gebhart/patrepeval huggingface dataset:
Free-form surface registration using surface signatures (1999)

The paper introduces a new free-form surface representation scheme for the purpose of fast and accurate registration and matching. Accurate registration of surfaces is a common task in computer vision. The proposed representation scheme captures the surface curvature information seen from certain points and produces images called surface signatures at these points. Matching signatures of different surfaces enables the recovery of the transformation parameters between these surfaces. We propose to use template matching to compare the signature images. To enable partial matching, another criterion, the overlap ratio, is used. This representation scheme can be used as a global representation of the surface as well as a local one and performs near real time registration. We show that the signature representation can be used to match objects in 3D scenes in the presence of clutter and occlusion. Applications presented include free-form object matching, multimodal medical volume registration and dental teeth reconstruction from intra-oral images.
VEGF Receptor Blockade Markedly Reduces Retinal Microglia/Macrophage Infiltration into Laser-Induced CNV (2013)

Although blocking VEGF has a positive effect in wet age-related macular degeneration (AMD), the effect of blocking its receptors remains unclear. This was an investigation of the effect of VEGF receptor (VEGFR) 1 and/or 2 blockade on retinal microglia/macrophage infiltration in laser-induced choroidal neovascularization (CNV), a model of wet AMD. CNV lesions were isolated by laser capture microdissection at 3, 7, and 14 days after laser and analyzed by RT-PCR and immunofluorescence staining for mRNA and protein expression, respectively. Neutralizing antibodies for VEGFR1 or R2 and the microglia inhibitor minocycline were injected intraperitoneally (IP). Anti-CD11b, CD45 and Iba1 antibodies were used to confirm the cell identity of retinal microglia/macrophage, in the RPE/choroidal flat mounts or retinal cross sections. CD11b(+), CD45(+) or Iba1(+) cells were counted. mRNA of VEGFR1 and its three ligands, PlGF, VEGF-A (VEGF) and VEGF-B, were expressed at all stages, but VEGFR2 were detected only in the late stage. PlGF and VEGF proteins were expressed at 3 and 7 days after laser. Anti-VEGFR1 (MF1) delivered IP 3 days after laser inhibited infiltration of leukocyte populations, largely retinal microglia/macrophage to CNV, while anti-VEGFR2 (DC101) had no effect. At 14 days after laser, both MF1 and DC101 antibodies markedly inhibited retinal microglia/macrophage infiltration into CNV. Therefore, VEGFR1 and R2 play differential roles in the pathogenesis of CNV: VEGFR1 plays a dominant role at 3 days after laser; but both receptors play pivotal roles at 14 days after laser. In vivo imaging demonstrated accumulation of GFP-expressing microglia into CNV in both CX3CR1(gfp/gfp) and CX3CR1(gfp/+) mice. Minocycline treatment caused a significant increase in lectin(+) cells in the sub-retinal space anterior to CNV and a decrease in dextran-perfused neovessels compared to controls. Targeting the chemoattractant molecules that regulate trafficking of retinal microglia/macrophage appears to be a compelling therapeutic strategy to control CNV and treat wet AMD.
Laser-Assisted Catalytic Growth of Single Crystal GaN Nanowires (1999)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTLaser-Assisted Catalytic Growth of Single Crystal GaN NanowiresXiangfeng Duan and Charles M. LieberView Author Information Department of Chemistry and Chemical Biology Harvard University, Cambridge, Massachusetts 02138 Cite this: J. Am. Chem. Soc. 2000, 122, 1, 188–189Publication Date (Web):December 18, 1999Publication History Received18 October 1999Published online18 December 1999Published inissue 1 January 2000https://pubs.acs.org/doi/10.1021/ja993713uhttps://doi.org/10.1021/ja993713urapid-communicationACS PublicationsCopyright © 2000 American Chemical SocietyRequest reuse permissionsArticle Views5248Altmetric-Citations755LEARN 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:Catalysts,Crystal structure,Crystallization,Nanowires,Nitrides Get e-Alerts
E1A Induces Phosphorylation of the Retinoblastoma Protein Independently of Direct Physical Association between the E1A and Retinoblastoma Products (1991)

We have studied the initial effects of adenovirus E1A expression on the retinoblastoma (RB) gene product in normal quiescent cells. Although binding of the E1A products to pRB could, in theory, make pRB phosphorylation unnecessary for cell cycle progression, we have found that the 12S wild-type E1A product is capable of inducing phosphorylation of pRB in normal quiescent cells. The induction of pRB phosphorylation correlates with E1A-mediated induction of p34cdc2 expression and kinase activity, consistent with the possibility that p34cdc2 is a pRB kinase. Expression of simian virus 40 T antigen induces similar effects. Induction of pRB phosphorylation is independent of the pRB binding activity of the E1A products; E1A domain 2 mutants do not bind detectable levels of pRB but remain competent to induce pRB phosphorylation and to activate cdc2 protein kinase expression and activity. Although the kinetics of induction are slower, domain 2 mutants induce wild-type levels of pRB phosphorylation and host cell DNA synthesis and yet fail to induce cell proliferation. These results imply that direct physical interaction between the RB and E1A products does not play a required role in the early stages of E1A-mediated cell cycle induction and that pRB phosphorylation is not, of itself, sufficient to allow quiescent cells to divide. These results suggest that the E1A products do not need to bind pRB in order to stimulate resting cells to enter the cell cycle. Indeed, a more important role of the RB binding activity of the E1A products may be to prevent dividing cells from returning to G0.
Oligocrystalline Shape Memory Alloys (2012)

Abstract Copper‐based shape memory alloys (SMAs) exhibit excellent shape memory properties in single crystalline form. However, when they are polycrystalline, their shape memory properties are severely compromised by brittle fracture arising from transformation strain incompatibility at grain boundaries and triple junctions. Oligocrystalline shape memory alloys (oSMAs) are microstructurally designed SMA structures in which the total surface area exceeds the total grain boundary area, and triple junctions can even be completely absent. Here it is shown how an oligocrystalline structure provides a means of achieving single crystal‐like SMA properties without being limited by constraints of single crystal processing. Additionally, the formation of oSMAs typically involves the reduction of the size scale of specimens, and sample size effects begin to emerge. Recent findings on a size effect on the martensitic transformation in oSMAs are compared and a new regime of heat transfer associated with the transformation heat evolution in these alloys is discussed. New results on unassisted two‐way shape memory and the effect of loading rate in oSMAs are also reported.
Synergistic regulation of serotonin and opioid signaling contributes to pain insensitivity in Nav1.7 knockout mice (2017)

Genetic loss of the voltage-gated sodium channel Na<sub>v</sub>1.7 (Na<sub>v</sub>1.7<sup>-/-</sup>) results in lifelong insensitivity to pain in mice and humans. One underlying cause is an increase in the production of endogenous opioids in sensory neurons. We analyzed whether Na<sub>v</sub>1.7 deficiency altered nociceptive heterotrimeric guanine nucleotide-binding protein-coupled receptor (GPCR) signaling, such as initiated by GPCRs that respond to serotonin (pronociceptive) or opioids (antinociceptive), in sensory neurons. We found that the nociceptive neurons of Na<sub>v</sub>1.7 knockout (Na<sub>v</sub>1.7<sup>-/-</sup>) mice, but not those of Na<sub>v</sub>1.8 knockout (Na<sub>v</sub>1.8<sup>-/-</sup>) mice, exhibited decreased pronociceptive serotonergic signaling through the 5-HT<sub>4</sub> receptors, which are Gα<sub>s</sub>-coupled GPCRs that stimulate the production of cyclic adenosine monophosphate resulting in protein kinase A (PKA) activity, as well as reduced abundance of the RIIβ regulatory subunit of PKA. Simultaneously, the efficacy of antinociceptive opioid signaling mediated by the Gα<sub>i</sub>-coupled mu opioid receptors was increased. Consequently, opioids inhibited more efficiently tetrodotoxin-resistant sodium currents, which are important for pain-initiating neuronal activity in nociceptive neurons. Thus, Na<sub>v</sub>1.7 controls the efficacy and balance of GPCR-mediated pro- and antinociceptive intracellular signaling, such that without Na<sub>v</sub>1.7, the balance is shifted toward antinociception, resulting in lifelong endogenous analgesia.
Comparison of ethanol and temperature tolerance of Zymomonas mobilis strain in glucose and molasses medium (2007)

The effect of temperature and exogenous ethanol was evaluated on the ethanol production potential of Zymomonas mobilis MTCC 2428 as an alternative to the classic and widespread use of Saccharomyces cerevisiae . At 30 °C, this strain produced the maximum amounts of ethanol, i.e. 4.0 and 3.3% (v/v) after utilizing 98 and 83% (w/v) sugar on glucose and molasses medium, respectively. While at higher temperatures (35 & 40 °C), the ethanol production by the strain decreased. Moreover, the strain was able to operate in the presence of 8% (v/v) ethanol in glucose medium at 30 °C; whereas it tolerated only 6 and 2% (v/v) ethanol at 35 and 40 °C, respectively. At the respective temperatures, further higher concentrations of the supplemented ethanol were found to be inhibitory to the isolate.
Human Immunodeficiency Virus Type 1 Neutralizing Antibody Serotyping Using Serum Pools and an Infectivity Reduction Assay (1996)

Classification of human immunodeficiency virus type 1 (HIV-1) by neutralization serotype may be important for the design of active and passive immunization strategies. Neutralizing antibody serotyping is hindered by the lack of standard reagents and assay format, and by the weak activity of many individual sera. To facilitate cross-clade neutralization analysis, we used an infectivity reduction assay (IRA) and selected clade-specific serum (or plasma) pools from subjects infected with clade B and E HIV-1, respectively. Several serum pools were utilized; some were selected for strong neutralizing activity against intraclade viruses and others were derived from conveniently available samples. Against a panel of 51 clade B and E viruses, serum pools displayed strong neutralization of most intraclade viruses and significantly diminished cross-clade neutralization. Results were confirmed against a blinded panel of 20 viruses. The data indicate that the phylogenetic classification of virus subtypes B and E corresponds to two distinct neutralization serotypes. This approach to neutralizing antibody serotyping may be useful in defining the antigenic relationship among viruses from other clades.
Exosome Research and Co-culture Study (2018)

In biological systems, extracellular vesicles including exosomes have recently been revealed to play a significant role in the communication between various cells, and the number of papers on this subject has dramatically increased. In current conventional exosome studies, the standard research method is to use liquid biopsies to analyze extracts of various disease exosomes. However, exosomes are only one of many key players in natural cellular interactions. Reproducing the phenomena occurring in vivo and investigating the interactions are required in order to examine their role fully. For exosome research, an alternative to the liquid biopsy method for observing natural interactions is the co-culturing technique. It does not require an exosome extraction procedure, and while the technique has been used in many studies thus far, its application to exosome research has been limited. However, the use of co-culturing technologies is necessary to examine the essential interactions of exosomes. An overview of exosome research methodologies and co-culturing systems is thus provided here.
N-Glycans on secretory component (2011)

Human beings live in symbiosis with billions of microorganisms colonizing mucosal surfaces. The understanding of the mechanisms underlying this fine-tuned intestinal balance has made significant processes during the last decades. We have recently demonstrated that the interaction of SIgA with Gram-positive bacteria is essentially based on Fab-independent, glycan-mediated recognition. Results obtained using mouse hybridoma- and colostrum-derived secretory IgA (SIgA) consistently show that N-glycans present on secretory component (SC) play a crucial role in the process. Natural coating may involve specific Gram-positive cell wall components, which may explain selective recognition at the molecular level. More widely, the existence of these complexes is involved in the modulation of intestinal epithelial cell (IEC) responses in vitro and the formation of intestinal biofilms. Thus, SIgA may act as one of the pillars in homeostatic maintenance of the microbiota in the gut, adding yet another facet to its multiple roles in the mucosal environment.
Peripheral nerve injury down‐regulates CNTF expression in adult rat sciatic nerves (1992)

Ciliary neurotrophic factor (CNTF) is a 200-amino acid protein expressed in high concentrations by peripheral nerves and is thought to be important for the survival and regeneration of injured motoneurons (Lin et al., J Biol Chem 265:8942-8947, 1990). To better understand CNTF's role in nerve injury we have characterized the effects of crush injury on the expression of CNTF in adult rat sciatic nerves using specific antibody and RNA probes. Following a crush injury, both the protein and mRNA levels undergo pronounced decreases distal to the crush. These changes in CNTF expression were qualitatively distinct from changes in the expression of the low-affinity NGF receptor (p75NGFR), which increases following crush. Thus, the changes in CNTF levels do not reflect an overall down-regulation of mRNA during degeneration, and are inconsistent with the proposed role of CNTF in neuronal injury, since its levels are decreasing at the same time as the requirement for neurotrophic support is increasing.
A unique spacer domain of synaptotagmin IV is essential for Golgi localization (2001)

Synaptotagmin (Syt) family members consist of six separate domains: a short amino terminus, a single transmembrane domain, a spacer domain, a C2A domain, a C2B domain and a short carboxyl (C) terminus. Despite sharing the same domain structures, several synaptotagmin isoforms show distinct subcellular localization. Syt IV is mainly localized at the Golgi, while Syt I, a possible Ca(2+)-sensor for secretory vesicles, is localized at dense-core vesicles and synaptic-like microvesicles in PC12 cells. In this study, we sought to identify the region responsible for the Golgi localization of Syt IV by immunocytochemical and biochemical analyses as a means of defining the distinct subcellular localization of the synaptotagmin family. We found that the unique C-terminus of the spacer domain (amino acid residues 73-144) between the transmembrane domain and the C2A domain is essential for the Golgi localization of Syt IV. In addition, the short C-terminus is probably involved in proper folding of the protein, especially the C2B domain. Without the C-terminus, Syt IVdeltaC proteins are not targeted to the Golgi and seem to colocalize with an endoplasmic reticulum (ER) marker (i.e. induce crystalloid ER-like structures). On the basis of these results, we propose that the divergent spacer domain among synaptotagmin isoforms may contain certain signals that determine the final destination of each isoform.
Thermoreversible Reactions on Inorganic Nanoparticle Surfaces: Diels–Alder Reactions on Sterically Crowded Surfaces (2012)

Organically surface-functionalized nanoparticles are important cross-linkers for nanocomposites. In the past, many cross-linking reactions were based on simple radical additions. However, novel smart materials require reversible reactions. These reactions, such as the Diels–Alder reaction, often have a specific sterical demand, e.g., a six-centered transition state. In this study, < 5 nm silica particles were functionalized with maleimide groups, and their reactivity with regard to Diels–Alder reactions were investigated, applying various techniques. A new method for the surface modification of silica nanoparticles is presented, minimizing agglomeration in organic solvents and thus increasing the accessibility of the functional groups on the particle surface. Kinetic studies of substituted model compounds were carried out to evaluate the reactivity of the maleimide functionality. The Diels–Alder reaction between 2,5-dimethylfuran and N-propylmaleimide, N-ethyl(N-propylcarbamato)maleimide, and N-phenylmaleimide was followed by UV/Vis spectroscopy. The reaction rate increases in this order, showing the effect of maleimide substitution. Afterwards N-((3-triethoxysilyl)propyl)maleimide was used to graft maleimidopropyl functional groups onto the nanoparticle surface. 3-Aminopropyltriethoxysilane, which could then be reacted with 1,1′-(methylenedi-4,1-phenylene)bismaleimide, was used to attach phenyl-substituted maleimide functionality to the surface. 3-Isocyanatopropyltriethoxysilane introduced the electron-drawing carbamato functionality into the system. The surface coverage of the samples was characterized applying CHN analysis, TGA-FTIR coupling, and FTIR spectroscopy. All analytical methods revealed that the functional groups are covalently bonded to the silica surface and the maleimide rings remain intact. Diels–Alder reactions of the surface groups show that the reactivity of the molecules attached to the particles depends on sterical crowding, but the reaction rate is not significantly changed by surface effects.
Antibiotics for Emerging Pathogens (2009)

Antibiotic-resistant strains of pathogenic bacteria are increasingly prevalent in hospitals and the community. New antibiotics are needed to combat these bacterial pathogens, but progress in developing them has been slow. Historically, most antibiotics have come from a small set of molecular scaffolds whose functional lifetimes have been extended by generations of synthetic tailoring. The emergence of multidrug resistance among the latest generation of pathogens suggests that the discovery of new scaffolds should be a priority. Promising approaches to scaffold discovery are emerging; they include mining underexplored microbial niches for natural products, designing screens that avoid rediscovering old scaffolds, and repurposing libraries of synthetic molecules for use as antibiotics.
Circumvention of Immunity to the Adenovirus Major Coat Protein Hexon (1998)

Immunity to adenoviruses is an important hurdle to be overcome for successful gene therapy. The presence of antibodies to the capsid proteins prevents efficacious adenovirus vector administration in vivo. We tested whether immunity to a particular serotype of adenovirus (Ad5) may be overcome with a vector that encodes the hexon sequences from a different adenovirus serotype (Ad12). We successfully constructed an adenovirus vector with a chimeric Ad5-Ad12 hexon which was not neutralized by plasma from C57BL/6 mice immunized with Ad5. The vector was also capable of transducing the livers of C57BL/6 mice previously immunized with Ad5.
Transient Expression of Chimeric Genes Delivered into Pollen by Microprojectile Bombardment (1989)

Chimeric genes containing a pollen-specific promoter from tomato (Lycopersicon esculentum) or the CaMV35S promoter were transiently expressed following their introduction into tobacco (Nicotiana tabacum) pollen using high velocity microprojectiles. Transient expression of the microprojectile-introduced genes in leaves and pollen was similar to that observed for these genes in stably transformed tobacco plants.
Construction of Recombinant Therapeutic Monoclonal Antibodies (1990)

This chapter describes recent progress in the generation of recombinant monoclonal antibodies (Mabs) with emphasis on the use of the polymerase chain reaction (PCR) to rapidly clone antibody variable regions. In the first part we review where Mab technology stands. The second part is devoted to experimental results using PCR.KeywordsHuman Monoclonal AntibodyRecombinant AntibodyTherapeutic Monoclonal AntibodyVariable Region SequenceConstant Region PrimerThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
MCPIP1/Regnase-1 Restricts IL-17A– and IL-17C–Dependent Skin Inflammation (2016)

The IL-17 family cytokines IL-17A and IL-17C drive the pathogenesis of psoriatic skin inflammation, and anti-IL-17A Abs were recently approved to treat human psoriasis. Little is known about mechanisms that restrain IL-17 cytokine-mediated signaling, particularly IL-17C. In this article, we show that the endoribonuclease MCP-1-induced protein 1 (MCPIP1; also known as regnase-1) is markedly upregulated in human psoriatic skin lesions. Similarly, MCPIP1 was overexpressed in the imiquimod (IMQ)-driven mouse model of cutaneous inflammation. Mice with an MCPIP1 deficiency (Zc3h12a<sup>+/-</sup>) displayed no baseline skin inflammation, but they showed exacerbated pathology following IMQ treatment. Pathology in Zc3h12a<sup>+/-</sup> mice was associated with elevated expression of IL-17A- and IL-17C-dependent genes, as well as with increased accumulation of neutrophils in skin. However, IL-17A and IL-17C expression was unaltered, suggesting that the increased inflammation in Zc3h12a<sup>+/-</sup> mice was due to enhanced downstream IL-17R signaling. Radiation chimeras demonstrated that MCPIP1 in nonhematopoietic cells is responsible for controlling skin pathology. Moreover, Zc3h12a<sup>+/-</sup>Il17ra<sup>-/-</sup> mice given IMQ showed almost no disease. To identify which IL-17RA ligand was essential, Zc3h12a<sup>+/-</sup>Il17a<sup>-/-</sup> and Zc3h12a<sup>+/-</sup>Il17c<sup>-/-</sup> mice were given IMQ; these mice had reduced but not fully abrogated pathology, indicating that MCPIP1 inhibits IL-17A and IL-17C signaling. Confirming this hypothesis, Zc3h12a<sup>-/-</sup> keratinocytes showed increased responsiveness to IL-17A and IL-17C stimulation. Thus, MCPIP1 is a potent negative regulator of psoriatic skin inflammation through IL-17A and IL-17C. Moreover, to our knowledge, MCPIP1 is the first described negative regulator of IL-17C signaling.