Clarithromycin ; therapeutic use ; Humans ; Lymphoma, B-Cell, Marginal Zone ; drug therapy ; Male ; Middle Aged ; Tomography, X-Ray Computed

Animals ; Female ; Injections, Intraventricular ; Male ; Maze Learning ; drug effects ; Memory ; drug effects ; Mice ; Mice, Inbred Strains ; Toluene ; administration & dosage ; toxicity

This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia.

Objective To observe the effect of midazolam plus propofol administered for colonoscopy on cognitive function in middle-aged and aged patients. Methods One hundred and thirty six patients, ASA I and II, aged 40~75 years and undergoing colonoscopy were randomized to propofol group (group P, n=68) and propofol plus midazolam group (group PM, n=68). Baseline cognitive function was measured using Mini mental state exami-nation (MMSE) before anesthesia and the cognitive testing was repeated 10 minutes after emerging from anesthesia. BP, HR, SpO2, analgesic effect and sedative drug doses in both groups were recorded. Procedure time, recovery time and Rasmay sedation score were both recorded. Results Recovery time was significantly longer in group PM than that in group P (P<0.05). The total dose of propofol was significantly smaller in group PM than that in group P (P<0.05). MMSE score of both groups decreased, but the incidence of cognitive decline and the level of cognition in group PM were more notable than those of group P (P<0.05). Conclusions Midazolam plus propofol and propo-fol alone administered for colonoscopy could both increase the incidence of cognitive decline, and the effect of the former is more notable, but midazolam added to propofol could reduce the dosage of propofol.

Animals ; Barbiturates ; Coloring Agents ; Fallopian Tubes ; cytology ; embryology ; physiology ; Female ; Isoxazoles ; Male ; Membrane Potentials ; Mice ; Mice, Inbred Strains

Objective To investigate the dynamic levels of autophagy after intimal injury of carotid artery. Meth-ods In this study ,40 male SD rats were randomly assigned to operated(n=20)and control groups(n=20). Balloon inju-ry was induced in the left carotid artery in operated groups .Rats in control groups just received carotid artery exposure without injury. Western blot was used to detect the levels of Beclin-1, LC3 and p62 at the third and seventh days. Immu-nofluorescence was used to examine the expression of Beclin-1 and LC3 at the third and seventh days. Results The ex-pression levels of Beclin-1 and LC3 were increased while the levels of P62 were decreased at the third and seventh days after carotid balloon injury. Beclin-1 and LC3 were present in neointima and medintima. The numbers of both Beclin-1 positive cells and LC3 positive cells were increased at the third and seventh days after carotid injury. The numbers of Be-clin-1 positive cells were 18.60 ± 1.34 in neointima and 6.40 ± 0.55 in medintima at third day, (27.6 ± 2.19 in neointima and 6.40±0.55 in medinitima at the seventh day,(all P=0.000,n=5). The numbers of LC3 positive cells were 10.60±1.52 in neointima and 3.00 ± 0.71 in medintima at third day, (P=0.000,n=5;at the seventh day 21.20 ± 2.49;3.00 ± 0.71,P=0.000,n=5). Conclusions This study domenstrates that autophagy was activated after carotid injury and the chang is dy-namic, which may contribute to neointima formation.

Objective To investigate the effects of the fibrin-derived peptide Bβ15-42 (FgBβ 15-42) on renal inflammation in acute kidney injury (AKI) induced by renal ischemia reperfusion (IR).Methods SD rats were randomly divided into sham group (the abdominal cavity were closed after separating the renal artery),IRI group (renal arteries of rats were occluded with microvascular clamps for 60 min),negative treated group (rats were injected with 3.6 mg/kg random peptide by tail vein) and FgBβ15-42 treated group (rats were injected with 3.6 mg/kg FgBβ15-42 by tail vein).Rats were sacrificed at 24 h or 48 h after reperfusion.Blood and kidney samples were collected and histological changes and renal function were examed.The mRNA and protein expressions of intercellular cell adhesion molecule-1 (ICAM-1) and interleukin-1β (IL-1β) were examined by immunohistochemistry,real-time PCR and Western blotting.Results Compared with sham group,Scr and BUN were obviously increased in IRI group (all P ＜ 0.05),pathologic changes of kidney were more serious (P ＜ 0.05).Compared with IRI group,in FgBβ15-42 treated group Scr and BUN were obviously decreased (all P ＜ 0.05),the injury of kidney tubulointerstitial was less serious (P ＜ 0.05).Compared with sham group,there was increased ICAM-1 and IL-1β in IRI group (all P ＜ 0.05),and they all peaked at 24 h.After treated with FgBβ15-42,the expression of ICAM-1,IL-1β were significantly decreased in kidneys compared to IRI group (all P ＜ 0.05).The above indexes had no significant differences between negative treated group and IRI group (all P ＞ 0.05).Conclusions FgBβ15-42 can protect kidneys against ischemia reperfusion injury in rats.The mechanism may be associated with down-regulated expressions of ICAM-1 and IL-1 β in the kidney.

Objective:To explore the relationship between pulmonary function and coronary artery disease (CAD) with the severity of coronary artery lesions in relevant patients.
Methods:A total of 200 patients received coronary angiography (CAG) in our hospital were studied. The patients were divided into 2 groups: Non-CAD group, n=88 and CAD group, n=112. The degree of coronary stenosis was assessed by GENSINI score;the pulmonary function, echocardiography and fasting blood level of brain natriuretic peptide(BNP) were examined in all patients.
Results:Forced expiratory volume in 1 second (FEV1) in CAD group (2.33±0.54) L/1s was lower than Non-CAD group (2.63±0.39) L/1s, P=0.04. Multivariate logistic regression analysis indicated that decreased FEV1 was the independent risk factor for CAD (OR=2.9, 95%CI 1.89-4.23, P<0.01). Spearman correlation analysis showed that FEV1 was negatively related to blood level of BNP (r=-0.54, P<0.01), positively related to the ratio of E/A (r=0.27, P=0.03). GENSINI score was positively related to smoking (r=0.31, P=0.01), diabetes (r=0.19, P=0.03) and negatively related to FEV1 (r=-0.40, P<0.01). With adjusted variables, partial correlation analysis presented that FEV1 was negatively related to GENSINI score (r=-0.21, P=0.01).
Conclusion:Decreased FEV1 is not only related to CAD occurrence, but also related to the degree of coronary stenosis in relevant patients.

Objective To retrospectively analyze the value of postoperative adjuvant therapy in the treatment of stageⅢthoracic esophageal squamous cell carcinoma ( ESCC) . Methods From 2008 to 2011, a total of 395 patients with stageⅢthoracic ESCC undergoing radical resection were enrolled as subjects. In those patients.97 received surgery alone (S).212 postoperative adjuvant chemotherapy (POCT),and 86 postoperative radiotherapy (PORT).Comparison of categorical data was made by chi?square test. The survival rates were calculated by the Kaplan?Meier method. The log?rank test was used for between?group comparison and univariate analysis. Results All patients were followed up for at least 3 years.125 cases were followed up for at least 5 years. The 5?year overall survival ( OS) rates in patients treated with S,POCT and PORT were 17. 1%,29. 2% and 36. 4%,respectively (P=0. 000).POCT and PORT could mainly increased OS in patients of males.upper?and middle?segment,severe ahhesion at surgery.well?or middle?differentiation,stageⅢa andⅢb(P=0. 000?0. 049);whenever ages.tumor lesion,two?/three field esophagectomy.and the number of removal lymph nodes. PORT could improved OS also (P=0. 001?0. 047).POCT could also improve OS in patients of ages≤60, tumor lesion<6 cm and removal lymph nodes<10 ( P=0. 002?0. 049 ) . The 5?year progression?free survival (PFS) were 19. 0% with S,28. 8% with POCT,36. 4% with PORT,respectively (P=0. 012).PORT could improve PFS (P=0. 012);especially for patients of males,ages ≤60,upper?and middle segment ESCC,tumor lesion ≥6 cm,severe ahhesion at surgery,removal lymph node<10 and ≥10,well or middle differentiation,stageⅢa andⅢb(P=0. 001?0. 042).But POCT could not increased PFS (P=0. 119) . Conclusions In the treatment of patients with stage Ⅲ thoracic ESCC undergoing radical resection,both POCT and PORT can improve the OS rate, particularly in patients with stage Ⅲa or Ⅲb middle and upper thoracic ESCC, severe adhesion formation during surgery. and moderately or well differentiated squamous cell carcinoma. The DFS rate is improved in patients treated with PORT,but not in those treated with POCT.

Objective To explore the significance of nuclear factor-?B(NF-?B)activation in peripheral blood mononuclear cells(PBMC)during acute Kawasaki disease(KD).Methods Peripheral blood was collected from children with acute KD(n=30)and healthy age-matched children(n=20).PBMC were cultured in vitro and divided into 3 groups:naturally cultured blank control group,protein kinase C(PKC)activator stimulated phorbol 12-myristate 13-acetate(PMA)group and PMA plus NF-?B inhibitor treated PMA plus pyrrolidine dithiocarbamate(PDTC)group.Percentages of NF-?B activation were detected by immunohistochemistry.Results Under natural culturing,the percentage of cells with activated NF-?B was significantly higher in acute KD blank control group than that in healthy blank control group.The percentage of cells with activated NF-?B was significantly higher in acute KD PMA group than that in acute KD blank group and that in normal control PMA group,respectively(Pa0.05).Conclusions NF-?B activation in PBMC during acute KD is markedly increased,which suggests that NF-?B activation plays an important role in the formation of vasulitis and CAL in this disease.NF-?B activation in PBMCs in children with KD is regulated by the PKC signaling pathway and PDTC obviously inhibits the activation of NF-?B.J Appl Clin Pediatr,2009,24(1):35-37