gebhart/patrepeval huggingface dataset:
Brain microdialysis of GABA and glutamate: What does it signify? (1997)

Microdialysis has become a frequently used method to study extracellular levels of GABA and glutamate in the central nervous system. However, the fact that the major part of GABA and glutamate as measured by microdialysis does not fulfill the classical criteria for exocytotic release questions the vesicular origin of the amino acids in dialysates. Glial metabolism or reversal of the (re)uptake sites has been suggested to be responsible for the pool of nonexocytotically released amino-acid transmitters that seem to predominate over the neuronal exocytotic pool. The origin of extracellular GABA and glutamate levels and, as a consequence, the implications of changes in these levels upon manipulations are therefore obscure. This review critically analyzes what microdialysis data signify, i.e., whether amino-acid neurotransmitters sampled by microdialysis represent synaptic release, carrier-mediated release, or glial metabolism. The basal levels of GABA and glutamate are virtually tetrodotoxin- and calcium-independent. Given the fact that evidence for nonexocytotic release mediated by reversal of the uptake sites as a release mechanism relevant for normal neurotransmission is so far limited to conditions of "excessive stimulation," basal levels most likely reflect a nonneuronal pool of amino acids. Extracellular GABA and glutamate concentrations can be enhanced by a wide variety of pharmacological and physiological manipulations. However, it is presently impossible to ascertain that the stimulated GABA and glutamate in dialysates are of neuronal origin. On the other hand, under certain stimulatory conditions, increases in amino-acid transmitters can be obtained in the presence of tetrodotoxin, again suggesting that aspecific factors not directly related to neurotransmission underlie these changes in extracellular levels. It is concluded that synaptic transmission of GABA and glutamate is strictly compartmentalized and as a result, these amino acids can hardly leak out of the synaptic cleft and reach the extracellular space where the dialysis probe samples.
Prolonged STAT1 Activation Related to the Growth Arrest of Malignant Lymphoma Cells by Interferon-α (1998)

Multiple biologic effects of interferon-alpha (IFN-alpha), including cell growth inhibition and antiviral protection, are initiated by tyrosine phosphorylation of STAT proteins. Although this signal pathway has been intensively investigated, the relevance of STAT signal persistence has received scant attention. Using paired isogenic lymphoma cells (Daudi), which either are sensitive or resistant to growth inhibition by IFN-alpha, we found comparable initial tyrosine phosphorylation of multiple STAT proteins; however, the phosphorylation durations and associated DNA-binding activities diverged. Phosphorylation and DNA-binding capacity of STAT1 decreased after 4 to 8 hours in resistant cells, as compared with 24 to 32 hours in sensitive cells, whereas phosphorylation of STAT3 and STAT5b was briefer in both lines. Functional significance of the prolonged STAT1 signal, therefore, was explored by experimental interruption of tyrosine phosphorylation, either by premature withdrawal of the IFN-alpha or deferred addition of pharmacologically diverse antagonists: staurosporine (protein kinase inhibitor), phorbol 12-myristate 13-acetate (growth promoter), or aurintricarboxylic acid (ligand competitor). Results indicated that an approximately 18-hour period of continued STAT1 phosphorylation was associated with growth arrest, but that antiviral protection developed earlier. These differences provide novel evidence of a temporal dimension to IFN-alpha signal specificity and show that duration of STAT1 activation may be a critical variable in malignant cell responsiveness to antiproliferative therapy.
Sindbis virus RNA polymerase is degraded by the N-end rule pathway. (1991)

Upon infection of animal cells by Sindbis virus, four nonstructural (ns) proteins, termed nsP1-4 in order from 5' to 3' in the genome, are produced by posttranslational cleavage of a polyprotein. nsP4 is believed to function as the viral RNA polymerase and is short-lived in infected cells. We show here that nsP4 produced in reticulocyte lysates is degraded by the N-end rule pathway, one ubiquitin-dependent proteolytic pathway. When the N-terminal residue of nsP4 is changed by mutagenesis, the metabolic stabilities of the mutant nsP4s follow the N-end rule, in that the half-life of nsP4 bearing different N-terminal residues decreases in the order Met greater than Ala greater than Tyr greater than or equal to Phe greater than Agr. Addition of dipeptides Tyr-Ala, Trp-Ala, or Phe-Ala to the translation mixture inhibits degradation of Tyr-nsP4 and Phe-nsP4, but not of Arg-nsP4. Conversely, dipeptides His-Ala, Arg-Ala, and Lys-Ala inhibit the degradation of Arg-nsP4 but not of Tyr-nsP4 or Phe-nsP4. We found that there is no lysine in the first 43 residues of nsP4 that is required for its degradation, indicating that a more distal lysine functions as the ubiquitin acceptor. Strict control of nsP4 concentration appears to be an important aspect of the virus life cycle, since the concentration of nsP4 in infected cells is regulated at three levels: translation of nsP4 requires read-through of an opal termination codon such that it is underproduced; differential processing by the virus-encoded proteinase results in temporal regulation of nsP4; and nsP4 itself is a short-lived protein degraded by the ubiquitin-dependent N-end rule pathway.
Revisiting immunosurveillance and immunostimulation: Implications for cancer immunotherapy (2005)

Experimental and clinical experience demonstrates that the resolution of a pathogenic challenge depends not only on the presence or absence of an immune reaction, but also on the initiation of the proper type of immune reaction. The initiation of a non-protective type of immune reaction will not only result in a lack of protection, but may also exacerbate the underlying condition. For example, in cancer, constituents of the immune system have been shown to augment tumor proliferation, angiogenesis, and metastases. This review discusses the duality of the role of the immune system in cancer, from the theories of immunosurveillance and immunostimulation to current studies, which illustrate that the immune system has both a protective role and a tumor-promoting role in neoplasia. The potential of using chemotherapy to inhibit a tumor-promoting immune reaction is also discussed.
Aliasing Reduction for Gain Control with Critically Sampled Filter Banks (2006)

Applications of audio playback and communication often require the possibility to shape the signal spectra. This can easily be implemented in conjunction with audio coding techniques which are based on a spectral decomposition. Here, this can be accomplished by simply multiplying the decoded spectral components with different gain factors. However, since the transforms or filter banks used in coding produce a critically sampled representation, this can lead to undesirable non-compensated aliasing components in the resulting output signal. The gain factor dependent aliasing compensation technique presented in this paper reduces these effects in a very efficient way. The remaining aliasing components are almost as low as for the approximation of a non-critically sampled complex filter bank, while the new technique is of lower computational complexity and introduces less delay.
Comparative Analysis of Chemically and Electrochemically Formed Porous Si Antireflection Coating for Solar Cells (2003)

From the viewpoint of the porous Si (PS) application as an antireflection coating (ARC) in crystalline Si solar cells, a comparative study has been made on the morphological, kinetic, and optical properties of both chemically and electrochemically etched PS. These results are correlated and interpreted in terms of a simplified empirical model for the simultaneous PS formation and dissolution of Si. The fact that PS mainly carries potential as an ARC stresses the importance of the reflectance study. Chemically etched (stain-etched) PS has a pronounced porosity gradient in depth which is the result of a simultaneous etching at the PS/Si interface and Si dissolution throughout the existing porous layer. This implies that a part of the solar cell emitter is removed during stain etching. The predominant etching at the PS/Si interface in the case of electrochemically etched PS only converts part of the solar cell emitter into a porous layer and results in a nearly constant porosity in the thickness range of interest (up to 200 nm) for solar cell applications. Multicrystalline Si (mc-Si) behaves strongly similar to monocrystalline Si when applying an electrochemical porous etching, while stain etching is intrinsically more sensitive to the Si surface structure. The typical reflectivity behavior of both types of PS is interpreted in terms of the morphological differences. The integrated reflectance of both electrochemically formed and stain-etched porous layers is comparable to the value obtained for a silicon nitride coating on textured mc-Si, which stresses the potential of a PS ARC for crystalline Si solar cells. © 2003 The Electrochemical Society. All rights reserved.
Expression of platelet-derived growth factor beta-receptors on stromal tissue cells in human carcinoid tumors. (1990)

Carcinoid tumors of the midgut type are slowly growing neoplasms which often present clinically and histologically pronounced fibrosis around the tumors. Cryosections from 41 neuroendocrine tumors (31 midgut carcinoid tumors, 8 endocrine pancreatic carcinomas, 1 parathyroid carcinoma, and 1 pheochromocytoma) and 22 nonneuroendocrine carcinomas were examined for the presence of platelet-derived growth factor (PDGF) beta-receptor by immunohistochemistry using the monoclonal antibody PDGFR-B2. Twenty midgut carcinoid tumor tissues (66%) and 4 endocrine pancreatic carcinomas (50%) and the parathyroid carcinoma stained positively with the antibody. In contrast, only 2 nonneuroendocrine tumor tissues (10%) were stained, and the staining in these cases was weak. The immunoreaction in the carcinoid tumors was observed in connective tissue cells adjacent to tumor cell clusters but not in the tumor cells themselves. The degree of positive PDGF beta-receptor expression in the carcinoid tissues seems to correlate positively with the presence of macrophages as determined by the monoclonal antibody anti-Leu-M5, but not with other infiltrated lymphocytes identified with the monoclonal antibody anti-Leu-4, or with anti-HLA-DR antibodies. Stromal cells adjacent to tumor cells, including small capillaries, stained more strongly than the stromal cells which were distant from tumor cell clusters. Furthermore, carcinoid tumor metastases from lymph nodes as well as from liver showed stronger immunoreactivity in the stromal cells with the PDGF beta-receptor antibody than the corresponding primary tumors. Our data suggest that carcinoid tumor cells may directly or indirectly induce expression of PDGF beta-receptor on adjacent stromal cells in the tumor tissue, which may contribute to the fibrosis that is often seen around carcinoid tumors.
NLRP3 inflammasome mediates contrast media-induced acute kidney injury by regulating cell apoptosis (2016)

Iodinated contrast media serves as a direct causative factor of acute kidney injury (AKI) and is involved in the progression of cellular dysfunction and apoptosis. Emerging evidence indicates that NLRP3 inflammasome triggers inflammation, apoptosis and tissue injury during AKI. Nevertheless, the underlying renoprotection mechanism of NLRP3 inflammasome against contrast-induced AKI (CI-AKI) was still uncertain. This study investigated the role of NLRP3 inflammasome in CI-AKI both in vitro and in vivo. In HK-2 cells and unilateral nephrectomy model, NLRP3 and NLRP3 inflammasome member ASC were significantly augmented with the treatment of contrast media. Moreover, genetic disruption of NLRP3 notably reversed contrast-induced expression of apoptosis related proteins and secretion of proinflammatory factors, similarly to the effects of ASC deletion. Consistent with above results, absence of NLRP3 in mice undergoing unilateral nephrectomy also protected against contrast media-induced renal cells phenotypic alteration and cell apoptosis via modulating expression level of apoptotic proteins. Collectively, we demonstrated that NLRP3 inflammasome mediated CI-AKI through modulating the apoptotic pathway, which provided a potential therapeutic target for the treatment of contrast media induced acute kidney injury.
Surgical management of uterine fibroids at Aminu Kano teaching hospital, Kano, Nigeria: a 5 year review (2009)

Background : Uterine fibroids are the most common pelvic tumors. They account for a significant number of gynecological consultations. Prevalence, presentation and outcome of treatment vary in different communities. Objectives : To determine the prevalence and clinical presentation of uterine fibroids, and the morbidity associated with surgical management of uterine fibroids at Aminu Kano Teaching Hospital, Kano. Study design : Retrospective study of all the cases of uterine fibroids that were surgically managed in Aminu Kano Teaching Hospital, Kano between 1st January 2006 and 31st December 2010. Results : The period prevalence of uterine fibroids found in this study was 3.1%, 8.3% of gynecological operations were for fibroids. Main presentations were menstrual irregularities 75.9%, abdominal swelling 51.9%, lower abdominal pain 46.5%, dysmenorrhea 29.1%, infertility 20.3%. The postoperative complication of anemia occurred in 34.1% of patients who had myomectomy and 14.6% of those who had hysterectomy. Anemia was 3 times more likely to occur with myomectomy (OR 3.02, CI 1.69-3.56, P  0.05 and for UTI OR 1.17, CI 0.42-3.23, P >0.05). Conclusion: The prevalence and presentation of uterine fibroids found in this study is similar to the finding of other studies from Northern Nigeria. The most common presentations were menorrhagia and lower abdominal swelling, and not infertility. Myomectomy was associated with higher complication rates compared to hysterectomy. Key words : Uterine fibroids, prevalence, presentation, postoperative morbidity.
Identification of a novel noncoding RNA gene, NAMA, that is downregulated in papillary thyroid carcinoma with BRAF mutation and associated with growth arrest (2007)

In search of tumor suppressor genes in papillary thyroid carcinoma (PTC), we previously used gene expression profiling to identify genes underexpressed in tumor compared with paired unaffected tissue. While searching for loss of heterozygosity (LOH) in genomic regions harboring candidate tumor suppressor genes, we detected LOH in a approximately 20 kb region around marker D9S176. Several ESTs flanking D9S176 were underexpressed in PTC tumors, and for one of the ESTs, downregulation was highly associated with the activating BRAF mutation V600E, the most common genetic lesion in PTC. A novel gene, NAMA, (noncoding RNA associated with MAP kinase pathway and growth arrest) containing the affected EST was cloned and characterized. NAMA is weakly expressed in several human tissues, and the spliced forms are primarily detected in testis. Several characteristics of NAMA suggest that it is a nonprotein coding but functional RNA; it has no long open reading frames (ORFs); the exons exhibit low sequence identity in the evolutionarily conserved regions; it is inducible by knockdown of BRAF, inhibition of the MAP kinase pathway, growth arrest and DNA damage in cancer cell lines. We suggest that NAMA is a noncoding RNA associated with growth arrest.
Identification and Characterization of cvHsp (1999)

Starting with computational tools that search for tissue-selective expression of assembled expressed sequenced tags, we have identified by focusing on heart libraries a novel small stress protein of 170 amino acids that we named cvHsp. cvHsp was found as being computationally selectively and highly (0.3% of the total RNA) expressed in human heart. The cvHsp gene mapped to 1p36.23-p34.3 between markers D1S434 and D1S507. The expression of cvHsp was analyzed with RNA dot, Northern blots, or reverse transcription-polymerase chain reaction: expression was high in heart, medium in skeletal muscle, and low in aorta or adipose tissues. In the heart of rat models of cardiac pathologies, cvHsp mRNA expression was either unchanged (spontaneous hypertension), up-regulated (right ventricular hypertrophy induced by monocrotaline treatment), or down-regulated (left ventricular hypertrophy following aortic banding). In obese Zucker rats, cvHsp mRNA was increased in skeletal muscle, brown, and white adipose tissues but remained unchanged in the heart. Western blot analysis using antipeptide polyclonal antibodies revealed two specific bands at 23 and 25 kDa for cvHsp in human heart. cvHsp interacted in both yeast two-hybrid and immunoprecipitation experiments with alpha-filamin or actin-binding protein 280. Within cvHsp, amino acid residues 56-119 were shown to be important for its specific interaction with the C-terminal tail of alpha-filamin.
Transforming Growth Factor β Receptor Type II Inactivation Promotes the Establishment and Progression of Colon Cancer (2004)

Deregulation of members of the transforming growth factor (TGF)-beta signaling pathway occurs often in colon cancers and is believed to affect the formation of primary colon cancer. Mutational inactivation of TGFBR2 is the most common genetic event affecting the TGF-beta signaling pathway and occurs in approximately 20-30% of all colon cancers. By mating Fabpl(4xat-132) Cre mice with Tgfbr2(flx/flx) mice, we have generated a mouse model that is null for Tgfbr2 in the colonic epithelium, and in this model system, we have assessed the effect of loss of TGF-beta signaling in vivo on colon cancer formation induced by azoxymethane (AOM). We have observed a significant increase in the number of AOM-induced adenomas and adenocarcinomas in the Fabpl(4xat-132) Cre Tgfbr2(flx/flx) mice compared with Tgfbr2(flx/flx) mice, which have intact TGF-beta receptor type II (TGFBR2) in the colon epithelium, and we have found increased proliferation in the neoplasms occurring in the Fabpl(4xat-132) Cre Tgfbr2(flx/flx) mice. These results implicate the loss of TGF-beta-mediated growth inhibition as one of the in vivo mechanisms through which TGFBR2 inactivation contributes to colon cancer formation. Thus, we have demonstrated that loss of TGFBR2 in colon epithelial cells promotes the establishment and progression of AOM-induced colon neoplasms, providing evidence from an in vivo model system that TGFBR2 is a tumor suppressor gene in the colon.
Isolation and sequencing of insecticidal peptides from the primitive hunting spider, Plectreurys tristis (Simon) (1994)

About 50 peptide toxins were purified from venom of the primitive hunting spider, Plectreurys tristis. Bioassay by injection into larval Heliothis virescens (tobacco budworm) allowed selection of nine toxins for analysis of amino acid sequences. Total sequences were determined for six of the more insecticidal peptides (46-49 amino acids) and three contained free carboxyl-terminal amino acids. These toxins (plectoxins) are paralytic and/or lethal when injected into insect pests such as the lepidopterous larvae H. virescens, Spodoptera exigua (beet armyworm), and Manduca sexta (tobacco hornworm). We expect these plectoxins to be useful in insect control after delivery by a suitable agent such as a recombinant baculovirus.
Empirical threshold values for quantitative trait mapping. (1994)

The detection of genes that control quantitative characters is a problem of great interest to the genetic mapping community. Methods for locating these quantitative trait loci (QTL) relative to maps of genetic markers are now widely used. This paper addresses an issue common to all QTL mapping methods, that of determining an appropriate threshold value for declaring significant QTL effects. An empirical method is described, based on the concept of a permutation test, for estimating threshold values that are tailored to the experimental data at hand. The method is demonstrated using two real data sets derived from F(2) and recombinant inbred plant populations. An example using simulated data from a backcross design illustrates the effect of marker density on threshold values.
The Knowledge Complexity of Interactive Proof Systems (1989)

Usually, a proof of a theorem contains more knowledge than the mere fact that the theorem is true. For instance, to prove that a graph is Hamiltonian it suffices to exhibit a Hamiltonian tour in it; however, this seems to contain more knowledge than the single bit Hamiltonian/non-Hamiltonian. In this paper a computational complexity theory of the “knowledge” contained in a proof is developed. Zero-knowledge proofs are defined as those proofs that convey no additional knowledge other than the correctness of the proposition in question. Examples of zero-knowledge proof systems are given for the languages of quadratic residuosity and 'quadratic nonresiduosity. These are the first examples of zero-knowledge proofs for languages not known to be efficiently recognizable.
The nitric oxide system in glucocorticoid-induced hypertension (2002)

The blood pressure-raising effects of adrenocortical steroids with predominantly glucocorticoid activity, both naturally occurring and synthetic, are well known. Recent evidence suggests that the nitric oxide system plays a key role in the hypertension produced by glucocorticoids. Glucocorticoid actions at various sites in the nitric oxide synthase (NOS) pathway may result in elevated blood pressure. These include: alterations in l-arginine availability or transport; NOS2 and NOS3 downregulation; reduced cofactor bioavailability; NOS uncoupling; a concomitant elevation in reactive oxygen species and removal of nitric oxide (NO) from the vascular environment; alterations in whole body antioxidant status; and erythropoietin induced resistance to NO.