gebhart/patrepeval huggingface dataset:
PROLONGATION OF RAT ISLET ALLOGRAFT SURVIVAL BY TREATMENT WITH MONOCLONAL ANTIBODIES AGAINST VLA-4 AND LFA-1 (1995)

In this study, we investigated the effects of treatment with monoclonal antibodies against the VLA-4 and LFA-1 adhesion molecules on rat islet allograft rejection. TA-2 and TA-3 are function-blocking mAb against rat VLA-4 and LFA-1, respectively. Lewis rats were made diabetic (plasma glucose levels > 22.2 mmol/L) with streptozotocin. One week later, 1500 freshly isolated Wistar Furth rat islets were transplanted under the left kidney capsule of each rat. Monoclonal antibodies were administered intravenously at a dosage of 2 mg on the day of islet transplantation and then intraperitoneally every second day for 3 weeks or until graft rejection. Plasma glucose levels were monitored at least 3 times a week and blood leukocyte counts were monitored every 4 days. Rejection was defined as 2 plasma glucose levels > 11.1 mmol/L. Mean graft survival times in untreated and control mAb-treated rats were 5.3 and 6.0 days, respectively. Treatment with anti-VLA-4 or anti-LFA-1 resulted in only modest prolongation of mean graft survival time (9.3 and 7.4 days, respectively). However, treatment with the combination of anti-VLA-4 plus anti-LFA-1 resulted in long-term (i.e., 60-day) graft survival in 5 of 7 rats. Graft nephrectomy and histology confirmed islet graft survival at 60 days. A second Wistar Furth rat islet graft under the opposite renal capsule after graft nephrectomy did not show full tolerance; however, the function of the second graft was significantly prolonged without any immunosuppression. Combined blockade of VLA-4 and LFA-1 also markedly prolonged islet graft survival when islets were transplanted via the portal vein. In conclusion, both VLA-4 and LFA-1 play a role in islet allograft rejection and blockade of both prevents or greatly delays graft rejection.
T helper type 1–specific Brg1 recruitment and remodeling of nucleosomes positioned at the IFN-γ promoter are Stat4 dependent (2006)

Transcriptional competence of the interferon-gamma (IFN-gamma) locus is enhanced as Th1 effectors develop from naive CD4 T lymphocytes; conversely, this gene is repressed during Th2 differentiation. We now show that the Switch (Swi)-sucrose nonfermenter (SNF) component Brahma-related gene 1 (Brg1) is recruited, and positioned nucleosomes are remodeled, in a Th1-specific manner that is dependent on the transcription factor Stat4 and calcineurin phosphatase activity. Interference with specific components of mammalian Swi-SNF complexes decreased CD4 T cell differentiation into IFN-gamma-positive Th1 cells. These findings reveal a collaborative mechanism of IFN-gamma gene regulation during Th1 differentiation and suggest that a Th1-specific chromatin structure is created by early recruitment of Swi-SNF complexes and nucleosome remodeling dependent on Stat4 and calcineurin activation.
Inhibition of Neovascularization by a Cartilage Factor (1983)

Neovascularization of developing, repairing or neoplastic tissues is regulated, at least partially, by a family of proteins of low molecular mass (1000 less than mol mass less than 50 000 Da) which can be extracted from avascular tissues, such as hyaline cartilage, aorta or bladder epithelium, by mild salt solutions. These extractable proteins, functionally defined as anti-invasion factor (AIF), act as local regulators for some of the major mechanistic pathways by which endothelial cells are thought to invade tissues during neovascularization, mainly by matrix-degrading enzymes and by increased rates of migration and proliferation. AIF contains a spectrum of proteinase (collagenase) inhibitory activities, as well as an endothelial cell growth inhibitor. The endothelial cell growth inhibitor is directed against actively dividing endothelial cells in culture but has no effect on endothelial cell monolayers or any other cell lines tested. In tumours, the AIF-derived endothelial cell growth inhibitor may limit tumour growth to less than 2 mm in diameter by inhibiting tumour neovascularization.
Mesenchymal stem cells ameliorate experimental peritoneal fibrosis by suppressing inflammation and inhibiting TGF-β1 signaling (2013)

Mesenchymal stem cells (MSCs) are multipotent adult stem cells that have regenerative capability and exert paracrine actions on damaged tissues. Since peritoneal fibrosis is a serious complication of peritoneal dialysis, we tested whether MSCs suppress this using a chlorhexidine gluconate model in rats. Although MSCs isolated from green fluorescent protein-positive rats were detected for only 3 days following their injection, immunohistochemical staining showed that MSCs suppressed the expression of mesenchymal cells, their effects on the deposition of extracellular matrix proteins, and the infiltration of macrophages for 14 days. Moreover, MSCs reduced the functional impairment of the peritoneal membrane. Cocultures of MSCs and human peritoneal mesothelial cells using a Transwell system indicated that the beneficial effects of MSCs on the glucose-induced upregulation of transforming growth factor-β1(TGF-β1) and fibronectin mRNA expression in the human cells were likely due to paracrine actions. Preincubation in MSC-conditioned medium suppressed TGF-β1-induced epithelial-to-mesenchymal transition, α-smooth muscle actin, and the decrease in zonula occludens-1 in cultured human peritoneal mesothelial cells. Although bone morphogenic protein 7 was not detected, MSCs secreted hepatocyte growth factor and a neutralizing antibody to this inhibited TGF-β1 signaling. Thus, our findings imply that MSCs ameliorate experimental peritoneal fibrosis by suppressing inflammation and TGF-β1 signaling in a paracrine manner.
Isolation of human cDNA clones ofmyb-related genes, A-myband B-myb (1988)

cDNA clones of the myb-related genes A-myb and B-myb were obtained by screening human cDNA libraries. The predicted open reading frame of B-myb could encode a protein of 700 amino acid residues. Although the C-terminal end has not been cloned yet, an almost entire coding region of A-myb, which is 745 amino acid long, was determined. The A-myb and B-myb proteins are highly homologous with the myb protein in three regions. Domain I, which is 161 amino acid long, is well conserved in the myb gene family. The homology between human-myb and A-myb in domain I is 90% at the amino acid level. Domain II, which is about 85 amino acid long, is less well conserved. Although it is a short stretch, domain III is found in the C-terminal region. The mRNAs of A-myb and B-myb were 5.0 and 2.6kb, respectively. The mRNA expression pattern of the myb gene family in various tumors is presented.
The Metabolic Syndrome, Circulating Oxidized LDL, and Risk of Myocardial Infarction in Well-Functioning Elderly People in the Health, Aging, and Body Composition Cohort (2004)

The object of this study was to establish the association between the metabolic syndrome and oxidized LDL (oxLDL) and to determine the risk for coronary heart disease (CHD) in relation to the metabolic syndrome and levels of oxLDL. OxLDL was measured in plasma from 3,033 elderly participants in the Health, Aging, and Body Composition study. The metabolic syndrome was defined according to criteria established in the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. We observed that the metabolic syndrome was associated with higher levels of oxLDL due to a higher fraction of oxLDL, not to higher levels of LDL cholesterol. Individuals with the metabolic syndrome had twice the odds of having high oxLDL (>1.90 mg/dl) compared with those not having the metabolic syndrome, after adjusting for age, sex, ethnicity, smoking status, and LDL cholesterol. Among those participants who had the metabolic syndrome at study entry, incidence rates of future CHD events were 1.6-fold higher, after adjusting for age, sex, ethnicity, and smoking status. OxLDL was not an independent predictor of total CHD risk. However, those with high oxLDL showed a greater disposition to myocardial infarction (relative risk 2.25, 95% confidence interval 1.22-4.15). We concluded that the metabolic syndrome, a risk factor for CHD, is associated with higher levels of circulating oxLDL that are associated with a greater disposition to atherothrombotic coronary disease.
Laser Diagnostics for Combustion Temperature and Species (2022)

1. Survey of Laser Diagnostics 2. Background Physics 3. Experimental Considerations 4. Application Considerations 5. Spontaneous Raman and Rayleigh Scattering 6. Coherent Anti-Stokes Raman Spectroscopy (CARS) 7. Laser-Induced Fluorescence (LIF) 8. Coherent Methods for Minor Species 9. Field Techniques
The Metastasis-Associated Gene CD24 Is Regulated by Ral GTPase and Is a Mediator of Cell Proliferation and Survival in Human Cancer (2006)

Ral GTPases are important mediators of transformation, tumorigenesis, and cancer progression. We recently identified the metastasis-associated protein CD24, a glycosyl phosphatidyl inositol-linked surface protein, as a downstream target of Ral signaling by profiling the expression of RalA/B-depleted bladder carcinoma cells. Because CD24 is highly expressed in bladder and many other tumor types, we sought to determine if this protein plays an essential role in maintaining the malignant phenotype. Here, we show that loss of CD24 function in cell lines derived from common tumor types is associated with decreased rates of cell proliferation, clonogenicity in soft agar, changes in the actin cytoskeleton, and induction of apoptosis. Given these phenotypes, we evaluated a human bladder cancer tissue microarray by immunohistochemistry for CD24 to determine if CD24 is a prognostic cancer biomarker. Multivariate analysis showed that increased CD24 expression correlated with shorter patient disease-free survival (P = 0.07). In conclusion, we show that CD24 is a novel and functionally relevant Ral-regulated target and a potentially important prognostic marker. We suggest that these insights may lead to future therapeutic approaches that seek to eliminate CD24 function in cancer cells.
Drop-in compatible entanglement  for optical-fiber networks (2009)

A growing number of quantum communication protocols require entanglement distribution among remote parties, which is best accomplished by exploiting the mature technology and extensive infrastructure of low-loss optical fiber. For this reason, a practical source of entangled photons must be drop-in compatible with optical fiber networks. Here we demonstrate such a source for the first time, in which the nonlinearity of standard single-mode fiber is utilized to yield entangled photon pairs in the 1310-nm O-band. Using an ultra-stable design, we produce polarization entanglement with 98.0% +/- 0.5% fidelity to a maximally entangled state as characterized via coincidence-basis tomography. To demonstrate the source's drop-in capability, we transmit one photon from each entangled pair through a telecommunications-grade optical amplifier set to boost classical 1550-nm (C-band) communication signals. We verify that the photon pairs experience no measurable decoherence upon passing through the active amplifier (the output state's fidelity with a maximally entangled state is 98.4% +/- 1.4%).
Platelet glycoprotein IIb gene expression as a model of megakaryocyte‐specific expression (1995)

Glycoprotein (GP)IIb/IIIa is an integrin complex normally restricted in its expression to platelets and the megakaryocytes from which they are derived. This complex functions as a receptor for fibrinogen and other ligands and is involved in platelet aggregation. The receptor complex is expressed at high levels during final megakaryocyte differentiation. Further, while GPIIIa is expressed in other tissues as part of the vitronectin receptor, GPIIb is only expressed on maturing megakaryocytes and the platelets derived from them. Thus studies of the GPIIb gene may serve as a model of gene regulation during this process. Over the past several years, the genes for both GPIIb and IIIa have been cloned and analyzed. The GPIIb gene contains 30 exons over 18 kilobases (kb). The transcriptional start site has been determined and there does not appear to be a TATA-box immediately upstream of this site. Studies have been done to define regulatory elements upstream of the transcriptional start site. Most of these studies focused on the human promoter and on studies using megakaryocytic cell lines. These studies have defined several important tissue-specific promoter elements including a GATA454 site (454 basepairs upstream of the transcriptional start site that involves a GATA-binding consensus sequence), a GATA54 site and an Ets35 site (that involves an Ets-binding consensus sequence). Expression studies with megakaryocytic cell lines suggest that each of these sites effects expression approximately threefold. Further, an Ets510 site was also described that had a similar effect. While these studies were underway, we pursued studies of the rat 5'-flanking region using a rat primary marrow expression system. Qualitatively, our data support the human data; however, quantitatively, we found significant differences from the human studies done in cell lines. We found that the major tissue-specific promoter element was the GATA454 site. Mutations altering this site result in an approximately fiftyfold drop in expression. In comparison, eliminating the Ets510 site by truncation or point mutation had only a twofold effect on expression. Mutations at the Ets35 site did effect expression at a high level, decreasing expression approximately fifteenfold, while mutations at the GATA54 site effected expression by approximately ninefold. In addition, using 50 bp deletions, we have preliminarily defined two domains from -450 to -351 bp and -150 to -101 bp upstream of the transcriptional start site that effected expression. The former appears to contain a positive regulatory element, while the latter appears to be a silencer element.(ABSTRACT TRUNCATED AT 400 WORDS)
Malondialdehyde-Altered Protein Occurs in Atheroma of Watanabe Heritable Hyperlipidemic Rabbits (1988)

It has been proposed that chemically reactive lipids released during lipid peroxidation convert low density lipoprotein (LDL), the major carrier of plasma cholesterol, to an abnormal form and that receptor-mediated clearance of this altered LDL produces cholesteryl ester deposition in macrophage-derived foam cells of atheroma. Immuno-cytochemical analyses now reveal the presence of protein modified by malondialdehyde, a peroxidative end product, which colocalizes with the extracellular deposition of apolipoprotein B-100 protein of LDL in atheroma from Watanabe heritable hyperlipidemic rabbits. These findings provide direct evidence for the existence in vivo of protein modified by a physiological product of lipid peroxidation within arterial lesions.
Surface Descriptors for Protein−Ligand Affinity Prediction (2002)

Molecular descriptors calculated by the VolSurf program have been extensively used to model pharmacokinetic properties, e.g., passive permeability through the gastrointestinal tract or through the blood-brain barrier. These descriptors quantify steric, hydrophobic, and hydrogen bond interactions between model compounds and different environments. Since these interactions are the same as those involved in the ligand-receptor binding, VolSurf descriptors could potentially be relevant in modeling this process as well. We obtained a significant model (r(2) = 0.85, q(2) = 0.75) using VolSurf descriptors derived from the ligand, the protein, and the ligand-protein complex for a diverse set of 38 structures previously used in the VALIDATE (ref 23) training set. Furthermore, a statistically significant model (r(2) = 0.94, q(2) = 0.89) was obtained using the same type of descriptors for a homogeneous set of glycogen phosphorylase inhibitors (ref 25). Using the VolSurf computational framework, both ligand-receptor binding and the ligand's pharmacokinetic behavior can be modeled simultaneously during the preclinical aspects of drug discovery.
Fatal Serotonin Syndrome Precipitated by Oxcarbazepine in a Patient Using an Selective Serotonin Reuptake Inhibitor (2012)

Oxcarbazepine, a metabolite of carbamazepine, is used as an antiepileptic, analgesic for neuropathic pain and in the treatment of affective disorders. It has been approved by the Food and Drug Administration for partial seizures in adults as both adjunctive and monotherapy, and as adjunctive therapy in children aged from 2 to 16 years (http://www.fda.gov/ohrms/dockets/ac/06/briefing/2006-4254b_07_05_KP%20OxcarbazepineFDAlabel102005.pdf). We present a case of serotonin syndrome, which was precipitated by this medicine in a patient who had been predisposed by long-term treatment with sertraline, a selective serotonin reuptake inhibitor. This is the first reported fatality due to this drug interaction and only the second case of serotonin syndrome reported with oxcarbazepine. Physicians should consider this risk when prescribing the above combination.
Tissue specificity of methylation of cytosines in regulatory regions of four genes located in the locus FXYD5-COX7A1 of human chromosome 19: Correlation with their expression level (2006)

In this study, we compared degree of methylation of selected CpG sites in CCGG sequences located in promoter regions of four human genes with expression level of these genes in several human cell lines and tissues. These genes were subdivided into two groups according to the dependence of their expression on CpG methylation in the 5 -regions. The first group, characterized by clear correlation of methylation with the transcription level, includes housekeeping gene COX6B (the absence of methylation unambiguously correlates with expression) and urothelium-specific uroplakin gene (the methylation coincides with absence of expression). The second group includes genes that are expressed in many, but not all tissues and cells. For these genes (LEAP-1 and ATP4A), there was no correlation between methylation and expression. It is possible that methylation provides some basal level of gene repression, which is overcome by binding of tissue-specific transcription factors, whereas lack of methylation gives the opportunity for gene expression in various cells and tissues.
Schlemm’s Canal and Trabecular Meshwork in Eyes with Primary Open Angle Glaucoma: A Comparative Study Using High-Frequency Ultrasound Biomicroscopy (2016)

We investigated in vivo changes in Schlemm's canal and the trabecular meshwork in eyes with primary open angle glaucoma (POAG). Relationships between Schlemm's canal diameter, trabecular meshwork thickness, and intraocular pressure (IOP) were examined. Forty POAG patients and 40 normal individuals underwent 80-MHz Ultrasound Biomicroscopy examinations. The Schlemm's canal and trabecular meshwork were imaged in superior, inferior, nasal and temporal regions. Normal individuals had an observable Schlemm's canal in 80.3% of sections, a meridional canal diameter of 233.0±34.5 μm, a coronal diameter of 44.5±12.6 μm and a trabecular meshwork thickness of 103.9±11.1 μm, in POAG patients, Schlemm's canal was observable in 53.1% of sections, a meridional canal diameter of 195.6±31.3 μm, a coronal diameter of 35.7±8.0 μm, and a trabecular meshwork thickness of 88.3±13.2 μm, which significantly differed from normal (both p <0.001). Coronal canal diameter (r = -0.623, p < 0.001) and trabecular meshwork thickness (r = -0.663, p < 0.001) were negatively correlated with IOP, but meridional canal diameter was not (r = -0.160, p = 0.156). Schlemm's canal was observable in 50.5% and 56.6% of POAG patients with normal (<21 mmHg) and elevated (>21 mmHg) IOP, respectively (χ = 1.159, p = 0.282). Coronal canal diameter was significantly lower in the elevated IOP group (32.6±4.9 μm) than in the normal IOP group (35.7±8.0 μm, p < 0.001). This was also true of trabecular meshwork thickness (81.9±10.0 μm vs. 97.1±12.0 μm, p < 0.001). In conclusion, eyes with POAG had fewer sections with an observable Schlemm's canal. Canal diameter and trabecular meshwork thickness were also lower than normal in POAG patients. Schlemm's canal coronal diameter and trabecular meshwork thickness were negatively correlated with IOP.
Human Body Temperature: Its Measurement and Regulation (1982)

The terminology used in thermal physiology is examined, and principles of heat transfer are discussed, taking into account heat quantity, heat flux, temperature, pressure, quantities used in physiology, a number of common definitions, the equivalence between different forms of energy, the release of potential energy in living tissues, heat transfer without change of state, and heat transfer with change of state. Temperature and humidity measurement are considered along with man and his environment, the temperature distribution in the systems and tracts of the human body, physiological changes affecting the temperature distribution, problems of temperature regulation, questions of heat loss and conservation, acclimatization to heat and cold, and disorders of thermoregulation. Attention is given to possible thermal imaging applications, causes of temperature irregularities in the head and neck, common causes of increased temperatures of upper limbs, and thermography in disease. 193 references.
Two Steps Forward in the Treatment of Colorectal Cancer (2004)

Until recently, fluorouracil was the only effective systemic treatment for colorectal cancer. It acts primarily by inhibiting thymidylate synthase, a key enzyme in DNA synthesis, and because leucovorin (folinic acid) enhances this effect, fluorouracil and leucovorin (FL) are given together. FL has been given in various dose schedules, with a continuous infusion appearing slightly more effective than a bolus.1 FL reduces tumor size by 50 percent or more (objective response) in approximately 20 percent of patients with advanced colorectal cancer and prolongs median survival from approximately 6 months (without treatment) to about 11 months.2 When given as adjuvant therapy after . . .