gebhart/patrepeval huggingface dataset:
Version 2 of the Protocol Operations for the Simple Network Management Protocol (SNMP) (2002)

2 of the protocol operations for the Simple Network Management Protocol (SNMP).It defines the syntax and elements of procedure for sending, receiving, and processing SNMP PDUs.This document obsoletes RFC 1905.
Mycoactive Acetate Esters from Apple Fruit Stimulate Adhesion and Germination of Conidia of the Gray Mold Fungus (2002)

Ethyl acetate, 2-methylbutyl acetate, butyl acetate (BA), and hexyl acetate were detected by solid-phase microextraction and gas-liquid chromatography inside slices of Golden Delicious apple and in water droplets on the skin of slices incubated in sealed glass jars. Conidial adhesion and germination of the gray mold fungus, Botrytis cinerea, was assessed on apple slices after exposure or no exposure to the esters in the headspaces of glass jars. Attached conidia were dislodged by sonication and remaining conidia on apple slices were counted by microscopy. Adhesion generally increased as BA increased to 7.2 microg mL(-1), but declined with greater concentrations. BA at 0-3.6 microg mL(-1) for 24 h stimulated adhesion 2-fold greater compared to that at 4 h. Adhesion stimulated by BA increased as a function of time (0-24 h), showing linear trends (r (2) = 0.99; p = 0.01) during 0-12 h. The four esters were similar in their ability to stimulate adhesion. Germination of conidia exposed to BA increased linearly (r (2) = 0.95-0.98; p = 0.01) during 4-12 h. Conidial adhesion stimulated by BA preceded conidial germination by 2 h. The four esters stimulated conidial germination to similar levels. Results indicated that acetate esters formed in apple fruit are mycoactive, influencing life-cycle events of B. cinerea important to its survival on the fruit. The similar responses of three B. cinerea isolates to four acetate esters suggests a common stimulation mechanism may operate in B. cinerea.
Prostate Cancer: Accurate Determination of Extracapsular Extension with High-Spatial-Resolution Dynamic Contrast-enhanced and T2-weighted MR Imaging—Initial Results (2007)

The combination of high-spatial-resolution dynamic contrast-enhanced MR imaging and T2-weighted MR imaging yields improved assessment of ECE and better results for prostate cancer staging compared with either technique independently.
Mass spectrometric methods for analysis of oligosaccharides in human milk (2009)

Establishing the analytical platforms for characterizing human milk oligosaccharides is important to fully assess their specific functionalities. The characterization of these biomolecules, however, is still considered challenging, owing to their overall complexity and diversity. Addressed here are the technical difficulties with an emphasis on the application of mass spectrometry to rapidly profile and quantify human milk oligosaccharides. Fundamental concepts and improvements in instrumentation and an overview of the biological functions and structures of these compounds are also discussed. Results reveal that small-chain oligosaccharides, evident in abundance in the early stage of lactation, are selectively consumed by specific stains of Bifidobacterium longum biovar, infantis.
A Class of Pantothenic Acid Analogs Inhibits Plasmodium falciparum Pantothenate Kinase and Represses the Proliferation of Malaria Parasites (2005)

The growth and proliferation of the human malaria parasite Plasmodium falciparum are dependent on the parasite's ability to obtain essential nutrients. One nutrient for which the parasite has an absolute requirement is the water-soluble vitamin pantothenic acid (vitamin B5). In this study, a series of pantothenic acid analogs which retain the 2,4-dihydroxy-3,3-dimethylbutyramide core of pantothenic acid but deviate in structure from one another and from pantothenic acid in the nature of the substituent attached to the amide nitrogen were synthesized using an efficient single-step synthetic route. Eight of 10 analogs tested inhibited the proliferation of intraerythrocytic P. falciparum parasites in vitro, doing so with 50% inhibitory concentrations between 15 and 200 microM. The compounds were generally selective, inhibiting the proliferation of a human cell line (the Jurkat cell line) only at concentrations severalfold higher than those required for inhibition of parasite growth. It was demonstrated that compounds in this series inhibited the phosphorylation of pantothenic acid by pantothenate kinase, the first step in the parasite's biosynthesis of the essential enzyme cofactor coenzyme A, doing so competitively, with K(i) values in the nanomolar range.
Lack of Evidence of Encephalopathy Related to Pertussis Vaccine : Active Surveillance by IMPACT, Canada, 1993–2002 (2004)

To assess whether pertussis-containing vaccines cause encephalitis or encephalopathy, the IMPACT network of Canadian pediatric centers screened more than 12,000 admissions for neurologic disorders between 1993 and 2002. Seven cases of encephalopathy began within 7 days after pertussis vaccination, but a more likely cause was found in each instance. No attributable case followed administration of >6.5 million doses of vaccine.
Toll-Like Receptor 9 Inhibition Confers Protection From Liver Ischemia–Reperfusion Injury (2009)

TLR9 serves as an endogenous sensor of tissue necrosis that exacerbates the innate immune response during liver I/R. Combined blockade of TLR9 and HMGB1 represents a clinically relevant, novel approach to limiting I/R injury.
Manganese superoxide dismutase gene therapy protects against irradiation-induced cystitis (2002)

Urinary bladder cystitis occurs in patients receiving radiation therapy for pelvic tumors. Radiation-induced formation of superoxide radicals is believed to damage the urothelium, exposing the underlying bladder smooth muscle to urine, culminating in nerve irritation and muscle dysfunction. We tested whether overexpression of MnSOD could decrease superoxide levels and protect the bladder from radiation damage. Pelvic irradiation led to sloughing of urothelial umbrella cells, with decreased transepithelial resistance, increased water and urea permeabilities, and increased expression of inducible nitric oxide synthase. Six months after irradiation, cystometrograms showed elevated intravesical pressures and prolonged voiding patterns. However, urothelia transfected with the MnSOD transgene recovered from radiation injury more rapidly, and detrusor function was much closer to that of control bladders than irradiated bladders without the transgene. We conclude that MnSOD gene therapy is protective, which could lead to its use in mitigating radiation cystitis and preventing dysfunction of the urinary bladder.
5A-3 Spatial and Temporal Controlled Tissue Heating on a Modified Clinical Ultrasound Scanner for Generating Mild Hyperthermia in Tumors (2007)

We present a new system for generating controlled tissue heating with a clinical ultrasound scanner and initial in vitro and in vivo results that demonstrate both transient and sustained heating in the mild- hyperthermia range of 37-42degC. The system consists of a Siemens Antarestrade ultrasound scanner, a custom dual-frequency 3-row transducer array, and an external temperature feedback control system. The transducer has 2 outer rows that operate at 1.5 MHz for tissue heating and a center row that operates at 5 MHz for B-mode imaging. Temperature measurement is accomplished using a thermocouple encased within a 29 gauge stainless steel needle. The temperature measurements are fed into a modified proportional-differential-integral (PID) control loop programmed in LabVIEWtrade running on an external PC. Modifications to the PID loop include a limited bandwidth differential section and integrator anti-windup. The PID loop controls duty cycle by varying the PRF on a SIEMENS Antares ultrasound scanner, and the resulting PRF update rate is approximately 3 Hz. The heating beam is directed using the pulsed-Doppler cursor with reference to a 5 MHz B-mode image. B-mode updates also occur at approximately 3 Hz. In vitro results show differential heating of chicken breast of 8degC at the beam focus. We show that the system is able to maintain the temperature to within 0.1degC of the desired temperature both in vitro and in vivo. In vivo tests of the system were performed on a mouse bearing Met-1 tumors, which is a model of aggressive, metastatic and highly vascular breast cancer. In superficially implanted tumors, we demonstrate controlled heating to temperatures in the 39-42degC range, which is ideal for releasing drugs from thermally-sensitive liposomes.
Heart rate variability (HRV) in kidney failure: measurement and consequences of reduced HRV (2007)

A common cause of death in end-stage renal disease (ESRD) patients on dialysis is sudden cardiac death (SCD). Compared to the general population, the percentage of cardiovascular deaths that are attributed to SCD is higher in patients treated by dialysis. While coronary artery disease (CAD) is the predominant cause of SCD in dialysis patients, reduced heart rate variability (HRV) may play a role in the higher risk of SCD among other risk factors. HRV refers to beat-to-beat alterations in heart rate as measured by periodic variation in the R-R interval. HRV provides a non-invasive method for investigating autonomic input into the heart. It quantifies the amount by which the R-R interval or heart rate changes from one cardiac cycle to the next. The autonomic nervous system transmits impulses from the central nervous system to peripheral organs and is responsible for controlling the heart rate, blood pressure and respiratory activity. In normal individuals, without cardiac disease, the heart rate has a high degree of beat-to-beat variability. HRV fluctuates with respiration: it increases with inspiration and decreases with expiration and is primarily mediated by parasympathetic activity. HRV has been used to evaluate and quantify the cardiac risk associated with a variety of conditions including cardiac disorders, stroke, multiple sclerosis and diabetes. In this narrative review, we will examine the association between HRV and SCD. This report explains the measurement of HRV and the consequences of reduced HRV in the general population and dialysis patients. Lastly, this review will outline the possible use of HRV as a clinical predictor for SCD in the dialysis population. The current understanding of SCD based on HRV findings among the ESRD population support the use of more aggressive treatment of CAD; greater use of angiotensin converting enzyme inhibitor (ACE-i)/angiotensin receptor blockers (ARBs) and beta-blockers and more frequent and/or nocturnal haemodialysis to improve the survival of a patient with kidney failure.
URINARY TRACT INFECTION PROPHYLAXIS USING ESCHERICHIA COLI 83972 IN SPINAL CORD INJURED PATIENTS (2000)

E. coli 83972 may be safely used to establish long-term asymptomatic bladder colonization in spinal cord injured subjects. Preliminary findings suggest that colonization with E. coli 83972 may reduce the frequency of urinary tract infection in patients with neurogenic bladder secondary to spinal cord injury.
Device challenges for near term superconducting quantum processors: frequency collisions (2018)

The outstanding progress in experimental quantum computing with superconducting Josephson-junction based qubits over the past few decades has pushed coherence times many orders of magnitude above that of the first measured. We are also in the midst of scaling towards complex architectures of multi-qubit processors where maintaining very low gate error rates at the limits supported by coherence times is extremely important. Here we will review some of the critical materials and device challenges for superconducting qubits from the perspective of improved coherence and improved error rates. In particular we will focus on the problem of frequency allocations in order to target multi-qubit lattices for fixed-frequency microwave-based gates.
Role of Histone H3 Lysine 9 Methylation in Epigenetic Control of Heterochromatin Assembly (2001)

The assembly of higher order chromatin structures has been linked to the covalent modifications of histone tails. We provide in vivo evidence that lysine 9 of histone H3 (H3 Lys9) is preferentially methylated by the Clr4 protein at heterochromatin-associated regions in fission yeast. Both the conserved chromo- and SET domains of Clr4 are required for H3 Lys9 methylation in vivo. Localization of Swi6, a homolog of Drosophila HP1, to heterochomatic regions is dependent on H3 Lys9 methylation. Moreover, an H3-specific deacetylase Clr3 and a beta-propeller domain protein Rik1 are required for H3 Lys9 methylation by Clr4 and Swi6 localization. These data define a conserved pathway wherein sequential histone modifications establish a "histone code" essential for the epigenetic inheritance of heterochromatin assembly.
MS-275 synergistically enhances the growth inhibitory effects of RAMBA VN/66-1 in hormone-insensitive PC-3 prostate cancer cells and tumours (2008)

Combining drugs, which target different signalling pathways, often decreases adverse side effects while increasing the efficacy of treatment. The objective of our study was to determine if the combination of our novel atypical retinoic acid metabolism-blocking agent (RAMBA) VN/66-1 and a promising histone deacetylase inhibitor N-(2-aminophenyl)4-[N-(pyridine-3-yl-methoxy-carbonyl)aminomethyl]benzamide (MS-275) would show enhanced antineoplastic activity on human PC-3 prostate cancer cells/tumours and also to decipher the molecular mechanisms of action. The combination of VN/66-1+MS-275 was found to be synergistic in inhibiting PC-3 cell growth, caused cell cytostaticity/cytotoxicity and induced marked G2/M phase arrest and apoptosis. In mice with well-established PC-3 tumours, VN/66-1 (5 and 10 mg kg(-1) day(-1)) caused significant suppression of tumour growth compared with mice receiving vehicle alone. Furthermore, treatment with VN/66-1 (10 mg kg(-1) day(-1))+MS-275 (2.5 mg kg(-1) day(-1)) for 18 days resulted in an 85% reduction in final mean tumour volume compared with control and was more effective than either agent alone. Mechanistic studies indicated that treatment of PC-3 cells/tumours with VN/66-1+MS-275 caused DNA damage (upregulation of gammaH2AX), hyperacetylation of histones H3 and H4, upregulation of retinoic acid receptor-beta, p21WAF1/CIP1, E-cadherin, and Bad and downregulation of Bcl-2. These data suggest that the mechanism of action of the combination of agents is DNA damage-induced p21 activation, resulting in inhibition of the Cdc2/cyclin B complex and accumulation of cells in G2/M phase. In addition, the combination caused modulation and induction of apoptosis. These results suggest that VN/66-1 or its combination with MS-275 may be a novel therapy for the treatment of prostate carcinoma.
Immunization with idiotypic immunoglobulin protects against development of B lymphocytic leukemia, but emerging tumor cells can evade antibody attack by modulation. (1983)

Immunization of strain 2 guinea pigs with idiotypic IgM obtained from serum of animals in the terminal phase of the L2C leukemia produced high levels of circulating anti-idiotypic antibody that was cytotoxic for the tumor cells in the presence of syngeneic C. Such animals showed good protection against injected tumor cells, but after a long delay, leukemia did develop. As tumor cells appeared in the blood, anti-idiotype was consumed, but the cells displayed little or no surface Ig and could not be killed in vitro by anti-idiotype and C. However, as serum antibody levels fell, the cells displayed increasing amounts of surface IgM lambda of the same idiotype and regained their susceptibility to the antibody and C in vitro. It appears, therefore, that the ability of tumor cells to modulate their target idiotype can present a considerable problem for antibody-mediated attack.
Amyloid plaque core protein in Alzheimer disease and Down syndrome. (1985)

We have purified and characterized the cerebral amyloid protein that forms the plaque core in Alzheimer disease and in aged individuals with Down syndrome. The protein consists of multimeric aggregates of a polypeptide of about 40 residues (4 kDa). The amino acid composition, molecular mass, and NH2-terminal sequence of this amyloid protein are almost identical to those described for the amyloid deposited in the congophilic angiopathy of Alzheimer disease and Down syndrome, but the plaque core proteins have ragged NH2 termini. The shared 4-kDa subunit indicates a common origin for the amyloids of the plaque core and of the congophilic angiopathy. There are superficial resemblances between the solubility characteristics of the plaque core and some of the properties of scrapie infectivity, but there are no similarities in amino acid sequences between the plaque core and scrapie polypeptides.
5-Aza-2′-deoxycytidine Activates the p53/p21Waf1/Cip1 Pathway to Inhibit Cell Proliferation (2004)

In addition to its demethylating function, 5-aza-2'-deoxycytidine (5-aza-CdR) also plays an important role in inducing cell cycle arrest, differentiation, and cell death. However, the mechanism by which 5-aza-CdR induces antineoplastic activity is not clear. In this study, we found that 5-aza-CdR at limited concentrations (0.01-5 microm) induces inhibition of cell proliferation as well as increased p53/p21(Waf1/Cip1) expression in A549 cells (wild-type p53) but not in H1299 (p53-null) and H719 cells (p53 mutant). The p53-dependent p21(Waf1/Cip1) expression induced by 5-aza-CdR was not seen in A549 cells transfected with the wild-type human papilloma virus type-16 E6 gene that induces p53 degradation. Furthermore, deletion analysis and site-directed mutagenesis of the p21 promoter reveals that 5-aza-CdR induces p21(Waf1/Cip1) expression through two p53 binding sites in the p21 promoter. Finally, 5-aza-CdR-induced p21(Waf1/Cip1) expression was dependent on DNA damage but not on DNA demethylation as demonstrated by comet assay and bisulfite sequencing, respectively. Our data provide useful clues for judging the therapeutic efficacy of 5-aza-CdR in the treatment of human cancer cells.
Minicell-forming mutants of Escherichia coli: production of minicells and anucleate rods (1988)

The Escherichia coli minB mutant originally isolated is known to septate at cell poles to form spherical anucleate minicells. Three new minicell-producing mutants were isolated during a screening by autoradiography for chromosome partition mutants giving rise spontaneously to normal-sized anucleate cells. These min mutants were affected close to or in the minB locus. Autoradiography analysis as well as fluorescent staining of DNA showed that in addition to minicells, these strains and the original minB mutant also spontaneously produced anucleate rods of normal size and had an abnormal DNA distribution in filaments. These aberrations were not associated with spontaneous induction of the SOS response. Inhibition of DNA synthesis in these mutants gave rise to anucleate cells whose size was longer than unit cell length, suggesting that the min defect allows septation to take place at normally forbidden sites not only at cell poles but also far from poles. Abnormal DNA distribution and production of anucleate rods suggest that the Min product(s) could be involved in DNA distribution.
Insulin action in cultured human myoblasts: contribution of different signalling pathways to regulation of glycogen synthesis (1996)

A key metabolic action of insulin is the stimulation of non-oxidative glucose utilization in skeletal muscle, by increasing both glucose uptake and glycogen synthesis. The molecular mechanism underlying this process has been investigated using a variety of experimental systems. We report here the use of cultured human myoblasts to study insulin control of glycogen synthesis in humans. In these cells insulin stimulates glycogen synthesis approx. 2.2-fold, associated with a similar activation of glycogen synthase (GS) which occurs within 5-10 min of the addition of insulin. Insulin also causes inactivation of glycogen synthase kinase-3 (GSK-3) and activation of protein kinase B, both processes being sufficiently rapid to account for the effects of insulin on GS. Activation by insulin of the protein kinases p70s6K, p90s6K and extracellular signal-regulated kinase 2 (ERK2) is observed, but is significantly slower than the activation of GS. Selective inhibitors of the p70s6K pathway (rapamycin), the ERK2/p90s6K pathway (PD98059) and phosphatidylinositol 3-kinase (wortmannin) have been used to probe the contribution of these components to insulin signalling in human muscle. Wortmannin blocks activation of both glycogen synthesis and GS and inactivation of GSK-3. PD98059 is without effect on these events, while rapamycin is without effect on inactivation of GSK-3 but partially blocks activation of glycogen synthesis and GS. Taken together, these findings suggest that protein kinase B is responsible for the inactivation of GSK-3, but that an additional rapamycin-sensitive mechanism may contribute to the activation of GS and stimulation of glycogen synthesis.
Tumor necrosis factor alpha-mediated tumor regression by the in vivo transfer of genes into the artery that leads to tumors. (1998)

We report that tumor necrosis factor (TNF) alpha induced a strong antitumor immune reaction when it was produced in arteries leading to tumors by gene transfer in vivo. We used a mouse model carrying a sarcoma-180 tumor in the right footpad and injected the fusogenic liposomes encapsulating the human TNF-alpha gene into the right femoral artery. Under this condition, human TNF-alpha was detected only in the artery leading to the tumor and in the tumor. There was a significant regression in tumor growth when the TNF-alpha gene was delivered into the right femoral artery, with 4 of 11 mice completely cured. No regression was observed when the TNF-alpha gene was delivered into the left femoral artery or into the tumor or when the luciferase gene was administered. Tumor regression was inhibited by the injection of anti-TNF-alpha, anti-CD4, or anti-CD8 monoclonal antibody, and CD8+ T cells accumulated in the tumors of TNF-alpha-treated mice. These results suggest that TNF-alpha expressed locally in the arteries leading to tumors efficiently suppresses tumor growth through reinforcement of an antitumor immune reaction. The significance of this phenomenon for cancer gene therapy was discussed.
Inhibition of tumor angiogenesis using a soluble receptor establishes a role for Tie2 in pathologic vascular growth. (1997)

Tie2 is a novel receptor tyrosine kinase that is expressed almost exclusively by vascular endothelium. Disruption of Tie2 function in transgenic mice resulted in embryonic lethality secondary to characteristic vascular defects; similar defects occurred after disruption of the Tie2 ligand. These findings indicate that the Tie2/Tie2 ligand pathway plays important roles during development of the embryonic vasculature. To determine whether the Tie2 pathway was involved in pathologic angiogenesis in adult tissues, a soluble form of the extracellular domain of murine Tie2 (ExTek.6His) was developed and used as a Tie2 inhibitor. After a single application of the ExTek.6His protein into a rat cutaneous window chamber, growth of a mammary tumor inside the chamber was reduced by > 75% (P < 0.005), and tumor vascular length density was reduced by 40% when compared with control-treated tumors (P < 0.01). In the rat cornea, ExTek.6His blocked angiogenesis stimulated by tumor cell conditioned media. ExTek.6His protein did not affect the viability of cultured tumor cells, indicating that the antitumor effect of ExTek.6His was due to the inhibition of tumor angiogenesis. These data demonstrate a role for the Tie2 pathway in pathologic angiogenesis, suggesting that targeting this pathway may yield effective antiangiogenic agents for treatment of cancer and other angiogenic diseases.