gebhart/patrepeval huggingface dataset:
Cyclins A and B1 in the Human Cell Cycle (2007)

Cyclins are a family of proteins involved in the regulation of the eukaryotic cell cycle. The first cyclins to be isolated were the A- and B-type cyclins and we have been studying their behaviour in human somatic cells. The levels of both cyclin A and B1 are regulated transcriptionally as well as post-translationally; both are rapidly and specifically degraded in mitosis. Cyclin A synthesis commences at the start of S phase and the protein is predominantly nuclear, whereas cyclin B1 appears during S phase and is primarily cytoplasmic. Cyclin B1 moves into the nucleus just at the start of mitosis and associates with condensed chromosomes and the mitotic spindle. Both cyclin A and cyclin B1 bind to and activate a protein serine/threonine kinase subunit; cyclin A associates with p33cdk2 and with p34cdc2, whereas cyclin B1 seems to bind exclusively to p34cdc2. Cyclin A-associated kinase activity appears much earlier in the cell cycle than that of cyclin B1, which appears only at the G2 to M transition. Therefore cyclin A may play a role in the events of S phase as well as G2 and M phases. Cyclin A forms a cell cycle-dependent complex with p33cdk2 and the transcription factor E2F, although the function of this complex is not yet clear. We conclude that cyclins A and B1 may differentially regulate the cell cycle in several ways. They form complexes with distinct protein kinases and these complexes are active at different times in the cell cycle; they form distinct multiprotein complexes, such as with the transcription factor E2F; and they are localized to different parts of the cell where different substrates will be available to them.
Protection against ischemic brain injury by protein therapeutics (2002)

Preventing massive cell death is an important therapeutic strategy for various injuries and disorders. Protein therapeutics have the advantage of delivering proteins in a short period. We have engineered the antiapoptotic bcl-x gene to generate the super antiapoptotic factor, FNK, with a more powerful cytoprotective activity. In this study, we fused the protein transduction domain (PTD) of the HIV/Tat protein to FNK and used the construct in an animal model of ischemic brain injury. When added into culture media of human neuroblastoma cells and rat neocortical neurons, PTD-FNK rapidly transduced into cells and localized to mitochondria within 1 h. It protected the neuroblastomas and neurons against staurosporine-induced apoptosis and glutamate-induced excitotoxicity, respectively. The cytoprotective activity of PTD-FNK was found at concentrations as low as 0.3 pM. Additionally, PTD-FNK affected the cytosolic movement of calcium ions, which may relate to its neuroprotective action. Immunohistochemical analysis revealed that myc-tagged PTD-FNK (PTD-myc-FNK) injected i.p. into mice can have access into brain neurons. When injected i.p. into gerbils, PTD-FNK prevented delayed neuronal death in the hippocampus caused by transient global ischemia. These results suggest that PTD-FNK has a potential for clinical utility as a protein therapeutic strategy to prevent cell death in the brain.
Markov Logic: A Unifying Framework for Statistical Relational Learning (2007)

Interest in statistical relational learning (SRL) has grown rapidly in recent years. Several key SRL tasks have been identified, and a large number of approaches have been proposed. Increasingly, a unifying framework is needed to facilitate transfer of knowledge across tasks and approaches, to compare approaches, and to help bring structure to the field. We propose Markov logic as such a framework. Syntactically, Markov logic is indistinguishable from first-order logic, except that each formula has a weight attached. Semantically, a set of Markov logic formulas represents a probability distribution over possible worlds, in the form of a log-linear model with one feature per grounding of a formula in the set, with the corresponding weight. We show how approaches like probabilistic relational models, knowledgebased model construction and stochastic logic programs can be mapped into Markov logic. We also show how tasks like collective classification, link prediction, linkbased clustering, social network modeling, and object identification can be concisely formulated in Markov logic. Finally, we develop learning and inference algorithms
Measurement of theabPlane Anisotropy of Microwave Surface Impedance of UntwinnedYBa2Cu3O6.95Single Crystals (1994)

The temperature dependence of the surface resistance ${R}_{s}$, and the penetration depth $\ensuremath{\lambda}$ has been measured in both $a$ and $b$ directions in ${\mathrm{Yba}}_{2}$${\mathrm{Cu}}_{3}$${\mathrm{O}}_{6.95}$. The overall temperature dependences are similar and show a linear behavior at low $T$. This argues against the chains playing a direct role in the unconventional behavior of the surface impedance. The residual ${R}_{s}$ of these twin-free crystals is very small, implying a residual conductivity of the order of the minimum value predicted by Lee Phys. Rev. Lett. 71 1837 1993 for a $d$-wave superconductor.
SHCBP1 is required for midbody organization and cytokinesis completion (2014)

The centralspindlin complex, which is composed of MKLP1 and MgcRacGAP, is one of the crucial factors involved in cytokinesis initiation. Centralspindlin is localized at the middle of the central spindle during anaphase and then concentrates at the midbody to control abscission. A number of proteins that associate with centralspindlin have been identified. These associating factors regulate furrowing and abscission in coordination with centralspindlin. A recent study identified a novel centralspindlin partner, called Nessun Dorma, which is essential for germ cell cytokinesis in Drosophila melanogaster. SHCBP1 is a human ortholog of Nessun Dorma that associates with human centralspindlin. In this report, we analyzed the interaction of SHCBP1 with centralspindlin in detail and determined the regions that are required for the interaction. In addition, we demonstrate that the central region is necessary for the SHCBP1 dimerization. Both MgcRacGAP and MKLP1 are degraded once cells exit mitosis. Similarly, endogenous and exogenous SHCBP1 were degraded with mitosis progression. Interestingly, SHCBP1 expression was significantly reduced in the absence of centralspindlin, whereas centralspindlin expression was not affected by SHCBP1 knockdown. Finally, we demonstrate that SHCBP1 depletion promotes midbody structure disruption and inhibits abscission, a final stage of cytokinesis. Our study gives novel insight into the role of SHCBP in cytokinesis completion.
Ruled Submanifolds of Finite Type (1992)

We show that a ruled submanifold of finite type in a Euclidean space is a cylinder on a curve of finite type or a generalized helicoid.
Rapid vascular regrowth in tumors after reversal of VEGF inhibition (2006)

Inhibitors of VEGF signaling can block angiogenesis and reduce tumor vascularity, but little is known about the reversibility of these changes after treatment ends. In the present study, regrowth of blood vessels in spontaneous RIP-Tag2 tumors and implanted Lewis lung carcinomas in mice was assessed after inhibition of VEGF receptor signaling by AG-013736 or AG-028262 for 7 days. Both agents caused loss of 50%-60% of tumor vasculature. Empty sleeves of basement membrane were left behind. Pericytes also survived but had less alpha-SMA immunoreactivity. One day after drug withdrawal, endothelial sprouts grew into empty sleeves of basement membrane. Vessel patency and connection to the bloodstream followed close behind. By 7 days, tumors were fully revascularized, and the pericyte phenotype returned to baseline. Importantly, the regrown vasculature regressed as much during a second treatment as it did in the first. Inhibition of MMPs or targeting of type IV collagen cryptic sites by antibody HUIV26 did not eliminate the sleeves or slow revascularization. These results suggest that empty sleeves of basement membrane and accompanying pericytes provide a scaffold for rapid revascularization of tumors after removal of anti-VEGF therapy and highlight their importance as potential targets in cancer therapy.
Sex Differences in Incidence, Mortality, and Survival in Individuals With Stroke in Scotland, 1986 to 2005 (2009)

We observed lower rates of incidence and mortality in younger women than men. However, higher numbers of older women in the population mean that the absolute burden of stroke is greater in women. Short-term case-fatality is greater in women of all ages and, worryingly, these differences have increased from 1986 to 2005.
Blocking the GABA transporter GAT‐1 ameliorates spinal GABAergic disinhibition and neuropathic pain induced by paclitaxel (2015)

Abstract Paclitaxel is a chemotherapeutic agent widely used for treating carcinomas. Patients receiving paclitaxel often develop neuropathic pain and have a reduced quality of life which hinders the use of this life‐saving drug. In this study, we determined the role of GABA transporters in the genesis of paclitaxel‐induced neuropathic pain using behavioral tests, electrophysiology, and biochemical techniques. We found that tonic GABA receptor activities in the spinal dorsal horn were reduced in rats with neuropathic pain induced by paclitaxel. In normal controls, tonic GABA receptor activities were mainly controlled by the GABA transporter GAT ‐1 but not GAT ‐3. In the spinal dorsal horn, GAT ‐1 was expressed at presynaptic terminals and astrocytes while GAT ‐3 was only expressed in astrocytes. In rats with paclitaxel‐induced neuropathic pain, the protein expression of GAT ‐1 was increased while GAT ‐3 was decreased. This was concurrently associated with an increase in global GABA uptake. The paclitaxel‐induced attenuation of GABA ergic tonic inhibition was ameliorated by blocking GAT ‐1 but not GAT ‐3 transporters. Paclitaxel‐induced neuropathic pain was significantly attenuated by the intrathecal injection of a GAT ‐1 inhibitor. These findings suggest that targeting GAT ‐1 transporters for reversing disinhibition in the spinal dorsal horn may be a useful approach for treating paclitaxel‐induced neuropathic pain. image Patients receiving paclitaxel for cancer therapy often develop neuropathic pain and have a reduced quality of life. In this study, we demonstrated that animals treated with paclitaxel develop neuropathic pain, have enhancements of GABA transporter‐1 protein expression and global GABA uptake, as well as suppression of GABAergic tonic inhibition in the spinal dorsal horn. Pharmacological inhibition of GABA transporter‐1 ameliorates the paclitaxel‐induced suppression of GABAergic tonic inhibition and neuropathic pain. Thus, targeting GAT‐1 transporters for reversing GABAergic disinhibition in the spinal dorsal horn could be a useful approach for treating paclitaxel‐induced neuropathic pain.
Characterization of monoclonal antibodies to a crystal protein of Bacillus thuringiensis subsp. kurstaki (1986)

Ten monoclonal antibodies were produced against a k-1-type crystal protein of Bacillus thuringiensis subsp. kurstaki. Eight of the antibodies belong to the immunoglobulin G1 (IgG1) subclass, with pI values ranging from 5.5 to 8.6, one could be assigned to the IgG2b subclass, and one could be assigned to the IgM class. Competitive antibody-binding assays and analysis of antibody specificity indicated that the 10 antibodies recognized at least nine distinct antigenic determinants. Eight antibodies bound to both protoxin and toxin, whereas the other two interacted with protoxin only. One antibody completely inhibited the biological activity of the delta-endotoxin, five antibodies reduced it by 15 to 82%, and four antibodies did not affect it at all. Based on cross-reaction studies, homologies and differences in the crystal protein structures of different B. thuringiensis subspecies were revealed. All of the monoclonal antibodies strongly cross-reacted with crystal proteins from strains of B. thuringiensis subsp. tolworthi, B. thuringiensis subsp. galleriae, B. thuringiensis subsp. dendrolimus, B. thuringiensis subsp. sotto, and B. thuringiensis subsp. subtoxicus. Some antibodies interacted only weakly with crystal proteins from strains of B. thuringiensis subsp. morrisoni and B. thuringiensis subsp. entomocidus, and some of these did not interact with B. thuringiensis subsp. kenyae and B. thuringiensis subsp. darmstadiensis. No cross-reaction was found with the parasporal inclusion protein of B. thuringiensis subsp. israelensis. Studies with the monoclonal antibodies also disclosed that crystal proteins from strains of the same subspecies can exhibit substantial differences in antigenic structure. In particular, striking strain-specific differences in the protoxins of B. thuringiensis subsp. kurstaki and B. thuringiensis subsp. thuringiensis were observed.
Induced Apoptosis Supports Spread of Adenovirus Vectors in Tumors (2001)

Selectively replicating viruses hold promise as anticancer agents. To eliminate the tumor, these viruses must efficiently spread throughout the tumor and induce oncolysis. We hypothesized that viral release and spread could be supported by apoptosis induced after assembly of de novo-produced virions in tumor cells. As a model to test this, we employed an adenovirus vector that replicated in human tumor cell lines. Expression of a dominant-negative I-kappaB from this vector sensitized tumor cells to recombinant human tumor necrosis factor alpha (TNF-alpha)-mediated apoptosis. We found that apoptosis induced during viral DNA replication compromised virus production, whereas apoptosis induced after virion assembly enhanced viral release from infected cells and dissemination. Electron microscopy demonstrated that viral particles were associated with or included in apoptotic bodies whose phagocytosis by neighboring cells provides a potential means for viral spread. Apoptosis induced after viral replication also supported spread in vivo, in subcutaneous tumors or liver metastases, resulting in a delay of tumor growth. Our findings could be applicable to other selectively replicating viruses or antitumor strategies that involve application of proapoptotic or cytolytic agents.
Palladium- and Nickel-Catalyzed Intramolecular Cyanoboration of Alkynes (2003)

Intramolecular addition of a boron-cyano bond across a carbon-carbon triple bond was achieved using palladium and nickel catalysts. Cyano(diisopropylamino)boryl homopropargyl ethers underwent regio- and stereoselective 5-exo cyclization, forming five-membered cyclic boryl ethers in high yields. The cyanoboration products thus obtained served as new precursors for the synthesis of highly substituted alpha,beta-unsaturated nitriles via transition-metal-catalyzed transformations.
Is Growth Differentiation Factor 11 a Realistic Therapeutic for Aging-Dependent Muscle Defects? (2016)

This "Controversies in Cardiovascular Research" article evaluates the evidence for and against the hypothesis that the circulating blood level of growth differentiation factor 11 (GDF11) decreases in old age and that restoring normal GDF11 levels in old animals rejuvenates their skeletal muscle and reverses pathological cardiac hypertrophy and cardiac dysfunction. Studies supporting the original GDF11 hypothesis in skeletal and cardiac muscle have not been validated by several independent groups. These new studies have either found no effects of restoring normal GDF11 levels on cardiac structure and function or have shown that increasing GDF11 or its closely related family member growth differentiation factor 8 actually impairs skeletal muscle repair in old animals. One possible explanation for what seems to be mutually exclusive findings is that the original reagent used to measure GDF11 levels also detected many other molecules so that age-dependent changes in GDF11 are still not well known. The more important issue is whether increasing blood [GDF11] repairs old skeletal muscle and reverses age-related cardiac pathologies. There are substantial new and existing data showing that GDF8/11 can exacerbate rather than rejuvenate skeletal muscle injury in old animals. There is also new evidence disputing the idea that there is pathological hypertrophy in old C57bl6 mice and that GDF11 therapy can reverse cardiac pathologies. Finally, high [GDF11] causes reductions in body and heart weight in both young and old animals, suggestive of a cachexia effect. Our conclusion is that elevating blood levels of GDF11 in the aged might cause more harm than good.
A Security Problem and Proposed Correction With Widely Deployed DNS Software (1993)

This document discusses a flaw in some of the currently distributed name resolver clients. The flaw exposes a security weakness related to the search heuristic invoked by these same resolvers when users provide a partial domain name, and which is easy to exploit (although not by the masses). This document points out the flaw, a case in point, and a solution.
Factors promoting acute and chronic diseases caused by yersiniae (1991)

The experimental system constructed with the medically significant yersiniae provides a powerful basic model for comparative study of factors required for expression of acute versus chronic disease. The system exploits the close genetic similarity between Yersinia pestis, the etiological agent of bubonic plague, and enteropathogenic Yersinia pseudotuberculosis and Yersinia enterocolitica. Y. pestis possesses three plasmids, of which one, shared by the enteropathogenic species, mediates a number of virulence factors that directly or indirectly promote survival within macrophages and immunosuppression. The two remaining plasmids are unique and encode functions that promote acute disease by enhancing bacterial dissemination in tissues and resistance to phagocytosis by neutrophils and monocytes. These properties are replaced in the enteropathogenic yersiniae by host cell invasins and an adhesin which promote chronic disease; the latter are cryptic in Y. pestis. Additional distinctions include specific mutational losses in Y. pestis which result in loss of fitness in natural environments plus gain of properties that facilitate transmission and infection via fleabite.
Purification, characterization, cloning, and amino acid sequence of the bifunctional enzyme 5,10-methylenetetrahydrofolate dehydrogenase/5,10-methenyltetrahydrofolate cyclohydrolase from Escherichia coli. (1991)

We have purified the enzyme 5,10-methylenetetrahydrofolate dehydrogenase (EC 1.5.1.5) from Escherichia coli to homogeneity by a newly devised procedure. The enzyme has been purified at least 2,000-fold in a 31% yield. The specific activity of the enzyme obtained is 7.4 times greater than any previous preparation from this source. The purified enzyme is specific for NADP. The protein also contains 5,10-methenyltetrahydrofolate cyclohydrolase (EC 3.5.4.9) activity. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and behavior on a molecular sieving column suggest that the enzyme is a dimer of identical subunits. We have cloned the E. coli gene coding for the enzyme through the use of polymerase chain reaction based on primers designed from the NH2 terminal analysis of the isolated enzyme. We sequenced the gene. The derived amino acid sequence of the enzyme contains 287 amino acids of Mr 31,000. The sequence shows 50% identity to two bifunctional mitochondrial enzymes specific for NAD, and 40-45% identity to the presumed dehydrogenase/cyclohydrolase domains of the trifunctional C1-tetrahydrofolate synthase of yeast mitochondria and cytoplasm and human and rat cytoplasm. An identical sequence of 14 amino acids with no gaps is present in all 7 sequences.
Measuring nursing quality (2009)

What outcomes distinguish good nursing care from poor nursing care vexed Florence Nightingale and many subsequent nurses. Indeed, much activity has been devoted to desirable attitudes, behaviours and actions of nurses but relatively little activity has been devoted to distilling out indicators which measure the nurse’s contribution to clinical outcome. This is an important deficit for nursing because it undermines claims from nurses that they make an indispensable contribution to patient care.
[A method based on image processing and analyzing technology for estimating the activity of mesenchymal stem cells]. (2006)

Cell culture is one of the usual methods for studying living cell and tissue, the method presented in this paper is based on image processing and analyzing technology for activity estimation of mesenchymal stem cells (MSCs). The existing activity estimation methods are costly, complex and invasive. In this method, thresholding is used to preprocess image and to separate out the growth hallow. Then the area is calculated by counting the pixels of the growth hallow. The changes of the activity estimated by this method are similar to those by corresponding cellular experiments. Compared with the existing methods in biology, medicine or medical cellular science, this method is easier, faster, cost-effective and non-invasive. The proposed method has been proved to be efficient by primary experiments of MSCs.
MODELLING THE RELATIONSHIP BETWEEN DRIVER IN-VEHICLE VISUAL DEMANS AND ACCIDENT OCCURRENCE (1998)

An investigation was carried out to determine if a relationship could be found between occurrences in a traffic accident data base and visual demands created by various in-vehicle systems. The idea was to determine whether or not the assumption of a relationship between accident rate and visual demands is justified and if so, how to model the relationship. The advantage of modelling the relationship is that accident rates of proposed new or modified in-vehicle devices can then be predicted and in addition, problems associated with existing devices can be uncovered. This paper describes the investigative procedure used and the models that were developed. These models appear to have reasonably accurate predictive capability, given the necessary visual demand and frequency-of-use input data. For the covering abstract see IRRD E102207.
Eukaryotic Initiation Factor 5A Activity and HIV-1 Rev Function (1997)

Eukaryotic initiation factor 5A (eIF-5A) is the only cellular protein known to contain the unusual amino acid hypusine, a modification that appears to be required for cell proliferation. This hypusine-modified protein stimulates synthesis of methionyl-puromycin in an in vitro assay which mimics the formation of the first peptide bond during protein synthesis, although the exact role of eIF-5A in vivo is still unknown. The unexpected finding that eIF-5A is a cellular cofactor of the HIV-1 Rev trans-activator protein may, however, provide a novel opportunity to reveal precisely what function eIF-5A performs in eukaryotic cells. In this review article, we first present a brief description of HIV-1 Rev function, followed by an overview of the data that identified eIF-5A as a Rev cofactor and, finally, discuss novel findings with respect to cellular eIF-5A activities.
Probing High Affinity Sequences of DNA Aptamer against VEGF165 (2012)

Vascular endothelial growth factor (VEGF(165)) is a potent angiogenic mitogen commonly overexpressed in cancerous cells. It contains two main binding domains, the receptor-binding domain (RBD) and the heparin-binding domain (HBD). This study attempted to identify the specific sequences of the VEa5 DNA aptamer that exhibit high binding affinity towards the VEGF(165) protein by truncating the original VEa5 aptamer into different segments. Using surface plasmon resonance (SPR) spectroscopy for binding affinity analysis, one of the truncated aptamers showed a >200-fold increase in the binding affinity for HBD. This truncated aptamer also exhibited high specificity to HBD with negligible binding affinity for VEGF(121), an isoform of VEGF lacking HBD. Exposing colorectal cancer cells to the truncated aptamer sequence further confirmed the binding affinity and specificity of the aptamer to the target VEGF(165) protein. Hence, our approach of aptamer truncation can potentially be useful in identifying high affinity aptamer sequences for the biological molecules and targeting them as antagonist for cancer cell detection.