Fault-tolerant analysis of augmented cubes

The augmented cube $AQ_n$, proposed by Choudum and Sunitha [S. A. Choudum, V. Sunitha, Augmented cubes, Networks 40 (2) (2002) 71-84], is a $(2n-1)$-regular $(2n-1)$-connected graph $(n\ge 4)$. This paper determines that the 2-extra connectivity of $AQ_n$ is $6n-17$ for $n\geq 9$ and the 2-extra edge-connectivity is $6n-9$ for $n\geq 4$. That is, for $n\geq 9$ (respectively, $n\geq 4$), at least $6n-17$ vertices (respectively, $6n-9$ edges) of $AQ_n$ have to be removed to get a disconnected graph that contains no isolated vertices and isolated edges. When the augmented cube is used to model the topological structure of a large-scale parallel processing system, these results can provide more accurate measurements for reliability and fault tolerance of the system

Covid-19 Diagnosis Based on CT Images Through Deep Learning and Data Augmentation

Coronavirus disease 2019(Covid-19) has made people around the world suffer. And there are many researchers make efforts on deep learning methods based on CT imgaes, but the limitation of  this work is the lackage of the dataset, which is not easy to obtain. In this study, we try to use data augmentation to compensate this weakness. In the first part, we use traditional DenseNet-169, and the result shows that data augmentation can help improve the calculating speed and the accuracy. In the second part, we combine Self-trans and DenseNet-169, and the result shows that when doing data augmentation, many model performance metrics have been improved. In the third part, we use UNet++, which reaches accuracy of 0.8645. Apart from this, we think GAN and CNN may also make difference

Demethyleneberberine alleviated the inflammatory response by targeting MD-2 to inhibit the TLR4 signaling

IntroductionThe colitis induced by trinitrobenzenesulfonic acid (TNBS) is a chronic and systemic inflammatory disease that leads to intestinal barrier dysfunction and autoimmunedisorders. However, the existing treatments of colitis are associated with poor outcomes, and the current strategies remain deep and long-time remission and the prevention of complications. Recently, demethyleneberberine (DMB) has been reported to be a potential candidate for the treatment of inflammatory response that relied on multiple pharmacological activities, including anti-oxidation and antiinflammation. However, the target and potential mechanism of DMB in inflammatory response have not been fully elucidated.MethodsThis study employed a TNBS-induced colitis model and acute sepsis mice to screen and identify the potential targets and molecular mechanisms of DMB in vitro and in vivo. The purity and structure of DMB were quantitatively analyzed by high-performance liquid chromatography (HPLC), mass spectrometry (MS), Hydrogen nuclear magnetic resonance spectroscopy (1H-NMR), and infrared spectroscopy (IR), respectively. The rats were induced by a rubber hose inserted approximately 8 cm through their anus to be injected with TNBS. Acute sepsis was induced by injection with LPS via the tail vein for 60 h. These animals with inflammation were orally administrated with DMB, berberine (BBR), or curcumin (Curc), respectively. The eukaryotic and prokaryotic expression system of myeloid differentiation protein-2 (MD-2) and its mutants were used to evaluate the target of DMB in inflammatory response.ReslutsDMB had two free phenolic hydroxyl groups, and the purity exceeded 99% in HPLC. DMB alleviated colitis and suppressed the activation of TLR4 signaling in TNBS-induced colitis rats and LPS-induced RAW264.7 cells. DMB significantly blocked TLR4 signaling in both an MyD88-dependent and an MyD88-independent manner by embedding into the hydrophobic pocket of the MD-2 protein with non-covalent bonding to phenylalanine at position 76 in a pi–pi T-shaped interaction. DMB rescued mice from sepsis shock induced by LPS through targeting the TLR4–MD-2 complex.ConclusionTaken together, DMB is a promising inhibitor of the MD-2 protein to suppress the hyperactivated TLR4 signaling in inflammatory response

The Change of Teleost Skin Commensal Microbiota Is Associated With Skin Mucosal Transcriptomic Responses During Parasitic Infection by Ichthyophthirius multifillis

Teleost skin serves as the first line of defense against invading pathogens, and contain a skin-associated lymphoid tissue (SALT) that elicit gut-like immune responses against antigen stimulation. Moreover, exposed to the water environment and the pathogens therein, teleost skin is also known to be colonized by diverse microbial communities. However, little is known about the interactions between microbiota and the teleost skin mucosal immune system, especially dynamic changes about the interactions under pathogen infection. We hypothesized that dramatic changes of microbial communities and strong mucosal immune response would be present in the skin of aquatic vertebrate under parasite infection. To confirm this hypothesis, we construct an infected model with rainbow trout (Oncorhynchus mykiss), which was experimentally challenged by Ichthyophthirius multifiliis (Ich). H & E staining of trout skin indicates the successful invasion of Ich and shows the morphological changes caused by Ich infection. Critically, increased mRNA expression levels of immune-related genes were detected in trout skin from experimental groups using qRT-PCR, which were further studied by RNA-Seq analysis. Here, through transcriptomics, we detected that complement factors, pro-inflammatory cytokines, and antimicrobial genes were strikingly induced in the skin of infected fish. Moreover, high alpha diversity values of microbiota in trout skin from the experimental groups were discovered. Interestingly, we found that Ich infection led to a decreased abundance of skin commensals and increased colonization of opportunistic bacteria through 16S rRNA pyrosequencing, which were mainly characterized by lose of Proteobacteria and increased intensity of Flavobacteriaceae. To our knowledge, our results suggest for the first time that parasitic infection could inhibit symbionts and offer opportunities for other pathogens' secondary infection in teleost skin

MicroRNA-34a Attenuates Paclitaxel Resistance in Prostate Cancer Cells via Direct Suppression of JAG1/Notch1 Axis

Background/Aims: Treatment options for metastatic castrate-resistant prostate cancer (mCRPC) are limited and typically centered on paclitaxel-based chemotherapy. In this study, we aimed to evaluate whether miR-34a attenuates chemoresistance to paclitaxel by regulating target genes associated with drug resistance. Methods: We used data from The Cancer Genome Atlas to compare miR-34a expression levels in prostate cancer (PC) tissues with normal prostate tissues. The effects of miR-34a inhibition and overexpression on PC proliferation were evaluated in vitro via Cell Counting Kit-8 (CCK-8) proliferation, colony formation, apoptosis, and cell-cycle assays. A luciferase reporter assay was employed to identify the interactions between miR-34a and specific target genes. To determine the effects of up-regulation of miR-34a on tumor growth and chemo-resistance in vivo, we injected PC cells overexpressing miR-34a into nude mice subcutaneously and evaluated the rate of tumor growth during paclitaxel treatment. We examined changes in the expression levels of miR-34a target genes JAG1 and Notch1 and their downstream genes via miR-34a transfection by quantitative reverse transcription PCR (qRT-PCR) and western blot assay. Results: miR-34a served as an independent predictor of reduced patient survival. MiR-34a was down-regulated in PC-3PR cells compared with PC-3 cells. The CCK-8 assay showed that miR-34a overexpression resulted in increased sensitivity to paclitaxel while miR-34a down-regulation resulted in chemoresistance to paclitaxel in vitro. A study of gain and loss in a series of functional assays revealed that PC cells expressing miR-34a were chemosensitive. Furthermore, the overexpression of miR-34a increased the sensitivity of PC-3PR cells to chemotherapy in vivo. The luciferase reporter assay confirmed that JAG1 and Notch1 were directly targeted by miR-34a. Interestingly, western blot analysis and qRT-PCR confirmed that miR-34a inhibited the Notch1 signaling pathway. We found that miR-34a increased the chemosensitivity of PC-3PR cells by directly repressing the TCF1/ LEF1 axis. Conclusion: Our results showed that miR-34a is involved in the development of chemosensitivity to paclitaxel. By regulating the JAG1/Notch1 axis, miR-34a or its target genes JAG1 or Notch1 might serve as potential predictive biomarkers of response to paclitaxel-based chemotherapy and/or therapeutic targets that will help to overcome chemoresistance at the mCRPC stage

The Transcription Factor T-Bet Is Required for Optimal Type I Follicular Helper T Cell Maintenance During Acute Viral Infection

Follicular helper T cells (TFH cells), known as the primary “helpers” of the germinal center (GC) reaction, promote the humoral immune response to defend against various pathogens. Under conditions of infection by different types of pathogens, many shared transcription factors (TFs), such as Bcl-6, TCF-1, and Maf, are selectively enriched in pathogen-specific TFH cells, orchestrating TFH cell differentiation and function. In addition, TFH cells also coexpress environmentally associated TFs as their conventional T cell counterparts (such as T-bet, GATA-3, or ROR-γt, which are expressed in Th1, Th2, or Th17 cells, respectively). These features likely indicate both the lineage-specificity and environmental adaption of the TFH cell responses. However, the extent to which the TFH cell response relies on these environmentally specific TFs is not completely understood. Here, we found that T-bet was specifically expressed in Type I TFH cells but not Type II TFH cells. While dispensable for the early fate commitment of TFH cells, T-bet was essential for the maintenance of differentiated TFH cells, promoting their proliferation, and inhibiting their apoptosis during acute viral infection. Microarray analysis showed both similarities and differences in transcriptome dependency on T-bet in TFH and TH1 cells, suggesting the distinctive role of T-bet in TFH cells. Collectively, our findings reveal an important and specific supporting role for T-bet in type I TFH cell response, which can help us gain a deeper understanding of TFH cell subsets

Recent advances on extracellular vesicles in central nervous system diseases

Extracellular vesicles (EVs) are particles released by multiple cells, encapsulated by lipid bilayers and containing a variety of biological materials, including proteins, nucleic acids, lipids and metabolites. With the advancement of separation and characterization methods, EV subtypes and their complex and diverse functions have been recognized. In the central nervous system (CNS), EVs are involved in various physiological and pathological processes, such as regulation of neuronal firing, synaptic plasticity, formation and maintenance of myelin sheath, propagation of neuroinflammation, neuroprotection, and spread and removal of toxic protein aggregates. Activity-dependent alteration of constituents enables EVs to reflect the change of cell and tissue states, and the wide distribution of EVs in biological fluids endows them with potential as diagnostic and prognostic biomarkers for CNS diseases, including neurodegenerative disease, cerebrovascular disease, traumatic brain disease, and brain tumor. Favorable biocompatibility, ability of crossing the blood-brain barrier and protecting contents from degradation, give promising therapeutic effects of EVs, either collected from mesenchymal stem cells culture conditioned media, or designed as drug delivery vehicles loaded with specific agents. In this review, we summarized EVs\u27 basic biological properties, and mainly focused on their applications in CNS diseases

Bending and Crack Evolution Behaviors of Cemented Soil Reinforced with Surface Modified PVA Fiber

To improve the flexural properties of cemented soils reinforced with fibers and avoid their brittle failure when subjected to complex loading conditions, a simple and cost-effective technique was explored to facilitate their application in retaining walls. In this study, how different fiber surface modifications, i.e., alkali treatment, acid treatment and silane coupling agent treatment, as well as different fiber contents, i.e., 0%, 0.25%, 0.5% and 1%, affect the bending properties of cemented soils was investigated by conducting three-point bending tests on notched beams. The digital image correlation (DIC) technology was used to examine the crack propagation process and the strain field distribution of cracks in specimens in the flexural tests. The results show that all fiber surface modifications increased peak strength and fracture energy, for example, the fracture energy of specimens AN1, AH1 and AK1 was increased by 180.4%, 121.5% and 155.4%, respectively, compared to PVA1. In addition, the crack tip strain, crack propagation rate and the initial crack width of the modified specimens were lower than those before modification. Lastly, scanning electron microscope (SEM) and mercury intrusion porosimetry tests were adopted to reveal the mechanism of bending performance in cemented soils reinforced by fiber surface modifications

Fault tolerance of augmented cubes

The augmented cube AQn, proposed by Choudum and Sunitha [S. A. Choudum, V. Sunitha, Augmented cubes, Networks 40 (2) (2002) 71-84], is a (2n − 1)-regular (2n − 1)-connected graph (n ≥ 4). This paper determines that the 2-extra connectivity of AQn is 6n − 17 for n ≥ 9 and the 2-extra edge-connectivity is 6n − 9 for n ≥ 4. That is, for n ≥ 9 (respectively, n ≥ 4), at least 6n − 17 vertices (respectively, 6n − 9 edges) of AQn have to be removed to get a disconnected graph that contains no isolated vertices and isolated edges. When the augmented cube is used to model the topological structure of a large-scale parallel processing system, these results can provide more accurate measurements for reliability and fault tolerance of the system