Objective:To compare the biomechanical effects between oblique Ban-pulling manipulation and lumbar erection-rotation manipulation in sitting position in treating lumbar intervertebral disc herniation (LIDH). Methods:A three-dimensional finite element model of L3-S1 was developed to carry out a comparative study between oblique Ban-pulling manipulation and lumbar erection and rotation manipulation in sitting position. The disc protrusion was assumed to be on the rear left of L4 disc, and the manipulations were performed on the right side. The loading process was simulated by two steps. In the first step, only the compression loading was imposed, and in the second step, both the compression loading and axial rotation moment were imposed. The displacement and stress distribution in L4 disc were investigated. Results:The values of stress and displacement in the second step were lower than those in the first step in each manipulation. The stress and displacement differences between the two steps were respectively 1.79 times and 3.03 times larger in oblique Ban-pulling manipulation than those in lumbar erection-rotation manipulation in sitting position. Conclusion: Oblique Ban-pulling manipulation may result in a better biomechanical effect than lumbar erection-rotation manipulation in sitting position for LIDH.

OBJECTIVETo study the effect of RAR-beta transfection plus treatment with the corresponding ligand ATRA on the proliferation and phenotype of platelet-derived growth factor (PDGF)-activated hepatic stellate cells (HSC).

METHODSPDGF-activated hepatic stellate cells of rats were transfected with eukaryotic expression vector pCMV-script-RAR-beta, which was verified by western blot. The proliferation of transfected HSC was assayed by BrdU incorporation as well as MTT methods. Their phenotype (alpha-SMA and desmin) was observed by immunocytochemistry assay with image analysis and RAR-beta protein expression was detected by western blot.

RESULTSTransfection of RAR-beta gene and treatment with ligand ATRA could increase the expression of RAR-beta protein for at least 144h and inhibit the proliferation and the expression of alpha-SMA and desmin in PDGF-activated HSC. Significant statistical differences were perceived comparing with sham-transfected, only-PDGF treated, non-ligand treated and irrelevant ligand-treated HSC.

CONCLUSIONSTransfected with RAR-beta gene as well as using related ligand ATRA could suppress the proliferation and reverse the activation phenotype of activated HSC.

Animals ; Blotting, Western ; Cell Division ; Liver ; cytology ; Phenotype ; Platelet-Derived Growth Factor ; pharmacology ; Rats ; Receptors, Retinoic Acid ; physiology ; Transfection ; Tretinoin ; pharmacology

This case report describes the diagnosis and endodontic therapy of maxillary fused second and third molars, using cone-beam computed tomography (CBCT). A 31-year-old Chinese male, with no contributory medical or family/social history, presented with throbbing pain in the maxillary right molar area following an unsuccessful attempted tooth extraction. Clinical examination revealed what appeared initially to be a damaged large extra cusp on the buccal aspect of the distobuccal cusp of the second molar. However, CBCT revealed that a third molar was fused to the second molar. Unexpectedly, the maxillary left third molar also was fused to the second molar, and the crown of an unerupted supernumerary fourth molar was possibly also fused to the apical root region of the second molar. Operative procedures should not be attempted without adequate radiographic investigation. CBCT allowed the precise location of the root canals of the right maxillary fused molar teeth to permit successful endodontic therapy, confirmed after 6 months.
Adult ; Cone-Beam Computed Tomography ; methods ; Follow-Up Studies ; Fused Teeth ; diagnostic imaging ; Humans ; Image Processing, Computer-Assisted ; methods ; Imaging, Three-Dimensional ; methods ; Male ; Maxilla ; Molar ; abnormalities ; Molar, Third ; abnormalities ; Pulpitis ; diagnostic imaging ; Root Canal Therapy ; Tooth Root ; abnormalities ; Tooth, Supernumerary ; diagnostic imaging ; Tooth, Unerupted ; diagnostic imaging

Objective Examination and evaluation of employee satisfaction index in the hospital performance evaluation.Methods Stratified sampling,field survey and telephone survey were used in customizing a questionnaire for two surveys in July and December 201 5 respectively.Results The standardized score of employee satisfaction was 86.252±1 5.1 53,and the lowest score was found in the canteen environment and food quality.Conclusion Employee satisfaction is found as good overall,and targeted measures are recommended to improve insufficiencies for better employee satisfaction.

AIMTo perpare and identify irisquinone hydroxypropyl-beta-cyclodextrin inclusion complex (irisquinone-HP-beta-CD), as well as to study the inclusion mechanism and molecule stoichiometry between irisquinone and hydroxypropyl-beta-cyclodextrin.

METHODSIrisquinone-HP-beta-CD was prepared by freeze-drying technique. The ratio of host and guest was also studied in inclusion process by mol gradient and continuing variational methods. At the same time, the inclusion complex was identified by X-ray diffraction (XRD) and differential scanning calorimetry (DSC).

RESULTSIt was demonstrated that the solubility of irisquinone was enhanced markedly by inclusion with HP-beta-CD when stoichiometry was 2:1 of host and guest at 25 degrees C, 35 degrees C and 45 degrees C.

CONCLUSIONThe solubility and stability of irisquinone could be increased by preparing the inclusion complex with hydroxypropyl-beta-cyclodextrin.

2-Hydroxypropyl-beta-cyclodextrin ; Benzoquinones ; administration & dosage ; chemistry ; Calorimetry, Differential Scanning ; Drug Compounding ; methods ; Drug Stability ; Freeze Drying ; Solubility ; X-Ray Diffraction ; beta-Cyclodextrins ; administration & dosage ; chemistry

OBJECTIVETo investigate the effect of semaphorin-3F (SEMA-3F) gene transient transfection on the proliferation of Tca8113 tongue carcinoma cells.

METHODSAfter construction of a full-length SEMA3F expression vector, Tca8113 cells were transient transfected with pEGFP-N1-SEMA3F by Lipofectamine 2000. The expression of SEMA-3F gene was detected by RT-PCR The differences of the expression in the transfected cell groups, empty vector groups and un-transfected cell groups were compared. The survival rates were assayed by methyl thiazolyl tetrazolium (MTT) enzymatic labeling technique. Cell cycle were assayed by flow cytometer (FCM).

RESULTSThe gene was transfected into Tca8113 cells. High expression of SEMA-3F was successfully detected in the transfected cell groups after gene transfection. The cell cycle percentage of G1 stage decreased and S stage increased.

CONCLUSIONSSEMA-3F gene transient transfection may inhibit the proliferation of Tca8113 cells.

Carcinoma, Squamous Cell ; genetics ; metabolism ; pathology ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Genetic Vectors ; Humans ; Membrane Proteins ; genetics ; metabolism ; Nerve Tissue Proteins ; genetics ; metabolism ; Tongue Neoplasms ; genetics ; metabolism ; pathology ; Transfection

The uracil in DNA comes from either the misincorporation of dUTP in place of dTTP or deamination of cytosine. In the latter case, it can result in a GC to AT transition mutation if the uracil is not removed before DNA replication. Base excision repair (BER) is a major pathway for removing DNA lesions arising from endogenous processes as well as those induced by exposure to exogenous chemicals or irradiation. BER is initiated by DNA glycosylases that excise aberrant bases from DNA by cleavage of the N-glycosidic bond linking to the base of its deoxyribose sugar. Uracil N-glycosylase (UNG) is the enzyme responsible for the first step in the BER pathway that specifically removes uracil from DNA. The UNG gene undergoes both temporal and spatial regulation mainly at the level of transcription. Normally cancer cells undergo over-proliferation and up-regulate their UNG during tumorigenesis. In this study we examine the correlation between UNG level and carcinogenesis, and explore the possibility of using UNG as a marker for cancer diagnosis. Human UNG gene was amplified from the total RNA of the human choriocarcinoma cell line, JEG-3, by RT-PCR. After purification, the 942bp full-length UNG cDNA coding sequence was digested with EcoR I and Sal I, and cloned into the digested pET-21 to construct a recombinant vector, pUNG. The UNG protein was expressed under the control of T7 promoter in E. coli BL21 (DE3) cells induced with IPTG. After ultrasonic treatment, the cell lysate and precipitate were analyzed by SDS-PAGE and a 39kD band was detected. The plasmid was serially diluted at appropriate concentrations and employed as standards in the subsequent quantification. Total RNAs were extracted from 18 pairs of clinical samples, each pair contains a sample of esophageal squamous cell carcinoma (ESCC) tissue and its surrounding normal esophageal epithelia. The copy numbers of UNG mRNA in these RNA samples were determined by real-time quantitative RT-PCR using a Lightcycler (Roche). UNG was present in 13 cases of ESCC (13/18, n = 18) but absent in all of the normal tissues. The results indicated that there was a correlation between high level of UNG expression and the carcinogenesis of ESCC.
Carcinoma, Squamous Cell ; genetics ; metabolism ; Cell Line, Tumor ; Cloning, Molecular ; Electrophoresis, Polyacrylamide Gel ; Esophageal Neoplasms ; genetics ; metabolism ; Humans ; In Vitro Techniques ; Reverse Transcriptase Polymerase Chain Reaction ; Uracil-DNA Glycosidase ; genetics ; metabolism

OBJECTIVESTo screen differential proteins in serum from hepatocellular carcinoma (HCC) patients by Proteomic Technology and to purify and identify them.

METHODSSurface enhanced laser desorption Ionization time of flight-mass spectrum (SELDI-TOF-MS) was employed to screen differential proteins in serum from 33 HCC patients and 33 control cases, and then to purify and identify them using isoelectric precipitation, Tricine sodium dodecyl sulphate polyacrylamide gel electrophoresis (Tricine-SDS-PAGE) and high performance liquid chromatography tandem Mass Spectrum (HPLC-MS).

RESULTS65 protein peaks in the range of relative molecular weight from 2,000 to 10,000 were found significant difference (P less than 0.05) between the patient group and control group. Based on these differential protein peaks, diagnostic model for HCC detection was established and its sensitivity and specificity were 100% and 96.97% respectively. Proteins with 8,706.5 and 8,579.2 relative molecular weights (the t value was 2.562 and 2.783 respectively, and P value was 0.013 and 0.015 respectively) out of the 65 differential proteins were purified and identified, and then recognized as Apolipoprotein AII (Apo AII).

CONCLUSIONApo AII is probably a differential protein of HCC and maybe related to the pathogenesis of HCC.

Apolipoprotein A-II ; isolation & purification ; Blood Proteins ; analysis ; Carcinoma, Hepatocellular ; blood ; Case-Control Studies ; Humans ; Liver Neoplasms ; blood ; Proteomics ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

Objective: To investigate the role of surfactant associated protein-A (SP-A) in the development and progression of silicosis, and its mechanism. Methods: Homozygous and heterozygous mice of SP-A knockout of specific pathogen free (SPF) grade were selected for mating, and mice with SP-A^-/- genotype were selected for subsequent experiments. SP-A wild-type (SP-A^+/+) and SP-A^-/- mice were divided into SP-A^+/+ control group, SP-A^-/- control group, SP-A^+/+ silicosis group and SP-A^-/- silicosis group with six mice in each group by random number table method. Mice in both silicosis groups were given 20.0 μL 250 g/L silica suspension by tracheal exposure, and mice in both control groups were injected with 0.9% sodium chloride solution at the same volume. On the 28th day after modeling, mice were sacrificed. Lung tissues were used for lung histopathology examination. The apoptosis of alveolar type Ⅱ epithelial cells of mice was detected by TUNEL method. The mRNA expression of B-lymphoblastoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), cysteinyl aspartate specific proteinase (Caspase)-3 and Caspase-9 in lung tissues of mice was detected by quantitative real-time polymerase chain reaction. Results: The histopathological result of mice showed that thickened alveolar septum, scattered silicon nodule and collagen fiber formation were observed in the mice lungs of SP-A^+/+ silicosis group, and a large number of inflammatory cells were observed in silicosis nodule, after exposure to silica dust. SP-A^-/- silicosis group resulted in a more severe pulmonary inflammation and interstitial fibrosis compared to SP-A^+/+ silicosis group. The apoptosis of alveolar type Ⅱ epithelial cells and the mRNA relative expression levels of Bax, Caspase-3 and Caspase-9 in lung tissues of mice in each silicosis groups were increased compared with their control groups (all P<0.05). The above four indexes of mice in SP-A^-/- silicosis group were higher than those in SP-A^+/+ silicosis group (all P<0.05). There was no significant difference in the expression of Bcl-2 mRNA in lung tissues of these four groups (P>0.05). Conclusion: Knockout of SP-A can aggravate inflammation and pulmonary fibrosis in silicosis model mice, and promote apoptosis of alveolar type Ⅱ epithelial cells. The mechanism may be related to the Bcl-2/Bax/Caspase-3 signaling pathway which affects the apoptosis of mitochondrial pathway.

OBJECTIVETo detect the adenomatous polyposis coli (APC) gene germline mutation in the proband and her family members with familial adenomatous polyposis (FAP).

METHODSThe diagnosis of a patient with FAP was validated by colonoscopy, pathology and the family history. The systematic screening with multiplex ligation-dependent probe amplification (MLPA), denaturing high-performance liquid chromatography (DHPLC) and DNA sequencing were carried out to detect APC gene germline mutations.

RESULTSA novel mutation c.1999 C >T (Q667X) of APC, which leads to premature termination of the protein, was identified in this family. This mutation manifested an aggressive form of FAP with early onset of colorectal adenocarcinoma and colonic adenoma.

CONCLUSIONThe mutation of APC Q667X is the cause of clinical phenotype of this family with FAP, and the prophylactic colectomy for the affected family members should be considered.

Adenomatous Polyposis Coli ; genetics ; Adenomatous Polyposis Coli Protein ; genetics ; Adolescent ; Adult ; Base Sequence ; Child ; Chromatography, High Pressure Liquid ; DNA Mutational Analysis ; Female ; Germ-Line Mutation ; Humans ; Male ; Middle Aged ; Pedigree ; Phenotype ; Polymerase Chain Reaction