gebhart/patrepeval huggingface dataset:
Structure and biosynthesis of surface polymers containing polysialic acid in Escherichia coli. (1980)

Membranous sialyltransferase complexes from Escherichia coli K-235 catalyze the synthesis of surface polymers containing alpha-2,8-ketosidically linked polysialic acid. Undecaprenyl phosphate functions as an intermediate carrier of sialic acid (NeuNAc) residues between cytidine 5'-monophospho-N-acetylneuraminic acid (CMP-NeuNAc) and an endogenous acceptor (Troy, F.A., and McCloskey, M.A. (1979) J. Biol. Chem 254, 7377-7387). In vitro pulse-chase experiments now confirm that polymer elongation occurs by the addition of sialyl residues to the nonreducing termini of growing nascent chains. Sequential periodate oxidation and borohydride reduction of radiolabeled polysialic acid was used to quantitatively convert the terminal, nonreducing sialic acid to the 7-carbon analogue, 5-acetamido-3,5-dideoxy-L-arabino-2-heptulosonic acid (NeuNAc7). After complete hydrolysis of the polymers by neuraminidase, the ratio between NeuNAc and NeuNAc7 was used to determine the average degree of polymerization (D.P.). The membrane preparations used as a source of enzyme contained endogenous sialyl polymers that averaged 165 residues in length. During the first phase of in vitro synthesis, lasting about 90 min, 40 to 45 sialyl residues were transferred onto these endogenous acceptors. Subsequent in vitro incorporation increased at a slower, constant rate for at least 16 h. During this second phase of synthesis, the D.P. of newly synthesized chains remained relatively constant while the number of nonreducing terminal end groups, a measure of the number of new sialyl chains, increased. These results establish that individual polymer chains are rapidly elongated in vitro to a defined length of about 200 sialyl residues, then terminated and new chains started. The mechanism signaling chain termination, translocation of the sialyltransferase to a new acceptor, and chain reinitiation remains to be determined. Endogenous and enzymatically synthesized sialyl polymers were solubilized with Triton X-100 and purified to apparent homogeneity. Sialic acid accounted for approximately 93% of the mass of these polymers which had no free reducing terminal sialic acid. This position of the molecule is presumably occupied by an as yet unidentified component which links the sialyl polymer to the membrane.
A high-frequency RFLP at the human TFE3 locus on the X chromosome (1991)

Source and Description of Clone: A single copy, human genomic 2.0 kb HindlE fragment, cloned from the chromosome 13 specific library of Lalande
Charge Multiplexing Readout for Position Sensitive Avalanche Photodiodes (2006)

A technique to charge-multiplex multiple position sensitive avalanche photodiodes (PSAPD) has been studied. We have observed that with multiplexing, the spatial resolution is slightly degraded, but the energy and time resolution are not affected. We are building high resolution PET systems that use numerous PSAPDs, and we would like to use multiplexing to reduce the number of electronic readout channels and complexity. This charge multiplexing technique will reduce the number of readout channels required by a factor of two. A PSAPD is a new silicon semiconductor photodetector that may be used to replace a photomultiplier tube in PET or SPECT systems. It is a planar avalanche photodiode with a resistive coating that allows continuous positioning over the entire active area. The resistive sheet of the PSAPD splits the charge signal amplified by an avalanche process of the diode into four spatial channels. The top contact contains the hole signal which is equal in magnitude to the sum of the 4 spatial channels. The PSAPD can be multiplexed in a way that sums the spatial channels but leaves the top channel independent. PSAPDs are currently fabricated with active areas that range from 8times8 mm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> and higher. The proposed PET system detectors comprise 1 mm lutetium oxyorthosilicate (LSO) crystals coupled to extra thin PSAPDs. Non-multiplexed, these detectors have achieved excellent spatial resolution (<1 mm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> ), energy resolution (<10%), and time resolution (<2 ns). Unlike a position-sensitive PMT, the electronic amplification of a PSAPD is only on the order of 1000, which makes it challenging to charge multiplex multiple devices
LATEXIN’S ROLE IN REGULATING HEMATOPOIETIC STEM AND PROGENITOR CELLS (2013)

Previous studies in our lab identified a novel gene, latexin (Lxn), that regulates murine hematopoietic stem cells through balancing apoptosis, self-renewal and proliferation. In these dissertation studies, I performed a series of experiments to examine the function of Lxn using a Lxn conventional knockout mouse, and characterize Lxn’s role in the presence of hematopoietic stresses such as ionizing radiation, cytokines induced-mobilization, and hematopoietic malignancy. The first series of experiments was designed to determine the role of Lxn in hematopoiesis under homeostatic conditions. I found that Lxn-/- mice exhibited hyperproliferative hematopoiesis, a repopulation advantage and elevated self-renewal capacity which was intrinsic to the Lxn-/- hematopoietic cells. Furthermore, I identified a reduction in apoptotic frequency in Lxn-/- hematopoietic progenitors, which may account for the expansion seen in the progenitor population. In a second series of experiments, I discovered a role of Lxn in the radio-sensitivity of hematopoietic cells. I found that loss of Lxn in mice confers resistance to ionizing radiation. Lxn-/- mice showed rapid hematological recoveries after radiation exposure at the stem and progenitor cell (HSPC) level. The ablation of Lxn hindered irradiation-induced apoptosis which may underlie the radiation resistance through regulating hematopoietic recovery. In a third series of experiments, I studied the interaction of Lxn-/- stem and progenitor cells with their microenvironment. Using a granulocyte colony-stimulating factor-induced mobilization model, I determined that the ability of HSPCs to mobilize into the bloodstream was significantly increased in Lxn-/- mice. The adhesive properties of hematopoietic cells were compromised in Lxn-/- animals. Gene expression studies on progenitor cells identified cell-to-ECM interactions were down-regulated upon Lxn deletion, implying the enhanced mobilization efficiency of hematopoietic cells from Lxn-/- mice correlated with reduced adhesion of hematopoietic progenitor cells to stroma. Last, but not least, I performed a series of experiments to study the putative tumor suppressor role of Lxn in hematological malignancy. I found that Lxn expression was down-regulated in primary tumor and tumor cell lines by promoter methylation. Overexpression of Lxn inhibited lymphoma cell growth both in vitro and in vivo. Overexpressed Lxn increased apoptosis frequency by suppressing the expression of several anti-apoptotic genes, and therefore reduced the tumor growth.
Identification of X-linked Inhibitor of Apoptosis-associated Factor-1 as an Interferon-stimulated Gene That Augments TRAIL Apo2L-induced Apoptosis (2002)

In the course of gene array studies aimed at identifying IFN-stimulated genes associated with interferon beta (IFN-beta)-induced apoptosis, we identified X-linked inhibitor of apoptosis-associated factor-1 (XAF1) as a novel IFN-stimulated gene. XAF1 mRNA was up-regulated by IFN-alpha and IFN-beta in all cells examined. However, IFNs induced high levels of XAF1 protein predominantly in cell lines sensitive to the proapoptotic effects of IFN-beta. In apoptosis-resistant cells including WM164 melanoma, WM35 melanoma, U937 pro-monocytic leukemia, and HT1080 fibrosarcoma cells, XAF1 mRNA was strongly up-regulated but XAF1 protein was up-regulated only weakly or not at all. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a critical mediator of IFN-beta-induced apoptosis, but most melanoma cell lines were resistant to recombinant TRAIL protein. For example, A375 melanoma cells were defective in TRAIL induction by IFN-beta and were resistant to TRAIL-induced apoptosis. However, IFN-beta pretreatment sensitized them to subsequent recombinant TRAIL-induced apoptosis. A375 cells expressing XAF1 constitutively were more sensitive to TRAIL-induced apoptosis compared with empty vector-transfected cells. The degree of sensitization by XAF1 was similar to that provided by IFN pretreatment and was correlated with the level of XAF1 expressed. Furthermore, the overexpression of the zinc-finger portion of XAF1 blocked IFN-dependent sensitization of A375 melanoma cells to the proapoptotic effects of TRAIL. These results suggested that IFN-dependent induction of XAF1 strongly influenced cellular sensitivity to the proapoptotic actions of TRAIL.
Drooling in Parkinson's disease is a motor disorder (2009)

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Permeability of Blast‐Furnace Refractories (1959)

The permeability of refractories is a governing factor in the deterioration of blast‐furnace linings by liquids and gases. Permeability tests there fore were performed on 17 carbon, 11 mullite, 85 castable, and 7 super‐duty and 11 high‐duty fire‐clay brands. The rate of gas flow was measured through a 2‐in. cube in three directions by using an improved laboratory permeameter. The range and mean of permeability in centidarcys for each class of refractory were as follows: carbon, 0.3 to 42 (20); mullite, 7 to 158 (48); castable, 0.2 to 43 (4.5); super‐duty fire‐clay, 28 to 207 (76); and high‐duty fire‐clay, 33 to 147 (72). The permeability of the different axes of the brick usually varied widely, with the face axis usually exhibiting the lowest values. The improved permeameter should prove to be especially valuable for determining resistance to gas flow and for controlling the quality of refractories.
Silk protein, sericin, suppresses DMBA-TPA-induced mouse skin tumorigenesis by reducing oxidative stress, inflammatory responses and endogenous tumor promoter TNF-alpha. (2003)

This study was conducted to assess protective effect of an antioxidant protein, sericin, on tumor promotion in the 7,12-dimethylbenz (alpha) anthracene (DMBA)-initiated and 12-O-tetradecanoylphorbol 13-acetate (TPA)-promoted mouse skin tumorigenesis model. In experiment 1, sericin was applied topically to DMBA-initiated female ICR mouse skin at the doses of 2.5 and 5 mg twice per week for 16 weeks, 30 min prior to each promotion treatment with TPA. The protective effect of sericin was evident in terms of significant reduction in tumor incidence and tumor multiplicity at the doses of 2.5 and 5 mg per application, compared to the control group without receiving sericin. The expression of tumor necrosis factor (TNF)-alpha protein and the level of 4-hydroxynonenal (4-HNE) in normal epidermis were significantly reduced in both sericin treatment groups. In experiment 2, sericin at the dose of 5 mg was applied topically to the dorsal mouse skin 30 min before application of a TPA, and the same doses of TPA and sericin were applied twice at an interval of 24 h. Sericin treatment inhibited double TPA treatment-induced morphological changes reflecting inflammatory response, including leukocyte infiltration, hyperplasia and cell proliferation. Furthermore, sericin treatment significantly suppressed the elevation in 4-HNE level and elevated expressions of c-fos, c-myc and cyclooxygenase-2 (COX-2) in normal epidermis induced by double application of TPA. The results suggest that sericin possesses protective effect against tumor promotion in mouse skin by suppressing oxidative stress, inflammatory responses and TNF-alpha.
Myocardial dysfunction in the patient with sepsis (2002)

The nature of myocardial dysfunction during sepsis and septic shock has been investigated for more than half a century. This review traces the evolution of scientific thought regarding this phenomenon during this period with particular emphasis on the current understanding of both the clinical manifestations and the molecular/cellular basis of septic myocardial dysfunction in critically ill patients. Current data suggest, contrary to older literature, that patients with septic shock develop a hyperdynamic circulatory state after fluid resuscitation and maintain this hyperdynamic circulatory state until death or recovery. Overt myocardial depression, as manifested by decreased cardiac output, is decidedly uncommon, even in the preterminal phase. Nonetheless, myocardial depression, as evidenced by biventricular dilation and depression of the ejection fraction, can be demonstrated in most patients with septic shock by using either radionuclide cineangiography or echocardiography. Depression is reversible over the course of 7 to 10 days in survivors. Available evidence suggests that myocardial hypoperfusion is not responsible for septic myocardial depression, because examination of humans with septic shock demonstrates increased myocardial perfusion, and animal models of septic shock appear to maintain myocardial high-energy phosphates. A circulating factor or factors, including the cytokines tumor necrosis factor alpha and interleukin-1beta, appear to have a significant role in the phenomenon. In addition, septic myocardial depression appears to be mediated in part through combinations of nitric oxide-dependent and -independent alterations of basal and catecholamine-stimulated cardiac myocyte contractility.
Continuous Spinning of a Single-Walled Carbon Nanotube−Nylon Composite Fiber (2005)

We report a chemical processing technology that allows the continuous spinning of single-walled carbon nanotubes (SWNTs)-nylon 6 (PA6) fibers by the in-situ polymerization of caprolactam in the presence of SWNTs, which simultaneously optimizes the morphology of the composite. We show that caprolactam is an excellent solvent for carboxylic-acid-functionalized SWNTs (SWNT-COOH) and that this allows the efficient dispersal of the SWNTs and subsequent grafting of PA6 chains to the SWNTs through condensation reactions between the carboxylic-acid group on SWNT-COOH and the terminal amine group of PA6. The existence of a graft copolymer between the PA6 chains and the SWNTs is demonstrated by IR, TGA, and AFM studies, and we show that the solubility of the polymerized material in formic acid is controlled by the degree of graft copolymerization. The amount of grafted PA6 chains that are attached to the SWNTs can be adjusted by controlling the concentration of the initiator (6-aminocaproic acid). The process leads to a uniform dispersion of the SWNTs, and the presence of the graft copolymer increases the polymer/SWNT compatibility while strengthening the interfacial interaction between the nanotube and matrix. The Young's modulus, tensile strength, and thermal stability of the SWNT-reinforced composite fibers produced by this process are significantly improved.
Airway anaesthesia and the cough reflex. (1987)

Topically and intravenously administered local anaesthetic agents are widely used to inhibit cough, but little quantitative, pharmacological data seems to be available. Various aspects of local anaesthetic agents as inhibitors of cough and other airway reflexes are discussed. Nebulized lidocaine dose-dependently inhibited both mechanically (trachea, carina) and ammonia vapour-induced cough. Lidocaine had a similar potency on each type of cough but inhibited that caused by mechanical stimulation for a significantly longer period of time. This observation supports the hypothesis of a more peripheral location for receptors mediating chemical cough. Nebulized tetracaine appeared to be more potent and to have a significantly longer duration of action than lidocaine. The Hering-Breuer inflation reflex was attenuated by both agents and in doses larger than those needed to inhibit cough. This observation is compatible with the view that the cough receptors are located close to the airway lumen and those mediating the Hering-Breuer reflex within the smooth muscle. Airway anaesthesia is commonly used to block the cough reflex during endoscopic procedures. Nebulized lidocaine has been reported also to suppress severe chronic cough but further studies on airway anaesthesia and cough in acute and chronic lung disease are warranted.
Atypical Mycobacterial Infection in the Pig-Tailed Macaque (Macaca nemestrina) (1970)

SUMMARY Mycobacterium tuberculosis of the group 3 avian type was isolated from a colony of macaques. The infection was not clinically observed and gross pathologic lesions were not distinguished in animals euthanatized and necropsied because of a positive tuberculin test. Acid-fast bacilli were cultured from lymph nodes of the pleural and peritoneal cavities.
Hematopoietic progenitor kinase 1 (HPK1) influences regulatory T cell functions (163.26) (2012)

Abstract HPK1 is a negative regulator of TCR-initiated signal transduction. HPK1-/- mice are more susceptible to experimental autoimmune encephalomyelitis, suggesting that the ability to enforce peripheral tolerance may have been compromised. Paradoxically, we observed that more natural regulatory T cells were found in the periphery of HPK1-/- mice than in wild type C57BL/6. We determined whether HPK1-/- Foxp3+ Tregs retained their ability to suppress TCR-induced effector T cell proliferation and found that they lack the ability to suppress. Because the ability to suppress T cell proliferation is a function conferred to Tregs by Foxp3-dependent suppression of IL-2 transcription, we assessed whether HPK1-/- Foxp3+ Tregs retain the ability to repress TCR-induced IL-2 production. We found that HPK1-/- Tregs produce a significant amount of IL-2 in response to TCR engagement, suggesting that Foxp3 is unable to carry out transcriptional repression. This aberrant phenotype implicates HPK1 as an important regulator of Treg functions.
A unified approach to bad pixel removal and adaptive CFA demosaicking (2012)

The fabrication process for today's digital cameras will inevitably produce some defective pixels in those mega-pixel image sensors. In the manufacturing process, these defective pixels, known as bad pixels, will normally be mapped out. However, more bad pixels could appear over time with camera usage, and some would only appear on a long exposure and/or at high ISO settings. It is therefore not desirable to permanently map out those bad pixels as they can still function at normal settings. As those bad pixels will interfere with the demosaicking process, in this paper, we propose an adaptive method to avoid inclusion of those bad pixels in the interpolation process. This is achieved by adaptively varying the order of interpolation so that the length of interpolation is shorter if a bad pixel is located closer to the pixel being interpolated. The bad pixels are located by using a median-based multi-shell filter structure. It has been shown that our proposed method outperforms other existing bad pixel correction techniques.
Electrical properties of pn junctions formed by plasma enhanced epitaxial growth (2002)

Properly functioning pn junction diodes have been fabricated by a low temperature plasma enhanced chemical vapor deposition (PECVD) technique. The diodes were constructed such that the metallurgical junction was coincident with the starting substrate surface. The electrical quality of the diodes was quantified by measuring their reverse bias leakage current. Contrary to popular opinion, it has been shown that the PECVD process is inherently capable of producing device quality material, and rather it is the in situ plasma cleaning technique typically associated with this method that is the cause of poor electrical performance. The chemical and physical nature of defects caused by the plasma cleaning step have been investigated by various experimental techniques including photoluminescence, secondary ion mass spectroscopy, and atomic force microscopy. The plasma cleaning step has been linked in certain cases to the production of a photoluminescence signal in Czochralski grown Si wafers. Results show that the plasma clean is neither required nor desired in the low temperature growth of device quality epitaxial Si thin films.
Electrospun Bioresorbable Heart Valve Scaffold for Tissue Engineering (2008)

Currently marketed mechanical or biological prosthetic heart valves are regarded as valid substitutes for native heart valves suffering from degenerative pathologies. These devices require strict follow-up due to dysfunctions or post-surgical complications. Potential drawbacks of these medical devices are calcification, tearing of the cusps, thromboembolism and hemolysis. In this context, a tissue engineering approach offers a promising alternative scenario. In this paper, a trileaflet poly(epsilon-caprolactone) (PCL) heart valve scaffold prototype has been manufactured by electrospinning technique using a custom-made rotating target. Process parameters were selected in order to achieve suitable microstructure and mechanical performance. The electrospun heart valve prototype was functionally characterized by means of a pulse duplicator in order to evaluate the mechanical/hydraulic response to the imposed testing conditions. Leaflets synchronously opened in the ejection phase and the proper apposition of the leaflets prevented high leakage volumes in the diastolic phase. This preliminary study suggests a successful perspective for the proposed approach in designing a novel tissue engineered bioresorbable heart valve.
Kinome expression profiling to target new therapeutic avenues in multiple myeloma (2019)

Multiple myeloma (MM) account for approximately 10% of hematological malignancies and is the second most common hematological disorder. Kinases inhibitors are widely used and their efficiency for the treatment of cancers has been demonstrated. Here, in order to identify kinases of potential therapeutic interest for the treatment of MM, we investigated the prognostic impact of the kinome expression profile in large cohorts of patients. We identified 36 kinome-related genes significantly linked with a prognostic value to MM, and built a kinome index based on their expression. The Kinome Index (KI) is linked to prognosis, proliferation, differentiation, and relapse in MM. We then tested inhibitors targeting seven of the identified protein kinas-es (PBK, SRPK1, CDC7-DBF4, MELK, CHK1, PLK4, MPS1/TTK) in human myeloma cell lines. All tested inhibitors significantly reduced the viability of myeloma cell lines, and we confirmed the potential clinical interest of three of them on primary myeloma cells from patients. In addition, we demonstrated their ability to potentialize the toxicity of conventional treatments, including Melphalan and Lenalidomide. This highlights their potential beneficial effect in myeloma therapy. Three kinases inhibitors (CHK1i, MELKi and PBKi) overcome resistance to Lenalidomide, while CHK1, PBK and DBF4 inhibitors re-sensitize Melphalan resistant cell line to this conventional therapeutic agent. Altogether, we demonstrate that kinase inhibitors could be of therapeutic interest especially in high-risk myeloma patients defined by the KI. CHEK1, MELK, PLK4, SRPK1, CDC7-DBF4, MPS1/TTK and PBK inhibitors could represent new treatment options either alone or in combination with Melphalan or IMiD for refractory/relapsing myeloma patients.