Shear Bond Strength of Self-etching Adhesive Systems with Different pH Values to Bleached and/or CPP-ACP-treated Enamel

Purpose: To compare shear bond strengths of three different self-etching adhesive systems of different pH values to enamel bleached with carbamide peroxide, treated with casein phosphopeptide-amorphous calcium phosphate (CPP-ACP), or treated with CPP-ACP subsequent to bleaching with carbamide peroxide. Materials and Methods: Thirty-six human third molars were cut into 4 sections and randomly assigned to 4 groups (n = 36): group I: no treatment; group II: bleaching; group III: CPP-ACP; group IV: bleaching and CPP-ACP. After surface treatments, the samples of each group were further divided into three subgroups (n = 12) based on the adhesive used. The adhesives Clearfil SE Bond (CSE), AdhesE (ADE), and Adper SE Plus (ADP) were applied, and resin composite cylinders with a diameter of 2 mm and a height of 4 mm were bonded to the enamel. Then the specimens were subjected to shear bond strength testing. Two-way ANOVA and a post-hoc Tukey's test were used for statistical analysis (α = 0.05). Results: There were significant differences between the adhesive systems (p < 0.001) and surface treatments (p < 0.001), but no significant interactions were observed between these variables (p = 0.78). The CSE adhesive system showed the highest bond strength, and the bleaching procedure reduced bond strengths (p = 0.001). Furthermore, there were no significant differences in shear bond strength values between the control and CPP groups. However, the differences between other groups were statistically significant (p < 0.05). Conclusion: Bleaching reduced shear bond strength to enamel, but CPP-ACP application did not affect the bond strength to intact and previously bleached enamel. The bond strength of adhesives with different pH values to enamel was material dependant.     

Detection of vertical root fractures using digitally enhanced images: reverse‐contrast and colorization

Abstract – Root fracture diagnosis is a clinical difficulty that in most cases can only be detected through radiography. The objective of this study was to compare the diagnostic accuracy of two types of digitally enhanced images (reverse‐contrast and colorization) with original digital radiographies in detecting experimental root fractures. Two hundred extracted single‐rooted human teeth were endodontically instrumented and then divided in two groups, one control group and one test group, including fractured teeth. Vertical root fractures were experimentally made in the fractured group. The digital image of each tooth was taken, using the paralleling technique. There were three groups of images: (i) original, (ii) reverse contrast, and (iii) colorized. Three experienced dental specialists examined the images with no prior knowledge of the distribution of the root fractures. Two‐way analysis of variance was used to assess the differences in accuracy, sensitivity, and specificity of each technique in detecting root fractures. Cohen’s kappa coefficients were calculated to investigate the degree of interobserver agreement. The accuracy, sensitivity, and specificity of original images were 67.4%, 66.7%, and 68%, respectively; these amounts were 61.5%, 61%, and 65.5% in reverse contrast images and 66.4%, 70.7%, and 62% in colorized digital radiography. The original images had the best inter observer kappa coefficients (between 0.45 and 0.55). The results showed that the accuracy of original images is better than reverse contrast and colorized images. Use of reverse‐contrast and colorization digital images in root fracture detection should be regarded as an adjunct to other diagnostic methods not as a highly critical diagnostic aid.     

Protective effects of copper against aluminum toxicity on acetylcholinesterase and catecholamine contents of different regions of rat’s brain

The probable protective effects of copper on the acetylcholinesterase activity and the catecholamine levels in cerebellum, cortex and mid-brain of rat, which was intoxicated by aluminum, were studied during short and long terms. In this respect, male Wistar rats weighing 200–250 g were received daily intraperitoneal doses of aluminum, copper and also combined doses of both metals for 15 days (Al 10 mg kg^?1 BW and Cu 1 mg kg^?1 BW), 30 days (Al 5 mg kg^?1 BW and Cu 0.5 mg kg^?1 BW) and 60 days (Al 1 mg kg^?1 BW and Cu 0.1 mg kg^?1 BW), respectively. The results obtained from the short period of exposure (15 days) showed that aluminum produced significant (P < 0.05) decreases in the acetylcholinesterase activity by 24.14, 23.30 and 25.81 %. Similarly, the catecholamine levels were reduced by 10.69, 12.25 and 12.64 % in cerebellum, cortex and mid-brain, respectively. Treatment with copper increases both acetylcholinesterase activity and catecholamine contents of cerebellum, cortex and mid-brain. Simultaneous injection of copper and aluminum increased both acetylcholinesterase activity and catecholamine contents in all three parts of rat brain when compared to aluminum-treated group. Same results were also observed following 30 and 60 days of exposures. In overall, it has been found that copper may have a protective-like ability to hinder aluminum toxicity in the brain.     

Histopathological changes of gastric mucosa following oral administration of fumonisin B1 in mice

Fumonisin B1 is a common secondary metabolite produced by Fusarium moniliforme that occurs in corn and corn-based foods. This mycotoxin is toxic to many species of laboratory and domestic animals and is known to induce a variety of diseases such as hepatic cancer and renal and hepatic dysfunction. The structure of fumonisin B1 (FB1) resembles sphingolipids so it can inhibit synthesis of ceramide, an enzyme in the sphingolipid biosynthetic pathway. This inhibition leads to the disruption of sphingolipid metabolism and increased levels of sphinganine and sphingosine (sphingoid bases) in the serum of treated animals. It is believed that the toxicity effect of fumonisin B1 is the result of these sphingoid bases. In the present research, mice were treated with FB1 to determine its pathological effects on gastric gland and gastric mucosa in the treated mice. For this purpose, the mice were randomly assigned into two groups, namely, control (n?=?14) and treatment (n?=?15). The treatment group was fed with prepared food containing FB1 (150 mg/kg) for a period of 4 months. One day after the last treatment, all animals in both groups were euthanized and their stomach were sampled and prepared for microscopic analysis. Histopathological analysis revealed a significant decrease in parietal cell number and a significant increase in the number of inflammatory cells in gastric mucosa. Also, atrophy of gastric glands was observed. The study confirmed that FB1 poisoning can have toxicopathological effects such as gastric gland atrophy and gastritis on mice gastric tissue.     

Small Nerve Fiber Damage and Langerhans Cells in Type 1 and Type 2 Diabetes and LADA Measured by Corneal Confocal Microscopy

PurposeIncreased corneal and epidermal Langerhans cells (LCs) have been reported in patients with diabetic neuropathy. The aim of this study was to quantify the density of LCs in relation to corneal nerve morphology and the presence of diabetic neuropathy and to determine if this differed in patients with type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM), and latent autoimmune diabetes of adults (LADA).MethodsPatients with T1DM (n = 25), T2DM (n = 36), or LADA (n = 23) and control subjects (n = 23) underwent detailed assessment of peripheral neuropathy and corneal confocal microscopy. Corneal nerve fiber density (CNFD), branch density (CNBD), length (CNFL) and total, immature and mature LC densities were quantified.ResultsLower CNFD (P < 0.001), CNBD (P < 0.0001), and CNFL (P < 0.0001) and higher LC density (P = 0.03) were detected in patients with T1DM, T2DM, and LADA compared to controls. CNBD was inversely correlated with mature (r = –0.5; P = 0.008), immature (r = –0.4; P = 0.02) and total (r = –0.5; P = 0.01) LC density, and CNFL was inversely correlated with immature LC density (r = –0.4; P = 0.03) in patients with T1DM but not in patients with T2DM and LADA.ConclusionsThis study shows significant corneal nerve loss and an increase in LC density in patients with T1DM, T2DM, and LADA. Furthermore, increased LC density correlated with corneal nerve loss in patients with T1DM.     

Proposing an ensemble learning model based on neural network and fuzzy system for keratoconus diagnosis based on Pentacam measurements

International Ophthalmology - The present study was done to evaluate efficiency of an ensemble learning structure for automatic keratoconus diagnosis and to categorize eyes into four different...     

Kidney Disease and Increased Mortality Risk in Type 2 Diabetes

Type 2 diabetes associates with increased risk of mortality, but how kidney disease contributes to this mortality risk among individuals with type 2 diabetes is not completely understood. Here, we examined 10-year cumulative mortality by diabetes and kidney disease status for 15,046 participants in the Third National Health and Nutrition Examination Survey (NHANES III) by linking baseline data from NHANES III with the National Death Index. Kidney disease, defined as urinary albumin/creatinine ratio ≥30 mg/g and/or estimated GFR ≤60 ml/min per 1.73 m², was present in 9.4% and 42.3% of individuals without and with type 2 diabetes, respectively. Among people without diabetes or kidney disease (reference group), 10-year cumulative all-cause mortality was 7.7% (95% confidence interval [95% CI], 7.0%–8.3%), standardized to population age, sex, and race. Among individuals with diabetes but without kidney disease, standardized mortality was 11.5% (95% CI, 7.9%–15.2%), representing an absolute risk difference with the reference group of 3.9% (95% CI, 0.1%–7.7%), adjusted for demographics, and 3.4% (95% CI, −0.3% to 7.0%) when further adjusted for smoking, BP, and cholesterol. Among individuals with both diabetes and kidney disease, standardized mortality was 31.1% (95% CI, 24.7%–37.5%), representing an absolute risk difference with the reference group of 23.4% (95% CI, 17.0%–29.9%), adjusted for demographics, and 23.4% (95% CI, 17.2%–29.6%) when further adjusted. We observed similar patterns for cardiovascular and noncardiovascular mortality. In conclusion, those with kidney disease predominantly account for the increased mortality observed in type 2 diabetes.In 2012, there were an estimated 346 million individuals with diabetes worldwide.¹ This number is expected to rise to >430 million by 2030.² Diabetes is associated with substantially increased risk of mortality, particularly due to cardiovascular disease.³Kidney disease, defined by increased urine albumin excretion and/or impaired GFR, is also strongly associated with increased risk of all-cause and cardiovascular mortality, both among persons with diabetes^4,5 and in the general population.^6–10 The critical effect of kidney disease on mortality in type 1 diabetes was emphasized in two recent reports.^11,12 Each study demonstrated that excess mortality was confined to the subgroup with kidney disease.The degree to which kidney disease captures risk of adverse health outcomes in type 2 diabetes has not been determined. The findings from type 1 diabetes may not extrapolate to type 2 diabetes because the latter is frequently associated with other comorbidities that affect mortality. This question has crucial public health implications because type 2 diabetes predominates among the 26 million US adults with diabetes^13,14 and identifying predictors of excess mortality in type 2 diabetes is essential in order to optimally target risk-reduction strategies. The primary objective of this study was to quantify and compare the excess risk of all-cause and cause-specific mortality among individuals with type 2 diabetes in presence or absence of kidney disease.