gebhart/patrepeval huggingface dataset:
Silver Impregnation of Degenerating Axons in the Central Nervous System: A Modified Technic (1954)

Frozen sections of formalin-fixed brains containing surgical lesions, were treated with 15% ethanol for 0.5 hr., soaked in 0.5% phosphomolybdic acid for 0.25–1.0 hr., and subsequently treated with 0.05% potassium permanganate for 4–10 min. (The duration of the latter treatment is critical and individually variable). Subsequent procedure is as follows: decolorize in a mixture of equal parts of 1% hydroquinone and 1% oxalic acid; wash thoroughly and soak sections in 1.5% silver nitrate for 20–30 min.; ammoniacal silver nitrate (silver nitrate 0.9 g., distilled water 20 ml., pure ethanol 10 ml., strong ammonia 1.8 ml., 2.5% sodium hydroxide 1.5 ml.) 0.5–1.0 min.; reduce in acidified formalin (distilled water 400 ml., pure ethanol 45 ml., 1% citric acid 13.5 ml., 10% formalin 13.5 ml.) 1 min.; wash, and pass section through 1 % sodium thiosulf ate (0.5–1.0 min.); wash thoroughly and pass sections through graded alcohols and xylene (3 changes); cover in neutral synthetic resin.
Physiological Action of Progesterone in Target Tissues* (1997)

I. Introduction II. Synthesis and Secretion of Progesterone III. The Progesterone Receptor A. PR expression and regulation IV. Progesterone Regulation of Gene Expression in the Uterus, Ovary, and Chick Oviduct A. Progesterone effects on proliferation and decidualization in the uterus during the menstrual cycle B. Progesterone regulation of insulin-like growth factor (IGF) pathways in the endometrium C. Control of ovulation D. Implantation, uterine proliferation, and early pregnancy E. Myometrial contractility F. Chick oviduct V. Progesterone Action in the Breast A. Effect of progesterone on proliferation of the normal breast B. Progesterone regulation of genes associated with cell cycle progression C. Progesterone regulation of growth factors and growth factor receptors in the breast D. Markers of progestin action in the breast E. Progesterone effects on lactation VI. Progesterone Effects in the Brain VII. Progesterone Effects on Bone VIII. Antiestrogen Action of Progesterone A. Inhibition of ER expressio...
Partial restoration of defective chloride conductance in ΔF508 CF mice by trimethylamine oxide (2001)

This study was designed to test the in vivo efficacy of the chemical chaperone trimethylamine oxide (TMAO) in correcting the Cl- transport defect in a mouse model of cystic fibrosis (CF). Rectal potential difference (RPD) measurements were done in matched wild-type and DeltaF508 CF mice. Mice were treated by subcutaneous injections of TMAO. Wild-type mice demonstrated a forskolin-stimulated, Cl--dependent hyperpolarization of -6.4 +/- 0.8 mV (n = 11), which was significantly increased to -13.1 +/- 1.4 mV after treatment with TMAO. DeltaF508 CF mice showed no significant responses to forskolin. Treatment with TMAO recovered a forskolin-activated RPD in DeltaF508 CF mice (-1.1 +/- 0.2 mV; n = 17) but not in CFTR null mice. The effects of TMAO were dose dependent, resulting in a slope of -0.4 +/- 0.1 mV x g(-1) x kg(-1) in DeltaF508 CF mice. The forskolin-stimulated RPD in TMAO-treated DeltaF508 CF mice was partially blocked by glibenclamide and further stimulated by apigenin. The total response to forskolin plus apigenin was -2.5 +/- 0.45 mV (n = 6 mice), corresponding to 39% of the response evoked by forskolin only in wild-type mice.
Dual-label one-step immunoassay for simultaneous measurement of free and total prostate-specific antigen concentrations and ratios in serum (1995)

We developed a simple one-step dual-label immunoassay for simultaneous measurement of the free, noncomplexed form of prostate-specific antigen (PSA) and total PSA. The assay is based on time-resolved fluorescence and includes a stable fluorescent chelate of Eu to label a monoclonal antibody (mAb) that detects only free PSA, whereas a second mAb labeled with a fluorescent chelate of Tb provides equimolar detection of both free PSA and PSA complexed to alpha 1-antichymotrypsin. A third mAb on a solid phase captures the free and complexed forms of PSA in an equimolar fashion. The simultaneous measurement of the free-to-total PSA ratio (F/T) with the one-step dual assay is not sensitive to variations in the sample volume. The discrimination between benign prostatic hyperplasia and prostate cancer patients, i.e., the area under the receiver-operating characteristic curve, increased from 0.64 (total PSA assay) to 0.78 and 0.81 when the F/T ratio was measured with single and dual assays, respectively.
Inflammatory response and retinal ganglion cell degeneration following intraocular injection of ME7 (1999)

Scrapie is a prion disease which occurs naturally in sheep and which can be transmitted experimentally to rodents. After intracerebral injection of ME7 into mouse, an atypical inflammatory response, characterized by T-lymphocytes and activated microglia is present early in the course of the disease. In the present work, we have investigated the relationship between this inflammatory response, astrocytosis and neuronal loss along the visual pathway after intraocular injection (intraocular) of ME7 in C57BL/6J mice. We have demonstrated that microglia activation and T-lymphocyte recruitment accompanies the spread of prion pathology along the visual pathway and in the early stages of the disease is restricted to the subcortical visual pathway. Inflammation was also present in non-visual areas in association with PrPsc deposition at late stages of the disease, possibily indicating that diffusion of the scrapie agent also contributes to the spread of the disease. After intraocular injection of the prion agent, the disease is believed to be transported into the brain via axons of retinal ganglion cells (RGCs). Despite the high levels of infectivity reported to be present in the retina early in the disease after intraocular injection of ME7, retinal pathology has not been extensively investigated. We have studied the RGCs response in whole mount retinas after intraocular injection of ME7. We have shown that RGCs degenerate after intraocular injection of ME7 whereas amacrine cells, retinal interneurones, are more resistant. Our results suggest that two distinct population of neurones, exposed in vivo at the same time to the same agent scrapie strain, show different susceptibility to the toxic effects of PrPsc.
Content-aware dynamic timeline for video browsing (2010)

When browsing a long video using a traditional timeline slider control, its effectiveness and precision degrade as a video's length grows. When browsing videos with more frames than pixels in the slider, aside from some frames being inaccessible, scrolling actions cause sudden jumps in a video's continuity as well as video frames to flash by too fast for one to assess the content. We propose a content-aware dynamic timeline control that is designed to overcome these limitations. Our timeline control decouples video speed and playback speed, and leverages video content analysis to allow salient shots to be presented at an intelligible speed. Our control also takes advantage of previous work on elastic sliders, which allows us to produce an accurate navigation control.
Electrochemical Formation of Polyaniline in Selenic Acid (1996)

The electrochemical formation of polyaniline (PAn) was investigated in selenic acid. The cyclic voltammetry of selenate in the potential window from −0.15 to 0.8 V, indicates that the electropolymerization of aniline is not affected by the oxidizing ability of selenic acid. The growth rate of PAn observed at a potential of 0.8 V in a solution of 0.1 M aniline in 0.2 M was comparable with that in 0.2 M . However, the PAn growth in during successive potential cycles between −0.15 and 0.8 V was much lower than that in . In cyclic voltammograms, the first reduction peak for PAn was enhanced by the presence of selenate ions, possibly due to the deposition of elemental selenium catalyzed by the polymer film. The deposition of metallic selenium on the PAn film greatly inhibited the growth of the polymer during successive potential cycling between −0.15 and 0.8 V.
The SNMMI Practice Guideline for Therapy of Thyroid Disease with 131I 3.0 (2012)

Preamble……1 I. Introduction: patient management, licensure.……2 II. Goals.……2 III. Definitions: risk levels……2 IV. Common clinical indications……3 V. Qualifications and responsibilities of personnel (in the United States).……3 VI. Procedure/specifications of the
Bacterial DNA and Lipopolysaccharide Induce Synergistic Production of TNF-α Through a Post-Transcriptional Mechanism (2001)

LPS is well recognized for its potent capacity to activate mouse macrophages to produce TNF-alpha, an important inflammatory mediator in bacterial infection-related diseases such as septic shock. We demonstrate here that while inducing only low levels of TNF-alpha alone, DNA from both Gram-negative and Gram-positive bacteria synergizes with subthreshold concentrations of LPS (0.3 ng/ml) to induce TNF-alpha in the RAW 264.7 macrophage-like cell line. The bacterial DNA effects are mimicked by synthetic CpG-containing oligodeoxynucleotides, but not non-CpG-containing oligodeoxynucleotides. Pretreatment of macrophages with either DNA for 2-8 h inhibits macrophage TNF-alpha production in responses to DNA/LPS. However, when pretreatment was extended to 24 h, DNA/LPS synergy on TNF-alpha is further enhanced. RT-PCR analysis indicates that mRNA levels of the TNF-alpha gene, however, are not synergistically induced by bacterial DNA and LPS. Analyses of the half-life of TNF-alpha mRNA indicate that TNF-alpha message has a longer half-life in bacterial DNA- and LPS-treated macrophages than that in bacterial DNA- or LPS-treated macrophages. These findings indicate that the temporally controlled, synergistic induction of TNF-alpha by bacterial DNA and LPS is not mediated at the transcriptional level. Instead, this synergy may occur via a post-transcriptional mechanism.
Envision (1995)

Project Envision is an early NSF-funded digital library effort to develop a multimedia collection of computer science literature with full-text searching and full-content retrieval capabilities. Envision was launched in 1991 in accordance with the ACM Publications Board's plans for encouraging research studies to develop an electronic archive for computer science.
Thermal stresses and cracking resistance of dielectric films (SiN, Si3N4, and SiO2) on Si substrates (1978)

In device-manufacturing technology, it is important to understand why dielectric films crack. With this objective in mind, we have constructed an apparatus for measurement of thermal stresses in thin films (25–500 °C), obtained results on various reactively plasma deposited (RPD) Si-N and CVD SiO2 films, and developed a model which quantifies the cracking resistance of different types of RPD Si-N films. Measurements were made of the coefficient of thermal expansion α (T), which increases on going from SiO2→Si3N4→SiN→Si and the intrinsic stress, which is compressive for RPD Si3N4, nearly zero for thermal SiO2 and tensile for RPD SiN and CVD SiO2. The cracking resistance of Si-N film at a given temperature is functionally related to its density, intrinsic stress, thermal mismatch with Si, and the deposition temperature.
Micro-thermal analysis: techniques and applications (2001)

The terms micro-thermal analysis and micro-spectroscopic analysis are used to include any form of localized characterization or analysis combined with microscopy that uses a near-field thermal probe to exploit the benefits of using thermal excitation. Individual regions of a solid sample are selected by means of surface or sub-surface imaging (atomic force microscopy and/or scanning thermal microscopy), so as to add spatial discrimination to four well-established methods of chemical fingerprinting, namely thermomechanometry, calorimetry, spectroscopy and analytical pyrolysis. We begin by describing the state of the art of scanning microscopy that uses resistive thermal probes, followed by an account of the various techniques of micro-thermal analysis.
Recombinant IκB Kinases α and β Are Direct Kinases of IκBα (1998)

Activation of the transcription factor NF-kappaB is regulated by the phosphorylation and subsequent degradation of its inhibitory subunit, IkappaB. A large multiprotein complex, the IkappaB kinase (IKK), catalyzes the phosphorylation of IkappaB. The two kinase components of the IKK complex, IKKalpha and IKKbeta, were overexpressed in insect cells and purified to homogeneity. Both purified IKKalpha and IKKbeta specifically catalyzed the phosphorylation of the regulatory serine residues of Ikappa Balpha. Hence, IKKalpha and IKKbeta were functional catalytic subunits of the IKK complex. Purified IKKalpha and IKKbeta also preferentially phosphorylated serine as opposed to threonine residues of Ikappa Balpha, consistent with the substrate preference of the IKK complex. Kinetic analysis of purified IKKalpha and IKKbeta revealed that the kinase activity of IKKbeta on Ikappa Balpha is 50-60-fold higher than that of IKKalpha. The primary difference between the two activities is the Km for Ikappa Balpha. The kinetics of both IKKalpha and IKKbeta followed a sequential Bi Bi mechanism. No synergistic effects on Ikappa Balpha phosphorylation were detected between IKKalpha and IKKbeta. Thus, in vitro, IKKalpha and IKKbeta are two independent kinases of Ikappa Balpha.
Epstein-Barr virus latent membrane protein 1 blocks p53-mediated apoptosis through the induction of the A20 gene (1996)

Two Epstein-Barr virus (EBV)-associated malignancies, nasopharyngeal carcinoma and posttransplant lymphoma, rarely have mutations in the p53 tumor suppressor gene, suggesting that a viral protein interferes with p53 function. The EBV oncogene, LMP1, induces expression of the cellular antiapoptotic genes bcl-2 and A20 and could in this way interfere with p53-mediated apoptosis. Two derivatives of the p53-null epithelial cell line H1299 were prepared, one of which (H1299-p53) stably expressed a temperature-sensitive (ts) p53 protein, and another (H1299-p53+LMP1) which stably expressed both ts-p53 and latent membrane protein 1 (LMP1). At the permissive temperature, the p53 protein in the H1299-p53 cell line transcriptionally activated two of its target genes, the cyclin-dependent kinase inhibitor p21 and the mdm2 gene product, in an LMP1-independent manner. Upon serum withdrawal at the permissive temperature, p53-mediated apoptosis was induced in 50 to 60% of the cells. In the H1299-p53 cell line which stably expressed LMP1, however, only 20 to 25% of the cells underwent apoptosis. While stable expression of LMP1 did not affect levels of bcl-2 family members in these cells, it did induce expression of A20. Stable expression of A20 in the H1299-p53 cell line inhibited p53-mediated apoptosis equivalent to inhibition by LMP1. The induction of A20 may underlie the ability of LMP1 to protect EBV-infected epithelial cells from p53-mediated apoptosis.
Actions of cytokines on the immune response and viral interactions: An overview (1996)

kinases (JAKs). 9,10They phosphorylate a newly de-
Receptor- and Carrier-Mediated Transport Systems for Folates and Antifolates (1999)

Eukaryotic cells lack the possibility of de novo biosynthesis of reduced folate cofactors that are required as one-carbon donors in the biosynthesis of thymidylate, purines, and amino acids (1).For this reason, cellular folate homeostasis depends on the delivery of reduced folate cofactors from extracellular fluids. At a physiological pH, the negatively charged α- and γ-carboxyl groups of the glutamate side chain of reduced folate cofactors change these molecules into divalent anions that cannot simply pass the plasma membrane but require (a) specific transport system(s) for their cellular entry. The importance of folate metabolism in tumor cells has been recognized for a long time as a potential target for chemotherapy (2–6). Historically, classical folate analogs such as aminopterin (AMT) and methotrexate (MTX) were recognized to disrupt folate metabolism through inhibition of dihydrofolate reductase (DHFR) (7). More recently, folate analogs were synthesized that could target other key enzymes in folate metabolism, including thymidylate synthase (TS) (8, 9) glycinamide ribonucleotide transformylase (GARTFase) (10, 11) and folylpolyglutamate synthetase (FPGS) (12). A number of these novel antifolates have demonstrated potential clinical activity (3,13–18). The majority of these folate analogs share the common feature that efficient membrane transport is the first determining factor in exerting their biological activity. This chapter will mainly focus on the role of two folate transport systems that are considered to be of the greatest relevance from the perspective of mediating folate homeostasis and the delivery of folate-based chemotherapeutic drugs into tumor cells. These transporters include the reduced folate carrier (RFC) (19–22) and a membrane-associated folate receptor (MFR) (22–25) also referred to as membrane-associated folate-binding protein (mFBP). A summary of some molecular, biochemical, and functional properties of these transporters will be given (see e.g., Table 1) along with a few examples how these properties (see Fig. 2A, B, below) may be translated into an improved biological/cytotoxic activity of antifolate drugs (see Table 2).
Graft-versus-host disease disrupts intestinal microbial ecology by inhibiting Paneth cell production of α-defensins (2012)

Allogeneic hematopoietic stem cell transplantation (SCT) is a curative therapy for various hematologic disorders. Graft-versus-host disease (GVHD) and infections are the major complications of SCT, and their close relationship has been suggested. In this study, we evaluated a link between 2 complications in mouse models. The intestinal microbial communities are actively regulated by Paneth cells through their secretion of antimicrobial peptides, α-defensins. We discovered that Paneth cells are targeted by GVHD, resulting in marked reduction in the expression of α-defensins, which selectively kill noncommensals, while preserving commensals. Molecular profiling of intestinal microbial communities showed loss of physiologic diversity among the microflora and the overwhelming expansion of otherwise rare bacteria Escherichia coli, which caused septicemia. These changes occurred only in mice with GVHD, independently on conditioning-induced intestinal injury, and there was a significant correlation between alteration in the intestinal microbiota and GVHD severity. Oral administration of polymyxin B inhibited outgrowth of E coli and ameliorated GVHD. These results reveal the novel mechanism responsible for shift in the gut flora from commensals toward the widespread prevalence of pathogens and the previously unrecognized association between GVHD and infection after allogeneic SCT.
Advances in Heart Failure Surgery (2005)

Heart failure is a major public health problem in the USA and in most Western countries. Nearly 5 million patients in the USA have heart failure with approximately 500,000 patients being diagnosed for the first time each year. Medical therapy is the first-line treatment, and surgery is considered when medical therapy fails or a clear mechanical cause of heart failure is identified and deemed correctable. Current surgical options include coronary revascularization, surgical correction of mitral regurgitation, left ventricular reconstruction, transmyocardial laser revascularization, ventricular assist devices, passive ventricular restraint devices, and cardiac transplantation. While a full discussion of cardiac transplantation is beyond the scope of this article, the other commonly performed procedures will be reviewed.
Critical Residues within the BTB Domain of PLZF and Bcl-6 Modulate Interaction with Corepressors (2002)

The PLZF (promyelocytic leukemia zinc finger) transcriptional repressor, when fused to retinoic acid receptor alpha (RARalpha), causes a refractory form of acute promyelocytic leukemia. The highly conserved N-terminal BTB (bric a brac, tramtrack, broad complex)/POZ domain of PLZF plays a critical role in this disease, since it is required for transcriptional repression by the PLZF-RARalpha fusion protein. The crystal structure of the PLZF BTB domain revealed an obligate homodimer with a highly conserved charged pocket formed by apposition of the two monomers. An extensive structure-function analysis showed that the charged pocket motif plays a major role in transcriptional repression by PLZF. We found that mutations of the BTB domain that neutralize key charged pocket residues did not disrupt dimerization, yet abrogated the ability of PLZF to repress transcription and led to the loss of interaction with N-CoR, SMRT, and histone deacetylases (HDACs). We extended these studies to the Bcl-6 protein, which is linked to the pathogenesis of non-Hodgkin's lymphomas. In this case, neutralizing the charged pocket also resulted in loss of repression and corepressor binding. Experiments with purified protein showed that corepressor-BTB interactions were direct. A comparison of the PLZF, Bcl-6, and the FAZF (Fanconi anemia zinc finger)/ROG protein shows that variations in the BTB pocket result in differential affinity for corepressors, which predicts the potency of transcriptional repression. Thus, the BTB pocket represents a molecular structure involved in recruitment of transcriptional repression complexes to target promoters.
Restoration of ß-Globin Gene Expression in Mammalian Cells by Antisense Oligonucleotides That Modify the Aberrant Splicing Patierns of Thalassemic Pre-mRNAs (1997)

Abstract Antisense 2′-methoxy-oligoribonucleotides targeted to aberrant splice sites in two thalassemic human ß-globin pre-mRNAs, IVS2-654 and IVS2-705, expressed in HeLa cells efficiently restore correct splicing with the use of Lipofectamine, Cellfectin and DMRIE-C, in effect reactivating a defective ß-globin gene.
Risk of anti-EGFR monoclonal antibody-related hypomagnesemia: systematic review and pooled analysis of randomized studies (2011)

The overall incidence of hypomagnesemia was 17% among the patients who received the treatment, whose risk of developing hypomagnesemia turned out to be significantly increased compared with the patients treated with control medication, with an overall relative risk of 5.83 (p < 0.00001), where 3.87 refers to cetuximab and 12.55 to panitumumab. The addition of anti-EGFR monoclonal antibodies to standard anticancer therapy showed a significantly increased risk of hypomagnesemia compared with controls. The risk seems to be even higher for panitumumab, probably correlated with the increased risk of other adverse events (e.g., diarrhea and dehydration). Hypomagnesemia does not seem to be linked with any serious complications.