gebhart/patrepeval huggingface dataset:
Existence of c-<i>kit</i> Receptor-Positive, Tryptase-Negative, IgE-Negative Cells in Human Allergic Nasal Mucosa: A Candidate for Mast Cell Progenitor (1997)

The accumulation of mast cells in the allergic nasal epithelium is well known, yet the mechanism remains unclear. We studied whether there is a candidate for mast cell progenitors in the allergic nasal mucosa tissue removed at the time of surgery. We first confirmed that most mast cells in nasal mucosae of 10 nasal allergic patients had c-kit receptor by immunohistochemistry using the mirror sectioning technique. We then investigated whether c-kit receptor+, tryptase-, IgE- cells existed in nasal mucosae of 15 nasal allergic patients and 15 nonallergic ones using sequential triple immunohistochemistry. We observed the area in which 1,000 to 1,100 tryptase-positive cells (mast cells) existed in both the subepithelial layer and the deep layer of each nasal lamina propria. The epithelial layer above this area was also examined. Some c-kit receptor+, tryptase- cells existed in the nasal mucosae of 11 patients with nasal allergy and of 5 patients with nonallergic rhinitis. From one to four of these cells in the nasal epithelium and subepithelial layer of the 4 allergic patients were IgE-negative. In contrast, no IgE-negative cells existed in the deep layer of allergic nasal mucosae or in any nonallergic nasal mucosae. Our results suggest that mast cell progenitors, hematopoietic progenitor cells or multipotential blood cells exist in the allergic nasal mucosa, and may contribute to the increase of mast cells in the epithelium and subepithelial layer of allergic nasal mucosa.
Recombinant human adenoviruses containing hybrid adenovirus type 5 (Ad5)/Ad12 E1A genes: characterization of hybrid E1A proteins and analysis of transforming activity and host range (1992)

Hybrid adenovirus type 12 (Ad12)/Ad5 E1A genes were constructed by homologous recombination in Escherichia coli, a technique which offers several advantages over conventional mutagenesis for genetic analysis of proteins. In particular, functional differences between the proteins can be mapped by correlating the replacement of specific sequences with the acquisition of new properties, and there is no requirement for common unique restriction sites or polymerase chain reaction strategies to construct the hybrids. Recombinant adenoviruses expressing these hybrid E1A proteins were capable of replicating efficiently in HeLa cells, with the exception of one construct which contained a hybrid transactivation domain. The transforming activity of the hybrid E1A constructs was assayed by DNA transfection of primary baby rat kidney cells. Plasmids containing Ad12 E1 were approximately 20-fold less efficient at transformation than those with E1 of Ad5, and it was found that two regions in exon 1 of E1A mediate this difference. No differences were found in the abilities of any hybrid E1A proteins to bind to cellular proteins previously determined to be important for transformation by E1A.
Differential Responsiveness of Human Bronchial Epithelial Cells, Lung Carcinoma Cells, and Bronchial Fibroblasts to Interferon-γ In Vitro (1994)

The present study examines interferon-gamma (IFN gamma)-induced changes in the expression of immunomodulatory genes, proliferation-associated genes, and squamous-specific genes in primary cultures of human bronchial epithelial cells and fibroblasts. IFN gamma induced the expression of guanylate binding protein (GBP or p67) and the MHC class II antigen, HLADR alpha, in both epithelial cells and fibroblasts. In contrast, the expression of complement component C3 was induced in bronchial epithelial cells but not in fibroblasts. Similarly, IFN gamma induced growth arrest (EC50 approximately 50 U/ml) only in bronchial epithelial cells. This growth arrest was accompanied by a down-regulation of cdc2, E2F-1, and p53 mRNA levels and was associated with expression of the squamous-specific marker genes, transglutaminase type I and cornifin. These findings are consistent with IFN gamma inducing squamous differentiation in bronchial epithelial cells. In contrast, several lung carcinoma cell lines did not respond to IFN gamma with respect to the down-regulation of proliferation-associated genes or the induction of squamous-specific genes. However, GBP expression was induced in all the cell lines in response to IFN gamma. The present study demonstrates that cultured human bronchial epithelial cells are sensitive to the immunomodulatory, growth-inhibitory, and differentiation-inducing properties of IFN gamma. In contrast, several lung carcinoma cell lines are insensitive to the growth-inhibitory and differentiation-inducing actions of IFN gamma, suggesting they may have acquired defects in certain IFN gamma signaling pathways. Although the growth of human bronchial fibroblasts is not altered, expression of certain immunomodulatory genes is induced by IFN gamma.(ABSTRACT TRUNCATED AT 250 WORDS)
Synthesis of 5,6‐dihydroxy‐2‐phenyl‐4‐pyrimidinecarboxylic acid, methyl ester, a corrected structure (1979)

Abstract Pyrolysis of the adduct of benzamide oxime and dimethyl acetylenedicarboxylate leads to 5,6‐dihydroxy‐2‐phenyl‐4‐pyrimidinecarboxylic acid methyl ester ( 4a ) rather than 4,5‐dihydro‐α,4‐dioxo‐2‐phenyl‐1 H ‐imidazole‐5‐acetic acid, methyl ester ( 1 ).
Detection and Characterization of Circulating Microsatellite‐DNA in Blood of Patients with Breast Cancer (2004)

Increased levels of circulating DNA have been reported in the blood of cancer patients but not healthy individuals. Tumor-specific genomic aberrations, such as loss of heterozygosity (LOH) and microsatellite instability (MSI), can be detected in this free extracellular DNA. Identification of these genetic aberrations may play an important role in cancer diagnosis and prediction of disease progression. Moreover, the genomic regions involved might harbor potential targets for therapies. To evaluate the incidence of microsatellite alterations in circulating DNA, we assessed the blood serum of 34 patients with primary (n = 8) and metastatic (n = 24) breast cancer. Samples were also analyzed for the presence of circulating tumor cells using an immunocytological cytokeratin assay, and the concentration of the tumor marker CA 15-3 was determined. Genomic DNA extracted from serum and normal blood leukocytes, as a control, was amplified by the polymerase chain reaction using markers at 4 microsatellite loci of chromosomes 10q22-23, 16q22-23, 17q11-12, and 17q21. In 17 of 34 cancer patients, tumor-specific alterations were detected in serum samples. In 16 patients, LOH at various loci was observed, whereas MSI was only detected in the serum of one patient. The pattern of LOH was very heterogeneous, and LOH was detected at chromosomal loci 10q22-23, 16q22-23, and 17q11-12 but not 17q21. No correlation was found between the detection of circulating tumor DNA and the presence of circulating tumor cells in the blood or serum concentration of CA 15-3. In conclusion, genomic aberrations on chromosomes 10, 16, and 17 are frequent in the circulating DNA of breast cancer patients. However, circulating tumor DNA does not reflect the presence of tumor cells in blood or the level of tumor-associated protein markers such as CA 15-3. Thus, screening for circulating tumor DNA may provide additional diagnostic information.
UBH 3: A Biologically Inspired Robotic Hand (2004)

This paper describes a work in progress at the Uni-versity of Bologna concerning the design of a new anthropomorphic robot hand. The overall hand is based on an innovative mechanical architecture, which adopts deformable elements as joint hinges. This de-sign leads to an endo-skeletal structure particularly suitable to host a distributed sensory equipment and a continuous compliant cover, allowing a high level of anthropomorphism together with great structural sim-plification, reliability enhancement and cost reduction. Furthermore, the proposed solution is very flexible, as it can be adapted to many different end-effector con-figurations and is not dependent on a particular type of actuation, being compatible with future availability of any kind of artificial muscles. 1
Plant Pathogens and Plant Diseases (1998)

This book, written by a team of Australian plant pathologists, is design to give students and researchers a background in the principles of plant pathology and of managing plant diseases. The book is divided into five sections. The first deals with the agents that cause disease and includes fungi, bacteria, phytoplasmas, viruses, viroids, nematodes, parasitic plants and abiotic agents. There is also a useful and up-to-date chapter on serological and molecular techniques to detect and identify plant pathogens. Part two deals with the survival and dispersal of plant pathogens, including airborne and soilborne inoculum, and the role played by vectors. Part three covers infection processes, epidemiology and crop-loss assessment and this is something of a mixed bag, as it includes chapters on plant defence, disease prediction, and biocontrol of weeds using plant pathogens. Quantitative concepts of epidemiology feature in the introduction to part four, which concerns disease management. This may not appeal to the purist or disease modellers but does have the virtue for students of introducing disease growth curves in the context of strategies for control. The remainder of this section covers all aspects of disease management including quarantine and sanitation, chemical, cultural, genetic and biological approaches to disease control. The final part gives specific examples of different types of plant diseases and their control, based on the different types of pathogens, as well as a chapter on disease in natural communities and another on postharvest pathology. Inevitably the book has an Australian emphasis in the examples chosen, but the principles developed are universal and it should prove very useful for a variety of plant pathology courses. The editors have done well to compile such a range of information from different authors in a uniform style. The book is strong on the biology of the different pathogens, and particularly on practical aspects of disease management, which occupy approximately one third of the 550 pages. It is well illustrated with tables, keys and diagrams, although the production standards are not as high as in some other recent texts where glossy paper and even colour photos are included. It is easy to read and accessible for students, and with the very wide range of topics covered deserves to be considered as a core text for both introductory and intermediate level plant pathology courses. At the price of $A49 it is good value.
A monoclonal antibody against an erythrocyte ontogenic antigen identifies fetal and adult erythroid progenitors (1986)

A murine monoclonal antibody (MoAb) designated FA6-152 has been obtained by immunizing mice with fetal erythrocytes. This antibody agglutinates fetal but not adult erythrocytes. Among blood cells, this antibody bound to both adult and fetal monocytes, platelets, and reticulocytes, but did not react with lymphocytes and granulocytes. Fluorescent labeling of marrow cells and of in vitro BFU-E, CFU-GM, and CFU-MK-derived colonies has shown that the antigen defined by FA6-152 MoAb was absent from the granulocytic precursors and was detected on the megakaryocytic lineage at a later stage of differentiation than the platelet-specific markers. In contrast, the antigen appeared as a very early marker of the erythroid differentiation since all erythroblasts, including proerythroblasts, were labeled even before the expression of glycophorin A. Cells from adult marrow and fetal liver were sorted with the FA6-152 MoAb and studied by electron microscopy and cell culture. The negative fraction contained granulocytic, monocytic, and megakaryocytic precursors, whereas the positive fraction was devoid of these precursors and contained monocytes, erythroblasts at all stages of maturation, and a homogeneous population of blasts. Cultures have shown that the only hematopoietic progenitors present in this positive fraction were CFU-E and some BFU-E. The antigenic density was related to the differentiation stage of the erythroid progenitors. In conclusion, this antibody is similar to the previously described 5F1 MoAb (Bernstein and Andrews, J Immunol 128:876, 1982; and Andrews et al, Blood 62:124, 1983) and provides a useful probe for studies leading to improved understanding of normal and malignant erythroid differentiation.
Structural Basis for Activation of Fibroblast Growth Factor Signaling by Sucrose Octasulfate (2002)

Sucrose octasulfate (SOS) is believed to stimulate fibroblast growth factor (FGF) signaling by binding and stabilizing FGFs. In this report, we show that SOS induces FGF-dependent dimerization of FGF receptors (FGFRs). The crystal structure of the dimeric FGF2-FGFR1-SOS complex at 2.6-A resolution reveals a symmetric assemblage of two 1:1:1 FGF2-FGFR1-SOS ternary complexes. Within each ternary complex SOS binds to FGF and FGFR and thereby increases FGF-FGFR affinity. SOS also interacts with the adjoining FGFR and thereby promotes protein-protein interactions that stabilize dimerization. This structural finding is supported by the inability of selectively desulfated SOS molecules to promote receptor dimerization. Thus, we propose that SOS potentiates FGF signaling by imitating the dual role of heparin in increasing FGF-FGFR affinity and promoting receptor dimerization. Hence, the dimeric FGF-FGFR-SOS structure substantiates the recently proposed "two-end" model, by which heparin induces FGF-FGFR dimerization. Moreover, the FGF-FGFR-SOS structure provides an attractive template for the development of easily synthesized SOS-related heparin agonists and antagonists that may hold therapeutic potential.
Circulation of Endemic Type 2 Vaccine-Derived Poliovirus in Egypt from 1983 to 1993 (2003)

From 1988 to 1993, 30 cases of poliomyelitis associated with poliovirus type 2 were found in seven governorates of Egypt. Because many of the cases were geographically and temporally clustered and because the case isolates differed antigenically from the vaccine strain, it was initially assumed that the cases signaled the continued circulation of wild type 2 poliovirus. However, comparison of sequences encoding the major capsid protein, VP1 (903 nucleotides), revealed that the isolates were related (93 to 97% nucleotide sequence identity) to the Sabin type 2 oral poliovirus vaccine (OPV) strain and unrelated (<82% nucleotide sequence identity) to the wild type 2 polioviruses previously indigenous to Egypt (last known isolate: 1979) or to any contemporary wild type 2 polioviruses found elsewhere. The rate and pattern of VP1 divergence among the circulating vaccine-derived poliovirus (cVDPV) isolates suggested that all lineages were derived from a single OPV infection that occurred around 1983 and that progeny from the initiating infection circulated for approximately a decade within Egypt along several independent chains of transmission. Complete genomic sequences of an early (1988) and a late (1993) cVDPV isolate revealed that their 5' untranslated region (5' UTR) and noncapsid- 3' UTR sequences were derived from other species C enteroviruses. Circulation of type 2 cVDPVs occurred at a time of low OPV coverage in the affected communities and ceased when OPV coverage rates increased. The potential for cVDPVs to circulate in populations with low immunity to poliovirus has important implications for current and future strategies to eradicate polio worldwide.
Overexpression and characterization of the chromosomal aminoglycoside 6'-N-acetyltransferase from Enterococcus faecium (1997)

The chromosomal gene aac(6')-Ii, encoding an aminoglycoside 6'-N-acetyltransferase in Enterococcus faecium, renders this organism resistant to moderate levels of many aminoglycoside antibiotics. The ubiquitous presence of aac(6')-Ii in E. faecium complicates the selection of antibiotics for treatment of infections caused by this organism. In view of the importance of this enzyme, we have initiated studies to gain an understanding of its molecular mechanism of acetyl transfer. The AAC(6')-Ii enzyme was overexpressed in Escherichia coli and purified in a simple three-step procedure which yields 55 mg of pure dimeric protein per liter of cell culture. Steady-state kinetic analyses revealed a broad substrate specificity and demonstrated that acetylation occurs exclusively at position N-6'. k(cat)/Km values were on the order of 10(4) M(-1) s(-1), which is relatively low compared to other aminoglycoside-modifying enzymes. In addition, MIC values were positively correlated with k(cat), the rate when the enzyme is saturated with the aminoglycoside substrate, and not with k(cat)/Km, the rate at low aminoglycoside (sub-Km) concentrations. These results describe an enzyme which is not optimally evolved for aminoglycoside inactivation and suggest that this chromosomally encoded enzyme may have an alternate physiological function.
Separation of gluco- and galactocerebrosides by means of borate thin-layer chromatography (1966)

Gluco- and galactocerebrosides can be separated by thin-layer chromatography on Silica Gel G prepared with sodium borate solution instead of water. The most successful developing system was chloroform-methanol-water-15 M NH(4)OH 280:70:6:1.
Activation of the Met Receptor by Cell Attachment Induces and Sustains Hepatocellular Carcinomas in Transgenic Mice (2001)

Overexpression is the most common abnormality of receptor tyrosine kinases (RTKs) in human tumors. It is presumed that overexpression leads to constitutive activation of RTKs, but the mechanism of that activation has been uncertain. Here we show that overexpression of the Met RTK allows activation of the receptor by cell attachment and that this form of activation can be tumorigenic. Transgenic mice that overexpressed Met in hepatocytes developed hepatocellular carcinoma (HCC), one of the human tumors in which Met has been implicated previously. The tumorigenic Met was activated by cell attachment rather than by ligand. Inactivation of the transgene led to regression of even highly advanced tumors, apparently mediated by apoptosis and cessation of cellular proliferation. These results reveal a previously unappreciated mechanism by which the tumorigenic action of RTKs can be mediated, provide evidence that Met may play a role in both the genesis and maintenance of HCC, and suggest that Met may be a beneficial therapeutic target in tumors that overexpress the receptor.
Clinical changes following four different periodontal therapies for the treatment of chronic periodontitis: 1‐year results (2007)

This study, demonstrated that periodontal therapy provides clinical benefits and that antibiotics provide a clinical benefit over SRP alone, particularly at initially deeper periodontal pockets.
In situ hybridization studies suggest a role for the basic region‐leucine zipper protein hXBP‐1 in exocrine gland and skeletal development during mouse embryogenesis (1993)

The spatial and temporal distribution of transcripts for the TRE/CRE-binding basic region-leucine zipper protein hXBP-1 was determined by in situ hybridization. Analysis of embryos from day 10.5 to 18.5 pc revealed high level expression of hXBP-1 RNA in two developing organ systems: 1) in bone and cartilage cells of the developing skeleton and toothbuds, and 2) in exocrine glands including the pancreas and the submandibular and salivary glands. High level expression was also found in whisker follicles and in selected cells in brown adipose tissue. In the developing skeleton, hXBP-1 RNA was expressed starting on day 11.5 pc in osteoblasts of newly formed intramembranous bone. Thereafter, hXBP-1 was expressed in both osteoblasts and preosteoblasts in bone formed directly by intramembranous formation as well as in bone formed during endochondral ossification. The most intense signal was observed in preosteoblasts and osteoblasts of newly forming bone. At day 11.5 pc low level hXBP-1 expression was also observed in matrix secreting chondroblasts of bones which are formed initially of cartilage, at the stage where they consist entirely of cartilage. Signal was also present in matrix producing chondroblasts of the mature zone of the growth region during endochondral ossification although at significantly lower level than in osteoblasts. hXBP-1 is thus the first transcription factor described, to our knowledge, whose level of expression is modulated during the osteoblast developmental sequence in vivo. The pattern of expression of hXBP-1 in the developing skeleton was found to be very similar to that of the genes encoding the tissue inhibitor of metalloproteinase and alkaline phosphatase throughout development. These observations suggest that hXBP-1 may play a role in regulating the expression of tissue specific genes (TIMP, osteonectin, osteopontin, osteocalcin) expressed in osteoblasts. It is intriguing that the promoter regions of several such genes contain potential hXBP-1 binding sites.
Leukotriene A4 Hydrolase – An Evolving Therapeutic Target (2012)

Leukotriene B4 is an important mediator of inflammation derived from successive metabolism of fatty acids by several enzymes including the terminal rate-limiting enzyme called leukotriene A4 hydrolase. Leukotriene A4 hydrolase is a soluble enzyme, and depending on its substrate can function as either an epoxide hydrolase or an aminopeptidase. Over the years, leukotriene B4 has been found to be highly associated with several human diseases, and most of the reported literature has focused on the biology of the epoxide hydrolase activity of the enzyme, which generates the lipid metabolite leukotriene B4. However, emerging data suggests that the aminopeptidase activity of the leukotriene A4 hydrolase enzyme may also play a crucial role in the process of antiinflammatory responses. Previous drug discovery efforts have focused on inhibition of the leukotriene B4 metabolite by indiscriminately blocking both the epoxide hydrolase and aminopeptidase functions of the enzyme. The co-existence of a dichotomous and directly opposing biological function of this enzyme as suggested by recent studies on the aminopeptidase activity of leukotriene A4 hydrolase is a radically paradigm-shifting and relevant concept. This manuscript will review these recent findings in the context of the classical understanding of the leukotriene A4 hydrolase enzyme.
Epidemic processes in complex networks (2015)

Complex networks arise in a wide range of biological and sociotechnical systems. Epidemic spreading is central to our understanding of dynamical processes in complex networks, and is of interest to physicists, mathematicians, epidemiologists, and computer and social scientists. This review presents the main results and paradigmatic models in infectious disease modeling and generalized social contagion processes.