Objective To explore the clinical diagnosis and treatment of nervous system damage caused by invasive fungi nasosinusitis.Methods 7 patients with nervous system damage caused by invasive fungi nasosinusitis were selected,and the clinical,imaging and pathological data of the patients were reviewed retrospectively.Laboratory tests were used in patients with cerebrospinal fluid (CSF).Imaging used CT or MRI examination.Results In the past history of the patients,no one with nasosinusitis.5 patients immunocompromised and 2 cases had no special medical history.All patients were diagnosed with neurological damage after admission.Under the microscope,fungal cultures showed Aspergillus in 4 cases,Mucor in 2 cases,Cryptococcus in 1 case.In the imaging,all patients had sinus lesions,base of skull destruction in 4 cases.Used surgical interventions and drug for 7 patients,6 cases recovered and 1 case died.Conclusion Using antibiotics and glucocorticoid for a long time or suffered from diabetes and tumour may have higher incidence of invasive fungi nasosinusitis and damage the nervous.It is one of the leading causes of patients with immune deficiencies deaths.

BACKGROUND:Because of their immunological properties, bone marrow mesenchymal stem cells transfusion is developed as a new treatment for refractory graft-versus-host disease. OBJECTIVE:To analyze the safety and curative effect of bone marrow mesenchymal stem cells transfusion on treating different organ damages in graft-versus-host disease after al ogeneic hematopoietic stem celltransplantation. METHODS:Eight patients with malignant hematologic disease were included in this study. The patients developed severe steroid-resistant graft-versus-host disease after al ogeneic hematopoietic stem celltransplantation and received transfusion of mesenchymal stme cell(1×106 of immunosuppressive agent. RESULTS AND CONCLUSION:For the total y eight patients, six got response (two cases of complete remission, and four cases of partial remission) and two showed no remission. Four of five cutaneous damages were ameliorated and one showed no effect. For three cases of oral graft-versus-host disease, two acquired complete remission and one showed partial remission. Two cases of liver graft-versus-host disease and two cases of astro-intestinal graft-versus-host disease obtained complete remission. No response was displayed to three cases of ocular graft-versus-host disease, one case of bronchiolitis obliterans, and one case of urinary graft-versus-host disease. In the median fol ow-up of 28 months (7-62 months), three patients developed posttransplant lymphoproliferative disorders within 3 months after mesenchymal stem cells transfusion. Administration of mesenchymal stem cells is safe for treatment of severe graft-versus-host disease after al ogeneic hematopoietic stem celltransplantation. Mesenchymal stem cells transfusion may be a promising/kg) together with the primary therapy therapy for refractory cutaneous , astro-intestinal, liver and oral graft-versus-host disease but not for pulmonary, ocular and urinary graft-versus-host disease. Whether mesenchymal stem cells transfusion is associated with posttransplant lymphoproliferative disorders needs more case data.

AIM:To investigate the activity change of voltage-dependent delayed rectifier potassium channel(Kv) on human airway smooth muscle cells(HASMCs) after transfection of Kv1.5 antisense oligonucleotides(AsOND),and to discuss the regulating mechanism of Kv1.5.METHODS: The mRNA and protein expressions of Kv1.5 in liposome-mediated Kv1.5 AsOND transfected HASMCs were measured with techniques of reverse transcriptase-polymerase chain reaction(RT-PCR) and Western blotting.Kv activities in transfected HASMCs were investigated with whole-cell patch clamp.RESULTS: After HASMC were transfected by liposome-mediated Kv1.5 AsOND,the mRNA and protein expressions of Kv1.5 were decreased,and Kv activity was inhibited,which made the cell membrane potential(Em) inclined to depolarization.CONCLUSION: Transfection of Kv1.5 AsOND made the function of Kv in HASMCs decreased.Kv1.5 may play a critical role in the regulation of Kv activity.

BACKGROUND: The rehabilitative intervention accelerates the recombination and reconstruction of cerebral structure and function and then promotes the amelioration of function.OBJECTIVE: To evaluate the influence of early and late rehabilitative interventions on the motor function and activities of daily living (ADL) with neurologic deficit score (NDS), Fugl-Meyer assessment (FMA) and modified Barthel index in patients with cerebral infarction.DESIGN: A randomized controlled trial.SETTING: Department of Neurology, Qilu Hospital of Shandong University; Department of Rehabilitation, Jinan Great Wall Hospital; Department of Neurology, the Third People' s Hospital of Heze.PARTICIPANTS: Totally 216 inpatients with cerebral infarction (125 males and 91 females, aged 60-75 years), who were selected from Qilu Hospital of Shandong University, Jinan Great Wall Hospital and the Third People's Hospital of Heze from December 2000 to December 2003, were randomly divided into early rehabilitation group (n=108) and late rehabilitation group (n=108) after admission.INTERVENTIONS: In the early rehabilitation group, the patients began to receive rehabilitation at 48 hours to 14 days after the stability of vital signs and absence of the progress of neurological signs. In the late rehabilitation group, the patients began to receive rehabilitation at 15-30 days after attack. They were trained with Bobath method and motor relearning program, once a day, 45 minutes for each time, and 6 times every week.Before and 30 days after the rehabilitative treatment, the rehabilitation was evaluated with modified Barthel index (100 points as normal, 0-20 as extremely severe functional defect, 25-45 as severe functional defect, 50 -70 as moderate functional defect, 75-95 as mild functional defect), FMA (total score was 100 points, including the highest scores of upper and lower limb movement were 66 and 34 points respectively) and NDS (the highest and lowest scores were 45 and 0 point, 0-15 as mild, 16-30 as moderate, 31-45as severe).ter treatment.RESULTS: All the 216 patients with cerebral infarction were involved in obviously lower than that before treatment in both groups (P ＜ 0.01), lower in the early rehabilitation group than in the late rehabilitation group score at 30 days after treatment was obviously higher than that before treat ment in both groups (P ＜ 0.01), higher in the early rehabilitation group than in the late rehabilitation group [upper limb: (32.43±21.52), (26.69±19.79)dex: The modified Barthel index at 30 days after treatment was obviously higher than that before treatment in both groups (P ＜ 0.01), higher in the early rehabilitation group than in the late rehabilitation group [(54.23±30.33),(46.57±29.85) points, P ＜ 0.05].CONCLUSION: Both early and late rehabilitative interventions can obviously accelerate the recovery of neurological function, motor function and ADL, but the effect of early rehabilitative intervention is superior to that of the late one.

Objective To investigate the anti-proliferation effect of peroxisome proliferator-activated receptor γ(PPARγ)agonist troglitazone(TGZ)on leukemic Raji cells and its mechanisms.Methods Raji cells in culture medium in vitro were given different concentrations of TGZ(0～60 μmol/L)for 24,48 and 72 h.The inhibitory rates of the cells were measured by MTT assay,cell apoptotic rate was detected by flow cytometry(FCM),agarose gel electrophoresis was used to observe the DNA ladder,and western blotting was used to analyzed the variation of apoptosis related proteins bcl-2,Bax and Survivin.Results TGZ(over 20 μmol/L)could inhibit the growth of Raji cells and cause apoptosis remarkably,the suppression was both in time-and dose-dependent manner.DNA ladder was observed after the cells treated by TGZ for 72 h,and western blotting analysis revealed that anti-apoptotie proteins Survivin and bcl-2 were decreased remarkably while pro-apoptotic protein Bax increased significantly after the cells were treated by TGZ for 48 h.Conclusion PPARγ agonist TGZ can inhibit the growth and induce apoptosis on Raji cells significantly,downregnlating the expression of Survivin and bcl-2 as well as upregulating of Bax expression of Raji cells may be one of its most important mechanisms.

Objective To investigate the brain protective effect of isoflurane preconditioning on the rat liver against ischemia-reperfusion through determining the content of S-100β protein in peripheral blood in combination with mitochondrial ultrastructure in rat brain.Methods A total of 45 SD rats were randomly divided into three groups,sham group (group S):the only separation of the hepatoduodenal ligament,but did not block the hepatic portal blood supply; ischemia-reperfusion group (group I/R):liver ischemia 60min,reperfusion 120 min; isoflurane preconditioning group (group ISO):60 min before liver I/R,ISO pretreatment for 30 min,elution in the air after 30 min; 24 h after recirculation the forebrain tissues were rapidly removed.The changes of mitochondrial ultrastructure were observed by electron microscopy.The content of S-100β protein in serum was measured before ischemia and reperfusion 120 min through the application of Elisa kit.Results Marked swelling of mitochondria with disrupted cristae and damaged matrix were observed in group I/R,while relative intact mitochondria were seen in sham and ISO groups.The content of S-100β protein in serum was significantly higher in I/R group [(1.52 ±0.26) μg/ml] than in sham [(0.31 ±0.05)μg/ml] and ISO [(0.79 ± 0.21) μg/ml] groups (P ＜0.05).Conclusions The liver ischemia-reperfusion may injure the brain of the rat and isoflurane preconditioning can protect the rat brain from injury.

AIM: To detect the protein expression of TIMP3 and RUNX3 in bone marrow mononuclear cells (BMMCs) from acute leukemia (AL) patients and to investigate the relationship between the methylation status of genes and their expressional levels. METHODS: Protein expression of TIMP3 and RUNX3 in 50 samples of BMMCs and 10 samples of peripheral blood mononuclear cells (PBMCs) from healthy volunteers was detected by Western blotting. The prognostic factors related to AL and data from methylation specific polymerase chain reaction were also analyzed. RESULTS: The expression level of RUNX3 with methylation was less than that without methylation in BMMCs from AL patients. The complete remission (CR) rate was related to RUNX3 expression and blasts in bone marrow (BM). BMMCs from patients with silencing of RUNX3 and higher blasts in BM had a lower CR rate. CONCLUSION: Absence of RUNX3 protein expression resulting from methylation of RUNX3 promoter probably plays a role in the pathogenesis of AL and is of value in prognosis. No relationship between methylation of TIMP3 promoter and the pathogenesis of AL is observed.

AIM:To investigate the expression of aplasia rashomolog member I ( ARHI) gene in acute myeloid leukemia cells (AML) and to study the effects of ARHI on the growth of AML cell line U937.METHODS:The mRNA ex-pression of ARHI in AML cells, 293FT cells, AML primary cells and healthy volunteer blood cells were detected by RT-PCR.After transfection with the MSCV-IRES-GFP-ARHI plasmid to the U937 cells, the growth curve was analyzed by MTT assay.U937 cells were re-suspended by fresh medium and cultured for 24 h, then the cell cycle distribution and ap-optotic rate were determined.RESULTS:The mRNA of ARHI was positively detectable in 293FT cells and healthy volun-teer blood cells instead of AML cell line and AML primary cells.The growth curve showed that cell viability in U937 cells with high expression of ARHI (U937-ARHI) was lower than that in the control cells (U937-GFP) on 6th~8th day.The ratio of G2/M phase and apoptotic rate in the U937-ARHI cells were increased compare with control group ( P<0.05 ) . CONCLUSION:The mRNA level of ARHI is low in AML cells.High expression of ARHI gene in U937 cells inhibits cell growth, arrests the cells at G2/M phase and induces apoptosis.

Objective To investigate the apoptosis inducing effect of peroxisome proliferator-activated receptor r(PPARr)agomst on leukemic K562 cells and its mechanisms of action.Methods K562 cells in culture medium in vitro were given different concentrations of PPARragonist rosiglitazone(RGZ)(20-80 umol/L)for O,24,48 and 72h The inhibitory rate of the cells were measured by MTT assay,cell apoptosis was detected by Annexin V/PI staining,and the expression of P53 protein as well as the activity of caspase-3 were also detected.Results RGZ(over 40umoL/L)could inhibit the growth of K562 cells and cause apopto-sis remarkably,the suppression Was both in time-and dose-dependent manner.The expression of P53 pmtein was upregulated and the activity of caspase-3 Was increased concomitantly after the cells werle treated by RGZ.Conclusion PPARr agonist RGZ(over 40 umol/L)can induce apoptosis on K562 cells signifieantly,upregu-lation the expression of P53 protein as well as increasing caspase-3 activity may be one of its most important mechamisms.

Objective To investigate the apoptosis inducing effects of oridonin on leukemic THP-1 cells and its mechanisms of action. Methods THP-1 cells in culture medium in vitro were given different concentrations of oridonin (16～56 μmol/L) for 24, 48 and 72 h. The inhibitory rate of the cells were measured by MTT assay, apoptotic morphology was observed by Hoechst 33258 staining, and Annexin V/PI staining was used to detect cell apoptosis by flow cytometry (FCM). Caspase-3 and poly (ADP-ribose) polymerase (PARP) expression were detected by Western blotting. Results Oridonin (over 32 μmol/L) could inhibit the growth of THP-1 cells and cause apoptosis remarkably, the suppression was both in time-and dose-dependentmanner. Marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Hoechst 33258 staining, and Annexin V/PI staining showed that apoptotic cells gradually increased after the cells treated with oridinon. Western blotting showed cleavage of the caspase-3 zymogen protein (32×103), with the appearance of its 20×103 subunit, and a cleaved 89×103 fragment of 116×103 PARP was also found. Conclusion Oridonin can inhibit cell growth and induce apoptosis in THP-1 cells via activation of caspase-3. The results indicated that oridonin might be an important potential anti-leukemia reagent.