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Poly-D-L lactide (PDLLA) biodegradable implants to heal fractures are widely applied in orthopedic surgeries. However, whether the process of fracture healing is regulated differently when PDLLA is used compared with traditional metal materials remains unclear. Runt-related transcription factor 2 (Runx2) and canonical Wnt signaling are essential and may interact reciprocally in the regulation of osteogenesis during bone repair. In the present study, a rat femoral open osteotomy model was used to compare the curative efficacy of a PDLLA rod and Kirschner wire under intramedullary fixation for fracture treatment. The dynamic expression of Runx2 and key components of the canonical Wnt signaling in callus tissue during fracture healing was also investigated. The results of the current study indicate that at weeks 4 and 6 following fixation, the callus bone structural parameters of microCT were significantly improved by PDLLA rod compared to that of Kirschner wire. In addition, at weeks 4 and 6 after fixation, the protein and mRNA expression of Runx2 and the positive regulators of canonical Wnt signaling, such as Wnts and ß-catenin, were significantly increased. However, the protein and mRNA expression levels of the negative regulators of canonical Wnt signaling, such as glycogen synthase kinase-3ß, were significantly decreased in callus tissue when treated with PDLLA rod compared with Kirschner wire. Collectively, these data indicate that compared to the traditional metal material, using PDLLA internal fixation for fracture treatment may further improve bone formation, which is associated with the increased expression of Runx2 and the enhancement of canonical Wnt signaling. [ABSTRACT FROM AUTHOR]

The aim of the present study was to select key genes that are associated with fibroblasts and keratinocytes during keloid scar progression and development. The gene expression profile of GSE44270, which includes 32 samples, was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) in case samples compared with control samples were screened using the Limma R package followed by hierarchical clustering analysis. Protein-protein interaction (PPI) networks of the total selected DEGs were constructed using Cytoscape. Moreover, the Gene Ontology biological processes and significant Kyoto Encyclopedia of Genes and Genomes pathways of the total selected DEGs were enriched using the Database for Annotation, Visualization and Integrated Discovery. Significant pathways that may be associated with keloid scar were analyzed using deviation analysis of dynamic capabilities. There were 658 DEGs in fibroblast keloid vs. normal, 112 DEGs in fibroblast non-lesion vs. normal, 439 DEGs in fibroblast keloid vs. non-lesion, 523 DEGs in keratocyte keloid vs. normal, 186 DEGs in keratocyte non-lesion vs. normal, and 963 DEGs in keratocyte keloid vs. non-lesion groups. HOXA9, BMP4, CDKN1A and SMAD2 in fibroblasts, and HOXA7, MCM8, PSMA4 and PSMB2 in keratinocytes were key genes in the PPI networks. Moreover, the amino sugar and nucleotide sugar metabolism pathway, cell cycle, and extracellular matrix (ECM)-receptor interaction pathway were significant pathways. This study suggests that several key genes (BMP4, HOXA9, SMAD2, CDKN1A, HOXA7, PSMA4 and PSMB2) that participate in some significant pathways (cell cycle and ECM-receptor interaction pathways) may be potential therapeutic targets for keloid scars. [ABSTRACT FROM AUTHOR]

The present study aimed to determine the effects of high mobility group box 1 protein (HMGB1) on myocardial ischemia reperfusion (I/R) injury in rats following acute myocardial ischemia and investigate the underlying molecular mechanisms of these effects. Male Wistar rats were randomly divided into the following groups (n=10/group): Sham operation; I/R; HMGB50 (50 ng/kg HMGB1 before I/R); HMGB100 (100 ng/kg HMGB1 before I/R); and HMGB200 (200 ng/kg HMGB1 before I/R). Serum cardiac troponin I (cTnI), interleukin (IL)-6 and tumor necrosis factor (TNF)-a levels were subsequently measured. Myocardial levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were also determined. Myocardial infarction size (IS) was determined by 2,3,5-triphenyltetrazolium chloride staining. Myocardial expression of hypoxia inducible factor (HIF)-1a and phosphorylated p38 mitogen-activated protein kinase (P-p38 MAPK) protein was measured using western blotting. The results demonstrated that HMGB1 significantly decreased serum levels of cTnI, IL-6 and TNF-a and myocardial IS in I/R rats compared with the sham group (all P<0.05). HMGB1 also significantly decreased and increased myocardial levels of MDA and SOD, respectively (both P<0.05). HMGB1 significantly increased myocardial expression of HIF-1α and decreased expression of P-p38 MAPK following I/R (both P<0.05). These effects of HMGB1 occurred in a dosedependent manner. The results of the current study indicate that the cardioprotective effects of intravenous HMGB1 are associated with increased myocardial expression of HIF-1a via inhibition of P-p38 MAPK expression, leading to inhibition of the P-p38 MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Cleidocranial dysplasia (CCD) is a rare autosomal dominant condition that affects ossification. The dental abnormalities associated with CCD present an obstacle to orthodontic treatment planning. Early diagnosis is crucial to provide the patient with different treatment modalities that will suit the particular patient. In the present case, combined surgical and orthodontic treatment were performed to guide multiple impacted teeth. A single nucleotide missense variation was identified in exon 3 of runt-related transcription factor 2 (RUNX2) in this patient. The current results suggest a correlation between dental alterations and mutations in the runt domain of RUNX2 in CCD patients. Further clinical and genetic studies may required to confirm the association between phenotypes and genotypes in CCD and to identify other factors that may influence the clinical features of this disease. Patients with cleidocranial dysplasia require a team approach which demands good communication and cooperation from the patient. Timing of the intervention is critical, and numerous surgeries may be required. The patient in the present case report was treated by a team of practitioners, which involved several dental specialties to achieve an optimal result. [ABSTRACT FROM AUTHOR]

The association between antibiotic resistance and SHV-12 extended-spectrum β-lactamase (ESBL) in Enterobacter cloacae remains unknown. The aim of the present study was to investigate the prevalence of both chromosome- and plasmid-borne SHV-12 ESBL genes in Enterobacter cloacae. Transmission of the SHV-12 ESBL gene was explored, and the risk factors for antibiotic resistance in E. cloacae were analyzed. Polymerase chain reaction (PCR) results showed that 58 out of the 100 isolates carried the SHV-12 ESBL gene: 34.48% of them occurred in the chromosome, 48.28% were plasmid-borne and 17.24% appeared in both. Enterobacterial repetitive intergenic consensus-PCR tests detected 82 chromosomal genotypes. Conjugation assays showed that 70.00% of plasmid-borne SHV-12 ESBL genes were successfully transconjugated into E. coli C600 and that the antibiotic resistance phenotype of E. cloacae was partially (84%) or completely (10%) transferred. A significantly higher SHV-12 ESBL detection rate was found in patients with underlying conditions and/or complications compared with those without (P<0.05). The detection of SHV-12 ESBL-producing E. cloacae from vertical transmission varied significantly across clinical departments and age groups (P<0.05), with the highest rates in the intensive care unit and the group of patients aged =60 years. The present results indicate that the location and transmission efficiency of SHV-12 ESBL are closely correlated with the antibiotic resistance of E. cloacae. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the acaricidal activity of Ligularia virgaurea. An extract was prepared by refluxing with ethanol and steam distillation, and its toxic effect was tested in vitro against Sarcoptes scabiei. The data from the toxicity tests were analyzed using a complementary log-log (CLL) model. The ethanol extract exhibited strong acaricidal activity against these mites; at a concentration of 2 g/ml it killed all S. scabiei within 2 h and at 1 g/ml it killed all S. scabiei within 6 h. Similarly, 2, 1, 0.5 and 0.25 g/ml concentrations of the extract had strong toxicity against S. scabiei, with median lethal time (LT50) values of 0.716, 1.741, 2.968 and 4.838 h, respectively. The median lethal concentration (LC50) values were 1.388, 0.624, 0.310 and 0.213 g/ml for Scabies mite in 1, 2, 4 and 6 h, respectively. The results indicate that the L. virgaurea extract has strong acaricidal activity and may be exploited as a novel treatment for the effective control of acariasis in animals. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate whether postconditioning with simvastatin attenuated myocardial ischemia reperfusion injury by inhibiting the expression of high mobility group box 1 (HMGB1) in rat myocardium following acute myocardial ischemia. In total, 30 male Sprague-Dawley rats were divided into sham operation (sham; n=10), acute myocardial infarction (AMI; n=10) and simvastatin (sim; n=10) groups. The AMI and sim groups were subjected to ischemia for 30 min, followed by reperfusion for 180 min. The rats in the sim group were administered 20 mg/kg simvastatin intravenously 5 min prior to reperfusion. Subsequently, the infarct size, serum cardiac troponin (c-TnI), tumor necrosis factor (TNF)-a and myocardial malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were measured. Western blot analysis was used to detect the protein expression of HMGB1. Postconditioning with simvastatin was shown to decrease the infarct size and HMGB1 expression levels in the myocardium following AMI (P<0.05). In addition, postconditioning with simvastatin not only decreased the serum levels of c-TnI and TNF-α (P<0.05), but also inhibited the increase in MDA levels and the reduction in SOD activity (P<0.05). Therefore, postconditioning with simvastatin was shown to attenuate myocardial injury. The underlying mechanism may be associated with the down-regulation of HMGB1 expression in the ischemic myocardium. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the effect of hydrogen sulfide (H2S) on kidney injury induced by urinary-derived sepsis. Rabbits were randomly divided into control, sham, sepsis, NaHS 2.8 μmol/kg and NaHS 8.4 μmol/kg groups, with six rabbits in each group. Upper urinary tract obstruction and acute infection was induced to establish the sepsis model. Blood was collected to carry out a white blood cell (WBC) count, and creatinine (Cr) and blood urea nitrogen (BUN) analysis. Morphological changes were observed by hematoxylin and eosin (H&E) staining and transmission electron microscopy. Immunohistochemical staining was used to detect the expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-10 and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB). Cystathionine-κ-lyase (CSE) activity was measured by the spectrophotometric methylene blue method and the blood H2S concentration was measured by deproteinization. WBC, Cr and BUN levels were significantly elevated in the sepsis group compared with those in the control group (P<0.05). Following treatment with NaHS, the WBC, Cr and BUN levels were significantly decreased in the NaHS groups compared with those in the sepsis group (P<0.05). The pathological features of kidney injury were also alleviated by NaHS. In the sepsis group, the levels of TNF-α, IL-10 and NF-κB were significantly increased compared with those in the control group (P<0.05). In the NaHS groups, the TNF-α and NF-κB levels were significantly reduced whereas the IL-10 level was significantly increased compared with the respective levels in the sepsis group (P<0.05). The H2S concentration was significantly decreased in the sepsis group and this reduction was attenuated in the NaHS groups (P<0.05). Furthermore, the NaHS 8.4 μmol/kg dose revealed a more potent effect than the NaHS 2.8 μmol/kg dose. Thus, exogenous H2S reduced kidney injury from urinary-derived sepsis by decreasing the levels of NF-κB and TNF-α, and increasing the level of IL-10. [ABSTRACT FROM AUTHOR]

The dihydropyridine-type calcium channel blocker, benidipine (BD) has been widely used in hypertension therapy. Previous studies have demonstrated that BD has a positive effect on bone metabolism. Inspired by this promoting phenomenon, the present study investigated the effects of BD on osteoblasts in vitro. Experiments were designed and performed, including an MTT assay, reverse transcription-polymerase chain reaction, western blot analysis, alkaline phosphatase activity measurements and alizarin red S staining. The results demonstrated that BD promoted osteoblast proliferation and osteogenic differentiation at concentrations from 1x10-6 to 1x10-9 M by upregulating Runx2, BMP2 and OCN gene expression levels. Overall, BD at appropriate concentrations has been demonstrated to have positive effects on osteoblast function in addition to its conventional clinical usage. [ABSTRACT FROM AUTHOR]