Background: Psychological status is a decisive factor for regulating the lung cancer chemotherapy patients’ levels of fatigue and hope. Using the PERMA (Positive Emotion, Engagement, Relationships, Meaning, and Accomplishment) framework. We aimed to explore the influences of the psychological intervention on the patients’ negative emotion, cancer-related fatigue, and level of hope. Method: A total of 100 lung cancer chemotherapy patients admitted in Wuhan No.4 Hospital, China, from Jan 2018 to Aug 2019 were enrolled as research objects divided into the control group and observation group. Positive psychological intervention using the PERMA framework was given to the observation group. The scores of Post-Traumatic Growth Inventory (PTGI), Self-rating Anxiety Scale (SAS), Self-rating Depression Scale (SDS), Cancer Fatigue Scale (CFS), and Herth Hope Index (HHI) were evaluated and compared in the two groups. Results: After the intervention, PTGI score in the observation group is higher than that in the control group, whereas the SAS and SDS scores are lower in the observation group than in the control group, and the differences are statistically significant (P<0.05). Score of each CFS dimension and total CFS score in the observation group are all lower than those in the control group, with statistically significant differences (P<0.05). Score of each HHI dimension and total HHI score are higher than those in the control group, and the differences are statistically significant (P<0.05). Conclusion: Positive psychological intervention using the PERMA framework can improve the emotional and fatigue state of lung cancer chemotherapy patients and elevate their level of hope.

Prudent corticosteroid use, vigilant microbiological surveillance and appropriate antibiotics coverage are the key to successful treatment.

Background This study aims to identify a prognostic biomarker to predict the disease prognosis and reduce the mortality rate of COVID-19, which has caused a worldwide pandemic. Methods COVID-19 patients were randomly divided into training and test groups. Univariate and multivariate Cox regression analyses were performed to identify the disease prognosis signature, which was selected to establish a risk model in the training group. Furthermore, the disease prognosis signature of COVID-19 was validated in the test group. Results The signature of COVID-19 was combined with five indicators, namely neutrophil count, lymphocyte count, procalcitonin, older age, and C-reactive protein. The signature stratified patients into high- and low-risk groups with significantly relevant disease prognosis (log-rank test, P&lt;0.001) in the training group. The survival analysis indicated that the high-risk group displayed substantially lower survival probability than the low-risk group (log-rank test P&lt;0.001). The area under ROC curve (AUC) showed that the signature of COVID-19 displayed the highest predictive accuracy regarding disease prognosis, which was 0.955 in the training group and 0.945 in the test group. The ROC analysis of both groups demonstrated that the predictive ability of the signature surpassed the use of each of the five indicators alone. Conclusion The signature of COVID-19 presents a novel predictor and prognostic biomarker for closely monitoring patients and providing timely treatment for those who are severely or critically ill.

Geniposide is a bioactive iridoid glucoside derived from Gardenia jasminoides that has proven anti-inflammatory effects against acute lung injury. The aim of this study was to determine whether geniposide could protect pulmonary arterial smooth muscle cells (PASMCs) from lipopolysaccharide (LPS)-induced injury and to explore the participation of α7 nicotinic acetylcholine receptor (α7nAChR), which was previously reported to suppress pro-inflammatory cytokine production in LPS-stimulated macrophages. In the present study, rat PASMCs were isolated and stimulated using LPS. The effect of geniposide on LPS-induced PASMC injury was then explored. Geniposide exerted anti-apoptotic and anti-inflammatory effects on LPS-treated PASMCs, as demonstrated by the downregulation of pro-apoptotic proteins and pro-inflammatory cytokines, respectively. Furthermore, the α7nAChR agonist PNU282987 accentuated the protective effect of geniposide against LPS-induced injury in PASMCs by inhibiting toll-like receptor-4/myeloid differentiation primary response 88 (TLR-4/MyD88) signaling and downregulating nuclear factor (NF)-κB expression. Conversely, methyllycaconitine, an inhibitor of α7nAChR, attenuated the effects of geniposide. These findings collectively suggested that in conjunction with geniposide, the activation of α7nAChR may contribute to further mitigating LPS-induced PASMC apoptosis and inflammation. In addition, the underlying mechanisms critically involve the NF-κB/MyD88 signaling axis. These results may provide novel insights into the treatment and management of lung diseases via geniposide administration.