gebhart/patrepeval huggingface dataset:
Entropically Driven Order in Crowded Solutions:  From Liquid Crystals to Cell Biology (1996)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTEntropically Driven Order in Crowded Solutions: From Liquid Crystals to Cell BiologyJudith HerzfeldJudith HerzfeldDepartment of Chemistry, Brandeis University, Waltham, Massachusetts 02254-9110 More by Judith HerzfeldCite this: Acc. Chem. Res. 1996, 29, 1, 31–37Publication Date (Web):January 10, 1996Publication History Received7 April 1995Published online10 January 1996Published inissue 10 January 1996https://pubs.acs.org/doi/10.1021/ar9500224https://doi.org/10.1021/ar9500224research-articleACS PublicationsCopyright © 1996 American Chemical SocietyRequest reuse permissionsArticle Views1301Altmetric-Citations92LEARN 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 SUBJECTS:Entropy,Filaments,Free energy,Peptides and proteins,Phase transitions Get e-Alerts
HIV-1 protease inhibitors based on hydroxyethylene dipeptide isosteres: An investigation into the role of the P1' side chain on structure-activity (1992)

A systematic investigation was undertaken to determine the role of the P1' sidechain in a series of hydroxyethylene isostere based inhibitors of HIV-1 protease. Substitution and homologation of the benzyl P1' side chain of the Phe-Phe isostere based pseudo peptides 1 (L-682,679) and 2 (L-685,434) with various heteroalkyl groups leads to a series of extremely potent inhibitors of the enzyme. Several examples of the most potent inhibitors were very effective in an ex vivo cell based viral spread assay using human H9 T-lymphocytes and the IIIb isolate of HIV-1. Compound 19 is 120 times more potent than 1 and 16 times more potent than 2 in inhibiting the spread of infection in this assay.
Leakage of periplasmic proteins from Escherichia coli mediated by polymyxin B nonapeptide (1986)

The effects of polymyxin B and polymyxin B nonapeptide (PMBN) on cell envelope integrity in Escherichia coli were compared. Both compounds caused loss of proteins from E. coli K-12 3300(pBR322), although PMBN released less protein than did polymyxin B. The origin of the released protein was determined both by polyacrylamide gel electrophoresis and by using specific enzyme markers (beta-lactamase in periplasm, beta-galactosidase in cytoplasm). The proteins released by both compounds were derived principally from the periplasm, accompanied in the case of polymyxin B by a low level of cytoplasmic proteins. Although polymyxin B and PMBN both caused release of periplasmic proteins, the individual proteins released by the compounds differed. The periplasmic fraction contained six principal polypeptides with molecular weights between 62,000 (polypeptide 1) and 29,000 (polypeptide 6). Polypeptide 6 was identified as the pBR322-encoded beta-lactamase, but the other proteins were not specifically identified. Polymyxin B caused considerable release of polypeptides 1, 2, and 5 with some release of polypeptides 4 and 6. PMBN released polypeptide 1 (trace), 3, 4, and 6 (trace). Scanning electron microscopy showed that polymyxin B and PMBN both caused surface damage in E. coli. However, polymyxin B produced greater morphological changes than PMBN.
Mast cells and the neurofibroma microenvironment (2010)

Neurofibromatosis type 1 (NF1) is the most common genetic disorder with a predisposition to malignancy and affects 1 in 3500 persons worldwide. NF1 is caused by a mutation in the NF1 tumor suppressor gene that encodes the protein neurofibromin. Patients with NF1 have cutaneous, diffuse, and plexiform neurofibromas, tumors comprised primarily of Schwann cells, blood vessels, fibroblasts, and mast cells. Studies from human and murine models that closely recapitulate human plexiform neurofibroma formation indicate that tumorigenesis necessitates NF1 loss of heterozygosity in the Schwann cell. In addition, our most recent studies with bone marrow transplantation and pharmacologic experiments implicate haploinsufficiency of Nf1 (Nf1(+/-)) and c-kit signaling in the hematopoietic system as required and sufficient for tumor progression. Here, we review recent studies implicating the hematopoietic system in plexiform neurofibroma genesis, delineate the physiology of stem cell factor-dependent hematopoietic cells and their contribution to the neurofibroma microenvironment, and highlight the application of this research toward the first successful, targeted medical treatment of a patient with a nonresectable and debilitating neurofibroma. Finally, we emphasize the importance of the tumor microenvironment hypothesis, asserting that tumorigenic cells in the neurofibroma do not arise and grow in isolation.
OligoWiz 2.0--integrating sequence feature annotation into the design of microarray probes (2005)

OligoWiz 2.0 is a powerful tool for microarray probe design that allows for integration of sequence annotation, such as exon/intron structure, untranslated regions (UTRs), transcription start site, etc. In addition to probe selection according to a series of probe quality parameters, cross-hybridization, T(m), position in transcript, probe folding and low-complexity, the program facilitates automatic placement of probes relative to the sequence annotation. The program also supports automatic placement of multiple probes per transcript. Together these facilities make advanced probe design feasible for scientists inexperienced in computerized information management. Furthermore, we show that probes designed using OligoWiz 2.0 give rise to consistent hybridization results (http://www.cbs.dtu.dk/services/OligoWiz2).
Type IX collagen proteoglycan from cartilage is covalently cross-linked to type II collagen. (1988)

Type IX collagen is a recently described component of cartilage. This nonfibril-forming molecule is composed of three helical (COL1-COL3) and four nonhelical domains (NC1-NC4) and also serves as a core protein for a single glycosaminoglycan side chain. To understand its spatial relationship with other matrix constituents, a peptide containing a lysine-derived cross-link was isolated and subjected to amino acid sequencing. The results show that type IX collagen is linked to type II collagen by a hydroxypyridinium cross-link. This cross-link connects the central triple helical (COL2) domain of one alpha 2(IX) chain to the amino telopeptides of two alpha 1(II) chains. The cross-link is very close to the glycosaminoglycan attachment site found in the nonhelical NC3 domain of the alpha 2(IX) chain. A model of the resulting assembly suggests that type IX collagen is located at the surface of the fibril with the short COL 3 domain and the basic globular NC4 domain projecting out from the surface of the fibril. The NC4 domain could, therefore, serve as a binding site for other matrix constituents. In this model, the glycosaminoglycan chain of type IX collagen would be located at the gap region of the fibril.
The Utility of the Emergency Department Observation Unit for Children With Abdominal Pain (2013)

The majority of children admitted to the EDOU with abdominal pain have nonsurgical causes of abdominal pain. The EDOU provides a reasonable alternative for monitoring these patients pending disposition.
The direction of gut looping is established by changes in the extracellular matrix and in cell:cell adhesion (2008)

The counterclockwise coiling of the intestines is initiated by a leftward tilt of the primitive gut tube, imparted by left-right asymmetries in the architecture of the dorsal mesentery. In silico analysis suggests that this is achieved by synergistic changes in its epithelium and mesenchyme. Within the mesenchymal compartment, cells are more densely packed on the left than on the right. In silico results indicate that this property can result from asymmetries in both extracellular matrix (ECM) and cell:cell adhesion. We find that the dorsal mesentery ECM is indeed left-right asymmetric and moreover that the adhesion molecule N-cadherin is expressed exclusively on the left side. These asymmetries are regulated by the asymmetrically expressed transcription factors Pitx2 and Isl1. Functional studies demonstrate that N-cadherin acts upstream of the changes in the ECM and is both necessary and sufficient to explain the asymmetric packing of the mesenchymal cells.
Recent Developments on the Optimization of Viscoelastic Coating (1995)

Viscoelastic coating is widely used to attenuate both vibrations and acoustic radiation of vibrating structures.A non exhausting number of papers have been published in the past to show the general performance of the technique.However, the effort made by manufacturers to build lighter and more powerful forces people to use the technique in an optimal manner.In fact, in many fields such as aerospace and aeronautics, the addition of extra weight due to the application of viscoelastic layers plays a critical role since it always drives to additional energy costs.Furthermore, the structures in these fields being frequently subject to a wide range of temperature and frequency variations, the optimization procedure should take these effects into account.In other more conventional industry applications, although the added weight is not necessarily a problem of primary concern, an overall layer setup may lead to the overheating of the machinery.This paper aims to illustrate such an issue using a simple vibrating structure.
Facilitated translocation of polypeptides through a single nanopore (2010)

The transport of polypeptides through nanopores is a key process in biology and medical biotechnology. Despite its critical importance, the underlying kinetics of polypeptide translocation through protein nanopores is not yet comprehensively understood. Here, we present a simple two-barrier, one-well kinetic model for the translocation of short positively charged polypeptides through a single transmembrane protein nanopore that is equipped with negatively charged rings, simply called traps. We demonstrate that the presence of these traps within the interior of the nanopore dramatically alters the free energy landscape for the partitioning of the polypeptide into the nanopore interior, as revealed by significant modifications in the activation free energies required for the transitions of the polypeptide from one state to the other. Our kinetic model permits the calculation of the relative and absolute exit frequencies of the short cationic polypeptides through either opening of the nanopore. Moreover, this approach enabled quantitative assessment of the kinetics of translocation of the polypeptides through a protein nanopore, which is strongly dependent on several factors, including the nature of the translocating polypeptide, the position of the traps, the strength of the polypeptide-attractive trap interactions and the applied transmembrane voltage.
Comparative development of Cryptosporidium parvum (Apicomplexa) in 11 continuous host cell lines (1994)

Using standardized media, incubation, and parasite inoculating procedures, we compared development of Cryptosporidium parvum between Madin-Darby bovine kidney (MDBK) cells and 10 additional host cell lines available through the American Type Culture Collection. Parasite development was assessed by counting parasite numbers atop monolayers in 25 random oil fields 68 h post-infection using Nomarski interference-contrast optics. Results revealed that the human ileocecal adenocarcinoma (HCT-8) cell line supported nearly twice the number of parasite developmental stages than MDBK cells or any of the other host cell types.
Identification and characterization of a novel cytoskeleton-associated pp60src substrate. (1991)

Transformation of cells by the src oncogene results in elevated tyrosine phosphorylation of two related proteins, p80 and p85 (p80/85). Immunostaining with specific monoclonal antibodies revealed a striking change of subcellular localization of p80/85 in src-transformed cells. p80/85 colocalizes with F-actin in peripheral extensions of normal cells and rosettes (podosomes) of src-transformed cells. Sequence analysis of cDNA clones encoding p80/85 revealed an amino-terminal domain composed of six copies of a direct tandem repeat, each repeat containing 37 amino acids, a carboxyl-terminal SH3 domain, and an interdomain region composed of a highly charged acidic region and a region rich in proline, serine, and threonine. The multidomain structure of p80/85 and its colocalization with F-actin in normal and src-transformed cells suggest that these proteins may associate with components of the cytoskeleton and contribute to organization of cell structure.
Pegylated Poly(Lactide) and Poly(Lactide-Co-Glycolide) Nanoparticles: Preparation, Properties and Possible Applications in Drug Delivery (2004)

The preparation, properties and potential applications in drug delivery of biocompatible and biodegradable PLA-PEG and PLGA-PEG nanoparticles are discussed. PLA-PEG and PLGA-PEG nanoparticles have been produced by emulsification-solvent evaporation, solvent displacement and salting out methods. The nanoparticles can be stored as freeze-dried powders, but an adequate amount of a suitable lyoprotectant should be added prior lyophilisation to prevent nanoparticle aggregation and retain nanoparticle redispersibility. The nanoparticles have a core-shell structure with a PLA core and a PEG coating. Their basic colloidal properties and degradation depend on copolymer composition. The PLA-PEG and PLGA-PEG nanoparticles exhibit prolonged blood circulation following intravenous administration to animals. The composition of the nanoparticles determine their biodistribution properties, probably through its effects on the effectiveness of the PEG steric barrier and the size of the nanoparticles. The ability of the PLA-PEG and PLGA-PEG nanoparticles to evade rapid phagocytocis has extended the range of sites within the body that the nanoparticles can reach, which has significant implications with regard to their application in controlled drug delivery and targeting. The PLA-PEG and PLGA-PEG nanoparticles can be loaded with a variety of bioactive agents achieving satisfactory loading, especially in the case of hydrophobic drugs. The nanoparticles have been investigated for the treatment of infectious diseases and cancer, the intravenous and mucosal delivery of proteins, and oligonucleotide and gene delivery. The results have been encouraging and PLA-PEG and PLGA-PEG nanoparticle formulations, improving the therapeutic potential of both established and new drugs, may be expected to be available in the near future.
NO synthase 2 ( NOS2 ) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease (2006)

Alzheimer's disease is characterized by two primary pathological features: amyloid plaques and neurofibrillary tangles. The interconnection between amyloid and tau aggregates is of intense interest, but mouse models have yet to reveal a direct interrelationship. We now show that NO may be a key factor that connects amyloid and tau pathologies. Genetic removal of NO synthase 2 in mice expressing mutated amyloid precursor protein results in pathological hyperphosphorylation of mouse tau, its redistribution to the somatodendritic compartment in cortical and hippocampal neurons, and aggregate formation. Lack of NO synthase 2 in the amyloid precursor protein Swedish mutant mouse increased insoluble beta-amyloid peptide levels, neuronal degeneration, caspase-3 activation, and tau cleavage, suggesting that NO acts at a junction point between beta-amyloid peptides, caspase activation, and tau aggregation.
Mediation of the DCC Apoptotic Signal by DIP13α (2002)

DCC (deleted in colorectal cancer) is a candidate tumor suppressor gene. However the function of DCC remains elusive. Previously, we demonstrated that forced expression of DCC induces apoptosis or cell cycle arrest (Chen, Y. Q., Hsieh, J. T., Yao, F., Fang, B., Pong, R. C., Cipriano, S. C. & Krepulat, F. (1999) Oncogene 18, 2747-2754). To delineate the DCC-induced apoptotic pathway, we have identified a protein, DIP13 alpha, which interacts with DCC. The DIP13 alpha protein has a pleckstrin homology domain and a phosphotyrosine binding domain. It interacts with a region on the DCC cytoplasmic domain that is required for the induction of apoptosis. Although ectopic expression of DIP13 alpha alone causes only a slight increase in apoptosis, co-expression of DCC and DIP13 alpha results in an approximately 5-fold increase in apoptosis. Removal of the DCC-interacting domain on DIP13 alpha abolishes its ability to enhance DCC-induced apoptosis. Inhibition of endogenous DIP13 alpha expression by small interfering RNA blocks DCC-induced apoptosis. Our data suggest that DIP13 alpha is a mediator of the DCC apoptotic pathway.
The role of VEGF-C/D and Flt-4 in the lymphatic metastasis of early-stage invasive cervical carcinoma (2009)

VEGF-C/D and Flt-4 may play an important role in the process of lymphatic metastasis of early-stage invasive cervical carcinoma through paracrine and autocrine mechanisms.
Cardiac Biomarkers for Detection of Myocardial Infarction: Perspectives from Past to Present (2004)

With great pleasure and anticipation in recognition of Clinical Chemistry's 50th anniversary, I have been able to arm-twist four talented scientists to document their impressive marks on the science of diagnostics in the field of cardiac biomarkers and detection of myocardial infarction. Their exciting discoveries and applications have dramatically influenced the fields of laboratory medicine and cardiology and have greatly influenced the care and management of thousands of patients suffering from coronary artery disease leading to acute myocardial infarction. As a matter of historical record, I owe a great deal of thanks to each one of the coauthors of this special report because each one has personally influenced my scientific career. I met Dr. Rosalki, during my postdoctoral training, at a national AACC meeting, where he kindly answered my numerous queries regarding creatine kinase enzymology and muscle physiology. Dr. Roberts, while serving as Director of the Coronary Care Unit at Washington University in St. Louis, generously allowed this fledgling fellow into his laboratory and shared many of his clinical and experimental findings with me. Dr. Katus, whom I first met at a scientific meeting sponsored by Boehringer Mannheim in 1986 in Bavaria, where I first became fascinated with cardiac troponin T, has remained a friend and colleague. Lastly, Dr. Ladenson, who as mentor, scientific colleague, and close friend remains ultimately responsible for both my professional growth as a clinical chemist (he was my postdoctoral fellowship advisor) and for stimulating and encouraging my goals and aspirations in the field of cardiac biomarkers. With the descriptions of the ground-breaking science described below, I am extremely excited and optimistic that the future of cardiac biomarkers is secure and open to new discoveries by the Rosalkis, Robertses, Katuses, and Ladensons of the future.
Extracellular matrix heparan sulfate proteoglycans modulate the mitogenic capacity of acidic fibroblast growth factor (1989)

Confluent cultures of human endothelial cells deposit into extracellular matrix (ECM) distinct heparan sulfate proteoglycans (HSPG) which modulate acidic fibroblast growth factor's (aFGF) ability to stimulate human endothelial cell mitogenic capacity. Extracellular matrix 35S-HSPG were isolated from cultures metabolically labelled with Na235SO4 by DEAE-Sepharose, Sepharose CL-4B, and aFGF-Affi-Gel 15 column chromatography and identified by resistance to chondroitinase ABC and sensitivity to nitrous acid. Fifty to sixty percent of the 35S-HSPG deposited into ECM do not bind aFGF. The bound 35S-HSGP (40-50% of the total counts applied) eluted from the aFGF-Affi-Gel column after the addition of buffer containing 2 M NaCl. aFGF-binding and aFGF-nonbinding 35S-HSPG were individually pooled and further purified by Sepharose CL-4B column chromatography. 35S-HSPG which bind aFGF, designated HSPGP, were 100-fold superior to heparin in augmenting the mitogenic efficacy of aFGF in sparse proliferating cultures. In contrast, however, 35S-HSPG, which did not bind aFGF, designated HSPG1, inhibited aFGF-stimulated proliferation in both sparse and subconfluent endothelial cell cultures. The majority of the biological activity of both aFGF-potentiating HSPGP and aFGF-inhibitory HSPG1 was contained in the glycosaminoglycan chains released by alkaline borohydride treatment of intact HSPGP or HSPG1, respectively. 3H-Core protein derived from HSPGP or HSPG1 contained only minor biological activity. The ability of heparitinase or heparinase (Flavobacterium heparinum) to abolish biological activity differed, depending upon the HSPG tested, also suggested that these are two distinct HSPGs.
Autoantibody From Women With Preeclampsia Induces Soluble Fms-Like Tyrosine Kinase-1 Production via Angiotensin Type 1 Receptor and Calcineurin/Nuclear Factor of Activated T-Cells Signaling (2008)

Preeclampsia is a pregnancy-specific hypertensive syndrome that causes substantial maternal and fetal morbidity and mortality. Recent evidence indicates that maternal endothelial dysfunction in preeclampsia results from increased soluble Fms-like tyrosine kinase-1 (sFlt-1), a circulating antiangiogenic protein. Factors responsible for excessive production of sFlt-1 in preeclampsia have not been identified. We tested the hypothesis that angiotensin II type 1 (AT(1)) receptor activating autoantibodies, which occur in women with preeclampsia, contribute to increased production of sFlt-1. IgG from women with preeclampsia stimulates the synthesis and secretion of sFlt-1 via AT(1) receptor activation in pregnant mice, human placental villous explants, and human trophoblast cells. Using FK506 or short-interfering RNA targeted to the calcineurin catalytic subunit mRNA, we determined that calcineurin/nuclear factor of activated T-cells signaling functions downstream of the AT(1) receptor to induce sFlt-1 synthesis and secretion by AT(1)-receptor activating autoantibodies. AT(1)-receptor activating autoantibody-induced sFlt-1 secretion resulted in inhibition of endothelial cell migration and capillary tube formation in vitro. Overall, our studies demonstrate that an autoantibody from women with preeclampsia induces sFlt-1 production via angiotensin receptor activation and downstream calcineurin/nuclear factor of activated T-cells signaling. These autoantibodies represent potentially important targets for diagnosis and therapeutic intervention.