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1.
Diagn Pathol ; 19(1): 110, 2024 Aug 15.
Artículo en Inglés | MEDLINE | ID: mdl-39143618

RESUMEN

AIMS: Compared to primary breast sarcoma (BSs), radiotherapy-induced sarcoma (RIS) is a less frequent type of secondary breast sarcoma. Undifferentiated pleomorphic sarcoma (UPS) is an even rarer occurrence within the RIS category. This study aimed to present the clinicopathologic and molecular features of breast radiotherapy-induced UPS. METHODS: A retrospective study was conducted at the Third Affiliated Hospital of Soochow University to analyze three patients with radiation-induced undifferentiated pleomorphic sarcoma (UPS) following breast cancer, spanning from 2006 to 2023. The clinical and pathological variables were extracted from the medical records, while immunohistochemistry was employed to analyze the immunophenotypes of these tumors. Genomic characteristics were assessed through DNA and RNA sequencing techniques. Another 15 cases from the literature were also reviewed to better characterize the tumor. RESULTS: The affected areas encompass the chest wall and breasts, with an incubation period ranging from 6 to 17 years. The tumor cells exhibit pleomorphism and demonstrate a high degree of pathological mitosis. Notably, two cases displayed an accelerated disease progression, characterized by recurrent tumors and metastases occurring within short intervals of 48 and 7 months respectively subsequent to the initial diagnosis. The two prevailing identified genes were TP53 (2/3, 66.7%) and RB1 (1/3, 33.3%). Through analysis of somatic copy number variation (CNV), it was discovered that two oncogenes, MCL1 (1/3, 33.3%) and MYC (1/3, 33.3%), had experienced gains in CNV. The Tumor Mutational Burden (TMB) values for case 1, case 2, and case 3 were 5.9 mut/Mb, 1.0 mut/Mb, and 3.0 mut/Mb, respectively. Moreover, the analysis of RNA-NGS (next-generation sequencing) revealed the presence of a novel gene fusion, named COL3A1-GULP1, in case 2. CONCLUSIONS: Based on our thorough analysis of research findings and previous reports, it is evident that radiotherapy-induced UPS exhibits a highly diverse and frequently severe clinical and biological behavior. Identifying tumor formation using genome sequencing can help understand its biological behavior and determine personalized treatments.


Asunto(s)
Neoplasias de la Mama , Neoplasias Inducidas por Radiación , Sarcoma , Humanos , Femenino , Neoplasias de la Mama/genética , Neoplasias de la Mama/patología , Neoplasias de la Mama/radioterapia , Sarcoma/genética , Sarcoma/patología , Neoplasias Inducidas por Radiación/genética , Neoplasias Inducidas por Radiación/patología , Persona de Mediana Edad , Estudios Retrospectivos , Adulto , Biomarcadores de Tumor/genética , Anciano , Proteínas de Unión a Retinoblastoma/genética , Ubiquitina-Proteína Ligasas
2.
Theranostics ; 14(6): 2345-2366, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38646645

RESUMEN

Rationale: Primordial follicles are limited in number and cannot be regenerated, dormant primordial follicles cannot be reversed once they enter a growth state. Therefore, the length of the female reproductive lifespan depends on the orderly progression and selective activation of primordial follicles, the mechanism of which remains unclear. Methods: We used human ovarian cortical biopsy specimens, granulosa cells from diminished ovarian reserve (DOR) patients, Hdac6-overexpressing transgenic mouse model, and RNA sequencing to analyze the crucial roles of histone deacetylase 6 (HDAC6) in fertility preservation and primordial follicle activation. Results: In the present study, we found that HDAC6 was highly expressed in most dormant primordial follicles. The HDAC6 expression was reduced accompanying reproductive senescence in human and mouse ovaries. Overexpression of Hdac6 delayed the rate of primordial follicle activation, thereby prolonging the mouse reproductive lifespan. Short-term inhibition of HDAC6 promoted primordial follicle activation and follicular development in humans and mice. Mechanism studies revealed that HDAC6 directly interacted with NGF, reducing acetylation modification of NGF and thereby accelerating its ubiquitination degradation. Consequently, the reduced NGF protein level maintained the dormancy of primordial follicles. Conclusions: The physiological significance of the high expression of HDAC6 in most primordial follicles is to reduce NGF expression and prevent primordial follicle activation to maintain female fertility. Reduced HDAC6 expression increases NGF expression in primordial follicles, activating their development and contributing to reproduction. Our study provides a clinical reference value for fertility preservation.


Asunto(s)
Histona Desacetilasa 6 , Ratones Transgénicos , Factor de Crecimiento Nervioso , Folículo Ovárico , Ubiquitinación , Animales , Femenino , Humanos , Ratones , Acetilación , Células de la Granulosa/metabolismo , Histona Desacetilasa 6/metabolismo , Histona Desacetilasa 6/genética , Factor de Crecimiento Nervioso/metabolismo , Folículo Ovárico/metabolismo
3.
Educ Inf Technol (Dordr) ; : 1-26, 2023 Mar 24.
Artículo en Inglés | MEDLINE | ID: mdl-37361730

RESUMEN

This study explored the interaction between cognition and emotion in blended collaborative learning. The participants (n = 30) of this study were undergraduate students enrolled in a 16-week course on information technology teaching. These students were divided into six groups of five people each. The behavior modes of the participants were analyzed using a heuristic mining algorithm and inductive miner algorithm. Compared with the groups with low task scores, the high-scoring groups exhibited more reflection phases and cycles in the interaction process and thus more frequent self-evaluation and regulation behavior for forethought and performance. Moreover, the frequency of emotion events unrelated with cognition was higher for the high-scoring groups than for the low-scoring groups. On the basis of the research results, this paper presents suggestions for developing online and offline blended courses.

4.
Front Psychol ; 13: 857709, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35558726

RESUMEN

The COVID-19 pandemic caused colleges and universities to rely heavily on online learning to continue knowledge dissemination to learners. This study used the second-generation model of unified theory of acceptance and use of technology (UTAUT2) to comprehensively analyze the mediating effects of self-efficacy, which affects learners' effective use of online tools for learning, and capability of metacognition and self-regulation, which can independently adjust learning progress into the UTAUT2 model, on the learner's willingness to continue online learning [i.e., their behavioral intention (BI)] by constructing a UTAUT2-based e-learning model. This study administered questionnaires to undergraduates in universities in East China to collect data. The effects of performance expectancy, effort expectancy (EE), social influence (SI), and facilitating conditions (FCs), hedonic motivation (HM), price value (PV), and habits on BI (directly or through mediators) were analyzed through data analysis and structural equation modeling, and the UTAUT2-based e-learning model was accordingly modified. The results indicated that the self-efficacy enhanced the effects of EE, SI, FCs, HM, and PV on learners' BI; that metacognition and self-regulation (MS) capabilities enhanced the effects of EE on learners' BI; and that habits had a direct and strong effect on BI. This study also provided some suggestions to enhance higher education learners' willingness to continue online learning, such as improving social recognition and support, careful design of teaching content, easy-to-use technology, financial support. These results and suggestions may guide colleges and universities in conducting, continuing, or enhancing online education, particularly as the pandemic continues.

5.
Endocrine ; 76(3): 526-535, 2022 06.
Artículo en Inglés | MEDLINE | ID: mdl-35194770

RESUMEN

PURPOSE: Pancreatic ß-cell failure is a central hallmark of the pathogenesis of diabetes mellitus; however, the molecular basis underlying chronic inflammation-caused ß-cell failure remains unclear. This study reported here specifically assessed the association between miR-25/miR-92b family and ß-cell failure in diabetes. METHODS: IL-1ß and two additional ER stress activators, palmitate and tunicamycin were applied to evaluate the expression level miR-25 by Taqman® RT-PCR. Glucose- and potassium-stimulated insulin secretion assays were performed to assess ß-cell function. Dual-luciferase activity, and western blotting assays were utilized for miR-25 target gene verification. CCK-8 and TUNEL staining were used to evaluate ß-cell viability and apoptosis. RESULTS: miRNA ChIP identified the increased level of miR-25 in INS-1 cells by IL-1ß treatment. Expression levels of miR-25 were significantly upregulated with the treatment of IL-1ß, palmitate or tunicamycin in both INS-1 cells and human islets. Ectopic elevation of miR-25 recapitulated most featured ß-cell defects caused by IL-1ß, including inhibition of insulin biosynthesis and increased ß-cell apoptosis. These detrimental effects of miR-25 relied on its seed sequence recognition and repressed expression of its target genes Neurod1 and Mcl1. The miR-25/NEUROD1 axis reduced insulin biosynthesis via transcriptional regulation of ß-cell specific genes. The miR-25/MCL1 axis caused ß-cell apoptosis in a CASPASE-3/PARP1-dependent manner. Comparable impairments were generated by miR-92b and miR-25, emphasizing the redundant biological roles of miRNA family members with the same seed sequence. CONCLUSION: MiR-25/miR-92b family plays a major role in ß-cell failure occurring under inflammation and diabetes states.


Asunto(s)
Células Secretoras de Insulina , MicroARNs , Apoptosis/genética , Humanos , Inflamación/metabolismo , Insulina/metabolismo , Células Secretoras de Insulina/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Proteína 1 de la Secuencia de Leucemia de Células Mieloides/metabolismo , Palmitatos/metabolismo , Palmitatos/farmacología , Tunicamicina/farmacología
6.
Int J Mol Med ; 41(2): 1096-1102, 2018 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-29207028

RESUMEN

The cofilin 2 (CFL2) and myosin heavy chain (MyHC) genes play a key role in muscle development and myofibrillar formation. The aim of the present study was to investigate the effect of CFL2 on genes involved in fiber formation and the mechanisms underlying this process. Undifferentiated and differentiated C2C12 cells (UDT and DT, respectively) were transfected with CFL2 small interfering RNA (siRNA). CFL2 mRNA and protein levels were assessed using reverse transcription polymerase chain reaction (RT-PCR) and western blotting, respectively. MyHC gene expression in UDT and signaling pathway-related factors were observed with quantitative PCR (RT­qPCR) and western blotting. Fluorescence microscopy was used to analyze the cytoskeletal effects of CFL2. The mRNA and protein expressions of CFL2, four MyHC isoforms (MyHC-I, MyHC-IIa, MyHC-IIb and MyHC-IIx), p38 mitogen-activated protein kinase, cAMP-response element-binding protein, AMP-activated protein kinase α1, and myocyte enhancer factor 2C, were significantly decreased in UDT. However, extracellular signal-regulated kinase 2 expression was significantly increased. Slightly decreased CFL2 protein and mRNA expression was observed in DT C2C12 cells transfected with CFL2 siRNA. Fluorescence microscopy revealed a significant decrease of CFL2 in the cytoplasm, but not the nucleus, of UDT, compared with normal cells. These results indicated that the mouse CFL2 gene may be involved in the regulation of MyHC via the key signaling molecules of CFL2-related signaling pathways.


Asunto(s)
Cofilina 2/genética , Desarrollo de Músculos/genética , Miofibrillas/genética , Cadenas Pesadas de Miosina/genética , Animales , Diferenciación Celular/genética , Regulación del Desarrollo de la Expresión Génica , Ratones , Proteína Quinasa 1 Activada por Mitógenos/genética , Mioblastos , Isoformas de Proteínas/genética , ARN Mensajero/genética , Proteínas Quinasas p38 Activadas por Mitógenos/genética
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