Risk factors for hyponatremia in acute exacerbation chronic obstructive pulmonary disease (AECOPD): a multicenter cross-sectional study.

BACKGROUND: Hyponatremia is an independent predictor of poor prognosis, including increased mortality and readmission, in COPD patients. Identifying modifiable etiologies of hyponatremia may help reduce adverse events in patients with AECOPD. Therefore, the aim of this study was to explore the risk factors and underlying etiologies of hyponatremia in AECOPD patients. METHODS: A total of 586 AECOPD patients were enrolled in this multicenter cross-sectional study. Finally, 323 had normonatremia, and 90 had hyponatremia. Demographics, underlying diseases, comorbidities, symptoms, and laboratory data were collected. The least absolute shrinkage and selection operator (LASSO) regression was used to select potential risk factors, which were substituted into binary logistic regression to identify independent risk factors. Nomogram was built to visualize and validate binary logistics regression model. RESULTS: Nine potential hyponatremia-associated variables were selected by LASSO regression. Subsequently, a binary logistic regression model identified that smoking status, rate of community-acquired pneumonia (CAP), anion gap (AG), erythrocyte sedimentation rate (ESR), and serum magnesium (Mg2+) were independent variables of hyponatremia in AECOPD patients. The AUC of ROC curve of nomogram was 0.756. The DCA curve revealed that the nomogram could yielded more clinical benefits if the threshold was between 10% and 52%. CONCLUSIONS: Collectively, our results showed that smoking status, CAP, AG, ESR, and serum Mg2+ were independently associated with hyponatremia in AECOPD patients. Then, these findings indicate that pneumonia, metabolic acidosis, and hypomagnesemia were the underlying etiologies of hyponatremia in AECOPD patients. However, their internal connections need further exploration.

Immunotherapy and Prognosis of Non-small Cell Lung Carcinoma by Monomethoxy polyethylene glycol-hyaluronic acid-platinum Combined with Immune CT4+ and CT8+ Detection.

To investigate the changes in CT4+ and CT8+ lymphocyte subpopulations of patients with non-small cell lung carcinoma (NSCLC) by monomethoxy polyethylene glycol-hyaluronic acid-platinum (MPEG-HA-Pt) and the correlation between efficacy evaluation and the changes in T lymphocyte subpopulation, 76 NSCLC patients treated at oncology department of Chengdu First People's Hospital were selected and randomly divided into the treatment group and the control group (38 cases in each). mPEG-HA-Pt was used for the treatment of the included patients in the research. The patients in the control group were performed with traditional chemotherapy for 2 treatment courses. The changes in the T-lymphocyte subpopulation before and after the treatment were detected and the therapeutic effects on the patients in the two groups were compared. The particle size of mPEG-HA-Pt ranged between 78nm and 100nm with an average of 84.6±7.5nm. After that, a transmission electron microscope (TEM) was used to observe the spheres with uniform size. The drug loading capacity and entrapped efficiency of mPEG-HA-Pt were 18.7% and 87.4%, respectively. After the treatment for NSCLC patients by nanomicelle, cellular immune functions were all improved. In particular, cellular immune functions of the patients with good efficacy evaluation were improved more apparently.

[Investigation of effect of bicuculline on expression of alpha-smooth muscle actin and airway remodeling in asthmatic mice].

OBJECTIVE: To observe the effect of bicuculline, which is a selective GABA receptor antagonist on expression of alpha-SMA in the lung tissue of rats with chronic asthma, to explore the role of the bicuculline on the airway remodeling in asthmatic mice. METHODS: Forty BALB/c mice were randomly divided into four groups: the control group (A), the asthma model group (B), the bicuculline group (C) and bicuculline with budesonide group (D). The asthmatic model was established by sensitization and challenge with ovalbumin. The expression of alpha-SMA in the lung tissue and the thickness of the airways of mice was detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical staining. RESULTS: There was little expression of alpha-SMA in the lung tissue of normal mice compared with the asthma model group (P < 0.05). The expressions of alpha-SMA in the group C and D decreased compared with that in group B (P < 0.01), but no significant difference (P > 0.05) was observed between group C and D. The WAt/Pbm, WAi/Pbm, and WAm/Pbm were significantly increased in the asthma group compared with that in normal group (P < 0.05), and the WAt/Pbm, WAi/Pbm, and WAm/Pbm were decrased in the group compared with that of group B (P < 0. 01), the wAm/Pbm was decreased in the group C (P < 0. 05). CONCLUSION: Over expression of alpha-SMA in asthmatic lung tissue is closely related to the onset of asthmatic. GABAAR antagonist bicuculline could inhibit the expression of alpha-SMA and alpha-SMA mRNA and alleviate airway remodeling with equivalent potency of inhaled corticosteroid. Our data suggest that GABAAR involve in the pathogenesis of asthmatic airway remodeling by upregulating the expression of alpha-SMA inducing the airway smooth muscle constriction and hyperplasia.

Downregulation of long non-coding RNA ZXF1 restricts cell survival by targeting miR-634-GRB2 in lung adenocarcinoma.

Increasing evidence demonstrates that long non-coding RNAs (lncRNAs) play important regulatory roles in mediating initiation and progression of lung adenocarcinoma (LA), which is one of the most lethal in humans. A previous study reported that lncRNAZXF1 was dysregulated in LA and enhanced expression of ZXF1 promoted the invasion and metastasis in LA. However, the effect of ZXF1 on LA progression and its underlying mechanisms were not thoroughly investigated. In our in vitro experiments, qRT-PCR revealed that the expression level of ZXF1 in LA tissues and tumor cells were significantly higher than that in adjacent normal tissues and normal cells. Furthermore, bioinformatics analysis, luciferase reporter assay, western blot and RNA immunoprecipitation (RIP) assay showed that ZXF1 could directly interact with miR-634, which targets GRB2. Therefore, we propose that ZXF1 could function as an oncogene partly by sponging miR-634 and therefore regulating GRB2 expression in LA. Overall, this study demonstrated, for the first time, that the lncRNA ZXF1/miR-634/GRB2 axis plays crucial roles in modulating LA progression. Moreover, lncRNA ZXF1 might potentially improve LA prognosis and serve as a therapeutic target for the treatment of LA.