Objective To discuss the influence of dental occlusion on mandibular movements. The characteristic tracings of mandibular movements at the condyle of unilateral posterior crossbite patients were investigated using a computerized axiography. The differences between patients with normal occlusion and unilateral posterior crossbite were compared by some recordings of condylar movements in three dimensions. Methods Seven unilateral posterior crossbite patients (at least two posterior teeth were crossbite) were chosen as experiment group, and five with normal occlusion without signs or symptoms of temporomandibular disorders (TMD) were chosen as controls. By computer-aided axiography (CADIAX) and gamma dental software for windows 2.3.2.22 (GDSW) from Grbh company (Germany), the tracings of condylar movements in right and left parasagittal planes during opening/closing were recorded, and the data were input into the computer and analyzed using GDSW software. The drifts in X, Y and Z coordinated with condylar movements, respectively, and the transverse condylar inclination from the orbital axis line and the horizontal condylar inclination were calculated, respectively. Results The lengths of the axiographical in opening/closing movement were significantly shorter in the experiment group than that in normal occlusion group; the bilateral condylar tracing of opening/closing movement was symmetric in younger cases but asymmetric in older cases; the lateral deviation of opening/closing movement was significantly larger in unilateral posterior crossbite than that in control group. Conclusion The condylar tracings of envelope of movement in unilateral posterior crossbite patients are significantly different in the patients with normal occlusion. With age increasing, tracings of the affected side and contralateral side vary from symmetry to asymmetry. The results suggest that the functional opening movements are limited in the patients with the unilateral posterior crossbite.

The association between psychogenic illness and human endogenous viruses (HEVs), including human endogenous retrovirus and Borna disease virus, remains unclear. As the component of human genome, HEVs may become the joint of various pathogenic factors of schizophrenia (SZ), such as heredity, environment, and immunity. In this review, we strive to uncover the clinical and laboratory evidence for the roles and possible pathogenic mechanism of HEVs in the development of SZ.
Animals ; Environment ; Humans ; Schizophrenia ; etiology ; genetics ; immunology ; virology ; Viruses ; genetics

Objective To develop a model of be nzene induced aplastic anemia in mice and to observe pathology of aplastic anemi a induced by benzene;Methods we tried to establish a model of benzene induced aplastic anemia in mice,then we studied pathology of aplastic anemia and the pr evention of amifostine on the model.(1) CD1 male mice were injected subcutaneou sly with benzene +corn oil three times a week,and randomly assigned to four gro ups according to the dose of benzene administrated:B1group(0.5ml/kg),B2group( 1.0ml/kg),B3group(1.5ml/kg),B4 group(2.0ml/kg),C group (injected intraperi toneally with 200mg/kg amifostine 30min before benzene administrated on the basi s of the aplastic anemia model as amifostine treated group),while A group treat ed with only corn oil as control,all the groups were complement with corn oil t o 4ml/kg;Before and 2 days after benzene were administrated 10,15,20 and 25 t imes respectively,all the groups mice were killed respectively ,the parameters tested were as following:general condition,peripheral blood smear,histopatho logy of bone marrow 、liver,spleen and PCNA,TUNEL.Results Compared with the control group,some parameters were changed in each model group,but only the pa rameters in B4 group were significantly different from the control group.After 25 times of benzene administration,compared with the control group (A group),B4 group mice showed 18.51% body and 63.86% spleen weight loss (P

Autophagy plays an important role in the regulation of activation and inflammation of microglia after ischemic stroke. The interaction between autophagy of microglia and the inflammation mediated by microglia after ischemic stroke was complex and a large num-ber of molecules were involved. The receptors of microglia activation and related substances may be possible mechanism in the regulation of microglia autophagy. Autophagy inhibitors and microglia receptor targeting therapy may provide new strategies for the clinical treatment of ischemic stroke. This paper summarized the progress of microglia autophagy after ischemic stroke.

Objective To investigate the therapeutic effects of givinostat , a histone deacetylase inhibitor (HDACI), on the development of chronic asthma with airway inflammation , airway remodeling and airway hyperresponsiveness ( AHR) .Methods BALB/C mice were randomly divided into control group , asthma group, dexamethasone group and givinostat group (n=12 per group).AHR was assessed.Total cell numbers and differential counts , interleukin-4 ( IL-4 ) , interleukin-5 ( IL-5 ) and interferon-γ( IFNγ) levels in the bronchoalveolar lavage fluid ( BALF) were measured in the above 4 groups.The pathology of lung tissue was evaluated .Immunohistochemical ( IHC) staining and Western blot were used to detect αsmooth muscle actin(α-SMA) and transforming growth factor-β1(TGFβ1).Results Compared with the asthma only group, givinostat treatment relieved airway resistance (2.96 ±1.01 vs 6.50 ±0.79,P<0.05).Total inflammatory cells [(33.04 ±5.62) ×104/ml vs (98.04 ±9.27) ×104/ml,P<0.01], eosinophil cells [(9.17 ±2.33) ×104/ml vs(37.64 ±6.98) ×104/ml, P <0.01], IL-4 [(10.12 ±2.98)ng/ml vs (16.88 ±2.78)ng/ml,P<0.05] and IL-5 [(27.09 ±3.62)ng/ml vs (37.86 ±7.34)ng/ml, P<0.05] levels were all reduced in givinostat group , while IFNγ[ ( 91.86 ±23.73 ) pg/ml vs ( 60.49 ±11.88 ) pg/ml, P>0.05] was enhanced in BALF.Inflammatory cell infiltration around the airway was reduced , with decreased inflammatory cell score [(1.60 ±0.69) points vs (3.40 ±0.68) points, P <0.01] and inflammatory cell number (111.65 ±31.41 vs 601.25 ±186.85, P<0.01).The goblet cell metaplasia [(26.36 ±2.33)%vs (57.21 ±11.56)%] and collagen deposition area [(52.77 ±7.58)μm2/μm vs (111.81 ±12.40)μm2/μm] were obviously reduced (P<0.01).The expressions of α-SMA and TGFβ1 in the lung tissue were both significantly decreased ( P<0.01 ) .Conclusion Givinostat treatment can reduce airway inflammation , airway remodeling and airway hyperresponsiveness in chronic asthma .Its effect is comparable to that of glucocorticoid hormone treatment .

Objective To investigate the relationships between vascular factors and plaque morphology in the patients with acute coronary syndrome(ACS). Methods lntravascular ultrasound(IVUS) was performed on 56 consecutively enrolled patients with ACS. Cytometric bead array for seven vascular factors(sPE,t-PA, MCP-I, IL-8,IL-6,sVCAM-1, and sCD40L) was measured by cytometry. The others biomarkers were tested by ELISA or biochemistry. Differences in bio-factors were compared between vulnerable plaque and non- vulnerable plaque groups, accte myocardial infarction (AMI) and ustable angina (UA) patients, and occurring plaque rupture. The relationship between the parameters of morphology and vascular factors was analyzed. Results There were positive correlations between sVCAM-1sPE, sVCAM-1-sCD40L, sCD40L-sPE, IL-6-IL8,IL8-MCP4, and MCPI-sVCAM-1; CRP (18.868±4.907mg/L vs 5.806±3.553 mg/L)and IL-6 (19.5 pg/ml [9.2±44.6 pg/ml]vs 5.3 pg/ml [2.3～ 13.4 pg/ml])were elevated in the vulnerable plaque group(P <0.05). sCD40L(473.82±126.11 vs 237.94±34.78 pg/mi),sPE (107.214±39.90 vs 49.06±5.61 μg/L) and MCP-1(132.42±17.85 vs 127.174±13.27 pg/ml) were increased in the plaque rupture group(P < 0.05);There was correlation between tPA and plaque morphology(P < 0.05). Increases in sCD40L, MCP-1, sPE, and TC were independent factors for plaque rupture. Conclusions IL-6 and CRP may be biomarkers for vulnerable plaque and for diagnosis ofAMI, sCD40L, MCP-1 and sPE are potential markers when for plaque rupture patient present with severe ACS.

Objective To explore the relationship of the level of serum selenium and infantile diarrhea,provide foundation for establishing the therapeutic criteria.Methods Seventy-eight diarrhea children was enrolled in this study,6 -24 months old.Thirty children with acute diarrhea (AD group),26 children with persistent diarrhea (PD group) and 22 children with chronic diarrhea (CD group).The level of serum selenium was measured and compared with another 30 healthy children (control group) of matched sex and age.The level of serum selenium of CD group was compared before and after the recovery.Results The level of serum selenium in AD group and PD group had no significant difference compared with control group [ (51.34 ± 4.84),(48.14 ± 3.05 ) μ g/L vs.(55.08 ± 5.59 ) μ g/L ] (P＞0.05 ).But the level of serum selenium in CD group was significantly lower than that in control group [ (42.13 ± 5.16) μ g/L vs.(55.08 ±5.59) μg/L] (P＜0.05).After treatment for 1 month,the level of serum selenium in CD group was significantly increased than before treatment [ (53.76 ± 8.38 ) μ g/L vs.(42.13 ± 5.16) μ g/L ] (P＜0.05 ).Conclusions The nosogenesis of chronic diarrhea may relate with the level of serum selenium decrease.Therapeutic selenium supplement is important in children with chronic diarrhea.

Objective To investigate the expression of the hypoxia-inducible factor (HIF)-1α in rat brain neurons and the intervention of β-sodium aescinate after restoration of spontaneous circulation (ROSC).Methods Sixty SD adult rats were randomly (random number) divided into 3 groups (n =20),namely experiment group,control group and sham operation group.(1) The rats of experiment group were injected intraperitoneally with β-sodium aescinate (5 mg/kg) immediately after ROSC.(2) The rats of control group received normal saline injected intraperitoneally instead of β-sodium aescinate solution.(3)The rats of sham operation group did not have cardiac arrest and β-sodium aescinate intervention.Cardiac arrest rat model was established by using asphyxiation and intra-venous potassium chloride solution.Blood samples were taken 1 h,6 h,12 h and 24 h after ROSC,and subsequently rats were sacrificed and their brain tissues were harvested.The expressions of HIF-1 α mRNA,vascular endothelial growth factor (VEGF)mRNA and erythropoitin (EPO) mRNA and their protein levels in rat brain neurons were detected by using RT-PCR and immunohistochemistry,and the levels of serum neuron-specific enolase (NSE) and S100β proteins were determined by using enzyme-linked immunosorbent assay.The t test or one-way ANOVA was used to assess overall differences among groups for each of the variables,followed by Bonferroni test for multiple comparisons.Pearson method was used for correlation analysis.Results Compared with the sham operation group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum S100β and NSE proteins were significantly increased in rats of the control group (P ＜ 0.05).Meanwhile,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in the control rats (P ＜0.05).Compared with the control group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum NSE and S100β proteins were significantly decreased in rats of the experiment group (P ＜ 0.05).Whereas,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in rats of the experiment group (P ＜0.05).HIF-1 α mRNA was positively correlated with EPO mRNA and VEGF mRNAs (r =O.866,P ＜0.05 ; r =0.952,P ＜ O.01).Conclusions The expression of hypoxia-inducible factor-1 α is increased in rat brain cells after ROSC,and β-sodium aescinate up-regulates the expression of hypoxia-inducible factor1 α mRNA and protein levels.The up-regulated expression of hypoxia-inducible factor-1α improves the resistance of brain cells to ischemia and hypoxia contributing neuronal protection,which might be due to upregulated EPO and VEGF expressions induced by hypoxia-inducible factor-1α.

Amifostine ; pharmacology ; Anemia, Aplastic ; chemically induced ; pathology ; prevention & control ; Animals ; Benzene ; toxicity ; Dose-Response Relationship, Drug ; Male ; Mice

Microglial cells are the resident immune cells of brain. The activated microglia produces a range of deleterious substances, which plays an important role in the inflammation of post-stroke, such as superoxide, nitric oxide, matrix metalloproteinases, etc. The activa-tion of microglia may involve triggering receptor expressed on myeloid cells-1, Toll-like receptors 4, peroxisome proliferator-activated re-ceptors, purinergic receptors, etc. Intervention targeted to microglial receptor is becoming a new strategy for ischemic stroke.