Evaluation of respiratory rate monitoring performance using a home oxygen monitoring device among patients with interstitial lung disease and chronic obstructive pulmonary disease

Background: Home monitoring devices have been developed to measure adherence to home oxygen therapy. In this study, we evaluated the performance of TeleOx®, a commercially available remote monitoring device, in comparison with polysomnography (PSG) in patients with interstitial lung disease (ILD) and chronic obstructive pulmonary disease (COPD) and the factors that affected TeleOx® correct use. Methods: TeleOx® was connected on the patient or concentrator side. The oxygen flow rates were set at 1, 3, and 5 L/min. Intraclass correlation coefficient (ICC) (2, 1) was used to determine the agreement between respiratory rate measured using TeleOx® and that measured using PSG, and the minimum acceptable level of reliability was >0.7. Results: In total, 22 patients (16 with ILD and 6 with COPD) were assessed. In patients with ILD, the detection rate of patients’ respiration assessed using TeleOx® did not change according to the device’s position. It increased from 53.5% to 79.0% by changing the position from the concentrator to the patient side in patients with COPD. The ICC (2, 1) value indicated that TeleOx® had acceptable reliability at oxygen flow rates of 1 and 3 L/min regardless of the device’s position in patients with ILD (the concentrator side: 0.9 and 0.82, respectively; the patient side: 0.95 and 0.82, respectively), whereas that did only at the oxygen flow rate of 1 L/min and in connecting TeleOx® on the patient side in patients with COPD (0.73). Conclusion: The monitoring performance of TeleOx® differed according to its position, oxygen flow rates, and patients’ diseases

Mixing time and simulated annealing for the stochastic cellular automata

Finding a ground state of a given Hamiltonian on a graph $G=(V,E)$ is an important but hard problem. One of the potential approaches is to use a Markov chain Monte Carlo to sample the Gibbs distribution whose highest peaks correspond to the ground states. In this paper, we investigate a particular kind of stochastic cellular automata, in which all spins are updated independently and simultaneously. We prove that (i) if the temperature is fixed sufficiently high, then the mixing time is at most of order $\log|V|$, and that (ii) if the temperature drops in time $n$ as $1/\log n$, then the limiting measure is uniformly distributed over the ground states.Comment: 16 pages, 8 figure

Bofutsushosan, an Oriental Herbal Medicine, Attenuates the Weight Gain of White Adipose Tissue and the Increased Size of Adipocytes Associated with the Increase in Their Expression of Uncoupling Protein 1 in High-Fat Diet-Fed Male KK/Ta mice

Bofutsushosan (BOF), an oriental herbal medicine, has been used as an anti-obesity drug in overweight patients. In the present study, to evaluate the anti-obesity and anti-diabetic effects of BOF, we investigated the effects of BOF on the white adipose tissue (WAT) weight, the size of adipocytes, adiponectin expression, and oral glucose tolerance test results in high-fat diet-fed male KK/Ta mice. In addition, the mRNA expression levels of uncoupling protein 1 (UCP1) and UCP2 mRNA in WAT and brown adipose tissue (BAT) were measured. 6-week-old KK/Ta mice were divided into four groups and fed a purified powdered basal diet (the BD group), a purified high-fat (HF) powdered diet containing suet powder at 37.5 g/100 g diet (the HF group), a high-fat diet plus 1.0% bofutsushosan (BOF) treatment (the HF + BOF group), or a high-fat diet plus 1.0% daisaikoto (DAI) treatment (the HF + DAI group) for 4 weeks. The weight of WAT and the size of adipocytes were increased in the HF group compared with those in the BD group, and these increases in the HF group were significantly inhibited in the HF + BOF group, but not affected in the HF + DAI group. There were no statistically significant differences in plasma levels and tissue mRNA levels of adiponectin among the four groups. There were no significant differences in UCP1 mRNA expression of BAT among the four groups. The expression of UCP1 mRNA in WAT was found in the HF + BOF group, but little expression was seen in the WAT of the BD, HF, or HF + DAI groups. The elevated plasma glucose levels and responses after the glucose loading in the HF group tended to decrease in the HF + BOF group. These results suggest that BOF decreases the weight and size gains of WAT along with up-regulating UCP1 mRNA in WAT in high-fat diet-fed mice

A Mouse Model of Metabolic Syndrome; Increase in Visceral Adipose Tissue Precedes the Development of Fatty Liver and Insulin Resistance in High-Fat Diet-Fed Male KK/Ta Mice

To determine the relative contribution of obesity and visceral white adipose tissue (WAT) to metabolic syndrome, we developed a model that is susceptible to high-fat diet-induced obesity and insulin resistance using male KK/Ta mice. The ratio of WAT weight to body weight was greater in the high-fat diet group compared with the control group in 10-, 14-, and 22-week-old mice. The increase in visceral WAT preceded development of fatty liver and insulin resistance. Adiponectin mRNA expression in WAT was markedly decreased before the decrease in its plasma levels or the development of insulin resistance. Insulin resistance appeared in association with fatty infiltration and TNF-α expression in the liver in 22-week-old mice. These data indicate that our mouse model would be useful for future studies that investigate the role of visceral WAT and its products in the development of metabolic syndrome

Transcriptome Analysis for Cytoprotective Actions of Rebamipide against Indomethacin-Induced Gastric Mucosal Injury in Rats

We have reported that rebamipide, a gastroprotective drug, suppresses indomethacin-induced gastric mucosal injury in humans and rats. However, the mechanisms of the cytoprotective actions of rebamipide have not been fully addressed. In the present study, we determined mRNA expression profile of the gastric mucosa treated with indomethacin in rats, and investigated the cytoprotective effects of rebamipide against indomethacin-induced injury with a high-density oligonucleotide array (Rat Toxicology U34 GeneChip array). Gastric epithelial cells were obtained by laser-assisted microdissection. Data analysis was performed with a GeneChip Operating Software, GeneSpring software 7.0, and Ingenuity Pathway Analysis. Among 1,031 probes, the expression of 160 probes (15.5%) showed at least 2.0-fold up-regulation (158 probes) and down-regulation (2 probes) 2 h after indomethacin administration in comparison with the vehicle-treated rats. The pathway analysis of the up-regulated 123 probes identified the network with a highly significant score, which consisted of known clusters of cell death, cancer, and endocrine system disorders. We succeeded in listing 10 genes that were up-regulated by the treatment with indomethacin and that were down-regulated by rebamipide, including growth arrest and DNA damage-induced 45α. In conclusion, we demonstrated that cell death, especially apoptosis, pathway is involved in the pathogenesis of indomethacin-induced gastric mucosal injury, and that inhibition of apoptosis-related genes is possibly important for the cytoprotective effect of rebamipide against this injury

Gastric peroxisome proliferator activator receptor-γ expression and cytoprotective actions of its ligands against ischemia-reperfusion injury in rats

The beneficial effects by peroxisome proliferator-activated receptor-γ (PPAR-γ) on gastric injury induced by ischemia-reperfusion have been confirmed, however, the precise mechanism of its cytoprotection is not elucidated thoroughly. The aim of the present study was to determine the gastric localization of PPAR-γ expression in the rat gastric mucosa, and to clarify the mechanism of its cytoprotective properties. The gastric expression of PPAR-γ was confirmed by RT-PCR and western blot, and localized on gastric epithelial cells. The protective effect of PPAR-γ ligands, pioglitazone or 15-deoxy-Δ12,14-prostaglandin J2, on gastric ischemia-reperfusion injury was reversed by the co-administration with PPAR-γ antagonist. The gastric expression of tumor necrosis factor-α and cytokine-induced neutrophil chemoattractant-1 increased significantly in rats treated ischemia-reperfusion, and these increases were significantly inhibited by treatment with pioglitazone. Among the 1,032 probes, 18 probes were up-regulated at least 1.5-fold, 17 were down-regulated at least 1.5-fold by pioglitazone. The network including calnexin, endoplasmic reticulum stress protein, heat shock proteins, and proteasome genes was induced by pioglitazone treatment. In conclusion, activation of gastric epithelial PPAR-γ receptor by its ligands may represent a novel therapeutic approach for gastric inflammation via up-regulation of heat shock proteins and endoplasmic reticulum-related proteins