gebhart/patrepeval huggingface dataset:
A Single-Phase Grid-Connected Inverter with a Power Decoupling Function (2007)

This paper presents a single-phase grid connected inverter with a power decoupling circuit. In the single-phase grid connected inverter, it is well known that a power pulsation with twice the grid frequency is contained in the input power. In a conventional inverter, electrolytic capacitors with large capacitance have been used in order to smooth the DC voltage. However, lifetime of those capacitors is shortened by the power pulsation with twice grid frequency. The authors have been studied a active power decoupling method that reduce the pulsating power on the input DC bus line, this enables to transfer the ripple energy appeared on the input DC capacitors into the energy in a small film capacitor on the additional circuit. Hence, extension of the lifetime of the inverter can be expected because the small film capacitor substitutes for the large electrolytic capacitors. Finally, simulation and experimental results are discussed.
Synthetic protein analogues in artificial surfactants (1996)

Today, airway instillation of surfactant preparations is a generally used treatment for respiratory distress syndrome in premature infants. Most commercially available surfactants are purified from animal lungs and contain lipids, mainly phospholipids, and about 2% of the hydrophobic surfactant proteins B and C (SP-B and SP-C). During the last half-decade the main structural properties of these proteins have been clarified and this knowledge now makes it possible to design synthetic analogues for future use in artificial surfactants.
The induction of matrix metalloproteinase and cytokine expression in synovial fibroblasts stimulated with immune cell microparticles (2005)

Rheumatoid arthritis is a chronic inflammatory disease characterized by destruction of cartilage and bone that is mediated by synovial fibroblasts. To determine the mechanisms by which these cells are activated to produce matrix metalloproteinases (MMPs), the effects of microparticles were investigated. Microparticles are small membrane-bound vesicles whose release from immune cells is increased during activation and apoptosis. Because microparticles occur abundantly in the synovial fluid in rheumatoid arthritis, they could represent novel stimulatory agents. Microparticles derived from T cells and monocytes strongly induced the synthesis of MMP-1, MMP-3, MMP-9, and MMP-13 in fibroblasts. The induction was time-dependent, with effects primarily observed after 36 h; under these conditions, MMP-2, MMP-14, and tissue inhibitor of MMP-1 (TIMP-1), TIMP-2, and TIMP-3 were not induced. Microparticles also increased the synthesis of inflammatory mediators including IL-6, IL-8, monocyte chemoattractant protein 1 (MCP-1), and MCP-2. In Ikappa-B-transfected synovial fibroblasts, MMPs were less inducible by microparticles compared with wild-type fibroblasts. Blocking of TNFalpha and IL-1beta with antibodies against TNFalpha and with IL-1 receptor antagonist did not abrogate stimulation by microparticles. These data provide evidence for a novel mechanism by which vesicles derived from activated or apoptotic immune cells can promote the destructive activity of synovial fibroblasts in rheumatoid arthritis.
The Effects of Treatment with Recombinant Human Growth Hormone on Body Composition and Metabolism in Adults with Growth Hormone Deficiency (1989)

In a double-blind, placebo-controlled trial, we studied the effects of six months of growth hormone replacement in 24 adults with growth hormone deficiency. Most of the patients had acquired growth hormone deficiency during adulthood as a consequence of treatment for pituitary tumors, and all were receiving appropriate thyroid, adrenal, and gonadal hormone replacement. The daily dose of recombinant human growth hormone (rhGH) was 0.07 U per kilogram of body weight, given subcutaneously at bedtime. The mean (+/- SE) plasma concentration of insulin-like growth factor I increased from 0.41 +/- 0.05 to 1.53 +/- 0.16 U per liter during rhGH treatment. Treatment with rhGH had no effect on body weight. The mean lean body mass, however, increased by 5.5 +/- 1.1 kg (P less than 0.0001), and the fat mass decreased by 5.7 +/- 0.9 kg (P less than 0.0001) in the group treated with growth hormone; neither changed significantly in the placebo group. The basal metabolic rate, measured at base line and after one and six months of rhGH administration, increased significantly; the respective values were 32.4 +/- 1.4, 37.2 +/- 2.2, and 34.4 +/- 1.6 kcal per kilogram of lean body mass per day (P less than 0.001 for both comparisons). Fasting plasma cholesterol levels were lower (P less than 0.05) in the rhGH-treated group than in the placebo group, whereas plasma triglyceride values were similar in the two groups throughout the study. We conclude that growth hormone has a role in the regulation of body composition in adults, probably through its anabolic and lipolytic actions.
Studies of the Selective O-Alkylation and Dealkylation of Flavonoids. VI. Demethylation of 8-Hydroxy-5,7-dimethoxyflavones with Anhydrous Aluminum Chloride or Bromide in Acetonitrile (1983)

Abstract The demethylation of seven 8-hydroxy-5,7-dimethoxyflavones with anhydrous aluminum chloride or bromide in acetonitrile was studied and the following results were obtained. (1) Anhydrous aluminum chloride in acetonitrile selectively split the 5-methoxyl group without cleavage of the 7-methoxyl group, and seven 5,8-dihydroxy-7-methoxy-flavones were quantitatively synthesized by the demethylation. (2) In the demethylation with anhydrous aluminum bromide, the 5- and 7-methoxyl groups on 4′,5,7-trimethoxy- and 3′,4′,5,7-tetramethoxy-8-hydroxyflavone were selectively split to give the corresponding 5,7,8-trihydroxyflavones in good yield. However, the demethylation was not accessible to the synthesis of 5,7,8-trihydroxy-3′,4′,5′-trimethoxyflavone, 4′,5,7,8-tetrahydroxy-3′-methoxy-, and 3′,5,7,8-tetrahydroxy-4′-methoxyflavone, because of the cleavage of the methoxyl groups on the B ring. The synthesized flavones were employed for the identification of the two natural flavones, which were proposed to be 4′,5,8-trihydroxy-7-methoxyflavone and 4′,5,8-trihydroxy-3′,7-dimethoxyflavone. The former, salvitin, was revised to 4′,5,7-trihydroxy-6-methoxyflavone and the latter seemed to be 4′,5,7-trihydroxy-3′,8-dimethoxyflavone.
The MEKK-JNK Pathway Is Stimulated by α1-Adrenergic Receptor and Ras Activation and Is Associated with in Vitro and in Vivo Cardiac Hypertrophy (1997)

In neonatal rat ventricular myocytes, stimulation of the alpha1-adrenergic receptor (alpha1-AdrR) activates a program of genetic and morphological changes characterized by transcriptional activation of the atrial natriuretic factor (ANF) gene and enlargement (hypertrophy) of the cells. The low molecular weight GTPase Ras has been established as an important regulator of hypertrophy both in vitro and in vivo. Ras activates a kinase cascade involving Raf, the mitogen-activated protein kinase kinase (MEK), and the extracellular signal-regulated protein kinase (ERK). However, the extent of involvement of this pathway in regulating hypertrophic responses is controversial. We demonstrate here that both alpha1-AdrR stimulation and Ras can also activate the c-Jun NH2-terminal kinase (JNK) in cardiomyocytes. The alpha1-AdrR effect on JNK occurs through a pathway requiring Ras and MEK kinase (MEKK). A constitutively activated mutant of MEKK that preferentially activates JNK, stimulates ANF reporter gene expression, while a dominant negative MEKK mutant inhibits ANF expression induced by PE. Furthermore, JNK activity is increased in the ventricles of mice overexpressing oncogenic Ras, whereas ERK activity is not. These results suggest that the alpha1-AdrR mediates ANF gene expression through a Ras-MEKK-JNK pathway and that activation of this pathway is associated with in vitro and in vivo hypertrophy.
A Reliability Study of Nanoparticles Reinforced Composite Lead-Free Solder (2010)

This work looks at the development and investigation of a reinforced composite solder with low melting point. The composite solder was prepared by adding Sn-3.0Ag-0.5Cu nanoparticles into Sn-58Bi solder paste. The Sn-3.0Ag-0.5Cu nanoparticles were manufactured using a self-developed Consumable-electrode Direct Current Arc (CDCA) technique. The test FR-4 Printed Circuit Board (PCB) with Cu pad and Electroless Nickel Immersion Gold (ENIG) surface finish were fabricated, and fifty SR1206 chip resistors were mounted on pads of test PCB with the reinforced composite solder paste by using conventional surface mount technology. The differential scanning calorimetry (DSC) was used to analyze the constituent of the composite solder joint after reflow. A scanning electron microscope (SEM), transmission electron microscope (TEM) and optical microscope (OM) were employed in order to observe the morphology of nanoparticles; the microstructure of reinforced composite solder joint; the crack initiation and propagation in solder joint; and the fracture mode after shear test. The thermal cycling (TC) was carried out with a temperature range of −40°C and 125°C. The contact resistance of the solder joint was measured during thermal cycling, and the shear test of solder joints was performed before and after 500 thermal cycles. After the shear test, all fracture surfaces were inspected to identify the fracture mode of the composite solder joint. The results of the experiments detailed in this work indicate that the shear strength of the composite solder increased 2 times in comparison to Sn-58Bi. Meanwhile, the thermomechanical fatigue (TMF) resistance of the composite solder with 1 mass% nanoparticles was 16 times stronger than Sn-58Bi and 4 times stronger than Sn-3.0Ag-0.5Cu. However, the tendency of forming micro-cracks between nanoparticles and solder matrix and the fracture within solder was increased for solder joints with more than 3 mass% nanoparticles after thermal cycling.
Characteristics and availability of commercially important woods (1999)

Contents Timber Resources and Uses 1--2 Hardwoods and Softwoods 1--2 Commercial Sources of Wood Products 1--2 Use Classes and Trends 1--3 Species Descriptions 1--3 U.S. Wood Species 1--3 Hardwoods 1--3 Softwoods 1--10 Imported Woods 1--17 Hardwoods 1--17 Softwoods 1--33 References 1--34 hroughout history, the unique characteristics and comparative abundance of wood have made it a natural material for homes and other structures, furniture, tools, vehicles, and decorative objects. Today, for the same reasons, wood is prized for a multitude of uses. All wood is composed of cellulose, lignin, hemicelluloses, and minor amounts (5% to 10%) of extraneous materials contained in a cellular structure. Variations in the characteristics and volume of these components and differences in cellular structure make woods heavy or light, stiff or flexible, and hard or soft. The properties of a single species are relatively constant within limits; therefore, selection of wood by species alone may
Survey of time-optimal attitude maneuvers (1994)

Introduction P pointing control and rapid maneuvering capabilities have long been part of many space missions; examples include military observation platforms, communications satellites, and exploratory space missions. Rapid retargeting may be an intrinsic part of the mission profile, as in military and exploratory applications, or it may be required to correct, periodically, the guidance and navigation sensors of a spacecraft. Consequently, research in attitude maneuvers and time-optimal controls has been a consistently strong field of study. Of particular interest is the time-optimal attitude maneuver; this problem combines aspects of many different fields, such as mathematics, optimal control theory, spacecraft dynamics, elasticity, and structural mechanics. In the study of attitude maneuvers and control, researchers have investigated the response of satellite control systems to disturbances caused by the influence of solar pressure, gravity gradients, the effectiveness of active control devices, and the best placement of actuators and sensors on a given structure. Numerous studies have been conducted for specific satellite configurations to determine a time-optimal attitude control for a predetermined maneuver. Further, the mathematical procedures required to investigate this problem have inspired a number of papers on techniques to address the difficulties which arise from time-optimal control. This survey reviews the literature of the last thirty years, including many of the more recent advances in the field, covers the aforementioned topics as well as specific attitude maneuvers, and traces the development of time-optimal and near time-optimal control algorithms. We begin by considering the formulation of the time-optimal control problem and the difficulties faced in obtaining the solution. The equations for the rotational motion of any rigid body (Ruler's equations) are quite elegant and compact; they are also coupled and highly nonlinear. In addition, the high angular velocities of time-optimal maneuvers will cause gyroscopic stiffness through the nonlinear terms. Ruler's equations are expressed as
Approval summary for imatinib mesylate capsules in the treatment of chronic myelogenous leukemia. (2002)

On May 10, 2001, imatinib mesylate (Gleevec, formerly known as STI-571 and Glivec), manufactured and distributed by Novartis Pharmaceuticals, East Hanover, NJ, was approved by the United States Food and Drug Administration for the treatment of CML in three clinical settings: CML-BC, CML-AP, and CML-CP. This report summarizes the Food and Drug Administration's review of the New Drug Application.
Analysis of a flow control system for a combined input-crosspoint buffered packet switch (2005)

A flow control mechanism is used in combined input-crosspoint buffered (CICB) switches to avoid buffer overflow and underflow. Credit-based flow control is widely used in CICB switches to reduce the required crosspoint-buffer size. For simplification, we analyze an flow control mechanism with active queue management (AQM) and a proportional controller. We show that the flow control mechanism is stable for small crosspoint buffer sizes and non-negligible round-trip times. In addition, we observe the effect of an input shaper combined with a proportional controller. We show that the input shaper reduces the response time of the flow control mechanism.
Evolution of hereditary non-polyposis colorectal cancer. (1992)

The prevalence of colorectal adenoma in 23 affected patients with hereditary non-polyposis colorectal cancer (HNPCC) was compared with that in an age matched forensic autopsy population. The mean ages at diagnosis of colorectal cancer in men (13) and women (10) were 39 and 37 years respectively. In HNPCC patients who presented below the age of 50 years, at least one adenoma was found in 3 of 10 (30%) men and in 4 of 9 (44%) women. In the age matched autopsy specimens of large bowel, a solitary adenoma was found in 2/42 (5%) men (p = 0.015) and 1/21 (5%) women (p = 0.0075). Of the 11 adenomas from HNPCC patients, nine were greater than 1 cm and six showed a pure villous architecture. Contiguous adenocarcinoma was observed with six adenomas. Adenomas do not occur in large numbers in HNPCC, but develop at a young age, attain a large size, often show a villous configuration, and are more prone to malignant conversion than sporadic adenomas.
Phosphorylation of extracellular signal-regulated kinase 1 and 2, protein kinase B, and signal transducer and activator of transcription 3 are differently inhibited by an epidermal growth factor receptor inhibitor, EKB-569, in tumor cells and normal human keratinocytes (2004)

Abstract EKB-569 is an irreversible inhibitor of epidermal growth factor receptor (EGF-R) tyrosine kinase. It inhibits EGF-induced phosphorylation of EGF-R and the growth of tumors that overexpress EGF-R in animal models. In clinical trials, EKB-569 and all other EGF-R inhibitors cause skin rashes. To understand the latter phenomenon, the effect of EKB-569 on EGF-R as well as downstream signaling to phosphoinositide 3-kinase-protein kinase B (AKT), extracellular signal-regulated kinase 1 and 2 (ERK1/2), or signal transducer and activator of transcription 3 (STAT3) pathways were compared in tumor cell lines and normal human keratinocytes (NHEK) grown in tissue culture. Tumor cell lines that have high (A431 epidermoid and MDA-468 breast carcinomas) and low (MCF-7 breast carcinoma) expression of EGF-R were used. NHEK cells express at least 15-fold less EGF-R than A431 cells. EKB-569 was a potent inhibitor of proliferation in NHEK, A431, and MDA-468 cells (IC50 = 61, 125, and 260 nm, respectively) but not MCF-7 cells (IC50 = 3600 nm). EKB-569 was also a potent inhibitor of EGF-induced phosphorylated EGF-R (pEGF-R) in A431 and NHEK cells (IC50 = 20–80 nm). The reduction in pEGF-R paralleled inhibition of phosphotyrosine-705 STAT3, while the inhibition of phosphorylated AKT and phosphorylated ERK1/2 occurred at higher concentrations of EKB-569 (75–500 nm) in both A431 and NHEK cells. The effects were specific because EKB-569 did not inhibit the nuclear factor-κB pathway. It is proposed that skin toxicity associated with EKB-569 is due to inhibition of EGF-R signaling. Downstream signal transduction markers, particularly the activation status of STAT3, may be useful surrogate markers to guide clinical development of EGF-R inhibitors.
A Region of Human CD14 Required for Lipopolysaccharide Binding (1995)

CD14, a glycosylphosphatidylinositol-anchored protein on the surface of monocytes, macrophages, and polymorphonuclear leukocytes, is a receptor for lipopolysaccharide (LPS). CD14 binding of LPS is enhanced by serum proteins, especially lipopolysaccharide binding protein. The serum-dependent binding of LPS to CD14 stimulates macrophages to make cytokines, which can cause septic shock in humans and animals. Here, we identify a region in human CD14 which is important in serum-dependent LPS binding and LPS-induced cellular activation. Four small regions (4-5 amino acids long) within the N-terminal 65 amino acids of CD14 were deleted singly or in combination. The deletion mutants were stably expressed in Chinese hamster ovary (CHO) cells. The mutants were characterized in three assays: reactivity with anti-CD14 monoclonal antibody, serum-dependent LPS binding, and LPS-induced activation of NF-kappa B. Some of the mutants selectively lost reactivity with the anti-CD14 monoclonal antibody that inhibited serum-dependent LPS binding and cellular activation. All of the mutants bound much less LPS than wild type CD14 in the presence of serum. None of the mutants bound more LPS than control CD14-CHO cells in the absence of serum. CD14-CHO cells respond to LPS by activation of NF-kappa B. All of the deletion mutants were less active LPS receptors than wild type CD14-CHO cells. The delta AVEVE mutant, the delta DDED and delta PQPD double mutant, and the delta DDED, delta PQPD, delta AVEVE, and delta DPRQY quadruple deletion mutants were essentially inactive LPS receptors in CHO cells. These studies suggest that the 65 N-terminal amino acids of CD14 are critical for serum-dependent binding of LPS to CD14 and subsequent signal transduction in CHO cells.
Myelin Basic Protein as an Encephalitogen in Encephalomyelitis and Polyneuritis Following Rabies Vaccination (1987)

Encephalitis and polyneuritis occurring after rabies vaccination are believed to be immunologically mediated. We studied antibody responses to neural antigens in 36 patients with major neurologic complications, 25 with minor complications, and 39 with no complications after immunization with a brain-derived, Semple rabies vaccine. Patients with major complications had significantly elevated levels of antibody to brain white matter as compared with the other groups (P less than 0.001). Assays for antibody to selected central nervous system antigens showed that high levels of serum and cerebrospinal fluid antibody to myelin basic protein correlated with the presence of major neurologic complications (both central and peripheral nervous systems). The level of antibody to cerebroside correlated best with the number of injections of vaccine, but like antibody to myelin basic protein, the antibody to cerebroside was present in the cerebrospinal fluid of patients with major complications. Some patients with major complications also had antibodies directed to the gangliosides GD1b and GT1b. No antibodies to myelin-associated glycoprotein were detected in any of the samples. These data implicate myelin basic protein as an encephalitogen in these autoimmune diseases of the human nervous system, but suggest that immune responses to cerebroside and certain gangliosides may have an augmentative role in severe disease.
Targeting Tumor-Initiating Cancer Cells with dCD133KDEL Shows Impressive Tumor Reductions in a Xenotransplant Model of Human Head and Neck Cancer (2011)

A novel anticancer agent was constructed by fusing a gene encoding the scFV that targets both glycosylated and unglycosylated forms of CD133 to a gene fragment encoding deimmunized PE38KDEL. The resulting fusion protein, dCD133KDEL, was studied to determine its ability to bind and kill tumor-initiating cells in vitro and in vivo. The anti-CD133 scFV selectively bound HEK293 cells transfected with the CD133 receptor gene. Time course viability studies showed that dCD133KDEL selectively inhibited NA-SCC and UMSCC-11B, 2 head and neck squamous cell carcinomas that contain a CD133 expressing subpopulation. Importantly, the drug did not inhibit the viability of hematopoietic lineages measured by long-term culture-initiating cell and colony-forming assays from sorted human CD34+ progenitor cells. In addition to in vitro studies, in vivo tumor initiation experiments confirmed that CD133-sorted cells implanted into the flanks of nude mice grew faster and larger than unsorted cells. In contrast, cells that were pretreated with dCD133KDEL before implantation showed the slowest and lowest incidence of tumors. Furthermore, UMSCC-11B-luc tumors treated with multiple intratumoral injections of dCD133KDEL showed marked growth inhibition, leading to complete degradation of the tumors that was not observed with an irrelevant control-targeted toxin. Experiments in immunocompetent mice showed that toxin deimmunization resulted in a 90% reduction in circulating antitoxin levels. These studies show that dCD133KDEL is a novel anticancer agent effective at inhibiting cell proliferation, tumor initiation, and eliminating established tumors by targeting the CD133 subpopulation. This agent shows significant promise for potential development as a clinically useful therapy.