Quality of life and its influencing factors on children with asthma in China: a comparative study before and during the COVID-19 pandemic.

OBJECTIVE: This study compares the level of quality of life (QoL) and its influencing factors on children with asthma before and during the COVID-19 pandemic. METHODS: The study carried out cross-sectional surveys on children with asthma and their parents in China before and during the epidemic. Data were collected using a demographic questionnaire, the Family Management Scale for Children with Asthma (FMSCA), and the Pediatric Asthma Quality of Life Questionnaire (PAQLQ). Participants from before the epidemic were matched by their propensity score in a 1:1 ratio with individuals from during the epidemic. The level of QoL of children with asthma was subsequently analyzed. Both univariate analysis and multiple linear regression were employed to identify the influencing factors. RESULTS: Compared to their level before the epidemic, the total score of PAQLQ and its three dimensions decreased during the epidemic. Regression analysis revealed that before the epidemic, the total score of PAQLQ was significantly associated with follow-up visits, attendance of asthma lectures, and the total score of FMSCA (p < 0.05). During the epidemic, the total score of the PAQLQ was significantly associated with three dimensions of the FMSCA (future expectation, children identity, and views of condition), and two classifications of the family management styles (FMS) (enduring and accommodating) (p < 0.05). CONCLUSION: The QoL of children with asthma deteriorated during the epidemic. Influencing factors changed during the epidemic, with more emphasis on the family environment. Future intervention strategies need to take into account the development of interactions between children and environmental forces.

Unraveling the G protein-coupled receptor superfamily in aphids: Contractions and duplications linked to phloem feeding.

The G Protein-Coupled Receptor (GPCR) superfamily is the largest and most diverse transmembrane receptor family, playing crucial roles in regulating various physiological processes. As one of the most destructive pests, aphids have been subject to previous studies, which revealed fewer GPCR superfamily members in Acyrthosiphon pisum and Aphis gossypii and the loss of multiple neuropeptide GPCRs. To elucidate the contraction patterns and evolutionary features of the aphid GPCR superfamily, we identified 97, 105, and 95 GPCR genes in Rhopalosiphum maidis, A. pisum, and A. gossypii, respectively. Comparative analysis and phylogenetic investigations with other hemipteran insects revealed a contracted GPCR superfamily in aphids. This contraction mainly occurred in biogenic amine receptors, GABA-B-R, and fz families, and several neuropeptide receptors such as ACPR, CrzR, and PTHR were completely lost. This phenomenon may be related to the parasitic nature of aphids. Additionally, several GPCRs associated with aphid feeding and water balance underwent duplication, including Lkr, NPFR, CCHa1-R, and DH-R, Type A LGRs, but the SK/CCKLR that inhibits feeding was completely lost, indicating changes in feeding genes that underpin the aphid's prolonged phloem feeding behavior. Furthermore, we observed fine-tuning in opsins, with reduced long-wavelength opsins and additional duplications of short-wavelength opsin, likely associated with daytime activity. Lastly, we found variations in the number of mthl genes in aphids. In conclusion, our investigation sheds light on the GPCR superfamily in aphids, revealing its association with diet lifestyle and laying the foundation for understanding and developing control strategies for the aphid GPCR superfamily.

Inhibition of autophagy potentiates the cytotoxicity of the irreversible FGFR1-4 inhibitor FIIN-2 on lung adenocarcinoma.

For patients with platinum-resistant lung adenocarcinoma (LUAD), the exploration of new effective drug candidates is urgently needed. Fibroblast growth factor receptors (FGFRs) have been identified as promising targets for LUAD therapy. The purpose of this study was to determine the exact role of the irreversible FGFR1-4 inhibitor FIIN-2 in LUAD and to clarify its underlying molecular mechanisms. Our results demonstrated that FIIN-2 significantly inhibited the proliferation, colony formation, and migration of A549 and A549/DDP cells but induced the mitochondria-mediated apoptosis of these cells. Meanwhile, FIIN-2 increased the autophagy flux of A549 and A549/DDP cells by inhibiting the mammalian target of rapamycin (mTOR) and further activating the class III PI3K complex pathway. More importantly, in vivo and in vitro experiments showed that autophagy inhibitors could enhance the cytotoxicity of FIIN-2 on A549 and A549/DDP cells, confirming that FIIN-2 induced protective autophagy. These findings indicated that FIIN-2 is a potential drug candidate for LUAD treatment, and its use in combination with autophagy inhibitors might be an efficient treatment strategy, especially for patients with cisplatin resistance.

Establishment and Evaluation of Artificial Intelligence-Based Prediction Models for Chronic Kidney Disease under the Background of Big Data.

Objective: To establish a prediction model for the risk evaluation of chronic kidney disease (CKD) to guide the management and prevention of CKD. Methods: A total of 1263 patients with CKD and 1948 patients without CKD admitted to the Tongde Hospital of the Zhejiang Province from January 1, 2008, to December 31, 2018, were retrospectively analyzed. Spearman's correlation was used to analyze the relationship between CKD and laboratory parameters. XGBoost, random forest, Naive Bayes, support vector machine, and multivariate logistic regression algorithms were employed to establish prediction models for the risk evaluation of CKD. The accuracy, precision, recall, F1 score, and area under the receiver operating curve (AUC) of each model were compared. The new bidirectional encoder representations from transformers with light gradient boosting machine (MD-BERT-LGBM) model was used to process the unstructured data and transform it into researchable unstructured vectors, and the AUC was compared before and after processing. Results: Differences in laboratory parameters between CKD and non-CKD patients were observed. The neutrophil ratio and white blood cell count were significantly associated with the occurrence of CKD. The XGBoost model demonstrated the best prediction effect (accuracy = 0.9088, precision = 0.9175, recall = 0.8244, F1 score = 0.8868, AUC = 0.8244), followed by the random forest model (accuracy = 0.9020, precision = 0.9318, recall = 0.7905, F1 score = 0.581, AUC = 0.9519). Comparatively, the predictions of the Naive Bayes and support vector machine models were inferior to those of the logistic regression model. The AUC of all models was improved to some extent after processing using the new MD-BERT-LGBM model. Conclusion: The new MD-BERT-LGBM model with the inclusion of unstructured data has contributed to the higher accuracy, sensitivity, and specificity of the prediction models. Clinical features such as age, gender, urinary white blood cells, urinary red blood cells, thrombin time, serum creatinine, and total cholesterol were associated with CKD incidence.

Autophagy Inhibition Enhances the Anti-Tumor Activity of Methylseleninic Acid in Cisplatin-Resistance Human Lung Adenocarcinoma Cells.

Cisplatin (DDP)-based chemotherapy remains one of the standard treatment options for patients with advanced lung adenocarcinoma (LUAD), and cisplatin resistance is the biggest challenge to this therapy. Autophagy is also closely associated with chemoresistance in LUAD. Desperately need to find a way to improve the treatment efficiency of cisplatin-resistant LUAD in clinical practice. Previous studies reported that methylseleninic acid (MSA) has good anti-proliferation and pro-apoptotic activities in tumor cells. However, the effectiveness of MSA on cisplatin-resistant LUAD and its effect on the induction of autophagy is still unclear. In the current study, we found that MSA effectively inhibited the proliferation of LUAD cell lines and triggered mitochondrial pathway-mediated apoptosis. This effect was more pronounced in cisplatin-resistant LUAD cells with high MDR1 expression. In contrast, the mitochondrial damage caused by MSA treatment can be degraded by inducing selective autophagy in LUAD cells, thereby exerting a self-protective effect on tumor cells. Mechanistically, MSA inhibits proliferation, promotes apoptosis, and induces autophagy in LUAD cells by inhibiting of the Akt/mTOR pathway. Combination with autophagy inhibitors reduces the effect of this selective autophagy-induced resistance, and thus enhancing even more the anti-tumor effect of MSA on cisplatin-resistant LUAD cells. Finally, We speculate that MSA in combination with autophagy inhibitors may be a promising new therapeutic strategy for the treatment of cisplatin-resistant LUAD.

The factors of family management affecting asthma control status in school-age children with asthma in China.

OBJECTIVE: To identify the factors of family management affecting asthma control status in school-age children with asthma in China. METHOD: The cross-sectional descriptive study was conducted among 139 children with asthma and their parents. The age range of the children was 7 to 14 years of age (Mage = 9.85; 76.26% boys). Eight dimensions (Children Identity, View of Condition, Management Mindset, Parental Mutuality, Parenting Philosophy, Management Approach, Family Focus, Future Expectation) of the Family Management Scale for Children with Asthma (FMSCA) were used as factors of family management. The Asthma Control Test (ACT) and the Children Asthma Control Test (C-ACT) were used to measure the asthma control status of children. A parental questionnaire was used to collect information regarding demographic data of familial socioeconomic status, general data about the child, and medical services status (Follow-Up Plan, received manual of asthma education, attended a lecture on asthma) received from medical institutions. A multivariate ordinal logistic regression model was performed. RESULTS: Factors significantly associated with asthma control were "Follow-Up Plan" (OR, 2.004; 95% CI, 1.009-3.981), "Attended a Lecture on asthma" (OR, 2.586; 95% CI, 1.103-6.066) and two dimensions of the FMSCA, "Children Identity" (OR = 1.133; 95% CI, 1.024-1.254) and "Family Focus" (OR = 1.114; 95% CI, 1.007-1.232). CONCLUSION: This study shows that asthma control status of school-age children in China is related to the parents' views of their child as having a "normal condition" and the parents' satisfaction with the balance between asthma related management and other aspects of family life.

Simiaosan alleviates the symptoms of gouty arthritis via the NALP3/IL­1ß pathway.

Previous studies have suggested that the herbal medicine simiaosan has beneficial effects on gouty arthritis (GA), for which conventional Western medicines are insufficient (particularly in cases of multiple episodes). The objective of the present study was to investigate the mechanism by which simiaosan alleviated the symptoms of GA. Sprague­Dawley rat models of acute GA were successfully established, as verified by pathological analyses. Additionally, an NLR family pyrin domain containing 3 (NLRP3) overexpression vector was constructed and a high transfection efficiency was confirmed by reverse transcription PCR. The following five treatment groups were established: i) Normal control; ii) model + saline; iii) model + simiaosan; iv) model + NALP3­overexpressing adenovirus + simiaosan; and v) model + empty vector adenovirus + simiaosan. The samples from mice in each group were subjected to hematoxylin and eosin (H&E) staining for assessing the histopathological changes, enzyme­linked immunosorbent assays for determining IL­1ß and TGF­ß1 levels and western blotting for evaluating NALP3 expression. H&E staining indicated that simiaosan could reduce the infiltration of inflammatory cells, while NALP3 overexpression aggravated the inflammatory response in tissues. Expression levels of IL­1ß, TGF­ß1 and NALP3 were significantly higher in the model and the model + NALP3­overexpressing adenovirus + simiaosan groups compared with the normal control group. Levels of IL­1ß, TGF­ß1 and NALP3 were significantly lower in the model + simiaosan and model + empty vector adenovirus + simiaosan groups compared with the model group. These results indicated that the effects of simiaosan were mediated through NALP3 inhibition. Therefore, the herbal medicine simiaosan was revealed to possess an ability to alleviate the symptoms of GA by regulating the NALP3/IL­1ß signaling pathway.

The expression and correlation of SIRT1 and Phospho-SIRT1 in colorectal cancer.

SIRT1 is the homologue of sir2 in mammals, which is a nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase. SIRT1 is involved in many physiological processes, such as metabolism, senescence, inflammatory response, neuroprotection, and tumorigenesis by acetylating histones and multiple transcription factors. However, the exact role of SIRT1 in tumor is still under controversial. Immunohistochemistry and Western blot were performed to investigate the expressions and subcellular localizations of SIRT1 and Phospho-SIRT1 in colorectal cancer tissues and adjacent normal tissues. The relationship between SIRT1 or Phospho-SIRT1 and clinicopathological characteristics was also analyzed. Real-Time PCR was performed to investigate the transcriptional level of SIRT1 mRNA in colorectal cancer tissues and adjacent normal tissues. SIRT1 and Phospho-SIRT1 were both localized in the nucleus. The expressions of SIRT1 and Phospho-SIRT1 were higher in colorectal cancer tissues than normal tissues. SIRT1 expression in cancer tissues was associated with patient age, TNM stage and mutant P53 loss. Phospho-SIRT1 expression in cancer tissues was associated with Ki67. SIRT1 and Phospho-SIRT1 were highly correlated in cancer tissues and normal tissues. The ratios of Phospho-SIRT1 and SIRT1 expression in cancer tissues were higher than normal tissues. SIRT1 mRNA level was no significant difference in cancer tissues and normal tissues. SIRT1 have a dual character in colorectal cancer, and Phospho-SIRT1 may determine the role of SIRT1 in colorectal cancer formation.