Influence of the Light-Curing Unit, Storage Time and Shade of a Dental Composite Resin on the Fluorescence

The aim of this study was to determine the influence of three light-curing units, storage times and colors of the dental composite resin on the fluorescence. The specimens (diameter 10.0 +/- 0.1 mm, thickness 1.0 +/- 0.1 mm) were made using a stainless steel mold. The mold was filled with the microhybrid composite resin and a polyethylene film covered each side of the mold. After this, a glass slide was placed on the top of the mold. To standardize the top surface of the specimens a circular weight (1 kg) with an orifice to pass the light tip of the LCU was placed on the top surface and photo-activated during 40 s. Five specimens were made for each group. The groups were divided into 9 groups following the LCUs (one QTH and two LEDs), storage times (immediately after curing, 24 hours, 7 and 30 days) and colors (shades: A(2)E, A(2)D, and TC) of the composite resin. After photo-activation, the specimens were storage in artificial saliva during the storage times proposed to each group at 37 C and 100% humidity. The analysis of variance (ANOVA) and Tukey's post-hoc tests showed no significant difference between storage times (immediately, 24 hours and 30 days) (P > 0.05). The means of fluorescence had difference significant to color and light-curing unit used to all period of storage (P < 0.05). The colors had difference significant between them (shades: A2D < A2E < TC) (P < 0.05). The Ultraled (LED) and Ultralux (QTH) when used the TC shade showed higher than Radii (LED), however to A2E shade and A2D shade any difference were found (P > 0.05).

A thin layer electrochemical cell for disinfection of water contaminated with Staphylococcus aureus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Surfactin reduces the adhesion of food-borne pathogenic bacteria to solid surfaces

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Proposal of Using Ozonated Water to Control Biofilm Formation on Mouth-Related Devices

The purpose of this study was to evaluate the antimicrobial effectiveness and dental applications of ozonated water generated by portable equipment (0.667 mg/L). Total elimination of C. albicans, E. coli and S. mutans planktonic cells was observed after 5 min. Reduction in the number of viable cells of biofilms formed on acrylic resin was observed for C. albicans, S. mutans and E. coli. The same effect was observed on biofilms of E. coli, S. aureus, S. mutans and C. albicans formed on stainless steel. Ozonated water was effective for the disinfection of experimentally contaminated toothbrushes.

Análise morfológica da corrosão por pites em aço inoxidável austenítico AISI 310S submetido à exposição em névoa salina

O artigo teve como objetivo estudar a evolução do crescimento, distribuição e classificação dos pites em aços inoxidáveis austeníticos AISI 310S no estado como recebida e tratado termicamente, submetidos a diferentes tempos de exposição em meio salino. A aplicabilidade deste trabalho baseou-se no desenvolvimento de uma técnica para caracterização morfológica da corrosão localizada, associado com os aspectos de descrição de formas, tamanho, parâmetros específicos e populacionais. A metodologia consistiu nas seguintes etapas: preparação dos corpos de prova, testes de corrosão via névoa salina em diferentes condições, análise microestrutural, análise dos perfis dos pites, processamento digital e análise de imagens, visando caracterizar a distribuição, morfologia e o tamanho dos pites. Os resultados obtidos no processamento digital e análise de imagens dos perfis foram submetidos á análise estatística, utilizando à mediana como parâmetro de avaliação na liga como recebido e tratada. A liga como recebido, exibe a seguinte morfologia: pites hemisféricos> região de transição A> região de transição B> irregulares> cônicos. A quantidade de pites na liga tratada a cada tempo de exposição é: região de transição B> hemisféricos> região de transição A> cônicos> irregulares.

Effects of the administration of a catalase inhibitor into the fourth cerebral ventricle on cardiovascular responses in spontaneously hypertensive rats exposed to sidestream cigarette smoke

OBJECTIVE: ,,,,,Previous studies have demonstrated a relationship between brain oxidative stress and cardiovascular regulation. We evaluated the effects of central catalase inhibition on cardiovascular responses in spontaneously hypertensive rats exposed to sidestream cigarette smoke. ,,,, ,,,, ,,,,,METHODS: ,,,,,Male Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SH) (16 weeks old) were implanted with a stainless steel guide cannula leading into the fourth cerebral ventricle (4th V). The femoral artery and vein were cannulated for arterial pressure and heart rate measurement and drug infusion, respectively. The rats were exposed to sidestream cigarette smoke for 180 minutes/day, 5 days/week for 3 weeks (CO: 100-300 ppm). The baroreflex was tested using a pressor dose of phenylephrine (8 μg/kg, bolus) and a depressor dose of sodium nitroprusside (50 μg/kg, bolus). Cardiovascular responses were evaluated before and 5, 15, 30 and 60 minutes after injection of a catalase inhibitor (3-amino-1,2,4-triazole, 0.001 g/100 μL) into the 4th V. ,,,, ,,,, ,,,,,RESULTS: ,,,,,Vehicle administration into the 4th V did not affect the cardiovascular response, whereas administration of the central catalase inhibitor increased the basal HR and attenuated the bradycardic peak (p<0.05) to a greater extent in WKY rats exposed to sidestream cigarette smoke than in WKY rats exposed to fresh air. However, in spontaneously hypertensive rats, the effect of the catalase inhibitor treatment was stronger in the fresh air condition (p<0.05). ,,,, ,,,, ,,,,,CONCLUSION: ,,,,,Administration of a catalase inhibitor into the 4th V combined with exposure to sidestream cigarette smoke has a stronger effect in WKY rats than in SH rats.

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

We investigated the role of alpha-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na+, K+ and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/µl) increased water intake (12.5 ± 1.7 ml/120 min). Clonidine (20 nmol/µl) injected into the MSA reduced the ANGII-induced water intake (2.9 ± 0.5 ml/120 min). Pretreatment with 80 nmol/µl yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 ± 0.4 and 3.1 ± 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGII-induced water intake (0.2 ± 0.1 and 0.2 ± 0.1 ml/120 min, respectively). ANGII reduced Na+ (23 ± 7 µEq/120 min), K+ (27 ± 3 µEq/120 min) and urine volume (4.3 ± 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of alpha1- and alpha2-antagonists decreased ANGII-induced water intake, and abolished the Na+, K+ and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal alpha1- and alpha2-adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII.

Role of nitric oxide of the median preoptic nucleus (MnPO) in the alterations of salivary flow, arterial pressure and heart rate induced by injection of pilocarpine into the MnPO and intraperitoneally

We investigated the effect of L-NAME, a nitric oxide (NO) inhibitor and sodium nitroprusside (SNP), an NO-donating agent, on pilocarpine-induced alterations in salivary flow, mean arterial blood pressure (MAP) and heart rate (HR) in rats. Male Holtzman rats (250-300 g) were implanted with a stainless steel cannula directly into the median preoptic nucleus (MnPO). Pilocarpine (10, 20, 40, 80, 160 µg) injected into the MnPO induced an increase in salivary secretion (P<0.01). Pilocarpine (1, 2, 4, 8, 16 mg/kg) ip also increased salivary secretion (P<0.01). Injection of L-NAME (40 µg) into the MnPO prior to pilocarpine (10, 20, 40, 80, 160 µg) injected into the MnPO or ip (1, 2, 4, 8, 16 mg/kg) increased salivary secretion (P<0.01). SNP (30 µg) injected into the MnPO or ip prior to pilocarpine attenuated salivary secretion (P<0.01). Pilocarpine (40 µg) injection into the MnPO increased MAP and decreased HR (P<0.01). Pilocarpine (4 mg/kg body weight) ip produced a decrease in MAP and an increase in HR (P<0.01). Injection of L-NAME (40 µg) into the MnPO prior to pilocarpine potentiated the increase in MAP and reduced HR (P<0.01). SNP (30 µg) injected into the MnPO prior to pilocarpine attenuated (100%) the effect of pilocarpine on MAP, with no effect on HR. Administration of L-NAME (40 µg) into the MnPO potentiated the effect of pilocarpine injected ip. SNP (30 µg) injected into the MnPO attenuated the effect of ip pilocarpine on MAP and HR. The present study suggests that in the rat MnPO 1) NO is important for the effects of pilocarpine on salivary flow, and 2) pilocarpine interferes with blood pressure and HR (side effects of pilocarpine), that is attenuated by NO.

CARDIOVASCULAR EFFECTS OF CENTRAL CLONIDINE IN CONSCIOUS RATS AFTER HYPOTHALAMIC-LESIONS

The central injection of clonidine (an alpha-2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and bradycardia. The present study was performed to investigate the effect of electrolytic lesions in the anteroventral third ventricle (AV3V) region or in the lateral hypothalamus (LH) on the pressor and bradycardic responses induced by central clonidine in rats. Mean arterial pressure and heart rate were recorded in sham or AV3V-lesioned rats with cerebral stainless steel cannulae implanted into the lateral cerebral ventricle (ICV) or LH. and in sham or bilateral LH-lesioned rats with cannulae-implanted ICV. The injection of clonidine (40 nmol) ICV or into the LH of sham rats produced a pressor response (37 +/- 2-48 +/- 3 mmHg) and bradycardia (-45 +/- 10--93 +/- 6 bpm). After AV3V-lesion (3 and 12 days) or LH-lesion (3 days) the pressor response was abolished and a small hypotensive response was induced by the injection of clonidine (-1 +/- 3--16 +/- 3 mmHg). The bradycardia (-27 +/- 6--57 +/- 11 bpm) was reduced, but not abolished by the lesions. These results show that the AV3V region and LH are important cerebral structures that participate in the excitatory pathways involved in the pressor response to central clonidine in rats. They also suggest that, in the absence of these pressor pathways, the hypotensive responses to central clonidine may appear in conscious rats.

LESIONS OF THE LATERAL HYPOTHALAMUS IMPAIR THE PRESSOR-RESPONSE TO CLONIDINE INJECTED INTO THE MEDIAL SEPTAL AREA OF CONSCIOUS RATS

The central injection of clonidine (an alpha-2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and bradycardia. The present study was performed to investigate the effect of electrolytic lesions of the lateral hypothalamus (LH) on the pressor and bradycardic responses induced by clonidine injected into the medial septal area (MSA) in conscious and unrestrained rats. Male Holtzman rats weighing 250-300 g were used. Mean arterial pressure and heart rate were recorded in sham- or bilateral LH-lesioned rats with a cerebral stainless steel cannula implanted into the MSA. The injection of clonidine (40 nmol/mu-l) into the MSA of sham rats (N = 8) produced a pressor response (36 +/- 7 mmHg, P<0.05) and bradycardia (-70 +/- 13 bpm, P<0.05) compared to saline. Fourteen days after LH-lesion (N = 9) the pressor response was reduced (9 +/- 10 mmHg, P<0.05) but no change was observed in the bradycardia (-107 +/- 24 bpm). These results show that LH is an important area involved in the pressor response to clonidine injected into the MSA of rats.

Involvement of the Central Nervous System in the Salivary Secretion Induced by Pilocarpine in Rats

The effect in rats of an anteroventral third ventricle (AV3V) electrolytic lesion on salivary secretion induced by intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) injection of a cholinergic agonist (pilocarpine) was investigated. Sham- or AV3V-lesioned rats anesthetized with urethane and with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The amount of salivary secretion was studied over a seven-minute period after i.c.v. or i.p. injection of pilocarpine. In sham-operated rats, i.p. injection of pilocarpine (1 mg/kg b.w.) (after 6 h, 2, 7, and 15 days) produced salivary secretion (486 +/- 21, 778 +/- 85, 630 +/- 50, and 560 +/- 55 mg/7 min, respectively). This effect was reduced 6 h, 2, and 7 days after an AV3V lesion (142 +/- 22, 113 +/- 32, and 290 +/- 62 mg/7 min, respectively), but not 15 days after an AV3V lesion (516 +/- 19 mg/7 min). I.c.v. injection of pilocarpine (120 mug in 1 muL), in sham-operated rats after 6 h, 2, 7, and 15 days also produced salivary secretion (443 +/- 20, 417 +/- 81, 496 +/- 14, and 427 +/- 47 mg/7 min, respectively). The effects of i.c.v. pilocarpine were also reduced 6 h, 2, and 7 days after an AV3V lesion (143 +/- 19, 273 +/- 14, and 322 +/- 17 mg/7 min, respectively), but not after 15 days (450 +/- 28 mg/7 min). The results demonstrate that the central nervous system, and particularly the AV3V region, is important for the effect of pilocarpine on salivary secretion in rats. Moreover, they suggest that activation of central pathways may play an important part in the salivary secretion to peripheral pilocarpine in rats.

Lateral parabrachial nucleus and serotonergic mechanisms in the control of salt appetite in rats

This study investigated the effects of bilateral injections of serotonergic receptor agonist and antagonist into the lateral parabrachial nucleus (LPBN) on the ingestion of water and 0.3 M NaCl induced by intracerebroventricular angiotensin II (ANG II) or by combined subcutaneous injections of the diuretic furosemide (Furo) and the angiotensin-converting enzyme inhibitor captopril (Cap). Rats had stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle. Bilateral LPBN pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (4 mu g/200 nl each site) increased 0.3 M NaCl and water intakes induced by intracerebroventricular ANG II (50 ng/mu l) and 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with bilateral LPBN injections of a serotonergic 5-HT2A/2C receptor agonist DOI (5 mu g/200 nl) significantly reduced 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with methysergide or DOI into the LPBN produced no significant changes in the water intake induced by subcutaneous Furo + Cap. These results suggest that serotonergic mechanisms associated with the LPBN may have inhibitory roles in water and sodium ingestion in rats.

AV3V-LESION IMPAIRS RESPONSES INDUCED BY CHOLINERGIC ACTIVATION OF SFO IN RATS

This study was performed to investigate the effect of lesion of the anteroventral third ventricle (AV3V) region on the pressor, bradycardic, dipsogenic, natriuretic, kaliuretic, and antidiuretic responses induced by cholinergic activation of the subfornical organ (SFO) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with a stainless steel cannula directly into the SFO. Microinjection of the cholinergic agonist carbachol (2 nmol) into the SFO of sham rats induced natriuresis (563 +/- 70 mueq/120 min), kaliuresis (205 +/- 13 mueq/120 min), antidiuresis (10.4 +/- 0.5 ml/120 min), water intake (9.3 +/-1.4 ml/h), bradycardia (-42 +/- 11 beats/min), and increased mean arterial pressure (53 +/- 3 mmHg). In AV3V-lesioned rats (1-5 and 14-18 days), there was a reduction of natriuresis (23 +/-11 and 105 +/- 26 mueq/120 min, respectively), kaliuresis (92 +/- 16 and 100 +/- 17 mueq/120 min), water intake (2.5 +/- 0.9 and 1.8 +/- 1.0 ml/h), and arterial pressure increase (17 +/- 2 and 16 +/- 2 mmHg) induced by carbachol into the SFO. Increased antidiuresis (6.0 +/- 1.0 and 5.2 +/- 0.7 ml/120 min, respectively) and tachycardia (39 +/- 4 and 15 +/- 12 beats/min) instead of bradycardia were also observed in both groups of AV3V-lesioned rats. These results show that cholinergic activation of the rat SFO produces marked natriuresis and kaliuresis in addition to the well-known pressor and dipsogenic responses. They also show that the AV3V region plays an important role in the cardiovascular, fluid, and electrolytic changes induced by cholinergic activation of the SFO in rats.

AV3V LESION SUPPRESSES THE PRESSOR, DIPSOGENIC AND NATRIURETIC RESPONSES TO CHOLINERGIC ACTIVATION OF THE SEPTAL AREA IN RATS

In the present study we investigated the effect of anteroventral third ventricle (AV3V) lesion on pressor, dipsogenic, natriuretic and kaliuretic responses induced by the injection of carbachol (a cholinergic agonist) into the medial septal area (MSA) of rats. Male rats with sham or AV3V lesion and a stainless-steel cannula implanted into the MSA were used. Carbachol (2 nmol) injected into the MSA in sham lesion rats produced pressor (43 +/- 2 mmHg), dipsogenic (9.6 +/- 1.2 ml/h), natriuretic (531 +/- 82-mu-Eq/120 min) and kaliuretic (164 +/- 14-mu-Eq/120 min) responses. In AV3V-lesioned rats (1-5 days and 14-18 days), the pressor (11 +/- 2 mmHg, respectively), dipsogenic (1.9 +/- 0.7 and 1.4 +/- 0.6 ml/h), natriuretic (21 +/- 5 and 159 +/- 44-mu-Eq/120 min) and kaliuretic (124 +/- 14 and 86 +/- 13-mu-Eq/120 min) responses induced by carbachol injection into the MSA were reduced. These results show that the AV3V region is essential for the pressor, dipsogenic, natriuretic and kaliuretic responses induced by cholinergic activation of the MSA in rats.

Ventromedial hypothalamus lesions increase the dipsogenic responses and reduce the pressor responses to median preoptic area activation

In this study, we investigated the participation of adrenergic receptors of the median preoptic area (MnPO) and the participation of ventromedial hypothalamus (VMH) in angiotensin II- (ANG II)-induced water intake and presser responses. Male rats with sham or electrolytic VMH lesions and a stainless steel cannula implanted into the MnPO were used. Noradrenaline, clonidine (an alpha(2)-adrenergic receptor agonist), or phenylephrine (an alpha(1)-adrenergic receptor agonist) injected into the MnPO of sham-lesioned rats reduced water ingestion induced by ANG II injected into the same area. In VMH-lesioned rats ANG II-induced water intake increased with a previous injection of noradrenaline, phenylephrine, or isoproterenol. The presser response induced by ANG II injected into the MnPO was reduced in VMH-lesioned rats, whereas the presser response induced by clonidine was abolished. Previous treatment with noradrenaline and phenylephrine into the MnPO of sham-lesioned rats produced a presser response, and a hypotensive response was obtained with the previous administration of noradrenaline, phenylephrine or isoproterenol into the MnPO of VMH-lesioned rats. These results show that VMH is essential for the dipsogenic and presser responses induced by adrenergic and angiotensinergic activation of the MnPO in rats. (C) 1997 Elsevier B.V.