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Chest. 2001 Jan;119(1):53-61.
Risk factors for sleep bruxism in the general population.

Ohayon MM, Li KK, Guilleminault C.

Stanford University School of Medicine, Sleep Disorders Center, Stanford, CA 94305, USA. mrcohayool.com

OBJECTIVE: Sleep bruxism can have a significant effect on the patient's quality of life. It may also be associated with a number of disorders. However, little is known about the epidemiology of sleep bruxism and its risk factors in the general population. DESIGN: Cross-sectional telephone survey using the Sleep-EVAL knowledge based system. SETTINGS: Representative samples of three general populations (United Kingdom, Germany, and Italy) consisting of 158 million inhabitants. PARTICIPANTS: Thirteen thousand fifty-seven subjects aged > or = 15 years (United Kingdom, 4,972 subjects; Germany, 4,115 subjects; and Italy, 3,970 subjects). INTERVENTION: None. MEASUREMENTS: Clinical questionnaire on bruxism (using the International Classification of Sleep Disorders [ICSD] minimal set of criteria) with an investigation of associated pathologies (ie, sleep, breathing disorders, and psychiatric and neurologic pathologies). RESULTS: Grinding of teeth during sleep occurring at least weekly was reported by 8.2% of the subjects, and significant consequences from teeth grinding during sleep (ie, muscular discomfort on awakening, disturbing tooth grinding, or necessity of dental work) were found in half of these subjects. Moreover, 4.4% of the population fulfilled the criteria of ICSD sleep bruxism diagnosis. Finally, subjects with obstructive sleep apnea syndrome (odds ratio [OR], 1.8), loud snorers (OR, 1.4), subjects with moderate daytime sleepiness (OR, 1.3), heavy alcohol drinkers (OR, 1.8), caffeine drinkers (OR, 1.4), smokers (OR, 1.3), subjects with a highly stressful life (OR, 1.3), and those with anxiety (OR, 1.3) are at higher risk of reporting sleep bruxism. CONCLUSIONS: Sleep bruxism is common in the general population and represents the third most frequent parasomnia. It has numerous consequences, which are not limited to dental or muscular problems. Among the associated risk factors, patients with anxiety and sleep-disordered breathing have a higher number of risk factors for sleep bruxism, and this must raise concerns about the future of these individuals. An educational effort to raise the awareness of dentists and physicians about this pathology is necessary.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11157584&dopt=Abstract



Circ Res. 2001 Feb 2;88(2):188-94.
Overexpression of FK506-binding protein FKBP12.6 in cardiomyocytes reduces ryanodine receptor-mediated Ca(2+) leak from the sarcoplasmic reticulum and increases contractility.

Prestle J, Janssen PM, Janssen AP, Zeitz O, Lehnart SE, Bruce L, Smith GL, Hasenfuss G.

Department of Cardiology and Pneumology, Georg-August-University Goettingen, Goettingen, Germany. prestled.uni-goettingen.de

The FK506-binding protein FKBP12.6 is tightly associated with the cardiac sarcoplasmic reticulum (SR) Ca(2+)-release channel (ryanodine receptor type 2 [RyR2]), but the physiological function of FKBP12.6 is unclear. We used adenovirus (Ad)-mediated gene transfer to overexpress FKBP12.6 in adult rabbit cardiomyocytes. Western immunoblot and reverse transcriptase-polymerase chain reaction analysis revealed specific overexpression of FKBP12.6, with unchanged expression of endogenous FKBP12. FKBP12.6-transfected myocytes displayed a significantly higher (21%) fractional shortening (FS) at 48 hours after transfection compared with Ad-GFP-infected control cells (4.8+/-0.2% FS versus 4+/-0.2% FS, respectively; n=79 each; P:=0.001). SR-Ca(2+) uptake rates were monitored in beta-escin-permeabilized myocytes using Fura-2. Ad-FKBP12.6-infected cells showed a statistically significant higher rate of Ca(2+) uptake of 0.8+/-0.09 nmol/s(-)(1)/10(6) cells (n=8, P:<0.05) compared with 0.52+/-0.1 nmol/s(-)(1)/10(6) cells in sham-infected cells (n=8) at a [Ca(2+)] of 1 micromol/L. In the presence of 5 micromol/L ruthenium red to block Ca(2+) efflux via RyR2, SR-Ca(2+) uptake rates were not significantly different between groups. From these measurements, we calculate that SR-Ca(2+) leak through RyR2 is reduced by 53% in FKBP12.6-overexpressing cells. Caffeine-induced contractures were significantly larger in Ad-FKBP12.6-infected myocytes compared with Ad-GFP-infected control cells, indicating a higher SR-Ca(2+) load. Taken together, these data suggest that FKBP12.6 stabilizes the closed conformation state of RyR2. This may reduce diastolic SR-Ca(2+) leak and consequently increase SR-Ca(2+) release and myocyte shortening.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11157671&dopt=Abstract



Circ Res. 2001 Feb 2;88(2):195-201.
Coordinated control of cell Ca(2+) loading and triggered release from the sarcoplasmic reticulum underlies the rapid inotropic response to increased L-type Ca(2+) current.

Trafford AW, Diaz ME, Eisner DA.

Unit of Cardiac Physiology, University of Manchester, Manchester, UK.trafforan.ac.uk

The aim of this study was to investigate how sarcoplasmic reticulum (SR) Ca(2+) content and systolic Ca(2+) are controlled when Ca(2+) entry into the cell is varied. Experiments were performed on voltage-clamped rat and ferret ventricular myocytes loaded with fluo-3 to measure intracellular Ca(2+) concentration ([Ca(2+)](i)). Increasing external Ca(2+) concentration ([Ca(2+)](o)) from 1 to 2 mmol/L increased the amplitude of the systolic Ca(2+) transient with no effect on SR Ca(2+) content. This constancy of SR content is shown to result because the larger Ca(2+) transient activates a larger Ca(2+) efflux from the cell that balances the increased influx. Decreasing [Ca(2+)](o) to 0.2 mmol/L decreased systolic Ca(2+) but produced a small increase of SR Ca(2+) content. This increase of SR Ca(2+) content is due to a decreased release of Ca(2+) from the SR resulting in decreased loss of Ca(2+) from the cell. An increase of [Ca(2+)](o) has two effects: (1) increasing the fraction of SR Ca(2+) content, which is released on depolarization and (2) increasing Ca(2+) entry into the cell. The results of this study show that the combination of these effects results in rapid changes in the amplitude of the systolic Ca(2+) transient. In support of this, the changes of amplitude of the transient occur more quickly following changes of [Ca(2+)](o) than following refilling of the SR after depletion with caffeine. We conclude that the coordinated control of increased Ca(2+) entry and greater fractional release of Ca(2+) is an important factor in regulating excitation-contraction coupling.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11157672&dopt=Abstract








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