Inhibition of experimental caries by plaque prevention

abstract – The purpose of this study was to test the hypothesis that a frequent intake of sucrose does not produce caries if the teeth are regularly treated with an antibacterial agent. Twenty-four students with clean teeth and normal gingivae were assigned to one of the following three groups: (1) eight individuals ceased all active oral hygiene measures and rinsed 9 times daily with 50% sucrose, (2) eight students refrained from all active oral hygiene procedures, rinsed 9 times daily with sucrose and twice daily with 10 ml 0.2% chlorhexidine gluconate, (3) the third group consisted of two subgroups each comprising 4 students. One subgroup ceased all oral hygiene procedures and rinsed twice daily with 0.2% chlorhexidine gluconate. The other was instructed to practice meticulous tooth brushing twice daily. The experiment lasted for 22 days. The group who rinsed with sucrose showed heavy plaque accumulation, those who rinsed with sucrose + chlorhexidine showed a drastic reduction in the formation of plaque. In the subgroup rinsing with chlorhexidine only and in that performing good oral hygiene, plaque was non-existent. The gingival state essentially paralleled the plaque formation. The sucrose group showed a definite increase in Caries Index. No significant changes occurred in the group rinsing with sucrose + chlorhexidine, with chlorhexidine only, or in the group performing good oral hygiene. It is concluded that prevention of plaque formation inhibits the development of gingivitis and dental caries, even with frequent rinses of sucrose.     

Fusion of dispatching centres into one entity: effects on performance

Background: Dispatching centres were fused into one of the 112 entity, which caused concerns regarding whether the medical calls could be processed effectively also in the new centre. We evaluated the effects of the reform on key performance criteria in medical calls. Methods: This observational study in the Helsinki Dispatching Centre consisted of two periods: Period I 2 years before the reform and Period II 2 years after. The main outcome measures were answering and call processing times, accuracy of risk assessment and appropriate use of ambulances. Results: In Period I (n=574,276), 92.2% of all incoming phone calls were answered within 10 s and in Period II (n=758,022) 82.8% (P<0.0001). Time to dispatch a first responding fire unit increased from 98 to 113 s (P<0.0001) and an advanced life support unit in category A calls increased from 73 to 84 s (P<0.0001). In Period I 47.7%, 34.8% and 17.5% of phone calls were completed in <3, 3–5 and >5 min and in Period II 29.8%, 36.1% and 34.1% (P<0.0001). The number of three studied non‐transportation call types and unnecessary lights‐and‐siren responses increased significantly (P<0.0001 and 0.0001, respectively). Neither the accuracy of risk assessment in the three studied call types nor the rate of telephone‐guided cardiopulmonary resuscitation changed. Conclusions: The reform increased the total number of ambulance dispatches, prolonged answering and call processing times and had a negative effect on the appropriate use of ambulances. The accuracy of risk assessment was not affected. Evidence‐based data should be the basis for the future as dispatching centre processes are shown to be vulnerable during organisational reforms.     

The relationship between audiogenic seizure (AGS) susceptibility and forebrain tone-responsiveness in genetically AGS-prone Wistar rats

The present study characterized the intensity-response functions of extracellular field responsiveness of different cortical/subcortical structures of the forebrain following the free-field presentation of tone stimuli, within a population of genetically audiogenic seizure (AGS)-prone KM-Wistar rats. The neural response properties of each case were compared to its propensity to exhibit AGSs during the continuous tone stimulation (15 kHz, 90 s at max.). The amplitudes or slope components of the evoked responses and their peak latencies showed significant positive (amplitude and slope) and negative (peak latency) Bolzmann's sigmoid relationships with the onset-latency of AGS. These relationships, with areal differences in the slopes of saturation functions, applied for the three different data sets recorded simultaneously from the stratum radiatum dendritic layer of the hippocampal CA1 area, primary auditory cortex layers II-IV, and frontal cortex surface. In addition, the similar type of functions between the evoked response variables and AGS onset latency held when all the areas were considered together. These data suggest that the neural responsiveness to acoustic stimulation of the primary sensory, multimodal and association cortices of the forebrain may altogether contribute to the seizure initiation by that modality in the genetically AGS-prone rats. It has been previously shown that there exist abundant and dispersed auditory projections from these forebrain areas to the brain stem and spinal cord, structures that are generally considered to be the key predisposing factors in the generation of AGS. Hence, the types of correlation found reflect the subject-specific stage of forebrain responsiveness, being either related or unrelated to genetic AGS-specific changes, and possibly its triggering impact upon the lower brain AGS network. Accordingly, the mere comparison of forebrain response measures of these AGS-prone animals with those of the AGS-resistant ones could not reveal the result presented.     

Effect of TCDD on mRNA expression of genes encoding bHLH/PAS proteins in rat hypothalamus

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) brings about a wide variety of toxic and biochemical effects via an AH receptor (AHR)-mediated signalling pathway. Wasting syndrome and acute lethality are TCDD-induced endpoints showing a striking sensitivity difference between two rat strains, TCDD-sensitive Long-Evans (Turku/AB) (L-E) and TCDD-resistant Han/Wistar (Kuopio) (H/W). These rat strains were used to study hypothalamic effects of TCDD on expression of genes encoding AHR-regulated bHLH/PAS proteins potentially involved in molecular pathogenesis of the wasting syndrome. In addition, two well-established target genes of TCDD, CYP1A1 and CYP1A2 were also examined. Quantitative RT-PCR was used to measure mRNA levels in hypothalamus, which is a major center of food intake and body weight regulation. At both 6 and 96 h after a single dose of 50 microg/kg TCDD, significant elevations were found in mRNA levels of AHR repressor (AHRR), CYP1A1 and CYP1A2, but not those of AHR, ARNT or ARNT2. Likewise, TCDD (100 microg/kg) did not alter the expression of SIM1, implicated in the suppressive impact of TCDD on food intake, nor that of PER2, involved in regulation of circadian rhythms. Differences between H/W and L-E rats appeared in constitutive levels of AHR and ARNT and in TCDD-induced levels of CYP1A2, AHRR, AHR and ARNT, which all were about two- to four-fold lower in H/W rats. Thus, although the changes found do not account for the wasting syndrome, expression of all principal genes of the AHR-signalling pathway in rat hypothalamus make it a candidate target for TCDD.     

Developmental dental aberrations after the dioxin accident in Seveso

Children's developing teeth may be sensitive to environmental dioxins, and in animal studies developing teeth are one of the most sensitive targets of toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Twenty-five years after the dioxin accident in Seveso, Italy, 48 subjects from the contaminated areas (zones A and B) and in patches lightly contaminated (zone R) were recruited for the examination of dental and oral aberrations. Subjects were randomly invited from those exposed in their childhood and for whom frozen serum samples were available. The subjects were frequency matched with 65 subjects from the surrounding non-ABR zone for age, sex, and education. Concentrations of TCDD in previously analyzed plasma samples (zone ABR subjects only) ranged from 23 to 26,000 ng/kg in serum lipid. Ninety-three percent (25 of 27) of the subjects who had developmental enamel defects had been < 5 years of age at the time of the accident. The prevalence of defects in this age group was 42% (15 of 36) in zone ABR subjects and 26% (10 of 39) in zone non-ABR subjects, correlating with serum TCDD levels (p = 0.016). Hypodontia was seen in 12.5% (6 of 48) and 4.6% (3 of 65) of the zone ABR and non-ABR subjects, respectively, also correlating with serum TCDD level (p = 0.05). In conclusion, developmental dental aberrations were associated with childhood exposure to TCDD. In contrast, dental caries and periodontal disease, both infectious in nature, and oral pigmentation and salivary flow rate were not related to the exposure. The results support our hypothesis that dioxins can interfere with human organogenesis.     

简易4步让全身肌肤柔滑过冬

冬天干冷的气候会令全身肌肤可能因此越来越干燥、粗糙，失去水分和光泽。选择有良好滋润功效的沐浴露和身体乳液，让你在寒冷冬天也能拥有一身光滑细腻的肌肤。[编者按]     

Pulse pressure in tests improves the prediction of left ventricular mass: 10 years of follow-up

Literature does not agree with the usefulness of exercise blood pressure (BP) in predicting hypertension or target organ damage. In this prospective 10 years of follow-up, we evaluated if exaggerated BP responses to tests may improve the prediction of left ventricular mass index (LVMI). At baseline, BP was recorded by casual measurements, and during tests using intra-arterial monitoring. The subjects were 97 healthy, untreated 35- to 45-year-old-men (34 normotensive, 29 borderline hypertensive, and 34 mild hypertensive). At 10-year follow-up, echocardiography was performed to 86 (89%) of them. Subjects not taking antihypertensive medication (n = 66) were included in the prediction of LVMI(g m-2). Echocardiography data at baseline was available from 70 (72%) of the subjects, of whom 52 did not use antihypertensive medication at follow-up. Pulse pressure (PP) at supine test (r = 0.337, P = 0.006), PP at dynamic exercise last work load (r = 0.332, P = 0.006), and PP after dynamic exercise (r = 0.316, P = 0.010) were the best BP variables achieved in tests in predicting future LVMI of the 66 subjects. Casual BP did not significantly correlate with future LVMI. The best model in predicting LVMI included PP achieved after dynamic exercise, family history of hypertension, and body mass index (BMI) (adj.R2 = 0.207). Baseline LVMI correlated significantly with future LVMI only among the 52 unmedicated subjects (r = 0.508, P<0.0001). The predictive value of baseline LVMI on future LVMI among them (adj.R2 = 0.243) was best improved by PP achieved in supine test and age (adj.R2 = 0.350). In conclusion, BP measurements during tests improved the prediction of LVMI compared with casual BP. For the first time, the pulsatile component of BP in tests was found to be the most significant BP parameter in predicting future LVMI.     

Effect of intracerebral 6-nitronoradrenaline, an endogenous catechol-O-methyltransferase (COMT) inhibitor, on striatal dopamine metabolism in anaesthetised rats

6-Nitronoradrenaline, a bioactive compound recently identified in the brain, is known to inhibit catechol-O-methyltransferase. To study its effect on dopamine metabolism, it was administered into rat striatum via a microdialysis probe. Other nitrated catechols (6-nitrodopamine, 6-nitro-DOPAC and 5-nitro-HVA) were studied for comparison. Tolcapone, a selective catechol-O-methyltransferase inhibitor, was used as a positive reference compound. Both 6-nitronoradrenaline and tolcapone increased striatal extracellular dopamine levels during the perfusion (at 100 microM concentration but not at 10 microM) and decreased the efflux of homovanillic acid. Tolcapone, but not other nitrated catechols, increased 3,4-dihydroxyphenylacetic acid efflux. None of the compounds inhibited MAO-B activity at 100 microM or lower. At 1 mM, 6-nitrodopamine inhibited MAO-B by 60%. Compared to tolcapone, other nitrated catechols were very weak COMT inhibitors in vitro. Neither tolcapone nor 6-nitronoradrenaline modified the metabolism of L-dopa which was given peripherally. In binding studies, both 6-nitronoradrenaline and other nitrocatechols failed to affect the dopamine transporter even at high micromolar concentrations. In conclusion, exogenous 6-nitronoradrenaline can act as a COMT inhibitor in the striatum and elevate striatal dopamine levels without inhibiting dopamine reuptake. Whether endogenous 6-nitronoradrenaline can be formed also in vivo in the striatum and act as a regulator of dopaminergic tone remains to be determined.