Gender and age differences among youth, in utilization of mental health services in the year preceding suicide in taiwan

The primary objective of this study was to explore gender and age differences in the use of medical services during the year preceding suicide. Data were obtained from the mortality dataset of Department of Health and National Health Insurance Database. Included in the sample were 862 persons aged 12-24?years who committed suicide in Taiwan between 2001 and 2004. We compared the records of medical service utilization of adolescents (ages 12-18?years) with young adults (ages 19-24?years). Persons in both age groups contacted general practitioners more often than other types of medical providers in the year preceding suicide, with the exception of the month before suicide. Females made greater use of medical services than males in both age groups. Suicide prevention strategies should increase the emphasis in training non-psychiatric medical practitioners to identify and treat young persons at suicide risk.     

Depression as a predictor of falls amongst institutionalized elders

Objective: In this study, we set out to examine the combined effects of medical condition and depression status on fall incidents amongst institutionalized elderly people.

Methods: A cross-sectional study was carried out to investigate the fall history of institutionalized elders involving 286 subjects. Experiences of falls over the previous year were recorded, with at least two falls during the prior one-year period, or one injurious fall defined as ‘fallers’. The Geriatric Depression Scale-15 was used as a screening instrument for depression status.

Results: Based on a multivariate logistic regression and stratification analysis, depression was found to have enhanced effects with various medical conditions on fall risk. As compared with the non-depressive reference group, a five-fold fall risk was discernible amongst depressed elders with multiple medications, whilst a six-fold risk was found amongst depressive elders using ancillary devices, along with a 11-fold amongst depressive elders with neural system diseases.

Conclusions: This study provides the evidence of enhancing effects between depression and medical conditions on the risk of falls amongst institutionalized elderly people. Thus, depressed elders with neural system diseases, using ancillary devices or multiple medications, should be specifically listed as very high risk of falling amongst institutionalized elderly, and strictly prevent them from falls. Screening and treatment of depression could also be a useful strategy in the prevention of falls amongst institutionalized elderly with poor medical condition.     

Genetic evidence for a contribution of EphA:ephrinA reverse signaling to motor axon guidance

Repulsive Eph forward signaling from limb-derived ephrins guides the axons of lateral motor column (LMC) motor neurons. LMC axons also express ephrinAs, while their EphA receptors are expressed in the limb mesenchyme. In vitro studies have suggested that reverse signaling from limb-derived EphA4 to axonal ephrinAs might result in attraction of LMC axons. However, genetic evidence for this function is lacking. Here we use the Dunn chamber turning assay to show that EphA proteins are chemoattractants and elicit fast turning responses in LMC neurons in vitro. Moreover, ectopic expression of EphA4 in chick hindlimb changes the limb trajectory of LMC axons. Nervous system-specific deletion of EphA4 in mice resulted in fewer LMC axon projection errors than the ubiquitous deletion of EphA4. Additionally, a signaling-incompetent EphA4 mutant partially rescued guidance errors in the hindlimb, suggesting that limb-derived EphA4 contributes to the establishment of LMC projections. In summary, we provide evidence for a role of EphA:ephrinA attractive reverse signaling in motor axon guidance and in vivo evidence of in-parallel forward Eph and reverse ephrin signaling function in the same neuronal population.     

Evaluation and management of osteochondral lesions of the knee

Osteochondral lesions of the knee is a common disorder in adolescents, although it may present in children and adults. Despite the fact that the disorder was discovered more than a century ago, no specific causes have been identified, although relationships with ischemia, irregular ossification of epiphyseal cartilage, genetic influences, trauma, and endocrine disorders have been postulated. Taking a thorough history and performing a thorough physical examination will facilitate diagnosis of this condition. Radiographic and magnetic resonance imaging are useful diagnostic tools that aid in the evaluation. A comprehensive knowledge of the relevant anatomy and clinical progression of osteochondral lesions allows for a better understanding of the classification systems and, ultimately management of this disorder. The size, location, and stability of the lesion, as well as the patient's age, are crucial in determining optimal treatment. The spectrum of injury ranges from small, stable lesions, which can be treated nonoperatively, to unstable or displaced lesions, which may require surgical management. Surgical options include drilling of subchondral bone, curettage and microfracture, refixation of detached lesions, autologous osteochondral autograft procedures (eg, mosaicplasty, osteochondral autograft transfer system), autologous chondrocyte implantation, and osteochondral allograft resurfacing. This article provides a basic approach to the evaluation and management of osteochondral lesions, as well as indications for surgery.     

Association of a fasting glucose genetic risk score with subclinical atherosclerosis: The Atherosclerosis Risk in Communities (ARIC) study

OBJECTIVE

Elevated fasting glucose level is associated with increased carotid intima-media thickness (IMT), a measure of subclinical atherosclerosis. It is unclear if this association is causal. Using the principle of Mendelian randomization, we sought to explore the causal association between circulating glucose and IMT by examining the association of a genetic risk score with IMT.

RESEARCH DESIGN AND METHODS

The sample was drawn from the Atherosclerosis Risk in Communities (ARIC) study and included 7,260 nondiabetic Caucasian individuals with IMT measurements and relevant genotyping. Components of the fasting glucose genetic risk score (FGGRS) were selected from a fasting glucose genome-wide association study in ARIC. The score was created by combining five single nucleotide polymorphisms (SNPs) (rs780094 [GCKR], rs560887 [G6PC2], rs4607517 [GCK], rs13266634 [SLC30A8], and rs10830963 [MTNR1B]) and weighting each SNP by its strength of association with fasting glucose. IMT was measured through bilateral carotid ultrasound. Mean IMT was regressed on the FGGRS and on the component SNPs, individually.

RESULTS

The FGGRS was significantly associated (P = 0.009) with mean IMT. The difference in IMT predicted by a 1 SD increment in the FGGRS (0.0048 mm) was not clinically relevant but was larger than would have been predicted based on observed associations between the FFGRS, fasting glucose, and IMT. Additional adjustment for baseline measured glucose in regression models attenuated the association by about one third.

CONCLUSIONS

The significant association of the FGGRS with IMT suggests a possible causal association of elevated fasting glucose with atherosclerosis, although it may be that these loci influence IMT through nonglucose pathways.Elevated fasting glucose level is associated with increased carotid intima-media thickness (IMT) (1,2), a measure of subclinical atherosclerosis. However, it is still unclear if this relation is causal, due to unmeasured confounding by other cardiovascular risk factors, or due to the metabolic derangements of diabetes—a disease defined by fasting glucose level.Several recent fasting glucose genome-wide association studies (GWAS) (3–5) and a large GWAS meta-analysis (6) have identified multiple genetic variants with strong associations to fasting plasma glucose level. A recent GWAS in the Atherosclerosis Risk in Communities (ARIC) study found five variants significantly associated with fasting glucose after correction for genome-wide testing (7). Consistent associations for all five of the variants have been reported in other fasting glucose GWAS (6). We demonstrated that these variants are much more strongly associated with fasting glucose in the normal or prediabetic range than in the diabetic range (7).The discovery of genetic variants reproducibly associated with fasting glucose provides the opportunity to investigate a causal association between fasting glucose and cardiovascular disease (CVD) using the theory of Mendelian randomization. Because of random assortment of alleles at the time of gamete formation, genetic variants should not be associated with known and unknown confounders in association analyses. Genetic variants can also be measured very accurately and are thus subject to little measurement error. Finally, genetic variants are also not susceptible to issues of reverse causality (8). Therefore, the proxy use of single nucleotide polymorphisms (SNPs) significantly associated with a trait instead of the trait itself in association analyses can help to explore a causal association between a trait and disease (9). This technique was recently used in a meta-analysis to examine the causal relationship of C-reactive protein to heart disease (10). In this paper, we applied principles of Mendelian randomization to explore whether there is a causal relation between fasting glucose in the nondiabetic range and subclinical atherosclerosis. In order to reduce problems with multiple testing, to create a genetic variable that accounted for a substantive amount of variation in fasting glucose, and to attempt to account for pleiotropic effects of individual SNPs, a composite genetic risk score was used. However, Mendelian randomization results from single SNPs associated with fasting glucose are also presented in the online appendix available at http://diabetes.diabetesjournals.org/cgi/content/full/db10-0839/DC1.