Evaluation of a group-based sensorimotor intervention programme to improve Chinese handwriting of primary school students.

Objective: Sensorimotor performance is influential in Chinese handwriting, but few studies have examined the efficacy of sensorimotor-based interventions on Chinese handwriting among primary school students with poor handwriting performance. The study aims to evaluate a sensorimotor-based intervention to improve handwriting in the mainstream primary schools. Methods: This study adopted a two-group pretest-posttest design. An 8-session group-based sensorimotor intervention was delivered to school-aged children (mean age = 8.1, 68% male). Group A had 2 sessions every week, while Group B had 4 sessions every week. Analysis of variance with repeated measures was used to test the effects. Results: The intervention had a significant time effect (p < .05) in terms of improving handwriting process (d = 0.33-1.10), manual dexterity (d = 0.57), visual memory (d = 0.70), visual-spatial perception (d = 0.37), and motor and postural skills (d = 0.73). The effect sizes ranged from medium to large. For the handwriting process, time per character had a significant group × time interaction, with post hoc analysis showing that Group A had a significantly large effect (d = 1.89, p < .001) while Group B did not. Conclusions: The group-based sensorimotor intervention programme appeared to show improvements in students with fair skills in writing Chinese characters. It appears that the effect is better if the training sessions are spaced out in one month rather than intensively conducted within two weeks. It might be related to more involvement from parents, and students need more time for practice after the training sessions.

Practice of breastfeeding and factors that affect breastfeeding in Hong Kong.

OBJECTIVES: To describe the patterns of and factors affecting breastfeeding and to find out any significant relationship between breastfeeding and health of the child. DESIGN: Cohort study. SETTING: Postnatal ward of the Prince of Wales Hospital. PARTICIPANTS: A total of 243 infants born in 1998 to 2001 at the hospital. Each infant was followed up for 3 years. Home visits were carried out at 3, 15, 24, and 36 months of age by medical students from the Chinese University of Hong Kong. A questionnaire was completed at each visit. Independent sample t-tests and Pearson Chi squared tests were used. RESULTS: Of the 243 subjects, 213 provided data on the method of infant feeding. There were 66.7% of mothers initiating breastfeeding, with a median duration of 1 month. Only 13.4% met the World Health Organization's recommendations on breastfeeding. Breastfeeding was found to have a statistically significant relationship with (i) the infant's birth order and (ii) the mother's and father's education level. During follow-up, 44.6% of the infants were hospitalised but there was no significant relationship between breastfeeding and number of hospitalisations. CONCLUSIONS: The current breastfeeding rate in Hong Kong falls below expectations when compared with other developed nations. To raise this rate, more support is needed for families with parents having a lower education level or more than two children, as they are the least likely to breastfeed. This might be achieved by encouraging antenatal class attendance, counselling of husbands, and more support for breastfeeding from doctors.

Programming of the macronucleus of Paramecium during asexual and sexual reproduction: A further study with cytidine analogues, dimethylsulfoxide, L-ethionine and N-butyric acid.

The control of the function of the macronucleus of Paramecium is studied, in connection with its role in the compensation for the asexual somatic function of the micronucleus. Following removal of the micronuclei, amicronucleate cell lines as a rule suffer a transient period of growth and developmental depression in the initial phase of asexual propagation. But they gradually recover to near-normal. Previous studies of treatment of amicronucleate cells with cytidine analogues have implicated the macronucleus in compensating for the somatic function of the micronucleus following the loss of the micronucleus, and the activation of this macronuclear function probably involves DNA-demethylation. The present study further tests this notion, by treating micronucleate cells with agents known to promote demethylation of 5-methylcytosine. After treatment, the cells were vegetatively propagated, and then enucleated to give rise to amicronucleate cell lines. Treatments with dimethylsulfoxide, L-ethionine, and 5-aza-2'-deoxycytidine promoted recovery in amicronucleate cell lines thus derived. Cells treated with 6-azacytidine did not produce such an effect. Hence, the compensatory mechanism, presumably residing in a repressed state in the macronucleus, can be activated or primed to activate by demethylating agents even before the loss of the micronucleus, and once established the new macronuclear programme perpetuates in succeeding asexual cell generations. This shows that during asexual propagation the macronuclear programme can be altered to 'pre-adapt' the cells for amicronuclearity. Treatment of micronucleate conjugants with 5-azacytidine, when the macronuclear anlagen develop, produced clones that had become similarly pre-adapted. There were also some indication of persistence of such effects of the analogue into the next clonal cycle following autogamy. The notion of macronuclear DNA-demethylation as a basis for the activation and maintenance of the compensatory mechanism is discussed.

Repressive function of the micronucleus during asexual reproduction in Paramecium tetraurelia: Experimental analysis with defective-micronucleates generated by laser microbeam irradiation.

The present paper reports on the experimental analysis of a novel regulatory function of the micronucleus of Paramecium tetraurelia. Previous studies have made clear that amicronucleate cell lines shortly after their generation generally suffer depression, in exhibiting low viability, slow growth and abnormal oral development in binary fission, but they eventually recover to near-normal. A compensatory mechanism is thus activated in the absence of the micronucleus, to allow recovery of the amicronucleate cell line. Implicit in this conclusion is the role of the micronucleus in repression of the compensatory mechanism. The present study tested this notion by perturbing the micronucleus with laser microbeam irradiation. This operation generated cell lines possessing defective micronuclei; during their asexual propagation, some cells lost the micronucleus and gave rise to amicronucleates. The viability of amicronucleate cell lines derived in this manner was found to be higher, compared to others generated by a different operation involving instantaneous removal of normal micronuclei from the cell with a microinjection needle. Some evidence also suggested that their oral development was less abnormal during the initial depression period. Hence, damage of the micronucleus has apparently facilitated the activation of the compensatory function, and the latter might have occurred even before the loss of the defective micronucleus. The present findings provide support for a regulatory role of the micronucleus during asexual propagation. Previous studies have indicated that the physical basis of the compensatory mechanism resides with the macronucleus. The micronuclear repressive function may be directed against this compensatory mechanism of the macronucleus.

Interleukin-17A differentially modulates BCG induction of cytokine production in human blood macrophages.

The pathogenesis of Mtb depends in part on cytokine cross-regulation between macrophages and T cells in host immunity. Th17 cells produce IL-17A to induce granuloma formation and to restrict mycobacterial dissemination. IL-17A also mediates cytokine responses induced by proinflammatory cytokines such as TNF-α. Our previous results showed that BCG induces IL-6, IL-10, and TNF-α via activity of protein kinases, including dsRNA-activated serine/threonine protein kinase and glycogen synthase kinase-3 in primary human monocytes. Therefore, we investigated whether IL-17A, upon its induction by BCG, plays an additional role to aid the production of downstream proinflammatory cytokines in macrophages. Here, we showed that IL-17A enhanced IL-6 mRNA and protein levels inducible by BCG in a time- and dose-dependent manner, whereas it had no effect on IL-10 and TNF-α production. We also demonstrated that IL-17A activated the phosphorylation of ERK1/2 triggered by BCG. With the use of a specific chemical inhibitor of a MAPK/ERK-activating kinase (MEK1/2), we confirmed the correlation between the enhanced ERK1/2 activation and augmented IL-6 production. Additionally, we revealed that IL-17A acts in concert with BCG-induced TNF-α to enhance the level of IL-6 synthesis. Taken together, our results suggest a significant role of IL-17A to serve as a modulator of cytokine expression in innate immune response during mycobacterial infection.