No nationally representative longitudinal data have been analyzed to evaluate the incidence of obesity in the transition between adolescence and adulthood. The objective was to examine dynamic patterns of change in obesity among white, black, Hispanic, and Asian US teens as they transitioned to young adulthood. We used nationally representative, longitudinally measured height and weight data collected from US adolescents enrolled in wave II (1996; ages 13-20 y) and wave III (2001; 19-26 y) of the National Longitudinal Study of Adolescent Health (n = 9795). Obesity incidence was defined on the basis of International Obesity Task Force (IOTF) cutoffs (wave II), which link childhood body mass index (BMI) centiles to adult cutoffs (BMI > or = 30; wave III), for comparability between adolescence and adulthood. In addition, the more commonly used cutoff of BMI > or = 95th percentile for age- and sex-specific cutoffs from the 2000 Centers for Disease Control and Prevention growth charts for adolescents (wave II) were compared with adult cutoffs (BMI > or = 30; wave III). On the basis of the IOTF cutoffs, obesity incidence over the 5-y study period was 12.7%; 9.4% of the population remained obese and 1.6% shifted from obese to nonobese. Obesity incidence was especially high in non-Hispanic black (18.4%) females relative to white females. The prevalence of obesity increased from 10.9% in wave II to 22.1% in wave III, and extreme obesity was 4.3% at wave III on the basis of a BMI > or = 40. During a 5-y transitional period between adolescence and young adulthood, the proportion of adolescents becoming and remaining obese into adulthood was very high. This upward trend is likely to continue. Effective preventive and treatment efforts are critically needed.

This protocol describes how to achieve optogenetics- and imaging-aided physiological analysis of synaptic interconnections among 4–30 simultaneously and sequentially recorded neurons. Deciphering neuronal circuitry is central to understanding brain function and dysfunction, yet it remains a daunting task. To facilitate the dissection of neuronal circuits, a process requiring functional analysis of synaptic connections and morphological identification of interconnected neurons, we present here a method for stable simultaneous octuple patch-clamp recordings. This method allows physiological analysis of synaptic interconnections among 4–8 simultaneously recorded neurons and/or 10–30 sequentially recorded neurons, and it allows anatomical identification of >85% of recorded interneurons and >99% of recorded principal neurons. We describe how to apply the method to rodent tissue slices; however, it can be used on other model organisms. We also describe the latest refinements and optimizations of mechanics, electronics, optics and software programs that are central to the realization of a combined single- and two-photon microscopy–based, optogenetics- and imaging-assisted, stable, simultaneous quadruple–viguple patch-clamp recording system. Setting up the system, from the beginning of instrument assembly and software installation to full operation, can be completed in 3–4 d.

Objective: This study aimed to understand how an increase in abdominal adiposity relative to overall adiposity is associated with blood pressure (BP) change.Methods: A sex‐stratified mixed linear model was used to examine the association (95% CI) between annual changes in waist circumference (WC) and systolic blood pressure and diastolic blood pressure, estimated from two to eight repeated measures across the 1993‐2015 China Health and Nutrition Survey, among 5,742 men and 5,972 women (18‐66 years) with no history of antihypertension medication use.Results: The association between annual WC change and BP change remained statistically significant but was attenuated after controlling for annual BMI change, regardless of baseline abdominal obesity or overweight status. Each 10‐cm annual WC gain in men and women was associated with a 0.98‐mm Hg (95% CI: 0.61‐1.35) and a 0.97‐mm Hg (95% CI: 0.62‐1.32) annual increase in systolic blood pressure and a 1.13‐mm Hg (95% CI: 0.87‐1.38) and a 0.74‐mm Hg (95% CI: 0.51‐0.97) annual increase in diastolic blood pressure, respectively, independent of annual BMI change.Conclusions: WC gain may elevate BP even in the absence of BMI gain. BP management that addresses only BMI gain could overlook individuals at risk of elevated BP who have increased WC but not BMI.

Epidemiological studies suggest a positive association between obesity and fecal short-chain fatty acids (SCFAs) produced by microbial fermentation of dietary carbohydrates, while animal models suggest increased energy harvest through colonic SCFA production in obesity. However, there is a lack of human population-based studies with dietary intake data, plasma SCFAs, gut microbial, and anthropometric data. In 490 Chinese adults aged 30–68 years, we examined the associations between key plasma SCFAs (butyrate/isobutyrate, isovalerate, and valerate measured by non-targeted plasma metabolomics) with body mass index (BMI) using multivariable-adjusted linear regression. We then assessed whether overweight (BMI ≥ 24 kg/m²) modified the association between dietary-precursors of SCFAs (insoluble fiber, total carbohydrates, and high-fiber foods) with plasma SCFAs. In a sub-sample (n = 209) with gut metagenome data, we examined the association between gut microbial SCFA-producers with BMI. We found positive associations between butyrate/isobutyrate and BMI (p-value < 0.05). The associations between insoluble fiber and butyrate/isobutyrate differed by overweight (p-value < 0.10). There was no statistical evidence for an association between microbial SCFA-producers and BMI. In sum, plasma SCFAs were positively associated with BMI and that the colonic fermentation of fiber may differ for adults with versus without overweight.

Animal studies have revealed gut microbial and metabolic pathways of blood pressure (BP) regulation, yet few epidemiological studies have collected microbiota and metabolomics data in the same individuals. In a population-based, Chinese cohort who did not report antihypertension medication use (30–69 years, 54% women), thus minimizing BP treatment effects, we examined multivariable-adjusted (eg, diet, physical activity, smoking, kidney function), cross-sectional associations between measures of gut microbiota (16S rRNA [ribosomal ribonucleic acid], N=1003), and plasma metabolome (liquid chromatography-mass spectrometry, N=434) with systolic (SBP, mean [SD]=126.0 [17.4] mm Hg) and diastolic BP (DBP [80.7 (10.7) mm Hg]). We found that the overall microbial community assessed by principal coordinate analysis varied by SBP and DBP (permutational multivariate ANOVA P <0.05). To account for strong correlations across metabolites, we first examined metabolite patterns derived from principal component analysis and found that a lipid pattern was positively associated with SBP (linear regression coefficient [95% CI] per 1 SD pattern score: 2.23 [0.72–3.74] mm Hg) and DBP (1.72 [0.81–2.63] mm Hg). Among 1104 individual metabolites, 34 and 39 metabolites were positively associated with SBP and DBP (false discovery rate–adjusted linear model P <0.05), respectively, including linoleate, palmitate, dihomolinolenate, 8 sphingomyelins, 4 acyl-carnitines, and 2 phosphatidylinositols. Subsequent pathway analysis showed that metabolic pathways of long-chain saturated acylcarnitine, phosphatidylinositol, and sphingomyelins were associated with SBP and DBP (false discovery rate–adjusted Fisher exact test P <0.05). Our results suggest potential roles of microbiota and metabolites in BP regulation to be followed up in prospective and clinical studies.

Chandelier cells (ChCs; also called axo-axonic cells) are a specialized GABAergic interneuron subtype that selectively innervates pyramidal neurons at the axon initial segment, the site of action potential generation. ChC connectivity allows for powerful yet precise modulation of large populations of pyramidal cells, suggesting ChCs have a critical role in brain functions. Dysfunctions in ChC connectivity are associated with brain disorders such as epilepsy and schizophrenia; however, whether it is causative, contributory or compensatory is not known. A likely stumbling block toward mechanistic discoveries and uncovering potential therapeutic targets is the apparent lack of rudimentary understanding of ChCs. For example, whether cortical ChCs are inhibitory or excitatory remains unresolved, and thus whether altered ChC activity results in altered inhibition or excitation is not clear. Recent studies have shed some light onto this excitation-inhibition controversy. In addition, new findings have identified preferential cell-type connectivities established by cortical ChCs, greatly expanding our understanding of the role of ChCs in the cortical microcircuit. Here we aim to bring more attention to ChC connectivity to better understand its role in neural circuits, address the controversy in ChC function in light of recent findings, and discuss the implications of ChC dysfunctions in brain disorders.