No abstract

ObjectivesObesity is reported to be closely relevant to early sexual development but the relationship between sexual precocity and obesity or central obesity is still inconsistent, especially in boys. We aimed to investigate the relationship between precocious puberty and obesity as well as central obesity.DesignA large population-based cross-sectional study using multistage, stratified cluster random sampling.SettingData from the Shanghai Children’s Health, Education and Lifestyle Evaluation (SCHEDULE) study in June 2014.Participants17 620 Chinese children aged 6–12 years.Primary and secondary outcome measuresObesity was defined by WHO Child Growth Standards. Central obesity was defined by sex-specific waist-to-height ratio (WHtR) cut-offs (WHtR ≥0.48 for boys, WHtR ≥0.46 for girls). Precocious puberty was identified by Tanner stage of breast, pubic hair and testicle development. A χ2 test was performed to compare rates. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the association between precocious puberty and general obesity and central obesity. Probit analysis was used for estimating the median age at entry into Tanner stage 2 or greater for breast, pubic hair and testicle development. Linear regression was utilised to compare the effects of WHtR and body mass index (BMI) on sex development indicators.Results25.98% and 38.58% of boys with precocious puberty were respectively accompanied by obesity (OR=2.15, 95% CI=1.31 to 3.50) or central obesity (OR=2.10, 95% CI=1.46 to 3.03); meanwhile, 13.86% and 29.42% of girls with precocious puberty were respectively accompanied by obesity (OR=9.00, 95% CI=5.60 to 14.46) or central obesity (OR=5.40, 95% CI=4.10 to 7.12). The median ages of breast, pubic hair and testicle development decreased with BMI increase and median ages of thelarche and testicular development rather than pubarche were earlier in children with central obesity.ConclusionsEarlier pubertal development was positively associated with obesity and central obesity in Chinese children.

Increasing dietary roughage level is a commonly used strategy to prevent subacute ruminal acidosis. We hypothesized that high-roughage diets could promote chewing activity, saliva secretion, and hence more alkaline to buffer rumen pH. To verify the hypothesis, 12 multiparous Holstein cows in mid lactation were randomly allocated to 4 treatments in a triplicated 4 × 4 Latin square experiment with one cow in each treatment surgically fitted with a ruminal cannula. Treatments were diets containing 40, 50, 60, or 70% of roughage on a DM basis. Increasing dietary roughage level decreased DM, CP, OM, starch, and NE intake, increased ADF intake, and decreased milk yield linearly. Intake of NDF was quite stable across treatments and ranged from 7.8 to 8.1 kg/d per cow. Daily eating time increased linearly with increased roughage level. The increase in eating time was due to increased eating time per meal but not number of meals per day, which was stable and ranged from 8.3 to 8.5 meals per day across treatments. Increasing dietary roughage level had no effect on ruminating time (min/d), the number of ruminating periods (rumination periods per d), and chewing time per ruminating period (min/ruminating period). Ruminating time per kilogram of NDF intake and total chewing time per kilogram of ADF intake were similar across treatments (57.4 and 183.8 min/kg, respectively). Increasing dietary roughage level linearly increased daily total chewing time; linearly elevated the mean, maximum, and minimum ruminal pH; and linearly decreased total VFA concentration and molar proportion of propionate in ruminal fluid. Saliva secretion during eating was increased, the secretion during rumination was unaffected, but the secretion during resting tended to decrease with increased dietary roughage level. As a result, total saliva secretion was not affected by treatments. In conclusion, the results of the present study did not support the concept that high-roughage diets elevated ruminal pH through increased salivary recycling of buffering substrates.

Single-cage TLIF approximates biomechanical stability and increases the stress of the bone graft. The use of a single cage may simplify the standard TLIF procedure, shorten operative times, decrease cost, and provide satisfactory clinical outcomes. Thus, single-cage TLIF is a useful alternative to traditional 2-cage TLIF.

The aim of the study was to evaluate the left ventricular systolic function of newborns with asphyxia using tissue Doppler imaging (TDI). Newborns with a history of asphyxia were divided into severe and mild groups based on their Apgar scores; normal newborns without asphyxia served as the controls. Left ventricular ejection fraction (LVEF), fraction shortening (FS), and stroke volume (SV) were measured by M-mode echocardiography at 24, 48, and 72 h after birth. The peak systolic velocity of the anterior mitral valve leaflet (Sm wave) was measured with TDI. Cardiac troponin I (CTnI) was measured. The results revealed that the LVEF and FS of the severe asphyxia group at 24 h were significantly lower than those at later time points (P < 0.01). These parameters were also significantly lower than those of the mild and control groups (P < 0.01). SV was not significantly different among the three groups. Sm wave of asphyxia groups was significantly lower than that of control group (P < 0.001). In the severe asphyxia group, Sm wave at 24 h was significantly lower than that at 48 or 72 h (P < 0.001). CTnI values of the severe asphyxia group were remarkably higher than those of the other two groups (P < 0.01). The findings of this study indicate decreased left ventricular systolic function of newborn children after asphyxia. Sm by TDI is a more sensitive indicator of left ventricular systolic function than LVEF, FS, or SV by M-mode echocardiography.

The TLIF procedure increases the approximate biomechanical stability and reduces stress at the cage-endplate interface, except for a slight increase in screw stress. Clinically, the TLIF procedure may reduce many of the risks and limitations associated with PLIF and offer a useful alternative to the PLIF procedure.

Two studies were undertaken to assess the effects of individual essential AA supplementation of a protein-deficient diet on lactational performance in mice using litter growth rates as a response variable. The first study was designed to establish a dietary protein response curve, and the second to determine the effects of Leu, Ile, Met, and Thr supplementation of a protein-deficient diet on lactational performance. In both studies, dams were fed test diets from parturition through d 17 of lactation, when the studies ended. Mammary tissue was collected on d 17 from mice on the second experiment and analyzed for mammalian target of rapamycin (mTOR) pathway signaling. Supplementation with Ile, Leu, or Met independently increased litter weight gain by 11, 9, and 10%, respectively, as compared with the protein-deficient diet. These responses were supported by independent phosphorylation responses for mTOR and eIF4E binding protein 1 (4eBP1). Supplementation of Ile, Leu, and Met increased phosphorylation of mTOR by 55, 34, and 47%, respectively, as compared with the protein-deficient diet. Phosphorylation of 4eBP1 increased in response to Ile and Met supplementation by 60 and 40%, respectively. Supplementation of Ile and Met increased phosphorylation of Akt/protein kinase B (Akt) by 41 and 59%, respectively. This work demonstrated that milk production responds nonlinearly to protein supply, and milk production and the mTOR pathway responded independently to supplementation of individual AA. The former demonstrates that a linear breakpoint model is an inappropriate description of the responses, and the latter demonstrates that no single factor limits AA for lactation. Incorporation of a multiple-limiting AA concept and nonlinear responses into milk protein response models will help improve milk yield predictions and allow derivation of diets that will increase postabsorptive N efficiency and reduce N excretion by lactating animals.

To investigate responses of milk protein synthesis and mammary AA metabolism to a graded decrease of postruminal Lys supply, 4 lactating goats fitted with jugular vein, mammary vein, and carotid artery catheters and transonic blood flow detectors on the external pudic artery were used in a 4 × 4 Latin square experiment. Goats were fasted for 24 h and then received a 9-h intravenous infusion of an AA mixture plus glucose. Milk yield was recorded and samples were taken in h 2 to 8 of the infusion period; a mammary biopsy was performed in the last hour. Treatments were graded decrease of lysine content in the infusate to 100 (complete), 60, 30, or 0% as in casein. Lysine-removed infusions linearly decreased milk yield, tended to decrease lactose yield, and tended to increase milk fat to protein ratio. Milk protein content and yield were linearly decreased by graded Lys deficiency. Mammary Lys uptake was concomitantly decreased, but linear regression analysis found no significant relationship between mammary Lys uptake and milk protein yield. Treatments had no effects on phosphorylation levels of the downstream proteins measured in the mammalian target or rapamycin pathway except for a tended quadratic effect on that of eukaryotic initiation factor 2, which was increased and then decreased by graded Lys deficiency. Removal of Lys from the infusate linearly increased circulating glucagon and glucose. Removal of Lys from the infusate linearly decreased arterial and venous concentrations of Lys. Treatments also had a significant quadratic effect on venous Lys, suggesting mechanisms to stabilize circulating Lys at a certain range. The 2 infusions partially removing Lys resulted in a similar 20% decrease, whereas the 0% Lys infusion resulted in an abrupt 70% decrease in mammary Lys uptake compared with that of the full-AA mixture infusion. Consistent with the abrupt decrease, mammary Lys uptake-to-output ratio decreased from 2.2 to 0.92, suggesting catabolism of Lys in the mammary gland could be completely prevented when the animal faced severe Lys deficiency. Mammary blood flow was linearly increased, consistent with the linearly increased circulating nitric oxide by graded Lys deficiency, indicating mechanisms to ensure the priority of the mammary gland in acquiring AA for milk protein synthesis. Infusions with Lys removed increased mammary clearance rate of Lys numerically by 2 to 3 fold. In conclusion, the decreased milk protein yield by graded Lys deficiency was mainly a result of the varied physiological status, as indicated by the elevated circulating glucagon and glucose, rather than a result of the decreased mammary Lys uptake or depressed signals in the mTOR pathway. Mechanisms of Lys deficiency to promote glucagon secretion and mammary blood flow and glucagon to depress milk protein synthesis need to be clarified by future studies.