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OBJECTIVE: This study aims to explore the effect of Internet + E-Coach chronic disease system intervention on fasting blood glucose (FPG), 2-hour postprandial blood glucose(2hPG), fasting serum insulin (FINS), triglyceride (TG), alanine transaminase (ALT) and quality of life in patients with chronic diabetic retinopathy. METHODS: 208 patients with chronic diabetic retinopathy who were treated in the hospital from March 2021 to March 2023 are chosen and separated into two groups by random number Table 104 patients in the control group received routine continuous intervention, and the research group received Internet + E-Coach chronic disease system intervention. The cognition of disease related knowledge, blood related indicators inflammatory factor levels and improvement of life quality between the two groups before intervention, 6 and 12 months after intervention were compared. RESULTS: Before the intervention, the comparison between the two groups in disease related knowledge scores, blood glucose, blood lipid, liver function indicators, inflammatory factor, and low vision quality of life scale (CLVQOL) scores was with P > 0.05. After 6 and 12 months of intervention, the research group had significantly higher scores for basic blood glucose intervention, healthy diet, reasonable exercise, and correct medication use compared to the control group (P < 0.05). FPG, 2hPG, TG and ALT in the research group were lower than those in the control group. FINS were higher in the control group, with P < 0.05. Interleukin-6 (IL-6), tumor necrosis factor (TNF-α), and hypersensitive C-reactive protein (Hs-CRP) in the research group were obviously lower than those in the control group (P < 0.05). The scores of far vision, movement and light perception, adjustment ability, reading and fine work, and daily living ability in the research group were higher than those in the control group, with P < 0.05. CONCLUSION: The intervention of Internet + E-Coach chronic disease system can improve the knowledge of chronic diabetic retinopathy patients about their own condition, stabilize the levels of blood sugar, blood lipid and liver function indicators, reduce the inflammatory reaction of the body, and improve the quality of life.
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Glicemia , Retinopatia Diabética , Lipídeos , Qualidade de Vida , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Glicemia/metabolismo , Retinopatia Diabética/terapia , Retinopatia Diabética/sangue , Retinopatia Diabética/fisiopatologia , Retinopatia Diabética/psicologia , Lipídeos/sangue , Doença Crônica , Gerenciamento Clínico , Fígado/metabolismo , Internet , Testes de Função Hepática , Idoso , AdultoRESUMO
Glioblastoma (GBM) is associated with a median survival rate of less than 15 months, necessitating innovative treatment approaches. This study investigates the safety and efficacy of the low-frequency magnetic field (LFMF) OM-100 instrument in GBM therapy. In vitro experiments utilized normal astrocyte and GBM cell lines, determining that OM-100 at 100 kHz for 72 h selectively targeted GBM cells without harming normal cells. Subsequent analyses revealed OM-100's impact on cell viability, apoptosis, migration, invasion, reactive oxide species levels, and PD-L1 expression. In vivo studies on mice with U87-induced GBM demonstrated OM-100's synergy with anti-PD-1 therapy, leading to significant tumor volume reduction and increased apoptosis. Notably, OM-100 exhibited safety in healthy mice. Overall, OM-100 could enhance anti-PD-1 immunotherapy effectiveness probably by directly inhibiting tumor proliferation and migration as well as promoting PD-L1 expression, offering a promising therapeutic strategy for GBM treatment.
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Proliferação de Células , Glioblastoma , Imunoterapia , Receptor de Morte Celular Programada 1 , Glioblastoma/terapia , Glioblastoma/tratamento farmacológico , Glioblastoma/patologia , Glioblastoma/metabolismo , Animais , Camundongos , Humanos , Linhagem Celular Tumoral , Receptor de Morte Celular Programada 1/antagonistas & inibidores , Receptor de Morte Celular Programada 1/metabolismo , Imunoterapia/métodos , Proliferação de Células/efeitos dos fármacos , Antígeno B7-H1/metabolismo , Antígeno B7-H1/antagonistas & inibidores , Neoplasias Encefálicas/tratamento farmacológico , Neoplasias Encefálicas/imunologia , Neoplasias Encefálicas/terapia , Apoptose/efeitos dos fármacos , Movimento Celular/efeitos dos fármacos , Inibidores de Checkpoint Imunológico/farmacologia , Inibidores de Checkpoint Imunológico/uso terapêutico , Ensaios Antitumorais Modelo de Xenoenxerto , Magnetoterapia/métodos , Sobrevivência Celular/efeitos dos fármacosRESUMO
BACKGROUND: Paranasal sinus angiosarcoma is an uncommon malignancy, with only a few reported cases worldwide. Although it exhibits multiple symptoms, facial paralysis has not been previously documented as a noticeable presentation. CASE PRESENTATION: In this case, we report a 40-year-old male who presented with facial numbness and pain for one month, weakness of his facial muscles for 15 days, and recurrent right epistaxis for 1 year. He had a history of nasal inflammatory polyps with chronic sinusitis. Computed tomography and magnetic resonance imaging showed space-occupying lesions in the right nasal cavity and maxillary sinus, with bone destruction occurring in the sinus wall and turbinate. This patient then underwent endoscopic surgery. According to the histopathological and immunohistochemical results, he was eventually diagnosed with paranasal sinus angiosarcoma in April 2021. To date, this patient has not initiated any radiotherapy or chemotherapy and has survived with lymphatic metastasis for at least 3 years. CONCLUSIONS: This manuscript suggests that paranasal sinus angiosarcoma can present with facial paralysis. Moreover, pathological and immunohistochemical tests are still vital for diagnosing paranasal sinus angiosarcoma and differential diagnosis. Additionally, regular follow-up is crucial for patients with paranasal sinus angiosarcoma, enabling monitoring of recurrence, metastasis, and recovery while contributing valuable clinical data to understanding this rare disease and associated research endeavours.
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Paralisia Facial , Hemangiossarcoma , Masculino , Humanos , Adulto , Hemangiossarcoma/diagnóstico , Hemangiossarcoma/diagnóstico por imagem , Paralisia Facial/etiologia , Seio Maxilar/diagnóstico por imagem , Seio Maxilar/patologia , Cavidade Nasal/patologia , Epistaxe/patologiaRESUMO
OBJECTIVES: To evaluate amide proton transfer-weighted (APTw)-derived whole-tumor histogram analysis parameters in predicting pathological extramural venous invasion (pEMVI) positive status of rectal adenocarcinoma (RA). METHODS: Preoperative MR including APTw imaging of 125 patients with RA (mean 61.4 ± 11.6 years) were retrospectively analyzed. Two radiologists reviewed each case's EMVI status based on the MR-based modified 5-point scale system with conventional MR images. The APTw histogram parameters of primary tumors were obtained automatically using whole-tumor volume histogram analysis. The independent risk factors markedly correlated with pEMVI-positive status were assessed using univariate and multivariate logistic regression analyses. Diagnosis performance was assessed by receiver operating characteristic curve (ROC) analysis. The AUCs were compared using the Delong method. RESULTS: Univariate analysis demonstrated that MR-tumor (T) stage, MR-lymph node (N) stage, APTw-10%, APTw-90%, interquartile range, APTw-minimum, APTw-maximum, APTw-mean, APTw-median, entropy, kurtosis, mean absolute deviation (MAD), and robust MAD were significantly related to pEMVI-positive status (all p < 0.05). Multivariate analysis demonstrated that MR-T stage (OR = 4.864, p = 0.018), MR-N stage (OR = 4.967, p = 0.029), interquartile range (OR = 0.892, p = 0.037), APT-minimum (OR = 1.046, p = 0.031), entropy (OR = 11.604, p = 0.006), and kurtosis (OR = 1.505, p = 0.007) were the independent risk factors enabling prediction of pEMVI-positive status. The AUCs for diagnostic ability of conventional MRI assessment, the APTw histogram model, and the combined model (including APTw histogram and clinical variables) were 0.785, 0.853, and 0.918, respectively. The combined model outperformed the APTw histogram model (p = 0.013) and the conventional MRI assessment (p = 0.006). CONCLUSIONS: Whole-tumor histogram analysis of APTw images combined with clinical factors showed better diagnosis efficiency in predicting EMVI involvement in RA. KEY POINTS: ⢠Rectal adenocarcinomas with pEMVI-positive status are typically associated with higher APTw-SI values. ⢠APTw-minimum, interquartile range, entropy, kurtosis, MR-T stage, and MR-N stage are the independent risk factors for EMVI involvement. ⢠The best prediction for EMVI involvement was obtained with a combined model of APTw histogram and clinical variables (area under the curve, 0.918).
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Adenocarcinoma , Neoplasias Retais , Humanos , Prótons , Amidas , Carga Tumoral , Estudos Retrospectivos , Imageamento por Ressonância Magnética/métodos , Neoplasias Retais/diagnóstico por imagem , Neoplasias Retais/patologia , Adenocarcinoma/diagnóstico por imagem , Adenocarcinoma/patologiaRESUMO
OBJECTIVES: Lymph node (LN) metastasis is an important prognostic factor in rectal cancer (RC). However, accurate identification of LN metastasis can be challenged for radiologists. The aim of our study was to assess the utility of MRI radiomics based on T2-weighted images (T2WI) and amide proton transfer-weighted (APTw) images for predicting LN metastasis in RC preoperatively. METHODS: A total of 125 patients with pathologically confirmed rectal adenocarcinoma (RA) from January 2019 to June 2021 who underwent preoperative MR were enrolled in this retrospective study. Radiomics features were extracted from high-resolution T2WI and APTw images of primary tumor. The most relevant radiomics and clinical features were selected using correlation and multivariate logistic analysis. Radiomics models were built using five machine learning algorithms including support vector machine (SVM), logical regression (LR), k- nearest neighbor (KNN), naive bayes (NB), and random forest (RF). The best algorithm was selected for further establish the clinical- radiomics model. The receiver operating characteristic curve (ROC) analysis was used to assess the performance of radiomics and clinical-radiomics model for predicting LN metastasis. RESULTS: The LR classifier had the best prediction performance, with AUCs of 0.983 (95% CI 0.957-1.000), 0.864 (95% CI 0.729-0.972), 0.851 (95% CI 0.713-0.940) on the training set, validation, and test sets, respectively. In terms of prediction, the clinical-radiomics combined model outperformed the radiomics model. The AUCs of the clinical-radiomics combined model in the validation and test sets were 0.900 (95% CI 0.785-0.986), and 0.929 (95% CI 0.721-0.943), respectively. CONCLUSION: The radiomics model based on high-resolution T2WI and APTw images can predict LN metastasis accurately in patients with RA.
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Adenocarcinoma , Neoplasias Retais , Humanos , Metástase Linfática/diagnóstico por imagem , Prótons , Estudos Retrospectivos , Teorema de Bayes , Imageamento por Ressonância Magnética/métodos , Neoplasias Retais/patologia , Adenocarcinoma/diagnóstico por imagem , Adenocarcinoma/secundárioRESUMO
OBJECTIVES: Melatonin (MT) is a pineal hormone with antineoplastic potential. This study aims to explore the therapeutic potential and mechanism of MT on glioblastoma (GBM). METHODS: A human GBM cell line, LN229, was used to evaluate the function of MT. Cell viability, apoptosis, and migration were detected by CCK-8, flow cytometry, and transwell assays, respectively. The mRNA and protein expressions of specific genes were measured by qRT-PCR and western blot, respectively. The regulatory relationship between miR-16-5p and PIM1 was validated by dual luciferase reporter gene assay. A mouse xenograft model was established to prove the anti-tumor effect and related mechanisms of MT in vivo. RESULTS: MT inhibited the viability and migration and promoted the apoptosis of LN229 cells in a dose-dependent manner. MiR-16-5p was dose-dependently up-regulated by MT in LN229 cells, negatively regulating its target PIM1. MiR-16-5p inhibitor eliminated the anti-tumor effect of MT in LN229 cells, while si-PIM1 reversed the effect of miR-16-5p inhibitor in MT-treated cells. MT inhibited the tumor growth in vivo and MT-induced PIM1 down-regulation was reversed by miR- 16-5p inhibition in tumor tissues. CONCLUSIONS: MT inhibits the malignant progression of GBM via regulating miR-16-5p-mediated PIM1.
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Glioblastoma , Melatonina , MicroRNAs , Animais , Apoptose/genética , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Glioblastoma/metabolismo , Humanos , Melatonina/farmacologia , Melatonina/uso terapêutico , Camundongos , MicroRNAs/genética , MicroRNAs/metabolismo , Proteínas Proto-Oncogênicas c-pim-1/genética , Proteínas Proto-Oncogênicas c-pim-1/metabolismoRESUMO
BACKGROUND: Tumor necrosis factor-α (TNF-α)-induced protein 3-interacting protein 2 (TNIP2) has been well demonstrated to act as a principal contributor to the development of inflammatory diseases; however, the role of TNIP2 in cerebral ischemic/reperfusion injury has never been studied. METHODS: Gene expression was examined by using quantitative real-time polymerase chain reaction and Western blot. The functional role of TNIP2 in oxygen and glucose deprivation/reoxygenation (OGD/R)-induced neuronal injury was evaluated using cell counting kit-8, terminal deoxynucleotidyl transferase dutp nick end labeling assay and enzyme-linked immunosorbent assay. Commercial kits were applied to evaluate the activity of NF-kappa-B (NF-κB) and caspase-3, as well as the release of lactate dehydrogenase release (LDH). RESULTS: TNIP2 expression was substantially declined in HT22 cells following OGD/R stimulation. TNIP2 overexpression attenuated ODG/R-induced inflammation in HT22 cells, as evidenced by reduced levels of TNF-α, interleukin (IL)-1ß, and intercellular cell adhesion molecule-1 (ICAM-1), and increased levels of IL-10. TNIP2 overexpression also reduced activity of NF-κB under ODG/R condition. Meanwhile, OGD/R treatment caused a reduction of cell viability and an elevation of cell apoptosis in HT22 cells, as indicated by the increase in LDH and caspase-3 activity. Whereas, OGD/R-induced HT22 cell injury was mitigated by TNIP2 overexpression in HT22 cells. Besides, we found the involvement of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/NF-κB pathway in the neuroprotective effect of TNIP2 on OGD/R-induced HT22 cell damage. CONCLUSION: TNIP2 overexpression mitigates OGD/R-induced inflammatory response and apoptosis. Moreover, TLR4/MyD88/NF-κB pathway participates in the protective effect of TNIP2 on OGD/R-induced neuronal damage.
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OBJECTIVES: To investigate the utility of 3D amide proton transfer (APT) MRI in predicting pathologic factors for rectal adenocarcinoma, in comparison with diffusion kurtosis imaging. METHODS: Sixty-one patients with rectal adenocarcinoma were enrolled in this prospective study. 3D APT and diffusion kurtosis imaging (DKI) were performed. Mean APT-weighted signal intensity (APTw SI), mean kurtosis (MK), mean diffusivity (MD), and ADC values of tumors were calculated on these maps. Pathological analysis included WHO grades, pT stages, pN stages, and extramural venous invasion (EMVI) status. Student's t test, Spearman correlation, and receiver operating characteristics (ROC) analysis were used for statistical analysis. RESULTS: High-grade rectal adenocarcinoma showed significantly higher mean APTw SI and MK values (2.771 ± 0.384 vs 2.108 ± 0.409, 1.167 ± 0.216 vs 1.045 ± 0.175, respectively; p < 0.05). T3 rectal adenocarcinoma demonstrated higher mean APTw SI and MK than T2 tumors (2.433 ± 0.467 vs 1.900 ± 0.302, p < 0.05). No kurtosis, diffusivity, and ADC differences were found between T2 and T3 tumors. Tumors with lymph node metastasis and EMVI involvement showed significantly higher mean APTw SI, MK. No difference was found in diffusivity and ADC between pN0 and pN1-2 groups, and EMVI-negative and EMVI-positive statuses. Mean APTw SI exhibited a significantly high positive correlation with WHO grades, demonstrating 92.31% sensitivity and 79.17% specificity for distinguishing low- from high-grade rectal adenocarcinoma, providing a better diagnostic capacity than MK, MD, and mean ADC values. CONCLUSION: 3D-APT could serve as a non-invasive biomarker for evaluating prognostic factors of rectal adenocarcinoma. KEY POINTS: ⢠Mean APTw SI was significantly higher in high-grade compared to low-grade rectal adenocarcinoma. ⢠Mean APTw SI was significantly higher in T3 stage rectal adenocarcinoma, with lymph node metastasis, or in EMVI-positive status. ⢠APTw SI exhibited greater diagnostic capability in discriminating low-grade from high-grade rectal adenocarcinoma, compared with kurtosis, diffusivity, and ADC.
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Adenocarcinoma , Prótons , Adenocarcinoma/diagnóstico por imagem , Amidas , Imagem de Difusão por Ressonância Magnética , Humanos , Imageamento por Ressonância Magnética , Prognóstico , Estudos Prospectivos , Sensibilidade e EspecificidadeRESUMO
BACKGROUND: The evaluation of prognostic factors in rectal carcinoma patients has important clinical significance. P53 status and the Ki-67 index have served as prognostic factors in rectal carcinoma. Amide proton transfer (APT) imaging has shown great potential in tumor diagnosis. However, few studies reported the value of APT imaging in evaluating p53 and Ki-67 status of rectal carcinoma. PURPOSE: To investigate the feasibility of amide proton transfer MRI in assessing p53 and Ki-67 expression of rectal adenocarcinoma, and compare it with conventional diffusion-weighted imaging (DWI). STUDY TYPE: Retrospective. POPULATION: Forty-three patients with rectal adenocarcinoma (age: 34-85 years). FIELD STRENGTH/SEQUENCE: 3T/APT imaging using a 3D turbo spin echo (TSE)-Dixon pulse sequence with chemical shift-selective fat suppression, 2D DWI, and 2D T2 -weighted TSE. ASSESSMENT: Mean tumor APT signal intensity (SImean ) and apparent diffusion coefficient (ADCmean ) were measured. Traditional tumor pathological analysis included WHO grades, pT (pathologic tumor) stages, and pN (pathologic node) stages. Expression levels of p53 and Ki-67 were determined by immunohistochemical assay. STATISTICAL TESTS: One-way analysis of variance (ANOVA); Student's t-test; Spearman's correlation coefficient; receiver operating characteristic (ROC) curve analysis. RESULTS: High-grade tumors, more advanced stage tumors, and tumors with lymph node involvement had higher APT SImean values: high grade (n = 15) vs. low-grade (n = 28), P < 0.001; pT2 (n = 10) vs. pT3 (n = 20) vs. pT4 (N = 13), P = 0.021; pN0 (n = 24) vs. pN1-2 (n = 19), P = 0.019. ADCmean differences were found in tumors with different pT stage: pT2 (n = 10) vs. pT3 (n = 20) vs. pT4 (N = 13), P = 0.013, but not in tumors with different histologic grade: high grade (n = 15) vs. low-grade (n = 28), P = 0.3536; or pN stage: pN0 (n = 24) vs. pN1-2 (n = 19), P = 0.624. Tumor with p53 positive status had higher APT SImean than tumor with negative p53 status (2.363 ± 0.457 vs. 2.0150 ± 0.3552, P = 0.014). There was no difference in ADCmean with p53 status (1.058 ± 0.1163 10-3 mm2 /s vs. 1.055 ± 0.128 10-3 mm2 /s, P = 0.935). APT SImean and ADCmean were significantly different in tumors with low and high Ki-67 status (1.7882 ± 0.11386 vs. 2.3975 ± 0.41586, P < 0.001; 1.1741 ± 0.093 10-3 mm2 /s vs. 1.0157 ± 0.10459 10-3 mm2 /s, P < 0.001, respectively). APT SImean exhibited a positive correlation with p53 labeling index and Ki-67 labeling index (r = 0.3741, P = 0.0135; r = 0.7048; P < 0.001, respectively). ADCmean showed no correlation with p53 labeling index, but a negative correlation with Ki-67 labeling index (r = -0.5543, P < 0.0001). ROC curves demonstrated that APT SImean had significantly higher diagnostic ability for differentiation of high Ki-67 expression of rectal adenocarcinoma than ADCmean (81.2% vs. 78.12%, 90.91% vs. 63.64; P < 0.001 vs. P = 0.017), while no difference was found in predicting p53 status (92.86% vs. 71.4%, 53.33% vs. 66.7%; P < 0.001 vs. P = 0.0471). DATA CONCLUSION: APT SImean was related to p53 and Ki-67 expression levels in rectal adenocarcinoma. APT imaging may serve as a noninvasive biomarker for assessing genetic prognostic factors of rectal adenocarcinoma. LEVEL OF EVIDENCE: 3 TECHNICAL EFFICACY STAGE: 2.
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Adenocarcinoma , Prótons , Adenocarcinoma/diagnóstico por imagem , Adulto , Idoso , Idoso de 80 Anos ou mais , Amidas , Imagem de Difusão por Ressonância Magnética , Humanos , Antígeno Ki-67/metabolismo , Imageamento por Ressonância Magnética , Pessoa de Meia-Idade , Estudos Retrospectivos , Proteína Supressora de Tumor p53RESUMO
BACKGROUND: Glioma is a common brain malignancy with high mortality. The competing endogenous RNA (ceRNA) networks may play key roles in cancer progression. This study was conducted to probe the role of long noncoding RNA (lncRNA) NCK1-AS1 in glioma progression and the involved mechanisms. METHODS: Microarray analyses were performed to explore the lncRNAs/miRNAs/genes with differential expression in glioma. NCK1-AS1 levels in glioma tissues and normal brain tissues, and in glioma cell lines and normal human glial cells were identified. The interactions among NCK1-AS1, miR-138-2-3p and TRIM24 were validated through luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. Gain- and loss-of functions of NCK1-AS1, miR-138-2-3p and TRIM24 were performed to identify their roles in the behaviors of glioma cells. The activity of the Wnt/ß-catenin pathway was measured. In vivo experiments were performed as well. RESULTS: High expression of NCK1-AS1 was found in glioma tissues and cells, especially in U251 cells. Online predictions and the integrated experiments identified that NCK1-AS1 elevated the TRIM24 expression through sponging miR-138-2-3p, and further activated the Wnt/ß-catenin pathway. Artificial silencing of NCK1-AS1 or up-regulation of miR-138-2-3p led to inhibited proliferation, invasion and migration but promoted cell apoptosis of U251 cells, while up-regulation of TRIM24 reversed these changes, and it activated the Wnt/ß-catenin pathway. The in vitro results were reproduced in in vivo experiments. CONCLUSIONS: Our study suggested that NCK1-AS1 might elevate TRIM24 expression and further activate the Wnt/ß-catenin pathway via acting as a ceRNA for miR-138-2-3p. Silencing of NCK1-AS1 might inhibit the progression of glioma.