gebhart/patrepeval huggingface dataset:
Heterogeneity of human T4+ inducer T cells defined by a monoclonal antibody that delineates two functional subpopulations. (1982)

A monoclonal antibody termed anti-T4 that detected approximately 60% of peripheral blood T lymphocytes was shown to define the human inducer population. In the present study, we characterized three additional monoclonal antibodies, anti-T4A, anti-T4B, and anti-TQ1, that were reactive with a similar percentage of T lymphocytes. Anti-T4A, anti-T4B, and anti-T4 delineated identical cell populations, while those defined by anti-TQ1 differed in several respects: 1) Anti-TQ1 stained a minority (less than 7%) of thymocytes, whereas the other antibodies stained a majority (80%); 2) Anti-TQ1 reacted with 70 to 85% of T4+ lymphocytes, but also stained 50% of T cells within the T4- (T8+) cytotoxic/suppressor subset; 3) The antigen defined by anti-TQ1 was not restricted in its expression to T cells; it defined a fraction of normal B and null lymphocytes as well as non-T cell lines. In vitro studies indicated that the subpopulations of T4+ T lymphocytes delineated by anti-TQ1 were functionally distinct. Although T4+TQ1+ and T4+TQ1- T cells proliferated in an equal fashion to soluble antigen and alloantigen, only the T4+TQ1+ subset was responsible for maximal proliferation in autologous MLR. This T4+TQ1+ subset contained a population of lymphocytes reactive with the previously defined JRA autoantibody. In contrast, the T4+TQ1-, but not the T4+TQ1+, subset provided the majority of T cell help for B cell immunoglobulin production in a pokeweed-driven system. We conclude that the subpopulation of T4+ inducer cells responsible for maximal helper activity in T-B interactions is restricted to a minor subpopulation of T4+ lymphocytes.
Identification of specific and cross-reactive antigens of Leishmania donovani chagasi by human infection sera. (1987)

Cloned Leishmania donovani chagasi (Ldc) promastigotes were analyzed by SDS-PAGE separation and immunoblotting with human infection sera. The patterns of antigen reactivity were compared by using sera from individuals with Ldc, Leishmania mexicana amazonensis (Lma), Trypanosoma cruzi, Mycobacterium tuberculosis, or Mycobacterium leprae infections. Sera from individuals with these infections recognized Ldc antigens in several m.w. ranges. Reactivity was due to recognition of Ldc molecules and not to Ldc culture medium components, as shown by comparing Ldc promastigotes grown in the presence or absence of fetal bovine serum (FBS), by immunoblotting of FBS, and by [35S]methionine labeling. The major findings of the study were as follows. Immunoblots with Ldc promastigotes could be used to distinguish individuals with Ldc infections from those with Lma infections. Persons with Ldc infections had antibodies to a Ldc antigen of approximately 32 to 35 kd not recognized by persons with Lma infections. Individuals cured of acute Ldc infection did not develop antibodies that differed in specificity to those present during their acute phase of infection. Ldc antigens in the 62 to 66 kd region were recognized by all individuals with Ldc or Lma infections but were not recognized by individuals in the other disease groups or by control sera. This region was found to contain at least four distinct bands, one of which appeared to be glycosylated as indicated by periodic acid-Schiff staining and concanavalin A labeling; an apparently nonglycosylated protein of 62 to 63 kd was eluted from SDS-PAGE gels and was used to diagnose Ldc infection by the ELISA. Whereas crude Ldc antigen gave false positive results with T. cruzi and mycobacteria infection sera, the eluted 62 to 63 kd protein was 100% specific and sensitive in the diagnosis of Ldc infection.
Antihyperglycemic Activity of Herb Extracts on Streptozotocin-Induced Diabetic Rats (2006)

We investigated the effects of herb extracts, Rhus verniciflua, Agrimonia pilosa, Sophora japonica, and Paeonia suffruticosa, on the lowering of blood glucose levels and thiobarbituric acid reactive substances (TBARS) in streptozotocin (STZ)-induced diabetic rats. After 4 weeks, oral administration of Rhus verniciflua extract (50 mg/kg) exhibited a significant decrease in blood glucose levels in diabetic rats (P<0.05). Blood TBARS concentrations, the products of glucose oxidation in blood, were also lowered by Rhus verniciflua extract supplementation. In addition, Sophora japonica and Paeonia suffruticosa extracts significantly reduced TBARS levels versus diabetic controls. Serum concentrations of liver-function marker enzymes, GOT and GPT, were also restored by Rhus verniciflua (50 mg/kg) supplementation in diabetic rats.
Composition of Forage and Grain from Second-Generation Insect-Protected Corn MON 89034 Is Equivalent to That of Conventional Corn (Zea mays L.) (2008)

Insect-protected corn hybrids containing Cry insecticidal proteins derived from Bacillus thuringiensis have protection from target pests and provide effective management of insect resistance. MON 89034 hybrids have been developed that produce both the Cry1A.105 and Cry2Ab2 proteins, which provide two independent modes of insecticidal action against the European corn borer ( Ostrinia nubilalis ) and other lepidopteran insect pests of corn. The composition of MON 89034 corn was compared to conventional corn by measuring proximates, fiber, and minerals in forage and by measuring proximates, fiber, amino acids, fatty acids, vitamins, minerals, antinutrients, and secondary metabolites in grain collected from 10 replicated field sites across the United States and Argentina during the 2004-2005 growing seasons. Analyses established that the forage and grain from MON 89034 are compositionally comparable to the control corn hybrid and conventional corn reference hybrids. These findings support the conclusion that MON 89034 is compositionally equivalent to conventional corn hybrids.
Improvements of the physical properties of fibroin membranes with sodium alginate (1992)

Abstract The effects of sodium alginate on the physical properties of fibroin membranes, such as rupture elongation, rupture strength, water absorption, and thermal properties, were investigated. The experimental results showed the β‐form crystal and β‐form molecular conformation increased due to the increase of intermolecular hydrogen bonds, such as CO‐‐‐HN and CO‐‐‐HO. The kind of intermolecular interaction and β‐form molecular conformation of polymer blends were clarified by 13 C–NMR and infrared spectroscopy. The increase in β‐form crystal was examined by X‐ray analysis. Further, membranes were characterized by thermogravimetric analysis (TGA) and by determining their water contents and tensile properties.
The synthesis of some substituted biphenyl-4-carboxylic acids, 4-biphenylylacetic acids, and 4-aminobiphenyls (1966)

The synthesis of a range of substituted biphenyl-4-carboxylic acids and 4-aminobiphenyls is described. Preparations are included for the parent biphenyl-4-carboxylic acid, and for 4-biphenylylacetic acid and three substituted 4-biphenylylacetic acids.
Solution Structure of the Human CC Chemokine 2:  A Monomeric Representative of the CC Chemokine Subtype, (1999)

HCC-2, a 66-amino acid residue human CC chemokine, was reported to induce chemotaxis on monocytes, T-lymphocytes, and eosinophils. The three-dimensional structure of HCC-2 has been determined by 1H nuclear magnetic resonance (NMR) spectroscopy and restrained molecular dynamics calculations on the basis of 871 experimental restraints. The structure is well-defined, exhibiting average root-mean-square deviations of 0.58 and 0.96 A for the backbone heavy atoms and all heavy atoms of residues 5-63, respectively. In contrast to most other chemokines, subtle structural differences impede dimer formation of HCC-2 in a concentration range of 0.1 microM to 2 mM. HCC-2, however, exhibits the same structural elements as the other chemokines, i.e., a triple-stranded antiparallel beta-sheet covered by an alpha-helix, showing that the chemokine fold is not influenced by quaternary interactions. Structural investigations with a HCC-2 mutant prove that a third additional disulfide bond present in wild-type HCC-2 is not necessary for maintaining the relative orientation of the helix and the beta-sheet.
MYELODYSPLASTIC SYNDROMES AND IRON CHELATION THERAPY (2017)

Over recent decades we have been fortunate to witness the advent of new technologies and of an expanded knowledge and application of chelation therapies to the benefit of patients with iron overload. However, extrapolation of learnings from thalassemia to the myelodysplastic syndromes (MDS) has resulted in a fragmented and uncoordinated clinical evidence base. We're therefore forced to change our understanding of MDS, looking with other eyes to observational studies that inform us about the relationship between iron and tissue damage in these subjects. The available evidence suggests that iron accumulation is prognostically significant in MDS, but levels of accumulation historically associated with organ damage (based on data generated in the thalassemias) are infrequent. Emerging experimental data have provided some insight into this paradox, as our understanding of iron-induced tissue damage has evolved from a process of progressive bulking of organs through high-volumes iron deposition, to one of 'toxic' damage inflicted through multiple cellular pathways. Damage from iron may, therefore, occur prior to reaching reference thresholds, and similarly, chelation may be of benefit before overt iron overload is seen. In this review, we revisit the scientific and clinical evidence for iron overload in MDS to better characterize the iron overload phenotype in these patients, which differs from the classical transfusional and non-transfusional iron overload syndrome. We hope this will provide a conceptual framework to better understand the complex associations between anemia, iron and clinical outcomes, to accelerate progress in this area.
Phagocytosis: receptors, signal integration, and the cytoskeleton (2014)

Phagocytosis is a remarkably complex and versatile process: it contributes to innate immunity through the ingestion and elimination of pathogens, while also being central to tissue homeostasis and remodeling by clearing effete cells. The ability of phagocytes to perform such diverse functions rests, in large part, on their vast repertoire of receptors. In this review, we address the various receptor types, their mobility in the plane of the membrane, and two modes of receptor crosstalk: priming and synergy. A major section is devoted to the actin cytoskeleton, which not only governs receptor mobility and clustering but also is instrumental in particle engulfment. Four stages of the actin remodeling process are identified and discussed: (i) the 'resting' stage that precedes receptor engagement, (ii) the disruption of the cortical actin prior to formation of the phagocytic cup, (iii) the actin polymerization that propels pseudopod extension, and (iv) the termination of polymerization and removal of preassembled actin that are required for focal delivery of endomembranes and phagosomal sealing. These topics are viewed in the larger context of the differentiation and polarization of the phagocytic cells.
Functional analysis of the human vascular cell adhesion molecule 1 promoter. (1992)

The vascular cell adhesion molecule 1 (VCAM-1) is a 110-kD member of the immunoglobulin gene superfamily expressed on the surface of interleukin 1 beta- or tumor necrosis factor alpha (TNF)-stimulated endothelial cells. The cell surface protein functions as an inducible adhesion receptor for circulating mononuclear leukocytes and some tumor cells. We have previously characterized the genomic organization of the VCAM1 gene and described its chromosomal localization. In this report, the promoter of the VCAM1 gene is characterized. New transcription of the VCAM1 gene occurred when endothelial cells were treated with TNF. Fusion plasmids containing the 5' flanking sequence of the VCAM1 gene and the chloramphenicol acetyltransferase reporter gene were used to identify cis-acting sequences that direct the cytokine-induced transcription. When transfected into bovine aortic endothelial cells, constructs containing 755 bp of the 5' flanking sequence were induced by TNF. Within the cytokine-responsive region of the core promoter were functional NF-kappa B and GATA elements. Upstream of the core promoter, the VCAM1 5' flanking sequence contained a negative regulatory activity. NF-kappa B-mediated activation of VCAM1 gene expression may lead to endothelial expression of a mononuclear leukocyte adhesion molecule associated with initial events in the development of an atherosclerotic lesion.
Glyphosate Resistance in a Johnsongrass (Sorghum halepense) Biotype from Arkansas (2011)

Johnsongrass is one of the most troublesome weeds of the world and is listed as a noxious weed in Arkansas. Reduced johnsongrass control with the recommended application rate of glyphosate (840 g ae ha −1 ) was reported in a continuous soybean field near West Memphis, AR, in the fall of 2007. A greenhouse study was conducted (1) to confirm and characterize glyphosate resistance in the johnsongrass biotype from West Memphis and (2) to determine whether resistant and susceptible biotypes have differential glyphosate absorption or translocation. Dose–response studies revealed that the resistant biotype was five- to seven-fold less sensitive to glyphosate than the susceptible biotype. Glyphosate absorption was similar in resistant and susceptible biotypes at 72 h after treatment (HAT). However, the treated leaf of the resistant biotype retained 28 percentage points more absorbed 14 C glyphosate compared to the susceptible biotype at 72 HAT. Additionally, the resistant biotype had less 14 C glyphosate translocated to the aboveground tissue below the treated leaf and to roots compared to the susceptible biotype at 24 and 72 HAT. Reduced translocation and increased retention of glyphosate in treated leaves is a probable mechanism of resistance in this glyphosate-resistant johnsongrass biotype.
Micron‐Size Drug Particles: Common and Novel Micronization Techniques (2004)

Drug powders containing micron-size drug particles are used in several pharmaceutical dosage forms. Many drugs, especially newly developed substances, are poorly water soluble, which limits their oral bioavailability. The dissolution rate can be enhanced by using micronized drugs. Small drug particles are also required in administration forms, which require the drug in micron-size size due to geometric reasons in the organ to be targeted (e.g., drugs for pulmonary use). The common technique for the preparation of micron-size drugs is the mechanical comminution (e.g., by crushing, grinding, and milling) of previously formed larger particles. In spite of the widespread use of this technique, the milling process does not represent the ideal way for the production of small particles because drug substance properties and surface properties are altered in a mainly uncontrolled manner. Thus, techniques that prepare the drug directly in the required particle size are of interest. Because physicochemical drug powder properties are decisive for the manufacturing of a dosage form and for therapeutic success, the characterization of the particle surface and powder properties plays an important role. This article summarizes common and novel techniques for the production of a drug in small particle size. The properties of the resulting products that are obtained by different techniques are characterized and compared.
Recombinant Human Osteogenic Protein‐1 (OP‐1) Stimulates Periodontal Wound Healing in Class III Furcation Defects (1998)

Osteogenic protein-1 (OP-1) is a member of the transforming growth factor beta superfamily and is a potent modulator of osteogenesis and bone cell differentiation. This preclinical study in dogs sought to assess the effects of OP-1 on periodontal wound healing in surgically created critical size Class III furcation defects. Eighteen male beagle dogs were subjected to the creation of bilateral mandibular 5 mm osseous defects. A split-mouth design was utilized which randomly assigned opposing quadrants to control therapy (surgery alone or collagen vehicle) or 1 of 3 ascending concentrations of OP-1 in a collagen vehicle (0.75 mg OP-1/g collagen, 2.5 mg/g, or 7.5 mg/g). Thus, 9 quadrants per test group received OP-1, 9 quadrants per control group received surgery alone, and 9 quadrants received collagen vehicle alone. Test articles were delivered by a surgeon masked to the treatment, and fluorogenic bone labels were injected at specified intervals post-treatment. Eight weeks after defect creation and OP-1 delivery, tissue blocks of the mandibulae were taken for masked histomorphometric analysis to assess parameters of periodontal regeneration (e.g., bone height, bone area, new attachment formation, and percent of defect filled with new bone). Histomorphometry revealed limited evidence of osteogenesis, cementogenesis, and new attachment formation in either vehicle or surgery-alone sites. In contrast, sites treated with all 3 concentrations of OP-1 showed pronounced stimulation of osteogenesis, regenerative cementum, and new attachment formation. Lesions treated with 7.5 mg/g of OP-1 in collagen regenerated 3.9+/-1.7 mm and 6.1+/-3.4 mm2 (mean +/-S.D.) of linear bone height and bone area, respectively. Furthermore, these differences were statistically different from both control therapies for all wound healing parameters (P < 0.0001). No significant increase in tooth root ankylosis was found among the treatment groups when compared to the surgery-alone group. We conclude that OP-1 offers promise as an attractive candidate for treating severe periodontal lesions.
Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice (2002)

Dual inactivation of PTEN and INK4a/ARF tumor suppressor genes is a common feature observed in a broad spectrum of human cancer types. To validate functional collaboration between these genes in tumor suppression, we examined the biological consequences of Pten and/or Ink4a/Arf deficiency in cells and mice. Relative to single mutant controls, Ink4a/Arf-/-Pten+/- mouse embryonic fibroblast cultures exhibited faster rates of growth in reduced serum, grew to higher saturation densities, produced more colonies upon low density seeding, and showed increased susceptibility to transformation by oncogenic H-Ras. Ink4a/Arf deficiency reduced tumor-free survival and shortened the latency of neoplasias associated with Pten heterozygosity, specifically pheochromocytoma, prostatic intraepithelial neoplasia, and endometrial hyperplasia. Compound mutant mice also exhibited an expanded spectrum of tumor types including melanoma and squamous cell carcinoma. Functional synergy between Ink4a/Arf and Pten manifested most prominently in the development of pheochromocytoma, prompting an analysis of genes and loci implicated in this rare human neoplasm. The classical pheochromocytoma genes Ret, Vhl, and Nf-1 remained intact, a finding consistent with the intersection of these genes with pathways engaged by Pten and Ink4a/Arf. Notably, conventional and array-comparative genomic hybridization revealed frequent loss of distal mouse chromosome 4 in a region syntenic to human chromosome 1p that is implicated in human pheochromocytoma. This study provides genetic evidence of collaboration between Pten and Ink4a/Arf in constraining the growth and oncogenic transformation of cultured cells and in suppressing a wide spectrum of tumors in vivo.
On lattices, learning with errors, random linear codes, and cryptography (2009)

Our main result is a reduction from worst-case lattice problems such as GapSVP and SIVP to a certain learning problem. This learning problem is a natural extension of the “learning from parity with error” problem to higher moduli. It can also be viewed as the problem of decoding from a random linear code. This, we believe, gives a strong indication that these problems are hard. Our reduction, however, is quantum. Hence, an efficient solution to the learning problem implies a quantum algorithm for GapSVP and SIVP. A main open question is whether this reduction can be made classical (i.e., nonquantum). We also present a (classical) public-key cryptosystem whose security is based on the hardness of the learning problem. By the main result, its security is also based on the worst-case quantum hardness of GapSVP and SIVP. The new cryptosystem is much more efficient than previous lattice-based cryptosystems: the public key is of size Õ( n 2 ) and encrypting a message increases its size by a factor of Õ( n ) (in previous cryptosystems these values are Õ( n 4 ) and Õ( n 2 ), respectively). In fact, under the assumption that all parties share a random bit string of length Õ( n 2 ), the size of the public key can be reduced to Õ( n ).
S2‐01‐02: Tau vaccine: Active immunization with misfolded tau protein attenuates tau pathology in the transgenic rat model of tauopathy (2009)

Hyperphosphorylation and truncation, the major pathological alterations of tau, are present both in Alzheimer's disease (AD) and in non-AD tauopathies. In order to analyze the role of misfolded tau protein in the neurodegenerative cascade we generated a rat model of tauopathy. We showed that non-mutated truncated tau derived from sporadic Alzheimer's disease is able to induce and drive neurofibrillary degeneration in rats when expressed as transgene. Transgenic rat were immunized with recombinant misfolded truncated tau before the onset of neurobehavioral alterations. Improvement of neurobehavioral functions was monitored by multi-test battery with novel sensitive scoring system - NeuroScale. Sarcosyl soluble and insoluble tau were detected by Western-blot analysis. Phosphorylated tau in cerebrospinal fluid (CSF) was detected by ELISA P181 (Innogenetics). Neurofibrillary pathology was identified by immunohistochemistry using phosphorylation dependent anti-tau antibodies. Immunization with misfolded truncated tau protein resulted in statistically significant delay of the progressive neurobehavioral impairment of transgenic rats. Moreover immunotherapy prevented the development of neurofibrillary tangles and formation of sarcosyl insoluble tau complexes. Immunization significantly reduced the levels of the phosphorylated as well as non-phosphorylated soluble misfolded tau protein in the brain. The ability of the misfolded tau based active immunotherapy to delay the onset of severe sensorimotor deficits in transgenic rat model, without obvious harmful side effects, would predict a favourable scenario for therapeutic intervention in Alzheimer's disease and related neurodegenerative tauopathies.
Analysis and control of transient torque response in engines with internal exhaust gas recirculation (1999)

We analyze the nonlinear dynamic behavior of an internal exhaust gas recirculation system based on a mean-value model of an experimental automotive engine equipped with a camshaft phaser. We develop a control scheme that adjusts camshaft timing to reduce feed-gas emissions while maintaining transient engine torque response similar to that of a conventional engine with zero exhaust gas recirculation. The control scheme consists of a feedforward map that specifies desired camshaft timing as a function of throttle position and engine speed in steady state, and a first-order lag that governs the transition of the camshaft timing to the desired value. The time constant of the first-order lag is adjusted based on engine speed and throttle position.