Effect of Enteral and Parenteral Nutrition Support on Pulmonary Function in Elderly Patients with Chronic Obstructive Pulmonary Disease Complicated by Respiratory Failure.

Objective: To investigate the effect of enteral and parenteral nutrition support (EPNS) on pulmonary function in elderly patients with chronic obstructive pulmonary disease (COPD) complicated by respiratory failure (RF). Methods: A total of 127 patients who underwent treatment for elderly patients with COPD complicated by RF in our hospital from February 2020 to May 2022 were collected for a retrospective analysis. There were 41 patients with enteral nutrition support (group A), 46 with parenteral nutrition support (group B), and 40 with EPNS (group C). The levels of serum albumin (ALB), prealbumin (PA), serum hemoglobin (Hb), and serum transferrin (TRF) were measured before and after nutritional support in the three groups, and the changes in pulmonary function of patients were compared. The changes in the levels of inflammatory factors and markers of oxidative stress (OS) in serum were also detected, and the incidence of adverse reactions and length of stay (LOS) were counted. Results: ALB, PA, Hb, and TRF levels were increased in all 3 groups after nutritional support, with the highest in group C (P < 0.05). Similarly, lung function was improved in all 3 groups and inflammatory factor levels and OS were suppressed, also most dramatically in group C (P < 0.05). There was no difference in the incidence of adverse reactions among the 3 groups, and the LOS in group C was shorter than those in groups A and B (P < 0.05). Conclusion: EPNS can effectively improve the lung function of patients with COPD combined with RF and reduce the inflammation and OS damage. It can effectively improve the therapeutic effect of patients and has great application prospects in the treatment of COPD combined with RH in the future.

LINC00941 Promotes Progression of Non-Small Cell Lung Cancer by Sponging miR-877-3p to Regulate VEGFA Expression.

Long noncoding RNAs (lncRNAs) play critical roles in carcinoma occurrence and metastasis. LINC00941 has been found to mediate the development of gastric cancer, and LINC00941 was negatively associated with the longer overall survival of lung adenocarcinoma patients. Herein, our aim was to investigate the effects and mechanisms of LINC00941 in NSCLC progression. Microarray was used to identify the change lncRNAs in NSCLC, LINC00941 was found to increase in tumor tissues and patients' plasma. Knockdown of LINC00941 didn't modulate the proliferation of NSCLC cells, but inhibition of LINC00941 in NSCLC cells suppressed the angiogenesis ability of human umbilical vein endothelial cells (HUVECs). Moreover, LINC00941 promoted tumorigenesis in vivo, while si-LINC00941 inhibited tumor development of NSCLC. VEGFA was should to be significantly modulated by LINC00941 in NSCLC cells, then luciferase assay proved that LINC00941 regulated VEGFA expression via interacting with miR-877-3p. Followed functional experiments indicated that overexpression of LINC00941 accelerated angiogenesis and NSCLC tumor progression via miR-877-3p/VEGFA axis both in vitro and in vivo. In conclusion, our results clarified the LINC00941 function for the first time, and LINC00941 promoted the progression of NSCLC, which was mediated by miR-877-3p/VEGFA axis. This study might provide new understanding and targets for NSCLC diagnosis and treatment.