To investigate the effects of Yiguanjian Decoction, a compound traditional Chinese herbal medicine, on rats with cirrhosis based on the method of differential proteomics.

OBJECTIVE: To explore the alteration and the clinical significance of QT dispersion in acute pulmonary embolism (PE). METHODS: From May 2011 to April 2012, 42 hospitalized PE patients in Xiangya Hospital of Central South University were enrolled, and divided into a high-risk group and a non-high-risk group according to the clinic state on admission. Another 30 healthy subjects with matched age and genders were enrolled as a normal control group. QT interval was measured manually in 12- lead conventional electrocardiogram within 24 hours on admission and after the treatment. QT dispersion (QTd) and heart rate-corrected QT dispersion (QTcd) were also calculated. All patients were followed up during hospitalization, and were divided to a death group and a survival group. RESULTS: QTd and QTcd in the high-risk group [(70.2±34.0), (88.1±43.3) ms] and the non-high-risk group [(49.3±21.8), (59.1±26.2) ms] were significantly higher than those in the normal control group[(33.2±12.4), (36.7±14.2) ms] (P<0.05), while QTd and QTcd in the high-risk group were significantly higher than those in the non-high-risk group (P<0.05). The interval of electrocardiogram was (5.6±2.5) days between 24 hours on admission and after the treatment (ECG). QTd and QTcd were reduced significantly after the treatment in the survival group [(41.0±16.4), (47.4±18.0)ms] compared with those on admission [(54.0±33.0), (67.2±40.5)ms] (P<0.05), but the QTd and QTcd after the treatment were also significantly higher than those in the normal control group (P<0.05). There was no significant difference in the QTd and QTcd between 24 hours on admission and after the treatment in the death group (P>0.05). Logistic regression showed that high-risk of PE, right ventricular dysfunction and high QTcd after the treatment were the main risk factors of hospital death. CONCLUSION QTd and QTcd are increased in PE. PE patients with right ventricular dysfunction, high-risk of PE, and high QTcd after the treatment suggest weak prognosis.
Adolescent ; Adult ; Aged ; Case-Control Studies ; Electrocardiography ; Female ; Heart Conduction System ; physiopathology ; Humans ; Male ; Middle Aged ; Prognosis ; Pulmonary Embolism ; complications ; physiopathology ; Ventricular Dysfunction, Right ; etiology ; physiopathology ; Young Adult

Objective: To investigate the effect of dopamine (DA) on the glutamate (Glu) uptake ability of neural cells, as well as its effect on cognitive impairment in rats with minimal hepatic encephalopathy (MHE) via related pathways. Methods: A total of 45 Sprague-Dawley rats were randomly divided into control group, MHE model group, and DA intervention model group, with 15 rats in each group. The rats in the MHE model group were given intraperitoneal injection of thioacetamide (TAA), those in DA intervention model group were given intraventricular injection of DA, and those in the control group were given intraperitoneal injection of physiological saline, with a frequency of twice a week for 8 weeks. Cerebral microdialysis was used to measure the change in the content of Glu in the brain in MHE rats and rats with DA intervention; RT-PCR and Western blotting were used to measure the relative mRNA and protein expression of trace amine-associated receptor 1 (TAAR1) and excitatory amino acid transporter 2 (EAAT2); the changes in the expression of EAAT2 and extracellular Glu level were measured after intracerebroventricular injection of TAAR1 siRNA and TAAR1 plasmid in MHE rats and rats with DA intervention. One- way analyses of variance for comparison among different groups were performed, categorical data between groups were compared using nonparametric tests. Results: Compared with the control group, the MHE model group had significant increases in the content of DA in liver tissue, plasma, and brain tissue (4.90 ± 0.13 ng/g vs 1.20 ± 0.13 ng/g, P < 0.05; 16.32 ± 1.01 pmol/ml vs 5.50 ± 0.82 pmol/ml, P < 0.05; 732.45 ± 78.85 ng/g vs 387.00 ± 23.36 ng/g, P < 0.05). There was a significant increase in the extracellular Glu level within 40-120 minutes after intracerebral injection of DA in the DA intervention model group. Compared with the control group, the MHE model group and the DA intervention model group had a significant increase in the relative protein expression of TAAR1 (3.72 ± 0.50/4.18 ± 0.43 vs 0.96 ± 0.40, both P < 0.05) and a significant reduction in the expression of EAAT2 (0.46 ± 0.16/0.51 ± 0.20 vs 0.92 ± 0.11, P = 0.013 and 0.036). Compared with the model group treated with empty vector, the MHE model group and the DA intervention model group had a significant increase in the relative protein expression of EAAT2 after TAAR1 siRNA intervention (0.86±0.142 vs 0.56 ± 0.060, P = 0.028; 0.99 ± 0.056 vs 0.43 ± 0.098, P = 0.0010) and a significant reduction in the extracellular Glu level in the brain at 60-120 minutes after injection, while after TAAR1 plasmid intervention, the MHE model group and the DA intervention model group had a significant reduction in the relative protein expression of EAAT2 (0.20 ± 0.040 vs 0.48 ± 0.08, P = 0.006; 0.24 ± 0.05 vs 0.54 ± 0.07, P = 0.004) and a significant increase in the extracellular Glu level in brain at 60-100 minutes after injection. Conclusion DA interacts with TAAR1 in brain tissue to induce extracellular accumulation of Glu, thus leading to the disorder of the TAAR1-EAAT2 signaling pathway in brain tissue and ultimately injuring the cognitive function of MHE rats.