The mononuclear cells in early skin lesions of 10 patients with extensive psoriasis vulgaris in progressive stage were studied by biotin-avidin-peroxidase method using monoclonal antibodies. The results show that increased mononuclear cells in the early skin lesions, expressing HLA-DR antigen mostly, consist of T lymphocytes and macrophases with a preponderance of T lymphocytes, B lymphocytes are absent, activated T lympocytes are usually in close proximity to DR~+ cells including dentritic cells and keratinocytes, indicating that the initial psoriatic lesion correlates closely with imbalance of cellular immunity.

BACKGROUND: Abnormal lipid metabolism is one of the risk factors in patients with ischemic cerebral disorders, and is correlated with the changes of lecithin cholesterol acyltransferase activity.OBJECTIVE: To observe the relationship between the changes of lecithin cholesterol acyltransferase activity and lipid content in red blood cell membrane.DESIGN: A case-control study(experimental group with control as standard level).SETTING: Department of clinical laboratory, emergency room and department of neurology of a hospital affiliated to a medical college of a university.PARTICIPANTS: Totally 105 inpatients and outpatients with cerebrovascular diseases were selected from the Department of Neurology, Affiliated Hospital of Medical College of Qingdao University, from March 2002 to December 2003. They accorded with the Diagnostic Criteria set at the Second National Conference on Cerebrovascular Diseases. A total of 42 patients with cerebral arteriosclerosis and 63 patients with cerebral infarction were selected as patients group consisting of 67 males and 38 females. Another 65 healthy people receiving physical examination in the hospital, 36 males and 29 females, were selected as control group.METHODS: Venous blood of 8 mL was drawn from the participants on an empty stomach. We assayed the activity of lecithin cholesterol acyltransferase,high density lipoprotein cholesterol, low density lipoprotein cholesterol,apolipoprotein A1 and apolipoprotein B. Red blood cell membrane cholesterol was determined by phthalyl aldehyde-acetometry and red blood cell membrane phospholipid was determined by chemical quantitative analysis.MAIN OUTCOME MEASURES: Changes of lecithin cholesterol acyltransferase activity and lipid content in red blood cell membrane in patients group and control group.RESULTS: According to intention analysis, all the 105 patients in patients group and 65 patients in control group entered the results analysis. Activity of lecithin cholesterol acyltransferase: Activity changes in cerebral arteriosclerosis group and cerebral infarction group were obvious lower than those in control group[(2.14±0.72) kat/L, (2.06±0.80) kat/L, and(2.61± 0. 74) kat/L, P ＜ 0.01 ] . Level of high density lipoprotein cholesterol and apolipoprotein A1: The level in cerebral arteriosclerosis group and cerebral infarction group was obvious lower than that in control group[ (1.32±0.33) mmol/L, (1.37±0.33) g/L, (1.28±0.33) mmol/L; (1.27±0.31) g/L, (1.60±0.43) mmol/L, (1.60±0.43) g/L, t=2.72 to 5.01, P ＜ 0.01 ]. Content of low density lipoprotein cholesterol and red blood cell membrane-cholesterol: The content in cerebral arteriosclerosis group and cerebral infarction group was obvious higher than that in control group [ (2.94 ± 0. 82) mmol/L, (0.63 ±0.05) mmol/g, (3.02 ±0.79) mmol/L;(0.60 ±0.07) mmol/g, (2.56 ±0. 58) mmol/L, (0.57 ±0.05) mmol/g, P ＜ 0. 01 ] . Moreover, the activity of lecithin cholesterol acyltransferase was positively correlated with high density lipoprotein cholesterol and apolipoprotein A1(r=0.247, P ＜0.05; r=0.303, P ＜0.01), but was negatively correlated with low density lipoprotein cholesterol and red blood cell membrane cholesterol(r= -0.212, P ＜0.05;r= -0.346, P ＜0.01).CONCLUSION: In patients with ischemic cerebral disorders, the major change of plasma lipid is the decrease of lecithin cholesterol acyltransferase,but it is not secondary to cerebral infarction. The activity of lecithin cholesterol acyltransferase is positively correlated with high density lipoprotein cholesterol and apolipoprotein A1, but is negatively correlated with low density lipoprotein cholesterol and red blood cell membrane cholesterol.

Objective To study the fecel-oral and blood transfusion of TT virus. Methods Paired feces and serum samples from 6 patients with type B and/or C hepatitis were tested for TTV DNA and its titers by PCR with seminested primers.Genotypes were determined after their sequences were compared with the original N22 and TA278 clone.Results TTV DNA was detected in sera from all patients,while it was detected in feces from 3 patients,including 2 with high viral titers in serum.The detection of fecal TTV DNA was dependent on the viral titers in serum.TTV isolates in 3 pairs of feces and serum had identical sequence of 222 base pairs.Their genotypes were 1a,1b and 2,respectively.Conclusion The excretion of TTV into feces indicates that TTV would be transmitted not only parenterally but also nonparenterally by a fecal-oral route.

Objective To investigate the effect of bone marrow mesenchymal stem cells (BMSCs) transplantation on angiogenesis and functional recovery after focal cerebral ischemia in rats.Methods BMSCs were isolated and cultured using the whole bone marrow adherent method,and conducted phenotypic identification using flow cytometry analysis of surface positive antigen of CD29,CD90 and the negative antigen of CD34,CD45.Rats were subjected to middle cerebral artery occlusion (MCAO) for 90 minutes,and divided into three groups randomly,the sham group,model group and BMSCs group.24 hours after cerebral ischemia,rats were injected with 1 ml BMSCs solution (1 × 106 cells/ml) or PBS via the tail vein.The modified neurological severity score(mNSS) test,the corner test and the adhesive tape test were used to evaluate sensorimotor function on the 1,7,14 and 28 days after ischemia.Infarcted volume was detected by toluidine blue staining,and the numbers of vWF positive microvessels and vascular endothelial growth factor (VEGF) positive cells in the ischemic boundary were determined by immunofluorescence.Results By flow cytometric analysis,the cell phenotype of passage 3 BMSCs showed that CD29,CD90,CD34 and CD45 were 98.3％,97.4％,0.2％ and 4.8％,respectively.Compared with the model group,BMSCs significantly reduced the score of mNSS(P＜0.01),the number of right turn of corner test(P＜0.05),latency of removal adhesive tape(P＜0.05) and the infarcted volume (P＜0.01).The numbers of vWF positive vesscls and the VEGF positive cells were (42.97±8.64)/mm2 and (54.83± 10.66)/mm2 at the boundary zone in model group 14 days after ischemia,respectively.BMSCs significantly increased the numbers of vWF positive vessels ((69.43± 7.29)/mm2) and VEGF positive cells ((78.70±6.16)/mm2,P＜0.01).Conclusion BMSCs can improve the functions of cerebral lesions after cerebral ischemia,which may be associated with the enhanced angiogenesis and VEGF expression in the ischemic boundary.

Objective To observe the effects of tetrandrine on the proliferation,migration,and invasion of melanoma cell B16,and to explore its effects on epithelial mesenchymal transition(EMT)and potential regulatory mechanisms.Methods(1)The proliferation of B16 cells was detected by CCK-8 assay after 0,2,4,6,8 and 10 μmol·L-1 of tetrandrine intervention for 24 and 48 hours.The colony formation ability of B16 cells was detected by plate clone formation assay after 1,2 and 4 μmol·L-1 of tetrandrine intervention;the migration and invasion ability of B16 cells was detected by cell scratch assay and Transwell invasion assay;the expressions of N-cadherin,Vimentin and E-cadherin related to EMT in B16 cells were detected by Western Blot assay.The mouse melanoma lung metastasis model was replicated by tail vein injection of B16 cells to observe the effects of tetrandrine(50 and 100 mg·kg-1)administered by gavage on the number of metastatic tumor nodules in the lungs of mice.(2)The CTD,SwissTargetPrediction and Similarity Ensemble Approach databases were used to predict the targets of tetrandrine;the GeneCards database was used to search for targets related to melanoma disease;the intersection of these two databases was taken as the potential target of tetrandrine for melanoma treatment.The intersected targets were imported into STRING database to construct protein-protein interaction(PPI)network and screen the core targets;the intersected targets were imported into DAVID database for GO function and KEGG pathway enrichment analysis;and molecular docking between tetrandrine and the core targets was verified by Autodock software.(3)In vivo experimental validation:after intervention of 1,2 and 4 μmol·L-1 tetrandrine,Western Blot method was used to detect the expression of the key pathway AKT/NF-κB/CREB pathway-related proteins;and AKT agonist SC79 was used to validate the replication experiments.Results(1)The IC50 of B16 cells intervened by tetrandrine was 4.273 and 4.085 μmol·L-1 at 24 and 48 hours.Compared with the control group,the colony forming ability,scratch healing rate and invasion rate of cells in the 1,2 and 4 μmol·L-1 tetrandrine group were all significantly reduced(P＜0.05,P＜0.01,P＜0.001);the expressions of cellular Vimentin and N-cadherin protein expressions were significantly down-regulated(P＜0.01,P＜0.001),and E-cadherin protein expression was significantly up-regulated(P＜0.01,P＜0.001).Compared with the model control group,the number of melanoma lung metastatic nodules was significantly reduced in the mice in the high-dose group of tetrandrine(P＜0.05).(2)A total of 60 potential targets were obtained for the treatment of melanoma with tetrandrine;core targets such as AKT1,TNF,CCND1,RELA,CASP9,CHUK,and CREBBP were further screened,among which AKT1 was the most strongly interacting target;the signaling pathways such as apoptosis,FoxO,TNF,PI3K-AKT,and NF-κB were mainly involved.The molecular docking showed that tetrandrine had strong binding activity with AKT1,TNF,RELA and other core targets.Compared with the control group,protein expressions of p-AKT/AKT,p-NF-κB p65/NF-κ B p65,and p-CREB/CREB were significantly down-regulated in the cells of the tetrandrine 1,2,and 4 μmol·L-1 groups(P＜0.05,P＜0.01);protein expressions of p-AKT and p-NF-κB p65 were significantly up-regulated in the cells of the SC79 group(P＜0.001).Compared with the SC79 group,protein expressions of p-AKT,p-NF-κB p65,and p-CREB were significantly down-regulated in the cells of the 2 μmol·L-1 tetrandrine+ SC79 group(P＜0.001).Conclusion Tetrandrine may inhibit the proliferation,migration,invasion and EMT of mouse melanoma by regulating the AKT/NF-κB/CREB pathway,and thus inhibit the lung metastasis of mouse melanoma.

BACKGROUNDSleep deprivation (SD) has been used in treatment of depression disorder, and could effectively improve the patients' depressive symptoms.The aim of the study was to explore the effects of SD on electroencephalographic (EEG) and executive function changes in patients with depression.

METHODSEighteen depression patients (DPs) and 21 healthy controls (HCs) were enrolled in the present study. The whole night polysomnography (PSG) was recorded by Neurofax-1518K (Nihon Kohden, Japan) system before and after 36 hours of SD. The level of subjects' depression state was assessed by Visual Analogue Scale (VAS), and the executive function was assessed by Wisconsin Card Sorting Test (WCST).

RESULTSSignificantly decreased sleep latency (SL; before SD: (31.8 ± 11.1) minutes, after SD: (8.8 ± 5.2) minutes, P < 0.01) and REM sleep latency (RL; before SD: (79.8 ± 13.5) minutes, after SD: (62.9 ± 10.2) minutes, P < 0.01) were found after SD PSG in depression patients. Decreased Stage 1 (S1; before SD: (11.7 ± 2.9)%, after SD: (7.3 ± 1.1)%, P < 0.01) and Stage 2 (S2, before SD: (53.8 ± 15.5)%, after SD: (42.3 ± 14.7)%, P < 0.05) of non-rapid eye movement (NREM) sleep, and increased Stage 3 (S3, before SD: (11.8 ± 5.5)%, after SD: (23.6 ± 5.8)%, P < 0.01) and Stage 4 (S4, before SD: (8.8 ± 3.3)%, after SD: (27.4 ± 4.8)%, P < 0.01) NREM sleep were also found. After SD, the depression level in patients decreased from 6.7 ± 2.1 to 2.9 ± 0.7 (P < 0.01). In WCST, the patients showed significantly decreased Response errors (Re, before SD: 22.3 ± 2.4, after SD: 18.3 ± 2.7, P < 0.01) and Response preservative errors (Rpe, before SD: 11.6 ± 3.6, after SD: 9.3 ± 2.9, P < 0.05). Depression patients' RE (t = 2.17, P < 0.05) and Rpe (t = 2.96, P < 0.01) also decreased significantly compared to healthy controls.

CONCLUSIONSD can improve depression symptom and executive function in depression patients.

Adult ; Depression ; physiopathology ; Female ; Humans ; Male ; Middle Aged ; Polysomnography ; methods ; Sleep Deprivation ; physiopathology