Objective To evaluate the clinical efficacy of percutaneous haemostat stroke-poking reduction and elastic intramedullary nailing for pediatric radial neck fractures of O'Brien types Ⅱ & Ⅲ.Methods From January 2014 to June 2016,38 children (23 boys and 15 girls) with radial neck fracture of O'Brien type u or Ⅲ were treated by percutaneous haemostat stroke-poking reduction and elastic intramedullary nailing in our department.We had 26 left and 12 right sides.Their ages ranged from 5 to 14 years,averaging 8.6 years.All fractures were fresh.According to O'Brien classification,22 cases were type Ⅱ and 16 type Ⅲ.The operation time,frequency of intraoperative C-arm fluoroscopy,frequency of percutaneous haemostat stroke-poking reduction,and union time were recorded.The elbow function was assessed one day before removal of internal implants according to the Métaizeau scoring system.Results All operations succeeded,lasting from 12 to 25 min (average,16.4 min).The frequency of intraoperative fluoroscopy ranged from 3 to 11 times (average,6.4 times);the frequency of intraoperative percutaneous reduction ranged from 1 to 4 times (average,2.3 times).The patients were followed up for 6 to 22 months (average,1 1.2 months).Postoperative X-ray films showed satisfactory alignment of the fracture ends.All fractures demonstrated clinical and radiographic evidence of complete healing after a mean time of 58 days (from 38 to 72 days).The Métaizeau scoring showed 33 excellent,4 good and one fair cases,yielding an excellent to good rate of 97.4％.Follow-ups revealed no infection,implants breakage,nonunion,fracture redisplacement,or iatrogenic radial nerve injury.Conclusions As percutaneous haemostat stroke-poking reduction can increase the probability of successful reduction at first attempt,reduce frequency of close reduction and X-ray exposure for both children and medical staff,and shorten operation time,the procedure is effective,simple,reliable and minimally invasive,leading to fewer complications.

Objective: To summarize the clinical data of elastic stable intramedullary nailing(ESIN) in the treatment of long bone fracture of children in a single medical center, and to analyze the problems occurred after the ESIN surgery and corresponding solutions. Methods: A retrospective analysis was conducted regarding the clinical data of 2 133 pediatric long bone fractures conforming to inclusion and exclusion criteria from June, 2005 to December, 2017 in Department of Orthopedics, Children′s Hospital of Nanjing Medical University.There were 1 191 boys and 942 girls, aged from 23 months to 14 years with mean age of (5.7 ± 3.1)years.There were 1 866 cases treated with closed reduction with ESIN, while 267 cases were treated with small incision assisted reduction with ESIN.Postoperative problems have been statistically analyzed. Results: There were altogether 2 133 children, including 603 cases of femur, 311 cases of tibia, 8 cases of fibula, 219 cases of humerus, and 992 cases of ulna/radius.The postoperative complications mainly consist of 62 cases of needle tail irritation reaction, 21 cases of misalignments of fracture alignment, 11 cases of intramedullary nail deformity or angular deformity, 7 cases of limb shortening, 14 cases of limited joint activity, 4 cases of nerve injury, 2 cases of tendon injury, 14 cases of difficult nail removal, 4 cases of cortical cleavage, 8 cases of delayed union, 1 case of nonunion, 6 cases of varus/valgus deformity, 5 cases of epiphyseal injury, 6 cases of ESIN exposure, and 2 cases of metal debris of ESIN′ end. Conclusions The complications of treatment for children with long bone fractures by ESIN cannot be ignored.To master the important biomechanical properties, to get familiar with the local anatomy and to avoid obvious technical errors can reduce the occurrence of postoperative complications.

Objective To investigate the relationship of-174G ＞ C polymorphism of interleukin 6 (IL-6) gene promoter region upstream-with coronary heart disease (CHD) of Chinese Han population in Nanjing area.Methods The polymorphism of IL-6-174G ＞C gene was confirmed in 235 patients with CHD and 175 healthy individuals by PCR-RFLP,and Hardy-Weinberg equilibrium was tested.DNA samples were selected for sequencing to verify their genotype.The concentration of blood sugar,lipid,C reaction protein (CRP) and glycosylated hemoglobin (HbAlc) in the samples were measured simultaneously.Results The genotype distributions of GG,GC and CC were 98.7％,1.3％ and 0 in CHD group and 97.7％,2.3％ and 0 in control group,respectively.The frequencies of G and C alleles were 99.4％,0.6％ and 98.9％,1.1％ in the two groups.There were no statistical significance for frequencies of genotype and alleles between the two groups (all P ＞ 0.05).Compared with the control group,the differences of smoking,systolic blood pressure (SBP),diastohc blood pressure (DBP),triglyceride (TG),cholesterol (CHOL),low-density lipoproteins-cholesterol (LDL-C),high-density lipoproteins-cholesterol (HDL-C),apolipoprotein A-I (ApoA-I),ApoB,CRP and HbA1 c were statistically significant (all P ＜ 0.05),while age,sex and blood glucose were not statistically significant (all P ＞ 0.05).Conclusion IL-6-174 G ＞ C gene polymorphism should not remarkably correlated with CHD in Chinese Han population in Nanjing area.

BACKGROUNDProstate stromal cells are known to regulate epithelial growth as well as support and maintain epithelial function. However, how stromal cells regulate epithelial cells and what differences among various histological/pathological prostate stromal cells in prostate cancer progression still remain unclear. This study aimed to investigate the different phenotypes of human various histological/pathological prostate stromal cells, and their role in tumor promotion.

METHODSThe different phenotypes of the human normal prostatic peripheral zonal primary stromal cells (NPPF), transitional zonal primary stromal cells (NPTF), and prostate cancer associated primary stromal cells (CAF) were examined with growth curves and Annexin V-fluorescein isothiocyanate (FITC) assay. The different effects on prostate cancer cell line C4-2B by NPPF, NPTF, and CAF were examined with MTT assay and Annexin V-FITC assay. The gene expression of different histological/pathological prostate stromal cells was profiled by microarray and hierarchical cluster analysis.

RESULTSThe growth rate of NPPF, NPTF and CAF gradually increased, followed by decreasing apoptosis. In vitro stromal-C4-2B cell line co-culture models, the proliferation and apoptosis of C4-2B cell line were differently affected by human various histological/pathological prostate stromal cells. CAF showed the most powerful effect to C4-2B cell line, as opposed to a weakest effect of NPTF. Microarray and hierarchical cluster analysis showed that the differentially expressed genes of CAF and NPPF were less than NPPF and NPTF, or CAF and NPTF. This was consistent with clinical observations that prostate cancer mostly derived from the peripheral zone and does not usually occur in the transitional zone.

CONCLUSIONNPPF, NPTF and CAF possess extremely different biological characteristics and gene expression, which may play an important role in genesis and development of prostate cancer.

Adult ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cells, Cultured ; Cluster Analysis ; Flow Cytometry ; Humans ; Immunohistochemistry ; Male ; Prostate ; cytology ; Prostatic Neoplasms ; pathology ; Stromal Cells ; cytology ; metabolism ; Tumor Cells, Cultured

Post-translational degradation of protein plays an important role in cell life. We employed chimeric molecules (dihydrotestosterone-based proteolysis-targeting chimeric molecule [DHT-PROTAC]) to facilitate androgen receptor (AR) degradation via the ubiquitin-proteasome pathway (UPP) and to investigate the role of AR in cell proliferation and viability in androgen-sensitive prostate cancer cells. Western blot analysis and immunohistochemistry were applied to analyse AR levels in LNCaP cells after DHT-PROTAC treatment. Cell counting and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) cell viability assay were used to evaluate cell proliferation and viability after AR elimination in both LNCaP and PC-3 cells. AR was tagged for elimination via the UPP by DHT-PROTAC, and this could be blocked by proteasome inhibitors. Degradation of AR depended on DHT-PROTAC concentration, and either DHT or an ALAPYIP-(arg)(8) peptide could compete with DHT-PROTAC. Inhibition of cell proliferation and decreased viability were observed in LNCaP cells, but not in PC-3 or 786-O cells after DHT-PROTAC treatment. These data indicate that AR elimination is facilitated via the UPP by DHT-PROTAC, and that the growth of LNCaP cells is repressed after AR degradation.
Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Dihydrotestosterone ; pharmacology ; Dose-Response Relationship, Drug ; Humans ; Male ; Prostatic Neoplasms ; drug therapy ; metabolism ; pathology ; Proteasome Endopeptidase Complex ; metabolism ; Receptors, Androgen ; metabolism ; Recombinant Fusion Proteins ; pharmacology ; therapeutic use ; Signal Transduction ; drug effects ; Ubiquitin ; metabolism

Cytokines are believed to be involved in a "vicious circle" of progressive interactions in bone metastasis. Iguratimod is a novel anti-rheumatic drug which is reported to have the capability of anti-cytokines. In this study, a rat model was constructed to investigate the effect of iguratimod on bone metastasis and it was found that iguratimod alleviated cancer-induced bone destruction. To further explore whether an anti-tumor activity of iguratimod contributes to the effect of bone resorption suppression, two human breast cancer cell lines MDA-MB-231 and MCF-7 were studied. The effect of iguratimod on tumor proliferation was detected by CCK-8 assay and flow cytometry. The effects of iguratimod on migration and invasion of cancer cells were determined by wound-healing and Transwell assays. Results showed that high dose (30 μg/mL) iguratimod slightly suppressed the proliferation of cancer cells but failed to inhibit their migration and invasion capacity. Interestingly, iguratimod decreased the transcription level of IL-6 in MDA-MB-231 cells in a concentration-dependent manner. Moreover, iguratimod partially impaired NF-κB signaling by suppressing the phosphorylation of NF-κB p65 subunit. Our findings indicated that iguratimod may alleviate bone destruction by partially decreasing the expression of IL-6 in an NF-κB-dependent manner, while it has little effect on the tumor proliferation and invasion.
Animals ; Apoptosis ; drug effects ; Bone Neoplasms ; complications ; drug therapy ; pathology ; secondary ; Bone Resorption ; complications ; drug therapy ; pathology ; Breast Neoplasms ; complications ; drug therapy ; genetics ; pathology ; Carcinogenesis ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Chromones ; administration & dosage ; Female ; Humans ; Interleukin-6 ; biosynthesis ; genetics ; MCF-7 Cells ; Neoplasm Invasiveness ; genetics ; pathology ; Rats ; Sulfonamides ; administration & dosage ; Transcription Factor RelA ; biosynthesis ; genetics

Depleted uranium (DU) has been widely applied in industrial and military activities, and is often obtained from producing fuel for nuclear reactors. DU may be released into the environment, polluting air, soil, and water, and is considered to exert both radiological and chemical toxicity. In humans and animals, DU can induce multiple health effects, such as renal tubular necrosis and bone malignancies. This review summarizes the known information on DU's routes of entry, mechanisms of toxicity, and health effects. In addition, we survey the chelating agents used in ameliorating DU toxicity.
Animals ; Chelating Agents ; pharmacology ; Humans ; Inactivation, Metabolic ; Radiation-Protective Agents ; pharmacology ; Uranium ; metabolism ; toxicity

Objective: To explore the relationship between pathogenic gene, mutation and phenotype of left ventricular noncompaction (LVNC) patients and their family members. Methods: The subjects were the proband with LVNC and her family members. The medical history including electrocardiogram, echocardiography and cardiac magnetic resonance examination of the proband and family members were collected. Whole exome sequencing of the proband was performed, bioinformatics analysis focused on the genes related to hereditary cardiomyopathy. Candidate pathogenic sites were validated by Sanger sequencing. The clinical interpretation of sequence variants were classified according to American College of Medical Genetics and Genomics (ACMG) guidelines. Results: The proband carried a heterozygous variation of the MYBPC3 gene c.C2827T and the MYH7 gene c.G2221C. The proband's sister carried heterozygous variation of MYBPC3 gene c.C2827T. According to the ACMG guidelines, the variant was determined to be pathogenic. Conclusion: The missense variant of MYBPC3 gene c.C2827T and MYH7 gene c.G2221C are identified from the proband with LVNC and her family member, which provides a genetic basis for clinical diagnosis and genetic counseling of the patients and the family members with LVNC.
Female ; Humans ; Cardiac Myosins/genetics* ; Heart Defects, Congenital ; Mutation ; Mutation, Missense ; Myosin Heavy Chains/genetics* ; Pedigree ; Phenotype

Objective: To explore the relationship between pathogenic gene, mutation and phenotype of left ventricular noncompaction (LVNC) patients and their family members. Methods: The subjects were the proband with LVNC and her family members. The medical history including electrocardiogram, echocardiography and cardiac magnetic resonance examination of the proband and family members were collected. Whole exome sequencing of the proband was performed, bioinformatics analysis focused on the genes related to hereditary cardiomyopathy. Candidate pathogenic sites were validated by Sanger sequencing. The clinical interpretation of sequence variants were classified according to American College of Medical Genetics and Genomics (ACMG) guidelines. Results: The proband carried a heterozygous variation of the MYBPC3 gene c.C2827T and the MYH7 gene c.G2221C. The proband's sister carried heterozygous variation of MYBPC3 gene c.C2827T. According to the ACMG guidelines, the variant was determined to be pathogenic. Conclusion: The missense variant of MYBPC3 gene c.C2827T and MYH7 gene c.G2221C are identified from the proband with LVNC and her family member, which provides a genetic basis for clinical diagnosis and genetic counseling of the patients and the family members with LVNC.
Female ; Humans ; Cardiac Myosins/genetics* ; Heart Defects, Congenital ; Mutation ; Mutation, Missense ; Myosin Heavy Chains/genetics* ; Pedigree ; Phenotype

To improve the diagnostic efficiency of prostate cancer (PCa) and reduce unnecessary biopsies, we defined and analyzed the diagnostic efficiency of peripheral zone prostate-specific antigen (PSA) density (PZ-PSAD). Patients who underwent systematic 12-core prostate biopsies in Shanghai General Hospital (Shanghai, China) between January 2012 and January 2018 were retrospectively identified (n = 529). Another group of patients with benign prostatic hyperplasia (n = 100) were randomly preselected to obtain the PSA density of the non-PCa cohort (N-PSAD). Prostate volumes and transition zone volumes were measured using multiparameter magnetic resonance imaging (mpMRI) and were combined with PSA and N-PSAD to obtain the PZ-PSAD from a specific algorithm. Receiver operating characteristic (ROC) curve analysis was used to assess the PCa detection efficiency in patients stratified by PSA level, and the area under the ROC curve (AUC) of PZ-PSAD was higher than that of PSA, PSA density (PSAD), and transition zone PSA density (TZ-PSAD). PZ-PSAD could amend the diagnosis for more than half of the patients with inaccurate transrectal ultrasonography (TRUS) and mpMRI results. When TRUS and mpMRI findings were ambiguous to predict PCa (PIRADS score ≤3), PZ-PSAD could increase the positive rate of biopsy from 21.7% to 54.7%, and help 63.8% (150/235) of patients avoid unnecessary prostate biopsy. In patients whose PSA was 4.0-10.0 ng ml