gebhart/patrepeval huggingface dataset:
Vom königlichen Hoftheater zum „Städtischen Opern- und Schauspielhaus“ (1995)

Die Revolutionsbewegung, die Deutschland in eine Republik verwandeln wird, erreicht die ehemals "Königliche Haupt- und Residenzstadt Hannover" bereits wenige Tage nach der Meuterei der Marinesoldaten in Wilhelmshafen am 6. November 1918. Ein rasch aus Politikern der Sozialdemokratischen Partei gebildeter Arbeiter- und Soldatenrat übernimmt die Kontrolle über die Stadt. Mit dem Ende der Monarchie geht in Hannover die wilhelminisch geprägte "Ära Tramm" zu Ende, deren Mittelpunkt das hannoversche Stadtoberhaupt, Stadtdirektor Heinrich Tramm, gebildet hat. Äußerliches Symbol dieser Periode ist der repräsentative Prachtbau des Neuen Rathauses, eine "eindrucksvolle Zurschaustellung spätbürgerlichen Selbstverständnisses".1 Nach fast drei Jahrzehnten Amtszeit trifft am 10. November das Rücktrittsgesuch des nach Berlin geflohenen Stadtdirektors Tramm ein. Zu seinem Nachfolger wird schon am folgenden Tag einstimmig Robert Leinert, SPD-Landtagsabgeordneter und Mitglied im Arbeiter- und Soldatenrat, gewählt.
beta-Trace protein as a marker for cerebrospinal fluid rhinorrhea. (2002)

Cerebrospinal fluid (CSF) leakage occurs mainly as a complication of head injuries or skull-base surgeries, but may also occur spontaneously or as a result of nontraumatic processes such as inflammatory disorders or tumors (1). Detection and management of CSF leakage is essential to prevent possible life-threatening infections of the central nervous system (2). Radiologic and invasive procedures may be used for the diagnosis of CSF leaks, but these procedures are laborious, expensive, and present potential risk to the patient. Therefore, noninvasive laboratory methods serve as screening procedures before definitive procedures are used to localize the site of the defect.

Laboratory assessment of CSF leakage relies on compositional differences between CSF and other body secretions. The β2-transferrin (β2Tr) τ-fraction, or asialotransferrin, is a brain-specific variant of transferrin that lacks neuraminic acid. It therefore can be distinguished from serum transferrin by electrophoretic procedures and used to detect CSF rhinorrhea (3)(4). However, β2Tr is present in aqueous humor and in perilymph fluid and can be detected in serum, especially in chronic alcohol abusers and in patients with inborn errors of glycoprotein metabolism or genetic variants of transferrin (5)(6).

β-Trace protein (βTP), recently identified as prostaglandin D2 synthase (7), is another brain-specific protein that is produced mainly in the leptomeninges and the choroid plexus and is secreted into the CSF. βTP is the second most abundant protein in CSF after albumin. However, it is also present in other body fluids, including serum, albeit at much lower concentrations than in CSF (8). Immunoelectrophoretic methods for βTP have been applied as a screening procedure for CSF leaks (9)(10). Recently, a nephelometric assay for the quantification of βTP was introduced that promised several advantages over current CSF detection methods, including enhanced sensitivity and reduced turnaround time (11 …
Survival After Bilateral Versus Single-Lung Transplantation for Idiopathic Pulmonary Fibrosis (2009)

None.
Intracellular delivery of mRNA to human primary T cells with microfluidic vortex shedding (2019)

Intracellular delivery of functional macromolecules, such as DNA and RNA, across the cell membrane and into the cytosol, is a critical process in both biology and medicine. Herein, we develop and use microfluidic chips containing post arrays to induce microfluidic vortex shedding, or μVS, for cell membrane poration that permits delivery of mRNA into primary human T lymphocytes. We demonstrate transfection with μVS by delivery of a 996-nucleotide mRNA construct encoding enhanced green fluorescent protein (EGFP) and assessed transfection efficiencies by quantifying levels of EGFP protein expression. We achieved high transfection efficiency (63.6 ± 3.44% EGFP + viable cells) with high cell viability (77.3 ± 0.58%) and recovery (88.7 ± 3.21%) in CD3 + T cells 19 hrs after μVS processing. Importantly, we show that processing cells via μVS does not negatively affect cell growth rates or alter cell states. We also demonstrate processing speeds of greater than 2.0 × 10<sup>6</sup> cells s<sup>-1</sup> at volumes ranging from 0.1 to 1.5 milliliters. Altogether, these results highlight the use of μVS as a rapid and gentle delivery method with promising potential to engineer primary human cells for research and clinical applications.
Fast projection algorithm and its step size control (2002)

Of the many adaptive filtering algorithms, the normalized LMS (NLMS) algorithm is generally used in practice because of its simplicity. The computational complexity of the NLMS algorithm is low, however, convergence is very slow and tracking is poor for a colored input signal such as speech. The projection algorithm was proposed as a generalization of the NLMS algorithm. This paper provides a fast projection algorithm and a step size control to obtain the same steady-state excess mean squared error (MSE) for various projection orders. Computer simulations for colored noise and speech input signal confirm the effectiveness of the projection algorithm and the step size control.
Tafazzin knockdown interrupts cell cycle progression in cultured neonatal ventricular fibroblasts (2013)

Mutation of the mitochondrial protein tafazzin causes dilated cardiomyopathy in Barth syndrome. Previous studies have shown that tafazzin knockdown promotes hypertrophy of neonatal cardiac myocytes. The current investigation was designed to show whether tafazzin knockdown affects cardiac fibroblast proliferation and collagen secretion, which contribute to fibrosis in dilated cardiomyopathy. In primary cultures of neonatal ventricular fibroblasts (NVFs) transduced with a tafazzin short hairpin RNA adenovirus, tafazzin knockdown increased production of reactive oxygen species and activation of mitogen-activated protein kinases and induced protein and DNA synthesis via cell cycle regulators. It also reduced intracellular ATP, activated AMPK, and caused multinucleation, hypertrophy, and enhanced collagen secretion. We concluded that tafazzin knockdown interrupts the NVF cell cycle and this in turn may contribute to fibrosis and dilated cardiomyopathy in Barth syndrome.
Magnetic Resonance Imaging of Fe<inf>3</inf>O<inf>4</inf> Nanoparticles Embedded in Living Magnetotactic Bacteria for Potential Use as Carriers for In Vivo Applications (2007)

MC-1 Magnetotactic Bacteria (MTB) are studied for their potential use as bio-carriers for drug delivery. The exploitation of the flagella combined with nanoparticles magnetite or magnetosomes chain embedded in each bacterium and used to change the swimming direction of each MTB through magnetotaxis provide both propulsion and steering in small diameters blood vessels. But for guiding these MTB towards a target, being capable to image these living bacteria in vivo using an existing medical imaging modality is essential. Here, it is shown that the magnetosomes embedded in each MTB can be used to track the displacement of these bacteria using an MRI system. In fact, these magnetosomes disturb the local magnetic field affecting T1 and T2-relaxation times during MRI. MR T1-weighted and T2-weighted images as well as T2-relaxivity of MTB are studied in order to validate the possibility of monitoring MTB drug delivery operations using a clinical MR scanner. This study proves that MTB affect much more the T2-relaxation than T1-relaxation rate and can be though as a negative contrast agent. The signal decay in the T2-weighted images is found to change proportionally to the bacterial concentration. These results show that a bacterial concentration of 2.2x10(7) cells/mL can be detected using a T2-weighted image, which is very encouraging to further investigate the application of MTB for in vivo applications.
Molecular Basis of Kell Blood Group Phenotypes (1997)

The molecular basis of different Kell blood group phenotypes is reviewed. Sequence analysis of the Kell gene (KEL) established that single base substitutions, resulting in amino acid changes, are responsible for the different phenotypes. Most of the amino acid substitutions, with the exception of the one responsible for expression of KEL6 (Jsa), occur at the amino-terminal half of the protein, a domain that has least amino acid homology with a family of zinc endopeptidases, which include neutral endopeptidase 24.11 and endothelin-converting enzyme-1. Some of the genes were expressed in transfected cells and typed with alloantibodies to confirm that the identified mutations are responsible for antigen expression. Clinical applications of Kell blood group genotyping which include prenatal diagnosis to monitor hemolytic disease of the newborn are discussed.
Fludarabine plus cyclophosphamide versus fludarabine alone in first-line therapy of younger patients with chronic lymphocytic leukemia (2005)

Combination chemotherapy with fludarabine plus cyclophosphamide (FC) was compared with the standard regimen of fludarabine monotherapy in first-line treatment of younger patients with chronic lymphocytic leukemia (CLL). Between 1999 and 2003, a total of 375 patients younger than 66 years who predominantly had advanced CLL were randomly assigned to receive either fludarabine (25 mg/m(2) for 5 days intravenously, repeated every 28 days) or FC combination therapy (fludarabine 30 mg/m(2) plus cyclophosphamide 250 mg/m(2) for 3 days intravenously, repeated every 28 days). Both regimens were administered to a maximum of 6 courses. FC combination chemotherapy resulted in significantly higher complete remission rate (24%) and overall response rate (94%) compared with fludarabine alone (7% and 83%; P < .001 and P = .001). FC treatment also resulted in longer median progression-free survival (48 vs 20 months; P = .001) and longer treatment-free survival (37 vs 25 months; P < .001). Thus far, no difference in median overall survival has been observed. FC caused significantly more thrombocytopenia and leukocytopenia but did not increase the number of severe infections. In summary, first-line treatment with FC increases the response rates and the treatment-free interval in younger patients with advanced CLL.
Development of an MRI-compatible needle insertion manipulator for stereotactic neurosurgery (1995)

A variety of medical robots for stereotactic neurosurgery has been developed in recent years. Almost of all these robots use computed tomography (CT) to scan the brain of the patient before and during surgery. Currently, we are developing a needle insertion manipulator for magnetic resonance imaging (MRI)-guided neurosurgery. MRI techniques, including MRI angiography and functional MRI, are attractive for the development of interventional MRI therapies and operations. If a robot were available, these therapies would be minimally invasive, with more accurate guidance than is possible with current CT-guided systems. Actuation of a robot in an MRI environment is difficult because of the presence of strong magnetic fields. Therefore, the robot must be constructed of nonmagnetic materials. The system frame was manufactured using polyethylene terephthalate (PET) and was actuated using ultrasonic motors. Accuracy-evaluation procedures and phantom tests have been performed. The total accuracy of the system was approximately 3.0 mm. No artifacts caused by the manipulator were observed in the images.
Hydrolysis of the brain dipeptide N-acetyl-L-aspartyl-L-glutamate. Identification and characterization of a novel N-acetylated alpha-linked acidic dipeptidase activity from rat brain. (1987)

High performance liquid chromatography studies documented the presence of an enzyme activity, N-acetylated alpha-linked acidic dipeptidase (NAALA dipeptidase), in rat brain membranes that cleaves the endogenous brain dipeptide, N-acetyl-L-aspartyl-L-glutamate to N-acetyl-aspartate and glutamate. With ion exchange chromatography, which quantitatively separated [3,4-3H]glutamate from N-acetyl-L-aspartyl-L-[3,4-3H]glutamate, we found that NAALA dipeptidase activity was essentially restricted to nervous tissue and kidney. We characterized NAALA dipeptidase activity in lysed synaptosomal membranes obtained from rat forebrain. Membrane-bound NAALA dipeptidase activity was optimal between pH 6.0 and 7.4 at 37 degrees C. Eadie-Hofstee analysis of kinetic data revealed a rather high apparent affinity for N-acetyl-L-aspartyl-L-glutamate with a Km = 540 nM and a Vmax = 180 nM/mg of protein/min. While NAALA dipeptidase showed a requirement for monovalent anions such as Cl-, the polyvalent anions phosphate and sulfate inhibited enzyme activity 50% at 100 microM and 1 mM, respectively. The divalent metal ion chelators EGTA, EDTA, and o-phenanthroline completely abolished activity, which was partially restored by manganese. Treatment of membranes with 1 mM dithiothreitol abolished NAALA dipeptidase activity. NAALA dipeptidase activity was also sensitive to the aminopeptidase inhibitors bestatin and puromycin, although not to the selective aminopeptidase A inhibitor amastatin. Structure-activity relationships inferred from inhibitor studies suggest that this enzyme shows specificity for N-acetylated alpha-linked acidic dipeptides. NAALA dipeptidase was also potently inhibited by the excitatory amino acid agonist L-quisqualate. Comparison of the properties of NAALA dipeptidase to those of previously characterized enzymes suggests that this is a novel peptidase which may be involved in the synaptic degradation of N-acetyl-L-aspartyl-L-glutamate.
Increased serum stromelysin-1 levels in systemic lupus erythematosus: lack of correlation with disease activity. (1999)

Serum concentrations of stromelysin-1 are increased in SLE, but the levels do not correlate with disease activity.
Induction of Protective CTL Responses in Newborn Mice by a Murine Retrovirus (1996)

The susceptibility of neonates to virus-induced disease is thought to reflect, in part, the immaturity of their immune systems. However, inoculation of newborn mice with low doses of Cas-Br-M murine leukemia virus induced a protective cytotoxic T lymphocyte (CTL) response. The inability of neonates to develop a CTL response to high doses of virus was not the result of immunological immaturity but correlated with the induction of a nonprotective type 2 cytokine response. Thus, the initial viral dose is critical in the development of protective immunity in newborns.
Hyperthermophilic microorganisms (1990)

Growth only up to about 70°C f mentioned due to their close relationship to hyperthermophiles b Contain also mesophilic species.
Enzymology and Structure of the GH13_31 Glucan 1,6-α-Glucosidase That Confers Isomaltooligosaccharide Utilization in the Probiotic Lactobacillus acidophilus NCFM (2012)

Isomaltooligosaccharides (IMO) have been suggested as promising prebiotics that stimulate the growth of probiotic bacteria. Genomes of probiotic lactobacilli from the acidophilus group, as represented by Lactobacillus acidophilus NCFM, encode α-1,6 glucosidases of the family GH13_31 (glycoside hydrolase family 13 subfamily 31) that confer degradation of IMO. These genes reside frequently within maltooligosaccharide utilization operons, which include an ATP-binding cassette transporter and α-glucan active enzymes, e.g., maltogenic amylases and maltose phosphorylases, and they also occur separated from any carbohydrate transport or catabolism genes on the genomes of some acidophilus complex members, as in L. acidophilus NCFM. Besides the isolated locus encoding a GH13_31 enzyme, the ABC transporter and another GH13 in the maltooligosaccharide operon were induced in response to IMO or maltotetraose, as determined by reverse transcription-PCR (RT-PCR) transcriptional analysis, suggesting coregulation of α-1,6- and α-1,4-glucooligosaccharide utilization loci in L. acidophilus NCFM. The L. acidophilus NCFM GH13_31 (LaGH13_31) was produced recombinantly and shown to be a glucan 1,6-α-glucosidase active on IMO and dextran and product-inhibited by glucose. The catalytic efficiency of LaGH13_31 on dextran and the dextran/panose (trisaccharide) efficiency ratio were the highest reported for this class of enzymes, suggesting higher affinity at distal substrate binding sites. The crystal structure of LaGH13_31 was determined to a resolution of 2.05 Å and revealed additional substrate contacts at the +2 subsite in LaGH13_31 compared to the GH13_31 from Streptococcus mutans (SmGH13_31), providing a possible structural rationale to the relatively high affinity for dextran. A comprehensive phylogenetic and activity motif analysis mapped IMO utilization enzymes from gut microbiota to rationalize preferential utilization of IMO by gut residents.
Frontline: GITR, a member of the TNF receptor superfamily, is costimulatory to mouse T lymphocyte subpopulations (2004)

GITR (glucocorticoid-induced TNFR family related gene) is a member of the TNFR superfamily (TNFRSF) that is expressed in different cell types, including T lymphocytes. Because of a high homology in its cytoplasmic region with other known costimulatory members of the TNFRSF, we investigated whether GITR played a costimulatory role in T lymphocyte subpopulations. Our results show that the proliferation response of CD8+ and CD4+ peripheral T cell subpopulations was potentiated when a GITR costimulus was added to an anti-CD3 stimulus. Furthermore, expression of the main activation-induced receptor (IL-2Ralpha) and production of IL-2 and IFN-gamma were increased more with a GITR costimulus than with anti-CD3 alone. GITR stimulation also enhanced anti-CD3-induced ERK phosphorylation, suggesting that GITR is involved in MAPK-pathway activation. Interestingly, CD4+CD25+ regulatory T cell (Treg cell) proliferation was triggered by the GITR costimulus; Treg cell proliferation was paralleled by the loss of the anergic phenotype and suppressor activity. Nevertheless, unstimulated GITR(-/-) CD4+CD25+ and GITR(+/+) CD4+CD25+ cells were equally able to exert suppressor activity on CD4+CD25- responder cells. These results indicate a novel function for GITR as costimulatory molecule of T cell subsets.
Characterization of serum platelet-activating factor (PAF) acetylhydrolase. Correlation between deficiency of serum PAF acetylhydrolase and respiratory symptoms in asthmatic children. (1988)

Platelet-activating factor (PAF) acetylhydrolase has been recognized as an enzyme that inactivates PAF. We developed a convenient and reproducible method for determining human serum PAF acetylhydrolase activity. The assay was based on measurement of [14C]acetate produced from 1-O-alkyl-2-[14C]-acetyl-sn-glycero-3-phosphocholine upon precipitation of the complex of radioactive substrate and albumin with TCA. The apparent Km value of PAF acetylhydrolase (near the physiological concentration of serum protein) was 1.5 X 10(-4) M PAF. 32 subjects with serum PAF acetylhydrolase deficiency were found among 816 healthy Japanese adults. The low PAF acetylhydrolase activity in the deficient serum might not be due to the presence of enzyme inhibitor. Both the sensitivity to PAF and the metabolism of PAF in platelets from PAF acetylhydrolase-deficient subjects were almost the same as those of normal subjects. Deficiency in serum PAF acetylhydrolase appeared to be transmitted by autosomal recessive heredity among five Japanese families. Among healthy adults, healthy children, and asthmatic children, who were grouped into five classes on the basis of respiratory symptoms (remission, wheezy, mild, moderate, and severe groups), the probability of PAF acetylhydrolase deficiency was significantly higher in groups with severe symptoms (moderate and severe) (P less than 0.01). These results suggest that deficiency of serum PAF acetylhydrolase might be one of the factors leading to severe respiratory symptoms in asthmatic children.
The pathogenesis of rheumatoid arthritis. (2006)

Rheumatoid arthritis (RA) is due to a combination of phagocytosis and anaphylaxis gone awry. Immune complexes create their havoc via Fc gamma III receptors that signal via the tyrosine phosphorylation immunoreceptor pathway. Anaphylatoxins, mainly C5a, signal via the MEK kinase cascade, and both engage in cross-talk via NF kappa B. Aspirin-III blocks signals sent by both: immune complexes via FCR, and anaphylatoxin via C5 receptors. Drugs that affect both pathways, for example anti-B cell monoclonal antibodies, such as rituximab, and anti-C5 monoclonal antibodies, such as pexelizumab are currently being investigated. We now appreciate that cytokines are important mediators of inflammation in RA but are downstream of the primary insults: immune complexes and anaphylatoxins. We can therefore begin to ask what the antigen or antigens might be that produce IgGs reactive to 7 S or 19 S rheumatoid factors. The primary antigens of RA could well be CPs, formed perhaps by oral bacteria. Once immunoglobulins become recognized by rheumatoid factors, immune complexes form, and these activate anaphylatoxins. Phagocytosis and anaphylaxis are the proximal events of RA.
Highly selective tripeptide thrombin inhibitors (1993)

Tripeptide aldehydes such as Boc-D-Phe-Pro-Arg-H (51) exhibit potent direct inhibition of thrombin. This distinction offers important insight for the design of more potent and selective serine protease inhibitors which may be useful pharmacological tools and hold promise for development of clinically useful agents. The structure-activity relationships (SAR) on a series of anticoagulant peptides with high selectivity for the enzyme thrombin are discussed. The SAR is centered on a series of di- and tripeptide arginine aldehydes based on the structure of 51. The structural and conformational role of the amino acid residue in position 1 was investigated by substitution with conformationally restricted aromatic amino acids, aromatic acids, and a dipeptide isostere containing the psi[CH2N] amide bond replacement. Many of these peptides demonstrate potent antithrombotic activity along with selectivity toward thrombin, determined by comparison of in vitro inhibitory effects on trypsin, plasmin, factor Xa, and tissue plasminogen activator. Compound 5f, D-1-Tiq-Pro-Arg-H.sulfate is highly active and the most selective tripeptide aldehyde inhibitor of thrombin reported to date.
DNA rearrangements in human follicular lymphoma can involve the 5' or the 3' region of the bcl-2 gene. (1987)

In most human follicular lymphomas, the chromosome translocation t(14;18) occurs within two breakpoint clustering regions on chromosome 18, the major one at the 3' untranslated region of the bcl-2 gene and the minor one at 3' of the gene. Analysis of a panel of follicular lymphoma DNAs using probes for the first exon of the bcl-2 gene indicates that DNA rearrangements may also occur 5' to the involved bcl-2 gene. In this case the IgH locus and the bcl-2 gene are found in the order 3' C gamma S gamma/mu JH 5'::5' bcl-2 3' (where C = constant, S = switch, and JH = joining segment of the heavy chain locus), suggesting that an inversion also occurred during the translocation process. The coding regions of the bcl-2 gene, however, are left intact in all cases of follicular lymphoma studied to date.