gebhart/patrepeval huggingface dataset:
Modale Analyse an rotierenden Maschinen mittels Magnetlager (1995)

Die experimentelle Modale Analyse ist eine Methode zur Bestimmung des dynamischen Verhaltens mechanischer Systeme. Bei rotierenden Maschinen ist in der Praxis die Messung der Ausgangsfrequenzspektren üblich. Zwar werden so die auftretenden Schwingungserscheinungen erfaßt, aber die Anregungsmechanismen, welche die Schwingungen hervorrufen, bleiben nach Art und Größe unbekannt. Um die modalen Parameter eines Systems identifizieren zu können, ist es unerläßlich eine rotierende Struktur gezielt mit einer bekannten Kraft anzuregen und die Übertragungsfunktion zwischen Aus-und Eingang zu ermitteln.
AC coupled PV hybrid systems and micro grids - state of the art and future trends (2022)

The consequent AC-coupling of generators, storage units and loads for setting up hybrid systems or hybrid micro grids is under investigation at ISET since more than ten years. After the development of suitable components like the PV-inverter Sunny Boy¿ and the battery inverter Sunny Island¿ and after the implementation of new control concepts for parallel operation, these systems can be easily set up with series produced components. This paper describes the principals of the Modular Systems Technology and shows some examples of operat-ing hybrid micro grids containing AC-PV, AC-battery power units, wind turbines and diesel gensets. Further developments and aims are described including the dis-tributed generation and energy storage in micro grids as well as the stepwise interconnection of micro grids. A first approach for the control and management of disconnecting houses or grid parts which make use of their distributed energy generators or storage units for emergency power will be outlined.
msaABCR operon positively regulates biofilm development by repressing proteases and autolysis in Staphylococcus aureus (2015)

Staphylococcus aureus is an important human pathogen that causes nosocomial and community-acquired infections. One of the most important aspects of staphylococcal infections is biofilm development within the host, which renders the bacterium resistant to the host's immune response and antimicrobial agents. Biofilm development is very complex and involves several regulators that ensure cell survival on surfaces within the extracellular polymeric matrix. Previously, we identified the msaABCR operon as an additional positive regulator of biofilm formation. In this study, we define the regulatory pathway by which msaABCR controls biofilm formation. We demonstrate that the msaABCR operon is a negative regulator of proteases. The control of protease production mediates the processing of the major autolysin, Atl, and thus regulates the rate of autolysis. In the absence of the msaABCR operon, Atl is processed by proteases at a high rate, leading to increased cell death and a defect in biofilm maturation. We conclude that the msaABCR operon plays a key role in maintaining the balance between autolysis and growth within the staphylococcal biofilm.
Assessing the validity of current mouse genetic models of obsessive–compulsive disorder (2009)

Obsessive-compulsive disorder (OCD) is a disorder characterized by unwanted and intrusive thoughts, images, or impulses and/or repetitive behavior. OCD is a major cause of disability; however, the genetic factors and pathophysiological mechanisms underlying this complex, heterogeneous disorder remain largely unknown. During the past decade, a number of putative mouse genetic models of OCD have been developed for the purpose of studying the neural mechanisms underlying this disorder and developing novel treatments. This review presents and evaluates these experimental preparations to date. Models using knockout or transgenic approaches, as well as those examining variation in genetically diverse populations, are evaluated and discussed.
Microwave induced alteration in the neuron specific enolase gene expression. (1993)

Exposure of pNGE7, a recombinant clone containing the coding and regulatory sequences for the expression of neuron specific enolase gene, cells to electromagnetic radiations (915 MHz, 16 Hz AM, SAR 0.05 mW/kg) resulted in the elevation of neuron specific enolase (NSE), a diagnostic marker for neuron and lung cancer. Using ion-exchange chromatography we separated the neuron specific enolase activity from the non-neuronal enolase (NNE) activity and observed an alteration in the expression of neuron specific enolase and non-neuronal enolase. The clinical applications of the present studies have been discussed.
Solid phase synthesis and structural analysis of novel A-chain dicarba analogs of human relaxin-3 (INSL7) that exhibit full biological activity (2009)

Replacement of disulfide bonds with non-reducible isosteres can be a useful means of increasing the in vivo stability of a protein. We describe the replacement of the A-chain intramolecular disulfide bond of human relaxin-3 (H3 relaxin, INSL7), an insulin-like peptide that has potential applications in the treatment of stress and obesity, with the physiologically stable dicarba bond. Solid phase peptide synthesis was used to prepare an A-chain analogue in which the two cysteine residues that form the intramolecular bond were replaced with allylglycine. On-resin microwave-mediated ring closing metathesis was then employed to generate the dicarba bridge. Subsequent cleavage of the peptide from the solid support, purification of two isomers and their combination with the B-chain via two intermolecular disulfide bonds, then furnished two isomers of dicarba-H3 relaxin. These were characterized by CD spectroscopy, which suggested a structural similarity to the native peptide. Additional analysis by solution NMR spectroscopy also identified the likely cis/trans form of the analogs. Both peptides demonstrated binding affinities that were equivalent to native H3 relaxin on RXFP1 and RXFP3 expressing cells. However, although the cAMP activity of the analogs on RXFP3 expressing cells was similar to the native peptide, the potency on RXFP1 expressing cells was slightly lower. The data confirmed the use of a dicarba bond as a useful isosteric replacement of the disulfide bond.
Inmunidad de enfermería a los efectos del Burnout (2003)

In 1977, Maslach used this term to describe a situation suffered relatively often by individuals who, as a result of their profession, maintained a direct and continued contact with people and whom, after a variable period of time, could end up being considerably worn out professionally speaking. For some authors, if to this we add the work environment of closed hospitalisations units, the rotation of working shifts and working hours that are quite often rather stressing, we are guaranteed to find burnout syndrome. Although there is no unanimity regarding this opinion, what appears to be clear is that among nursing professionals this influence is greater. We sought out to investigate this subject by conducting a study on the nursing personnel working at the Intensive Care Unit of the Torrecardenas hospital in Almeria, with the aim of measuring the work stress levels experienced by the nursing staff at the ICU of the Torrecardenas hospital with over 5 years seniority as opposed to the burnout experienced by other nursing professionals who left voluntarily after 5 or more years of active service.
NADP(H) Phosphatase Activities of Archaeal Inositol Monophosphatase and Eubacterial 3′-Phosphoadenosine 5′-Phosphate Phosphatase (2007)

NADP(H) phosphatase has not been identified in eubacteria and eukaryotes. In archaea, MJ0917 of hyperthermophilic Methanococcus jannaschii is a fusion protein comprising NAD kinase and an inositol monophosphatase homologue that exhibits high NADP(H) phosphatase activity (S. Kawai, C. Fukuda, T. Mukai, and K. Murata, J. Biol. Chem. 280:39200-39207, 2005). In this study, we showed that the other archaeal inositol monophosphatases, MJ0109 of M. jannaschii and AF2372 of hyperthermophilic Archaeoglobus fulgidus, exhibit NADP(H) phosphatase activity in addition to the already-known inositol monophosphatase and fructose-1,6-bisphosphatase activities. Kinetic values for NADP+ and NADPH of MJ0109 and AF2372 were comparable to those for inositol monophosphate and fructose-1,6-bisphosphate. This implies that the physiological role of the two enzymes is that of an NADP(H) phosphatase. Further, the two enzymes showed inositol polyphosphate 1-phosphatase activity but not 3'-phosphoadenosine 5'-phosphate phosphatase activity. The inositol polyphosphate 1-phosphatase activity of archaeal inositol monophosphatase was considered to be compatible with the similar tertiary structures of inositol monophosphatase, fructose-1,6-bisphosphatase, inositol polyphosphate 1-phosphatase, and 3'-phosphoadenosine 5'-phosphate phosphatase. Based on this fact, we found that 3'-phosphoadenosine 5'-phosphate phosphatase (CysQ) of Escherichia coli exhibited NADP(H) phosphatase and fructose-1,6-bisphosphatase activities, although inositol monophosphatase (SuhB) and fructose-1,6-bisphosphatase (Fbp) of E. coli did not exhibit any NADP(H) phosphatase activity. However, the kinetic values of CysQ and the known phenotype of the cysQ mutant indicated that CysQ functions physiologically as 3'-phosphoadenosine 5'-phosphate phosphatase rather than as NADP(H) phosphatase.
A phase 1 study investigating DX-2930 in healthy subjects (2014)

ClinicalTrials.gov identifier: NCT01923207.
NEUTROPHIL-DERIVED CIRCULATING FREE DNA (cf-DNA/NETs) (2008)

The release of "neutrophil extracellular traps" (NETs) has been identified as a novel immune response in innate immunity. Neutrophil extracellular traps are composed of neutrophil-derived circulating free DNA (cf-DNA), histones, and neutrophil cytoplasm-derived proteins such as proteases. Here, we studied the putative predictive value of plasma cf-DNA/NETs for the development of sepsis and mortality after multiple trauma. In a prospective pilot study with 45 multiple trauma (Injury Severity Score>16) patients, cf-DNA was directly quantified in plasma. Blood samples were sequentially obtained daily from admission to our Trauma Center until day 10. Because of limited intensive care unit (ICU) stay of less than 3 days, 8 patients have been excluded, resulting in 37 patients that were evaluated. Time kinetics of cf-DNA/NETs was compared with C-reactive protein (CRP), interleukin (IL) 6, leukocyte counts, and myeloperoxidase. The severity of the injury was calculated on the basis of the Injury Severity Score, as well as Multiple Organ Dysfunction Score, Sequential Organ Failure Assessment, and Simplified Acute Physiology Score II on ICU. Initially high cf-DNA/NETs values (>800 ng/mL) with recurrent increased values between days 5 to 9 were associated with subsequent sepsis, multiple organ failure, and death. In conjunction with cf-DNA/NETs, IL-6 was significantly elevated after admission. However, the development of a second hit was not indicated by IL-6. In contrast to cf-DNA/NETs, no difference in CRP kinetics was observed between patients with and without development of sepsis. Circulating free DNA/NETs kinetics rather followed kinetics of Multiple Organ Dysfunction Score, Sepsis-related Organ Failure Assessment, leukocyte counts, and partially of myeloperoxidase. Circulating free DNA/NETs seems to be a valuable additional marker for the calculation of injury severity and/or prediction of inflammatory second hit on ICU. However, a large clinical trial with severely injured patients should confirm the prognostic value of neutrophil-derived cf-DNA/NETs.
Two novel multiway circuit partitioning algorithms using relaxed locking (1997)

All the previous Kernighan-Lin-based (KL-based) circuit partitioning algorithms employ the locking mechanism, which enforces each cell to move exactly once per pass. In this paper, we propose two novel approaches for multiway circuit partitioning to overcome this limitation. Our approaches allow each cell to move more than once. Our first approach still uses the locking mechanism but in a relaxed way. It introduces the phase concept such that each pass can include more than one phase, and a phase can include at most one move of each cell. Our second approach does not use the locking mechanism at all. It introduces the mobility concept such that each cell can move as freely as allowed by its mobility. Each approach leads to KL-based generic algorithms whose parameters can be set to obtain algorithms with different performance characteristics. We generated three versions of each generic algorithm and evaluated them on a subset of common benchmark circuits in comparison with Sanchis' algorithm (FMS) and the simulated annealing algorithm (SA). Experimental results show that our algorithms are efficient, they outperform FMS significantly, and they perform comparably to SA. Our algorithms perform relatively better as the number of parts in the partition increases as well as the density of the circuit decreases. This paper also provides guidelines for good parameter settings for the generic algorithms.
Effect of Oral Alendronate on Bone Mineral Density and the Incidence of Fractures in Postmenopausal Osteoporosis (1995)

Daily treatment with alendronate progressively increases the bone mass in the spine, hip, and total body and reduces the incidence of vertebral fractures, the progression of vertebral deformities, and height loss in postmenopausal women with osteoporosis.
MIC-1, a novel macrophage inhibitory cytokine, is a divergent member of the TGF-β superfamily (1997)

Macrophages play a key role in both normal and pathological processes involving immune and inflammatory responses, to a large extent through their capacity to secrete a wide range of biologically active molecules. To identify some of these as yet not characterized molecules, we have used a subtraction cloning approach designed to identify genes expressed in association with macrophage activation. One of these genes, designated macrophage inhibitory cytokine 1 (MIC-1), encodes a protein that bears the structural characteristics of a transforming growth factor beta (TGF-beta) superfamily cytokine. Although it belongs to this superfamily, it has no strong homology to existing families, indicating that it is a divergent member that may represent the first of a new family within this grouping. Expression of MIC-1 mRNA in monocytoid cells is up-regulated by a variety of stimuli associated with activation, including interleukin 1beta, tumor necrosis factor alpha (TNF-alpha), interleukin 2, and macrophage colony-stimulating factor but not interferon gamma, or lipopolysaccharide (LPS). Its expression is also increased by TGF-beta. Expression of MIC-1 in CHO cells results in the proteolytic cleavage of the propeptide and secretion of a cysteine-rich dimeric protein of Mr 25 kDa. Purified recombinant MIC-1 is able to inhibit lipopolysaccharide -induced macrophage TNF-alpha production, suggesting that MIC-1 acts in macrophages as an autocrine regulatory molecule. Its production in response to secreted proinflammatory cytokines and TGF-beta may serve to limit the later phases of macrophage activation.
Polymer–drug conjugates: towards a novel approach for the treatment of endrocine-related cancer (2005)

The last decade has seen successful clinical application of polymer-protein conjugates (e.g. Oncaspar, Neulasta) and promising results in clinical trials with polymer-anticancer drug conjugates. This, together with the realisation that nanomedicines may play an important future role in cancer diagnosis and treatment, has increased interest in this emerging field. More than 10 anticancer conjugates have now entered clinical development. Phase I/II clinical trials involving N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer-doxorubicin (PK1; FCE28068) showed a four- to fivefold reduction in anthracycline-related toxicity, and, despite cumulative doses up to 1680 mg/m2 (doxorubicin equivalent), no cardiotoxicity was observed. Antitumour activity in chemotherapy-resistant/refractory patients (including breast cancer) was also seen at doxorubicin doses of 80-320 mg/m2, consistent with tumour targeting by the enhanced permeability (EPR) effect. Hints, preclinical and clinical, that polymer anthracycline conjugation can bypass multidrug resistance (MDR) reinforce our hope that polymer drugs will prove useful in improving treatment of endocrine-related cancers. These promising early clinical results open the possibility of using the water-soluble polymers as platforms for delivery of a cocktail of pendant drugs. In particular, we have recently described the first conjugates to combine endocrine therapy and chemotherapy. Their markedly enhanced in vitro activity encourages further development of such novel, polymer-based combination therapies. This review briefly describes the current status of polymer therapeutics as anticancer agents, and discusses the opportunities for design of second-generation, polymer-based combination therapy, including the cocktail of agents that will be needed to treat resistant metastatic cancer.
Carbonic Acid from Decarboxylation by “Malic” Enzyme in Lactic Acid Bacteria (1970)

Carbonic anhydrase studies were used to determine the primary form of carbonic acid produced from decarboxylation of l-malic acid by "malic" enzyme in malolactic strains of five different species of lactic acid bacteria. Addition of carbonic anhydrase to the reaction mixture containing crude bacterial extract and l-malic acid, at pH 7, in all five cases resulted in an increase (13 to 23%) in the rate of carbon dioxide evolution over the control. The results indicated that the primary form of carbonic acid released from "malic" enzyme was not anhydrous carbon dioxide as previously supposed and as has been shown for other decarboxylating enzymes. The standard free-energy changes of the malo-lactic reaction with the various forms of carbonic acid as the primary decarboxylation product were calculated. The reaction is less exergonic when carbonic acid, bicarbonate ion, or carbonate ion is the primary decarboxylation product compared to anhydrous carbon dioxide. The free-energy of the reaction is not biologically available to the bacteria; with carbon dioxide not the primary decarboxylation product, the potential energy lost in a malo-lactic fermentation is not as great as previously considered. Endogenous carbonic anhydrase activity was not found.
Etanercept in systemic juvenile idiopathic arthritis. (2003)

Etanercept, in combination with MTX, demonstrated benefit soon after initiation of treatment in patients with refractory SJIA, but flares and progressive loss of effectiveness were observed with continued treatment in most patients. Sharp decreases in the dose of MTX and corticosteroids may have contributed to subsequent occurrence of flares. Changes in MTX and corticosteroids doses should probably need to be made gradually, and it is possible that patients on SJIA should continue on therapeutic doses of MTX while being on etanercept in order to maintain therapeutic benefit.
A multicenter, randomized, double-blind, placebo-controlled trial evaluating the efficacy and safety of Huangqi Guizhi Wuwutang granule in patients with rheumatoid arthritis (2019)

ClinicalTrials.gov ID: NCT03593837.
Oxidative Stress and Vascular Disease (2004)

Growing evidence indicates that chronic and acute overproduction of reactive oxygen species (ROS) under pathophysiologic conditions is integral in the development of cardiovascular diseases (CVD). These ROS can be released from nicotinamide adenine dinucleotide (phosphate) oxidase, xanthine oxidase, lipoxygenase, mitochondria, or the uncoupling of nitric oxide synthase in vascular cells. ROS mediate various signaling pathways that underlie vascular inflammation in atherogenesis: from the initiation of fatty streak development through lesion progress to ultimate plaque rupture. Various animal models of oxidative stress support the notion that ROS have a causal role in atherosclerosis and other cardiovascular diseases. Human investigations also support the oxidative stress hypothesis of atherosclerosis. Oxidative stress is the unifying mechanism for many CVD risk factors, which additionally supports its central role in CVD. Despite the demonstrated role of antioxidants in cellular and animal studies, the ineffectiveness of antioxidants in reducing cardiovascular death and morbidity in clinical trials has led many investigators to question the importance of oxidative stress in human atherosclerosis. Others have argued that the prime factor for the mixed outcomes from using antioxidants to prevent CVD may be the lack of specific and sensitive biomarkers by which to assess the oxidative stress phenotypes underlying CVD. A better understanding of the complexity of cellular redox reactions, development of a new class of antioxidants targeted to specific subcellular locales, and the phenotype-genotype linkage analysis for oxidative stress will likely be avenues for future research in this area as we move toward the broader use of pharmacological and regenerative therapies in the treatment and prevention of CVD.
The Electrical Conductivity and Isothermal Hall Effect in Cuprous Sulfide, Semi-Conductor (1951)

The experimental measurements of the isothermal Hall effect on the γ-cuprous sulfide were performed with the following results. In the stoichiometric specimens, the values of Hall constant R are about \(3{\sim}4{\times}10^{9}\left[\frac{\text{Volt}{\cdot}\text{cm}}{\text{Gauss}{\cdot}\text{amp}}\right]\), mobility µ and mean free path l are about 12[cm 2 /Volt·sec], 9[cm], respectively. These values of R , µ and l decrease in the β-phase. As compared with the stoichiometric specimens, the values of µ and l in the sulphur excess specimens do not increase so much as the conductivities do. On the contrary, in the sulphur deficient specimens, the decrease of µ and l is not so remarkable in comparison with that of conductivities. These phenomena may be considered that the impurity scattering due to the free electrons and holes makes the values of µ and l reduce.
Differential effects of imatinib on PDGF‐induced proliferation and PDGF receptor signaling in human arterial and venous smooth muscle cells (2006)

Platelet-derived growth factor (PDGF) has been implicated in smooth muscle cell (SMC) proliferation, a key event in the development of myointimal hyperplasia in vascular grafts. Recent evidence suggests that the PDGF receptor (PDGFR) tyrosine kinase inhibitor, imatinib, can prevent arterial proliferative diseases. Because hyperplasia is far more common at the venous anastomosis than the arterial anastomosis in vascular grafts, we investigated whether imatinib also inhibited venous SMC (VSMC) proliferation, and examined possible differences in its mechanism of action between VSMC and arterial SMC (ASMC). Human ASMC and VSMC were stimulated with PDGF-AB, in the presence or absence of imatinib (0.1-10 microM). Proliferation was assayed using the 5-bromo-2'-deoxyuridine (BrdU) incorporation assay, while PDGFR, Akt and ERK1/2-mitogen activated protein kinase (MAPK) signaling pathways were investigated by immunoblotting. The proliferative response to PDGF at 50 and 100 ng/ml was 32 and 43% greater, respectively, in VSMC than in ASMC. Similarly, PDGF-stimulated proliferation was more sensitive to inhibition by imatinib in VSMC than ASMC (IC(50) = 0.05 microM vs. 0.4 microM; P < 0.01). Imatinib also more effectively inhibited PDGF-induced phosphorylation of PDGFRbeta and Akt in VSMC, compared to ASMC. These data highlight inherent pharmacodynamic differences between VSMC and ASMC in receptor and cell signaling functions and suggest that imatinib therapy may be useful for the prevention of venous stenosis in vascular grafts.