Effects of varying the carbohydrate:fat ratio in a hot lunch on postprandial variables in male volunteers.

1. Healthy male volunteers consumed at noon, hot test meals with four different carbohydrate:fat ratios varying between 2.64 and 0.50, and composed of fried beefsteak, mashed potatoes, French beans, and a dessert of custard with mashed peaches. The energy content of the meals was 40% of the daily intake of the volunteers, estimated from their individual dietary histories. 2. Before, and at different times after the start of the meal, blood samples were taken and a number of indices of carbohydrate and lipid metabolism were determined in the samples, i.e. glucose, insulin, free fatty acid, free and total glycerol, free and total cholesterol, high-density-lipoprotein (HDL)-cholesterol and low-density-lipoprotein (LDL)-cholesterol. 3. Increasing the carbohydrate:fat ratio resulted in higher postprandial peaks of glucose and insulin. In addition, the peak area under the postprandial glucose curve showed a significant increase. The peak area under the postprandial insulin curve had also increased, indicating that a larger amount of insulin was secreted by the pancreas on increasing the carbohydrate content in the meal. There was no significant correlation between the height of the postprandial peak of blood glucose and the size of the meal. 4. All four meals caused elevated postprandial blood triacylglycerol levels. However, the decline of this elevated level took a much longer time after the meals with the lower carbohydrate:fat ratios, i.e. containing larger amounts of triacylglycerols. There was a significant decreasing linear relation between the carbohydrate content of the meals and the peak area under the postprandial triacylglycerol curve. Free glycerol and free fatty acids showed lower postprandial levels in the blood after the meals with the higher carbohydrate:fat ratios, and the peak areas of the postprandial curves of both variables displayed a significant decrease. Little or no effect of the meal carbohydrate:fat ratio was observed on the postprandial concentrations of total cholesterol, unesterified cholesterol, HDL-cholesterol or LDL-cholesterol.

Periodontal conditions in patients after molar uprighting.

Fifteen patients who had mandibular molars uprighted unilaterally and seven patients who had mandibular molars uprighted bilaterally were examined an average of 3 1/2 years after treatment had been completed. The investigation focused on differences in clinical observations between the treated teeth and the controls on the contralateral side at the time of the recall examination. Pretreatment radiographs provided longitudinal observations. After elimination of significant but unrelated factors, including surgical pocket elimination and the presence or absence of subgingival margins, the following appeared. Changes in alveolar bone height mesial to the uprighted molars were not different from changes mesial to control teeth. Gingival inflammation scores around uprighted molars were not different from those around control teeth. Pockets mesial to uprighted molars were shallower than those mesial to control teeth. Observations on pocket depth distal to the teeth considered were inconclusive.

Exposure time and the effect of hexylresorcinol on bacterial aggregates.

The bactericidal effect of hexylresorcinol was assessed using bacterial aggregates. Increased drug concentration resulted in decreased survival of bacteria when the aggregates were exposed to hexylresorcinol for at least eight hours. This indicates that this drug may be effective against dental plaque only when available for long periods of time.

Crown-to-root ratio: its significance in restorative dentistry.

The definition of the crown-to-root ratio, its manifestation as a clinical problem, and associated problems were reviewed. Treatment possibilities were discussed in terms of plaque control, periodontal surgery, occlusal adjustment by selective grinding, splinting, restorative considerations, and extraction. The original guidelines for crown-to-root ratio in the selection of abutments were found to be exceptionally conservative and treatment limiting. New treatment modalities were considered in light of increased understanding of periodontal inflammation and its control. With inflammation controlled and with a carefully designed occlusion, some degree of mobility may be tolerated, thereby permitting the retention of teeth with minimal alveolar support.

Chlorhexidine feeding and its effect on growth and intestinal microflora in rats.

Chlorhexidine digluconate was administered to rats by incorporating the drug in drinking water and by regular gastric intubation. Incorporating the drug in the drinking water resulted in feed and water rejection. Relatively high doses (30 mg/day) could be administered over a period of 30 to 45 days without apparent effect on feed and water intake and growth. The total number of bacteria as well as the number of colony-forming units from cecal samples were determined. Chlorhexidine intake did not reduce the cultivable or total intestinal flora.

Effects of cigarette smoke components on in vitro chemotaxis of human polymorphonuclear leukocytes.

Some ciliostatic components of cigarette smoke were studied as inhibitors of in vitro chemotaxis of human polymorphonuclear leukocytes (PMNs). In comparison to their concentration in an inhibitory level of cigarette smoke, the unsaturated aldehydes acrolein and crotonaldehyde were the most potent inhibitors, whereas nicotine, cyanide, acetaldehyde, and furfural were the next strongest inhibitors. In contrast, sulfide, propionaldehyde, butyraldehyde, and the phenols (phenol and o-, m-, and p-cresol) were relatively weak inhibitors of PMN chemotaxis. Acrolein and crotonaldehyde mimicked whole cigarette smoke in their effects on PMNs by not causing loss of PMN viability, yet their effects were prevented by the addition of cysteine. On the other hand, addition of nicotine, cyanide, acetaldehyde, and furfural to PMN suspensions resulted in a limited loss of cellular viabilities, and their effects on PMNs were not prevented by cysteine. Of the tested components, only cyanide significantly altered PMN glucose metabolism by increasing carbon flow via the glycolytic and hexose monophosphate pathways in a manner similar to that observed with whole cigarette smoke. The results of this study suggest that the unsaturated aldehydes, including acrolein and crotonaldehyde, are major contributors to the inhibitory properties of cigarette smoke. The inhibitory effects of these unsaturated aldehydes are probably due to a direct interaction of these oxidants and/or thiol-alkylating agents with PMNs, yet the glucose metabolism of these cells is unaffected. One interpretation of these data is that PMN chemotaxis is dependent upon particular cellular proteins containing one or more essential thiol group(s) but that these proteins are unrelated to glucose metabolism.

Effects of tobacco smoke on chemotaxis and glucose metabolism of polymorphonuclear leukocytes.

The effect of tobacco smoke on in vitro chemotaxis of human polymorphonuclear leukocytes (PMN) was determined. Whole tobacco smoke, gas phase of smoke, and water-soluble fraction were potent inhibitors of PMN chemotaxis. The results indicated that PMN chemotaxis was inhibited in a dose-dependent manner by water-soluble fraction and that this suppression was not a result of cytotoxicity. In an attempt to determine the mechanism of chemotaxis inhibition, the effect of tobacco smoke on glucose metabolism of PMN was studied. Exposure of PMN to whole smoke, gas phase, or water-soluble fraction resulted in an increase (twofold) in glucose catabolism via both glycolysis and the hexose monophosphate shunt, with no apparent effects on the metabolism of glucose via the tricarboxylic acid cycle. These results suggest that the inhibitory effects of tobacco smoke on PMN chemotaxis were not directly attributable to effects on glucose metabolism of these cells. Further, the inhibitory effects of water-soluble fraction on PMN chemotaxis were shown to be largely irreversible and preventable in the presence of cysteine. Thus, the major inhibitory effects of tobacco smoke probably result from the direct action of oxidants and/or thiol-reactive substances on PMN.