gebhart/patrepeval huggingface dataset:
Development of a Patient-Specific Multi-Scale Model to Understand Atherosclerosis and Calcification Locations: Comparison with In vivo Data in an Aortic Dissection (2016)

Vascular calcification results in stiffening of the aorta and is associated with hypertension and atherosclerosis. Atherogenesis is a complex, multifactorial, and systemic process; the result of a number of factors, each operating simultaneously at several spatial and temporal scales. The ability to predict sites of atherogenesis would be of great use to clinicians in order to improve diagnostic and treatment planning. In this paper, we present a mathematical model as a tool to understand why atherosclerotic plaque and calcifications occur in specific locations. This model is then used to analyze vascular calcification and atherosclerotic areas in an aortic dissection patient using a mechanistic, multi-scale modeling approach, coupling patient-specific, fluid-structure interaction simulations with a model of endothelial mechanotransduction. A number of hemodynamic factors based on state-of-the-art literature are used as inputs to the endothelial permeability model, in order to investigate plaque and calcification distributions, which are compared with clinical imaging data. A significantly improved correlation between elevated hydraulic conductivity or volume flux and the presence of calcification and plaques was achieved by using a shear index comprising both mean and oscillatory shear components (HOLMES) and a non-Newtonian viscosity model as inputs, as compared to widely used hemodynamic indicators. The proposed approach shows promise as a predictive tool. The improvements obtained using the combined biomechanical/biochemical modeling approach highlight the benefits of mechanistic modeling as a powerful tool to understand complex phenomena and provides insight into the relative importance of key hemodynamic parameters.
Cancer statistics, 2017 (2017)

Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics. In 2017, 1,688,780 new cancer cases and 600,920 cancer deaths are projected to occur in the United States. For all sites combined, the cancer incidence rate is 20% higher in men than in women, while the cancer death rate is 40% higher. However, sex disparities vary by cancer type. For example, thyroid cancer incidence rates are 3-fold higher in women than in men (21 vs 7 per 100,000 population), despite equivalent death rates (0.5 per 100,000 population), largely reflecting sex differences in the "epidemic of diagnosis." Over the past decade of available data, the overall cancer incidence rate (2004-2013) was stable in women and declined by approximately 2% annually in men, while the cancer death rate (2005-2014) declined by about 1.5% annually in both men and women. From 1991 to 2014, the overall cancer death rate dropped 25%, translating to approximately 2,143,200 fewer cancer deaths than would have been expected if death rates had remained at their peak. Although the cancer death rate was 15% higher in blacks than in whites in 2014, increasing access to care as a result of the Patient Protection and Affordable Care Act may expedite the narrowing racial gap; from 2010 to 2015, the proportion of blacks who were uninsured halved, from 21% to 11%, as it did for Hispanics (31% to 16%). Gains in coverage for traditionally underserved Americans will facilitate the broader application of existing cancer control knowledge across every segment of the population. CA Cancer J Clin 2017;67:7-30. © 2017 American Cancer Society.
beta-Amyloid fibrils activate parallel mitogen-activated protein kinase pathways in microglia and THP1 monocytes. (1998)

The senile plaques of Alzheimer's disease are foci of local inflammatory responses, as evidenced by the presence of acute phase proteins and oxidative damage. Fibrillar forms of beta-amyloid (Abeta), which are the primary constituents of senile plaques, have been shown to activate tyrosine kinase-dependent signal transduction cascades, resulting in inflammatory responses in microglia. However, the downstream signaling pathways mediating Abeta-induced inflammatory events are not well characterized. We report that exposure of primary rat microglia and human THP1 monocytes to fibrillar Abeta results in the tyrosine kinase-dependent activation of two parallel signal transduction cascades involving members of the mitogen-activated protein kinase (MAPK) superfamily. Abeta stimulated the rapid, transient activation of extracellular signal-regulated kinase 1 (ERK1) and ERK2 in microglia and ERK2 in THP1 monocytes. A second superfamily member, p38 MAPK, was also activated with similar kinetics. Scavenger receptor and receptor for advanced glycated end products (RAGE) ligands failed to activate ERK and p38 MAPK in the absence of significant increases in protein tyrosine phosphorylation, demonstrating that scavenger receptors and RAGE are not linked to these pathways. Importantly, the stress-activated protein kinases (SAPKs) were not significantly activated in response to Abeta. Downstream effectors of the MAPK signal transduction cascades include MAPKAP kinases, such as RSK1 and RSK2, as well as transcription factors. Exposure of microglia and THP1 monocytes to Abeta resulted in the activation of RSK1 and RSK2 and phosphorylation of cAMP response element-binding protein at Ser133, providing a mechanism for Abeta-induced changes in gene expression.
Effect of Depot Oral Cholecalciferol Treatment on Secondary Hyperparathyroidism in Stage 3 and Stage 4 Chronic Kidney Diseases Patients (2008)

By the time patients require dialysis replacement therapy, nearly all chronic kidney diseases (CKD) patients are affected with uremic bone diseases. High-turnover osteodystrophy can be prevented; patients with CKD should be monitored for imbalances in calcidiol (25 OH vitamin D), calcium, and phosphate homeostasis. We aimed to determine the effect of a monthly oral 300,000 IU vitamin D(3) (cholecalciferol) supplementation on the uremic bone diseases (UBD) markers such as iPTH and alkaline phosphatase in CKD patients. Among a total of 70 patients under treatment in the nephrology unit, 40 predialysis CKD patients (mean age of 49 +/- 14, male/female 20/20) were included the study. The patients were randomly divided into two groups. Treatment group included 20 patients (mean age of 51 +/- 14, male/female 9/11), and the control group comprised 20 patients (mean age of 47 +/- 14, male/female 9/11). Treatment group patients were given a single dose of Devit3 ampoule (300,000 U cholecalciferol) per month orally way. Patients in the control group did not take any vitamin D for a month. The level of calcidiol was lower than normal range in two groups. After a month, treatment group patient's calcidiol increased statistically significant (6.8 +/- 3.5 to 17.8 +/- 21.4 ng/mL, p < 0.001). After a month, iPTH level decreased in the treatment group statistically significantly (368 +/- 274 to 279 +/- 179 pg/ml, p < 0.001). At the 30(th) day of the treatment, in 9/20 of the treatment group patients (45%), the iPTH value decreased at least 30% (p < 0.001). We suggest that oral depot cholecalciferol treatment causes a statistically significant decrease of serum iPTH level but does not cause a statistically significant change in Ca, P, ratio of Ca x P, or urinary calcium creatinine rate in UBD predialysis CKD. This treatment can be used safely for the predialysis CKD patients, along with the cautious control of serum calcium and phosphor.
Suzuki-Miyaura coupling of arylboronic acids to (2015)

Gold(III) is prominent in catalysis, but its organometallic chemistry continues to be restricted by synthesis. Metal–carbon bond formation often relies on organometallic complexes of electropositive elements, including lithium and magnesium. The redox potential of gold(III) interferes with reactions of these classic reagents. Resort to toxic metals is common, including reagents based on mercury and thallium. We report that the palladium-catalyzed Suzuki–Miyaura coupling of arylboronic acids extends to cyclometalated gold(III) chlorides. Both monoarylation and diarylation are achieved. We propose a mechanism where oxidative addition to palladium with rearrangement at gold(III) fixes the stereochemistry of monoarylated intermediates. Singly arylated species form as thermodynamic isomers. These entities then go on to form diarylated complexes. Reactions proceed at room temperature, and the products are stable to air, moisture, and chromatography.
Functional leukemia-associated antigen-specific memory CD8+ T cells exist in healthy individuals and in patients with chronic myelogenous leukemia before and after stem cell transplantation (2003)

Antigens implicated in the graft-versus-leukemia (GVL) effect in chronic myeloid leukemia (CML) include WT1, PR1, and BCR-ABL. To detect very low frequencies of these antigen-specific CD8+ T cells, we used quantitative polymerase chain reaction (qPCR) to measure interferon-gamma (IFN-gamma) mRNA production by peptide-pulsed CD8+ T cells from HLA-A*0201+ healthy volunteers and from patients with CML before and after allogeneic stem cell transplantation (SCT). Parallel assays using cytomegalovirus (CMV) pp65 tetramers demonstrated the IFN-gamma copy number to be linearly related to the frequency of tetramer-binding T cells, sensitive to frequencies of 1 responding CD8+ T cell/100 000 CD8+ T cells. Responses to WT1 and PR1 but not BCR-ABL were detected in 10 of 18 healthy donors. Responses to WT1, PR1, or BCR-ABL were observed in 9 of 14 patients with CML before SCT and 5 of 6 after SCT, often to multiple epitopes. Responses were higher in patients with CML compared with healthy donors and highest after SCT. These antigen-specific CD8+ T cells comprised central memory (CD45RO+CD27+CD57-) and effector memory (CD45RO-CD27-CD57+) T cells. In conclusion, leukemia-reactive CD8+ T cells derive from memory T cells and occur at low frequencies in healthy individuals and at higher frequencies in patients with CML. The increased response in patients after SCT suggests a quantitative explanation for the greater effect of allogeneic SCT.
Biochemical and Morphological Characterization of the Intra-Acrosomal Antigen SP-1O from Human Sperm1 (1990)

The human sperm protein SP-10 was previously defined as a "primary vaccine candidate" by a World Health Organization Taskforce on Contraceptive Vaccines. By one- and two-dimensional immunoblots, we show that SP-10, extracted from ejaculated human sperm, demonstrated a polymorphism of immunogenic peptides from 18 to 34 kDa, a pattern that was conserved from individual to individual and was not altered by reducing agents. The majority of the antigenic peptides possessed isoelectric points of approximately 4.9. Immunocytochemistry on testis sections indicated that SP-10 was localized to round spermatids and spermatozoa within the adluminal compartment of the seminiferous epithelium. Immunofluorescence showed that SP-10 was not associated with the surface of acrosome-intact, ejaculated sperm. Light and electron microscopic immunocytochemistry localized SP-10 throughout the acrosome, and electron microscopic evidence demonstrated a bilaminar array in association with the inner aspect of the outer acrosomal membrane and the outer aspect of the inner acrosomal membrane. After induction of the acrosome reaction with the ionophore A23187, SP-10 remained displayed on the sperm head in association with the inner acrosomal membrane and equatorial segment. The results indicate that the MHS-10 monoclonal antibody may be used as a marker of acrosome development in the human and as a probe to evaluate acrosome status. The results also support the hypothesis that inhibition of sperm-egg interaction by anti-SP-10 monoclonal antibody may occur as a result of antigen exposure following the acrosome reaction.
Novel α-Amylase That Is Highly Resistant to Chelating Reagents and Chemical Oxidants from the Alkaliphilic Bacillus Isolate KSM-K38 (2001)

A novel alpha-amylase (AmyK38) was found in cultures of an alkaliphilic Bacillus isolate designated KSM-K38. Based on the morphological and physiological characteristics and phylogenetic position as determined by 16S ribosomal DNA gene sequencing and DNA-DNA reassociation analysis, it was suggested that the isolate was a new species of the genus Bacillus. The enzyme had an optimal pH of 8.0 to 9.5 and displayed maximum catalytic activity at 55 to 60 degrees C. The apparent molecular mass was approximately 55 kDa, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the isoelectric point was around pH 4.2. This enzyme efficiently hydrolyzed various carbohydrates to yield maltotriose, maltohexaose, maltoheptaose, and, in addition, maltose as major end products after completion of the reaction. The activity was not prevented at all by EDTA and EGTA at concentrations as high as 100 mM. Moreover, AmyK38 was highly resistant to chemical oxidation and maintained more than 80% of its original activity even after incubation for 1 h in the presence of excess H2O2 (1.8 M).
Differential free-radical activity after successful and unsuccessful thrombolytic reperfusion in acute myocardial infarction (1993)

Successful early reperfusion and non-Q-wave myocardial infarction are both associated with a significantly greater increase in the levels of markers of serum free-radical activity immediately after infarction. The results support present concepts of free-radical-mediated reperfusion injury. Use of these assays may identify those patients who may be at risk from free-radical-mediated reperfusion injury.
Ligation of CD11b and CD11c β2 integrins by antibodies or soluble CD23 induces macrophage inflammatory protein 1α (MIP-1α) and MIP-1β production in primary human monocytes through a pathway dependent on nuclear factor–κB (2001)

Chemokines and adhesion molecules such as integrins play a major part in the trafficking, extravasation, and recruitment of leukocytes to inflammatory sites. This study investigated the effects of beta(2) integrin engagement on chemokine production by freshly isolated human monocytes. We found that ligation of CD11b or CD11c but not CD11a alpha chains of beta(2) integrins by antibodies or soluble CD23 (sCD23) fusion proteins rapidly induced transcription and secretion of interleukin 8, macrophage inflammatory protein (MIP) 1alpha, and MIP-1beta. Because the promoters of these chemokine genes contain kappaB binding sites, we assessed the possible role of nuclear factor-kappaB (NF-kappaB) in controlling induction of the genes through beta(2) integrin engagement. Electrophoretic mobility shift assays showed that sCD23 or antibodies to CD11b or to CD11c up-regulated DNA-binding activity of NF-kappaB. Activation of NF-kappaB was accompanied by degradation of its cytosolic inhibitor IkappaB-alpha. Blockade of depletion of IkappaB-alpha by proteasome inhibitors (proteasome inhibitor I or acetyl-leucinyl-leucinyl-norleucinal) led to concomitant inhibition of NF-kappaB DNA-binding activity and expression of MIP-1alpha and MIP-1beta messenger RNA induced by beta(2) integrin ligation. These results suggest that triggering of CD11b or CD11c beta(2) integrin on primary human monocytes provides activation signals leading to nuclear translocation of NF-kappaB and subsequent secretion of MIP-1alpha and MIP-1beta that may have an important role in recruitment of other inflammatory cells during initiation of an inflammatory response.
Lack of plasminogen activator inhibitor-1 effect in a transgenic mouse model of metastatic melanoma. (1996)

Tumor cell invasion and metastasis is a complex, multistep process that is postulated to require degradation of extracellular matrix at several steps. Urokinase-type plasminogen activator (uPA) is expressed on the cell surface of B16 murine melanoma cells and is thought to contribute to the pericellular proteolysis necessary for tumor cell migration. In vitro modification of B16 melanoma cell surface uPA activity has been shown to alter the invasive and metastatic potential of these murine melanoma cells in vivo. Plasminogen activator inhibitor-1 (PAI-1), a rapid inhibitor of both uPA and tissue-type plasminogen activator (tPA) is the major physiologic regulator of plasminogen activator activity. To test the role of host PAI-1 in the invasive and metastatic capacity of B16 melanoma cells we analyzed local tumor growth and pulmonary metastasis in transgenic mice engineered to overexpress murine PAI-1 in multiple tissues including lung, and in mice completely deficient in PAI-1. No significant difference in the number of pulmonary metastases was observed after intravenous inoculation of tumor cells into PAI-1-overexpressing and PAI-1-deficient mice when compared with wild-type controls. Similarly, in a spontaneous metastasis model, PAI-1-overexpressing and PAI-1-deficient mice demonstrated no difference in primary tumor size or overall survival. These data demonstrate that wide variations of host PAI-1 expression, from complete absence to marked overexpression, does not significantly influence the metastatic potential of B16 melanoma cells in a murine model.
Case Report (2014)

Pediatric Perspectives| April 01 2014 Case Report: Pulmonary Edema Induced by Breath Holding in an Adolescent Patient Serena Phromsivarak Kelly, MS, FNP, CCRN; Serena Phromsivarak Kelly, MS, FNP, CCRN Serena Phromsivarak Kelly is Nurse Practitioner, Pediatric Intensive Care Unit, Doernbecher Children’s Hospital, Oregon Health & Science University, Portland, Oregon. Ashley Jones is Pediatric Critical Care Fellow, Pediatric Intensive Care Unit, Doernbecher Children’s Hospital, Oregon Health & Science University, Portland, Oregon. Robert Steelman is Associate Professor, Pediatric Critical Care Medicine/Anesthesiology Oregon Health & Science University, 700 SW Campus Drive, Portland, OR 97239 (steelmar@ohsu.edu). Search for other works by this author on: This Site PubMed Google Scholar Ashley Jones, MD; Ashley Jones, MD Serena Phromsivarak Kelly is Nurse Practitioner, Pediatric Intensive Care Unit, Doernbecher Children’s Hospital, Oregon Health & Science University, Portland, Oregon. Ashley Jones is Pediatric Critical Care Fellow, Pediatric Intensive Care Unit, Doernbecher Children’s Hospital, Oregon Health & Science University, Portland, Oregon. Robert Steelman is Associate Professor, Pediatric Critical Care Medicine/Anesthesiology Oregon Health & Science University, 700 SW Campus Drive, Portland, OR 97239 (steelmar@ohsu.edu). Search for other works by this author on: This Site PubMed Google Scholar Robert Steelman, MD, DMD Robert Steelman, MD, DMD Serena Phromsivarak Kelly is Nurse Practitioner, Pediatric Intensive Care Unit, Doernbecher Children’s Hospital, Oregon Health & Science University, Portland, Oregon. Ashley Jones is Pediatric Critical Care Fellow, Pediatric Intensive Care Unit, Doernbecher Children’s Hospital, Oregon Health & Science University, Portland, Oregon. Robert Steelman is Associate Professor, Pediatric Critical Care Medicine/Anesthesiology Oregon Health & Science University, 700 SW Campus Drive, Portland, OR 97239 (steelmar@ohsu.edu). Search for other works by this author on: This Site PubMed Google Scholar AACN Adv Crit Care (2014) 25 (2): 101–103. https://doi.org/10.4037/NCI.0000000000000021 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Cite Icon Cite Get Permissions Citation Serena Phromsivarak Kelly, Ashley Jones, Robert Steelman; Case Report: Pulmonary Edema Induced by Breath Holding in an Adolescent Patient. AACN Adv Crit Care 1 April 2014; 25 (2): 101–103. doi: https://doi.org/10.4037/NCI.0000000000000021 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search nav search search input Search input auto suggest search filter All ContentAACN Advanced Critical Care Search Advanced Search You do not currently have access to this content.
The Exploration of Tissue pH and its Relationship to Bacterial Contamination (2000)

Presently, plastic surgeons do not have a methodology for non-invasive, real-time assessment of wound tissue properties. It is of extreme importance to objectively determine the health of wound tissue and the level of bacterial infection before surgical closure of the wound is attempted. Wounds that possess significant areas of low blood perfusion and high levels of bacteria will not be successfully grafted. Thus, this research aims at identifying and testing a measurable parameter for the assessment of tissue properties in acute and chronic wounds. Tissue pH, which is easily measured, has been proven to detect the presence of tissue ischemia. In this research, the variations of tissue pH levels in patient wounds and the relationship between tissue pH and bacteria levels were explored. Micro-combination pH electrodes were tested; software algorithms for acquiring and processing raw tissue pH data were developed; and calibration, sterilization, animal, and clinical protocols were designed. Animal and clinical studies were performed. Small variations in tissue pH values were found within patient wounds and between patient cases. A qualitative relationship between tissue pH levels and bacterial contamination was identified. As the bacterial contamination, rises, the averaage tissue pH level tends to decrease. A methodology that clinicians can use to efficiently measure tissue pH in wounds was developed. This research provides preliminary work in an area that has not been previously explored. It was shown that tissue pH measurements can be acquired efficiently, non-invasively, and with no discomfort to the patient. The incorporation of tissue pH measurements into the evaluation of wounds will contribute to providing an objective measure of the health of the tissue and aid plastic surgeons in the development of patient treatments.
SOLVATOCHROMIC SOLVENT POLARITY MEASUREMENTS OF ALCOHOL SOLVENT MODIFIERS AND CORRELATION WITH CESIUM EXTRACTION STRENGTH1† (2001)

Solvatochromic solvent polarity measurements reveal that the cesium extraction strength afforded by solutions composed of calix[4]arene-bis-(tert-octylbenzocrown-6) at 0.005 M in 1,2-dichloroethane containing a variety of novel alcohol phase modifiers at 0.25 M correlates well with the hydrogen-bond donor (HBD) ability of the alcohol. The alcohols comprise a small library of derivatives of 2-(4-tert-octylphenoxy)-1-ethanol, in which the alcohol carbon atom contains a substituent of variable electron-withdrawing ability. The betaine dye 4-(2,4,6-triphenylpyridinium)-2,6-diphenylphenoxide, also known as Dimroth-Reichardt dye #30, was used to obtain ET(30) and ET N values. Alcohols containing substituents with fluorine atoms gave rise to both higher ET N values and higher cesium distribution values. The trend observed in HDB parallels the expected trend in alcohol acidity. †This research was sponsored by the Office of Science, Office of Basic Energy Sciences, U.S. Department of Energy, under contract number ...
The ghosts of Florida (1994)

Cutaneous botryomycosis is a chronic focal infection characterized by a granulomatous inflammatory response to bacterial pathogens such as Staphylococcus aureus. Treatment requires antibiotic therapy and may also require surgical debridement. We employed topical heat therapy and oral minocycline. The lesions became flattened and pigmented after 1 month. We consider that this simple treatment can be an effective and harmless complementary therapy for cutaneous botryomycosis.