Complex Organ Mask Guided Radiology Report Generation

The goal of automatic report generation is to generate a clinically accurate and coherent phrase from a single given X-ray image, which could alleviate the workload of traditional radiology reporting. However, in a real-world scenario, radiologists frequently face the challenge of producing extensive reports derived from numerous medical images, thereby medical report generation from multi-image perspective is needed. In this paper, we propose the Complex Organ Mask Guided (termed as COMG) report generation model, which incorporates masks from multiple organs (e.g., bones, lungs, heart, and mediastinum), to provide more detailed information and guide the model's attention to these crucial body regions. Specifically, we leverage prior knowledge of the disease corresponding to each organ in the fusion process to enhance the disease identification phase during the report generation process. Additionally, cosine similarity loss is introduced as target function to ensure the convergence of cross-modal consistency and facilitate model optimization.Experimental results on two public datasets show that COMG achieves a 11.4% and 9.7% improvement in terms of BLEU@4 scores over the SOTA model KiUT on IU-Xray and MIMIC, respectively. The code is publicly available at https://github.com/GaryGuTC/COMG_model.Comment: 12 pages, 7 images. Accepted by WACV 202

Mechanisms of Volatile Anesthetic-Induced Myocardial Protection

Volatile anesthetics protect myocardium against reversible and irreversible ischemic injury. Experimental evidence from several in vitro and in vivo animal models demonstrates that volatile agents enhance the recovery of stunned myocardium and reduce the size of myocardial infarction after brief or prolonged coronary artery occlusion and reperfusion, respectively. This protective effect persists after the anesthetic has been discontinued, a phenomenon known as anesthetic-induced preconditioning (APC). Recent clinical data also demonstrates evidence of APC in patients during cardiac surgery. Thus, administration of volatile anesthetics may represent a novel therapeutic approach that reduces morbidity and mortality associated with perioperative myocardial ischemia and infarction. The mechanisms responsible for APC appear to be similar to those implicated in ischemic preconditioning, but nonetheless have subtle differences. Accumulating evidence indicates that APC is characterized by complex signal transduction pathways that may include adenosine receptors, G proteins, protein kinase C, reactive oxygen species, and sarcolemmal or mitochondrial KATP channels. Opioid analgesics may further enhance APC as well. This article will review recent advances in the understanding of mechanisms responsible for volatile anesthetic-induced myocardial protection

A Distance-Heuristic Tree Building Approach in Application Layer Multicast

In the application layer multicast (ALM), clustering nearby nodes can effectively improve the multicast performance. However, it is difficult for the ALM solution to quickly and accurately position the newcomer, because group members have no direct knowledge of underlying network topology. Additionally, ALM delivery trees with different performances are built when group members join the group in different join sequences. To alleviate the above problems, this paper proposes a distance-heuristic tree building protocol (called DHTB). DHTB uses our proposed distance-constrained cluster model and close-member-first-receive (CF) rule. In the model, most nearby nodes are grouped into some distance-constrained clusters, with little cluster organization and maintenance overhead. The CF rule arranges or rearranges the locations of group members according to related distances, and effectively positions the newcomer with the help of on-demand landmarks. Both the distance-constrained cluster model and CF rule are distance-heuristic. Therefore DHTB can alleviate the join sequence problem, and build the ALM tree with desirable performance

Scorpion in Combination with Gypsum: Novel Antidiabetic Activities in Streptozotocin-Induced Diabetic Mice by Up-Regulating Pancreatic PPARγ and PDX-1 Expressions

The management of diabetes without any side effects remains a challenge in medicine. In this study, antidiabetic activity and the mechanism of action of scorpion combined with gypsum (SG) were investigated. Streptozotocin-induced diabetic mice were orally administrated with scorpion (200 mg kg−1 per day) in combination with gypsum (200 mg kg−1 per day) for 5 weeks. SG treatment resulted in decreased body weight, blood glucose and lipid levels, and increased serum and pancreatic insulin levels in diabetic mice. Furthermore, SG significantly increased the number and volume of beta cells in the Islets of Langerhans and promoted peroxisome proliferator-activated receptor gamma and pancreatic duodenal homeobox 1 expressions in pancreatic tissues. However, scorpion or gypsum alone had no significant effect in this animal model. Metformin showed a slight or moderate effect in this diabetic model, but this effect was weak compared with that of SG. Taken together, SG showed a new antidiabetic effect in streptozotocin-induced diabetic mice. This effect may possibly be involved in enhancing beta-cell regeneration and promoting insulin secretion by targeting PPARγ and PDX-1. Moreover, this new effect of SG offers a promising step toward the treatment of diabetic patients with beta-cell failure as a complementary and alternative medicine

Id2 promotes the invasive growth of MCF-7 and SKOV-3 cells by a novel mechanism independent of dimerization to basic helix-loop-helix factors

<p>Abstract</p> <p>Background</p> <p>Inhibitor of differentiation 2 (<it>Id2</it>) is a critical factor for cell proliferation and differentiation in normal vertebrate development. Most of the biological function of Id2 has been ascribed to its helix-loop-helix motif. Overexpression of Id2 is frequently observed in various human tumors, but its role for invasion potential in tumor cells is dispute. We aimed to reveal the role of Id2 in invasion potential in poorly invasive and estrogen receptor α (ERα)-positive MCF-7 and SKOV-3 cancer cells.</p> <p>Methods</p> <p>MCF-7 and SKOV-3 cells were stably transfected with the wild-type, degradation-resistant full-length or helix-loop-helix (HLH)-deleted Id2, respectively. Protein levels of Id2 and its mutants and E-cadherin were determined by western blot analysis and mRNA levels of Id2 and its mutants were determined by RT-PCR. The effects of Id2 and its mutants on cell proliferation were determined by [³H]-thymidine incorporation assay and the 3- [4, 5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) dye method. The <it>in vitro </it>invasion potential of cells was evaluated by Transwell assay. Cell motility was assessed by scratch wound assay. The promoter activity of <it>E-cadherin </it>was determined by cotransfection and luciferase assays.</p> <p>Results</p> <p>Ectopic transfection of the wild-type Id2 markedly increased the protein and mRNA expression of <it>Id2 </it>in MCF-7 and SKOV-3 cells; the protein level but not mRNA level was further increased by transfection with the degradation-resistant Id2 form. The ectopic expression of Id2 or its mutants did not alter proliferation of either MCF-7 or SKOV-3 cells. Transfection of the wild-type Id2 significantly induced the invasion potential and migratory capacity of cells, which was further augmented by transfection with the degradation-resistant full-length or HLH-deleted Id2. E-cadherin protein expression and transactivation of the proximal E-cadherin promoter were markedly suppressed by the degradation-resistant full-length or HLH-deleted Id2 but not wild-type Id2. Ectopic expression of E-cadherin in MCF-7 and SKOV-3 cells only partially blunted the invasion potential induced by the degradation-resistant HLH-deleted Id2.</p> <p>Conclusion</p> <p>Overexpression of Id2 in ERα-positive epithelial tumor cells indeed increases the cells' invasive potential through a novel mechanism independent of dimerization to basic helix-loop-helix factors. E-cadherin contributes only in part to Id2-induced cell invasion when Id2 is accumulated to a higher level in some specific cell types.</p