Objective: To assess the impact of urbanisation on the prevalence of the metabolic syndrome in Chinese adults.Design: As part of a community-based cross-sectional survey conducted in 2002, a sample from rural and urban populations in East China was obtained. The metabolic syndrome is defined by the National Cholesterol Education Program Adult Treatment Panel III criteria (ATP III) and the modified ATP III, which recommended a lower waist circumference cut-off for Asians.Setting: Field sites in Jiangxi and Anhui provinces and the Jing'an District of Shanghai, China.Subjects: A total of 529 non-pregnant, non-lactating urban and rural adults, aged 20–64 years without diagnosed diabetes.Results: Dwelling in urban areas was associated with higher dietary fat intake and slightly lower total energy intake, and with significantly lower occupational physical activity. Using the ATP III criteria, the prevalence of the metabolic syndrome was significantly higher for urban than rural men (12.7 vs. 1.7%, P < 0.001), and was similar between urban and rural women (10.1 vs. 9.7%, P = 0.17). These urban–rural differences were greatly enhanced when the modified ATP III criteria for the syndrome were used, for men (34.3 vs. 2.7%, P < 0.01) and women (24.1 vs. 11.4%, P = 0.07). The Asian waist circumference cut-offs (90 and 80 cm for men and women, respectively) had a better combination of sensitivity and specificity in identifying other metabolic disorders, which included high glucose, high blood pressure, high triglycerides and low high-density lipoprotein cholesterol, for this population.Conclusion: For the Chinese population, urban dwelling was associated with higher prevalence of the metabolic syndrome, especially in men.

Linear growth retardation (stunting) is prevalent (10–80%) in developing countries. It takes place between 6 and 18 mo of age and can be characterized by the delayed onset of the childhood phase of growth. The objective of this work was to study the existence of stunting in early life and, when present, its lifelong effects on final height in a normal healthy population in a developed country. A total of 2432 children with longitudinal height data from birth to adulthood were analyzed. The series represents a normal healthy population-based sample of full-term children born around 1974 in Göteborg, Sweden. We found the incidence of stunting to be about 10% as indicated by delayed onset of the childhood phase of growth (>12 mo of age): 14% in boys and 8% in girls. In a multiple linear regression model, final height was described by length at 6 mo of age, age at onset of the childhood phase of growth, and age at peak height velocity during puberty. All three measures contributed significantly (p < 0.05) to final height with a total R² of 0.33. A final height difference of 5.0 cm could be explained by abnormal onset of the childhood phase of growth in this normal population. The timing of the childhood onset of growth did not correlate with the timing of puberty. For the first time, we can conclude that stunting in early life is not only a problem in developing countries. Its importance on final height achieved is clearly shown, even after controlling for the timing of puberty.

J. Neurochem. (2012) 121, 932–943. Vitamin A (VA) is important for postnatal brain development, and VA deficiency (VAD) can cause learning and spatial memory deficits in rats. Most of the biological functions of VA are mediated by retinoic acid (RA). To investigate the mechanisms underlying VA deficits, mother rats were fed elemental diets to achieve blood VA levels classified as normal, deficient or severely deficient. Shuttle box and Morris water maze tests revealed impairments in learning ability and spatial memory, respectively, in adolescent VAD rats (p 30–35). Electrophysiology showed weaker long‐term potentiation in VAD rats compared to VA normal rats. Examination of NMDA‐induced calcium (Ca²⁺) excitability revealed decreased excitability in hippocampal slices from VAD rats during postnatal development. Relative to VA normal rats, VAD rats also had decreased NMDA receptor NR1 mRNA and protein expression in later stages of postnatal development (p 10–30), as well as differences in retinoic acid receptor (RARα) mRNA and protein expression. Furthermore, primary hippocampal neurons in culture showed increased neuronal Ca²⁺ excitability in response to all‐trans‐RA or 9‐cis‐RA, coupled with increases in RARα and NR1 expression similar to those observed in vivo. We also found weaker calcium excitability and lower expression of NR1 mRNA and protein after specific silencing of RARα. Finally, we found that RA signals affected the expression of NR1 do not directly through transcriptional regulation. These data support the new idea that continuous postnatal VAD inhibits RARα expression, which decreases NR1 expression via no direct transcriptional regulation and then inhibits hippocampal neuronal Ca²⁺excitability which affects long‐term potentiation, finally producing deficits in active learning and spatial memory in adolescence.

Mesenchymal stem cells (MSCs) can differentiate into neurons in an appropriate cellular environment. Retinoid signaling pathway is required in neural development. However, the effect and mechanism through retinoid signaling regulates neuronal differentiation of MSCs are still poorly understood. Here, we report that all‐trans‐retinoic acid (ATRA) pre‐induction improved neuronal differentiation of rat MSCs. We found that, when MSCs were exposed to different concentrations of ATRA (0.01–100 μmol/L) for 24 h and then cultured with modified neuronal induction medium (MNM), 1 μmol/L ATRA pre‐induction significantly improved neuronal differentiation efficiency and neural‐cell survival. Compared with MNM alone induced neural‐like cells, ATRA/MNM induced cells expressed higher levels of Nestin, neuron specific enolase (NSE), microtubule‐associated protein‐2 (MAP‐2), but lower levels of CD68, glial fibrillary acidic protein (GFAP), and glial cell line‐derived neurotrophic factor(GDNF), also exhibited higher resting membrane potential and intracellular calcium concentration, supporting that ATRA pre‐induction promotes maturation and function of derived neurons but not neuroglia cells from MSCs. Endogenous retinoid X receptors (RXR) RXRα and RXRγ (and to a lesser extent, RXRβ) were weakly expressed in MSCs. But the expression of RARα and RARγ was readily detectable, whereas RARβ was undetectable. However, at 24 h after ATRA treatment, the expression of RARβ, not RARα or RARγ, increased significantly. We further found the subnuclear redistribution of RARβ in differentiated neurons, suggesting that RARβ may function as a major mediator of retinoid signaling during neuronal differentiation from MSCs. ATRA treatment upregulated the expression of Vimentin and Stra13, while it downregulated the expression of Brachyury in MSCs. Thus, our results demonstrate that pre‐activation of retinoid signaling by ATRA facilitates neuronal differentiation of MSCs.