[The role of cell-crystal reaction mediated inflammation in the formation of intrarenal calcium oxalate crystals].

Calcium oxalate nephrolithiasis is the common disease of urinary surgery, its exact pathogenesis is still unclear.It is believed that the renal inflammatory injury induced by cell-crystal reaction plays an important role in the formation of intrarenal calcium oxalate crystals. Recent studies indicated that inflammation induced by cell-crystal reaction can cause renal cell damage, stimulate intracellular expression of NADPH oxidase, trigger the massive production of reactive oxygen species, activate nuclear factor-κB signaling pathway, release a large number of inflammatory factors, and cause inflammatory cascade effect of the kidney, thus promoting the accumulation, nucleation and growth of calcium salt crystals, eventually leading to the formation of intrarenal crystals and even stones. In this process, the regulatory factors and mechanisms involved include macrophages, NLRP3-high mobility group box-1 protein inflammation network, fetuin A, autophagy activation and other factors.

Evaluation on the impact of spontaneous reperfusion on cardiac muscle of acute myocardial infarction by three-dimensional speckle tracking imaging.

OBJECTIVE: To explore the effect of spontaneous reperfusion (SR) on three-dimensional myocardial strain in patients with acute anterior myocardial infarction by three-dimensional speckle tracking imaging (3D-STI) technology. PATIENTS AND METHODS: Patients diagnosed with acute anterior myocardial infarction during 2013 to 2016 were consecutively selected and divided into SR group and non-spontaneous reperfusion (Non-SR) group based on whether there was SR. Patients in both groups received direct percutaneous coronary intervention (PCI) in time window. Baseline information, patency rates of culprit vessel, durations of operation, intraoperative non-reflow phenomenon ratios, and thrombolysis in myocardial infarction (TIMI) blood flows after reperfusion of patients in each group were recorded. Hospital stays of patients were compared between the two groups. Before discharge, left ventricular ejection fraction (LVEF) and left ventricular end-diastolic diameter (LVEDd) were measured. Global longitudinal strain (GLS), global radial strain (GRS), and global circumferential strain (GCS) of left ventricular (LV) were also detected by 3D-STI, so as to assess movement situations of ventricular wall and cardiac muscle in occlusive blood vessel distribution area. LVEF, LVEDd and various 3D-STI parameters were reexamined and compared one year after discharge. RESULTS: There were no significant differences between the Non-SR group and the SR group regarding the patency rate of culprit vessel, duration of operation, intraoperative non-reflow phenomenon ratio, TIMI blood flow after reperfusion, and LVEDd (p>0.05). Both LVEF before discharge and LV three-dimensional strain indexes of the SR group, were clearly higher than those of the Non-SR group (p<0.05). After one-year follow-up, the SR group had a remarkably lower LVEDd than the Non-SR group (p<0.05). LVEF of the SR group was overtly higher than that of the Non-SR group (p<0.05). LV three-dimensional strain indexes were also distinctly higher in the SR group than in the Non-SR group (p<0.05). There were good correlations between GLS, GRS, GCS and LVEF (r values were -0.620, -0.674 and 0.723, respectively). CONCLUSIONS: SR can improve nosocomial and long-term LV remodeling in patients with acute anterior myocardial infarction, and 3D-STI is able to assess ventricular remodeling after myocardial infarction.

Attenuation of myocardial injury due to oxygen free radicals (OFR) by pretreatment with OFR or calcitonin gene-related peptide.

AIM: To study the cardioprotective effects of oxygen free radicals (OFR) and calcitonin gene-related peptide (OGRP) pretreatment on myocardial damages due to OFR in isolated perfused rat heart. METHODS: The hearts were perfused in a Langendorff mode. OFR were generated by electrolysis of Krebs-Henseleit (K-H) solution. RESULTS: OFR pretreatment reduced the impairment of cardiac contractile function, the decrease of coronary flow and the increase of creatinine kinase (CK) release due to OFR, and the effect exhibited period dependence and cycle-dependence. 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C, abolished the protection of OFR pretreatment (CK release = 110 +/- 7, 215 +/- 23, 169 +/- 14, 240 +/- 30, and 113 +/- 19 kU.L-1 for control, OFR, OFR pretreatment, OFR pretreatment plus H-7, and H-7, respectively). CGRP pretreatment also protected the myocardium damages elicited by OFR in isolated perfused rat heart. CONCLUSIONS: OFR or CGRP pretreatment protected myocardium against injury elicited by OFR, and the effect of OFR pretreatment was related to the activation of PKC.