bluuebunny/crossref_metadata_2025_split huggingface dataset:
Capture–recapture estimation of unreported work‐related musculoskeletal disorders in Connecticut
Authors: Morse Timothy , Dillon Charles , Warren Nicholas , Hall Charles , Hovey Deborah 
Published: August 2002

AbstractBackgroundEstimates of the extent of musculoskeletal disorders (MSD) are usually based upon workers' compensation reports, although recent reports indicate that there may be widespread under‐reporting of MSD.MethodsAn estimate of the incidence of arm and hand work‐related MSD was made using capture–recapture analysis of the overlap between state workers' compensation reports and physician reports in Connecticut for 1995. The resulting estimate was compared to a population‐based survey of MSD.ResultsThere was very small overlap between the two state injury reporting systems: 6.7% of 793 reported workers' compensation cases, or 8% of 661 physician's reports. The estimate for MSD not captured by either system was 13,285, resulting in 14,686 (95% CI: 9,733–18,453) total reported and non‐reported cases. This compares to an estimate of 13,775 cases (95% CI: 8,800–18,800) based on a phone survey.ConclusionsThis analysis points to substantial under‐reporting of MSD in Connecticut: estimates of unreported cases exceed those officially reported by a factor of 11:1. The findings have an important bearing on injury prevention programs and policy making. Am. J. Ind. Med. 39:636–642, 2001. © 2001 Wiley‐Liss, Inc.
Advent of occupational health services research*
Authors: Deitchman Scott , Dembe Allard E. , Himmelstein Jay 
Published: August 2002

AbstractAfter lagging behind health services research in general health care, research is now examining health services provided to workers suffering occupational injuries and illnesses. The National Institute for Occupational Safety and Health, the Robert Wood Johnson Foundation Workers' Compensation Health Initiative, the Agency for Health Care Policy and Research (now the Agency for Healthcare Research and Quality), and the Canadian Institute for Work and Health co‐sponsored a June, 1999, conference to explore research needs in this area. Fundamental tenets for advancing occupational health services research include: adopting the goal of improving occupational health care, including better integration of preventive and curative care; creating standardized interstate occupational health care data sets that include medical, economic, and patient perspectives; better defining quality in occupational care and developing appropriate performance measures; in addition to medical costs, assessing social, economic, medical and functional outcomes of care; considering the connections between work and health, including general health services; and addressing the need to train qualified occupational health services researchers. Am. J. Ind. Med. 40:291–294, 2001. Published 2001 Wiley‐Liss, Inc.
Determinants of duration of disability and return‐to‐work after work‐related injury and illness: Challenges for future research
Authors: Krause Niklas , Frank John W. , Dasinger Lisa K. , Sullivan Terry J. , Sinclair Sandra J. 
Published: August 2002

AbstractBackgroundThe purpose of this review was to identify critical data and research needs in addressing the following question: What are the primary factors that affect the time lost from work, return‐to‐work (RTW), subsequent unemployment, and changes in occupation after disabling illness or injury?MethodsReview of the literature to identify research challenges originating from the multitude of disciplines, data sources, outcome measures, and methodological and analytical problems.ResultsAbout 100 different determinants of RTW outcomes were identified. Their impact varies across different phases of the disablement process. Recommendations are provided for addressing five selected research challenges.ConclusionInterdisciplinary research needs to develop a comprehensive conceptual framework. Priority should be given to studies on specific domains of risk factors meeting five selection criteria: amenability to change; relevance to users of research; generalizability across health conditions, disability phases, and settings; “degree of promise” as derived from qualitative exploratory studies; and capacity to improve measurement instruments. Combining qualitative and quantitative research methods is necessary to bridge existing knowledge gaps. Am. J. Ind. Med. 40:464–484, 2001. © 2001 Wiley‐Liss, Inc.
Different familial transmission patterns in bipolar I disorder with onset before and after age 25
Authors: Grigoroiu‐Serbanescu Maria , Martinez Maria , Nöthen Markus M. , Grinberg Mihaela , Sima Dorina , Propping Peter , Marinescu Elvira , Hrestic Mihaela 
Published: August 2002

AbstractGene identification in common disorders such as Alzheimer disease and breast cancer has greatly profited from the use of age of onset as criterion to delineate subgroups of disease characterized by different inheritance patterns. In bipolar affective disorder, where the majority of linkage studies have produced conflicting results, studies reporting clinical characteristics and familial occurrence of disease have suggested that age of onset might serve as an indicator for identifying more homogeneous subgroups of disease. Our study was the first to examine this hypothesis by the means of segregation analysis. We investigated a sample of 177 bipolar I probands recruited from consecutive admissions and their first‐ and second‐degree relatives (2,407 subjects). Probands were subdivided into an early‐onset (n = 107) and a late‐onset group (n = 70) using an age of onset of 25 as a cut‐off point. This age was chosen because the observed age of onset distribution was bimodal with a cut‐off of 25 years. Morbid risks for affective disorder were found significantly higher (P = 0.01) in relatives of probands with an early onset than in probands with late onset of disease. The segregation analysis showed that the disease is transmitted differently in early‐ and late‐onset groups. In the early‐onset group, a non‐Mendelian major gene with a polygenic component was favored while the data in the late‐onset group were compatible with a multifactorial model. This result may have important implications for future molecular studies aiming at the identification of disease‐associated genes. © 2001 Wiley‐Liss, Inc.
Serotonin transporter promoter polymorphism, peripheral indexes of serotonin function, and personality measures in families with alcoholism
Authors: Stoltenberg Scott F. , Twitchell Geoffrey R. , Hanna Gregory L. , Cook Edwin H. , Fitzgerald Hiram E. , Zucker Robert A. , Little Karley Y. 
Published: August 2002

AbstractA functional polymorphism in the regulatory region of the serotonin transporter gene (5‐HTTLPR) is considered to be a plausible candidate gene for anxiety‐related personality traits and for alcoholism. Empirical support for the association between 5‐HTTLPR and psychological traits has been somewhat inconsistent; however, observations of the functional dominance of the low‐activity s‐allele over the l‐allele have been more consistent. When studying the influence of particular genes on psychological traits, it seems useful also to assess more biological intermediate traits that may mediate the effects of those genes on the traits of interest. The present study examined relationships between 5‐HTTLPR genotype, whole blood serotonin (5‐HT) level, and platelet 5‐HT binding in 150 Caucasian subjects from 50 biological families. Individuals with the s‐allele had lower average platelet 5‐HT binding availability than those with the l/l genotype (P < 0.025). Whole blood 5‐HT level was not associated with 5‐HTTLPR genotype. In adult men, those with the s‐allele had higher mean scores on the NEO‐FFI personality trait of openness than did those with the l/l genotype (P = 0.002). The effect was not statistically significant in women (P = 0.42), although it was in the same direction. Our findings do not support an association of 5‐HTTLPR genotype with alcoholism diagnosis, alcoholism subtype, or the personality trait of neuroticism. The results of this pilot study suggest that further work should examine the mediation of the genetic effects on personality traits by biochemical measures and their moderation by gender. © 2002 Wiley‐Liss, Inc.
Genetic study of Apolipoprotein E gene, alpha‐1 antichymotrypsin gene in sporadic Parkinson disease
Authors: Tang Guomei , Xie Huijun , Xu Lin , Hao Yixin , Lin Dayu , Ren Daming 
Published: August 2002

AbstractSeveral lines of evidence have suggested some common genetic risk factors for Alzheimer disease (AD) and Parkinson disease (PD) because there are some overlapping pathologies in these two neurodegenerative diseases. In the present study, we investigated the role of Apolipoprotein E gene polymorphism and the signal peptide polymorphism in alpha‐1 antichymotrypsin (ACT) gene in idiopathic sporadic PD. The study was performed in a sample consisting of 68 PD cases and 160 healthy subjects in Shanghai China. We found no significant differences of ACT gene polymorphic distribution between PD cases and controls. The ApoE gene ε2/ε4 genotype was significantly more frequent in PD subjects (χ2 = 7.126, df = 1, P = 0.008) and conferred a 12.70 times susceptibility for PD (OR = 12.62, 95% CI: 1.445–110.17, χ2 = 5.259, P < 0.05, AF = 4.59%). No interaction of ApoE and ACT genes was detected in PD. Therefore, our data suggested that the ApoE ε2/ε4 genotype might be a susceptibility variant of moderate effect for sporadic idiopathic PD in our samples, whereas the ACT gene signal peptide polymorphism might not. © 2002 Wiley‐Liss, Inc.
Segregation analysis of Parkinson disease revealing evidence for a major causative gene
Authors: Maher N.E. , Currie L.J. , Lazzarini A.M. , Wilk J.B. , Taylor C.A. , Saint‐Hilaire M.H. , Feldman R.G. , Golbe L.I. , Wooten G.F. , Myers R.H. 
Published: August 2002

AbstractThe role of genetics in Parkinson disease (PD) continues to be an area of considerable interest and controversy. We collected information involving the nuclear families of 948 consecutively ascertained PD index cases from the University of Virginia (UVA) Health System, the University of Medicine and Dentistry of New Jersey–Robert Wood Johnson (RWJ) School of Medicine, and Boston University (BU) School of Medicine. We performed a segregation analysis to assess evidence for the presence of a Mendelian pattern of familial transmission. The proportion of male (60.4%) and female (39.6%) cases, the mean age of onset (57.7 years), and the proportion of affected fathers (4.7%), mothers (6.6%), brothers (2.9%), and sisters (3.2%) were similar across the three sites. While most of the index cases were male, modestly more of the reported affected relatives were female. These analyses support the presence of a rare major Mendelian gene for PD in both the age‐of‐onset and susceptibility model. The age‐of‐onset model provides evidence for a gene that influences age‐dependent penetrance of PD, influencing age of onset rather than susceptibility. We also found evidence for a Mendelian gene influencing susceptibility to the disease. It is not evident whether these two analyses are modeling the same gene or different genes with different effects on PD. The finding of significant genes influencing penetrance for PD raises the question of whether these may interact with environmental factors or other genes to increase the risk for PD. Such gene environment interactions, involving reduced penetrance in PD, may explain the low concordance rates among monozygotic twins for this disease. © 2002 Wiley‐Liss, Inc.
Polymorphism R25P in the gene encoding transforming growth factor‐beta (TGF‐β1) is a newly identified risk factor for proliferative diabetic retinopathy
Authors: Beránek Michal , Kan̆ková Kater̆ina , Benes̆ Petr , Izakovic̆ová‐Hollá Lydie , Znojil Vladimír , Hájek Dobroslav , Vlková Eva , Vácha Jir̆í 
Published: August 2002

AbstractAssociations of the genetic polymorphisms in the promoter region and the signal peptide sequence of the transforming growth factor‐beta (TGF‐β1) gene with proliferative diabetic retinopathy (PDR) in patients with non‐insulin‐dependent diabetes mellitus (NIDDM) were studied. A total of 245 Caucasian subjects comprised the two groups: NIDDM patients with PDR (n = 73) and NIDDM patients without PDR (n = 172). Allele frequencies of common TGF‐β1 polymorphisms (at positions −988C/A, −800G/A, −509C/T, +869T/C (L10P), and +915G/C (R25P)) were determined by PCR‐based methodology. All polymorphisms were in strong linkage disequilibrium (P < 10−2). Significantly higher frequencies of both the L allele and the R allele of the signal sequence polymorphisms in PDR subjects were found (after a correction for multiple comparisons, Pcorr < 10−2 and Pcorr < 10−4, respectively). Calculated odds ratios (ORs) for the LL and RR genotypes were 2.89 (95% confidence interval (CI), 1.6–5.1) and 19.73 (95% CI, 2.6−146.8), respectively. No significant differences between groups were found for the −800G/A and −509C/T polymorphisms. The −988A allele was not represented in our sample. Multiple logistic regression identified age, diabetes duration, and R25P polymorphism as significant predictors (P = 0.002, P = 0.000003, and P = 0.007, respectively). The frequencies of genotype combinations of the −800G/A, −509C/T, L10P, and R25P TGF‐β1 polymorphisms were significantly different between the PDR and non‐PDR groups (χ2 = 37.83, df = 20, P < 10−2). The frequency of haplotype consisting of majority alleles was found significantly associated with PDR (P < 0.03). The presented data indicate that the R25P polymorphisms in the TGF‐β1 gene could be regarded as a strong genetic risk factor for PDR. © 2002 Wiley‐Liss, Inc.
CUX2, a potential regulator of NCAM expression: Genomic characterization and analysis as a positional candidate susceptibility gene for bipolar disorder
Authors: Jacobsen Nick J.O. , Elvidge Gareth , Franks Emily K.E. , O'Donovan Michael C. , Craddock Nick , Owen Michael J. 
Published: August 2002

AbstractWe have previously reported cosegregation of bipolar affective disorder and Darier disease, a dominant skin disorder with a neuropsychiatric component. The gene for Darier disease was mapped to chromosome 12q23–q24.1 and linkage studies have subsequently implicated this region as harboring a susceptibility gene for bipolar affective disorder. We have genomically characterized the human homologue of murine Cux‐2, a neuronal‐specific transcription factor potentially involved in the regulation of neural cell adhesion molecule expression that maps to this region. Also, in a panel of 15 unrelated bipolar patients from multiply affected families showing increased allele sharing at markers in the 12q23–q24.1 region, we performed mutational screening of the CUX2 coding sequence, and 5′ untranslated region (5′ UTR). Resulting sequence were analyzed in a large sample of bipolar patients (n = 218) and control subjects (n = 218). No evidence was found for the involvement of variants within the CUX2 coding, or 5′ UTR sequence in producing susceptibility to bipolar disorder. © 2001 Wiley‐Liss, Inc.
Association of a polymorphism of the dopamine transporter gene with externalizing behavior problems and associated temperament traits: A longitudinal study from infancy to the mid‐teens
Authors: Jorm Anthony F. , Prior Margot , Sanson Ann , Smart Diana , Zhang Yafei , Easteal Simon 
Published: August 2002

AbstractThere have been reports that a variable number of tandem repeats (VNTR) polymorphism situated in the 3′ untranslated region of the dopamine transporter gene is associated with attention‐deficit hyperactivity disorder. On the basis of these findings, we predicted an association of this polymorphism with hyperactivity, other externalizing behavior problems, and related temperament traits in a general population sample. The association was investigated using children participating in a longitudinal study of childhood temperament and development. DNA was taken from 660 children who had been assessed for temperament from 4–8 months to 15–16 years, and for behavior problems from 3–4 to 15–16 years. No significant associations were found at any age. There are a number of methodological differences from earlier studies that might explain the lack of associations with hyperactivity. It is also possible that the earlier findings are not replicable. © 2001 Wiley‐Liss, Inc.
Malignancy of recurrent, early‐onset major depression: A family study
Authors: Zubenko George S. , Zubenko Wendy N. , Spiker Duane G. , Giles Donna E. , Kaplan Barry B. 
Published: August 2002

AbstractCoordinated efforts to identify susceptibility genes for unipolar major depressive disorder (MDD) and related disorders are now underway. These studies have focused on recurrent, early‐onset MDD (RE‐MDD), the most heritable form of this disorder. The goal of this study was to characterize the burden of MDD and other mood disorders, comorbid mental disorders, and excess mortality in RE‐MDD families. A total of 81 families were identified through probands over the age of 18, who met criteria for recurrent (≥ 2 episodes), early‐onset (≤ 25 years), nonpsychotic, unipolar MDD (RE‐MDD), and included 407 first‐degree relatives and 835 extended relatives. Psychiatric diagnoses for probands and their family members who provided blood samples were formulated from structured personal interviews, structured family history assessments, and available medical records. The remaining family members who participated and those who were deceased were evaluated through the family history method augmented by available medical records. Best estimate diagnoses were made during a consensus conference according to established diagnostic criteria. Approximately half of the first‐degree relatives and a quarter of extended relatives of RE‐MDD probands suffered from at least one mood disorder, typically MDD. As commonly observed for other oligogenic, multifactorial disorders, the severity of MDD reflected by age at onset and number of episodes attenuated with increasing familial/genetic distance from the proband. A substantial fraction of RE‐MDD probands and their first‐degree relatives met diagnostic criteria for additional psychiatric disorders that include prominent disturbances of mood. The deceased relatives of RE‐MDD probands died at a median age that was 8 years earlier than for the local population; over 40% died before reaching age 65. These differences in mortality statistics resulted from a shift toward younger ages at death across the lifespan, including a fivefold increase in the proportion of individuals who died in the first year of life. Several‐fold increases in the proportion of deaths by suicide, homicide, and liver disease were observed among the relatives of RE‐MDD probands. However, the rank order of the three most common causes of death—heart disease, cancer, and stroke—remained unchanged and differences in the proportions of deaths from the remaining causes were small. RE‐MDD is a strongly familial condition with a high rate of psychiatric comorbidity, whose malignant effects have a significant negative impact on the health and longevity of patients and their family members. © 2001 Wiley‐Liss, Inc.
Motor immaturity and specific speech and language impairment: Evidence for a common genetic basis
Authors: Bishop Dorothy V.M. 
Published: August 2002

AbstractPrevious studies have found an association between motor immaturity and specific language impairment in children. Data from two twin studies were used to address the question of whether these linked deficits have a common etiology. Study 1 involved 57 MZ and 22 DZ pairs where one or both twins had specific speech/language impairment. A control group of 173 single‐born children was also tested. Motor skill was assessed using a tapping task, which was carried out with left and right hands. Tapping scores were converted to scaled scores adjusted for age and sex. Unaffected twins and single‐born controls did not differ in motor skill, but twins with speech and/or language impairments obtained significantly poorer tapping scores than controls. Bivariate DeFries‐Fulker analysis pointed to shared genetic influence on tapping speed and a measure of speech production accuracy. In study 2, 37 twin pairs from study 1 were retested 2–3 years later and combined with 100 twin pairs from a general population sample. A timed peg‐moving task was used to assess motor skill. Children with combined speech and language impairments obtained poorer peg‐moving scores than unaffected children. Bivariate DeFries‐Fulker analysis found significant shared genetic variance for impairments on peg‐moving and on a test of nonword repetition. It is concluded that genes that put the child at risk for communicative problems also affect motor development, with the association being most evident when speech production is affected. © 2001 Wiley‐Liss, Inc.
Fecal analysis of ovarian cycles in female black‐handed spider monkeys (Ateles geoffroyi)
Authors: Campbell C.J. , Shideler S.E. , Todd H.E. , Lasley B.L. 
Published: August 2002

AbstractAn enzyme immunoassay (EIA) was applied to characterize the reproductive endocrinology of adult female black‐handed spider monkeys (Ateles geoffroyi). Analysis of paired urine and fecal samples, collected from two females housed at San Diego Zoo, confirmed that the EIAs employed provided quantitative measurements of ovarian sex steroid hormones. Fecal metabolite levels were significantly correlated with those in urine, confirming that feces are a valid source of steroid metabolites in this species. The excretion of these metabolites in feces lagged urinary excretion by 1–2 days. The ovarian cycle profiles of the two captive females and five free‐ranging females are comparable, with an average length of approximately 20–23 days. Cyclical bleeding, as previously reported, was observed in one of the two captive females. Pregnancy was detected in four free‐ranging females, and early fetal loss for one female was indicated by hormonal data. Am. J. Primatol. 54:79–89, 2001. © 2001 Wiley‐Liss, Inc.
Status and distribution of golden langurs (Trachypithecus geei) in Assam, India
Authors: Srivastava A. , Biswas J. , Das J. , Bujarbarua P. 
Published: August 2002

AbstractThe distribution of golden langurs (Trachypithecus geei) is limited to a small area of western Assam in northeast India and Bhutan between the rivers Manas in the east, Sankosh in the west, and Brahmaputra in the south. It is one of the most seriously endangered primate species of India. A comparative analysis based on satellite images taken in 1988 and 1998 showed a 50% loss of original golden langur habitat. Data on population dynamics collected using line transect and total count methods are presented here. An average group size of 8.2 (range 4.0–22.0) individuals was recorded. A total of 1,064 individuals were counted living in 130 groups. The sex ratio was 1.9–2.5 adult females for each adult male. A low percentage of juveniles and infants suggests that the population is unstable. Most of the groups had only one adult male. Small group sizes, isolated distribution, proportionately few infants and juveniles, and degrading habitat are all causes of concern. Demographic trends indicate a decline in the golden langur population. Am. J. Primatol. 55:15–23, 2001. © 2001 Wiley‐Liss, Inc.