The effects of a 0.12% chlorhexidine-digluconate-containing mouthrinse versus a placebo on plaque and gingival inflammation over a 3-month period

Abstract Several previous studies have evaluated the effects of 0.12% chlorhexidine digluconate (ChD) mouthrinses on plaque and gingival inflammation. However, previously, none have been based in general dental practices. The aim of this study was to evaluate the potential to conduct controlled periodontal clinical trials in co-operation with general dental practitioners (gdps). The project took place in 5 general dental practices in the South of England. 121 healthy subjects (24 at 4 sites and 25 at the 5th). aged 18-65 years, mean 35 ± 12) years participated in a double-blind, randomised study during which they received full mouth assessments for plaque and gingival bleeding at baseline, 6 and 12 weeks. 60 subjects were randomly asigned to use the 0.12% ChD mouth wash and 6i the placebo. The assessments were carried out by 5 gpds, who had previously achieved inter-examiner κ scores of 0.78–0.85 (mean 0.81) for the plaque index (PlI), and of 0.73–0.94 (mean 0.87) for a modified gingival index (mGI), and who maintained κ scores of 0.51–0.90 for PII and of 0.73–1.00 for mGI during the 12 months required to complete the study. 98 subjects (48 ChD and 50 placebo) completed the study. Even though the baseline levels of plaque and gingivitis were low, by week 12, mean whole mouth piaque score of the ChD mouthwash users had fallen from 1.33 at baseline to 0.96 and was significantly lower (p < 0.001) than for the placebo users, 1.31 at baseline to 1.13. Whole-mouth gingival bleeding score fell from 0.56 to 0.42 in the ChD mouthwash group but was unchanged (0.54–0.55) in the placebo group. A subsidiary data analysis which considered the effects at sites indicated that within these overall differences, the ChD users experienced almost 2× the reduction from plaque score 2 at baseline at proximal molar sites over a 12-week period (50.6% ChD versus 27.6% placebo). It was concluded that 0.12% ChD mouthwash reduced plaque accumulation fay 28% and gingival inflammation by 25% over a 12–week period, that it is feasible for a group of gdps to maintain high levels of inter–examiner consistency in the use of PlI and mGI, that it is also feasible to carry out such a multicentre study in general dental practice, and that the use of mean mouth scores per subject to analyse the effects of mouthrinses may well mask variations in response throughout the mouth.     

A study of diazepam binding inhibitor (DBI) processing products in human cerebrospinal fluid and in postmortem human brain

Diazepam binding inhibitor (DBI) is a neuropeptide of 11 kDa molecular size and is unevenly distributed in human and rat brain. It appears to function as a negative allosteric modulator of GABAA receptors. In the present paper, using antibodies directed against several synthetic peptides, which correspond to selective regions of human DBI (DBI 51-70, DBI 37-50, DBI 81-101), it is shown that DBI is processed into at least 6 peptide fragments in both postmortem human brain and in cerebrospinal fluid (CSF). One of these fragments was identified as the synthetic DBI 51-70 fragment (an eikosaneuropeptide, ENP) by combined chromatographic procedures. Immunoblotting analysis of the other fragments, by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (PAGE), revealed an apparent molecular size, ranging from 3-4 kDa for four of them and a larger molecular form of 8 kDa. On the basis of the immunological properties, a tentative amino acid sequence was deduced.     

The Fort McMurray demonstration project in social marketing: health- and safety-related behaviour among oil sands workers

This is the first round in a series of surveys conducted inFort McMurray as part of the Fort McMurray Demonstration Projectin social marketing. This component of the survey was intendedto focus on the most prominent group of employed workers inthe community and to compare their patterns of response withthe community as a whole. Respondents to the survey were overwhelminglymale (96%), married (72.9%) and living in households of twoto five persons (87.9%). They were predominantly aged 30–44(55%) and graduates of high school (53.5%). Younger male workers(below age 30) were more likely to have a high school diploma(78.3%) or some additional technical or vocational training(21.7% compared to 12.5% overall) and to be unmarried or separated.Attitudes toward safety-related behaviours were stronger thanfor respondents from the community as a whole. Approximately70–100% of all age groups and both sexes showed strongagreement with attitudes involving child car seats and the unacceptabilityof drinking and driving. These attitudes include strong advocacyof vigorous enforcement of occupational health and safety standards.However, they showed a variability similar to the communityas a whole in behaviour at home compared to work, generallyreporting more consistent use of personal protection on thejob than in their own homes, particularly hearing protection.Even so, they were much less likely to perform stretching andwarm-up exercises prior to exertion than community residentsin general. The potential may exist to transfer the technologyand attitudes from workplace health and safety to communitysafety. One possible strategy to accomplish this is to involveworkers in this industry directly in community initiatives.This strategy may be generalizable to any community in whichthere are major employers who place a heavy emphasis on riskcontrol and occupational health and safety.     

Human factors in firefighting: ergonomic-, cardiopulmonary-, and psychogenic stress-related issues

Summary There are many issues in firefighting that involve human factors and cardiopulmonary conditioning. Population-based mortality and disability surveillance studies suggest a relatively small but significant excess of disability but not mortality from nonmalignant cardiovascular disease for fire fighters. More targeted cohort and case-control studies do not support such an excess and instead suggest a strong healthy worker effect. Pulmonary function among fire fighters has been extensively studied, with contradictory findings. Extreme exposures and long-term exposure in combination with cigarette smoking may be risk factors for respiratory disorders and accelerated decline in airflow. It appears likely that individual fire fighters who show early signs of illness are often selectively transferred out of active firefighting positions. Despite exposure to substances such as carbon monoxide that may predispose to cardiovascular mortality and morbidity, excesses are not consistently shown in mortality studies. Clinical studies of individual fire fighters do suggest an elevated risk for myocardial ischemia. The ergonomic demands of firefighting are extreme at peak activity because of high energy costs for activities such as climbing aerial ladders, the positive heat balance from endogenous and absorbed environmental heat, and encumbrance by bulky but necessary protective equipment. The psychological stresses of firefighting include long periods of relative inactivity punctuated by highly stressful alarms and extremely stressful situations such as rescues, as reflected in physiological and biochemical indicators. Fire fighters are at risk for depression and posttraumatic stress disorder, although morale overall is generally much higher than in comparable occupations. Women firefighter candidates as a group perform less well on selection test simulating the demands of active firefighting, but some individual women perform very well.     

Delayed increase of Ca2+ influx elicited by glutamate: role in neuronal death

The mechanism of delayed neurotoxicity, triggered by glutamate, was studied in 7-8-day-old primary cultures of rat cerebellar granule cells. Treatment of cultures for 15 min with 50 microM glutamate in Mg2+ -free medium, followed by removal of the excitoxin, resulted in neuronal death, which started to appear 2-3 hr after the termination of glutamate treatment. The number of dead neurons increased gradually in the next few hours and 80-85% of neurons were found dead 24 hr later. Antagonists of N-methyl-D-aspartate-sensitive glutamate receptors (phencyclidine) or 1.2 mM MgCl2, but not the antagonist of N-methyl-D-asparatate-insensitive glutamate receptors (6-cyano-7-nitroquinoxaline-2,3-dione), abolished the neurotoxic effect of kainate. Development of glutamate-induced neuronal death depends strongly on Ca2+. Removal of extracellular Ca2+ (with 1mM ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid) immediately after the termination of glutamate exposure and before the appearance of the early signs of neuronal death (post-glutamate period) dramatically reduced neuronal degeneration. Neurotoxic concentrations of glutamate induced sustained increase of 45Ca2+ uptake in the post-glutamate period. The delayed increase of 45Ca2+ uptake, as well as the delayed neurotoxicity, were not affected by post-glutamate treatment with phencyclidine, dibenzocyclohepteneimine; DL-2-amino-5-phosphonovalerate, or MgCl2 or with voltage-dependent Ca2+ channel blockers (nitrendipine, verapamil, diltiazem). Neurotoxic concentrations of glutamate also induced a delayed sustained increase of [3H]phorbol-12,13-dibutyrate binding, reflecting an increased translocation of protein kinase C (PKC) from cytosol to the cell membrane during the post-glutamate period. Pretreatment of neurons with the ganglioside GT1b (trisialosylgangliotetraglycosylceramide), followed by removal of free GT1b from the incubation medium, prevented PKC translocation, the sustained increase of 45Ca2+ uptake in the post-glutamate period, and the delayed neuronal death. We suggest that the sustained activation and translocation of PKC primed by glutamate receptor stimulation may be the triggering event causing the protracted increase of neuronal Ca2+ influx. This influx is insensitive to voltage-dependent Ca2+ channel blockers and glutamate receptor antagonists. It appears that this delayed increase of Ca2+ influx may be important in causing neuronal death.     

Retrovirus-mediated enzymatic correction of Tay-Sachs defect in transduced and non-transduced cells

Tay-Sachs disease is a severe neurodegenerative disorder due to mutations in the HEXA gene coding for the alpha-chain of the alpha-beta heterodimeric lysosomal enzyme beta-hexosaminidase A (HexA). Because no treatment is available for this disease, we have investigated the possibility of enzymatic correction of HexA-deficient cells by HEXA gene transfer. Human HEXA cDNA was subcloned into a retroviral plasmid generating to G.HEXA vector. The best Psi-CRIP producer clone of G.HEXA retroviral particles was isolated, and murine HexA-deficient fibroblasts derived from hexa -/- mice were transduced with the G.HEXA vector. Transduced cells overexpressed the alpha-chain, resulting in the synthesis of interspecific HexA (human alpha-chain/murine beta- chain) and in a total correction of HexA deficiency. The alpha-chain was secreted in the culture medium and taken up by HexA-deficient cells via mannose-6-phosphate receptor binding, allowing for the restoration of intracellular HexA activity in non-transduced cells.      

Charcot-Marie-Tooth phenotype produced by a duplicated PMP22 gene as part of a 17P trisomy-translocation to the X chromosome

The Charcot-Mane-Tooth disease type 1A (CMTlA) phenotype is most often associated with a 1.5 megabase (mb), tandem duplication of chromosome 17 band p12 (17˜12). The prevailing hypothesis is that the demyelinating neuropathy results from a dosage effect of the peripheral myelin protein gene PMP22 which is included within this duplication. We present a patient with clinical and electrophysiological features ofCMTlA in whom an extra PMP22 gene resulted from a rare unbalanced translocation of 17p to the X chromosome. This finding further supports the hypothesis of gene dosage as the basis for CMTlA. More-over, this case highlights the importance of fluorescence in siiu hybridization (FISH) as an alternative molecular technique in the diagnosis of CMTlA.