gebhart/patrepeval huggingface dataset:
Immunologic Features of Porcine Circovirus Type 2 Infection (2002)

Clinical expression of porcine circovirus 2 (PCV-2) infection in swine may result in two distinct high mortality disease syndromes. In North America, postweaning multisystemic wasting syndrome (PMWS), while still sporadic in incidence, predominates. In Europe and elsewhere, both PMWS and a second syndrome, porcine dermatitis and nephropathy syndrome (PDNS), occur in endemic and epidemic forms. PMWS but not PDNS has been reproduced in piglets by inoculations with PCV-2 alone or in PCV-2-infected swine co-infected with porcine parvovirus (PPV) or porcine respiratory and reproductive syndrome (PRRS) virus and also if PCV-2-infected piglets are immunostimulated by injections with an immunogen emulsified in an oil-based macrophage-targeted adjuvant. Subclinical but active infection has been achieved by direct inoculation of piglets with cloned PCV-2 DNA and/or progeny virus derived from cloned DNA. Morphologic changes in lymphoid tissues and preliminary functional data suggest that immunosuppression may occur in PMWS-affected swine. This phenomenon appears to be mediated by generalized lymphoid depletion and replacement by infiltrating and proliferating histiocytes and macrophages. Accumulation of virus in both mononuclear phagocytes and follicular dendritic cells is characteristic of PCV-2 infection. Exogenous immunosuppression of PCV-2-infected gnotobiotic piglets with cyclosporine (Cys), but not corticosteroid (St), potentiates PCV-2 replication and promotes productive virus infection of hepatocytes in Cys-treated piglets, a tropism not previously apparent in experimentally induced PMWS in gnotobiotic swine. In the Cys-treated piglets, inflammatory lesions characteristic of PMWS are absent, even though tissues contain high titers of infectious virus, a finding which suggests that the granulomatous inflammatory lesions characteristic of PMWS are immune mediated.
Spatiotemporal relation between gap junctions and fascia adherens junctions during postnatal development of human ventricular myocardium. (1994)

Changes in the spatiotemporal patterns of the intercellular junctions responsible for electrical and mechanical coupling are closely coordinated in postnatal human ventricular myocardium and continue to about 6 years of age. Over this period there is a close and increasing association between the gap junctions and fascia adherens junctions. These changes in the distribution of intercellular electrical and adhering junctions may parallel the changing functional requirements of the ventricle, from a distribution that facilitates the remodeling necessitated by rapid growth and changing hemodynamics to that of the relatively stable and rapidly conducting adult myocardium. These age-related changes may also diminish the ability for appropriate myocardial remodeling in response to physiological, pathological, or surgical hemodynamic alterations.
Zwischenmolekulare Energiewanderung und Fluoreszenz (1948)

Abstract In Weiterentwicklung früherer Theorien von J. und F. Perrin und klassischphysikalischer Überlegungen des Verfassers wird eine quantenmechanische Behandlung des Übergangs von Elektronenanregungsenergie zwischen gleichartigen Molekülen in Lösung gegeben. Der kritische Molekülabstand, unterhalb dessen der übergang während der Anregungsdauer stattfindet, läßt sich aus den Absorptions‐ und Fluoreszenzspektren und der Anregungsdauer der Moleküle berechnen. Für Fluorescein und Chlorophyll a ergeben sich Werte von 50 bzw. 80 ÅE, entsprechend den mittleren Molekülabständen in Lösungen von 3,2 · 10 −3 bzw. 7,7 · 10 −4 Molen/Liter. Für die Bereiche oberhalb und unterhalb der kritischen Konzentration werden Formeln zur Berechnung der Energieabwanderung vom Primärmolekül angegeben, die mit den vorliegenden Messungen der Konzentrationsdepolarisation der Fluoreszenz gut übereinstimmen. Die Anwendung auf analoge Energiewanderungsprobleme in Molekülkristallen und im Assimilationsapparat der Pflanze wird diskutiert.
Resistance of Weeds to Herbicides (2011)

Herbicides are the most widely used group of pesticides worldwide. The widespread use of herbicides has allowed tremendous gains in agricultural productivity worldwide. Since the 1950’s herbicides have progressively replaced mechanical weed control because herbicides are more cost effective (Gianessi & Reigner, 2007). In 2009 over 95% of all the major agronomic crops grown in the U. S. were treated with herbicides (USDA-NASS, 2009). Transgenic herbicide-resistant crops were commercially introduced in the U. S. in 1996 when glyphosate-resistant (Roundup Ready®) soybean was released. Use of the very broadspectrum herbicide, glyphosate, provided outstanding weed control (Dill, 2005; Dill et al. 2008). The most recent data indicates that the percent of the total acres of each of the following crops planted with glyphosate-resistant cultivars is soybeans 91%, canola 91%, cotton 71%, and corn 68% (Brookes & Barfoot 2009). Herbicides are used on >90% of arable farmland in the U.S. and herbicide-resistant crops has been used widely since the mid1990’s. Herbicide resistance in weeds was first discovered in 1968 (Ryan 1970) and there are currently 347 confirmed weed biotypes worldwide (Heap 2010). When discussing pest resistance, whether it is weeds, pathogens, or insects, it is important to define the resistance. Some of the basic differences in the definitions of pest resistance depend on the basic definitions. The most basic unit of biological classification is the species, defined as a group of individual organisms displaying common characteristics and having the ability to mate and produce fully viable progeny. A population is a group of organisms within a species that co-occur in time and space (Radosevich et al. 1997) and share a distinct range of genetic variation. A species is usually composed of several to many populations. A genotype is the sum of the genetic coding or the genome of an individual. A biotype may not be fully coincident with genotype, as an individual has many genes. Certain genes may be expressed or unexpressed and not pertain to the phenotype associated with the biotype. A biotype is a phenotype that consistently expresses or exhibits a specific trait or set of traits. Weed scientists tend to refer to a biotype as a group of individuals with distinctive biochemical or morphological traits (e.g. resistance to a specific herbicide mechanism of action; growth and morphological traits). A phenotype refers to the physiological and morphological profile of the expressed genes in an individual. A single genotype can produce different phenotypes in response to environmental conditions present. This fundamental property of organisms is known as phenotypic plasticity. The alteration of phenotype (morphological or biochemical) without change in either the coding sequence of a gene or the upstream promoter region is classified as epigenetic change (Rapp & Wendel 2005). There is some controversy over whether
Tissue levels of tumor necrosis factor-alpha correlates with grade of inflammation in untreated ulcerative colitis (2007)

TNF-alpha is highly expressed in UC and correlates to the grade of inflammation. The sources of TNF-alpha were observed both in CD3+ lymphocytes and in macrophages. Cytokine expression (mRNA) profiles seem to be similar in patients with moderate to severe UC and CD.
Nonlinear extension to a moment method iterative reconstruction algorithm for microwave tomography (1986)

An iterative nonlinear algorithm for microwave image reconstruction based on moment method solutions to field problems has been suggested. The algorithm has been simplified significantly considering the effects due to the dominant nonlinear terms only. The results obtained using it have been compared with those reported earlier using a simpler algorithm.
Structural Characterization of Phospholipids and Peptides Directly from Tissue Sections by MALDI Traveling-Wave Ion Mobility-Mass Spectrometry (2010)

Ion mobility-mass spectrometry (IM-MS) provides rapid two-dimensional separations based on analyte apparent surface area or collision cross section (CCS, A(2)) and mass-to-charge, respectively. Recently, traveling-wave (t-wave) IM-MS was developed which uses electrodynamic rather than electrostatic fields commonly used in drift cell IM-MS instruments. The underlying theory for obtaining CCS data is well developed for drift cell IM-MS, while strategies for obtaining CCS values from t-wave IM-MS data remains an active area of research. In this report, methods were developed and validated to obtain CCS values of phospholipids and peptides directly from thin tissue sections by MALDI t-wave IM-MS using CCS calibrants measured by MALDI drift cell IM-MS. Importantly, the average percent difference between t-wave and drift cell CCS measurements is minimized by calibrating with the same biomolecular class. Calibrating t-wave phospholipid CCS values with drift cell peptide CCS measurements results in an average percent difference of ca. 7% between the same lipids measured using t-wave and drift cell IM-MS, while this improves to <0.5% when drift cell phospholipid CCS values are used for calibrating t-wave data. A suite of CCS values are reported for lipids and peptides that were determined directly from tissue, i.e. without the need for tissue extraction and further purification steps.
Multivariate calibration for assays in clinical chemistry using attenuated total reflection infrared spectra of human blood plasma (1989)

A spectral analysis of human blood plasma was undertaken by use of a Fourier-transform infrared spectrometer with a circular attenuated total reflection cell. The concentrations of total protein, glucose, triglycerides, total cholesterol, urea, and uric acid were measured by chemical or enzymatic methods. For these constituents the partial least-squares (PLS) algorithm was used for a multivariate calibration including the infrared fingerprint region of the plasma spectra. Best results were achieved for total protein with an average prediction error (PRESS based on cross validation) of 2.1 g/L; other PRESS results were for glucose 22 mg/dL, triglycerides 33 mg/dL, cholesterol 31 mg/dL, urea 4.4 mg/dL, and uric acid 1.6 mg/dL.
Mechanistic Aspects of the Alternating Copolymerization of Propene with Carbon Monoxide Catalyzed by Pd(II) Complexes of Unsymmetrical Phosphine−Phosphite Ligands (1997)

The reaction steps responsible for the highly enantioselective asymmetric copolymerization of propene with carbon monoxide catalyzed by a cationic Pd(II) complex bearing an unsymmetrical chiral bidentate phosphine−phosphite, (R,S)-BINAPHOS [(R,S)-2-(diphenylphosphino)-1,1‘-binaphthalen-2‘-yl 1,1‘-binaphthalene-2,2‘-diyl phosphite = L1], have been studied. Stepwise identification and characterization were carried out for catalyst precursors (SP-4-2)- and (SP-4-3)-Pd(CH3)Cl(L1) (1a and 1b) and (SP-4-3)-[Pd(CH3)(CH3CN)(L1)]·X1 (X1 = B{3,5-(CF3)2C6H3}4) (2), and complexes related to the reaction steps, (SP-4-3)-[Pd(COCH3)(CH3CN)(L1)]·X1 (3), (SP-4-3)- and (SP-4-4)-[Pd{CH2CH(CH3)COCH3}(L1)]·X1 (4a and 4b), (SP-4-3)-[Pd{COCH2CH(CH3)COCH3}(CH3CN)(L1)]·X1 (5), and (SP-4-3)-[Pd{CH2CH(CH3)COCH2CH(CH3)COCH3}(L1)]·X1 (6). An X-ray structure of alkyl complex 4a has been obtained. Studies on [Pt(CH3)2(L1)] (8) reveal that the methyl group is more stabilized at a position trans to the phosphine than at the cis position. This is consistent with the structures of 1−6 in which all carbon substituents are trans to the phosphine moiety in their major forms. On the basis of analogous studies using platinum complexes, an isomerization from (SP-4-3)-[Pd(CH3)(CO)(L1)]·X1 (13a) to the (SP-4-4) isomer (13b) is suggested to occur for the CO-insertion process 2 → 3, which results in the activation of the methyl group for the migration to the coordinated CO. Rapid equilibrium was observed between the two isomers 4a and 4b during the CO insertion process to give 5. Theoretical studies have been carried out on the transformation of 3 to 4a and 4b. The B3LYP and MPn calculations indicated that the alkene insertion into the Pd−acyl bond trans to a phosphine is more favorable than that into the Pd−acyl bond trans to a phosphite. The MM3 calculations demonstrated that one specific transition structure is more favorable than the other possible transition structures for the transformation of (SP-4-4)-[Pd(COCH3)(propene)(L1)]·X1 (14b) to 4b. The difference originates from the steric effects of the BINAPHOS ligand, and the results account for high enantio- and regioselectivities experimentally observed. The two key steps, propene insertion into 3 and CO insertion into 4, were monitored by 1H NMR spectroscopy. The activation energies for these two steps were estimated to be 19.0−19.6 kcal/mol at −20 to 0 °C, their difference being insignificant. The living nature of the copolymerization was proved. Some related chiral ligands were examined for the copolymerization. Copolymerization of other olefins with CO was also investigated.
Gene therapy for hemophilia (2001)

Hemophilia A and B are X-chromosome linked recessive bleeding disorders that result from a deficiency in factor VIII (FVIII) and factor IX (FIX) respectively. Though factor substitution therapy has greatly improved the lives of hemophiliac patients, there are still limitations to the current treatment that have triggered interest in alternative treatments by gene therapy. Significant progress has recently been made in the development of gene therapy for the treatment of hemophilia A and B. These advances parallel the technical improvements of existing vector systems including MoMLV-based retroviral, adenoviral and AAV vectors, and the development of new delivery methods such as lentiviral vectors, helper-dependent adenoviral vectors and improved non-viral gene delivery methods. Therapeutic and physiologic levels of FVIII and FIX could be achieved in FVIII- and FIX-deficient mice and hemophilia dogs by different gene therapy approaches. Long-term correction of the bleeding disorders and in some cases a permanent cure has been realized in these preclinical studies. However, the induction of neutralizing antibodies often precludes stable phenotypic correction. Another complication is that certain promoters are prone to transcriptional inactivation in vivo, precluding long-term FVIII or FIX expression. Several gene therapy phase I clinical trials are currently ongoing in patients suffering from severe hemophilia A or B. No significant adverse side-effects were reported, and semen samples were negative for vector sequences by sensitive PCR assays. Most importantly, some subjects report fewer bleeding episodes and occasionally have very low levels of clotting factor activity detected. The results from the extensive preclinical studies in normal and hemophilic animal models and encouraging preliminary clinical data indicate that the simultaneous development of different strategies is likely to bring a permanent cure for hemophilia one step closer to reality.
uPAR induces epithelial–mesenchymal transition in hypoxic breast cancer cells (2007)

Hypoxia activates genetic programs that facilitate cell survival; however, in cancer, it may promote invasion and metastasis. In this study, we show that breast cancer cells cultured in 1.0% O(2) demonstrate changes consistent with epithelial-mesenchymal transition (EMT). Snail translocates to the nucleus, and E-cadherin is lost from plasma membranes. Vimentin expression, cell migration, Matrigel invasion, and collagen remodeling are increased. Hypoxia-induced EMT is accompanied by increased expression of the urokinase-type plasminogen activator receptor (uPAR) and activation of cell signaling factors downstream of uPAR, including Akt and Rac1. Glycogen synthase kinase-3beta is phosphorylated, and Snail expression is increased. Hypoxia-induced EMT is blocked by uPAR gene silencing and mimicked by uPAR overexpression in normoxia. Antagonizing Rac1 or phosphatidylinositol 3-kinase also inhibits development of cellular properties associated with EMT in hypoxia. Breast cancer cells implanted on chick chorioallantoic membranes and treated with CoCl(2), to model hypoxia, demonstrate increased dissemination. We conclude that in hypoxia, uPAR activates diverse cell signaling pathways that cooperatively induce EMT and may promote cancer metastasis.
Genetic background affects susceptibility to mammary hyperplasias and carcinomas in Apc(min)/+ mice. (2001)

Treatment of female C57BL/6J (B6) mice carrying the mutant Min allele of the adenomatous polyposis coli (Apc) gene with ethylnitrosourea (ENU) results in approximately 90% of mice developing an average of three mammary tumors within 65 days. As a first step in the identification of loci modifying susceptibility to ENU-induced mammary tumors and hyperplasias, we have tested ENU-treated Apc(Min)/+ (Min/+) mice on several hybrid backgrounds for susceptibility to mammary and intestinal tumors. C57BR/cdJxB6 (BRB6) Min/+ mice were more sensitive to development of mammary squamous cell carcinomas than B6 Min/+ mice. In contrast, Min/+ hybrids between B6 and FVB/NTac (FVB), 129X1/SvJ (129X1), and 129S6/SvEvTac (129S6) were all significantly more resistant to mammary carcinoma development. However, mice from these three crosses developed more focal mammary hyperplasias than did the B6 or BRB6 Min/+ mice. Susceptibility to intestinal tumors was independent of mammary tumor susceptibility in most hybrids. These results indicate that genetic background can affect independently the phenotypes conferred by the Min allele of APC:
Attributions, Involuntariness, and Hypnotic Rapport (1987)

Abstract Subjects' attributions of their hypnotic responsiveness to the hypnotist's abilities and efforts were associated with reports of suggestion-related involuntariness. In addition, rapport with the hypnotist was found to correlate with experienced involuntariness. As predicted, high-susceptible subjects expressed greater positive rapport and liking for the hypnotist and experienced greater involuntariness than their low-susceptible counterparts; they also attributed more of their responsiveness to the hypnotist's ability and efforts. Medium susceptibles were distinguishable from both highs and lows on all measures except liking for the hypnotist, in which case they were similar to the highs. Subjects viewed ability and effort as independent sources of hypnotic responsiveness.
Distributed form management (1990)

An open architecture for distributed form management is described. The model employs object-orientation in describing organizational units as well as individual users as entities with uniform external interfaces. Each entity is represented by an autonomous user agent which operates on local and migrating forms . The form concept encapsulates data, layout, and rules into a unified object which is the basic unit of presentation, processing, storage, and communication. All functionality of the system appears in rules of form classes and all data in instances of these form classes. This approach applies the techniques of computer supported cooperative work to provide a flexible mechanism for interpersonal, intraoffice, and interoffice procedures. The main challenge is to organize the collaboration without affecting the autonomy of individual user agents. In this respect, the contribution of the model is the mechanism for form migration. The dynamic integration of forms into different agents is solved with the coordinated interchange of form classes. A specific inheritance scheme provides the desired flexibility by separating the interrelated private and public form operations within each agent. The paper first describes the architecture by starting from a single agent and moving progressively towards a set of cooperating agents. Then an agent implementation called PAGES is described, experiences reported, and the open issues discussed. A typical distributed ordering procedure is used as an example throughout the text.
Demystified … (2000)

Apoptosis is the genetically regulated form of cell death that permits the safe disposal of cells at the point in time when they have fulfilled their intended biological function. Examples of apoptosis can be cited throughout the whole of the animal and plant kingdoms. It is a vitally important process during normal development and the adult life of many living organisms. In humans, dysregulation of apoptosis can result in inflammatory, malignant, autoimmune, and neurodegenerative diseases. In addition, infectious agents, including viruses, exploit cellular apoptosis in the host to evade the immune system. This review gives a brief historical perspective of some of the landmark discoveries in apoptosis research. The morphological and biochemical stages of apoptosis are then covered, followed by an overview of how it can be studied in the laboratory. Finally, the implications for therapeutic intervention in disease treatment are discussed.
Repeat administration of an adenovirus vector encoding cystic fibrosis transmembrane conductance regulator to the nasal epithelium of patients with cystic fibrosis. (1996)

Cystic fibrosis (CF) is a common autosomal recessive disease caused by mutations in the CF transmembrane conductance regulator gene. Recombinant adenoviruses have shown promise as vectors for transfer of CF transmembrane conductance regulator cDNA to airway epithelia and correction of the Cl- transport defect. However, because adenovirus-mediated gene transfer is transient, use of adenovirus as a vector for treatment of CF would require repeated administration. Therefore, we evaluated repeat administration of an adenovirus vector to the nasal epithelium of patients with CF with five escalating doses of up to 10(10) infectious units. There were no detectable adverse affects. All subjects were initially seropositive but developed additional humoral immune responses. The vector partially corrected the defect in airway epithelial Cl- transport in some subjects, although there was variability between subjects and there was less correction with subsequent administration, perhaps because the immune response limited gene transfer. Future work must focus on vectors with increased efficiency and with the ability to evade host defenses.
Nitric oxide-sensing mechanisms in Escherichia coli (2006)

Exposure of Escherichia coli to nitric oxide (NO) or nitrosating agents causes significant changes in patterns of gene expression. Three recent studies have used microarrays to analyse the response of the E. coli transcriptome to NO and nitrosative stress. Drawing on the array data, I review our current understanding of the E. coli regulatory systems that are involved.
Miniaturizing VEGF: Peptides mimicking the discontinuous VEGF receptor-binding site modulate the angiogenic response (2016)

The angiogenic properties of VEGF are mediated through the binding of VEGF to its receptor VEGFR2. The VEGF/VEGFR interface is constituted by a discontinuous binding region distributed on both VEGF monomers. We attempted to reproduce this discontinuous binding site by covalently linking into a single molecular entity two VEGF segments involved in receptor recognition. We designed and synthesized by chemical ligation a set of peptides differing in length and flexibility of the molecular linker joining the two VEGF segments. The biological activity of the peptides was characterized in vitro and in vivo showing a VEGF-like activity. The most biologically active mini-VEGF was further analyzed by NMR to determine the atomic details of its interaction with the receptor.