BACKGROUND: After tooth extraction, residual ridge resorption is a complicate process, while stress is one of the main causes. Recent studies have demonstrated that osteopontin (OPN) is a kind of agent that is sensitive to mechanical stress.OBJECTIVE: To study the role of OPN in mediating mechanical stress effect on bone, and to investigate the relationship of OPN and bone rebuilding, action mechanism of OPN and cell surface receptor and the relationship of OPN and osteoblast and osteoclast, in order to reveal the molecule mechanism of residual ridge resorption mainly caused by stress, and also to be a basic theory for clinical molecule therapy or gene therapy.RETRIEVE STRATEGY: PubMed was searched from January 1985 to June 2007 for English literatures with the searching words of "OPN, mechanical stress and bone resorption" and China Journal Full-text Database was also searched from January 1995 to June 2007 for Chinese literatures with the searching words of "OFN, mechanical stress and bone resorption". Fifty-two literatures were retrieved. The data were primarily selected. Inclusive criteria: being relative to role of OPN in mediating mechanical stress effect on bone. Exclusive criteria: repetitive studies.LITERATURE EVALUATION: Among the 52 literatures, including 6 Chinese and 46 English, 5 were rejected for objective independent from this study, 13 for repetitive contents, and so 34 literatures were involved for further analysis on the role of OPN in mediating mechanical stress effect on bone, 6 being review and the others being clinical or basic studies.DATA SYNTHESIS: ①After tooth extraction, residual ridge resorption is a complicate process. It also influences the effect of artificial denture, while stress is the main cause. ② OPN is widely distributed throughout the body, and has many physiologic functions. Recent studies have demonstrated that OPN is a kind of agent that is sensitive to mechanical stress. ③Bone is a special kind of biological tissue, bone resorption and bone rebuilding both can take place when it is lack of mechanical stress (atrophy of disuse),or endures mechanical stress. ④Bone rebuilding can be seen as the results of these molecule events. OPN, as a main protein, participates in the bone resorption and bone rebuilding. ⑤These OPN can be seen as a chemotatic factor to guide prosoma osteoclast to migrate to the surface of the bone, and mediate it to combine with the integrin on the surface of osteoclast so to promote the resorption of bone. So, OPN is a necessary factor in mechanical stress induced bone loss. ⑥OPN is a signal of transmission between osteoblast and osteoclast. ⑦OPN can be seen as a long acting feedback inhibition signal to inhibit bone mineralization.CONCLUSION: OPN is a kind of agent that is sensitive to mechanical stress. It plays an important role in mediating mechanical stress effect on bone.

Objective To study the antitumor effectivity of special cytotoxic T lymphocytes(CTLs) induced by B lymphocytes in mice.Methods B lymphocytes were collected,isolated and purfied.Cells were initially activated by CD40L and rmIL-4,then cocultivated with T lymphocytes.T lymphocyte proliferation was examined.Total RNA,which was extracted from Hepal-6(a hepatocelluar carcinoma cell line),were transfected into B lymphocytes,as experimental group;while transfected with RNA of mice liver cells,liposimes and 1640 were as control groups,The expression of antigen presenting cell(APC) markers(CD40,CD80 and CD86) and major histocomability complex(MHC) on B cell surface after transfection were deteced.CTL were obtained by stimulating T lymphocytes with transfected B lymphocytes.Hepal-6 was cell-targeted and examined as index of CTL killing activity.The IFN-r secretion of stimulated CTL was quantified.Results T cell proliferation in experimental group had a higher degree than that in RNA control group(P

Objective To explore the efficacy of low dosage of olanzapine combined with fluoxetine in the treatment of depression.Methods A 8-week study was conducted in 130 patients met the diagnostic criteria for de- pression.Subjects were randomly assigned to two groups:fluoxetine(20mg/d)alone and olanzapine(2.5～5 mg/d) plus fluoxetine(20mg/d).They were evaluated with Hamilton depression scale(HAMD).Hamilton anxiety scale (HAMA)at baseline,the 1 week,2 weeks,4 weeks and 8 weeks subsequently.Results(1)There were significant differences in the total scores and reduction rates of HAMD between two groups in every interview.(2)The combi- nation group had greater reduction in depressive and anxiety symptoms than that in fluoxetine group.(3)The re- sponse rate in combination group was higher than that of fluoxetine group in 1 week,2 weeks and 4 weeks.There were no significant differences in response and remission rate between combination group and fluoxetine group.Con- clusion The combination of olanzapine with fluoxetine demonstrated a rapid,effective antidepressant action.

Adolescent ; Adult ; Aged ; Blood Coagulation Disorders ; Blood Coagulation Factors ; Case-Control Studies ; Child ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Vitamin K ; Vitamin K Deficiency ; Young Adult

Aged ; Esophagus ; Foreign Bodies ; complications ; diagnosis ; Hoarseness ; diagnosis ; etiology ; Humans ; Male

Humans ; Polyomavirus ; classification ; Polyomavirus Infections ; virology

Objective To determine the expression of glial fibrillary acidic protein(GFAP) and vascular endothelial growth factor(VEGF) in the hippocampus of rats with Alzheimer's disease(AD), and to determine the effect of butylphthalide on them and its significance. Methods Sixty male adult rats were randomly divided into a model group, a Butylphthalide group, and a control group. AD models were established by injecting β-amyloid protein 1-42 into the hippocampus of rats. Sixty days later,the rats were sacrificed and both sides of the hippocampus were sectioned for immunohistochemistry. Results Positive cells of GFAP in the hippocampus of the model group increased and the expression of VEGF decreased statistically, compared with the control group(P<0.01). The positive cells of GFAP in the hippocampus of the butylphthalide group decreased and the expression of VEGF increased significantly, compared with the model group(P<0.05). Conclusion Butylphthalide may protect the neuron-vascular unit of the hippocampus of Alzheimer model rats by inhibiting the expression of GFAP and increasing the expression of VEGF.

Objective To investigate the molecular mechanisms of cross-resistance to azoles in a clinical isolate of Aspergillus fumigatus. Methods A. fumigatus was isolated from a patient with invasive aspergillosis.Clinical Laboratory Standard Institute M38-A2 broth microdilution method and E-test method were used to determine the minimum inhibitory concentrations (MICs) or minimum effective concentration (MEC) of itraconazole, voriconazole, amphotericin B, posaconazole and caspofungin for the A. fumigatus isolate. DNA was extracted from the isolate and subjected to the amplification of cyp51A gene encoding the target enzyme of azole antifungal agents followed by sequence analysis. Results The broth microdilution test showed that the MEC of caspofungin was 0.5 mg/L, and MICs of itraconazole, voriconazole and amphotericin B were ≥ 16 mg/L,8 mg/L and 1 mg/L, respectively, for this isolate; while E-test assay revealed that the MICs of caspofungin,itraconazole, voriconazole, amphotericin B and posaconazole were 0.047 mg/L, ≥32 mg/L,≥32 mg/L, 12 mg/L and ≥32 mg/L, respectively. Sequence analysis showed an insertion of a 34-bp tandem sequence in the promoter region of the cyp51A gene as well as a T364A point mutation causing the substitution of leucine 98 (L98H). In addition, there were some other mutations in the cyp51A gene of this isolate, such as A137T,G585A, C814A, G836C, T991C and A1350G, which could result in corresponding amino acid substitutions.Conclusions An A. fumigatus strain with cross-resistance to azole antifungal agents is isolated. There is an insertion of a 34-bp tandem sequence into the promoter region as well as a T364A point mutation in the cyp51A gene, which contribute to the cross resistance to azole antifungal agents including itraconazole, voriconazole,and posaconazole. In addition, other mutations causing amino acid substitutions have also been detected in the cyp51 A gene of this isolate.

Objective To investigate the relationship of the activation of nuclear factor kappa B(NF-kB) with myocardial neutrophil infiltration and injury in human open heart surgery,and to observe the inhibiting effect on the activation of NF-kB and protecting effect on myocardium of the coenzyme Q10,a scavenger of oxygen free radicals.Methods Forty-seven adult patients undergoing open heart surgery were randomly divided into two groups,the control and the treatment.CoenzymeQ10 tablets were given to the treatment group 5 days before operation.Biopsy of right atrium for myocardial pathology,activated NF-kB detection and ultrastructure observation were done prior to cardiopulmonary bypass,45 minutes of ischemia and 45 minutes of reperfusion.The dynamic indexes,vasomotor drug dosage,and outcomes were observed postoperatively.Results Upon 45 minutes of ischemia and 45 minutes of reperfusion,in control group there were neutrophil accumulation and adhesion of vascular endothelium,ultrastructural damages,and positive expression of NF-kB both in nuclei and cytoplasm,in myocardium.In treatment group,there were only mild neutrophil infiltration and ultrastructural damages,and weak positive expression of NF-kB both in nuclei and cytoplasm.However,the dynamic indexes,vasomotor drug dosage,and outcomes of two groups were not significantly different.Conclusion NF-kB plays an important role in pathophysiological process of myocardial ischemia and reperfusion in open heart surgery.CoenzymeQ10 has obvious inhibiting effect on activation of NF-kB and protecting effect on myocardium.

Objective To observe the cerebral activation pattern in patients with cervical dystonia (CD) during finger movements and the changes caused by botulinum toxin injection by functional MRI.The possible etiological mechanism of CD and effect of peripheral botulinum toxin treatment on the level of central nerves system are investigated.Methods A designed functional MRI block with complex finger movements was applied and 11 patients with CD as well as 11 age and gender matched controls were scanned.Compare the activation pattern of CD pre/post treatment groups versus health controls.Evaluate and compare the symtom severity with Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS).Make a correlation analysis between activation pattern alteration and TWSTRS change in CD pre/post treatment groups.Results An reduced extent of activation in patients with CD was demonstrated compared to healthy controls in ipsilateral putamen,prefrontal cortex and contralateral somatosensory cortex to the direction of the head deviation,while an elevated extent of activation in ipsilateral precuneus and fusiform with statistic significance.At the time point of 4 weeks after botulinum toxin treatment patients showed no evident difference with healthy controls except for the decreased activation in contralateral precuneus to the direction of the head deviation.TWSTRS of patients with CD decreased from (20.02 ± 5.52) to (4.11 ± 4.34) with statistic significance (t =11.71,P =0.000) after botulinum toxin treatment.There was a positive correlation between cerebral activation pattern change in some cerebral areas (ipsilateral primary somatosensory cortex,premotor cortex,supplementary motor cortex,insula,fusiform,hippocampus with parahippocampa as well as contralateral middle temporal cortex and hippocampus with parahippocampa to the direction of the head deviation) and TWSTRS score decrease.Conclusions There are widespread abnormalities in cortical and subcortical activation pattern in patients with CD,which might due to dysfunction of sensory-motor integration.We speculate a basic pre-dystonic state is present in affected body parts prior to clinical symptoms appear.Botulinum toxin fulfills its subsequent central effect by reorganizing and normalizing the cerebral cortex in patients with CD.