Nickel-Catalyzed Exhaustive Hydrodefluorination of Perfluoroalkyl Arenes.

Perfluoroalkyl compounds are persistent environmental pollutants due to their strong C(sp3)-F bonds. Hydrodefluorination has emerged as a potential alternative disposal method for perfluoroalkyl compounds. Although the transformation of trifluoromethyl arenes into the corresponding methyl arenes has been studied by several research groups, hydrodefluorination reactions of longer perfluoroalkyl chains remain rare. Herein, we report exhaustive hydrodefluorination reactions of pentafluoroethyl arenes and longer-chain analogues using molecular nickel catalysis. Despite the cleavage of multiple C(sp3)-F bonds, the reaction already proceeds upon gentle heating (60 °C). A mechanistic investigation indicated that the reaction proceeds via benzylic hydrodefluorination reactions followed by homobenzylic ones. We reveal the multiple roles of the Ni catalyst, which include C-F bond cleavage, promotion of HF elimination, and hydrosilylation.

Drosophila transcription factor NF-Y suppresses transcription of the lipase 4 gene, a key gene for lipid storage.

The CCAAT motif-binding factor NF-Y consists of three different subunits, NF-YA, NF-YB, and NF-YC. Although it is suggested that NF-Y activity is essential for normal tissue homeostasis, survival, and metabolic function, its precise role in lipid metabolism is not clarified yet. In Drosophila, eye disc specific knockdown of Drosophila NF-YA (dNF-YA) induced aberrant morphology of the compound eye, the rough eye phenotype in adults and mutation of the lipase 4 (lip4) gene suppressed the rough eye phenotype. RNA-seq analyses with dNF-YA knockdown third instar larvae identified the lip4 gene as one of the genes that are up-regulated by the dNF-YA knockdown. We identified three dNF-Y-binding consensuses in the 5'flanking region of the lip4 gene, and a chromatin immunoprecipitation assay with the specific anti-dNF-YA IgG demonstrated dNF-Y binding to this genomic region. The luciferase transient expression assay with cultured Drosophila S2 cells and the lip4 promoter-luciferase fusion genes with and without mutations in the dNF-Y-binding consensuses showed that each of the three dNF-Y consensus sequences negatively regulated lip4 gene promoter activity. Consistent with these results, qRT-PCR analysis with the dNF-YA knockdown third instar larvae revealed that endogenous lip4 mRNA levels were increased by the knockdown of dNF-YA in vivo. The specific knockdown of dNF-YA in the fat body with the collagen-GAL4 driver resulted in smaller oil droplets in the fat body cells. Collectively, these results suggest that dNF-Y is involved in lipid storage through its negative regulation of lip4 gene transcription.

Unexpected formation of poly-functionalized fulvenes by the reaction of a tetraaryl[5]cumulene with iodine.

Longer cumulenes have come to draw considerable attention due to their unique properties and reactivities, leading to various hydrocarbons. In this manuscript, we describe the reaction of tetrakis(p-methoxyphenyl)[5]cumulene with iodine to afford poly-functionalized fulvenes via unexpected migration of a terminal aryl ring under ambient conditions. The obtained iodinated fulvenes were utilized in Suzuki-Miyaura cross-coupling reactions affording penta- and fully-arylated fulvenes successfully.

The Pseudomonas aeruginosa dnaK gene is involved in bacterial translocation across the intestinal epithelial cell barrier.

Pseudomonas aeruginosa can penetrate through polarized epithelial cell monolayers produced by the human adenocarcinoma cell line Caco-2. We previously identified genes associated with bacterial translocation through Caco-2 cell monolayers by analysing transposon insertion mutants with dramatically reduced penetration activity relative to that of the wild-type P. aeruginosa PAO1 strain. In this study, we focused on the dnaK mutant because the association between this gene and penetration activity is unknown. Inactivation of dnaK caused significant repression of bacterial penetration through Caco-2 cell monolayers, with decreased swimming, swarming and twitching motilities; bacterial adherence; and fly mortality rate; as well as dramatic repression of type III effector secretion and production of elastase and exotoxin A. However, type IV pilus protein PilA expression was not affected. These results suggest that dnaK is associated with bacterial motility and adherence, which are mediated by flagella and pili, and with toxin secretion, which plays a key role in the penetration of P. aeruginosa through Caco-2 cell monolayers. Inactivation of P. aeruginosa dnaK function may interfere with bacterial translocation and prevent septicaemia caused by P. aeruginosa.

Identification of genes associated with the penetration activity of the human type of Edwardsiella tarda EdwGII through human colon epithelial cell monolayers.

Edwardsiella tarda is a Gram-negative pathogen with a broad host range including fish and humans. E. tarda causes gastrointestinal and extraintestinal infections in humans. In present study, the penetration activities of 22 strains of E. tarda, including 10 human isolates and 12 diseased fish isolates, through Caco-2 cell monolayers were evaluated. All the human isolates exhibited penetration activity in contrast to the fish isolates, which did not. In order to identify genes responsible for penetration activity, we screened transposon (Tn) insertion mutants for reduced penetration activity. Two Tn insertion mutants showed markedly reduced penetration activity, and we identified the wecC and fliF genes as Tn insertion sites. The wecC and fliF genes encode UDP-N-acetyl-d-mannosamine dehydrogenase, which is involved in synthesis of enterobacterial common antigen and flagellar basal body M-ring protein, respectively. Motility activity, including swarming and swimming, by the wecC mutant was weaker than that by the wild-type strain, while the fliF mutant was immotile. These results indicated that the swarming and swimming abilities mediated by the wecC and fliF genes appeared to be essential for penetration activity of E. tarda through Caco-2 cell monolayers. We also demonstrated that it was possible to group E. tarda strains into two types of human isolates and diseased fish isolates based on distribution of the wecC gene, type III and type VI secretion system genes. PCR detection of the wecC gene may represent a useful method for detecting the human type of E. tarda, which may have the ability to cause human infection.

ORF13 in the Type III secretion system gene cluster of Edwardsiella tarda binds to the mammalian factor Cugbp2.

The Type III secretion system (TTSS) is essential for the intracellular replication of Edwardsiella tarda in phagocytes of fish and mammals, and a hypothetical gene (orf13) located in the TTSS gene cluster is required for intracellular replication and virulence of E. tarda. Here, we show that under TTSS-inducing conditions, the protein ORF13 was secreted into culture supernatant. Then, using a yeast 2-hybrid screen, we show that the mammalian factor Cugbp2, which regulates apoptosis in breast cancer cells, directly interacts with ORF13. A pull-down assay revealed that ORF13 binds to the C-terminal region of Cugbp2. Our results suggest that ORF13 may facilitate E. tarda replication in phagocytes by binding to Cugbp2.

Potential role of the NADPH oxidase NOX1 in the pathogenesis of 5-fluorouracil-induced intestinal mucositis in mice.

Although NADPH oxidase 1 (NOX1) has been shown to be highly expressed in the gastrointestinal tract, the physiological and pathophysiological roles of this enzyme are not yet fully understood. In the present study, we investigated the role of NOX1 in the pathogenesis of intestinal mucositis induced by the cancer chemotherapeutic agent 5-fluorouracil (5-FU) in mice. Intestinal mucositis was induced in Nox1 knockout (Nox1KO) and littermate wild-type (WT) mice via single, daily administration of 5-FU for 5 days. In WT mice, 5-FU caused severe intestinal mucositis characterized by a shortening of villus height, a disruption of crypts, a loss of body weight, and diarrhea. In Nox1KO mice, however, the severity of mucositis was significantly reduced, particularly with respect to crypt disruption. The numbers of apoptotic caspase-3- and caspase-8-activated cells in the intestinal crypt increased 24 h after the first 5-FU administration but were overall significantly lower in Nox1KO than in WT mice. Furthermore, the 5-FU-mediated upregulation of TNF-α, IL-1ß, and NOX1 and the production of reactive oxygen species were significantly attenuated in Nox1KO mice compared with that in WT mice. These findings suggest that NOX1 plays an important role in the pathogenesis of 5-FU-induced intestinal mucositis. NOX1-derived ROS production following administration of 5-FU may promote the apoptotic response through upregulation of inflammatory cytokines.

Dual role of serotonin in the pathogenesis of indomethacin-induced small intestinal ulceration: pro-ulcerogenic action via 5-HT3 receptors and anti-ulcerogenic action via 5-HT4 receptors.

Serotonin (5-HT) exerts multiple physiological functions not only in the central and peripheral nervous systems but also in the gastrointestinal tract, and these multiple functions are accounted for by a variety of 5-HT receptor subtypes. We investigated the role of 5-HT in the pathogenesis of indomethacin-induced intestinal lesions in mice, in relation to 5-HT receptor subtypes. A single oral administration of indomethacin (10 mg/kg) provoked damage in the small intestine of mice 24 h later, and this response was prevented by pretreatment with p-chlorophenylalanine (a 5-HT synthesis inhibitor). The administration of 5-HT3 receptor antagonists, such as ondansetron and ramosetron, dose-dependently reduced the severity of the intestinal lesions, whereas a high dose of GR113808 (a 5-HT4 receptor antagonist) significantly aggravated these lesions. In contrast, NAN-190 (a 5-HT1 receptor antagonist), ketanserin (a 5-HT2 receptor antagonist), and SB269970 (a 5-HT7 receptor antagonist) had no effect on these lesions. Mosapride (a 5-HT4 receptor agonist) significantly reduced the severity of indomethacin-induced intestinal lesions, and this protective effect was totally prevented by either GR113808 or methyllycaconitine (an α7-nicotinic acetylcholine receptor antagonist). Indomethacin increased the activity of myeloperoxidase and the expression of inducible nitric oxide synthase, inflammatory cytokines, and chemokines in the small intestine; these responses were significantly attenuated by ondansetron and mosapride. These findings suggest that endogenous 5-HT exerts a dual role in the pathogenesis of indomethacin-induced intestinal lesions: pro-ulcerogenic action via 5-HT3 receptors and anti-ulcerogenic action via 5-HT4 receptors, and the latter effect via 5-HT4 receptors may be mediated by activation of α7-nicotinic acetylcholine receptors.

Carbon monoxide involved in modulating HCO3- secretion in rat duodenum.

We examined the effect of the tricarbonyl-dichlororuthenium (II) dimer (CORM-2), a carbon monoxide (CO) donor, on duodenal HCO(3)(-) secretion in rats and investigated whether endogenous CO produced by heme oxygenase (HO) is involved in the regulation of this secretion. Under urethane anesthesia, a duodenal loop was perfused with saline, and HCO(3)(-) secretion was measured at pH 7.0 using a pH stat method. CORM-2, biliverdin, FeCl(2), or ruthenium (III) chloride hydrate (RuCl(3)) was applied to the loop for 5 min. The mucosal application of CORM-2 dose-dependently increased HCO(3)(-) secretion, whereas neither RuCl(3), FeCl(2), nor biliverdin had an effect. The stimulatory effect was significantly attenuated by indomethacin but not N(G)-nitro-L-arginine methyl ester. The application of CORM-2 increased the mucosal prostaglandin (PG) E(2) content of the duodenum. The acid-induced HCO(3)(-) response was markedly inhibited by indomethacin and Sn(IV) protoporphyrin IX dichloride (SnPP; an inhibitor of HO) but not Cu(II) protoporphyrin dichloride, and the inhibitory effect of SnPP was significantly reversed by pretreatment with hemin, a substrate of HO. Perfusion of the duodenal loop with 100 mM HCl for 2 h caused a few hemorrhagic lesions in the mucosa, and this response was significantly worsened by the prior administration of SnPP and indomethacin. The expression of HO-1 but not HO-2 protein was up-regulated in the duodenum after the acid treatment. These results suggest that CO, generated endogenously or exogenously, stimulates HCO(3)(-) secretion in the duodenum, and this effect is mediated by endogenous PGs. It is assumed that HO/CO plays a role in maintaining the integrity of the duodenal mucosa.

Dopamine D2-receptor antagonists ameliorate indomethacin-induced small intestinal ulceration in mice by activating α7 nicotinic acetylcholine receptors.

We have reported that nicotine and the specific α7AChR agonist ameliorate indomethacin-induced intestinal lesions in mice by activating α7 nicotinic acetylcholine receptors (α7nAChR). Dopamine D2-receptor antagonists, such as domperidone and metoclopramide, enhance the release of ACh from vagal efferent nerves. The present study examined the effects of domperidone and metoclopramide on indomethacin-induced small intestinal ulceration in mice, focusing on the α7AChR. Male C57BL/6 mice were administered indomethacin (10 mg/kg, s.c.) and sacrificed 24 h later. Domperidone (0.1-10 mg/kg) and metoclopramide (0.03-0.3 mg/kg) were administered i.p. twice, at 0.5 h before and 8 h after indomethacin treatment, while methyllycaconitine (a selective antagonist of α7nAChR, 30 mg/kg) was administered twice, at 0.5 h before each domperidone treatment. Indomethacin caused severe hemorrhagic lesions in the small intestine, mostly to the jejunum and ileum, with a concomitant increase in myeloperoxidase (MPO) activity. Domperidone suppressed the severity of lesions and the increase in MPO activity at low doses (0.1-3 mg/kg), but not at a high dose (10 mg/kg). Similar effects were also observed by metoclopramide. The protective effects of domperidone and metoclopramide were totally abolished by prior administration of methyllycaconitine. Indomethacin treatment markedly enhanced inducible nitric oxide synthase and chemokine mRNA expression in the small intestine, but these responses were all significantly attenuated by either domperidone or metoclopramide. These findings suggest that dopamine D2-receptor antagonists ameliorate indomethacin-induced small intestinal ulceration through the activation of endogenous anti-inflammatory pathways mediated by α7nAChR.

Dependence of electric power flow on solar radiation power in compact photovoltaic system containing SiC-based inverter with spherical Si solar cells.

A photovoltaic power generation system suitable for mobile applications was developed. A SiC integrated converter with the maximum power point tracking circuit provided the smallest photovoltaic inverter in ~200 W level. The SiC-based inverter exhibited a peak direct current (DC)-alternating current (AC) conversion efficiency higher than that of conventional Si inverters. A Li-ion laminated battery was mounted in the same housing as the inverter. The weight of entire system containing spherical Si solar cell panels was well below 6 kg. Continuous operation measurements of this system were carried out using four solar cell modules connected in parallel under irradiation by natural sunlight. The total inverter efficiencies under realistic operation conditions were slightly decreased compared with the DC-AC converter values because of loss by the maximum power point tracking device. Even under unstable weather conditions, the system provided power stability without ripples. The behaviors of the output powers of the solar cell, storage battery, and inverter modules were analyzed as a function of the solar radiation power density. The substantial efficiencies of the solar cell modules were dependent on the weather conditions and were approximately 10% on cloudy days. The present compact photovoltaic power generation system with SiC device and spherical Si solar cells is viable for sub kW-class inverter.

Aggravation of cold-restraint stress-induced gastric lesions in adjuvant arthritic rats: pathogenic role of inducible and endothelial nitric oxide.

It was reported previously that non-steroidal anti-inflammatory drugs (NSAID)-induced gastric damage was markedly aggravated in rats during arthritis, and this response was mediated by the overproduction of nitric oxide (NO) derived from endothelial NO synthase (eNOS) in addition to inducible NO synthase (iNOS). The present study examined the gastric ulcerogenic response to cold-restraint stress in adjuvant arthritic rats, particularly in relation to NO/NOS isozymes. Exposure of normal rats to cold-restraint stress (13 degrees C) produced slight gastric damage 3 h later, but the ulcerogenic response was markedly aggravated in arthritic rats. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME) (a nonselective inhibitor of NOS) slightly increased the cold-restraint stress-induced gastric lesions in normal rats, but dose-dependently prevented the aggravation of these lesions in arthritic rats. The increased ulcerogenic response in arthritic rats was significantly suppressed by 1400 W (a selective inhibitor of iNOS) and L-iminoethyl ornithine (L-NIO) (a selective inhibitor of eNOS), but not by N(G)-propyl-L-arginine (L-NPA) (a selective inhibitor of nNOS), and almost totally abolished by the co-administration of 1400 W and L-NIO. The mucosal expression levels of eNOS and iNOS but not nNOS mRNAs were enhanced in arthritic rats compared with normal rats. The aggravation of stress-induced gastric lesions in arthritic rats was also significantly suppressed by pretreatment with glutathione. These results suggest that the gastric ulcerogenic response to cold-restraint stress is enhanced in arthritic rats, similar to that induced by NSAIDs, and this phenomenon may be causally associated with the upregulation of eNOS/NO in addition to iNOS/NO.

Validating the inhibitory effects of d- and l-serine on the enzyme activity of d-3-phosphoglycerate dehydrogenases that are purified from Pseudomonas aeruginosa, Escherichia coli and human colon.

BACKGROUND: We previously demonstrated that the serA gene is associated with bacterial pathogenicity, including bacterial penetration through the Caco-2 cell monolayers, bacterial motility, bacterial adherence, and fly mortality. l-Serine is known to inhibit the d-3-phosphoglycerate dehydrogenase (PGDH) activity of the SerA protein, and it significantly reduced the bacterial pathogenicity as described above. We also demonstrated that in a PGDH assay using crude extracts isolated from overnight cultures of E. coli overexpressing the P. aeruginosa serA gene, l-serine inhibited the PGDH activity of the SerA protein. The basal PGDH activity of the negative control strain was high, presumably due to contamination of unknown proteins in the crude extracts. Therefore, to further confirm the direct inhibition of PGDH activity of P. aeruginosa SerA by l-serine, we purified and characterized the PGDH from P. aeruginosa and compared it with the previously characterized PGDHs from E. coli, and the human colon as controls. RESULTS: Optimum pH and ionic strength of the purified PGDHs were different depending on the three species; optimal activity of P. aeruginosa PGDH was at pH 7.5 with 50-100 mM Tris-HCl, E. coli PGDH was at pH 8.5 with 100-200 mM Tris-HCl, and human PGDH was at pH 9.0 with 100-200 mM Tris-HCl. The addition of l-serine reduced the activity of PGDH from P. aeruginosa and E. coli, but not the PGDH from human colon. The median inhibitory concentration (IC50) of l-serine was 630 µM for P. aeruginosa and 250 µM for E. coli, while IC50 of d-serine was much higher than that of l-serine; 76 mM in P. aeruginosa PGDH and 45 mM in E. coli PGDH. CONCLUSIONS: These results suggest that l-serine significantly repressed P. aeruginosa pathogenicity through direct inhibition of the PGDH activity, but was not able to inhibit the human PGDH activity. Oral administration of l-serine to compromised hosts might interfere with bacterial translocation and prevent gut-derived sepsis caused by P. aeruginosa through inhibition of the function of the serA gene product.

Electrochemical treatment of human urine for its storage and reuse as flush water.

We proposed the electrochemical treatment of human urine to enable its storage without the accompanying unpleasant odor. This urine can then be reused as flush water in toilets as a means to tackle water shortage problems. In laboratory-scale experiments, the time-dependent variation in the pH of human urine, after the addition of urease, could be suppressed by chlorine produced via the electrochemical treatment of diluted human urine. Ureolysis was quantified by pH increase within 100 h. This suppression occurred as a result of an irreversible change in the conformation of urease that resulted in its inactivation at an oxidation-reduction potential (ORP) of ca. 240 mV or above. Due to the electrochemical inactivation of urease during the entire storage period of urine, the hydrolysis of urea in urine, which results in the production of the unpleasant odor due to ammonia formation, can be avoided. Thus, the treatment enables the storage of urine for its reuse as flush water in toilets.

Pseudomonas aeruginosa serA Gene Is Required for Bacterial Translocation through Caco-2 Cell Monolayers.

To specify critical factors responsible for Pseudomonas aeruginosa penetration through the Caco-2 cell epithelial barrier, we analyzed transposon insertion mutants that demonstrated a dramatic reduction in penetration activity relative to P. aeruginosa PAO1 strain. From these strains, mutations could be grouped into five classes, specifically flagellin-associated genes, pili-associated genes, heat-shock protein genes, genes related to the glycolytic pathway, and biosynthesis-related genes. Of these mutants, we here focused on the serA mutant, as the association between this gene and penetration activity is yet unknown. Inactivation of the serA gene caused significant repression of bacterial penetration through Caco-2 cell monolayers with decreased swimming and swarming motilities, bacterial adherence, and fly mortality rate, as well as repression of ExoS secretion; however, twitching motility was not affected. Furthermore, L-serine, which is known to inhibit the D-3-phosphoglycerate dehydrogenase activity of the SerA protein, caused significant reductions in penetration through Caco-2 cell monolayers, swarming and swimming motilities, bacterial adherence to Caco-2 cells, and virulence in flies in the wild-type P. aeruginosa PAO1 strain. Together, these results suggest that serA is associated with bacterial motility and adherence, which are mediated by flagella that play a key role in the penetration of P. aeruginosa through Caco-2 cell monolayers. Oral administration of L-serine to compromised hosts might have the potential to interfere with bacterial translocation and prevent septicemia caused by P. aeruginosa through inhibition of serA function.

Activation of α7 nicotinic acetylcholine receptors ameliorates indomethacin-induced small intestinal ulceration in mice.

Cholinergic anti-inflammatory actions have been shown to result mainly from the activation of α7 nicotinic acetylcholine receptors. Here, we investigated the possible role of α7 nicotinic acetylcholine receptors in the pathogenesis of indomethacin-induced small intestinal ulceration in mice. Male C57BL/6 mice were given indomethacin (10mg/kg, s.c.), and sacrificed 24h later. Nicotine (0.3-3mg/kg) and PNU-282987 (a selective agonist of α7 nicotinic acetylcholine receptors; 1-10mg/kg) were administered i.p. twice, at 0.5h before and 8h after indomethacin treatment, while methyllycaconitine (a selective antagonist of α7 nicotinic acetylcholine receptors; 10mg/kg was administered twice, at 0.5h before each nicotine treatment. Indomethacin caused severe hemorrhagic lesions in the small intestine with marked increases in myeloperoxidase (MPO) activity and inducible nitric oxide synthase (iNOS) expression in the mucosa. Pretreatment with nicotine reduced the severity of intestinal lesions in a dose-dependent manner. The protective effect of nicotine was mimicked by PNU-282987 and significantly attenuated by methyllycaconitine. The increases in MPO activity and iNOS expression induced by indomethacin were also significantly suppressed by nicotine and PNU-282987. Immunohistochemical study showed that the expression of α7 nicotinic acetylcholine receptors was clearly enhanced in the submucosa of the damaged area following indomethacin treatment. These results suggest that the activation of α7 nicotinic acetylcholine receptors ameliorates indomethacin-induced small intestinal ulceration, and that this effect may result from the inhibition of iNOS expression and neutrophil migration.

Alternation of gene expression in trigeminal ganglion neurons following complete Freund's adjuvant or capsaicin injection into the rat face.

The hyperexcitability of trigeminal ganglion (TG) neurons following inflammation or C-fiber stimulation is known to be involved in a variety of changes in gene expression in TG neurons, resulting in pain abnormalities in orofacial regions. We analyzed nocifensive behavior following complete Freund's adjuvant (CFA) or capsaicin injection into the maxillary whisker pad, and gene expression in the TG neurons using microarray analysis. The head-withdrawal latency to capsaicin injection or the head-withdrawal threshold to mechanical stimulation of the whisker pad skin in CFA-treated rats was significantly decreased compared to vehicle-treated rats. Many up-regulated and down-regulated genes in the TG neurons of each model were reported. Genes which have not been linked to peripheral inflammation or C-fiber activation were detected. Moreover, microarray chip containing a number of non-coding sequences was also up-regulated by C-fiber activation. These findings suggest that the diverse gene expressions in TG neurons are differentially involved in the inflammatory chronic pain and the acute pain induced by C-fiber activation, and the hyperexcitation of C-fibers are associated with the activation of certain non-coding RNAs.

Non-restrictive heart rate monitoring using an acceleration sensor.

Daily long-term monitoring of heart rates is important for health management. An analysis of heart rate variability can facilitate the early discovery of illnesses. In this study, we paid attention to the method of measuring resting heart rate over long term. An acceleration sensor was set inside the down kilt as it opposing to subject's left chest. Mechanical vibration from heart activity is carried to the acceleration sensor through the down quilt. As a result, periodic vibration was measured successfully and this vibration was proved to be in high correlation with the R wave of ECG. The same results were obtained even in case of lying in a left lateral position.

Proposal for a method of non-restrictive measurement of resting heart rate in a lying position.

Daily monitoring of heart rates is important in health management. Many researchers have analysed heart rate variability by using the resting heart rate because such an analysis can facilitate the early discovery of a variety of illnesses and health conditions. Some problems that arise in measuring heart rate are the feeling of confinement. Therefore, we required a system that could measure the resting heart rate in a static position in such a way that the subject is completely unaware that the measurement is being recorded. We propose a non-restrictive measurement method that uses only an acceleration sensor placed inside a down quilt. This method is easy for home use. The acceleration sensor was placed inside the quilt such that it was positioned opposite to the left-hand side of the subject's chest. Six healthy subjects were requested to lie in the supine position and were covered with the quilt equipped with the acceleration sensor. Mechanical vibrations that resulted from heart activity were carried through the quilt to the acceleration sensor. As a result, periodic vibrations were measured successfully, and in the six subjects, these vibrations were proved to be highly correlated with the R wave of electrocardiograms. The same results were obtained even when the subjects were lying in the left lateral position. The results indicated that our new method, which used an acceleration sensor placed inside a down quilt, was simple and could be used to measure the resting heart rate in a lying position.