Implicit government guarantees and bank risk

We develop a model on bank risk and implicit government guarantees. This model concerns the willingness and capacity of implicit government guarantees. Using the Option Pricing Theory, we derive a mathematical formulation of maximizing the bank’s net present value (NPV) with implicit government guarantees. Unlike previous work, both the loan portfolio and the bank’s NPV are regarded as a combination of options underlying the risky project. We conduct comparative static analyses and numerical examples to examine how implicit government guarantees and capital control affect bank risk and its asset scale. The main insight of our analysis is that implicit government guarantees have some unintended consequences: (a) Inefficient and excessive risk taking (including bank’s asset and overall risk); (b) Inefficient investment if there is no binding capacity constraint. We show that it is mainly due to the bank’s excessive reliance on contingent assets. In addition, we demonstrate the ineffectiveness of capital constraint on risk control under certain circumstances. Therefore, we suggest that the gradual withdrawal of implicit government guarantees should be accompanied by multiple combinations of regulatory measures and proper institutional reform to avoid risk surges

The boundedness of commutators of sublinear operators on Herz Triebel-Lizorkin spaces with variable exponent

In this paper, the authors first discuss the characterization of Herz Triebel-Lizorkin spaces with variable exponent via two families of operators. By this characterization, the authors prove that the Lipschitz commutators of sublinear operators is bounded from Herz spaces with variable exponent to Herz Triebel-Lizorkin spaces with variable exponent. As an application, the corresponding boundedness estimates for the commutators of maximal operator, Riesz potential operator and Calder\'on-Zygmund operator are established.Comment: commutator; sublinear operator; Lipschitz spaces; Herz Triebel-Lizorkin spaces; variable exponen

Dual-Crystallizable Silk Fibroin/Poly(L-lactic Acid) Biocomposite Films: Effect of Polymer Phases on Protein Structures in Protein-Polymer Blends

Biopolymer composites based on silk fibroin have shown widespread potential due to their brilliant applications in tissue engineering, medicine and bioelectronics. In our present work, biocomposite nanofilms with different special topologies were obtained through blending silk fibroin with crystallizable poly(L-lactic acid) (PLLA) at various mixture rates using a stirring-reflux condensation blending method. The microstructure, phase components, and miscibility of the blended films were studied through thermal analysis in combination with Fourier-transform infrared spectroscopy and Raman analysis. X-ray diffraction and scanning electron microscope were also used for advanced structural analysis. Furthermore, their conformation transition, interaction mechanism, and thermal stability were also discussed. The results showed that the hydrogen bonds and hydrophobic interactions existed between silk fibroin (SF) and PLLA polymer chains in the blended films. The secondary structures of silk fibroin and phase components of PLLA in composites vary at different ratios of silk to PLLA. The β-sheet content increased with the increase of the silk fibroin content, while the glass transition temperature was raised mainly due to the rigid amorphous phase presence in the blended system. This results in an increase in thermal stability in blended films compared to the pure silk fibroin films. This study provided detailed insights into the influence of synthetic polymer phases (crystalline, rigid amorphous, and mobile amorphous) on protein secondary structures through blending, which has direct applications on the design and fabrication of novel protein–synthetic polymer composites for the biomedical and green chemistry fields

Effects of suppressor of cytokine signaling 3 (SOCS3) on the development of colon cancer via regulation of HIF-1α

Purpose: To investigate the influence of suppressor of cytokine signaling 3 (SOCS3) on rats with colon cancer (CC). Methods: Sprague-Dawley (SD) rats were randomly divided into CC group and control group. CC models were constructed. The expression of SOCS3 in CC tissues was determined by quantitative real time-polymerase chain reaction (qRT-PCR). Hematoxylin-eosin staining (H&E) was used to examine colon tissue morphology, while immunohistochemistry (IHC) staining assay was performed to determine the expression of SOCS3 protein in colon tissues. The content of HIF-1α, phosphorylated phosphatidylinositol 3-hydroxy kinase (p-PI3K), and phosphorylated protein kinase B (p-AKT) proteins was determined by Western blotting (WB). Results: Compared with that in the control group, the number of tumors in the CC group was significantly increased (p < 0.05). Protein and messenger ribonucleic acid (mRNA) expressions of SOCS3 were down-regulated in CC group (p < 0.05), while protein expressions of p-PI3K, p-AKT and HIF-1α were significantly elevated in CC group (p < 0.05). Conclusion: SOCS3 is poorly expressed in CC rats, and promotes the expression of HIF-1α by activating PI3K/AKT signaling pathway. The findings, thus, provide a probable strategy for management of colon cancer

Effects of SOCS3 on the development of colon cancer via regulation of HIF-1α

Purpose: To investigate the influence of suppressor of cytokine signaling 3 (SOCS3) on rats with colon cancer (CC). Methods: Sprague-Dawley (SD) rats were randomly divided into CC group and control group, and then CC rat model was constructed. The expression of SOCS3 in CC tissues was determined by quantitative real time-polymerase chain reaction (qRT-PCR). Hematoxylin-eosin staining (H&E) was used to examine colon tissue morphology. Immunohistochemistry (IHC) staining assay was performed to determine the expression of SOCS3 protein in colon tissues. The contents of HIF-1α, phosphorylated phosphatidylinositol 3-hydroxy kinase (p-PI3K), and phosphorylated protein kinase B (p-AKT) proteins were determined by Western blotting (WB). Results: Compared with that in the control group, the number of tumors in CC group was significantly increased (p < 0.05). 2). On the other hand, protein and message ribonucleic acid (mRNA) expressions of SOCS3 were down-regulated in CC group (p < 0.05). 3), while protein expressions of p-PI3K, p-AKT and HIF-1α were raised in CC group (p < 0.05). Conclusion: SOCS3 is lowly expressed in CC rats, and promotes the expression of HIF-1α by activating PI3K/AKT signaling pathway. Thus, SOCS3 provides a therapeutic strategy for the management of colon cancer. Keywords: Colon cancer; Suppressor of cytokine signaling protein 3 (SOCS3); Hypoxia inducible factor-1

Dynamic Multimodal Information Bottleneck for Multimodality Classification

Effectively leveraging multimodal data such as various images, laboratory tests and clinical information is gaining traction in a variety of AI-based medical diagnosis and prognosis tasks. Most existing multi-modal techniques only focus on enhancing their performance by leveraging the differences or shared features from various modalities and fusing feature across different modalities. These approaches are generally not optimal for clinical settings, which pose the additional challenges of limited training data, as well as being rife with redundant data or noisy modality channels, leading to subpar performance. To address this gap, we study the robustness of existing methods to data redundancy and noise and propose a generalized dynamic multimodal information bottleneck framework for attaining a robust fused feature representation. Specifically, our information bottleneck module serves to filter out the task-irrelevant information and noises in the fused feature, and we further introduce a sufficiency loss to prevent dropping of task-relevant information, thus explicitly preserving the sufficiency of prediction information in the distilled feature. We validate our model on an in-house and a public COVID19 dataset for mortality prediction as well as two public biomedical datasets for diagnostic tasks. Extensive experiments show that our method surpasses the state-of-the-art and is significantly more robust, being the only method to remain performance when large-scale noisy channels exist. Our code is publicly available at https://github.com/ayanglab/DMIB.Comment: WACV 202

Swin transformer for fast MRI

Magnetic resonance imaging (MRI) is an important non-invasive clinical tool that can produce high-resolution and reproducible images. However, a long scanning time is required for high-quality MR images, which leads to exhaustion and discomfort of patients, inducing more artefacts due to voluntary movements of the patients and involuntary physiological movements. To accelerate the scanning process, methods by k-space undersampling and deep learning based reconstruction have been popularised. This work introduced SwinMR, a novel Swin transformer based method for fast MRI reconstruction. The whole network consisted of an input module (IM), a feature extraction module (FEM) and an output module (OM). The IM and OM were 2D convolutional layers and the FEM was composed of a cascaded of residual Swin transformer blocks (RSTBs) and 2D convolutional layers. The RSTB consisted of a series of Swin transformer layers (STLs). The shifted windows multi-head self-attention (W-MSA/SW-MSA) of STL was performed in shifted windows rather than the multi-head self-attention (MSA) of the original transformer in the whole image space. A novel multi-channel loss was proposed by using the sensitivity maps, which was proved to reserve more textures and details. We performed a series of comparative studies and ablation studies in the Calgary-Campinas public brain MR dataset and conducted a downstream segmentation experiment in the Multi-modal Brain Tumour Segmentation Challenge 2017 dataset. The results demonstrate our SwinMR achieved high-quality reconstruction compared with other benchmark methods, and it shows great robustness with different undersampling masks, under noise interruption and on different datasets. The code is publicly available at https://github.com/ayanglab/SwinMR.This work was supported in part by the UK Research and Inno- vation Future Leaders Fellowship [MR/V023799/1], in part by the Medical Research Council [MC/PC/21013], in part by the European Research Council Innovative Medicines Initiative [DRAGON, H2020-JTI-IMI2 101005122], in part by the AI for Health Imaging Award [CHAIMELEON, H2020-SC1-FA-DTS-2019-1 952172], in part by the British Heart Foundation [Project Number: TG/18/5/34111, PG/16/78/32402], in part by the NVIDIA Academic Hardware Grant Program, in part by the Project of Shenzhen International Cooper- ation Foundation [GJHZ20180926165402083], in part by the Bas- que Government through the ELKARTEK funding program [KK- 2020/00049], and in part by the consolidated research group MATHMODE [IT1294-19

MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice

MiR-455 has been verified a key regulator of brown adipose tissue and adipose tissue-specific overexpression of miR-455 (ap2-miR-455) mice could combat high-fat-diet-induced obesity. This study is to verify overexpression of miR-455 could ameliorate the lipid accumulation and metabolism in the liver of db/db diabetic mice and explore the potential mechanisms. Diabetic mice (db/db) and control mice (db/m) were randomly divided into four groups. After overexpression of miR-455 in the liver of db/db mice, the triglycerides level in both serum and liver decreased, the lipid deposit in liver was improved, the expression of fatty acid synthase, stearoyl-CoA desaturase 1, sterol regulatory element binding protein 1c (SREBP-1c) and acetyl-CoA carboxylase (ACCα) was also significantly down-regulated. TargetScan indicated that suppressor of cytokine signalling 3 (SOCS3) is predicated to target miR-455 and the protein of SOCS3 in the liver of db/db mice after intervention was significantly decreased. The dual luciferase reporter assay showed that SOCS3 was target gene of miR-455. In vitro, in Palmitate (PA)-stimulated human normal liver (LO2) cells, transfected miR-455 mimic could significantly inhibit the expression of SOCS3, while transfected miR-455 inhibitor could up-regulate the expression of SOCS3. Transfecting LO2 cells with siRNA of SOCS3 could significantly down-regulate the protein expression of SREBP-1c and ACCα. Our study showed that overexpression of miR-455 in the liver could improve lipid metabolism in diabetic mice by down-regulating its target gene SOCS3