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Adversarial examples are artificially crafted to mislead deep learning systems into making wrong decisions. In the research of attack algorithms against multi-class image classifiers, an improved strategy of applying category explanation to the generation control of targeted adversarial example is proposed to reduce the perturbation noise and improve the adversarial robustness. On the basis of C&W adversarial attack algorithm, the method uses Grad-Cam, a category visualization explanation algorithm of CNN, to dynamically obtain the salient regions according to the signal features of source and target categories during the iterative generation process. The adversarial example of non-global perturbation is finally achieved by gradually shielding the non-salient regions and fine-tuning the perturbation signals. Compared with other similar algorithms under the same conditions, the method enhances the effects of the original image category signal on the perturbation position. And it makes up for the shortcomings of the adversarial example algorithm in terms of interpretability and teaching intuitiveness. Experimental results show that the improved adversarial examples have higher PSNR. In addition, in a variety of different defense processing tests, the examples can keep high adversarial performance and show strong attacking robustness. [ABSTRACT FROM AUTHOR]

The virtual teaching and research platform is a cognitive and practical activity for relevant teachers engaged in education and teaching research to improve and improve the quality of education and teaching, relying on the unique functions and resource advantages of the network, using information technology and various network tools to carry out teaching, feedback, etc., and to carry out education and teaching exchange, discussion and other education and teaching research with other administrative organizations or teachers in space regions. It can break the constraints of time, space, organization and other factors. It is an effective form of educational and teaching activities carried out for common goals. It integrates teaching, guidance, discussion, exchange, resource sharing and other functions, and is an important part of the "double training plan". The collaborative innovation ability training mode selection of virtual teaching and research platforms as a multi-attribute group decision making (MAGDM) problem. In this paper, the Evaluation Based on Distance from Average Solution (EDAS) method is extended to the single-valued neutrosophic sets (SVNSs) and single-valued neutrosophic EDAS method (SVN-EDAS) is proposed to solve MAGDM problem. Finally, the collaborative innovation ability training mode selection of virtual teaching and research platforms is given to show the SVN-EDAS model and some comparative analysis is conduct to depict the advantages of SVN-EDAS. [ABSTRACT FROM AUTHOR]

(J) ChIP-qPCR assay in 293T cells that ectopically overexpress Flag-tagged HMGA1-WT or HMGA1-S3A, and with siSP1 in these Flag-HMGA1 expressing cells. (B) Western blotting for pan-phospho-serine levels in 293T cells transduced with MOCK, Flag-tagged HMGA1-WT, HMGA1-S99A, HMGA1-S102A, HMGA1-S103A or HMGA1-S3A. ChIP analysis using anti-flag antibodies or control normal mouse IgG was performed in four groups: HMGA1-WT/siCtrl, HMGA1-WT/siSP1, HMGA1-S3A/siCtrl and HMGA1-S3A/siSP1. [Extracted from the article]

Adversarial examples have begun to receive widespread attention owning to their potential destructions to the most popular DNNs. They are crafted from original images by embedding well-calculated perturbations. In some cases, the perturbations are so slight that neither human eyes nor detection algorithms can notice them, and this imperceptibility makes them more covert and dangerous. For the sake of investigating the invisible dangers in the applications of traffic DNNs, we focus on imperceptible adversarial attacks on different traffic vision tasks, including traffic sign classification, lane detection and street scene recognition. We propose a universal logits map-based attack architecture against image semantic segmentation and design two targeted attack approaches on it. All the attack algorithms generate the micro-noise adversarial examples by the iterative method of C&W optimization and achieve 100% attack rate with very low distortion, among which, our experimental results indicate that the MAE (mean absolute error) of perturbation noise based on traffic sign classifier attack is as low as 0.562, and the other two algorithms based on semantic segmentation are only 1.503 and 1.574. We believe that our research on imperceptible adversarial attacks has a certain reference value to the security of DNNs applications. [ABSTRACT FROM AUTHOR]

By incorporating the interface energy effect into a classical micromechanics framework, effective elastic moduli of a composite material containing randomly distributed nanosized prolate spheroidal inhomogeneities are investigated in this paper. The effect of interface energy, which is usually neglected in classical micromechanics theories, becomes important when the size of the reinforcement phase in the composite enters the nanometer range. The interface energy effect is simulated by inducing interface stress on the zero-thickness membrane interface between the matrix and the inhomogeneities. The interfacial stress discontinuity equations are formulated in accordance with the equilibrium conditions on the idealized interface, from which the interfacial strain discontinuity is solved. Subsequently, the effective elastic moduli are derived based on the classical micromechanics homogenization approaches. Comparisons are made of the effective moduli under the current nanomechanical framework and under classical micromechanical theory. The effective moduli are shown to be dependent upon the size of the inhomogeneities and the interface properties when the interface energy effect is considered. [ABSTRACT FROM AUTHOR]

Mammalian target of rapamycin complex 1 (mTORC1) plays important roles in regulating cell growth and proliferation, and the aberrant activation of mTORC1 has been observed in many human diseases. However, the proteins regulated by mTORC1 activation and their roles in mTORC1 downstream functions are still poorly understood. Using proteomic analysis, we found that proteins regulated by mTORC1 in MEFs could be categorized into eight functional groups including protein nuclear import and glycolysis. The positive regulation of Karyopherin subunit alpha-2 (KPNA2), an importer protein involved in protein nuclear import, by mTORC1 was verified in several other mouse and human cell lines. The regulation occurred at the transcriptional level, rather than at the level of S6K1- and 4E-BP1-dependent protein synthesis. KPNA2 knockdown partially blocked upregulation of glycolytic genes by mTORC1 activation, indicating that mTORC1 activation enhanced expression of glycolytic genes by increasing KPNA2 abundances. Furthermore, KPNA2 knockdown had no effects on the expression and subcellular localization of HIF1α, a transcription factor involved in regulating glycolytic genes downstream of mTORC1. In conclusion, our results proved that KPNA2 regulated the expression of glycolytic genes downstream of mTORC1 in a HIF1α-independent manner. Significance Identifying mTORC1-regulated proteins through proteomic method is a feasible way to study the downstream functions of mTORC1. In this study, we identified many mTORC1-regulated proteins using proteomic analysis by overlapping two different high vs low/no mTORC1 activity comparisons, TSC2 −/− vs WT MEFs and TSC2 −/− with/without rapamycin treatment. We found the abundances of many enzymes in glycolysis pathway and several proteins involved in protein nuclear import were positively regulated by mTORC1. More importantly, we first discovered that mTORC1 positively regulated the importer protein KPNA2, which participated in glycolysis regulation downstream of mTORC1 in a HIF1α-independent manner, indicating that mTORC1 regulates glycolysis through multiple ways. [ABSTRACT FROM AUTHOR]

Lycium barbarum has been used as a traditional Chinese medicine to nourish liver, kidneys and the eyes. However, the underlying mechanisms of its hepatic-protective properties remain uncertain. In this study, we aimed to investigate whether thioredoxin-interacting protein (TXNIP) and NOD-like receptor 3 (NLRP3) inflammasome mediated the attenuation of ethanol-induced hepatic injury by Lycium barbarum polysaccharide (LBP). Rat normal hepatocyte line BRL-3A was pre-treated with LBP prior to ethanol incubation. Hepatic damages, including apoptosis, inflammation, and oxidative stress, were measured. Then the inhibition of endogenous TXNIP expression was achieved by using its specific siRNA to test its possible involvement in the injury attenuation. We found that 50 μg/ml LBP pre-treatment significantly alleviated 24-h ethanol exposure-induced overexpression of TXNIP, increased cellular apoptosis, secretion of inflammatory cytokines, activation of NLRP3 inflammasome, production of ROS, and reduced antioxidant enzyme expression. Silence of TXNIP suppressed the activated NLRP3 inflammasome, increased oxidative stress and worsened apoptosis in the cells. Further addition of LBP did not influence the effects of TXNIP inhibition on the cells. In conclusion, inhibition of hepatic TXNIP by LBP contributes to the reduction of cellular apoptosis, oxidative stress and NLRP3 inflammasome-mediated inflammation. [ABSTRACT FROM AUTHOR]

• The interface energy effect is considered to predict the elastoplastic properties of nanocomposites. • Randomly located and randomly oriented spheroidal particles in the nanocomposites are investigated. • The orientational averaging procedures are applied to evaluate the effect of the particle orientations. • The interface elasticity and interface residual stress are studied simultaneously in considering the interface energy effect. • Effective secant moduli are demonstrated to be dependent on the particle size and the interface residual stress. A nanomechanical framework is proposed to predict the effective elastoplastic behavior of the metal matrix nanocomposites (MMNCs) containing randomly distributed and randomly oriented spheroidal particles. The interface energy effect is investigated by considering both of the interface elastic stress and the interface residual stress on the idealized zero-thickness membrane interphase between the matrix and the inhomogeneities. The orientational average is performed to obtain the effective constitutive relations of the MMNCs with randomly oriented spheroidal particles. By employing the micromechanical homogenization approaches, an effective yield criterion is formulated, and the effective secant moduli of the MMNCs are derived. Comparisons are made between the present framework and the classical micromechanics theory. The interface energy effect on the effective secant moduli are discussed, and the particle size dependence of the effective secant moduli is revealed. Furthermore, the effects of the interface elastic stress and the interface residual stress on the plastic yielding of the nanocomposites are discussed. Lastly, the theoretical predictions obtained by the present framework are compared with the relevant experiments and numerical simulations. [ABSTRACT FROM AUTHOR]

Today, with the rapid development of science and technology, the era of big data has been proposed and triggered reforms in all walks of life. Face recognition is a biometric recognition method with the characteristics of non-contact, non mandatory, friendly and harmonious, which has a good application prospect in the fields of national security and social security. With the deepening of the research on face recognition, small-scale face recognition has achieved good recognition results, but in the era of big data, the existing small-scale face recognition methods have gradually failed to meet the social needs, and how to get a good face recognition effect in the era of big data has become a new research hotspot. Based on this, this paper aims to optimize the existing face recognition algorithm, study the face recognition method driven by big data, and propose a deep learning multi feature fusion face recognition algorithm driven by big data. First, for the problem that 2DPCA (Two-dimensional Principle Component Analysis) can well extract the global features of the face under large samples, but the local features of the face are difficult to process, this paper uses the LBP (Local Binary Pattern, LBP) algorithm to extract the texture features of the face, and the extracted texture features are integrated with the global features extracted by 2DPCA to multi-feature fusion, so that the fused features can take into account both global and local features, and have better recognition results. Then using the obtained fusion features as input, training in a convolutional neural network, and measuring the similarity based on the feature vectors of the sample set and the training set after the training, can realize multi-feature fusion face recognition. Through the analysis of simulation experiments, it is found that, compared with the use of global features or local features alone, the fusion features obtained by multi-feature fusion of global features extracted by 2DPCA and local features extracted by LBP algorithm have better recognition effect in the big data environment. After convolutional neural network trains and recognizes this feature, a high recognition accuracy rate is obtained, which can show that the face recognition method designed in this paper has good application potential in the era of big data. In the background of big data, the accuracy of face recognition can reach more than 90%, which can meet the needs of society well. • This paper aims to optimize the existing face recognition algorithm. • This paper uses the LBP algorithm to extract the texture features of the face. • This method fuse local & global features of human face in big data background. • The accuracy of face recognition reaches more than 90%. [ABSTRACT FROM AUTHOR]

• our study emphasizes the clinical relevance of QAlb in detecting individuals with an elevated risk of cognitive decline. • heightened BBB permeability could contribute to clinical deterioration and serves as a plausible therapeutic target. • investigations are required to elucidate the underlying mechanisms of BBB permeability elevation and to devise efficient treatment approaches addressing BBB dysfunction in individuals with cognitive impairment. The breakdown of the blood-brain barrier (BBB) is intricately linked to the onset and advancement of cognitive impairment and dementia. This investigation explores the correlation between blood-brain barrier permeability, assessed through the cerebrospinal fluid/serum albumin ratio (QAlb), in a clinical cohort and the evolution of cognitive decline. This prospective observational cohort study included 295 participants. Cognitive decline progression was characterized by an escalation in the overall deterioration scale and/or clinical dementia rating scores. The investigation delves into the correlation between blood-brain barrier permeability and the advancement of cognitive impairment among patients. The APOE 4 allele and diabetes mellitus among individuals exhibited increased BBB permeability (P < 0.05). Moreover, AD patients exhibited the highest QAlb levels, signifying elevated BBB permeability compared to individuals with MCI and SCD (P < 0.05). After mean 17 months following up, 117 patients (51.31 %) were identified as experiencing cognitive decline progression, and we found that only AD diagnosis, CDR, and QAlb (All P < 0.05) were significant predictors of cognitive decline progression. Our study emphasizes the clinical relevance of QAlb in detecting individuals with an elevated risk of cognitive decline. It suggests that heightened BBB permeability could contribute to clinical deterioration and serves as a plausible therapeutic target. [ABSTRACT FROM AUTHOR]

The serine protease inhibitor clade E member 1 (SERPINE1) is a major inhibitor of tissue plasminogen activator and urokinase, and has been implicated in the development and progression of a variety of tumors. In this study, mRNA microarray and TCGA database were used to comprehensively analyze the upregulation of SERPINE1 in gastric cancer (GC) tissues compared with the normal stomach tissues. Kaplan-Meier results confirmed that patients with high SERPINE1 expression exhibited worse overall survival and disease-free survival. In addition, cell proliferation, cell scratches, transwell migration and invasion assay showed that SERPINE1 knockdown inhibited the proliferation, migration and invasion of GC ells. Western blot showed that the expression of VEGF and IL-6 was significantly upregulated after overexpression of SERPINE1. Meanwhile, SERPINE1 was positively correlated with the level of immune infiltration using the online analysis tools TISIDB and TIMER. And SERPINE1 expression increased with the increase of malignancy of GC which were detected by Immunohistochemistry. Finally, tumorigenesis experiments in nude mice further demonstrated that SERPINE1 could promote the occurrence and development of GC, while deletion of SERPINE1 inhibited the progression of GC. In summary, SERPINE1 was highly expressed in GC tissues, and SERPINE1 was helpful for differential diagnosis of pathological grade of gastric mucosal lesions. SERPINE1 might regulate the expression of VEGF and IL-6 through the VEGF signaling pathway and JAK-STAT3 inflammatory signaling pathway, thus ultimately affecting the invasion and migration of GC cells. [ABSTRACT FROM AUTHOR]

The cementitious composites with microencapsulated healing agents have become a class of hotspots in the field of construction materials, and they have very broad application prospects and research values. The in-depth study on multi-scale mechanical behaviors of microencapsulated self-healing cementitious composites is critical to quantitatively account for the mechanical response during the damage-healing process. This paper proposes a three-dimensional evolutionary micromechanical model to quantitatively explain the self-healing effects of microencapsulated healing agents on the damage induced by microcracks. By virtue of the proposed 3 D micromechanical model, the evolutionary domains of microcrack growth (DMG) and corresponding compliances of the initial, extended and repaired phases are obtained. Moreover, the elaborate studies are conducted to inspect the effects of various system parameters involving the healing efficiency, fracture toughness and preloading-induced damage degrees on the compliances and stress-strain relations. The results indicate that relatively significant healing efficiency, preloading-induced damage degree and the fracture toughness of polymerized healing agent with the matrix will lead to a higher compressive strength and stiffness. However, the specimen will break owing to the nucleated microcracks rather than the repaired kinked microcracks. Further, excessive higher values of healing efficiency, preloading-induced damage degree and the fracture toughness of polymerized healing agent with the matrix will not affect the compressive strength of the cementitious composites. Therefore, a stronger matrix is required. To achieve the desired healing effects, the specific parameters of both the matrix and microcapsules should be selected prudently. [ABSTRACT FROM AUTHOR]

Resistance to chemotherapy remains a formidable obstacle in acute myeloid leukemia (AML) therapeutic management, necessitating the exploration of optimal strategies to maximize therapeutic benefits. Venetoclax with 3+7 daunorubicin and cytarabine (DAV regimen) in young adult de novo AML patients is evaluated. 90% of treated patients achieved complete remission, underscoring the potential of this regimen as a compelling therapeutic intervention. To elucidate underlying mechanisms governing response to DAV in AML, quantitative phosphoproteomics to discern distinct molecular signatures characterizing a subset of DAV‐sensitive patients is used. Cluster analysis reveals an enrichment of phosphoproteins implicated in chromatin organization and RNA processing within DAV‐susceptible and DA‐resistant AML patients. Furthermore, kinase activity profiling identifies AURKB as a candidate indicator of DAV regimen efficacy in DA‐resistant AML due to AURKB activation. Intriguingly, AML cells overexpressing AURKB exhibit attenuated MCL‐1 expression, rendering them receptive to DAV treatment and maintaining them resistant to DA treatment. Moreover, the dataset delineates a shared kinase, AKT1, associated with DAV response. Notably, AKT1 inhibition augments the antileukemic efficacy of DAV treatment in AML. Overall, this phosphoproteomic study identifies the role of AURKB as a predictive biomarker for DA, but not DAV, resistance and proposes a promising strategy to counteract therapy resistance in AML. [ABSTRACT FROM AUTHOR]

Nucleophosmin (NPM1) is a widely expressed nucleocytoplasmic shuttling protein with prominent nucleolar localization. It is estimated that 25–35% of adult patients with acute myeloid leukemia (AML) carry NPM1 mutations. The classic NPM1 type A mutation occurs in exon 12, which accounts for 75–80% of adult patients with NPM1-mutated AML. It produces an additional leucine and valine-rich nuclear export signal (NES) at the C-terminus, and causes aberrant cytoplasmic dislocation of NPM1 protein. Notably, emerging evidence indicates that besides the classic type A mutation, rare mutants occurring in other exons may also lead to the imbalance of the nucleocytoplasmic shuttle of NPM1. Identification of novel non-type A mutants is crucial for the diagnosis, prognosis, risk stratification and disease monitoring of potential target populations. Here we reported a novel NPM1 mutation in exon 5 identified from a de novo AML patient. Similar to the classic type A mutation, the exon 5 mutation had the NPM1 mutant bound to exportin-1 and directed the mutant into the cytoplasm by generating an additional NES sequence, resulting in aberrant cytoplasmic dislocation of NPM1 protein, which could be reversed by exportin-1 inhibitor leptomycin B. Our findings strongly support that besides the exon 12 mutation, the exon 5 mutant is another NPM1 "born to be exported" mutant critical for leukemogenesis. Therefore, similar to the classic type A mutation, the identification of our novel NPM1 mutation is beneficial for clinical laboratory diagnosis, genetic risk assessment and MRD monitoring. [ABSTRACT FROM AUTHOR]

Lack of training samples always affects the performance and robustness of face recognition. Generating virtual samples is one of effective methods to expand the training set. When the virtual samples are able to simulate the variations of facial images including variations of illuminations, facial postures and the facial expressions, the robustness will be enhanced and the accuracy will be improved obviously in the face recognition problem. In this paper, an improved linear representation-based classification combined virtual samples (ILRCVS) is proposed. First, we design a new objective function that simultaneously considers the information of the virtual training samples and the virtual test sample. Second, an alternating minimization algorithm is proposed to solve the optimization problem of the objective function. Finally, a new classification criterion combined with the virtual training and test sample is proposed. Experimental results on the Georgia Tech, FERET and Yale B face databases show that the proposed method is more robust than three state-of-the-art face recognition methods, LRC, SRC and CRC. [ABSTRACT FROM AUTHOR]

The epidermal growth factor (EGF) receptor (EGFR) pathway is one of the most dysregulated and extensively investigated signaling pathways in human cancers and plays important roles in the regulation of nuclear functions through both cytoplasmic and nuclear EGFR pathways. However, the current understanding of the nuclear phosphorylation responses to activated EGFR pathways remains limited. In the present study, phosphoproteomics analysis revealed the increased phosphorylation of 90 nuclear proteins, primarily involved in RNA processing, pre-mRNA splicing and cell cycle regulation, upon EGF stimulation in MDA-MB-468 cells. Cellular splicing assays of the β-globin (HBB) minigene confirmed that EGF induced constitutive pre-mRNA splicing. Further analysis of phosphoproteomics data identified multiple CDK1/2 substrates in pre-mRNA splicing-related proteins, and both CDK1/2 inhibitors and CDK1/2 knockdowns reduced EGF-regulated pre-mRNA splicing. In conclusion, the results of the present study provide evidence that CDK1/2 participate in the regulation of constitutive pre-mRNA splicing by EGF stimulation in MDA-MB-468 cells. Significance In this study, we successfully carried out a survey of nuclear phosphorylation changes in response to EGF stimulation. The results from the functional category analysis and pre-mRNA splicing assay strongly indicated that EGFR activation increased constitutive pre-mRNA splicing in MDA-MB-468 cells, revealing additional role of EGFR on regulation of mRNA maturation beyond alternative pre-mRNA splicing reported by previous studies. Furthermore, we found that CDK1/2 participated in constitutive pre-mRNA splicing regulation by EGF in MDA-MB-468 cells. Our study provides new knowledge for understanding the regulation of constitutive pre-mRNA splicing by EGF stimulation. [ABSTRACT FROM AUTHOR]

Oxidative stress is thought to contribute to cancer development. Epstein–Barr virus (EBV) and its encoded oncoprotein, latent membrane protein 1 (LMP1), are closely associated with the transformation of nasopharyngeal carcinoma (NPC) and Burkitt’s lymphoma (BL). In this study, we used LMP1-transformed NP cells and EBV-related malignant cell lines to assess the effects of LMP1 on reactive oxygen species (ROS) accumulation and glycolytic activity. Using NPC tissue samples and a tissue array to address clinical implications, we report that LMP1 activates NAD(P)H oxidases to generate excessive amount of ROS in EBV-related malignant diseases. By evaluating NAD(P)H oxidase (NOX) subunit expression, we found that the expression of the NAD(P)H oxidase regulatory subunit p22phox was significantly upregulated upon LMP1-induced transformation. Furthermore, this upregulation was mediated by the c-Jun N-terminal kinase (JNK) pathway. In addition, LMP1 markedly stimulated anaerobic glycolytic activity through the PI3K/Akt pathway. Additionally, in both NPC cells and tissue samples, p22phox expression correlated with LMP1 expression. The NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI) also exerted a marked cytotoxic effect in LMP1-transformed and malignant cells, providing a novel strategy for anticancer therapy. [ABSTRACT FROM AUTHOR]

• Ferrostatin-1 prevented Ang II- induced expression of AT1R. • Ferrostatin-1 reduced Ang II- induced IL-6, IL-1β, COX-2, PGE2, and GFAP. • Ferrostatin-1 prevented Ang II- induced oxidative stress and Ferroptosis. • Ferrostatin-1 increased the expression of Nrf2/HO-1. Inflammation and ferroptosis in astrocytes can be induced by external injuries, which results in excessive production of inflammatory factors and further injury on neurons. Alleviating ferroptosis might be an effective way to protect the brain from external injuries. The present study aims to explore the protective effects of Ferrostatin-1 against ferroptosis induced by Angiotensin II and the underlying mechanism. The mouse primary astrocytes were isolated from the cortices of mice. The astrocytes were stimulated using 10 µM angiotensin II in the presence or absence of 1 or 2 μM Ferrostatin-1. The gene expression levels of AT1R, IL-6, IL-1β, COX-2, GFAP, and GPx4 were evaluated using qRT-PCR. Western Blot was used to determine the protein levels of AT1R, COX-2, GFAP, GPx4, Nrf2, and HO-1 and ELISA was used to detect the concentrations of IL-6, IL-1β, and PGE 2. The ROS levels were evaluated using DHE staining and the reduced GSH level was determined using GSH detection kits. The expression levels of AT1R, IL-6, IL-1β, COX-2, and GFAP in the astrocytes were significantly elevated by stimulation with Ang II and greatly suppressed by the introduction of Ferrostatin-1 in a dose-dependent manner. The promoted ROS level and inhibited GSH level in the astrocytes by the stimulation with Ang II were significantly reversed by Ferrostatin-1. Down-regulated GPx4, Nrf2, and HO-1 in the astrocytes induced by Ang II were extremely up-regulated by the treatment of Ferrostatin-1 in a dose-dependent manner. Ferrostatin-1 alleviates angiotensin II (Ang II)- induced inflammation and ferroptosis by suppressing the ROS levels and activating the Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to characterize clinical features, etiologies, and mechanisms of strokes due to bilateral middle cerebellar peduncle infarction (BMCPI). Methods: Cases diagnosed as BMCPI in our hospital were retrieved, and a literature review was performed. Data on clinical features and brain MRI were obtained. Extracranial and intracranial segments of the vertebrobasilar artery were assessed by using digital subtraction angiography, magnetic resonance angiography, or computed tomography angiography. Results: Thirteen cases (11 men and 2 women) of BMCPI were identified. A high-intensity signal of diffusion-weighted imaging sequence involving the bilateral middle cerebellar peduncle was observed in all patients. Most patients experienced vertigo, dysarthria, ataxia, and hearing disorders. Eleven of these cases were classified as large artery atherosclerosis, one as traumatic vertebral artery (VA) dissection, and one as giant cell arteritis. Conclusion: BMCPI is a rare cerebrovascular disease characterized by vertigo, ataxia, and dysarthria, which may also be accompanied by a hearing deficit or clinical signs of brainstem damage. BMCPI may be associated with hypoperfusion secondary to occlusive disease of the bilateral VA or proximal basilar artery. [ABSTRACT FROM AUTHOR]

Isolated bilateral cerebral peduncular infarctions (BCPI) presenting as acute pseudobulbar palsy are rarely reported and, to the best of our knowledge, most of the previous reports of BCPI were related to locked-in syndrome and disturbance of consciousness. Herein, we described a case of a 55-year-old man who presented with acute pseudobulbar palsy and mild tetraparesis, but preserved eye movements, with no consciousness disturbance. DWI revealed an acute infarction involving the central portion of the cerebral peduncle with a characteristic “traditional Chinese eight character” sign. The relationship between the infarcted range in the cerebral peduncle and the clinical manifestation was discussed in our report. [ABSTRACT FROM AUTHOR]

Nasopharyngeal carcinoma (NPC) is an endemic malignant disease of the head and neck region with unique features including striking ethnic and geographic variations as well as multifactorial etiology. Previous studies have demonstrated the anticancer properties of genistein, the major soy isoflavonoid, in several human cancer cells such as breast, prostate, colon, gastric, lung, and hepatoma. However, the action of genistein in NPC cells has not been determined. In this study, we investigated the inhibitory effects of genistein on NPC cells and its possible underlying mechanisms. We found that genistein dose-dependently inhibited the proliferation of human NPC cell line CNE2 cells. DNA flow cytometric analysis revealed that 30 to 120 μM genistein induced dramatic G2/M phase arrest in NPC cells. The mRNA expression levels, as shown by gene expression array and quantitative real-time polymerase chain reaction, and the protein expression levels of the cell cycle regulators p21Cip1 and ATR (Ataxia telangiectasia and Rad3 related) were elevated following genistein treatment. Interestingly, we also observed concomitant induction of p15Ink4b in genistein induced inhibitory effects in NPC cells. Moreover, selective estrogen receptor modulators did not affect genistein induced growth inhibition. These findings provide new insights into the potential intervention of NPC with genistein. [ABSTRACT FROM AUTHOR]

• A 3D micromechanical model for self-healing cementitious composites is established. • The evolutionary domains of microcrack growth (DMG) are obtained. • The evolutionary compliances and constitutive relations are investigated. • The healing effect is demonstrated on the mesoscale under tensile loading. • The effects of various model parameters on self-healing effect are studied. For the past several years, research in the field of self-healing construction materials becomes a hotspot with broad application prospects. This paper mainly focuses on the self-healing cementitious composites with microcapsules. To quantitatively interpret the self-healing effect of micro-encapsulated healing agents on microcrack-induced damage, a three-dimensional evolutionary micromechanical model is established to predict the mechanical response of the cementitious composites with the microcapsules subjected to tensile loading during the damage-healing process. The evolutionary domains of microcrack growth (DMG) and the corresponding compliances at the initial, activated and repaired stages are obtained. On the basis of the proposed 3D micromechanical model of the self-healing cementitious composites with microcapsules, elaborate studies of constitutive relations and compliance are conducted to investigate the effects of various system parameters involving the healing efficiency, fracture toughness and preloading-induced damage degrees on the compliances and stress-strain relations. The results indicate that relatively significant healing efficiency, preloading-induced damage degree and the fracture toughness of polymerized healing agent with the matrix will lead to higher tensile strength and stiffness. However, based on the two different failure modes of self-healing concrete, the excessive values of healing efficiency, preloading-induced damage degree and the fracture toughness of polymerized healing agent with the matrix will not affect the tensile strength of the cementitious composites. For the sake of the desired optimal healing effect, the specific parameters of both the matrix and the microcapsules should be selected carefully. [ABSTRACT FROM AUTHOR]

By using cDNA microarray analysis, we identified cornulin (CRNN) gene was frequently downregulated in esophageal squamous cell carcinoma (ESCC). In the present study, we investigated the role of CRNN in ESCC development. The results showed that CRNN was frequently downregulated in primary ESCCs in both mRNA level (26/56, 46.4%) and protein level (137/249, 55%), which was significantly associated with lymph node metastases (P=0.027), advanced clinical stage (P=0.039), and overall survival rate (P<0.001). Multivariate analysis indicated that the CRNN downregulation was an independent prognostic factor for ESCC. Functional studies with both in vitro and in vivo assays demonstrated that CRNN had strong tumor suppressive ability in ESCC cells. The tumor-suppressive mechanism of CRNN was associated with its role in cell cycle arrest at G1/S checkpoint by upregulating expressions of P21WAF1/CIP1 and Rb. Silencing CRNN expression by RNA interference could effectively inhibit its tumor suppressive effect. In conclusion, our findings demonstrate that CRNN is a tumor suppressor gene that plays a critical tumor suppressive role in ESCC. [ABSTRACT FROM AUTHOR]

Background: We previously found that r-hu-IFNgamma exerts a potent anti-tumor effect on human nasopharyngeal carcinoma xenografts in vivo. Considering the fact that the clinical use of recombinant IFNgamma is limited by its short half-life and systemic side effects, we developed a recombinant adenovirus, Ad-IFNgamma.Methods: Dynamic distribution of the adenovirus vector and expression of IFNgamma were evaluated by Q-PCR and ELISA after intratumoral administration of Ad-IFNgamma into CNE-2 xenografts.Results: Ad-IFNgamma DNA was mainly enriched in tumors where the Ad-IFNgamma DNA was injected (P < 0.05, compared to blood or parenchymal organs), as well as in livers (P < 0.05). Concentrations of Ad-IFNgamma DNA in other organs and blood were very low. Intratumoral Ad-IFNgamma DNA decreased sharply at high concentrations (9 x 10(5) copies/microg tissue DNA), and slowly at lower concentrations (1.7-2.9 x 10(5) copies/microg tissue DNA). IFNgamma was detected in the tumors and parenchymal organs. The concentration of IFNgamma was highest in the tumor (P < 0.05), followed by the liver and kidney (P < 0.05). High-level intratumoral expression of IFNgamma was maintained for at least 7 days, rapidly peaking on day 3 after injection of Ad-IFNgamma DNA.Conclusion: An IFNgamma gene delivered by an adenoviral vector achieved high and consistent intratumoral expression. Disseminated Ad-IFNgamma DNA and the transgene product were mainly enriched in the liver. [ABSTRACT FROM AUTHOR]