gebhart/patrepeval huggingface dataset:
Cooking procedure recognition and support system by intelligent environments (2009)

In this paper, we propose cooking support system by using ubiquitous sensors. We developed machine learning algorithm that recognizes cooking procedures by taking account of various and numerous sensor information and past human behaviors. In order to provide appropriate instructions to a user, we also developed Markov-model based human behavior prediction algorithm. By employing these algorithms, we developed cooking support system that automatically displays cooking instruction movies according to users progresses. We conducted experiments with subjects and the experimental results confirmed the feasibility of the proposed cooking support system.
Sub-100 nm lithography using ultrashort wavelength of surface plasmons (2004)

The development of a nanolithography technique utilizing ultrashort wavelength of surface plasmons (SPs) is presented in this article. The mask consists of silver thin film perforated with two-dimensional hole arrays exhibiting superior confinement due to SPs with a wavelength equal to 14 of that of the illuminating light (365 nm). This short wavelength of SPs can confine the field on an area much smaller compared to the excitation light wavelength, leading to the higher resolution lithography than conventional photolithography methods. Finite-difference time-domain simulations show significantly enhanced electric field and tight confinement of the near-field profile obtained from silver plasmonic masks, where features as small as 30 nm can be resolved. Furthermore, the lithography experiments have been performed with demonstration of sub-100 nm spatial resolution.
G protein-coupled receptors as therapeutic targets for obesity and type 2 diabetes. (2004)

The prevalence of obesity and type 2 diabetes, two strongly correlated disorders, is increasing worldwide. Weight loss can reduce the risk of developing type 2 diabetes and the pharmacological treatments normally required to manage this disorder. Even though dietary and lifestyle changes may eventually reduce obesity for some individuals, new safe and more efficacious drugs are required for successful weight reduction and treatment of type 2 diabetes in a large proportion of obese individuals. In addition to targeting known G protein-coupled receptors (GPCRs), several orphan GPCRs expressed in central nervous system areas known to regulate feeding may provide new targets for the treatment of obesity. Similarly, the pancreas contains numerous islet GPCRs as well as an abundance of orphan GPCRs that potentially could emerge as targets for future antidiabetic compounds. One of the major challenges facing the pharmaceutical industry is how to rapidly establish the function and therapeutic relevance of orphan GPCRs, some of which may represent novel targets for the discovery of the next generation of drugs to effectively treat obesity and type 2 diabetes. This review will focus on the significant potential of known and orphan GPCRs as targets for the discovery of new drugs to successfully treat these serious disorders.
Engineering smooth muscle tissue with a predefined structure (1998)

Nonwoven meshes of polyglycolic acid (PGA) fibers are attractive synthetic extracellular matrices (ECMs) for tissue engineering and have been used to engineer many types of tissues. However, these synthetic ECMs lack structural stability and often cannot maintain their original structure during tissue development. This makes it difficult to design an engineered tissue with a predefined configuration and dimensions. In this study, we investigated the ability of PGA fiber-based matrices bonded at their fiber crosspoints with a secondary polymer, poly-L-lactic acid (PLLA), to resist cellular contractile forces and maintain their predefined structure during the process of smooth muscle (SM) tissue development in vitro. Physically bonded PGA matrices exhibited a 10- to 35-fold increase in the compressive modulus over unbonded PGA matrices, depending on the mass of PLLA utilized to bond the PGA matrices. In addition, the bonded PGA matrices degraded much more slowly than the unbonded matrices. The PLLA bonding of PGA matrices had no effect on the ability of cells to adhere to the matrices. After 7 weeks in culture, the bonded matrices maintained 101 +/- 4% of their initial volume and an approximate original shape while the unbonded matrices contracted to 5 +/- 1% of their initial volume with an extreme change in their shape. At this time the bonded PGA matrices had a high cellularity, with smooth muscle cells (SMCs) and ECM proteins produced by these cells (e.g., elastin) filling the pores between PGA fibers. This study demonstrated that physically bonded PGA fiber-based matrices allow the maintenance of the configuration and dimensions of the original matrices and the development of a new tissue in a predefined three-dimensional structure. This approach may be useful for engineering a variety of tissues of various structures and shapes, and our study demonstrates the importance of matching both the initial mechanical properties and the degradation rate of a matrix to the specific tissue one is engineering.
Myocardial angiotensin II receptor expression and ischemia-reperfusion injury (1998)

The renin-angiotensin system plays an important role in myocardial ischemia-reperfusion injury. Angiotensin II (Ang II) contributes to the evolution of ischemic coronary events through its hemodynamic, hemostatic and mitogenic effects. Angiotensin-converting enzyme (ACE) inhibitors and Ang II receptor antagonists have been shown to be cardioprotective in experimental animal models, with ischemia-reperfusion injury and in patients with congestive heart failure. Ang II receptors include at least two different subtypes, AT1 and AT2. Both AT1 and AT2 are expressed in the rat heart. Myocardial AT1 receptor density increases in association with ACE expression, and AT1 receptor activation is related to collagen formation following myocardial infarction in rats. Studies from the authors' laboratory have shown significant myocardial dysfunction in association with a concurrent increase in AT1 receptor expression in the rat myocardium immediately following a brief period of ischemia and reperfusion. Application of antisense oligodeoxynucleotides (AS-ODN) directed at AT1 receptor messenger RNA and AT1 receptor antagonist, losartan, significantly attenuates myocardial dysfunction induced by ischemia-reperfusion in the isolated rat heart. These observations suggest that myocardial AT1 receptor expression is involved in myocardial dysfunction following ischemia-reperfusion. Unlike losartan, which upregulates the plasma Ang II level, administration of AS-ODN does not affect plasma Ang II level. Although the reason for this is not clear, the difference in plasma Ang II levels implies that AS-ODN may be, at least theoretically, more beneficial than losartan in limiting ischemia-reperfusion-induced cardiac dysfunction. Apoptosis, or programmed cell death, also contributes to the outcome of myocardial ischemia-reperfusion injury. Recent studies from the authors' laboratory have demonstrated that Ang II induces apoptosis in cultured human coronary artery endothelial cells via activation of AT1 receptors and this can be blocked by losartan. These observations collectively underscore the importance of myocardial AT1 receptor expression in ischemia-reperfusion injury.
StarT-Voyager: A Flexible Platform for Exploring Scalable SMP Issues (1998)

This paper describes StarT-Voyager, a machine designed as an experimental platform for research in cluster system communication. The heart of StarT-Voyager is a network interface unit (NIU) that connects the memory bus of a PowerPC-based SMP to the MIT Arctic network. The NIU is highly flexible, with its set of functions easily modified by firmware or by programmable hardware, making it possible to compare different communication interfaces and implementation strategies on a common platform. Its flexibility comes from a fast embedded processor and large, fast FPGAs that surround a high-speed protected communication core. Its efficiency comes from a set of primitive operations that are implemented in hardware and are designed to reduce the firmware overhead. Our initial configuration of StarT-Voyager implements four forms of message passing along with S-COMA and NUMA shared memory support. With experimentation on the machine, it can be reconfigured to introduce new mechanisms improving usability and performance.
Developing Sybase applications (1995)

This guide covers Sybase, Powerbuilder 4 and Visual Basic. It shows how things happen in the Sybase environment and why they happen. The book also shows how to select a tool set and bullet-proof and test applications.
Designer Assays for Antimicrobial Peptides Disputing the "One-Size-Fits-All" Theory (2003)

Some travelers believe that the difficulties of a voyage become its most pleasurable memories. Others doubt this maxim or believe that it operates only in retrospect, and take a guidebook and compass along. This chapter is written for the second type of traveler.
In vivo imaging of light-emitting probes (2001)

In vivo imaging of cells tagged with light-emitting probes, such as firefly luciferase or fluorescent proteins, is a powerful technology that enables a wide range of biological studies in small research animals. Reporters with emission in the red to infrared (>600 nm) are preferred due to the low absorption in tissue at these wavelengths. Modeling of photon diffusion through tissue indicates that bioluminescent cell counts as low as a few hundred can be detected subcutaneously, while approximately 10(6) cells are required to detect signals at approximately 2 cm depth in tissue. Signal-to-noise estimates show that cooled back-thinned integrating charge coupled devices (CCDs) are preferred to image-intensified CCDs for this application, mainly due to their high quantum efficiency (approximately 85%) at wavelengths >600 nm where tissue absorption is low. Instrumentation for in vivo imaging developed at Xenogen is described and several examples of images of mice with bioluminescent cells are presented.
Virtual Locomotion: Walking in Place through Virtual Environments (1999)

This paper presents both an analysis of requirements for user control over simulated locomotion and a new control technique designed to meet these requirements. The goal is to allow the user to move through virtual environments in as similar a manner as possible to walking through the real world. We approach this problem by examining the interrelationships between motion control and the other actions people use to act, sense, and react to their environment. If the interactions between control actions and sensory feedback can be made comparable to those of actions in the real world, then there is hope for constructing an effective new technique. Candidate solutions are reviewed once the analysis is developed. This analysis leads to a promising new design for a sensor-based virtual locomotion called Gaiter. The new control allows users to direct their movement through virtual environments by stepping in place. The movement of a person's legs is sensed, and in-place walking is treated as a gesture indicating the user intends to take a virtual step. More specifically, the movement of the user's legs determines the direction, extent, and timing of their movement through virtual environments. Tying virtual locomotion to leg motion allows a person to step in any direction and control the stride length and cadence of his virtual steps. The user can walk straight, turn in place, and turn while advancing. Motion is expressed in a body-centric coordinate system similar to that of actual stepping. The system can discriminate between gestural and actual steps, so both types of steps can be intermixed.
Schottky barrier height modulation using dopant segregation in schottky-barrier SOI-MOSFETs (2005)

The effect of dopant segregation (DS) on the electrical behavior of silicon-on-insulator Schottky barrier MOSFETs (SB-MOSFETs) is investigated. Ion implantation with arsenic and boron and subsequent silicidation is used to create highly n- and p-doped interface layers at the silicide-silicon interface. As a result, a strong band bending occurs at the silicide-silicon interface giving rise to a lowering of the effective Schottky barrier height. In turn, an increased electron as well as hole injection into the channel leads to improvements of the off- and on-state of the SB-MOSFETs. Using dopant segregation n-type as well as p-type SB-MOSFETs with nickel silicide source/drain electrodes have been fabricated exhibiting an inverse sub-threshold slope close to the thermal limit and showing one order of magnitude higher on-currents if compared to SB-MOSFETs without DS. In essence, the use of dopant segregation allows the fabrication of high performance Schottky barrier MOSFETs.
Topology of the Membrane-Associated Hepatitis C Virus Protein NS4B (2003)

Hepatitis C virus (HCV) belongs to the Hepacivirus genus in the Flaviviridae family. Among the least known viral proteins in this family is the nonstructural protein NS4B, which has been suggested to be a part of the replication complex. Hydrophobicity plots indicate a common profile among the NS4B proteins from different members of the Flaviviridae family, suggesting a common function. In order to gain a deeper understanding of the nature of HCV NS4B, we have determined localization and topology of this protein by using recombinant HCV NS4B constructs. The protein localized to the endoplasmic reticulum (ER), but also induced a pattern of cytoplasmic foci positive for markers of the ER. Computer predictions of the membrane topology of NS4B suggested that it has four transmembrane segments. The N and C termini were anticipated to be localized in the cytoplasm, because they are processed by the cytoplasmic NS3 protein. By introducing glycosylation sites at various positions in HCV NS4B, we show that the C terminus is cytoplasmic and the loop around residue 161 is lumenal as predicted. Surprisingly, the N-terminal tail was translocated into the lumen in a considerable fraction of the NS4B molecules, most likely by a posttranslational process. Interestingly, NS4B proteins of the yellow fever and dengue viruses also have their N termini located in the ER lumen due to an N-terminal signal peptide not found in NS4B of HCV. A shared topology achieved in two different ways supports the notion of a common function for NS4B in FLAVIVIRIDAE:
Virus‐Based Chemical and Biological Sensing (2009)

Viruses have recently proven useful for the detection of target analytes such as explosives, proteins, bacteria, viruses, spores, and toxins with high selectivity and sensitivity. Bacteriophages (often shortened to phages), viruses that specifically infect bacteria, are currently the most studied viruses, mainly because target-specific nonlytic phages (and the peptides and proteins carried by them) can be identified by using the well-established phage display technique, and lytic phages can specifically break bacteria to release cell-specific marker molecules such as enzymes that can be assayed. In addition, phages have good chemical and thermal stability, and can be conjugated with nanomaterials and immobilized on a transducer surface in an analytical device. This Review focuses on progress made in the use of phages in chemical and biological sensors in combination with traditional analytical techniques. Recent progress in the use of virus-nanomaterial composites and other viruses in sensing applications is also highlighted.
Measurement of hepatocellular function, cardiac output, effective blood volume, and oxygen saturation in rats (1989)

The available techniques do not permit the measurement of hepatocellular function, cardiac output, effective blood volume, and oxygen saturation in small animals without the need of blood or tissue sampling. We present methodology that permits us to measure the above variables in the rat. Multiple doses of indocyanine green (ICG; 0.16-2.6 mg/kg) were given to pentobarbital-anesthetized rats, and [ICG] was continuously measured by an in vivo hemoreflectometer. Initial velocity of clearance (Vo) was determined from the [ICG] vs. time plot for each dose by nonlinear regression. The maximal velocity of clearance (Vmax; indicating hepatocellular function) was calculated. Vmax was 1) accurately determined using two, three, or four doses of ICG; 2) it was 1.09 +/- 0.16 mg.kg-1.min-1, not different from the Vo of the near-saturating dose of 25 mg/kg; and 3) it decreased after partial hepatectomy. Cardiac output was 41.89 +/- 1.46 ml.100 g-1.min-1, effective blood volume was 6.12 +/- 0.34 ml/100 g, and oxygen saturation was 92 +/- 2%. These methodologies may prove useful in the evaluation of hepatocellular dysfunction and hemodynamic parameters in the rat during and after various diseased states.
Study of the costs and morbidities of late-preterm birth (2012)

Late-preterm infants are at higher risk of specific morbidities compared with term infants. Their mean total costs fall from almost double that of term infants during the first 2 years of life, to just 46% greater in the third year of life.
Human Pancreatic Islets Produce and Secrete MCP-1/CCL2: Relevance in Human Islet Transplantation (2002)

We investigated the capacity of human islets to produce monocyte chemoattractant protein-1 (MCP-1). Primary cultures of pancreatic islets expressed and secreted MCP-1, as determined by Northern blot, immunohistochemistry, in situ hybridization, and enzyme-linked immunosorbent assay. The produced MCP-1 was biologically active as it attracted monocytes in chemotaxis assay, and chemotactic activity was almost abrogated by a neutralizing anti-MCP-1 monoclonal antibody. Expression of MCP-1 was increased by primary inflammatory cytokines (interleukin-1 beta, tumor necrosis factor-alpha) and lipopolysaccharide at both the mRNA and protein levels but not by glucose. However, MCP-1 did not modulate insulin secretion. MCP-1 secreted by pancreatic islets plays a relevant role in the clinical outcome of islet transplant in patients with type 1 diabetes. In fact, low MCP-1 secretion resulted as the most relevant factor for long-lasting insulin independence. This finding opens new approaches in the management of human islet transplantation. Finally, the finding that MCP-1 appears constitutively present in normal human islet beta-cells (immunohistochemistry and in situ hybridization), in the absence of an inflammatory infiltrate, suggests that this chemokine could have functions other than monocyte recruitment and opens a new link between the endocrine and immune systems.
Selective Modification of Antigen-Specific T Cells by RNA Electroporation (2008)

It has been observed that the efficient transfection of T cells by RNA electroporation requires prior activation of T cells with mitogens or by anti-CD3 antibody stimulation. We hypothesized that this requirement for T cell activation could be leveraged to express marker genes within activated T cells responding to antigen-pulsed dendritic cells and allow for the selective enrichment and modification of antigen-specific T cells. Using electroporation of mRNA encoding green fluorescent protein as a marker gene, we demonstrate that RNA electroporation can efficiently allow for the separation of cytomegalovirus-specific CD8+ and CD4+ T cells from bulk culture responding to cytomegalovirus pp65 antigen-pulsed dendritic cells. Furthermore, we demonstrate that cytomegalovirus-specific T cells can be functionally modified by RNA transfection of the C-X-C chemokine receptor, CXCR2, to migrate efficiently toward a variety of CXCR2-specific chemokines in vitro and in vivo. These studies demonstrate the utility of RNA transfection as a simple method by which to purify and selectively modify the function of antigen-specific T cells for use in adoptive immunotherapy, and importantly provide evidence that transient expression of proteins by RNA transfection is an efficient means of modulating the in vivo function of activated T cells.
Ribonucleotide reductase R2 gene expression and changes in drug sensitivity and genome stability. (1997)

Ribonucleotide reductase is a highly regulated, cell cycle-controlled activity that plays an important role in DNA synthesis and repair. Recent studies have shown that elevated expression of the rate-limiting R2 component of ribonucleotide reductase increases Raf-1 protein activation and mitogen-activated protein kinase activity and acts as a novel malignancy determinant in cooperation with activated oncogenes like H-ras. We show that hydroxyurea-resistant mouse L cells with elevated R2 gene expression and increased ribonucleotide reductase activity exhibit significantly decreased sensitivities to the chemotherapeutic compounds N-(phosphonacetyl)-L-aspartate (PALA) and methotrexate (MTX). Furthermore, BALB/c 3T3 cells containing a retroviral expression vector encoding the R2 sequence also showed decreased sensitivity to PALA and MTX when compared to cells containing the same vector but without the R2 coding region. Colonies that developed in the presence of PALA or MTX contained amplifications of the CAD or dihydrofolate reductase genes and exhibited wild-type p53 function as determined in sequence-specific p53 binding activity assays. NIH-3T3 cells containing the R2 retroviral expression vector also showed significantly decreased sensitivity to hydroxyurea and MTX but not to PALA. Furthermore, NIH-3T3 cells transfected with a vector containing the R2 sequence in antisense orientation exhibited increased sensitivity to hydroxyurea, PALA, and MTX. Similarly, mouse 10T1/2 cells that are highly transformed and drug resistant due to alterations in H-ras and a mutant oncogenic form of p53 exhibited significant increases in sensitivity to hydroxyurea, PALA, and MTX when transfected with a vector containing the R2 sequence in antisense orientation and compared to cells containing the same vector without the antisense sequence. These results indicate that altered expression of the R2 component is capable of significantly modifying drug sensitivity properties of tumor cells. We hypothesize that this occurs, at least in part, through a mechanism of increased genetic instability that is independent of direct p53 mutation or loss and involves R2 stimulation of the mitogen-activated protein kinase signal pathway.
Cellular mechanisms of insulin resistance (2000)

It is estimated that by the year 2020 there will be approximately 250 million people affected by type 2 diabetes mellitus worldwide (1). Although the primary factors causing this disease are unknown, it is clear that insulin resistance plays a major role in its development. Evidence for this comes from (a) the presence of insulin resistance 10–20 years before the onset of the disease (2, 3); (b) cross-sectional studies demonstrating that insulin resistance is a consistent finding in patients with type 2 diabetes (3–6); and (c) prospective studies demonstrating that insulin resistance is the best predictor of whether or not an individual will later become diabetic (2, 3). Here, I focus on some recent advances in our understanding of human insulin resistance that have been made using nuclear magnetic resonance spectroscopy (NMR). This technique takes advantage of the spin properties of the nuclei of certain isotopes, such as 1H, 13C, and 31P, which endow the isotopes with a magnetic component that can be used to measure the concentration of intracellular metabolites noninvasively and to assess biochemical differences between normal and diabetic subjects. Drawing on NMR studies from my laboratory and others, I first consider the control of glucose phosphorylation and transport in regulating muscle responses to insulin. I then turn to the effects of fatty acids on insulin responses, showing that commonly accepted models that attempt to explain the association of insulin resistance and obesity are incompatible with recent findings. Finally, I propose an alternative model that appears to fit these and other available data.