Meta-analysis of defibrase in treatment of acute cerebral infarction.

BACKGROUND: Fibrinogen-depleting agents are promising in the treatment of cerebral ischemic disease. They were studied by many trials, and the outcomes were different because of different regimens and different doses. In this study, we assessed the efficacy and safety of defibrase on acute cerebral infarction in China. METHODS: A search using Chinese hospital knowledge database (CHKD) and MEDLINE database for randomized controlled trials was carried out. A CHKD (1994 June 2005) search was performed with the keyword "defibrase", then a second search for the keyword "acute cerebral infarction"; a MEDLINE search (1950 June 2005) was performed with the following keywords: [(cerebral ischemia), OR (acute cerebral infarction), OR (stroke)], AND [defibrase]. Meta-analysis was performed with RevMan software 4.2. RESULTS: Included were 14 studies comparing the efficiency and safety of defibrase with other drugs in the treatment of acute cerebral infarction. Patients' records were pooled (total 646 patients; defibrase, n = 328, no defibrase n = 318). Neurological deficit score (NDS) before treatment showed weighted mean differences (WMD) = 0.95, 95% confidence interval (CI) = (-0.60, 2.50), P = 0.23; NDS after treatment showed WMD = -2.20, 95% CI = (-4.21, -0.18), P = 0.03; Barthel index at 3 months showed WMD = 4.45, 95% CI = (-0.13, 9.03), P = 0.06; the plasma fibrinogen level before treatment showed WMD = 0.02, 95% CI = (-0.16, 0.19), P = 0.86; plasma fibrinogen level after treatment showed WMD = -1.51, 95% CI = (-1.88, -1.15), P < 0.00 001. CONCLUSIONS: With the given dose and regimen of defibrase in China, defibrase may play a role of anticoagulation. It might inhibit the progression of stroke and prevent the recurrence of stroke.

Inducible Nitric Oxide Synthase in the Duodenal Mucosa Is Associated with Mast Cell Degranulation in Patients with Functional Dyspepsia.

AIM: Functional dyspepsia (FD) is a clinical syndrome with chronic gastroduodenal symptoms without noticeable organic or systemic diseases. According to the Rome III consensus, FD can be subdivided into PDS (postprandial distress syndrome) and EPS (epigastric pain syndrome). Neurotransmitters are involved in the development and pathology of FD. However, the expression profiles of neurotransmitters in FD patients are not clear. This study aimed to investigate the expression profile of neurotransmitters in the duodenal mucosa of FD patients. METHODS: A total of 48 FD patients treated at our hospital were included in this study: 23 patients with PDS and 25 patients with EPS. Another 21 healthy volunteers served as normal controls. The duodenal mucosa was biopsied with gastroscopy and examined with immunohistochemical staining against serotonin, substance P, inducible nitric oxide synthase (iNOS), and vasoactive intestinal peptide (VIP). Mast cells were identified with toluidine blue staining. RESULTS: The duodenal iNOS levels were significantly higher in PDS patients than the normal controls (P<0.05). The expression of serotonin, substance P, and VIP did not differ significantly among the groups. Mast cell counts and the percentage of mast cells with degranulation were significantly higher in PDS and EPS patients than normal controls (P<0.001) In addition, iNOS expression levels were positively correlated with percentage of degranulating mast cells (r=0.321, P=0.008). CONCLUSIONS: In conclusion, duodenal iNOS may be involved in the pathogenesis of PDS.

Anxiety and depression are associated with increased counts and degranulation of duodenal mast cells in functional dyspepsia.

BACKGROUND: Patients with functional dyspepsia (FD) have increased risks for psychological dysfunction than healthy peoples. This study aimed to explore the roles of psychosocial factors and duodenal mast cells in the pathogenesis of FD. MATERIAL AND METHODS: We prospectively included 48 FD patients and 21 age- and sex-match healthy volunteers. There were 23 patients with postprandial distress syndrome (PDS) and 25 patients with epigastric pain syndrome (EPS). The Hospital Anxiety Depression Scale (HADS) was administered to evaluate their psychosocial status. Upper endoscopy was performed with biopsy of the mucosa from the bulb of duodenum. Mast cells counts and degranulation rates were identified by toluidine blue staining. The relationship among the scores of HADS-A (anxiety) and HADS-D (depression) and the mast cell counts and degranulation rates were analyzed. RESULTS: The scores of HADS-A and HADS-D were significantly higher in PDS and EPS patients than the normal controls (P<0.05). The mast cell counts and degranulation rates in the duodenum were significantly increased in PDS and EPS patients than the controls (P<0.05). In either PDS or EPS patients, the HADS-A and HADS-D scores were positively correlated with the mast cell counts and degranulation rate. CONCLUSION: FD patients had significantly higher risks for anxiety and depression, which may lead to FD through the increased mast cell counts and degranulation.

The expression of matrix metalloproteinases-9, transforming growth factor-beta1 and transforming growth factor-beta receptor I in human atherosclerotic plaque and their relationship with plaque stability.

BACKGROUND: Transforming growth factor-beta (TGF-beta) and matrix metalloproteinases-9 (MMP-9) have been implicated in the pathogenesis of human atherosclerosis but their relationship during lesion progression are poorly understood. The objective of this study was to investigate the expression of MMP-9, TGF-beta1 and TGF-beta receptor I (TbetaR-I) in human atherosclerotic plaque and their relationship and plaque stability. METHODS: Specimens of human coronary artery atherosclerotic plaques were obtained from 41 patients undergoing coronary endarterectomy, and were paraffin embedded, sectioned at 4 microm intervals then stained with haematoxylin and eosin. They were divided into stable (with no or only little lipid core) and unstable plaque groups (with lipid core size > 40%): the immunohistochemical staining were performed for MMP-9, TGF-beta1 and TbetaR-I. RESULTS: The expression of MMP-9 in the unstable plaques was much higher than in the stable ones, but the expression of TGF-beta1 was higher in the stable plaques. There was no similar significant difference for TbetaR-I. Correlation analysis showed that there was a negative correlation between the expression of MMP-9 and TGF-beta1 (r = -0.332, P = 0.034 for average areal density; r = -0.373, P = 0.016 for average optical density). CONCLUSIONS: There were close relationships between MMP-9, TGF-beta1 and plaque stability. Enhanced production of MMP-9 may participate in the formation of unstable plaque, while TGF-beta1 maybe an important stabilizing factor in preventing transition into an unstable plaque phenotype.