rs4770359, COGA-AA P = 2.92E-08). Chromosome 11 was replicated in an EA dataset from the National Institute on Alcohol Abuse and Alcoholism intramural program. In silico functional analyses and RNA expression analyses suggest that the chromosome 6 locus is an eQTL for KIF25. Polygenic risk scores derived using the COGA SRE-T and SRE-5 GWAS predicted 0.47% to 2.48% of variances in AD and DSM-IV AD criterion count in independent datasets. This study highlights the genetic contribution of alcohol response phenotypes to the etiology of alcohol use disorders

Stress-response pathways are altered in the hippocampus of chronic alcoholics

The chronic high-level alcohol consumption seen in alcoholism leads to dramatic effects on the hippocampus, including decreased white matter, loss of oligodendrocytes and other glial cells, and inhibition of neurogenesis. Examining gene expression in post mortem hippocampal tissue from 20 alcoholics and 19 controls allowed us to detect differentially expressed genes that may play a role in the risk for alcoholism or whose expression is modified by chronic consumption of alcohol. We identified 639 named genes whose expression significantly differed between alcoholics and controls at a False Discovery Rate (FDR) ≤ 0.20; 52% of these genes differed by at least 1.2-fold. Differentially expressed genes included the glucocorticoid receptor and the related gene FK506 binding protein 5 (FKBP5), UDP glycosyltransferase 8 (UGT8), urea transporter (SLC14A1), zinc transporter (SLC39A10), Interleukin 1 receptor type 1 (IL1R1), thioredoxin interacting protein (TXNIP), and many metallothioneins. Pathways related to inflammation, hypoxia, and stress showed activation, and pathways that play roles in neurogenesis and myelination showed decreases. The cortisol pathway dysregulation and increased inflammation identified here are seen in other stress-related conditions such as depression and post-traumatic stress disorder and most likely play a role in addiction. Many of the detrimental effects on the hippocampus appear to be mediated through NF-κB signaling. Twenty-four of the differentially regulated genes were previously identified by genome-wide association studies of alcohol use disorders; this raises the potential interest of genes not normally associated with alcoholism, such as suppression of tumorigenicity 18 (ST18), BCL2-associated athanogene 3 (BAG3), and von Willebrand factor (VWF)

ADH1B is associated with alcohol dependence and alcohol consumption in populations of European and African ancestry.

A coding variant in alcohol dehydrogenase 1B (ADH1B) (rs1229984) that leads to the replacement of Arg48 with His48 is common in Asian populations and reduces their risk for alcoholism, but because of very low allele frequencies the effects in European or African populations have been difficult to detect. We genotyped and analyzed this variant in three large European and African-American case-control studies in which alcohol dependence was defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, and demonstrated a strong protective effect of the His48 variant (odds ratio (OR) 0.34, 95% confidence interval (CI) 0.24, 0.48) on alcohol dependence, with genome-wide significance (6.6 × 10(-10)). The hypothesized mechanism of action involves an increased aversive reaction to alcohol; in keeping with this hypothesis, the same allele is strongly associated with a lower maximum number of drinks in a 24-hour period (lifetime), with P=3 × 10(-13). We also tested the effects of this allele on the development of alcoholism in adolescents and young adults, and demonstrated a significantly protective effect. This variant has the strongest effect on risk for alcohol dependence compared with any other tested variant in European populations