The effects of obstructive sleep apnea on blood pressure variability and load in patients with hypertension.

BACKGROUND: Hypertension frequently coexists with obstructive sleep apnea (OSA), and their interplay substantially impacts the prognosis of affected individuals. Investigating the influence of OSA on blood pressure variability (BPV) and blood pressure load (BPL) in hypertensive patients has become a focal point of clinical research. METHODS: This cross-sectional study recruited hypertensive patients (n = 265) without discrimination and classified them into four groups based on their apnea-hypopnea index (AHI): control group (n = 40), AHI < 5; mild group (n = 74), 5 ≤ AHI ≤ 15; moderate group (n = 68), 15 < AHI ≤ 30; severe group (n = 83), AHI > 30. All participants underwent comprehensive assessments, including polysomnography (PSG) monitoring, 24-h ambulatory blood pressure (ABP) monitoring, cardiac Doppler ultrasound, and additional examinations when indicated. RESULTS: BPV and BPL exhibited significant elevations in the moderate and severe OSA groups compared to the control and mild OSA groups (P < 0.05). Moreover, interventricular septum thickness and left ventricular end-diastolic volume (LVEDV) demonstrated higher values in the moderate and severe OSA groups (P < 0.05). Multiple stepwise regression analysis identified noteworthy risk factors for elevated BPV in hypertensive patients with OSA, including AHI, maximum apnea time, total times of oxygen reduction, and mean time of apnea. CONCLUSION: Hypertensive patients with moderate to severe OSA exhibited substantially increased BPV and BPL. Moreover, BPV was correlated with AHI, maximum apnea time, total times of oxygen reduction, and mean time of apnea in hypertensive patients with OSA.

Prognostic Prediction Value and Biological Functions of Non-Apoptotic Regulated Cell Death Genes in Lung Adenocarcinoma / 中国医学科学杂志(英文版)

Objective To explore the potential biological functions and prognostic prediction values of non-apoptotic regulated cell death genes (NARCDs) in lung adenocarcinoma.Methods Transcriptome data of lung adenocarcinoma were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases. We identified differentially expressed NARCDs between lung adenocarcinoma tissues and normal tissues with R software. NARCDs signature was constructed with univariate Cox regression analysis and the least absolute shrinkage and selection operator Cox regression. The prognostic predictive capacity of NARCDs signature was assessed by Kaplan-Meier survival curve, receiver operating characteristic curve, and univariate and multivariate Cox regression analyses. Functional enrichment of NARCDs signature was analyzed with gene set variation analysis, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes. In addition, differences in tumor mutational burden, tumor microenvironment, tumor immune dysfunction and exclusion score, and chemotherapeutic drug sensitivity were analyzed between the high and low NARCDs score groups. Finally, a protein-protein interaction network of NARCDs and immune-related genes was constructed by STRING and Cytoscape software. Results We identified 34 differentially expressed NARCDs associated with the prognosis, of which 16 genes (ATIC, AURKA, CA9, ITGB4, DDIT4, CDK5R1, CAV1, RRM2, GAPDH, SRXN1, NLRC4, GLS2, ADRB2, CX3CL1, GDF15, and ADRA1A) were selected to construct a NARCDs signature. NARCDs signature was identified as an independent prognostic factor (P < 0.001). Functional analysis showed that there were significant differences in mismatch repair, p53 signaling pathway, and cell cycle between the high NARCDs score group and low NARCDs score group (all P < 0.05). The NARCDs low score group had lower tumor mutational burden, higher immune score, higher tumor immune dysfunction and exclusion score, and lower drug sensitivity (all P < 0.05). In addition, the 10 hub genes (CXCL5, TLR4, JUN, IL6, CCL2, CXCL2, ILA, IFNG, IL33, and GAPDH) in protein-protein interaction network of NARCDs and immune-related genes were all immune-related genes. Conclusion The NARCDs prognostic signature based on the above 16 genes is an independent prognostic factor, which can effectively predict the clinical prognosis of patients of lung adenocarcinoma and provide help for clinical treatment.

Protective effects of hydrogen on monoarthritis rats / 第二军医大学学报

Objective: To explore the protective effect of hydrogen (H2) inhalation through respiratory tract on monoarthritis (MA) rats. Methods: Forty male SD rats were randomly divided into 5 groups: MA group, MA+H2 0-14 d group, MA+H2 0-3 d group, MA+H2 4-14 d group, and sham+H2 0-14 d group (n = 8). Complete Freund's adjuvant (CFA) was injected into the left ankle joint of rats to construct MA model. The rats in the MA group did not inhale H2, and the rats in other four groups inhaled 65% H2 1.5 h per day on the day of modeling and 1-14 days after modeling, 1.5 h per day on the day of modeling and 1-3 days after modeling, 1.5 h per day on the 4th-14th day after modeling, and 1.5 h per day on the day of sham operation and 1-14 days after modeling, respectively. Paw withdrawal threshold (PWT) was detected by von Frey method 0, 1, 3, 5, 7, 10, and 14 d after modeling. Another 15 rats were randomly divided into 5 groups and there were 3 rats in each group. Lumbar enlargement tissues were taken from the spinal cord of the inflammatory side on the 10th day after modeling or sham operation. The contents of superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were detected. Results: In the MA group, the posterior paw PWT of the inflammatory side was lower than that of the healthy side on the first day after modeling, reached the lowest on the 3th day and remained stable until the 14th day (P0.05). The levels of SOD and CAT in the spinal cord of the inflammatory side in the MA+H2 0-14 d group were higher than those in the MA group (all P0.05). Conclusion: Inhalation of 65% H2 via the respiratory tract at the initial stage of MA rat modeling can alleviate mechanical hyperalgesia and oxidative stress. Pre-administration of H2 can inhibit the formation of mechanical hyperalgesia in MA.