LightBTSeg: A lightweight breast tumor segmentation model using ultrasound images via dual-path joint knowledge distillation

The accurate segmentation of breast tumors is an important prerequisite for lesion detection, which has significant clinical value for breast tumor research. The mainstream deep learning-based methods have achieved a breakthrough. However, these high-performance segmentation methods are formidable to implement in clinical scenarios since they always embrace high computation complexity, massive parameters, slow inference speed, and huge memory consumption. To tackle this problem, we propose LightBTSeg, a dual-path joint knowledge distillation framework, for lightweight breast tumor segmentation. Concretely, we design a double-teacher model to represent the fine-grained feature of breast ultrasound according to different semantic feature realignments of benign and malignant breast tumors. Specifically, we leverage the bottleneck architecture to reconstruct the original Attention U-Net. It is regarded as a lightweight student model named Simplified U-Net. Then, the prior knowledge of benign and malignant categories is utilized to design the teacher network combined dual-path joint knowledge distillation, which distills the knowledge from cumbersome benign and malignant teachers to a lightweight student model. Extensive experiments conducted on breast ultrasound images (Dataset BUSI) and Breast Ultrasound Dataset B (Dataset B) datasets demonstrate that LightBTSeg outperforms various counterparts.Comment: 7 pages, 7 figures, conferenc

PO-099 Effects of long-term high-intensity exercise training on renal local renin-angiotensin system in rats

Objective Exercise stimulation to the body of the first stress: blood changes, regulated by the renin-angiotensin system. Long-term high-intensity exercise training will lead to changes in kidney structure and function, resulting in renal injury. This will not only affect training and competition, but also affect the health of athletes, thus it is becoming an influential factor in the occurrence and development of excessive fatigue. At present, the mechanism of renal injury and proteinuria caused by exercise is not very clear. Therefore, this study conducted an in-depth study on the upstream mechanism of renal blood flow changes from the molecular level and explored the effects of 6-week high-intensity exercise training on the renal local renin-angiotensin system in rats. Methods 30 SD male rats (8 weeks old) were randomly divided into control group (10) and exercise group (20). Then according to different time, the exercise group (20) was divided into two groups on average, which are 0h group and 24h group. The rats in the control group did not do any exercise, and the rats in the exercise group were trained to run on the platform with high intensity for 6 weeks. At the beginning of the sixth week, the urine of rats from different group were selected randomly, and the urine NGAL, urinary microalbumin (mAlb), urinary creatinine (UCr) and total urine protein (TP) were tested, to determine the rat model of exercise-induced renal injury with proteinuria. After training on the 6th weekend, the renal tissue renin activity and angiotensin Ⅱ (Ang Ⅱ) content in right kidney were tested. At the same time, the left kidney of the rat was taken to make HE staining sections. Results (1) The mAlb, Alb/Cr and TP of the exercise group were higher than those of the control group, while the UCr content was lower than that of the control group. There was a significant difference between mAlb and TP in the exercise group and the control group(p<0.05). UCr, mAlb/Cr were significantly different from the control group(p<0.01). The urine NGAL concentration in the exercise group was higher than that in the control group, and the difference was significant(p<0.05). (2) The glomerulus of the rats in the 0h group showed obvious congestion, swelling and erythrocyte exudation. The tissue morphology of rats in the 24h group recovered slightly, but it was still different from the control group. (3) The renin activity and Ang Ⅱ were the lowest in the 0h group, and the renin activity and Ang Ⅱ were highest in the 24h group. There is a very significant difference between the groups(p<0.01). Conclusions (1) The 6-week high-intensity training used in this study increased the levels of NGAL, TP, and mAlb in the urine of rats, and successfully established a rat model of exercise-induced renal injury with proteinuria. (2) Long-term high-intensity exercise training can cause obvious congestion, swelling, erythrocyte exudation in rat glomeruli, which can’t return to the quiet level 24 hours after exercise. (3) Renal injury caused by exercise decreased the expression of local renin activity and angiotensin II in the kidney, and the recovery of renal renin activity and angiotensin II was increased 24h after exercise

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Background/Aims: This study aims to examine the effect of long noncoding RNA HOST2 (LncRNA HOST2) on epithelial-mesenchymal transition (EMT), proliferation, invasion and migration of hepatocellular carcinoma (HCC) cells via activation of the JAK2-STAT3 signaling pathway. Methods: HCC and para-cancerous tissues were collected from 136 HCC patients. Immunohistochemistry was used to detect the expression of JAK2 and STAT3. HCC SMMC7721 cells were grouped into blank, negative control (NC), HOST2 mimic and HOST2 inhibitor groups. The mRNA and protein expression levels of HOST2, JAK2, STAT3, E-cadherin, vimentin, Snail, Slug, Twist and Zeb1 in tissues and cells were determined by reverse transcription -quantitative polymerase chain reaction (RT-qPCR) and Western blotting, respectively. An MTT assay, scratch test and Transwell assay were applied to measure cell proliferation, migration and invasion, respectively. Results: The levels of JAK2, STAT3 and vimentin were higher in HCC tissues, while the expression of E-cadherin was lower in HCC tissues compared with para-cancerous tissues. The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. HOST2 silencing also decreased the levels of Snail, Slug and Twist but increased the level of Zeb1 protein, while the opposite findings were observed in the HOST2 mimic group. Conclusion: These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway

Epidemiology of Schistosomiasis in the People’s Republic of China, 2004

Although the number of human infections decreased, human prevalence increased from 4.9% in 1995 to 5.1% in 2004

MicroRNA profiling associated with non-small cell lung cancer: next generation sequencing detection, experimental validation, and prognostic value

[EN] Background: The average five-year survival for non-small cell lung cancer (NSCLC) patients is approximately 15%. Emerging evidence indicates that microRNAs (miRNAs) constitute a new class of gene regulators in humans that may play an important role in tumorigenesis. Hence, there is growing interest in studying their role as possible new biomarkers whose expression is aberrant in cancer. Therefore, in this study we identified dysregulated miRNAs by next generation sequencing (NGS) and analyzed their prognostic value. Methods: Sequencing by oligo ligation detection technology was used to identify dysregulated miRNAs in a training cohort comprising paired tumor/normal tissue samples (N = 32). We validated 22 randomly selected differentially-expressed miRNAs by quantitative real time PCR in tumor and adjacent normal tissue samples (N = 178). Kaplan-Meier survival analysis and Cox regression were used in multivariate analysis to identify independent prognostic biomarkers. Results: NGS analysis revealed that 39 miRNAs were dysregulated in NSCLC: 28 were upregulated and 11 were downregulated. Twenty-two miRNAs were validated in an independent cohort. Interestingly, the group of patients with high expression of both miRNAs (miR-21(high) and miR-188(high)) showed shorter relapse-free survival (RFS) and overall survival (OS) times. Multivariate analysis confirmed that this combined signature is an independent prognostic marker for RFS and OS (p = 0.001 and p < 0.0001, respectively). Conclusions: NGS technology can specifically identify dysregulated miRNA profiles in resectable NSCLC samples. MiR-21 or miR-188 overexpression correlated with a negative prognosis, and their combined signature may represent a new independent prognostic biomarker for RFS and OS.This work was supported by the RD12/0036/0025 and RD06/0020/1024 PI12-02838, ISCIII, grants from the Fondo Europeo de Desarrollo Regional (FEDER), by funds from the Proyecto de Investigacion Fundamental Orientada a la Transmision de Conocimiento a la Empresa (TRACE; TRA09-0132) and Beca Roche Oncohematologia.Gallach-Garcia, S.; Jantus-Lewintre, E.; Calabuig-Fariñas, S.; Montaner, D.; Alonso, S.; Sirera Pérez, R.; Blasco, A.... (2017). MicroRNA profiling associated with non-small cell lung cancer: next generation sequencing detection, experimental validation, and prognostic value. Oncotarget. 8(34):56143-56157. https://doi.org/10.18632/oncotarget.18603S561435615783

DNA demethylation pathways: Additional players and regulators.

DNA demethylation can occur passively by "dilution" of methylation marks by DNA replication, or actively and independently of DNA replication. Direct conversion of 5-methylcytosine (5mC) to cytosine (C), as originally proposed, does not occur. Instead, active DNA methylation involves oxidation of the methylated base by ten-eleven translocations (TETs), or deamination of the methylated or a nearby base by activation induced deaminase (AID). The modified nucleotide, possibly together with surrounding nucleotides, is then replaced by the BER pathway. Recent data clarify the roles and the regulation of well-known enzymes in this process. They identify base excision repair (BER) glycosylases that may cooperate with or replace thymine DNA glycosylase (TDG) in the base excision step, and suggest possible involvement of DNA damage repair pathways other than BER in active DNA demethylation. Here, we review these new developments

Search for chargino-neutralino production with mass splittings near the electroweak scale in three-lepton final states in √s=13 TeV pp collisions with the ATLAS detector

A search for supersymmetry through the pair production of electroweakinos with mass splittings near the electroweak scale and decaying via on-shell W and Z bosons is presented for a three-lepton final state. The analyzed proton-proton collision data taken at a center-of-mass energy of √s=13  TeV were collected between 2015 and 2018 by the ATLAS experiment at the Large Hadron Collider, corresponding to an integrated luminosity of 139  fb−1. A search, emulating the recursive jigsaw reconstruction technique with easily reproducible laboratory-frame variables, is performed. The two excesses observed in the 2015–2016 data recursive jigsaw analysis in the low-mass three-lepton phase space are reproduced. Results with the full data set are in agreement with the Standard Model expectations. They are interpreted to set exclusion limits at the 95% confidence level on simplified models of chargino-neutralino pair production for masses up to 345 GeV

Regulation of AMP-activated protein kinase by natural and synthetic activators

AbstractThe AMP-activated protein kinase (AMPK) is a sensor of cellular energy status that is almost universally expressed in eukaryotic cells. While it appears to have evolved in single-celled eukaryotes to regulate energy balance in a cell-autonomous manner, during the evolution of multicellular animals its role has become adapted so that it also regulates energy balance at the whole body level, by responding to hormones that act primarily on the hypothalamus. AMPK monitors energy balance at the cellular level by sensing the ratios of AMP/ATP and ADP/ATP, and recent structural analyses of the AMPK heterotrimer that have provided insight into the complex mechanisms for these effects will be discussed. Given the central importance of energy balance in diseases that are major causes of morbidity or death in humans, such as type 2 diabetes, cancer and inflammatory disorders, there has been a major drive to develop pharmacological activators of AMPK. Many such activators have been described, and the various mechanisms by which these activate AMPK will be discussed. A particularly large class of AMPK activators are natural products of plants derived from traditional herbal medicines. While the mechanism by which most of these activate AMPK has not yet been addressed, I will argue that many of them may be defensive compounds produced by plants to deter infection by pathogens or grazing by insects or herbivores, and that many of them will turn out to be inhibitors of mitochondrial function