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700 | Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of L-alanine for aminopeptidase N, 4-methoxy-2-naphthylamide of L-leucine for leucine aminopeptidase, 4-methoxy-2-naphthylamide of L-glutamic acid for aminopeptidase A and << 4-methoxy-2-naphthylamide >> of L-arginine for [[ aminopeptidase B ]]. | 700 | 5 |
701 | The inhibition of << aminopeptidase >> activity in the presence of [[ bestatin ]] and puromycin inhibitors was also investigated. | 701 | 0 |
702 | The inhibition of << aminopeptidase >> activity in the presence of bestatin and [[ puromycin ]] inhibitors was also investigated. | 702 | 0 |
703 | Here, we demonstrate that << peptidyl-prolyl cis/trans-isomerase A1 >> (Pin1), an enzyme that catalyzes the conversion of the peptide bond of [[ pSer ]]/pThr-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification. | 703 | 5 |
704 | Here, we demonstrate that peptidyl-prolyl cis/trans-isomerase A1 (<< Pin1 >>), an enzyme that catalyzes the conversion of the peptide bond of [[ pSer ]]/pThr-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification. | 704 | 5 |
705 | Here, we demonstrate that << peptidyl-prolyl cis/trans-isomerase A1 >> (Pin1), an enzyme that catalyzes the conversion of the peptide bond of pSer/[[ pThr ]]-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification. | 705 | 5 |
706 | Here, we demonstrate that peptidyl-prolyl cis/trans-isomerase A1 (<< Pin1 >>), an enzyme that catalyzes the conversion of the peptide bond of pSer/[[ pThr ]]-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification. | 706 | 5 |
707 | Here, we demonstrate that << peptidyl-prolyl cis/trans-isomerase A1 >> (Pin1), an enzyme that catalyzes the conversion of the peptide bond of pSer/pThr-[[ Pro ]] moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification. | 707 | 5 |
708 | Here, we demonstrate that peptidyl-prolyl cis/trans-isomerase A1 (<< Pin1 >>), an enzyme that catalyzes the conversion of the peptide bond of pSer/pThr-[[ Pro ]] moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification. | 708 | 5 |
709 | Withdrawal from free-choice << ethanol >> consumption results in increased packing density of [[ glutamine synthetase ]]-immunoreactive astrocytes in the prelimbic cortex of alcohol-preferring rats. | 709 | 7 |
710 | Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released glutamate and its conversion to << glutamine >> through the enzyme [[ glutamine synthetase ]] (GS). | 710 | 4 |
711 | Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released glutamate and its conversion to << glutamine >> through the enzyme glutamine synthetase ([[ GS ]]). | 711 | 4 |
712 | Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released << glutamate >> and its conversion to glutamine through the enzyme [[ glutamine synthetase ]] (GS). | 712 | 5 |
713 | Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released << glutamate >> and its conversion to glutamine through the enzyme glutamine synthetase ([[ GS ]]). | 713 | 5 |
714 | << All-trans retinoic acid >> protects hepatocellular carcinoma cells against serum-starvation-induced cell death by upregulating [[ collagen 8A2 ]]. | 714 | 7 |
715 | The protein exhibited modest << H(2)O(2) >>-dependent [[ peroxidase ]] activities with guaiacol, potassium iodide, and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS). | 715 | 9 |
716 | The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with [[ guaiacol ]], potassium iodide, and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS). | 716 | 5 |
717 | The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with guaiacol, [[ potassium iodide ]], and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS). | 717 | 5 |
718 | The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with guaiacol, potassium iodide, and [[ 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid ]] (ABTS). | 718 | 5 |
719 | The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with guaiacol, potassium iodide, and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid ([[ ABTS ]]). | 719 | 5 |
720 | Ferredoxin 1 (<< FDX1 >>; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid ]] hormone synthesis in mammalian tissues. | 720 | 4 |
721 | Ferredoxin 1 (FDX1; << adrenodoxin >>) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid ]] hormone synthesis in mammalian tissues. | 721 | 4 |
722 | << Ferredoxin 1 >> (FDX1; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid ]] hormone synthesis in mammalian tissues. | 722 | 4 |
723 | Ferredoxin 1 (<< FDX1 >>; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid hormone ]] synthesis in mammalian tissues. | 723 | 4 |
724 | Ferredoxin 1 (FDX1; << adrenodoxin >>) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid hormone ]] synthesis in mammalian tissues. | 724 | 4 |
725 | << Ferredoxin 1 >> (FDX1; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid hormone ]] synthesis in mammalian tissues. | 725 | 4 |
726 | Luciferase reporter assays showed that transcription of << FDX1 >> was synergistically activated by the NR5A family and [[ 8Br-cAMP ]] treatment through two SF-1 binding sites and a CRE-like sequence in a human ovarian granulosa cell line, KGN. | 726 | 6 |
727 | These results indicate transcription of << FDX1 >> is regulated by the NR5A family and [[ cAMP ]] signaling, and participates in steroid hormone production in ovarian granulosa cells. | 727 | 6 |
728 | These results indicate transcription of << FDX1 >> is regulated by the NR5A family and cAMP signaling, and participates in [[ steroid ]] hormone production in ovarian granulosa cells. | 728 | 4 |
729 | << Flutamide >>, an effective competitive inhibitor of the [[ androgen receptor ]] used orally for palliative treatment of prostatic carcinoma and regulation of prostatic hyperplasia was evaluated for its genotoxic effects in the intact rat and in primary cultures of human hepatocytes. | 729 | 0 |
730 | In the liver of rats given << flutamide >> as initiating agent at the dose of 500 mg/kg/week for 6 successive weeks, [[ gamma-glutamyltraspeptidase ]]-positive foci were detected only in 3 of 10 rats. | 730 | 6 |
731 | << Cycloxygenase-2 >> (COX-2)-derived [[ prostaglandin E2 ]] (PGE2) has been shown to be important in esophageal tumorigenesis. | 731 | 4 |
732 | Cycloxygenase-2 (<< COX-2 >>)-derived [[ prostaglandin E2 ]] (PGE2) has been shown to be important in esophageal tumorigenesis. | 732 | 4 |
733 | << Cycloxygenase-2 >> (COX-2)-derived prostaglandin E2 ([[ PGE2 ]]) has been shown to be important in esophageal tumorigenesis. | 733 | 4 |
734 | Cycloxygenase-2 (<< COX-2 >>)-derived prostaglandin E2 ([[ PGE2 ]]) has been shown to be important in esophageal tumorigenesis. | 734 | 4 |
735 | We have shown that << COX-2 >> mediates acid-induced [[ PGE2 ]] production. | 735 | 4 |
736 | We conclude that << mPGES1 >> mediates acid-induced increase in [[ PGE2 ]] production and cell proliferation. | 736 | 4 |
737 | << Butein >> also increased [[ heme oxygenase-1 ]] (HO-1) protein expression and HO activity. | 737 | 6 |
738 | << Butein >> also increased heme oxygenase-1 ([[ HO-1 ]]) protein expression and HO activity. | 738 | 6 |
739 | << Butein >> also increased heme oxygenase-1 (HO-1) protein expression and [[ HO ]] activity. | 739 | 7 |
740 | Furthermore, << butein >> treatment caused nuclear accumulation of nuclear factor-E2-related factor 2 (Nrf2) and increased the promoter activity of [[ antioxidant response elements ]] (AREs). | 740 | 6 |
741 | Furthermore, << butein >> treatment caused nuclear accumulation of nuclear factor-E2-related factor 2 (Nrf2) and increased the promoter activity of antioxidant response elements ([[ AREs ]]). | 741 | 6 |
742 | Furthermore, << butein >> treatment caused nuclear accumulation of [[ nuclear factor-E2-related factor 2 ]] (Nrf2) and increased the promoter activity of antioxidant response elements (AREs). | 742 | 6 |
743 | Furthermore, << butein >> treatment caused nuclear accumulation of nuclear factor-E2-related factor 2 ([[ Nrf2 ]]) and increased the promoter activity of antioxidant response elements (AREs). | 743 | 6 |
744 | Treatment of HDP cells with a c-Jun NH2-terminal kinase (JNK) inhibitor also reduced butein-induced HO-1 expression, and << butein >> treatment led to increased [[ JNK ]] phosphorylation. | 744 | 9 |
745 | Treatment of HDP cells with a c-Jun NH2-terminal kinase (JNK) inhibitor also reduced << butein >>-induced [[ HO-1 ]] expression, and butein treatment led to increased JNK phosphorylation. | 745 | 6 |
746 | The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its << proline-42-to-alanine >> mutant (Pro42Ala) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding. | 746 | 0 |
747 | The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its proline-42-to-alanine mutant (<< Pro42Ala >>) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding. | 747 | 0 |
748 | The refolding kinetics of guanidine-denatured disulfide-intact << bovine pancreatic ribonuclease A >> (RNase A) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding. | 748 | 0 |
749 | The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (<< RNase A >>) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding. | 749 | 0 |
750 | The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its << proline-42-to-alanine >> mutant (Pro42Ala) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding. | 750 | 0 |
751 | The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its proline-42-to-alanine mutant (<< Pro42Ala >>) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding. | 751 | 0 |
752 | The refolding kinetics of guanidine-denatured disulfide-intact << bovine pancreatic ribonuclease A >> (RNase A) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding. | 752 | 0 |
753 | The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (<< RNase A >>) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding. | 753 | 0 |
754 | The folding rate for wild-type << RNase A >> is faster in the presence of the inhibitor [[ 2'CMP ]] than in its absence, indicating that the transition-state structure in the rate-determining step is stabilized by 2'CMP. | 754 | 0 |
755 | During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce << prostaglandins >> (PG) via [[ PG synthase 2 ]] (PTGS2) and cortisol via hydroxysteroid (11-β) dehydrogenase 1 (HSD11B1). | 755 | 4 |
756 | During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce << prostaglandins >> (PG) via PG synthase 2 ([[ PTGS2 ]]) and cortisol via hydroxysteroid (11-β) dehydrogenase 1 (HSD11B1). | 756 | 4 |
757 | During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce prostaglandins (PG) via PG synthase 2 (PTGS2) and << cortisol >> via [[ hydroxysteroid (11-β) dehydrogenase 1 ]] (HSD11B1). | 757 | 4 |
758 | During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce prostaglandins (PG) via PG synthase 2 (PTGS2) and << cortisol >> via hydroxysteroid (11-β) dehydrogenase 1 ([[ HSD11B1 ]]). | 758 | 4 |
759 | The primary aim of these studies was to test the hypothesis that << HSD11B1 >>-derived [[ cortisol ]] has a biological role in endometrial function and conceptus development during early pregnancy in sheep. | 759 | 4 |
760 | In study 1, cyclic ewes received vehicle, cortisol, << PF 915275 >> (PF; a selective inhibitor of [[ HSD11B1 ]]), cortisol and PF, meloxicam (a selective inhibitor of PTGS2), cortisol and meloxicam, recombinant ovine IFNT, or IFNT and PF into the uterus from day 10 to day14 after estrus. | 760 | 0 |
761 | In study 1, cyclic ewes received vehicle, cortisol, PF 915275 (PF; a selective inhibitor of HSD11B1), cortisol and PF, << meloxicam >> (a selective inhibitor of [[ PTGS2 ]]), cortisol and meloxicam, recombinant ovine IFNT, or IFNT and PF into the uterus from day 10 to day14 after estrus. | 761 | 0 |
762 | << Cortisol >> and IFNT stimulated endometrial [[ HSD11B1 ]] expression and activity, increased endometrial PTGS2 activity and the amount of PG in the uterine lumen, and up-regulated many conceptus elongation-related genes in the endometrium. | 762 | 9 |
763 | << Cortisol >> and IFNT stimulated endometrial HSD11B1 expression and activity, increased endometrial [[ PTGS2 ]] activity and the amount of PG in the uterine lumen, and up-regulated many conceptus elongation-related genes in the endometrium. | 763 | 9 |
764 | << Cortisol >> and IFNT stimulated endometrial [[ HSD11B1 ]] expression and activity, increased endometrial PTGS2 activity and the amount of PG in the uterine lumen, and up-regulated many conceptus elongation-related genes in the endometrium. | 764 | 6 |
765 | These results suggest that << HSD11B1 >>-derived [[ cortisol ]] mediates, in part, actions of ovarian progesterone and the conceptus on endometrial function and support the hypothesis that IFNT, PG, and cortisol coordinately regulate endometrial functions important for conceptus elongation and implantation during early pregnancy in sheep. | 765 | 4 |
766 | << 2-(2-Aminoethyl)-quinoline >> (D-1997): a novel agonist at [[ 5-hydroxytryptamine1-like receptors ]] in the canine basilar artery. | 766 | 2 |
767 | 2-(2-Aminoethyl)-quinoline (<< D-1997 >>): a novel agonist at [[ 5-hydroxytryptamine1-like receptors ]] in the canine basilar artery. | 767 | 2 |
768 | The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the << beta-adrenoceptor >> blocker with high affinity for 5-HT1A and 5-HT1B binding sites [[ (+/-)-pindolol ]] (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM). | 768 | 0 |
769 | The effects of D-1997 in the basilar artery were not modified by incubation with either the << 5-HT2 receptor >> antagonist [[ ketanserin ]] (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM). | 769 | 1 |
770 | The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the << 5-HT3 >> and 5-HT4 receptor antagonist ICS205930 ([[ tropisetron ]]; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM). | 770 | 1 |
771 | The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and << 5-HT4 >> receptor antagonist ICS205930 ([[ tropisetron ]]; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM). | 771 | 1 |
772 | The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the << 5-HT1A >> receptor antagonist [[ spiroxatrine ]] (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM). | 772 | 1 |
773 | The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the << alpha 1-adrenoceptor >> antagonist [[ prazosin ]] (0.01-1 microM). | 773 | 1 |
774 | In contrast, the << D-1997 >>-induced responses were potently and concentration-dependently antagonized by the mixed [[ 5-HT1-like ]] and 5-HT2 receptor antagonist methiothepin (0.01-1 microM). | 774 | 2 |
775 | In contrast, the << D-1997 >>-induced responses were potently and concentration-dependently antagonized by the mixed 5-HT1-like and [[ 5-HT2 receptor ]] antagonist methiothepin (0.01-1 microM). | 775 | 2 |
776 | In contrast, the D-1997-induced responses were potently and concentration-dependently antagonized by the mixed << 5-HT1-like >> and 5-HT2 receptor antagonist [[ methiothepin ]] (0.01-1 microM). | 776 | 1 |
777 | In contrast, the D-1997-induced responses were potently and concentration-dependently antagonized by the mixed 5-HT1-like and << 5-HT2 receptor >> antagonist [[ methiothepin ]] (0.01-1 microM). | 777 | 1 |
778 | It is concluded that << D-1997 >> contracts the canine basilar artery by stimulating [[ 5-HT1-like receptors ]] unrelated to either the 5-HT1A or 5-HT1B receptor subtypes. | 778 | 9 |
779 | It is concluded that << D-1997 >> contracts the canine basilar artery by stimulating 5-HT1-like receptors unrelated to either the [[ 5-HT1A ]] or 5-HT1B receptor subtypes. | 779 | 9 |
780 | It is concluded that << D-1997 >> contracts the canine basilar artery by stimulating 5-HT1-like receptors unrelated to either the 5-HT1A or [[ 5-HT1B ]] receptor subtypes. | 780 | 9 |
781 | Although Bak and Bcl-2-associated X protein (Bax), another member of the Bcl-2 family, are generally thought to be functionally redundant, only Bak is necessary and sufficient for << VK2 >>-induced [[ cytochrome c ]] (cyt c) release and cell death. | 781 | 6 |
782 | Although Bak and Bcl-2-associated X protein (Bax), another member of the Bcl-2 family, are generally thought to be functionally redundant, only Bak is necessary and sufficient for << VK2 >>-induced cytochrome c ([[ cyt c ]]) release and cell death. | 782 | 6 |
783 | In muscle and liver, << TCDD >> (10 ng/kg/day) induced increases in methylation and decreases in mRNA expression of [[ Igf2r ]]. | 783 | 8 |
784 | << Rasagiline >> is a propargylamine and irreversible [[ monoamine oxidase (MAO) B ]] inhibitor used for the treatment of Parkinson's disease (PD). | 784 | 0 |
785 | Rasagiline is a << propargylamine >> and irreversible [[ monoamine oxidase (MAO) B ]] inhibitor used for the treatment of Parkinson's disease (PD). | 785 | 0 |
786 | << Tolvaptan >> is a selective [[ arginine vasopressin (AVP) V(2) receptor ]] blocker used to induce free water diuresis in the treatment of euvolemic or hypervolemic hyponatremia. | 786 | 0 |
787 | Prolonged use of << tolvaptan >> leads to increased endogenous levels of AVP and perhaps over-stimulation of [[ V(1A) receptors ]]. | 787 | 9 |
788 | Prolonged use of << tolvaptan >> leads to increased endogenous levels of [[ AVP ]] and perhaps over-stimulation of V(1A) receptors. | 788 | 6 |
789 | In addition, << tolvaptan >> is metabolized by the [[ CYP3A4 ]] system; thus physicians should be aware of the potential for increased interactions with other medications. | 789 | 5 |
790 | << Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), NF-kB p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma [[ insulin ]]. | 790 | 6 |
791 | << Fisetin >> treatment showed a significant decline in the levels of blood glucose, [[ glycosylated hemoglobin ]] (HbA1c), NF-kB p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin. | 791 | 8 |
792 | << Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin ([[ HbA1c ]]), NF-kB p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin. | 792 | 8 |
793 | << Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), [[ NF-kB ]] p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin. | 793 | 8 |
794 | << Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), NF-kB [[ p65 ]] unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin. | 794 | 8 |
795 | << Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), NF-kB p65 unit (in pancreas) and [[ IL-1β ]] (plasma), serum nitric oxide (NO) with an elevation in plasma insulin. | 795 | 8 |
796 | High-<< glucose >> environment enhanced oxidative stress and increased [[ interleukin-8 ]] secretion from keratinocytes: New insights on impaired diabetic wound healing. | 796 | 6 |
797 | Using cultured human keratinocytes and diabetic rat model, the current study showed that high-<< glucose >> environment enhanced [[ IL-8 ]] production via epidermal growth factor receptor (EGFR) -extracelluar signal-regulated kinase (ERK) pathway in a reactive oxygen species (ROS)-dependent manner in keratinocytes. | 797 | 6 |
798 | In conclusion, << IL-8 >> production and neutrophil infiltration are increased in high-[[ glucose ]] environment due to elevated ROS level and contributed to impaired wound healing in diabetic skin. | 798 | 6 |
799 | The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) << PhIP >> (10 and/or 15mg/kg) significantly decreased superoxide dismutase (SOD) and glutathioneperoxidase (GPx) activities, while increased [[ catalase ]] (CAT) activity compared with the control. | 799 | 7 |
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