Miracle-dz/UniFAR-FTUs huggingface dataset:
Comprehensive electrochemical imaging with local redox cycling-based electrochemical chip device for evaluation of three-dimensional culture cells

In this study, we have developed a novel electrochemical detection system containing many electrochemical sensors. The detection system is based on local redox cycling to incorporate many electrochemical sensors into small chip device. The density of the electrochemical sensors is the highest in the field of the electrochemical lab-on-a-chip devices. By using the chip device, comprehensive electrochemical imaging can be achieved. In this study, the chip device was applied for cell analysis of three-dimensional culture cells.
Postsynaptic muscarinic m2 receptors at cholinergic and glutamatergic synapses of mouse brainstem motoneurons

In many brain areas, few cholinergic synapses are identified. Acetylcholine is released into the extracellular space and acts through diffuse transmission. Motoneurons, however, are contacted by numerous cholinergic terminals, indicating synaptic cholinergic transmission on them. The muscarinic m2 receptor is the major acetylcholine receptor subtype of motoneurons; therefore, we analyzed the localization of the m2 receptor in correlation with synapses by electron microscopic immunohistochemistry in the mouse trigeminal, facial, and hypoglossal motor nuclei. In all nuclei, m2 receptors were localized at the membrane of motoneuronal perikarya and dendrites. The m2 receptors were concentrated at cholinergic synapses located on the perikarya and most proximal dendrites. However, m2 receptors at cholinergic synapses represented only a minority (<10%) of surface m2 receptors. The m2 receptors were also enriched at glutamatergic synapses in both motoneuronal perikarya and dendrites. A relatively large proportion (20–30%) of plasma membrane–associated m2 receptors were located at glutamatergic synapses. In conclusion, the effect of acetylcholine on motoneuron populations might be mediated through a synaptic as well as diffuse type of transmission. J. Comp. Neurol. 521:2008–2024, 2013. © 2012 Wiley Periodicals, Inc.
Prioritized energy optimal management for home-to-home in smart grid

This paper proposes a prioritized energy optimal management for home-to-home in smart grid. As this proposed mechanism configures the prioritized optimal energy, if there is a surplus of energy from the energy provider of home, the energy broker in smart grid distributes the optimal energy to the requesting user for the purpose of maximizing the user's payoff.
Testing Stenting and Flow Diversion Using a Surgical Elastase-Induced Complex Fusiform Aneurysm Model

BACKGROUND AND PURPOSE: Rabbit elastase-induced saccular aneurysms have been commonly used for preclinical testing of endovascular devices, including flow diverters. However, all tested devices have been shown to be capable of aneurysm occlusion with this model. We aimed to create a more challenging model to test and discriminate among neurovascular devices of varying efficacies. MATERIALS AND METHODS: With a surgical approach that included elastase infusion and balloon dilation, we attempted the creation of complex fusiform aneurysms in 16 rabbits, with standard saccular carotid aneurysms created in 15 other animals. Aneurysms were randomly allocated to one of the following treatments: flow diversion (n = 8), high-porosity stent (n = 6), double high-porosity stent (n = 5), and control (n = 6). Angiographic assessment and pathologic analyses were performed at 3 months. RESULTS: Creation of complex fusiform and standard saccular aneurysms was successful in 12/16 and 13/15 attempts, respectively. All saccular (n = 4) or complex fusiform (n = 4) aneurysms treated with flow diverters were successfully occluded. Three of 3 saccular compared with 0/2 complex fusiform aneurysms were occluded by double high-porosity stents. One of 3 saccular and 0/3 complex fusiform aneurysms were occluded by a single high-porosity stent. Both aneurysm types shared the same pathologic findings when untreated: The aneurysm wall lacked an elastic layer and smooth muscle cells, while the lumen was lined with neointima of varying thickness. Neointimal coverage of the devices was complete when aneurysms were occluded, while leaks were always associated with aneurysm remnants. CONCLUSIONS: Challenging fusiform aneurysms can be created in rabbits by using a surgical modification of the elastase method.
Late Archean rise of aerobic microbial ecosystems

We report the 13C content of preserved organic carbon for a 150 million-year section of late Archean shallow and deepwater sediments of the Hamersley Province in Western Australia. We find a 13C enrichment of ≈10‰ in organic carbon of post-2.7-billion-year-old shallow-water carbonate rocks relative to deepwater sediments. The shallow-water organic-carbon 13C content has a 29‰ range in values (−57 to −28‰), and it contrasts with the less variable but strongly 13C-depleted (−40 to −45‰) organic carbon in deepwater sediments. The 13C enrichment likely represents microbial habitats not as strongly influenced by assimilation of methane or other 13C-depleted substrates. We propose that continued oxidation of shallow settings favored the expansion of aerobic ecosystems and respiring organisms, and, as a result, isotopic signatures of preserved organic carbon in shallow settings approached that of photosynthetic biomass. Facies analysis of published carbon-isotopic records indicates that the Hamersley shallow-water signal may be representative of a late Archean global signature and that it preceded a similar, but delayed, 13C enrichment of deepwater deposits. The data suggest that a global-scale expansion of oxygenated habitats accompanied the progression away from anaerobic ecosystems toward respiring microbial communities fueled by oxygenic photosynthesis before the oxygenation of the atmosphere after 2.45 billion years ago.
Label information-based weighted regularized sparsity preserving embedding for face recognition

Graph learning framework has become a popular method of dimensional reduction. However, the traditional graph construction heavily relies on the selection of parameters, resulting in unstable performance in real-world face recognition applications. To address this, a label information-based weighted regularized sparsity preserving embedding for face recognition is proposed in this paper. Different from the existing L1-graph, we adaptively construct both intrinsic graph and penalty graph with label information-based L1-graph in the graph embedding framework. In order to preserve the local structure, Gaussian kernel distances between the samples are used as weight matrix to weight graph. In addition, the problem of irreversible matrix is alleviated by regularization instead of PCA that loses some discrimination information. At last, an objective function combining globality and locality is created to reduce dimensionality. Meanwhile, Schmidt orthogonalization is used to obtain the orthogonal basis vectors. The experimental results on public face database illustrate that the proposed algorithm has high recognition rate.
The Ratio of Messenger RNA Levels of Receptor Activator of Nuclear Factor κB Ligand to Osteoprotegerin Correlates with Bone Remodeling Indices in Normal Human Cancellous Bone but Not in Osteoarthritis

The determinants of cancellous bone turnover and trabecular structure are not understood in normal bone or skeletal disease. Bone remodeling is initiated by osteoclastic resorption followed by osteoblastic formation of new bone. Receptor activator of nuclear factor κB ligand (RANKL) is a newly described regulator of osteoclast formation and function, the activity of which appears to be a balance between interaction with its receptor RANK and with an antagonist binding protein osteoprotegerin (OPG). Therefore, we have examined the relationship between the expression of RANKL, RANK, and OPG and indices of bone structure and turnover in human cancellous bone from the proximal femur. Bone samples were obtained from individuals with osteoarthritis (OA) at joint replacement surgery and from autopsy controls. Histomorphometric analysis of these samples showed that eroded surface (ES/BS) and osteoid surface (OS/BS) were positively associated in both control (p < 0.001) and OA (p < 0.02), indicating that the processes of bone resorption and bone formation remain coupled in OA, as they are in controls. RANKL, OPG, and RANK messenger RNA (mRNA) were abundant in human cancellous bone, with significant differences between control and OA individuals. In coplotting the molecular and histomorphometric data, strong associations were found between the ratio of RANKL/OPG mRNA and the indices of bone turnover (RANKL/OPG vs. ES/BS: r = 0.93, p < 0.001; RANKL/OPG vs. OS/BS: r = 0.80, p < 0.001). These relationships were not evident in trabecular bone from severe OA, suggesting that bone turnover may be regulated differently in this disease. We propose that the effective concentration of RANKL is related causally to bone turnover.
Accumulation of Myeloperoxidase-Positive Neutrophils in Atherosclerotic Lesions in LDLR−/− Mice

Objective—Atherosclerosis is a chronic inflammatory disease in which the immune system plays an important role. Neutrophils have not been thoroughly studied in the context of atherogenesis. Here, we investigated neutrophils in the development of murine atherosclerotic lesions. Methods and Results—LDLR−/− mice were given a high-fat diet for different time periods and subsequently atherosclerotic lesions were studied by immunohistochemistry. Staining with anti–Ly-6G monoclonal antibody, a specific marker for neutrophils, revealed a marked accumulation of neutrophils during atherosclerosis development. Neutrophils were observed in the lesion, attached to the cap, and in the arterial adventitia. In addition, at some sites, neutrophil accumulation colocalized with endothelial E-selectin expression. Immunofluorescence double staining with anti-myeloperoxidase and anti–Ly-6G antibodies demonstrated the presence of myeloperoxidase in atherosclerotic lesions and its colocalization with neutrophils. After introducing the high-fat diet, levels of circulating myeloperoxidase in plasma strongly increased, with a peak at 6 weeks and a subsequent decrease to almost normal levels after 16 weeks of diet. Conclusions—We here demonstrate for the first time the presence of neutrophils and myeloperoxidase in murine atherosclerotic lesions. As a major cell type in inflammatory responses the neutrophil may also be an important mediator in the development of atherosclerosis.
Hepatitis C virus genotypes: An investigation of type‐specific differences in geographic origin and disease

Because of the nucleotide sequence diversity of different isolates of hepatitis C virus, it has become important to clarify whether distinct genotypes of hepatitis C virus vary with respect to pathogenicity, infectivity, response to antiviral therapy and geographic clustering. We assessed nucleotide sequence variability in the 5′ noncoding region of hepatitis C virus, using restriction enzymes to analyze the distribution of hepatitis C virus genotypes, in 80 patients with chronic hepatitis C virus infection. Genotypes were correlated with demographic, clinical and histological features. Thirty‐seven patients were infected with type 1, 10 had type 2 and 8 had type 3, and another 23 were infected with a new distinct hepatitis C virus type now classified as type 4. Two were infected with variants whose classification are uncertain. Types 1, 2 and 3 were found in patients from the United Kingdom, southern Europe, Asia, Africa and South America. Nineteen of 23 type 4 genotype isolates were from Middle Eastern patients, compared with 0 of 37 type 1 isolates (p < 0.001). Of 21 Middle Eastern patients, 19 (90.4) had type 4 hepatitis C virus (p = 0.001, odds ratio = 9). We found no significant difference between the mean ages or mean serum aminotransferase concentrations between the various types. Types 1,2,3 and 4 were found in patients with mild‐to‐moderate disease or severe disease. However, 21 of 29 (72.4) patients with type 1 who underwent liver biopsy had severe chronic hepatitis, cirrhosis or hepatocellular carcinoma histologically; 8 had mild or moderate chronic hepatitis without cirrhosis (p = 0.03, odds ratio = 2.6). Poor response to interferon‐α was noted in patients with type 1 disease. Our data suggest significant geographic clustering of type 4 disease in the Middle East area. Although different hepatitis C virus genotypes can be encountered in both mild and severe disease, type 1 hepatitis C virus may have important clinical implications. The prognostic importance of these genotypes will require prolonged follow‐up studies. (Hepatology 1994;19:13–18).
Assay for IkappaB kinases using an in vivo biotinylated IkappaB protein substrate.

IkappaB kinases (IKK)-1 and -2 are related kinases that are induced by stimuli such as TNF or IL-1 to phosphorylate serines 32 and 36 of IkappaBalpha, the regulatory subunit of the transcription factor NF-kappaB. A procedure for an IKK protein kinase assay is described that uses an in vivo biotinylated IkappaB protein substrate, [gamma-(33)P]ATP, and capture onto a streptavidin membrane. Residues 1-54 of the IkappaBalpha substrate were expressed as a fusion with glutathione S-transferase (GST) and a short (22 amino acid) biotinylation sequence that allowed modification during bacterial expression. Using the streptavidin capture assay the phosphorylation activities of recombinant IKK-1 and -2 were characterized. The assay provided a convenient way to compare IKK protein and peptide substrate preferences; biotinylated GST-IkappaBalpha(1-54) was more readily phosphorylated by both IKK-1 and IKK-2 compared to biotinylated myelin basic protein or a 20-mer biotinylated peptide containing serines 32 and 36 of IkappaBalpha. IKK-1 had 83-fold less activity than IKK-2, and the IKK-1+2 complex had approximately 2-fold more activity than IKK-2. IKK-1+2 and IKK-2 had similar K(m) values for ATP and GST-biotin-IkappaB(1-54) and were similarly inhibited by staurosporine and two of its analogues K252a and K252b, suggesting that most of the IkappaBalpha kinase activity in the IKK-1+2 complex may be attributed to IKK-2. Several features of the assay including the broad linear binding range of the streptavidin membranes for the protein substrate GST-biotin-IkappaB(1-54) (1-4000 pmol of protein/cm(2)), the low background, and its capacity for both biotinylated peptides and proteins make it a useful tool for quantitating IKK activity. These factors and the ease of expressing in vivo biotinylated GST fusions will make this assay approach suitable for a wide variety of protein kinases.
Immunogenicity of genetically engineered glutathione S-transferase fusion proteins containing a T-cell epitope from diphtheria toxin

Glutathione S-transferase (GST) has been shown to induce a marginal antibody response in experimental animals as well as partial protection against a number of parasitic worms, including Schistosoma and Fasciola species. The objective of our study was to increase the immunogenicity of GST by adding heterologous T-cell epitopes at the carboxy terminus of the protein. We generated recombinant GST proteins by attaching one or three tandem repeats of a T-cell epitope of CRM197, a nontoxic variant of diphtheria toxin. This T-cell epitope encoding the region of amino acids 366 to 383 of CRM197, when contained in a GST fusion protein and/or after purification as a recombinant peptide, retained the ability to induce a CRM197-specific T-cell response. The fusion protein containing a single T-cell epitope induced a strong T-cell proliferative response to GST and also enhanced anti-GST antibody production in mice. The addition of three repeats of the epitope did not augment the responses when compared with the responses of GST itself. The results suggest that the addition of a single T-cell epitope to a larger protein like GST increases the immunogenicity of the protein.
Dependence of the hazard of AIDS on markers

Objective:To investigate the dependence of the hazard of symptomatic AIDS on various markers using a non-parametric method. The markers we consider are measures of time (time since infection and calendar date), measures of immune function (numbers and percentage of CD4 T cells) and serological activation markers (neopterin and β2-microglobulin). Methods:We adapted a non-parametric statistical method to estimate the hazard of AIDS. We considered both univariate analyses, in which each marker was considered separately and bivariate analyses of pairs of markers. Conclusions:Using data from 356 seroconverters from the Multicenter AIDS Cohort Study, we found that in the univariate analyses the hazard of AIDS is dependent on all markers, with the strongest dependence for CD4 count and CD4 percentage. In the bivariate analyses we found that the time since infection is of little importance in determining the hazard of AIDS if the CD4 count or percentage are known, and is of minor additional value if one of the serological markers is known. In contrast, we found that both β2-microglobulin and neopterin do add some additional information to the hazard of AIDS if CD4 count or CD4 percentage are known.
Interleukin‐6 dependence of advanced malignant plasma cell dyscrasias

The authors, and others, clearly have established that interleukin‐6 (IL‐6) is the major growth factor for human myeloma cells in vitro. It is a critical conceptual point whether or not IL‐6 remains involved in the final phases of disease progression in malignant plasma cell dyscrasias. To answer this question, the authors evaluated the in vitro IL‐6 dependence of the proliferation of myeloma cells from the bone marrow of 13 patients with advanced multiple myeloma (MM) and from the peripheral blood of 13 patients with plasma cell leukemia (seven primary and six secondary cases). Their results show that myeloma cell growth was totally dependent on IL‐6 in 25 of 26 patients. Myeloma cells of only one patient did not respond to IL‐6 in vitro. Actually, the cells from this patient were not proliferating in vivo. Identical patterns of IL‐6 dependence of myeloma cells were found in the peripheral blood and bone marrow from four patients with PCL. The authors conclude that, in the terminal phase of malignant plasma cell dyscrasias, tumoral growth is totally dependent on IL‐6 in vitro. This observation is critical in considering the investigation of anti‐IL‐6 therapy in patients with advanced MM. Cancer 1992; 69:1373‐1376.
Salmonella Pathogenicity Island 2-Dependent Expression of Suppressor of Cytokine Signaling 3 in Macrophages

ABSTRACT Salmonella pathogenicity island 2 (SPI-2), which is located at centisome 30.7 on the chromosome of Salmonella enterica serovar Typhimurium, is required for growth within macrophages and systemic infection in mice. We recently reported that the infection of macrophages with Salmonella induces the expression of cyclooxygenase-2 in a manner dependent on SPI-2 (K. Uchiya and T. Nikai, Infect. Immun. 72:6860-6869, 2004). In the present study, gene expression analysis using a cDNA array further showed the involvement of SPI-2 in the expression of suppressor of cytokine signaling 3 (SOCS-3), which is involved in the inhibition of cytokine signaling via the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. A high level of SOCS-3 expression was induced in J774 macrophages infected with wild-type Salmonella compared to that in macrophages infected with a strain carrying a mutation in the spiC gene within SPI-2. Other members of the SOCS family were not detected in Salmonella-infected macrophages. The SPI-2-induced up-regulation of SOCS-3 expression was dependent on activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Furthermore, the inhibition of gamma-interferon-induced STAT-1 and interleukin-6-induced STAT-3 tyrosine phosphorylation correlated with the expression of SOCS-3. Taken together, these results indicate that Salmonella causes SPI-2-dependent activation of ERK1/2, leading to SOCS-3 expression, which in turn inhibits cytokine signaling via the JAK/STAT pathway.
Unity power factor control of hybrid excited axial field flux-switching permanent magnet machine

Hybrid excited axial field flux-switching permanent magnet (AFFSPM) (HEAFFSPM) machine is a novel stator-excitation hybrid excited synchronous machine, which combines the advantages of AFFSPM machine and wound-field excitation machine. In this paper, the structure feature of HEAFFSPM machine is analyzed, and the mathematical model is established. In order to improve the power factor of drive system for the HEAFFSPM machine and make full use of the inverter capability, a kind of unity power factor (UPF) control method is proposed, and the operating performance of HEAFFSPM machine is investigated. The validity of the proposed control method is verified by the simulation and experimental research. The results indicate the UPF can be achieved at different speed and load while the constant torque region is extended by using the UPF control method compared with the zero d-axis current control.
Genomic imbalances in human lung adenocarcinomas and squamous cell carcinomas

Comparative genomic hybridization analysis was performed on 67 non‐small‐cell lung cancers (NSCLCs), including 32 squamous cell carcinomas (SCCs) and 35 adenocarcinomas (ACs), to identify differences in the patterns of genomic imbalance between these two histologic subtypes. Among the entire tumor set, the chromosome arms most often overrepresented were 1q, 3q, 5p, and 8q, each detected in 50–55% of cases. The most frequently underrepresented arms were 9q, 3p, 8p, and 17p. The number of imbalances was similar in SCCs and ACs (median number/case: 12 and 11, respectively). Moreover, many imbalances, such as gains of 1q, 5p, and 8q, occurred at a high frequency in both histologic subgroups. Several statistically significant differences, however, were found. The most prominent difference was gain of 3q24‐qter, seen in 81% of SCCs compared with 31% of ACs (P < 0.0001), with amplification at 3q25‐26 being detected in eight of 32 (25%) SCCs but in only two of 35 (6%) ACs. Gain of 20p13 and loss of 4q also were seen at a significantly higher rate in SCCs than in ACs, whereas overrepresentation of 6p was more common in ACs. Gains of 7q and 8q each were associated with higher‐stage tumors and either positive nodal involvement or higher tumor grade. These data suggest that genes located in several chromosomal regions, particularly 3q25‐26, may be associated with phenotypic properties that differentiate lung SCCs from ACs. Furthermore, certain imbalances, prominent among them gains of 7q and 8q, may be indicative of tumor aggressiveness in NSCLCs. © 2001 Wiley‐Liss, Inc.