The urban morphology on our planet - Global perspectives from space.

Urbanization is the second largest mega-trend right after climate change. Accurate measurements of urban morphological and demographic figures are at the core of many international endeavors to address issues of urbanization, such as the United Nations' call for "Sustainable Cities and Communities". In many countries - particularly developing countries -, however, this database does not yet exist. Here, we demonstrate a novel deep learning and big data analytics approach to fuse freely available global radar and multi-spectral satellite data, acquired by the Sentinel-1 and Sentinel-2 satellites. Via this approach, we created the first-ever global and quality controlled urban local climate zones classification covering all cities across the globe with a population greater than 300,000 and made it available to the community (https://doi.org/10.14459/2021mp1633461). Statistical analysis of the data quantifies a global inequality problem: approximately 40% of the area defined as compact or light/large low-rise accommodates about 60% of the total population, whereas approximately 30% of the area defined as sparsely built accommodates only about 10% of the total population. Beyond, patterns of urban morphology were discovered from the global classification map, confirming a morphologic relationship to the geographical region and related cultural heritage. We expect the open access of our dataset to encourage research on the global change process of urbanization, as a multidisciplinary crowd of researchers will use this baseline for spatial perspective in their work. In addition, it can serve as a unique dataset for stakeholders such as the United Nations to improve their spatial assessments of urbanization.

CNR1 may reverse progesterone-resistance of endometrial cancer through the ERK pathway.

Endocrine therapy is a promising treatment for endometrial cancer (EC) that preserves fertility, however, progesterone-resistance is currently the major challenges. The Cancer Genome Atlas (TCGA) database analysis showed that CNR1 was closely have a negative correlation with overall survival (OS) and relapse-free survival (RFS) in endometrial cancer. To explore the role of CNR1 in progesterone resistance and possible molecular regulation mechanism, we established stable progesterone-resistant cell lines (IshikawaPR) via progesterone tolerance of ordinary cancer cells (Ishikawa). The difference of CNR1 level in two cell lines was assessed by MTT, RT-PCR, Western blot, immunofluorescence. Then, lentiviruses constructed CNR1-knockdown with GV248 as the tool vector were used to transfect IshikwaPR cells, and the changes of biological behavior and progesterone sensitivity was verified respectively through plate cloning experiment, EdU assay, flow cytometry cycle analysis, transwell, Scratch test, etc. We founded after CNR1 was knocked down, the proliferative activity and ability to migrate of IshikawaPR cells decreased, progesterone-response sensitivity could be improved. Moreover, knockdown of CNR1 can also down-regulate ERK and NFκ B expression and activation. Furthermore, subcutaneous xenograft in nude mice was tested similarly in vivo. The above datas suggest that targeting CNR1 may reverse the progesterone resistance in endometrial cancer and may coordinate the role of ERK pathway activation.

MiR-501 promotes tumor proliferation and metastasis by targeting HOXD10 in endometrial cancer.

BACKGROUND: Several studies have shown the crucial role of miR-501 in regulating cellular pathology in various cancers. However, the function and expression of miR-501 in endometrial cancer (EC) remain obscure. METHODS: The expression of miR-501 was determined using quantitative real-time PCR. MTT assay, colony formation assay and cell cycle analysis were used to evaluate the proliferation ability. Migration and invasion were assessed using transwell assay. Tumor formation in nude mice was used to observe the effects of miR-501 on cell proliferation and migration in vivo. Luciferase assay, quantitative real-time PCR and western blot were applied to determine that HOXD10 was the target gene of miR-501. RESULTS: In this study, we observed significantly up-regulated expression of miR-501 in endometrial cancer, which correlated with higher pelvic lymph node metastasis and shorter overall survival in high-grade endometrial cancer. High expression of miR-501 was also found in the copy-number-high group than other groups. Moreover, in vitro and in vivo assay showed that overexpression of miR-501 can promote proliferation and metastasis. Mechanistically, we found that miR-501 promotes tumor progression by directly targeting HOXD10. Further study also indicated that miR-501 overexpression can activate the AKT/mTOR pathway. CONCLUSIONS: MiR-501, which functions as an oncomir in endometrial cancer, might be a potential therapeutic target in high grade endometrial cancer.

The diagnosis and treatment of adrenocortical carcinoma in pregnancy: a case report.

BACKGROUND: Pregnancy complicated with adrenocortical carcinoma (ACC) is a sporadic syndrome that is characterized by hypertension, uncontrolled hypokalemia, severe heart failure, premature delivery and other adverse effects. The clinical presentation of adrenocortical carcinoma is vague and nonspecific, it is challenging to identify complications of pregnancy with adrenocortical carcinoma. Here we present a case of adrenocortical carcinoma during pregnancy. We describe how to distinguish secondary hypertension from other conditions and the importance of timely detection and treatment of such patients. CASE PRESENTATION: A 22-year-old woman 30 weeks pregnant was hospitalized with uncontrolled hypertension and hypokalemia. An ultrasound examination of the right adrenal gland revealed a large mass. She underwent transabdominal adrenalectomy, and histopathology from the sample removed revealed an adrenocortical carcinoma. Five days after surgery, the patient had a premature rupture of the fetal membranes and gave birth to a newborn girl via vaginal delivery at 32 weeks of gestation. The newborn was transferred to the neonatal pediatrics ward, and the woman started receiving chemotherapy. CONCLUSIONS: Pregnancy with adrenocortical carcinoma is a rare condition. This case alerts the obstetricians that analysis of hypertension, hypokalemia, the plasma level and circadian rhythm of plasma cortisol provides a strategy to diagnose adrenocortical carcinoma during pregnancy.

A framework for large-scale mapping of human settlement extent from Sentinel-2 images via fully convolutional neural networks.

Human settlement extent (HSE) information is a valuable indicator of world-wide urbanization as well as the resulting human pressure on the natural environment. Therefore, mapping HSE is critical for various environmental issues at local, regional, and even global scales. This paper presents a deep-learning-based framework to automatically map HSE from multi-spectral Sentinel-2 data using regionally available geo-products as training labels. A straightforward, simple, yet effective fully convolutional network-based architecture, Sen2HSE, is implemented as an example for semantic segmentation within the framework. The framework is validated against both manually labelled checking points distributed evenly over the test areas, and the OpenStreetMap building layer. The HSE mapping results were extensively compared to several baseline products in order to thoroughly evaluate the effectiveness of the proposed HSE mapping framework. The HSE mapping power is consistently demonstrated over 10 representative areas across the world. We also present one regional-scale and one country-wide HSE mapping example from our framework to show the potential for upscaling. The results of this study contribute to the generalization of the applicability of CNN-based approaches for large-scale urban mapping to cases where no up-to-date and accurate ground truth is available, as well as the subsequent monitor of global urbanization.

Comprehensive bioinformatics analysis of acquired progesterone resistance in endometrial cancer cell line.

BACKGROUND: Progesterone resistance is a problem in endometrial carcinoma, and its underlying molecular mechanisms remain poorly understood. The aim of this study was to elucidate the molecular mechanisms of progesterone resistance and to identify the key genes and pathways mediating progesterone resistance in endometrial cancer using bioinformatics analysis. METHODS: We developed a stable MPA (medroxyprogesterone acetate)-resistant endometrial cancer cell subline named IshikawaPR. Microarray analysis was used to identify differentially expressed genes (DEGs) from triplicate samples of Ishikawa and IshikawaPR cells. PANTHER, DAVID and Metascape were used to perform gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and cBioPortal for progesterone receptor (PGR) coexpression analysis. GEO microarray (GSE17025) was utilized for validation. The protein-protein interaction network (PPI) and modular analyses were performed using Metascape and Cytoscape. Further validation were performed by real-time polymerase chain reaction (RT-PCR). RESULTS: In total, 821 DEGs were found and further analyzed by GO, KEGG pathway enrichment and PPI analyses. We found that lipid metabolism, immune system and inflammation, extracellular environment-related processes and pathways accounted for a significant portion of the enriched terms. PGR coexpression analysis revealed 7 PGR coexpressed genes (ANO1, SOX17, CGNL1, DACH1, RUNDC3B, SH3YL1 and CRISPLD1) that were also dramatically changed in IshikawaPR cells. Kaplan-Meier survival statistics revealed clinical significance for 4 out of 7 target genes. Furthermore, 8 hub genes and 4 molecular complex detections (MCODEs) were identified. CONCLUSIONS: Using microarray and bioinformatics analyses, we identified DEGs and determined a comprehensive gene network of progesterone resistance. We offered several possible mechanisms of progesterone resistance and identified therapeutic and prognostic targets of progesterone resistance in endometrial cancer.

Squamous cell carcinoma transformation in mature cystic teratoma of the ovary: a systematic review.

BACKGROUND: 0.17-2% of mature cystic teratoma of the ovary (MCTO) undergo malignant transformation, of which 80% are squamous cell carcinoma (SCC) transformation in MCTO. We aim to investigate the clinical characteristics and treatment of SCC transformation in MCTO METHODS: We systematically searched PubMed database and individual patient data about SCC transformation in MCTO were extracted. The published cases were combined with 6 cases of SCC transformation in MCTO from Qilu Hospital, Shandong University. RESULTS: The incidence of SCC transformation in MCTO was 0.3%. A total of 435 cases of SCC transformation in MCTO were enrolled in the analysis. The mean age of diagnosis was 53.5 (range 19-87) years old. The most common clinical manifestations were abdominal pain (47.3%) and abdominal mass (26.0%). StageI,II, III and IV accounted for 50.0, 18.8, 26.8 and 4.4% of all cases, respectively. Patients with stage I had significantly better prognosis than stage II, III and IV patients (P < 0.01). Hysterectomy can improve overall survival (P < 0.01). For patients younger than 45 years old with stageIA orIC, there was no difference in mortality between fertility-sparing and radical surgery (P = 1.00). Adjuvant chemotherapy can improve survival in patients with advanced stage (P = 0.02), and chemotherapy with platinum was related to better prognosis (P = 0.02). CONCLUSION: SCC transformation in MCTO is a rare malignancy mainly occurs in older age. FIGO stage is an independent prognostic factor. Hysterectomy and platinum-based chemotherapy are associated with better survival. Fertility-sparing surgery is feasible for young patients with early stage.

SUSD2 promotes cancer metastasis and confers cisplatin resistance in high grade serous ovarian cancer.

The activation of Notch3 is associated with potential progression of ovarian cancer, tumor invasion, metastasis and chemoresistance, which account for poor prognosis of high grade serous ovarian cancer (HGSOC). However, the underlying mechanisms of Notch3 are not yet very clear. Here we show that SUSD2 is one of Notch3-regulating genes and the elevated protein expression of SUSD2 in HGSOC. We also found that its high expression level was significantly correlated with worse overall survival, early recurrence and lymph nodes metastasis. Moreover, overexpression of SUSD2 in ovarian cancer cells promoted epithelial-mesenchymal transition (EMT) and the metastatic capacity of malignant cells. In contrast, silencing SUSD2 in aggressive ovarian cancer cells inhibited these processes both in vitro and in vivo. Mechanistically, we found SUSD2 promoted EMT through regulating the expression of EpCAM and EpCAM silencing reversed SUSD2-induced E-cadherin reduction and cells migration. Further experiments indicated a role of SUSD2 in conferring cisplatin resistance in ovarian cancer probably through enhancing autophagy in vitro. Collectively, these findings shed a new insight into the role of Notch3 downstream gene SUSD2 and provided a new therapeutic target for HGSOC.

Effect of monoacylglycerol lipase on the tumor growth in endometrial cancer.

AIM: Abnormal lipid metabolism plays a dual role in tumorigenesis, specifically in the occurrence and development of cancers. Monoacylglycerol lipase (MAGL), a hydrolase that is important for lipid metabolism, plays a vital role in different aspects of tumorigenesis. Many studies have shown that MAGL is highly elevated in a variety of cancers and plays an active role. However, its potential role in supporting endometrial cancer (EC) growth and progression has not yet been explored in depth. METHODS: Immunohistochemistry and quantitative real-time reverse transcription polymerase chain reaction were performed to estimate the protein and messenger RNA (mRNA) levels of MAGL in tumor tissues. Then, JZL184 and small interfering RNA (siRNA) were used to decrease the expression of MAGL in EC cells. The gene and protein expression levels of MAGL were measured using quantitative real-time PCR and western blotting, respectively. Additionally, the effect of MAGL on tumor growth in EC was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide , cell cycle and western blotting assay in vitro. RESULTS: We found that MAGL was overexpressed in EC and was significantly correlated with surgical-pathological stage, myometrial invasion, number of pregnancies and body mass index. The growth and cell cycle progression of tumor cells were significantly impaired in vitro by the pharmacological and siRNA-mediated MAGL inhibition. In addition, MAGL inhibition seemed to repress two target genes, Cyclin D1 and Bcl-2. CONCLUSION: In summary, we have demonstrated that MAGL is involved in EC growth and progression. Our results suggest that targeting MAGL may be a novel and valid treatment for EC.

Local climate zone-based urban land cover classification from multi-seasonal Sentinel-2 images with a recurrent residual network.

The local climate zone (LCZ) scheme was originally proposed to provide an interdisciplinary taxonomy for urban heat island (UHI) studies. In recent years, the scheme has also become a starting point for the development of higher-level products, as the LCZ classes can help provide a generalized understanding of urban structures and land uses. LCZ mapping can therefore theoretically aid in fostering a better understanding of spatio-temporal dynamics of cities on a global scale. However, reliable LCZ maps are not yet available globally. As a first step toward automatic LCZ mapping, this work focuses on LCZ-derived land cover classification, using multi-seasonal Sentinel-2 images. We propose a recurrent residual network (Re-ResNet) architecture that is capable of learning a joint spectral-spatial-temporal feature representation within a unitized framework. To this end, a residual convolutional neural network (ResNet) and a recurrent neural network (RNN) are combined into one end-to-end architecture. The ResNet is able to learn rich spectral-spatial feature representations from single-seasonal imagery, while the RNN can effectively analyze temporal dependencies of multi-seasonal imagery. Cross validations were carried out on a diverse dataset covering seven distinct European cities, and a quantitative analysis of the experimental results revealed that the combined use of the multi-temporal information and Re-ResNet results in an improvement of approximately 7 percent points in overall accuracy. The proposed framework has the potential to produce consistent-quality urban land cover and LCZ maps on a large scale, to support scientific progress in fields such as urban geography and urban climatology.

PCNA-associated factor P15PAF , targeted by FOXM1, predicts poor prognosis in high-grade serous ovarian cancer patients.

Activation of the FOXM1 signaling pathway and the PI3K/AKT/mTOR signaling pathway is associated with poor prognosis in ovarian cancer. In this study, we demonstrated that P15PAF (KIAA0101) was significantly upregulated in high-grade serous ovarian cancer (HGSOC) and that high KIAA0101 expression was associated with poor prognosis. FOXM1 transcriptionally activated KIAA0101 to drive proliferation and metastasis of ovarian cancer cells. KIAA0101 activated the PI3K/AKT/mTOR signaling pathway to inhibit cisplatin-induced apoptosis and autophagy in ovarian cancer cells resulting in cisplatin resistance. Thus, KIAA0101 was closely related to the FOXM1 and PI3K/AKT/mTOR signaling pathways. Collectively, these findings provide insights into the mechanisms of poor prognosis of ovarian cancer and have implications for the development of both predictive and therapeutic biomarkers for the treatment of ovarian cancer.

Spliceosome-associated factor CTNNBL1 promotes proliferation and invasion in ovarian cancer.

Ovarian cancer is the most lethal gynecologic malignancy and the molecular pathogenesis of high-grade serous ovarian carcinoma has not been completely characterized. Numerous studies have shown that altered splicing patterns and splicing factors were found to contribute to tumor development and progression. In this study, we demonstrated that spliceosome-associated factor CTNNBL1 was significantly upregulated in high-grade serous ovarian carcinoma, the elevated level of CTNNBL1 indicates poor prognosis in patients with high-grade serous ovarian carcinoma. Functional characterization revealed that CTNNBL1 promoted the proliferation and invasion of ovarian cancer cells in vitro. Furthermore, through transcriptome analysis, we found CTNNBL1 regulates multiple splicing events and gene expression in ovarian cancer cells. Importantly, we identified IFI16 and FOXM1 splicing was regulated by CTNNBL1. To our knowledge, this is the first study exploring the expression, functional roles and regulated splicing events of CTNNBL1 in ovarian cancer.

Towards automatic SAR-optical stereogrammetry over urban areas using very high resolution imagery.

In this paper we discuss the potential and challenges regarding SAR-optical stereogrammetry for urban areas, using very-high-resolution (VHR) remote sensing imagery. Since we do this mainly from a geometrical point of view, we first analyze the height reconstruction accuracy to be expected for different stereogrammetric configurations. Then, we propose a strategy for simultaneous tie point matching and 3D reconstruction, which exploits an epipolar-like search window constraint. To drive the matching and ensure some robustness, we combine different established hand-crafted similarity measures. For the experiments, we use real test data acquired by the Worldview-2, TerraSAR-X and MEMPHIS sensors. Our results show that SAR-optical stereogrammetry using VHR imagery is generally feasible with 3D positioning accuracies in the meter-domain, although the matching of these strongly hetereogeneous multi-sensor data remains very challenging.

Gene expression profiles of ovarian low-grade serous carcinoma resemble those of fallopian tube epithelium.

OBJECTIVE: The cell of origin of ovarian low-grade serous carcinoma (LGSC) remains unclarified. Our recent morphologic and immunophenotypic study suggests that most LGSCs may be derived from the fallopian tube. The purpose of the current study was to gain further insight into the origin of LGSC at the molecular level. METHODS: RNA-seq analysis was performed on a total of 31 tissue samples including LGSC (n=6), serous borderline tumors (SBT, n=6), fallopian tube epithelia (FTE, n=5), ovarian surface epithelia (OSE, n=4), and human peritoneal mesothelia (HPM, n=4). HGSC cases (n=6) served as a positive control. Gene expression profiles were compared and analyzed. To validate the findings from the gene expression array study, we selected the highly differentially expressed genes (PAX8, CDH1, FOXA2, and ARX) as well as those corresponding proteins and examined their expression levels in tissue samples of ovarian serous tumors, fallopian tube, ovarian surface epithelia, and peritoneal mesothelia. RESULTS: Dendrograms revealed that OSE samples clustered with HPM, while ovarian serous tumors, including LGSC, SBT and high-grade serous carcinoma (HGSC), clustered with FTE. Furthermore, LGSC showed a significantly closer relationship with FTE than with OSE and HPM samples. PAX8, CDH1, and FOXA2 were highly and specifically expressed in serous tumors and FTE samples but not in OSE samples. In contrast, ARX was mainly expressed in OSE samples but not in FTE and serous tumors. CONCLUSIONS: The findings of the current study provide further evidence at a molecular level that the fallopian tube is likely the cellular source of LGSC. This finding may enable new prevention strategies, improve early detection, and allow novel therapies to be tested.

Biglycan enhances the ability of migration and invasion in endometrial cancer.

OBJECTIVE: This study aimed to confirm that biglycan (BGN) can promote the migration and invasion in endometrial cancer both in vitro and in vivo and the possible therapeutic value of BGN in endometrial cancer. METHODS: Western blot was used to screen out the higher protein level of BGN in human endometrial cancer cells; BGN knocked down cells were constructed by lentiviral transfection; The effect of BGN in endometrial cancer detected by wound healing, transwell migration, and invasion, endothelial tube formation assay in vitro, and xenograft model in vivo. RESULTS: (1) We found that BGN expression level is higher in the Ishikawa (ISK, high differentiation) and AN3CA (poor differentiation) cells than other endometrial cancer cells. (2) BGN enhances endometrial cancer cell wound healing, invasion, and migration ability and formation ability of endothelial cells in vitro. Xenograft model has confirmed the outcome in vivo. CONCLUSIONS: BGN might play an important role on metastasis in human endometrial cancer and it might be a target marker for the molecular therapy of advanced and recurrence endometrial cancer.

Sterol regulatory element-binding protein-1/fatty acid synthase involvement in proliferation inhibition and apoptosis promotion induced by progesterone in endometrial cancer.

BACKGROUND: The number of endometrial cancer (EC) cases is escalating rapidly, with no evident improvements in survival rates. The downregulation of progesterone receptor, resulting in progestin resistance, is presently a major problem regarding the therapeutic aspect. On the basis of this, we can focus more on the downstream signaling pathways that are controlled by progesterone. Lipid biosynthesis mediated by sterol regulatory element-binding protein-1/fatty acid synthase (SREBP-1/FASN) is of utmost importance to the growth and the proliferation of EC cells, so we hypothesize that SREBP-1/FASN might be involved in suppressing the proliferation and promoting apoptosis in EC cells through the effects induced by progesterone. MATERIAL AND METHODS: The Cell Counting Kit-8 was used to analyze the growth inhibition ratio of Ishikawa cells upon treatment with megestrol acetate (MA; MA is a progesterone derivative, also known as 17α-acetoxy-6-dehydro-6-methylprogesterone) and to determine the 50% inhibitory concentration. Apoptosis ratio was analyzed by treatment of the cells with MA at 50% inhibitory concentration at different time intervals using Annexin V-FITC/propidium iodide. The protein and messenger RNA levels of SREBP-1 and FASN were compared between the experimental and control groups (MA-treated Ishikawa cells were considered to be the experimental group). RESULTS: The experimental group showed obvious growth inhibition that was time and concentration dependent. The apoptosis ratio was also significantly higher in the experimental group compared with the control group (P < 0.01). The protein and messenger RNA levels of SREBP-1 and FASN were significantly reduced by MA too. CONCLUSIONS: Sterol regulatory element-binding protein-1/FASN is involved in the proliferation suppression and apoptosis promotion brought about by MA in Ishikawa cells.

Progress of immunotherapies in gestational trophoblastic neoplasms.

BACKGROUND: Different from other malignant gynecologic tumors, gestational trophoblastic neoplasms (GTNs) exhibit an exceptionally high cure rate primarily through chemotherapeutic interventions. However, there exists a small subset of refractory GTNs that do not respond to conventional chemotherapies. In such cases, the emergence of immunotherapies has demonstrated significant benefits in managing various challenging GTNs. PURPOSE: This article aims to provide a comprehensive and systematic review of the immune microenvironment and immunotherapeutic approaches for GTNs. The purpose is to identify potential biomarkers that could enhance disease management and summarize the available immunotherapies for ease of reference. METHODS: We reviewed the relevant literatures toward immunotherapies of GTNs from PubMed. CONCLUSION: Current immunotherapeutic strategies for GTNs mainly revolve around immune checkpoint inhibitors (ICIs) targeting programmed death receptor 1 (PD-1) and programmed cell death ligand 1 (PD-L1). Prominent examples include avelumab, pembrolizumab, and camrelizumab. However, existing researches into the underlying mechanisms are still limited.

Novel insights into tumorigenesis and prognosis of endometrial cancer through systematic investigation and validation on mitophagy-related signature.

In-depth studies on the pathogenesis of endometrial cancer (EC) are critical because of the increasing global incidence of EC. Mitophagy, a mitochondrial quality control process, plays an important role in carcinogenesis and tumor progression. This study aimed to develop a novel mitophagy-based signature to predict the tumorigenesis and prognosis of EC. Data was downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases, and 29 mitophagy-related genes were downloaded from the Pathway Unification Database. EC patients were classified into two risk groups based on the two-key- gene signature, TOMM40 and MFN1, which were constructed using Cox regression analysis. A better prognosis was noted in the low-risk group. The model was validated for four aspects: clinical features, mutation status, clinical therapeutic response, and immune cell infiltration status. Moreover, according to the contribution to the risk model, TOMM40 was selected for further in vitro experiments. The silencing of TOMM40 inhibited mitochondrial degradation; suppressed cell proliferation; induced cell apoptosis and G1 phase cell cycle arrest; inhibited migration, invasion, and epithelial-mesenchymal transition; and suppressed cell stemness. In conclusion, the mitophagy-related risk score provides a novel perspective for survival and drug selection during the individual treatment of EC patients. TOMM40 serves as an oncogene in EC and promotes tumor progression via a mitophagy-related pathway. Thus, TOMM40 is a potential therapeutic target in EC.

Multi-granularity knowledge distillation and prototype consistency regularization for class-incremental learning.

Deep neural networks (DNNs) are prone to the notorious catastrophic forgetting problem when learning new tasks incrementally. Class-incremental learning (CIL) is a promising solution to tackle the challenge and learn new classes while not forgetting old ones. Existing CIL approaches adopted stored representative exemplars or complex generative models to achieve good performance. However, storing data from previous tasks causes memory or privacy issues, and the training of generative models is unstable and inefficient. This paper proposes a method based on multi-granularity knowledge distillation and prototype consistency regularization (MDPCR) that performs well even when the previous training data is unavailable. First, we propose to design knowledge distillation losses in the deep feature space to constrain the incremental model trained on the new data. Thereby, multi-granularity is captured from three aspects: by distilling multi-scale self-attentive features, the feature similarity probability, and global features to maximize the retention of previous knowledge, effectively alleviating catastrophic forgetting. Conversely, we preserve the prototype of each old class and employ prototype consistency regularization (PCR) to ensure that the old prototypes and semantically enhanced prototypes produce consistent prediction, which excels in enhancing the robustness of old prototypes and reduces the classification bias. Extensive experiments on three CIL benchmark datasets confirm that MDPCR performs significantly better over exemplar-free methods and outperforms typical exemplar-based approaches.

LncRNA HOXB-AS3 binding to PTBP1 protein regulates lipid metabolism by targeting SREBP1 in endometrioid carcinoma.

Endometrial cancer (EC) is a malignant tumor with a high incidence in women, and the survival rate of high-risk patients decreases significantly after disease progression. The regulatory role of long non-coding RNAs (LncRNAs) in tumors has been widely appreciated, but there have been few studies in EC. To investigate the effect of HOXB-AS3 in EC, we used bioinformatics tools for prediction and collected clinical samples to detect the expression of HOXB-AS3. Colony formation assay, MTT assay, flow cytometry and apoptosis assay, and transwell assay were used to verify the role of HOXB-AS3 in EC. HOXB-AS3 was upregulated in EC, promoted the proliferation and invasive ability of EC cells, and inhibited apoptosis. In addition, the ROC curve illustrated its diagnostic value. We explored experiments via lentiviral transduction, FISH, Oil Red O staining, TC and FFA content detection, RNA-pulldown, RIP, and other mechanisms to reveal that HOXB-AS3 can bind to PTBP1 and co-regulate the expression of SREBP1, thereby regulating lipid metabolism in EC cells. To the best of our knowledge, this is the first study on HOXB-AS3 in disorders of lipid metabolism in EC. In addition, we believe HOXB-AS3 has the potential to be a neoplastic marker or a therapeutic target.