gebhart/patrepeval huggingface dataset:
The induction of prostatic hypertrophy in the dog with androstanediol. (1976)

The effects of androstanediol and estradiol on prostatic growth were investigated in castrate dogs. Estrogens along resulted in no significant change in prostatic weight, whereas androstanediol produced growth comparable to that in uncastrated controls. Androstanediol plus estradiol resulted in an even more striking increase in prostate growth. Approximately half the animals receiving androstanediol alone and all of those receiving androstanediol plus estradiol fulfill the weight and histological criteria for prostatic hypertrophy in the dog. Since both these steroid hormones are presumed to be normal secretory products of the testis, it is possible that they are involved in the pathogenesis of prostatic hypertrophy in the dog.
The dominant flocculation genes of Saccharomyces cerevisiae constitute a new subtelomeric gene family (1995)

The quality of brewing strains is, in large part, determined by their flocculation properties. By classical genetics, several dominant, semidominant and recessive flocculation genes have been recognized. Recent results of experiments to localize the flocculation genes FLO5 and FLO8, combined with the in silicio analysis of the available sequence data of the yeast genome, have revealed that the flocculation genes belong to a family which comprises at least four genes and three pseudogenes. All members of this gene family are located near the end of chromosomes, just like the SUC, MEL and MAL genes, which are also important for good quality baking or brewing strains. Transcription of the flocculation genes is repressed by several regulatory genes. In addition, a number of genes have been found which cause cell aggregation upon disruption or overexpression in an as yet unknown manner. In total, 33 genes have been reported that are involved in flocculation or cell aggregation.
Protein Kinase C α/β Inhibitor Go6976 Promotes Formation of Cell Junctions and Inhibits Invasion of Urinary Bladder Carcinoma Cells (2004)

Changes in activation balance of different protein kinase C (PKC) isoenzymes have been linked to cancer development. The current study investigated the effect of different PKC inhibitors on cellular contacts in cultured high-grade urinary bladder carcinoma cells (5637 and T24). Exposure of the cells to isoenzyme-specific PKC inhibitors yielded variable results: Go6976, an inhibitor of PKCalpha and PKCbeta isoenzymes, induced rapid clustering of cultured carcinoma cells and formation of an increased number of desmosomes and adherens junctions. Safingol, a PKCalpha inhibitor, had similar but less pronounced effects. In contrast, a PKCdelta inhibitor, rottlerin, had an opposite effect on cell clustering and caused dissociation of cell junctions. A broad-spectrum PKC inhibitor bisindolylmaleimide I did not have any apparent effect on the morphology of the cultures or on the number of cell junctions. Additional studies with Go6976 demonstrated that inhibition of PKCalpha and beta isoenzymes induced translocation of beta1-integrin from the cell-matrix junctions and that beta4-integrin was translocated to face the culture substratum. Go6976 was also highly effective in inhibiting migration of carcinoma cells and inhibited invasion through artificial basement membrane. Our results on urinary bladder carcinoma cells emphasize that Go6976 is a potential anticancer drug due to its effects on cell-cell and cell-matrix junctions, migration, and invasion. Furthermore, the results may be explained by changes in PKC activation balance promoted by inhibition of PKCalpha/beta.
Apoptosis of T lymphocytes in experimental autoimmune encephalomyelitis. Evidence for programmed cell death as a mechanism to control inflammation in the brain. (1993)

In experimental autoimmune encephalomyelitis (EAE) myelin-specific T lymphocytes attack the myelinated tissue of the central nervous system (CNS). In the Lewis rat, EAE as a rule has an acute, monophasic course. With spontaneous clinical recovery the inflammatory CNS infiltrates are cleared from the nervous tissue within a few days. This is well in line with the remarkably low incidence of myelin-specific T cells present in EAE infiltrate. Combining immunocytochemical techniques, ultrastructural criteria and in situ nick translation we found up to 49% of T lymphocytes in EAE lesions showing signs of apoptosis at the time of recovery from disease. Our results suggest that apoptosis of T lymphocytes may be one possible mechanism to eliminate T lymphocytes from inflammatory brain lesions.
Differences between melphalan and nitrogen mustard in the formation and removal of DNA cross-links. (1978)

The formation of DNA cross-links is thought to represent the lethal lesion following exposure of cells to bifunctional alkylating agents. Since differences in rates of formation and repair of cross-links may explain differences in activity of these agents, we have studied these events following exposure of L1210 cells to nitrogen mustard (HN2) and melphalan. With the technique of alkaline elution, it was possible to measure cross-linking at doses that result in relatively little cell kill. Following a 30-min exposure to HN2, DNA cross-links increased for 1 to 2 hr and were then removed by a process that was virtually complete in 24 hr. In contrast, following a 30-min exposure to melphalan, cross-link formation increased for 12 hr and removal was much slower than it was for HN2. Comparison of cell survival with cross-linking kinetics suggests that persistence of the cross-links with time is an important factor in determining lethality.
Joint scheduling of distributed complex periodic and hard aperiodic tasks in statically scheduled systems (2002)

In this paper we present algorithms for the joint scheduling of periodic and aperiodic tasks in statically scheduled distributed real-time systems. Periodic tasks are precedence constrained, distributed, and communicating over the nodes of the systems. Both soft and hard aperiodic tasks are handled. After a static schedule has been created in a first step, the algorithms determine the amount and distribution of unused resources and leeway in it. These are then used to incorporate aperiodic tasks into the schedule by shifting the periodic tasks' execution, without violating their feasibility. Run-time mechanisms are simple and require only little memory. Processors and communication nodes can be utilized fully. The algorithm performs on optimal online guarantee algorithm for hard aperiodic tasks of O(N). An extensive simulation study exhibits very high guarantee ratios for various load and deadline scenarios, which underlines the efficiency of our method.
Metabolic Biomarker and Kinase Drug Target Discovery in Cancer Using Stable Isotope-Based Dynamic Metabolic Profiling (SIDMAP) (2003)

Tumor cells respond to growth signals by the activation of protein kinases, altered gene expression and significant modifications in substrate flow and re-distribution among biosynthetic pathways. This results in a proliferating phenotype with altered cellular function. These transformed cells exhibit unique anabolic characteristics, which includes increased and preferential utilization of glucose through the non-oxidative steps of the pentose cycle for nucleic acid synthesis but limited de novo fatty acid synthesis and TCA cycle glucose oxidation. This primarily non-oxidative anabolic profile reflects an undifferentiated highly proliferative aneuploid cell phenotype and serves as a reliable metabolic biomarker to determine cell proliferation rate and the level of cell transformation/differentiation in response to drug treatment. Novel drugs effective in particular cancers exert their anti-proliferative effects by inducing significant reversions of a few specific non-oxidative anabolic pathways. Here we present evidence that cell transformation of various mechanisms is sustained by a unique disproportional substrate distribution between the two branches of the pentose cycle for nucleic acid synthesis, glycolysis and the TCA cycle for fatty acid synthesis and glucose oxidation. This can be demonstrated by the broad labeling and unique specificity of [1,2-(13)C(2)]glucose to trace a large number of metabolites in the metabolome. Stable isotope-based dynamic metabolic profiles (SIDMAP) serve the drug discovery process by providing a powerful new tool that integrates the metabolome into a functional genomics approach to developing new drugs. It can be used in screening kinases and their metabolic targets, which can therefore be more efficiently characterized, speeding up and improving drug testing, approval and labeling processes by saving trial and error type study costs in drug testing.
Radionuclide Peptide Cancer Therapy (2013)

THEORY AND PRODUCTION OF PEPTIDES FOR RADIONUCLIDE THERAPY. Peptide Structure and Analysis. Molecular Pharmacology of Receptors. Receptors Distribution and Biochemical Characterization. RADIOLABELING MECHANISMS AND STRATEGIES. Developments of Radiolabeled Peptides. Receptor Targeting for Tumor Therapy with Radiopeptides. New Radionuclides for Peptide Therapy. Pre-Clinical Comparison of Radiolabeled Peptides for Radionuclide Therapy. CLINICAL THERAPEUTIC APPLICATIONS. Phase I Therapeutic Studies. Response to Treatment with Radiolabeled Peptides. Receptor Radionuclide Therapy: From 90Y to 177Lu Labeled Peptides. Therapeutic Potential of Radiolabeled Peptides with Beta and Alpha Emitters. Receptor-Mediated Radionuclide Therapy: The European Institute of Oncology Experience. DOSIMETRIC ASPECTS AND REGULATORY REQUIREMENTS. Radiation Dosimetry in Preparation to Therapy. Dosimetry and Critical Organs. Regulatory Requirements for Therapy Trials. FUTURE PERSPECTIVES. Advances in the Field of Radiopeptides for Therapy
Time-reversal symmetry-breaking superconductivity (1999)

We study time-reversal symmetry-breaking superconductivity with ${\ensuremath{\Delta}}_{k}={\ensuremath{\Delta}}_{{x}^{2}\ensuremath{-}{y}^{2}}{(k)+e}^{i\ensuremath{\theta}}{\ensuremath{\Delta}}_{\ensuremath{\alpha}}(\ensuremath{\alpha}=s$ or ${d}_{\mathrm{xy}})$ symmetries. It is shown that the behavior of such superconductors could be qualitatively different depending on the minor component $(\ensuremath{\alpha})$ and its phase at lower temperatures. It is argued that such qualitatively different behaviors in thermal as well as in angular dependences could be a source of consequences in transport and Josephson physics. Orthorhombicity is found to be a strong mechanism for the mixed phase (in the case of $\ensuremath{\alpha}=s).$ We show that due to electron correlation the order parameter is more like a pure ${d}_{{x}^{2}\ensuremath{-}{y}^{2}}$ symmetry near optimum doping.
Epidermal growth factor and transforming growth factor α induce c‐fos gene expression in retinal muller cells in vivo (1991)

Epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha) are peptides that act at a common receptor and are mitogenic for immature astrocytes and trophic for developing brain neurons in vitro. However, a role for these growth factors in the mature nervous system has not been established. To investigate the actions of EGF and TGF alpha in the adult central nervous system (CNS) in vivo, the growth factors were injected into the vitreous cavity of adult male rabbits. After varying intervals, the retinas were examined for c-fos mRNA by Northern blot hybridization or Fos (and Fos-related antigen) protein by immunocytochemistry. EGF induction of c-fos mRNA occurs within 30 min and persists more than 4 hr. Fos nuclear immunostaining is induced selectively in nuclei of Muller cells by both EGF and TGF alpha. Fos-like immunoreactivity appears within 1 hr and persists more than 9 hr after EGF injection. These observations demonstrate that mature retinal Muller cells respond to exogenously applied EGF and TGF alpha in vivo, although the effect of the growth factors is not necessarily direct. The expression of c-fos and other immediate early genes provides a short-term marker that can be used to investigate the role of growth factors in normal retinal physiology and responses to injury.
Médailles de Prix des Écoles et des Facultés mixtes de Médecine et de Pharmacie (1992)

Preismedaillen der Schulen un der gemischten medizinischen und pharmazeutischen Fakultäten . Der Verfasser beschreibt sechs Preismedaillen der Vorbereitungsschulen, der vollständigen Schulen und der gemischten medizinisch-pharmazeutischen Fakultäten.
In vitro neutralization of the Shwartzman-inducing activity of endotoxins by immune serum. (1970)

The Shwartzman-inducing activity in rabbits of purified endotoxin from four O serotypes of Escherichia coli, one strain of Salmonella typhi and one of Serratia marcescens was completely abolished by mixture, before intradermal injection, with homologous rabbit antiserum. The neutralization was highly specific since the same sera had no effect, under the conditions used, on endotoxin of heterologous serotypes or heterologous species. Neutralization of inducing activity did not require incubation or complement and was demonstrable independently of the species of endotoxin used for provocation. Inducing activity could be restored by extraction of the endotoxin—antiserum mixture with aqueous phenol, but not with trichloracetic acid.
Fully Homomorphic SIMD Operations. (2011)

Abstract. At PKC 2010 Smart and Vercauteren presented a variant of Gentry’s fully homomorphic public key encryption scheme and mentioned that the scheme could support SIMD style operations. The slow key generation process of the Smart–Vercauteren system was then addressed in a paper by Gentry and Halevi, but their key generation method appears to exclude the SIMD style operation alluded to by Smart and Vercauteren. In this paper, we show how to select parameters to enable such SIMD operations, whilst still maintaining practicality of the key generation technique of Gentry and Halevi. As such, we obtain a somewhat homomorphic scheme supporting both SIMD operations and operations on large finite fields of characteristic two. This somewhat homomorphic scheme can be made fully homomorphic in a naive way by recrypting all data elements seperately. However, we show that the SIMD operations can be used to perform the recrypt procedure in parallel, resulting in a substantial speed-up. Finally, we demonstrate how such SIMD operations can be used to perform various tasks by studying two use cases: implementing AES homomorphically and encrypted database lookup. 1
Handbook of Psychopathy (2007)

Part I: Theoretical and Empirical Foundations. Lykken, Psychopathic Personality: The Scope of the Problem. Fowles, Dindo, A Dual-Deficit Model of Psychopathy. Blackburn, Other Theoretical Models of Psychopathy. Hare, Neumann, The PCL-R Assessment of Psychopathy: Development, Structural Properties, and New Directions. Part II: Issues in Conceptualization and Assessment. Cooke, Michie, Hart, Facets of Clinical Psychopathy: Toward Clearer Measurement. Lilienfeld, Fowler, The Self-Report Assessment of Psychopathy: Problems, Pitfalls, and Promises. Lynam, Derefinko, Psychopathy and Personality. Widiger, Psychopathy and DSM-IV Psychopathology. Poythress, Skeem, Disaggregating Psychopathy: Where and How to Look for Subtypes. Krueger, Perspectives on the Conceptualization of Psychopathy: Toward an Integration. Part III: Etiological Mechanisms. Waldman, Rhee, Genetic and Environmental Influences on Psychopathy and Antisocial Behavior. Farrington, Family Background and Psychopathy. Minzenberg, Siever, Neurochemistry and Pharmacology of Psychopathy and Related Disorders. Raine,Yang, The Neuroanatomical Bases of Psychopathy: A Review of Brain Imaging Findings. Blair, Subcortical Brain Systems in Psychopathy: The Amygdala and Associated Structures. Rogers, The Functional Architecture of the Frontal Lobes: Implications for Research with Psychopathic Offenders. Hiatt, Newman, Understanding Psychopathy: The Cognitive Side. Frick, Marsee, Psychopathy and Developmental Pathways to Antisocial Behavior in Youth. MacDonald III, Iacono, Toward an Integrated Perspective on the Etiology of Psychopathy. Part IV: Psychopathy in Specific Subpopulations. Salekin, Psychopathy in Children and Adolescents. Verona,Vitale, Psychopathy in Women: Assessment, Manifestations, and Etiology. Sullivan, Kosson, Ethnic and Cultural Variations in Psychopathy. Hall, Benning, The Successful Psychopath: Adaptive and Subclinical Manifestations of Psychopathy in the General Population. Part V: Clinical and Applied Issues. Porter, Woodworth, Psychopathy and Aggression. Taylor, Lang, Psychopathy and Substance Use Disorders. Knight, Guay, The Role of Psychopathy in Sexual Coercion against Women. Douglas,Vincent, Edens, Risk for Criminal Recidivism: The Role of Psychopathy. Harris, Rice, Treatment of Psychopathy: A Review of Empirical Findings. Edens, Petrila, Legal and Ethical Issues in the Assessment and Treatment of Psychopathy. Seto, Quinsey, Toward the Future: Translating Basic Research into Prevention and Treatment Strategies. Part VI: Conclusions and Future Directions. Patrick, Back to the Future: Cleckley as a Guide to the Next Generation of Psychopathy Research.
Generation of neural progenitor cells by chemical cocktails and hypoxia (2014)

Neural progenitor cells (NPCs) can be induced from somatic cells by defined factors. Here we report that NPCs can be generated from mouse embryonic fibroblasts by a chemical cocktail, namely VCR (V, VPA, an inhibitor of HDACs; C, CHIR99021, an inhibitor of GSK-3 kinases and R, Repsox, an inhibitor of TGF-β pathways), under a physiological hypoxic condition. These chemical-induced NPCs (ciNPCs) resemble mouse brain-derived NPCs regarding their proliferative and self-renewing abilities, gene expression profiles, and multipotency for different neuroectodermal lineages in vitro and in vivo. Further experiments reveal that alternative cocktails with inhibitors of histone deacetylation, glycogen synthase kinase, and TGF-β pathways show similar efficacies for ciNPC induction. Moreover, ciNPCs can also be induced from mouse tail-tip fibroblasts and human urinary cells with the same chemical cocktail VCR. Thus our study demonstrates that lineage-specific conversion of somatic cells to NPCs could be achieved by chemical cocktails without introducing exogenous factors.
An Ultrasonically Powered Implantable Micro-Oxygen Generator (IMOG) (2011)

In this paper, we present an ultrasonically powered implantable micro-oxygen generator (IMOG) that is capable of in situ tumor oxygenation through water electrolysis. Such active mode of oxygen generation is not affected by increased interstitial pressure or abnormal blood vessels that typically limit the systemic delivery of oxygen to hypoxic regions of solid tumors. Wireless ultrasonic powering (2.15 MHz) was employed to increase the penetration depth and eliminate the directional sensitivity associated with magnetic methods. In addition, ultrasonic powering allowed for further reduction in the total size of the implant by eliminating the need for a large area inductor. IMOG has an overall dimension of 1.2 mm × 1.3 mm × 8 mm, small enough to be implanted using a hypodermic needle or a trocar. In vitro and ex vivo experiments showed that IMOG is capable of generating more than 150 μA which, in turn, can create 0.525 μL/min of oxygen through electrolytic disassociation. In vivo experiments in a well-known hypoxic pancreatic tumor models (1 cm (3) in size) also verified adequate in situ tumor oxygenation in less than 10 min.
The Herbicide Dicamba (2-Methoxy-3,6-dichlorobenzoic Acid) Is a Peroxisome Proliferator in Rats (1995)

The widely used broad leaf herbicide, dicamba, or Banvel, is similar in structure to xenobiotics which induce hepatic drug metabolism or proliferation of hepalic peroxisomes in rodents. The ability of xenobiotics to effect these hepatic changes often portends their positive outcomes in chronic bioassays. Dicamba's ability to induce hepatomegaly and peroxisome proliferation was studied in male and female Sprague-Dawley rats. Rats were placed on feed containing 0, 0.001, 0.01, 0.1, or 1% dicamba or 0.01% ciprofibrate for 3 weeks. Dicamba had no effect on relative liver weights or feed efficiency in either female or male rats at all doses tested. Dicamba, however, caused a statistically significant increase in peroxisomal β-oxidation activity in liver homogenates from rats of both sexes fed 1% dicamba Fatty acyl CoA-oxidase activity was increased in male rats fed 1% dicamba. A protein of Mr 80 kDa was visible when liver homogenates of female or male rats fed 1% dicamba were subjected to SDS-PAGE. Lauric acid hydroxylase activity and CYP4A-reactive protein were increased in microsomes from male rats fed the highest level of dicamba. Moreover, dicamba was observed to transcriptionally upregulate the peroxisome proliferator-activated receptor (PPAR), a peroxisome proliferator sensitive receptor previously shown to be linked to the transcriptional regulation of a variety of peroxisome specific enzymes. These studies show that dicamba is a peroxisome proliferator in rats. Although dicamba was not an efficacious inducer of peroxisomal enzymes in these rats, dicamba's ability to transcriptionally activate the PPAR and induce peroxisomal and related enzymes must be considered in the safety evaluation of this herbicide.
Possible involvement of neuropeptidergic sensory nerves in alopecia areata (1997)

Alopecia areata (AA) is a dermatosis involving the sudden occurrence of bald patches on the scalp. Although the aetiology is unknown, experimental data indicate that cutaneous microcirculation plays an important role. The skin is richly innervated by neuropeptidergic sensory nerves that help regulate microvascular circulation. This study shows a reduction of cutaneous levels of substance P and calcitonin gene-related peptide (CGRP) but not of vasoactive intestinal polypeptide in scalp biopsies from patients with AA. Laser-Doppler flowmetry was used to study microcirculation of the scalp. Results indicate that patients with AA have lower basal blood flow and greater vasodilatation following intradermal CGRP injection than control subjects. A vascular hyper-reactivity to vasodilatatory substances such as neuropeptides, probably because of the lack of these substances, is hypothesized.
On the mechanisms of the internalization of S413-PV cell-penetrating peptide (2005)

Cell-penetrating peptides have been shown to translocate across eukaryotic cell membranes through a temperature-insensitive and energy-independent mechanism that does not involve membrane receptors or transporters. Although cell-penetrating peptides have been successfully used to mediate the intracellular delivery of a wide variety of molecules of pharmacological interest both in vitro and in vivo, the mechanisms by which cellular uptake occurs remain unclear. In the face of recent reports demonstrating that uptake of cell-penetrating peptides occurs through previously described endocytic pathways, or is a consequence of fixation artifacts, we conducted a critical re-evaluation of the mechanism responsible for the cellular uptake of the S4(13)-PV karyophilic cell-penetrating peptide. We report that the S4(13)-PV peptide is able to accumulate inside live cells very efficiently through a rapid, dose-dependent and non-toxic process, providing clear evidence that the cellular uptake of this peptide cannot be attributed to fixation artifacts. Comparative analysis of peptide uptake into mutant cells lacking heparan sulphate proteoglycans demonstrates that their presence at the cell surface facilitates the cellular uptake of the S4(13)-PV peptide, particularly at low peptide concentrations. Most importantly, our results clearly demonstrate that, in addition to endocytosis, which is only evident at low peptide concentrations, the efficient cellular uptake of the S4(13)-PV cell-penetrating peptide occurs mainly through an alternative, non-endocytic mechanism, most likely involving direct penetration across cell membranes.