Healthy Eating Report Card for Pre-school Children in Hong Kong.

INTRODUCTION: This study aimed to develop the Healthy Eating Report Card for Pre-school Children in Hong Kong for evaluating the prevalence of healthy eating behaviours and favourable family home food environments (FHFEs) among pre-school children in Hong Kong. METHODS: In this cross-sectional study, 538 parent-child dyads from eight kindergartens in Hong Kong were recruited. Parents or guardians completed a questionnaire comprising Report Card items. The Report Card included two indicators of Children's Eating Behaviours (ie, Children's Dietary Patterns and Children's Mealtime Behaviours) and three indicators of FHFEs (ie, Parental Food Choices and Preparation, Avoidance of Unhealthy Foods, and Family Mealtime Environments). Each indicator and its specific items were assigned a letter grade representing the percentage of participants achieving the predefined benchmarks. The grades were defined as A (≥80%, Excellent); B (60%-79%, Good); C (40%-59%, Fair); D (20%-39%, Poor); and F (<20%, Very poor). Plus (+) and minus (-) signs were used to indicate the upper or lower 5% of each grade. RESULTS: Overall, Children's Eating Behaviours were classified as Fair (average grade of 'C'), whereas FHFEs were classified as Good (average grade of 'B'). The sub-grades ranged from 'C' to 'A-', as follows: Children's Dietary Patterns, 'C+'; Children's Mealtime Behaviours, 'C'; Parental Food Choices and Preparation, 'C+'; Avoidance of Unhealthy Foods, 'B'; and Family Mealtime Environments, 'A-'. CONCLUSION: The findings highlight areas for improvement in healthy eating among children. The Healthy Eating Report Card could offer novel insights into intervention tools that promote healthy eating.

Identification of a nonselective cation channel in isolated lens fiber cells that is activated by cell shrinkage.

The initiation of lens cataract has long been associated with the development of a membrane "leak" in lens fiber cells that depolarizes the lens intracellular potential and elevates intracellular Na(+) and Ca(2+) concentrations. It has been proposed that the leak observed in cataractous lenses is due to the activation of a nonselective cation (NSC) conductance in the normal electrically tight fiber cells. Studies of the membrane properties of isolated fiber cells using the patch-clamp technique have demonstrated a differentiation-dependent shift in membrane permeability from K(+)-dominated in epithelial and short fiber cells toward larger contributions from anion and NSC conductances as fiber cells elongate. In this study, the NSC conductances in elongating lens fiber cells are demonstrated to be due to at least two distinct classes: a Gd(3+)-sensitive, mechanosensitive channel whose blockade is essential for obtaining viable isolated fiber cells, and a second Gd(3+)-insensitive, La(3+)-sensitive conductance that appears to be activated by cell shrinkage. This second conductance was eliminated by the replacement of extracellular Na(+) with the impermeant cation N-methyl-d-glucamine and was potentiated by both hypertonic stress and isosmotic cell shrinkage evoked by the replacement of extracellular Cl(-) with the impermeant anion gluconate. This additional cation conductance may play a role in normal lens physiology by mediating regulatory volume increase under osmotic or other physiological challenges. Since the inappropriate activation of NSC channels is implicated in the initiation of lens cataract, they represent potential targets for the development of novel anticataract therapies.

Pilot study of vascular health in survivors of Hodgkin lymphoma.

BACKGROUND: Vascular-related toxicities have been reported among survivors of Hodgkin lymphoma (HL), but their genesis is not well understood. PROCEDURE: Fasting blood samples from 25 previously irradiated HL survivors were analyzed for biomarkers that can reveal underlying inflammation and/or endothelial cell activation: high-sensitivity C-reactive protein (hsCRP), triglycerides, total cholesterol, high-density lipoprotein (HDL), apolipoprotein ß, lipoprotein (a), fibrinogen, circulating endothelial cells (CECs), and vascular cell adhesion molecule-1 (VCAM-1) expression. Values were compared to subjects in the Coronary Artery Risk Development in Young Adults (CARDIA) study. CECs and VCAM-1 were compared to healthy controls. RESULTS: Survivors (76% male), median age 17.6 years (5-33) at diagnosis, 33.0 years (19-55) at follow-up, included stages IA (n = 6), IIA (n = 10), IIB (n = 2), IIIA (n = 4), and IVA (n = 3) patients. Twenty-four received at least chest radiation therapy (RT) (median dose 3,150 cGy; range: 175-4,650 cGy), one received neck only; 14 (56%) had a history of anthracycline exposure (median dose: 124 mg/m(2) range: 63-200 mg/m2). Compared to CARDIA subjects, mean hsCRP (3.0 mg/L ± 2.0 vs. 1.6 ± 1.9), total cholesterol (194.1 mg/dl ± 33.2 vs. 179.4 ± 32.9), lipoprotein (a) (34.2 mg/dl ± 17.5 vs. 13.8 ± 17.5), and fibrinogen (342.0 mg/dl ± 49.1 vs. 252.6 ± 48.4) were significantly elevated. CECs (2.3 cells/ml ± 1.5 vs. 0.34 ± 1.4) were significantly elevated compared to controls. No difference in VCAM-1 expression (51.1% ± 36.8 vs. 42.3 ± 35.6) was detected. CONCLUSION: HL survivors exposed to RT have evidence of vascular inflammation, dyslipidemia, and injury suggestive of early atherogenesis.

p32 regulates mitochondrial morphology and dynamics through parkin.

Mutations in parkin were first identified in a group of Japanese patients who developed autosomal recessive juvenile Parkinsonism with clinical symptoms similar to idiopathic Parkinson's disease (PD). Parkin is an E3 ligase that targets a number of substrates for ubiquitination. Recent studies show that parkin together with PINK1, another familial-linked PD gene product, is involved in the regulation of mitochondrial dynamics in the cell. In this study, we have identified a mitochondrial protein p32 as a novel interactor of parkin in the brain. We found that p32 can regulate mitochondrial morphology and dynamics by promoting parkin degradation through autophagy. These results suggest that parkin might be an important effector in the regulation of morphology and dynamics of mitochondria.

Necrotizing leukoencephalopathy following CHOP chemotherapy.

Toxic leukoencephalopathy syndromes are rare disorders of cerebral injury characterized by changes in the white matter and accompanying neurologic dysfunction. They have been reported in association with a variety of clinical etiologies, most commonly including severe hypertension, cranial irradiation, and environmental toxins. However, they have also been described in conjunction with immunosuppressive and chemotherapeutic agents. There has been one case of fatal leukoencephalopathy reported following CHOP chemotherapy for non-Hodgkin lymphoma. We report a second case of fatal necrotizing leukoencephalopathy following the administration of CHOP chemotherapy.

Nitric oxide, S-nitrosylation and neurodegeneration.

Nitric oxide is a critically important signaling molecule, controlling a wide range of pathways and biological processes. Highly reactive nitric oxide mediates its function through reaction with different molecules directly or indirectly. One of these modifications is the S-nitrosylation of cysteine residues in proteins. S-nitrosylation is emerging as an important redox signaling mechanism and has been found to regulate a broad range of biologic, physiologic and cellular functions. One of the major findings in this area recently is the linkage of nitrosative stress to various neurodegenerative disorders. Oxidative stress has long been regarded as a prime mediator in the development of neurodegeneration as various indices of oxidative stress are readily observed in postmortem studies. A causative role for nitrosative stress in neurodegeneration is just now being appreciated. The direct connection of S-nitrosylation to the pathogenesis of Parkinson's disease in recent studies further provide insights into how imbalance in nitric oxide metabolism can contribute to the development of selective injury and disease.

SEPT5_v2 is a parkin-binding protein.

Mutations in parkin are associated with various inherited forms of Parkinson's disease (PD). Parkin is a ubiquitin ligase enzyme that catalyzes the covalent attachment of ubiquitin moieties onto substrate proteins destined for proteasomal degradation. The substrates of parkin-mediated ubiquitination have yet to be completely identified. Using a yeast two-hybrid screen, we isolated the septin, human SEPT5_v2 (also known as cell division control-related protein 2), as a putative parkin-binding protein. SEPT5_v2 is highly homologous to another septin, SEPT5, which was recently identified as a target for parkin-mediated ubiquitination. SEPT5_v2 binds to parkin at the amino terminus and in the ring finger domains. Several lines of evidence have validated the putative link between parkin and SEPT5_v2. Parkin co-precipitates with SEPT5_v2 from human substantia nigra lysates. Parkin ubiquitinates SEPT5_v2 in vitro, and both SEPT5_v1 and SEPT5_v2 accumulate in brains of patients with ARJP, suggesting that parkin is essential for the normal metabolism of these proteins. These findings suggest that an important relationship exists between parkin and septins.

Parkin ubiquitinates the alpha-synuclein-interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease.

Parkinson disease is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons and the presence of intracytoplasmic-ubiquitinated inclusions (Lewy bodies). Mutations in alpha-synuclein (A53T, A30P) and parkin cause familial Parkinson disease. Both these proteins are found in Lewy bodies. The absence of Lewy bodies in patients with parkin mutations suggests that parkin might be required for the formation of Lewy bodies. Here we show that parkin interacts with and ubiquitinates the alpha-synuclein-interacting protein, synphilin-1. Co-expression of alpha-synuclein, synphilin-1 and parkin result in the formation of Lewy-body-like ubiquitin-positive cytosolic inclusions. We further show that familial-linked mutations in parkin disrupt the ubiquitination of synphilin-1 and the formation of the ubiquitin-positive inclusions. These results provide a molecular basis for the ubiquitination of Lewy-body-associated proteins and link parkin and alpha-synuclein in a common pathogenic mechanism through their interaction with synphilin-1.

The role of the ubiquitin-proteasomal pathway in Parkinson's disease and other neurodegenerative disorders.

A unifying feature of neurodegenerative diseases is the abnormal accumulation and processing of mutant or damaged intra- and extracellular proteins; this leads to selective neuronal vulnerability and dysfunction. The ubiquitin-proteasomal pathway (UPP) is poised to play a central role in the processing of damaged and toxic proteins by ubiquitin-dependent proteolysis. The UPP can be overwhelmed in several neurodegenerative diseases. This results in the accumulation of toxic proteins and the formation of inclusions, and ultimately to neuronal dysfunction and cell death. Further analysis of the cellular and molecular mechanisms by which the UPP influences the detoxification of damaged and toxic proteins in neurodegenerative diseases could provide novel concepts and targets for the treatment and understanding of the pathogenesis of these devastating disorders.

Parkin functions as an E2-dependent ubiquitin- protein ligase and promotes the degradation of the synaptic vesicle-associated protein, CDCrel-1.

Parkinson's disease is a common neurodegenerative disorder in which familial-linked genes have provided novel insights into the pathogenesis of this disorder. Mutations in Parkin, a ring-finger-containing protein of unknown function, are implicated in the pathogenesis of autosomal recessive familial Parkinson's disease. Here, we show that Parkin binds to the E2 ubiquitin-conjugating human enzyme 8 (UbcH8) through its C-terminal ring-finger. Parkin has ubiquitin-protein ligase activity in the presence of UbcH8. Parkin also ubiquitinates itself and promotes its own degradation. We also identify and show that the synaptic vesicle-associated protein, CDCrel-1, interacts with Parkin through its ring-finger domains. Furthermore, Parkin ubiquitinates and promotes the degradation of CDCrel-1. Familial-linked mutations disrupt the ubiquitin-protein ligase function of Parkin and impair Parkin and CDCrel-1 degradation. These results suggest that Parkin functions as an E3 ubiquitin-protein ligase through its ring domains and that it may control protein levels via ubiquitination. The loss of Parkin's ubiquitin-protein ligase function in familial-linked mutations suggests that this may be the cause of familial autosomal recessive Parkinson's disease.

c-fos expression, behavioural, endocrine and autonomic responses to acute social stress in male rats after chronic restraint: modulation by serotonin.

The effects in male rats of serotonin depletion (using the neurotoxin 5,7-dihydroxytryptamine) on the cross-sensitization of an acute social stress (defeat by a larger resident male) by previous repeated restraint stress (10 days, 60 min per day) was studied. Previous restraint increased freezing responses during social defeat in sham-operated rats, but this was not observed in those with depleted serotonin (83% or more in different regions of the brain). In contrast, neither heart rate (tachycardia) nor core temperature responses (hyperthermia) were accentuated in previously restrained rats (i.e. neither showed heterotypical sensitization), and neither adapted to repeated restraint (there is a hypothermic core temperature response during restraint). Corticosterone levels, which did adapt, nevertheless did not show accentuated responses to social defeat in previously restrained rats, though samples could only be taken 60 min after defeat. c-fos expression in the central nucleus of the amygdala 60 min after social defeat was increased by previous restraint. No other areas examined in the hypothalamus (e.g., paraventricular nucleus) or brainstem (e.g., solitary nucleus) showed differences related to previous restraint. Serotonin depletion reduced the expression of c-fos in the frontal cortex, lateral preoptic area, medial amygdala, central gray, medial and dorsal raphe, and locus coeruleus after social stress, but this was not altered by previous restraint. These results show that serotonin depletion has selective effects on the cross-sensitization of responses in previously stressed rats to a heterotypical stressor.

Central serotonin depletion modulates the behavioural, endocrine and physiological responses to repeated social stress and subsequent c-fos expression in the brains of male rats.

Intraspecific confrontation has been used to study effect of depleting central serotonin on the adaptation of male rats to repeated social stress (social defeat). Four groups of adult male rats were used (serotonin depletion/sham: stressed; serotonin depletion/sham: non-stressed). Central serotonin was reduced (by 59-97%) by a single infusion of the neurotoxin 5,7-dihydroxtryptamine (150 microg) into the cerebral ventricles; levels of dopamine and noradrenaline were unaltered (rats received appropriate uptake blockers prior to neurotoxic infusions). Sham-operated animals received solute only. Rats were then either exposed daily for 10 days to a second larger aggressive male in the latter's home cage, or simply transferred to an empty cage (control procedure). Rats with reduced serotonin failed to show the increased freezing behaviour during the pre-defeat phase of the social interaction test characteristic of sham animals. There was no change in the residents' behaviour. Core temperature increased during aggressive interaction in sham rats, and this did not adapt with repeated stress. By contrast, stress-induced hyperthermia was accentuated in serotonin-reduced rats as the number of defeat sessions increased. Basal core temperature was unaffected by serotonin depletion. Heart rate increased during social defeat, but this did not adapt with repeated stress; serotonin depletion had no effect on this cardiovascular response. Basal corticosterone was increased in serotonin-depleted rats, but the progressive reduction in stress response over days was not altered. C-fos expression in the brain was not altered in control (non-stressed) rats by serotonin reduction in the areas examined, but there was increased expression after repeated social stress in the medial amygdala of 5-HT depleted rats. These experiments show that reduction of serotonin alters responses to repeated social stress in male rats, and suggests a role for serotonin in the adaptive process.

The effects of prolonged passive heat exposure and basic military training on thermoregulatory and cardiovascular responses in recruits from a tropical country.

This study investigates the effects of long-term passive heat exposure and a 16-week basic military training program on heat acclimatization. Thirty recruits were tested on the zero (T1), 2nd (T2), 6th (T3), and 16th (T4) weeks of the basic military training program. The trials involved 1 hour of marching on a treadmill at 5.5 km h-1, with a 5% gradient. The subjects wore their camouflage uniforms during the trials, with simulated combat loads. The trials were conducted in a climatic chamber programmed at 32 degrees C, 60% relative humidity, 900 Wm-2 of simulated solar radiation, and wind speed of 3 m s-1. There was no fluid replacement during the trials. Because only 9 subjects attended all the trials, the results presented are based on these subjects. No significant difference was found in mean skin temperature in all the four trials. Tympanic temperature was significantly reduced (p < 0.05) only at 20 minutes. Pairwise analysis was significant (p < 0.05) only between T1 (37.18 +/- 0.38 degrees C) and T4 (36.48 +/- 0.53 degrees C). Average body temperature was significantly different only at 10 and 60 minutes (p < 0.05). A significant pairwise difference (p < 0.05) was found only between T1 (36.61 +/- 0.33 degrees C) and T4 (36.07 +/- 0.46 degrees C) in 10 minutes. No pairwise difference was found at 60 minutes. Mean heart rate (HR) was significantly reduced during the 16 weeks at 10, 20, and 30 minutes. Mean HR at 10 minutes was reduced from 152.11 +/- 14.18 beats min-1 in T1 to 130.78 +/- 10.43 beats min-1 in T4 (p < 0.001). Mean HR at 20 and 30 minutes was reduced from 156.11 +/- 17.74 beats min-1 (T1) to 137.25 +/- 11.42 beats min-1 (T4) (p < 0.001), and from 157.14 +/- 15.77 beats min-1 (T1) to 146.11 +/- 12.64 beats min-1 (T4) (p < 0.05). There was no significant difference in sweat loss and mean sweat rate during the 16 weeks. This study concluded that long-term passive heat exposure was effective at inducing heat acclimatization in terms of tympanic temperature, average body temperature, mean skin temperature, sweat loss, and mean sweat rate, but not in terms of HR. Physical training was still necessary to induce further adaptation in HR. The limiting factor to task completion during the trials was physical fitness rather than beat fitness.

The antigenic sites of trichosanthin, a ribosome-inactivating protein with multiple pharmacological properties.

Trichosanthin (TCS) fragments were produced by Tn1000 deletion mutagenesis and by cyanogen bromide (CNBr) cleavage and their immunoreactivity was examined by incubating with various antibodies. Twelve C-terminally truncated TCS variants were successfully synthesized under the control of a T7 RNA driven promoter. The smallest antigenic fragment mapped corresponded to the N-terminal 20 amino acids (aa). Six CNBr fragments of TCS were created and identified by electrospray mass spectrometry and N-terminal sequencing. Three antigenic fragments corresponding to aa 1-72, 101-152 and 153-246, respectively were mapped. Fragments corresponding to aa 1-72 and 153-246 were immunoreactive to the same monoclonal antibody showing they are components of a discontinuous epitope. On the other hand, the fragment containing aa 73-100 was not detected by any of the antibodies used.

Interaction between clients and grass-root family planning workers in Korea: implications for program performance.

PIP: The main purpose of this study is to assess the effects of the interaction patterns between family planning workers and potential clients upon acceptance of family planning. The study was carried out as part of an intercountry collaborative study and guided by UN-ESCAP in 1991. For data collection, a random sampling procedure was applied in picking up the final units of areas (9 "dongs" in Choonchon city, 1 county in Kyeonggi Province, and 2 counties in Kangwon Province, Korea). 1383 married eligible women and 66 family planning workers in these areas were interviewed. Among the survey respondents, 75.3% were currently practicing family planning (77.7% in urban and 72.1% in rural areas), and only 19.2% of the urban respondents and 45.8% of the rural respondents had ever been exposed to a family planning worker; those who had met a worker within the 3 current months comprised 3.1% among the urban dweller and 22.9% among those in rural areas. The focal point of this study was to review the correlation between the interaction of clients and grass-root family planning workers, and the adoption of family planning practices. Family planning practice as a dependent variable was applied to tabulate multiple regression analysis in order to explain the power of the variables including interaction-related factors. The variables appearing to explain the nonadoption of family planning at a highly significant level were: 1) time and distance to service institutions, 2) friendliness of service institutions, 3) frequency of meetings with a family planning workers, 4) support of friends, 5) visits to friends, 6) wife's occupation, 7) number of living sons, 8) number of living daughters, and 9) friendliness of family planning workers. The study suggested that the training programs for field workers should be strengthened to provide a greater proportion of special sessions in the curriculum to develop the human interaction skills of workers in helping clients to identify their own problems and solve them.^ieng

Health-related behaviors in Korea: smoking, drinking, and perinatal care.

The prevalence of major health-related behaviors and the relationship of these factors with selected sociodemographic factors were studied in South Korea. Subjects studied were household heads and their wives from 989 households. Age-standardized prevalences of smoking were 74.8% and 2.9% for men and women respectively, with no urban-rural difference. There was a tendency of younger or less-educated men smoking more heavily. The prevalence of use of alcoholic drinks were 79.8% and 26.0% for men and women respectively. More drinking was associated with a younger age and higher level of education. The mean prevalences of prenatal care, clinic or hospital delivery, and breastfeeding were 75.0%, 62.6%, and 75.2% respectively in the urban area, whereas the corresponding rates were 63.0%, 50.9%, and 81.1% in the rural area. Higher rates in prenatal care and hospital delivery were associated with a younger age and higher educational level, while breastfeeding showed the opposite trend.