gebhart/patrepeval huggingface dataset:
Isolation of tobacco mesophyll cells in intact and active state (1968)

Journal Article Isolation of tobacco mesophyll cells in intact and active state Get access ITARU TAKEBE, ITARU TAKEBE Institute for Plant Virus ResearchAobacho, Chiba Search for other works by this author on: Oxford Academic Google Scholar YOSHIAKI OTSUKI, YOSHIAKI OTSUKI Institute for Plant Virus ResearchAobacho, Chiba Search for other works by this author on: Oxford Academic Google Scholar SHIGEJI AOKI SHIGEJI AOKI Institute for Plant Virus ResearchAobacho, Chiba Search for other works by this author on: Oxford Academic Google Scholar Plant and Cell Physiology, Volume 9, Issue 1, 1968, Pages 115–124, https://doi.org/10.1093/oxfordjournals.pcp.a079318 Published: 01 January 1968 Article history Received: 14 December 1967 Published: 01 January 1968
Expression and development of a functional plasmalemmal 5-hydroxytryptamine transporter by thyroid follicular cells. (1996)

5-Hydroxytryptamine (5-HT) is synthesized and secreted by thyroid parafollicular (PF) cells. As all PF granules contain 5-HT, it is released whenever PF cells secrete. Because 5-HT stimulates follicular (F) cells and can modulate their response to TSH, 5-HT has been proposed to be a paracrine PF to F cell transmitter. This role would require a thyroid mechanism to rapidly inactivate 5-HT. A 5-HT transporter (SERT) in the plasma membrane of serotonergic neurons inactivates neuronal 5-HT. We thus tested the hypothesis that this molecule is expressed in the thyroid. Messenger RNA encoding SERT was demonstrated in both the human thyroid and a rat F cell line (FRTL-5). SERT immunoreactivity was detected in rat F, but not PF, cells. Transporter-mediated uptake of [3H]5-HT by F cells arose early in development (E13 in mice) and was maintained in adult life in mice, guinea pigs, bats, and rats (FRTL-5 cells). These observations indicate that a functional SERT is expressed in the thyroid, not by the 5-HT-secreting PF cells, but by their putative F cell targets.
Mucosal and systemic immunizations with killed Pseudomonas aeruginosa protect against acute respiratory infection in rats (1994)

The aim of this study was to determine the efficacies of prior mucosal (oral, intra-Peyer's patch, or intratracheal) and systemic (subcutaneous) immunizations with killed Pseudomonas aeruginosa in clearance of an acute P. aeruginosa respiratory infection in rats. Rats were immunized with paraformaldehyde-killed P. aeruginosa at various doses, and 2 weeks later, the rats were challenged with a log10 dose of 8.7 live bacteria. This dose was fatal for unimmunized rats, with death occurring approximately 12 h after challenge. The numbers of surviving bacteria in the airways and lung tissue were determined by analyses of bronchoalveolar lavage fluid (BAL) and lung homogenate samples, respectively. Enhanced bacterial clearance was associated with survival of intra-Peyer's patch-immunized rats. Determination of bacterial clearance in BAL 4 h after challenge demonstrated that the use of all immunization routes led to significant clearance compared with the bacterial levels in unimmunized controls (the order of effectiveness was intra-Peyer's patch > oral-intratracheal > intratracheal > subcutaneous > oral). Bacterial clearance in the lung homogenate was also significantly greater for all immunization routes than in the unimmunized controls (the order of effectiveness was intra-Peyer's patch > subcutaneous > oral-intratracheal > oral = intratracheal). Prior oral immunization with killed P. aeruginosa also induced enhanced bacterial clearance of heterologous strains of P. aeruginosa, Haemophilus influenzae, and to a lesser extent, Klebsiella pneumoniae. Because of the ease of antigen delivery, oral immunization with killed P. aeruginosa may be an important route of immunization for induction of enhanced bacterial clearance of subsequent acute respiratory infection with P. aeruginosa and other gram-negative bacteria.
Studies on the Constituents of Fructus Momordicae. III. Structure of Mogrosides (1983)

The structure of mogroside V (1), C60H102O29·2H2O, the sweet principal of Fructus Momordicae, has been established by chemical and spectroscopic evidence as mogrol-3-O-[β-D-glucopyranosyl (1→6)-β-D-glucopyranoside]-24-O-{[β-D-glucopyranosyl (1→2)]-[β-D-glucopyranosyl (1→6)]-β-D-glucopyranoside}.
Signaling pathways involved in LPS induced TNFalpha production in human adipocytes (2010)

This study clearly demonstrates that the LPS induced activation pathway is an integral part of the inflammatory process linked to obesity, and that adipocytes are responsible for most of the secreted TNFalpha in inflamed adipose tissue, through TLR4 activation.
Embryo cloning in cattle: the use of in vitro matured oocytes (1993)

In vitro matured (IVM) bovine oocytes were examined to determine their potential viability in embryo cloning. Activation competence, as monitored by pronuclear formation, increased with oocyte age. Oocytes readily formed a pronucleus when challenged with an electrical pulse 30 h after the onset of maturation. Developmental competence of IVM oocytes tended to increase with oocyte age (P = 0.079). Selection of IVM oocytes on the basis of the presence of a polar body 24 h after the onset of maturation and the size of the follicle from which the oocyte was derived improved development of nuclear transfer embryos (polar body positive 25% versus polar body negative 10%, P < 0.05; large follicle oocytes 31% versus small follicle oocytes 14%, P < 0.05). When selected, IVM oocytes were compared with in vivo matured oocytes recovered from superovulated cows and heifers; no difference was detected for the frequency of embryos produced, pregnancies confirmed between days 50 and 60 of gestation, or the number of calves born. We conclude that selected IVM oocytes are equivalent to in vivo matured oocytes when used for bovine embryo cloning.
Overview: neurobiology of OB protein (leptin) (1998)

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Crystal structure of the disulfide‐stabilized Fv fragment of anticancer antibody B1: Conformational influence of an engineered disulfide bond (1998)

A recombinant Fv construct of the B1 monoclonal antibody that recognizes the LewisY-related carbohydrate epitope on human carcinoma cells has been prepared. The Fv is composed of the polypeptide chains of the VH and VL domains expressed independently and isolated as inclusion bodies. The Fv is prepared by combining and refolding equimolar amounts of guanidine chloride solubilized inclusion bodies. The Fv is stabilized by an engineered interchain disulfide bridge between residues VL100 and VH44. This construct has a similar binding affinity as that of the single-chain construct (Benhar and Pastan, Clin. Cancer Res. 1:1023–1029, 1995). The B1 disulfide-stabilized Fv (B1dsFv) crystallizes in space group P6122 with the unit cell parameters a = b = 80.1 Å, and c = 138.1 Å. The crystal structure of the B1dsFv has been determined at 2.1-Å resolution using the molecular replacement technique. The final structure has a crystallographic R-value of 0.187 with a root mean square deviation in bond distance of 0.014 Å and in bond angle of 2.74°. Comparisons of the B1dsFv structure with known structures of Fv regions of other immunoglobulin fragments shows closely related secondary and tertiary structures. The antigen combining site of B1dsFv is a deep depression 10-Å wide and 17-Å long with the walls of the depression composed of residues, many of which are tyrosines, from complementarity determining regions L1, L3, H1, H2, and H3. Model building studies indicate that the LewisY tetrasaccharide, Fuc–Gal–Nag–Fuc, can be accommodated in the antigen combining site in a manner consistent with the epitope predicted in earlier biochemical studies (Pastan, Lovelace, Gallo, Rutherford, Magnani, and Willingham, Cancer Res. 51:3781–3787, 1991). Thus, the engineered disulfide bridge appears to cause little, if any, distortion in the Fv structure, making it an effective substitute for the B1 Fab. Proteins 31:128–138, 1998. Published 1998 Wiley-Liss, Inc.1 This article is a US Government work and, as such, is in the public domain in the United States of America.
Biochemistry and Biology of Anaphylatoxins (1986)

The molecular architecture of anaphylatoxins has been explored on several levels. Primary, secondary and tertiary structural parameters that dictate function of the C3a, C4a and C5a molecules are being elucidated with the aid of comparative sequence analyses, physical measurements and organic syntheses. Although C3a, C4a and C5a are biologically distinct mediators, as defined by their unique receptor systems, a common genetic origin is apparent from conserved features in their primary structures. Evidence is now available which suggests that similarities in the folding pattern of the anaphylatoxins may dictate a concensus conformation for each factor. We have learned from synthetic peptide studies that the binding (e.g. effector) site in anaphylatoxin molecules exists as a linear sequence contained in the C-terminal portion of the polypeptide. What is also evident is that a preferred conformation is defined for the binding site requiring a proper side chain orientation for optimal bioactivity. It is proposed that folding of the native structure stabilizes this conformation at the binding site. The binding site in C3a contains the essential residues LGLAR folded in an irregular or pseudo-beta-turn and stabilized by an adjacent alpha-helical segment. It is proposed that the alpha-helical segment influences orientation of the side chain residues in the 'binding site'. A similar model is evolving for C5a based on synthetic C5a peptides that express both spasmogenic and chemotactic activities. This helix turn model promises to be representative of an essential structural feature that determines anaphylatoxin activity. We believe that these models contribute significantly to our understanding of the molecular relationships between structure and function for these humoral mediators of inflammation.
Alternative splicing of tropomyosin pre-mRNAs in vitro and in vivo. (1988)

A single rat gene encodes both fibroblast TM-1 and skeletal muscle beta-tropomyosin by an alternative RNA-processing mechanism. The gene contains 11 exons: Exons 1-5 and exons 8 and 9 are constitutive exons common to all mRNAs expressed from this gene; exons 6 and 11 are used in fibroblasts as well as smooth muscle; exons 7 and 10 are used exclusively in skeletal muscle. We have studied the internal alternative RNA splice choice (exons 6 and 7) of the rat tropomyosin 1 gene in vitro, using nuclear extracts obtained from HeLa cells. Use of alternative splice sites in vitro is dependent on the ionic conditions of the assay, and correct splicing occurs only under well-defined salt conditions. Splicing of exon 5 to exon 6 (fibroblast-type splice) and exon 5 to exon 7 (skeletal muscle-type splice) was dependent on precursors in which exon 6 or 7 was first joined to exon 8. The same patterns of alternatively spliced RNAs were formed when similar templates were introduced in HeLa cells by transfection. Thus, there appears to be an ordered pathway of splicing in which the internal alternatively spliced exons must first be joined to the downstream constitutive exon before they can be spliced to the upstream constitutive exon. The data are consistent with a model in which the critical event in alternative splicing occurs during the joining of exon 6 to exon 8 (fibroblast-type splice) or exon 7 to exon 8 (skeletal muscle-type splice).
Dysregulation of X‐linked gene expression in Klinefelter's syndrome and association with verbal cognition (2007)

Klinefelter's Syndrome (KS) is a chromosomal karyotype with one or more extra X chromosomes. KS individuals often show language impairment and the phenotype might be due to overexpression of genes on the extra X chromosome(s). We profiled mRNA derived from lymphoblastoid cell lines from males with documented KS and control males using the Affymetrix U133P microarray platform. There were 129 differentially expressed genes (DEGs) in KS group compared with controls after Benjamini-Hochberg false discovery adjustment. The DEGs included 14 X chromosome genes which were significantly over-represented. The Y chromosome had zero DEGs. In exploratory analysis of gene expression-cognition relationships, 12 DEGs showed significant correlation of expression with measures of verbal cognition in KS. Overexpression of one pseudoautosomal gene, GTPBP6 (GTP binding protein 6, putative) was inversely correlated with verbal IQ (r = -0.86, P < 0.001) and four other measures of verbal ability. Overexpression of XIST was found in KS compared to XY controls suggesting that silencing of many genes on the X chromosome might occur in KS similar to XX females. The microarray findings for eight DEGs were validated by quantitative PCR. The 14 X chromosome DEGs were not differentially expressed in prior studies comparing female and male brains suggesting a dysregulation profile unique to KS. Examination of X-linked DEGs, such as GTPBP6, TAF9L, and CXORF21, that show verbal cognition-gene expression correlations may establish a causal link between these genes, neurodevelopment, and language function. A screen of candidate genes may serve as biomarkers of KS for early diagnosis.
The Stille Reaction of 1,1-Dibromo-1-alkenes:  Preparation of Trisubstituted Alkenes and Internal Alkynes (1999)

The Stille reaction of 1,1-dibromo-1-alkenes 1 with aryl- and vinylstannanes produces different products depending on the reaction conditions. When the reaction is run in toluene or 1,4-dioxane with tris(2-furyl)phosphine (TFP) as the ligand, (Z)-bromoalkenes 2 are obtained stereospecifically in good to excellent yields with most substrates. However, 2-aryl-1,1-dibromo-1-alkenes (1e,1g) having an electron-donating methoxy group in the para- or ortho- position give poor yields. This method has been applied to the one-pot syntheses of stereospecifically trisubstituted alkenes 5. When the Stille reaction is conducted in a highly dipolar solvent (DMF), monobromides 2 and/or internal alkynes 4 are the products. The less reactive phenylstannane favors the formation of alkynes 4, regardless of which ligand is used. More reactive organostannanes (vinyl, furyl) require a very electron rich ligand, tris(4-methoxyphenyl)phosphine, for the formation of alkynes 4. This new method for internal alkyne preparation is general, requires very mild reaction conditions, and gives high yields.
Nucleotide sequences and comparison of the hemolysin determinants of Vibrio cholerae El Tor RV79(Hly+) and RV79(Hly-) and classical 569B(Hly-) (1988)

We determined the nucleotide sequences of the hemolysin structural gene, hlyA, of Vibrio cholerae El Tor biotype strains RV79(Hly+) and RV79(Hly-) and the hly determinant of the nonhemolytic classical biotype strain 569B(Hly-). The sequences of the hlyA gene from El Tor strains RV79(Hly+) and RV79(Hly-) have an identical 2,223-base open reading frame which is predicted to encode an 81,977-dalton precursor form of hemolysin. This value is in excellent agreement with the 84,000-Mr hemolysin described in the earlier report of Goldberg and Murphy (S. L. Goldberg and J. R. Murphy, J. Bacteriol. 162:35-41, 1985). In contrast, the sequence of the hly determinant of the classical 569B(Hly-) strain has an 11-base-pair deletion within the hlyA structural gene. In this instance the hly determinant is predicted to encode a 26,765-dalton precursor form of a truncated hemolysin. In each case, the regulatory region encoding the putative hlyA promoter and the predicted 25-amino-acid signal sequence are identical.
The Effects of Wall Populations on Coexistence of Bacteria in the Liquid Phase of Chemostat Cultures (1985)

We have examined the effects of wall populations on coexistence between strains of Escherichia coli in the liquid phase of mixed (two-strain) chemostats. The wall populations of the two competing strains became established soon after the start of the cultures and, although the relative abundance of the strains in the liquid phase could change over time by several orders of magnitude, the composition of an established wall population did not change markedly. The bacterial strains examined could not displace an established wall population of a competing strain. The presence of a permanent wall population allowed a strain that was less fit in the liquid phase to coexist with a superior strain. The resulting coexistence did not require that the inferior strain attached to the vessel wall better than the superior strain. We believe that the coexistence developed because the inferior strain survived and reproduced on the vessel wall. The progeny from that wall population then provided replacements for the bacteria that the inferior strain lost through a selective disadvantage in the liquid phase of the culture. By replacing the chemostat vessel, hence eliminating the wall populations, we could distinguish between cases where the coexistence depended on the presence of a wall population and where it resulted from some alternative mechanism.
Rapid targeted mutational analysis of human tumours: a clinical platform to guide personalized cancer medicine (2010)

Targeted cancer therapy requires the rapid and accurate identification of genetic abnormalities predictive of therapeutic response. We sought to develop a high-throughput genotyping platform that would allow prospective patient selection to the best available therapies, and that could readily and inexpensively be adopted by most clinical laboratories. We developed a highly sensitive multiplexed clinical assay that performs very well with nucleic acid derived from formalin fixation and paraffin embedding (FFPE) tissue, and tests for 120 previously described mutations in 13 cancer genes. Genetic profiling of 250 primary tumours was consistent with the documented oncogene mutational spectrum and identified rare events in some cancer types. The assay is currently being used for clinical testing of tumour samples and contributing to cancer patient management. This work therefore establishes a platform for real-time targeted genotyping that can be widely adopted. We expect that efforts like this one will play an increasingly important role in cancer management.
Interleukin-5 and its receptor: a drug target for eosinophilia associated with chronic allergic disease (1995)

A characteristic feature of chronic allergic diseases such as asthma is the increase in eosinophil numbers in the inflamed tissue. In light of its specificity for the development of eosinophils, interleukin-5 (IL-5) is considered the most important cytokine involved in the regulation of eosinophilia. Hence, an antagonist for IL-5 activity is a new target for drug discovery programs. We have examined the opportunity for both a random and a rational approach for the identification of such an antagonist. The elucidation of the structure of IL-5 and the initial structure/function analysis of the ligand/receptor complex constitute a first step towards the design of antagonistic compounds. The identification of a small compound by random screening able to inhibit the IL-5/IL-5 receptor interaction indicated an important domain in the receptor. We examine here protein-based IL-5 antagonists, such as IL-5-muteins, soluble IL-5 receptor constructs, and monoclonal antibodies, for their potential as IL-5/IL-5 receptor antagonists, and the use of a murine model of eosinophil airway inflammation for their evaluation.
Cereblon is a direct protein target for immunomodulatory and antiproliferative activities of lenalidomide and pomalidomide (2012)

Thalidomide and the immunomodulatory drug, lenalidomide, are therapeutically active in hematological malignancies. The ubiquitously expressed E3 ligase protein cereblon (CRBN) has been identified as the primary teratogenic target of thalidomide. Our studies demonstrate that thalidomide, lenalidomide and another immunomodulatory drug, pomalidomide, bound endogenous CRBN and recombinant CRBN-DNA damage binding protein-1 (DDB1) complexes. CRBN mediated antiproliferative activities of lenalidomide and pomalidomide in myeloma cells, as well as lenalidomide- and pomalidomide-induced cytokine production in T cells. Lenalidomide and pomalidomide inhibited autoubiquitination of CRBN in HEK293T cells expressing thalidomide-binding competent wild-type CRBN, but not thalidomide-binding defective CRBN(YW/AA). Overexpression of CRBN wild-type protein, but not CRBN(YW/AA) mutant protein, in KMS12 myeloma cells, amplified pomalidomide-mediated reductions in c-myc and IRF4 expression and increases in p21(WAF-1) expression. Long-term selection for lenalidomide resistance in H929 myeloma cell lines was accompanied by a reduction in CRBN, while in DF15R myeloma cells resistant to both pomalidomide and lenalidomide, CRBN protein was undetectable. Our biophysical, biochemical and gene silencing studies show that CRBN is a proximate, therapeutically important molecular target of lenalidomide and pomalidomide.
Southern blot analysis of DNA extracted from formalin-fixed pathology specimens. (1986)

We have developed a method for the extraction of DNA from formalin-fixed, paraffin-embedded pathology specimens. High-molecular-weight DNA was recovered from well-fixed nonautolyzed samples of viable tissue. DNA recovered from samples exposed to picric acid or mercuric chloride containing fixatives was not intact. Increasing the formalin fixation time decreased the amount of intact DNA available. When these limitations were taken into consideration, the procedure allowed for the removal of degraded and chemically modified DNA from the preparation, and the final product was suitable for quantitative and qualitative analysis by Southern or dot blotting techniques. Digestion with methylation-sensitive restriction endonucleases showed that DNA methylation patterns were not altered after formalin fixation.
Heat shock regulatory gene htpR influences rates of protein degradation and expression of the lon gene in Escherichia coli. (1984)

Upon a shift to high temperature, Escherichia coli increase their rate of protein degradation and also the expression of a set of "heat shock" genes. Nonsense mutants of htpR (also called hin), suppressed by a temperature-sensitive suppressor, show lower expression of heat shock genes at 30 degrees C and fail to respond to a shift to 42 degrees C. These mutants were found to have a lower capacity to degrade abnormal or incomplete proteins than that of wild-type cells. This reduction in proteolysis equals or exceeds that in lon mutants, which encode a defective ATP-dependent protease, protease La, and is particularly large in htpR lon double mutants. The activity of protease La was higher in wild-type cells than in htpR mutants grown at 30 degrees C and increased upon shift to 42 degrees C only in the wild type. To determine whether htpR influences transcription of the lon gene, a lon-lacZ operon fusion was utilized. Introduction of the htpR mutation reduced transcription from the lon promoter at 30 degrees C and 37 degrees C. This defect was corrected by a plasmid (pFN97) carrying the wild-type htpR allele. Induction of the heat shock response with ethanol had little or no effect in htpR mutants but stimulated lon transcription 2-3 fold in wild-type cells and htpR cells carrying pFN97. Thus, lon appears to be a heat shock gene, and increased synthesis of protease La under stressful conditions may help to prevent the accumulation of damaged cellular protein.