gebhart/patrepeval huggingface dataset:
Enhanced Uptake of a Heterologous Protein with an HIV-1 Tat Protein Transduction Domains (PTD) at Both Termini (2003)

Poor membrane permeability of proteins is a major limitation of protein therapy. In a previous study, we showed that the minimal sequence required for efficient transduction of Tat-GFP is the basic domain from 49-57 of HIV-1 Tat called the protein transduction domain (PTD. Here we have generated HIV-1 Tat PTD GFP fusion proteins in which HIV-1 Tat PTD is fused with the N- and/or C-termini of GFP. The various GFP fusion proteins were purified from Escherichia coli and characterized for their ability to enter mammalian cells using Western blot analysis, confocal microscopy and flow cytometry. The GFP fusion protein with Tat PTD at its C-terminus was taken up as efficiently as the GFP fusion protein with Tat PTD at its N-terminus. However, the same protein with PTDs at its both termini was taken up even more efficiently. All the GFP fusion proteins were present in both the nucleus and cytosol of the transduced cells. Uptake was lower at 4 degrees C than at 37 degrees C. The availability of the expression vectors developed in this study may help to devise novel strategies in the rational development of protein-based drugs.
Recombineering: Genetic Engineering in Bacteria Using Homologous Recombination (2005)

Abstract The bacterial chromosome and plasmids can be engineered in vivo by homologous recombination using PCR products and synthetic oligonucleotides as substrates. This is possible because bacteriophage‐encoded recombination functions efficiently recombine sequences with homologies as short as 35 to 40 bases. This recombineering allows DNA sequences to be inserted or deleted without regard to location of restriction sites. This unit first describes preparation of electrocompetent cells expressing the recombineering functions and their transformation with double‐stranded DNA (dsDNA) or single‐stranded DNA (ssDNA). Support protocols describe a two‐step method of making genetic alterations without leaving any unwanted changes, and a method for retrieving a genetic marker (cloning) from the E. coli chromosome or a coelectroporated DNA fragment and moving it onto a plasmid. A method is also given to screen for unselected mutations. Additional protocols describe removal of defective prophage, methods for recombineering.
Air-Stable All-Inorganic Nanocrystal Solar Cells Processed from Solution (2005)

We introduce an ultrathin donor-acceptor solar cell composed entirely of inorganic nanocrystals spin-cast from solution. These devices are stable in air, and post-fabrication processing allows for power conversion efficiencies approaching 3% in initial tests. This demonstration elucidates a class of photovoltaic devices with potential for stable, low-cost power generation.
ScheduleNanny: Using GPS to Learn the User's Significant Locations, Travel Times and Schedule (2004)

As computing technology becomes more pervasive, personal devices such as the PDA, cell-phone, and notebook should use context to determine how to act. Location is one form of context that can be used in many ways. We present a multiple-device system that collects and clusters GPS data into significant locations. These locations are then used to determine travel times and a probabilistic model of the user's schedule, which is used to intelligently alert the user. We evaluate our system and suggest how it should be integrated with a variety of applications.
Low counts of Faecalibacterium prausnitzii in colitis microbiota (2009)

The fecal microbiota of patients with IBD differs from that of HS. The phylum Firmicutes and particularly the species F. prausnitzii, are underrepresented in A-IBD patients as well as in IC patients. These bacteria could be crucial to gut homeostasis since lower counts of F. prausnitzii are consistently associated with a reduced protection of the gut mucosa.
Cell-Mediated Immune System Regulation in Periodontal Diseases (1997)

The adaptive immune system consists of humoral and cell-mediated immunity. T-lymphocytes are the key components of cell-mediated immunity. CD4+ helper T-lymphocytes facilitate B-cells to differentiate and produce specific antibodies, whereas CD8+ cytotoxic T-lymphocytes kill virally infected cells. Periodontal diseases have been associated with a variety of imbalances in the regulation of immune responses. Changes in the ratios of peripheral blood CD4+ and CD8+ T-lymphocytes, depressed proliferative responses of peripheral blood lymphocytes, and increased frequency of CD45RO+ memory T-lymphocytes in diseased tissues have been reported in individuals with various forms of periodontal disease. While some studies have shown an increased frequency of γδ+ T-cells in periodontal lesions, the role of γδ+ T-cells in periodontal disease remains controversial. The ability of putative periodontopathic bacteria selectively to stimulate certain V(3-expressing T-cells is intriguing and could determine whether a CD4+ Th I or a CD4+ Th2 cell response is elicited. The prominence of a particular subset of helper T-cells within the periodontal lesion could be a reflection of the stage and activity of the disease, or the types of bacteria present. Regardless, longitudinal studies of the involvement of T-cell subsets and cytokines in periodontal disease are clearly needed.
Potential use of lipoxygenase inhibitors for cancer chemoprevention (2000)

Increasing evidence suggests that lipoxygenase (LO)-catalysed metabolites have a profound influence on the development and progression of human cancers. Compared with normal tissues, significantly elevated levels of LO products have been found in breast tumours, colon cancers, lung, skin and prostate cancers, as well as in cells from patients with both acute and chronic leukaemias. LO-mediated products elicit diverse biological activities needed for neoplastic cell growth, influencing growth factor and transcription factor activation, oncogene induction, stimulation of tumour cell adhesion and regulation of apoptotic cell death. Agents that block LO catalytic activity may be effective in preventing cancer by interfering with signalling events needed for tumour growth. In the past ten years, pharmaceuticals agents that specifically inhibit the 5-LO metabolic pathway have been developed to treat inflammatory diseases such as asthma, arthritis and psoriasis. Some of these compounds possess anti-oxidant properties and may be effective in preventing cancer by blocking free radical-induced genetic damage or by preventing the metabolic activation of carcinogens. Other compounds may work by negatively modulating DNA synthesis. Pharmacological profiles of potential chemopreventive agents are compiled from enzyme assays, in vitro testing (e.g., cell proliferation inhibition in human cancer cells) and in vivo animal carcinogenesis models (e.g., N-methyl-N-nitrosourea-induced rat mammary cancer, benzo(a)pyrene-induced lung tumours in strain A/J mice and hormone-induced prostate tumours in rats). In this way, compounds are identified for chemoprevention trials in human subjects. Based on currently available data, it is expected that the prevention of lung and prostate cancer will be initially studied in human trials of LO inhibitors.
Cellular distribution of 92-kd type IV collagenase/gelatinase B in human hepatocellular carcinoma. (1996)

To examine the possible involvement of gelatinase B in human hepatocellular carcinoma (HCC), cellular localization of transcripts and protein of gelatinase B were studied by using in situ hybridization and immunohistochemistry. Transcripts for gelatinase B were observed in tumor cells in 22 cases of 27 HCCs and also in dysplastic nodules. However, there was no significant difference in the expression among histological grades of HCC. The expression was mostly homogeneous, but the intensity varied with the nodules. Of 13 cases with capsular invasion, 12 expressed gelatinase B, whereas 10 of 14 without capsular invasion did (P < 0.05). Gelatinase B transcripts were commonly observed in the sinusoidal cells of the hepatic lobules, in mesenchymal cells both in fibrous capsules and around the necrosis, and also in some undefined cells of the portal tracts of noncancerous liver. Localization of gelatinase B protein was mostly similar to but sometimes different from that of the transcripts in cancer nodules. In conclusion, the expression of gelatinase B appears to be an important characteristic of malignant transformation of hepatocytes. The findings suggest that gelatinase B synthesized by cancer cells plays an important role in the growth and invasion of HCC by degrading surrounding extracellular matrices.
Pneumococcal Neuraminidases A and B Both Have Essential Roles during Infection of the Respiratory Tract and Sepsis (2006)

We examined the role of the neuraminidases NanA and NanB in colonization and infection in the upper and lower respiratory tract by Streptococcus pneumoniae, as well as the role of these neuraminidases in the onset and development of septicemia following both intranasal and intravenous infection. We demonstrated for the first time using outbred MF1 mouse models of infection that both NanA and NanB were essential for the successful colonization and infection of the upper and lower respiratory tract, respectively, as well as pneumococcal survival in nonmucosal sites, such as the blood. Our studies have shown that in vivo a neuraminidase A mutant is cleared from the nasopharynx, trachea, and lungs within 12 h postinfection, while a neuraminidase B mutant persists but does not increase in either the nasopharynx, trachea, or lungs. We also demonstrated both neuraminidase mutants were unable to cause sepsis following intranasal infections. When administered intravenously, however, both mutants survived initially but were unable to persist in the blood beyond 48 h postinfection and were progressively cleared. The work presented here demonstrates the importance of pneumococcal neuraminidase A and for the first time neuraminidase B in the development of upper and lower respiratory tract infection and sepsis.
On the Role of Helix 0 of the Tryptophan Synthetase α Chain of (1996)

The role of helix 0 of the alpha chain (TrpA) of the tryptophan synthetase alpha2beta2 multi-functional enzyme complex of Escherichia coli was examined by deleting amino-terminal residues 2-6, 2-11, or 2-19 of TrpA. Selected substitutions were also introduced at TrpA positions 2-6. The altered genes encoding these polypeptides were overexpressed from a foreign promoter on a multicopy plasmid and following insertion at their normal chromosomal location. Each deletion polypeptide was functional in vivo. However all appeared to be somewhat more labile and insoluble and less active enzymatically than wild type TrpA. The deletion polypeptides were overproduced and solubilized from cell debris by denaturation and refolding. Several were partially purified and assayed in various reactions in the presence of tryptophan synthetase beta2 (TrpB). The purified TrpADelta2-6 and TrpADelta2-11 deletion polypeptides had low activity in both the indole + serine --> tryptophan reaction and the indoleglycerol phosphate + serine --> tryptophan reaction. Poor activity in each reaction was partly due to reduced association of TrpA with TrpB. The addition of the TrpA ligands, alpha-glycerophosphate or indoleglycerol phosphate, during catalysis of the indole + serine --> tryptophan reaction increased association and activity. These findings suggest that removal of helix 0 of TrpA decreases TrpA-TrpB association as well as the activity of the TrpA active site. Alignment of the TrpA sequences from different species indicates that several lack part or all of helix 0. In some of these polypeptides, extra residues at the carboxyl end may substitute for helix 0.
MECHANISM BY WHICH ADDITIONAL MONOCLONAL ANTIBODY (mAB) INJECTIONS OVERCOME THE REQUIREMENT FOR THYMIC IRRADIATION TO ACHIEVE MIXED CHIMERISM IN MICE RECEIVING BONE MARROW TRANSPLANTATION AFTER CONDITIONING WITH ANTI-T CELL mABs AND 3-GY WHOLE BODY IRRADIATION1 (1996)

A relatively nontoxic method of conditioning mice has been developed recently that allows allogeneic bone marrow engraftment and specific skin allograft tolerance induction. This regiment included anti-CD4 and anti-CD8 mAbs administered on day -5, followed by 3-Gy whole body irradiation (WBI) and 7-Gy thymic irradiation (TI) on day 0. We have recently shown that the potential toxicity of this regimen can be further reduced by replacing TI with additional anti-T cell mAb injections before and after bone marrow transplantation. Mixed chimerism and prolonged donor-specific skin graft acceptance are induced in 90% of B10 mice conditioned with anti-CD4 and anti-CD8 mAbs on days -6 and -1 and 3-Gy WBI on day 0 without TI, but only in a small fraction of mice receiving a similar regimen, except that mAbs are given on day -5 only. To determine the mechanism of tolerance induction in the former group, we compared the two groups for the extent of thymocyte depletion, for the timing of development of intrathymic and extrathymic chimerism, and for clonal deletion of host-type thymocytes with TCR recognizing superantigens presented by donor class II molecules. The results suggest that administration of a second mAb injection depletes or inactivates residual host thymocytes that are capable of causing intrathymic rejection of donor hematopoietic cells even when peripheral engraftment is achieved. The presence of donor class II+ hematopoietic cells in the thymus on day 14 correlated with marked deletion of mature host-type V beta 11+ thymocytes that recognize donor I-E plus endogenous superantigen. This suggests that tolerance is achieved primarily through a central deletional mechanism when peripheral and intrathymic host T cells are adequately inactivated or depleted by mAbs and 3-Gy WBI. In addition, the higher incidence of early failure of peripheral chimerism in mice conditioned with a single injection rather than than two mAb injections prior to bone marrow transplantation suggests that nontolerant residual host thymocytes can also induce early peripheral rejection after mAbs have cleared from the circulation. This early rejection is prevented by the longer persistence of anti-T cell mAbs observed in mice receiving two pretransplant mAb injections. Thus, administration of sufficient depleting anti-T cells mAbs followed by 3-Gy WBI allows the induction of central deletional tolerance while minimizing the toxicity of the conditioning regimen.
Biochemical properties of glycoproteins involved in lymphocyte recognition of high endothelial venules in man. (1988)

Lymphocyte interactions with high endothelial venules (HEV) are important to the in vivo migration of normal and neoplastic lymphocyte populations. We have previously described an 85- to 95-kDa lymphocyte surface glycoprotein(s) defined by mAb Hermes-1, that is involved in the recognition of HEV by human lymphocytes: antibodies against distinct epitopes of the Hermes-1 Ag differentially inhibit lymphocyte binding to lymph node, mucosal, or synovial HEV. Here we characterize further the Hermes-1-defined glycoproteins. No well defined differences were observed between the Hermes-1 Ag immunoprecipitated from PBL and from mucosa- vs lymph HEV-specific cell lines. The Ag is an acidic (isoelectric point = 4.2) sulfated molecule bearing both O-linked and (3,4) N-linked oligosaccharide side chains. A subset of the Hermes-1-immunoprecipitated species is modified by covalent linkage to chondroitin sulfate, yielding a Mr of approximately 180 to 200 kDa. Pulse-chase labeling reveals a major precursor of 76 kDa that appears to be processed either to the 85- to 95-kDa form or, by addition of chondroitin sulfate, to a 180- to 200-kDa form. The potential role of these structural modifications, and particularly of chondroitin sulfate, in the function of the putative adhesion molecules is discussed.
Fully coherent growth of Ge on free-standing Si(001) nanomesas (2014)

We investigate the structural properties of Ge nanostructures selectively grown on Si. Defect-free nanostructures with a lateral size of 100 nm and surrounded by a thick (\ensuremath{\sim}20 times larger than the coherent-film limit) Ge layer are achieved as demonstrated by transmission electron microscopy. As demonstrated by modeling based on elasticity theory solved by finite element methods, the peculiar combination of morphology and chemical composition of the nanostructures allows for a very efficient elastic relaxation of the heteroepitaxial strain. We demonstrate that, despite the relatively large size of the nanostructures, even a single dislocation would raise the energy of the system. A direct comparison between the strain field predicted by modeling and measured by energy-dispersive synchrotron-radiation grazing incidence x-ray diffraction shows substantial agreement.
Hydroxyarginine-containing Polyphenolic Proteins in the Adhesive Plaques of the Marine Mussel Mytilus edulis (1995)

An unusual polymorphic protein family of nine or more variants has been isolated from the byssal adhesive plaques and foot of the marine mussel Mytilus edulis. In accordance with established terminology, the family is referred to as M. edulis foot protein 3 or simply Mefp-3. Variants of Mefp-3 have molecular masses of about 6 kDa, isoelectric points greater than 10.5, and an amino acid composition dominated by six amino acids: glycine, asparagine, 3,4-dihydroxyphenylalanine (Dopa), tryptophan, arginine, and an unknown basic amino acid. The latter has been isolated and identified as 4-hydroxyarginine using fast atom bombardment mass spectrometry and appropriate standards. The primary structure of variant Mefp-3F has been determined by peptide mapping using automated Edman sequencing in combination with fast atom bombardment and matrix-assisted laser desorption ionization mass spectrometry: ADYYGPNYGPPRRYGGGNYNRYNRYGRRYGGYKGWNNGWNRGRRGKYW where Y represents Dopa, and R represents hydroxyarginine. Notably, the 4 occurrences of RY are marked by a resistance to trypsin digestion. Although the conversion of tyrosines to Dopa is essentially complete, hydroxylation of arginines varies between 40 and 80%. In contrast to other mussel adhesive proteins such as Mefp-1 and -2 which have large numbers of highly conserved, tandemly repeated peptide motifs, Mefp-3 has only short sporadic repeats. The specific function of Mefp-3 in byssal adhesion is unknown.
Introduction of a selectable gene into different animal tissue by a retrovirus recombinant vector. (1984)

The potential use of retrovirus vectors to transduce foreign genetic information into cells of different tissues of an animal was explored by introducing a recombinant genome carrying the Eco gpt gene into postimplantation mouse embryos. To obviate the need for preparing concentrated virus stocks, psi 2-2-5 cells producing the replication-defective murine sarcoma virus (MSV)-gpt virus were microinjected directly into embryos. The psi 2-2-5 cells were mixed with cells producing replication-competent Moloney murine leukemia virus (Mo-MuLV) to facilitate spread of the vector. A high percentage of the manipulated embryos continued to develop without disturbance and were analyzed either prior to birth or as adults for expression of both helper and Eco gpt virus. Microinjection of as few as 10 Mo-MuLV-producing cells resulted in viremia of greater than 50% of the embryos or adults, 25%-30% of which produced MSV-gpt recombinant virus in a variety of organs including thymus, spleen, lung, kidney, and brain. The fraction of vector-producing cells, however, was 3 to 5 orders of magnitude lower than that of helper-virus-producing cells. Our results demonstrate that a selectable gene can be introduced by retroviral vectors into animals and can be expressed in a wide variety of different somatic tissues.
Diisopropylsilyl-linked oligonucleotide analogs: solid-phase synthesis and physicochemical properties (1993)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTDiisopropylsilyl-linked oligonucleotide analogs: solid-phase synthesis and physicochemical propertiesAshis K. Saha, Mark Sardaro, Cheryl Waychunas, Daniel Delecki, L. I. Kruse, Rusty Kutny, Paul Cavanaugh, Anne Yawman, and Donald A. UpsonCite this: J. Org. Chem. 1993, 58, 27, 7827–7831Publication Date (Print):December 1, 1993Publication History Published online1 May 2002Published inissue 1 December 1993https://pubs.acs.org/doi/10.1021/jo00079a030https://doi.org/10.1021/jo00079a030research-articleACS PublicationsRequest reuse permissionsArticle Views199Altmetric-Citations15LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Aberrant Localization of FUS and TDP43 Is Associated with Misfolding of SOD1 in Amyotrophic Lateral Sclerosis (2012)

We conclude that cytosolic mislocalization of FUS or TDP43 in vitro and ALS in vivo may kindle wtSOD1 misfolding in non-SOD1 FALS and SALS. The lack of immunohistochemical compartmental co-localization of misfolded SOD1 with cytosolic TDP43 or FUS suggests an indirect induction of SOD1 misfolding followed by propagation through template directed misfolding beyond its site of inception. The identification of a final common pathway in the molecular pathogenesis of ALS provides a treatment target for this devastating disease.
The nature of carrier localisation in polar and nonpolar InGaN/GaN quantum wells (2016)

In this paper, we compare and contrast the experimental data and the theoretical predictions of the low temperature optical properties of polar and nonpolar InGaN/GaN quantum well structures. In both types of structure, the optical properties at low temperatures are governed by the effects of carrier localisation. In polar structures, the effect of the in-built electric field leads to electrons being mainly localised at well width fluctuations, whereas holes are localised at regions within the quantum wells, where the random In distribution leads to local minima in potential energy. This leads to a system of independently localised electrons and holes. In nonpolar quantum wells, the nature of the hole localisation is essentially the same as the polar case but the electrons are now coulombically bound to the holes forming localised excitons. These localisation mechanisms are compatible with the large photoluminescence linewidths of the polar and nonpolar quantum wells as well as the different time scales and form of the radiative recombination decay curves.