OBJECTIVE: To investigate the effect of periostin on hypoxia-induced oxidative stress and apoptosis in human periodontal ligament fibroblasts and the molecular mechanism involved. METHODS: cultured human periodontal ligament fibroblasts were placed in an anaerobic gas-producing bag for hypoxia treatment for 48 h followed by treatment with periostin at low (25 ng/mL), moderate (50 ng/mL) or high (100 ng/mL) doses. MTT assay was used to measure the cell viability, and the cell apoptosis rate was determined using flow cytometry. The contents of IL-1β, IL-6 and TNF-α in the cells were determined with ELISA, and ROS levels were measured using a fluorescent plate reader. The intracellular SOD activity was detected using ELISA. The expressions of HIF-1α, P21, cyclin D1, Bax, cleaved caspase-3, Bcl-2, P38MAPK and p-p38 MAPK proteins in the cells were detected with Western blotting. RESULTS: Hypoxia treatment significantly reduced the cell viability ( < 0.05), increased P21, Bax, and cleaved caspase-3 protein levels ( < 0.05), promoted cell apoptosis ( < 0.05), and decreased cyclin D1 and Bcl-2 protein levels ( < 0.05) in the cells. Compared with the hypoxic group, the cells treated with periostin at different concentrations showed significantly increased cell viability ( < 0.05) with significantly lowered apoptotic rates ( < 0.05) and decreased expression levels of Bax and cleaved caspase-3 ( < 0.05) but significantly increased expression levels of cyclin D1 and Bcl-2 ( < 0.05). Hypoxic exposure of the cells resulted in significantly increased expression levels of HIF-1α and p-p38 MAPK ( < 0.05) and increased levels of IL-1β, IL-6, TNF-α and ROS ( < 0.05) but decreased SOD activity ( < 0.05). Periostin treatment at different concentrations significantly lowered the expression levels of HIF-1α and p-p38 MAPK ( < 0.05) and the levels of IL-1β, IL-6, TNF-α and ROS ( < 0.05) and significantly increased SOD activity in the hypoxic cells ( < 0.05). CONCLUSIONS Periostin promotes the proliferation, inhibits apoptosis, enhances cellular antioxidant capacity, and reduces inflammatory damage in human periodontal ligament fibroblasts exposed to hypoxia possibly by inhibiting the activation of the p38 MAPK signaling pathway.
Apoptosis ; drug effects ; Cell Adhesion Molecules ; administration & dosage ; Cell Hypoxia ; Fibroblasts ; drug effects ; Humans ; Oxidative Stress ; drug effects ; Periodontal Ligament ; cytology ; Signal Transduction ; drug effects ; p38 Mitogen-Activated Protein Kinases

OBJECTIVE: To investigate the effect of periostin on hypoxia-induced oxidative stress and apoptosis in human periodontal ligament fibroblasts and the molecular mechanism involved. METHODS: cultured human periodontal ligament fibroblasts were placed in an anaerobic gas-producing bag for hypoxia treatment for 48 h followed by treatment with periostin at low (25 ng/mL), moderate (50 ng/mL) or high (100 ng/mL) doses. MTT assay was used to measure the cell viability, and the cell apoptosis rate was determined using flow cytometry. The contents of IL-1β, IL-6 and TNF-α in the cells were determined with ELISA, and ROS levels were measured using a fluorescent plate reader. The intracellular SOD activity was detected using ELISA. The expressions of HIF-1α, P21, cyclin D1, Bax, cleaved caspase-3, Bcl-2, P38MAPK and p-p38 MAPK proteins in the cells were detected with Western blotting. RESULTS: Hypoxia treatment significantly reduced the cell viability ( < 0.05), increased P21, Bax, and cleaved caspase-3 protein levels ( < 0.05), promoted cell apoptosis ( < 0.05), and decreased cyclin D1 and Bcl-2 protein levels ( < 0.05) in the cells. Compared with the hypoxic group, the cells treated with periostin at different concentrations showed significantly increased cell viability ( < 0.05) with significantly lowered apoptotic rates ( < 0.05) and decreased expression levels of Bax and cleaved caspase-3 ( < 0.05) but significantly increased expression levels of cyclin D1 and Bcl-2 ( < 0.05). Hypoxic exposure of the cells resulted in significantly increased expression levels of HIF-1α and p-p38 MAPK ( < 0.05) and increased levels of IL-1β, IL-6, TNF-α and ROS ( < 0.05) but decreased SOD activity ( < 0.05). Periostin treatment at different concentrations significantly lowered the expression levels of HIF-1α and p-p38 MAPK ( < 0.05) and the levels of IL-1β, IL-6, TNF-α and ROS ( < 0.05) and significantly increased SOD activity in the hypoxic cells ( < 0.05). CONCLUSIONS Periostin promotes the proliferation, inhibits apoptosis, enhances cellular antioxidant capacity, and reduces inflammatory damage in human periodontal ligament fibroblasts exposed to hypoxia possibly by inhibiting the activation of the p38 MAPK signaling pathway.
Apoptosis ; Fibroblasts ; Humans ; Hypoxia ; Oxidative Stress ; Periodontal Ligament ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases

Objective:To investigate the association between the parameters of thin-section computed tomography and the invasion and histological subtypes of subsolid nodules measuring 1-2 centimeters in diameter as lung adenocarcinoma.Methods:We retrospectively reviewed the cases with subsolid nodules measuring 1-2 centimeters on thin-section computed tomography and histologically confirmed as lung adenocarcinoma.Results:A total of 135 patients were enrolled in this study, including 23 with pure ground glass nodules and 112 with part-solid ground glass nodule. We observed significant differences of nodule size, solid component size, consolidation-to-tumor ratio, nodule attenuation and attenuation ratio( P<0.0001). The receiver operating curve indicated certain predictive value of solid component size, nodule attenuation and attenuation ratio: AUC were 0.838(0.756-0.919)、0.823(0.729-0.917) and 0.820(0.726-0.914), respectively. Of the invasive adenocarcinoma, those with solid or micropapillary components merely showed a significance in solid component size( P=0.024). Conclusion:The parameters of thin-section computed tomography of 1-2 centimeters subsolid nodules showed significant differences in varied invasiveness of lung adenocarcinoma, and these could have certain predictive value.

Objective : To explore diagnostic value of ankle brachial index (ABI) combined carotid intima‐media thickness (IMT) for CHD in aged patients with DM.Methods :A total of 198 aged DM patients were selected ,including 101 patients complicated with CHD (complicated CHD group ) and 97 non‐CHD patients (pure DM group ).According to number of diseased coronary vessels ,complicated CHD group was further divided into single vessel group (n＝29) ,double vessel group (n＝41) and multi‐vessel group(n＝31).Another 104 healthy aged people were enrolled as healthy control group simultane‐ously.Abnormal ABI rate (percentage of ABI＜0.9) and IMT were measured and compared among all groups .With coro‐nary angiography (CAG) as gold standard ,diagnostic value of single and combined detection of ABI and IMT for CHD were analyzed .Results :Compared with healthy control group ,there were significant rise in abnormal ABI rate (30.7% vs. 53.6% vs.69.3%) and IMT [(0.78 ± 0.46)mmvs.(1.14 ± 0.53)mm vs.(1.46 ± 0.38)mm]in pure DM group and com‐plicated CHD group ,and those of complicated CHD group were significantly higher than those of pure DM group , P＜0.05 or ＜0.01. Compared with single vessel group ,there was significant rise in abnormal ABI rate (51.7% vs.87.1%) in multi‐vessel group , P＝0.003 ;significant rise in IMT [(1.21 ± 0.42)mmvs.(1.42 ± 0.34)mmvs.(1.68 ± 0.36) mm]in double vessel group and multi‐vessel group ,and that of multi‐vessel group was significantly higher than that of double vessel group , P＜0.05 or ＜0.01. Sensitivity and specificity of single detection of ABI＜0.9 was 55.6% and 82.2% respectively in diagnosing CHD ;it′s 59.1% and 71.4% respectively for single detection of thickened IMT ;for combined detection ,sen‐sitivity can reach 84.51%(ABI＜0.9 or thickened IMT) and sensitivity can reach 88.91%(ABI＜0.9 combined thickened IMT).Conclusion :ABI combined IMT possesses high diagnostic value screening CHD in aged DM patients ,which is worth extending.

It is not fully clear why there is a higher contribution of pluripotent stem cells (PSCs) to the chimera produced by injection of PSCs into 4-cell or 8-cell stage embryos compared with blastocyst injection. Here, we show that not only embryonic stem cells (ESCs) but also induced pluripotent stem cells (iPSCs) can generate F0 nearly 100% donor cell-derived mice by 4-cell stage embryo injection, and the approach has a "dose effect". Through an analysis of the PSC-secreted proteins, Activin A was found to impede epiblast (EPI) lineage development while promoting trophectoderm (TE) differentiation, resulting in replacement of the EPI lineage of host embryos with PSCs. Interestingly, the injection of ESCs into blastocysts cultured with Activin A (cultured from 4-cell stage to early blastocyst at E3.5) could increase the contribution of ESCs to the chimera. The results indicated that PSCs secrete protein Activin A to improve their EPI competency after injection into recipient embryos through influencing the development of mouse early embryos. This result is useful for optimizing the chimera production system and for a deep understanding of PSCs effects on early embryo development.
Activins ; metabolism ; Animals ; Cells, Cultured ; Embryonic Development ; Germ Layers ; metabolism ; Mice ; Pluripotent Stem Cells ; cytology ; metabolism

Objective To study the effects of serum C-type natriuretic peptide (CNP) ,insulin-like growth factor II (IGF-Ⅱ ) , endothelin (ET) ,neuron-specific enolase (NSE) and S100B protein(S100B) on the prognosis of the patients with traumatic brain injury .Methods A total of 110 patients with craniocerebral trauma admitted in our hospital from January 2016 to January 2017 se-lected as the craniocerebral trauma group and further divided into the mild ,moderate and severe craniocerebral trauma groups ac-cording to the Glasgow Coma Scale (GCS) .Then the levels of serum CNP ,IGF-Ⅱ ,ET ,NSE and S100B in all cases were analyzed by enzyme-linked immunosorbent assay (ELISA) .Their influence on the prognosis of the patients with craniocerebral trauma and the correlation among various indicators were analyzed .Results The levels of CNP and IGF-Ⅱat admission in the craniocerebral trauma group were significantly decreased ,while the levels of ET ,NSE and S100B were significantly increased ,the difference com-pared with the control group was statistically significant (P<0 .05) .Serum CNP and IGF-Ⅱlevels in the death group ,plant survival group and disabled group were significantly decreased .The difference was statistically significant (P<0 .01) .Serum CNP and IGF-Ⅱlevels in the moderate and severe craniocerebral trauma groups were gradually increased with the disease course progress ,while serum ET ,NSE and S100B levels were gradually decreased with the disease course progress ,the difference was statistically signifi-cant(P<0 .05) .In the patients with craniocerebral trauma ,the positive correlation existed between CNP and IGF-Ⅱ ,between ET and S100B ,between ET and NSE ,and between NSE and S100B(P<0 .01) ,while the negative correlation existed between IGF-Ⅱand ET ,between IGF-Ⅱ and S100B ,between CNP and ET ,and between IGF-Ⅱand NSE (P<0 .01) .Conclusion Serum CNP , IGF-Ⅱ ,ET ,NSE and S100B are correlated to the severity of craniocerebral trauma ,which has a higher clinical application value for judging the disease condition ,evaluating the prognosis in cradiocerebral trauma .

OBJECTIVETo conduct genetic diagnosis for a family in which no exonic deletions and duplications of the dystrophin gene were detected.

METHODSPotential exonic deletions and duplications of the dystrophin gene were initially analyzed with using multiplex ligation-dependent probe amplification (MLPA). Subsequently, all of the 79 exons of the dystrophin gene of the proband and a pregnant woman from the family were analyzed with PCR amplification and DNA sequencing. Following identification of the causative mutation, prenatal diagnosis was provided.

RESULTSMLPA analysis had detected no exonic deletions and duplications of the dystrophin gene. Sequence analysis has identified a C>T mutation on the 22nd nucleotide position of the 70th exon of the dystrophin gene (c.10108 C>T), which has replaced the codon CGA to a stop codon (TGA). The patient's mother and sister were both heterozygous for the same mutation. Upon prenatal diagnosis, the fetus was found to be positive for the Y chromosome sex-determining gene (SRY) and has carried above mutation. The result of short tandem repeat linkage analysis also confirmed that the fetus has inherited the mutant X chromosome.

CONCLUSIONThe causative mutation of the dystrophin gene has been discovered in an affected family, which has enabled prenatal diagnosis of the disease.

Child, Preschool ; Dystrophin ; genetics ; Exons ; Gene Deletion ; Gene Duplication ; Humans ; Male ; Microsatellite Repeats ; Multiplex Polymerase Chain Reaction ; Mutation

Objective To analysis the role of adiponectin, insulin like growth factor -1 in elderly chronic heart failure.Methods 92 elderly patients with chronic heart failure were selected and divided into control group and experiment group.46 cases of the control group were treated with conventional treatment including strong heart, diuresis, vasodilator,lowering blood pressure, the experimental group was on the basis of routine treatment with catechin, 50 mg/kg orally, 1 times a day.2 weeks as a course, 1 course of treatment.Adiponectin, insulin like growth factor -1,BNP,LVEDD, LVESD and LVEF were compared before and after treatment.Results After treatment, the total effective rate of observation group was 93.48%, the control group total effective rate was 76.09%.The total effective rate of observation group was significantly higher than that of the control group (χ2 =5.39, P <0.05 ).After treatment, BNP, Adp in two groups decreased, IGF-1 increased, compared with control group, BNP, Adp level of the experiment group were lower, IGF-1 was higher(P<0.05),and LVEDD and LVESD of the experiment were lower, LVEF was higher, (P<0.05). Conclusion Catechins can decrease the serum levels of adiponectin, elevate insulin like growth factor-1, improve the degree of heart failure, is worthy of clinical application.

The quality of traditional Chinese medicine (TCM) is the concentrated reflection of its pharmaceutical value. We should pay attention to the quality of Chinese medicine because it is the core problem for the development of traditional Chinese medicine. Thequality of traditional Chinese medicine is the important connotation of Chinese medicine professional high-level personnel training. Thequality of Chinese medicine has become a priority of degree and diploma education in different levels of traditional Chinese medicine class specialized courses. The quality of Chinese medicine is an important content of traditional Chinese medicine curriculum system and includes the knowledge of Chinese traditional medicine quality factor, quality requirements, quality characteristics, quality management and quality evaluation, etc. This paper mainly discusses thequality of Chinese traditional medicine curriculum structure, textbook compilation and talent cultivation.