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AIM: Evaluate the effectiveness of biannual 38% SDF in arresting early childhood caries (ECC) compared to atraumatic restorative treatment (ART). METHODS: One hundred children (aged 2-5 years) with ECC were (2-5 years) divided equally and randomly into two groups. Test group: 38% SDF biannually; Control group: ART. The primary outcome was caries arrestarrest, which was assessed at the 3,6,9, and 12 months interval. Oral health- related quality of life (OHRQoL) was evaluated at base line and after 12 months using the Parental-Caregiver Perceptions Questionnaire (P-CPQ) and Family Impact Scale (FIS). CONCLUSION: SDF was considerably more effective in arresting ECC after 12 months compared to ART. An overall significant improvement of OHRQoL was reported for both groups with SDF being faintly superior to ART.

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AIM: To evaluate and compare the surface roughness and colour change of microhybrid and nanocomposite after exposure to beverages commonly used by children. METHODS: Thirty discs were prepared using Filtek Z250 and Filtek Supreme composites. Discs were immersed in distilled water, orange juice and Coca-Cola. Colour and surface roughness were measured at baseline and on days 15 and 30. RESULTS: Filtek Z250 and Filtek Supreme showed no significant difference in surface roughness and colour change at all measurement times. Immersion solution had a significant effect on surface roughness as well as colour change. Specimens immersed in Coca-Cola demonstrated the highest effect, followed by those immersed in orange juice, while specimens immersed in distilled water had the least effect. There was a significant increase in surface roughness and colour change over time. The change in colour was more evident in the period between baseline measurements and after 15 days. There was a significant interaction between media type and time. CONCLUSIONS: Both composites showed no significant difference in roughness and colour change at all measurement times. There was a significant increase in surface roughness and colour change in all immersion solutions tested over time. Coca-Cola caused unacceptable colour change.

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The clinical effectiveness of mandibular block anesthesia was compared to that of buccal infiltration anesthesia. A total of eighty patients three to nine years old was selected with identical bilateral lesions. The anesthetic used was mepacaine HCL 2 percent. The treatments performed were restorations, pulpotomies, and extractions. Child behavior and pain reaction were recorded and rated at certain intervals of treatment, using the Frankl behavioral scale and the SEM scale. The Eland color scale was also used in another sample of twenty patients to determine which type of anesthesia was more acceptable to children. The paired t-test was used to compare results. Buccal infiltration anesthesia was found to be as effective as block anesthesia in all situations, except when pulpotomies were performed in the mandibular second primary molar, where it proved to be unreliable regardless of age. Block anesthesia was significantly more painful than buccal infiltration anesthesia, and behavior of children three through five years old sometimes turned negative following the block injection.

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The pharmacokinetics of 2-[(2,6-dichlorophenyl)-amino]phenyl acetic acid (diclofenac sodium) was studied after a single oral dose of 10 mg/kg in rabbits, using a developed HPLC method. The observed serum levels of rabbits were fitted to a one-compartment open model, with first-order absorption and elimination. The mean values of t1/2e, ke, 51/2a, ka and tmax were 1.98 h, 0.3455 h-1, 1.2357 h, 1.2357 h, 0.5653 h-1 and 2.2267 h, respectively. This high-performance liquid chromatographic method for the rapid (about 10 min), sensitive (1 microgram/ml) and specific determination of diclofenac sodium in serum and urine was developed using acetaminophen as the internal standard, a reversed-phase C 18 column, and ethanol: water (1:2) as the mobile phase.

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Alloxan diabetes caused a marked stimulation of endogenous oxygen uptake by rat testis tissues. However, the oxygen uptake in the presence of added glucose or pyruvate as substrate was significantly reduced. The ability of the testis tissues to utilize these substrates and to produce lactate was significantly inhibited in the diabetic animals. Alloxan diabetes also increased the levels of cholesterol, cholesterol esters, non-esterified fatty acids, triglycerides and phospholipids in rat testis tissues. Treatment of the diabetic rats with ascorbic acid caused more or less a normalization of all the parameters tested.

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The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenate of non infected mice were determined. In vitro, niridazole was found to inhibit the succinate and pyruvate oxidation at the high concentration tested (10(-3)M). The rate of gluconeogenesis from alpha-ketoglutarate was unaffected. In vivo, niridazole showed a stimulatory effect on the rate of gluconeogenesis from alpha-ketoglutarate and on the rate of oxidation of pyruvate at a dosage level of 100 mg/kg for 5 days. The observed changes were discussed and the differences observed between the in vivo and in vitro work were assumed to be due to exposure of the tissues to the unmetabolized drug in vitro and to the drug and its metabolites in vivo.

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The effects of the antischistosomal drug, niridazole, on the rate of gluconeogenesis in kidney cortex slices and on the rate of oxidation of pyruvate and some Krebs cycle intermediates in liver homogenates of infected mice were described. The effect of schistosoma mansoni infection on the previously mentioned parameters was also described. The infection per se did not affect the rate of gluconeogenesis from pyruvate, succinate and alpha-ketoglutarate when used as gluconeogenic precursors. In case of the rates of oxidation of pyruvate, succinate alpha-ketoglutarate and citrate, the infection decreased them significantly. In vitro, niridazole did not increase the inhibition of the rate of oxidation of different substances studied caused by the infection per se. The rate of gluconeogenesis from alpha-ketoglutarate was also unaffected. In vivo, niridazole did not affect the oxidoreductases more than did the infection per se. In fact in many cases, the drug tended to normalize the inhibitory effect of the infection on some of the enzyme systems, particularly in the case of the citrate succinate and pyruvate. On administration of 100 mg/kg of niridazole for 5 days (i.e. low dosage only) the rate of gluconeogenesis from pyruvate and alpha-ketoglutarate was stimulated. Such effects seem to be related to the presence of metabolites rather than to the parent drug.

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BILHARCID inhibited malate and pyruvate oxidation. The degree of inhibition reached 50% when the concentration of Bilharcid was 10(-3) M. The mechanisms of the inhibitory action of the drug are discussed with reference to the effects of both adenine and pyridine nucleotides on the activity of the oxidoreductase enzymes.

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IN THIS INVESTIGATION, the effects of the examined antibilharzial agents are as follows: Bilharcid and tartar-emetic similarly affected succinate oxidation. 50% inhibition could be obtained at a concentration of 10(-3) of both drugs. Malate oxidation was differently affected by the drugs. Bilharcid and tartar-emetic at a concentration of 10(-3) M induced 50% and 70% inhibition respectively, while tartar-emetic stimulated malate oxidation if added in a concentration of 10(-5) M. Pyruvate oxidation was affected in the same manner and to the same extent as malate oxidation. Citrate oxidation was slightly inhibited by Bilharcid and tartar-emetic. 10% and 30% inhibition could be obtained if the concentration was 10(-3) M of both drugs respectively. Bilharcid had a biphasic effect on citrate oxidation. Stimulation could be observed at low concentrations (up to 10(-8) M and inhibition at higher ones (up to 10(-3) M. Piperazine hexahydrate was nearly without effect on the rate of oxidation of the four mentioned substrates.

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THE INHIBITION of succinate oxidation by Piperazine diantimonyl tartarate (Bilharcid) could be in part attributed to accumulation of oxaloacetate. This is discussed with reference to the effect of ATP, glutamate and cysteine on the reversal of the inhibitory action, of the drug on succinate oxidation.

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Two colorimetric methods are presented for determining reserpine. In the first method, an iron hydroxamate complex is formed through the ester group in position 16 in the reserpine molecule. The color is measured at 535 nm (0.5-6 mg/25 ml). This method is useful for routine and control analyses of reserpine formulations. In the second method the tertiary amino group of reserpine reacts with 2% citric acid in acetic anhydride to form a red-violet complex which is measured at 505 nm (5-400 mug/10 ml). This method could be useful in measuring trace amounts of reserpine present in biological fluids.

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A sensitive method is presented for determining aconitine. Aconitine is complexed with Co2+, the aconitine-cobalt complex is extracted with chloroform, and the absorbance is measured at 320 nm. The sensitivity of the method ranged between 0.06 and 3 mg/25 ml, and the color was stable for 6 hr. The method was successfully applied for the quantitative determination of aconitine in animal tissues.

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Bilharcid inhibited citrate oxidation and the inhibition was decreased by time. The inhibition is not restored or reduced by increasing citrate concentration. NAD stimulated citrate oxidation in the presence of Bilharcid. Cysteine slightly stimulated citrate oxidation, while ATP had no effect. Addition of citrate before Bilharcid protected the enzyme against the inhibitory action of the drug.

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The effects of the organophosphorous insecticide, Dursban, on aerobic oxidation, glycolysis, glucose utilization and gluconeogenesis in snails tissues were determined. Dursban had a biphasic effect on the aerobic oxidation of succinate, glutamate + malate and TMPD + ascorbate while it had only an inhibitory action on pyruvate oxidation. The compound significantly inhibited glycolysis, glucose utilization and gluconeogenesis when used at high concentrations (ten times higher than its LC50). However, it had a slight effect on thepreviously mentioned process when its concentration was equal to or approximated its LC50. The relationship between the metabolic effect of Dursban and its molluscicidal activity is discussed.

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Previous work has shown that the aerobic oxidation of certain intermediates of Krebs cycle by the snail B. alexandrina and B. truncatusis inhibited by TPT. This paper reports data on the effect of TPT on glucose utilization, glycolysis, glycogen content, and glucone ogenesis in snail tissue preparations. The compounds at its LC50 inhibited gluconeogenesis, stimulated glycolysis and markedly reduced the glycogen content and glucose utilization in both snails. However, the effects were more pronounced in B. truncatus than in B. alexandrina. Possible interpretations of these findings are discussed with reference to published arrangements for regulation of gluconeogenesis and glycolysis, coupling of electorn transport to ATP synthesis and also to our present knowledge of the chemical and biological specificity of TPT.

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