gebhart/patrepeval huggingface dataset:
Quantum computing by color-code lattice surgery (2014)

We demonstrate how to use lattice surgery to enact a universal set of fault-tolerant quantum operations with color codes. Along the way, we also improve existing surface-code lattice-surgery methods. Lattice-surgery methods use fewer qubits and the same time or less than associated defect-braiding methods. Furthermore, per code distance, color-code lattice surgery uses approximately half the qubits and the same time or less than surface-code lattice surgery. Color-code lattice surgery can also implement the Hadamard and phase gates in a single transversal step---much faster than surface-code lattice surgery can. Against uncorrelated circuit-level depolarizing noise, color-code lattice surgery uses fewer qubits to achieve the same degree of fault-tolerant error suppression as surface-code lattice surgery when the noise rate is low enough and the error suppression demand is high enough.
Nearly Linear Time Algorithms for Preconditioning and Solving Symmetric, Diagonally Dominant Linear Systems (2014)

We present a randomized algorithm that on input a symmetric, weakly diagonally dominant $n$-by-$n$ matrix $A$ with $m$ nonzero entries and an $n$-vector $b$ produces an ${\tilde{x}} $ such that $\|{\tilde{x}} - A^{\dagger} {b} \|_{A} \leq \epsilon \|A^{\dagger} {b}\|_{A}$ in expected time $O (m \log^{c}n \log (1/\epsilon))$ for some constant $c$. By applying this algorithm inside the inverse power method, we compute approximate Fiedler vectors in a similar amount of time. The algorithm applies subgraph preconditioners in a recursive fashion. These preconditioners improve upon the subgraph preconditioners first introduced by Vaidya in 1990. For any symmetric, weakly diagonally dominant matrix $A$ with nonpositive off-diagonal entries and $k \geq 1$, we construct in time $O (m \log^{c} n)$ a preconditioner $B$ of $A$ with at most $2 (n - 1) + O ((m/k) \log^{39} n)$ nonzero off-diagonal entries such that the finite generalized condition number $\kappa_{f} (A,B)$ is at most $k$, for some other constant $c$. In the special case when the nonzero structure of the matrix is planar the corresponding linear system solver runs in expected time $O (n \log^{2} n + n \log n \ \log \log n \ \log (1/\epsilon))$. We hope that our introduction of algorithms of low asymptotic complexity will lead to the development of algorithms that are also fast in practice.
End extension repair of introduced targeting vectors mediated by homologous recombination in mammalian cells (1992)

We have studied the mechanism of targeted recombination in mammalian cells using a hemizygous adenine phosphoribosyltransferase-deficient (APRT-) Chinese hamster ovary (CHO) cell mutant as a recipient. Three structurally different targeting vectors with a 5' or a 3', or both, end-deleted aprt sequence, in either a closed-circular or linear form, were transfected to the cells with a mutated aprt gene by electroporation. APRT-positive (APRT+) recombinant clones were selected and analyzed to study the gene correction events of the deletion mutation. Some half of 58 recombinant clones obtained resulted from corrections of the deleted chromosomal aprt gene by either gene replacement or gene insertion, a mechanism which is currently accepted for homologous recombination in mammalian cells. However, the chromosomal sequence in the remaining half of the recombinants remained uncorrected but their truncated end of the aprt gene in the incoming vectors was corrected by extending the end beyond the region of homology to the target locus; the corrected vector was then randomly integrated into the genome. This extension, termed end extension repair, was observed with all three vectors used and was as far as 4.6-kilobase (kb) or more long. It is evident that the novel repair reaction mediated by homologous recombination, in addition to gene replacement and gene insertion, is also involved in gene correction events in mammalian cells. We discuss the model which may account for this phenomenon.
Mechanisms of caspase-1 activation by P2X7 receptor-mediated K+ release (2004)

The mechanisms underlying caspase-1 activation and IL-1beta processing during inflammatory activation of monocytes and macrophages are not well defined. Here, we describe an in vitro proteolytic processing assay that allows for comparison of caspase-1 regulatory components in a cell-free system separately from the confounding issue of IL-1beta secretion. Analysis of in vitro IL-1beta and caspase-1 processing in lysates from unstimulated Bac1 murine macrophages indicated a slow rate of basal caspase-1 activation and proteolytic maturation of IL-1beta. In contrast, brief (5 min) treatment of intact macrophages with extracellular ATP (as an activator of the P2X(7) receptor) or nigericin before cell lysis markedly accelerated the in vitro processing of caspase-1 and IL-1beta. This acceleration of in vitro processing was strictly dependent on loss of intracellular K(+) from the intact cells. The induction of in vitro caspase-1 activation by lysis per se or by K(+) loss before lysis was sensitive to pretreatment of intact macrophages with the tyrphostin AG-126 or bromoenol lactone, an inhibitor of Ca(2+)-independent phospholipase A(2). Caspase-1 activation and IL-1beta processing in lysates from unstimulated macrophages were also accelerated by addition of recombinant ASC, a previously identified adapter protein that directly associates with caspase-1. These data indicate that increased K(+) efflux via P2X(7) nucleotide receptor stimulation activates AG-126- and bromoenol lactone-sensitive signaling pathways in murine macrophages that result in stably maintained signals for caspase-1 regulation in cell-free assays.
Characterization of the thyroid Na + /I − symporter with an anti-COOH terminus antibody (1997)

The Na+/I- symporter (NIS) is the plasma membrane protein that catalyzes active I- transport in the thyroid, the first step in thyroid hormone biogenesis. The cDNA encoding NIS was recently cloned in our laboratory and a secondary structure model proposed, suggesting that NIS is an intrinsic membrane protein (618 amino acids; approximately 65.2 kDa predicted molecular mass) with 12 putative transmembrane domains. Here we report the generation of a site-directed polyclonal anti-COOH terminus NIS antibody (Ab) that immunoreacts with a approximately 87 kDa-polypeptide present in membrane fractions from a rat thyroid cell line (FRTL-5). The model-predicted cytosolic-side location of the COOH terminus was confirmed by indirect immunofluorescence experiments using anti-COOH terminus NIS Ab in permeabilized FRTL-5 cells. Immunoreactivity was competitively blocked by the presence of excess synthetic peptide. Treatment of membrane fractions from FRTL-5 cells, Xenopus laevis oocytes, and COS cells expressing NIS with peptidyl N-glycanase F converted the approximately 87 kDa-polypeptide into a approximately 50 kDa-species, the same relative molecular weight exhibited by NIS expressed in E. coli. Anti-NIS Ab immunoprecipitated both the NIS precursor molecule (approximately 56 kDa) and the mature approximately 87 kDa form. Furthermore, a direct correlation between circulating levels of thyroid-stimulating hormone and NIS expression in vivo was demonstrated.
Somatostatin Receptor Gene Therapy Combined With Targeted Therapy With Radiolabeled Octreotide (2002)

The authors showed an impressive antitumor effect of SSR (subtype 2)-transfected colon carcinoma cells with PRRT in a rat liver metastasis model. Moreover, rats with mixed liver metastases had significantly fewer liver metastases compared with control rats, which may be due to a radiologic bystander effect of [177 Lu-DOTA0, Tyr3 ]octreotate. This phenomenon is beneficial in the concept of in vivo gene therapy.
Expression of programmed cell death factor 4 and its pathological significance in gastric cancer (2006)

OBJECTIVE: To investigate the expression of programmed cell death factor 4 (PDCD4) protein and its clinicopathological significance in gastric cancer.METHODS:PDCD4 expression in 5 fresh specimens of gastric cancer and relevant adjuvant non-cancerous tissue were detected by Western blot with PDCD4 specific antibody; immunohistochemistry was used to examine the expression of PDCD4 in 61 paraffin embedded specimens of gastric cancer, among which 26 specimens had adjacent normal gastric tissue. Correlations of PDCD4 expression with clinico-pathological data were analyzed.RESULTS:The expression of PDCD4 was significantly lower in all 5 fresh gastric cancer tissues than in non-cancerous tissues detected by Western blot. Compared with adjuvant normal gastric tissue (80% of positive cells), low PDCD4 expression was shown in 61 gastric cancer tissues (30% of positive cells in 40 cases and 30%-80% of positive cells in 21 cases). In the 21 cases that positive cells was between 30% and 80%, the rates of well, moderately, and poorly differentiated patients were 57.1%, 33.3% and 9.6%, respectively. However, in the 40 cases that positive cells was less than 30%, the rates of well, moderately, and poorly differentiated patients were 2.5%, 37.5% and 60%, respectively. In moderately and poorly differentiated patients, 68.2% and 92.3% showed positive cells less than 30%, however, only 7.7% well differentiated patients showed positive cells less than 30%, indicating low PDCD4 level was associated with histological grade, P0.01. There is no relationship between PDCD4 expression and other clinicopathological parameters including sex, age and TNM status. CONCLUSION: Progressive down-regulation of PDCD4 in gastric cancer is correlated with histological grade. PDCD4 may play an important role in occurrence and development of gastric cancer.
Identification of non-amplifying CYP21 genes when using PCR-based diagnosis of 21-hydroxylase deficiency in congenital adrenal hyperplasia (CAH) affected pedigrees (1996)

Steroid 21-hydroxylase deficiency is among the most common inborn errors of metabolism in man. Characterization of mutations in the 21-hydroxylase gene (CYP21) has permitted genetic diagnosis, facilitated by the polymerase chain reaction (PCR). The most common mutation is conversion of an A or C at nt656 to a G in the second intron causing aberrant splicing of mRNA. Homozygosity for nt656G is associated with profoundly deficient adrenal cortisol and aldosterone synthesis, secondary hypersecretion of adrenal androgens, and a severe form of congenital adrenal hyperplasia (CAH) characterized by ambiguous genitalia and/or sodium wasting in newborns. During the course of genetic analysis of CYP21 mutations in CAH families, we and others have noticed a number of relatives genotyped as nt656G homozygotes, yet showing no clinical signs of disease. A number of lines of evidence have led us to propose that the putative asymptomatic nt656G/G individuals are incorrectly typed due to dropout of one haplotype during PCR amplification of CYP21. For prenatal diagnosis, we recommend that microsatellite typing be used as a supplement to CYP21 genotyping in order to resolve ambiguities at nt656.
Sol‐Gel Synthesized Magnetic MnFe2O4 Spinel Ferrite Nanoparticles as Novel Catalyst for Oxidative Degradation of Methyl Orange (2013)

The MnFe 2 O 4 spinel ferrite nanoparticles with sensitive magnetic response properties and high specific surface area were prepared from metal nitrates by the sol‐gel process as catalysts for oxidative degradation of methyl orange (MO). The nanoparticles were characterized by X‐ray powder diffraction (XRD), scanning electron microscopy (SEM), BET surface area analysis, H 2 ‐Temperature programmed reduction (H 2 ‐TPR), X‐ray photoelectron spectra (XPS), and vibration sample magnetometer (VSM). The catalytic activity experimental results showed that the MnFe 2 O 4 spinel ferrite nanoparticles possess very high MO degradation activity. It is expected that this kind of MnFe 2 O 4 spinel ferrite nanoparticles has a potential application in water treatment fields due to its sensitive magnetic response properties and high catalytic activity.
Isolation and transmission of the Lyme disease spirochete from the southeastern United States. (1993)

The isolation of the Lyme disease spirochete (Borrelia burgdorferi) from the southeastern United States is reported. Three isolates, two from cotton mice (Peromyscus gossypinus) and one from the black-legged tick (Ixodes scapularis), were recovered from Sapelo Island, Georgia, in July and September 1991. The spirochetes were characterized by indirect fluorescent antibody assay using a battery of five monoclonal antibodies, by sodium dodecyl sulfate/polyacrylamide gel electrophoresis (SDS/PAGE) of whole cell lysates, and by the polymerase chain reaction (PCR) assay using primers for three DNA target sequences found in B. burgdorferi reference strain B-31. Transmission experiments indicate that the three Georgia isolates can infect experimentally inoculated hamsters and mice. Tick transmission of one of the isolates has been attempted so far; I. scapularis transmitted isolate SI-1 from hamsters to mice, but the lone-star tick, Amblyomma americanum, did not.
Obligatory heterotetramerization of three previously uncharacterized Kv channel α-subunits identified in the human genome (2002)

Voltage-gated K(+) channels control excitability in neuronal and various other tissues. We identified three unique alpha-subunits of voltage-gated K(+)-channels in the human genome. Analysis of the full-length sequences indicated that one represents a previously uncharacterized member of the Kv6 subfamily, Kv6.3, whereas the others are the first members of two unique subfamilies, Kv10.1 and Kv11.1. Although they have all of the hallmarks of voltage-gated K(+) channel subunits, they did not produce K(+) currents when expressed in mammalian cells. Confocal microscopy showed that Kv6.3, Kv10.1, and Kv11.1 alone did not reach the plasma membrane, but were retained in the endoplasmic reticulum. Yeast two-hybrid experiments failed to show homotetrameric interactions, but showed interactions with Kv2.1, Kv3.1, and Kv5.1. Co-expression of each of the previously uncharacterized subunits with Kv2.1 resulted in plasma membrane localization with currents that differed from typical Kv2.1 currents. This heteromerization was confirmed by co-immunoprecipitation. The Kv2 subfamily consists of only two members and uses interaction with "silent subunits" to diversify its function. Including the subunits described here, the "silent subunits" represent one-third of all Kv subunits, suggesting that obligatory heterotetramer formation is more widespread than previously thought.
A Novel Type II NAD+-Specific Isocitrate Dehydrogenase from the Marine Bacterium Congregibacter litoralis KT71 (2015)

In most living organisms, isocitrate dehydrogenases (IDHs) convert isocitrate into ɑ-ketoglutarate (ɑ-KG). Phylogenetic analyses divide the IDH protein family into two subgroups: types I and II. Based on cofactor usage, IDHs are either NAD+-specific (NAD-IDH) or NADP+-specific (NADP-IDH); NADP-IDH evolved from NAD-IDH. Type I IDHs include NAD-IDHs and NADP-IDHs; however, no type II NAD-IDHs have been reported to date. This study reports a novel type II NAD-IDH from the marine bacterium Congregibacter litoralis KT71 (ClIDH, GenBank accession no. EAQ96042). His-tagged recombinant ClIDH was produced in Escherichia coli and purified; the recombinant enzyme was NAD+-specific and showed no detectable activity with NADP+. The Km values of the enzyme for NAD+ were 262.6±7.4 μM or 309.1±11.2 μM with Mg2+ or Mn2+ as the divalent cation, respectively. The coenzyme specificity of a ClIDH Asp487Arg/Leu488His mutant was altered, and the preference of the mutant for NADP+ was approximately 24-fold higher than that for NAD+, suggesting that ClIDH is an NAD+-specific ancestral enzyme in the type II IDH subgroup. Gel filtration and analytical ultracentrifugation analyses revealed the homohexameric structure of ClIDH, which is the first IDH hexamer discovered thus far. A 163-amino acid segment of CIIDH is essential to maintain its polymerization structure and activity, as a truncated version lacking this region forms a non-functional monomer. ClIDH was dependent on divalent cations, the most effective being Mn2+. The maximal activity of purified recombinant ClIDH was achieved at 35°C and pH 7.5, and a heat inactivation experiment showed that a 20-min incubation at 33°C caused a 50% loss of ClIDH activity. The discovery of a NAD+-specific, type II IDH fills a gap in the current classification of IDHs, and sheds light on the evolution of type II IDHs.
Permanent, Nonleaching Antibacterial Surfaces. 1. Synthesis by Atom Transfer Radical Polymerization (2004)

We have grown an antimicrobial polymer directly on the surfaces of glass and paper using atom transfer radical polymerization (ATRP). The method described here results in potentially permanent nonleaching antibacterial surfaces without the need to chemically graft the antimicrobial material to the substratum. The tertiary amine 2-(dimethylamino)ethyl methacrylate was polymerized directly onto Whatman #1 filter paper or glass slides via atom transfer radical polymerization. Following the polymerization, the tertiary amino groups were quaternized using an alkyl halide to produce a large concentration of quaternary ammonium groups on the polymer-modified surfaces. Incubating the modified materials with either Escherichia coli or Bacillus subtilis demonstrated that the modified surfaces had substantial antimicrobial capacity. The permanence of the antimicrobial activity was demonstrated through repeated use of a modified glass without significant loss of activity. Quaternary amines are believed to cause cell death by disrupting cell membranes allowing release of the intracellular contents. Atomic force microscopic imaging of cells on modified glass surfaces supports this hypothesis.
Studies on the synthesis and anti-inflammatory activity of 2,6-di-tert-butylphenols with a heterocyclic group at the 4-position. I. (1983)

A number of 2, 6-di-tert-butylphenols with a heterocyclic group at the 4-position were prepared. The heterocyclic groups were as follows : benzoxazole, benzothiazole, benzimidazole, indole, imidazo [1, 2-a] pyridine and imidazo [1, 2-a] pyrimidine. Anti-inflammatory activity of these compounds was examined by using the adjuvant-induced arthritis (A. A) assay. Some compounds were further tested in carrageenin-induced rat paw edema (CIPE) assay and AcOH-induced writhing (AIW) assay in mice. The anti-inflammatory activity was greatly dependent on the value of the heterocyclic group. Among these compounds, 2-(3, 5-di-tert-butyl-4-hydroxyphenyl)-benzoxazole (IIa) and 2-(3, 5-di-tert-butyl-4-hydroxyphenyl) indole (Xg) showed very potent activity. Both IIa and Xg had a minimum effective dose of 5 mg/kg (p. o.) in A. A assay and showed stronger activity than phenylbutazone in CIPE assay but weaker analgesic activity than aminopyrine in AIW assay.
The improved lytic function and in vivo efficacy of monovalent monoclonal CD3 antibodies (1989)

A series of hybrid-hybridomas were derived by the cell fusion of a CD3 antibody-secreting hybridoma with other Ig-producing cell lines. The Ig molecules secreted by these hybrid-hybridomas were fractionated by ion-exchange chromatography, and fractions containing monovalent CD3 antibodies were tested for complement-mediated lysis of T cells. Two monovalent CD3 antibodies with mixed heavy chain isotypes were very poor in lysis but, in contrast, a monovalent antibody possessing two identical rat gamma 2b heavy chains but two non-identical light chains was found to be more lytic with human complement than the parental bivalent CD3 antibody. The difference in lysis was not readily explicable in terms of a difference in complement activation at the level of C1q binding or cell-associated C3. A highly purified batch of this lytic monovalent CD3 antibody was prepared in a form suitable for in vivo therapy. In a preliminary clinical study in one patient with a T lymphoma in leukemic phase this monovalent CD3 antibody was found to be very effective in depleting CD3+ tumor cells in the peripheral blood and bone marrow. The cells in the peripheral blood were completely cleared and there was no evidence for antigenic modulation. In addition the antibody was able to reverse cell-mediated kidney rejection in three kidney graft patients. These results suggest that monovalent antibody may be effective in vivo as well as in vitro and that a fuller clinical evaluation is justified.
HIV infectivity is not augmented by treatment with trypsin, Factor Xa or human mast-cell tryptase (1992)

Departments of Medicine and Pathology, University of California San Diego School of Medicine and Veterans Affairs Medical Center, 3350 La Jolla Village Drive, San Diego, California 92161, USA.
Gpd1 and Gpd2 Fine-Tuning for Sustainable Reduction of Glycerol Formation in Saccharomyces cerevisiae (2011)

Gpd1 and Gpd2 are the two isoforms of glycerol 3-phosphate dehydrogenase (GPDH), which is the rate-controlling enzyme of glycerol formation in Saccharomyces cerevisiae. The two isoenzymes play crucial roles in osmoregulation and redox balancing. Past approaches to increase ethanol yield at the cost of reduced glycerol yield have most often been based on deletion of either one or two isogenes (GPD1 and GPD2). While single deletions of GPD1 or GPD2 reduced glycerol formation only slightly, the gpd1Δ gpd2Δ double deletion strain produced zero glycerol but showed an osmosensitive phenotype and abolished anaerobic growth. Our current approach has sought to generate "intermediate" phenotypes by reducing both isoenzyme activities without abolishing them. To this end, the GPD1 promoter was replaced in a gpd2Δ background by two lower-strength TEF1 promoter mutants. In the same manner, the activity of the GPD2 promoter was reduced in a gpd1Δ background. The resulting strains were crossed to obtain different combinations of residual GPD1 and GPD2 expression levels. Among our engineered strains we identified four candidates showing improved ethanol yields compared to the wild type. In contrast to a gpd1Δ gpd2Δ double-deletion strain, these strains were able to completely ferment the sugars under quasi-anaerobic conditions in both minimal medium and during simultaneous saccharification and fermentation (SSF) of liquefied wheat mash (wheat liquefact). This result implies that our strains can tolerate the ethanol concentration at the end of the wheat liquefact SSF (up to 90 g liter(-1)). Moreover, a few of these strains showed no significant reduction in osmotic stress tolerance compared to the wild type.
A novel class of potent topical antiinflammatory agents: 17-benzoylated, 7 alpha-halogeno substituted corticosteroids. (1979)

As part of continued efforts in the synthesis of structurally novel corticosteroids, a number of 17 alpha-benzoylated, 7 alpha-halogeno substituted prednisolones were tested for topical antiinflammatory activity. 7 alpha-Chloro, 7 alpha-bromo, and 7 alpha-iodo corticosteroids were synthesized by hydrogen halide addition to 1,4,6-triene-3-ones. The 7 alpha-fluoro substituted steroid was obtained by reaction of the appropriate 7 beta-hydroxy compound with N,N-diethyl(2-chloro-1,1,2-trifluoroethyl)amine. Antiinflammatory potencies were obtained using a croton oil-induced inflammation in the ears of mice. In this assay the greatest effect of a 7 alpha-halogen was observed in the 16 alpha-methylprednisolone series, where 7 alpha-fluoro and 7 alpha-bromo substitution yielded corticosteroids with topical potencies significantly higher than those of the corresponding 17,21-dipropionate analogs. Surprisingly, little potency enhancement due to 7 alpha-halogenation was discerned in the 16 beta-methylprednisolone series.