gebhart/patrepeval huggingface dataset:
Enzymatic Fractionation of Carbon Isotopes by Phosphoenolpyruvate Carboxylase from C4 Plants (1973)

The carbon atoms of glucose and malate in C(4) plants are 2 to 3 per thousand enriched in (12)C with respect to atmospheric CO(2); whereas these intermediates in C(3) plants are 15 to 18 per thousand enriched with (12)C with respect to atmospheric CO(2). The enzymatic synthesis of malate from phosphoenolpyruvate and bicarbonate in preparations of leaves of Sorghum bicolor, Haygrazer result in a carbon isotope fractionation of about 3 per thousand. The enzymatic synthesis of phosphoglyceric acid from ribulose 1,5-diP and CO(2) in these preparations (contaminated with carbonic anhydrase) at 24 C and 37 C result in a carbon isotope fractionation of 33.7 per thousand and 18.3 per thousand, respectively. These data are consistent with the conclusion that the small enrichment of (12)C in the carbon atoms of malate and glucose (with respect to atmospheric CO(2)) in leaves of Sorghum bicolor, Haygrazer occurs at the phosphoenolpyruvate carboxylase step.
Application of time-reversal with MMSE equalizer to UWB communications (2005)

We propose to apply a technique called time-reversal to UWB communications. In time-reversal a signal is precoded such that it focuses both in time and in space at a particular receiver. Spatial focusing reduces interference to other co-existing systems. Due to temporal focusing, the received power is concentrated within a few taps and the task of equalizer design becomes much simpler than without focusing. Furthermore, temporal focusing allows a large increase in transmission rate compared to schemes that let the impulse response ring out before the next symbol is sent. Our paper introduces time-reversal, investigates the benefit of temporal focusing, and examines the performance of an MMSE-TR equalizer in an UWB channel.
Inhibition of Keratinocyte Apoptosis by IL-15: A New Parameter in the Pathogenesis of Psoriasis? (2000)

Keratinocytes (KC) are important source of and targets for several cytokines. Although KC express IL-15 mRNA, the functional effects of IL-15 on these epithelial cells remain to be dissected. Investigating primary human foreskin KC and HaCaT cells, we show here by semiquantitative RT-PCR and flow cytometric analysis that both translate IL-15 and IL-15R mRNA and express IL-15 and IL-15Ralpha protein on the cell surface, suggesting that human KC can employ IL-15 for juxtacrine signaling. While IL-15 exerted no significant effect on KC proliferation and IL-6 or IL-8 secretion, IL-15 inhibited both anti-Fas and methylcellulose-induced KC apoptosis in vitro. This is in line with the recognized potent anti-apoptotic effects of IL-15. IL-2, whose receptor shares two components with the IL-15R, failed to inhibit KC apoptosis. Together with the role of IL-15 in sustaining chronic immune reactions, this invited the question of whether a reduction of KC apoptosis by IL-15 may be involved in the pathogenesis of psoriasis, a chronic hyperproliferative inflammatory skin disease characterized by abnormally low KC apoptosis in the epidermis. Remarkably, compared with nonlesional psoriatic skin and skin of healthy volunteers, lesional psoriatic epidermis showed high IL-15 protein expression in the epidermis and enhanced binding activity for IL-15. Therefore, antagonizing the inhibitory effects of IL-15 on KC apoptosis deserves exploration as a novel therapeutic strategy in psoriasis management.
Immunohistochemical localization and molecular characteristics of three monoclonal antibody‐defined epitopes detectable on carcinoembryonic antigen (CEA) (1985)

Three murine monoclonal antibodies (MAbs) reactive to different epitopes on CEA were selected according to their ability to bind to various human tissue sections. The most selective MAb, BW 431/31, bound to the majority of colon carcinomas but only faintly to normal colon mucosa. In addition to the tissues stained by MAb BW 431/31, MAb BW 250/183 reacted with granulocytes, colon mucosa and faintly with pancreatic ducts. The third MAb, BW 374/14, reacted with granulocytes, colon mucosa, strongly with pancreatic ducts and with alveolar and bronchial epithelium. The antigenic determinants recognized by the 3 MAbs in human tissue sections were resistant to formaldehyde fixation and paraffin embedding as well as to periodic acid oxidation and neuraminidase treatment. The last two treatments suggest that the epitopes are protein in nature. Using MAb affinity chromatography, 3 antigen preparations were isolated from a human colon carcinoma xenograft with an approximate molecular weight of 180 kd. These preparations were shown to bear the epitopes from each of the MAbs and from a polyclonal antiserum specific for purified CEA. Furthermore, the ability of MAb BW 431/31 to localize its antigenic determinant in vivo on a human colon carcinoma xenograft is evaluated and its possible application in the patient is suggested.
Animal Models of Bone Metastasis (2015)

Bone is one of the most common sites of cancer metastasis in humans and is a significant source of morbidity and mortality. Bone metastases are considered incurable and result in pain, pathologic fracture, and decreased quality of life. Animal models of skeletal metastases are essential to improve the understanding of the molecular pathways of cancer metastasis and growth in bone and to develop new therapies to inhibit and prevent bone metastases. The ideal animal model should be clinically relevant, reproducible, and representative of human disease. Currently, an ideal model does not exist; however, understanding the strengths and weaknesses of the available models will lead to proper study design and successful cancer research. This review provides an overview of the current in vivo animal models used in the study of skeletal metastases or local tumor invasion into bone and focuses on mammary and prostate cancer, lymphoma, multiple myeloma, head and neck squamous cell carcinoma, and miscellaneous tumors that metastasize to bone.
Recent advances in peanut allergy (2002)

Peanut remains preeminent as the food allergen most associated with severe and fatal allergic reactions. Reactions are frequent despite patients' best efforts to avoid peanut. In the future, better information sharing and communication between families and both schools and restaurants may lead to a decrease in the rate of severe reactions induced by exposure to peanut outside the home. Reaction severity may increase over time but up to 25% of young peanut allergic individuals may outgrow their peanut allergy. Personalized care plans and education programmes may have an impact on avoidance of peanut and on the appropriate responses of caregivers. Peanut's allergenicity may be affected by the method of cooking, with roasted peanuts appearing more allergenic than boiled or fried peanuts. Immunotherapy with modified peanut allergens and DNA based vaccines may soon move from animal studies to clinical trials.
Polony DNA Sequencing (2006)

Abstract Polony DNA sequencing provides an inexpensive, accurate, high‐throughput way to resequence genomes of interest by comparison to a reference genome. Mate‐paired in vitro shotgun genomic libraries are produced and clonally amplified on microbeads by emulsion PCR. These serve as templates for sequencing by fluorescent nonamer ligation reactions on a microscope slide. Each sequencing run results in millions of 26‐bp reads that can be aligned to the reference genome, allowing the identification of differences between sequences.
Evidence for a polypeptide segment at the carboxyl terminus of recombinant human .gamma. interferon involved in expression of biological activity (1988)

A panel of 18 murine monoclonal antibodies was raised in BALB/c mice to the full-length, 146 amino acid residue recombinant human gamma interferon (rHuIFN gamma-A). Two monoclonal antibodies, designated 47N3-6 and 30N47-1, were purified from ascites tumors and further characterized. Antibody 47N3-6 neutralized both the antiviral and antiproliferative activities of rHuIFN gamma-A. Both Western blotting and enzyme-linked immunosorbent assays indicated that antibody 47N3-6 could bind to rHuIFN gamma-A as well as to a genetically engineered truncated form lacking the first three amino-terminal residues (rHuIFN gamma-D) but did not recognize a genetically engineered variant terminating at residue 131 (rHuIFN gamma-B). This antibody also demonstrated binding to a 15 amino acid residue oligopeptide, designated F-1, corresponding to residues 132-146 at the carboxyl terminus of rHuIFN gamma-A. Chemical cleavage of peptide F-1 with cyanogen bromide produced two fragments that were separated by reversed-phase high-pressure liquid chromatography. Dot-blot analysis indicated that antibody 47N3-6 could bind to a fragment, KRKRSQHse, derived from residues 132-137 of rHuIFN gamma-A, but could bind only weakly to the cyanogen bromide fragment corresponding to residues 138-146. It was consistent with these results that antibody 47N3-6 demonstrated binding to a form lacking the five carboxyl-terminal amino acids (rHuIFN gamma-D') but did not bind to a synthetic polypeptide corresponding to residues 138-146. Peptide F-1 exhibited neither antiviral nor antiproliferative activity, and it did not antagonize the antiviral activity of rHuIFN gamma-A.(ABSTRACT TRUNCATED AT 250 WORDS)
Generation and Measurement of Shear Waves In Situ (1978)

Field procedures used to measure in situ shear wave velocity by cross-hole and downhole seismic methods are presented along with typical travel time records. Identification of the initial shear wave arrival is enhanced by use of a reversible torsional source in the crosshole method and a reversible embedded source in the downhole method. Correct triggering of recording equipment is critical in these measurements. Characteristics of three triggering systems—a velocity transducer, a resistance-capacitance (RC) circuit, and an electrical step trigger—are presented. Incorrect triggering can cause errors greater than 50 percent in field measurement of shear wave velocity. Other variables such as borehole casing, borehole disturbance, and source and sensor configuration also affect velocity measurement. The effects of many of the variables can be minimized by basing wave velocity computations on interval travel times of the initial arrival. It is recommended that any ASTM standards for crosshole and downhole seismic methods include field check procedures for correct timing and triggering of recording equipment and field measurement of borehole verticality.
Kernel-based object tracking (2003)

A new approach toward target representation and localization, the central component in visual tracking of nonrigid objects, is proposed. The feature histogram-based target representations are regularized by spatial masking with an isotropic kernel. The masking induces spatially-smooth similarity functions suitable for gradient-based optimization, hence, the target localization problem can be formulated using the basin of attraction of the local maxima. We employ a metric derived from the Bhattacharyya coefficient as similarity measure, and use the mean shift procedure to perform the optimization. In the presented tracking examples, the new method successfully coped with camera motion, partial occlusions, clutter, and target scale variations. Integration with motion filters and data association techniques is also discussed. We describe only a few of the potential applications: exploitation of background information, Kalman tracking using motion models, and face tracking.
Influence of heat and moisture exchanger respiratory load on transcutaneous oxygenation in laryngectomized individuals: A randomized crossover study (2007)

In contrast to earlier suggestions, there is no evidence of increased tcpO(2) levels by high-resistance HMEs in laryngectomized individuals. Thus, using such HMEs has no added clinical value in this respect.
Src Inhibitors in Metastatic Bone Disease (2006)

Src tyrosine kinase was the first gene product shown to have an essential function in bone using recombinant DNA technology after its expression was knocked out in mice approximately 15 years ago. Since then, our understanding of the regulation of bone catabolism has advanced significantly with the identification of other key enzymes that regulate osteoclast formation, activation, and survival after their knockout in mice or recognition of mutations in them in humans. This led to the discovery or development of specific inhibitors of some of these key enzymes, including Src, as proof-of-concept lead compounds or potential clinical candidates for the prevention of diseases associated with increased bone resorption, such as osteoporosis and metastatic bone disease. Although bisphosphonates have been prescribed with proven and improving efficacy for the prevention of bone loss for >30 years, adverse effects, such as upper gastrointestinal tract symptoms, and the requirement to take them at least 2 hours before food have limited patient compliance. Thus, with growing knowledge of the pathways regulating osteoclast function and the appreciation that some of these are active also in tumor cells, drug companies have made efforts to identify small-molecular lead compounds for development into new therapeutic agents for the prevention of bone loss with efficacy that matches or supersedes that of bisphosphonates. In this article, we review our current understanding of the signaling pathways that regulate osteoclast formation, activation, and survival with specific reference to the role of Src tyrosine kinase and downstream signaling and highlight in a variety of models of increased bone resorption the effects of Src kinase inhibitors that have been targeted to bone to limit potential adverse effects on other cells.
Calling name delivery (2003)

The development and implementation of the name and number delivery of a caller-ID service are reviewed. The process of identification of customer needs and implementation of the requirements is discussed. The service trial test results and market environment for the service are described.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Versatile insertion plasmids for targeted genome manipulations in bacteria: isolation, deletion, and rescue of the pathogenicity island LEE of the Escherichia coli O157:H7 genome (1997)

A system of versatile insertion plasmids was constructed that permits efficient delivery of the target sites of an ultra-rare-cutting endonuclease and the recombinase FLP into preselected sites of the bacterial genome. With the help of this system, the pathogenicity island LEE of the Escherichia coli O157:H7 genome was excised and isolated in vitro, deleted in vivo, rescued as a plasmid, and transferred into another strain.
Effect of Replacing the Aspartic Acid/Glutamic Acid Residues of Bullfrog Sialic Acid Binding Lectin with Asparagine/Glutamine and Arginine on the Inhibition of Cell Proliferation in Murine Leukemia P388 Cells. (2002)

The sialic acid binding lectin from bullfrog oocytes (cSBL) is known to have anti-tumor activity. In a previous report, to elucidate the relationship between the net charge and anti-tumor activity of cSBL, we examined the effect of chemical modifications of cSBL with a water-soluble carbodiimide in the presence of various nucleophiles. The results suggested that the anti-tumor activity and internalization into tumor cells increased with an increase in the net charge of cSBL. However, in the chemically modified cSBL, a modification site was observed on average in two of the carboxyl groups of cSBL. To confirm these previous results and to determine which modified carboxyl group contributes to the increase in anti-tumor activity, we prepared mutants with substitutions of Asn/Gln and Arg at three acidic amino acid residues of cSBL and studied their anti-tumor activity and internalization efficiency. The results showed the enhancing effect of charge on anti-tumor activity and internalization, and suggested that the replacement of D24 and E88 of cSBL with arginine is more effective than that of E97. The double mutant D24RE88R showed comparable anti-tumor activity to the ethylenediamine-modified cSBL reported previously. The mutant was well-characterized as a pure cSBL derivative suitable for studying the mechanism of the anti-tumor action of cSBL.
Effect of Stimulation of the Host Defense System by Coenzyme Q 10 on Dibenzpyrene-Induced Tumors and Infection with Friend Leukemia Virus in Mice (1973)

Members of the coenzyme Q group increase the phagocytic activity in rats, as measured by the carbon clearance technique, and increase the hemolytic antibody formation in mice. In addition, prior treatment with low doses of chloroquine hydrochloride combined with coenzyme Q(10) results in increased numbers of survivors, prolonged survival time, and reduced parasitemia in blood-transferred Plasmodium berghei infection in miceIn an extension of these studies, using emulsions of coenzyme Q(10), I demonstrated the following effects on two tumor systems in mice: (i) Treatment with coenzyme Q(10) decreased splenomegaly and hepatomegaly and increased the number of surviving mice infected with Friend leukemia virus. (ii) Treatment with coenzyme Q(10) reduced the percentage of mice with tumors, increased the number of survivors, and reduced the tumor size in mice with tumors induced by 3,4,9,10-dibenzpyrene. The effect on both tumor systems was dose-dependent. These studies support the hypothesis that the host defense system plays a definitive role in the defense of the host against invasion by various agents, including neoplasia.
Platelet-activating factor-induced ischemic bowel necrosis. An investigation of secondary mediators in its pathogenesis. (1986)

The authors have previously reported a model of ischemic bowel necrosis produced in the rat by synthetic platelet-activating factor (PAF) or a combination of PAF and bacterial endotoxin. Because rat platelets are refractory to PAF and thromboemboli were not found in the mesenteric or intestinal microvasculature, they suspected that secondary mediators were involved in the pathogenesis of bowel necrosis. They have found the following lipoxygenase products of arachidonic acid, especially leukotrienes (LT), probably played an important role in the pathogenesis of bowel necrosis, because diethylcarbamazine (an inhibitor for LTA synthesis) and FPL55712 (LT antagonist) ameliorated, and at times completely prevented, the lesions. NDGA (a nonspecific lipoxygenase inhibitor) was less effective, probably because of its additional effect on cyclooxygenase inhibition. Verapamil, a calcium channel blocker, ameliorated the disease. Thromboxane A2, a potent vasoconstrictor, was probably not responsible for the ischemia of the gastrointestinal tract. This is suggested by the ineffectiveness of OKY-046 in preventing bowel necrosis. Prostaglandin (PG) E1 infusion often prevented the bowel necrosis, which suggested beneficial effects of vasodilating PGs, probably released as a defense mechanisms. Indomethacin aggravated the disease, probably by inhibiting PG release and shifting the metabolic pathway toward the lipoxygenase pathway. Antihistamine and antiserotonin had no effect, which suggested that these mediators were not involved in the pathogenesis of bowel necrosis. Shock produced by PAF was probably not the only cause of bowel necrosis, because reversal of the hypotension did not always prevent the development of bowel necrosis. Hemoconcentration (increased vasopermeability) and leukopenia induced by PAF did not correlate with the development or severity of bowel necrosis.
Cultured mouse marrow stromal cell lines. II. Distinct subtypes differing in morphology, collagen types, myelopoietic factors, and leukemic cell growth modulating activities (1985)

A series of stromal cell lines were studied for their growth properties, electron microscopic morphology, cytochemical profile, collagen types, production of myelopoietic factors, and modulation of leukemic cell growth. Three cell types were identified in addition to the previously described macrophages (14M and 14M1) and preadipocytes (14F). MBA-1 cells were found to be fibroblasts by their ability to synthesize collagen types I and III, while the cell line MBA-13 shared properties in common with both fibroblasts and endothelial cells (collagen types I, III, IV, V). The third cell type, represented by the stromal cell line MBA-2, produced mainly collagen types IV and V and exhibited junctional complexes between adjacent cells. All of the cell lines tested produced and secreted a macrophage-colony-stimulating factor, CSF-1. MBA-2 and to a lesser extent, MBA-13, produced an additional activity resistant to anti-CSF-1 antiserum. Trypsin extraction of outer surface components from two clones of the MBA-2 cell line (MBA-2.1 and MBA-2.4) yielded high molecular weight factor(s) that specifically inhibited the growth of a plasmacytoma cell line (MPC-11). Such inhibitory activity was not detected in other stromal cell lines. It is possible that this variability in the nature of stromal cell lines represents corresponding diversity of cell types comprising the hematopoietic microenvironment in vivo.
Abrupt changes in prostate-specific antigen concentration in acute renal failure (1993)

Journal Article Abrupt changes in prostate-specific antigen concentration in acute renal failure Get access A Price A Price Search for other works by this author on: Oxford Academic Google Scholar Clinical Chemistry, Volume 39, Issue 1, 1 January 1993, Pages 161–162, https://doi.org/10.1093/clinchem/39.1.161 Published: 01 January 1993
Allele‐specific silencing of mutant Huntington’s disease gene (2008)

Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder caused by a poly-glutamine expansion in huntingtin, the protein encoded by the HD gene. PolyQ-expanded huntingtin is toxic to neurons, especially the medium spiny neurons of the striatum. At the same time, wild-type huntingtin has important - indeed essential - protective functions. Any effective molecular therapy must preserve the expression of wild-type huntingtin, while silencing the mutant allele. We hypothesized that an appropriate siRNA molecule would display the requisite specificity and efficacy. As RNA interference is incapable of distinguishing among alleles with varying numbers of CAG (glutamine) codons, another strategy is needed. We used HD fibroblasts in which the pathogenic mutation is linked to a polymorphic site: the Delta2642 deletion of one of four tandem GAG triplets. We silenced expression of the harmful Delta2642-marked polyQ-expanded huntingtin without compromising synthesis of its wild-type counterpart. Following this success in HD fibroblasts, we obtained similar results with neuroblastoma cells expressing both wild-type and mutant HD genes. As opposed to the effect of depleting wild-type huntingtin, specifically silencing the mutant species actually lowered caspase-3 activation and protected HD cells under stress conditions. These findings have therapeutic implications not only for HD, but also for other autosomal dominant diseases. This approach has great promise: it may lead to personalized genetic therapy, a holy grail in contemporary medicine.
EVIDENCE FOR A PREVIOUSLY UNIDENTIFIED UPSTREAM EXON IN THE HUMAN OESTROGEN RECEPTOR GENE. (1991)

The presence of a previously unidentified exon upstream of the originally described human oestrogen receptor (hOR) gene is demonstrated. This is shown to be spliced to the 5' untranslated region of the previously designated exon I. The resulting genomic structure of the human gene is thus in agreement with the structure of the mouse OR gene and highlights the conservation of an 18 amino acid upstream open-reading frame formed from the above splicing event. Taken in conjunction with previous publications this would suggest that the hOR gene is a complex transcriptional unit that contains two promoters.