gebhart/patrepeval huggingface dataset:
Improved mechanical load transfer between shells of multiwalled carbon nanotubes (2004)

Ultra-low friction between shells of multiwalled carbon nanotubes indicates that, when the nanotubes are used as reinforcement agents, the mechanical load is carried by the outermost shell of the tube only. We suggest using small-dose electron or ion irradiation to partially transfer the load to the nanotube inner shells. Employing analytical potential molecular dynamics, we simulate the response of multiwalled nanotubes to an external force acting on one of the shells with irradiation-induced defects which bridge adjacent shells. We demonstrate that a small number of defects can increase the interlayer shear strength by several orders of magnitude. We further discuss how the irradiation-induced load transfer can be measured experimentally and how, by manipulating the particle beam characteristics, one can improve the load transfer between preselected shells.
IMAP4 Authentication Mechanisms (1994)

The Internet Message Access Protocol, Version 4 [IMAP4] contains the
AUTHENTICATE command, for identifying and authenticating a user to an
IMAP4 server and for optionally negotiating a protection mechanism for
subsequent protocol interactions. This document describes several
authentication mechanisms for use by the IMAP4 AUTHENTICATE command.
[STANDARDS-TRACK]
Efficient cell delivery mediated by lipid‐specific endosomal escape of supercharged branched peptides (2018)

Various densely charged polycationic species, whether of biological or synthetic origin, can penetrate human cells, albeit with variable efficiencies. The molecular underpinnings involved in such transport remain unclear. Herein, we assemble 1, 2 or 3 copies of the HIV peptide TAT on a synthetic scaffold to generate branched cell-permeable prototypes with increasing charge density. We establish that increasing TAT copies dramatically increases the cell penetration efficiency of the peptides while simultaneously enabling the efficient cytosolic delivery of macromolecular cargos. Cellular entry involves the leaky fusion of late endosomal membranes enriched with the anionic lipid BMP. Derivatives with multiple TAT branches induce the leakage of BMP-containing lipid bilayers, liposomal flocculation, fusion and an increase in lamellarity. In contrast, while the monomeric counterpart 1TAT binds to the same extent and causes liposomal flocculation, 1TAT does not cause leakage, induce fusion or a significant increase in lamellarity. Overall, these results indicate that an increase in charge density of these branched structures leads to the emergence of lipid specific membrane-disrupting and cell-penetrating activities.
MTA1 overexpression correlates significantly with tumor grade and angiogenesis in human breast cancers (2006)

Metastasis associated antigen 1 (MTA1) is a recently identified candidate metastasis-associated gene that plays an important role in tumorigenesis and tumor aggressiveness, especially tumor invasiveness and metastasis. We analyzed the relationship between MTA1 expression and variable clinicopathological features and characterized its role in tumor angiogenesis in human breast cancers. Two hundred and sixty-three breast cancer cases that successfully underwent surgery at Hanyang University Hospital (Seoul, Korea) between January 1989 and December 1997 were enrolled. MTA1 expression was observed by immunohistochemical staining and correlated with intratumoral microvessel density (MVD) and other clinicopathological parameters. MTA1 overexpression correlated significantly with higher tumor grade (grades 1 and 2 vs grade 3, P = 0.009). However, MTA1 expression did not correlate with tumor stage, status of estrogen and progesterone receptors, or axillary lymph node metastasis. Interestingly, MTA1 expression was found to correlate significantly with tumor MVD (P = 0.002). Survival analysis did not show a significant difference between MTA1 overexpression and poorer survival. In conclusion, MTA1 overexpression was found to be closely associated with higher tumor grade and increased tumor angiogenesis. These findings suggest MTA1 as a predictor of aggressive phenotype and a possible target molecule for anti-angiogenic drugs in breast cancer treatment.
CD38-Mediated Signaling Events in Murine Pro-B Cells Expressing Human CD38 With or Without Its Cytoplasmic Domain (1999)

To elucidate the signaling mechanism of CD38 (a transmembrane molecule highly expressed in immature hemopoietic cells), we transfected Ba/F3 murine pro-B cells with a cDNA encoding human CD38. CD38 ligation with anti-CD38 Abs caused rapid, transient, dose-dependent tyrosine phosphorylation of several proteins, including the tyrosine kinase TEC and the adaptor molecule CBL, and association of tyrosine-phosphorylated proteins with phosphatidylinositol 3-kinase p85. Exposure to anti-CD38 Abs or their F(ab')2 and Fab also induced tight aggregation of CD38-transfected Ba/F3 cells, which appeared to be Ca2+ and Mg2+ independent and did not involved LFA-1. Aggregation was abrogated by addition of the tyrosine kinase inhibitor herbimycin A and was delayed by the phosphatidylinositol 3-kinase inhibitor wortmannin, suggesting a link between biochemical events and cellular effects induced by CD38. Cell aggregation was accompanied by a decrease in cell recovery. After 3 days of culture on bone marrow-derived stroma, the mean (+/-SD) cell recovery in the presence of anti-CD38 (T16) was 10.5 +/- 9.2% (n = 7) of that in parallel cultures with an isotype-matched nonreactive Ab. Finally, CD38 ligation in Ba/F3 cells expressing a mutant human CD38 lacking the cytoplasmic domain induced tyrosine phosphorylation with intensity and kinetics similar to those seen with the entire protein. It also induced cell aggregation and decreased cell recovery. We conclude that CD38 triggers remarkably similar signaling pathways in human and murine immature B cells. This signaling is independent of the CD38 cytoplasmic domain, suggesting the existence of accessory transmembrane molecules associated with CD38.
Delineation of active marrow by whole-body scanning with radioactive colloids. (1966)

The bone-marrow organ is difficult to delineate. Although kinetic aspects of hematopoiesis have been clarified by a variety of valuable studies, until recently, the clinical determination of marrow size and location in diseases affecting hematopoiesis has been limited to local sampling by aspiration or biopsy. The bone-marrow distribution now can be detected by radioisotopic scan ning techniques. We have in earlier papers (1,2) demonstrated marrow patterns using intravenous colloidal gold-198 and a research scanner with a gold-tungsten collimator, confirming and extending the observations of Engstedt (3), et al and Larsson (4), et al. Although the uptake of the colloid is by reticuloendothelial cells, we and others (3 ) have observed that correlation exists in the bone marrow between reticuloendothelial function and hematopoiesis, and this method has proved of value in studying marrow distribution. In this paper, marrow described as functioning, or active, refers to reticuloendothelial activity.
Interleaving for combating bursts of errors (2004)

To ensure data fidelity, a number of random error correction codes (ECCs) have been developed. ECC is, however, not efficient in combating bursts of errors, i.e., a group of consecutive (in one-dimensional (1-D) case) or connected (in two- and three- dimensional (2-D and 3-D) case) erroneous code symbols owing to the bursty nature of errors. Interleaving is a process to rearrange code symbols so as to spread bursts of errors over multiple code-words that can be corrected by ECCs. By converting bursts of errors into random-like errors, interleaving thus becomes an effective means to combat error bursts. In this article, we first illustrate the philosophy of interleaving by introducing a 1-D block interleaving technique. Then multi-dimensional (M-D) bursts of errors and optimality of interleaving are defined. The fundamentals and algorithms of the state of the art of M-D interleaving - the t-interleaved array approach by Blaum, Bruck and Vardy and the successive packing approach by Shi and Zhang-are presented and analyzed. In essence, a t-interleaved array is constructed by closely tiling a building block, which is solely determined by the burst size t. Therefore, the algorithm needs to be implemented each time for a different burst size in order to maintain either the error burst correction capability or optimality. Since the size of error bursts is usually not known in advance, the application of the technique is somewhat limited. The successive packing algorithm, based on the concept of 2 /spl times/ 2 basis array, only needs to be implemented once for a given square 2-D array, and yet it remains optimal for a set of bursts of errors having different sizes. The performance comparison between different approaches is made. Future research on the successive packing approach is discussed. Finally, applications of 2-D/3-D successive packing interleaving in enhancing the robustness of image/video data hiding are presented as examples of practical utilization of interleaving.
The epitope recognized by rituximab (2006)

Rituximab is a monoclonal antibody widely used in the treatment of malignant lymphoma and autoimmunity. Its epitope within the B-cell antigen CD20 is largely unknown. We used phage display libraries to select peptides binding to rituximab. Enriched peptides showed 2 sequence patterns: one motif (CALMIANSC) is related to (170)ANPS(173) within CD20, while another motif (WEWTI) may mimic the CD20 segment (182)YCYSI(185). Phages displaying either motif specifically bound rituximab. Binding to rituximab by the CD20 peptides ANPS and YCYSI was weak when used separately and enhanced when both peptides were linked. Recombinant CD20 extracellular loop proteins blocked binding of the selected CWWEWTIGC phage to rituximab, suggesting that CWWEWTIGC mimics the epitope. Blocking capacity was strongly reduced upon mutation of the CD20 strings ANPS or YCYSI. We conclude that rituximab binds a discontinuous epitope in CD20, comprised of (170)ANPS(173) and (182)YCYSI(185), with both strings brought in steric proximity by a disulfide bridge between C(167) and C(183).
Vector analysis of astigmatism correction after toric intraocular lens implantation (2015)

No author has a financial or proprietary interest in any material or method mentioned.
The Ribosomal Intergenic Spacer and Domain I of the 23S rRNA Gene Are Phylogenetic Markers for Chlamydia spp. (1997)

Current methods used to classify Chlamydia strains, including biological, morphological, and DNA hybridization techniques and major outer membrane protein (omp1) gene analysis, can be imprecise or difficult to perform. To facilitate classification, 2.8-kb partial ribosomal DNA (rDNA) segments from a Chlamydia trachomatis strain and a Chlamydia psittaci strain were amplified by PCR and sequenced. Subsequently, a 1,320-bp region in this segment, including both the 16S/23S intergenic spacer (232 +/- 11 bp) and domain I (620 +/- 2 bp) of the 23S gene, was sequenced from 41 additional strains and from the chlamydia-like organisms Simkania sp. strains "Z" and "Z1." When both parsimony and distance analyses were performed, these sequences were found to have variable regions that grouped the isolates into two lineages (C. trachomatis and non-C. trachomatis) and nine distinct genotypic groups. The C. trachomatis lineage included human, swine, and mousehamster groups. The non-C. trachomatis lineage included Chlamydia pecorum, Chlamydia pneumoniae, and C. psittaci abortion, avian, feline, and guinea pig groups. These nine groups were essentially equidistant from the genetic root and were congruent with groups identified previously by using DNA-DNA homology, genomic restriction endonuclease analysis, host specificity, tissue specificity, and/or disease production. Phylogenetic trees based on the intergenic spacer or on domain I were congruent with trees previously derived from ompI sequences. DNA sequence analysis of either the intergenic spacer or domain I provides a rapid and reproducible method for identifying, grouping, and classifying chlamydial strains.
Characteristics of Cold-sensitive Cell Division Mutant ofEscherichia coliK-12 (1977)

The culture of cold-sensitive division mutant, cs 2–29 consists of many normal cells and some filaments at 37°C. When an exponentially growing culture of cs 2–29 at 37°C was shifted to 20°C, the number of viable cells increased about 1.5-fold and the cells formed multinucleated filaments lacking septa. After the increase in optical density terminated at 20°C, normal cells separated from the end of filaments and the number of colony formers gradually increased. The number of viable cells of cs 2–29 increased normally at 25°, 30° and 37°C but not at 20°C in NBT medium. When chloramphenicol was added to the culture simultaneously with the temperature shift to 37°C after 6 hr of incubation at 20°C, the filamentous cells of cs 2–29 failed to divide. Strain cs 2–29 could divide at 20°C in NBT medium containing d-pantoyl lactone and also in semi-synthetic medium supplemented with sodium acetate as a carbon source. The mutant accepted both chromosomal and plasmid markers at reduced frequencies. The cs gene has been located between met E and rha, a previously undescribed region involved in septation. The mutated gene in this strain was designated as fcsA. The decrease of conjugation ability of cs 2–29 appears to be co-transducible with the cs gene.
Effects of central cholinergic blockade on striatal dopamine release measured with positron emission tomography in normal human subjects. (1993)

Previously we demonstrated that positron emission tomography (PET) can be used to measure changes in the concentrations of synaptic dopamine and acetylcholine. Whether induced directly or indirectly through interactions with other neurotransmitters, these studies support the use of PET for investigating the functional responsiveness of a specific neurotransmitter to a pharmacologic challenge. In an extension of these findings to the human brain, PET studies designed to measure the responsiveness of striatal dopamine release to central cholinergic blockade were conducted in normal male volunteers using high-resolution PET and [11C]raclopride, a D2-dopamine receptor antagonist. [11C]Raclopride scans were performed prior to and 30 min after systemic administration of the potent muscarinic cholinergic antagonist, scopolamine (0.007 mg/kg). After scopolamine administration, [11C]raclopride binding decreased in the striatum (specific binding) but not in the cerebellum (nonspecific binding) resulting in a significant decrease, exceeding the test/retest variability of this ligand (5%), in the ratio of the distribution volumes of the striatum to the cerebellum (17%). Furthermore, scopolamine administration did not alter the systemic rate of [11C]raclopride metabolism or the metabolite-corrected plasma input function. These results are consistent not only with the known inhibitory influence that acetylcholine exerts on striatal dopamine release but also with our initial 18F-labeled N-methylspiroperidol and benztropine studies. Thus these data support the use of PET for measuring the functional responsiveness of an endogenous neurotransmitter to an indirect pharmacologic challenge in the living human brain.
Differentially Charged Hollow Core/Shell Lipid–Polymer–Lipid Hybrid Nanoparticles for Small Interfering RNA Delivery (2011)

Speedy delivery: Biodegradable and biocompatible polymers and lipids form hybrid core/shell nanoparticles (see picture, left) that show promising in vitro and in vivo results for delivering siRNA. The unique lipid–polymer–lipid nanostructure is elucidated by electron and fluorescence microscopy (right) and provides the delivery system with distinct functional features. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
The Surface of Dendritic Cells in the Mouse as Studied with Monoclonal Antibodies (1990)

A family of dendritic cells has been identified in situ and in vitro by microscopy and immunolabeling. The members of this family include the dendritic cells isolated from lymphoid organs, Langerhans cells [LC] of the epidermis, veiled cells in afferent lymph, and interdigitating cells [IDC] in the T-cell areas. Some common features to all members of the family are high levels of MHC class II antigens, a lack of most B and T cell markers, and an absence or low levels of macrophage/granulocyte antigens. This review summarizes the markers of mouse dendritic cells as assessed by a panel of monoclonal antibodies, and stresses a few recent findings. 1) In spleen, there are two populations of dendritic cells. More than 75% of isolated cells are 33D1+, NLDC145-, and J11d-, while the remainder have the reciprocal phenotype and thus share the NLDC145 antigen of IDC. Thymic dendritic cells, released by collagenase digestion, and epidermal LC also are 33D1-, NLDC145+, J11d+. 2) When epidermal LC are placed in culture, there are changes in cell function and phenotype. There is a decrease in Fc gamma receptors and the F4/80 macrophage antigen, an increase in class I and II MHC products and p55 IL-2 receptors, and persistence of the NLDC145 IDC antigen. The cultured LC thereby resembles the IDC. 3) A new antibody N418 shows that dendritic cells express the p150/90 member of the leukocyte beta 2 integrin family. Immunolabeling of tissue sections of spleen indicates that N418+ dendritic cells not only are present in the periarterial sheaths, the location of IDC, but also in "nests" at the periphery of the T area where 33D1 has been found. The peripheral collections interrupt the marginal zone of macrophages that separates white and red pulp, and places the dendritic cells in the path of T cells as they move through the white pulp. Therefore the members of the dendritic cell family have important markers in common, as well as differences that are associated with state of immunologic function and location.
Periodontitis and Diabetes Interrelationships: Role of Inflammation (2001)

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifically immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes-induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes-induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic beta cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes-induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes.
Kinase Mutations and Imatinib Response in Patients With Metastatic Gastrointestinal Stromal Tumor (2003)

Activating mutations of KIT or PDGFRA are found in the vast majority of GISTs, and the mutational status of these oncoproteins is predictive of clinical response to imatinib. PDGFRA mutations can explain response and sensitivity to imatinib in some GISTs lacking KIT mutations.
Dynamic Standby Prediction for Leakage Tolerant Microprocessor Functional Units (2006)

Leakage power is projected to comprise approximately 50% of the processor's power for sub 65 nm technologies. Much of this power is consumed in the processor's functional units. Accordingly, leakage control techniques are employed to reduce leakage in these functional units. Many of these techniques are dynamic and are based on an input sleep signal to initiate a low leakage mode. However, since most of these leakage control techniques are based on circuit level schemes, such techniques inherently lack information about the operational profile of the functional units they manage. This limitation is usually handled statically by using a fixed length counter that generates the sleep signal when the functional unit is idle for a specified number of cycles. In this paper, the limitations of the static sleep signal generation approach are identified, and the use of a dynamic alternative that is capable of adopting the counter length to the running application is proposed. In order to assess the accuracy of the proposed dynamic sleep signal generator, the length of the sleep period following the sleep signal generation is used as a metric to identify the usefulness of utilizing the dynamic approach. Experimental results for the dynamic alternative shows up to 98% accuracy in predicting the length of the standby period compared to an average of 40-60% in the static case, which translates into increased leakage savings. This is achieved while consuming 360 muW of overhead power at 1 GHz