Dietary calcium and nonphosphate phosphorus interaction influences tibiotarsus development and related gene expression of broilers from 1 to 21 days of age

ABSTRACT: The dietary needs of calcium (Ca) and phosphorus (P) are interdependent, thus accurate evaluation of Ca and P requirements of broilers to support skeleton health and optimal growth is critical. The present study was carried out to investigate the effects of dietary Ca and nonphytate P (NPP) levels and their interactions on growth performance, tibiotarsus characteristics, tibiotarsus metabolism-related enzyme and proteins, and their gene expression of broilers, so as to provide a rational recommendation for Ca and NPP levels in diet. A total of 540 one-day-old Arbor Acres male broilers were randomly allotted to 1 of 15 treatments with 6 replicate cages of 6 birds per cage for each treatment in a completely randomized design involving a 5 × 3 factorial arrangement of treatments (5 levels of Ca × 3 levels of NPP). The birds were fed the corn–soybean meal diet containing 0.60%, 0.70%, 0.80%, 0.90%, or 1.00% Ca and 0.35%, 0.40%, or 0.45% NPP for 21 d. Dietary Ca level affected (P 0.05) were found between 0.40% and 0.45% NPP. Broilers that received 0.40% NPP had higher (P = 0.02) tibia FGF23 mRNA level than those that received 0.35% NPP, but no differences (P > 0.05) were detected between 0.40% and 0.45% NPP or 0.45% and 0.35% NPP. The interactions between dietary Ca and NPP affected (P < 0.05) ADG, ALP activity, bone gal protein, FGF23 contents, and the mRNA expression levels ALP and bone gal protein in tibia of broilers. Results from the present study indicate that dietary Ca and NPP interaction influences growth, tibiotarsus development, and related gene expression of broiler chickens. Considering all the criteria, the dietary levels of 0.90% Ca and 0.45% NPP would be optimal for both growth and tibiotarsus development of broilers fed a conventional corn–soybean meal diet from 1 to 21 d of age

Nerve growth factor protects retinal ganglion cells against injury induced by retinal ischemia-reperfusion in rats

In this study, we investigated the protective effect of mouse nerve growth factor (NGF) on retinal ganglion cell (RGC) injury induced by retinal ischemia–reperfusion (RIR) in rats and explored its possible mechanisms of action. RIR caused a significant injury to RGCs and an obvious impairment of the inner retina functions, which could be seen from flash electroretinogram and flash visual evoked potential recordings. RIR also increased the expression of the apoptotic protein Bax while decreasing the expression of Bcl-2 and the phosphorylation of protein kinase B (Akt) in RGCs. Preinjection (i.m.) of NGF for 22 d reversed the injury induced by RIR and ameliorated the inner retina functions. NGF also reduced the expression of Bax and reversed the reduction of Bcl-2 and the phosphorylated Akt induced by RIR. These results indicate that NGF produces a neuroprotective effect on RGCs against RIR injury and the protective effect of NGF is mainly mediated by the PI-3K/Akt signaling pathway

IGF-1 signaling via the PI3K/Akt pathway confers neuroprotection in human retinal pigment epithelial cells exposed to sodium nitroprusside insult

The pathological increase in the levels of the second messenger nitric oxide (NO) in the vitreous cavity and retina leads to injury and cell death of the retinal pigment epithelium (RPE) cells and eventually may contribute to the occurrence and development of diabetic retinopathy. In this study, we developed a cellular model of retinopathy using D407 cells (a human RPE cell line) exposed to sodium nitroprusside (SNP) and investigated the protective effect of the insulin-like growth factor-1 (IGF-1) towards this insult. Cell death and apoptosis were examined by the methyl thiazolyl tetrazolium assay and Hoechst staining, respectively. Specific inhibitors were used and phosphorylation of relevant signaling proteins was determined by Western blotting. SNP, in a concentration-dependent fashion, increased the production of reactive oxygen species (ROS) and lipid peroxidation process causing cell death by apoptosis of D407 cells. IGF-1, in a time- and dose-dependent manner, conferred protection towards SNP-mediated insult. Both phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and mitogen-activated protein kinase (MAPK) were activated by IGF-1 in relation to the protective effect. Blockade of the PI3K/Akt pathway abolished the protective effect of IGF-1 whereas inhibition of the MAPK pathway was ineffective. SNP decreased the phosphorylation of Akt in the cells while IGF-1 reversed this inhibitory effect. These results indicate that the protective effect of IGF-1 on D407 exposed to SNP insult is mediated by the PI3K/Akt pathway. This proposal may be exploited in the clinic to improve the viability of insulted retinal cells for maintaining physiological vision

Stereoselective reduction of 1-O-isopropyloxygenipin enhances its neuroprotective activity in neuronal cells from apoptosis induced by sodium nitroprusside

Genipin is a Chinese herbal medicine with both neuroprotective and neuritogenic activity. Because of its unstable nature, efforts have been to develop more stable genipin derivatives with improved biological activities. Among the new compounds reported in the literature, (1R)-isopropyloxygenipin (IPRG001) is a more stable but less active compound compared with the parent, genipin. Here, two new IPRG001 derivatives generated by stereoselective reduction of the C=C double bond were synthesized. The 1R and 1S isomers of (4aS,7S,7aS)-methyl-7-(hydroxymethyl)-1-isopropoxy-1,4a,5, 6,7,7a-hexahydrocyclopenta[c]pyran-4-carboxylate (CHR20 and CHR21) were shown to be very stable both in high-glucose cell culture medium and in mice serum at 37 °C. Evaluation using an MTT assay and Hoechst staining showed that CHR20 and CHR21 promote the survival of rat adrenal pheochromocytoma (PC12) and retinal neuronal (RGC-5) cells from injury induced by sodium nitroprusside (SNP). The neuroprotective effects of CHR20 and CHR21 were greater than both isomers of IPRG001, the parent compounds. These results indicate that reduction of 1-O-isopropyloxygenipin enhances its neuroprotective activity without affecting its stability. Remastering Chinese herbal medicine: Genipin is known to have neuroprotective activity but problematic stability under physiological conditions. Isomeric derivatives of isopropyloxygenipin, a synthetic genipin analogue, were synthesized by stereoselective reduction of the C =C double bond and found to exhibit improved neuroprotective activity and stability over the parent compounds

Astrometric Support for the Lunar-based Ultraviolet Telescope

The Lunar-based Ultraviolet Telescope (LUT) is an astronomical instrument aboard Chang&#39;e 3, the lunar probe of China&#39;s Lunar Exploration Program that successfully landed on the northern part of the Moon&#39;s Mare Imbrium (340.4884E, 44.1214N) in late 2013. LUT is charting an ultraviolet map of the plane of the Milky Way and is also providing long-term light variability monitoring for a sample of RR Lyrae stars. However, the principal goal of the computer-controlled landing of the probe was a safe descent to a stable resting-place, and therefore, the precise orientation of LUT was never a priority. For this reason, at least theoretically, touch-down could have occurred anywhere and, for LUT, at any attitude, which would make the pointing and tracking of the wanted celestial objects practically impossible. Moreover, to reduce the data transmission load, the whole frame of every exposure could not be downloaded: only the image data containing the objects can make it to the ground; also, in order to save on electricity, the telescope does not usually track objects, which means that targets&#39; accurate positions and velocities (within the focal plane CCD) are both needed. This paper presents the astrometric solution devised to solve these problems: feasibility is first shown with experiments done from Earth, and then confirmed with actual LUT observations from the Moon&#39;s surface

Genistein inhibits PDGF-stimulated proteoglycan synthesis in vascular smooth muscle without blocking PDGFβ receptor phosphorylation

The signaling pathways that regulate the synthesis and structure of proteoglycans secreted by vascular smooth muscle cells are potential therapeutic targets for preventing lipid deposition in the early stage of atherosclerosis. PDGF stimulates both core protein expression and elongation of glycosaminoglycan (GAG) chains on proteoglycans. In this study we investigated the effects of the tyrosine kinase inhibitor genistein on PDGF mediated receptor phosphorylation and proteoglycan synthesis in human vascular smooth muscle cells. We demonstrate that genistein does not block phosphorylation of the activation site of the PDGF receptor at Tyr857 and two other downstream sites Tyr 751 and Tyr1021. Genistein blocked PDGF-mediated proteoglycan core protein synthesis however it had no effect on GAG chain elongation. These results differ markedly to two other tyrosine kinase inhibitors, imatinib and Ki11502, that block PDGF receptor phosphorylation and PDGF mediated GAG elongation. We conclude that the action of genistein on core protein synthesis does not involve the PDGF receptor and that PDGF mediates GAG elongation via the PDGF receptor