The impact of reconditioned orthodontic brackets on bond strength / Faisal Ismail El-Sayed Bahnasi

Introduction: Orthodontic bracket bond failure is common during orthodontic treatment. Objectives: To evaluate the Shear Bond Strength (SBS) of new orthodontic brackets, and the SBS after reconditioning and repeating the reconditioning procedure for such brackets, with and without bonding; and to evaluate the bond failure rate of new and reconditioned orthodontic brackets during orthodontic treatment. Methods: A total of 120-extracted human premolar teeth and 120 premolar stainless-steel brackets were used and were randomly divided into six groups of 20 each. Five methods of reconditioning were used in each of the first five groups while the last group was used as a control. The six groups (I-VI) were subjected to shear force for half an hour until the brackets debonded. SBS was measured and the methods showing the highest SBS were selected. Two groups were selected and then reconditioned for a second time using the previous steps. The SBS of all subgroups were examined with and without the application of a primer. For the clinical experiment, a total of 60-patients were selected from the waiting list of the orthodontic clinic of the Faculty of Dentistry, UNIVERSITY TEKNOLOGI MARA, Malaysia. The patients were randomly divided into three main groups of 20-patients each. 60-sets of 3M Unitek™ Gemini Brackets were used. The first group was reconditioned using 50μm aluminium oxide particle grit-blasting before bonding, the second group was reconditioned using the Er,Cr3+:YSGG laser and the last was used as a control group

The effect of curing methods and loading time on shear bond strength of orthodontic brackets / Faisal Ismail El-Sayed Bahnasi

The introduction of light cured materials in dentistry had led to the development of different curing devices with different curing times. Objectives: to evaluate the effect of light curing units. curing times and the effect of delay loading on shear bond strength (SBS) of orthodontic brackets. Methods: 120-extracted human teeth were divided into 12-groups of 10-teeth each and bonded with stainless-steel brackets by using 3M linitek Transhond XT composite. Specimens NNerc cured with halogen. LED and plasma arc lights with different times. 6-groups of the specimens were tested after 5rnin in shear with Shimadzu Precision Universal Tester at a cross-head speed of Irnm/min until brackets dehonded. The rest of specimen were stored in distilled water at 37°C for 2411 and then subjected to the same loading. The bond strength was calculated by dividing the force in Newton to the surface area. Data were subjected to statistical analysis to identify differences in mean SE3S with respect to curing time and time of force loading. Results: There was no significant dif1rcnce between 6-groups with dehonded fbrce after 5mm. However the other 6- groups with debonded force after 24h showed a statistically significant difference, group 10. LED 20s was significantl y higher than LED lOs. plasma arc 6s and plasma arc lOs. Conclusion: SBS of all curing light devices with applied force after 5 min gave values more than the normal range: therefore arch wire can be inserted at the same visit. Within limit of this study. halogen (20 and 40s). LED (10 and 20s) and plasma arc (6 and lOs) can be used to bond brackets, however if high is needed. LED 20s with loading time after 2411 is recommended

Natural and synthetic flavonoid modulation of TRPC5 channels

Background and Purpose The TRPC5 proteins assemble to create calcium-permeable, non-selective, cationic channels. We sought novel modulators of these channels through studies of natural products. Experimental Approach Intracellular calcium measurements and patch clamp recordings were made from cell lines. Compounds were generated by synthetic chemistry. Key Results Through a screen of natural products used in traditional Chinese medicines, the flavonol galangin was identified as an inhibitor of lanthanide-evoked calcium entry in TRPC5 overexpressing HEK 293 cells (IC50 0.45 μM). Galangin also inhibited lanthanide-evoked TRPC5-mediated current in whole-cell and outside-out patch recordings. In differentiated 3T3-L1 cells, it inhibited constitutive and lanthanide-evoked calcium entry through endogenous TRPC5-containing channels. The related natural flavonols, kaempferol and quercetin were less potent inhibitors of TRPC5. Myricetin and luteolin lacked effect, and apigenin was a stimulator. Based on structure–activity relationship studies with natural and synthetic flavonols, we designed 3,5,7-trihydroxy-2-(2-bromophenyl)-4H-chromen-4-one (AM12), which inhibited lanthanide-evoked TRPC5 activity with an IC50 of 0.28 μM. AM12 also inhibited TRPC5 activity evoked by the agonist (−)-Englerin A and was effective in excised outside-out membrane patches, suggesting a relatively direct effect. It inhibited TRPC4 channels similarly, but its inhibitory effect on TRPC1–TRPC5 heteromeric channels was weaker. Conclusions and Implications The data suggest that galangin (a natural product from the ginger family) is a TRPC5 inhibitor and that other natural and synthetic flavonoids contain antagonist or agonist capabilities at TRPC5 and closely related channels depending on the substitution patterns of both the chromone core and the phenyl ring

Molecular physiology and pharmacolgy of TRPC5 ion channels

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Shalat Sebagai Terapi Psikologi

301 hal.; 23.5 c

Madkhal al-Fiqh al-Jina i al-Islami, 4th.ed./ Bahnasi

211 hal.; 21 cm

al Manzdur al Handasi

123 hal.; 24 C

Cardiac Adaptive Responses After Hypoxia in an Experimental Model

The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (Delta P/Delta t(max)) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P LT .001), RPP (P LT .001), and Delta P/Delta t(max) (P LT .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms

Rapid and Contrasting Effects of Rosiglitazone on Transient Receptor Potential TRPM3 and TRPC5 ChannelsS⃞

The aim of this study was to generate new insight into chemical regulation of transient receptor potential (TRP) channels with relevance to glucose homeostasis and the metabolic syndrome. Human TRP melastatin 2 (TRPM2), TRPM3, and TRP canonical 5 (TRPC5) were conditionally overexpressed in human embryonic kidney 293 cells and studied by using calcium-measurement and patch-clamp techniques. Rosiglitazone and other peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists were investigated. TRPM2 was unaffected by rosiglitazone at concentrations up to 10 μM but was inhibited completely at higher concentrations (IC50, ∼22.5 μM). TRPM3 was more potently inhibited, with effects occurring in a biphasic concentration-dependent manner such that there was approximately 20% inhibition at low concentrations (0.1–1 μM) and full inhibition at higher concentrations (IC50, 5–10 μM). PPAR-γ antagonism by 2-chloro-5-nitrobenzanilide (GW9662) did not prevent inhibition of TRPM3 by rosiglitazone. TRPC5 was strongly stimulated by rosiglitazone at concentrations of ≥10 μM (EC50, ∼30 μM). Effects on TRPM3 and TRPC5 occurred rapidly and reversibly. Troglitazone and pioglitazone inhibited TRPM3 (IC50, 12 μM) but lacked effect on TRPC5, suggesting no relevance of PPAR-γ or the thiazolidinedione moiety to rosiglitazone stimulation of TRPC5. A rosiglitazone-related but nonthiazolidinedione PPAR-γ agonist, N-(2-benzoylphenyl)-O-[2-(methyl-2-pyridinylamino)ethyl]-l-tyrosine (GW1929), was a weak stimulator of TRPM3 and TRPC5. The natural PPAR-γ agonist 15-deoxy prostaglandin J2, had no effect on TRPM3 or TRPC5. The data suggest that rosiglitazone contains chemical moieties that rapidly, strongly, and differentially modulate TRP channels independently of PPAR-γ, potentially contributing to biological consequences of the agent and providing the basis for novel TRP channel pharmacology