|1.||Chen, Xi: 8 articles (07/2008 - 01/2007)|
|2.||Nielsen, Vance G: 7 articles (12/2014 - 01/2010)|
|3.||Cepinskas, Gediminas: 5 articles (05/2011 - 11/2007)|
|4.||Sun, Bing-Wei: 5 articles (01/2008 - 01/2007)|
|5.||George, James F: 4 articles (04/2011 - 07/2009)|
|6.||Sun, Yan: 4 articles (04/2010 - 12/2007)|
|7.||Chen, Zhao-Yong: 4 articles (12/2007 - 01/2007)|
|8.||Sun, Bing-wei: 3 articles (12/2014 - 07/2008)|
|9.||Leánez, Sergi: 3 articles (08/2014 - 08/2013)|
|10.||Pol, Olga: 3 articles (08/2014 - 08/2013)|
01/01/2014 - "In both human and mouse cells, CORM-2 inhibited endogenous and exogenous ligand-dependent TLR4 activation, which indicates that CORM-2 could be therapeutic for both early and late stages of AP, which involve sterile- and endotoxin-mediated inflammation, respectively. "
07/01/2015 - "We conclude that Nrf2 is indispensable for CORM-2 inhibition of LPS-induced inflammation."
03/01/2014 - "The increased NOS1 expression induced by inflammation in WT mice was abolished by CORM-2 treatment, while there was no effect of the inflammation in neither CORM-2 treatment in the expression of NOS2 in WT and NOS1-KO mice. "
03/01/2014 - "In all genotypes, inflammation increased the dorsal root ganglia and paw expression of HO-1, but CORM-2 treatment only over-expressed this enzyme in the paw of all genotypes. "
03/01/2014 - "Effects of CORM-2 treatment on the expression of HO-1, NOS1, and NOS2 at 14 days after inflammation induction were assessed by Western blot. "
01/01/2008 - "In parallel, burn-induced granulocytes infiltration in renal tissue was markedly decreased by treatment with CORM-2. "
12/14/2007 - "In parallel, burn-induced granulocyte infiltration in mid-ileum was markedly decreased in the burn mice treated with CORM-2. "
06/01/2007 - "Additionally, the adhesion of PMN on HSEC after stimulation of serum in burn group was enhanced, while it was markedly inhibited after stimulation of serum in burn + CORM-2 group (P < 0.05). "
07/01/2008 - "The mice in the sham group (n=7) underwent sham thermal injury, whereas the mice in the burn group (n=7) received 15% total body surface area full-thickness thermal injury, the mice in the burn+CO-releasing molecules (CORM)-2 group (n=7) underwent the same injury with immediate administration of CORM-2 (8 mg/kg, i.v.), and the mice in the burn+inactivated CORM (iCORM)-2 group (n=7) underwent the same injury with immediate administration of iCORM-2. "
01/28/2008 - "In each experiment, mice in sham group (n=4) received sham thermal injury, whereas mice in burn group (n=4) received a 15% of total body surface area (TBSA) full-thickness thermal injury, and mice in burn+CORM-2 group (n=4) received the same thermal injury with immediate administration of CORM-2 (8 mg/kg, iv). "
04/01/2011 - "In contrast, although CORM-2 exposure improved coagulation kinetics, dilution with VOL markedly degraded thrombus formation kinetics. "
01/01/2010 - "In FVIII-deficient plasma, CORM-2 exposure significantly (P < 0.05) increased the velocity of thrombus formation (84%) and strength (48%) compared with plasma not exposed to CORM-2. "
12/01/2014 - "CORM-2 and CORM-3 enhanced the velocity of clot formation and thrombus strength in a similar manner, whereas CORM-A1 did not affect coagulation. "
01/01/2011 - "Thus, our goals were to discern the effects of hypothermia on fibrinolysis in human plasma, and secondarily determine if a new procoagulant/antifibrinolytic molecule, carbon monoxide releasing molecule (tricarbonyldichlororuthenium (II) dimer; CORM-2) would modify thrombus growth/disintegration under hypothermic conditions. "
07/01/2011 - "Thrombus growth was monitored with thrombelastography for 15 min. LC-MS/MS did not detect any direct modifications of amino acids in fibrinogen, but detection of small regions of both the alpha and gamma chains was lost following exposure to CORM-2 and endoproteinase digestion with trypsin and Glu-C. "
|4.||Wounds and Injuries (Trauma)
04/01/2011 - "Extensive preclinical investigation remains to be performed to determine the route of administration, safety, and efficacy of CORM-2 and other CORMs to treat trauma-associated bleeding."
01/01/2011 - "Further investigation is warranted to determine if CORM-2 administration can improve hemostasis in preclinical models of hypothermia and trauma."
07/01/2015 - "Moreover, HO-1 inhibitor, ZnppIX and CO scavenger, hemoglobin impaired HT-dependent wound healing while CORM-2, a CO generator, accelerated wound closure. "
03/01/2014 - "CORM-2 treatment may represent a new approach for management chronic inflammatory pain."
03/01/2014 - "CORM-2 treatment inhibits inflammatory pain through enhancing HO-1 paw expression in all genotypes and reducing NOS1 over-expression in WT mice. "
03/01/2014 - "Main inflammatory pain symptoms induced by CFA in WT, NOS1-KO, and NOS2-KO mice were significantly reduced in a time-dependent manner by CORM-2 treatment. "
08/01/2013 - "Moreover, while CORM-2 or CoPP treatments did not alter or reduced the antinociceptive effects of morphine during acute and visceral pain, both treatments improved the local antiallodynic and antihyperalgesic effects of morphine after chronic inflammatory or neuropathic pain in WT, but not in KO mice. "
08/15/2014 - "The effects of CORM-2 and CoPP treatments on the local antinociceptive actions of morphine and their interactions with nitric oxide during acute pain were evaluated by using wild type (WT), neuronal (nNOS-KO) or inducible (iNOS-KO) nitric oxide synthase knockout mice and assessing their thermal nociception to a hot stimulus with the hot plate test. "
|2.||Intercellular Adhesion Molecule-1 (Intercellular Adhesion Molecule 1)
|3.||NF-kappa B (NF-kB)
|4.||Nitric Oxide (Nitrogen Monoxide)
|5.||Morphine (MS Contin)
|6.||Protein Isoforms (Isoforms)
|7.||Vascular Cell Adhesion Molecule-1 (Vascular Cell Adhesion Molecule 1)
|9.||Transcription Factors (Transcription Factor)
|10.||salicylhydroxamic acid (SHAM)
|1.||Transplantation (Transplant Recipients)