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1.
Meat Sci ; 83(4): 768-74, 2009 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20416624

RESUMO

This experiment investigated the combined effects of two dry-aging methods (unpackaged and in a bag), two loin-cut styles (bone-in shell loins and boneless strip loins), and two aging times (21 and 28days) on the physical, chemical, sensory, and microbial properties of dry-aged beef. Sections from shell and strip loin were assigned randomly to be aged unpackaged or aged packaged in a bag with high moisture permeability. Weight losses increased with aging time. Shell loins lost more (P<0.05) weight during aging compared with strip loins; dry aging in a bag had less (P<0.05) weight loss than unpackaged aging. There were no differences (P>0.05) in any of the sensory traits between shell and strip loins or dry aging using a traditional method or in a bag. Dry aging in a bag creates positive effects on yields, no negative effects on product quality, and adds flexibility and control of the aging environment.

2.
Meat Sci ; 77(4): 562-9, 2007 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22061942

RESUMO

Previous research has shown that beef quality decreased with the age of cattle. In this study, beef trimmings from nine mature cows (n=9), equally representing three animal age groups (2-4, 6-8, and 10-12yr), were restructured into steaks formulated with propyl gallate, alone or in combination with a beefy flavoring agent, to enhance palatability and stability during 6months of frozen storage at -29°C. Lipid oxidation, rancidity, and loss of beefy flavor in restructured steaks during extended storage were reduced by propyl gallate. The beefy flavoring agent inclusion masked mature, forage-fed beef off-flavors, intensified beefy flavor, and improved steak tenderness, juiciness and cooking yield. Thus, the combination of propyl gallate and beefy flavoring offers an effective means to enhance the palatability and storage stability of restructured beef prepared from mature cows.

3.
Eur J Pharmacol ; 424(1): 1-11, 2001 Jul 13.
Artigo em Inglês | MEDLINE | ID: mdl-11470254

RESUMO

We investigated whether and how could various modulators of arachidonic acid metabolism affect apoptosis induced by tumour necrosis factor-alpha (TNF-alpha) in human myeloid leukaemia HL-60 cells. These included arachinonyltrifluoromethyl ketone (AACOCF3; cytosolic phospholipase A2 inhibitor), indomethacin (cyclooxygenase inhibitor), MK-886 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2-dimethyl propanoic acid; 5-lipoxygenase-activating protein inhibitor), nordihydroguaiaretic acid (general lipoxygenase inhibitor), and arachidonic acid itself. Incubation of HL-60 cells with nordihydroguaiaretic acid resulted in apoptosis and it was characterised by mitochondria membrane depolarisation, release of cytochrome c from mitochondria into cytosol and activation of caspase-3. Indomethacin and nordihydroguaiaretic acid synergistically potentiated TNF-alpha-induced apoptosis, while arachidonic acid, AACOCF3 and MK-886 did not modulate its effects. Furthermore, indomethacin potentiated apoptosis in cells treated with a differentiating agent, all-trans retinoic acid, which induces resistance to TNF-alpha. However, the observed effects were probably not associated either with the cyclooxygenase- or lipoxygenase-dependent activities of indomethacin and nordihydroguaiaretic acid, respectively. Since indomethacin may reportedly activate peroxisome proliferator-activated receptors (PPARs), the effects of specific ligands of PPARs on apoptosis were studied as well. It was found that selective PPARs ligands had no effects on TNF-alpha-induced apoptosis. The findings suggest that arachidonic acid metabolism does not play a key role in regulation of apoptosis induced by TNF-alpha in the present model. Nevertheless, our data raise the possibility that indomethacin could potentially be used to improve the treatment of human myeloid leukaemia.


Assuntos
Apoptose/efeitos dos fármacos , Ácido Araquidônico/antagonistas & inibidores , Tiazolidinedionas , Fator de Necrose Tumoral alfa/farmacologia , Ácido Araquidônico/metabolismo , Caspase 3 , Caspases/efeitos dos fármacos , Caspases/metabolismo , Ciclo-Oxigenase 2 , Inibidores de Ciclo-Oxigenase 2 , Inibidores de Ciclo-Oxigenase/farmacologia , Grupo dos Citocromos c/efeitos dos fármacos , Grupo dos Citocromos c/metabolismo , Citosol/efeitos dos fármacos , Citosol/enzimologia , Relação Dose-Resposta a Droga , Sinergismo Farmacológico , Células HL-60 , Humanos , Indometacina/farmacologia , Isoenzimas/efeitos dos fármacos , Isoenzimas/metabolismo , Masoprocol/farmacologia , Proteínas de Membrana , Proliferadores de Peroxissomos/farmacologia , Fosfolipases A/efeitos dos fármacos , Fosfolipases A/metabolismo , Fosfolipases A2 , Prostaglandina-Endoperóxido Sintases/efeitos dos fármacos , Prostaglandina-Endoperóxido Sintases/metabolismo , Pirimidinas/farmacologia , Receptores Citoplasmáticos e Nucleares/efeitos dos fármacos , Receptores Citoplasmáticos e Nucleares/metabolismo , Tiazóis/farmacologia , Fatores de Transcrição/efeitos dos fármacos , Fatores de Transcrição/metabolismo , Tretinoína/farmacologia
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