Association between 19 Allergens and Chronic Constipation in Adults: NHANES 2005-2006.

INTRODUCTION: There are increasing reports of a link between chronic constipation and allergies in children. However, similar epidemiological evidence is limited in the general adult population. Therefore, in this study, we attempted to assess the association between chronic constipation and allergy in adults aged ≥20 years in the USA. METHODS: We established a logistic regression model to test the relationship between chronic constipation and 19 specific immunoglobulin E (sIgE) types in adults aged ≥20 years using large-sample data from the National Health and Nutrition Examination Survey database (2005-2006). The weekly defecation times of the allergic and non-allergic groups were compared using the t test. RESULTS: We found that sIgE-sensitized participants had a 0.723 lower risk of chronic constipation than the general population (95% confidence interval (CI) = 0.566-0.923). There was a negative association between chronic constipation and sensitizations to peanut (odds ratio (OR) = 0.579, 95% CI = 0.381-0.935), egg (OR = 0.335, 95% CI = 0.134-0.838), dog (OR = 0.723, 95% CI = 0.522-0.965), and cockroach (OR = 0.540, 95% CI = 0.373-0.784). In addition, the frequency of defecation per week increased significantly in people allergic to peanuts and cockroaches (p < 0.05). DISCUSSION/CONCLUSION: The results of this study demonstrate an inverse relationship between sIgE sensitization and chronic constipation in adults. However, the specific association mechanism needs to be further studied.

Verbascoside protects from LPS-induced septic cardiomyopathy via alleviating cardiac inflammation, oxidative stress and regulating mitochondrial dynamics.

BACKGROUND: Verbascoside (VB), as an active component of multiple medicinal plants, has been proved to exert anti-oxidative, anti-aging and neuroprotective effects. This study was designed to investigate whether VB could play a cardioprotective role in septic heart injury. METHODS: Mice were injected with lipopolysaccharide (LPS; 10 mg/kg) to induce sepsis. The treatment group received an intraperitoneally injection of VB (20 mg/kg) before LPS challenge. Transthoracic echocardiography, ELISA, immunofluorescence, and qPCR were performed to assess the effect of VB on heart function, oxidative stress, inflammation and apoptosis. Transmission electronic microscopy and immunoblotting were used to evaluate the mitochondrial morphology and biogenesis of the septic heart. In vitro experiments were also performed to repeat above-mentioned assays. RESULTS: Compared with LPS group, the VB treatment group showed improved cardiac function in sepsis. VB alleviated oxidative stress and inflammatory cell infiltration, as well as cardiomyocyte apoptosis. Specifically, VB could restore sepsis-induced mitochondrial alterations via regulating mitochondrial biogenesis. These results were also confirmed in in vitro experiments. CONCLUSION: Verbascoside could protected from sepsis-induced cardiomyopathy by inhibiting oxidative stress, inflammation, and apoptosis, as well as promoting mitochondrial biogenesis.

Joint association of cigarette smoking and PM2.5 with COPD among urban and rural adults in regional China.

BACKGROUND: Cigarette smoking and PM2.5 are important risk factors of Chronic Obstructive Pulmonary Disease (COPD). However, the joint association of cigarette smoking and PM2.5 with COPD is unknown. METHODS: A community-based study was conducted among urban and rural adults aged 40 + years between May and December of 2015 in Jiangsu Province, China. The outcome variable was spirometry-defined COPD. Explanatory measures were smoking status (non-smokers or smokers) and PM2.5 exposure [low level (< 75 µg/m3) or high level (≥ 75 µg/m3)]. Mixed-effects logistic regression models were applied to calculate the odds ratio (OR) and 95% confidence interval (CI) to investigate the associations of cigarette smoking and PM2.5 with COPD. RESULTS: The prevalence of COPD was 11.9% (95% CI = 10.9%, 13.0%) within the overall 3407 participants in this study. After adjustment for potential confounders and community-level clustering effect, smokers tended to develop COPD relative to non-smokers (OR = 2.46, 95% CI 1.76, 3.43), while only smokers exposed to high level PM2.5 were more likely to experience COPD (OR = 1.36; 95% CI 1.01, 1.83) compared to their counterparts exposed to low level PM2.5. Meanwhile, compared to non-smokers who exposed to low level PM2.5, non-smokers who exposed to high level PM2.5 (OR = 1.10, 95% CI 0.74, 1.64), smokers who exposed to low (OR = 2.22, 95% CI 1.51, 3.27) or high level PM2.5 (OR = 3.14, 95% CI 2.15, 4.59) were, respectively, more like to develop COPD. CONCLUSIONS: Cigarette smoking was positively associated with COPD among overall participants, while PM2.5 was in positive relation to COPD among smokers only. Moreover, cigarette smoking and PM2.5 might have an additive effect on the risk of COPD among adult smokers aged 40 years or older in China.

Coexistence of OSA may compensate for sleep related reduction in neural respiratory drive in patients with COPD.

BACKGROUND: The mechanisms underlying sleep-related hypoventilation in patients with coexisting COPD and obstructive sleep apnoea (OSA), an overlap syndrome, are incompletely understood. We compared neural respiratory drive expressed as diaphragm electromyogram (EMGdi) and ventilation during stage 2 sleep in patients with COPD alone and patients with overlap syndrome. METHODS: EMGdi and airflow were recorded during full polysomnography in 14 healthy subjects, 14 patients with OSA and 39 consecutive patients with COPD. The ratio of tidal volume to EMGdi was measured to indirectly assess upper airway resistance. RESULTS: Thirty-five patients with COPD, 12 healthy subjects and 14 patients with OSA completed the study. Of 35 patients with COPD, 19 had COPD alone (FEV1 38.5%±16.3%) whereas 16 had an overlap syndrome (FEV1 47.5±16.2%, AHI 20.5±14.1 events/hour). Ventilation (VE) was lower during stage 2 sleep than wakefulness in both patients with COPD alone (8.6±2.0 to 6.5±1.5 L/min, p<0.001) and those with overlap syndrome (8.3±2.0 to 6.1±1.8 L/min). Neural respiratory drive from wakefulness to sleep decreased significantly for patients with COPD alone (29.5±13.3% to 23.0±8.9% of maximal, p<0.01) but it changed little in those with overlap syndrome. The ratio of tidal volume to EMGdi was unchanged from wakefulness to sleep in patients with COPD alone and healthy subjects but was significantly reduced in patients with OSA or overlap syndrome (p<0.05). CONCLUSIONS: Stage 2 sleep-related hypoventilation in COPD alone is due to reduction of neural respiratory drive, but in overlap syndrome it is due to increased upper airway resistance.

Mitochondria related peptide MOTS-c suppresses ovariectomy-induced bone loss via AMPK activation.

Therapeutic targeting bone loss has been the focus of the study in osteoporosis. The present study is intended to evaluate whether MOTS-c, a novel mitochondria related 16 aa peptide, can protect mice from ovariectomy-induced osteoporosis. After ovary removal, the mice were injected with MOTS-c at a dose of 5 mg/kg once a day for 12 weeks. Our results showed that MOTS-c treatment significantly alleviated bone loss, as determined by micro-CT examination. Mechanistically, we found that the receptor activator of nuclear factor-κB ligand (RANKL) induced osteoclast differentiation was remarkably inhibited by MOTS-c. Moreover, MOTS-c increased phosphorylated AMPK levels, and compound C, an AMPK inhibitor, could partially abrogate the effects of the MOTS-c on osteoclastogenesis. Thus, our findings provide evidence that MOTS-c may exert as an inhibitor of osteoporosis via AMPK dependent inhibition of osteoclastogenesis.

Synthesis of N-heterocyclic carbene-PdCl2-(iso)quinoline complexes and their application in arylamination at low catalyst loadings.

A new type of N-heterocyclic carbene-PdCl2-(iso)quinoline complexes 3 were successfully achieved in acceptable to good yields from easily available starting materials under mild conditions, and their structures were unambiguously confirmed using X-ray single crystal diffraction. Furthermore, their catalytic activity toward Buchwald-Hartwig arylamination of aryl chlorides with primary and secondary amines was fully tested. Under the optimal reaction conditions, the expected arylated amines can be obtained in high to excellent yields at low catalyst loadings (0.005-0.05 mol%). It may be worth noting here that comparison of these complexes with other well-defined and easily available NHC-Pd(ii) complexes bearing different N-containing ancillary ligands was also carried out, showing their superior catalytic activity over all others.

Adiponectin protects the kidney against chronic intermittent hypoxia-induced injury through inhibiting endoplasmic reticulum stress.

PURPOSE: The current study was carried out to assess the effects of chronic intermittent hypoxia (CIH) on the kidney, the intervention roles of adiponectin (Ad), and the associated mechanisms. METHODS: Sixty Wistar rats were randomly divided into four groups: the normal control (NC), normal control plus Ad supplement (NC + Ad), CIH, and CIH plus Ad supplement (CIH + Ad) groups. The rats in both CIH and CIH + Ad groups were submitted to a CIH environment for 4 months, while the rats in NC and NC + Ad groups were housed with the normal air for 4 months. In addition, the rats in NC + Ad and CIH + Ad groups were treated with an intravenous injection of Ad at a dosage of 10 µg per injection, twice a week, for four successive months. RESULTS: The production level of reactive oxygen species (ROS) and the protein levels of endoplasmic reticulum (ER) stress, as well as the cell apoptosis level in kidney, were all higher in the CIH group than in the NC and NC + Ad groups (all p < 0.05). However, the ROS production, the protein of ER stress, and cell apoptosis levels in kidney were all lower in the CIH + Ad group than those in the CIH group (all p < 0.05). CONCLUSION: Ad could protect against CIH-induced renal cell apoptosis through inhibiting ROS-related ER stress.

Association between the -1438G/A and T102C polymorphisms of 5-HT2A receptor gene and obstructive sleep apnea: a meta-analysis.

The serotonin 2A (5-HT2A) receptor has been implicated in obstructive sleep apnea (OSA). Single nucleotide polymorphisms (SNPs) in the 5-HT2A gene have been found in OSA, the most common being -1438G/A and T102C; however, studies of the association between 5-HT2A SNPs and OSA risk have reported inconsistent findings. A meta-analysis was performed to quantitatively review the association between -1438G/A and T102C SNPs and OSA. Five studies, including 791 subjects for -1438G/A genotype and 1,068 subjects for T102C genotype, were selected. Pooled data analysis of the -1438G/A genotype indicated a significantly increased OSA risk was associated with two variant genotypes (AA vs. AG+GG: OR 3.023, 95 % CI 2.169-4.213, P = 0.506 for heterogeneity; A allele carriers vs. GG: OR 1.938, 95 % CI 0.879-4.274, P = 0.012 for heterogeneity). Stratification analysis by gender supported the association in males, but not females. For the T102C genotype, no significantly increased OSA risk was associated with the two variant genotypes (CC vs. CT+TT: OR 1.065, 95 % CI 0.787-1.442, P = 0.361 for heterogeneity; C allele carriers vs. TT: OR 0.979, 95 % CI 0.737-1.3, P = 0.9 for heterogeneity).In conclusions, meta-analysis indicated that the -1438G/A, and not T102C, polymorphism of 5-HT2A is a positive risk factor of OSA, especially in males.

Fasting Plasma Glucose and Glycohemoglobin with Allergic Symptoms and Specific Sensitization: Results from NHANES 2005-2006.

OBJECTIVE: The National Health and Nutrition Examination Survey (NHANES) data has been used to study the relationship between fasting plasma glucose (FPG) and glycohemoglobin (A1c) in patients with allergic symptoms and specific sensitization, respectively. METHODS: A total of 1,687 participants and a variety of logistic regression models were selected based on the 2005-2006 NHANES (n = 10,348) for our study to describe the relationship between FPG and A1c in subjects with the sensitivity of allergic symptoms, specific sensitization and specific sensitization of 19 allergens, respectively. On this basis, a variety of logistic regression models were further established for hierarchical analysis to study the limiting conditions when FPG and A1c were related to allergic symptoms. RESULTS: We adjusted the confounding factors and found that the risk of specific sensitization increased with the increase in FPG and A1c. Stratified analysis showed that the risk of allergic symptoms increased with the increase in FPG and A1c when born elsewhere other than in the U.S. and Mexico or underweight or overweight or with hypertension. Furthermore, we found that the risk of egg sensitization increased with the increase in FPG and A1c, while the risk of rat sensitization decreased with the increase in FPG. CONCLUSION: Under certain conditions, FPG and A1c were risk factors for allergic symptoms. FPG and A1c were risk factors for specific sensitization, especially egg sensitization. These findings indicate a possible link between diabetes and allergies.

The impact of E-cadherin expression on non-small cell lung cancer survival: a meta-analysis.

E-cadherin has been implicated in invasiveness and metastasis. However, the clinical prognostic value of decreased E-cadherin expression in patients with non-small cell lung cancer (NSCLC) remains unsettled. A meta-analysis of eligible studies was performed to quantitatively review the correlation of decreased E-cadherin expression with survival in patients with NSCLC. Thirteen studies, including 2,274 patients, were subjected to final analysis. The rate of decreased E-cadherin expression was 47.6 % overall and 41.4 % for stage I disease. The combined hazard ratio (HR) was 1.41 (95 % CI 0.18-1.65; P = 0.001), indicating that decreased E-cadherin expression had an unfavorable impact on the survival of patients with NSCLC. Further, in the stratified analysis by ethnicity, the combined HR in Asians was 1.49 (95 % CI 1.27-1.71) and in non-Asians was 1.01 (95 % CI 1.00-1.02). However, when only the stage I studies were considered, the combined HR was 1.19 (95 % CI 0.90-1.47; P = 0.576), suggesting that decreased E-cadherin expression has no impact on survival. Decreased E-cadherin expression was associated with poor survival in patients with NSCLC, especially among Asians, but was not significantly correlated with survival for stage I NSCLC patients.

Breaking a chaotic direct sequence spread spectrum communication system using interacting multiple model-unscented Kalman filter.

In this paper, a new method to break chaotic direct sequence spread spectrum (CD3S) communication systems is proposed. Here, the CD3S communication system transmitting different information symbols is considered as a combination of two subsystems which are driven by two different chaotic dynamic models, respectively. At every single time moment, the CD3S signal can be regarded as generated by the subsystem corresponding to the information symbol transmitted. Then, based on the multiple model form of CD3S signals, an interacting multiple model unscented Kalman filter with model switching detection mechanism is exploited to track the CD3S signals. The l(2)-norm of tracking errors is used to choose the model which best matches the intercepted signals. Thus, the information symbols are recovered indirectly. Compared with the existing methods, the proposed algorithm can: (1) reduce the influence of a low spreading factor; (2) calculate the spreading factor using the length of time intervals between model switching; and (3) be more effective under scenarios of low signal-to-noise ratio or multipath fading. Simulation results verify the superiority of the proposed method.

Allergy-related outcomes and sleep-related disorders in adults: a cross-sectional study based on NHANES 2005-2006.

BACKGROUND: Epidemiological evidence between the sleep disorders and allergy-related outcomes is limited. OBJECTIVES: The purpose of the present study was to estimate the relationship between sleep disorders and allergy-related outcomes in adults. METHODS: We built logistic regression models to examine the associations between sleep disorders and allergy-related outcomes in adult participants using the 2005-2006 NHANES database. Allergy-related outcomes included sIgE levels, asthma, hay fever, sneezing, wheezing, and eczema. Sleep disorders included sleep latency, sleep length, sleep problems, OSA symptoms, and daytime sleepiness. A t-test was used for between-group comparisons. RESULTS: Participants with OSA symptoms had 2.72 × higher odds of experiencing hay fever and 1.54 × higher odds of having eczema compared to Non-OSA symptoms participants. Participants with insufficient sleep (≤ 6 h/night) had 1.27 × higher odds of developing allergic sensitisation compared to participants with adequate sleep (7-8 h/night). Sneezing was positively associated with sleep problems (OR: 1.706; 95% CI 1.386, 2.099), OSA symptoms (OR: 1.297; 95% CI 1.049, 1.605), and daytime sleepiness (OR: 1.569; 95% CI 1.205, 2.04). CONCLUSION: Our findings suggest a positive association between allergy-related outcomes and sleep disorders. In particular, OSA symptoms, daytime sleepiness, and sleep problems are strongly associated with allergic conditions.

C1q/tumor necrosis factor-related protein-3 improves microvascular endothelial function in diabetes through the AMPK/eNOS/NO· signaling pathway.

The repair of vascular endothelial cell dysfunction is an encouraging approach for the treatment of vascular complications associated with diabetes. It has been demonstrated that members of C1q/tumor necrosis factor-related protein (CTRP) family may improve endothelial function. Nevertheless, the protective properties of CTRPs in diabetic microvascular complications continue to be mostly unknown. Here, we demonstrate that the C1q-like globular domain of CTRP3, CTRP5, and CTRP9 (gCTRP3, 5, 9) exerted a vasorelaxant effect on the microvasculature, of which gCTRP3 was the most powerful one. In a murine model of type 2 diabetes mellitus, serum gCTRP3 level and endothelial function decreased markedly compared with controls. Two weeks of gCTRP3 treatment (0.5 µg/g/d) enhanced endothelium-dependent relaxation in microvessels, increased nitric oxide (NO·) production, and reduced retinal vascular leakage. In addition, Western blotting in human retinal microvascular endothelial cells indicated that gCTRP3 triggered AMP-activated protein kinase-α (AMPKα), hence increasing the endothelial NO synthase (eNOS) level and NO· production. In addition, incubation with gCTRP3 in vitro ameliorated the endothelial dysfunction induced by high glucose in the branch of the mesenteric artery. Blockade of either eNOS or AMPKα completely abolished the effects of gCTRP3 described above. Taken together, we demonstrate for the first time that gCTRP3 improves impaired vasodilatation of microvasculature in diabetes by ameliorating endothelial cell function through the AMPK/eNOS/NO· signaling pathway. This finding may suggest an effective intervention against diabetes-associated microvascular complications.

Targeted Anti-Hepatocellular Carcinoma Research of Targeted Peptides Combined with Drug-Loaded Cell-Derived Microparticles.

To conduct an anti-tumor research by using targeted drug-loaded cell-derived microparticles to target the tumor microenvironment and enhance NK cell killing function. In this experiment, we obtained HepG2 tumor cell-derived microparticles by physical extrusion, high speed centrifugation and filtration, modified the hepatocellular carcinoma targeting peptide SP94 on the surface of microparticles and encapsulated the TGF-ß inhibitor SB505124. Finally we validated and analyzed whether the new drug delivery system can target to tumor site and enhance the anti-tumor function of NK cells. This type of novel targeted cell-derived microparticles drug delivery system will provide a novel idea for tumor immunotherapy.

Aqua-trinitrato[2,4,6-tris-(pyridin-2-yl)-1,3,5-triazine]neodymium(III) dihydrate.

In the title compound, [Nd(NO(3))(3)(C(18)H(12)N(6))(H(2)O)]·2H(2)O, the Nd(3+) ion is in a distorted bicapped square-anti-prismatic geometry formed by three N atoms from the 2,4,6-tris-(pyridin-2-yl)-1,3,5-triazine (TPTZ) ligand, six O atoms from the three nitrate anions and one O atom from the aqua ligand. The mol-ecules are linked by O-H⋯O and O-H⋯N hydrogen bonds. Two types of π-π stacking inter-actions occur between the TPTZ ligands of adjacent complexes [centroid-to-centroid distances = 3.760 (4) and 3.870 (3) Å].

Cannabis Seed Oil Alleviates Experimental Atherosclerosis by Ameliorating Vascular Inflammation in Apolipoprotein-E-Deficient Mice.

In recent decades, epidemiological, clinical, and experimental studies have demonstrated that a diet with antioxidant or anti-inflammatory function plays a central role in the prevention of atherosclerosis (AS). The purpose of this study was to explore the effects of Cannabis seed oil (CO) administration on in vitro antioxidant capacity as well as blood lipid profiles, lipid peroxidation, inflammatory response, and endothelial cell integrity. Female ApoE-/- mice were fed a high-cholesterol diet and administrated with CO or phosphate-buffered saline (PBS) and seal oil by gavage for 8 weeks. The results show that CO administration reduced the levels of serum triglycerides and low-density lipoprotein cholesterol at week 6. Additionally, a decrease in serum tumor necrosis factor α and nitric oxide was also observed. Moreover, results from CD31 staining and scanning electron microscopy revealed that CO treatment alleviated the endothelial cell damage and lipid deposition induced by a high-cholesterol diet. The ratio of lesion area to the total aorta area was 19.57% for the CO group, which was lower than the PBS control group (24.67%). Collectively, CO exerted anti-atherosclerotic effects by modulating serum lipid profiles and inflammatory responses and improving endothelial cell integrity and arterial lipid deposition. The results provide a promising preventive strategy for the early progression of AS.

Association between socioeconomic status and chronic obstructive pulmonary disease in Jiangsu province, China: a population-based study.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a common public health problem worldwide. Recent studies have reported that socioeconomic status (SES) is related to the incidence of COPD. This study aimed to investigate the association between SES and COPD among adults in Jiangsu province, China, and to determine the possible direct and indirect effects of SES on the morbidity of COPD. METHODS: A cross-sectional study was conducted among adults aged 40 years and above between May and December of 2015 in Jiangsu province, China. Participants were selected using a multistage sampling approach. COPD, the outcome variable, was diagnosed by physicians based on spirometry, respiratory symptoms, and risk factors. Education, occupation, and monthly family average income (FAI) were used to separately indicate SES as the explanatory variable. Mixed-effects logistic regression models were introduced to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for examining the SES-COPD relationship. A pathway analysis was conducted to further explore the pulmonary function impairment of patients with different SES. RESULTS: The mean age of the 2421 participants was 56.63 ±â€Š9.62 years. The prevalence of COPD was 11.8% (95% CI: 10.5%-13.1%) among the overall sample population. After adjustment for age, gender, residence, outdoor and indoor air pollution, body weight status, cigarette smoking, and potential study area-level clustering effects, educational attainment was negatively associated with COPD prevalence in men; white collars were at lower risk (OR: 0.60, 95% CI: 0.43-0.83) of experiencing COPD than blue collars; compared with those within the lower FAI subgroup, participants in the upper (OR: 0.68, 95% CI: 0.49-0.97) tertiles were less likely to experience COPD. Such negative associations between all these three SES indicators and COPD were significant among men only. Education, FAI, and occupation had direct or indirect effects on pulmonary function including post-bronchodilator forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC), FEV1, FVC, and FEV1 percentage of predicted. Education, FAI, and occupation had indirect effects on pulmonary function indices of all participants mainly through smoking status, indoor air pollution, and outdoor air pollution. We also found that occupation could affect post-bronchodilator FEV1/FVC through body mass index. CONCLUSIONS: Education, occupation, and FAI had an adverse relationship with COPD prevalence in Jiangsu province, China. SES has both direct and indirect associations with pulmonary function impairment. SES is of great significance for COPD morbidity. It is important that population-based COPD prevention strategies should be tailored for people with different SES.

Identification of target genes of transcription factor activator protein 2 gamma in breast cancer cells.

BACKGROUND: Activator protein 2 gamma (AP-2gamma) is a member of the transcription factor activator protein-2 (AP-2) family, which is developmentally regulated and plays a role in human neoplasia. AP-2gamma has been found to be overexpressed in most breast cancers, and have a dual role to inhibit tumor initiation and promote tumor progression afterwards during mammary tumorigensis. METHODS: To identify the gene targets that mediate its effects, we performed chromatin immunoprecipitation (ChIP) to isolate AP-2gamma binding sites on genomic DNA from human breast cancer cell line MDA-MB-453. RESULTS: 20 novel DNA fragments proximal to potential AP-2gamma targets were obtained. They are categorized into functional groups of carcinogenesis, metabolism and others. A combination of sequence analysis, reporter gene assays, quantitative real-time PCR, electrophoretic gel mobility shift assays and immunoblot analysis further confirmed the four AP-2gamma target genes in carcinogenesis group: ErbB2, CDH2, HPSE and IGSF11. Our results were consistent with the previous reports that ErbB2 was the target gene of AP-2gamma. Decreased expression and overexpression of AP-2gamma in human breast cancer cells significantly altered the expression of these four genes, indicating that AP-2gamma directly regulates them. CONCLUSION: This suggested that AP-2gamma can coordinate the expression of a network of genes, involving in carcinogenesis, especially in breast cancer. They could serve as therapeutic targets against breast cancers in the future.

Neural Respiratory Drive Measured Using Surface Electromyography of Diaphragm as a Physiological Biomarker to Predict Hospitalization of Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients.

BACKGROUND: Neural respiratory drive (NRD) using diaphragm electromyography through an invasive transesophageal multi-electrode catheter can be used as a feasible clinical physiological parameter in patients with chronic obstructive pulmonary disease (COPD) to provide useful information on the treatment response. However, it remains unknown whether the surface diaphragm electromyogram (EMGdi) could be used to identify the deterioration of clinical symptoms and to predict the necessity of hospitalization in acute exacerbation of COPD (AECOPD) patients. METHODS: COPD patients visiting the outpatient department due to acute exacerbation were enrolled in this study. All patients who were subjected to EMGdi and classical parameters such as spirometry parameters, arterial blood gas analysis, COPD assessment test (CAT) score, and the modified early warning score (MEWS) in outpatient department, would be treated effectively in the outpatient or inpatient settings according to the Global Initiative for Chronic Obstructive Lung Disease guideline. When the acute exacerbation of the patients was managed, all the examination above would be repeated. RESULTS: We compared the relationships of admission-to-discharge changes (Δ) in the normalized value of the EMGdi, including the change of the percentage of maximal EMGdi (ΔEMGdi%max) and the change of the ratio of minute ventilation to the percentage of maximal EMGdi (ΔVE/EMGdi%max) with the changes of classical parameters. There was a significant positive association between ΔEMGdi%max and ΔCAT, ΔPaCO2, and ΔpH. The change (Δ) of EMGdi%max was negatively correlated with ΔPaO2/FiO2in the course of the treatment of AECOPD. Compared with the classical parameters including forced expiratory volume in 1 s, MEWS, PaO2/FiO2, the EMGdi%max (odds ratio 1.143, 95% confidence interval 1.004-1.300) has a higher sensitivity when detecting the early exacerbation and enables to predict the admission of hospital in the whole cohort. CONCLUSIONS: The changes of surface EMGdi parameters had a direct correlation with classical measures in the whole cohort of AECOPD. The measurement of NRD by surface EMGdi represents a practical physiological biomarker, which may be helpful in detecting patients who should be hospitalized timely.