gebhart/patrepeval huggingface dataset:
Induction of tyrosine phosphorylation by the erythropoietin receptor correlates with mitogenesis. (1991)

A role for tyrosine phosphorylation in the signal-transducing mechanisms of several hematopoietic growth factors has been hypothesized. To extend these observations, we have examined the effects of erythropoietin (Epo) on tyrosine phosphorylation in an Epo-responsive cell that was obtained by transfecting the murine erythropoietin receptor (EpoR) into an interleukin-3 (IL-3)-dependent cell line. By two-dimensional analysis of phosphotyrosine-containing proteins isolated with a monoclonal antibody (1G2) against phosphotyrosine, Epo and IL-3 were found to rapidly induce tyrosine phosphorylation of comparable substrates of 92, 70, and 56 kDa. In addition, Epo uniquely induced phosphorylation of a 72-kDa substrate while IL-3 uniquely induced phosphorylation of a 140-kDa substrate. Immunoprecipitation and mixing experiments indicated that the 72-kDa substrate may represent a small fraction of the EpoR. To explore the significance of tyrosine phosphorylation, we generated two mutants of the EpoR that lacked 108 or 146 amino acids at their carboxyl termini. In addition we constructed an internally deleted mutant that lacked 20 amino acids in a region of sequence homology with the IL-2 receptor beta chain. Although all mutants were expressed at comparable levels and had comparable binding affinities for Epo, only the mutant lacking 108 amino acids at the carboxyl terminus retained significant mitogenic activity or the ability to induce tyrosine phosphorylation.
Cell-to-Cell Transmission of α-Synuclein Aggregates (2012)

It is now recognized that the cell-to-cell transmission of misfolded proteins such as α-synuclein contributes to the neurodegenerative phenotype in neurological disorders such as idiopathic Parkinson's disease, Dementia with Lewy bodies, and Parkinson's disease dementia. Thus, establishing cell-based models for the transmission of α-synuclein is of importance to understand the mechanisms of neurodegeneration in these disorders and to develop new therapies. Here we describe methods to study the neuron-to-neuron propagation of α-synuclein in an in vitro setting that also has in vivo applications.
Characterization of the inward current induced by metabotropic glutamate receptor stimulation in rat ventromedial hypothalamic neurones (1997)

1. Whole-cell patch clamp recordings were made from rat ventromedial hypothalamic neurones in slices of brain tissue in vitro. Bath application of 50 microM (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) depolarized all neurones tested by activation of an inward current of approximately 55 pA at -60 mV. 2. The inward current elicited by 1S,3R-ACPD was unaffected by K+ channel blockade with external Cs+, Ba2+ or TEA. However, the current was significantly reduced by replacement of the external NaCl with either Tris-HCl or LiCl. 3. The 1S,3R-ACPD-induced current was reduced by the heavy metal ions Ni2+ or La3+ and also by the Na(+)-Ca2+ exchange current inhibitor 3',4'-dichlorobenzamil. 4. The effects of 1S,3R-ACPD were mimicked by the group I metabotropic agonist 3,5-dihydroxyphenylglycine (DHPG) but not by the group III selective agonist, L-2-amino-4-phosphonobutanoate (L-AP4). Furthermore, the effects of 1S,3R-ACPD were inhibited by the metabotropic antagonists alpha-methyl-4-carboxyphenylglycine (MCPG) and 1-aminoindan-1,5-dicarboxylic acid (AIDA) but not by the presynaptic metabotropic receptor antagonists alpha-methyl-4-phosphonophenylglycine (MPPG) or alpha-methyl-4-tetrazolylphenylglycine (MTPG). 5. Photorelease of caged GDP beta S inside neurones irreversibly blocked the 1S,3R-ACPD-induced current whilst photolysis of caged GTP gamma S inside neurones irreversibly potentiated this current. 6. The PLC inhibitor U-73,122 significantly reduced the size of the inward current induced by 1S,3R-ACPD. This effect was not mimicked by the inactive analogue U-73,343. 7. Flash photolysis of the caged calcium chelator diazo-2 inside neurones diminished the response to 1S,3R-ACPD. 8. It is concluded that group I metabotropic glutamate receptors depolarize neurones in the VMH by activation of a Na(+)-Ca2+ exchange current through a G-protein coupled increase in intracellular Ca2+.
Improved Line Heat Source Thermal Conductivity Probe (1981)

ABSTRACT An improved line heat source thermal conductivity probe was made to simplify the construction and extend the life of thermal conductivity probes. The accuracy of thermal conductivity measurement is also improved. The better linearity of temperature versus logarithm of time was obtained as compared to published techniques. The probe made with the heater wire and thermocouple on the outside of a sewing needle instead of inside of a hypodermic needle was checked by measuring the thermal conductivity of known samples. Results obtained with the improved probe show lower temperature rise and lower standard deviation.
α-Aminosulfonopeptides as possible functional analogs of penicillin; evidence for their extreme instability (1996)

Sulfonopeptide analogs of acyl-D-Ala-D-Ala bearing an α-aminosulfonic acid moiety in the penultimate position have been synthesized using a Curtius rearrangement step. The sulfonopeptides were prepared and examined in aprotic solvents, but they proved to be exceedingly labile in protic solvents; for example, α-acylaminosulfonodipeptide 31 proved to be too unstable to isolate in pure form and its methyl ester, 34, decomposed with a half-life of ca. 8 min in 50% methanol at pD=5 and at 25°C. A mechanistic study relating to the stability of the α-sulfonopeptides is delineated, including an analysis of the decomposition products in aqueous solution.
Selection of functional T cell receptor mutants from a yeast surface-display library (1999)

The heterodimeric alphabeta T cell receptor (TCR) for antigen is the key determinant of T cell specificity. The structure of the TCR is very similar to that of antibodies, but the engineering of TCRs by directed evolution with combinatorial display libraries has not been accomplished to date. Here, we report that yeast surface display of a TCR was achieved only after the mutation of specific variable region residues. These residues are located in two regions of the TCR, at the interface of the alpha- and beta-chains and in the beta-chain framework region that is thought to be in proximity to the CD3 signal-transduction complex. The mutations are encoded naturally in many antibody variable regions, indicating specific functional differences that have not been appreciated between TCRs and antibodies. The identification of these residues provides an explanation for the inherent difficulties in the display of wild-type TCRs compared with antibodies. Yeast-displayed mutant TCRs bind specifically to the peptide/MHC antigen, enabling engineering of soluble T cell receptors as specific T cell antagonists. This strategy of random mutagenesis followed by selection for surface expression may be of general use in the directed evolution of other eukaryotic proteins that are refractory to display.
Dendritic cells are the principal stimulators of the primary mixed leukocyte reaction in mice (1983)

Clone 33D1 is a mouse-rat hybridoma that secretes a specific anti-dendritic cell (DC) monoclonal antibody (14). Because the antibody kills DC in the presence of rabbit complement, it can be used to study the functional consequences of selective DC depletion. Previous data on the cell specificity of 33D1 were first extended. By cytotoxicity (rabbit complement) and indirect immunofluorescence (biotin-avidin technique), 33D1 reacted with DC but not with macrophages nor other splenocytes. In contrast, the monoclonal antibody, F4/80 (15), reacted with macrophages but not DC. The functional assay evaluated in this paper was stimulation of the primary mixed leukocyte reaction (MLR). 33D1 antibody itself did not inhibit stimulation by enriched populations of DC. In the presence of complement, 33D1 killed DC and ablated stimulatory function. The effect of 33D1 and complement on MLR stimulation by heterogenous cell mixtures was then evaluated. Removal of DC from unfractionated spleen suspensions reduced stimulatory capacity 75-90 percent, comparable to that produced with specific anti-Ia antibody and complement. Stimulation of both proliferative and cytotoxic responses was reduced. DC depletion had similar effects on MLR generated across full strain differences, or across selected subregions (H2I, H-2K/D) of the major histocompatibility complex. To further compare the functional properties of spleen DC and macrophages, MLR stimulation by adherent and nonadherent fractions of spleen were tested separately. 62 +/- 8 percent of the total stimulatory capacity of spleen was in the plastic adherent population. Activity was ablated greater than 90 percent after elimination of DC. MLR stimulation by 24-h cultures of spleen adherent cells, which contained a three- to sixfold excess of Ia(+) macrophages, was also ablated when DC were removed. Stimulation by nonadherent spleen was more resistant, but was reduced 50-75 percent by 33D1 and complement. The function of spleen cells treated with 33D1 or anti-Ia antibody and complement was restored with a small inoculum of purified DC. The latter corresponded to 0.5 percent of total stimulator cells and were enriched by previously described techniques that did not require the 33D1 antibody. We conclude that the DC, a trace component of mouse spleen, is the principal cell type required for stimulation of the primary MLR. Because other cells are not immunogenic, but do express Ia and H-2 alloantigens, DC likely represent the critical accessory cell required for the induction of lymphocyte responses.
Multiparty micropayments for ad hoc networks (2004)

The majority of ad hoc networks and their associated applications have been designed with closed user groups in mind. In such scenarios all the nodes in the network usually belong to a single authority and are configured to cooperate in the relaying of packets within the network. In recent years however, ad hoc networks have also found their way into everyday networking environments, where mobile devices may be under the administrative control of individual users. These users may not necessarily be motivated to provide services for free to others in the network. A typical situation could be where a node may wish to relay packets through a number of intermediate nodes in the ad hoc network, to access services in the fixed network. In this paper we present a lightweight payment scheme based on hash chains, which allows a node to pay others who relay packets on its behalf in real-time. Also due to the dynamic nature of an ad hoc network, the topology of the network can change unpredictably. The design of the payment scheme is flexible enough to be able to cope with such route changes, without the need to contact a trusted third party such as a bank or broker to pay the nodes in the new path.
Construction and characterization in vivo of Bordetella pertussis aroA mutants (1990)

A DNA fragment encoding a kanamycin resistance determinant was used to insertionally inactivate the cloned aroA gene of Bordetella pertussis in Escherichia coli K-12, and a conjugative shuttle vector system based on the suicide vector pRTP1 was used to deliver the mutations from E. coli back into B. pertussis CN2992FS and BP1. The aroA mutation was introduced by allelic exchange into the chromosome of B. pertussis, resulting in otherwise isogenic parental and aroA mutant pairs. The B. pertussis aroA mutants grew well on laboratory medium supplemented with aromatic compounds but failed to grow on unsupplemented medium. The B. pertussis aroA mutants expressed the normal B. pertussis extracellular, virulence-associated proteins; inactivated, whole-cell vaccines prepared from the mutants protected mice as efficiently as vaccines made from the parent strains against intracerebral challenge with the virulent B. pertussis 18323. Live B. pertussis aroA bacteria inefficiently colonized the lungs of NIH/S mice after they were challenged with aerosol, unlike the wild-type B. pertussis organism. Mice exposed to three separate aerosols of live B. pertussis aroA bacteria were protected against lung colonization after being exposed to an aerosol containing the virulent parental B. pertussis strain. High-level antibodies against B. pertussis rapidly appeared in the sera of mice immunized by aerosol with the B. pertussis aroA strains and challenged with the virulent parent.
Characteristics of MSM photodetectors with trench electrodes on p-type Si wafer (1998)

U-grooved metal-semiconductor-metal photodetectors (UMSM-PD's) having various trench depths of interdigitated electrodes and an intrinsic hydrogenated amorphous silicon (i-a-Si:H) to c-Si heterojunction have been fabricated successfully on a p-type [100] Si wafer. The U-grooved structures on c-Si were achieved with a simple orientation-dependent etching (ODE) process. Some important characteristics of the obtained UMSM-PDs are presented and discussed. An UMSM-PD with a 70 nm i-a-Si:H overlayer, 1.45 /spl mu/m-deep recessed electrodes, and 3 /spl mu/m finger width and spacing, had a full width at half maximum (FWHM) of 50.6 ps and a full-time of 132 ps for its temporal response under a bias of 15 V. The significant improvements of transient response for UMSM-PD, as compared to the conventional one, were attributed to the trench electrodes resulted in a stronger lateral electric field in the light absorption region of photodetector. At a bias of 20 V, this UMSM-PD had a responsivity of 0.25 A/W as measured with an 0.83-/spl mu/m incident semiconductor laser, a high photo/dark current ratio about 2000, and an internal quantum efficiency of 36%. This high photo/dark current ratio would be due to the additional i-a-Si:H overlayer on Si wafer. These mentioned performances were much better than those of the conventional Si-based planar MSM-PD.
Active Surface Architectures of Large Radio Telescopes (2002)

The active surface architectures of all three large radio telescopes either built or under active development are reviewed, with
Activation of aldosterone secretion in primary aldosteronism (1969)

Angiotensin infusion evokes marked increases in aldosterone secretion in primary aldosteronism and little change in secondary aldosteronism. The low plasma renin activity of primary aldosteronism and the elevated plasma renin activity of secondary aldosteronism are thought to account for this differential response. The effect of angiotensin on aldosterone and 18-hydroxycorticosterone secretion was studied during adrenal vein catheterization in seven patients with primary aldosteronism (whose plasma renin activity had been elevated following spironolactone therapy), one hypertensive patient with normal plasma renin activity and normal aldosterone secretion, two patients with secondary aldosteronism who had elevated plasma renin activity, and one anephric patient whose plasma renin activity was 0. Adrenal venous aldosterone and 18-hydroxycorticosterone were measured before and after a ten min sub-pressor angiotensin infusion. The cells of the aldosterone-producing adenoma (APA) respond to small increases in plasma angiotensin with large increases in secretion of aldosterone and 18-hydroxycorticosterone. The dose of angiotensin capable of evoking this response from the aldosterone-producing adenoma produces little or no change in the secretion of the steroids from nontumorous glands. The augmentation of aldosterone secretion, induced by angiotensin, in primary aldosteronism is due solely to increased secretion by the adenoma and not by the contralateral zona glomerulosa. The increased sensitivity of the aldosterone-producing adenoma is characteristic of the tumor. This response is independent of fluctuations in endogenous plasma renin activity. This sensitivity is not blunted by high plasma renin activity, nor is it a function of tumor mass for the effect is observed in aldosterone-producing adenomas regardless of size. ACTH injection after angiotensin infusion resulted in a marked increase in aldosterone concentration in the effluent from the nontumorous adrenal, but was not capable of producing further increases in aldosterone concentration in the effluent from the APA. In view of this exquisite sensitivity to infused angiotensin, it may be that the small variations in endogenous plasma renin activity that have been observed in primary aldosteronism may be capable of evoking large changes in aldosterone secretion in patients with aldosterone-producing adenomas.
Current Concepts Review - Acetabular and Femoral Anteversion (1999)

†Departments of Orthopedics and Diagnostic Radiology, Städtische Kliniken, Syburger Strasse 14, D-44265, Dortmund, Germany. ‡Institute of Medical Informatics and Biomathematics, University of Münster, Domack Strasse 9, D-48149 Münster, Germany.
Crizotinib in ROS1-Rearranged Non–Small-Cell Lung Cancer (2014)

In this study, crizotinib showed marked antitumor activity in patients with advanced ROS1-rearranged NSCLC. ROS1 rearrangement defines a second molecular subgroup of NSCLC for which crizotinib is highly active. (Funded by Pfizer and others; ClinicalTrials.gov number, NCT00585195.).
Correlation between reversing of multidrug resistance and inhibiting of [3H]azidopine photolabeling of P-glycoprotein by newly synthesized dihydropyridine analogues in a human cell line. (1989)

Ten synthetic dihydropyridine analogues were investigated for their ability to reverse drug resistance in a multidrug-resistant human carcinoma cell line, KB-Cl. Four dihydropyridine analogues completely reversed the resistance, three lowered the resistance, and three had little effect. The radioactive photoactive dihydropyridine calcium channel blocker, [3H]azidopine, photolabels P-glycoprotein in membrane vesicles from KB-Cl cells. This photolabeling was almost completely inhibited by excess dihydropyridine analogues that reversed or lowered drug resistance. In contrast, the labeling was not significantly inhibited by analogues that do not reverse resistance. Among other reversing agents, cepharanthine and reserpine inhibited the [3H]azidopine photolabeling, but thioridazine did not. N-Solanesyl-N,N'-bis(3,4-dimethoxybenzyl)ethylenediamine slightly inhibited the labeling at 100 microM. An anticancer agent, vinblastine, also inhibited the labeling. The correlation between the reversing of the drug resistance and the inhibition of the [3H]azidopine photolabeling of P-glycoprotein by dihydropyridine analogues suggests a role for P-glycoprotein in multidrug resistance and also the reversing of the resistance by dihydropyridine analogues.
Functional Dendrimers for Nonlinear Optics (2001)

Novel nonlinear optical (NLO) building blocks can be placed into the periphery, branch, or core of a dendrimer to construct precise molecular architecture with predetermined chemical composition. The site-isolation effect, through the encapsulation of active moieties by dendrons, or the cooperative effect, through the coherent interaction among the same or different kinds of active blocks in the dendrimer, can greatly enhance the performance of NLO materials. This paper provides a review of recent developments in dendrimers for NLO applications, such as electro-optics (E-O), photorefractive (PR) materials, second harmonic generation (SHG), and two-photon absorption (TPA).
Between explosive crystallization and amorphous regrowth: Inhomogeneous solidification upon pulsed-laser annealing of amorphous silicon (1987)

Si amorphized by Cu implantation has been irradiated by spatially uniform pulses of 7.5 ns duration from a frequency-doubled neodymium:yttrium aluminum garnet laser. After irradiation the samples were examined by cross-section transmission electron microscopy. A laterally random pattern of polycrystalline Si patches was found imbedded in amorphous material. At low-energy densities a considerable fraction of the regrown Si was polycrystalline. With increasing energy density the amount of polycrystalline Si decreased, both at the surface and in total. These results are discussed in terms of the time available for the nucleation of polycrystalline Si at a liquid-solid interface and the temperature profile in both the liquid and the solid material.
The Bacterial Enhancer-Dependent ς54(ςN) Transcription Factor (2000)

The initiation of transcription is a complex process involving many different steps. These steps are all potential control points for regulating gene expression, and many have been exploited by bacteria to give rise to sophisticated regulatory mechanisms that allow the cell to adapt to changing
Differential sensitivity of oligodendrocytes and motor neurons to reactive nitrogen species: implications for multiple sclerosis (2009)

Depending on its concentration, nitric oxide (NO) has beneficial or toxic effects. In pathological conditions, NO reacts with superoxide to form peroxynitrite, which nitrates proteins forming nitrotyrosine residues (3NY), leading to loss of protein function, perturbation of signal transduction, and cell death. 3NY immunoreactivity is present in many CNS diseases, particularly multiple sclerosis. Here, using the high flux NO donor, spermine-NONOate, we report that oligodendrocytes are resistant to NO, while motor neurons are NO sensitive. Motor neuron sensitivity correlates with the NO-dependent formation of 3NY, which is significantly more pronounced in motor neurons when compared with oligodendrocytes, suggesting peroxynitrite as the toxic molecule. The heme-metabolizing enzyme, heme-oxygenase-1 (HO1), is necessary for oligodendrocyte NO resistance, as demonstrated by loss of resistance after HO1 inhibition. Resistance is reinstated by peroxynitrite scavenging with uric acid further implicating peroxynitrite as responsible for NO sensitivity. Most importantly, differential sensitivity to NO is also present in cultures of primary oligodendrocytes and motor neurons. Finally, motor neurons cocultured with oligodendrocytes, or oligodendrocyte-conditioned media, become resistant to NO toxicity. Preliminary studies suggest oligodendrocytes release a soluble factor that protects motor neurons. Our findings challenge the current paradigm that oligodendrocytes are the exclusive target of multiple sclerosis pathology.
[Poxvirus vectors for gene transfer]. (1997)

A promising approach to cancer immunotherapy is immunization with modified tumor cells carrying cytokine or immunomodulatory genes. Cytokine genes (tumor necrosis factor-alpha, interleukin 2, interferon gamma) and costimulatory molecule, B7-1, were incorporated into canarypox virus, ALVAC, which does not replicate in infected mammalian cells, and highly attenuated vaccinia virus, NYVAC. We examined the effect of local cytokine production on the growth of the mouse prostate tumor, RM-1, and the mouse bladder tumor, MBT-2. The vectors expressed the high levels of cytokines and B7-1 and the tumor growth of infected cells was significantly inhibited. The mice immunized with irradiated MBT-2 cells infected with ALVAC-interleukin 2 were protected against the subsequent challenge of parental tumor cells. We conclude that poxvirus vectors are useful for gene delivery in immunotherapy studies because of their infection efficiency, their capability of high gene product expression, their safety, and their case of handling.
Acridine Orange Stain for Determining Intracellular Enteropathogens in HeLa Cells (1991)

Green-fluorescent intracellular enteropathogenic bacteria were observed after infected HeLa cell monolayers were stained with acridine orange and counterstained with crystal violet at least 3 h after infection.