Continuous positive airway pressure improves respiratory mechanics and efficiency of neural drive in stable COPD: an exploratory study.

BACKGROUND: Continuous positive airway pressure (CPAP) is a major treatment strategy for severe chronic obstructive pulmonary disease (COPD), especially with respiratory failure. However, it remains inconclusive whether CPAP affects respiratory mechanics and neural drive in stable COPD patients without respiratory failure. METHODS: Twenty-two COPD patients without respiratory failure received CPAP starting from 4 to 10 cmH2O in 1 cmH2O increments. Respiratory pattern, end expiatory lung volume (EELV), dynamic PEEPi (PEEPidyn), airway resistance (Raw), pressure-time product of diaphragmatic pressure (PTPdi) and esophageal pressure (PTPeso), root mean square (RMS) of diaphragm electromyogram (EMGdi) and ratio of ventilation (Ve) to EMGdi (i.e., Ve/RMS) were measured before and at each level of continue positive airway pressure (CPAP). A subgroup analysis was performed between patients with and without inspiratory muscle weakness. RESULTS: Nineteen patients completed the treatment. The respiratory pattern improved significantly after CPAP. Raw, PTPdi, and Pdi decreased significantly. ΔEELV decreased at 4 cmH2O (P<0.05), but increased significantly at >8 cmH2O. PEEPidyn decreased from 2.18±0.98 to 1.37±0.55 cmH2O. RMS increased while Ve/RMS improved significantly after CPAP (P<0.05). Besides, CPAP could significantly improve respiratory mechanics in patients with inspiratory muscle weakness. CONCLUSIONS: CPAP improves respiratory pattern, PEEPi, Raw, work of breathing and efficiency of neural drive in COPD patients without respiratory failure, but easily increases dynamic pulmonary hyperinflation. These effects on respiratory mechanics are significant in patients with inspiratory muscle weakness.

[VOCs Emission Inventory and Impact Range Simulation of Antibiotic Enterprises].

Drug production consumes a large amount of raw materials and is recognized as a "high-pollution, high-energy-consumption" industry. In consideration of the small amount of emission inventory research in the pharmaceutical industry, firstly, based on the actual monitoring data and production information of typical antibiotic enterprises, the emission factors of various volatile organic compounds (VOCs) were determined using the field measurement method. Then, combined with the activity level information of antibiotics from A to G plant in the same park, the emission factor method was used to calculate and obtain the emissions of each plant, and an emission list was established. Uncertainty analysis of the list was carried out using the Monte Carlo method. Finally, the CALPUFF model was used to simulate the environmental impact range of the A-G plants in spring, summer, autumn, and winter. The results showed that the total VOCs emission factor in the production of antibiotic enterprises was 6655.61 g·t-1, and the crystallization process emission factor was the largest, at 3603.476 g·t-1. The A to G plants produce 6655.610, 7454.283, 998.342, 11980.098, 4492.537, 42462.792, and 18302.928 kg, respectively, of VOCs each year for the production of antibiotics, and the four substances with the largest emissions are butyl acetate, n-butanol, n-hexane, and acetone, respectively. Through the verification of the Monte Carlo model for plant A, it was found that the emissions of plant A basically presented as a lognormal distribution, and the uncertainty of 95% confidence interval was (-60.62%, 131.78%), which was within the acceptable range. Through CALPUFF simulation, the diffusion direction and range of VOCs were found to be different in each season, and an aggregation phenomenon occurs in summer.

Parathyroid Hormone-Related Protein (1-40) Enhances Calcium Uptake in Rat Enterocytes Through PTHR1 Receptor and Protein Kinase Cα/ß Signaling.

BACKGROUND/AIMS: Parathyroid hormone-related protein (PTHrP) is implicated in regulating calcium homeostasis in vertebrates, including sea bream, chick, and mammals. However, the molecular mechanism underlying the function of PTHrP in regulating calcium transport is still not fully investigated. This study aimed to investigate the effect of PTHrP on the calcium uptake and its underlying molecular mechanism in rat enterocytes. METHODS: The rat intestinal epithelial cell line (IEC-6) was used. Calcium uptake was determined by using the fluo-4 acetoxymethyl ester fluorescence method. The expression levels of RNAs and proteins was assessed by RT-PCR and Western-blot, respectively. RESULTS: PTHrP (1-40) induced rapid calcium uptake in enterocytes in a dose-dependent manner. PTHrP (1-40) up-regulated parathyroid hormone 1 receptor (PTHR1) protein but not 1,25D3-MARRS receptor. Pre-treatment of anti- PTHR1 antibody abolished the PTHrP (1-40)-induced calcium uptake. PTHrP (1-40) significantly up-regulated four transcellular calcium transporter proteins, potential vanilloid member 6 (TRPV6), calbindin-D9k (CaBP-D9k), sodium-calcium exchanger 1 (NCX1) and plasma membrane calcium ATPase 1 (PMCA1), in a dose- and time-dependent manner. Pre-treatment with TRPV6 or CaBP-D9k antibodies or knockout of rat TRPV6 or CaBP-D9k markedly inhibited PTHrP (1-40)-induced calcium uptake, whereas inhibition of NCX or PMCA1 by antibodies or inhibitors had no effect on PTHrP(1-40)-induced calcium uptake. Furthermore, PTHrP (1-40) treatment up-regulated protein levels of protein kinase C (PKC α/ß) and protein kinase A (PKA). Pretreatment of PKC α/ß inhibitor (but not PKA inhibitor) inhibited PTHrP (1-40)-induced calcium uptake. CONCLUSION: PTHrP (1-40) stimulates calcium uptake via PTHR1 receptor and PKC α/ß signaling pathway in rat enterocytes, and calcium transporters TRPV6 and CaBP-D9k are necessary for this stimulatory effect.

Online learning algorithms for principal component analysis applied on single-lead ECGs.

This article evaluates several adaptive approaches to solve the principal component analysis (PCA) problem applied on single-lead ECGs. Recent studies have shown that the principal components can indicate morphologically or environmentally induced changes in the ECG signal and can be used to extract other vital information such as respiratory activity. Special interest is focused on the convergence behavior of the selected gradient algorithms, which is a major criterion for the usability of the gained results. As the right choice of learning rates is very data dependant and subject to movement artifacts, a new measurement system was designed, which uses acceleration data to improve the performance of the online algorithms. As the results of PCA seem very promising, we propose to apply a single-channel independent component analysis (SCICA) as a second step, which is investigated in this paper as well.

Effect of expiratory load on neural inspiratory drive.

BACKGROUND: Neural respiratory drive is usually measured during inspiration, even in patients with chronic obstructive pulmonary disease (COPD) in whom the primary physiological deficit is expiratory flow limitation. The purpose of the study was to test the hypothesis that inspiratory muscle neural respiratory drive could be used to assess expiratory load. METHODS: Ten healthy young men, (26 ± 4) years old, were asked to expire through a tube immersed in water where an expiratory load was required. The load was judged by the depth of the tube in water and the different loads (0 cmH2O, 10 cmH2O, 20 cmH2O and 30 cmH2O) were randomly introduced. Each expiratory load lasted for 3 - 5 minutes and inspiration was unimpeded throughout. Diaphragm electromyogram (EMG) and transdiaphragmatic pressure were recorded by a catheter with 10 metal coils and two balloons. Incremental cycle exercise with and without an expiratory load at 30 cmH2O was also performed. RESULTS: Neural drive during expiratory loaded breathing was larger than during unloaded breathing but neural drive did not increase proportionally with increasing expiratory load; neural drive during expiratory loading at 0, 10, 20 and 30 cmH2O was (10.1 ± 3.1) µV, (16.7 ± 7.3) µV, (18.4 ± 10.7) µV and (22.9 ± 13.2) µV, respectively. Neural drive as a percentage of maximum at the end of exercise with or without load was similar ((57.4 ± 11.0)% max vs. (62.7 ± 16.4)% max, P > 0.05). CONCLUSION: Neural respiratory drive measured at inspiration does not accurately quantify expiratory load either at rest or during exercise.

[Respiratory effort assessed by surface diaphragm EMG in patients with sleep apnea].

OBJECTIVE: Measurement of esophageal pressure is considered to be the gold standard for assessing respiratory effort and neural respiratory drive but this requires placement of an esophageal catheter. We hypothesized that neural drive could be reflected by the diaphragm EMG recorded from chest wall surface electrodes. METHODS: We simultaneously recorded esophageal pressure and the chest wall diaphragm EMG in 11 patients with suspected obstructive sleep apnea/hypopnea syndrome during full night polysomnography. We also recorded the diaphragm EMG from esophageal electrode in 5 of the 11 subjects. RESULTS: Diaphragm EMG could be satisfactorily recorded from 9 of the 11 subjects. The root mean square of the chest wall diaphragm EMG increased gradually during the obstructive sleep apnea events and reached a maximal value at arousal. Similarly, the esophageal pressure increased gradually over the obstructive sleep apnea events and reached a maximal value at the end of apnea. There was a relation between the RMS of the diaphragm EMG recorded from the chest wall surface electrodes and esophageal pressure (r = 0.66) and the diaphragm EMG (r = 0.72) recorded from esophageal electrode during obstructive event. CONCLUSION: The diaphragm EMG could be recorded from the chest wall surface electrodes in most subjects and can be used to demonstrate the presence of respiratory effort during apnoea/hypopnea events.