gebhart/patrepeval huggingface dataset:
FemtoCaching: Wireless video content delivery through distributed caching helpers (2012)

We suggest a novel approach to handle the ongoing explosive increase in the demand for video content in wireless/mobile devices. We envision femtocell-like base stations, which we call helpers, with weak backhaul links but large storage capacity. These helpers form a wireless distributed caching network that assists the macro base station by handling requests of popular files that have been cached. Due to the short distances between helpers and requesting devices, the transmission of cached files can be done very efficiently. A key question for such a system is the wireless distributed caching problem, i.e., which files should be cached by which helpers. If every mobile device has only access to a exactly one helper, then clearly each helper should cache the same files, namely the most popular ones. However, for the case that each mobile device can access multiple caches, the assignment of files to helpers becomes nontrivial. The theoretical contribution of our paper lies in (i) formalizing the distributed caching problem, (ii) showing that this problem is NP-hard, and (iii) presenting approximation algorithms that lie within a constant factor of the theoretical optimum. On the practical side, we present a detailed simulation of a university campus scenario covered by a single 3GPP LTE R8 cell and several helpers using a simplified 802.11n protocol. We use a real campus trace of video requests and show how distributed caching can increase the number served users by as much as 400 - 500%.
Fatty acid metabolism in obesity and type 2 diabetes mellitus (2003)

Disturbances in pathways of lipolysis and fatty acid handling are of importance in the aetiology of obesity and type 2 diabetes mellitus. There is evidence that a lowered catecholamine-mediated lipolytic response may play a role in the development and maintenance of increased adipose tissue stores. Increased adipose tissue stores, a disturbed insulin-mediated regulation of lipolysis and subnormal skeletal muscle non-esterified fatty acid (NEFA) uptake under conditions of high lipolytic rate may increase circulating NEFA concentrations, which may promote insulin resistance and cardiovascular complications. In addition, a disturbance of NEFA uptake by adipose tissue postprandially is also a critical determinant of plasma NEFA concentration. Furthermore, evidence is increasing that insulin-resistant muscle is characterised by a lowered ability to oxidise fatty acids. A dysbalance between fatty acid uptake and fatty acid oxidation may in turn be a factor promoting accumulation of lipid intermediates and triacylglycerols within skeletal muscle, which is strongly associated with skeletal muscle insulin resistance. The present review describes the reported disturbances in pathways of lipolysis and skeletal muscle fatty acid handling, and discusses underlying mechanisms and metabolic consequences of these disturbances.
Identification of a MAGE-2-encoded human leukocyte antigen-A24-binding synthetic peptide that induces specific antitumor cytotoxic T lymphocytes. (1999)

Because MAGE-2 gene is expressed in a wide variety of malignant tumors and HLA-A24 is the most common allele in the Japanese population and is also frequently present in Caucasians, the identification of MAGE-2-encoded peptide presented by HLA-A24 is, therefore, considered to be important in order to develop specific immunotherapy for malignant tumors using peptides as a vaccine. By using a MHC-binding assay, eight peptides derived from MAGE-2 were found to bind with sufficient affinity to the HLA-A24 molecule. When the induction of specific cytotoxic T lymphocytes (CTLs) was examined using a simplified method, the highest human lymphocyte antigen (HLA) binder (EYLQLVFGI) in these peptides was able to elicit CTLs from unseparated peripheral blood mononuclear cells in HLA-A24 healthy donors by stimulation with freshly isolated, peptide-pulsed peripheral blood mononuclear cells as antigen-presenting cells and also by using interleukin 7 and keyhole-limpet hemocyanin in a primary culture. The induced CTL could, thus, lyse HLA-A24 tumor cells expressing MAGE-2, as well as the peptide-pulsed target cells, with antigen specificity in a HLA class I-restricted manner. The identification of this peptide may, thus, be of therapeutic value in peptide-based vaccines for the treatment of several types of malignant tumors expressing MAGE-2.
Dendritic Cell-Directed CTLA-4 Engagement during Pancreatic β Cell Antigen Presentation Delays Type 1 Diabetes (2010)

The levels of expression of alternatively spliced variants of CTLA-4 and insufficient CTLA-4 signaling have been implicated in type 1 diabetes. Hence, we hypothesized that increasing CTLA-4-specific ligand strength on autoantigen-presenting dendritic cells (DCs) can enhance ligation of CTLA-4 on T cells and lead to modulation of autoreactive T cell response. In this study, we show that DC-directed enhanced CTLA-4 engagement upon pancreatic beta cell Ag presentation results in the suppression of autoreactive T cell response in NOD mice. The T cells from prediabetic NOD mice treated with an agonistic anti-CTLA-4 Ab-coated DC (anti-CTLA-4-Ab DC) showed significantly less proliferative response and enhanced IL-10 and TGF-beta1 production upon exposure to beta cell Ags. Furthermore, these mice showed increased frequency of Foxp3+ and IL-10+ T cells, less severe insulitis, and a significant delay in the onset of hyperglycemia compared with mice treated with control Ab-coated DCs. Further analyses showed that diabetogenic T cell function was modulated primarily through the induction of Foxp3 and IL-10 expression upon Ag presentation by anti-CTLA-4-Ab DCs. The induction of Foxp3 and IL-10 expression appeared to be a consequence of increased TGF-beta1 production by T cells activated using anti-CTLA-4-Ab DCs, and this effect could be enhanced by the addition of exogenous IL-2 or TGF-beta1. Collectively, this study demonstrates the potential of a DC-directed CTLA-4 engagement approach not only in treating autoimmunity in type 1 diabetes, but also in altering diabetogenic T cell function ex vivo for therapy.
Bronchoalveolar Lavage and Transbronchial Biopsy for the Diagnosis of Pulmonary Infections in the Acquired Immunodeficiency Syndrome (1985)

The efficacy of bronchoalveolar lavage and transbronchial biopsy in diagnosing lung infection was determined in 276 fiberoptic bronchoscopic examinations done on 171 patients with known or suspected acquired immunodeficiency syndrome. Of 173 pathogens (Pneumocystis carinii, cytomegalovirus, Mycobacterium avium-intracellulare, Cryptococcus neoformans, M. tuberculosis, Coccidioides immitis, and Histoplasma capsulatum) identified during the initial evaluation or in the subsequent month, the initial bronchoscopic examination detected 166 (96%). Bronchoalveolar lavage and transbronchial biopsy had sensitivities of 86% and 87%, respectively. When bronchoscopy included both bronchoalveolar lavage and transbronchial biopsy, the yield for all pathogens was 98% and the sensitivity for P. carinii infections was 100%. Follow-up for at least 3 weeks after examination failed to detect any additional false-negative results. Fiberoptic bronchoscopy is extremely accurate for the detection of pathogens in patients with the acquired immunodeficiency syndrome, especially when bronchoalveolar lavage and transbronchial biopsy are combined. In patients at high risk of complications from transbronchial biopsy, bronchoalveolar lavage is sufficiently accurate to be used alone.
Frequency selective signal extrapolation for compensation of missing data in sinograms (2008)

We present a method to compensate for missing projection data in positron emission tomography (PET), which may result from gaps between adjacent detectors or from malfunctioning detectors. To prevent artifacts in the reconstruction when using Fourier rebinning (FORE) or analytical reconstruction algorithms, filling the data gaps is required. This new approach for sinogram data interpolation prior to reconstruction is based on a simple iterative frequency selective signal extrapolation method initially proposed and successfully applied for error concealment in image and video communication. In this work the method has been improved taking advantage of well known restrictions in the allowed region of frequencies of the sinograms. We compare quantitatively the results of this technique with previously proposed gap filling procedures in both the sinograms and in their reconstructed images. The proposed technique outperforms those methods without requiring too much computational time.
Leukotriene A4 Hydrolase in Rat and Human Esophageal Adenocarcinomas and Inhibitory Effects of Bestatin (2003)

LTA4H overexpression appears to be an early event in esophageal adenocarcinogenesis and is a potential target for the chemoprevention of EAC.
Alpha 3, alpha 5, and beta 4: three members of the rat neuronal nicotinic acetylcholine receptor-related gene family form a gene cluster. (1990)

We have identified two additional members of the neuronal nicotinic acetylcholine receptor (nAChR)-related gene family. cDNA clones for one new gene, designated alpha 5, were isolated from rat hippocampus and rat PC12 cell line cDNA libraries. The alpha 5 gene encodes a protein of 48,800 daltons (424 amino acids) which exhibits significant overall amino acid sequence identity with the previously cloned rat nAChR subunits alpha 1 (49%), alpha 2 (55%), alpha 3 (52%), and alpha 4 (49%). Features characteristic of other nAChR alpha-subunits are present such as conserved cysteine residues at positions 127, 141, 191, and 192, and four strongly hydrophobic domains. A second addition to the nAChR-related gene family, designated beta 4, is encoded in overlapping rat genomic clones lambda DD15 and lambda RG518A. The beta 4 gene, encoding a mature protein of 53,300 daltons (475 amino acids), consists of 6 exons and has a transcription unit length of approximately 18 kilobase pairs. The beta 4 gene encoded protein shows considerable amino acid sequence identity with nAChR beta 1 (43%), beta 2 (64%), and beta 3 (44%) subunits. Northern blots showed that, along with alpha 3 and beta 2, transcripts for both the alpha 5 and beta 4 genes are present in the PC12 cell line, while in situ hybridization experiments demonstrated expression of the alpha 5 and beta 4 genes in a small number of nuclei in the central nervous system. Finally, the genes that encode the beta 4, alpha 3, and alpha 5 proteins are transcribed with convergent polarities and form a tightly linked gene cluster spanning approximately 60 kilobase pairs.
Drugs derived from cannabinoids. 6. Synthesis of cyclic analogues of dimethylheptylpyran (1976)

Two cyclic analogues 8 and 9 of dimethylheptylpyran (DMHP, 1) were synthesized by the Pechmann condensation of the resorcinol 4 with ethyl 4-methyl-2-cyclohexanone-1-carboxylate followed by Grignard addition with MeMgI. In selected pharmacological tests both analogues 8 and 9 were considered inactive compared to DMHP as CNS and cardiovascular agents.
Defects Engineered Monolayer MoS2 for Improved Hydrogen Evolution Reaction (2016)

MoS2 is a promising and low-cost material for electrochemical hydrogen production due to its high activity and stability during the reaction. However, the efficiency of hydrogen production is limited by the amount of active sites, for example, edges, in MoS2. Here, we demonstrate that oxygen plasma exposure and hydrogen treatment on pristine monolayer MoS2 could introduce more active sites via the formation of defects within the monolayer, leading to a high density of exposed edges and a significant improvement of the hydrogen evolution activity. These as-fabricated defects are characterized at the scale from macroscopic continuum to discrete atoms. Our work represents a facile method to increase the hydrogen production in electrochemical reaction of MoS2 via defect engineering, and helps to understand the catalytic properties of MoS2.
Fenretinide (4-HPR) in chemoprevention of oral leukoplakia (1993)

A controlled clinical trial has been underway at the Istituto Nazionale Tumori (INT) of Milan since 1988. The goal of the trial is to evaluate the effectiveness of fenretinide (4-HPR) in preventing relapses, new localizations, and carcinomas in patients with benign postoperative diagnoses who have been surgically treated for oral leukoplakias. This paper presents the design and the preliminary results of this study. To date, 137 patients have been randomized, following surgical excision of oral leukoplakia, to receive either 200 mg 4-HPR daily for 52 weeks or no intervention. Twenty local relapses or new localizations have occurred so far in the control group and 9 in the 4-HPR group. Seven patients have interrupted the intervention because of toxicity. No impaired dark adaptation has been observed. We conclude that 4-HPR is well-tolerated and appears to be effective in preventing relapses and new localizations during the treatment period.
Alteration of aldolase isozymes in serum and tissues of patients with cancer and other diseases (1994)

We studied the alteration of aldolase isozymes in the serum and tissues of patients with cancer and other diseases using radioimmunoassays specific for aldolase A, B, and C subunits. Aldolase B was predominantly found in adult liver, where aldolase A and C were distinctly low. Aldolase A and B showed almost the same concentration in fetal liver, while in neonatal liver aldolase B protein concentrations were much higher than aldolase A. In contrast, aldolase A was the predominant isozyme found in hepatoma and gastric cancer tissues, whereas aldolase B was distinctly low in hepatoma tissues, and extremely low in gastric cancer tissues. These results suggest that the aldolase A is a more fetal type of liver isozyme than the aldolase B and C, and aldolase B is a more differentiated type of liver isozyme than aldolase A and C. Serum FDP aldolase activities were elevated in half of patients with liver diseases, all patients with muscle diseases and a few patients with cancer. Serum aldolase A levels were elevated in patients with muscle diseases and cancer, but not elevated in patients with liver diseases. In contrast, serum aldolase B levels were elevated in patients with liver disease, but not elevated in patients with muscle diseases and other diseases without liver injury. Serum aldolase B levels showed a trend to decrease in cancer patients with normal GPT levels. Serum aldolase A/B ratios were significantly increased in cancer patients with normal GPT levels, whereas they showed the decreased levels in patients with liver diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
Omega-3 Fatty Acid Treatment of Women With Borderline Personality Disorder: A Double-Blind, Placebo-Controlled Pilot Study (2002)

The results of this study suggest that E-EPA may be a safe and effective form of monotherapy for women with moderately severe borderline personality disorder.
Symmetry and molecular structure of a DNA triple helix: d(T)n.cntdot.d(A)n.cntdot.d(T)n (1993)

A structure for the triple helix d(T)n.d(A)n.d(T)n consistent with recent infrared spectral data is proposed, and its salient features are discussed. The present structure preserves the pseudodyad between the Watson-Crick base-paired adenine and thymine strands and in addition has a pseudorotational symmetry relating the Hoogsteen-paired adenine and thymine strands. The simultaneous presence of these two symmetries gives rise to a dyad between the two thymine polynucleotides. These symmetries result in identical backbone conformations for all three strands, unlike any previously proposed model for a triple helix. The proposed structure has an axial rise per residue of 3.26 A and 12 residues per turn obtained from X-ray fiber diffraction [Arnott S., & Selsing, E. (1974) J. Mol. Biol. 88, 509-521]. The present structure is structurally and conformationally similar to double helical B-form DNA and has sugar pucker in the C2'-endo region. This structure is fundamentally different from the one proposed by Arnott and co-workers, which was based on structural and conformational features similar to double helical A-form DNA with C3'-endo sugar pucker. It is stereochemically satisfactory, and it does not have the disallowed nonbonded distances present in the earlier model of Arnott and co-workers. It is energetically much more favorable than their structure. Coordinates of the present structure are given.
Characterization and Heterologous Expression of the Oxalyl Coenzyme A Decarboxylase Gene from Bifidobacterium lactis (2004)

Oxalyl coenzyme A (CoA) decarboxylase (Oxc) is a key enzyme in the catabolism of the highly toxic compound oxalate, catalyzing the decarboxylation of oxalyl-CoA to formyl-CoA. The gene encoding a novel oxalyl-CoA decarboxylase from Bifidobacterium lactis DSM 10140 (oxc) was identified and characterized. This strain, isolated from yogurt, showed the highest oxalate-degrading activity in a preliminary screening with 12 strains belonging to Bifidobacterium, an anaerobic intestinal bacterial group largely used in probiotic products. The oxc gene was isolated by probing a B. lactis genomic library with a probe obtained by amplification of the oxalyl-CoA decarboxylase gene from Oxalobacter formigenes, an anaerobic bacterium of the human intestinal microflora. The oxc DNA sequence analysis revealed an open reading frame of 1,773 bp encoding a deduced 590-amino-acid protein with a molecular mass of about 63 kDa. Analysis of amino acid sequence showed a significant homology (47%) with oxalyl-CoA decarboxylase of O. formigenes and a typical thiamine pyrophosphate-binding site that has been reported for several decarboxylase enzymes. Primer extension experiments with oxc performed by using RNA isolated from B. lactis identified the transcriptional start site 28 bp upstream of the ATG start codon, immediately adjacent to a presumed promoter region. The protein overexpressed in Escherichia coli cross-reacted with an anti-O. formigenes oxalyl-CoA decarboxylase antibody. Enzymatic activity, when evaluated by capillary electrophoresis analysis, demonstrated that the consumption substrate oxalyl-CoA was regulated by a product inhibition of the enzyme. These findings suggest a potential role for Bifidobacterium in the intestinal degradation of oxalate.
Archaeal Flagella, Bacterial Flagella and Type IV Pili: A Comparison of Genes and Posttranslational Modifications (2006)

The archaeal flagellum is a unique motility organelle. While superficially similar to the bacterial flagellum, several similarities have been reported between the archaeal flagellum and the bacterial type IV pilus system. These include the multiflagellin nature of the flagellar filament, N-terminal sequence similarities between archaeal flagellins and bacterial type IV pilins, as well as the presence of homologous proteins in the two systems. Recent advances in archaeal flagella research add to the growing list of similarities. First, the preflagellin peptidase that is responsible for processing the N-terminal signal peptide in preflagellins has been identified. The preflagellin peptidase is a membrane-bound enzyme topologically similar to its counterpart in the type IV pilus system (prepilin peptidase); the two enzymes are demonstrated to utilize the same catalytic mechanism. Second, it has been suggested that the archaeal flagellum and the bacterial type IV pilus share a similar mode of assembly. While bacterial flagellins and type IV pilins can be modified with O-linked glycans, N-linked glycans have recently been reported on archaeal flagellins. This mode of glycosylation, as well as the observation that the archaeal flagellum lacks a central channel, are both consistent with the proposed assembly model. On the other hand, the failure to identify other genes involved in archaeal flagellation by homology searches likely implies a novel aspect of the archaeal flagellar system. These interesting features remain to be deciphered through continued research. Such knowledge would be invaluable to motility and protein export studies in the Archaea.
Process design and emission properties of gated n+ polycrystalline silicon field emitter arrays for flat-panel display applications (1997)

The gated n+ polycrystalline silicon (poly-Si) field emitter arrays (FEAs) have been designed and successfully fabricated on an oxidized silicon wafer for large display applications. The proposed structure of the FEAs eliminates the difficulty of having the cathode electrode (n+ diffusion layer)-to-cathode electrode isolation, which is common to crystalline silicon (c-Si) field emitter arrays. Compared with c-Si field emitters, poly-Si emitters showed poor uniformity in device structure such as emitter shape and gate hole, which was thought to be due to the variation of the grain size of poly-Si and the oxide thickness associated with grain boundaries of poly-Si in the sharpening oxidation step. The anode current of 0.1 μA/tip was measured at the gate bias of 82 V from poly-Si emitters with gate hole diameter of 1.2 μm under the vacuum pressure of 3×10−9 Torr. The same anode current was obtained at 80 V from c-Si emitters with the gate hole diameter of 1.6 μm. The gate leakage current for both the c-Si FEA and the poly-Si FEA was much less than 1% of the anode current. Long-term fluctuation characteristics in emission current of the poly-Si FEA are also studied under different sample treatments. In spite of much room for improvement, the emission characteristics of poly-Si FEAs are outstanding in terms of emission current and gate leakage current, compared with those of previously reported poly-Si FEAs.
Molecular cloning and characterization of murine ICOS and identification of B7h as ICOS ligand (2000)

Human ICOS (huICOS) is a T cell-specific molecule structurally related to CD28 and CTLA-4 with potent co-stimulatory activities on T cell proliferation, cytokine induction and T cell help for B cells. We have now cloned and characterized murine ICOS (muICOS). muICOS mRNA of 1.5 kb and 3.3 kb encodes a protein with a deduced molecular mass of 20.3 kDa, which is 71.7 % identical to huICOS. On the cell surface, muICOS is expressed as a disulfide-linked, glycosylated homodimer of 47-57 kDa, with subunits of approximately 26 kDa. With a panel of monoclonal antibodies we have determined the expression of muICOS in vitro and in vivo. Following activation of splenic T cells via CD3, muICOS became detectable at 12 h and reached a maximum of expression at around 48 h, thus exhibiting expression kinetics similar to huICOS. In vivo, muICOS was found to be substantially expressed in the thymic medulla and in the germinal centers and T cell zones of lymph nodes and Peyer's patches. Non-lymphoid tissue was ICOS negative. The muICOS gene was mapped to a region of chromosome 1 also harboring the CD28 and CTLA-4 genes. Using recombinant chimeric muICOS-Ig we determined that B7h, a recently cloned B7-like molecule, is a ligand for muICOS.