Z. Yu, H. Liao, G. Wu, Y. Liu, G. Zhang, L. Xiao, S. Yang, J. Liu, G. Yang, “ SIRT3 Inhibits Cell Proliferation of Nonsmall Cell Lung Carcinoma by Inducing ROS Production,” Clinical Respiratory Journal 18, no. 11 (2024), https://doi.org/10.1111/crj.70033.
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For critically ill patients in the intensive care unit (ICU), acute respiratory failure (ARF) stands as a prominent cause of mortality. Anion gap (AG) denotes the disparity between unmeasured cations and anions. Adjusting AG for albumin levels results in the albumin corrected anion gap (ACAG), which provides a more accurate representation of the body's acid–base status. Elevated ACAG may arise from ARF-induced cellular hypoxia and metabolic acidosis. However, limited research has investigated the association between ACAG and the 28-day all-cause mortality of ARF patients in critical care.
Using the Medical Information Mart for Intensive Care (MIMIC-IV 2.2) database, a retrospective data analysis was conducted, specifically targeting critically ill patients diagnosed with ARF. Serum ACAG was collected within 24 hours of the patient's admission to the ICU. The association between ACAG levels and 28-day all-cause mortality was investigated using smooth curve fitting, a multivariate Cox proportional hazard regression model, and Kaplan–Meier survival curve analysis. Furthermore, the consistency of these relationships was assessed through interaction and subgroup analyses.
The study involved the enrollment of 3888 eligible participants in total. After adjusting for confounding variables in the multivariable Cox regression analysis model, we noticed a positive linear relationship between the ACAG value and the ICU's 28-day all-cause mortality rate. When ACAG was used as a continuous variable, a 3.1% increase in 28-day all-cause mortality was associated with a 1.0-mmol/L increase in ACAG (adjusted HR = 1.037, 95% CI: 1.025–1.048, p < 0.001). In the 28-day all-cause mortality, the highest and intermediate ACAG groups (adjusted HR 1.483, 95% CI: 1.244–1.768 and adjusted HR 1.244, 95% CI: 1.062–1.457, respectively) were notably higher than the lowest ACAG group when ACAG was utilized as a tertiles categorical variable. The substantial association between ACAG and 28-day all-cause mortality in the ICU was consistently demonstrated through subgroup analysis.
Among ICU patients with ARF, an elevated ACAG is linked to an elevated risk of 28-day all-cause mortality. There exists a linearly positive relationship between the 28-day all-cause mortality and ACAG.
Interstitial lung disease (ILD) is a group of diseases involving diffuse pulmonary parenchymal lesions and alveolar inflammation and interstitial fibrosis. Telomeres are repetitive DNA sequences at the end of chromosomes to maintain structural integrity and telomerase can prevent telomere shortening. Telomerase abnormalities such as related gene mutations lead to decrease in telomerase activity and telomere shortening. It has been proven that telomere shortening and telomerase abnormalities are related to the occurrence and development of ILD. Telomere shortening occurs in different types of ILD patients and is associated with prognosis. Gene therapy targeting telomerase exhibits therapeutic potential. The paper elaborates on the progress of telomere shortening in the diagnosis, differential diagnosis, treatment, and prognosis of ILD in recent years, in order to demonstrate its potential and promises and to be helpful for clinical diagnosis and treatment.
Asthma is a chronic airway inflammatory disease that significantly affects patients' quality of life and mental health. This study aims to compare the differences between acupoint embedding auxiliary therapy and traditional auxiliary therapy in asthma control, immune response, sleep quality, and quality of life, as well as evaluate their therapeutic effects on patients with asthma.
A retrospective analysis of 300 patients with asthma was conducted, divided into acupoint catgut embedding and conventional treatment groups. Key assessments included asthma control (ACQ score), exacerbation frequency, HADS, PSQI, and SF-36 for quality of life. Immune markers (IgE, eosinophil count, IL-4, IL-5, IL-10) were measured. Univariate and multivariate logistic regression analyses and ROC curves were used to identify predictors of asthma control and sleep quality. Stratified analysis evaluated differences by asthma severity.
The acupoint catgut embedding group showed significant improvements in asthma control (p < 0.001), exacerbation frequency (p < 0.05), and anxiety and depression (p = 0.0359) compared to the conventional treatment group. IgE (p = 0.00656), eosinophil count (p = 0.0214), and IL-5 (p = 0.0187) were significantly lower, while IL-10 (p = 0.0226) was higher in the acupoint group. Sleep quality (PSQI score, p = 0.0117) and deep sleep (NREM 3, p < 0.05) improved. Asthma severity (p < 0.001) and treatment method (p < 0.001) were significant predictors of outcomes, with model 2 (AUC = 0.731) outperforming model 1 (AUC = 0.649). Stratified analysis showed acupoint therapy was more effective in intermittent and mild asthma.
As an auxiliary treatment, acupoint embedding therapy has shown a good effect in improving the sleep quality of patients with asthma and controlling asthma symptoms, especially in patients with mild-to-moderate asthma.
The dramatic increase in antidepressant prescribing over the past decade has sparked debate about the possible contribution of antidepressants to elevated cancer risk. In this study, we investigate whether antidepressant use has a causal relationship with lung cancer risk.
Genome-wide association study (GWAS) data for antidepressant use were acquired from the FinnGen Biobank, while GWAS data for overall lung cancer and specific histological subtypes were obtained from the UK Biobank (UKBB) and IEU databases. The causal impact was evaluated using inverse variance weighting (IVW), MR-Egger regression, and weighted median (WM) approaches. Multiple sensitivity analyses were conducted to validate the findings. Results are expressed as ORs and 95% CIs.
No causal relationship between antidepressant use and lung cancer risk was observed in the IVW (OR = 1.001, 95% CI = 0.999, p = 0.279), MR-Egger (OR = 1.002, 95% CI = 0.992, p = 0.700), and WM analyses (OR = 1.000, 95% CI: 0.997, p = 0.889). Similar results were found across lung cancer subtypes, including lung adenocarcinoma (LUAD) (OR = 1.197, 95% CI = 0.884–1.619, p = 0.247), lung squamous cell carcinoma (LUSC) (OR = 1.052, 95% CI = 0.822, p = 0.688), and small cell lung carcinoma (SCLC) (OR = 1.874, 95% CI = 0.737, p = 0.187). Sensitivity tests confirmed the robustness of these results.
This analysis indicates antidepressant use is not significantly associated with lung cancer risk.
Nebulized inhalation therapy is an important method in the prevention and treatment of respiratory diseases, and inactivated mycobacterial vaccine nebulized inhalation has received a wide attention recently, but the roles and mechanisms are still not fully understood. A literature search showed there is a strong scientific rationale and evidence that nebulized inhalation of inactivated mycobacterial vaccine is effective in the prevention and treatment of respiratory diseases. Clinically available mycobacterial vaccines include Mycobacterium phlei (M. phlei), BCG, and Mycobacterium vaccae (M. vaccae). Nebulized inhalation of inactivated mycobacterial vaccine, especially M. vaccae, has been used in the prevention and treatment of respiratory diseases, such as asthma, respiratory syncytial virus (RSV), coronavirus disease 2019 (COVID-19), and sepsis. It acts on the respiratory tract directly, thus stimulating the body to produce an immune response, enhance respiratory immunity, and achieve prevention and treatment effects. Nebulized inhalation of inactivated mycobacterial vaccine will be an effective therapy in the prevention and treatment of respiratory diseases.
Volume OXygenation (VOX) index has good efficacy in predicting the failure of high-flow nasal cannula therapy. However, its predictive value for treatment failure in patients receiving noninvasive ventilation (NIV) remains uncertain.
Patients who underwent early NIV treatment were grouped based on their 2-h NIV VOX Youden index. The low-risk group consisted of patients with a VOX value > 20.45 (n = 188), while the high-risk group included those with a VOX value ≤ 20.45 (n = 200). Baseline data and arterial blood gas values were collected at 2, 12, and 24 h after NIV initiation.
Compared to the low-risk group, the high-risk group exhibited higher SOFA scores, respiratory rates, and heart rates, along with a lower oxygenation index (P/F) (all p < 0.05). Following NIV treatment, the low-risk group showed a more significant increase in P/F values at 2 h, 12 h, and 24 h after NIV initiation. The low-risk group showed a lower VT and MV (minute ventilation volume) at 2 h, 12 h, and 24 h of NIV (p < 0.05). Moreover, the low-risk group had a lower intubation rate (7.98% vs. 77%, p < 0.05) and mortality rate (4.79% vs. 17.5%, p < 0.05). At 2 h of NIV, the area under the receiver operating characteristic curve for predicting NIV failure using the VOX index was 0.843 (95% CI 0.805–0.882). Using a VOX value threshold of 20.45 to predict NIV failure, the sensitivity was 69.1%, and the specificity was 94.4%. Furthermore, a VOX value ≤ 20.45 was identified as an independent risk factor for tracheal intubation and death.
VOX index shows promise to serve as an effective evaluation index to predict early NIV efficacy in patients with AHRF; a VOX value > 20.45 after 2 h of NIV treatment can better predict improvements in hypoxia, respiratory drive, and NIV outcomes, guide early tracheal intubation in cases of NIV failure, and have a certain predictive effect on patient outcomes.
Considerable evidence suggests a strong link between immune cell traits (ICTs) and asthma development via plasma metabolites (PMs), but the causality between ICTs and asthma is still unclear, mainly due to issues like selection bias. Our research was designed to investigate the causality between ICTs, PMs, and asthma and to provide a clearer explanation of these relationships.
Utilizing the GWAS database, this study employed a two-step, two-sample Mendelian randomization (MR) approach and the inverse variance weighted (IVW) method to investigate the causality between ICTs and asthma, as well as between PMs and asthma. Lastly, we calculated the mediated proportion of PMs as mediators in the link between ICTs and asthma.
Excluding heterogeneity and pleiotropy, MR analysis identified 13 ICTs (CD14 on CD33br HLA DR+ CD14dim, etc.) and asthma causality, and no reverse causality was observed. In addition, 27 PMs (androsterone sulfate levels, succinate levels, etc.) were also causally associated with asthma. Mediate MR indicated −9.81% (−1.2%, −18.4%) of the effect of CD24 on IgD+ CD38br on asthma is mediated by S-methylcysteine sulfoxide levels, with a mediated effect value (p = 0.006) is 0.003 (0.0004, 0.006); 21.4% (6.2%, −36.6%) of the effect of CD3 on CD28+ CD4+ on asthma is mediated by 1-myristoyl-2-arachidonoyl-GPC (14:0/20:4) levels, with a mediated effect value (p = 0.025) is 0.004 (0.001, 0.007).
We identified two pathways by which ICTs can impact asthma through PMs, which might help in identifying potential targets for personalized treatment approaches.
This case report features a patient with an invasive thymoma. The patient presented with an anterior mediastinal mass that invaded the left brachiocephalic trunk vein, resulting in the formation of a carcinoma thrombus in the right atrium, superior vena cava, left brachiocephalic trunk vein, and left internal jugular vein (Masaoka stage IV). No indication for surgery was assessed by surgical consultation. After six cycles of chemotherapy and chest radiotherapy, the tumor size decreased from 72.43 to 24 mm, showing a significant improvement in patient efficacy. After a follow-up of 50 months, the patient remained well, without local recurrence or distal metastasis, and maintained a partial response (PR).
G. Liu, H. Shi, H. Zheng, W. Kong, X. Cheng, L. Deng, “ Circular RNA NFIX Functions as an Oncogene in Non-Small Cell Lung Cancer by Modulating the miR-214-3p/TRIAP1 Axis,” Clinical Respiratory Journal 18, no. 8 (2024). https://doi.org/10.1111/crj.13801.
Figures 4 and 7 are incorrect. Below are the correct figures.
FIGURE 4 | Effect of circRNA NFIX interference in NSCLC by targeting miRNA-214-3p. A549 cells were transfected with control-siRNA, circRNA NFIX-siRNA, circRNA NFIX-siRNA + inhibitor control, or circRNA NFIX-siRNA + miR-214-3p inhibitor for 48 h. (A) Cell proliferation was counted by MTT assay. (B and C) The apoptosis ratio of cancer cells was detected by flow cytometry. (D and E) The level of cleaved-caspase3 was detected by western blot assay, and cleaved-caspase3/caspase3 ratio was calculated. ** indicates p < 0.01 versus control-siRNA, ## indicates p < 0.01 circRNA NFIX-siRNA + inhibitor control. Data are exhibited as average ± SD of triple single experiments.
FIGURE 7 | Overexpression of miRNA-214-3p suppressed cell growth and promoted cell apoptosis via TRIAP1 in NSCLC cells. A549 cells were transfected with mimic control, miRNA-214-3p mimic, miRNA-214-3p mimic + control-plasmid, or miRNA-214-3p mimic + TRIAP1-plasmid for 48 h. (A) Cell proliferation was counted by MTT assay. (B and C) The apoptosis of A549 cells was analyzed by flow cytometry. (D and E) The level of cleaved-caspase3 was detected by western blot assay, and the ratio of cleaved-caspase3/caspase3 was determined. ** indicates p < 0.01 versus mimic control, ## indicates p < 0.01 versus miR-214-3p mimic + control-plasmid. Data are exhibited as average ± SD of triple single experiments.
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