This study was conducted to evaluate the effects of exogenous enzymes on Nile tilapia (Oreochromis niloticus) growth and general health status. Tilapia (38.7 g) were fed one of four plant-based diets (408 g kg(-1) protein, 78 g kg(-1) lipid); one of which was a control and the remaining three were supplemented with exogenous enzymes (phytase, protease and carbohydrase at 300 mg kg(-1), 200 mg kg(-1), and 300 mg kg(-1), respectively). Tilapia fed the phytase supplemented diet displayed higher final body weight, FBW (94.9 g fish(-1)) and specific growth rate, SGR (2.48% day(-1)) compared to tilapia fed the control diet (82.6 g fish(-1) FBW and 2.11% day(-1) SGR) (P < 0.05). In terms of feed conversion ratio, FCR and protein efficiency ratio, PER, tilapia fed diet supplemented with phytase (1.36 FCR and 1.08 PER) performed better (P < 0.05) than tilapia fed the control diet (1.68 FCR and 0.80 PER). However, the dietary treatments had no significant effect on tilapia somatic indices (P square 0.05). The level of circulatory red blood cells was higher (P < 0.05) in tilapia fed the carbohydrase supplemented diet (1.98 x 10(6) mu L-1) compare to those fed the control diet. Dietary treatments did not affect the mid-intestinal perimeter ratio, goblet cell abundance and intraepithelial leucocytes abundance. However, the microvilli density of the mid-intestine was higher (P < 0.05) in tilapia fed the phytase (15.6) and carbohydrase (16.0) supplemented diets compared to those fed the control (10.4) and protease (11.5) supplemented diets. The intestinal bacterial community profile of tilapia fed the carbohydrase supplemented diet was significantly altered in contrast to those fed the control diet (P < 0.05). The supplementation of diets with phytase has the potential to enhance tilapia growth without detrimental impacts on intestinal health. (C) 2016 Elsevier B.V. All rights reserved.

Previous articleNext article No AccessNew Biological BooksBeyond the Power of Science? The Mystery of Life's Origin: Reassessing Current Theories. Charles B. Thaxton , Walter L. Bradley , Roger L. Olsen Sidney W. FoxSidney W. Fox Search for more articles by this author PDFPDF PLUS Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by The Quarterly Review of Biology Volume 60, Number 2Jun., 1985 Published in association with Stony Brook University Article DOIhttps://doi.org/10.1086/414316 Copyright 1985 Stony Brook Foundation, Inc.PDF download Crossref reports no articles citing this article.

Fishmeal (FM) is increasingly being replaced by plant proteins which are a relatively poor phosphorous source for mineralized tissues. To promote P availability plant-based feedstuffs are supplemented with exogenous phytase. However, the effect of phytase on skeletal development in juvenile rainbow trout (Oncorhynchus mykiss) which have distinct mineral requirements is poorly understood. To address this juvenile trout were fed FM diet, a replacement feed (soybean meal, SBM) in which 50% (460 g kg(-1)) of crude protein (from FM) was substituted with soybean-meal or SBM supplemented with microbial or corn-expressed phytase. Vertebral and scale morphology, remodelling and mineralization were then assessed by histomorphometric and colorimetric assays. Body weight and SGR of trout fed SBM was lower than FM fed fish with no improvement noted with any phytase supplement. Vertebral mineral content and autocentrum morphology were similar in trout fed SBM or FM and supplementation with microbial-phytase did not enhance these parameters at any concentration. However, scale and vertebral mineral content were significantly enhanced in trout fed SBM supplemented with corn-expressed phytase 1500 FTU kg(-1) (vertebral phosphorus P - 0.014, Ca P = 0.026; scale phosphorus P = 0.012). Thus, SBM feeds supplemented with corn-expressed phytase could help reduce FM usage and generate a more robust skeleton less prone to deformity.

Variations in the composition of thermal copolyamino acids inhibitory for glyoxalase I have been studied. Those produced from both tryptophan and cysteine are the most active. The activity requires the polymeric state since the free amino acids are devoid of activity. On the basis of these studies and others elsewhere, hydrophobicily appears to be a significant physical property contributing to the activity of some of the inhibitors.

International Journal of Quantum ChemistryVolume 22, Issue S9 p. 195-204 Article The updated experimental proteinoid model† Sidney W. Fox, Sidney W. Fox Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this authorTadayoshi Nakashima, Tadayoshi Nakashima Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this authorAleksander Przybylski, Aleksander Przybylski Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this authorRobert M. Syren, Robert M. Syren Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this author Sidney W. Fox, Sidney W. Fox Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this authorTadayoshi Nakashima, Tadayoshi Nakashima Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this authorAleksander Przybylski, Aleksander Przybylski Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this authorRobert M. Syren, Robert M. Syren Laboratory of the National Foundation for Cancer Research, Institute for Moleular and Cellular Evolution, University of Miami, Coral Gables, Florida 33134, U.S.A.Search for more papers by this author First published: 4/6 March 1982 https://doi.org/10.1002/qua.560220719Citations: 5 † Dedicated to the memory of a young tennis partner (with S.W.F.), Max Delbrück, who said in 1978, “Ridiculous or not, to look for the origin of the mind is no longer an idle question. It has become an approachable, a natural, indeed an unavoidable, question” [from The Nature of Life, W. H. Heidcamp, Ed. (University Park Press, Baltimore, 1978), p. 146]. The late Dr. Delbrück was also one who saw the origin of the mind as coincident with the origin of life from appropriate matter. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract The experimental proteinoid model includes new results indicating that polymers sufficiently rich in basic amino acid catalyze the synthesis of peptides from ATP and amino acids and of oligonucleotides from ATP. The need for simulation syntheses of amino acids yielding significant proportions of basic amino acids is now in focus. The modeled simultaneous protocellular synthesis of peptides and polynucleotides is part of a more comprehensive proposal for the origin of the coded genetic mechanism. The finding of membrane and action potentials in proteinoid microspheres, with or without added lecithin, is reported. The crucial nature of a nonrandom matrix for protocells is developed. Citing Literature Volume22, IssueS9Supplement: Proceedings of the International Symposium on Quantum Biology and Quantum Pharmacology4/6 March 1982Pages 195-204 RelatedInformation

Osteoclastogenesis is dependent on distinct stimuli that prime and activate osteoclast differentiation. One cytokine needed to prime monocytes for osteoclastogenesis is TGF-beta, which enables and augments RANKL and TNF-alpha-induced osteoclast differentiation. However, the precise time-period during which this occurs and the molecular mechanism mediating this action are unknown. We report here TGF-beta prime monocytes for osteoclast formation within 24h by regulating expression of NFATc1, a key osteoclastic transcription factor. TGF-beta directly induces cytoplasmic NFATc1 expression within 24h, but is unable to stimulate NFATc1 nuclear translocation. Furthermore, RANKL-induced NFATc1 expression is dependent on the presence of TGF-beta during the early stages of osteoclastogenesis. Similarly, TNF-alpha activates osteoclastogenesis by stimulating translocation of TGF-beta-induced NFATc1. In light of these findings, it is apparent that osteoclast formation is dependent on coordinated interactions between TGF-beta and RANKL/TNF-alpha that regulate the expression and intracellular distribution of NFATc1 during early stages of osteoclast differentiation.

Osteoclast differentiation is dependent on TGF-β to prime precursors to the osteoclast lineage. The mechanism by which TGF-β enables osteoclast formation is unknown. One possibility is that TGF-β opposes pro-inflammatory JAK/STAT signalling. Recently, we showed that TGF-β-induces SOCS3, an inhibitor of the JAK/STAT pathway, in precursors and enhances SOCS3 in RANKL-induced osteoclasts. We therefore elected to test the role of SOCS3 in the effect of other regulators of osteoclastic differentiation. We found that TNF-α-induced osteoclasts also express SOCS3 and TGF-β strongly up-regulates this. Moreover, TNF-α-induced osteoclast differentiation and total resorbed bone area were enhanced in SOCS3-retrovirally infected precursors, whereas antisense knockdown of SOCS3 suppressed formation and the augmentative effect of TGF-β. Furthermore, SOCS3 overexpression blunted the anti-osteoclastic effect of IFN-β but not IL-10. This suggests that TGF-β-induced expression of SOCS3 may represent a crucial mechanism by which TGF-β antagonizes specific anti-osteoclastic JAK/STAT signals, priming precursors for resorption rather than inflammatory functions.

TNFalpha is pivotal to the pathogenesis of inflammatory and possibly postmenopausal osteolysis. Much recent work has clarified mechanisms by which TNFalpha promotes osteoclastogenesis, but the means by which it activates osteoclasts to resorb bone remain uncertain. We found that very low concentrations of TNFalpha promoted actin ring formation, which correlates with functional activation in osteoclasts, both in osteoclasts formed in vitro and extracted from newborn rats. TNFalpha was equipotent with RANKL for this action. Activation by TNFalpha was unaffected by blockade of RANKL by OPG, its soluble decoy receptor, suggesting that this was due to a direct action on osteoclasts. Bone resorption was similarly directly and potently stimulated, in a RANKL-independent manner in osteoclasts, whether these were formed in vitro or in vivo. Interestingly, TNFalpha promoted actin ring formation at concentrations an order of magnitude below those required for osteoclastic differentiation. Moreover, TNFalpha strongly synergized with RANKL, such that miniscule concentrations of TNFalpha were sufficient to substantially augment osteoclast activation. The extreme sensitivity of osteoclasts to activation by TNFalpha suggests that the most sensitive osteolytic response of bone to TNFalpha is through activation of existing osteoclasts; and the strong synergy with RANKL provides a mechanism whereby increased osteolysis can be achieved without disturbance to the underlying pattern of osteoclastic localization.

Osteoclast formation from hemopoietic precursors is induced by TRANCE (also called RANKL, ODF, and OPGL), a membrane-bound ligand expressed by bone marrow stromal cells. Because soluble recombinant TRANCE is a suboptimal osteoclastogenic stimulus, and to eliminate the need for such dependence on stromal cells, membrane-bound TRANCE was expressed in hematopoietic precursors using retroviral gene transfer. Four TRANCE-expressing osteoclast cell lines were established that continuously generate large numbers of multinucleated cells and express tartrate-resistant acid phosphatase and calcitonin receptors. The multinuclear cells are long-lived and either fuse continuously with each other and with mononuclear cells to form enormous syncytia, or separate to form daughter multinuclear cells. When formed on bone, but not on plastic, the majority of multinuclear cells develop actin rings on bone, and resorb bone, suggesting that bone matrix may provide additional signals that facilitate osteoclastic functional maturation. Surprisingly, multinuclear cells originate from fusion of proliferating mononuclear cells that strongly express the mature macrophage markers F4/80 and Fc receptor, which are not expressed by osteoclasts. These results indicate that osteoclasts can be derived from F4/80-positive and Fc receptor-positive cells, and that TRANCE induces osteoclastic differentiation partly by suppressing the macrophage phenotype.

The immune system has profound effects on bone remodeling. IFN-gamma, a major product of immune cells, potently inhibits bone resorption, but its mechanism of action is unknown. We found in cultures of stroma-free mononuclear precursors that IFN-gamma strongly suppresses TRANCE/RANKL-induced osteoclast formation in a dose-dependent manner. This direct effect on osteoclast progenitors was not due to stimulation of NO production by IFN-gamma, as the NOS inhibitors 1400W and L-NAME were unable to reverse the suppression. However, TGFbeta(1), which has opposing actions to IFN-gamma on diverse cellular functions, was able to antagonize the effect of IFN-gamma. This suggests that IFN-gamma prevents osteoclast formation by actively directing the differentiation of osteoclastic progenitors toward an alternative cytocidal lineage to the osteoclast.