Analyzing brain tumours is important for prompt diagnosis and efficient patient care. The morphology of tumours, which includes their size, location, texture, and heteromorphic appearance in medical pictures, makes them difficult to analyse. A unique two-phase deep learning-based framework is suggested in this respect to recognise and classify brain cancers in magnetic resonance images (MRIs). A new DTA approach is suggested in the first phase to successfully identify tumour MRI images from healthy persons. DTA are specifically designed and perform well are used to create the deep boosted feature space, which is then fed into the group of machine learning (ML) classifiers. In the second stage, a brand-new hybrid features fusion-based brain tumour classification technique is put forward, one that makes use of both static and dynamic features as well as an ML classifier to classify various tumour kinds. The proposed algorithm, which can recognise the heteromorphic and variable behaviour of different tumours, is where the dynamic characteristics are taken.In this paper, many segmentation algorithms for MRI and PET are reviewed together with their performance evaluations in order to detect brain tumours. There are numerous segmentation methods available for the diagnosis of medical images. The features of the image, such as the capacity to distinguish between similarities and discontinuities, are often used to classify the segmentation techniques. Neuroradiologists have a difficult issue in trying to quickly identify the abnormal region, which is essential in the medical field. In order to overcome this problem, the efficiency of different segmentation procedures is assessed. The segmentation methods considered here are Ant Colony Optimization (ACO), Wavelet Transform (WT), Gradient Vector Flow (GVF), Gray level Co-occurrence matrix (GLCM), and Artificial Bee Colony (ABC). The various performance metrics are used to evaluate the suggested segmentation algorithms. The GVF strategy works better with MRI images, whereas the ABC and ACO approaches perform similarly with PET scans, according to the data acquired.

Wilms tumor (WT) is the commonest cause of renal cancer in children. In Europe, a diagnosis is made for most cases on typical clinical and radiological findings, prior to pre-operative chemotherapy. Here, we describe a case of a young boy presenting with a large abdominal tumor, associated with raised serum alpha-fetoprotein (AFP) levels at diagnosis. Given the atypical features present, a biopsy was taken, and histology was consistent with WT, showing triphasic WT, with epithelial, stromal, and blastemal elements present, and positive WT1 and CD56 immunohistochemical staining. During pre-operative chemotherapy, serial serum AFP measurements showed further increases, despite a radiological response, before a subsequent fall to normal following nephrectomy. The resection specimen was comprised of ~55% and ~45% stromal and epithelial elements, respectively, with no anaplasia, but immunohistochemistry using AFP staining revealed positive mucinous intestinal epithelium, consistent with the serum AFP observations. The lack of correlation between tumor response and serum AFP levels in this case highlights a more general clinical unmet need to identify WT-specific circulating tumor markers.

UNASSIGNED: Wilms tumour (WT) is caused by aberrant embryonic kidney development and associated with dysregulated expression of short, non-protein-coding RNAs termed microRNAs (miRNAs). At present, there is no reliable circulating biomarker of WT, and this remains an urgent unmet clinical need. Such biomarkers may assist diagnosis, subtyping/prognostication, and disease-monitoring. Here, we established the list of dysregulated circulating miRNAs in WT from the existing published literature.
UNASSIGNED: Regardless of publication date, PubMed, Scopus, Web-of-Science, and Wiley online library databases were searched for English/French studies on WT circulating miRNAs. The PRISMA-compliant search was registered in PROSPERO. The QUADAS tool measured retained article quality. The meta-analysis assessed the sensitivity and specificity of miRNAs for WT diagnosis.
UNASSIGNED: Qualitative analysis included 280 samples (172 WT patients; 108 healthy controls) from five of 450 published articles. The study uncovered 301 dysregulated miRNAs (144 up-regulated, 143 down-regulated, 14 conflicting). The pooled sensitivity, specificity, and AUC of the 49 significantly dysregulated microRNAs from two studies was 0.67 [0.62; 0.73], 0.95 [0.92; 0.96] and 0.77 [0.73; 0.81] respectively, indicating a stronger diagnostic potential for WT.
UNASSIGNED: Circulating miRNAs show promise for WT diagnosis and prognosis. More research is needed to confirm these findings and determine associations with tumour stage/subtype.
UNASSIGNED: CRD42022301597.

Diabetic nephropathy (DN) is one of the most established microvascular complications of diabetes and a key cause of end-stage renal disease. It is well established that gene susceptibility to DN plays a critical role in disease pathophysiology. Therefore, many genetic studies have been performed to categorize candidate genes in prominent diabetic cohorts, aiming to investigate DN pathogenesis and etiology. In this study, we performed a meta-analysis on the expression profiles of GSE1009, GSE30122, GSE96804, GSE99340, GSE104948, GSE104954, and GSE111154 to identify critical transcriptional factors associated with DN progression. The analysis was conducted for all individual datasets for each kidney tissue (glomerulus, tubules, and kidney cortex). We identified distinct clusters of susceptibility genes that were dysregulated in a renal compartment-specific pattern. Further, we recognized a small but a closely connected set of these susceptibility genes enriched for podocyte differentiation, several of which were characterized as genes encoding critical transcriptional factors (TFs) involved in DN development and podocyte function. To validate the role of identified TFs in DN progression, we functionally validated the three main TFs (DACH1, LMX1B, and WT1) identified through differential gene expression and network analysis using the hyperglycemic zebrafish model. We report that hyperglycemia-induced altered gene expression of the key TF genes leads to morphological abnormalities in zebrafish glomeruli, pronephric tubules, proximal and distal ducts. This study demonstrated that altered expression of these TF genes could be associated with hyperglycemia-induced nephropathy and, thus, aids in understanding the molecular drivers, essential genes, and pathways that trigger DN initiation and development.

Light detection and ranging (LIDAR) is an active remote sensing system. Lidar echo signal is non-linear and non-stationary, which is often accompanied by various noises. In order to filter out the noise and extract valid signal information, a suitable method should be chosen for noise reduction. Some denoising methods are commonly used, such as the wavelet transform (WT), the empirical mode decomposition (EMD), the variational mode decomposition (VMD), and their improved algorithms. In this paper, a new denoising method named the WT-VMD joint algorithm based on the sparrow search algorithm (SSA), for lidar signal is selected by comparative experiment analysis. It is shown that this method is the most suitable one with the maximum signal-to-noise ratio (SNR), the minimum root-mean-square error (RMSE), and a relatively small indicator of smoothness when it is used in three kinds (50, 100, and 1000 pulses) of simulate lidar signals. The SNR is increased by 138.5%, 77.8% and 42.8% and the RMSE is decreased by 81.8%, 72.0% and 68.8% when being used to the three kinds of cumulative signal without pollution. Then, the SNR is increased by 83.3%, 60.4% and 24.0% and the RMSE is decreased by 70.8%, 66.0% and 50.5% when being used to the three kinds of cumulative signal with aerosol and clouds. The WT-VMD joint algorithm based on SSA is used in the denoising process for the actual lidar signal, showing extraordinary denoising effect and will improve the inversion accuracy of the lidar signal.

Dysferlin (DYSF) has drawn much attention due to its involvement in dysferlinopathy and was reported to affect monocyte functions in recent studies. However, the role of DYSF in the pathogenesis of atherosclerotic cardiovascular diseases (ASCVD) and the regulation mechanism of DYSF expression have not been fully studied. In this study, Gene Expression Omnibus (GEO) database and epigenome-wide association study (EWAS) literatures were searched to find the DNA methylation-driven genes (including DYSF) of ASCVD. The hub genes related to DYSF were also identified through weighted correlation network analysis (WGCNA). Regulation of DYSF expression through its promoter methylation status was verified using peripheral blood leucocytes (PBLs) from ASCVD patients and normal controls, and experiments on THP1 cells and Apoe-/- mice. Similarly, the expressions of DYSF related hub genes, mainly contained SELL, STAT3 and TMX1, were also validated. DYSF functions were then evaluated by phagocytosis, transwell and adhesion assays in DYSF knock-down and overexpressed THP1 cells. The results showed that DYSF promoter hypermethylation up-regulated its expression in clinical samples, THP1 cells and Apoe-/- mice, confirming DYSF as a DNA methylation-driven gene. The combination of DYSF expression and methylation status in PBLs had a considerable prediction value for ASCVD. Besides, DYSF could enhance the phagocytosis, migration and adhesion ability of THP1 cells. Among DYSF related hub genes, SELL was proven to be the downstream target of DYSF by wet experiments. In conclusion, DYSF promoter hypermethylation upregulated its expression and promoted monocytes activation, which further participated in the pathogenesis of ASCVD.

Paediatric malignant renal neoplasms are subjected to neoadjuvant chemotherapy as per Societe Internationale d\'Oncologie Pediatrique; International Society of Pediatric Oncology (SIOP) protocol. An accurate tissue diagnosis is required prior to institution of chemotherapy, and hence the aim of this study was to evaluate the diagnostic accuracy of fine needle aspiration biopsy cytology (FNABC) along with cell block histology.
A retrospective audit of all paediatric renal neoplasms diagnosed by FNABC between 2015 and 2019 was performed. Histopathology correlation was done wherever available. WT cases were subjected to detailed cytomorphological evaluation.
A total of 121 cases of paediatric renal neoplasms including 109 WT, four clear cell sarcoma, one malignant rhabdoid tumour and three mesoblastic nephroma were evaluated. The age range was 4 weeks to 8 years. FNABC samples were adequate for diagnosis in 120 of 121 cases (99.18%) and a definitive cytological diagnosis was achieved in 117 cases (96.7%). The specificity and sensitivity for a cytopathological diagnosis of WT were 98.7% and 97.4%, respectively. On detailed cytomorphological analysis of 68 histopathology-proven WT, 40 (58.8%) cases were triphasic, 23 (35.3%) were biphasic and four were composed of blastema only. The corresponding cell blocks provided additional information over the conventional smears in 23 (33.8%) cases, with epithelial or mesenchymal elements recognised and evidence of rhabdomyoblastic differentiation.
FNABC along with cell block histology is highly accurate for diagnosis of WT and other malignant paediatric renal neoplasms and is recommended as the technique of choice in centres with cytopathology expertise for establishing a cellular diagnosis prior to commencement of neoadjuvant chemotherapy.

The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) chromatin remodeling subunit, plays a critical role in regulating immune responses. We have previously shown that ubiquitous SRG3 overexpression attenuates the progression of Th1/Th17-mediated experimental autoimmune encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a Th2-type immune disorder. Thus, to elucidate the effects of SRG3 overexpression in AD development, we bred NC/Nga (NC) mice with transgenic mice where SRG3 expression is driven by the β-actin promoter (SRG3β-actin mice). We found that SRG3β-actin NC mice exhibit increased AD development (e.g., a higher clinical score, immunoglobulin E (IgE) hyperproduction, and an increased number of infiltrated mast cells and basophils in skin lesions) compared with wild-type NC mice. Moreover, the severity of AD pathogenesis in SRG3β-actin NC mice correlated with expansion of interleukin 4 (IL4)-producing basophils and mast cells, and M2 macrophages. Furthermore, this accelerated AD development is strongly associated with Treg cell suppression. Collectively, our results have identified that modulation of SRG3 function can be applied as one of the options to control AD pathogenesis.

Micro ribonucleic acid (miR)-21 in the proliferation and apoptosis of Wilms\' tumor (WT) cells was explored. SK-NEP-1 cells were transfected with miR-21 inhibitor to silence the expression of miR-21. Then, the effects of miR-21 silencing on the proliferation and apoptosis of WT SK-NEP-1 cells were detected through cell counting kit-8 (CCK-8), colony formation assay and flow cytometry. The targets of miR-21 were analyzed via TargetScan database. Fluorescence real-time quantitative polymerase chain reaction (RT-qPCR) assay and western blot analysis were conducted to detect the changes in messenger RNA (mRNA) and protein expression levels of gene of phosphate and tension homology deleted on chromosome ten (PTEN) after silencing miR-21. Whether miR-21 directly binds to PTEN was examined by activity detection via dual luciferase reporter gene assay. Western blotting was employed to detect the correlation of miR-21 with PTEN and protein kinase B (Akt). Compared with normal control (NC) group, miR-21 inhibitor group had significantly inhibited proliferation of SK-NEP-1 cells (P<0.05), notably reduced number of clones (P<0.05) and overtly raised proportion of apoptotic cells (P<0.05). The suppression of miR-21 expression upregulated the mRNA and protein expression levels of PTEN, and the results of activity detection via dual luciferase reporter gene assay indicated that miR-21 bound to PTEN 3\'-untranslated region (UTR) to repress its expression (P<0.05). PTEN silencing increased phosphorylated Akt (p-Akt) level in SK-NEP-1 cells, but there was no changes in Akt protein level. After silencing both PTEN and miR-21, the decrease in p-Akt was reversed, thereby reversing the inhibitory effect of miR-21 on the proliferation of SK-NEP-1 cells (P<0.05). miR-21 affects the proliferation and apoptosis of WT SK-NEP-1 cells via the PTEN/Akt pathway.

Wilms tumor (WT) is the most common solid childhood tumors all over the world. MicroRNAs (miRs) contribute to tumorigenesis of various cancers through targeting gene. The present study investigated the vital role of miR-194-5p and its underlying mechanism in the progression of WT. Immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR) assay indicated downregulation of miR194-5p and upregulation of Crk, in WT tissues compared to adjacent normal tissues. Transfection with miR-194-5p mimics into nephroblastoma cells showed a significant decline in cell migration and invasion, which was detected by Transwell assay. Luciferase assay confirmed that Crk was a direct target gene of miR-194-5p. More important, the mesenchymal to epithelial transition (EMT) biomarkers containing E-cadherin, N-cadherin and Zeb1 were examined by Western blot, and revealed that miR-194-5p mimics decreased the levels of N-cadherin and Zeb1 but increased E-cadherin, which suggested that miR-194-5p inhibited EMT. Crk knockdown could reverse the increased nephroblastoma cell invasion, migration and EMT caused by miR-194-5p inhibitor. Interestingly, qRT-PCR and Western blot analysis showed that overexpression of miR-194-5p deactivated HGF/c-Met/Scr signaling pathway via targeting Crk. In conclusion, miR-194-5p inhibited nephroblastoma cell metastasis and EMT in the progression of WT by targeting Crk. Thus, miR-194-5p might be a potential target in WT particularly for the prevention of metastasis and EMT.