BACKGROUND:Age and dental age are shown to have some limitations in predicting skeletal maturity.
OBJECTIVE:To compare the mandibular length in boys and girls with Class I and Class II skeletal patterns by using the cervical vertebrae maturation, and to provide valid reference index for orthodontical treatment.
METHODS:The lateral cephalograms of the 160 cases of Class I (40 males and 40 females) and Class II (40 males and 40 females) skeletal patterns, aged 8-15 years, were taken before orthodontic treatment. The sample was grouped according to stages of the cervical vertebrae maturation (Hasse and Farman method), and the mandibular length was measured separately. The results were statistical y analyzed by the independent-sample t test.
RESULTS AND CONCLUSION:No matter you are a male or female, the mandibular length of Class I was greater than that of Class II at the early stages of growth and development. In the Class I pattern, the mandibular lengths of boys were greater than those of girls at accelerated, transition, and deceleration stages (P<0.05), whereas in the Class II pattern, the mandibular lengths of boys were greater than those of girls at accelerated, transition, and deceleration stages (P<0.05). The present results indicate a sexual dimorphism in the mandibular length at almost al stages of bone maturation, but the possibility of a later“catch up”growth period occurs on Class II girls. And this information has important orthodontic clinical implications.

The palliative care has become an important part of social civilization. Its treatment of advanced patients with no response to the treatment of patients with positive and comprehensive care, paying attention to the people-oriented conforms to the Chinese nationHeperfectly. In palliative care practice,Heconcept penetrates in the happening of the disease and development, treatment and special and complex and changeful in interpersonal relationship. The ultimate goal of He is also a palliative care. The concept of reconciliation will promote the development of palliative care.

Carrying out researches in urban community health service centers can effectively promote the improvement of management system, the cultivation of talents and the formation of characteristic service, leading to the institutional development.This paper summarizes the role and significance of researches in promoting the overall development of urban community health service center in order to provide reference for the relevant medical institutions based on the experiences in Shanghai Fenglin Community Health Service Center.

Aim To explore the effect of survivin in PC12 cells against injuries induced by cobalt chloride(CoCl_2).Methods PC12 cells were exposed to CoCl_2 at different doses in different time to set up the chemical hypoxia induced PC12 cells injuries model.Cell viability was tested by using cell counter kit-8.Dose-effect(200～1 000 μmol·L~(-1))and time-effect(0～48 h)relationship between hypoxia induced by CoCl_2 and the expression of survivin was evaluated by western blot.Results PC12 cells viability was inhibited significantly by CoCl_2 in a dose and time dependent manners;At the concentrations from 200 to 600 μmol·L~(-1) CoCl_2 for 24 h,survivin expression was upregulated in a dose dependent manner,peaking at 600 μmol·L~(-1) CoCl_2 treatment,exceeding this concentration of CoCl_2,with dose increasing,survivin expression decreased.At the dose of CoCl_2 up to 1 000 μmol·L~(-1),survivin did not express basically;Treatment with 600 μmol·L~(-1) CoCl_2 in different time,within the range of 0～36 h,the expression of survivin enhanced in time dependent manner.But with the extension of time,survivin expression was declining; 17-allylamino-17-demethoxygeldanamycin (2 μmol·L~(-1)),an inhibitor of Hsp90,not only decreased survivin overexpression but also obviously enhanced the injuries of PC12 cells induced by CoCl_2,which didn't damage PC12 cells alone.Conclusion Upregulation of survivin expression may be one of the endogenous defense mechanisms for PC12 cells against chemical hypoxia.

[Objective] To explore the cytoprotecfion of hydrogen sulfide (H_2S) against cobalt chloride (CoCl_2)-induced apeptosis in PC12 cells and the underlying mechanisms. [Methods] CoCl_2 (a chemical hypoxia-mimetic agent) was used to establish the chemical hypoxia-induced PC12 cell injuries model. Sodium hydrosulfide (NaHS) was used as a H_2S donor. The viability of PC12 cells was measured by CCK-8 assay. The percentage of apeptotic cells was assessed by propidium iodide stain flow cytometry (FCM). The morphological change of apeptotic cells was tested by using the chromatin dye Hoechst 33258. The mitochondrial membrane potential (MMP) was analyzed by rhodamine 123 staining and photofluorography. The level of reactive oxygen species (ROS) in PC12 cells was measured by DCFH-DA staining and photofluorography. [Results] CoCl_2 induced a decrease in cell viability and an increase in percentage of apeptosis in PC12 cells along with dissipation of MMP as well as overproduction of ROS. When PC12 cells were treated with Naris 30 min before CoCl_2 treatment a decrease in viability of PC12 cells induced by 600 μmol/L CoCl_2 was concentration-dependently blocked by NaHs (100, 200, and 400 μmol/L). Pretreatment with NaHS at 200 and 400 μmol/L obviously reduced the apepetotic percentage of PC12 cells induced by 600 μmol/L CoCl_2 and inhibited the dissipation of MMP and overproduction of ROS. [Conclusion] H_2S protected PC12 cells against CoCl_2-induced apeptosis, which may be associated with the inhibition of H_2S on the dissipation of MMP and overproduction of ROS induced by CoCl_2.

Objective To estimate the influences of N-acetyl cysteine (NAC) on a chemical hypoxiamimetic agent CoCl2 induced-injury to, and expressions of inflammatory factors by, an immortal human skin keratinocyte line HaCaT. Methods HaCaT cells were treated with CoCl2 of 2000 μmol/L for 4 hours to set up a chemical hypoxia-induced cell model of skin injury. NAC of various concentrations ( 1000, 2000, 3000 μmol/L)was used to pretreat HaCaT cells for 2 hours prior to the establishment of cell model. After these treatments,cell viability was detected by cell counting kit 8 (CCK-8), the levels of interleukin 6 and 8 (IL-6 and -8) and tumor necrosis factor α (TNF-α) in culture supernatant by ELISA kits, mitochondrial membrane potential (MMP) by rhodamine 123 (Rh123) staining and photofluorography, intracellular reduced glutathione (GSH)content by glutathione detection kit. Results An obvious decline was observed in HaCaT cell viability after pretreatment with various concentrations of NAC for 2 hours. The treatment with CoCl2 of 2000 μmol/L for 4 hours induced an elevation in the supernatant levels of IL-6, IL-8 and TNF-α and a decrease in GSH content and MMP, while the pretreatment with NAC for 2 hours retarded the CoCl2-induced increase in IL-6 and IL-8 levels as well as decrease in GSH content and MMP. Conclusion The reactive oxygen species (ROS) scavenger NAC can protect against CoCl2-induced injury to and inflammatory reaction in HaCaT cells, which may be associated with a decrement in oxidative stress.

AIM:To investigate the role of canonical transient receptor potential channel 1 ( TRPC1 ) in the migration of human bronchial epithelial cells (16HBE) induced by transforming growth factor-β1 ( TGF-β1).METH-ODS:Silencing of TRPC1 gene expression was performed by siRNA.The cell activity and apoptosis were measured by CCK-8 assay and flow cytometry, respectively.The migration and invasion abilities of the 16HBE cells were detected by wound-healing assay and Transwell assay.The protein expression of E-cadherin and vimentin was determined by Western blot.RESULTS:TGF-β1 treatment significantly enhanced the cell migration distance compared with control groups ( P<0.01 ) .The results of CCK-8 assay and flow cytometry indicated that there were no significant difference in proliferation and apoptosis among TRPC1 siRNA group, TGF-β1 group and control group (P>0.05).The results of wound-healing and Tr-answell assays showed that migration and invasion abilities in TRPC1 siRNA +TGF-β1 group were markedly suppressed compared with TGF-β1 group (P<0.01).The protein expression of E-cadherin and vimentin induced by TGF-β1 was in-hibited by TRPC1 silencing compared with TGF-β1 group (P<0.05).CONCLUSION:TRPC1 is involved in the migra-tion of human bronchial epithelial cells induced by TGF-β1 through regulating the protein expression of E-cadherin and vim-entin.

[ ABSTRACT] AIM:To investigate the effect of hydrogen sulfide ( H2 S) on airway inflammation induced by ozone (O3) exposure and its mechanisms.METHODS:C57BL/6 mice (n=32) were randomly divided into control group, O3 group, NaHS+O3 group and NaHS group.The mice in O3 group and O3 +NaHS group were exposed to 2.14 mg/m3 O3 for 3 h on days 1, 3 and 5, while the mice in control group and NaHS group were exposed to filtered air .NaHS (14μmol/kg) was administered intraperitoneally to the mice in NaHS group and O 3 +NaHS group 30 min before each exposure .After the last exposure for 24 h, the airway responsiveness was determined , and bronchoalveolar lavage fluid ( BALF) was collected for counting inflammatory cells and measuring total protein concentration .The lung tissues were collected for observing the morphological changes with HE staining .The levels of interleukin-6 ( IL-6 ) , interleukin-8 ( IL-8 ) , malondialdehyde ( MDA) and NF-κB p65 protein in the lungs were determined .RESULTS: Compared with control group , the airway re-sponsiveness, inflammatory cells, protein concentration, inflammation score, levels of IL-6, IL-8, MDA and NF-κB p65 in O3 group increased significantly , but these in NaHS+O3 group decreased compared with O 3 group.CONCLUSION: The present findings suggest that H 2 S attenuates O3 induced airway inflammation by inhibiting NF-κB expression and preventing lipid peroxidation .

AIM:To investigate the ability of a metal complex ammonium tetrathiomolybdate (ATTM) to re-lease H2 S and its cytoprotective effect on an oxidative injury model .METHODS:Released H2 S was absorbed in a reaction flask from ATTM dissolved in the cell medium .Staining with dichlorodihydrofluorescein diacetate or rhodamine 123 fol-lowed by photofluorography was conducted for the observation of reactive oxygen species ( ROS) and mitochondrial mem-brane potential (ΔΨm) levels, respectively.Cell viability and release of lactate dehydrogenase (LDH) from the cells were measured with commercial kits.RESULTS:Similar to another H2S donor GYY4137, ATTM had an ability to release H2S in the cell medium in a dose-dependent manner .Treatment of human skin HaCaT cells with ATTM at concentrations of 25~400 μmol/L didn’ t significantly alter cell viability .Exposure of the cells to ultraviolet rays or a ROS donor H 2 O2 in-creased the intracellular ROS levels .Treatment with 400 μmol/L H2 O2 significantly reduced the viability of HaCaT cells (P<0.01).However, before the treatment with H2O2, pretreatment with ATTM at 100 and 200 μmol/L markedly pre-vented the H2O2-induced cell injury (P<0.01).In addition, the treatment with H2O2 triggeredΔΨm loss (P<0.01) and LDH release from the cells (P<0.01).Prior to suffering from H2O2 injury, the preconditioning with 200 μmol/L ATTM significantly improved ΔΨm levels ( P<0.05 ) and attenuated LDH release from the cells ( P<0.01 ) .CONCLUSION:ATTM is capable of releasing H 2 S and protecting human skin cells against oxidative injury .

[ ABSTRACT] AIM:To investigate the role of canonical transient receptor potential channel 1 ( TRPC1 ) in the epithelial-mesenchymal transition ( EMT) of human bronchial epithelial ( HBE) cells induced by transforming growth fac-tor-β1 (TGF-β1).METHODS:EMT of 16HBE cells induced by TGF-β1 were identified by microscopy, immunofluores-cence and Western blotting.Immunofluorescence, real-time PCR and Western blotting were applied to detect the mRNA and the protein expression of TRPC1 in the 16HBE cells.The influence of SKF96365 (a TRPC1 blocker) and siRNA-me-diated silencing of TRPC1 on the EMT of the 16HBE cells were detected by microscopy and Western blotting.RESULTS:Treatment with TGF-β1 induced significant morphological changes of the 16HBE cells.Exposure to TGF-β1 decreased the expression of E-cadherin protein (P<0.01) and increased the expression of α-SMA protein (P<0.05) in the 16HBE cells.Immunofluorescence observation indicated that TRPC1 expression in the 16HBE cells was positive.The expression of TRPC1 at mRNA and protein levels was significantly increased in the 16HBE cells after stimulation with TGF-β1 ( P<0.05).The morphological changes of the 16HBE cells induced by TGF-β1 were inhibited by SKF96365 and TRPC1 silen-cing compared with TGF-β1 group.The protein expression of E-cadherin andα-SMA induced by TGF-β1 were inhibited by SKF96365 and TRPC1 silencing compared with TGF-β1 group (P<0.05).CONCLUSION:TGF-β1 induces EMT with the mechanism of up-regulating TRPC1 in human bronchial epithelial cells.