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Objective: To evaluate the accuracy of simple anthropometric parameters in diagnosing obesity in children in Guangzhou. Methods: A cross-sectional study, including 465 children aged 6-9 years, was carried out in Guangzhou. Their body height and weight, waist circumference (WC) and hip circumference were measured according to standard procedure. Body mass index (BMI), waist to hip ratio (WHR) and waist-to-height ratio (WHtR) were calculated. Body fat percentage (BF%) was determined by dual-energy X-ray absorptiometry. Multiple regression analysis was applied to evaluate the correlations between age-adjusted physical indicators and BF%, after the adjustment for age. Obesity was defined by BF%. Receiver operating characteristic (ROC) curve analyses were performed to assess the diagnostic accuracy of the indicators for childhood obesity. Area under-ROC curves (AUCs) were calculated and the best cut-off point that maximizing 'sensitivity + specificity-1' was determined. Results: BMI showed the strongest association with BF% through multiple regression analysis. For 'per-standard deviation increase' of BMI, BF% increased by 5.3% (t=23.1, P<0.01) in boys and 4.6% (t=17.5, P<0.01) in girls, respectively. The ROC curve analysis indicated that BMI exhibited the largest AUC in both boys (AUC=0.908) and girls (AUC=0.895). The sensitivity was 80.8% in boys and 81.8% in girls, and the specificity was 88.2% in boys and 87.1% in girls. Both the AUCs for WHtR and WC were less than 0.8 in boys and girls. WHR had the smallest AUCs (<0.8) in both boys and girls. Conclusion: BMI appeared to be a good predicator for BF% in children aged 6-9 years in Guangzhou.

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BACKGROUND: Anaesthetics may target ionotropic glutamate receptors in brain cells to produce their biological actions. Membrane-bound ionotropic glutamate receptors undergo dynamic trafficking between the surface membrane and intracellular organelles. Their subcellular distribution is subject to modulation by changing synaptic inputs and determines the efficacy and strength of excitatory synapses. It has not been explored whether anaesthesia has any impact on surface glutamate receptor expression. In this study, the effect of general anaesthesia on expression of N-methyl-D-aspartate (NMDA) receptors in the surface and intracellular pools of cortical neurones was investigated in vivo. METHODS: General anaesthesia was induced by intraperitoneal injection of chloral hydrate in adult male mice. Surface protein cross-linking assays were performed to detect changes in distribution of NMDA receptor subunits (NR1, NR2A, and NR2B) in the surface and intracellular compartments of cerebral cortical neurones. RESULTS: Chloral hydrate did not alter the total amounts of NR1, NR2A, and NR2B proteins in cortical neurones. However, the drug reduced NR1 proteins in the surface pool of these neurones, and induced a proportional increase in NR1 in the intracellular pool. Similar redistribution of NR2B subunits was observed between the two distinct pools. The changes in NR1 and NR2B were rapid and remained throughout the duration of anaesthesia. NR2A proteins were not altered in the surface or intracellular pool in response to chloral hydrate. CONCLUSIONS: These data demonstrate that subcellular expression of NR1 and NR2B in cortical neurones is sensitive to anaesthesia. Chloral hydrate reduces surface-expressed NMDA receptors (specifically NR2B-containing NMDA receptors) in these neurones in vivo.

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BACKGROUND: The ionotropic glutamate receptor is a potential molecular site in the central nervous system that general anaesthetics may interact with to produce some of their biological actions. Protein phosphorylation has been well documented to occur in the intracellular C-terminal domain of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) subtype of glutamate receptors, which represents a pivotal mechanism for the post-translational modulation of AMPA receptor functions. In this study, we investigated a possible influence of an i.v. anaesthetic agent propofol on the phosphorylation of AMPA receptor GluR1 subunits in cultured neurons. METHODS: The effect of propofol on phosphorylation of GluR1 subunits at serine 831 and 845 was assayed in cultured rat striatal and cortical neurons by western blot with phospho- and site-specific antibodies. RESULTS: Propofol consistently elevated phosphorylation of GluR1 subunits at the C-terminal serine 845 site in both striatal and cortical neurons. The elevation in phosphorylation was concentration-dependent and started at a low concentration (3 microM). This increase in serine 845 phosphorylation was rapid and sustained during the entire course of propofol exposure. In contrast to serine 845, phosphorylation of GluR1 at serine 831 was not altered by propofol in striatal and cortical neurons. Total GluR1 abundance remained unchanged in response to propofol incubation. CONCLUSIONS: These data indicate that propofol possesses the ability to upregulate AMPA receptor GluR1 subunit phosphorylation at a specific serine 845 site in neurons and provide evidence supporting the AMPA receptor as a molecular target for general anaesthetics.

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Metabotropic glutamate receptors (mGluR) are densely expressed by striatal medium spiny neurons. Activation of mGluR in this brain region alters local transmitter release and behaviors of experimental animals. In particular, mGluR regulate transcription factor and neuropeptide gene expression in striatal neurons through their connections with multiple intracellular effectors. This prominent involvement of mGluR in overall cellular activity is pivotal for the development of neuronal plasticity underlying long-term adaptive changes in cellular physiology related to a variety of neurologic disorders. Accumulating evidence demonstrates that the subtypes of mGluR have distinct effects on gene expression: group I subtypes facilitating, and group II/III subtypes inhibiting, gene expression. Thus, the mGluR can be considered as promising targets in the development of novel therapeutic drugs that can relieve neurologic disorders resulting from dysfunction of the striatum.

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Continued pursuit of market-oriented reforms in China seems to have resulted in increasing income disparities. This has raised concerns about possible declines in the use of health services by the poor. Using data from three waves of the China Health and Nutrition Survey (1989, 1991, 1993), we examine whether people age 20-45 in eight provinces became less likely to seek care when ill. We carried out three probit estimations of seeking care when ill; the predictor variables include individual and workplace characteristics, a measure of the severity of illness and community level factors. Health care is broadly defined to include basic level clinics as well as urban hospitals. We find no evidence that health care utilization is decreasing. Rather, for people in a community survey reporting mainly mild or moderate illness, health care continues to be accessible. We consider possible limits of our study and discuss extensively the implications of the use of illness reports from the three cross-sectional surveys as health status indicators.

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In lightly pentobarbital-anesthetized and acutely-prepared rats, electrical stimulation within the arcuate nucleus of the hypothalamus consistently inhibited the tail-flick responses to noxious heating of the tail. The opioid receptor antagonist, naloxone hydrochloride applied intrathecally at the lumbar level, at dose of 20 micrograms, reversed this inhibition without affecting the baseline pain threshold. The same dose of naloxone, applied to the cervical subarachnoid space, had no effect on the inhibitory modulation by the arcuate nucleus. Naloxone, at doses 2- to 4-fold greater than the intrathecal dose, did not modify the suppression of the tail-flick, when given systemically. With the doses ranging from 5 to 40 micrograms, naloxone showed a dose-dependent blockade of the inhibition produced by stimulation of the arcuate nucleus. These results indicate that an endogenous opioid system is most likely involved in the descending inhibition of spinal nociceptive reflexes, resulting from stimulation of the arcuate nucleus of the hypothalamus.

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In lightly pentobarbital-anesthetized and acutely prepared rats, electrical stimulation within the arcuate nucleus of the hypothalamus (ARH) consistently inhibited the tail-flick responses to noxious heating of the tail. The peptide ICI174864, a delta-opioid receptor antagonist applied intrathecally at the lumbar level at a dose of 1 nmol, markedly attenuated this inhibition without affecting the baseline nociceptive threshold. Normal saline injected by the same approach had no effect on the ARH inhibitory modulation. This is the first report showing an involvement of the delta-opioid receptor in the descending inhibition of spinal nociceptive reflex resulting from ARH stimulation.

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Inhibition of noxious heat-induced tail flick by electrical stimulation of the arcuate nucleus of the hypothalamus (ARH) was examined and characterized in pentobarbital-anesthetized rats. Systematic mapping studies revealed that inhibition of the tail flick reflex could be induced by stimulating widespread areas in the ventromedial parts of the hypothalamus, which include the paraventricular nucleus, ventromedial nucleus, dorsomedial nucleus, anterior hypothalamic area as well as the ARH areas. The ARH stimulation-produced tail flick suppression could be completely blocked by systemic naloxone (2 mg/kg) which shows the involvement of an opiate mechanism in this effect. Although the tail flick reflex in the lightly anesthetized state is of significantly shorter latency than in the unanesthetized state, thresholds of the ARH stimulation for suppressing spinal nociceptive reflexes in the lightly anesthetized state were not significantly different from the thresholds at the same ARH sites in the awake state.

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The marked suppression of noxious heat-evoked tail flick reflex was produced in conscious rats by low (2 Hz) or high (100 Hz) frequency electroacupuncture (EA) stimulation at acupoints S36 and Sp6. Electrolytic and kainate lesions in the ventral periaqueductal gray (vPAG) led to significant attenuation of the low and high frequency EA analgesia as measured 4 and 6 days following the lesion. In sham-operated animals, analgesia induced by either low or high frequency EA remained intact. The role of vPAG in organization of different EA analgesia is discussed in detail.

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Transections at two levels of the forebrain were undertaken in the rat to investigate the neural structures indispensable for the mediation of tail flick reflex suppression (TFRS) induced by low (2 Hz) and high (100 Hz) frequency electroacupuncture (EA) stimulation. Removal of the telencephalic structures did not affect TFRS produced by high frequency EA, although a mild and temporal attenuation was observed for low frequency EA-induced TFRS. Ablation of the whole forebrain (the telencephalon and diencephalon) resulted in a total abolishment of 2-Hz EA effect as measured 5, 24 and 72 h after surgery. In the meantime there was a moderate attenuation (-32.8%, P less than 0.05) of 100-Hz EA effect, which appeared 5 h after the operation and recovered after 24 h. The results indicate that (1) high frequency EA effect persisted in animals devoid of the whole forebrain structures; (2) an intact diencephalon is indispensable for the neural circuitry controlling low frequency EA-induced TFRS.

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Suppression of the tail flick response to noxious heat and paw withdrawal response to noxious pressure were produced by electrical stimulation of arcuate nucleus of the hypothalamus (ARH) in pentobarbital anesthetized rats. Systemic administration of naloxone (2 mg/kg) greatly antagonized the ARH stimulation-produced inhibition of both algesic reflexes. The thresholds of stimulation for inhibition of two spinal nociceptive reflexes in the lightly anesthetized state were not significantly different from the thresholds of stimulation at the same ARH sites in the awake state in the same animals. These findings provide evidence establishing the (1) usefulness of the anesthetized rat model for investigation of antinociceptive mechanisms; (2) the involvement of endogenous opioid mechanisms in mediating ARH stimulation-produced analgesia.

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