gebhart/patrepeval huggingface dataset:
Suppression of Autocrine and Paracrine Functions of Basic Fibroblast Growth Factor by Stable Expression of Perlecan Antisense cDNA (1997)

Heparan sulfate proteoglycans (HSPG) play a critical role in the formation of distinct fibroblast growth factor (FGF)-HS complexes, augmenting high-affinity binding and receptor activation. Perlecan, a secreted HSPG abundant in proliferating cells, is capable of inducing FGF-receptor interactions in vitro and angiogenesis in vivo. Stable and specific reduction of perlecan levels in mouse NIH 3T3 fibroblasts and human metastatic melanoma cells has been achieved by expression of antisense cDNA corresponding to the N-terminal and HS attachment domains of perlecan. Long-term perlecan downregulation is evidenced by reduced levels of perlecan mRNA and core protein as indicated by Northern blot analysis, immunoblots, and immunohistochemistry, using DNA probes and antibodies specific to mouse or human perlecan. The response of antisense perlecan-expressing cells to increasing concentrations of basic FGF (bFGF) is dramatically reduced in comparison to that in wild-type or vector-transfected cells, as measured by thymidine incorporation and rate of proliferation. Furthermore, receptor binding and affinity labeling of antisense perlecan-transfected cells with 125I-bFGF is markedly inhibited, indicating that eliminating perlecan expression results in reduced high-affinity bFGF binding. Both the binding and mitogenic response of antisense-perlecan-expressing clones to bFGF can be rescued by exogenous heparin or perlecan. These results support the notion that perlecan is a major accessory receptor for bFGF in mouse fibroblasts and human melanomas and point to the possible use of perlecan antisense constructs as specific modulators of bFGF-mediated responses.
Acidities of carbon and nitrogen acids: the aromaticity of the cyclopentadienyl anion (1981)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTAcidities of carbon and nitrogen acids: the aromaticity of the cyclopentadienyl anionFrederick G. Bordwell, George E. Drucker, and Herbert E. FriedCite this: J. Org. Chem. 1981, 46, 3, 632–635Publication Date (Print):January 1, 1981Publication History Published online1 May 2002Published inissue 1 January 1981https://pubs.acs.org/doi/10.1021/jo00316a032https://doi.org/10.1021/jo00316a032research-articleACS PublicationsRequest reuse permissionsArticle Views2444Altmetric-Citations216LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Correction of liver dysfunction in DNA repair-deficient mice with an ERCC1 transgene (2001)

The ERCC1 gene is essential for the repair of UV-induced DNA damage. Unlike most genes in the nucleotide excision repair (NER) pathway, ERCC1 is also involved in recombinational repair. Perhaps for this reason, ERCC1 knockout mice are not a model for the human NER deficiency disorder, xeroderma pigmentosum. Instead, ERCC1 null mice are severely runted and die before weaning from liver failure with accelerated hepatocyte polyploidy that is more reminiscent of a premature ageing disorder. To permit study of the role of ERCC1 in other tissues we have corrected the liver ERCC1 deficiency with a transgene under the control of a liver-specific promoter. The transgene alleviated runting and extended the lifespan. The elevated level of oxidative DNA damage and premature liver polyploidy were reversed and liver function was corrected. A widespread mitochondrial dysfunction was identified and an essential role for ERCC1 in the kidney was also revealed with transgene-containing ERCC1-deficient animals going on to die of renal failure. The nuclei of kidney proximal tubule cells became polyploid in a similar way to the premature liver polyploidy observed in younger ERCC1-deficient animals. We believe that this is a response to the accumulation of endogenous DNA damage in these particularly susceptible tissues which cannot be repaired in ERCC1-deficient animals.
Intranasal immunization of a DNA vaccine with IL-12- and granulocyte-macrophage colony-stimulating factor (GM-CSF)-expressing plasmids in liposomes induces strong mucosal and cell-mediated immune responses against HIV-1 antigens (1997)

A DNA vaccine constructed with the CMV promoter conjugated to env gp160 and rev genes has been shown to induce an effective Th1-type immune response when inoculated via an intramuscular route. In the present study, we obtained high levels of both humoral and cell-mediated immune activity by intranasal administration of this DNA vaccine. The production of mucosal IgA Ab in feces and vaginal fluid was stimulated significantly by intranasal DNA administration. This route of administration resulted in a significant level of HIV-1-neutralizing Abs in feces and serum. Cytokine assays revealed that intranasal administration of this DNA vaccine induces a Th2-type immune response. Interestingly, cationic liposomes greatly enhanced these activities. Abs against HIV-1 were present for at least 10 mo. Coadministration of the DNA vaccine with IL-12- and granulocyte/macrophage-CSF-expressing plasmids induced high levels of HIV-specific CTLs and an increase in delayed type hypersensitivity when administered by the intranasal route. These results clearly demonstrate that intranasal administration of this DNA vaccine with liposomes, together with IL-12- and/or granulocyte/macrophage-CSF-expressing plasmids, induces a strong level of anti-HIV-1 immune response.
The spectrum of mutations in UBE3A causing Angelman syndrome (1999)

Angelman syndrome (AS) is characterized by mental retardation, absence of speech, seizures and motor dysfunction. AS is caused by maternal deletions for chromosome 15q11-q13, paternal uniparental disomy (UPD), imprinting defects or loss-of-function mutations in the UBE3A locus which encodes E6-AP ubiquitin-protein ligase. The UBE3A gene is imprinted with paternal silencing in human brain and similar silencing of the Ube3a locus in Purkinje cells and hippocampal neurons in the mouse. We have sequenced the major coding exons for UBE3A in 56 index patients with a clinical diagnosis of AS and a normal DNA methylation pattern. The analysis identified disease-causing mutations in 17 of 56 patients (30%) including 13 truncating mutations, two missense mutations, one single amino acid deletion and one stop codon mutation predicting an elongated protein. Mutations were identified in six of eight families (75%) with more than one affected case, and in 11 of 47 isolated cases (23%); no mutation was found in one family with two siblings, one with a typical and one with an atypical phenotype. Mutations were de novo in nine of the 11 isolated cases. An amino acid polymorphism of threonine substituted for alanine at codon 178 was identified, and a 3 bp length polymorphism was found in the intron upstream of exon 8. In all informative cases, phenotypic expression was consistent with imprinting with a normal phenotype when a mutation was on the paternal chromosome and an AS phenotype when a mutation was on the maternal chromosome. Laboratory diagnosis and genetic counseling for AS are complex, and mutation analysis is valuable in clinically typical AS patients with a normal methylation analysis.
Mupirocin application at the exit site in peritoneal dialysis patients: five years of experience (2010)

Mupirocin application at the exit sites reduces peritonitis and ESI to a considerable amount, and thrice-weekly application of mupirocin seems to be more efficient compared to once-weekly application.
CpG Oligodeoxynucleotides Enhance Host Defense during Murine Tuberculosis (2002)

Oligodeoxynucleotides (ODNs) containing unmethylated CpG motifs activate immune cells to produce cytokines. CpG ODNs protect mice against infections with intracellular bacteria by the induction of a T helper 1 (Th1) response. To determine the effect of CpG ODNs in pulmonary tuberculosis, mice were treated with CpG ODNs or control ODNs at the time of intranasal infection. CpG ODNs reduced mycobacterial outgrowth for up to 5 weeks after Mycobacterium tuberculosis infection and were associated with a decrease in inflammation in lung tissue. CpG treatment was also associated with elevated levels of gamma interferon (IFN-gamma) and decreased levels of interleukin 4 in the lungs and an increased capacity of splenocytes to secrete Th1-type cytokines. CpG ODNs given 2 weeks after infection were still able to reduce mycobacterial outgrowth and to enhance a Th1 response 5 weeks postinfection. Administration of CpG ODNs to IFN-gamma-gene-deficient mice failed to reduce mycobacterial outgrowth. These data suggest that CpG ODNs improve host defense during pulmonary tuberculosis by an IFN-gamma-dependent mechanism.
Representing the Relationships Between Field Collected Carbon Exchanges and Surface Reflectance Using Geospatial and Satellite-Based Techniques (2017)

Carbon exchanges between the atmosphere and the land surface vary in space and time, and are highly dependent on land cover type. It is important to quantify these exchanges to understand how landscapes affect the carbon budget, which will have a significant impact on future climate change and will inform climate change projections. However, how do you represent regional carbon exchanges from a single meteorological station? A single observing station will represent a limited area around the station, but each individual observation will sample a different physical land area in time due to varying wind speeds, wind direction, and atmospheric stability. The methods and techniques presented address the challenges, limitations, and future work that is needed to properly scale and model carbon exchanges in four dimensions for varying agricultural and transitioning ecotones. Seasonal variability of carbon exchanges can be modeled in agricultural land covers using satellite-based techniques, but due to physiological differences in crop types the values must be modeled by crop species. The spatially varying atmospheric conditions must also be considered when modeling carbon exchanges from a single point in the spatial realm because of the dependency of carbon exchange on temperature and humidity conditions. In summary, field-based carbon exchange observations are used to quantify whether a specific land cover in a region is a carbon source to carbon sink to the atmosphere, however, it is important to consider the spatially varying variables that limit the ability of a single point measurement to represent carbon exchanges of an entire region.
Role of RT-PCR and FISH in diagnosis and monitoring of acute promyelocytic leukemia (2011)

Both RT-PCR and FISH are important for the diagnosis of APL cases, as both techniques complement each other in the absence or failure of any one of them. However, RT-PCR is more sensitive than FISH for the detection of minimal residual disease in the long-term monitoring of these patients. The present study shows that the predictive value of relapse is more associated with minimal residual disease (MRD) results by RT-PCR than that by FISH.
Site-Specific Antibody–Drug Conjugates: The Nexus of Bioorthogonal Chemistry, Protein Engineering, and Drug Development (2014)

Antibody-drug conjugates (ADCs) combine the specificity of antibodies with the potency of small molecules to create targeted drugs. Despite the simplicity of this concept, generation of clinically successful ADCs has been very difficult. Over the past several decades, scientists have learned a great deal about the constraints on antibodies, linkers, and drugs as they relate to successful construction of ADCs. Once these components are in hand, most ADCs are prepared by nonspecific modification of antibody lysine or cysteine residues with drug-linker reagents, which results in heterogeneous product mixtures that cannot be further purified. With advances in the fields of bioorthogonal chemistry and protein engineering, there is growing interest in producing ADCs by site-specific conjugation to the antibody, yielding more homogeneous products that have demonstrated benefits over their heterogeneous counterparts in vivo. Here, we chronicle the development of a multitude of site-specific conjugation strategies for assembly of ADCs and provide a comprehensive account of key advances and their roots in the fields of bioorthogonal chemistry and protein engineering.
Laser micromanipulation systems as universal tools in cellular and molecular biology and in medicine. (1998)

The UV-laser microbeam has been established as a valuable tool in a wide area of molecular biology as well as in medical research and applications. This system allows to cut or fuse microscopically small specimen. An important application of the cutting laser is laser microbeam microdissection (LMM) combined with laser pressure catapulting (LPC), which allows to procure single cells or small homogeneous cell areas for subsequent molecular analysis in an entirely "non-contact" manner. With LMM minute tissue areas, single cells or chromosomes are microdissected and separated from their surroundings. Subsequently, LPC ejects the dissectates directly into the cap of a sample tube without any mechanical contact. This enables the rapid procurement of homogeneous specimen from less than one up to several hundreds of micrometers in diameter without encroachment of the adjacent region. The mRNA information of the selected specimen as well as of the remaining probe are well preserved, as demonstrated with laser isolated samples from a routinely prepared tissue section of a differentiated colorectal adenocarcinoma. Reverse transcription of specific mRNA coding for cytoplasmic beta-actin and subsequent hemi-nested PCR amplification was not impaired. Any kind of tissue, as well as single cells from different sources and even subcellular structures can be captured using this laser method. Wherever homogeneous samples are required to analyze cell or chromosome-specific genetic alterations such as in cancer research or prenatal diagnosis this unique and rapid laser micropreparation method will become a key technology of great value.
Chemotherapy and Angiogenesis in Advanced Cancer: Vascular Endothelial Growth Factor (VEGF) Decline as Predictor of Disease Control during Taxol Therapy in Metastatic Breast Cancer (2000)

Angiogenesis is essential for tumor growth. Since vascular endothelial growth factor (VEGF) represents the main angiogenic factor, the control of VEGF secretion could constitute the most important mechanism to achieve the inhibition of angiogenesis-related processes. High blood concentrations have been proven to correlate with poor prognosis in advanced cancer. In experimental conditions, chemotherapeutic agents such as taxol appeared to inhibit VEGF-induced angiogenesis, while at present there are no data about the influence of chemotherapy on VEGF secretion in cancer patients. This preliminary study was performed to evaluate the effect of taxol therapy on VEGF secretion in advanced cancer patients in relation to the clinical response. The study included 14 patients with metastatic breast cancer who were treated with taxol monochemotherapy (175 mg/m2 i.v. every 21 days for three cycles). Serum levels of VEGF were measured by ELISA in blood samples collected before therapy and at 21-day intervals. The clinical response consisted of partial response (PR) in three and stable disease (SD) in six patients, whereas the other five patients had progressive disease (PD). Abnormally high pre-treatment levels of VEGF were seen in 8/14 patients. VEGF mean values significantly decreased during taxol therapy in patients with PR or SD, whereas no decline was observed in patients with PD. Moreover, the percent of normalization or decline greater than 50% in VEGF levels was significantly higher in patients with PR or SD than in those with PD (5/9 vs. 0/5). This preliminary study would suggest that the efficacy of taxol therapy in metastatic breast cancer - at least in terms of disease stabilization - may be associated with a decrease in VEGF blood levels followed by potential inhibition of cancer-related neovascularization.
Über Oxide des neuen Formeltyps A[T4O4]: Zur Kenntnis von KLi3GeO4, KLi3SiO4 und KLi3TiO4 (1984)

Abstract Die Kristallstruktur von KLi 3 GeO 4 wurde aus Einkristalldaten bestimmt. Die Elementarzelle ist triklin, Raumgruppe P 1 , a = 10,278(2), b = 7,511(1), c = 5,849(1) Å, α = 100,33(2), β = 110,07(2), γ = 90,32(2)°; Z = 4, R = 0,086 7 , R w = 0,079 3 . Stränge aus KO 8/2 ‐Würfeln parallel zu [1 1 1] werden durch tetraedrisch umgebene Li + und Ge 4+ miteinander verknüpft. KLi 3 SiO 4 und KLi 3 TiO 4 sind isotyp. Effektive Koordinationszahlen (ECoN) und der Madelunganteil der Gitterenergie (MAPLE) wurden berechnet.
Cellular interactions in the generation of cytolytic T lymphocyte responses Analysis of the helper T cell pathway (1981)

Murine splenic lymphocytes exhibit a requirement for helper T cells for the induction of a cytolytic T lymphocyte response to suboptimal doses of allogeneic cells, membranes from allogeneic cells, or purified H-2 antigen in liposomes. The conditions where a requirement for help is apparent are the same conditions where a dependence on splenic adherent cells (SAC) has been demonstrated (Weinberger, O. et al., PROC. Natl. Acad, Sci, USA 1980. 77: 6091). Help can be provided in the form of primed, radioresistant, Ly-1+ spleen or lymph node cells or helper factor (interleukin 2, IL-2). A factor generated from phytohemagglutinin-stimulated human lymphocytes, when added to culture in the presence of antigen, bypassed the requirement for Ia+ SAC and helper cells. IL-2 reconstituted the response to H-2K(k) in liposomes in cultures depleted of SAC, strongly suggesting that the helper cell must see antigen re-expressed by an antigen-presenting cell, whereas the prekiller does not. IL-2 could be generated by culturing Ly-1+ murine spleen cells with H-2K(k) pulsed on SAC.
Printed antennas for dual-band GSM/DCS 1800 mobilehandsets (1998)

The recent developments of dual-band dual-mode D-AMPS/AMPS mobile handsets and radiostations has increased pressure on GSM service providers to follow similar technology breakthroughs as a first step towards IMT2000. A frequency-agile device accommodating both GSM standard frequency bands would serve more than 25 million GSM subscribers, with expectations as high as 100 million subscribers by the year 2000. Novel dual-band printed bow-tie antenna elements developed for dual-mode GSM/DCS 1800 handsets are described.
Face annotation for personal photos using collaborative face recognition in online social networks (2009)

Automatic face annotation (or tagging) facilitates improved retrieval and organization of personal photos in online social networks. In this paper, we present a new collaborative face recognition (FR) method that aims to improve face annotation accuracy. The proposed method makes efficient use of multiple FR engines and databases that are distributed over an online social network. The performance of our collaborative face recognition method was successfully evaluated using the standard MPEG-7 VCE-3 data set and a set of real-world personal photos from the Web. The efficacy of the proposed method is demonstrated in terms of comparative annotation performance against non-collaborative approaches utilizing a single FR engine and a single database only.
Glypican-6, a New Member of the Glypican Family of Cell Surface Heparan Sulfate Proteoglycans (1999)

The glypicans compose a family of glycosylphosphatidylinositol-anchored heparan sulfate proteoglycans. Mutations in dally, a gene encoding a Drosophila glypican, and in GPC3, the gene for human glypican-3, implicate glypicans in the control of cell growth and division. So far, five members of the glypican family have been identified in vertebrates. By sequencing expressed sequence tag clones and products of rapid amplifications of cDNA ends, we identified a sixth member of the glypican family. The glypican-6 mRNA encodes a protein of 555 amino acids that is most homologous to glypican-4 (identity of 63%). Expression of this protein in Namalwa cells shows a core protein of approximately 60 kDa that is substituted with heparan sulfate only. GPC6, the gene encoding human glypican-6, contains nine exons. Like GPC5, the gene encoding glypican-5, GPC6 maps to chromosome 13q32. Clustering of the GPC5/GPC6 genes on chromosome 13q32 is strongly reminiscent of the clustering of the GPC3/GPC4 genes on chromosome Xq26 and suggests GPCs arose from a series of gene and genome duplications. Based on similarities in sequence and gene organization, glypican-1, glypican-2, glypican-4, and glypican-6 appear to define a subfamily of glypicans, differing from the subfamily comprising so far glypican-3 and glypican-5. Northern blottings indicate that glypican-6 mRNA is widespread, with prominent expressions in human fetal kidney and adult ovary. In situ hybridization studies localize glypican-6 to mesenchymal tissues in the developing mouse embryo. High expressions occur in smooth muscle cells lining the aorta and other major blood vessels and in mesenchymal cells of the intestine, kidney, lung, tooth, and gonad. Growth factor signaling in these tissues might in part be regulated by the presence of glypican-6 on the cell surface.
Genetic studies in idiopathic short stature (2000)

Idiopathic short stature (ISS) refers to a heterogeneous group of children with marked growth failure of unknown cause, and encompasses familial short stature and constitutional delay of growth. It has been postulated that specific genetic mutations may explain certain cases of growth failure. Some patients with growth hormone (GH) deficiency have mutations in the GH-releasing hormone receptor or GH gene, whereas patients with GH insensitivity syndrome have mutations in the GH receptor or insulin-like growth factor-I gene. It appears that heterozygous mutations of the GH receptor may cause partial GH insensitivity in a subset of patients with ISS. Defects in the short stature homeobox-containing gene (SHOX) in the pseudoautosomal region of the sex chromosomes may cause the growth failure seen in the Leri-Weill and Turner syndromes, and in some familial cases of ISS. Further research into stature-related genes will likely contribute to our understanding of this population.