gebhart/patrepeval huggingface dataset:
Shape and nonrigid motion estimation through physics-based synthesis (1993)

A physics-based framework for 3-D shape and nonrigid motion estimation for real-time computer vision systems is presented. The framework features dynamic models that incorporate the mechanical principles of rigid and nonrigid bodies into conventional geometric primitives. Through the efficient numerical simulation of Lagrange equations of motion, the models can synthesize physically correct behaviors in response to applied forces and imposed constraints. Applying continuous Kalman filtering theory, a recursive shape and motion estimator that employs the Lagrange equations as a system model is developed. The system model continually synthesizes nonrigid motion in response to generalized forces that arise from the inconsistency between the incoming observations and the estimated model state. The observation forces also account formally for instantaneous uncertainties and incomplete information. A Riccati procedure updates a covariance matrix that transforms the forces in accordance with the system dynamics and prior observation history. Experiments involving model fitting and tracking of articulated and flexible objects from noisy 3-D data are described.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Mutation Patterns of the Reverse Transcriptase and Protease Genes in Human Immunodeficiency Virus Type 1-Infected Patients Undergoing Combination Therapy: Survey of 787 Sequences (1999)

The aim of the present study was to evaluate the resistance-associated mutations in 302 human immunodeficiency virus type 1 (HIV-1)-infected patients receiving combination therapy and monitored in Marseille, France, hospitals from January 1997 to June 1998. In the reverse transcriptase (RT) gene, the most frequent mutations were found at codons 215 (53%), 41 (34%), and 67, 70, 184, and 210 (>20%). One deletion and two insertions in the beta3-beta4 hairpin loop of the finger subdomain (codon 69) were detected. Interesting associations and/or exclusions of specific mutations were observed. In 96% of RT genes, a mutation at codon 70 (most frequently, K70R) was associated with a wild-type genotype at position 210 (P < 10(-5)). Similarly, a mutation at codon 210 (most frequently, L210W) was generally associated with mutations at codons 41 (92%) and 215 (96%) but not at codon 219 (16%) or codon 70 (4%) (P < 10(-5)). In the protease gene, the most prevalent mutations were at codons 63 (84%), followed by codons 10, 36, 71, 77, and 93 (ca. 20%). As for RT, pairwise associations of mutations were observed. Analysis of the mutation patterns for patients with undetectable HIV-1 loads revealed a high proportion (65%) of wild-type RT genotypes but only 18% wild-type protease genotypes. For patients with high viral loads (>100,000 copies/ml), more than 50% of the RT and protease genes displayed three or more mutations. The significant correlation between the level of viremia in plasma and the number of resistance mutations in the protease (P = 0.007) and RT (P = 0.00078) genes strengthens the importance of defining the genotype of the predominant HIV-1 quasispecies before initiating antiretroviral therapy.
The Role of Serotonin in Schizophrenia and the Place of Serotonin-Dopamine Antagonist Antipsychotics (1995)

After four decades of the use of antipsychotic drugs that target the dopamine D2 receptor as the initial site of action, a new strategy for antipsychotic therapy has emerged and, with it, new hope for greater efficacy and fewer side effects. This new strategy involves identifying drugs with strong serotonin (5-hydroxytryptamine) 5-HT2A receptor relative to dopamine D2 receptor blocking properties. Clozapine is now known to have these properties, but risperidone is the first drug to be designed intentionally to have these properties. Others are being developed. These drugs, the serotonin-dopamine antagonists (SDAs), may prove to have many other uses in psychiatry beyond schizophrenia because of their low propensity to cause extrapyramidal symptoms. Their pharmacologic mechanism of action may be more complex than only strong 5-HT2A and weak D2 block, e.g., 5-HT2C and D4 receptor blockade. Nevertheless, the SDAs are proving to be valuable tools in the analysis of both normal brain function and the etiology of schizophrenia.
B Cell Developmental Requirement for the G α i2 Gene (2003)

Null mutation of the Galphai2 trimeric G protein results in a discrete and profound mucosal disorder, including inflammatory bowel disease (IBD), attenuation of IL-10 expression, and immune function polarized to Th1 activity. Genetic and adoptive transfer experiments have established a role for B cells and IL-10 in mucosal immunologic homeostasis and IBD resistance. In this study, we addressed the hypothesis that Galphai2 is required for the development of IL-10-producing B cells. Galphai2(-/-) mice were reduced in the relative abundance of marginal zone (MZ), transitional type 2 (T2), and B-1a B cells and significantly increased in follicular mature and B-1b B cells. Reconstitution of RAG2(-/-) mice with Galphai2(-/-) bone marrow induced an IBD-like colitis and a deficiency in absolute numbers of MZ, T2, and B-1 B cells. Thus, the Galphai2(-/-) genotype in colitis susceptibility and B cell development involved a cis effect within the hemopoietic compartment. In vitro, the B cell population of Galphai2(-/-) mice was functionally deficient in LPS-induced proliferation and IL-10 production, consistent with the exclusive capacity of T2 and MZ cell subpopulations for LPS responsiveness. In vivo, Galphai2(-/-) mice were selectively impaired for the IgM response to T-independent type II, consistent with the relative depletion of MZ and peritoneal B-1 subpopulations. Collectively, these results reveal a selective role for Galphai2 in MZ and B-1 B cell development. Disorders of this Galphai2-dependent process in B cell development may represent a mechanism for IBD susceptibility.
Characterization of a Mucin cDNA Clone Isolated from HT-29 Mucus-secreting Cells. (1995)

A 3310base pair mucin eDNA clone (L31) was isolated from an HT29-MTX expression library using a polyclonal serum specific for normal gastric mucosa. It shows a high level of identity (98.6%) to clone NP3a isolated from a nasal polyp eDNA library (Meerzaman, D., Charles, P., Daskal, E., Polymeropoulos, M. H., Martin, B. M., and Rose, M
Prostaglandin I2-IP Signaling Blocks Allergic Pulmonary Inflammation by Preventing Recruitment of CD4+ Th2 Cells into the Airways in a Mouse Model of Asthma (2007)

PGI(2) plays a key role in limiting Th2-mediated airway inflammation. In studies to investigate the mechanism underlying such regulation, we found that the PGI(2) receptor, IP, is preferentially expressed by effector CD4(+) Th2 cells, when compared with Th1 cells. Adoptive transfer of DO11.10 Th2 cells pretreated with PGI(2) resulted in considerably attenuated pulmonary inflammation and airway hyperreactivity in BALB/c recipient mice in response to OVA inhalation. This suppression was independent of increased cAMP levels, because pretreatment of Th2 cells with dibutyryl cAMP before transfer had no effect on airway inflammation. Moreover, PGI(2) pretreatment of Th2 cells suppressed the ability of the cells to infiltrate the lungs but not the spleen. In vitro studies showed that PGI(2) did not affect IL-4 and IL-5 production or the level of IFN-gamma by the T cells. However, the prostanoid strongly inhibited CCL17-induced chemotaxis of CD4(+) Th2 but not Th1 cells. The IP was implicated in this process since migration of wild-type Th2 cells in response to CCL17 was markedly reduced following treatment with PGI(2), whereas IP-deficient Th2 cells were unaffected and migrated effectively. Collectively, these experiments suggest that PGI(2), which is generated by endothelial cells during lung inflammatory response, serves to limit the influx of Th2 cells to the airways. Our results identify PGI(2)-IP as an important pathway for inhibiting allergic pulmonary inflammation by controlling recruitment of CD4(+) Th2 cells into the inflammatory site.
Optical waveguide biosensors constructed with subwavelength gratings (2006)

The reflection resonance spectrum of a subwavelength diffraction-grating-coupled waveguide is used to analyze biomolecular interactions in real time. By detecting this resonance wavelength shift, the optical waveguide biosensor provides the ability to identify the kinetics of the biomolecular interaction on an on-line basis without the need for extrinsic labeling of the biomolecules. A theoretical analysis of the subwavelength optical waveguide biosensor is performed. A biosensor with a narrow reflection resonance spectrum, and hence an enhanced detection resolution, is then designed and fabricated. Currently, the detection limit of the optical waveguide sensor is approximately 10(-5) refractive-index units. The biosensor is successfully applied to study of the dynamic response of an antibody interaction with protein G adsorbed on the sensing surface.
The legal and ethical aspects of telemedicine. 2: Data protection, security and European law (1998)

The electronic record may be subject to abuses that can be carried out on a large scale and cause great damage. A wide range of data protection and information security measures will need to be taken to ensure the quality and integrity of such records. A European Union directive was formally adopted in 1995 which sets the obligations of those responsible for data processing as well as a number of important rights for individuals. The responsible teleconsultant or medical officer, as the data controller, must make sure these measures are enforced. In the case of the transmission of medical records to another location, the original data controller may remain liable for abuses. But as different elements of the records are spread throughout the different departments of a hospital or across different geographical locations, it may become difficult to ascertain who is responsible for protecting and controlling what. To this end, the designation of liability by contractual means, between the hospital and remote users of a telemedicine network, would be the clearest and most straightforward way of achieving uniformity and predictability in terms of the distribution of responsibility for data protection and security.
Tumor Necrosis Factor-α Induces Serum Amyloid A3 in Mouse Granulosa Cells (2004)

TNF-alpha has significant inhibitory effects on steroidogenesis and folliculogenesis and is associated with several inflammatory responses. Because ovulation is an inflammatory reaction, the effects of TNF on the family of acute-phase proteins in granulosa cells were investigated. Granulosa cells from immature mice at 28 d of age were cultured in the presence of 10 ng TNF/ml for 24 h. Serum amyloid A3 (SAA3), a main acute-phase protein, was induced by TNF in granulosa cells. The other isoforms of serum amyloid proteins SAA1, SAA2, and SAA4 were neither expressed in granulosa cells nor induced by TNF. TNF did not induce SAA3 mRNA in granulosa cells from TNF receptor type 1 (TNFR1) knockout mice, although SAA3 mRNA was induced within 3 h after TNF treatment in wild-type cells. Two SAA3 promoters, -617/+73 and -198/+73, were responsive to TNF and to p65, a component of the TNF signaling molecule nuclear factor (NF)-kappaB. The -106/+73 promoter of SAA3 lacking a NF-kappaB-like site was not responsive to TNF or p65. In granulosa cells from TNFR1 knockout mice, the SAA3 promoter (-198/+73) was responsive to transfection with the p65 component of NF-kappaB, but neither TNF treatment nor overexpression of the p50 component of NF-kappaB increased promoter activity. Similar results were observed in the murine ovarian granulosa tumor cell line (OV3121-1). Overexpression of the inhibitor of NF-kappaB (called IkappaB) blocked SAA3 promoter activity induced by TNF and by p65 in OV3121-1 cells. Closer analysis of deletion mutants of the SAA3 promoter revealed the necessity of a NF-kappaB like site for responsiveness to TNF in the OV3121-1 cells. TNF rapidly increased p65 in OV3121-1 nuclei when compared with controls not treated with TNF. TNF also increased phospho-IkB and SAA3 in whole-cell homogenates as determined by Western blots. Thus, TNF likely increased SAA3 promoter activity and protein by activating NF-kappaB signaling via TNFR1 in mouse granulosa cells. SAA3 is a novel gene in granulosa cells with yet unknown functions in the ovary.
Surfactant Protein-D Regulates Surfactant Phospholipid Homeostasis in Vivo (1998)

Surfactant protein D (SP-D) is a 43-kDa member of the collectin family of collagenous lectin domain-containing proteins that is expressed in epithelial cells of the lung. The SP-D gene was targeted by homologous recombination in embryonic stem cells that were used to produce SP-D (+/-) and SP-D (-/-) mice. Both SP-D (-/-) and SP-D (+/-) mice survived normally in the perinatal and postnatal periods. Whereas no abnormalities were observed in SP-D (+/-) mice, alveolar and tissue phosphatidylcholine pool sizes were markedly increased in SP-D (-/-) mice. Increased numbers of large foamy alveolar macrophages and enlarged alveoli were also observed in SP-D (-/-) mice. Phospholipid composition was unaltered in SP-D (-/-) mice, but surfactant morphology was abnormal, consisting of dense phospholipid membranous arrays with decreased tubular myelin. The pulmonary lipoidosis in the SP-D (-/-) mice was not associated with accumulation of surfactant proteins B or C, or their mRNAs, distinguishing the disorder from alveolar proteinosis syndromes. Surfactant protein A mRNA was reduced and, SP-A protein appeared to be reduced in SP-D (-/-) compared with wild type mice. Targeting of the mouse SP-D gene caused accumulation of surfactant lipid and altered phospholipid structures, demonstrating a previously unsuspected role for SP-D in surfactant lipid homeostasis in vivo.
Bacterial flagellar structure and function (1988)

Historical introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 442 Some salient features of flagellar motility. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .442 Structure of the filament, hook, and basal body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ,443 Image analysis of flagellar structures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ,444 Components of the filament hook basal-body complex . . . . . . . . . . . . . . . . . . . . . . . . 447 TheMotproteins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447 Flagellar switch components. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ,448 Relationship to the cell surface. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ,448 Organelle assembly. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .449 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 450
STUDIES ON CHITAN (β-(1 → 4)-LINKED 2-ACETAMIDO-2-DEOXY-D-GLUCAN) FIBERS OF THE DIATOM THALASSIOSIRA FLUVIATILIS HUSTEDT: II. PROTON MAGNETIC RESONANCE, INFRARED, AND X-RAY STUDIES (1966)

The extracellular fibers attached to the diatom Thalassiosirafluviatilis have been shown to be pure β-(1 → 4)-linked 2-acetamido-2-deoxy-D-glucan. This polysaccharide was given the systematic trivial name chitan to distinguish it from chitin, which is not a chemically distinct species and which has a radically different X-ray diffraction pattern and infrared spectrum. Proton magnetic resonance studies on the acid hydrolysis of chitan have established that the hydrolysis occurred in three distinct steps: (a) the degradation of the polysaccharide to smaller polymeric units, (b) the production of N-acetylglucosamine from the latter, and (c) the conversion of N-acetylglucosamine into glucosamine and acetic acid. X-ray and infrared studies have shown that chitan has a different macrostructure from that of arthropod chitin. Chitan is completely crystalline and can be converted irreversibly into a form indistinguishable from that of chitin by treatment with hot aqueous lithium thiocyanate. Boiling chitan in water converts it into a second crystalline modification, possibly a hydrate, which can be reconverted into the starting material by drying invacuo. The exceptionally sharp infrared spectrum of chitan allows a more unequivocal assignment of a number of bands common to chitan and chitin, and provides information about the nature of the bands at 1 626 and 1 656 cm −1 in the spectrum of chitin. The correlation of the bands in the region of 840 to 890 cm −1 with the configuration at the anomeric center of glycopyranose derivatives is discussed.
Microsatellite instability and promoter hypermethylation of MLH1 and MSH2 in patients with sporadic colorectal cancer. (2011)

Our data suggest that sporadic CRCs with MSI/LOH are more aggressive, develop earlier and progress faster to more advanced stage. The most frequent cause of failure of DNA MMR system appeared to be the hypermethylation of CpG islands of the promoter region of MLH1, whereas the methylation of MSH2 was a rare event.
Endothelial Extracellular Matrix (2005)

The extracellular matrix (ECM) is critical for all aspects of vascular biology. In concert with supporting cells, endothelial cells (ECs) assemble a laminin-rich basement membrane matrix that provides structural and organizational stability. During the onset of angiogenesis, this basement membrane matrix is degraded by proteinases, among which membrane-type matrix metalloproteinases (MT-MMPs) are particularly significant. As angiogenesis proceeds, ECM serves essential functions in supporting key signaling events involved in regulating EC migration, invasion, proliferation, and survival. Moreover, the provisional ECM serves as a pliable scaffold wherein mechanical guidance forces are established among distal ECs, thereby providing organizational cues in the absence of cell-cell contact. Finally, through specific integrin-dependent signal transduction pathways, ECM controls the EC cytoskeleton to orchestrate the complex process of vascular morphogenesis by which proliferating ECs organize into multicellular tubes with functional lumens. Thus, the composition of ECM and therefore the regulation of ECM degradation and remodeling serves pivotally in the control of lumen and tube formation and, finally, neovessel stability and maturation.
Identification and Characterization of the Immunodominant Rat HER-2/neu MHC Class I Epitope Presented by Spontaneous Mammary Tumors from HER-2/neu-Transgenic Mice (2003)

The HER-2/neu (neu-N)-transgenic mice are a clinically relevant model of breast cancer. They are derived from the parental FVB/N mouse strain and are transgenic for the rat form of the proto-oncogene HER-2/neu (neu). In this study, we report the identification of a MHC class I peptide in the neu protein that is recognized by CD8(+) T cells derived from vaccinated FVB/N mice. This 10-mer was recognized by all tumor-specific FVB/N T cells generated regardless of the TCR Vbeta region expressed by the T cell or the method of vaccination used, establishing it as the immunodominant MHC class I epitope in neu. T cells specific for this epitope were able to cure FVB/N mice of transplanted neu-expressing tumor cells, demonstrating that this is a naturally processed peptide. Altered peptide analogs of the epitope were analyzed for immunogenicity. Vaccination with dendritic cells pulsed with a heteroclitic peptide provided FVB/N and neu-N mice with increased protection against tumor challenge as compared with mice immunized with dendritic cells loaded with either wild-type or irrelevant peptide. Discovery of this epitope allows for better characterization of the CD8(+) T cell responses in the neu-N mouse model in which neu-specific tolerance must be overcome to produce effective antitumor immunity.
Enzymatic Preparation of (S)-3-Hydroxytetradecanoic Acid and Synthesis of Unnatural Analogues of Lipid A Containing the (S)-Acid (1997)

Abstract Synthesis of unnatural analogues, that contain (S)-3-hydroxytetradecanoyl moieties in place of the corresponding natural (R)-isomers, of both lipid A and its biosynthetic precursor, designated precursor Ia or lipid IVA, has been achieved through our recently developed procedure. (S)-3-Hydroxytetradecanoic acid was prepared from its racemate through the optical resolution by the use of a lipase and subsequent fractional recrystallization. The (S)-acyl analogue of lipid A exhibited slightly stronger interleukin-6 inducing activity than the corresponding natural lipid A, and the (S)-acyl analogue of the biosynthetic precursor was far more active than the natural precursor in inhibiting the induction of interleukin-6 by lipopolysaccharide.
Gene expression profiling of human prostate cancer stem cells reveals a pro-inflammatory phenotype and the importance of extracellular matrix interactions (2008)

We describe an expression signature of 581 genes whose levels are significantly different in prostate cancer stem cells. Functional annotation of this signature identified the JAK-STAT pathway and focal adhesion signaling as key processes in the biology of cancer stem cells.
Aminoacyl-tRNA Synthesis (2000)

Aminoacyl-tRNAs are substrates for translation and are pivotal in determining how the genetic code is interpreted as amino acids. The function of aminoacyl-tRNA synthesis is to precisely match amino acids with tRNAs containing the corresponding anticodon. This is primarily achieved by the direct attachment of an amino acid to the corresponding tRNA by an aminoacyl-tRNA synthetase, although intrinsic proofreading and extrinsic editing are also essential in several cases. Recent studies of aminoacyl-tRNA synthesis, mainly prompted by the advent of whole genome sequencing and the availability of a vast body of structural data, have led to an expanded and more detailed picture of how aminoacyl-tRNAs are synthesized. This article reviews current knowledge of the biochemical, structural, and evolutionary facets of aminoacyl-tRNA synthesis.