Hesspaul7555
Our results showed that the ResNet-50 method based on TL (ResNet-50-TL) obtained the highest diagnostic accuracy, with a rate of 82.7% and a recall rate of 79.1% for COVID-19. These results showed that applying deep learning technology to COVID-19 screening based on chest CT images is a very promising approach. This study inspired us to work towards developing an automatic diagnostic system that can quickly and accurately screen large numbers of people with COVID-19.
We tested a deep learning algorithm to accurately detect COVID-19 and differentiate between healthy control samples, COVID-19 samples, and common pneumonia samples. We found that TL can significantly increase accuracy when the sample size is limited.
We tested a deep learning algorithm to accurately detect COVID-19 and differentiate between healthy control samples, COVID-19 samples, and common pneumonia samples. We found that TL can significantly increase accuracy when the sample size is limited.
A redox-sensitive nanoscale delivery system was developed, based on the hydrophilic chitosan oligosaccharide-ss-hydrophobic curcumin conjugate (CSO-ss-CUR) loaded with docetaxel (DTX), for the targeting and synergistic treatment of gliomas.
Redox-sensitive nanoparticles were loaded with DTX (DTX/CSO-ss-CUR) using the improved ultrasonic-dialysis approach. The morphology and particle size of the loaded nanoparticles were examined by transmission electron microscopy (TEM) and dynamic light scattering (DLS), respectively. The cytotoxicity and cellular uptake of the nanoparticles were assessed
using the C6 glial cell line. The
antitumor efficacy and
biodistribution studies were evaluated using the C6 tumor-bearing Balb/c female mouse model.
The DTX/CSO-ss-CUR nanoparticles were generally spherical in shape and exhibited desirable particle size (under 250 nm) with high drug loading efficiency (DL) (8.96%±0.56%) and encapsulation efficiency (EE) (35.23%±3.26%).
, the drug was released from the nanoatment of gliomas.
Chitosan oligosaccharide (CSO); curcumin (CUR); docetaxel (DTX); glioma.
Chitosan oligosaccharide (CSO); curcumin (CUR); docetaxel (DTX); glioma.
Lung cancer is the leading cause of cancer-associated mortality worldwide, and most lung cancers are classified as non-small cell lung cancer (NSCLC). MiR-328 influence the progression of multiple tumors, but the role of miR-328-5p in NSCLC has not been elucidated. The aim of this study was to illuminate the oncogenic role and potential molecular mechanisms of the miR-328-5p and lysyl oxidase like 4 (LOXL4) in NSCLC.
Expression of miR-328-5p was detected by real-time quantitative polymerase chain reaction (qRT-PCR) in tumor and non-tumor adjacent tissues. After Lentivirus-miR-328-5p was employed to intervene this miRNA in NSCLC cell lines, RT-qPCR was used to detect the expression levels of miR-328-5p. Cell Counting Kit-8 (CCK-8), cell colony formation, flow cytometry, wound healing, Transwell assays were used to determine the malignant phenotypes of NSCLC cells. Nude mice models of subcutaneous tumors were established to observe the effect of miR-328-5p on tumorigenesis. Targeting the 3'UTR of LOXL4 by miR-328-5p was verified by integrated analysis including transcriptome sequencing, dual-luciferase and western-blot assays.
High miR-328-5p level was observed in NSCLC cells from The Cancer Genome Atlas (TCGA) database and tumor tissues collected from NSCLC patients. Overexpressed miR-328-5p promoted NSCLC cell proliferation, survival, and migration, and promoted tumor growth
. Knockdown of miR-328-5p suppressed tumorigenic activities. Transcriptome sequencing analysis revealed that LOXL4 was downregulated by miR-328-5p, which was confirmed by dual-luciferase reporter and western-blot assays.
miR-328-5p showed targeted regulation of LOXL4 to promote cell proliferation and migration in NSCLC.
miR-328-5p showed targeted regulation of LOXL4 to promote cell proliferation and migration in NSCLC.
Dilated cardiomyopathy (DCM) is currently the major cause of systolic heart failure. This study explored potential therapeutic targets and investigated the role of immune cell infiltration in DCM.
Three DCM datasets (GSE3585, GSE9800, and GSE84796) from the Gene Expression Omnibus (GEO) database were merged into an integrated dataset, and batch effects were removed. Differentially expressed genes (DEGs) were screened and the associations between gene co-expression modules and clinical traits were assessed by weighted gene co-expression network analysis (WGCNA) in R software. Any DEGs from the integrated dataset overlapped with the significant module genes were defined as common genes (CGs). Enrichment analysis of the CGs was performed. Enzalutamide The protein-protein interaction (PPI) network of the CGs was visualized and the hub gene was identified by using Cytoscape 3.8.2 software. The miRNA-transcription factor-mRNA (miRNA-TF-mRNA) network was constructed using Cytoscape to unveil the regulatory relationships in Din ECM remodeling and eventually lead to DCM.
In conclusion, we speculate that miR-129-5p might target ASPN in regulating DCM via the ECM signaling pathway. Macrophage infiltration may be involved in ECM remodeling and eventually lead to DCM.
Gemcitabine is among the most commonly utilized chemotherapeutic agents for treating pancreatic cancer (PC), yet patients ultimately develop chemoresistance and thus exhibit a poor prognosis. Long noncoding RNAs (lncRNAs) can function as key regulators of PC progression and may serve as prognostic biomarkers in individuals with gemcitabine-resistant PC. This study sought to explore the role of the lncRNA DBH-AS1 in this oncogenic setting.
Based on public databases and qRT-PCR analyses the expression of lncRNA DBH-AS1 in PC tissues and cell lines. The effects of lncRNA DBH-AS1 on proliferation and gemcitabine resistance were determined by
and
experiments. Luciferase reporter assay and RNA immunoprecipitation (RIP) were carried out to reveal the interaction between lncRNA DBH-AS1, miR-3163 and USP44.
We found that PC tissues exhibited DBH-AS1 downregulation that was particularly pronounced in gemcitabine-resistant PC tissues and cells. This DBH-AS1 downregulation was negatively correlated with the malignancy of PC tumors and with patient survival outcomes. Additionally, decreased DBH-AS1 expression in PC was found to be linked to the METTL3-dependent m
A methylation of the lncRNA, with functional analyses revealing that DBH-AS1 was able to suppress the growth of PC cells. Mechanistically, DBH-AS1 was able to increase PC cell sensitivity to gemcitabine by sequestering miR-3163 and thus upregulating USP44 in these tumor cells. Clinically, patient-derived PC tumor xenografts exhibiting high levels of DBH-AS1 expression were found to be responsive to gemcitabine treatment.
Overall, these data underscore a key role for DBH-AS1 as a regulator of PC tumor growth and a promising therapeutic target capable of predicting PC patient responsiveness to gemcitabine treatment.
Overall, these data underscore a key role for DBH-AS1 as a regulator of PC tumor growth and a promising therapeutic target capable of predicting PC patient responsiveness to gemcitabine treatment.
Emerging evidence suggests that secreted phosphoprotein 1 (SPP1) is involved in tumor cell progression in multiple cancer types. However, the role of SPP1 in different cancers is still not clear.
We used data from The Cancer Genome Atlas (TCGA) to analyze the multiomic roles of SPP1, including RNA expression, DNA methylation, protein phosphorylation, immune infiltration, and overall survival (OS) in 33 tumor types.
SPP1 is highly expressed in most cancer types, and its methylation variability and mRNA expression level are both correlated with prognosis in multiple cancer types. A higher S234 phosphorylation level was observed in 4 types of tumors, including colon adenocarcinoma (COAD) and lung adenocarcinoma (LUAD). SPP1 expression level was positively associated with the infiltration level of dendritic cells, neutrophils, and macrophages in multiple cancer types. It was also significantly positively correlated with hepatitis A virus cellular receptor 2 (HAVCR2), which was observed in most tumor types, including brain lower grade glioma (LGG) and ovarian serous cystadenocarcinoma (OV). Moreover, myeloid cell differentiation and leukocyte migration were observed in the enrichment analysis, suggesting that SPP1 might induce immune escape.
Pan-cancer analysis using a multiomic approach offered a comprehensive overview of SPP1. This protein plays an important role in most of the analyzed tumor types and could be a valuable prognostic marker across different types of cancer.
Pan-cancer analysis using a multiomic approach offered a comprehensive overview of SPP1. This protein plays an important role in most of the analyzed tumor types and could be a valuable prognostic marker across different types of cancer.
The timely addition of anlotinib to the nab-paclitaxel/gemcitabine regimen may further increase the treatment efficacy for pancreatic adenocarcinoma (PDAC), which has not yet been reported. Therefore, we aimed to compare the efficacy and safety of anlotinib plus nab-paclitaxel/gemcitabine in the first-line treatment of patients with unresectable or metastatic PDAC.
This was a retrospective cohort of patients with unresectable or metastatic PDAC performed in The First Affiliated Hospital of Anhui Medical University from August 17, 2019 to April 3, 2021. Patients who received anlotinib plus nab-paclitaxel/gemcitabine treatment were defined as the anlotinib plus chemotherapy group and patients who received nab-paclitaxel/gemcitabine were defined as the chemotherapy group. The primary outcomes were progression-free survival (PFS) and overall survival (OS). Secondary outcomes were the objective response rate (ORR), the disease control rate (DCR), and toxic side effects. Clinical data and follow-up information or metastatic PDAC. Randomized controlled trials with large sample sizes are warranted to further evaluate the treatment effects of anlotinib in PDAC.
Pancreatic adenocarcinoma (PDAC); anlotinib; nab-paclitaxel/gemcitabine; progression-free survival (PFS); overall survival (OS).
Pancreatic adenocarcinoma (PDAC); anlotinib; nab-paclitaxel/gemcitabine; progression-free survival (PFS); overall survival (OS).
With long-term pharmacotherapy, Parkinson's disease (PD) is expectedly to incur a significant healthcare burden. However, drug utilization and costing study is limited, so is the cost composition and its impact on resource allocation. This study took a healthcare provider's perspective to quantify medical and drug expenses and the utilization of drugs for managing PD and its complications.
Medical resources use and associated cost of outpatient visits and inpatient admission episodes for PD patients were extracted from electronic medical records at a tertiary hospital in China from 1 January 2016 to 15 August 2018. Total and average direct medical (costs of outpatient visits and inpatient admission episodes) and drug costs were calculated during the study period and each calendar year. Drug cost was quantified by defined daily dose cost (DDDc) and levodopa equivalent dose cost (LEDc) per outpatient visit or inpatient admission episode for PD in Chinese yuan (¥), stratified by medication categories, and presented in descriptive statistics.
