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  • Combined efficacy of nisin and pediocin with sodium lactate, citric acid, phytic acid, and potassium sorbate and EDTA in reducing the Listeria monocytogenes population of ... 16013374

    The inability of chlorine to completely inactivate human bacterial pathogens on whole and fresh-cut produce suggests a need for other antimicrobial washing treatments. Nisin (50 microg/ml) and pediocin (100 AU/ml) individually or in combination with sodium lactate (2%), potassium sorbate (0.02%), phytic acid (0.02%), and citric acid (10 mM) were tested as possible sanitizer treatments for reducing the population of Listeria monocytogenes on cabbage, broccoli, and mung bean sprouts. Cabbage, broccoli, and mung bean sprouts were inoculated with a five-strain cocktail of L. monocytogenes at 4.61, 4.34, and 4.67 log CFU/g, respectively. Inoculated produce was left at room temperature (25 degrees C) for up to 4 h before antimicrobial treatment. Washing treatments were applied to inoculated produce for 1 min, and surviving bacterial populations were determined. When tested alone, all compounds resulted in 2.20- to 4.35-log reductions of L. monocytogenes on mung bean, cabbage, and broccoli, respectively. The combination treatments nisin-phytic acid and nisin-pediocin-phytic acid caused significant (P < 0.05) reductions of L. monocytogenes on cabbage and broccoli but not on mung bean sprouts. Pediocin treatment alone or in combination with any of the organic acid tested was more effective in reducing L. monocytogenes populations than the nisin treatment alone. Although none of the combination treatments completely eliminated the pathogen on the produce, the results suggest that some of the treatments evaluated in this study can be used to improve the microbial safety of fresh-cut cabbage, broccoli, and mung bean sprouts.
    Document Type:
    Reference
    Product Catalog Number:
    04-409

  • Water in Citric acid

    Document Type:
    Application
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • c-Myc Alters Substrate Utilization and O-GlcNAc Protein Posttranslational Modifications without Altering Cardiac Function during Early Aortic Constriction. 26266538

    Hypertrophic stimuli cause transcription of the proto-oncogene c-Myc (Myc). Prior work showed that myocardial knockout of c-Myc (Myc) attenuated hypertrophy and decreased expression of metabolic genes after aortic constriction. Accordingly, we assessed the interplay between Myc, substrate oxidation and cardiac function during early pressure overload hypertrophy. Mice with cardiac specific, inducible Myc knockout (MycKO-TAC) and non-transgenic littermates (Cont-TAC) were subjected to transverse aortic constriction (TAC; n = 7/group). Additional groups underwent sham surgery (Cont-Sham and MycKO-Sham, n = 5 per group). After two weeks, function was measured in isolated working hearts along with substrate fractional contributions to the citric acid cycle by using perfusate with 13C labeled mixed fatty acids, lactate, ketone bodies and unlabeled glucose and insulin. Cardiac function was similar between groups after TAC although +dP/dT and -dP/dT trended towards improvement in MycKO-TAC versus Cont-TAC. In sham hearts, Myc knockout did not affect cardiac function or substrate preferences for the citric acid cycle. However, Myc knockout altered fractional contributions during TAC. The unlabeled fractional contribution increased in MycKO-TAC versus Cont-TAC, whereas ketone and free fatty acid fractional contributions decreased. Additionally, protein posttranslational modifications by O-GlcNAc were significantly greater in Cont-TAC versus both Cont-Sham and MycKO-TAC. In conclusion, Myc alters substrate preferences for the citric acid cycle during early pressure overload hypertrophy without negatively affecting cardiac function. Myc also affects protein posttranslational modifications by O-GlcNAc during hypertrophy, which may regulate Myc-induced metabolic changes.
    Document Type:
    Reference
    Product Catalog Number:
    ABS204
    Product Catalog Name:
    Anti-phospho-PDHE1-A type I (Ser293) Antibody

  • Differential stimulation pathways of progesterone secretion from newly formed corpora lutea in rats treated with ethylene glycol monomethyl ether, sulpiride, or atrazine. 21427058

    Ethylene glycol monomethyl ether (EGME), sulpiride, and atrazine are known ovarian toxicants, which increase progesterone (P4) secretion and induce luteal cell hypertrophy following repeated administration. The aim of this study was to define the pathways by which these compounds exerted their effects on the ovary and hypothalamic-pituitary-gonadal (HPG) axis. In the ovary, changes in the steroidogenic activity of new and old corpora lutea (CL) were addressed. EGME (300 mg/kg), sulpiride (100 mg/kg), or atrazine (300 mg/kg) were orally given daily for four times from proestrus to diestrus in normal cycling rats. Treatment with all chemicals significantly increased serum P4 levels, and EGME as well as sulpiride induced increases in prolactin (PRL) levels. In new CL, at both the gene and the protein levels, all three chemicals upregulated the following steroidogenic factors: scavenger receptor class B type I, steroidogenic acute regulatory protein, P450 cholesterol side-chain cleavage, and 3β-hydroxysteroid dehydrogenase (HSD) and downregulated the luteolytic gene, 20α-HSD. Coadministration of EGME and bromocriptine, a D2 agonist, completely inhibited PRL but not P4 secretion. Additionally, steroidogenic factor expression levels were upregulated, and 20α-HSD level was downregulated in new CL. These results suggest that EGME both directly and indirectly stimulates P4 production in luteal cells, whereas sulpiride elevates P4 through activation of PRL secretion in the pituitary. Atrazine may directly activate new CL by stimulating steroidogenic factor expressions. The present study suggests that multiple pathways mediate the effects of EGME, sulpiride, and atrazine on the HPG axis and luteal P4 production in female rats in vivo.
    Document Type:
    Reference
    Product Catalog Number:
    AB1244

  • Propofol compared with isoflurane inhibits mitochondrial metabolism in immature swine cerebral cortex. 24398942

    Anesthetics used in infants and children are implicated in the development of neurocognitive disorders. Although propofol induces neuroapoptosis in developing brain, the underlying mechanisms require elucidation and may have an energetic basis. We studied substrate utilization in immature swine anesthetized with either propofol or isoflurane for 4 hours. Piglets were infused with 13-Carbon-labeled glucose and leucine in the common carotid artery to assess citric acid cycle (CAC) metabolism in the parietal cortex. The anesthetics produced similar systemic hemodynamics and cerebral oxygen saturation by near-infrared spectroscopy. Compared with isoflurane, propofol depleted ATP and glycogen stores. Propofol decreased pools of the CAC intermediates, citrate, and α-ketoglutarate, while markedly increasing succinate along with decreasing mitochondrial complex II activity. Propofol also inhibited acetyl-CoA entry into the CAC through pyruvate dehydrogenase, while promoting glycolytic flux with marked lactate accumulation. Although oxygen supply appeared similar between the anesthetic groups, propofol yielded a metabolic phenotype that resembled a hypoxic state. Propofol impairs substrate flux through the CAC in the immature cerebral cortex. These impairments occurred without systemic metabolic perturbations that typically accompany propofol infusion syndrome. These metabolic abnormalities may have a role in the neurotoxity observed with propofol in the vulnerable immature brain.
    Document Type:
    Reference
    Product Catalog Number:
    ABS204
    Product Catalog Name:
    Anti-phospho-PDHE1-A type I (Ser293) Antibody