Objective To explore the clinical and imaging features of reversible posterior leukoencephalopathy syndrome (RPLS). Methods The etiology, clinical manifestations, imaging features, treatment and prognosis of 6 patients with RPLS, admitted to our hospital from December 2007 to August 2010, were retrospectively analyzed. Results Among the 6 patients with RPLS, 1 was secondary to leukemia, 1 secondary to nephrotic syndrome, 1 secondary to renal transplantation, 1 secondary to pheochromocytoma, and 2 secondary to primary hypertention. The clinical manifestations of patients included seizure, dizziness, headache, nausea, vomit, conscious disturbance, behavioral and psychological abnormalities, and visual disorder. Cranial CT showed that 4 patients had low-density white matter lesions; cranial MRI mainly indicated posterior cerebral hemisphere white matter lesions,and the lesions showed low or iso-signal in T1WI, high signal in T2WI and FLAIR, low or iso-signal in diffusion-weighted magnetic imaging (DWI) and high signal in apparent diffusion coefficient (ADC)map. Five patients received the right treatment got rapid improvement of clinical symptoms with normal imaging examinations. One patient with renal transplantation who refused to disable cyclosporin A and mycophenolate mofetil eventually died. Conclusion The diagnosis of RPLS relys on history, clinical features and imaging characteristics. Most patients have a better prognosis, but a few patients have poor prognosis due to various reasons.

OBJECTIVETo observe the effect of volatile oil of amomum (VOA) on the expressions of mastocarcinoma-related peptide (PS2) and platelet activating factor (PAF) in helicobacter pyloriassociated gastritis (HPG) and to analyze its potential mechanism.

METHODSEighty patients with HPG were randomly assigned to two groups, 42 patients in the treated group treated with 0.5 mL VOA, thrice per day; and the 38 patients in the control group receiving Western tertiary medicinal treatment. Gastroscopic picture and helicobacter pylori (HP) infection (by quick urease and Warthin-Starry stain) of the gastro-membrane, expressions of PS2 and PAF (by immunohistochemical assay and Western blotting) as well as the contents of aminohexose and phospholipid (by Neuhaus method) in the gastric membrane of all patients were detected before treatment and 4 weeks after treatment. The clinical efficacy in the two groups was compared.

RESULTSThe total effective rate in the treated group was 88.1%, which was significantly higher than that in the control group (78.9%, P<0.05). After treatment, in the treated group, gastric membranous contents of aminohexose and phospholipid was increased, expression of PS2 elevated but that of PAF lowered, all showing significant difference as compared with those in the control group (P<0.01). In the control group, the expressions of PS2 and PAF changed insignificantly. The radical eliminating rate of HP in the treated group and the control group was insignificantly different between them (76.1% vs. 65.8%, P>0.05).

CONCLUSIONThe mechanism of VOA for anti-gastritis might be related with its action in increasing the expression of PS2 and decreasing the expression of PAF, and thus regulating the hydrophobicity of the gastric membrane.

Adult ; Aged ; Amomum ; Blotting, Western ; Chronic Disease ; Female ; Gastric Mucosa ; chemistry ; Gastritis ; drug therapy ; metabolism ; Helicobacter Infections ; drug therapy ; metabolism ; Helicobacter pylori ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Oils, Volatile ; adverse effects ; therapeutic use ; Peptides ; analysis ; Phospholipids ; analysis ; Platelet Activating Factor ; analysis

OBJECTIVETo investigate the role of AT2 receptors in the secretion of tumor necrosis factor alpha (alpha-TNF) and interleukin 1 beta (IL1 beta) in adult rat cardiac fibroblasts.

METHODSAdult rat cardiac fibroblasts in in vitro culture were divided into control, Ang II, AngII + Losartan, and AngII + PD123319 groups with corresponding treatments. Radioimmunoassay was used to determine alpha-TNF and IL1 beta levels in the supernatant of the treated cardiac fibroblasts.

RESULTSAng II treatment resulted in significantly increased alpha-TNF and IL1 beta levels. Compared with AngII group, IL1 beta level was decreased by 69.1% and 78.7% and alpha-TNF by 58.7% and 65.9% after blocking AT1 and AT2 receptors, respectively.

CONCLUSIONAT2 receptors are involved in alpha-TNF and IL1 beta secretions in cardiac fibroblasts.

Angiotensin II ; pharmacology ; Animals ; Fibroblasts ; drug effects ; metabolism ; secretion ; Gene Expression Regulation ; drug effects ; Interleukin-1beta ; secretion ; Male ; Myocardium ; cytology ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 2 ; metabolism ; Tumor Necrosis Factor-alpha ; secretion

Objective To explore the relationship between post-traumatic stress disorder (PTSD) and perceived social support (PSS)ability among middle school students in earthquake-stricken areas after the Wenchuan earthquake accident. Methods A total of 1966 students from three secondary schools of Wenchuan earthquake-stricken areas were evaluated by PTSD Checklist-Civilian Version (PCL-C) and Perceived Social Support Scale (PSSS). Results The overall incidence rate of PTSD was 78.3%, with severe PTSD as 24.38%. Significant differences on the incidence rates of PTSD were found among the students who were in different PSS levels (P<0.05) and significant negative correlation existed between the levels of severity on PTSD and PSS (γ=-0.226, P<0.05). Significant differences on PTSD incidence rates were found among those students who were from different families or out-family PSS levels (P=0.009, P<0.05). Significant negative correlation existed between the severity of PTSD and family or out-family PSS level (γ=-0.176, P<0.05, γ=-0.214, P<0.05). Conclusion Relationships between the incidence rate, severity of PTSD and PSS levels existed among the middle school students in Wenchuan earthquake-stricken areas, with higher PSS, lower incidence rate and lighter severity of PTSD. Psychological intervention for earthquake-stricken students should be carried out.

Objective To explore the distribution of water with high level arsenic and prevalence of arsenism along Huai'he River and the surrounding area of Hong'ze lake in Huai'an of Jiangsu. Methods Wate rsamples were collected and tested in 2008 from 18 villages of 6 towns according to history data in 3 counties like Xuyi,Jinhu and Hongze. Samples having arsenic level higher than 0.05 mg/L were investigated by epidemiological method and the patients were diagnosed by Standard of Diagnosis for Endemic Arsenism. Results All 5199 water samples were determined,and 260 water samples were exceeding the national drinking water quality level (0.05 mg/L) in 3 counties,the rates of exceeding diagnosis were 5.6%(247/4454),0.7%(4/597),6.0%(9/148) respectively. Total detected rate of endemic arsenic disease was 5.94%(128/2155). The detected rates of age group of 0 ～ ,20 ～,30 ～ ,40 ～ ,50 ～ ,60 ～ ,70 ～ ,80 ～ were 2.86%(1/35),2.11%(2/95),1.26%(3/239),3.10%(16/516),5.53% (32/579),10.07%(41/407),11.84%(27/228),10.71%(6/56) respectively. The detected rate of male (9.10%,78/857) was higher than that of female(3.85%,50/1298,χ~2 = 25.46,P < 0.01). Conclusions Huai'he River and the surrounding areas of Hong'ze lake like Xuyi,Jinhu and Hongze are identified existing endemic arsenic disease area. The prevention of arsenism should be strengthened in these areas.

OBJECTIVECytokine mediated cell immunity is the main mode of anti-tumor immunity in organism, and the disequilibrium of cytokine network is the main cause of tumor cells escaping immunologic surveillance. High mobility group box 1 (HMGB1), a nuclear protein, has recently been identified as an important mediator of local and systemic inflammatory diseases when released into the extracellular milieu. In the present study, the investigators explored the clinical significance of alteration in the serum levels of HMGB1 in childhood acute lymphocytic leukemia (ALL) and the mechanism of HMGB1-induced tumor necrosis factor (TNF)-alpha secretion in leukemic cells.

METHODSThe serum levels of HMGB1 in healthy children and childhood ALL were assayed by Western blotting. K562 leukemic cells were stimulated with recombinant HMGB1 protein in vitro, and the secretion of TNF-alpha was determined by using ELISA. The effects of HMGB1 on activation of p38, c-Jun amino-terminal kinase (JNK), and extracellular-signal regulated protein kinase (ERK) and mitogen-activated protein kinase (MAPK) in K562 cells were assayed by using Western blotting. The effects of inhibitors specific for the MAPK on HMGB1-induced TNF-alpha secretion were assayed by using ELISA.

RESULTSThe serum levels of HMGB1 were significantly higher in ALL initial treatment group (n = 15, 43.78 +/- 4.62 microg/ml) than those in healthy control group (n = 15, 0.60 +/- 0.48 microg/ml, P < 0.01) and ALL complete remission group (n = 15, 0.89 +/- 0.62 microg/ml, P < 0.01). No significant difference was found between the healthy control group and ALL complete remission group in HMGB1 levels (P > 0.05). TNF-alpha started to become detectable at 2 h and was still increasing at 16 h after HMGB1 (1 microg/ml) treatment in K562 cell culture. TNF-alpha was also secreted from K562 cells in a dose-dependent manner after HMGB1 (1 ng/ml-1 microg/ml) exposure. HMGB1 induced the phosphorylation of p38, JNK and ERK in k562 cells. Inhibitors specific for the JNK (SP600125), MEK (PD98059), and p38 MAPK (SB203580), abrogated HMGB1-induced TNF-alpha secretion.

CONCLUSIONSThe measurement of serum HMGB1 is helpful to evaluate the prognosis of the childhood ALL. HMGB1 stimulates leukemic cells to secrete TNF-alpha through a MAPK-dependent mechanism.

Cell Line, Tumor ; Child ; Cytokines ; metabolism ; HMGB1 Protein ; metabolism ; Humans ; Imidazoles ; pharmacology ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Mitogen-Activated Protein Kinase Kinases ; metabolism ; Mitogen-Activated Protein Kinases ; metabolism ; Phosphorylation ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; enzymology ; metabolism ; Protein Kinase Inhibitors ; pharmacology ; Pyridines ; pharmacology ; Signal Transduction ; drug effects ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo explore the effects of survivin antisense RNA and HSP70 double gene transfection on breast cancer cell line MCF-7.

METHODSMCF-7 cells was transfected with the double-gene vector pIRES2-EGFP-survivin antisense RNA/HSP70 via liposome. After a 72-h transfection, the cells were collected for observation under inverted fluorescent microscope. The changes of survivin mRNA and HSP70 protein expressions in the cells were detected with real-time PCR and Western-blot before and after the cell transfection, and the apoptotic rate of the transfected MCF-7 cells was detected by flow cytometry analysis with Annexin-V-cy5/7AAD double staining.

RESULTSGreen fluorescence was detected in MCF-7 cells transfected with the double-gene expression vector and the empty vector under inverted fluorescent microscope. The expression level of survivin mRNA in the cells was reduced effectively after the transfection with the double-gene expression vector, which also induced obvious cell apoptosis and enhanced the expression level of HSP70 protein as compared with those in MCF-7 cells transfected with the empty vector and the untransfected MCF-7 cells.

CONCLUSIONSurvivin antisense RNA can interfere with the expression of endogenous survivin and induce apoptosis of MCF-7 cells. HSP70 can increase the expression of HSP70 protein in MCF-7 cells.

Apoptosis ; drug effects ; Female ; HSP70 Heat-Shock Proteins ; genetics ; pharmacology ; Humans ; Inhibitor of Apoptosis Proteins ; genetics ; pharmacology ; MCF-7 Cells ; RNA, Antisense ; genetics ; pharmacology ; RNA, Messenger ; genetics ; Transfection

Objective To investigate the effect of silment information regulator factor related enzymes 1 (SIRT1) on the apoptosis of retinal ganglion cells (RGCs) in rats with diabetic retinopathy and its downstream molecular mechanisms.Methods Together 60 healthy male Sprague-Dawley rats were collected and randomly divided into normal group,diabetic group,SIRTI activator-resveratrol treatment group (treatment group),and diabetic rat model was induced by intraperitoneal injection of streptozotocin at 60 mg · kg-1 in the latter two group rats,while the normal group was injected with sodium citrate buffer at 60 mg · kg-1.Then,after 72 h,rats with blood glucose ＞ 16.7 mmol · L-1 were designated as diabetic rats by blood glucose test.Then each rat in the treatment group was treated with SIRT1 activator-resveratrol at 20 g · kg-1 once a day at the 2nd day after the success of the model,and the normal group and diabetic group were given methylene chloride.Finally,after immunohistochemical staining for retina,TUNEL assay was used to evaluate the apoptosis of RGCs,while the expression of SIRTI,p38 MAPK and Caspase-3 protein was detected by Western blot.Results The apoptotic index of RGCs in the normal group,diabetic group and treatment group was (0.848+0.131)％,(19.038 + 1.327)％,(10.461 + 1.089)％ respectively at 8 weeks,and the difference among the three groups was statistically significant (F =670.497,P =0.000),while the differences between each two groups were also statistically significant (all P =0.000).Furthermore,when compared with the normal group (0.132 ± 0.043),the expression of SIRT1 protein in the diabetic group (0.060 ± 0.028) and the treatment group (0.073 ± 0.026) was significantly decreased,and the overall difference among the three groups was statistically significant (F =1 310.663,P =0.000),while the differences between each two groups were also statistically significant (all P =0.000).The expression levels of p38 MAPK and Caspase-3 were increased in diabetic group (1.121 ± 0.082,0.266 ± 0.005) and treatment group (0.574 ± 0.012,0.190 ±0.060) respectively,and the overall difference and pairwise comparison in the three groups approached statistically significance (all P =0.000,0.000).Conelusion Up-regulation of SIRT1,can inhibit the apoptosis of RGCs,and protect RGCs against apoptosis in rat model of diabetic retinopathy,which may be correlated with the downregulation of p38 MAPK signal pathway.

OBJECTIVE: To evaluate the effect of intrathecal pumping tramadol on cell-mediated immunity in rats with formalin inflammatory pain. METHODS: Thirty-two Sprague-Dawley adult male rats weighting 250 approximately 300 g were randomly divided into 4 groups (n=8 in each group):Saline group (NS) and 3 tramadol groups (T1,T2,and T3). The rats were anesthetized with intraperitoneal chloral hydrate (300 approximately 350)mg/kg. Microspinal catheter was inserted into the subarachnoid space at the lumber region according to modified Yaksh techniques. In the tramadol groups,after 5 days tramadol was continuously infused through the spinal catheter at 50 (T1),25 (T2), and 12.5 microg/h (T3) for 7 days. In the NS group normal saline was continuously infused instead of tramadol. On Day 7 formalin (5%, 50 microL) was injected into the plantar surface of the left hindpaw. The number of flinches, lickings and total time of licking was recorded for 60 min.Pain intensity scoring(PIS)(0 approximately 3;0= no pain, 3=severe pain) was used to assess the antinociceptive effect of intrathecal tramadol. The rats were killed after the evaluation of pain intensity. Body weight and spleen weight were measured and spleen index (spleen weight/body weight) was calculated. T-lymphocyte function was evaluated based on Concanavalin-A(ConA) induced splenocyte proliferation. A modified lactic acid dehydrogenase(LDH) release assay was done to assess the NK cell activity. Phenotypic expressions of cell surface markers of T lymphocyte subsets (CD3+, CD3+ CD4+, CD3+ CD8+, and CD4+/ CD8+) and NK cell(CD161+) in the spleen were analyzed by flow cytometry. RESULTS: The PIS scores were significantly lower in the T1,T2,and T3 groups than those in the NS group. The spleen index and splenocyte proliferation induced by ConA were significantly suppressed in the T1 group,and the phenotypes of T lymphocyte subsets were significantly changed,but no significant difference was found in the T2 and T3 groups compared with the NS group. There were no differences in NK cell activity in the 3 tramadol groups from the control group. CONCLUSION Intrathecal pumping tramadol has significantly antinociceptive effect. Intrathecal pumping higher dosage tramadol (50microg/h) suppresses T lymphocyte proliferation and alteres T lymphocyte subset phenotype but does not affect NK cell activity. General analgesic dosage tramadol (25 and 12.5 microg/h) has no effect on the immune function.
Analgesics, Opioid ; pharmacology ; Animals ; Dose-Response Relationship, Drug ; Formaldehyde ; Injections, Spinal ; Killer Cells, Natural ; immunology ; Male ; Pain ; chemically induced ; immunology ; Pain Measurement ; drug effects ; Rats ; Rats, Sprague-Dawley ; T-Lymphocyte Subsets ; immunology ; Tramadol ; administration & dosage ; pharmacology

OBJECTIVETo investigate the differences about RNA interference (RNAi) technique which focuses on single or multiple sites to suppress colon cancer LoVo cell line's epidermal growth factor receptor (EGFR) mRNA and protein expression, induce cell apoptosis and enhance 5-fluorouracil (5-FU) sensitivity.

METHODSThe human colon cancer LoVo cells were transfected by liposome with pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 expressive vectors which were established by p Genesil-1 plasmid and EGFR short hairpin RNA (shRNA) synthesized in vitro, then were selected for 4 weeks by using G418. Five groups were selected for the study: Group 1: the normal cultured LoVo cells; Group 2: the negative control plasmid HK; Group 3: pU6-EGFR-shRNA-1 plasmid vector; Group 4: pU6-EGFR-shRNA-2 plasmid vector; Group 5: pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2, half for each. The mRNA and protein expression were assessed using Real Time PCR and Western blot, the cell apoptosis was determined via flow cytometry, and the suppressive rate and IC(50) to LoVo cells by 5-FU of different concentrations and time points were carried out by using Cell Counting Kit-8 (CCK-8).

RESULTSExpression plasmids encoding shRNA were successfully established and transfected into the LoVo cells. In group 3, 4 and 5, the mRNA expression was decreased by (80.2 +/- 3.4)%, (81.3 +/- 2.8)% and (90.6 +/- 2.8)%, respectively, and protein expression was decreased by (74.1 +/- 4.0)%, (73.4 +/- 2.3)% and (90.4 +/- 3.3)%, respectively; meanwhile, cell apoptosis increased by (10.4 +/- 0.5)%, (10.1 +/- 0.4)% and (14.2 +/- 0.5)%, respectively. The IC(50) of 5-FU and cell suppressive rate analysis demonstrated that there were significant differences among group 5, groups 3 and 4, and groups 1 and 2, but there were no significant difference between group 1 and group 2, as well as group 3 and group 4.

CONCLUSIONSBoth pU6-EGFR-shRNA-1 and pU6-EGFR-shRNA-2 were capable of suppressing EGFR expression of LoVo cells, and therefore promoting apoptosis and increasing the cell toxicity of 5-FU. The targeting double combined sites RNAi technique was significantly better than single site interference. The new therapeutic modalities in the treatment of human colon cancer are suggested by this study.

Apoptosis ; genetics ; Cell Line, Tumor ; Colonic Neoplasms ; genetics ; metabolism ; pathology ; therapy ; Combined Modality Therapy ; Fluorouracil ; pharmacology ; Genetic Therapy ; Humans ; RNA ; genetics ; RNA Interference ; Receptor, Epidermal Growth Factor ; biosynthesis ; genetics ; Transfection