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Wang, Jianhong,Diao, Qiyu,Tu, Yan,Zhang, Naifeng,Xu, Xiancha Asian Australasian Association of Animal Productio 2012 Animal Bioscience Vol.25 No.2
The limiting sequence and relative ratio of lysine (Lys), methionine (Met), and threonine (Thr) for calves about 2 mo of age fed milk replacers (MR) containing soy protein are not clearly defined. The objective of the study was to investigate the effect of supplementing MR containing 22% CP, half from soy protein concentrate (SPC, 40.56% CP, flour) and half from whey proteins, with Lys, Met, and Thr to estimate amino acid (AA) sequence and their relative ratio for calves about 2 mo of age. A method of partial deduction of AA was adopted. Twenty-four newborn calves (half males and half females, $40.7{\pm}0.9$ kg of BW) were fed 1 of 4 MR diets for 56 d (n = 6/diet). The diets were supplemented with all (positive control) or with 2 of the 3 AAs: Lys, Met and Thr, (i.e., PC (22% CP, 2.34% Lys, 0.72% Met and 1.80% Thr), PC-Lys (22% CP, 1.64% Lys, 0.72% Met and 1.80% Thr), PC-Met (22% CP, 2.34% Lys, 0.50% Met and 1.80% Thr), and PC-Thr (22% CP, 2.34% Lys, 0.72% Met and 1.26% Thr)). Calves were fed thrice daily; starter (20% CP, 1.03% Lys, 0.30% Met and 0.69% Thr), hay (3.23% CP, 0.29% Lys, 0.12% Met and 0.23% Thr) and water were offered free choice. Starter and hay were only offered beginning on d 36 (after 5 wk) and d 43 (after 6 wk), respectively. BW, body size and blood samples measures were taken every two weeks. Three-day total collection of feed refusals, feces, and urine were recorded starting at d 33 and d 54 of age, respectively. From the results, the limiting sequence and relative ratio between the 3 AAs in calves with different diet structures were calculated. The limiting sequence of the 3 AAs were ranked as Lys, Met and Thr; the proper ratio was 100:29:70 for MR-only diet and 100:30:60 for diets consisted of MR, starter and hay. Nitrogen digestion and utilization and nutrient digestibility were negatively affected by AA deletion treatments. From the evidence of this experiment, it did not appear that the AA limiting sequence was selectively altered by differences in diet structures such as would be encountered in practice. The relative ratio between the 3 AAs varied with the offer of starter and hay to calves, and the average ratio was 100:29.5:65 for calves during 2 to 10 wk of age.
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Net Phosphorus Requirements of Dorper×Thin-tailed Han Crossbred Ram Lambs
Ji, Shoukun,Xu, Guishan,Jiang, Chenggang,Deng, Kaidong,Tu, Yan,Zhang, Naifeng,Ma, Tao,Lou, Can,Diao, Qiyu Asian Australasian Association of Animal Productio 2013 Animal Bioscience Vol.26 No.9
A comparative slaughter trial was conducted to estimate the phosphorus (P) requirement for maintenance and growth of crossbred lambs of Dorper with a Chinese indigenous sheep breed, thin-tailed Han sheep. Thirty-five Dorper${\times}$thin-tailed Han crossbred, noncastrated ram lambs ($20.3{\pm}0.22kg$ of shrunk body weight (SBW)) were used. Seven lambs were randomly chosen and slaughtered at 20 kg SBW as the baseline group for measuring initial body composition. Another seven lambs were also randomly chosen and offered a pelleted mixed diet for ad libitum intake and slaughtered at 28 kg SBW. The remaining 21 sheep were randomly divided into 3 groups with 7 sheep each and subject to the same diet of either 70 or 40% of ad libitum intake. The 3 groups were slaughtered when the sheep fed ad libitum reached 35 kg of SBW. Body P contents were determined after slaughter. The results showed that the net P requirement for maintenance was 30.0 mg/kg of empty body weight (EBW) or 23.4 mg/kg body weight (BW), and the P requirement for growth decreased from 5.3 to 5.0 g/kg of EBW gain as the lamb grew from 20 to 35 kg. The net P requirement for growth of Dorper${\times}$thin-tailed Han crossbred ram lambs was lower than that of sheep adopted by the American nutritional system.
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Jianle Wang,Majid Nisar,Chongan Huang,Xiangxiang Pan,Dongdong Lin,Gang Zheng,Haiming Jin,Deheng Chen,Naifeng Tian,Qianyu Huang,Yue Duan,Yingzhao Yan,Ke Wang,Congcong Wu,Jianing Hu,Xiaolei Zhang,Xiangy 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Oxidative stress-induced mitochondrial dysfunction is implicated in the pathogenesis of intervertebral disc degeneration (IVDD). Sirtuin 3 (SIRT3), a sirtuin family protein located in mitochondria, is essential for mitochondrial homeostasis; however, the role of SIRT3 in the process of IVDD has remained elusive. Here, we explored the expression of SIRT3 in IVDD in vivo and in vitro; we also explored the role of SIRT3 in senescence, apoptosis, and mitochondrial homeostasis under oxidative stress. We subsequently activated SIRT3 using honokiol to evaluate its therapeutic potential for IVDD. We assessed SIRT3 expression in degenerative nucleus pulposus (NP) tissues and oxidative stressinduced nucleus pulposus cells (NPCs). SIRT3 was knocked down by lentivirus and activated by honokiol to determine its role in oxidative stress-induced NPCs. The mechanism by which honokiol affected SIRT3 regulation was investigated in vitro, and the therapeutic potential of honokiol was assessed in vitro and in vivo. We found that the expression of SIRT3 decreased with IVDD, and SIRT3 knockdown reduced the tolerance of NPCs to oxidative stress. Honokiol (10 μM) improved the viability of NPCs under oxidative stress and promoted their properties of anti-oxidation, mitochondrial dynamics and mitophagy in a SIRT3-dependent manner. Furthermore, honokiol activated SIRT3 through the AMPKPGC- 1α signaling pathway. Moreover, honokiol treatment ameliorated IVDD in rats. Our study indicated that SIRT3 is involved in IVDD and showed the potential of the SIRT3 agonist honokiol for the treatment of IVDD.
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Haiming Jin,Zengjie Zhang,Chengui Wang,Qian Tang,Jianle Wang,Xueqin Bai,Qingqing Wang,Majid Nisar,Naifeng Tian,Quan Wang,Cong Mao,Xiaolei Zhang,Xiangyang Wang 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Wound healing is delayed in diabetic patients. Increased apoptosis and endothelial progenitor cell (EPC) dysfunction are implicated in delayed diabetic wound healing. Melatonin, a major secretory product of the pineal gland, promotes diabetic wound healing; however, its mechanism of action remains unclear. Here, EPCs were isolated from the bone marrow of mice. Treatment of EPCs with melatonin alleviated advanced glycation end product (AGE)-induced apoptosis and cellular dysfunction. We further examined autophagy flux after melatonin treatment and found increased light chain 3 (LC3) and p62 protein levels in AGE-treated EPCs. However, lysosome-associated membrane protein 2 expression was decreased, indicating that autophagy flux was impaired in EPCs treated with AGEs. We then evaluated autophagy flux after melatonin treatment and found that melatonin increased the LC3 levels, but attenuated the accumulation of p62, suggesting a stimulatory effect of melatonin on autophagy flux. Blockage of autophagy flux by chloroquine partially abolished the protective effects of melatonin, indicating that autophagy flux is involved in the protective effects of melatonin. Furthermore, we found that the AMPK/mTOR signaling pathway is involved in autophagy flux stimulation by melatonin. An in vivo study also illustrated that melatonin treatment ameliorated impaired wound healing in a streptozotocin-induced diabetic wound healing model. Thus, our study shows that melatonin protects EPCs against apoptosis and dysfunction via autophagy flux stimulation and ameliorates impaired wound healing in vivo, providing insight into its mechanism of action in diabetic wound healing.
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