Evaluation of Microtensile Bond Strength of Universal Self-etch Adhesive System to Wet and Dry Dentin

BACKGROUND: The durability of dentin-resin interfaces with the universal adhesive system is a crucial characteristic with chemical interactions between the exposed collagen and the adhesive monomers, but it is still compromised with wet and dry mode. AIM: The present study evaluated the effect of dentin wetness and solvents containing of one-step self-etch adhesives on the microtensile bond strength (μTBS) of dentin at different storage times. METHODS: Occlusal dentin of 54 extracted human molars was exposed. Each adhesive agent was applied according to manufacturer instructions to wet and dry dentin surfaces. Composite resin was incrementally built up. Bond strengths to dentin were determined using the μTBS test after water storage for 24 h, 1 month, and 6 months. One-way ANOVA was used to compare between more than two non-related samples. The significance level was set at p ≤ 0.05. RESULTS: Dryness of dentin increases the μTBS with solvent-containing adhesives while decrease the μTBS with solvent-free adhesive. There was an increase in microtensile bond strength values in the case of ethanol water-based self-etch adhesive over time. No statistically significant difference was found among different storage times regarding μTBS for solvent-free adhesive, while a statistically significant difference was found among different storage times in μTBS for solvent-containing adhesives. CONCLUSION: Universal adhesive systems improve the durability and stability of dentin bond strength

Surface Roughness of Bulk Fill Composite after Simulated Toothbrushing with Different Dentifrices

AIM: The aim of the current in vitro study was to evaluate the changes in surface roughness of bulk fill composites after simulated toothbrushing with different dentifrices. MATERIALS AND METHODS: Three types of bulk fill resin composites were used in this study; 27 specimens of each composite resin were randomly divided into three main groups (n = 9). Each main group was further subdivided into three subgroups (n = 3). Each group was subjected to simulated toothbrushing with three different dentifrices. One-way analysis of variance was used to evaluate the effect of brushing using dentifrices on the surface roughness of each type of composite resin, followed by Tukey’s test at a significance level of p ≤ 0.5%. RESULTS: Results revealed that different effects on composite surface roughness were detected after simulating toothbrushing with different dentifrices. Lacalut toothpaste abrades more with Filtek Bulk Fill, Tetric N-Ceram then Bulk Fill SDR. Crest 3D toothpaste abrades more with Tetric N-Ceram, Bulk Fill SDR then Filtek Bulk Fill. BlanX toothpaste abrades more with Tetric N-Ceram, Bulk Fill SDR then Filtek Bulk Fill. CONCLUSION: Chemical composition of both resin composites and dentifrices plays an important role in influencing the degree of surface roughness of bulk fill composite resin restorations

Induction of Hemeoxygenase-1 Reduces Renal Oxidative Stress and Inflammation in Diabetic Spontaneously Hypertensive Rats

The renoprotective mechanisms of hemeoxygenase-1 (HO-1) in diabetic nephropathy remain to be investigated. We hypothesize that HO-1 protects the kidney from diabetic insult via lowering renal oxidative stress and inflammation. We used control and diabetic SHR with or without HO-1 inducer cobalt protoporphyrin (CoPP) treatment for 6 weeks. Urinary albumin excretion levels were significantly elevated in diabetic SHR compared to control and CoPP significantly attenuated albumin excretion. Immuno-histochemical analysis revealed an elevation in TGF-β staining together with increased urinary collagen excretion in diabetic versus control SHR, both of which were reduced with CoPP treatment. Renal oxidative stress markers were greater in diabetic SHR and reduced with CoPP treatment. The increase in renal oxidative stress was associated with an elevation in renal inflammation in diabetic SHR. CoPP treatment also significantly attenuated the markers of renal inflammation in diabetic SHR. In vitro inhibition of HO with stannous mesoporphyrin (SnMP) increased glomerular NADPH oxidase activity and inflammation and blocked the anti-oxidant and anti-inflammatory effects of CoPP. These data suggest that the reduction of renal injury in diabetic SHR upon induction of HO-1 are associated with decreased renal oxidative stress and inflammation, implicating the role of HO-1 induction as a future treatment of diabetic nephropathy

12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

The purpose of the current study was to evaluate the effect of 12/15- lipoxygenase (12/15-LOX) metabolites on retinal endothelial cell (REC) barrier function. FITC-dextran flux across the REC monolayers and electrical cell-substrate impedance sensing (ECIS) were used to evaluate the effect of 12- and 15-hydroxyeicosatetreanoic acids (HETE) on REC permeability and transcellular electrical resistance (TER). Effect of 12- or 15-HETE on the levels of zonula occludens protein 1 (ZO-1), reactive oxygen species (ROS), NOX2, pVEGF-R2 and pSHP1 was examined in the presence or absence of inhibitors of NADPH oxidase. In vivo studies were performed using Ins2Akita mice treated with or without the 12/15-LOX inhibitor baicalein. Levels of HETE and inflammatory mediators were examined by LC/MS and Multiplex Immunoassay respectively. ROS generation and NOX2 expression were also measured in mice retinas. 12- and 15- HETE significantly increased permeability and reduced TER and ZO-1expression in REC. VEGF-R2 inhibitor reduced the permeability effect of 12-HETE. Treatment of REC with HETE also increased ROS generation and expression of NOX2 and pVEGF-R2 and decreased pSHP1 expression. Treatment of diabetic mice with baicalein significantly decreased retinal HETE, ICAM-1, VCAM-1, IL-6, ROS generation, and NOX2 expression. Baicalein also reduced pVEGF-R2 while restored pSHP1 levels in diabetic retina. Our findings suggest that 12/15-LOX contributes to vascular hyperpermeability during DR via NADPH oxidase dependent mechanism which involves suppression of protein tyrosine phosphatase and activation of VEGF-R2 signal pathway.Qatar National Research Fund (NPRP 4 - 1046 - 3 -284), American Heart Association (AHA00104) and Vision Discovery Institute (VDI002010) and Bridge Fund (BFP00018) from the Georgia Health Sciences University.Scopu

Development of Epoxyeicosatrienoic Acid Analogs with in Vivo Anti-Hypertensive Actions

Epoxyeicosatrienoic acids (EETs) contribute importantly to the regulation of vascular tone and blood pressure control. The purpose of this study was to develop stable EET analogs and test their in vivo blood pressure lowering effects in hypertensive rats. Using the pharmacophoric moiety of EETs, ether EET analogs were designed with improved solubility and resistance to auto-oxidation and metabolism by soluble epoxide hydrolase. Ether EET analogs were chosen based on their ability to dilate afferent arterioles and subsequently tested for blood pressure lowering effects in rodent models of hypertension. Initially, 11,12-ether-EET-8-ZE failed to lower blood pressure in angiotensin hypertension or spontaneously hypertensive rats (SHR). Esterification of the carboxylic group of 11,12-ether-EET-8-ZE prevented blood pressure increase in SHR when injected at 2 mg/day for 12 days (MAP Δ change at day 8 of injection was −0.3 ± 2 for treated and 12 ± 1 mmHg for control SHR). Amidation of the carboxylic group with aspartic acid produced another EET analog (NUDSA) with a blood pressure lowering effect when injected at 3 mg/day in SHR for 5 days. Amidation of the carboxylic group with lysine amino acid produced another analog with minimal blood pressure lowering effect. These data suggest that esterification of the carboxylic group of 11,12-ether-EET-8-ZE produced the most effective ether-EET analog in lowering blood pressure in SHR and provide the first evidence to support the use of EET analogs in treatment of cardiovascular diseases

Is inflammation the cause of pre-eclampsia?

It has been proposed that either excessive inflammation or an imbalance in angiogenic factors cause pre-eclampsia. In the present review, the arguments for and against the role of inflammation and/or angiogenic imbalance as the cause of pre-eclampsia are discussed on the basis of the Bradford–Hill criteria for disease causation. Although both angiogenic imbalance and systemic inflammation are implicated in pre-eclampsia, the absence of temporality of inflammatory markers with pre-eclampsia challenges the concept that excessive inflammation is the cause of pre-eclampsia. In contrast, the elevation of anti-angiogenic factors that precede the clinical signs of pre-eclampsia fulfils the criterion of temporality. The second most important criterion is the dose–response relationship. Although such a relationship has not been proven between pro-inflammatory cytokines and pre-eclampsia, high levels of anti-angiogenic factors have been shown to correlate with increased incidence and disease severity, hence satisfying this condition. Finally, as the removal of circulating sFlt-1 (soluble Fms-like tyrosine kinase receptor-1) from pre-eclamptic patients significantly improves the clinical outcome, it fulfils the Hill's experiment principle, which states that removal of the cause by an appropriate experimental regimen should ameliorate the condition. In contrast, treatment with high doses of corticosteroid fails to improve maternal outcome in pre-eclampsia, despite suppressing inflammation. Inflammation may enhance the pathology induced by the imbalance in the angiogenic factors, but does not by itself cause pre-eclampsia. Development of therapies based on the angiogenic and cytoprotective mechanisms seems more promising

Correction: Curcumin attenuates iron accumulation and oxidative stress in the liver and spleen of chronic iron-overloaded rats.

[This corrects the article DOI: 10.1371/journal.pone.0134156.]