gebhart/patrepeval huggingface dataset:
Variation in lipid A structure in the pathogenic yersiniae (2004)

Important pathogens in the genus Yersinia include the plague bacillus Yersinia pestis and two enteropathogenic species, Yersinia pseudotuberculosis and Yersinia enterocolitica. A shift in growth temperature induced changes in the number and type of acyl groups on the lipid A of all three species. After growth at 37 degrees C, Y. pestis lipopolysaccharide (LPS) contained the tetra-acylated lipid IV(A) and smaller amounts of lipid IV(A) modified with C10 or C12 acyl groups, Y. pseudotuberculosis contained the same forms as part of a more heterogeneous population in which lipid IV(A) modified with C16:0 predominated, and Y. enterocolitica produced a unique tetra-acylated lipid A. When grown at 21 degrees C, however, the three yersiniae synthesized LPS containing predominantly hexa-acylated lipid A. This more complex lipid A stimulated human monocytes to secrete tumour necrosis factor-alpha, whereas the lipid A synthesized by the three species at 37 degrees C did not. The Y. pestis phoP gene was required for aminoarabinose modification of lipid A, but not for the temperature-dependent acylation changes. The results suggest that the production of a less immunostimulatory form of LPS upon entry into the mammalian host is a conserved pathogenesis mechanism in the genus Yersinia, and that species-specific lipid A forms may be important for life cycle and pathogenicity differences.
Epidemiology of Pertussis (2005)

The World Health Organization recommended that a pertussis incidence of <1 case per 100,000 population be achieved in Europe by 2000. Available data indicate that this goal has generally not been achieved, and the incidence is actually rising in some countries. Understanding the reasons for this increased incidence may lead to better global control of pertussis. In the majority of countries where pertussis is a notifiable disease, a case-based national surveillance system is in place. However, different case definitions, methods of diagnosis and reporting and surveillance systems make direct intercountry comparisons difficult, and pertussis is not a statutory notifiable disease in every country. Nevertheless the general consensus is that reported incidences are probably considerably lower than the actual incidence of pertussis; underreporting is common. Prolonged cough may be the only clinical feature in adolescents or adults, who may present for diagnosis late (precluding laboratory confirmation) or not at all. When they do present, their condition is often misdiagnosed because, in part, clinicians continue to perceive pertussis as a childhood disease. Despite underreporting, an increased incidence of infant, adolescent and adult pertussis has been observed worldwide since the introduction of widespread vaccination. This is of concern because adolescents and adults have been identified as a source of transmission of pertussis to very young infants who are unimmunized or partially immunized and thus more vulnerable to disease-related complications and higher mortality. In recent years, acellular pertussis vaccines have been incorporated into the immunization schedules of many developed countries, gradually replacing whole cell vaccines. Dosing schedules vary between countries, although primary immunization with 3 doses of the pertussis vaccine within the first 6 months of life exists in most countries. Only Australia, Austria, Canada, France and Germany have incorporated an adolescent booster dose into their current immunization schedules, in recognition of the rising incidence of pertussis in adolescents and adults. Despite high coverage rates for primary immunization in infants and children, pertussis continues to be a global concern, with increased incidence widely noted. This global epidemiologic summary highlights differences worldwide in pertussis reporting, incidence and approaches to prevention. It underscores a general shift in the age distribution of pertussis toward older groups. Understanding the link between these observations may lead to better informed global control strategies, especially those pertaining to immunization schedules and use of pertussis vaccine.
Two New p73 Splice Variants, γ and δ, with Different Transcriptional Activity (1998)

p73 has been recently identified as a new structural and functional homologue of the transcription factor p53. It is expressed in either a full-length form, α, or a shorter β mRNA variant, with exon 13 spliced out. Here we report the identification and functional characterization of two new p73 splicing variants, γ (splicing out exon 11) and δ (splicing out exons 11, 12, and 13). Both γ and δ p73 variants are expressed in human peripheral blood lymphocytes, primary keratinocytes, and different tumor cell lines, including neuroblastoma, glioblastoma, melanoma, hepatoma, and leukemia. The expression pattern of the four p73 splicing variants differs in both primary cells of different lineage and established cell lines even within the same type of tumor. A two-hybrid assay was used to characterize the homodimeric and heterodimeric interactions between the p73 variants, and showed that neither p73γ nor p73δ interact with p53, whereas p73γ showed strong interactions with all p73 isoforms, and p73δ binds efficiently p73α and p73γ but only weakly p73β. At the functional level, p73γ is significantly less efficient in activating transcription of the p21Waf1/Cip1 promoter than p53 or p73β, whereas the effect of p73δ is intermediate and comparable to that of p73α. The ability of the different p73 variants to affect cell growth in p53 null osteosarcoma SAOS-2 cells correlates with their transcriptional activity on the p21Waf1/Cip1 promoter: p73β is the most efficient in inhibiting colony formation, whereas p73γ is almost ineffective. Our results suggest that p73 isoforms may be differentially regulated, with four different isoforms capable of interacting among themselves and with p53. The relative expression level of each splice variant may modulate p73 transcriptional and growth suppression activities by affecting heterodimer formation.
Purification and characterization of a mitochondrial isozyme of C1-tetrahydrofolate synthase from Saccharomyces cerevisiae. (1986)

C1-Tetrahydrofolate synthase is a trifunctional polypeptide found in eukaryotic organisms that catalyzes 10-formyltetrahydrofolate synthetase (EC 6.3.4.3), 5,10-methenyltetrahydrofolate cyclohydrolase (EC 3.5.4.9), and 5,10-methylenetetrahydrofolate dehydrogenase (EC 1.5.1.5) activities. In Saccharomyces cerevisiae, C1-tetrahydrofolate synthase is encoded by the ADE3 locus, yet ade3 mutants have low but detectable levels of these enzyme activities. Synthetase, cyclohydrolase, and dehydrogenase activities in an ade3 deletion strain co-purify 4,000-fold to yield a single protein species as seen on sodium dodecyl sulfate-polyacrylamide gels. The native molecular weight of the isozyme (Mr = 200,000 by gel exclusion chromatography) and the size of its subunits (Mr = 100,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis) are similar to those of C1-tetrahydrofolate synthase. Cell fractionation experiments show that the isozyme, but not C1-tetrahydrofolate synthase, is localized in the mitochondria. Genetic studies indicate that the isozyme is encoded in the nuclear genome. Peptide mapping experiments show that C1-tetrahydrofolate synthase and the isozyme are not structurally identical. However, immunotitration experiments and amino acid sequence analysis suggest that C1-tetrahydrofolate synthase and the isozyme are structurally related. We propose to call the isozyme "mitochondrial C1-tetrahydrofolate synthase."
Control Theory: Multivariable and Nonlinear Methods (2000)

Preface. Introduction. 1. Representation of linear systems 2. Properties of linear systems 3. Sampled data systems 4. Disturbance models 5. The closed loop system 6. Limitations and conflicts 7. Controller structures and design 8. Minimization of quadratic criteria 9. Shaping the loop again 10. Descriptions of nonlinear systems 11. Stability of nonlinear systems 12. Qualitative beviour. Phase Plane 13. Oscillations and describing functions 14. Controller synthesis for nonlinear systems 15. Model predictive control : MPC, GPC, and DMM 16. To compensate exactly for nonlinearities 17. Optimal control 18. Conclusion. Literature. Index. Index of examples.
New photometric assay for chymotrypsin in stool. (1984)

Abstract In this new photometric assay fecal samples are pretreated with detergent and high concentrations of salts. The subsequent kinetic enzyme determination step involves the chromogenic substrate succinyl-Ala-Ala-Pro-Phe-4-nitroanilide. The sample pretreatment assures a nearly complete solubilization of the formerly particle-bound enzyme, thus permitting determination of the enzyme activity in either the suspension or the supernate after centrifugation. Furthermore this pretreatment enhances the enzyme activity and decreases the Km value. Results by this assay correlate well with those by classical titrimetry and the method is easily adapted to automated systems.
<italic>Laser Communications in Space</italic> (1996)

Past, present, and future architecture and applications system design methodology optical design the communication receiver the acquisition receiver the tracking receiver key technologies configuring the system trading RF and laser communications for your system size, weight, and power trends in laser crosslinks laser communications applications.
AvrXa10 Contains an Acidic Transcriptional Activation Domain in the Functionally Conserved C Terminus (1998)

The avrXa10 gene of Xanthomonas oryzae pv. oryzae, the causal agent of bacterial blight of rice, is a member of the avrBs3 avirulence gene family and directs the elicitation of resistance in a gene-for-gene manner on rice lines carrying the resistance gene Xa10. The carboxyl (C) terminus of AvrXa10 has a previously undescribed domain that is structurally similar to the acidic activation domain of many eukaryotic transcription factors in addition to three nuclear localization signal (NLS) sequences. Removal of the C-terminal 38 codons containing the putative activation domain, but retaining the NLS sequences, was concomitant with the loss of avirulence activity. The C-terminal coding regions of avrBs3 and avrXa7 can be replaced by the corresponding region of avrXa10, and the genes retained specificity for the resistance genes Bs3 in pepper and Xa7 in rice, respectively. The avrBs3 and avrXa7 avirulence activities of the hybrid genes were also lost upon removal of the terminal 38 codons. When fused to the coding sequence of the Gal4 DNA binding domain, AvrXa10 activated transcription in yeast and Arabidopsis thaliana. Removal of the carboxyl region severely reduced transcriptional activation. AvrXa10 would have to be localized to the host cell nucleus to function autonomously in transcriptional activation. Consistent with this requirement, mutations in all three NLS sequences of avrXa10 caused a loss in avirulence activity. The findings demonstrate the requirement of the C terminus for AvrXa10 function and the potential for the members of this family of avirulence gene products to enter the host nucleus and alter host transcription.
Loss-of-Function of Nkx3.1 Promotes Increased Oxidative Damage in Prostate Carcinogenesis (2005)

Despite the significance of oxidative damage for carcinogenesis, the molecular mechanisms that lead to increased susceptibility of tissues to oxidative stress are not well-understood. We now report a link between loss of protection against oxidative damage and loss-of-function of Nkx3.1, a homeobox gene that is known to be required for prostatic epithelial differentiation and suppression of prostate cancer. Using gene expression profiling, we find that Nkx3.1 mutant mice display deregulated expression of several antioxidant and prooxidant enzymes, including glutathione peroxidase 2 and 3 (GPx2 and GPx3), peroxiredoxin 6 (Prdx6), and sulfyhydryl oxidase Q6 (Qscn6). Moreover, the formation of prostatic intraepithelial neoplasia in these mutant mice is associated with increased oxidative damage of DNA, as evident by increased levels of 8-hydroxy-2'-deoxyguanosine. We further show that progression to prostate adenocarcinoma, as occurs in compound mutant mice lacking Nkx3.1 as well as the Pten tumor suppressor, is correlated with a further deregulation of antioxidants, including superoxide dismutase enzymes, and more profound accumulations of oxidative damage to DNA and protein, the latter manifested by increased levels of 4-hydroxynonenal. We propose that the essential role of Nkx3.1 in maintaining the terminally differentiated state of the prostate epithelium provides protection against oxidative damage and, thereby, suppression of prostate cancer. Thus, our findings provide a molecular link between a gene whose inactivation is known to be involved in prostate carcinogenesis, namely Nkx3.1, and oxidative damage of the prostatic epithelium.
Redirecting the complete T cell receptor/CD3 signaling machinery towards native antigen via modified T cell receptor (1996)

We show that a chimeric T cell receptor (TCR) beta chain consisting of a single-chain Fv portion derived from a monoclonal antibody and the full TCR beta chain is able to assemble functionally with endogenous TCR/CD3 components and transfer the antibody specificity as well as the TCR specificity into TCR beta- as well as into TCR beta+ T cells. This allows the incorporation new non-major histocompatibility complex-restricted ligand specificities into the intact TCR/CD3 complex which can exploit the full range of biological activities of the endogenous TCR signaling machinery. This approach can provide wider opportunities to redirect T cells to virus or tumor antigen-bearing cells.
AdapterRemoval: easy cleaning of next-generation sequencing reads (2012)

AdapterRemoval is a comprehensive tool for analyzing next-generation sequencing data. It exhibits good performance both in terms of sensitivity and specificity. AdapterRemoval has already been used in various large projects and it is possible to extend it further to accommodate application-specific biases in the data.
Complement and cell mediated cytotoxicity by antiendothelial cell antibodies in Takayasu's arteritis. (2001)

AECA in TA mediate CDC against endothelial cells and may have a pathogenic role in the perpetuation of vascular damage in this disease.
Protecting a private network: the AltaVista Firewall (1997)

Connecting an organization’s private network to the Internet offers many advantages but also exposes the organization to the threat of an electronic break-in. The AltaVista Firewall 97 for DIGITAL UNIX protects a private network from malicious attack or casual infiltration by screening all internetwork communication. It enforces the organization’s network security policy so that only allowed network traffic can cross the firewall. When installed on a dual- or multihomed host, the AltaVista Firewall applies the principle “that which is not expressly permitted is denied” and uses patented technology to screen each IP packet that attempts to cross it. A highly flexible access control grammar and a comprehensive reporting and alarm system enable the AltaVista Firewall to detect and react to harmful or dangerous events. The AltaVista Firewall also includes an HTML-based user interface to ease configuration and management of the firewall.
Genetically modified skin fibroblasts persist long after transplantation but gradually inactivate introduced genes. (1991)

Genetically engineered fibroblasts have been successfully used to produce therapeutic proteins in animals, but sustained production of the proteins has not been achieved. This limits the potential of fibroblast-mediated gene therapy in humans. We have studied the phenomenon of decreased production in rats by using retroviral vectors carrying genes encoding human adenosine deaminase and neomycin phosphotransferase. While transplanted skin fibroblasts containing vector sequences persisted at constant levels for at least 8.5 mo, vector expression decreased by greater than 1500-fold after 1 mo. Cellular or antibody-mediated immune responses were not detected in transplanted animals, and expression could not be restored in fibroblasts recultivated from the grafts. This phenomenon is reminiscent of sequence-specific gene inactivation observed in other cell types. Because genetic manipulation and expression of foreign proteins did not affect survival of the transplanted cells, effective long-term therapy may be possible with the use of alternative gene regulatory elements.
Direct binding to antigen‐coated beads refines the specificity and cross‐reactivity of four monoclonal antibodies that recognize polymorphic epitopes of HLA class I molecules (2013)

Monoclonal antibodies with specificity for human leukocyte antigen (HLA) class I determinants of HLA were originally characterized using serological assays in which the targets were cells expressing three to six HLA class I variants. Because of this complexity, the specificities of the antibodies were defined indirectly by correlation. Here we use a direct binding assay, in which the targets are synthetic beads coated with 1 of 111 HLA class I variants, representing the full range of HLA-A, -B and -C variation. We studied one monoclonal antibody with monomorphic specificity (W6/32) and four with polymorphic specificity (MA2.1, PA2.1, BB7.2 and BB7.1) and compared the results with those obtained previously. W6/32 reacted with all HLA class I variants. MA2.1 not only exhibits high specificity for HLA-A*02, -B*57 and -B*58, but also exhibited cross-reactivity with HLA-A*11 and -B*15:16. At low concentration (1 µg/ml), PA2.1 and BB7.2 were both specific for HLA-A*02 and -A*69, and at high concentration (50 µg/ml) exhibited significant cross-reactions with HLA-A*68, -A*23 and -A*24. BB7.1 exhibits specificity for HLA-B*07 and -B*42, as previously described, but reacts equally well with HLA-B*81, a rare allotype defined some 16 years after the description of BB7.1. The results obtained with cell-based and bead-based assays are consistent and, in combination with amino acid sequence comparison, increase understanding of the polymorphic epitopes recognized by the MA2.1, PA2.1, BB7.2 and BB7.1 antibodies. Comparison of two overlapping but distinctive bead sets from two sources gave similar results, but the overall levels of binding were significantly different. Several weaker reactions were observed with only one of the bead sets.
Section Review Central & Peripheral Nervous Systems: P2-Purinoceptors: Advances and therapeutic opportunities (1995)

The recent cloning of a number of distinct receptors belonging to the P<sub>2</sub>-purinoceptor superfamily has provided conclusive evidence for a pivotal role for ATP and other nucleotides as effector molecules involved in cell-to-cell communication and the modulation of many basic aspects of tissue function. ATP itself is being clinically evaluated as a cytotoxic agent for the treatment of cancer and as an adjunct to inhalation anaesthetic use. The pyrimidine nucleotide, UTP, is in clinical trials for the treatment of cystic fibrosis. The stable ATP bioisostere, ARL 67085, is being developed as a novel antithrombotic agent, blocking with a superior safety profile and increased efficacy as compared to other agents. The diversity of P<sub>2</sub> receptors, with eleven having been defined using both pharmacological and molecular cloning criteria, indicates considerable additional potential and subtlety in regard to the effects of ATP on tissue function and pathophysiology.
Laparoscopic Adjustable Gastric Banding for the Treatment of Morbid (Grade 3) Obesity and its Metabolic Complications: A Three-Year Study (2002)

Weight loss ameliorates arterial hypertension and glucose metabolism in obese patients, but the dietary approach is unsatisfactory because obesity relapses. Durable reduction of body weight, obtained through major nonreversible surgical procedures, such as jejunal and gastric bypass, allows improvement of glucose metabolism and arterial blood pressure in morbid (grade 3) obesity. Laparoscopic adjustable gastric banding (LAGB) is a minimally invasive and reversible surgical procedure that yields a significant reduction of gastric volume and hunger sensation. In this study, 143 patients with grade 3 obesity [27 men and 116 women; age, 42.9 +/- 0.83 yr; body mass index (BMI), 44.9 +/- 0.53 kg/m(2); normal glucose tolerance (NGT; n = 77); impaired glucose tolerance (IGT; n = 47); type 2 diabetes mellitus (T2DM; n = 19)] underwent LAGB and a 3-yr follow-up for clinical (BMI, waist circumference, waist to hip ratio, and arterial blood pressure) and metabolic variables (glycosylated hemoglobin, fasting insulin and glucose, insulin and glucose response to oral glucose tolerance test, homeostasis model assessment index, total and high-density lipoprotein cholesterol, triglycerides, uric acid, and transaminases). At baseline and 1 yr after LAGB, patients underwent computerized tomography and ultrasound evaluation of visceral and sc adipose tissue. One-year metabolic results were compared with 120 obese patients (51 men and 69 women; age, 42.9 +/- 1.11 yr; BMI, 43.6 +/- 0.46 kg/m(2); NGT, n = 66; IGT, n = 8; T2DM, n = 46) receiving standard dietary treatment. LAGB induced a significant and persistent weight loss and decrease of blood pressure. Greater metabolic effects were observed in T2DM patients than in NGT and IGT patients, so that at 3 yr glycosylated hemoglobin was no longer different in NGT and T2DM subjects. Clinical and metabolic improvements were proportional to the amount of weight loss. LAGB induced a greater reduction of visceral fat than sc fat. At 1-yr evaluation, weight loss and metabolic improvements were greater in LAGB-treated than diet-treated patients. We conclude that LAGB is an effective treatment of grade 3 obesity in inducing long-lasting reduction of body weight and arterial blood pressure, modifying body fat distribution, and improving glucose and lipid metabolism, especially in T2DM.
T cells reactive with a small synthetic peptide of the acetylcholine receptor can provide help for a clonotypically heterogeneous antibody response and subsequently impaired muscle function. (1990)

The influence of T cell specificity was evaluated with regard to its role in the antibody response against the acetylcholine receptor (AChR) and resulting AChR-dependent muscle dysfunction. The reactivity of immune Th cells was restricted to a small region of the AChR alpha-subunit (amino acid residues 100-116) reported to be highly immunogenic. T cells primed to this peptide were found to demonstrate significant proliferation when challenged in vitro with either the homologous peptide or the intact AChR. Adoptive transfer of the peptide-immune T cells into immunologically naive recipient rats followed by AChR challenge resulted in the production of anti-AChR antibodies very similar to those produced under the regulation of T cells immune to the entire intact AChR with regard to overall clonotypic heterogeneity (measured by IEF) and their ability to interfere with AChR-dependent muscle contraction. Interestingly, when the threonine at position 106 was substituted with a proline, the resulting peptide continued to be equally, if not exceedingly, capable of stimulating T cell-proliferative responses, but was found to be ineffective at stimulating the levels of anti-AChR antibodies necessary for producing neuromuscular dysfunction.