Objective To observe the changes in OLETF kideys at different stage and the beneficial influences by modulating serum lipids. Methods OLETF rats aged 8 wks were randomly divided into treated group and untreated group,and LETO rats served as normal control.Fenofibrate 20 mg/kg was given daily to the treated group.OGTT was performed at the age of 8,16 and 24 wks.Blood glucose,serum lipids and 24 h urine albumin excretion(UA) were investigated.The rats were killed at 16 and 24 wks of age,and the kidney sections were stained with PAS.Transforming growth factor-?_1(TGF?_1),vascular endothelial growth factor(VEGF) and fibronectin(FN) were investigated by immunohistochemistry assay.The electron microscope(EM) sections were made to measure GBM width and to observe the mesangial matrix.Results(1) Blood glucose had no significant difference between untreated and treated groups at 16 and 24 wks of age;(2) Fenofibrate decreased serum TG, increased HDL-C markedly but had no influence on LDL-C;(3) As aging,24hrs UA increased in untreated group,and reduced significantly in fenofibrate group at 24 wks of age;(4) TGF-?_1,VEGF and FN expressions were all higher in untreated group than in treated group at 24 wks of age.(5) EM revealed GBM obviously thickened and mesangial matrix widened in untreated group.Fenofibrate attenuated the kidney lesion greatly in EM picture.Conclusions (1) Dyslipidemia occurs prior to glucose metabolism abnormity in OLETF rats;(2) As aging,dyslipidemia progresses accompanying markedly the increased UA,enlarged glomeruli,thickened GBM and widened masangial matrix;(3) Modulating lipids early couldn′t improve glucose metabolism,but corrects dyslipidemia and reveals beneficial influence on kidneys;(4) The possible mechanism is that modulating lipids decreases TGF-?_1 and VEGF expressions.

Objective To investigate the effects of dexmedetomidine on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n =18 each): shame operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was produced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg).In group D dexmedetomidine 3 μg/kg was injected iv immediately after I/R,followed by infusion of dexmedetomidine at a rate of 3 μg· kg- 1 · h- 1 until 2 h of reperfusion.The neurological deficit score (NDS) was assessed (0 =normal,100 =brain death) at 6 h (T1),24 h (T2)and 72 h (T3) of reperfusion.Then six rats were sacrificed in each group and brain tissues were removed for microscopic examination of hippocampus CA1 region and determination of activity of myeloperoxidase (MPO),contents of TNF-α and IL-1β and expression of glial fibrillary acidic protein ( GFAP).Results Compared with group S,NDS,MPO activity and the contents of TNF-α and IL-1β at T1-3 were significantly increased,the expression of GFAP was up-regulated at T2,3 in groups I/R and D ( P ＜ 0.05 or 0.01).Compared with group I/R,NDS,MPO activity and TNF-α concent were significantly decreased at T1-3,IL-1β concent was decreased at T1,2,the expression of GFAP was down-regulated at T2,3 in group D (P ＜ 0.05 or 0.01 ).The pathologic changes were significantly attenuated in group D as compared with group I/R.Conclusion Dexmedetomidine can attenuate global cerebral I/R injury in rats,and the inhibition of inflammatory response may be involved in the mechanism.

Objective To investigate the safety of different intensity anticoagulation therapy of warfarin in preventing thromboembolism in octogenarian patients with nonvalvular atrial fibrillation (NVAF). Methods The 130 patients with persistent or permanent NVAF were randomly divided into three groups: low-intensity warfarin group (35 cases, international normalized ratio, INR (1.5-2.0), moderate-intensity warfarin group (32 cases, INR 2.1-2.5) and aspirin control group (63 cases). The rate of hemorrhagic events and the effect on renal function were observed. Results The incidence of hemorrhage was the lowest in low-intensity warfarin group compared to the other groups with slight bleeding in one case. life-threatening bleeding in one case, severe bleeding in one case and slight bleeding in four cases occurred in moderate-intensity warfarin group. Life-threatening bleeding in three cases, severe bleeding in two cases and slight bleeding in six cases occurred in aspirin control group. There were significant differences in bleeding incidence among the three groups (χ2=5.13,P＜0.05). The low-intensity warfarin group and moderate-intensity warfarin group were superior to the aspirin control group in the effect on renal function (P＜0.05). Conclusions It is safe that the dose of warfarin is maintained at low anticoagulation intensity between INR 1.5 and 2.0 in octogenarians with NVAF.

Pregnant women with subacute thyroiditis (SAT) are rare.One case was reported and the clinical features and management principles of SAT during pregnancy were reviewed.In pregnant women with SAT,the illness is usually not serious.If subclinical or clinical hypothyroidism develops,L-T4 must be given and thyroid function be monitored routinely,and the medication be adjusted carefully to ensure the maternal-fetal safety.

Objective To evaluate the effects of dexmedetomidine on the permeability of blood-brain barrier in rats subjected to global cerebral ischemia-reperfusion (I/R).Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP was maintained at 35-45 mm Hg) in anesthetized rats.In group D,dexmedetomidine was infused at a rate of 3μg· kg-1 · h-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was injected intravenously immediately after onset of I/R.The rats were sacrificed at 24 h of reperfusion and their brains were immediately removed for microscopic examination of hippocampal CA1 region and for determination of the cell apoptosis,brain water content,Evans blue content and aquaporin 4 (AQP4) expression.Results The number of apoptotic cells was significantly larger,and brain water content,Evans blue content and AQP4 expression were higher in groups I/R and D than in group S (P ＜ 0.05 or 0.01).The number of apoptotic cells was significantly smaller,and brain water content,and Evans blue content and AQP4 expression were lower in group D than in group I/R (P ＜ 0.05 or 0.01).Global cerebral I/R-induced pathological changes were significantly attenuated in group D.Conclusion Dexmedetomidine can decrease the permeability of blood-brain barrier and attenuate global cerebral I/R injury in rats,and down-regulation of AQP4 expression may be involved in the mechanism.

Objective To observe the suppressing effect of topical nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids on ultraviolet ray (UV)-induced erythema.Methods A solar simulator and an UV phototherapy device were used as light sources,respectively.Erythema reaction was induced on the back skin of 30 healthy volunteers by 1,2 and 3 minimal erythema doses (MED) of irradiation.Five preparations including butyl flufenamate 2.5％ ointment,butyl flufenamate 5％ ointment,the base of butyl flufenamate ointment,halometasone ointment,and diclofenac 1％ ointment,were applied to the irradiation sites respectively half an hour before or immediately after the irradiation.One irradiation site remained untreated and served as the control.The degree of erythema was evaluated by a chromameter at 4,24,and 48 hours after the irradiation.Intragroup and intergroup comparisons were done by t test and analysis of variance,respectively.Results When applied half an hour before solar-simulated irradiation,both 2.5％ and 5％ butyl flufenamate ointment totally suppressed the erythema reaction induced by 1-3 MED of UV irradiation,with no significant increase in erythema index at all the three time points after irradiation (all P ＞ 0.05); diclofenac 1％ only inhibited the erythema induced by 1 MED of UV irradiation at 4 and 48 hours,with no difference observed in erythema index between the baseline and these time points after irradiation; however,halometasone significantly aggravated the erythema reaction (P ＜ 0.05).Neither NSAIDs nor corticosteroids applied immediately after solar-simulated irradiation showed statistical effect on the degree of UV-induced erythema.When applied immediately after irradiation using the phototherapy device,butyl flufenamate 2.5％ ointment,butyl flufenamate 5％ ointment and halometasone ointment all induced a significant reduction in erythema reaction at 4 hours after 1 MED of irradiation (all P ＜ 0.05),and diclofenac caused a statistical decrease in erythema reaction at all the time points after 1-3 MED of irradiation (all P ＜0.05).Conclusions Topical use of butyl flufenamate before UV irradiation can effectively inhibit erythema reaction induced by 1-3 MED of irradiation.When applied immediately after irradiation,diclofenac shows the strongest erythema-suppressive effect,followed sequentially by butyl flufenamate and halometasone.

Objective To investigate the effects of lipoxin A4 (LXA4) on the inflammatory response to focal cerebral ischemia-reperfusion(I/R) inmy in rats.Methods Fifty-six healthy male SD rats weighing 200-250 g were randomly divided into 3 groups:group Ⅰ sham operation(group S,n=8);group Ⅱ cerebral I/R(n=24)and group Ⅲ lipoxin A4+I/R(group LXA4,n=24).Right mid-cerebral artery was occluded for 2 h by inserting cranially a nylon thread with rounded tip into internal carotid artery.LXA4 0.03 nmol/5 μl was injected into cerebral ventricle at 5 min after cerebral ischemia.Neurological deficit was scored at 24 h of reperfusion.Then four animals in each group were killed and their brains were removed for microscopic examination and expression of MPO at 24 h of reperfusion.Meantime,content of IL-1β,TNF-α,TGF-β1,and IL-10 in the brain tissue were measured at 1,6,12,24 and 48 h of reperfusion by ELISA.Glial cell activity was examined at 24 h of reperfusion by immuno-histochemistry.Results Intra-cerebroventricular administrated LXA4 0.03 nmol/5 μl provided mild neuroprotection against focal cerebral I/R injury,improved neurological deficits,and reduced morphological brain damages and PMN infiltration.LXA4 also decreased the content of TNF-α and IL-1β,and increased the content of IL-10 and TGF-β1.The numbers of activated astroglia and microglia were decreased in group LXA4 compared with group I/R.Conclusion LXA4 protects the brain against I/R injury by inhibiting inflammatory response.

Objective To investigate the expression of serum B factor in the peripheral blood of patients with systemic lupus erythematosus (SLE),and explore its role in the pathogenesis.Methods Seventy eight patients with SLE in our hospital and 46 healthy persons were eligible to participate in this study.Rate nphelometyr was used to test serum B factor for 78 patients with SLE and 46 healthy controls.According to systemic lupus erythematosus disease activity index (SLEDAI),participants were divided into steady SLE group (SLEDAI ＜ 5) and active SLE group (SLEDAI ≥5),which was further divided into mild,moderate,and serious subgroups.The differences in serum B factor between SLE patients and healthy controls,including SLE patients with different severity,were all compared.Then we analyzed the differences in serum B factor and other laboratory and clinical indexes between active and steady SLE patients.The correction of serum B factor and other laboratory and clinical indexes were also analyzed.Results Compared to healthy controls,patients with SLE had significantly lower value of serum B factor [(27.13 ± 8.98) mg/dl vs (36.73 ± 5.47) mg/dl,t =7.4,P ＜ 0.01].Compared to steady SLE group,SLE active group had significantly lower level of serum factor B,C3 and C4,and also had significant higher level of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) (all P ＜ 0.05).Moreover,There were significant differences in the lower level of serum B factor between subgroups.Correlation analysis showed that the level of serum B factor was negatively associated with the levels of CRP and SLEDAI scores,whereas serum B factor was positively associated with the levels of C3 and C4 (all P ＜ 0.05).Conclusions Serum B factor is related to SLE.Serum B factor might be involved in the pathogenesis of SLE.Detection of serum B factor is helpful for diagnosis and evaluation of SLE disease activity.

Objective To explore the expression and the role of Toll-like receptor(TLR3 and TLR4) in rats with nephrotic syndrome induced by respiratory syncytial virus(RSV).Methods SD rats were inoculated intranasally and intraperitoneally with 6?106 plaque for-ming unit(PFU) RSV to construct RSV-induced nephropathy in rat model.Rats were anesthetized and blood was withdrawn from cardiac on day 4,14,30,60 after inoculation.The normal ones without intervention were set as control group.The renal histology was observed by light microscope and electron microscope.The urinary protein collected in 24 hours were measured.Meanwhile,the expressions of TLR3 and TLR4 were detected by indirect immunofluorescence staining and flow cytometry in peripheral blood mononuclear cells of rats.The results were analyzed by SPSS 13.0 softwore.Results After inoculation,the proteinuria increased and under the electron microscope the foot processes of glomerular epithelial cells were fused which resembled human minimal change nephrotic syndrome.Proteinuria reached the peak and the fusion of foot processes were most extensive in rats of RSV at 60 d.The expressions of TLR3 and TLR4 in each group of RSV-induced nephropathy in rat models were significantly higher than those in normal control group(Pa0.05).Conclusions TLR3 and TLR4 in peripheral blood mononuclear cells of RSV-induced nephropathy rat mo-dels had being significantly activated until 60 d after RSV inoculation.TLR signaling pathway may play an important role in nephrotic syndrome of rats induced by RSV.

Objective To study dIe ESBLs and plasmid-mediated AmpC enzymes in E.Coli and Klebsiella spp. with CLSI ESBL-screening test positive,confirmation test negative but cefepime susceptible.Methods Antimierobial susceptibility testing were performed by Kirby-Bauer(K-B)method.The genes encoding ESBLs and plasmid-mediated AmpC enzymes were detected by PCR Transfer of ESBLs or plagmid-mediated AmpC resistance was studied by conjugation experiments.The homology of donor (E.coli),recipient(E.coli J53)and their transconjugants were analyzed by ERIC-PCR DNA fingerprints of E.coli and Klebsiella pneumoniae were analyzed by PFGE as recommended bv PulseNet protocoL Results Of 18 isolates from Huashan Hospital,11 were E.coli.6 were Klebsiella pneumoniae and 1 was Klebsiella oxytoca.Antimicrobial susceptibility testing indicated all of 18 isolates were positive on the CLSI ESBL screening test but negative on the confirmation test.and all of isolates were susceptible to cefepime(a zoneof-inhibition diameter of≥18 mm wag considered to indicate susceptible).PCR results indicated that 9 of the 11 E.coli isolates predued CMY-2 AmpC enzyme.TEM,SHV,CTX-M,PER,VEB or SFO type β-lactamages were not identified.Of 6 Klebsiella pneumoniae isolates.5 were DHA-1 AmpC-producing strains.4 of the 5 DHA-1 AmpC-producing strains were coexistence of broad-speetrumβ-lactamaae or extended-spectrumβ-lactamase.including two producing SHV-11 and two producing CTX-M-14 and SHV-62 type ESBL respectively.One Klebsiella oxytoca wag also DHA-1 AmpC producing strain.Conjugation experiments indicated that both ESBLs and AmpC enzymes could be transfefred from donor to recipient.PFGE indicated that the DNA fingerprints of K.pneumoniae were difierent but seven CMY-2 AmpC-producing E.coli isolates from general surgieal ward were similar.Concluslons The main mechanism of antibiotic resistance in CLSI ESBLs-screening test-positive but eefepime.susceptible E.coli and KIebsiellaspp.is production of plagmid-mediated AmpC enzymes.Some strains produce both AmpC enzyme and ESBLs.Such strains should be reported as resistant to cefepime.The results suggest that laboratories should routinely conduct research on the ESBLs and plnsmid.mediated AmpC enzymes in Enterobacteriaceae in order to report antimicrobial susceptibility testing results more correcdy.