Motor skill learning in children with Developmental Coordination Disorder

Children with Developmental Coordination Disorder (DCD) are characterized as having motor difficulties and learning impairment that may last well into adolescence and adulthood. Although behavioral deficits have been identified in many domains such as visuo-spatial processing, kinesthetic perception, and cross-modal sensory integration, recent studies suggested that the functional impairment of certain brain areas, such as cerebellum and basal ganglia, are the underlying causes of DCD. This review focuses on the “motor learning deficits” in DCD and their possible neural correlates. It presents recent evidence from both behavioral and neuroimaging studies and discusses dominant neural hypotheses in DCD. Given the heterogeneity of this disorder, a successful intervention program should target the specific deficits on an individual basis. Future neuroimaging studies are critical steps in enhancing our understanding of learning deficits in DCD.     

Molecular mechanisms responsible for microglia-derived protection of Sprague-Dawley rat brain cells during in vitro ischemia

Microglia-derived protection of brain cells (microglia, astrocytes, and neurons) during in vitro ischemic stress (deprivation of glucose, oxygen, and serum) was determined. Trypan blue exclusion assay, immunoblocking assay, Western blot analysis, and ELISA assay were used to determine the molecular mechanisms responsible for the microglia-derived protection. Results demonstrated that supernatants from the ischemic microglia protected all three cell-types from ischemia-induced damage by releasing the transforming growth factor-beta1 (TGF-beta1) and glial cell line-derived neurotrophic factor (GDNF). The protection of microglia was TGF-beta1 related, whereas astrocytes protection was GDNF-dependent. The protection of neurons was TGF-beta1 and GDNF independent, and the molecular nature responsible for their protection remains to be determined. These results indicate contribution from the surrounding cells and the types of receptors expressed on different brain cells probably also play an important role in determining their fate against ischemia.     

Attenuation of lipopolysaccharide-induced acute lung injury by treatment with IL-10

Background and objective:   The aim of this study was to characterize the changes in neutrophils and cytokines in BAL fluid following acute lung injury (ALI), and to determine the protective effect of post-injury treatment with IL-10.
Methods:   A rat model of ALI was established by evenly spraying LPS (16 mg/kg) into the lungs followed by observation for 48 h. Histological changes and the kinetics of neutrophil infiltration were evaluated in the injured lungs. The cytokines (TNF-α, IL-6, IL-10 and interferon-γ) and macrophage-inflammatory protein (MIP-2) were measured in BAL fluid by ELISA. The activation of BAL fluid neutrophils was investigated after treatment with IL-10 in vitro . The protective effect on histology and MIP-2 levels of intra-tracheal instillation of IL-10 12 and 16 h after LPS treatment was studied in vivo.
Results:   Intra-tracheal instillation of LPS caused significant lung injury and the activation of neutrophils. The levels of TNF-α and IL-6 in BAL fluid peaked at 8 and 16 h after LPS instillation respectively. IL-10 levels reached a maximum at 16–24 h, at the beginning of resolution of tissue injury. IL-10 inhibited the activation of neutrophils in vitro and MIP-2 induction in vivo . IL-10 had a protective effect if it was administered 12 but not 16 h after LPS.
Conclusions:   Neutrophils appeared to play an important role in ALI. Time-dependent treatment with IL-10 after intra-tracheal instillation of LPS was effective in protecting rats from ALI, probably by suppressing pulmonary infiltration with activated neutrophils.     

An exploratory study of psychiatric patients' needs and nurses' current practices related to sexual counseling

The purpose of this study was to explore psychiatric patient needs and current nursing practice with regard to sexual counseling and to understand differences in individual patient characteristics. A total of 182 psychiatric patients and 44 psychiatric nurses were purposively selected from a mental hospital in northern Taiwan. Results revealed that 63.2% of subjects had not been given sexuality information and 81.9% had not been approached by nurses to discuss such issues. While 35.2% of study patients treated sexual issues as psychological or private issues that should only be discussed with psychologists, 33.5% expressed a desire to discuss issues related to sexuality with nurses. Even so, most subjects preferred to discuss sexual issues in a private way, and asked for assistance from same-gender professionals. Also, patients with higher education levels placed greater attention on the counseling topics of how to express sexual needs and the impacts of mental illness on sexuality. With regard to nurses participating in the study, female nurses had a generally more conservative attitude toward sexual values than males. Those who were married, older, or had received continuing sexuality education were more comfortable with conducting sexual counseling. Those with clinical experience and continuing sexuality education were able to take more responsibility and a more professional role in sexual counseling. Data collected on the specific subject groups in order to provide effective comparisons can be employed to refine current sexual counseling training programs for nurses in order to improve patient care.     

Who needs myopia control?

Myopia has become a major visual disorder among school-aged children in East Asia due to its rising prevalence over the past few decades and will continue to be a leading health issue with an annual incidence as high as 20%-30%. Although various interventions have been proposed for myopia control, consensus in treatment strategies has yet to be fully developed. Atropine and orthokeratology stand out for their effectiveness in myopia progression control, but children with rapid progression of myopia require treatment with higher concentrations of atropine that are associated with increased rates of side effects, or with orthokeratology that carries risk of significant complication. Therefore, improved risk assessment for myopia onset and progression in children is critical in clinical decision-making. Besides traditional prediction models based on genetic effects and environmental exposures within populations, individualized prediction using machine learning and data based on age-specific refraction is promising. Although emerging treatments for myopia are promising and some have been incorporated into clinical practice, identifying populations who require and benefit from intervention remains the most important initial step for clinical practice.     

Protection of ischemic brain cells is dependent on astrocyte-derived growth factors and their receptors

An in vitro ischemia model (oxygen, glucose, and serum deprivation) is used to investigate the possible cellular and molecular mechanisms responsible for cerebral ischemia. We have previously demonstrated that supernatants derived from ischemic microglia can protect ischemic brain cells by releasing GDNF and TGF-beta1. In the present study, we investigate whether products of ischemic astrocytes can also protect ischemic microglia, astrocytes, and neurons in a similar manner. Supernatants from ischemic astrocytes were collected after various periods of ischemia and incubated with microglia, astrocytes, or neurons individually, under in vitro ischemic conditions. The components responsible for the protective effects of astrocyte-derived supernatants were then identified by Western blot, ELISA, trypan blue dye exclusion, and immunoblocking assays. Results showed that under conditions of in vitro ischemia the number of surviving microglia, astrocytes, and neurons was significantly increased by the incorporation of the astrocyte-derived supernatants. Astrocyte supernatant-mediated protection of ischemic microglia was dependent on TGF-beta1 and NT-3, ischemic astrocytes were protected by GDNF, and ischemic neurons were protected by NT-3. In addition, protein expression of TGF-beta1 and NT-3 receptors in microglia, GDNF receptors in astrocytes, and NT-3 receptors in neurons was increased by in vitro ischemia. These results suggest that astrocyte-derived protection of ischemic brain cells is dependent not only on factors released from the ischemic astrocytes, but also on the type of receptor present on the responding cells. Therapeutic potential of TGF-beta1, GDNF, and NT-3 in the control of cerebral ischemia is further suggested.     

HTRA2 variations in Taiwanese Parkinson’s disease

Mutations in HTRA2 have been reported to associate with Parkinson’s disease (PD). This study investigates if the genetic variants in HTRA2 contribute to Taiwanese PD. HTRA2 cDNA fragments from 80 patients with early-onset PD (onset ≤50 years) were sequenced. The identified variants were further examined for a cohort of PD and ethnically matched controls. A novel heterozygous R36W was identified in one early-onset and two late-onset PD patients, which was absent in 606 normal controls. The clinical features and 99mTc-TRODAT-1 SPECT image of the early-onset patient carrying R36W were similar to that of idiopathic PD. The R36W mutation of the patient was inherited from his mother whose SPECT revealed asymmetric reduction of 99mTc-TRODAT-1 uptake in the left striatum, suggesting that the defect of the nigrostriatal pathway may be attributable to the R36W in this family. Protein subcellular fractionation further revealed that R36W affected the processing of the proprotein after transport into mitochondria. Although the functional assays are promising, a larger cohort of both cases and controls should be screened to clarify the role of R36W in Taiwanese PD pathogenicity.     

Berberine inhibits platelet-derived growth factor-induced growth and migration partly through an AMPK-dependent pathway in vascular smooth muscle cells

Platelet-derived growth factor (PDGF) is released from vascular smooth muscle cells (VSMCs), endothelial cells, or macrophages after percutaneous coronary intervention and is related with neointimal proliferation and restenosis. Berberine is a well-known component of the Chinese herb medicine Huanglian (Coptis chinensis), and is capable of inhibiting growth and endogenous PDGF synthesis in VSMCs after in vitro mechanical injury. We analyzed the effects of berberine on VSMC growth, migration, and signaling events after exogenous PDGF stimulation in vitro in order to mimic a post-angioplasty PDGF shedding condition. Pretreatment of VSMCs with berberine inhibited PDGF-induced proliferation. Berberine significantly suppressed PDGF-stimulated Cyclin D1/D3 and Cyclin-dependent kinase (Cdk) gene expression. Moreover, berberine increased the activity of AMP-activated protein kinase (AMPK), which led to phosphorylation activation of p53 and increased protein levels of the Cdk inhibitor p21(Cip1). Compound C, an AMPK inhibitor, partly but significantly attenuated berberine-elicited growth inhibition. In addition, stimulation of VSMCs with PDGF led to a transient increase in GTP-bound, active form of Ras, Cdc42 and Rac1, as well as VSMC migration. However, pretreatment with berberine significantly inhibited PDGF-induced Ras, Cdc42 and Rac1 activation and cell migration. Co-treatment with farnesyl pyrophosphate and geranylgeranyl pyrophosphate drastically reversed berberine-mediated anti-proliferative and migratory effects in VSMCs. Based on these findings, we conclude that berberine inhibited PDGF-induced VSMC growth via activation of AMPK/p53/p21(Cip1) signaling while inactivating Ras/Rac1/Cyclin D/Cdks and suppressing PDGF-stimulated migration via inhibition of Rac1 and Cdc42. These observations offer a molecular explanation for the anti-proliferative and anti-migratory properties of berberine.     

Sleep problems in children with autism, attention-deficit hyperactivity disorder, and epilepsy

This study aimed to examine sleep problems in children with autism spectrum disorders (ASD), attention-deficit/hyperactivity disorder (ADHD), and epilepsy in clinical settings. We assessed 64 children with ASD, 64 with ADHD, 64 with epilepsy, and 64 typically developing children without any neuropsychiatric disorders by using a sex-and age-matched case-control study design. The parents reported their children's sleep problems. Parents of children with ASD and ADHD reported more current and lifetime sleep problems of their children than parents of children with epilepsy, especially in snoring and restless legs syndrome. Current or lifetime sleep problems did not differ between children with ASD and children with ADHD, or between children with epilepsy and typically developing children. Demographic characteristics and medication status could not fully explain the increased risk of sleep problems in children with ASD and ADHD. Our findings lend evidence to support more sleep problems in children with ASD and ADHD than typically developing children. Our study adds that children with epilepsy do not. These findings emphasize the importance to assess sleep problems in children with neurodevelopmental disorders highly comorbid with ASD or ADHD in clinical practice.