Enamel microhardness and shear bond strength after treatment with an 18% carbamide peroxide bleaching varnish

PURPOSE: To evaluate the microhardness and shear bond strength of human enamel treated with an 18% carbamide peroxide bleaching varnish. METHODS: 40 dental enamel slabs were embedded and ground flat, dividing them into four groups (n=10) which received the varnish application for 14 consecutive days: (G1) one daily varnish application; (G2) two daily varnish applications with an interval of 15 minutes; (G3) two daily varnish applications with an interval of 5 hours. After varnish application, the slabs were immersed in artificial saliva changed daily. The control group (G4) consisted of slabs (n=10) that did not receive any varnish treatment and were maintained in artificial saliva for 14 days. Microhardness tests were performed with Knoop indentation with a load of 25 grams for 5 seconds at the beginning of the treatment (baseline values) and after 7 and 14 days. Cylinders were made with microhybrid resin composite and one-bottle adhesive system for shear bond strength tests. Using a universal testing machine with a speed of 0.5 mm/minute to obtain the values in MPa. RESULTS: The Kruskal-Wallis test showed no changes in microhardness values among groups after 7-day varnish application, although there was a decrease in microhardness values when using an 18% carbamide peroxide varnish twice a day with a time-interval of 5 hours between applications (P < 0.05). For enamel shear bond strength, ANOVA test (P > 0.05) did not show significant differences among the groups (G1=15.8; G2=15.2; G3=19.0; G4=15.1).     

Transgenic angiotensin-converting enzyme 2 overexpression in vessels of SHRSP rats reduces blood pressure and improves endothelial function

Rat models of hypertension, eg, spontaneously hypertensive stroke-prone rats (SHRSP), display reduced angiotensin-converting enzyme 2 (ACE2) mRNA and protein expression compared with control animals. The aim of this study was to investigate the role of ACE2 in the pathogenesis of hypertension in these models. Therefore, we generated transgenic rats on a SHRSP genetic background expressing the human ACE2 in vascular smooth muscle cells by the use of the SM22 promoter, called SHRSP-ACE2. In these transgenic rats vascular smooth muscle expression of human ACE2 was confirmed by RNase protection, real-time RT-PCR, and ACE2 activity assays. Transgene expression leads to significantly increased circulating levels of angiotensin-(1-7), a prominent product of ACE2. Mean arterial blood pressure was reduced in SHRSP-ACE2 compared to SHRSP rats, and the vasoconstrictive response to intraarterial administration of angiotensin II was attenuated. The latter effect was abolished by previous administration of an ACE2 inhibitor. To evaluate the endothelial function in vivo, endothelium-dependent and endothelium-independent agents such as acetylcholine and sodium nitroprusside, respectively, were applied to the descending thoracic aorta and blood pressure was monitored. Endothelial function turned out to be significantly improved in SHRSP-ACE2 rats compared to SHRSP. These data demonstrate that vascular ACE2 overexpression in SHRSP reduces hypertension probably by locally degrading angiotensin II and improving endothelial function. Thus, activation of the ACE2/angiotensin-(1-7) axis may be a novel therapeutic strategy in hypertension.     

Interleukin-6 enhances growth factor-dependent proliferation of the blast cells of acute myeloblastic leukemia

The effects of recombinant interleukin-6 (IL-6) on the proliferation of blast precursors present in the peripheral blood of patients with acute myeloblastic leukemia (AML) was investigated. IL-6 had little effect by itself; however, it synergized with granulocyte macrophage colony- stimulating factor (GM-CSF) and interleukin-3 (IL-3) in the stimulation of AML blast colony formation. Responsiveness of blast progenitors to IL-6 was heterogeneous. On normal bone marrow cells the same synergy was observed on granulocyte and monocyte precursors (GM-CFC), while there was no significant effect on erythroid and multipotential precursors.     

Control by cations of opioid binding in guinea pig brain membranes.

In membrane suspensions from guinea pig brain or cerebellum, NaCl, LiCl, NH4Cl, and KCl inhibit the equilibrium binding at 25 degrees C of the selective mu-agonist [3H][2-D-alanine,4-methylphenylalanine,5-glycinol]enkephalin ([D-Ala2,MePhe4,Gly-ol5]EK), the selective delta-agonist [3H][2-D-penicillamine,5-D-penicillamine]enkephalin ([D-Pen2,D-Pen5]-EK), and the selective kappa-agonist [3H]dynorphin A-(1-9). Choline chloride inhibits mu- and kappa-binding but not delta-binding. The relative activities of these monovalent salts and the slopes of the dose-response curves are site-dependent. Binding at the kappa-binding site is also inhibited by CaCl2, MnCl2, and MgCl2. On the other hand, these divalent salts potentiate delta-binding, and MnCl2 and MgCl2 have both potentiating and inhibitory effects on mu-binding; CaCl2 inhibits but does not potentiate mu-binding. Thus, the mechanisms by which monovalent cations inhibit opioid binding differ from those of divalent cations, and the mechanisms of action of both monovalent and divalent cations may differ at each site. When the antagonist [3H]naloxone, rather than the agonist [3H][D-Ala2,MePhe4,Gly-ol5]EK, is used to label the mu-binding site, the main effect of NaCl is to potentiate binding; a 22-fold higher concentration of LiCl is required to inhibit binding. The effects of NH4Cl, KCl, MnCl2, MgCl2, CaCl2, and choline chloride are little changed when [3H]naloxone is the ligand.     

Recurring patterns in stationary intervals of abdominal uterine electromyograms during gestation

Abdominal uterine electromyograms (uEMG) studies have focused on uterine contractions to describe the evolution of uterine activity and preterm birth (PTB) prediction. Stationary, non-contracting uEMG has not been studied. The aim of the study was to investigate the recurring patterns in stationary uEMG, their relationship with gestation age and PTB, and PTB predictivity. A public database of 300 (38 PTB) three-channel (S1–S3) uEMG recordings of 30 min, collected between 22 and 35 weeks’ gestation, was used. Motion and labour contraction-free intervals in uEMG were identified as 5-min weak-sense stationarity intervals in 268 (34 PTB) recordings. Sample entropy (SampEn), percentage recurrence (PR), percentage determinism (PD), entropy (ER), and maximum length (L _MAX) of recurrence were calculated and analysed according to the time to delivery and PTB. Random time series were generated by random shuffle (RS) of actual data. Recurrence was present in actual data (p < 0.001) but not RS. In S3, PR (p < 0.005), PD (p < 0.01), ER (p < 0.005), and L _MAX (p < 0.05) were higher, and SampEn lower (p < 0.005) in PTB. Recurrence indices increased (all p < 0.001) and SampEn decreased (p < 0.01) with decreasing time to delivery, suggesting increasingly regular and recurring patterns with gestation progression. All indices predicted PTB with AUC ≥0.62 (p < 0.05). Recurring patterns in stationary non-contracting uEMG were associated with time to delivery but were relatively poor predictors of PTB.     

Effect of candesartan on the expression of sclera-choroidal intercellular adhesion molecule-1 in hypercholesterolemic models

OBJECTIVE:

To evaluate the effect of blocking the angiotensin II AT-1 receptor by the systemic administration of candesartan on the expression of intercellular adhesion molecule-1 in the sclera and choroid of hypercholesterolemic rabbits.

METHODS:

New Zealand rabbits were divided into 3 groups, as follows: GI, which was fed a rabbit standard diet; GII, which was fed a hypercholesterolemic diet; and GIII, which received hypercholesterolemic diet plus candesartan. Samples of the rabbits'' sclera and choroid were then studied by hematoxylin-eosin staining and histomorphometric and immunohistochemical analyses for intercellular adhesion molecule-1 expression.

RESULTS:

Histological analysis of hematoxylin- and eosin-stained sclera and choroid revealed that macrophages were rarely present in GI, and GII had significantly increased macrophage numbers compared to GIII. Moreover, in GII, the sclera and choroid morphometry showed a significant increase in thickness in comparison to GI and GIII. GIII presented a significant increase in thickness in relation to GI. Sclera and choroid immunohistochemical analysis for intercellular adhesion molecule-1 expression revealed a significant increase in immunoreactivity in GII in relation to GI and GIII. GIII showed a significant increase in immunoreactivity in relation to GI.

CONCLUSION:

Candesartan reduced the expression of intercellular adhesion molecule-1 and consequently macrophage accumulation in the sclera and choroid of hypercholesterolemic rabbits.     

Three-dimensional strain-rate imaging

Strain-rate imaging uses large velocity encoding gradients to obtain measurements of velocity that are extremely insensitive to the effects of random noise. The spatial differential of velocity yields the velocity gradient from which the strain-rate and twist-rate tensors can be determined. These tensors represent the distortion of the material and are of interest in the analysis of the dynamic behavior of living tissue (e.g., that of the myocardium). This work presents a new technique that uses the magnitude of the signal in the velocity encoded data to measure through-plane velocity variations at the resolution of the voxel size. The magnitude of the MR signal contains information about the range of phases present within a voxel. When the phase is dependent on the velocity (as in phase velocity imaging), the magnitude contains information about the range of velocities within a voxel. The method presented in this work uses unbalanced slice-refocusing gradients to sample the magnitude variation introduced by the interaction of velocity encoding gradients with spatially dependent velocities. The previously developed in-plane velocity gradient methods can be easily integrated with this new through-plane measurement to characterize the deformation of the myocardium in three spatial dimensions with high accuracy. The applicability of these methods is demonstrated theoretically, in phantoms and in vivo.