PubMed · 13835645
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J M SULLIVAN, R E POLLARD. 1960. Acute appendicitis.. https://pubmed.ncbi.nlm.nih.gov/13835645/
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AIM: To investigate the relationship between the polymorphism of class II transactivator (CIITA) gene promoters and chronic hepatitis B (CHB). METHODS: Genomic DNA was prepared from peripheral blood leukocytes. Promoters I, III and IV of gene were analyzed respectively with polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) in 65 patients with CHB, 26 patients with acute hepatitis B (AHB) and 85 normal controls. RESULTS: No abnormal migration was found in PCR-SSCP analysis of the three promoters in the three groups. Also, no sequential difference was observed at the three promoters among the CHB patients, AHB patients and normal controls. CONCLUSION: No polymorphism in promoters I, III and IV of CIITA gene exists in CHB patients, ABH patients and normal controls, suggesting that the promoter of CIITA gene might be a conserved domain.
Previous studies have demonstrated increased expression and phosphorylation of tyrosine kinase receptor (TrkA, TrkB) in lumbosacral DRG after chronic (6 weeks) spinal cord (T8-T10) injury. This study examined the effects of acute SCI (48 hours, 2 weeks) on TrkA and TrkB expression and phosphorylation, and CREB and c-Jun expression in DRG. A significant increase in the number of TrkA- (1.5-3-fold; P < or = 0.05), TrkB- (1.3-2.0-fold; P < or = 0.05), and phosphorylated Trk (pTrk)-immunoreactive (1.5-3-fold; P < or = 0.05) cells was observed in the L1, L6, and S1 DRG 48 hours, 2, or 6 weeks after SCI. A significant increase in the number of phosphorylated (p-) CREB-immunoreactive cells was observed in the L1, L2, L6, and S1 DRG 48 hours, 2, or 6 weeks after SCI. The largest changes in p-CREB-immunoreactivity were in L1 and L2 DRG (10-fold; P <or= 0.01) at 48 hours after SCI; however, changes were modest in bladder afferent neurons. After SCI, the overall number of c-Jun-immunoreactive cells in L1, L2, and S1 DRG was dramatically increased (3-10-fold; P < or = 0.01); however, only a low percentage of bladder afferent cells expressed c-Jun-IR before or after SCI. In summary, these results suggest that TrkA or TrkB may be involved in reorganization of micturition pathways after SCI. However, CREB or c-Jun may not be downstream transcription factors in Trk-mediated signaling cascades in micturition reflex pathways after SCI but may play a role in other, nonbladder SCI-induced changes.
AIM: To investigate the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1) expression on polymorphonuclear leukocytes (PMNs) in peripheral circulation and pancreatic microcirculation in cerulein-induced acute edematous pancreatitis (AEP). METHODS: Fifty Wistar rats were randomly divided into control group (n = 10) and AEP group (n = 40). A model of AEP was established by subcutaneous injection of cerulein 5.5 and 7.5 mug/kg at 0 and 1 h after the beginning of experiment respectively. PECAM-1 expression on PMNs from splenic vein and inferior vena cava was determined by RT-PCR at mRNA level and determined by flow cytometry at protein level. RESULTS: In experimental rats, an increased PECAM-1 mRNA expression was seen from 4 to 8 h of AEP in peripheral circulation (0.77+/-0.25%, 0.76+/-0.28%, 0.89+/-0.30%, 1.00+/-0.21%), while in pancreatic microcirculation, expression decreased from 2 h and reached the lowest level at 6 h of AEP (0.78+/-0.29%, 0.75+/-0.26%, 0.62+/-0.28%, 0.66+/-0.20%). There were significant differences at 8-h time point of AEP between peripheral circulation and pancreatic microcirculation (1.00+/-0.21% vs 0.66+/-0.20%, P<0.05). Meanwhile, the difference at protein level was also found. CONCLUSION: A reverse expression of PECAM-1 on PMNs was found between peripheral circulation and pancreatic microcirculation, suggesting that inhibition of PECAM-1 expression may improve the pathological change of AEP.