1.Effect of C1-Esterase-inhibitor in angiotensin-converting enzyme inhibitor-induced angioedema.
Greve J1, Bas M2, Hoffmann TK1, Schuler PJ1, Weller P3, Kojda G4, Strassen U2. Laryngoscope. 2015 Jun;125(6):E198-202. doi: 10.1002/lary.25113. Epub 2015 Jan 13.
OBJECTIVES/HYPOTHESIS: The study objective was to generate pilot data to evaluate the effectiveness and safety of C1-esterase-inhibitor concentrate (C1-INH) compared to standard treatment in patients with angiotensin-converting enzyme inhibitor (ACEi)-induced angioedema affecting the upper aerodigestive tract.
2.Kinetic and thermodynamic characterization of the interactions between the components of human plasma kinin-forming system and isolated and purified cell wall proteins of Candida albicans.
Seweryn K1, Karkowska-Kuleta J1, Wolak N1, Bochenska O1, Kedracka-Krok S2, Kozik A1, Rapala-Kozik M1. Acta Biochim Pol. 2015;62(4):825-35. doi: 10.18388/abp.2015_1142. Epub 2015 Dec 4.
Cell wall proteins of Candida albicans, besides their best known role in the adhesion of this fungal pathogen to host's tissues, also bind some soluble proteins, present in body fluids and involved in maintaining the biochemical homeostasis of the human organism. In particular, three plasma factors - high-molecular-mass kininogen (HK), factor XII (FXII) and prekallikrein (PPK) - have been shown to adhere to candidal cells. These proteins are involved in the surface-contact-catalyzed production of bradykinin-related peptides (kinins) that contribute to inflammatory states associated with microbial infections. We recently identified several proteins, associated with the candidal cell walls, and probably involved in the binding of HK. In our present study, a list of potential FXII- and PPK-binding proteins was proposed, using an affinity selection (on agarose-coupled FXII or PPK) from a whole mixture of β-1,3-glucanase-extrated cell wall-associated proteins and the mass-spectrometry protein identification.
3.Genome-wide investigation of schizophrenia associated plasma Ndel1 enzyme activity.
Gadelha A1, Coleman J2, Breen G3, Mazzoti DR4, Yonamine CM5, Pellegrino R6, Ota VK7, Belangero SI7, Glessner J6, Sleiman P8, Hakonarson H8, Hayashi MA9, Bressan RA10. Schizophr Res. 2016 Apr;172(1-3):60-7. doi: 10.1016/j.schres.2016.01.043. Epub 2016 Feb 2.
Ndel1 is a DISC1-interacting oligopeptidase that cleaves in vitro neuropeptides as neurotensin and bradykinin, and which has been associated with both neuronal migration and neurite outgrowth. We previously reported that plasma Ndel1 enzyme activity is lower in patients with schizophrenia (SCZ) compared to healthy controls (HCs). To our knowledge, no previous study has investigated the genetic factors associated with the plasma Ndel1 enzyme activity. In the current analyses, samples from 83 SCZ patients and 92 control subjects that were assayed for plasma Ndel1 enzyme activity were genotyped on Illumina Omni Express arrays. A genetic relationship matrix using genome-wide information was then used for ancestry correction, and association statistics were calculated genome-wide. Ndel1 enzyme activity was significantly lower in patients with SCZ (t=4.9; p<0.001) and was found to be associated with CAMK1D, MAGI2, CCDC25, and GABGR3, at a level of suggestive significance (p<10(-6)), independent of the clinical status.
4.Nitric oxide modulation of endothelium-derived hyperpolarizing factor in agonist-induced depressor responses in anesthetized rats.
Kobuchi S1, Miura K2, Iwao H3, Ayajiki K4. Eur J Pharmacol. 2015 Sep 5;762:26-34. doi: 10.1016/j.ejphar.2015.04.053. Epub 2015 May 8.
Vasodilators, such as prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF), released from the vascular endothelium are important in the maintenance of systemic blood pressure. Some studies have shown that NO affects EDHF-induced vasodilator responses in isolated perfused blood vessel segments. However, the effects of NO on EDHF-mediated dilation, and their contribution to systemic blood pressure, have not been clarified. Therefore, in the present study we investigated the mechanisms underlying acetylcholine- and bradykinin-induced depressor responses, as well as the interaction between NO and EDHF, by measuring systemic blood pressure in anesthetized rats. In the presence of indomethacin and N(G)-nitro-l-arginine (l-NA; an NO synthase inhibitor), apamin plus charybdotoxin significantly inhibited depressor responses to acetylcholine and bradykinin, whereas glibenclamide, iberiotoxin, quinacrine, catalase, and combination of ouabain plus BaCl2 failed to inhibit EDHF-induced depressor responses.
