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BACKGROUND: Most patients with splenosis have no clinical symptoms and do not need intervention. Hematospermia and testicular pain occurred in this patient, which was considered to be related to the huge pelvic implantation of the spleen, which was relatively rare in clinical practice, so we hereby report this case. CASE PRESENTATION: A 28-year-old male patient with a history of splenectomy was admitted to the Urology Department of the Second Affiliated Hospital of Anhui Medical University with the chief complaint of "Hematospermia for 1 month and testicular pain for 2 days". Preoperative imaging examination indicated pelvic mass. Combined with the patient's history of splenectomy for splenic rupture in childhood, the possibility of pelvic spleen implantation was considered. Laparoscopic pelvic exploration was performed. During the operation, multiple grayish-brown nodular tissues were observed in the space between the posterior bladder and rectum, and a lobulated grayish-brown mass with a diameter of about 9 cm was observed in the posterior upper part of the prostate gland and seminal vesicle at the pelvic floor. Two nodular tissues were removed intraoperatively and sent for quick frozen pathology, which was reported as spleen tissue. Further resection of the huge mass was performed, and the postoperative pathological results were consistent with the diagnosis of splenosis. CONCLUSION: We report a rare case of splenosis presenting with hemospermia and testicular pain.
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Hemospermia , Esplenose , Masculino , Humanos , Adulto , Esplenose/complicações , Esplenose/diagnóstico , Esplenose/cirurgia , Hemospermia/diagnóstico , Hemospermia/etiologia , Esplenectomia/métodos , DorRESUMO
The relaxation of field-line tension during magnetic reconnection gives rise to a universal Fermi acceleration process involving the curvature drift of particles. However, the efficiency of this mechanism is limited by the trapping of energetic particles within flux ropes. Using 3D fully kinetic simulations, we demonstrate that the flux-rope kink instability leads to strong field-line chaos in weak-guide-field regimes where the Fermi mechanism is most efficient, thus allowing particles to transport out of flux ropes and undergo further acceleration. As a consequence, both ions and electrons develop clear power-law energy spectra that contain a significant fraction of the released energy. The low-energy bounds are determined by the injection physics, while the high-energy cutoffs are limited only by the system size. These results have strong relevance to observations of nonthermal particle acceleration in space and astrophysics.
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BACKGROUND Growing evidence indicates an association between microfibril-associated protein 2 (MFAP2) and a number of physiological and pathological mechanisms. The potential role of MFAP2 in cancer requires further elucidation. The present study investigated the biological behavior of MFAP2 in melanoma patients. MATERIAL AND METHODS MFAP2 inhibition was established in the B16 melanoma cell line through the use of RNA interference and was assessed by quantitative real-time PCR (qRT-PCR) and Western blot analysis. Wound-healing analysis, transwell assay, and in vivo imaging were performed to investigate the roles of MFAP2 reducing cell mobility, migration, and invasion abilities in vitro and in vivo. RESULTS We found substantially higher MFAP2 expression in B16 melanoma cells. The knockdown of MFAP2 inhibited B16 melanoma cells migration and invasion. Western blot analysis was used to assess changes in biomarkers of EMT, indicating the function of MFAP2 in EMT. We found that downregulation of MFAP2 altered the expression of Wnt/ß-catenin-linked protein. CONCLUSIONS Our results suggest that MFAP2 has potential as a molecular target to treat melanoma and suppress metastasis of melanoma cells.
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Melanoma Experimental/metabolismo , Fatores de Processamento de RNA/metabolismo , Via de Sinalização Wnt , Animais , Apoptose/fisiologia , Linhagem Celular Tumoral , Movimento Celular/fisiologia , Proliferação de Células/fisiologia , Transição Epitelial-Mesenquimal , Masculino , Melanoma Experimental/patologia , Camundongos , Camundongos Endogâmicos BALB C , Microfibrilas/metabolismo , Microfibrilas/patologia , Invasividade Neoplásica , Interferência de RNA , Fatores de Processamento de RNA/genética , RNA Interferente Pequeno/administração & dosagemRESUMO
Gastric cancer remains a malignancy with poor survival outcome. We herein report that GSE1, a proline-rich protein, possesses a role in the progression of human gastric cancer. The expression of GSE1 was observed to be much higher in human gastric cancer tissues compared with normal gastric tissues, and GSE1 expression correlated positively with lymph node metastasis, histological grade, depth of invasion, and clinical stage in gastric cancer patients. Moreover, GSE1 expression was also associated with decreased post-operative relapse-free survival and overall survival in the cohort. The forced expression of GSE1 in gastric cancer cell lines resulted in increased cell proliferation, increased colony formation, enhanced cell migration, and invasion. Furthermore, forced expression of GSE1 also increased tumor size and enhanced lung metastasis in xenograft models. The depletion of endogenous GSE1 with shRNAs decreased the oncogenicity and invasiveness of gastric cancer cells both in vitro and in vivo In addition, GSE1 was determined to be a direct target of miR-200b and miR-200c. Furthermore, GSE1 positively regulated the downstream gene SLC7A5 (also known as LAT-1), which was scanned and verified from mRNA sequencing. GSE1 therefore possesses an oncogenic role in human gastric cancer, and targeted therapeutic approaches to inhibit GSE1 function in gastric cancer warrant further consideration.
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Adenocarcinoma/mortalidade , Movimento Celular , Proliferação de Células , Transportador 1 de Aminoácidos Neutros Grandes/metabolismo , Proteínas de Neoplasias/metabolismo , Recidiva Local de Neoplasia/mortalidade , Neoplasias Gástricas/mortalidade , Adenocarcinoma/secundário , Adenocarcinoma/cirurgia , Animais , Apoptose , Biomarcadores Tumorais/metabolismo , Estudos de Casos e Controles , Feminino , Seguimentos , Regulação Neoplásica da Expressão Gênica , Humanos , Metástase Linfática , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Invasividade Neoplásica , Recidiva Local de Neoplasia/patologia , Recidiva Local de Neoplasia/cirurgia , Prognóstico , Neoplasias Gástricas/patologia , Neoplasias Gástricas/cirurgia , Taxa de Sobrevida , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
Deep neural networks (DNNs) have made great breakthroughs and seen applications in many domains. However, the incomparable accuracy of DNNs is achieved with the cost of considerable memory consumption and high computational complexity, which restricts their deployment on conventional desktops and portable devices. To address this issue, low-rank factorization, which decomposes the neural network parameters into smaller sized matrices or tensors, has emerged as a promising technique for network compression. In this article, we propose leveraging the emerging tensor ring (TR) factorization to compress the neural network. We investigate the impact of both parameter tensor reshaping and TR decomposition (TRD) on the total number of compressed parameters. To achieve the maximal parameter compression, we propose an algorithm based on prime factorization that simultaneously identifies the optimal tensor reshaping and TRD. In addition, we discover that different execution orders of the core tensors result in varying computational complexities. To identify the optimal execution order, we construct a novel tree structure. Based on this structure, we propose a top-to-bottom splitting algorithm to schedule the execution of core tensors, thereby minimizing computational complexity. We have performed extensive experiments using three kinds of neural networks with three different datasets. The experimental results demonstrate that, compared with the three state-of-the-art algorithms for low-rank factorization, our algorithm can achieve better performance with much lower memory consumption and lower computational complexity.
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Purpose: Positive interpersonal interactions are indispensable for employees to engage in organizational citizenship behavior (OCB) that benefits teamwork; however, co-worker ostracism triggers interpersonal isolation, inhibiting OCB. This research aims to leverage the intervention of ethical leadership in the ostracism-OCB relationship to moderate the harmful ostracism and promote ostracized employees' OCB through employee self-identity. Methods: This research chose 122 MBA to participate in Study 1's scenario experiment to verify the causality between variables. Study 2 used 295 valid questionnaires from full-time employees to generalize the experimental results to field settings and compensate for external validity. Two studies used Hayes's conditional process model to test the conditional direct and indirect relationships. Findings: This research revealed that high levels of ethical leadership effectively transitioned the harmful ostracism and promoted ostracized employees' OCB by satisfying ostracized employees' needs for identity recognition. Accordingly, the direct and indirect effects of co-worker ostracism on OCB through employee self-identity would be positive at high levels of ethical leadership, but negative at low levels. Originality: This research first introduces an identity perspective on ethical leadership in moderating the ostracism-OCB relationship. Based on the social identity theory of leadership, this research fills the gap in ostracism and OCB research calling for leadership interventions. It extends a novel insight into inspiring ostracized employees' participation in OCB through employee self-identity. Practical Implications: This research provides the managerial applications of ethical leadership for China organizations to reduce inadvertent inactions, accept employees' identities, and value interpersonal communication for effectively transitioning harmful ostracism.
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It is well known that collisionless systems are dissipation free from the perspective of particle collision and thus conserve entropy. However, processes such as magnetic reconnection and turbulence appear to convert large-scale magnetic energy into heat. In this paper, we investigate the energization and heating of collisionless plasma. The dissipation process is discussed in terms of fluid entropy in both isotropic and gyrotropic forms. Evolution equations for the entropy are derived and they reveal mechanisms that lead to changes in fluid entropy. These equations are verified by a collisionless particle-in-cell simulation of multiple reconnecting current sheets. In addition to previous findings regarding the pressure tensor, we emphasize the role of heat flux in the dissipation process.
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Breast cancer is the leading cause of cancer-related mortality in women worldwide. Trastuzumab (Herceptin) is an effective antibody drug for HER2 positive breast cancer; de novo or acquired trastuzumab resistance retarded the use of trastuzumab for at least 70% of HER2 positive breast cancers. In this study, we reported LMO4 (a member of LIM-only proteins) promoted trastuzumab resistance in human breast cancer cells. Over-expression of LMO4 was observed in acquired trastuzumab resistance breast cancer cells SKBR3 HR and BT474 HR. Depletion of LMO4 partly abolished the trastuzumab resistance of SKBR3 HR and BT474 HR cells. Forced expression of LMO4 significantly increased trastuzumab resistance of HER2 positive breast cancer cells both in vitro and in vivo. BCL-2 was regulated by LMO4 and mediated the promoting role of LMO4 in trastuzumab resistance of HER2 positive breast cancer cells. High level of LMO4 was associated with worse clinicopathological parameters (including tumor size and histological grade) and lower survival rate in HER2 positive breast cancer patients. LMO4 therefore could be used as a target to develop diagnostic and therapeutic methods for human HER2 positive breast cancer.
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Papillary thyroid carcinoma (PTC) is the most common endocrine cancer with a significantly increase of the incidence recently. Several cytokines, such as thyroid peroxidase (TPO), cluster of differentiation 56 (CD56), Galectin-3, mesothelial cell (MC), cytokeratin 19 (CK19) and BRAF (B-raf) were recommended to be tested by immunohistochemistry (IHC) for a definitive diagnosis, but were still limited in clinical use because of their relative lower sensitivity and specificity. MicroRNA (miRNA), as a new molecular biomarkers, however, has not been reported yet so far. To address this, hsa-miR-200a-5p, a miRNA, was selected and detected in PTC patients by in situ hybrization with benign thyroid tumor with papillary hyperplasia as a control, and the differential expression of hsa-miR-200a-5p between fresh PTC tissues and control was detected by qRT-PCR. Expressive levels of cytokines of TPO, CD56, Galectin-3, MC, CK19 and B-raf were also detected by immunohistochemistry. The correlation was analyzed by SPSS software using Spearman methods. As expected, the hsa-miR-200a-5p expressive level was significantly increased in PTC patients, compared to that of control, and was consistent with that of TPO, CD56, Galectin-3, MC, CK19 and B-raf. In addition, expression of hsa-miR-200a-5p showed negative correlation to that of TPO (rs = - 0.734; **: P < 0.01) and CD56 (rs = - 0.570; **: P < 0.01), but positive correlation to that of Galectin-3 (rs = 0.601; **: P < 0.01), MC (rs = 0.508; **: P < 0.01), CK19 (rs = 0.712; **: P < 0.01) and B-raf (rs = 0.378; **: P < 0.01). PTC and papillary benign thyroid papillary hyperplasia are difficult to distinguish in morphology, so requiring immunohistochemistry to further differentiate the diagnosis, however, for the existing clinical common diagnostic marker for immunohistochemistry, the sensitivity and accuracy are low, it is easy to miss diagnosis. Therefore, there is an urgent need for a rapid and sensitive molecular marker. So miR-200a-5p can be used to assist in the diagnosis of PTC at the molecular level, and as a biomarker, can be effectively used to distinguish between PTC and benign thyroid tumor with papillary hyperplasia.
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MicroRNAs/genética , Câncer Papilífero da Tireoide/genética , Glândula Tireoide/patologia , Neoplasias da Glândula Tireoide/genética , Marcadores Genéticos/genética , Humanos , Hiperplasia/diagnóstico , Hiperplasia/genética , Hibridização In Situ , Reação em Cadeia da Polimerase em Tempo Real , Câncer Papilífero da Tireoide/diagnóstico , Neoplasias da Glândula Tireoide/diagnósticoRESUMO
Glioma is the most common and aggressive type of human primary brain tumor with a poor outcome. The molecular mechanisms underlying glioma development and progression are still poorly understood. Recent studies have reported a novel role of ARPP-19 in the regulation of cell mitosis and cancer progression. However, no study has been carried out to determine the role of ARPP-19 in human glioma cells and assess the expression and clinical significance of ARPP-19 in human glioma. In this study, we systematically examined the role of ARPP-19 in glioma A172 cells and examined the expression of ARPP-19 and CD147 in 81 cases of human glioma tissue specimens and correlated them to clinicopathological parameters and patient survival. We found that ARPP-19 promoted both proliferation and metastasis of human glioma cells and the expression of ARPP-19 and CD147 in high-grade glioma was significantly higher than that in the low-grade glioma. Patients whose tumors were positive for expression of ARPP-19 or CD147 showed lower relapse-free survival and overall survival than patients whose tumors were negative for ARPP-19 or CD147, respectively. Pearson correlation analysis indicated that there was a statistically significant correlation between ARPP-19 and CD147. Expressions of ARPP-19 and CD147 may serve as biomarkers for high-grade glioma and poor patient survival.