gebhart/patrepeval huggingface dataset:
Acetylcholine Stimulates α-Melanocyte-Stimulating Hormone Release from Frog Pituitary Melanotrophs through Activation of Muscarinic and Nicotinic Receptors* (1989)

The release of alpha MSH from the pars intermedia of amphibians is regulated by multiple factors, including classical neurotransmitters and neuropeptides. In this study we have examined the possible involvement of acetylcholine (ACh) in the regulation of alpha MSH secretion from the pars intermedia of the frog (Rana ridibunda) using the perifusion technique. When intact neurointermediate lobes (NIL) were exposed to graded doses of ACh (3 X 10(-7) to 3 X 10(-4) M), a dose-dependent stimulation of alpha MSH release was observed. Repeated administration of ACh (10(-4) M) induced reproducible responses of NIL without any desensitization phenomenon. ACh was also capable of stimulating alpha MSH release from dispersed intermediate lobe cells, indicating that the neurotransmitter exerts its effect by acting directly on frog melanotrophs. Using the monoclonal antibody M-35 against calf muscarinic receptors we have visualized, by the immunofluorescence technique, the presence of muscarinic receptor-like immunoreactivity in the frog pars intermedia. The stimulatory action of ACh was mimicked by both nicotine and muscarine (10(-5) M each). Nicotine-induced stimulation of alpha MSH release was partially abolished by alpha-bungarotoxin (10(-6) M) and hexamethonium (10(-4) M). The stimulatory effect of muscarine was suppressed by atropine and the M1-muscarinic antagonist pirenzepine (10(-5) M), but not by the M2-muscarinic antagonist gallamine. We have investigated the effect of ACh during administration of specific nicotinic and muscarinic antagonists. While hexomethonium or atropine could block only part of the stimulatory effect of ACh, concomitant administration of these antagonists totally abolished the response of NIL to ACh. Finally, the stimulatory effect of ACh was not impaired during prolonged administration of the beta-adrenergic antagonist propranolol. These data show that ACh stimulates in vitro alpha MSH secretion by frog NIL. Our results also indicate that amphibian pars intermedia cells possess two types of cholinergic receptors, an M1-muscarinic receptor sensitive to pirenzepine and nicotinic receptors sensitive to hexamethonium and alpha-bungarotoxin.
Microfluidic Networks for Chemical Patterning of Substrates:  Design and Application to Bioassays (1998)

This article describes the design, function, and application of simple microfluidic networks as conduits for the patterned delivery of chemical reactants onto a substrate. It demonstrates how such networks, made in an elastomer, allow simultaneous delivery of functionally distinct molecules onto targeted regions of a surface (Delamarche, E. et al. Science 1997, 276, 779−781). Microfluidic networks generally consume less than microliter quantities of solution and are thus well suited for use when the required reagents are scarce or precious, as often occurs in experiments and technologies that place biochemicals on solid planar substrates. We illustrate some of the particular challenges of doing chemistry inside the narrow confines of capillaries defined by fluidic networks, in addition to the advantages attendant to this approach, in the context of forming patterned arrays of different, and functional, immunoglobulins useful in highly localized biological assays.
Reticulum Cell Sarcoma: An Effector Cell in Antibody-Dependent Cell-Mediated Immunity (1975)

A transplantable, murine reticulum cell sarcoma is described which exhibits the cytologic, adherence, and phagocytic properties of macrophages. It forms specific rosettes with erythrocytes in the presence of the corresponding anti-serum. The ascites cells mediate antibody-dependent cellular immunity as assayed by release of radioactivity from 51Cr-labeled erythrocytes. The contribution of contaminating host cells in the cytotoxic reaction was ruled out by growing the tumor in F1 mice and removing the host cells by anti-H2 serum and complement. The tumor cells have receptors for IgG2a and IgG2b immunoglobulins. The availability of a pure population of effector cells in the immune system allows study of the biochemical processes pursuant to lysis of foreign cells.
Evolving concepts in molecular pathology (1994)

During the last decade, an understanding of the causes of many human diseases has progressed rapidly, in large measure because of the development of technologies that allow us to identify the genes that are involved. Identification of a gene that is suspected to play an important role in a particular disease opens up a whole new dimension of research to understand the molecular events that underlie the cause of that disorder. A crucial step in this process is often the development of an animal model of the disease. Again, the last decade has seen rapid advances in our ability to create such models, particularly in mice. Technologies that allow for the addition, alteration, or elimination of individual genes from the genome to create a transgenic mouse are now routine. The advantages of having a transgenic mouse model of a human disease are many. These animals often provide the first unequivocal proof that a particular gene is responsible for causing the pathological changes that occur with disease. They also can provide a system to carefully dissect the successive events that lead to the disease state, and can provide a custom-designed whole animal system to test potential therapies to treat and eventually cure the disease. Most important, new concepts relating to gene expression and gene function in disease often emerge from such transgenic studies. This review will illustrate several examples in which transgenic animals have contributed significantly to the evolution of concepts of the underlying mechanisms of human disease.
Detailed deletion mapping of chromosome 9q in bladder cancer: evidence for two tumour suppressor loci. (1995)

Loss of heterozygosity (LOH) at loci on chromosome 9p and/or 9q is the most frequent genetic alteration in transitional cell carcinoma (TCC) of the bladder. However, localisation of the tumour suppressor locus or loci on 9q has been hampered by the relative infrequency of tumours with subchromosomal deletions. We have used 24 microsatellite markers to examine LOH in 70 new cases of TCC of the bladder and upper urinary tract. Forty tumours (57%) showed LOH at one or more loci on 9q and partial deletions were detected in five tumours (7%). Combined data from the five cases with partial deletions place one tumour suppressor locus at 9q34 between D9S61 and D9S66 (an estimated distance of 13-14 cM). This region is frequently deleted in other sporadic tumours and encompasses one of the loci for tuberous sclerosis (TSC1). One tumour contained a distinct deletion between D9S153 and D9S109 (9q13-q31), which encompasses the locus for the familial nevoid basal cell carcinoma syndrome (Gorlin syndrome). This may indicate the presence of another tumour suppressor locus on 9q for TCC. Our findings significantly reduce the regions of 9q within which suppressor genes for TCC may reside. The possible involvement of two deletion targets on 9q in addition to the locus at 9p21 implicated in TCC may explain why LOH at all loci on chromosome 9 is frequent in TCC.
A CONDENSATION OF ACETOPHENONE WITH ISATIN BY THE KNOEVENAGEL METHOD1 (1932)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTA CONDENSATION OF ACETOPHENONE WITH ISATIN BY THE KNOEVENAGEL METHOD1H. G. Lindwall and J. S. MaclennanCite this: J. Am. Chem. Soc. 1932, 54, 12, 4739–4744Publication Date (Print):December 1, 1932Publication History Published online1 May 2002Published inissue 1 December 1932https://pubs.acs.org/doi/10.1021/ja01351a034https://doi.org/10.1021/ja01351a034research-articleACS PublicationsRequest reuse permissionsArticle Views1271Altmetric-Citations66LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
A Brief Review of Krill Oil History, Research, and the Commercial Market (2014)

In the last few years there has been a noticeable increase in both the promotion and research of krill oil for its purported health benefits, including the management and treatment of conditions, such as hyperlipidemia, inflammation, and arthritis. Additionally, because krill oil contains the same omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in fish and fish oil, krill oil is viewed as a viable alternative to fish oil to deliver the health benefits associated with EPA and DHA. The following review provides an overview of the currently available 10 peer-reviewed human clinical studies on krill oil, its safety, as well as a brief summary of the commercial krill oil market.
Rapid pacing results in changes in atrial but not in ventricular refractoriness (2002)

It is well known that atrial tachycardia causes atrial electrical remodeling, characterized by shortening of atrial effective refractory periods (AERPs) and loss of physiological adaptation of AERP to rate. However, the nature and time course of changes in ventricular effective refractory periods (VERP) caused by rapid rates are to be established. After being instrumented with epicardial electrodes on both atria and both ventricles nine goats were subjected to 1 week of rapid AV pacing with a rate of 240 beats/min and an AV delay of 100 ms. Pacing was only interrupted for measurement of left and right AERPs and VERPs at three basic cycle lengths (BCL) of 400 ms, 300 ms, and 200 ms during sinus rhythm in the conscious animal. Left and right AERPs decreased at all BCLs, reaching minimum values after 3 days (right AERP at BCL of 400 ms, 96+/-16 ms after 3 days vs 144+/-16 ms at baseline, P
Tau phosphorylation by GSK-3β promotes tangle-like filament morphology (2007)

These results suggest that phosphorylation of tau by GSK-3beta promotes formation of tangle-like filament morphology. The in vitro cell-free experiments described here provide a new model system to study mechanisms of NFT development. Although the severity of dementia has been found to correlate with the presence of NFTs, there is some question as to the identity of the neurotoxic agents involved. This model system will be beneficial in identifying intermediates or side reaction products that might be neurotoxic.
Efficacy of Fremanezumab in Migraine Patients Who Have Failed at Least One Prior Migraine Preventive Medication (P1.10-011) (2019)

To assess the efficacy of fremanezumab in migraine patients who failed at least one prior preventive migraine medication.
Importance of the cysteine-rich carboxyl-terminal half of V protein for Sendai virus pathogenesis (1997)

The Sendai virus V protein is a nonstructural trans-frame protein whose cysteine-rich C-terminal half is fused to the acidic N-terminal half of the P protein via mRNA editing. We recently created a mutant by disrupting the editing motif, which is devoid of mRNA editing and hence unable to produce the V protein, and demonstrated that this V(-) virus replicated normally or even faster with augmented gene expression and cytopathogenicity in cells in vitro, but was strongly attenuated in pathogenicity for mice (A. Kato, K. Kiyotani, Y. Sakai, T. Yoshida, and Y. Nagai, EMBO J. 16:578-587, 1997). Thus, although categorized as a nonessential protein, the V protein appeared to encode a luxury function required for the viral in vivo pathogenesis. Here, we created another version of a V-deficient mutant, VdeltaC, encoding only the N-terminal half but not the V-specific C-terminal half, by introducing a stop codon in the trans-V frame, and then we compared its in vitro and in vivo phenotypes with those of the V(-) and wild-type viruses. The VdeltaC virus was found to be similar to the wild-type virus in vitro with no augmented gene expression and cytopathogenicity, but in vivo, it resembled the V(-) virus, displaying a similarly attenuated phenotype. Thus, the pathogenicity determinant in the V protein was mapped to the C-terminal half. The N-terminal half was likely sufficient to confer normal (wild-type) in vitro phenotypes.
Thioredoxin-dependent peroxide reductase from yeast. (1994)

A 25-kDa antioxidant enzyme that provides protection against oxidation systems capable of generating reactive oxygen and sulfur species has previously been identified. The nature of the oxidant eliminated by, and the physiological source of reducing equivalents for, this enzyme, however, were not known. The 25-kDa enzyme is now shown to be a peroxidase that reduces H2O2 and alkyl hydroperoxides with the use of hydrogens provided by thioredoxin, thioredoxin reductase, and NADPH. This protein is the first peroxidase to be identified that uses thioredoxin as the immediate hydrogen donor and is thus named thioredoxin peroxidase (TPx). TPx exists as a dimer of identical 25-kDa subunits that contain 2 cysteine residues, Cys47 and Cys170. Cys47-SH appears to be the site of oxidation by peroxides, and the oxidized Cys47 probably reacts with Cys170-SH of the other subunit to form an intermolecular disulfide. Mutant TPx proteins lacking either Cys47 or Cys170, therefore, do not exhibit thioredoxin-coupled peroxidase activity. The TPx disulfide is specifically reduced by thioredoxin, but can also be reduced (less effectively) by a small molecular size thiol. The Saccharomyces cerevisiae thioredoxin reductase gene was also cloned and sequenced, and the deduced amino sequence was shown to be 51% identical with that of the Escherichia coli enzyme.
Compelling mechanistic data and identification of the active species in tungsten-catalyzed alkyne polymerizations: conversion of a trianionic pincer into a new tetraanionic pincer-type ligand (2012)

Complex [tBuOCO]WC(tBu)(THF)2 (1) {where tBuOCO = [2,6-(tBuC6H3O)2C6H3]3−, THF = tetrahydrofuran} polymerizes acetylenes (R-phenylacetylene (R = H, p-OMe, p-F, 3,5-diCF3), 1-decyne, 3,3-dimethyl-1-butyne, and trimethylsilylacetylene) to form π-conjugating polymers. Upon treating 1 with 2 equiv. of phenylacetylene in toluene-d8 at −35 °C, two isolable products form. These two products are [O2C(tBuC)W(η2-HCCPh)] (2-tttBu) and [O2C(PhC)W(η2-HCCtBu)] (2-Ph) {where OC(tBuC)O = [2,6-(tBuC6H3O)2C6H3(tBuC)]4−, OC(PhC)O = [2,6-(tBuC6H3O)2C6H3(PhC)]4−} and derived from an apparent reductive alkylidyne migratory insertion into a metal–arene bond. Complexes 2-tttBu and 2-Ph polymerize acetylene and a wide variety of monosubstituted acetylenes including phenylacetylene derivatives, 1-decyne, 3,3-dimethyl-1-butyne and trimethylsilylacetylene. With a substrate to catalyst loading ratio of 25 000 : 1, complex 2-tttBu polymerizes phenylacetylene with a turnover number (TON) of 17 233. Additionally, 2-tttBu polymerizes phenylacetylene and 1-decyne with catalytic activities up to 5.64 × 106 gPPA mol−1 h−1 and 7.98 × 106 gPA mol−1 h−1, respectively. 2-tttBu also polymerizes the disubstituted acetylene, 1-phenyl-1-propyne. NMR spectroscopic and single crystal X-ray structural studies provide compelling evidence for polymer chain growth via an insertion ring-expansion mechanism.
[Protective immunity against HIV infection]. (2002)

The clinical manifestation of HIV infection varies among HIV-exposed individuals. Most HIV infected people will develop AIDS after 8-10-yr exposure. However, long-term nonprogressors (LTNP) can remain asymptomatic and keep normal CD4 cell in the absence of treatment even after more than 10-yr of infection. In addition there are some exposed yet uninfected individuals (EU) despite repeated exposure of HIV among high risk group. Although HIV-specific IgG antibodies and small amount of viral RNA could be observed among the former LTNP group, no HIV-specific IgG and virions could be detected in the latter EU cohort. In contrast, the fact that cellular immune responses, in particular HIV-specific CD8+ CTL immunity could be seen in both groups strongly indicates their importance for the establishment of protective immunity. Together with the cellular immunity, the effect of mucosal immune components such as secretory IgA, gamma delta T cells and dendritic cells toward HIV infection will be discussed.
Y1 and Y2 Receptor Selective Neuropeptide Y Analogs: Evidence for a Y1 Receptor Subclass (1995)

Neuropeptide Y (NPY), a 36-residue polypeptide produced abundantly in both nervous and peripheral tissues, appears to play a significant role in the regulation of diverse biological processes, including feeding behavior and cardiovascular and psychotropic functions. The actions of NPY are mediated through effective binding to specific receptors of which two, designated Y1 and Y2, have been well characterized. A shortened cyclic analogue of NPY, des-AA10-17-cyclo-7/21[Cys7,21]NPY, was shown to retain high affinity for both human neuroblastoma SK-N-MC and SK-N-BE2 cell types (expressing Y1 and Y2 receptors, respectively). Increasing the size of the ring (des-AA10-17-cyclo-2/27[Cys2,27]NPY) in the present study produced a high-affinity analogue (Ki = 3.0 vs 0.3 nM for NPY) that bound exclusively to Y2 receptors. Using the feedback from structure-activity relationships, we also describe the optimization of specific substitutions and bridging arrangements leading to the production of other truncated, high-affinity Y1 selective analogues which bind, as does NPY itself, in the low-nanomolar range. Of greatest significance, des-AA10-17-cyclo-7/21[Cys7,21,Pro34]NPY (11) was found to possess agonistic properties with an affinity comparable to that of the native NPY molecule when tested for its ability to inhibit norepinephrine-stimulated cAMP release in SK-N-MC human neuroblastoma cells. Compound 11 also caused an increase in blood pressure in anesthetized rats. However, in two central nervous system models of Y1 receptor function, stimulation of feeding and anxiolytic activity, this analogue was inactive, which suggests the presence of a new subclass of receptors. In summary, the present results demonstrate that residues 10-17 of NPY are not directly involved in either Y1 or Y2 receptor recognition or activation. This suggests that the selectivity of NPY receptors is highly dependent on subtle conformational changes such as the substitution of residue 34 to a proline or the introduction of intramolecular constraints. Additionally, we have produced an analogue of NPY that selectively activates peripheral NPY Y1 receptors.
Self-assembled growth and optical emission of silver-capped silicon nanowires (2004)

Structured silver-capped silicon nanowires were fabricated via electroless metal deposition on a silicon wafer in an ionic silver HF solution through selective chemical etching. Their formation mechanism was explained on the basis of self-assembled localized microscopic electrochemical cell model. The metal–semiconductor composite nanostructure was found to have a strong ultraviolet-emitting property with an emission peak position at 330 nm. The intensity of the peak nonmonotonously varies with annealing temperature and time, but its position remains unchanged. Emission and excitation spectral analyses suggest that the ultraviolet emission is closely related to the existence of silver vacancy defects in silver nanocaps formed during sample fabrication. A specific vacancy density is required to produce the strong ultraviolet emission.
A GSM/GPRS Receiver front-end with discrete-time filters in a 90nm Digital CMOS (2006)

An RF receiver front-end for a GSM/GPRS radio system-on-chip in a 90 nm digital CMOS technology is presented. The circuit consisting of low noise amplifier, transconductance amplifier and switching mixer, offers 32.5 dB dynamic range with digitally-configurable voltage gain of 40 dB down to 7.5 dB. A series of decimation and discrete-time filtering follows the mixer and performs a highly-linear second-order low-pass filtering to reject close-in interferers. The front-end gains can be configured with an automatic-gain-control to select an optimal setting to form a trade-off between noise figure and linearity and to compensate the process and temperature variations. Even under the digital switching activity, noise figure at the 40 dB maximum gain is 1.8 dB and +50 dBm IIP/sub 2/ at the 34 dB gain. The variation of the input matching versus multiple gains is less than 1 dB. The circuit in total occupies 3.1 mm/sup 2/. The LNA, TA and mixer consume less than 15.3 mA at a supply voltage of 1.4 V.
Oncogenic aberrations of p16INK4/CDKN2 and cyclin D1 cooperate to deregulate G1 control. (1995)

The p16INK4/CDKN2, D-type cyclins, their partner cyclin-dependent kinases, and retinoblastoma protein constitute a G1 regulatory pathway commonly targeted in oncogenesis. We show that, unexpectedly, abnormalities of p16INK4/CDKN2 occur concomitantly in two-thirds of cancer cell lines harboring aberrations of cyclin D1. Gene and protein transfer experiments demonstrated that concurrent alterations of cyclin D1 and p16 levels cooperate to (de)regulate G1 control in diploid fibroblasts, and that both events influence growth of retinoblastoma (RB)-positive, but not RB-deficient cancer cells. These results show that biological consequences of deregulating individual components along the pathway are unequal, reflecting their hierarchical roles in the G1 checkpoint control. Whereas RB defects eliminate the checkpoint completely, aberrations of the upstream components, such as cyclin D1 and p16INK4/CDKN2, can cooperate in multistep tumorigenesis.
The Representation of Function in Computer-Based Design (1999)

Abstract This paper proposes a standardized representation of function for use by the research community, industry, and eventually commercial software vendors. This includes schemata (information models) for representation of function and associated flows, as well as an initial attempt at developing taxonomies of functions and flows. The objective of the latter effort is to generate taxonomies that are as small as possible, yet generic enough to allow modeling of a broad variety of engineering artifacts. This representation is intended to provide a generic infrastructure that will facilitate the capture and exchange of function information among researchers at present, and eventually in industry by contributing to interoperability between design systems, be they commercial or developed internally within a company.
Digital video transmission and coding for the broadband ISDN (1988)

An overview of visual communication in the broadband network is presented with particular attention to the transmission aspect of full-motion video. A detailed analysis of the quality requirements for digital video transmission is provided. Some significant coding algorithms presently under investigation by international bodies are reviewed.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>