gebhart/patrepeval huggingface dataset:
Analysis of the activating receptors and cytolytic function of human natural killer cells undergoing in vivo differentiation after allogeneic bone marrow transplantation (2004)

Patients undergoing allogeneic bone marrow transplantation offer a unique system to analyze NK cell development in vivo. We analyzed NK cells from 23 such patients to assess the acquisition of activating receptors. Four patients displayed an immature NK cell surface phenotype at engraftment, as their cells were CD16(-)KIR(-) and NKG2D(-) but expressed low levels of NKp46, NKp30, 2B4 and NKG2A. These NK cells had particularly low cytolytic activity against the HLA-class-I(-) melanoma F01 cell line and the 721-221 EBV-infected B cell line. Moreover, cytoxicity was inhibited upon mAb-mediated crosslinking of 2B4. Analysis of NK cells at day 30 after bone marrow transplantation revealed the occurrence of both phenotypic and functional maturation. These data are in agreement with a previous in vitro study showing that immature NK cell precursors express CD16, NKG2D and KIR only at a late stage of differentiation and also express inhibitory 2B4. Our present study allows a better understanding of the NK cell differentiation in vivo.
Automatic personalization based on Web usage mining (2000)

article Free Access Share on Automatic personalization based on Web usage mining Authors: Bamshad Mobasher De Paul Univ., Chicago, IL De Paul Univ., Chicago, ILView Profile , Robert Cooley View Profile , Jaideep Srivastava Univ. of Minnesota, Minneapolis Univ. of Minnesota, MinneapolisView Profile Authors Info & Claims Communications of the ACMVolume 43Issue 8Aug. 2000 pp 142–151https://doi.org/10.1145/345124.345169Published:01 August 2000Publication History 758citation11,301DownloadsMetricsTotal Citations758Total Downloads11,301Last 12 Months396Last 6 weeks78 Get Citation AlertsNew Citation Alert added!This alert has been successfully added and will be sent to:You will be notified whenever a record that you have chosen has been cited.To manage your alert preferences, click on the button below.Manage my Alerts New Citation Alert!Please log in to your account Save to BinderSave to BinderCreate a New BinderNameCancelCreateExport CitationPublisher SiteView all FormatsPDF
The Participation of IL-8 in the Synovial Lesions at an Early Stage of Rheumatoid Arthritis. (1999)

Synovial tissues from Rheumatoid Arthritis (RA) were divided into three groups based on their histopathological findings and compared for their expression of IL-8 and monocyte chemotactic and activating factor (MCAF) by using immunohistochemistry and in situ hybridization. The levels of IL-8 as well as those of MCAF were markedly higher in the synovial fluid from RA joints. Synovial lining cells (SLC) and macrophages had an ability to produce IL-8 at an early phase of the disease. The presence of MCAF was restricted in macrophages at this stage. On the other hand, the production of IL-8 as well as MCAF were prominent in most components of the joints such as SLC, migrated monocytes, sublining fibroblastoid cells, endothelial cells or migrated neutrophils at an active phase. The expression of IL-8 or MCAF was low in fibrotic synovitis of RA. These data indicate that IL-8 generated from SLC and macrophages may participate to the inflammatory process in the early synovitis of RA.
The structural integrity exerted by N-terminal pyroglutamate is crucial for the cytotoxicity of frog ribonuclease from Rana pipiens (2003)

Onconase, a cytotoxic ribonuclease from Rana pipiens, possesses pyroglutamate (Pyr) at the N-terminus and has a substrate preference for uridine-guanine (UG). To identify residues responsible for onconase's cytotoxicity, we cloned the rpr gene from genomic DNA and expressed it in Escherichia coli BL21(DE3). The recombinant onconase with Met at the N-terminus had reduced thermostability, catalytic activity and antigenicity. Therefore, we developed two methods to produce onconase without Met. One relied on the endogeneous E.coli methionine aminopeptidase and the other relied on the cleavage of a pelB signal peptide. The Pyr1 substitutional variants maintained similar secondary structures to wild-type onconase, but with less thermostability and specific catalytic activity for the innate substrate UG. However, the non-specific catalytic activity for total RNAs varied depending on the relaxation of base specificity. Pyr1 promoted the structural integrity by forming a hydrogen bond network through Lys9 in alpha1 and Val96 in beta6, and participated in catalytic activity by hydrogen bonds to Lys9 and P(1) catalytic phosphate. Residues Thr35 and Asp67 determined B(1) base specificity, and Glu91 determined B(2) base specificity. The cytotoxicity of onconase is largely determined by structural integrity and specific catalytic activity for UG through Pyr1, rather than non-specific activity for total RNAs.
Activation of the renal renin-angiotensin system in diabetes--new concepts (2008)

The incidence of diabetes mellitus, obesity and the metabolic syndrome is rapidly rising to epidemic levels worldwide. Hyperglycemia, the metabolic hallmark of the pathology, is a significant causative factor for the complications of diabetes mellitus which result in significant morbidity and mortality for millions. Hyperglycemia is clearly associated with microvascular complications in many organs including the kidney, and diabetic nephropathy is the leading cause of end-stage renal disease (ESRD) in developed countries [1,2]. In addition, diabetes may lead to other vascular complications, including systemic hypertension [1,2]. Recent advances on the cellular and kidney-specific effects of hyperglycemia place activation of the local, intrarenal renin–angiotensin system (RAS) as a strong candidate for the core abnormality that leads to renal tissue injury [1–3]. The nature of RAS activation in diabetes is, however, controversial [3]. It has been difficult to isolate the acute and direct actions of hyperglycemia per se from the many other systemic factors and intra-renal, macula densa-mediated feedback mechanisms that can indirectly activate the intrarenal RAS. Therefore, the primary cause and exact mechanism of RAS activation in early diabetes have been unknown. The prevailing paradigm, the ‘tubular hypothesis of glomerular filtration’ [4], argues that the two hallmarks of early changes, glomerular hyperfiltration and renin activation, originate from the primary effects of glucose on proximal tubule salt reabsorption that secondarily activate macula densa-mediated feedback mechanisms. However, the development of diabetes-induced glomerular hyperfiltration was intact, or even augmented, in mice that lacked tubuloglomerular feedback (TGF), demonstrating that the TGF mechanism could not be the major cause of the development of hyperfiltration [5,6].
T cell-derived B cell growth factor(s) can induce stimulation of both resting and activated B cells. (1985)

The effects of a preparation containing partially purified, EL4-derived B cell growth factor(s) (BCGF) on B cell growth and proliferation have been examined by using B lymphocyte subpopulations separated on the basis of size. BCGF was found to maintain and enhance proliferation of a significant proportion of large activated B cells. In contrast, small resting B cells required the presence of BCGF and a second stimulus such as anti-IgM antibody (anti-mu) to be induced to proliferate. This disparity was not due to a lack of an effect of BCGF on small resting B cells. A factor contained within the partially purified EL4 supernatant produced time-dependent increases in cell size and RNA content in all subpopulations. These effects were independent of possible effects due to contaminating lymphokines such as interleukin 2 (IL 2), concanavalin A (Con A), and phorbol myristate acetate (PMA). Nonmitogenic doses of lipopolysaccharide (LPS) failed to show similar effects. Our data suggest that B cells at all levels of in vivo activation are responsive to stimulation by a growth factor present in EL4 supernatant, as manifested by cell growth and RNA synthesis. This activity has not previously been described for BCGF preparations. However, because the partially purified, EL4-derived supernatant used as BCGF in these studies has not been purified to homogeneity, we cannot conclude whether the factors that induce resting B cells to increase in size are the same as the growth factors that synergize with anti-mu to induce B cell proliferation or that maintain the proliferation of activated B cells.
Nitric Oxide Is Necessary for Multiple Memory Processes after Learning That a Food Is Inedible inAplysia (2002)

Nitric oxide (NO) signaling was inhibited via N(omega)-nitro-L-arginine methyl ester (L-NAME) during and after training Aplysia that a food is inedible. Treating animals with L-NAME 10 min before the start of training blocked the formation of three separable memory processes: (1) short-term, (2) intermediate-term, and (3) long-term memory. The treatment also attenuated, but did not block, a fourth memory process, very short-term memory. L-NAME had little or no effect on feeding behavior per se or on most aspects of the animals' behavior while they were being trained, indicating that the substance did not cause a pervasive modulation or poisoning of many aspects of feeding and other behaviors. Application of L-NAME within 1 min after the training had no effect on short- or long-term memory, indicating that NO signaling was not needed during memory consolidation. Treating animals with the NO scavenger 2-phenyl-4,4,5,5-tetramethyl-imidazdine-1-oxy-3-oxide before training also blocked long-term memory. Memory was not blocked by D-NAME, or by the simultaneous treatment with L-NAME and the NO donor S-nitroso-N-acetyl-penicillamine, confirming that the effect of L-NAME is attributable to its effect as a competitive inhibitor of L-arginine for NO synthase in the production of NO rather than to possible effects at other sites. These data indicate that NO signaling during training plays a critical role in the formation of multiple memory processes.
The meso substitution of chlorophyll derivatives: direct route for transformation of bacteriopheophorbides d into bacteriopheophorbides c. (1985)

In order to develop a procedure for direct methylation of methyl bacteriopheophorbides d (Bmph-d) to afford methyl bacteriopheophorbides c (Bmph-c), several reactions involving meso substitution of chlorophyll derivatives were investigated. Treatment of zinc(II) methyl mesopyropheophorbide a (7b) with bromine in chloroform accomplished oxidation, presumably via the π-cation radical, to the corresponding porphyrin, phylloerythrin methyl ester (16); meso bromination (to give 17) resulted when metal-free methyl mesopyropheophorbide a (7) was treated with bromine in chloroform. Friedel-Crafts cyanation (cyanogen bromide/aluminum chloride) of copper(II) methyl mesopyropheophorbide a (7a) gave 40-50% yields of the mesocyanochlorin 18 after demetalation, but attempts to transform the cyano group into methyl were unsuccessful. Oxidation reactions of 7 using thallium(III) trinitrate resulted in formation of the corresponding mesonitrochlorins 20. Treatment of copper(II) methyl mesopyropheophorbide a (7a) with chloromethyl methyl sulfide and titanium tetrachloride afforded the meso-methylthiomethyl derivative 19a (74-77% yields); use of the nickel(II) complex 7d likewise gave 80-84% yields of 19b. With Raney nickel, both 19a and 19b gave good yields of the required meso-methyl metallochlorins 3a and 3b, respectively, the former being readily demetalated with HC1 gas in dichloromethane to give the meso-methylchlorin 3. Thus, the Bmph-d to Bmph-c transformation was accomplished by initially protecting the vinyl group in methyl pyropheophorbide a (9) as the corresponding 2-chloroethyl group; the copper(II) complex 25a was then methylthiomethylated, treated with Raney nickel (to give 26a), and finally demetalated with HC1 gas to give 27. Compound 27 has previously been converted into Bmph-c [Et, Me] (4) by treatment with base (to give the 2-vinyl derivative) followed by hydration of the vinyl with HBr in acetic acid. © 1985, American Chemical Society. All rights reserved.
Targeted SARS-CoV-2 treatment is associated with decreased mortality in immunocompromised patients with COVID-19 (2022)

Our results suggest that targeted COVID-19 treatment, including direct antivirals or monoclonal antibodies, is safe and efficient and could be proposed in high-risk immunocompromised patients.
SV40-based Escherichia coli shuttle vectors infectious for monkey cells (1987)

We describe SV40-based Escherichia coli shuttle vectors which can be packaged as pseudovirions without excision of plasmid sequences and which can be rescued in bacteria. These vectors replicate and are transmitted as virus in monkey COS cells without requiring a helper virus. Extrachromosomal vector DNA isolated from infected cells can be rescued in E. coli, so that DNA alterations can be easily screened. Indeed, some of the constructions give rise to very stable plasmids with no detectable rearrangements after multiple lytic cycles in COS cells. The spontaneous mutation frequency measured in bacteria, on the lacO target, is smaller than those usually found with shuttle vectors. We also constructed an expression vector derived from one of our infectious viruses by inserting the chloramphenicol acetyl transferase gene, expressed from the SV40 early promoter, which is efficiently transduced to cells by infection. In this system, the shuttle virus combines the convenience of plasmid rescue and analysis in bacteria, with the advantages of infectious virus.
Dipeptidyl peptidase IV: a cell surface peptidase involved in regulating T cell growth (review). (1999)

The CD26 antigen is identical with the cell surface ectopeptidase dipeptidyl peptidase IV (DP IV, EC 3.4.14.5). The post proline cleaving substrate specificity makes DP IV relatively unique among other proteases. Numerous cytokines, chemokines and other bioactive peptides are potential substrates of DP IV, but knowledge about the real in vivo substrates is still very limited. CD26 represents an accessory surface molecule playing an important role in the process of activation and proliferation of human lymphocytes. The molecular events mediated by this ectoenzyme are only partly established and the necessity of DP IV enzymatic activity for its signalling capacity has been controversial. This review out-lines evidence for an involvement of DP IV in the regulation of immune response and focuses on the putative role of the catalytic domain of this peptidase. Inhibition of the catalytic activity can provoke many cellular effects, including induction of tyrosine phosphorylations and p38 MAP kinase activation as well as suppression of DNA synthesis and reduced production of various cytokines. TGF-beta1, the production and secretion of which is increased after DP IV inhibition, supposedly mediates the observed suppressive effects by maintaining p27kip expression levels which leads to a cell cycle arrest in G1. Moreover, anti-CD3-induced signalling pathways can be strongly affected by DP IV inhibition. Thus, the enzymatic activity or at least the interaction of effectors with the catalytic domain of CD26 seem to be important for crucial functions of this cell surface antigen.
Characterization of hydrogenated amorphous boron films prepared by electron cyclotron resonance plasma chemical vapor deposition method (1990)

This paper presents characterization of amorphous boron (a-B) films prepared by the electron cyclotron resonance plasma chemical vapor deposition method using diborane (B2H6) and hydrogen mixtures. Compositional analyses show that hydrogen is the only impurity which influences film properties appreciably. The infrared absorption study shows that the hydrogen is incorporated into the film in the terminal bonding form. The hydrogen concentration has been estimated using the semiempirical equation given by Blum, Feldman, and Satkiewicz [Phys. Status Solidi A 41, 481 (1977)], which can be verified by the more fundamental principle. The infrared absorption study also shows that the amorphous films possess some short-range order related with the icosahedral structure. These observations allow us to consider that this film belongs to one of alloyed materials and is true hydrogenated a-B. In order to study the contributions of hydrogen to the film properties, variations of the color and the electrical resistivity of the film have been examined with changing the substrate temperature and the B2H6 concentration in source gases. These variations can be described with consistency in terms of the optical absorption edge. The films are a-B:H at substrate temperatures below 350 °C. The hydrogen incorporation results in increase in the resistivity and increase in the optical transparency. At substrate temperatures above 350 °C, the hydrogen is evolved from the film regardless of the B2H6 concentration, and intrinsic a-B films are obtained.
Product Layer Diffusion during the Reaction of Calcium Oxide with Carbon Dioxide (1999)

The carbonation rate of 15−20 μm, nonporous, calcium oxide crystals has been studied over a temperature range of 550−1100 °C and a CO2 pressure range of 1−11.7 atm. At temperatures greater than 600 °C, the carbonation rate decreases more rapidly with time than would be expected from diffusion through a uniform product layer and the activation energy is initially low but increases with conversion. The product layer consists of crystalline grains, and these product layer grains grow by coalescence from less than one μm diameter to the approximate dimension of the particle. The carbonation rate can be described by a model where CO2 pressure-independent grain boundary diffusion and diffusion through the carbonate crystals act in parallel. The relative importance of bulk diffusion through the product layer crystals increases with time relative to transport through the grain boundaries and has an effective activation energy of 57 kcal/mol. Diffusion through the crystal boundaries has low activation energy and low dependence on CO2 pressure. At temperatures greater than 900 °C and times greater than 600 min, bulk diffusion through the product layer becomes dominant and the rate approaches first order in CO2 pressure.
Motility assays using myosin attached to surfaces through specific binding to monoclonal antibodies. (1995)

We have analyzed the dependence of actin filament movement on the mode of myosin attachment to surfaces. Monoclonal antibodies that bind to three distinct sites were used to tether myosin to nitrocellulose-coated glass. One antibody reacts with an epitope on the regulatory light chain located at the head-rod junction. The other two react with sites in the rod domain, one in the S2 region near the S2-LMM hinge, and the other at the C terminus of the myosin rod. These monoclonal antibodies were used to provide increasing flexibility in the mode of attachment. Fast skeletal muscle myosin monomers were bound to the surfaces through the specific interaction with these monoclonal antibodies and the sliding movement of fluorescently labeled actin filaments analyzed by video microscopy. Each of these antibodies produced stable, myosin-coated surfaces that supported uniform movement of actin over the course of several hours. Attachment of myosin through the anti-S2 and anti-LMM monoclonal antibodies yielded a maximum velocity of 10 microns/s at 30 degrees C, whereas attachment through anti-LC2 produced a lower velocity of 4-5 microns/s. Each antibody showed a characteristic minimum myosin density below which sliding movement was no longer supported and an exponential dependence of actin filament velocity on myosin surface density below Vmax. Maximum sliding velocity was achieved over a range of myosin surface densities. Thus, the specific mode of attachment can influence the characteristic velocity of actin filament movement and the surface density needed to support movement. These data are being used to analyze the dynamics of sliding filament assays and evaluate estimates of the average number of motor molecules per unit length of actin required to support movement.
HELLP! A cry for laboratory assistance: a comprehensive review of the HELLP syndrome highlighting the role of the laboratory. (1998)

The HELLP syndrome is a dangerously severe form of preeclampsia associated with multiorgan system damage and occurs in 0.2-0.6% of all pregnancies. It usually presents with abdominal pain, often in the setting of preeclampsia. In most cases, HELLP is initiated by inadequate placental vessel development with subsequent placental ischemia, leading to the release of circulating vasoconstrictors. These powerful vasoconstrictors include thromboxane A2, angiotensin, prostaglandin F2, and endothelin-1. The ischemic placenta also produces fewer vasodilators, such as prostacyclin, prostaglandin, E2, and nitric oxide. The ensuing imbalance in vasoactive substances causes intense systemic vasospasm and multiorgan endothelial damage. Multiple genetic, coagulation, and immunologic disorders also appear to contribute to the endothelial damage. Fibrin and platelets are then deposited on the endothelial surfaces leading to the hemolytic anemia, elevated liver enzymes, and low platelets of the HELLP syndrome. The most reliable laboratory tests for the diagnosis of HELLP are a complete blood count with peripheral smear, lactate dehydrogenase, serum transaminases, and urinalysis. Supportive tests include serum haptoglobin, D-dimer fragment levels, lactate dehydrogenase isoenzymes, total bilirubin, prothrombin times, and activated partial thromboplastin times. Lactate dehydrogenase and the platelet count are the two best tests to monitor the course of the disease. Prompt delivery is the treatment of choice. The intensity of the HELLP syndrome peaks 24 hours after delivery. Extended atypical HELLP has been successfully treated with plasma exchange. The clinical laboratory professional plays an important role in the diagnosis, follow-up, and treatment of patients with the HELLP syndrome.
Critical Role of l -Arginine in Endothelial Cell Survival During Oxidative Stress (2003)

Our data demonstrate that arginine concentrations corresponding to physiological serum levels do not allow for optimal endothelial iNOS activity. Thus, decreases in systemic arginine concentrations, or locally within atherosclerotic plaques, will impair the endothelial iNOS-mediated stress response and will significantly increase the risk of endothelial dysfunction.
Dependence of Mouse Embryonic Stem Cells on Threonine Catabolism (2009)

Measurements of the abundance of common metabolites in cultured embryonic stem (ES) cells revealed an unusual state with respect to one-carbon metabolism. These findings led to the discovery of copious expression of the gene encoding threonine dehydrogenase (TDH) in ES cells. TDH-mediated catabolism of threonine takes place in mitochondria to generate glycine and acetyl-coenzyme A (CoA), with glycine facilitating one-carbon metabolism via the glycine cleavage system and acetyl-CoA feeding the tricarboxylic acid cycle. Culture media individually deprived of each of the 20 amino acids were applied to ES cells, leading to the discovery that ES cells are critically dependent on one amino acid--threonine. These observations show that ES cells exist in a high-flux backbone metabolic state comparable to that of rapidly growing bacterial cells.