gebhart/patrepeval huggingface dataset:
The film formation of acrylic latexes: A comprehensive model of film coalescence (1994)

Abstract A comprehensive model of film formation that was proposed in an earlier article by the present authors was evaluated for latexes having a wide range of physical properties. In this model, capillary force and interfacial forces act in tandem to promote film coalescence. The emulsion polymers studied were all based on poly(methyl methacrylate‐ co ‐butyl acrylate). The viscoelastic nature of the copolymer was varied by the addition of molecular weight modifiers (CBr 4 chain‐transfer agent and ethylene glycol dimethacrylate cross‐linking monomer) during synthesis. In contrast to the simplifications of the previous analysis, the experimental system was well characterized. The effect of water plasticization was investigated. The surface energetics of the system were studied. Also, drying kinetics were considered. Results showed that the degree of coalescence ranged from complete fusion to superficial fusion. The minimum film temperature was found to increase with increasing polymer rigidity, as is expected. Comparison of the model predictions and experimental observations validated the model. © 1994 John Wiley &amp; Sons, Inc.
Hansen Solubility Parameters (2007)

Hansen solubility parameters (HSPs) are used to predict molecular affinities, solubility, and solubility-related phenomena. Revised and updated throughout, Hansen Solubility Parameters: A User's Handbook, Second Edition features the three Hansen solubility parameters for over 1200 chemicals and correlations for over 400 materials including p
Regulation of cytokine and growth factor gene expression in human bone marrow stromal cells transformed with simian virus 40. (1990)

Marrow stromal cells are thought to regulate hematopoiesis by producing colony-stimulating factors (CSFs) and other cytokines, either constitutively or in response to mediators such as interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF alpha). The mechanisms by which these inflammatory cytokines induce CSF expression in stromal cells are not fully defined. In this study, we used human marrow stromal cells transformed by simian virus 40 (SV-MSCs) to study growth factor and cytokine gene regulation in response to IL-1 alpha and TNF alpha. IL-1 alpha induced significant and prolonged increases in steady-state mRNA levels for interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), granulocyte-macrophage CSF (GM-CSF), and, to a lesser extent, granulocyte-CSF (G-CSF); this induction was not dependent on new protein synthesis. Nuclear run-on analyses showed that IL-1 alpha transcriptionally activated the genes for IL-6, GM-CSF, and IL-1 beta, while TNF alpha transcriptionally induced expression of IL-6 and IL-1 beta. Furthermore, mRNA for IL-6 and IL-1 beta was dramatically superinduced by the combination of cycloheximide and TNF alpha. When SV-MSCs were cultured in semisolid medium, they formed colonies of blast-like cells that, when replated on plastic, resumed adherent growth. These "colony-derived" cell lines, unlike the parental SV-MSCs from which they were derived, constitutively expressed colony-stimulating activity and mRNA for GM-CSF, G-CSF, IL-6, and IL-1 beta. In this report, we show that the expression of IL-6 and IL-1 beta mRNA in the colony-derived cell lines was due, at least in part, to constitutive transcriptional activation of these genes (similar to the findings in IL-1 alpha- and/or TNF alpha-stimulated parental SV-MSCs). However, in contrast to the transcriptional activation of the GM-CSF gene seen in cytokine-induced parental SV-MSCs, GM-CSF transcripts accumulated in the colony-derived cell lines by a posttranscriptional mechanism.
Mitochondrion and Neurodegenerative Disease (2008)

The structural and functional changes of mitochondria is the early common pathological phenomena found in many neurodegenerative diseases.This article reviews mitochondria about its morphosis abnormality(including its morphosis and structural abnomalities,gene mutation),functional abnormality(including energy metabolic disorder,β-amyloid cascade reaction,oxidative stress,calcium overload,excitatory toxicity,cell apoptosis) and so on,in order to provide direction for further study of this diseases.
Gemcitabine Combined With Oxaliplatin in Advanced Pancreatic Adenocarcinoma: Final Results of a GERCOR Multicenter Phase II Study (2002)

PURPOSE: Based on preclinical in vitro synergy data, this study evaluated the activity and toxicity of a gemcitabine/oxaliplatin combination in patients with metastatic and locally advanced pancreatic adenocarcinoma. PATIENTS AND METHODS: Previously untreated metastatic and locally advanced unresectable pancreatic adenocarcinoma patients were enrolled onto this multicenter phase II study. Patients received gemcitabine 1,000 mg/m 2 as a 10-mg/m 2 /min infusion on day 1 and oxaliplatin 100 mg/m 2 as a 2-hour infusion on day 2 every 2 weeks. Patients with metastatic disease were treated until evidence of progressive disease, whereas patients with locally advanced disease received six cycles in the absence of progression, followed when appropriate by concomitant radiochemotherapy. RESULTS: Among 64 eligible patients included in eight centers, 30 had locally advanced and 34 had metastatic disease. Response rate for the 62 patients with measurable disease was 30.6% (95% confidence interval, 19.7% to 42.3%), 31.0% for locally advanced and 30.3% for metastatic patients. Among 58 assessable patients, 40% had clinical benefit. Median progression-free survival and median overall survival (OS) were 5.3 and 9.2 months, respectively, with 36% of patients alive at 1 year. Median OS for patients with metastatic disease and locally advanced disease were 8.7 and 11.5 months, respectively. With 574 treatment cycles (median per patient, nine; range, zero to 27), grade 3/4 toxicity per patient was 11% for neutropenia and thrombocytopenia, 14% for nausea or vomiting, 6.2% for diarrhea, and 11% for peripheral neuropathy, with no toxic deaths. CONCLUSION: Palliative effects, response rate, and survival observed with this well-tolerated gemcitabine/oxaliplatin combination deserve additional evaluation. A comparative study of combination therapy versus gemcitabine alone is ongoing.
Body conformable 915 MHz microstrip array applicators for large surface area hyperthermia (1992)

The optimal treatment with hyperthermia of superficially located tumors which involve large surface areas requires applicators which can physically conform to body contours, and locally alter their power deposition patterns to adjust for nonuniform temperature caused by tissue inhomogeneities and blood flow variations. A series of 915-MHz microstrip array applicators satisfying these criteria have been developed and clinically tested. Clinical and engineering design tradeoff's for practical devices are discussed. Measurements taken in tissue equivalent phantoms and a summary of clinical experiences with these microstrip arrays are presented.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Class I histocompatibility antigens and insulin receptors: evidence for interactions. (1986)

We provide evidence for an interaction between mouse class I major histocompatibility complex antigens and insulin receptors. Antibodies against class I but not class II major histocompatibility complex antigens immunoprecipitate photoaffinity-labeled hepatic insulin receptors. Haplotype specificity is demonstrated by reciprocal precipitation using anti-class I antibodies and three strains of mice. Antibodies against the 45-kDa products of either the H-2K or H-2D locus and rabbit anti-mouse beta 2-microglobulin antibodies were shown to precipitate insulin receptors. We also demonstrate the specific binding of 125I-labeled insulin and 125I-labeled epidermal growth factor, but not 125I-labeled glucagon or 125I-labeled atrial natriuretic factor, to solubilized plasma membranes immunoprecipitated with anti-H-2K antibody. These observations suggest a specific interaction between class I major histocompatibility complex antigens and certain hormone receptors.
Interleukin 12 Gene Therapy of Cancer by Peritumoral Injection of Transduced Autologous Fibroblasts: Outcome of a Phase I Study (2001)

A phase I dose-escalation clinical trial of peritumoral injections of interleukin 12 (IL-12)-transduced autologous fibroblasts was performed in patients with disseminated cancer for whom effective treatment does not exist. The goals of this study were to assess the safety and toxicities as well as the efficacy, and ancillarily the immunomodulatory effects, of peritumoral IL-12 gene transfer. Primary dermal fibroblasts cultured from the patients were transduced with retroviral vector carrying human IL-12 genes (p35 and p40) as well as the neomycin phosphotransferase gene (TFG-hIL-12-Neo). Patients received four injections at intervals of 7 days. Nine patients were enrolled in this dose-escalation study, with secreted IL-12 doses ranging from 300 ng/24 hr for the first three patients to 1000, 3000, and 5000 ng/24 hr for two patients in each subsequent dosage level. Although a definite statement cannot be made, there appears to be perturbation of systemic immunity. Also, the locoregional effects mediated by tumor necrosis factor alpha (TNF-alpha) and CD8+ T cells were observed with tumor regression. Treatment-related adverse events were limited to mild to moderate pain at the injection site; clinically significant toxicities were not encountered. Transient but clear reductions of tumor sizes were observed at the injected sites in four of nine cases, and at noninjected distant sites in one melanoma patient. Hemorrhagic necrosis of tumors was observed in two melanoma patients. These data indicate that gene therapy by peritumoral injection of IL-12-producing autologous fibroblasts is feasible, and promising in patients with advanced cancer.
Serum markers for the staging of disease activity of sarcoidosis and other interstitial lung diseases of unknown etiology. (1998)

Immunopathogenic mechanisms in sarcoidosis, idiopathic pulmonary fibrosis, and pulmonary manifestations of collagen-vascular diseases maintain an alveolitis which may lead to irreversible organ damage. The classical parameters used in the management of pulmonary involvement of these disorders are chest X-ray and pulmonary function test which do not gauge alveolitis but rather pulmonary impairment. From the immunopathogenesis several serological parameters have been delineated estimating different aspects of inflammatory processes. Cytokines, soluble cytokine receptors, metabolites, enzymes, extracellular matrix components, soluble adhesion molecules, and other serum components have been evaluated to serve as serological markers of alveolitis. The mechanisms gauged by these markers, and their clinical usefulness are discussed in this review.
Combinatorial engineering of a gene therapy vector: directed evolution of adeno‐associated virus (2005)

Our results demonstrate that combinatorial engineering overcomes the limitations of rational design approaches posed by incomplete understanding of the infectious process and at the same time offers a powerful tool to dissect basic viral biology by reverse genetics.
Treatable neurotransmitter deficiency in mild phenylketonuria (2001)

The authors describe a case of neurologic involvement in mild hyperphenylalaninemia (HPA), not due to tetrahydrobiopterin (BH(4)) deficiency, with low levels of monoamine neurotransmitter metabolites in CSF. The combined BH(4)-Phe loading test suggested a BH(4) response, confirmed by clinical improvement after BH(4) therapy. Molecular study revealed a compound heterozygosity of the phenylalanine hydroxylase alleles: a mild HPA-associated mutation (T380M) and the new mutation D151E. This case demonstrates that even mild HPA, generally considered a benign disorder, may present neurologic impairment.
Glial and neuronal proteins in serum predict outcome after severe traumatic brain injury (2004)

These results suggest that determination of serum levels of glial and neuronal proteins may add to the clinical assessment of the primary damage and prediction of outcome after severe traumatic brain injury.
Two‐component photoresists containing thermally crosslinkable photoacid generators (2000)

Abstract Bis{4‐[2′‐(vinyloxy)ethoxy]phenyl}‐4‐methoxyphenylsulfonium triflate (TPS‐2VE‐Tf) and tris{4‐[2′‐(vinyloxy)ethoxy]phenyl}sulfonium triflate (TPS‐3VE‐Tf) were synthesized as thermally crosslinkable photoacid generators (PAGs) and used in a two‐component chemically amplified photoresist system. The photoresist films formulated with poly( p ‐hydroxystyrene) (PHS) as a binder polymer and a thermally crosslinkable PAG are insolubilized in aqueous base by prebaking due to the thermal crosslinking reaction between PHS and the PAG. The insolubilization temperature of the resists and conversion of vinyl ether groups are greatly influenced by the PAG concentration and prebaking temperature, respectively. Upon exposure to deep UV and subsequent postexposure bake, the crosslinks are cleaved by photogenerated acid, leading to effective solubilization of the exposed areas. Photoresists containing TPS‐2VE‐Tf and TPS‐3VE‐Tf exhibited sensitivities of 12 and 45 mJ/cm 2 , respectively. Positive‐tone images were obtained using a 2.38 wt% aqueous tetramethylammonium hydroxide developer.
Internalization of human lactoferrin by the Jurkat human lymphoblastic T-cell line. (1996)

Binding of either iron-saturated or iron-free lactoferrin to the Jurkat human lymphoblastic T-cell line was saturable with a dissociation constant Kd of 40 nM. The total number of binding sites was estimated to be approximately 300,000. Non-specific binding did not exceed 30% of the total binding. Removal of the 4 clustered arginine residues of lactoferrin at position 2 to 5, which are involved in the interactions with heparan sulfate, did not modify the binding parameters. Therefore, the high number of low affinity binding sites previously described as responsible for the interaction of lactoferrin with either hepatocytes, enterocytes or the U937 monocytic cell line, is not involved in the binding of lactoferrin to Jurkat cells. After binding at 4 degrees C, a shift to 37 degrees C causes cell to internalize lactoferrin, with the maximum intracellular concentration found at 3 to 8 and 5 to 15 min for iron-saturated and iron-free forms, respectively. Addition of colchicine had no effect on binding or internalization. These results suggest that endocytosis of lactoferrin by Jurkat cells occurs through a receptor-mediated process. Jurkat cells internalize lactoferrin monophasically with a first-order endocytic constant K(in) of 0.060 min-1 at 37 degrees C. Confocal microscopic analysis, using fluorescein-carbohydrate-labeled lactoferrin showed that lactoferrin was mainly localized in intracellular vesicles. Following uptake, the endocytic path utilized by fluorescein-carbohydrate-labeled lactoferrin was shown to diverge from that of rhodamine-labeled serum transferrin; after internalization, lactoferrin and serum transferrin did not fully colocalize. Intracellular lactoferrin was found in endosome vesicles as assessed by electron microscopy. Raising the pH in endosomes using chloroquine led to the accumulation of lactoferrin into endosomes (acidic compartment). After internalization, Jurkat cells released both degraded and intact lactoferrin into the culture medium, suggesting that a fraction (30-40%) of the ligand is degraded at each round of endocytosis.
Structural Aspects of Troponin-Tropomyosin Regulation of Skeletal Muscle Contraction (1987)

PERSPECTIVES AND OVERVIEW . . . . . . . . . . . . ..... ... . . . . ... . . . . . . . . . . . . . . . . . . . .. . . . ... . . ... . . . . . . . . . . . . . . . . . . . . . ... . . . . . 535 THE THIN FILAMENT . ..... , .... , .... , ... .. ,., ,., .. .. ,', ... .. , ....... •.. .. 536 TROPONIN 537 Troponin C . . . ... . ..... . . . . . . ... ... . . . . . . . . . . . . . . . . ... . .... . . ... . . ........ . . ... . . . . . . ..... 537 Troponin ! ........ ... . . . .... . 543 Troponin T , 544 TROPOMYOSIN . . . ..... 545 INTERACTIONS OF REGULATORY PROTEINS . . . . . . . . ... . . ... . . . . . . . ... . ... . . . . . . . . . ...... 547 Tropomyosin-Actin ...... .... 547 TnT-Tropomyosin . ... . . ... . ... . . .... . ... . . ... . .... . ... . . ... . . .... . . . . . . ... . ......... . ... . .... . ... . .... . .... 548 TnT-TnC and TnT-Tn! 550 TnCTn! and Tn!-Actin . . . . . . . . ... 552 REGULATORY MECHANiSMS 553
Hydrophobic moments and protein structure (1982)

The structure of a protein can be analysed in terms of what may be called the “hydrophobic moments” of (1) the entire molecule and (2) of the segments of secondary structure that make up the polypeptide chain. The zeroth moment is defined as the sum of the hydrophobicities of the amino-acid residues of the structure under consideration; it is the analogue of the net charge of a cluster of point charges. The first moment, or hydrophobic dipole moment, is the analogue of the electric dipole moment of a cluster of charges. Just as the electric dipole moment measures the asymmetry of the charge distribution, the hydrophobic dipole moment measures the amphiphilicity (asymmetry of hydrophobicity) of the structure. A large hydrophobic dipole moment indicates that a structure is predominantly hydrophobic on one side and predominantly hydrophilic on the other. A quadrupole hydrophobic moment may be similarly defined. It indicates whether a protein is more hydrophobic in its interior (as for a globular protein in aqueous solution) or at its surface (as for a membrane protein).The hydrophobic dipole moment is useful in two separate applications. The first, which we have discussed elsewhere [D. Eisenberg, R. M. Weiss and T. C. Terwilliger, Nature (London), 1982, 299, 371] relates the function and secondary structure of a region of protein structure to its amino-acid sequence. For example, sequences that form surface-seeking helices have large hydrophobic dipole moments. The second application is in the analysis of interactions of a segment or domain of a protein with neighbouring regions in the protein and with other parts of the environment. In this paper we examine the hydrophobic dipole moments in the known structures of nine globular proteins and find that the moments of neighbouring segments tend to point towards each other. This suggests that the hydrophobic dipole can serve as a simple and pictorial summary of some of the forces at work in the folding of proteins. We have also found that the interactions of some macromolecules with an apolar–polar interface can be conveniently described in terms of the hydrophobic moments of the molecule and a “hydrophobic field” which reflects the hydrophobicity of the environment.
High-performance charge transfer device detectors (1988)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTHigh-performance charge transfer device detectorsJonathan V. Sweedler, Robert B. Bilhorn, Patrick M. Epperson, Gary R. Sims, and M. Bonner DentonCite this: Anal. Chem. 1988, 60, 4, 282A–291APublication Date (Print):February 15, 1988Publication History Published online22 September 2008Published inissue 15 February 1988https://pubs.acs.org/doi/10.1021/ac00155a002https://doi.org/10.1021/ac00155a002research-articleACS PublicationsRequest reuse permissionsArticle Views400Altmetric-Citations67LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
A zebrafish bmyb mutation causes genome instability and increased cancer susceptibility (2005)

A major goal of cancer research has been to identify genes that contribute to cancer formation. The similar pathology between zebrafish and human tumors, as well as the past success of large-scale genetic screens in uncovering human disease genes, makes zebrafish an ideal system in which to find such new genes. Here, we show that a zebrafish forward genetic screen uncovered multiple cell proliferation mutants including one mutant, crash&burn (crb), that represents a loss-of-function mutation in bmyb, a transcriptional regulator and member of a putative proto-oncogene family. crb mutant embryos have defects in mitotic progression and spindle formation, and exhibit genome instability. Regulation of cyclin B levels by bmyb appears to be the mechanism of mitotic accumulation in crb. Carcinogenesis studies reveal increased cancer susceptibility in adult crb heterozygotes. Gene-expression signatures associated with loss of bmyb in zebrafish are also correlated with conserved signatures in human tumor samples, and down-regulation of the B-myb signature genes is associated with retention of p53 function. Our findings show that zebrafish screens can uncover cancer pathways, and demonstrate that loss of function of bmyb is associated with cancer.
Protein‐misfolding diseases and chaperone‐based therapeutic approaches (2006)

A large number of neurodegenerative diseases in humans result from protein misfolding and aggregation. Protein misfolding is believed to be the primary cause of Alzheimer's disease, Parkinson's disease, Huntington's disease, Creutzfeldt-Jakob disease, cystic fibrosis, Gaucher's disease and many other degenerative and neurodegenerative disorders. Cellular molecular chaperones, which are ubiquitous, stress-induced proteins, and newly found chemical and pharmacological chaperones have been found to be effective in preventing misfolding of different disease-causing proteins, essentially reducing the severity of several neurodegenerative disorders and many other protein-misfolding diseases. In this review, we discuss the probable mechanisms of several protein-misfolding diseases in humans, as well as therapeutic approaches for countering them. The role of molecular, chemical and pharmacological chaperones in suppressing the effect of protein misfolding-induced consequences in humans is explained in detail. Functional aspects of the different types of chaperones suggest their uses as potential therapeutic agents against different types of degenerative diseases, including neurodegenerative disorders.
Signaling to NF- B: Regulation by Ubiquitination (2009)

The NF-kappaB pathway is a ubiquitous stress response that activates the NF-kappaB family of transcription factors. Antigen receptors, receptors of the innate immune system, and certain intracellular stressors are potent activators of this pathway. The transcriptional program that is activated is both antiapoptotic and highly proinflammatory. Indeed, any compromise in engagement of the pathway results in immunodeficiency, whereas constitutive activation generates a sustained inflammatory response that may promote malignancy. As such, NF-kappaB activation is under tight regulation by a number of post-translational modifications, including phosphorylation and ubiquitination. This article attempts to synthesize our current knowledge regarding the regulation of NF-kappaB signaling by ubiquitination, specifically highlighting the biochemical basis for both positive and negative feedback loops that function in unison to generate coordinated signals that are essential for the viability of metazoan animals.