gebhart/patrepeval huggingface dataset:
Increases in neutrophil counts by purified human urinary colony- stimulating factor in chronic neutropenia of childhood (1988)

Clinical effects of purified human urinary colony-stimulating factor (CSFHU) were studied in nine patients with chronic neutropenia of childhood who ranged in age from 1 to 18 years. The patients were given CSFHU at a dose of 6 x 10(6) U/m2/d for seven consecutive days, and their peripheral neutrophil counts were serially followed for 6 to 12 months. In addition, changes in bone marrow morphology and granulocyte- macrophage colony-forming cells (GM-CFUs) were studied. Transient increases in neutrophil counts occurred during the first 4 weeks in all patients except one. Repeated increases were seen in a cyclic fashion in five patients. Three of the patients recovered from the neutropenia after several cycles of fluctuation of neutrophil counts; the counts (per microliter) reached 5,880, 5,640, and 2,000 as compared with pretreatment levels (mean +/- 2 SD) of 80 +/- 164, 182 +/- 250, and 2 +/- 14, respectively. The percentage (mean +/- SE) of marrow neutrophilic cells increased from 30.4% +/- 7.0% to 34.9% +/- 6.9% (P less than .05) and the ratio of the later neutrophil precursors to the earlier ones from 1.02 +/- 0.27 to 1.42 +/- 0.36 (P less than .02) 2 weeks after CSFHU infusion. There were no changes in GM-CFU numbers. These results indicate that CSFHU can increase neutrophil counts by increasing the number and maturity of the marrow neutrophil precursors in some types of childhood chronic neutropenia.
Treatment with cisplatin and etoposide in patients with neuroendocrine tumors (2001)

The combination of cisplatin and etoposide can produce significant responses in patients with heavily pretreated and poorly differentiated/rapidly progressing neuroendocrine tumors. The toxicity is considerable, and nephrotoxicity is the dose limiting factor.
Lactosylated Poly(ethylene glycol)-siRNA Conjugate through Acid-Labile β-Thiopropionate Linkage to Construct pH-Sensitive Polyion Complex Micelles Achieving Enhanced Gene Silencing in Hepatoma Cells (2005)

The remarkably enhanced gene silencing in hepatoma cells was achieved by assembling lactosylated-PEG-siRNA conjugates bearing acid-labile beta-thiopropionate linkages into polyion complex (PIC) micelles through the mixing with poly(l-lysine). The PIC micelles with clustered lactose moieties on the periphery were successfully transported into hepatoma cells in a receptor-mediated manner, releasing hundreds of active siRNA molecules into the cellular interior responding to the pH decrease in the endosomal compartment. Eventually, almost 100 times enhancement in gene silencing activity compared to that of the free conjugate was achieved for the micelle system, facilitating the practical utility of siRNA therapeutics.
Critical issues for the growth of high-quality (Al,Ga)N/GaN and GaN/(In,Ga)N heterostructures on SiC(0001) by molecular-beam epitaxy (1999)

We identify and discuss the essential strategies for the growth of (Al,Ga)N/GaN and GaN/(In,Ga)N heterostructures on SiC(0001) by both plasma-assisted and reactive molecular-beam epitaxy. Substrate preparation, nucleation, and growth conditions are optimized for simultaneously satisfying the requirements of high structural, morphological, optical, and electrical quality. The results demonstrate that molecular-beam epitaxy is a competitive technique for the growth of group-III nitrides.
The DNA Damage Response Induces IFN (2011)

This study reveals a new complexity in the cellular response to DNA damage: activation of IFN signaling. The DNA damage response involves the rapid recruitment of repair enzymes and the activation of signal transducers that regulate cell-cycle checkpoints and cell survival. To understand the link between DNA damage and the innate cellular defense that occurs in response to many viral infections, we evaluated the effects of agents such as etoposide that promote dsDNA breaks. Treatment of human cells with etoposide led to the induction of IFN-stimulated genes and the IFN-α and IFN-λ genes. NF-κB, known to be activated in response to DNA damage, was shown to be a key regulator of this IFN gene induction. Expression of an NF-κB subunit, p65/RelA, was sufficient for induction of the human IFN-λ1 gene. In addition, NF-κB was required for the induction of IFN regulatory factor-1 and -7 that are able to stimulate expression of the IFN-α and IFN-λ genes. Cells that lack the NF-κB essential modulator lack the ability to induce the IFN genes following DNA damage. Breaks in DNA are generated during normal physiological processes of replication, transcription, and recombination, as well as by external genotoxic agents or infectious agents. The significant finding of IFN production as a stress response to DNA damage provides a new perspective on the role of IFN signaling.
Persistent personal names for globally connected mobile devices (2006)

The Unmanaged Internet Architecture (UIA) provides zero-configuration connectivity among mobile devices through personal names. Users assign personal names through an ad hoc device introduction process requiring no central allocation. Once assigned, names bind securely to the global identities of their target devices independent of network location. Each user manages one namespace, shared among all the user's devices and always available on each device. Users can also name other users to share resources with trusted acquaintances. Devices with naming relationships automatically arrange connectivity when possible, both in ad hoc networks and using global infrastructure when available. A UIA prototype demonstrates these capabilities using optimistic replication for name resolution and group management and a routing algorithm exploiting the user's social network for connectivity.
The lactic dehydrogenase of Propionibacterium pentosaceum (1960)

Research Article| April 01 1960 The lactic dehydrogenase of Propionibacterium pentosaceum R. Molinari; R. Molinari 1Department of Biochemistry, Faculty of Medicine of Ribeirão Prêto, University of São Paulo, Ribeirão Prêto, São Paulo, Brazil Search for other works by this author on: This Site PubMed Google Scholar F. J. S. Lara F. J. S. Lara 1Department of Biochemistry, Faculty of Medicine of Ribeirão Prêto, University of São Paulo, Ribeirão Prêto, São Paulo, Brazil Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1960) 75 (1): 57–65. https://doi.org/10.1042/bj0750057 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation R. Molinari, F. J. S. Lara; The lactic dehydrogenase of Propionibacterium pentosaceum. Biochem J 1 April 1960; 75 (1): 57–65. doi: https://doi.org/10.1042/bj0750057 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1960 CAMBRIDGE UNIVERSITY PRESS1960 Article PDF first page preview Close Modal You do not currently have access to this content.
New fadB homologous enzymes and their use in enhanced biosynthesis of medium‐chain‐length polyhydroxyalkanoates in fadB mutant Escherichia coli (2004)

Recombinant Escherichia coli harboring the medium-chain-length (MCL) polyhydroxyalkanoate (PHA) synthase gene has been shown to accumulate MCL-PHAs from fatty acids when FadB is inactive. However, the enzymes in fadB mutant E. coli responsible for channeling the beta-oxidation intermediates to PHA biosynthesis have not been fully elucidated. Only recently, two enzymes encoded by yfcX and maoC have been found to be partially responsible for this. In this study, we identified five new FadB homologous enzymes in E. coli: PaaG, PaaF, BhbD, SceH, and YdbU, by protein database search, and examined their roles in the biosynthesis of MCL-PHAs in an fadB mutant E. coli strain. Coexpression of each of these genes along with the Pseudomonas sp. 61-3 phaC2 gene did not allow synthesis of MCL-PHA from fatty acid in recombinant E. coli W3110, which has a fully functional beta-oxidation pathway, but allowed MCL-PHA accumulation in an fadB mutant E. coli WB101. In particular, coexpression of the paaG, paaF, and ydbU genes resulted in a MCL-PHA production up to 0.37, 0.25, and 0.33 g/L, respectively, from 2 g/L of sodium decanoate, which is more than twice higher than that obtained with E. coli WB101 expressing only the phaC2 gene (0.16 g/L). These results suggest that the newly found FadB homologous enzymes, or at least the paaG, paaF, and ydbU genes, are involved in MCL-PHA biosynthesis in an fadB mutant E. coli strain and can be employed for the enhanced production of MCL-PHA.
Demonstration of Nonpolar m-Plane InGaN/GaN Laser Diodes (2007)

The first nonpolar m-plane (1-100) nitride laser diodes (LDs) have been realized on low extended defect bulk m-plane GaN substrates. The LDs were grown by metal organic chemical vapor deposition (MOCVD) using conditions similar to that of c-plane device growth. Broad area lasers were fabricated and tested under pulsed conditions. Lasing was observed at duty cycles as high as 10%. These laser diodes had threshold current densities (Jth) as low as 7.5 kA/cm2. Stimulated emission was observed at 405.5 nm, with a spectral line-width of 1 nm.
Dasatinib as a Bone-Modifying Agent: Anabolic and Anti-Resorptive Effects (2012)

Low dasatinib concentrations show convergent bone anabolic and reduced bone resorption effects, which suggests its potential use for the treatment of bone diseases such as osteoporosis, osteolytic bone metastasis and myeloma bone disease.
Sequence-specific recognition, photocrosslinking and cleavage of the DNA double helix by an oligo-(α]-thymidylate covalently linked to an azidoproflavine derivative (1987)

A 3-azidoproflavine derivative was covalently linked to the 5'-end of an octathymidylate synthesized with the [alpha]-anomers of the nucleoside. Two target nucleic acids were used for this substituted oligo-[alpha]-thymidylate: a 27-mer single-stranded DNA fragment containing an octadeoxyadenylate sequence and a 27-mer duplex containing eight contiguous A.T base pairs with all adenines on the same strand. Upon visible light irradiation the octa-[alpha]-thymidylate was photocrosslinked to the single-stranded 27-mer. Chain breaks were induced at the crosslinked sites upon piperidine treatment. From the location of the cleavage sites on the 27-mer sequence it was concluded that a triple helix was formed by the azidoproflavine-substituted oligo-[alpha]-thymidylate with its complementary oligodeoxyadenylate sequence. When the 27-mer duplex was used as a substrate cleavage sites were observed on both strands after piperidine treatment of the irradiated sample. They were located at well defined positions which indicated that the octathymidylate was bound to the (dA)8.(dT)8 sequence in parallel orientation with respect to the (dA)8-containing strand. Specific binding of the [alpha]-octathymidylate involved local triple strand formation with the duplex (dA)8.(dT)8 sequence. This result shows that it is possible to synthesize sequence-specific molecules which specifically bind oligopurine-oligopyrimidine sequences in double-stranded DNA via recognition of the major groove hydrogen bonding sites of the purines.
The inhibition of tissue type plasminogen activator by plasminogen activator inhibitor-1. The effects of fibrinogen, heparin, vitronectin, and lipoprotein(a). (1991)

Plasminogen activator inhibitor-1 (PAI-1) regulates fibrinolysis by inhibiting tissue type plasminogen activator (t-PA). Fibrinogen, heparin, and vitronectin enhance the rate of inhibition of t-PA by PAI-1. Kinetic studies indicate that both fibrinogen and heparin increase the second-order inhibition constant by a maximum of approximately 4-fold, whereas vitronectin increases the rate constant by a maximum of approximately 6-fold. The dissociation constants of fibrinogen, heparin, and vitronectin for the inhibition reaction were 200 nM, 20 nM, and 600 pM, respectively. In addition, PAI-1 inhibition of t-PA may be regulated by the presence of lipoprotein(a) (Lp(a)). Previous studies demonstrated that Lp(a) competes with plasminogen for the active site of fibrinogen- and heparin-bound t-PA. Kinetic studies described here demonstrate that Lp(a) prevents the inhibition of t-PA by PAI-1 in the presence of fibrinogen and heparin, but has no effect on the reaction in the presence of vitronectin or in the absence of either fibrinogen or heparin. The data suggest that fibrinogen and heparin may enhance the rate of inhibition through an interaction with t-PA, and that vitronectin may enhance the inhibition through an interaction with PAI-1. In addition, these experiments indicate that Lp(a) may regulate fibrinolysis by competing with PAI-1 and plasminogen for fibrinogen- and heparin-bound t-PA. These data suggest that PAI-1 inhibition of t-PA in vivo is primarily mediated via interaction with fibrinogen, heparin, vitronectin, and Lp(a), and therefore, the functional levels of PAI-1 activity in the vasculature may be regulated by the presence of these components.
Cerebral hypoxia: some new approaches and unanswered questions (1990)

The apoplexy of Hippocrates’ time remains with us today, unchanged and untreated. We call this syndrome of acute brain damage “stroke”; we know that it most commonly reflects localized tissue hypoxia attributable to reduced blood flow (ischemia). Focal hypoxia-ischemia also occurs in such contexts as traumatic insults, or cerebral hemorrhages, while global hypoxia-ischemia occurs in cardiac arrest, near-drowning, and carbon monoxide poisoning. The centuries since Thomas Willis, Johann Wepfer, and Giovanni Morgagni have brought precise definition of cerebral vascular anatomy and the neurological consequences of focal brain lesions, permitting full comprehension of functional deficits; we can prognosticate with sad accuracy. But the medical management of stroke patients in 1990 is still the management of symptoms and associated conditions. Despite its status as a major worldwide cause of death and disability, we are no more able than Hippocrates to treat cerebral hypoxia itself. Nevertheless, hope for the development of effective therapy has endured, and in the last few years has been encouraged by the emergence of some promising strategies for reducing the brain’s intrinsic susceptibility to hypoxic insults. These tissuelevel approaches, sometimes referred to as “parenchymal” approaches to distinguish them from other strategies aimed at influencing blood how, are based on recent information suggesting that central neurotransmitter mechanisms, especially those related to the excitatory neurotransmitter glutamate, may play an important role in the pathogenesis of hypoxic neuronal death (Meldrum, 1985; Rothman and Olney, 1986; Choi, 1988b). In this essay I will comment on the possibility of new therapies for cerebral hypoxia directed at glutamate-mediated injury mechanisms, and will briefly mention some other potential approaches. Glutamate and hypoxic neuronal injury The brain is critically dependent on its blood flow for a continuous supply of oxygen and glucose. The oscillations of the electroencephalogram cease within seconds of cardiac arrest, and only a few minutes of severe ischemia can induce the selective degeneration of certain neuronal populations, including pyramidal neurons in the CA1 region of the hippocampal formation, striatal medium-sized neurons, neocortical neurons in layers 3,
Real-time shaded NC milling display (1986)

The real-time shaded display of a solid model being milled by a cutting tool following an NC path is attained by the image-space Boolean subtraction of solid objects. The technique is suitable for implementation in microcode in a raster graphic display processor. Update rates of 10 cutting operations per second are typical.
Automated three‐dimensional registration of magnetic resonance and positron emission tomography brain images by multiresolution optimization of voxel similarity measures (1997)

Approaches using measures of voxel intensity similarity are showing promise in fully automating magnetic resonance (MR) and positron emission tomography (PET) image registration in the head, without requiring extraction and identification of corresponding structures. In this paper a method of multiresolution optimization of these measures is described and five alternative measures are compared: cross correlation, minimization of corresponding PET intensity variation, moments of the distribution of values in the intensity feature space, entropy of the intensity feature space and mutual information. Their ability to recover registration is examined for ten clinically acquired image pairs with respect to the size of initial misregistration, the precision of the final result, and the accuracy assessed by visual inspection. The mutual information measure proved the most robust to initial starting estimate, successfully registering 98.8% of 900 trial misregistrations. Success is defined as providing a visually acceptable solution to a trained observer. A high resolution search (1/16 mm step size) of 30 trial misregistrations showed that optimization using the mutual information measure provided solutions with 0.13 mm, 0.11 mm and 0.17 mm standard deviations in the three Cartesian axes of the translation vector and 0.2 degree, 0.3 degree and 0.2 degree standard deviations for rotations about the three axes. The algorithm takes between 4 and 8 minutes to run on a typical workstation, including visual inspection of the result.
Hybrid Cell Line from a Cloned Immunoglobulin-Producing Mouse Myeloma and a Nonproducing Mouse Lymphoma (1971)

A hybrid cell line was established by cell fusion between a cloned Balbic myeloma that is resistant to 8-azaguanine and produces immunoglobulin (gammaG and free kappa chain) and C57BL/6N lymphoma that is resistant to bromo-deoxyuridine and does not produce immunoglobulins. The hybrid cells contained the membrane antigens of both parents; they synthesized free kappa chain; no synthesis of gammaG (gamma(2a)) heavy chain was detected.
Observing middle and inner ear mechanics with novel intracochlear pressure sensors (1998)

Intracochlear pressure was measured in vivo in the base of the gerbil cochlea. The measurements were made over a wide range of frequencies simultaneously in scalae vestibuli and tympani. Pressure was measured just adjacent to the stapes in scala vestibuli and at a number of positions spaced by tens of micrometers, including a position within several micrometers of the basilar membrane, in scala tympani. Two findings emerged from the basic results. First, the spatial variation in scala tympani pressure indicated that the pressure is composed of two modes, which can be identified with fast and slow waves. Second, at frequencies between 2 and 46 kHz (the upper frequency limit of the measurements) the scala vestibuli pressure adjacent to the stapes had a gain of approximately 30 dB with respect to the pressure in the ear canal, and a phase which decreased linearly with frequency. Thus, over these frequencies the middle ear and its termination in the cochlea operate as a frequency independent transmission line. A subset of the data was analyzed further to derive the velocity of the basilar membrane, the pressure difference across the organ of Corti complex (defined to include the tectorial and basilar membranes) and the specific acoustic impedance of the organ of Corti complex. The impedance was found to be tuned in frequency.
Immunogenic Properties of Structurally Modified Human Tissue Plasminogen Activators in Chimpanzees and Mice (1992)

Immunogenic properties of second generation human tissue plasminogen activator (tPA) derivatives were examined in chimpanzee and mouse systems. Five species of modified tPAs (mtPAs) (designated 2660, 2663, 2810, 8000, and 9200), recombinant native tPA or bovine serum albumin (BSA) as a positive control were subcutaneously injected nine times at suitable intervals into chimpanzees, genetically the closest species to man. These animals were tested for antigen(Ag)-specific antibodies to the corresponding proteins by means of enzyme-linked immunosorbent assay and Western blot analysis. Neither 9200, one of the five mtPAs tested, nor tPA was immunogenic, although BSA and the other four mtPAs were immunogenic under these conditions. Thus, an antigenic deter minant was not exposed by the modification on 9200 and this modified tPA is expected not to be immunogenic in humans. In the mouse studies, mice were immunized with mtPAs. Serum sam-pies from these animals were tested for antibodies to the mtPAs which did not concomitantly recognize native tPA by immune ad sorption of the antibodies to tPA. The amount of such antibodies alter the elimination of native tPA-reactive antibodies was little or none when the serum samples from 9200 and from the other mtPAs, except 8000, were tested. Taking into consideration the results of the chimpanzee studies, it can be concluded that Ag-specific antibodies are dominantly produced to unchanged epitopes present in modified proteins in the mouse system, in which the native protein is immunogenic. These results suggest that the chimpanzee model should be useful to predict immunogenicity of second generation recombinant proteins in man, while the mouse system adopted by us, which determines the newly generated epitopes of the modified proteins, is not sufficient.
Defective TCR expression in transgenic mice constructed using cDNA‐based α‐ and β‐chain genes under the control of heterologous regulatory elements (1998)

We describe the generation of ovalbumin (OVA)-specific, MHC class II-restricted alpha beta T cell receptor (TCR) transgenic mice. Initial attempts at generating these transgenic mice utilized heterologous regulatory elements to drive the expression of cDNA genes encoding the separate alpha- and beta-chains of the TCR. Unexpectedly, T cells bearing the transgenic alpha beta TCR failed to emerge from the thymus in these mice, although the transgenes did modify endogenous TCR expression. However, subsequent modification of the approach which enabled expression of the TCR beta-chain under the control of its natural regulatory elements generated mice whose peripheral T cells expressed the transgenic TCR and were capable of antigen-dependent proliferation. These results show that successful generation of MHC class II-restricted, OVA-specific alpha beta TCR transgenic mice was dependent upon combining cDNA- and genomic DNA-based constructs for expression of the respective alpha- and beta-chains of the TCR.
Battery Powered BION FES Network (2005)

The Alfred Mann Foundation is completing development of a coordinated network of BION microstimulator/sensor (hereinafter implant) that has broad stimulating, sensing and communication capabilities. The network consists of a master control unit (MCU) in communication with a group of BION implants. Each implant is powered by a custom lithium-ion rechargeable 10 mW-hr battery. The charging, discharging, safety, stimulating, sensing, and communication circuits are designed to be highly efficient to minimize energy use and maximize battery life and time between charges. The stimulator can be programmed to deliver pulses in any value in the following range: 5 microA to 20 mA in 3.3% constant current steps, 7 micros to 2000 micros in 7 micros pulse width steps, and 1 to 4000 Hz in frequency. The preamp voltage sensor covers the range 10 microV to 1.0 V with bandpass filtering and several forms of data analysis. The implant also contains sensors that can read out pressure, temperature, DC magnetic field, and distance (via a low frequency magnetic field) up to 20 cm between any two BION implants. The MCU contains a microprocessor, user interface, two-way communication system, and a rechargeable battery. The MCU can command and interrogate in excess of 800 BlON implants every 10 ms, i.e., 100 times a second.