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KIF2A mRNA and protein expression levels were elevated in NCI-H1299, NCI-H385, NCI-H1650, and A549 cells compared to BEAS-2B cells. KIF2A overexpression elevated proliferation, migration, invasion, stemness, and resistance to cisplatin but did not affect apoptosis or resistance to pemetrexed in A549 cells. Furthermore, KIF2A knock-down repressed proliferation, migration, invasion, stemness, and resistance to cisplatin, but not to pemetrexed, and it enhanced apoptosis in NCI-H1299 cells. Rescue experiments showed that the PI3K/AKT/VEGF pathway compensated for KIF2A effects on cell functions and sensitivity to cisplatin in A549 and NCI-H1299 cells. In conclusion, KIF2A advocates NSCLC cell viability, mobility, stemness, and chemoresistance to cisplatin by activating the PI3K/AKT/VEGF signaling pathway.Gynecologic cancer is a serious global healthcare issue with high rates of mortality and morbidity. In recent years, tumor immunity and immunotherapy have attracted extensive attention for treatment of gynecological cancers. Indoleamine 2, 3-dioxygenase 1 (IDO1) plays a critical role in cancer immune escape, and its inhibition has been explored for immune-targeted therapies for many malignancies. However, knowledge about IDO1 involvement in the pathogenesis of gynecological cancers and its therapeutic potential is still evolving. Selleck ARV-825 In the current study, we integrated bioinformatics analysis of the prognostic value and immune function of IDO1 in gynecologic malignancies using Oncomine, GEPIA, HPA, TIMER, TISIDB, SurvExpress and Metascape database. Comprehensive analysis revealed that the transcription levels of IDO1 were significantly overexpressed in patients with gynecologic cancers, and IDO1-co-expressed gene signatures may be useful potential prognostic markers for gynecologic cancers. Furthermore, increased IDO1 expression correlated with immune infiltration cells, immune marker sets, and immunomodulators in gynecological cancers. These findings suggest that IDO1 plays an important role in immune infiltration and could potentially be an immunotherapeutic target for gynecological cancers. However, future large-scale and comprehensive research is required to validate our results.EGb 761 has some protective effects on AD and can improve the cognitive functions of AD mice. However, the underlying molecular mechanisms are unknown. Here, we investigated the function of bilobalide, the effective component of EGb 761, in neuroinflammation and autophagy during AD. LPS-treated BV-2 cells were used as an in vitro model for neuroinflammation. The APP/PS1 AD mouse line was used to examine the function of bilobalide in AD. ELISA and qRT-PCR were used to measure the levels of proinflammatory cytokines, including TNF-α, IL-6 and IL-1β. Western blotting was employed to determine the protein levels of p-p65, iNOS, COX-2, LC3, beclin-1, p62 and p-STAT3. Immunostaining was applied to examine the number of autophagosomes. LPS treatment induced inflammatory responses and inhibited autophagy in BV-2 cells. Bilobalide suppressed LPS-induced neuroinflammation and promoted autophagy. Furthermore, bilobalide treatment increased the lincRNA-p21 levels, which suppressed STAT3 signalling. Knockdown of lincRNA-p21 reversed the effects of bilobalide. Overexpression of lincRNA-p21 promoted autophagy and inhibited neuroinflammation as well while STAT3 inhibitor blocked the effects of si-lincRNA-p21. In vivo experiments revealed that bilobalide improved the learning and memory capabilities of APP/PS1 AD mice. Bilobalide improves the cognitive functions of APP/PS1 AD mice. Mechanistically, bilobalide suppresses inflammatory responses and promotes autophagy possibly by upregulating lincRNA-p21 levels.Apigenin (APG), a natural flavonoid with anti-inflammatory and anti-fibrosis properties, has been shown to play a protective role in diabetic nephropathy (DN), but their molecular protection mechanism for miRNA has not been elucidated in detail. This study was designed to focus on exploring its protective role in DN and whether miR-423-5p-upstream stimulating factor 2 (USF2) axis was involved in its protective mechanism. The in vivo model of rat was induced by streptozotocin (STZ) and the in vitro model of renal tubular epithelial cell (RTEC) was induced by high glucose (HG). Our in vivo study revealed that APG had different protective effects on inflammation, renal fibrosis and epithelial mesenchymal transition (EMT) in DN rats, which is mainly reflected in that the inflammatory factors (IL-6, IFN-γ, TNF-α) were obviously down-regulated, the renal fibrosis markers (IV-C, FN, Col I) were significantly inhibited, the E-cadherin (EMT factors) was significantly up-regulated, while the vimentin and α-SMA (EMT factors) were significantly down-regulated, and the renal function indexes (serum Cr, BUN) were significantly improved. In terms of mechanism, the protective effect of APG was related to the regulation of the expression of miR-423-5p-USF2 axis, and there was a targeted relationship between miR-423-5p and USF2. Down-regulating miR-423-5p or up-regulating USF2 could significantly aggravate the disease progression of in vitro model and eliminate DN resistance under APG intervention. The above results revealed that the protective role of APG on DN was mediated by miR-423-5p-USF2 axis.Tissue engineering has become an important therapeutic method for injuries. This study aimed to generate collagen-like matrix constructed by hUCMSCs combining self-assembled polypeptide and evaluate differentiated capacity, safety and biocompatibility. Human umbilical cord tissues were isolated and used to primarily culture hUCMSCs. hUCMSCs were identified using immunofluorescence and flow cytometry. Adipogenic- and osteogenic-differentiation of hUCMSCs were evaluated using Oil-red O and Alizarin-Red staining. Self-assembling collagen peptide RAD16-I hydrogel and substance P (SP) were prepared and combined together to form RAD16-I/SP complex. Surface morphology and ultrastructures were observed with scanning electron microscopic (SEM). hUCMSCs in simulated collagen-like matrix environment were plane-cultured and stereo-cultured. Cell viability was examined using CCK-8 and fluorescent staining assay. Osteogenic genes were detected with qRT-PCR and western blot assay. HE staining and Masson staining were used tbers. This established cell-collagen-like matrix complex (RAD16-I/SP/hUCMSCs) injection exhibited better biocompatibility, without cytotoxicity.Cancer-induced bone pain (CIBP) represents the pain induced by bone metastases from malignancies. The role of extracellular vesicles (Evs) has been underscored in bone metastasis. However, the function of Evs, especially these derived from M2 macrophages (M2φ-Evs) in CIBP is unclear. Therefore, this investigation aimed to probe the possible antinociceptive effect of M2φ-Evs in CIBP and the underlying mechanism of action. Using the C57bl/6 mice, a CIBP animal model was established by the administration of Walker 256 mammary gland carcinoma cells, followed by M2φ-Evs administration. It was found that CIBP mice treated with M2φ-Evs had significantly reduced nociception and serum inflammatory factors. Microarray sequencing revealed that microRNA-216a (miR-216a) was the most upregulated miRNA in Evs-treated mouse spinal cord tissues. Subsequent bioinformatics, GSEA and KEGG enrichment analyses demonstrated that HMGB1 and TLR4-NF-κB pathway were the downstream effectors of miR-216a and were both downregulated in spinal cord tissues of CIBP mice treated with M2φ-Evs. Rescue experiments displayed that after we reduced miR-216a expression in M2φ-Evs, the antinociceptive effect of M2φ-Evs on CIBP mice was inhibited, and the HMGB1 expression and the TLR4-NF-κB signaling were significantly activated. Together, M2φ-Evs relieve CIBP by carrying miR-216a, which was elicited through the HMGB1/TLR4-NF-κB axis.DNA repair-related genes (DRGs) have attracted much attention in the field of oncology. However, the prognostic role of DRGs and their biological function in lung adenocarcinoma (LUAD) remains rudimentary and inconclusive. In this study, 716 LUAD cases from two different cohorts were collected. Samples from The Cancer Genome Atlas (TCGA) were used as the training set, and data from Gene Expression Omnibus (GEO) datasets were used for validation. Using multivariate Cox analysis and LASSO regression, we constructed a DRG signature and used it, together with clinical indices, to develop a nomogram to predict 1-, 3-, and 5-year survival rates. We identified a six-DRG signature to estimate the survival of LUAD patients, which distinguished high-risk from low-risk patients with LUAD in both the training and validation cohorts. We also observed elevated levels of infiltrating CD4 memory activated T cells, resting NK cells, M0 and M1 macrophages, and activated mast cells in the high-risk group. Finally, a nomogram incorporating the signature and clinical parameters was superior to the American Joint Committee on Cancer (AJCC) staging system in predicting the survival of LUAD patients. The DRG prognostic signature and integrated nomogram could be a useful tool to predict prognosis in patients with LUAD.Tracheal, bronchus, and lung (TBL) cancer is the most common malignant tumor worldwide. link2 This study aims to grasp the characteristics of the TBL cancer burden in China and the United States (USA). Data included incidence, deaths, and disability-adjusted life years (DALYs) as well as their age-standardized rates (ASRs) among different gender, age and risk factors. Joinpoint Regression Model and Age-period-cohort (APC) analysis were used to evaluate the variation tendency and effect of the risk factors. link3 China and USA bore almost half of the TBL cancer burden, especially for males. ASRs of TBL cancer increased in China, but decreased in USA. In China, three factors related to TBL cancer deaths and DALYs related were tobacco, air pollution, and diet low in fruits; in USA, these are tobacco, occupational carcinogens, and high fasting plasma glucose. The younger the population, the less impact of birth cohort on morbidity and mortality. According to APC analysis, age effect played a key role in morbidity and mortality of TBL cancer, and the risk increased with age. Period effect kept increasing over time, while cohort effect decreased with the time of birth. Tobacco was always the top risk factor of death and DALYs in both countries. The policy should be tilted towards air pollution and a diet low in fruits in China, as well as occupational carcinogens and high fasting plasma glucose in USA. Healthcare reform in both countries should focus on planning how its health system could effectively prevent and manage TBL cancer at low cost.

In this study, we estimated the predictive factors of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission in anesthesiologists performing endotracheal intubation in patients with confirmed SARS-CoV-2.

We analyzed data from a survey conducted by the Chinese Society of Anesthesiology Task Force on Airway Management on endotracheal intubation in 98 patients with SARS-CoV-2 confirmed through nucleic acid testing and chest computed tomography. The multivariate logistic model with stepwise selection was used for selecting the predictive factors significantly associated with SARS-CoV-2 infection in the corresponding anesthesiologists.

SARS-CoV-2 prevalence in the corresponding anesthesiologists was 20.41% after intubation in patients with SARS-CoV-2. Univariate analysis indicated that intubation for elective treatment, intubation in an operating room or isolation ward, and routine rapid induction with continuous positive-pressure ventilation (PPV) for intubation were associated with a lower SARS-CoV-2 risk in the anesthesiologists.

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