Aspirin reduces the mortality risk of patients with community-acquired pneumonia: a retrospective propensity-matched analysis of the MIMIC-IV database.

Background: Community-acquired pneumonia (CAP) is a common infectious disease characterized by inflammation of the lung parenchyma in individuals who have not recently been hospitalized. It remains a significant cause of morbidity and mortality worldwide. Aspirin is a widely used drug, often administered to CAP patients. However, the benefits of aspirin remain controversial. Objective: We sought to determine whether aspirin treatment has a protective effect on the outcomes of CAP patients. Methods: We selected patients with CAP from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Propensity score matching (PSM) balanced baseline differences. A multivariate Cox regression model assessed the relationship between aspirin treatment and 28-day mortality. Results: A total of 3,595 patients were included, with 2,261 receiving aspirin and 1,334 not. After PSM, 1,219 pairs were matched. The 28-day mortality rate for aspirin users was 20.46%, lower than non-users. Multivariate Cox regression indicated aspirin use was associated with decreased 28-day mortality (HR 0.75, 95% CI 0.63-0.88, p < 0.001). No significant differences were found between 325 mg/day and 81 mg/day aspirin treatments in terms of 28-day mortality, hospital mortality, 90-day mortality, gastrointestinal hemorrhage, and thrombocytopenia. However, intensive care unit (ICU) stay was longer for the 325 mg/day group compared to the 81 mg/day group (4.22 vs. 3.57 days, p = 0.031). Conclusion: Aspirin is associated with reduced 28-day mortality in CAP patients. However, 325 mg/day aspirin does not provide extra benefits over 81 mg/day and may lead to longer ICU stays.

Prolonged elevated heart rate is association with adverse outcome in severe pulmonary embolism: A retrospective study.

BACKGROUND: Pulmonary embolism (PE) is a critical condition characterized by the obstruction of pulmonary arteries by thrombi, which significantly contributes to morbidity and mortality globally. Although prolonged elevated heart rate (peHR) is recognized as a risk factor for adverse outcomes in critically ill patients, its specific impact on severe PE has remained unexplored. METHODS: This retrospective cohort study analyzed data from the Medical Information Mart for Intensive Care (MIMIC)-IV database. Patients diagnosed with PE were included in the study. peHR was defined as heart rates exceeding 100 beats per minute on at least 11 occasions within any 12-h interval. Cox proportional hazards regression models were used to evaluate the impact of peHR on 30-day and 90-day mortality rates, adjusting for a broad range of demographic and clinical variables. RESULTS: A total of 1248 patients were included in this study, of whom 540 exhibited peHR. These patients experienced significantly longer hospital and intensive care unit (ICU) stays, as well as higher mortality rates at both 30 days (25.93 % vs. 14.97 %, P < 0.001) and 90 days (33.89 % vs. 22.74 %, P < 0.001) compared to patients without peHR. Multivariate Cox regression analysis confirmed peHR as an independent predictor of increased mortality at 30 days (HR 1.56, 95 % CI 1.19-2.07; P = 0.0014) and 90 days (HR 1.66, 95 % CI 1.32-2.10; P < 0.001). CONCLUSION: peHR significantly worsens outcomes in severe PE patients, underscoring the need for stringent heart rate monitoring and management. These findings advocate for integrating heart rate control within management strategies for severe PE, potentially improving survival outcomes.

Gitogenin suppresses lung cancer progression by inducing apoptosis and autophagy initiation through the activation of AMPK signaling.

Lung cancer is a leading cause of tumor-associated death worldwide. Autophagy plays a key role in regulating lung cancer progression, and is a promising option for lung cancer treatment. Saponins are a group of naturally occurring plant glycosides, characterized by their strong foam-forming properties in aqueous solution, and exert various biological properties, such as anti-inflammation and anti-cancer. In the present study, we for the first time explored the effects of gitogenin (GIT), an important saponin derived from Tribulus longipetalus, on lung cancer progression both in vitro and in vivo. We found that GIT markedly reduced the proliferation and induced apoptosis in lung cancer cells through increasing the cleavage of Caspase-3 and poly (ADP-ribose) polymerases (PARPs). In addition, GIT-incubated lung cancer cells exhibited clear accumulation of autophagosome, which was essential for GIT-suppressed lung cancer. Mechanistically, GIT-induced autophagy initiation was mainly through activating AMP-activated protein kinase (AMPK) and blocking protein kinase B (AKT) signaling pathways, respectively. Moreover, the autophagic flux was disrupted in GIT-treated lung cancer cells, contributing to the accumulation of impaired autophagolysosomes. Importantly, we found that suppressing autophagy initiation could abolish GIT-induced cell death; however, autophagosomes accumulation sensitized lung cancer cells to cell death upon GIT treatment. More in vitro experiments showed that GIT led to reactive oxygen species (ROS) production in lung cancer cells, which was also involved in the modulation of apoptosis. The in vivo findings confirmed the effects of GIT against lung cancer progression with undetectable toxicity to organs. In conclusion, we provided new insights into the treatment of lung cancer, and GIT might be an effective strategy for future clinical application.

Pulmonary rehabilitation focusing on the regulation of respiratory movement can improve prognosis of severe patients with COVID-19.

BACKGROUND: Since the coronavirus disease 2019 (COVID-19) emerged in Wuhan, China, it has become a global public health emergency. Besides conventional care, pulmonary rehabilitation (PR) is an equally important treatment for patients with COVID-19 suffering from respiratory, physical and psychological disease. The aim of this study is to investigate the role of PR on the inpatients with severe COVID-19. METHODS: This study was a self-pre- and post-control prospective clinical trial, which totally recruited 31 inpatients confirmed COVID-19 by RT-PCR. They were performed 3-week PR. The demographic data, medical records, symptoms, laboratory findings and chest computed tomographic (CT) scans of patients were collected at baseline. The effect of PR was assessed by questionnaires before PR as well as after 2- and 3-week PR. RESULTS: After 3-week PR and treatment, neutrophil percentage decreased, while lymphocyte percentage and lymphocyte count increased (before vs. 2 weeks after PR respectively: P=0.001; P=0.001; P<0.0001). Besides, CRP and procalcitonin reduced significantly (before vs. after respectively: P<0.0001; P=0.023). Patients' oxygen intake decreased and oxygen saturation increased significantly. Meanwhile, PR relieved the patients' symptoms of cough and dyspnea, improved the patients' self-care ability, physical fitness and mental state significantly. Activities of daily living (ADL) score increased and Modified Medical Research Council Dyspnea Scale (mMRC) decreased after PR. CONCLUSIONS: PR can relieve symptoms, enhance health-related quality of life, improve respiratory muscle function and alleviate disease-related anxiety and depression of severe patients with COVID-19. PR should be provided throughout the diseases management process, regardless of whether the patient is hospitalized or at home.

Engeletin suppresses lung cancer progression by inducing apoptotic cell death through modulating the XIAP signaling pathway: A molecular mechanism involving ER stress.

Lung cancer is a leading cause of human death worldwide. Nevertheless, the outcome of present therapeutic options is still not satisfying. Engeletin (ENG, dihydrokaempferol 3-rhamnoside) is a flavanonol glycoside, showing anticancer activities in some tumors. But the exact molecular mechanism of ENG is not fully understood. In our present study, we found that ENG significantly induced apoptotic cell death in lung cancer cells through reducing X-linked inhibitor apoptosis (XIAP) expression from the post-translational levels. However, the XIAP ubiquitination was obviously up-regulated by ENG. In addition, second mitochondria-derived activator of caspase (SMAC) expression levels were increased by ENG in lung cancer cells. Notably, SMAC inhibition significantly abrogated ENG-inhibited expression of XIAP. Furthermore, ENG enhanced the interaction between XIAP and SMAC through increasing SMAC secretion from mitochondria to the cytoplasm. Moreover, endoplasmic-reticulum (ER) stress was highly induced by ENG, and we found that inhibiting C/-EBP homologous protein (CHOP), the transcription factor of ER stress, eliminated the regulatory effects of ENG on the expression of SMAC and XIAP. The in vitro analysis showed that ENG treatment caused apparent mitochondrial dysfunction in lung cancer cells. Finally, we showed that ENG effectively reduced the growth of xenograft tumors derived from cell lines with limited toxicity. Taken together, ENG had therapeutic potential against lung cancer progression.