gebhart/patrepeval huggingface dataset:
Molecular Cloning of the Full-length cDNA of (S)-Hydroxynitrile Lyase from Hevea brasiliensis (1996)

The full-length cDNA of (S)-hydroxynitrile lyase (Hnl) from leaves of Hevea brasiliensis (tropical rubber tree) was cloned by an immunoscreening and sequenced. Hnl from H. brasiliensis is involved in the biodegradation of cyanogenic glycosides and also catalyzes the stereospecific synthesis of aliphatic, aromatic, and heterocyclic cyanohydrins, which are important as precursors for pharmaceutical compounds. The open reading frame identified in a 1. 1-kilobase cDNA fragment codes for a protein of 257 amino acids with a predicted molecular mass of 29.2 kDa. The derived protein sequence is closely related to the (S)-hydroxynitrile lyase from Manihot esculenta (Cassava) and also shows significant homology to two proteins of Oryza sativa with as yet unknown enzymatic function. The H. brasiliensis protein was expressed in Escherichia coli and Saccharomyces cerevisiae and isolated in an active form from the respective soluble fractions. Replacement of cysteine 81 by serine drastically reduced activity of the heterologous enzyme, suggesting a role for this amino acid residue in the catalytic action of Hnl.
Protective effects of liposome‐entrapped superoxide dismutase on posttraumatic brain edema (1987)

Oxygen-derived free radicals and membrane lipid peroxidation have been postulated to be involved in brain edema and cell death, secondary to ischemia and traumatic injury. Using a model of brain edema induced by cold-induced injury, we have demonstrated an early elevation of superoxide radicals followed by permeability changes in the blood-brain barrier and development of edema in injured brain. Intravenous injection of liposome-entrapped copper-zinc-superoxide dismutase 5 minutes before the injury-enhanced entry of the enzyme into endothelial cells of the blood-brain barrier of injured brain reduced the brain level of superoxide radicals and ameliorated blood-brain barrier permeability changes and brain edema. Identical treatment 5 minutes after injury was also effective. These data demonstrate that superoxide radicals play an important role in the delayed development of vasogenic brain edema following brain injury.
Activation of the SH2-containing phosphotyrosine phosphatase SH-PTP2 by its binding site, phosphotyrosine 1009, on the human platelet-derived growth factor receptor. (1993)

Much progress has been made in elucidating early events in signal transduction by growth factor receptors with intrinsic tyrosine kinase activity. Upon ligand addition, these receptors dimerize and activate, becoming phosphorylated at a number of tyrosyl residues. These phosphorylation sites serve as docking points for proteins containing src homology-2 (SH2) domains. However, little is known about how phosphotyrosine phosphatases (PTPs), participate in these events. Recently, we and others molecularly cloned a ubiquitously expressed SH2 domain-containing PTP, SH-PTP2 (Syp, PTP1D, PTP2C), and found that it interacts directly with several activated growth factor receptors via its SH2 domains. Using a peptide competition assay, we now demonstrate that the major binding site for SH-PTP2 on the platelet-derived growth factor receptor is phosphotyrosine 1009. Immunoprecipitation studies indicate that SH-PTP2 is the previously unidentified "64-kDa" protein known to bind at this site. Addition of a phosphotyrosyl peptide comprising the region around Tyr-1009 stimulates SH-PTP2 activity 5-10-fold, whereas other phosphotyrosyl peptides from the platelet-derived growth factor receptor have no stimulatory effect. Our data suggest that binding of SH-PTP2 to the activated receptor in vivo should result in stimulation of SH-PTP2 activity.
<title>Low-density plasmas below the optical breakdown threshold: potential hazard for multiphoton microscopy, and a tool for the manipulation of intracellular events</title> (2002)

Irradiance values employed in multiphoton microscopy are only one order of magnitude below the irradiance threshold for femtosecond optical breakdown in aqueous media (approximately equals 1.0 x 10<SUP>13</SUP> W cm<SUP>-2</SUP>). At the breakdown threshold, a plasma with a free electron density of about 10<SUP>21</SUP> cm<SUP>-3</SUP> is generated, and the energy density in the breakdown region is sufficiently high to cause the formation of a bubble at the laser focus. We found previously that plasmas with a free electron density &lt;10<SUP>21</SUP> cm<SUP>-3</SUP> are formed also in a fairly large irradiance range below the breakdown threshold. The present study investigates the chemical, thermal, and thermomechanical effects produced by these low-density plasmas, and their consequences for multiphoton microscopy. We use a rate equation model considering multiphoton ionization and avalanche ionization to numerically simulate the plasma formation. The value of the plasma energy density created by each laser pulse is then used to calculate the temperature distribution in the focal region. The results of the temperature calculations yield, finally, the starting point for calculations of the thermoelastic stresses that are generated during the formation of the low-density plasmas. We found that with femtosecond pulses a large 'tuning range' exists for the creation of spatially extremely confined chemical, thermal and mechanical effects via free electron generation through nonlinear absorption. Photochemical effects dominate at the lower end of this irradiance range, whereas at the upper end they are mixed with thermal effects and modified by thermoelastic stresses. Above the breakdown threshold, the spatial confinement is partly destroyed by cavitation bubble formation, and the laser-induced effects become more disruptive. Our simulations revealed that the highly localized ablation of subcellular structures recently demonstrated by other researchers are probably mediated by free-electron-induced chemical bond breaking and not related to heating or thermoelastic stresses. At the irradiance values employed in multiphoton microscopy (about 1/20 of the breakdown threshold), the model predicts, for (lambda) =800 nm wavelength, an electron density of about 10<SUP>11</SUP> cm<SUP>-3</SUP>, sufficient to produce free electrons in the focal volume. Multiphoton microscopy may, hence, be accompanied by chemical effects arising from these electrons. We conclude that low density plasmas below the optical breakdown threshold can be a versatile tool for the manipulation of transparent biological media and other transparent materials but may also be a potential hazard in multiphoton microscopy and higher harmonic imaging.
PATHOLOGIC ANALYSIS OF PHOTOTHERMAL AND PHOTOMECHANICAL EFFECTS OF LASER–TISSUE INTERACTIONS (1991)

Pathologic analysis of the biologic effects and mechanisms of laser-tissue interactions requires correlation of the irradiation parameters with the biologic status and response of the target tissues over time. The photobiologic mechanisms of laser-induced tissue injury can be separated into three categories, photochemical, photothermal and photomechanical. Anatomic pathologic analysis of laser-induced lesions reveals alterations that represent either specific markers of the photobiologic mechanism or non-specific reactions to tissue injury. Repair, regeneration and wound healing of laser induced lesions appear to be non-specific responses to the type of tissue damage rather than the photobiologic mechanism producing the lesion.
Substance P and vasoactive intestinal peptide in bullous and inflammatory skin disease (1986)

Immunoreactivity (IR) of substance P (SP) and Vasoactive Intestinal Peptide (VIP) were determined by radioimmunoassay in serum of 56 patients with inflammatory skin diseases, in blister fluid of 40 patients with spontaneous blisters and 31 subjects with induced skin blisters. Serum concentrations of SP-IR and VIP-IR were mostly low or non-detectable. Spontaneous blisters contained high amounts of SP-IR, particularly in bullous pemphigoid and in some inflammatory dermatoses, while VIP-IR levels usually were low. Suction blisters from inflamed but not from normal skin often contained SP-IR but more seldom VIP-IR.
Transparent X-Ray Lithography Masks (1982)

With a view to producing a rigid and optically-transparent mask for use in X-ray lithography, the membrane strength was theoretically analyzed as a function of the residual stress in films. In silicon nitride films, reduction of the residual stress resulted in an increase in membrane strength accompanied by a decrease in optical Transparency. Silicon nitride film was then combined with transparent silicon dioxide film and an Si 3 N 4 /SiO 2 /Si 3 N 4 sandwich-structure membrane was developed. In this membrane, the compressive film force approached the tensile film force closely, keeping the membrane under tension. This produced an optically-transparent, rigid, smoothly stretched-out membrane. An X-ray lithography mask with 0.8 µm thick gold absorber patterns on this membrane was successfully used for four-level multiple-pattern replications using an optical auto-alignment system.
Induction of TNF-.ALPHA. Gene Expression by Heat Inducible Promoter gadd 153. (2000)

We demonstrated the effectiveness of inducible expression of the TNF-α gene. The TNF-α gene located under the heat-inducible promoter, gadd 153, was introduced into the human glioma cell line, U251-SP. Without heat treatment, no cytotoxicity for the transfected cells was observed. When the transfected cells were treated with hyperthermia at 43°C for 1 h or 45°C for 1 h, inducible expression of the TNF-α gene was observed. The pattern of enhancement of the gene expression varied with temperature. The TNF-α production per cell on treatment at 43°C reached 4.3 times the basal level at one day after the heat treatment while the maximum production on treatment at 45°C was observed at 4 days after the heating. The cytotoxicity of the transfected cells treated at 43°C and at 45°C was 81% at 3 days after the heating and 99.9% at 4 days after the heating, respectively.
Technique of pudendal Nerve Localization for Block or Stimulation (1989)

A diagnostic technique is described for study of the pudendal nerve via a dorsal rather than perineal approach. The method offers unique advantages for the urodynamic study of sphincteric function. The patient is placed in the prone position with slight flexion of the hips. The position of the ischial spine is identified topographically using the ischial tuberosities, greater trochanter and lower edge of the ischial-tuberous ligament. Local anesthesia and electrical stimulation then are used to position a needle tip adjacent to the pudendal nerve. This approach allows for specific localization of the nerve for accurate temporary or permanent nerve block. It also permits continuous urodynamic monitoring of pelvic floor behavior with stimulation of the pudendal nerve to assess functional integrity of the nerve and the pelvic floor striated muscles.
The Mechanical Properties of Human Flexor Tendons in Relation to Artificial Tendons (1985)

The continuation of an unacceptable failure rate with tendon repair or grafting procedures, largely due to adhesions, suggested that an artificial flexor tendon could be an attractive alternative. A literature search found no published data of the mechanical properties of fresh human finger flexor tendons, so a study of the strength and extensibility of 153 tendons was carried out. The bone insertion strength of twenty middle finger tendons was also examined. The results showed that an artificial tendon should have a strength of approximately 1500N, and that it should extend 13% at that load, an elongation of 26mm for a tendon 200mm long. The insertion strength was less than a half of the tendon strength. This data will allow an artificial flexor tendon to be designed with sufficient strength and the correct elastic properties to allow its function to integrate reliably with natural tendons in adjacent fingers.
Improved Arteriogenesis with Simultaneous Skeletal Muscle Repair in Ischemic Tissue by SCL+ Multipotent Adult Progenitor Cell Clones from Peripheral Blood (2004)

These data suggest that molecularly primed hem-/mesangioblast-type adult progenitor cells can circulate in the peripheral blood improving perfusion of tissues with chronic ischemia and extending beyond the vascular compartment.
Regulation of gene expression in the mouse oocyte and early preimplantation embryo: developmental changes in Sp1 and TATA box-binding protein, TBP (1994)

We previously demonstrated that an Sp1-dependent reporter gene is preferentially expressed in G2 of the 1-cell mouse embryo following microinjection of the male pronucleus when compared to microinjection of the female pronucleus (P.T. Ram and R.M. Schultz, 1993, Dev. Biol. 156, 552-556). We also noted that expression of the reporter gene is not observed following microinjection of the germinal vesicle of the fully grown oocyte. In the present study, we examined expression of this reporter gene during oocyte growth, as well as the nuclear concentration of two transcription factors, Sp1 and the TATA box-binding protein, TBP, during oocyte growth and the first cell cycle. The extent of reporter gene expression decreases during oocyte growth and this decrease correlates with the decrease in nuclear concentration of Sp1, as determined by confocal immunofluorescent microscopy. In addition, results of immunoblotting experiments also indicate a similar decrease in the total concentration of Sp1 during oocyte growth. The nuclear concentration of TBP also decreases during oocyte growth, as determined by confocal immunofluorescent microscopy. Following fertilization, the pronuclear concentration of these two transcription factors increases in a time-dependent fashion and the concentration of each is greater in the male pronucleus as compared to the female pronucleus. For each pronucleus and for each transcription factor, this increase in nuclear concentration is inhibited by aphidicolin, which inhibits DNA synthesis. Last, the increase in nuclear concentration of these two proteins observed between the 1-cell and 2-cell stages does not require transcription or cytokinesis.
Idiotype vaccines against human T cell leukemia. II. Generation and characterization of a monoclonal idiotype cascade (Ab1, Ab2, and Ab3). (1988)

Previously, we had generated anti-Id mAb (Ab2) binding to a hybridoma SN2 (Ab1), which recognizes a glycoprotein, gp37, expressed by human leukemic T cells. To characterize these anti-idiotopes further, they were used to immunize mice and rabbits. Several murine anti-anti-Idiotype mAb (Ab3), mostly of IgM-k isotype, were obtained. mAb3 and sera from rabbits immunized with Ab2 contained antibodies that bind to gp37 Ag and leukemic MOLT-4 and JM cells. Also, mAb3 and immune sera from rabbits competed with Ab1 for binding to MOLT-4 cells. They inhibited the binding of iodinated Ab1 to Ab2 indicating that Ab3 in mice and rabbits shares idiotopes with Ab1 (SN2). Furthermore, both the murine mAb3 and rabbit polyclonal Ab3 immunoprecipitated the same gp37 Ag as SN2 (Ab1). The production of Ag-specific Ab3 (Ab1') in mice and rabbits in absence of any exposure to gp37 indicates that these Ab2 may indeed carry the internal image of the gp37 Ag. Such anti-idiotopes (Ab2 beta) may be useful as Ag substitute for the induction of therapeutic immunity in T cell leukemia patients.
Diazo transfer reactions under mildly basic conditions (1990)

A. M. P. Koskinen and L. Muñoz, J. Chem. Soc., Chem. Commun., 1990, 652 DOI: 10.1039/C39900000652
Activation and Regioselective Ortho-Functionalization of the A-Ring of β-Estradiol Promoted by “Cp*Ir”:  An Efficient Organometallic Procedure for the Synthesis of 2-Methoxyestradiol (1997)

5,6,7,8-Tetrahydro-2-naphthol (3) and β-estradiol (1) gave η6-arene complexes using [Cp*Ir(solvent)3][BF4]2 (4) prepared in situ; subsequent O-deprotonation with NEt3 produced the corresponding complexes [Cp*Ir(oxo-η5-dienyl)][BF4] (5 and 6a,b). In the case of the complexed hormone, the Cp*Ir moiety coordinates the A-ring either α (metal down, 6a) or β (metal up, 6b) relative to the methyl group at C(13). The X-ray molecular structure of the α-isomer 6a was determined. These (oxo-η5-dienyl)iridium derivatives 5 and 6a react with NaOMe in methanol at −40 °C to give respectively the novel iridium cyclohexadienone complexes [Cp*Ir(methoxy-η4-dienone)] (7a and 8a) in 95 and 91% yields, respectively, with nucleophilic attack occurring exclusively at the ortho-position relative to the CO function. The novel iridium cyclohexadienone compound of the complexed steroid 8a can be oxidized easily by iodine to produce 2-methoxyestradiol (2) in 60% overall yield from β-estradiol. This efficient organometallic procedure is preferable to the classical organic procedure, which requires five steps and affords 2 in less than 5% yield.
Microsomal enzymes of cholesterol biosynthesis from lanosterol. Purification and characterization of delta 7-sterol 5-desaturase of rat liver microsomes. (1985)

Microsomal delta 7-sterol 5-desaturase of cholesterol biosynthesis is a multienzyme system which catalyzes the introduction of the delta 5-bond into delta 7-cholestenol to form 7-dehydrocholesterol. The detergent-solubilized 5-desaturase has been purified more than 70-fold and resolved from electron carriers and other rat liver microsomal enzymes of sterol biosynthesis by chromatography on DEAE-Sephacel, CM-Sepharose, and immobilized cytochrome b5; the 5-desaturase had not been fully resolved from cytochrom b5 reductase in earlier work. A functional electron transport system for the 5-desaturase has been reconstituted by combining the purified 5-desaturase and electron carriers with egg phosphatidylcholine liposomes. Optimizations of conditions for reconstitution have been obtained; both cytochrome b5 and NADH-cytochrome b5 reductase serve as electron carriers. A pyridine nucleotide-dependent flavoprotein is required and the requirement can be satisfied with either purified cytochrome b5 reductase or cytochrome P-450 reductase. Cyanide and iron-chelators strikingly inhibit the 5-desaturase activity, thus suggesting that 5-desaturase is a metalloenzyme as are other well-characterized cytochrome b5-dependent oxidases. 5-Desaturase is resolved from 4-methyl sterol oxidase activity of cholesterol biosynthesis by chromatography on the immobilized cytochrome b5. This resolution of the two oxidases not only indicates that introduction of the delta 5-bond and oxidation of 4 alpha-methyl groups are catalyzed by different terminal oxidases, but resolution affords enzymes of sufficient purity to carry out reconstitution experiments. A novel assay based on substrate-dependent increments of oxidation of alpha-NADH has been developed for measurement of 5-desaturase activity. Measurement of stoichiometry of 5-desaturase demonstrates that for each equivalent of cis-desaturation of delta 7-cholestenol, 1 eq of NADH is consumed. Along with strict dependence upon oxygen, this observation confirms, as suggested by previous workers, that the 5-desaturation is catalyzed by a mixed function oxidase rather than a dehydrogenase.
La Rosa C et al (J Infect Dis 2012; 205:1294-304) (2013)

In “Clinical Evaluation of Safety and Immunogenicity of PADRE-Cytomegalovirus (CMV) and Tetanus-CMV Fusion Peptide Vaccines With or Without PF03512676 Adjuvant” (J Infect Dis2012; 205:1294–304), Sanjeet Dadwal was mistakenly omitted from the coauthor list.

The authors regret the error. A corrected author list is below.
Does innate immune privilege exist? (2000)

Immune privilege in the eye is believed to originate from the eye's need to avoid the sight-destroying consequences of inflammation. Over the past 25 years, many of the anatomical, cellular, and molecular mechanisms by which the eye avoids inflammation secondary to adaptive immune responses have been elucidated. In the recent past, it has become increasingly clear that innate immune responses play a critical role in activating the adaptive immune response. Moreover, innate immunity itself carries a heavy burden of inflammation, thereby posing a threat to vision if it should occur intraocularly. Ocular immunologists have now begun to inquire into the extent to which the eye regulates the expression of innate immunity in oculi. Evidence is presented which indicates that factors found in normal aqueous humor (1) prevent NK cells from lysing their targets, (2) inhibit neutrophil activation by CD95 ligand, (3) suppress nitric oxide production by activated macrophages, and (4) interfere with complement activation via the alternative pathway. These factors include transforming growth factor-beta2, alpha-melanocyte-stimulating hormone, calcitonin gene-related peptide, and migration inhibitory factor. The ability of the eye to prevent intraocular activation of innate immune effectors spares the corneal endothelium (which expresses CD95 ligand constitutively, but low levels of MHC class I molecules) from destruction by NK cells and neutrophils, and protects the visual axis from distortion by macrophage and complement-mediated inflammation. Thus, privilege exists in the eye for both adaptive and innate immunity.
Vascular Endothelial Growth Factor Up-regulates ICAM-1 Expression via the Phosphatidylinositol 3 OH-kinase/AKT/Nitric Oxide Pathway and Modulates Migration of Brain Microvascular Endothelial Cells (2000)

Endothelium of the cerebral blood microvessels, which constitutes the major component of the blood-brain barrier, controls leukocyte and metastatic cancer cell adhesion and trafficking into the brain parenchyma. In this study, using rat primary brain microvascular endothelial cells (BMEC), we demonstrate that the vascular endothelial growth factor (VEGF), a potent promoter of angiogenesis, up-regulates the expression of the intracellular adhesion molecule-1 (ICAM-1) through a novel pathway that includes phosphatidylinositol 3 OH-kinase (PI3K), AKT, and nitric oxide (NO), resulting in the migration of BMEC. Upon VEGF treatment, AKT is phosphorylated in a PI3K-dependent manner. AKT activation leads to NO production and release and activation-deficient AKT attenuates NO production stimulated by VEGF. Transfection of the constitutive myr-AKT construct significantly increased basal NO release in BMEC. In these cells, VEGF and the endothelium-derived NO synergistically up-regulated the expression of ICAM-1, which was mediated by the PI3K pathway. This activity was blocked by the PI3K-specific inhibitor, wortmannin. Furthermore, VEGF and NO significantly increased BMEC migration, which was mediated by the up-regulation of ICAM-1 expression and was dependent on the integrity of the PI3K/AKT/NO pathway. This effect was abolished by wortmannin, by the specific ICAM-1 antibody, by the specific inhibitor of NO synthase, N(G)-l-monomethyl-arginine (l-NMMA) or by a combination of wortmannin, ICAM-1 antibody, and l-NMMA. These findings demonstrate that the angiogenic factor VEGF up-regulates ICAM-1 expression and signals to ICAM-1 as an effector molecule through the PI3K/AKT/NO pathway, which leads to brain microvessel endothelial cell migration. These observations may contribute to a better understanding of BMEC angiogenesis and the physiological as well as pathophysiological function of the blood-brain barrier, whose integrity is crucial for normal brain function.
The Association of Pericardial Fat with Coronary Artery Plaque Index at MR Imaging: The Multi-Ethnic Study of Atherosclerosis (MESA) (2011)

Pericardial fat volume, rather than BMI and waist circumference, was more strongly related to plaque eccentricity as a measure of coronary atherosclerotic plaque burden. The results support the proposed role of pericardial fat in association with atherosclerosis.
Nephrotoxic Effects in High-Risk Patients Undergoing Angiography (2003)

Nephropathy induced by contrast medium may be less likely to develop in high-risk patients when iodixanol is used rather than a low-osmolar, nonionic contrast medium.