Biomedical subjects

T Arima

Publications and source records attributed to T Arima.

At least 37 records · Page 2Linked to original sources

PubMed2002

Charge/orbital ordering structure of Pr(1-x)Ca(x)MnO(3)(x = 3/8) examined by low-temperature transmission electron microscopy.

The structural phase transition of Pr(1-x)Ca(x)MnO(3)(x = 3/8) was investigated by means of low-temperature transmission electron microscopy. Superlattice reflection spots with a modulation wave vector q(1) = (0,1/2,0) appeared below 230 K, indicating formation of the d(3x(2-r(2))/d(3y(2)-r(2)) type of charge/orbital ordering. Below 150 K, a new series of superlattice reflection spots with a modulation wave vector q(2) = (1/4,1/4,1/2) appeared, suggesting an additional ordering of excess 1/8 Mn(3+), necessary due to the deviation of x from 1/2, with the occupation of the d(3z(2-r(2)) type of e(g) orbital.

Journal Article↗

PubMed2002

Growth-associated gene expression profiles by microarray analysis of trophoblast of molar pregnancies and normal villi.

We used microarray analysis to investigate expression profiles of 589 known genes committed to cell growth control to characterize regulatory circuitry for cell proliferation in complete moles (CMs). CMs are characterized by hyperplastic trophoblast and have a high propensity to give rise to choriocarcinoma. Characteristic alterations in gene expression profiles were observed when compared with normal villi. Fifty-seven genes were significantly up-regulated in CMs and involved the Ras-Map kinase 3, Jak-STAT5, and Wnt signal pathways, implicating growth factor or cytokine-mediated signal pathways in the trophoblastic hyperplasia of CMs. Several genes associated with anti-apoptosis, cell structuring, and/or cell attachment were also up-regulated in CMs. In contrast, relatively fewer genes were down-regulated and these involved IGFBPs, versican, interleukin-1, tumor necrosis factor receptor, CD44, and RAD52. Genes identified in this study may elucidate regulation mechanisms of trophoblastic proliferation and mechanisms causing a pathological phenotype in CMs.

Apoptosis↗

PubMed2001

Expression of functional lung resistance--related protein predicts poor outcome in adult T-cell leukemia.

Chemotherapy of patients with adult T-cell leukemia (ATL) has been unsuccessful. The poor outcome is thought to be caused mainly by the drug resistance of ATL cells. Lung resistance-related protein (LRP) is a novel protein associated with drug resistance. The expression of LRP messenger RNA (mRNA) was evaluated by slot blot analysis in 55 patients with ATL. Of these patients, 36 had acute, 12 chronic, and 7 lymphoma-type ATL. The expression levels of LRP mRNA were significantly higher in chronic ATL than in lymphoma-type ATL (P =.007). The expression of LRP mRNA was higher in patients with white blood cell counts above 30,000/microL (P =.038) or with abnormal lymphocyte counts above 10,000/microL (P =.007) than in the remaining patients. The enhanced efflux of [(14)C]doxorubicin from nuclei isolated from ATL cells that expressed high levels of LRP was inhibited by a polyclonal antibody against LRP, and the accumulation of doxorubicin in the isolated nuclei was increased by the anti-LRP antibody. In acute and lymphoma-type ATL patients, high expression of LRP mRNA at diagnosis correlated with shorter survival, and a Cox proportional hazards model showed that LRP expression is an independent prognostic factor. These findings suggest that functionally active LRP is expressed in some ATL cells and that it is involved in drug resistance and poor prognosis in ATL. (Blood. 2001;98:1160-1165)

Active Transport, Cell Nucleus↗

PubMed2001

A conserved imprinting control region at the HYMAI/ZAC domain is implicated in transient neonatal diabetes mellitus.

Transient neonatal diabetes mellitus (TNDM) is associated with intra-uterine growth retardation, dehydration and a lack of insulin. Some TNDM patients exhibit paternal uniparental disomy (UPD) of chromosome 6q24, where at least two imprinted genes, HYMAI and ZAC, have so far been characterized. Here we show that the differentially methylated CpG island that partially overlaps mZac1 and mHymai at the syntenic mouse locus is a likely imprinting control region (ICR) for the approximately 120--200 kb domain. The region is unmethylated in sperm but probably methylated in oocytes, a difference that persists between parental alleles throughout pre- and post-implantation development. We also show that within this ICR, there is a region that exhibits a high degree of homology between mouse and human. Using a reporter expression assay, we demonstrate that this conserved region acts as a strong transcriptional repressor when methylated. Finally, we provide in vivo evidence that in the majority of TNDM patients with a normal karyotype, there is a loss of methylation within the highly homologous region. We propose that this ICR regulates expression of imprinted genes within the domain; epigenetic or genetic mutations of this region probably result in TNDM, possibly by affecting expression of ZAC in the pancreas and/or the pituitary.

Alleles↗

PubMed2001

Organ transplant specificity of tolerance to skin grafts with heart or kidney grafts plus nondepleting anti-CD4 monoclonal antibody (RIB 5/2) and intravenous donor alloantigen administration.

BACKGROUND: CD4+ T cells play an essential role in allograft rejection. Monoclonal anti-rat CD4 antibody, RIB 5/2, has been shown to modulate the CD4 glycoprotein without eliminating recipient T cells. A single dose of monoclonal anti-rat CD4 antibody RIB 5/2 plus donor splenocytes results in donor-specific unresponsiveness to heart and kidney allografts, but not skin allografts. This study examined whether tolerance to the more resistant skin graft could also be achieved with RIB 5/2. METHODS: Buffalo (RT1(b)) recipients were given a single dose (20 mg/kg) of monoclonal antibody RIB 5/2 IP plus IV Lewis (RT1(l)) splenocytes (25 x 10(6)) 21 days before Lewis heart, kidney, or skin grafts. In addition, Lewis skin was grafted either simultaneously with or after long- term Lewis heart or kidney allograft acceptance (>50 days). RESULTS: While IV alloantigen plus RIB 5/2 results in long-term acceptance of both heart and kidney, skin allografts are rejected when transplanted alone. Simultaneous transplantation with a Lewis kidney, but not with a Lewis heart, resulted in long-term Lewis skin graft acceptance. However, recipients tolerant to Lewis kidney or heart alone will not accept subsequent Lewis skin grafts, while recipients of simultaneous Lewis skin and kidney grafts subsequently accept a second Lewis, but not third-party Brown Norway (RT1(n)), skin graft. CONCLUSION: RIB 5/2 plus Lewis donor splenocytes tolerize for donor-specific heart and kidney but not skin grafts. However, Lewis skin grafted simultaneously with a Lewis kidney, but not Lewis heart, is accepted and protects a subsequent donor-specific Lewis skin graft.

Animals↗

PubMed2001

Efficient repetitive gene delivery to skeletal muscle using recombinant adenovirus vector containing the Coxsackievirus and adenovirus receptor cDNA.

To improve adenovirus-mediated gene delivery to skeletal muscle, we have used a recombinant adenovirus vector encoding the human Coxsackievirus and adenovirus receptor (hCAR). Because CAR is expressed at a lower level in rodent myoblasts and muscle fibers than in other tissues, we expected that elevated expression of CAR in skeletal muscle would improve the efficacy of adenovirus-mediated gene transfer. Since the mouse myoblasts, C2C12 cells, showed low sensitivity to infection by recombinant adenovirus 5, we initially infected these cells at a high multiplicity of infection (MOI) of 250 with the recombinant adenovirus containing hCAR cDNA and LacZ gene. Subsequent infection by recombinant adenovirus containing the marker gene, green fluorescence protein, became efficient even at a low MOI of 25. Thus, elevated hCAR expression in mouse muscle fibers made a second virus inoculation at low doses possible. We also demonstrated that the elevated hCAR expression did not influence muscle membrane integrity. Our results suggest that co-expression of CAR and a therapeutic gene by adenovirus vector constitutes a novel strategy to advance gene therapy for hereditary muscle diseases.

Adenoviridae↗

PubMed2001

Bcl-2 expression by retrograde transport of adenoviral vectors with Cre-loxP recombination system in motor neurons of mutant SOD1 transgenic mice.

We investigated genes expression by retrograde axonal transport of replication-defective adenoviruses carrying genes for LacZ (AdLacZ) and Bcl-2 in motor neurons of transgenic mice expressing mutant human Cu/Zn superoxide dismutase (SOD1) gene containing a substitution of alanine for glycine at position 93. We found that intramuscular injection of AdLacZ into the tongue of mutant SOD1 transgenic mice and their wild-type littermates at various ages results in high expression of the transgene and similar time course of expression in hypoglossal cranial nerve nuclei, suggesting no difference in the behavior of the transgene expression between the two groups. Subsequently, we employed a molecular switching cassette for Bcl-2 designed to express Bcl-2 by Cre-loxP recombination using adenoviral vectors, and examined the COS7 and primary neuronal cells with the mutant SOD1 gene. The overexpression of Bcl-2 in both cells and the neuronal protection against staurosporine-induced apoptosis were observed, after dual infection of adenoviral vectors with cassette for Bcl-2 (AxCALNLBcl-2) and Cre recombinase (AxCANCre). After inoculation of AxCALNLBcl-2 followed by AxCANCre into the tongue of both mutant SOD1 transgenic mice and wild-type littermates, Bcl-2 was detected in both the injection site and the hypoglossal nuclei of brainstems, suggesting that this was the result of retrograde transport of AxCALNLBcl-2 and AxCANCre and expression of Bcl-2 by Cre recombinase in the hypoglossal nuclei. This strategy for delivery of exogenous genes such as Bcl-2 will be useful for studying neuronal death/survival and introducing foreign genes into postmitotic motor neurons, and in gene therapy for motor neuron diseases such as ALS.

Adenoviridae↗

PubMed2001

The relationship between selective sleep deprivation, nocturnal jaw-muscle activity and pain in healthy men.

The relationship between nocturnal jaw-muscle activity and temporomandibular disorders (TMD) is still controversial. The aim of this study was to investigate the effect of selective slow wave sleep (SWS = non-rapid-eye-movement (NREM) stage 3 + 4) deprivation on jaw-muscle activity using a new automatic system. Ten healthy men without signs of symptoms of TMD participated. The subjects slept in the laboratory for six continuous nights including one adjustment night, one baseline night, three nights with experimental sleep deprivation and one recovery night. Polysomnographic recordings of electroencephalography (EEG) and electromyography (EMG) were obtained for recognition of sleep stages and masseter muscle activity. During the three experimental nights, computer-controlled sound stimulation (60--90 dB(A), 1000 Hz) were given as long as the subjects were in SWS. Maximum voluntary occlusal force (MVOF), pain pressure threshold (PPT) and visual analogue scales (VAS) were used to assess the state of the masseter muscles every morning and evening during the study period. The results showed that the time spent in SWS was significantly decreased during the first sleep deprivation night, but there were no significant effects on nocturnal EMG activity (i.e. the numbers of bruxism episodes per hour of sleep, bruxism bursts per episodes bruxism bursts per hour of sleep), MVOF, VAS or PPT. Furthermore, the automatic system only deprived the SWS in five subjects for the following two nights although the sound stimulation was given at the maximum intensity. These results suggest that deprivation of SWS may not interact immediately with nocturnal jaw-muscle activity and jaw-muscle pain.

Adult↗

PubMed2001

Heart rate decline after exercise in patients with hypertrophic cardiomyopathy.

To evaluate the heart rate recovery, submaximal exercise, echocardiographic examination, and Holter monitoring were performed on 30 patients with hypertrophic cardiomyopathy and 11 controls. The time constant of heart rate decline after exercise was calculated. Spectral analysis was performed on Holter recordings. The time constant did not correlate with heart rate, left ventricular end-diastolic pressure, ejection fraction, or wall thickness. There was no correlation between the time constant and any mean spectral indices over 24 hours in patients. However, the time constant correlated with high frequency component in the night. Nocturnal high frequency component in patients with short time constant was significantly less than in those with long time constant, but did not significantly differ from that in controls. In conclusion, the heart rate decline after exercise does not primarily reflect the severity of hypertrophy or hemodynamic impairment but is associated with nocturnal parasympathetic modulation in patients with hypertrophic cardiomyopathy.

Adult↗

PubMed2001

Effect of FR167653 on pancreatic ischemia-reperfusion injury in dogs.

BACKGROUND: The role of inflammatory cytokines is still unclear in ischemia-reperfusion injury of the pancreas. We investigated the effect of FR167653 (FR), a newly developed compound that is a potent suppressor of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha on ischemia-reperfusion injury of the isolated pancreatic tail in dogs. METHODS: The tail of the pancreas was subjected to ischemia for 90 minutes. During occlusion of the vascular inflow, the head of the pancreas was removed. A control group (n = 14) and an FR treatment group (n = 11) were evaluated for survival rate, tissue blood flow, arterial oxygen pressure (Pao(2)), serum amylase and lipase levels, glucose and insulin, liver enzymes, creatinine, IL-1beta mRNA in the peripheral blood, and histopathology. RESULTS: Six of the 14 control animals and 2 of the 11 FR-treated animals died. The FR treatment group showed lower amylase (P=.037) and lipase (P =.030) levels, lower IL-1beta mRNA expression (P =.033), and less pancreatic tissue damage (P =.041) than did the control group, but there was no remarkable change in endocrine function (P =.422). Pao(2) during the acute phase in the FR treatment group was maintained (P=.009), but pulmonary tissue was damaged. Results of biochemical and histologic examinations of the liver and kidneys were unremarkable. CONCLUSIONS: FR ameliorates ischemia-reperfusion injury of the pancreas and reduces the production of inflammatory cytokines that may contribute to secondary damage to distant organs.

Animals↗

PubMed2001

The combined use of prostaglandin I2 analogue (OP-2507) and thromboxane A2 synthetase inhibitor (OKY-046) strongly inhibits atherosclerosis of aortic allografts in rats.

BACKGROUND: Atherosclerosis is the main lesion in allografts undergoing chronic rejection. We investigated the effect of OP-2507 (prostaglandin I2 analogue) and OKY-046 (thromboxane A2 synthetase inhibitor) on graft atherosclerosis morphologically and the production of eicosanoids in grafts in a rat aortic allograft model. METHODS: Abdominal aortic allografts of Lewis (RT-1(l)) rats were transplanted orthotopically into fully major histocompatibility complex mismatched Wistar King A/Qdj (RT-1(u)) rats that were subcutaneously administered OP-2507 (0.1 mg/kg/d) or OKY-046 (125 mg/kg/d), or both, with an osmotic pump. Four, 8, or 12 weeks later, the grafts were harvested and examined histologically, and the concentration of eicosanoids in the grafts were analyzed. RESULTS: Lewis aortic allografts in Wistar King A recipients with no treatment displayed atherosclerosis, which involved gradual intimal thickening and medial thinning with continuous inflammation in adventitia. Neither OP-2507 nor OKY-046 treatment affected the intensity of adventitial inflammation. Although inhibition of medial thinning or a decrease in medial nuclear density was not observed, OKY-046 administration alone significantly inhibited an increase in intimal thickness. OP-2507 administration alone significantly inhibited a decrease in medial nuclear density and intimal thickening. Combined treatment with OP-2507 and OKY-046 further decreased the alteration of media and intima. The ratio of thromboxane B2 and 6-keto-prostaglandin F(1alpha) in the grafts was significantly reduced by OKY-046 but not by OP-2507 alone. CONCLUSIONS: We have demonstrated that atherosclerosis in aortic allografts is inhibited by the continuous administration of either OP-2507 or OKY-046, and a combination of both agents strongly increases this inhibitory effect. Amelioration of balance in eicosanoid production in the grafts by the use of thromboxane A2 synthetase inhibitor and the simultaneous usage of stable prostaglandin I2 analogue may be a strategy for preventing atherosclerosis that results from chronic rejection.

6-Ketoprostaglandin F1 alpha↗

PubMed2001

The clp1 gene of the mushroom Coprinus cinereus is essential for A-regulated sexual development.

Sexual development in the mushroom Coprinus cinereus is under the control of the A and B mating-type loci, both of which must be different for a compatible, dikaryotic mycelium to form between two parents. The A genes, encoding proteins with homeodomain motifs, regulate conjugate division of the two nuclei from each mating partner and promote the formation of clamp connections. The latter are hyphal configurations required for the maintenance of the nuclear status in the dikaryotic phase of basidiomycetes. The B genes encode pheromones and pheromone receptors. They regulate the cellular fusions that complete clamp connections during growth, as well as the nuclear migration required for dikaryosis. The AmutBmut strain (326) of C. cinereus, in which both A- and B-regulated pathways are constitutively activated by mutations, produces, without mating, dikaryon-like, fertile hyphae with clamp connections. In this study we isolated and characterized clampless1-1 (clp1-1), a mutation that blocks clamp formation, an essential step in A-regulated sexual development, in the AmutBmut background. A genomic DNA fragment that rescues the clp1-1 mutation was identified by transformations. Sequencing of the genomic DNA, together with RACE experiments, identified an ORF interrupted by one intron, encoding a novel protein of 365 amino acids. The clp1-1 mutant allele carries a deletion of four nucleotides, which is predicted to cause elimination of codon 128 and frameshifts thereafter. The clp1 transcript was normally detected only in the presence of the A protein heterodimer formed when homokaryons with compatible A genes were mated. Forced expression of clp1 by promoter replacements induced clamp development without the need for a compatible A gene combination. These results indicate that expression of clp1 is necessary and sufficient for induction of the A-regulated pathway that leads to clamp development.

Amino Acid Sequence↗

PubMed2001

Vitamin E inhibits proliferation of primary cultured human mesangial and endothelial cells.

BACKGROUND: Vitamin E (VE) has been used as an antioxidant and has been suggested to inhibit the proliferation of mesangial cells in rat and vascular endothelial cells. The direct effect of VE on primary cultures of mesangial cells (MC) and endothelial cells (EC) from the human glomerulus was studied. METHODS: (1) MC (in 17 or 2.5% FCS DMEM) or EC (in 10 or 5% FCS CSC) at 5,000 cells/well was incubated with serial concentrations of VE from 0.05 to 50 microg/ml (0.06 to 60 IU/l). (2) MC was cocultured with 160, 80, 40 or 20 microg/ml of low-density lipoprotein (LDL) or oxidized LDL (ox-LDL) in 17 or 2.5% FCS DMEM with or without VE. After 3 days of incubation at 37 degrees C in 5% CO(2), cell proliferation was measured by the Premix WST-1 Assay System. RESULTS: The concentration of VE that significantly inhibited the proliferation of MC cultured in 17 or 2.5% FCS DMEM was 50 or 2.5 microg/ml (60 or 3.0 IU/l), respectively, and that of EC in 10 or 5% FCS medium was 50 or 25 microg/ml (60 or 30 IU/l). VE at 25 microg/ml (30 IU/l) inhibited the LDL proliferative effect on MC cultured in 2.5 FCS DMEM by 21.79-93.21% in a LDL concentration-dependent manner. There was little difference between the effects of LDL and ox-LDL on the VE inhibitory effect on MC under our experimental conditions. CONCLUSION: VE at low concentrations had no effect on the proliferation of both MC and EC, but at high concentrations, it showed an inhibitory effect on both cells.

Cell Division↗

PubMed2001

Hepatic necrosis with cholestasis induced by long-term voglibose administration.

A 76-year-old woman admitted to our hospital for jaundice had been treated for diabetes mellitus with insulin for 9 years and voglibose had been added for the 39 months preceding admission. Elevated serum bilirubin and transaminase concentration began to normalize with initiation of corticosteroid treatment 1 week after discontinuation of voglibose. In the in vitro testing of the patient's peripheral blood, lymphocytes showed stimulation by voglibose. In dramatic contrast to an initial liver biopsy specimen that demonstrated cholestasis with submassive and zonal necrosis, the follow-up specimen was normal 1 year later. We believe that patients treated with voglibose should be monitored long-term with monthly determinations of transaminases and bilirubin in serum.

Aged↗

PubMed2001

A new hypoglycemic agent, JTT-608, evokes protein kinase A-mediated Ca(2+) signaling in rat islet beta-cells: strict regulation by glucose, link to insulin release, and cooperation with glucagon-like peptide-1(7-36)amide and pituitary adenylate cyclase-activating polypeptide.

A new nonsulfonylurea oral hypoglycemic agent, JTT-608, has been reported to stimulate insulin release at elevated, but not low, glucose concentrations and consequently not to induce hypoglycemia in rats. Accordingly, this drug is potentially a safer antidiabetic agent than sulfonylureas. To explore the mechanisms underlying this glucose-dependent insulinotropism, the present study investigated the effects of JTT-608 on cytosolic free Ca(2+) concentration ([Ca(2+)](i)) and protein kinase A (PKA) activity in rat islet beta-cells by microfluorometry using, respectively, fura-2 and a fluorescence PKA substrate, DR II. In the presence of glucose at normal and elevated concentrations (5.0-16.7 mM) JTT-608 (30-1000 microM) concentration dependently increased [Ca(2+)](i) in up to 88% of single beta-cells, whereas at lower glucose concentrations (2.8 and 4.2 mM) it had little effect. The [Ca(2+)](i) responses were inhibited under Ca(2+)-free conditions and by nitrendipine, an L-type Ca(2+) channel blocker. JTT-608 rapidly activated PKA and a PKA inhibitor, H89, inhibited [Ca(2+)](i) responses to JTT-608. JTT-608 also stimulated insulin release from rat islets in a glucose- and Ca(2+)-dependent manner. The glucose-unresponsive beta-cells, which failed to respond to 8.3 mM glucose with increases in [Ca(2+)](i), were frequently recruited to [Ca(2+)](i) increases by JTT-608. JTT-608 also induced oscillations of [Ca(2+)](i). Glucagon-like peptide-1(7-36)amide (GLP-1), pituitary adenylate cyclase-activating polypeptide (PACAP), and acetylcholine (ACh) enhanced the action of JTT-608 on [Ca(2+)](i). In conclusion, JTT-608 evokes PKA-mediated Ca(2+) influx and Ca(2+) signaling in rat islet beta-cells in a glucose-regulated manner, which may account for its glucose-dependent insulinotropism. JTT-608 and neurohormones may cooperatively activate islet beta-cells under physiological conditions.

Acetylcholine↗

PubMed2001

Long-term outcome of patients with ergonovine induced coronary constriction not associated with ischemic electrocardiographic changes.

OBJECTIVES: This study investigated the long-term outcome of patients with coronary artery constriction induced with ergonovine but not associated with ischemic electrocardiographic changes. METHODS: The ergonovine provocation test was performed in 419 patients with suspected but unproven variant angina. Ergonovine maleate was administered into the coronary arteries at 8 micrograms/min for 5 min during cardiac catheterization. Patients were categorized into three groups according to their response to ergonovine. The positive group contained patients who developed coronary constriction of more than 90% in diameter associated with ischemic electrocardiographic changes and chest pain. The intermediate group contained patients who had coronary constriction of more than 90% but no electrocardiographic changes. The negative group contained patients who had neither significant coronary constriction nor ST segment changes. RESULTS: There were 305 patients, 49, and 65 in the negative, intermediate, and positive groups, respectively. Death occurred in six patients (2%), one (2%), and one (2%) in the negative, intermediate, and positive groups, respectively. Sudden cardiac death occurred in one patient in the negative group. Recurrence of chest pain with effectiveness of sublingual administration of nitroglycerine was observed in 26 patients (9%), 10 (20%), and 11 (17%) in the negative, intermediate, and positive groups, respectively. CONCLUSIONS: Some patients in the intermediate group might show "false negative" response to ergonovine so careful treatment with calcium antagonists should be continued in patients in the intermediate group as well as patients with vasospastic angina.

Coronary Angiography↗

PubMed2001

Cornelia de Lange syndrome associated with cecal volvulus: report of a case.

UNLABELLED: Cornelia de Lange syndrome is known to be occasionally associated with gastrointestinal malformation. However, the occurrence of cecal volvulus in such anomalies is very rare. We report a 15-y-old Japanese boy with Cornelia de Lange syndrome associated with a cecal volvulus secondary to non-fixation of the cecum and ascending colon. The patient was admitted to our hospital because of abdominal pain and bilious vomiting. At emergent laparotomy, cecal volvulus with non-fixation of the ascending colon and cecum was diagnosed. Release of the cecal volvulus and the fixation of the cecum and ascending colon to the right retroperitonium were performed. The postoperative course was uneventful, except for sepsis caused by aspiration pneumonia soon after the operation. CONCLUSION: Clinicians treating patients with this syndrome should be aware that such patients may be at risk for developing severe gastrointestinal anomalies, including cecal volvulus.

Adolescent↗

PubMed2001

Effect of jaw muscle pain and soreness evoked by capsaicin before sleep on orofacial motor activity during sleep.

AIMS: Sleep bruxism, which is a form of orofacial motor activity (OMA), and jaw muscle pain and soreness have for a long time been thought to be mutually linked. The aim of this study was to investigate the effect of clinical and experimental jaw muscle pain and soreness on sleep OMA. METHODS: Twelve healthy subjects aged 21 to 31 years old participated in this study. All of them were aware of signs or symptoms of sleep OMA and were subdivided into a group with clinical pain complaints (n = 5) and a group without pain (n = 7). All subjects slept in the laboratory for 3 consecutive nights, including a habituation night, a baseline night, and an experimental night. Electroencephalographic (EEG) activity and electromyographic (EMG) activity from the masseter muscles were recorded during sleep. On the experimental night, before sleep, all subjects received an injection of capsaicin (0.1 mL, 100 micrograms/mL) into the masseter muscle that had demonstrated the most EMG activity during the previous recordings. The OMA events and episodes were quantified and were compared between the baseline night and the experimental night. Every evening and morning during the study period, pain intensity, unpleasantness, and soreness were scored by the subjects on a visual analog scale (VAS), and pain detection thresholds (PDTs) in the masseter muscles and maximal voluntary occlusal force (MVOF) were also measured. RESULTS: Pre-sleep injection of capsaicin did not cause significant differences between groups in peak pain intensity on the VAS. The PDT and MVOF did not show any significant differences between groups, injection and non-injection sides, or baseline and experimental nights and mornings. The number of EMG episodes/hour sleep, the number of bursts/hour sleep, and total area of all bursts and episodes during the baseline night were significantly higher in the subjects without pain than in the subjects with pain. However, the capsaicin injection did not cause any significant changes in these parameters. CONCLUSION: This study suggests that an acute pre-sleep painful stimulus does not have any effect on OMA during sleep, but the study extends previous findings that clinical jaw muscle pain and soreness are associated with less EMG activity in the masticatory muscles.

Adult↗