Effects of non-thermal atmospheric plasma treatment on dentin wetting and surface free energy for application of universal adhesives

Objectives

The study aims to evaluate the effects of non-thermal atmospheric plasma (NTAP) treatments on dentin wetting and surface free energy (SFE) and compare the effects of NTAP treatment, etch-and-rinse, and self-etch protocols for application of universal adhesives.

Materials and methods

Mid-coronal dentin of intact third molars was used to measure contact angles of distilled water, ethylene-glycol, and diiodomethane and calculate SFE following different NTAP preset treatments (feeding gas consisting of pure He, He + 1% O₂, He + 1.5% O₂), power input (1 or 3 W), and tip-to-surface distance (2, 4, or 8 mm). Contact angles of reference liquids and SFE of dentin following He + 1.5% O₂ at 3-W and 4-mm treatment was compared to phosphoric acid etching. Contact angles of Single Bond Universal (SBU; 3M ESPE) and Clearfil Universal Bond (CUB; Kuraray Noritake) were measured following NTAP, etch-and-rinse, and self-etch protocols.

Results

NTAP significantly reduced contact angles of reference liquids and increased dentin SFE compared to untreated dentin (p < 0.05). O₂ intensified the effect of He NTAP (p < 0.05). NTAP and phosphoric acid increased dentin polarity and Lewis base surface characteristics. Phosphoric acid increased contact angles of adhesives compared to the self-etch protocol (p < 0.05). NTAP resulted in lower adhesive contact angles than phosphoric acid, the difference being statistically significant for CUB (p < 0.05). Compared to the self-etch protocol, NTAP slightly reduced CUB contact angle but not that of SBU (p > 0.05).

Conclusions

He NTAP with and without O₂ increased dentin wetting and SFE, surpassing the effect of phosphoric acid and lowering adhesive contact angles. NTAP produced no apparent micro-morphological changes on dentin surface comparable to acid etching.

Clinical significance

NTAP treatment of dentin prior to adhesive application increases dentin wetting and surface free energy facilitating better adhesive distribution on dentin surface compared to phosphoric acid etching and similar to the “self-etch” application protocol.

     

Effect of taste and smell on secretion rate of salivary IgA in elderly and young persons

Two experiments were performed to determine the effect of taste and odor stimuli on secretion rate of salivary IgA in young and elderly individuals. In Experiment 1, three stimuli were applied to the tongue: 1) "flavor" drops (60% sugar, 5% cocoa powder, and 0.1 % Irish cream odor); 2) sugar (60%); and 3) water. In Experiment 2, four different foods (chicken broth, onion soup, corn, and carrots) were tested with and without monosodium glutamate (MSG). The stimuli in both experiments were delivered three times in a one hour period: t=0, t=30 minutes, t=60 minutes. The results of Experiment 1 indicated that application of sugar (taste alone) and flavor (taste and odor combined) to the tongue induced significantly higher secretion rates of sIgA than the application of water in both elderly and young subjects. In addition, flavor application produced significantly higher secretion rates of sIgA than sugar application alone. Secretion rates of sIgA in young persons were significantly higher than those in elderly persons. In Experiment 2, the increase in secretion rate of sIgA at 30 and 60 minutes for each food with MSG was greater than the same food without MSG for the elderly subjects. The increases in secretion rates of sIgA were produced by elevated salivary flow (Experiments 1 and 2) as well as increased absolute concentrations of sIgA (Experiment 1). The elevation of absolute concentrations of sIgA by chemosensory stimuli may involve neural-immune connections. The improvements in salivary flow and secretory immunity by repeated taste and smell stimulation found here have clinical potential for treatment of immune deficiencies and dry mouth which frequently occur in elderly individuals.     

Delineation of brain tumor extent with [11C]L-methionine positron emission tomography: local comparison with stereotactic histopathology.

PURPOSE: Methyl-[11C]L-methionine ([11C]MET) positron emission tomography (PET) in brain tumors reflects amino acid transport and has been shown to be more sensitive than magnetic resonance imaging in stereotactic biopsy planning. It remains unclear whether the increased [11C]MET uptake is limited to solid tumor tissue or even detects infiltrating tumor parts. EXPERIMENTAL DESIGN: In 30 patients, a primary or recurrent brain tumor was suspected on magnetic resonance imaging. Patients were investigated with [11C]MET-PET before stereotactic biopsy. The biopsy trajectories were plotted into the [11C]MET-PET images with a newly designed C-based software program. The exact local [11C]MET uptake was determined within rectangular regions of interest of 4 mm in width and length aligned with the biopsy specimen. Individual histologic specimens were rated for the presence of solid tumor tissue, infiltration area, and nontumorous tissue changes. RESULTS: Receiver operating characteristics analysis demonstrated a sensitivity of 87% and specificity of 89% for the detection of tumor tissue at a threshold of 1.3-fold [11C]MET uptake relative to normal brain tissue. At this threshold, only 13 of 100 tumor positive specimen were false negative mainly in grade 2 astrocytoma. In grade 2 astrocytoma, mean [11C]MET uptake in the infiltration area was significantly higher than in solid tumor tissue (P < 0.003). CONCLUSIONS: [11C]MET-PET detects solid parts of brain tumors, as well as the infiltration area at high sensitivity and specificity. High [11C]MET uptake in infiltrating tumor of astrocytoma WHO grade 2 reflects high activity in this tumor compartment. Molecular imaging, with [11C]MET, will guide improved management of patients with brain tumors.     

Astrocytes enhance glioblastoma growth

Glioblastoma (GBM) is a deadly disease with a need for deeper understanding and new therapeutic approaches. The microenvironment of glioblastoma has previously been shown to guide glioblastoma progression. In this study, astrocytes were investigated with regard to their effect on glioblastoma proliferation through correlative analyses of clinical samples and experimental in vitro and in vivo studies. Co-culture techniques were used to investigate the GBM growth enhancing potential of astrocytes. Cell sorting and RNA sequencing were used to generate a GBM-associated astrocyte signature and to investigate astrocyte-induced GBM genes. A NOD scid GBM mouse model was used for in vivo studies. A gene signature reflecting GBM-activated astrocytes was associated with poor prognosis in the TCGA GBM dataset. Two genes, periostin and serglycin, induced in GBM cells upon exposure to astrocytes were expressed at higher levels in cases with high “astrocyte signature score”. Astrocytes were shown to enhance glioblastoma cell growth in cell lines and in a patient-derived culture, in a manner dependent on cell–cell contact and involving increased cell proliferation. Furthermore, co-injection of astrocytes with glioblastoma cells reduced survival in an orthotopic GBM model in NOD scid mice. In conclusion, this study suggests that astrocytes contribute to glioblastoma growth and implies this crosstalk as a candidate target for novel therapies.     

Increased levels of Homer1b/c and Shank1a in the post-synaptic density of spinal dorsal horn neurons are associated with neuropathic pain in rats

Activity-dependent plasticity in the spinal dorsal horn may underlie the development of neuropathic pain following peripheral nerve injury. In this study we examined whether the expression and loss of behavioral signs of neuropathic pain were associated with changes in the content of the scaffolding proteins Homer and Shank in the post-synaptic density (PSD) of the spinal dorsal horn. In animals exhibiting thermal hyperalgesia and differential weight-bearing behavior 7 days after loose ligation of the sciatic nerve the levels of Homer1b/c and Shank1a were significantly greater than in control, uninjured or sham-operated animals. These greater levels were specifically a reflection of increases in the injured, ipsilateral and not contralateral dorsal horn. In contrast, there were no differences in the PSD content of Homer1b/c and Shank1a in the dorsal horn of control or sham-operated animals and ligated animals in which the thermal hyperalgesia and differential weight-bearing behavior had disappeared 28 days after the loose ligation. These data revealed a close association between the expression and loss of allodynia and hyperalgesia with changes in the levels of Homer1b/c and Shank1a in the spinal dorsal horn. The reversible shift in the content of scaffolding proteins in the PSD may have important implications for the development of injury-elicited neuropathic pain.     

Chronic exposure to lead acetate affects the development of protein kinase C activity and the distribution of the PKCgamma isozyme in the rat hippocampus.

This study has examined the effect of chronic inorganic lead exposure on phospholipid-dependent protein kinase C (PKC) activity, and the distribution of its alpha (alpha), beta II (betaII), gamma (gamma), and zeta (zeta) isozymes in subcellular fractions of the developing rat hippocampus. Dams were exposed to either 0 or 1000 ppm lead acetate in their drinking water for one week and mated. Offspring were exposed to lead in utero, via lactation, and directly in the drinking water after weaning. The offspring were sacrificed at postnatal days 1 (P1), 8 (P8), 15 (P15), and 29 (P29). PKC activity was determined in the post-synaptosomal supernatant (PSS) and synaptosomal (P-2) membrane fractions by an in vitro assay using histone as the phosphate acceptor. The selected PKC isozymes were detected by immunoblotting techniques. In control animals, PKC activity (pmole/min/mg total protein) in both subcellular fractions substantially increased between P1 and P8. In chronically exposed rats exhibiting clinically relevant blood lead concentrations, this marked increase in PKC activity on P8 was significantly attenuated in both subcellular fractions. On this postnatal day, the amount of immunodetectable PKC gamma was significantly higher in the synaptosomal membrane fraction of lead-exposed rats. Other isozymes were unaffected. These results imply that in lead-exposed animals the PKC gamma isozyme was inactive even though it was associated with the membrane. These results also suggest that prolonged exposure to the heavy metal attenuated PKC activity at an important developmental time to potentially adversely affect normal hippocampal function.