gebhart/patrepeval huggingface dataset:
Role of Cellular Magnesium in Human Diseases. (2014)

Magnesium is required for many of the major organs to function and plays a crucial role in human and mammalian physiology. Magnesium is essential for the structure of bones and teeth, acts as a cofactor for more than 300 enzymes in the body, including binding to ATP for kinase reactions, and affects permeability of excitable membranes and neuromuscular transmission. Despite these essential roles, much is still unknown about magnesium physiology and homeostasis. Currently, nutritionists believe that the general population intakes insufficient magnesium daily through the diet. The effects of magnesium deficiency are, for the most part undetected, and simple, widespread assessments of magnesium intake remain unavailable for humans. Many of the patients admitted to hospitals or medical care facilities are unaware of their low magnesium levels. Moreover, because magnesium is predominantly an intracellular cation (>99%), serum magnesium levels remain a poor predictor of tissue magnesium content and availability. This review will discuss the effects of magnesium deficiency in various pathologies affecting the human population. The underlying causes for magnesium depletion in major physiological systems will be examined along with the involved signaling pathways and the main roles of magnesium homeostasis. Where possible (e.g. alcoholism), the implications of administering supplemental magnesium will be discussed. Ultimately, this review will advocate for the necessity of identifying easy and reproducible methods to assess serum and cellular magnesium levels and to identify magnesium deficiency in order to alleviate related pathological conditions.
Reciprocal actions of ATF5 and Shh in proliferation of cerebellar granule neuron progenitor cells (2011)

Precise regulation of neuroprogenitor cell proliferation and differentiation is required for successful brain development, but the factors that contribute to this are only incompletely understood. The transcription factor ATF5 promotes proliferation of cerebral cortical neuroprogenitor cells and its down regulation permits their differentiation. Here, we examine the expression and regulation of ATF5 in cerebellar granule neuron progenitor cells (CGNPs) as well as the role of ATF5 in the transition of CGNPs to postmitotic cerebellar granule neurons (GCNs). We find that ATF5 is expressed by proliferating CGNPs in both the embryonic and postnatal cerebellar external granule layer (EGL) and in the rhombic lip, the embryonic structure from which the EGL arises. In contrast, ATF5 is undetectable in postmitotic GCNs. In highly enriched dissociated cultures of CGNPs and CGNs, ATF5 is expressed only in CGNPs. Constitutive ATF5 expression in CGNPs does not affect their proliferation or exit from the cell cycle. In contrast, in presence of sonic hedgehog (Shh), a mitogen for CGNPs, constitutively expressed ATF5 promotes CGNP proliferation and delays their cell cycle exit and differentiation. Conversely, ATF5 loss-of-function conferred by a dominant-negative form of ATF5 significantly diminishes Shh-stimulated CGNP proliferation and promotes differentiation. In parallel with its stimulation of CGNP proliferation, Shh enhances ATF5 expression by what appeared to be a posttranscriptional mechanism involving protein stabilization. These findings indicate a reciprocal interaction between ATF5 and Shh in which Shh stimulates ATF5 expression and in which ATF5 contributes to Shh-stimulated CGNP expansion.
Predictors of Psychiatric Disorders Following Traumatic Brain Injury (2010)

Findings suggest that long-term screening and support are important for individuals with TBI, regardless of preinjury psychiatric status.
Stenting for coronary artery spasm (2002)

We evaluated coronary stenting in nine patients with clinically severe, angiographically documented spasm refractory to aggressive pharmacologic management. No patient subsequently developed unstable ischemia requiring hospitalization as a consequence of recurrent spasm within the stent. Mechanisms of therapeutic failure included both persistent spasm and spasm in a different artery in one patient. Restenosis occurred in three patients who subsequently underwent repeat revascularization. In the rare, carefully selected patient, stents may represent an adjunct in the management of focal coronary artery spasm, although currently medical therapy remains the standard initial approach.
Use of concentrated fibrinogen in experimental tracheal repair (1986)

Tracheal stenosis is a devastating complication of tracheal resection that may be related to improper suture selection and technique, as well as extensive surgical devascularization. This study evaluated Fibrin Sealant (FS) (Immuno AG, Vienna, Austria), a two-component biologic adhesive, as a method for reducing the need for sutures in tracheal surgery. This adhesive has been found to be effective in face-to-face sealing of tissues, wound healing, and in establishing hemostasis. Six adult mongrel dogs underwent tracheal repair with FS. Three had tracheal hemitransections (approximately three quarters of the circumference) and were repaired using one absorbable suture and FS, and three had complete transections (with resection of two tracheal rings each) repaired using five absorbable sutures and FS. The animals were killed at varying intervals ranging from 6 h to 6 weeks. No animal had gross evidence of significant tracheal stenosis, and the endotracheal mucosa appeared well healed. We conclude that the use of FS in tracheal reconstruction results in a stable, leakless trachea, and that it significantly reduces the number of sutures needed; this may lead to a decreased potential for anastomotic ischemia and tracheal stenosis.
Increased prevalence of intestinal inflammation in patients with liver cirrhosis (1999)

目的: 与肝 cirrhosis.METHODS 在病人调查消化道的病理生理学: 在 42 个肝脏硬化症的病人和 20 个控制题目，，下列烘便的蛋白质被连接酶的免疫测量吸着剂试金：白朊(白长袍的)，转铁蛋白( Tf )，和高山哈( 1 )反胰岛素(高山哈( 1 )是的-AT)为肠的蛋白质损失的一个标记，为流血的血红素( Hb )，为肠的发炎的 PMN-elastase ，并且为肠的 immunity.RESULTS 的能分泌的 IgA : Hb 的烘便的集中，白长袍的， Tf ，高山哈( 1 )-AT,和 PMN-elastase 在 13 被增加(31%)， 8 (19%)， 10 (24%)， 6 (14%)，并且 11 (26%)在 42 个病人之中的案例分别地。能分泌的 IgA 的烘便的集中在 7 被减少(17%) 42 个病人。然而，这些烘便的集中不与肝肝硬化的严厉或病原学有关。没有肠的蛋白质 loss.CONCLUSION，浆液白长袍的水平显著地在病人与那相比与肠的蛋白质损失在病人被减少: 这些调查结果建议那：(1 ) 除著名病理学的条件以外，肠的发炎和减少的肠的免疫例如流血和蛋白质损失，在肝脏硬化症的病人被发现；(2 ) 肠的蛋白质损失在肝脏硬化症的病人贡献血白蛋白减少，并且(3 ) 肠的发炎不应该完了在肝脏硬化症的病人看了，后来，它可以贡献或引起肠的蛋白质损失和另外的各种各样的病理学的条件。
Soluble Vascular Endothelial Growth Factor Receptor-1 (sFLT-1) Mediates Downregulation of FLT-1 and Prevents Activated Neutrophils From Women With Preeclampsia From Additional Migration by VEGF (2005)

Neutrophil activation and increased migration is associated with preeclampsia and is resolved after delivery. Preeclampsia is an inflammatory disorder where altered levels of vascular endothelial growth factor (VEGF) and the circulating soluble fms-like tyrosine kinase 1 (sFlt-1) have a pathogenic role. VEGF, by binding to FLT-1, induces leukocytic chemotaxis. We studied expression and function of FLT-1 in maternal neutrophils during preeclampsia and normal pregnancies. Analysis of maternal neutrophils showed the relationship between FLT-1 expression and week of gestation. Preeclamptic women express lower FLT-1 and sFLT-1 in neutrophils. In contrast, serum levels of sFLT-1 in patients with preeclampsia are increased and, therefore, inhibit upregulation of FLT-1 in neutrophils by neutralizing VEGF. VEGF-dependent FLT-1 expression is regulated by changing FLT-1-promoter activity. Promoter activity is decreased by sFLT-1. In vitro experiments demonstrated that migration of neutrophils is regulated by VEGF via FLT-1 and excess of sFLT-1. Thus, VEGF-dependent migration of neutrophils is decreased during preeclampsia as a consequence of excess circulating sFlt1. But, they still increase migration by fMLP and, therefore, migration of neutrophils from preeclamptic women is highly activated when compared with the normotensive group. In conclusion, besides being involved in inducing an antiangiogenic state in the serum, excess of sFLT-1 seems to prevent activated neutrophils from women with preeclampsia from additional migration by VEGF. We provide evidence that neutrophils may be involved in the pathophysiology of pregnancy-related hypertensive disorders.
Hyaluronan-CD44 Interaction with Leukemia-associated RhoGEF and Epidermal Growth Factor Receptor Promotes Rho/Ras Co-activation, Phospholipase Cϵ-Ca2+ Signaling, and Cytoskeleton Modification in Head and Neck Squamous Cell Carcinoma Cells (2006)

In this study we have examined the interaction of CD44 (a major hyaluronan (HA) receptor) with a RhoA-specific guanine nucleotide exchange factor (leukemia-associated RhoGEF (LARG)) in human head and neck squamous carcinoma cells (HNSCC-HSC-3 cell line). Immunoprecipitation and immunoblot analyses indicate that CD44 and the LARG protein are expressed in HSC-3 cells and that these two proteins are physically associated as a complex. HA-CD44 binding induces LARG-specific RhoA signaling and phospholipase C epsilon (PLC epsilon) activity. In particular, the activation of RhoA-PLC epsilon by HA stimulates inositol 1,4,5-triphosphate production, intracellular Ca2+ mobilization, and the up-regulation of Ca2+/calmodulin-dependent kinase II (CaMKII), leading to phosphorylation of the cytoskeletal protein, filamin. The phosphorylation of filamin reduces its interaction with filamentous actin, promoting tumor cell migration. The CD44-LARG complex also interacts with the EGF receptor (EGFR). Most importantly, the binding of HA to the CD44-LARG-EGFR complex activates the EGFR receptor kinase, which in turn promotes Ras-mediated stimulation of a downstream kinase cascade including the Raf-1 and ERK pathways leading to HNSCC cell growth. Using a recombinant fragment of LARG (the LARG-PDZ domain) and a binding assay, we have determined that the LARG-PDZ domain serves as a direct linker between CD44 and EGFR. Transfection of the HSC-3 cells with LARG-PDZcDNA significantly reduces LARG association with CD44 and EGFR. Overexpression of the LARG-PDZ domain also functions as a dominant-negative mutant (similar to the PLC/Ca2+-calmodulin-dependent kinase II (CaMKII) and EGFR/MAPK inhibitor effects) to block HA/CD44-mediated signaling events (e.g. EGFR kinase activation, Ras/RhoA co-activation, Raf-ERK signaling, PLC epsilon-mediated inositol 1,4,5-triphosphate production, intracellular Ca2+ mobilization, CaMKII activity, filamin phosphorylation, and filamin-actin binding) and to abrogate tumor cell growth/migration. Taken together, our findings suggest that CD44 interaction with LARG and EGFR plays a pivotal role in Rho/Ras co-activation, PLC epsilon-Ca2+ signaling, and Raf/ERK up-regulation required for CaMKII-mediated cytoskeleton function and in head and neck squamous cell carcinoma progression.
Dielectric breakdown of TMR sensors and the role of Joule heating (2016)

For voltage (V) stress of TMRs, the log of the dielectric breakdown time is found to be linear in (H-γZaV/t <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">B</sub> )/(k <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">B</sub> T), where H, γ, Z, a, t <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">B</sub> and k <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">B</sub> are an activation energy, a parameter, charge, tunnel barrier lattice constant and thickness, and Boltzmann constant. T is the ambient plus Joule heating temperature of the tunnel barrier.
Control of bacterial biofilms with marine alkaloid derivatives (2008)

Bacterial biofilms are defined as a community of surface-attached bacteria that are protected by an extracellular matrix of biomolecules. We have recently reported the synthesis of a small molecule, denoted TAGE, based on the natural product bromoageliferin and demonstrated that TAGE has anti-biofilm activity against Pseudomonas aeruginosa. Herein we demonstrate that TAGE: (1) does not have selective toxicity against cells within the biofilm state, (2) will inhibit biofilm development under flow conditions, indicating that the CV staining protocol correlates with the ability to be active under biomimetic conditions, and (3) will disperse preformed P. aeruginosa biofilms. We also present preliminary toxicity work that indicates that TAGE is devoid of cytotoxicity in rat and mice cell lines. Advanced derivatives of TAGE have generated compounds shown to be exceedingly effective as biofilm inhibitors against the gamma-proteobacteria in this study (P. aeruginosa strains PAO1, PA14, PDO300, and Acinetobacter baumannii). TAGE derivatives also possessed anti-biofilm activity against the beta-proteobacterium Bordetella bronchiseptica (Rb50) and the Gram-positive bacterium Staphylococcus aureus;TAGE derivatives inhibited the formation of biofilms, however, some of this activity is attributed to microbicidal activity. The TAGE derivatives presented in this study, however, do not disperse pre-formed biofilms with the same efficiency as TAGE.
Performance of two-stage massive correlator architecture for fast acquisition of GPS signals (2006)

A typical operation of GPS receivers assumes a search of the satellites visible on the sky by synchronizing locally generated replica with the transmitted pseudo-random noise (PRN) code sequence. This synchronization is initially performed by finding the highest correlation between the incoming signal and replica, a process known as “acquisition”. Highest correlation is observed as a correlator peak response which is compared with a certain threshold to identify availability and values of unknown code phase and frequency of a residual carrier modulation. If the peak is not detected or the decision is wrong then acquisition stage should be repeated many times which is quite a time consuming task. State-of-the-art advanced receivers use massive correlators which parallelize the acquisition process. While massive correlators improve significantly the sensitivity of the receivers, so-called multiple peak selection approach provides an opportunity to save computations by sharing tasks between the massive correlator and validation system [1]. In this paper we study a performance of two stage correlator consisting of massive and supplementary implementations. The massive correlator is not making firm decisions each time it finds a peak, but provides several possible options (a limited set of highest peaks) to supplementary system.
Physiological response to anaerobicity of glycerol-3-phosphate dehydrogenase mutants of Saccharomyces cerevisiae (1997)

Mutants of Saccharomyces cerevisiae, in which one or both of the genes encoding the two isoforms of NAD-dependent glycerol-3-phosphate dehydrogenase had been deleted, were studied in aerobic batch cultures and in aerobic-anaerobic step change experiments. The respirofermentative growth rates under aerobic conditions with semisynthetic medium (20 g of glucose per liter) of two single mutants, gpd1 delta and gpd2 delta, and the parental strain (mu = 0.5 h-1) were almost identical, whereas the growth rate of a double mutant, gpd1 delta gpd2 delta, was approximately half that of the parental strain. Upon a step change from aerobic to anaerobic conditions in the exponential growth phase, the specific carbon dioxide evolution rates (CER) of the wild-type strain and the gpd1 delta strain were almost unchanged. The gpd2 delta mutant showed an immediate, large (> 50%) decrease in CER upon a change to anaerobic conditions. However, after about 45 min the CER increased again, although not to the same level as under aerobic conditions. The gpd1 delta gpd2 delta mutant showed a drastic fermentation rate decrease upon a transition to anaerobic conditions. However, the CER values increased to and even exceeded the aerobic levels after the addition of acetoin. High-pressure liquid chromatographic analyses demonstrated that the added acetoin served as an acceptor of reducing equivalents by being reduced to butanediol. The results clearly show the necessity of glycerol formation as a redox sink for S. cerevisiae under anaerobic conditions.
Sulforaphane, an activator of Nrf2, suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes (2006)

Sulforaphane (SFN) is an activator of the transcription factor Nrf2, which plays a critical role in metabolism and excretion of xenobiotics. Exposure of primary mouse hepatocytes to SFN resulted in activation of Nrf2 and significant elevation of protein expressions responsible for excretion of arsenic into extracellular space. Pretreatment with SFN 24 h prior to arsenite exposure reduced not only arsenic accumulation in the cells but also cellular toxicity of this metalloid. Therefore, our findings indicate a potential function of SFN in reducing cellular arsenic levels, thereby diminishing arsenic toxicity.
MEASUREMENT OF ACTIVITY OF SINGLE MOLECULES OF β-D-GALACTOSIDASE (1961)

Proceedings of the National Academy of Sciences (PNAS), a peer reviewed journal of the National Academy of Sciences (NAS) - an authoritative source of high-impact, original research that broadly spans the biological, physical, and social sciences.
Longitudinal study of clinical and radiological progression in psoriatic arthritis. (1990)

Our aim was to document the progression of psoriatic arthritis in 126 patients prospectively evaluated for a minimum of 5 years. Clinical and laboratory variables and radiographs of the hands and feet, recorded at first and last assessment, were compared to document change in the degree of joint inflammation and damage. During followup there was a significant increase in the use of a number of therapeutic modalities, in particular, gold, PUVA, retinoids and intraarticular glucocorticoid injections. Evidence of inflammatory arthritis was decreased at last assessment relative to presentation. The rate of progression of joint damage, calculated by the ratio of the number of damaged joints to the duration of arthritis in years, actually decreased during followup from 1.97/year to 0.5/year. Nevertheless the proportion of patients with at least 5 damaged joints doubled from 19 to 41% during the study. Thus, despite active treatment and a reduction in joint inflammation and in rate of damage, psoriatic arthritis may be a progressively deforming arthritis, even during 5 years of followup.
Whole Blood Capcellia CD4/CD8 Immunoassay for Enumeration of CD4+ and CD8+ Peripheral T Lymphocytes (1999)

We evaluated the Whole Blood Capcellia(R) CD4/CD8, an immunoenzymatic method that provides absolute counts of CD4+ and CD8+ T cells in peripheral blood. The assay is based on the separation of T cells by use of an anti-CD2 magnetic bead suspension, followed by reaction of the CD4 or CD8 molecules with the corresponding monoclonal antibody coupled to peroxidase. CD4-positive monocytes were excluded from the assay. Freeze-dried magnetic bead-T-cell complexes were used as calibrators. Capcellia counts from HIV-1-infected patients were compared with those obtained by flow cytometry as the comparison method. The results by Capcellia correlated well with those by flow cytometric analysis: r2 = 0.95; P <0.001; (y = 0.96x - 22.1); Sy|x = 64 for CD4; r2 = 0.81; P <0.001; (y = 1.26x - 76.4); Sy|x = 139 for CD8; n = 76. The correlation between CD4+ T-cell counts determined by two trained experimenters was significant (r2 = 0.96). Our results indicate that this new ELISA technique for lymphocyte immunophenotyping is an efficient alternative to flow cytometry.
Notch: Implications of endogenous inhibitors for therapy (2010)

Soluble components of Notch signalling can be applied to manipulate a central pathway essential for the development of metazoans and often deregulated in illnesses such as stroke, cancer or cardiovascular diseases. Commonly, the Notch cascade is inhibited by small compound inhibitors, which either block the proteolysis of Notch receptors by gamma-secretases or interfere with the transcriptional activity of the Notch intracellular domain. Specific antibodies can also be used to inhibit ligand-induced activation of Notch receptors. Alternatively, naturally occurring endogenous inhibitors of Notch signalling might offer a specific way to block receptor activation. Examples are the soluble variants of the canonical Notch ligand Jagged1 and the non-canonical Notch ligand Dlk1, both deprived of their transmembrane regions upon ectodomain shedding, or the bona fide secreted molecule EGFL7. We present frequently used methods to decrease Notch signalling, and we discuss how soluble Notch inhibitors may be used to treat diseases.
Mammalian DNA ligases (1997)

DNA joining enzymes play an essential role in the maintenance of genomic integrity and stability. Three mammalian genes encoding DNA ligases, LIG1, LIG3 and LIG4, have been identified. Since DNA ligase II appears to be derived from DNA ligase III by a proteolytic mechanism, the three LIG genes can account for the four biochemically distinct DNA ligase activities, DNA ligases I, II, III and IV, that have been purified from mammalian cell extracts. It is probable that the specific cellular roles of these enzymes are determined by the proteins with which they interact. The specific involvement of DNA ligase I in DNA replication is mediated by the non-catalytic amino-terminal domain of this enzyme. Furthermore, DNA ligase I participates in DNA base excision repair as a component of a multiprotein complex. Two forms of DNA ligase III are produced by an alternative splicing mechanism. The ubiqitously expressed DNA ligase III-alpha forms a complex with the DNA single-strand break repair protein XRCC1. In contrast, DNA ligase III-beta, which does not interact with XRCC1, is only expressed in male meiotic germ cells, suggesting a role for this isoform in meiotic recombination. At present, there is very little information about the cellular functions of DNA ligase IV.
Only the Tip of the Iceberg (1995)

This paper gives an historical account of a consumer perspective on breast cancer screening in Australia from the viewpoint of a rural woman from New South Wales who has represented consumers on the National Advisory Committee for the Early Detection of Breast Cancer. The account includes reasons why I started to research breast cancer screening and how the research was conducted as well as a summary of the research findings. Over the 5 year period of consumer representation, advocacy and research, my views on breast cancer screening have changed very little despite my role in national breast cancer screening policy development and in the management of the North West Breast Cancer Screening Service. My role in the development, implementation and evaluation of breast cancer screening policy in Australia is then discussed in terms of consumer advocacy versus bureaucratic cooption.