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

AIM: To study the effect of activated protein C(APC) at different concentrations on apoptosis of human umbilical vein endothelial cells(HUVECs) induced by lipopolysaccharide(LPS).METHODS: The HUVECs were induced by LPS(1.0 mg/L) as apoptotic model that was administered by different concentration of APC(10 ?g/L or 50 ?g/L).Meanwhile,the control group and induced apoptosis group induced by LPS(1.0 mg/L) stimulation were also set up.The changes of cellular ultrastructures were observed under electron microscope.The DNA ladder and TUNEL fluorescent staining were measured in cells.Annexin-Ⅴ/PI double staining was used to measure the cell apoptosis rate by flow cytometry.Cell survival rate was measured by MTT assay.The proliferating cell nuclear antigen(PCNA) expression levels in cells were also measured by Western blotting to reflect the proliferation of the cells.RESULTS: There were significant apoptotic changes in the cells induced by LPS,but the apoptotic changes were reduced and apoptosis rates were decreased in the cells treated with APC.Meanwhile,cell survival rate and the protein levels of PCNA were increased after APC treatment,particularly at the concentration of 50 ?g/L,which showed difference when compared with those induced apoptosis group by LPS(P

Objective To study the protective effects of activated protein C (AFC) on the apoptosis of endothelial cells induced by lipopolysaccharide (LPS) in order to clarify the mechanisms associated with the expression of some genes related to apoptosis. Method The human umbilical vein endothelial cells were incubated with LPS (1.0 μg/mL) for one hour to make the models of cell apoptosis, and then the different concentrations of AFC (10 ng/mL and 50 ng/mL) were added to the models of cell apoptosis as treatment group. Therefore, there were two groups, model group and APC treated group. The factors related with apoptosis such as P53, Bax, Bcl-2, and caspase-3 mRNA or protein level were measured by using RT-PCR and Western blotting. Results Compared with LPS stimulated cells, the expressions of P53, Bax and caspase-3 mRNA and levels of protein were decreased and the expression of Bcl-2 mRNA and protein level were increased in APC treated cells particularly in APC 50 ng/mL treated cells (P <0.05). Conclusions The APC inhibits the apoptosis of HUVECs induced by LPS via regulating the mitochondrial-dependent apoptosis pathway, and it may become a novel therapeutic agent for infection disease.

Objective To investigate the relationship between the activity of Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in cerulein-induced pancreatic acinar cell line AR42J. Methods The in vivo model of AP was induced by cerulean treated pancreatic acinar cell line AR42J, then RPM and AG490 were given for intervention. Western blot was used to determine theexpressions of JAK1 and phosphorylation JAK1 ( P JAK1 ) , STAT1, PSTAT1 and TNFα, IL-1β, IL-6. The expressions of IL-6, IL-1 β, and TNFα mRNA were measured by RT-PCR. Survival rate of cells was evaluated by trypan blue stain. Results The relative expressions of JAK1, P JAK1, STAT1, P STAT1 and TNF-o, IL-1β, IL 6 without cerulean treatment were 0.09 ±0.04,0.14 ±0.08,0.21 ±0.09,0.12 ±0.12,0.10 ±0.02,0.08 ± 0.03,0.02 ± 0.02. After cerulean treatment, the expressions of abovementioned protein increased in a time-dependant manner, the expressions at 24h were 0.53 ± 0.09,0.53 ± 0.13,0.56 ± 0.09,0.55 ± 0.10,0.25 ± 0.04,0.25 ±0.09,0.27 ±0.07, which were significantly higher than those in the control group (P ＜0.05). 2 4 h after RPM and AG 4 9 0 inhibition, the expressions of TNF-α, IL-1 β, IL-6 proteins significantly decreased to 0.17 ± 0.03and 0.17 ± 0.01,0.15 ± 0.05 and 0.14 ± 0.07,0.19 ± 0.04 and 0.19 ± 0.05; their expressions of mRNA significantly decreased ( P ＜ 0.05 ). The cell survival rates in RPM and AG490 treatment group were (72.4 ± 11.2) %, (69.7 ± 9.8 ) %, and in cerulein-stimulated cells (42.2 ± 12.3 ) % ( P ＜ 0.05 ).Conclusions The JAK1/STAT1 signaling pathway was involved in pancreatic inflammatory response with cerulein stimulation. Early treatment with inhibitors to the JAK1/STAT1 signaling pathway might control the inflammatory response in acute pancreatitis.

Adolescent ; Diagnosis, Differential ; Humans ; Male ; Sturge-Weber Syndrome ; pathology

Objective To compare the clinical outcomes of gonadotropin-releasing hormone (GnRH) antagonist (GnRH-ant) fixed protocol with GnRH agonist (GnRH-a) long protocol in infertile patients with normal ovarian reserve function in their first in vitro fertilization-embryo transfer (IVF-ET) cycle,and to explore the feasibility and advantage of GnRH antagonist protocol performed in normal responders.MethodsFrom January 2011 to June 2011,771 infertile women with normal ovarian reserve function underwent their first IVF or intracytoplasmic sperm injection (ICSI) cycles in Peking University Third Hospital,which were divided into 245 cycles in GnRH-ant fixed protocol group ( GnRH-ant group) and 526 cycles in GnRH-a long protocol group ( GnRH-a group).The data of general demographic,treatment and clinical outcome were compared between two groups.ResultsAge,infertile duration,body mass index (BMI),baseline serum follicle-stimulating hormone (FSH) and estradiol levels between two groups did not reached statistical difference (P ＞ 0.05 ).The level of estradiol was (12 289 ± 6856) pmol/L in GnRH-ant group and (14934±8007)pmol/L in GnRH-a group at day of hCG injection.The mean length of stimulation was ( 10.3 ± 1.2) days in GnRH-ant group and ( 12.8 ± 1.6) days in GnRH-a group.The dose of gonadotropin was (2013 ± 607 ) U in GnRH-ant group and (2646 ± 913 ) U in GnRH-a group.The number of ovum was 15 ± 7 in GnRH-ant group and 17 ± 8 in GnRh-a group.Those clinical parameter all reached statistical difference (P ＜0.05 ).The number of embryo was 7 ±4 in GnRH-ant group and 8 ± 5 in GnRH-a group,the rate of clinical pregnancy was 40.9％ (94/230) in GnRH-ant group and 45.6％ (216/474)in GnRH-a group,the rate of implantation was 26.1％ (128/490)in GnRH-ant group and 30.9％ (307/994) in GnRH-a group,the rate of continuing pregnancy was 38.7％ ( 89/230 ) in GnRH-ant group and 42.6％ (202/474) in GnRH-a group,those parameter did not reach statistical difference (P ＞ 0.05).The rate of moderate or severe ovarian hyperstimulation syndrome was 2.4％ ( 6/245 ) in GnRH-ant group and 4.2％ (22/526) in GnRH-a group,which did not show significant difference ( P ＞ 0.05 ).ConclusionIn the first IVF or ICSI cycle of the patients with normal ovarian reserve function,the fixed GnRH-ant protocol could get the same satisfied clinical outcome,and it is more economic,convenient and safer compared with low dose depot GnRH-a long protocol.

Objective To investigate the effect of protein inhibitor of activated signal transducer and activator of transcription 1 ( PIAS1 ) gene silencing on the inflammatory response of rat pancreatic acinar cell lines AR42J with cerulein stimulation, to study its role in the pathogenesis of acute pancreatitis.Methods The siRNA targeting PIASI was designed, synthesized, transfected into AR42J cells by lipofectmine 2000.24 h later, cerulean was added and cultured for another 24 h.Subsequent AR42J cells with cerulein stimulation were divided into 4 groups: cerulein, liposome, negative-siRNA and PIAS1-siRNA groups.In addition, a group with PBS was as control group.The activity of p38 mitogen- activated protein kinase (p38MAPK) was detected by western blotting.TNF-α, IL-1β, IL-6, matrix metalloproteinase (MMP) 9 expression were analyzed by RT-PCR and western blotting, respectively.Results The expression of p38MAPK in PIAS1-siRNA, negative-siRNA, liposome, cerulein,and control group was 1.93 ±0.11, 1.22 ±0.10, 1.30 ±0.17,1.32 ± 0.21, 0.12 ± 0.02;while the expression of phosphorylated p38MAPK was 2.10 ± 0.25, 1.36 ± 0.20,1.26 ±0.15, 1.23 ±0.25, 0.58 ±0.48, the expression in PIAS1-siRNA group was significantly increased when compared with other groups (P＜0.05).The levels of TNF-α, IL-1β, IL-6, MMP-9 mRNA were 1.66 ±0.15,1.66 ± 0.15,1.90 ±0.01, 1.56 ±0.20 in PIAS1-siRNA group, while the expression of protein was 2.06 ±0.37,2.20 ±0.34, 1.80 ±0.10, 1.17 ±0.05, which was markedly higher than those in other group (P ＜0.05).Conclusions PIAS1 gene silencing could enhance p38MAPK activity, and improve inflammatory mediator expression in pancreatic acinar cells with cerulein stimulation.

AIM: To determine the effect of endogenous histamine on transient forebrain ischemia-induced neuronal injury at the late phase of reperfusion using histidine decarboxylase knockout ( HDC-KO) mice.METHODS:Wild-type (WT) and HDC-KO mice were subjected to bilateral common carotid artery occlusion for 30 min followed by 3 d or 15 d of reperfusion.At different time points after reperfusion, the body weight, mortality rate, learning and memory in fear conditioning test and hippocampal CA 1 neuronal density were evaluated .RESULTS: At 1 d after reperfusion , the body weight loss was observed in both WT and HDC-KO mice.At 4 d, 5 d, 6 d and 7 d after reperfusion, the increment in the body weight of the HDC-KO mice was significantly smaller than that of the WT mice .During the period between 8 d and 14 d after reperfusion, the mortality rate of the HDC-KO mice was higher than that of the WT mice (P<0.05).At 14 d after reperfusion , the HDC-KO mice exhibited more aggravated deficits in contextual and cue memory compared with the WT mice.Correspondingly , a more severe CA1 neuronal injury in the HDC-KO mice than that in the WT mice was ob-served at 15 d but not at 3 d after reperfusion (P<0.05).CONCLUSION:Endogenous histamine may attenuate learn-ing/memory deficits and neuronal injury at the late phase of ischemia /reperfusion.However, the involved mechanisms need to be further investigated .

Objective To assess the effectiveness of treatment of meniscal injuries of knee joints by arthroscopy.Methods 33 patients 35 joints were followed up and the parts,types and treatment under arthroscopy were analysed.Results 33 patients were followed up from six months to six years,the mean preoperative Lysholm score was 60.5 points,and the mean postoperative one was 86.7 points.Conclusion The advantage of treating meniscal injuries by arthroscopy was the result of correct examination and little wound of arthroscopy operation,and arthroscopic repair or partial menisectomy could effectively restore the function of the injured knee.

OBJECTIVE To investigate the mechanism of nicotinamide mononucleotide (NMN) on inflammation and fibrosis between endogenous nicotinamide phosphoribosyltransferase (NAMPT) and bone morphogenetic protein 7 (BMP-7) in diabetic glomerular cells.METHODS ① In vivo,spontaneous diabetic C57/BL6 mice and wild C57/BL6 mice were divided into two groups.When blood glucose was above (34.2±1.9) mmol· L-1,renal histology of diabetic mice became obvious.The protein expressions of Nampt and nuclear transcription factors-kappa B p65 (NF-κB p65),silent mating type information regulation 2 homolog 1 (SIRT1) and BMP7 were analyzed by lengths of immunofluorescence.② In vitro,rats' glomerular cells HBZY-1 were incubated with glucose 200 mmol· L-1 for different lengths of time (0,24,48 and 72 h) and at different concentrations of NMN (0,50,100 and 200 iμmol· L-1).The protein levels of Nampt and BMP7 were detected by Western blotting and the protein expressions of NF-κB p65 and α-SMA were measured by immunofluorescence assay.The protein levels of Nampt,BMP7 and NF-κB p65 were detected by Western blotting after HBZY-1 cells were treated with NMN 100 μmol· L-1 and FK866 10 μmol· L-1 for 24 h.RESULTS ① In vivo,the glomeruli of diabetic C57/BL6 mice showed obvious atrophy.Fluorescence intensity of Nampt was increased (P＜0.05),but that of BMP7 and SIRT1 in renal glomeruli cells was decreased compared with the wild type (P＜0.01).② In vitro,HBZY-1 cells were cultured in glucose 200 mmol· L-1 for 48 and 72 h.The protein expression of NAMPT was increased,but that of BMP7 was decreased (P＜0.05,P＜0.01).Expressions of NF-κB p65 and α-SMA were increased (P＜0.01) by immunofluorescence.The expression of BMP7 was increased after treatment with glucose 200 mmol· L-1,followed by NMN 50,100 and 200 μmol · L-1 for 24 h (P＜0.01).The expressions of NAMPT and NF-κB p65 were decreased (P＜0.01).The expressions of Nampt and NF-κB p65 in glucose 5.6 mmol· L1 +FK866 and glucose 5.6 mmol· L-1+ NMN groups were increased (P＜0.01),but the expression of BMP7 did not change.CONCLUSION Upregulation of endogenous Nampt obviously intervenes in BMP7 expression in the process of glomerular inflammatory fibrosis in severe diabetes.NMN can affect the protein expression of BMP7 via a special Nampt signaling pathway.