ABSTRACT Two experiments were conducted to evaluate the effects of β-mannanase on egg production performance, egg quality, intestinal microbiota, viscosity, and ammonia concentration in laying hens. In Exp. 1, two hundred and seventy 30-wk-old Hy-Line Brown laying hens were assigned to 6 diets arranged in a 3 × 2 factorial of three levels of MEn and CP [(a corn-soybean meal based diet (HEHP), a diet containing 50 kcal of MEn/kg and 1.0% less energy and CP than the HEHP (MEMP), and a diet containing 80 kcal of MEn/kg and 1.5% less energy and CP than HEHP (LELP)], and β-mannanase supplementation (0 or 0.04%). In Exp. 2, A total of two hundred and sixteen62-wk-old Hy-Line Brown laying hens were assigned to 6 dietary treatments in a 3 × 2 factorial arrangement. In Exp. 1, β-mannanase supplementation increased egg production rate in hens fed LELP diet, but not in those fed HEHP or MEMP diet (interaction, p<0.01), and the interaction was significant (p<0.01) for egg mass. β-mannanase supplementation decreased (p<0.05) ammonia concentration. In Exp. 2, the supplementation of β-mannanase increased egg production rate and egg mass in hens fed LELP diet, whereas no differences were found in those fed HEHP or MELP diet (interaction, p<0.01). The supplementation of β-mannanase in a lower energy and protein diet resulted in similar production performance when compared to high-energy and high-protein diet during early and late stages of egg production.

This study proposed a decision tree model to screen upper urinary tract damage (UUTD) for patients with neurogenic bladder (NGB). Thirty-four NGB patients with UUTD were recruited in the case group, while 78 without UUTD were included in the control group. A decision tree method, classification and regression tree (CART), was then applied to develop the model in which UUTD was used as a dependent variable and history of urinary tract infections, bladder management, conservative treatment, and urodynamic findings were used as independent variables. The urethra function factor was found to be the primary screening information of patients and treated as the root node of the tree; Pabd max (maximum abdominal pressure, >14 cmH2O), Pves max (maximum intravesical pressure, ≤89 cmH2O), and gender (female) were also variables associated with UUTD. The accuracy of the proposed model was 84.8%, and the area under curve was 0.901 (95%CI=0.844-0.958), suggesting that the decision tree model might provide a new and convenient way to screen UUTD for NGB patients in both undeveloped and developing areas.

The levels of serum inflammatory cytokines and the activation of nuclear factor kappa B (NF-κB) and hypoxia inducible factor-1α (HIF-1α) in heart tissues in response to different frequencies of intermittent hypoxia (IH) and the antioxidant tempol were evaluated. Wistar rats (64 males, 200-220 g) were randomly divided into 6 experimental groups and 2 control groups. Four groups were exposed to IH 10, 20, 30, or 40 times/h. The other 2 experimental groups were challenged with IH (30 times/h) plus tempol, either beginning on day 0 (IH30T0) or on day 29 (IH30T29). After 6 weeks of challenge, serum levels of tumor necrosis factor (TNF)-α, intracellular adhesion molecule (ICAM)-1, and interleukin-10 were measured, and western blot analysis was used to detect NF-κB p65 and HIF-1α in myocardial tissues. Serum levels of TNF-α and ICAM-1 and myocardial expression of NF-κB p65 and HIF-1α were all significantly higher in IH rats than in controls (P<0.001). Increased IH frequency resulted in more significant changes. Administration of tempol in IH rats significantly reduced levels of TNF-α, ICAM-1, NF-κB and HIF-1α compared with the non-tempol-treated group (F=16.936, P<0.001). IH induced an inflammatory response in a frequency-dependent manner. Additionally, HIF-1α and NF-κB were increased following IH administration. Importantly, tempol treatment attenuated this effect.

ABSTRACTThis experiment was conducted to evaluate the combination effect of low dietary non-phytate phosphorus (NPP) concentrations, phytase (PHY) levels, and 25-hydroxycholecalciferol (25-OH-D3) levels on the growth performance and meat quality of broilers. Two levels of NPP, two levels of PHY, and two levels of 25-OH-D3 resulted in a 2�2�2 factorial arrangements, with eight treatments (TRT). The birds on TRT 1-4 were fed diet 1 (NRC NPP was reduced by 0.1) and the birds on TRT 5-8 were fed with diet 2 (NRC NPP was reduced by 0.2). Each diet was mixed with different levels PHY and 25-OH-D3. Performance and meat quality parameters were measured. Results showed that during entire experiment the most advantageous effects were obtained with TRT 3 (NRC NPP reduced by 0.1 + 600 U/kg phytase + 34.5�g/kg 25-OH-D3) and TRT 4 (NRC NPP reduced by 0.1 + 600 U/kg phytase + 69�g/kg 25-OH-D3). The lowest body weight gain (BWG) and feed intake(FI) were observed with TRT 5 (NRC NPP reduced by 0.2 + 300 U/kg phytase + 34.5�g/kg 25-OH-D3). Lowering NRC NPP by 0.1 to 0.2 significantly reduced weight gain (WG) (p< 0.05) and FI (p< 0.05) during the starter phase (ST), while during grower phase (GF) lowering NRC NPP by 0.1 to 0.2 did not affect WG (p>0.05) and produced small decrease in FI. BWG, FI and feed conversion ratio were not influenced (p>0.05) by different PHY or 25-OH-D3 levels. In addition, the meat color, pH, and shear force were not affected by the different NPP, PHY or 25-OH-D3levels.

Tissue engineering encapsulated cells such as chondrocytes in the carrier matrix have been widely used to repair cartilage defects. However, chondrocyte phenotype is easily lost when chondrocytes are expanded in vitro by a process defined as “dedifferentiation”. To ensure successful therapy, an effective pro-chondrogenic agent is necessary to overcome the obstacle of limited cell numbers in the restoration process, and dedifferentiation is a prerequisite. Gallic acid (GA) has been used in the treatment of arthritis, but its biocompatibility is inferior to that of other compounds. In this study, we modified GA by incorporating sulfamonomethoxine sodium and synthesized a sulfonamido-based gallate, JJYMD-C, and evaluated its effect on chondrocyte metabolism. Our results showed that JJYMD-C could effectively increase the levels of the collagen II, Sox9, and aggrecan genes, promote chondrocyte growth, and enhance secretion and synthesis of cartilage extracellular matrix. On the other hand, expression of the collagen I gene was effectively down-regulated, demonstrating inhibition of chondrocyte dedifferentiation by JJYMD-C. Hypertrophy, as a characteristic of chondrocyte ossification, was undetectable in the JJYMD-C groups. We used JJYMD-C at doses of 0.125, 0.25, and 0.5 µg/mL, and the strongest response was observed with 0.25 µg/mL. This study provides a basis for further studies on a novel agent in the treatment of articular cartilage defects.