Effect of topology of poly(L-lactide-co-ε-caprolactone) scaffolds on the response of cultured human umbilical cord Wharton’s jelly-derived mesenchymal stem cells and neuroblastoma cell lines

In this study, for the first time, a biodegradable poly(L-lactide-co-ε-caprolactone), PLC 67:33 copolymer was developed for use as temporary scaffolds in reconstructive nerve surgery. The effect of the surface topology and pore architecture were studied on the biocompatibility for supporting the growth of human umbilical cord Wharton’s jelly-derived mesenchymal stem cells (hWJ-MSCs) and human neuroblastoma cells (hNBCs) as cell models. Porous PLC membranes were prepared by electrospinning and phase immersion precipitation with particulate leaching and nonporous PLC membranes were prepared by solvent casting. From the results, the porous PLC membranes can support hWJ-MSCs and hNBCs cells better than the nonporous PLC membrane, and the interconnected pore scaffold prepared by electrospinning exhibited a more significant supporting attachment of the cells than the open pore and nonporous membranes. We can consider that these electrospun PLC membranes with 3-D interconnecting fiber networks and a high porosity warrant a potential use as nerve guides in reconstructive nerve surgery.     

The effect of different etching times of acidulated phosphate fluoride gel on the shear bond strength of high-leucite ceramics bonded to composite resin

STATEMENT OF PROBLEM: A 10-minute treatment with acidulated phosphate fluoride (APF) gel has been used as an alternative in ceramic surface etching before repairing with composite resin. However, the optimal etching time for APF gel is still unknown. PURPOSE: The purpose of this study was to determine the in vitro shear bond strengths of composite resin on high-leucite ceramics after APF gel treatment over different time periods. MATERIAL AND METHODS: One hundred and twenty high-leucite ceramic (Empress 1) specimens (12 mm in diameter and 1.5 mm thick) were prepared and divided into 12 groups (n=10). Ten experimental groups were surface treated with 1.23% APF gel, each group receiving 1 to 10 minutes of etching time in 1 minute increments. One group was treated with 9.6% hydrofluoric acid for 4 minutes and the final group received no treatment and served as a control. The surface condition of the treated specimens was analyzed under a scanning electron microscope (SEM). All specimens received a silane application and were bonded to a composite resin Filtek (Z250) cylinder with an adhesive system (Scotchbond Multi-Purpose Plus adhesive) and then stored in 100% humidity at 37 degrees C for 24 hours before shear bond strength testing in a universal testing machine. Mean bond strengths (MPa) were analyzed with 1-way ANOVA and the Tukey HSD test (alpha=.05). RESULTS: Hydrofluoric acid etching produced the highest mean shear bond strength (SD) between composite resin and the ceramic (17.64 (1.48) MPa). Overall, APF gel etching produced lower bond strengths. No significant difference in mean bond strength (SD) was observed between etching with hydrofluoric acid and etching with APF gel for 7 to 10 minutes (15.21 (1.93) to 17.33 (1.43)). The lowest mean shear bond strengths (SD) were recorded in the untreated group (7.61 (1.03) MPa) (P<.05). CONCLUSIONS: Within the limitations of this study, shear bond strength values between composite resin and high-leucite ceramics after etching with 1.23% APF gel for 7 to 10 minutes were not significantly different than that after etching with 9.6% hydrofluoric acid for 4 minutes.     

Effect of novel chitosan-fluoroaluminosilicate glass ionomer cement with added transforming growth factor beta-1 on pulp cells

Introduction

Vital pulp therapy might benefit from the sustained release of transforming growth factor beta-1 (TGF-β1) from dental restorative materials. Chitosan has previously been shown to enable sustained release of bovine serum albumin (BSA) from glass ionomer cement (GIC). Because BSA can prolong release of growth factor, chitosan-fluoroaluminosilicate GIC with albumin (BIO-GIC) should sustain the effect of growth factor. This study investigated the effect of BIO-GIC with added TGF-β1 on pulp cells.

Methods

BIO-GIC was prepared from GIC (conventional type) incorporated with 15% of chitosan and 10% of BSA. TGF-β1 (100 ng) was added in BIO-GIC+TGF-β1 and GIC+TGF-β1 groups during each disk specimen (10 mm diameter, 1 mm high) preparation. Two control groups were BIO-GIC and GIC. The effect of each specimen on pulp cells was investigated by using the Transwell plate technique. Cell proliferation was determined by MTT assay at 2 time periods (each period lasting 3 days). Pulp cell differentiation was examined by alkaline phosphatase activity and also by cell mineralization, which was measured by calculating the area of mineralization with von Kossa staining.

Results

Percentage of viable cells of GIC+TGF-β1 group was the highest after the first period. This might suggest an initial rapid release of TGF-β1 from GIC. After the second period, BIO-GIC, BIO-GIC+TGF-β1, and GIC+TGF-β1 had more than 90% cell survival. It was significantly greater than GIC (82% ± 2%). There was no significant difference in alkaline phosphatase activity. BIO-GIC+TGF-β1 had the highest mineralization area during 21 days.

Conclusions

BIO-GIC could retain the effect of TGF-β1.     

Cardiac and lung point‐of‐care ultrasound in pediatric anesthesia and critical care medicine: Uses,pitfalls, and future directions to optimize pediatric care

Point‐of‐care ultrasound (POCUS) has found many relevant applications in pediatric anesthesia and critical care medicine. Specifically, the cardiac and pulmonary POCUS examinations provide a wealth of information from physical examination assistance to diagnostic evaluation and assessment of treatment response. However, as with any adjunct, potentially dangerous pitfalls exist when POCUS is performed, interpreted, and applied by the novice sonographer. Using case illustrations, we highlight the clinical application of POCUS in addition to potential dangers. Additionally, suggestions for learning POCUS, assessing competency and credentialing are reviewed.     

Association of Abnormal Pap Smear with Occult Cervical Stromal Invasion in Patients with Endometrial Cancer

Objective: The purpose of this study was to determine the association between abnormal preoperative Pap smearresults and occult cervical stromal invasion in endometrial cancer patients. Methods: Medical records were reviewed ofpatients with endometrial cancer who had undergone surgical staging at Srinagarind Hospital. Patients with gross cervicalinvolvement, with an unsatisfactory Pap smear, without available Pap smear results, with no cervical intraepitheliallesion/invasive cervical cancer, or who had previously undergone pelvic radiation therapy were excluded. The patientswere assigned to one of two groups according their Pap smear results (negative and epithelial cell abnormalities).Logistic regression was used to determine the independent association between an abnormal Pap smear and the riskof cervical stromal invasion. Results: All cervical smears in this study were performed as conventional Pap smears.Smears were abnormal in 50 (21.0%) of the 238 patients enrolled and normal in the remaining 188 (79.0%). The typesof Pap smear abnormalities included adenocarcinoma (n=22); atypical endometrial cells (n=2); atypical glandular cells(n=17); high-grade squamous intraepithelial lesions (n=4); atypical squamous cells, cannot exclude high-grade squamousintraepithelial lesions (n=2); and atypical squamous cells of undetermined significance (n=3). After controlling for type ofendometrial cancer, abnormal Pap smear results were found to be a significant independent factor that indicated cervicalstromal invasion (adjusted OR 2.65; 95% CI 1.35 to 5.21). Conclusion: Endometrial cancer patients with abnormalPap smears were strongly and independently associated with histopathologically diagnosed cervical stromal invasion.     

Role of macrophages in LPS-induced osteoblast and PDL cell apoptosis

In periradicular lesions and periodontal disease, bacterial invasion leads to chronic inflammation resulting in disruption of the structural integrity of the periodontal ligament and progressive alveolar bone destruction. The pathogenesis of these conditions has been attributed not only to bacterial-induced tissue destruction but also to a defect in periodontal tissue repair. Accumulated data have also shown that lipopolysaccharide (LPS) can directly induce cell death or apoptosis in many cell types, including macrophages, osteoblasts, vascular endothelial cells, hepatocytes and myocytes. The present study hypothesized that bacterial LPS-induced apoptosis in osteoblasts and periodontal ligament fibroblasts (PDL cells) is an important contributing factor to the defect in periodontal tissue repair in periodontal and periapical disease. Macrophages have been shown to respond to bacterial LPS by increasing the production of proinflammatory cytokines. In addition, large numbers of macrophages are present in inflamed periodontal tissue. We speculated that macrophages were a potential candidate cell for mediating apoptosis in osteoblasts and PDL cells in response to bacteria-derived LPS. The macrophage-like cell line, RAW 264.7, was stimulated with LPS, and the conditioned medium was used to treat osteoblasts and PDL cells. Bacterial LPS had no direct apoptotic effect on mouse osteoblasts or PDL cells, whereas the conditioned medium from LPS-activated macrophages was able to induce apoptosis in these cells. To evaluate the contribution of tumor necrosis factor-alpha (TNF-) released from macrophages on osteoblast and PDL cell apoptosis, cells were incubated with conditioned medium from LPS-treated macrophages in the presence and absence of anti-TNF- neutralizing antibodies. TNF- neutralizing antibody pretreatment inhibited the effect of conditioned medium from LPS-treated macrophages on osteoblast and PDL cell apoptosis in a dose-dependent manner. These results suggest that LPS could indirectly induce apoptosis in osteoblasts and PDL cells through the induction of TNF- release from macrophages. These studies provide insight into a potential mechanism by which bacterial-derived LPS could contribute to defective periodontal and bone tissue repair in periodontal and periapical disease.