gebhart/patrepeval huggingface dataset:
Standardized peripheral blood mononuclear cell culture assay for determination of drug susceptibilities of clinical human immunodeficiency virus type 1 isolates. The RV-43 Study Group, the AIDS Clinical Trials Group Virology Committee Resistance Working Group (1993)

A standardized antiviral drug susceptibility assay for clinical human immunodeficiency virus type 1 (HIV-1) isolates has been developed for use in clinical trials. The protocol is a two-step procedure that first involves cocultivation of patient infected peripheral blood mononuclear cells (PBMC) with seronegative phytohemagglutinin-stimulated donor PBMC to obtain an HIV-1 stock. The virus stock is titrated for viral infectivity (50% tissue culture infective dose) by use of serial fourfold virus dilutions in donor PBMC. A standardized inoculum of 1,000 50% tissue culture infective doses per 10(6) cells is used in the second step of the procedure to acutely infect seronegative donor PBMC in a 7-day microtiter plate assay with triplicate wells containing zidovudine (ZDV) concentrations ranging from 0 to 5.0 microM. The ZDV 50% inhibitory concentrations (IC50) for reference ZDV-susceptible and ZDV-resistant HIV-1 isolates ranged from 0.002 to 0.113 microM and from 0.15 to > 5.0 microM, respectively. Use of this consensus protocol reduced interlaboratory variability for ZDV IC50 determinations with reference HIV-1 isolates. Among eight laboratories, the coefficient of variation ranged from 0.85 to 1.25 with different PBMC protocols and was reduced to 0.39 to 0.98 with the standardized assay. Among the clinical HIV-1 isolates assayed by the standardized drug susceptibility assay, the median ZDV IC50 increased gradually with more ZDV therapy. This protocol provides an efficient and reproducible means to assess the in vitro susceptibility to antiretroviral agents of virtually all clinical HIV-1 isolates.
In Vitro Activity of Hepatitis C Virus Protease NS3 Purified from Recombinant Baculovirus-infected Sf9 Cells (1996)

A recombinant Baculovirus expression system was used for the production of a 20-kDa protein encompassing the hepatitis C virus NS3 protease domain. The protein was purified to apparent homogeneity after detergent extraction of cell homogenates. It was shown to be a monomer in solution and to cleave the in vitro translated precursor proteins NS4A-NS4B and NS5A-NS5B, but not the NS4B-NS5A or the NS3-NS4A precursors. The enzyme also cleaved a 20-mer peptide corresponding to the NS4A-NS4B junction with kcat/Km = 174 m(-1) s(-1). Peptides harboring NS4A sequences comprising amino acids 21-54 (Pep4A21-54) and 21-34 (Pep4A21-34) were found to induce an up to 2.8-fold acceleration of cleavage. Kinetic analysis revealed that this acceleration was due to an increase in kcat whereas no significant effect on Km could be detected. Pep4A21-54 was also an absolute requirement for cleavage of in vitro translated NS4B-NS5A by the purified protease. From these data we conclude that: (i) the purified protease domain shows substrate specificity and cleavage requirements similar to those previously reported on the basis of transfection experiments, (ii) activation of the purified protease by the NS4A co-factor can be mimicked by synthetic peptide analogs, and (iii) a central hydrophobic region of NS4A with a minimum core of 14 amino acids is responsible for the interaction with NS3.
Sphenopalatine ganglion block: clinical use in the pain management clinic. (1990)

Clinical experience with the sphenopalatine ganglion (SPG) block combined with a review of prior studies led to conducting a retrospective evaluation of four patients with chronic pain treated with the SPG block. The review of case reports suggests the usefulness of SPG blocks in the pain management clinic.
Preparation of porcine carotid arteries for vascular tissue engineering applications (2004)

Biomaterials derived from tissue continue to offer viable alternatives to synthetic materials when autologous materials are unavailable for transplantation due to their unique chemical and mechanical properties. Tissue processing aims to stabilize the material against host degradation and render it immunologically inert by removing cellular material and crosslinking the structural proteins. It is clear that different approaches taken to achieve these goals have very different chemical and mechanical effects on the material. We describe herein the development of a tissue processing methodology to generate acellular scaffolds for tissue engineering small-diameter vascular grafts. Carotid arteries were isolated from Great White pigs and exposed to various solvent treatments, xylene, butanol, and ethanol to determine optimal parameters for the extraction of host lipids. The tissue was then exposed to a limited proteolysis with trypsin to disrupt cellular protein. This resulted in a controlled digestion that disrupted porcine nuclear DNA and cleared bulk cellular protein, leaving the more resistant structural proteins largely intact and retaining the bulk mechanical properties of the matrix. Histological analysis and scanning electron microscopy illustrated the complete removal of intact cells and nuclear material. The decellularized graft was stabilized by crosslinking with the photooxidative dye methylene green in the presence of 30,000 LUX of broad-band light energy. High-performance liquid chromatography analysis showed that the crosslinked tissue yielded 78.6% less hydroxyproline, compared with control tissue, after 20 h incubation with pepsin. Analysis of the crosslinked vessels' burst-pressure and stress-strain characteristics have shown comparable mechanical properties to those of control vessels. Assessment of in vitro cell adhesion and compatibility was conducted by seeding primary human umbilical vein endothelial cells and adult human vascular smooth muscle cells onto the lumenal and ablumenal surfaces, respectively; these cells were shown to adhere and proliferate under traditional static culture conditions.
Bcl6 Acts as an Amplifier for the Generation and Proliferative Capacity of Central Memory CD8+ T Cells (2004)

Central memory CD8(+) T cells (T(CM)) are considered to be more efficient than effector ones (T(EM)) for mediating protective immunity. The molecular mechanism involved in the generation of these cells remains elusive. Because Bcl6 plays a role in the generation and maintenance of memory CD8(+) T cells, we further examined this role in the process in relation to T(CM) and T(EM) subsets. In this study, we show that T(CM) and T(EM) were functionally identified in CD62L(+) and CD62L(-) memory (CD44(+)Ly6C(+)) CD8(+) T cell subsets, respectively. Although T(CM) produced similar amounts of IFN-gamma and IL-2 to T(EM) after anti-CD3 stimulation, the cell proliferation capacity after stimulation and tissue distribution profiles of T(CM) differed from those of T(EM). Numbers of T(CM) were greatly reduced and elevated in spleens of Bcl6-deficient and lck-Bcl6 transgenic mice, respectively, and those of T(EM) were constant in nonlymphoid organs of these same mice. The majority of Ag-specific memory CD8(+) T cells in spleens of these mice 10 wk after immunization were T(CM), and the number correlated with Bcl6 expression in T cells. The proliferation of Ag-specific memory CD8(+) T cells upon secondary stimulation was dramatically up-regulated in lck-Bcl6 transgenic mice, and the adoptive transfer experiments with Ag-specific naive CD8(+) T cells demonstrated that some of the up-regulation was due to the intrinsic effect of Bcl6 in the T cells. Thus, Bcl6 is apparently a crucial factor for the generation and secondary expansion of T(CM).
Tumor Immunity Induced by Preimmunization With BALB/c Mouse Myeloma Protein2 (1976)

Prior sc immunization of BALB/c mice with 1 mg isolated M component of MOPC-11 mouse myeloma resulted in significant relative immunity to subsequent sc or ip challenge with 10(4) living cells from the same plasmacytoma. However, challenges of 10(5) and 10(6) tumor cells overcame immune status engendered by preimmunization with M component. Despite evidence for the specificity of the immunity induced by one isolated M component as opposed to another, no clear cytotoxic antibody, cell-mediated tumor-cell lysis, or predominance of either humoral or cell-mediated immune mechanisms were demonstrated. These findings were compatible with a relatively slight tumor-specific antigenicity of M components expressed on tumor surfaces, compared with the tumor specificity of other tumor-related, cell-surface antigens.
Curved Periacetabular Osteotomy for Treatment of Dysplastic Hip (2005)

Therapeutic study, Level IV (case series--no, or historical control group). See the Guidelines for Authors for a complete description of levels of evidence.
Plasma simulation using the massively parallel processor (1987)

Two dimensional electrostatic simulation codes using the particle-in-cell model are developed on the Massively Parallel Processor (MPP). The conventional plasma simulation procedure that computes electric fields at particle positions by means of a gridded system is found inefficient on the MPP. The MPP simulation code is thus based on the gridless system in which particles are assigned to processing elements and electric fields are computed directly via Discrete Fourier Transform. Currently, the gridless model on the MPP in two dimensions is about nine times slower that the gridded system on the CRAY X-MP without considering I/O time. However, the gridless system on the MPP can be improved by incorporating a faster I/O between the staging memory and Array Unit and a more efficient procedure for taking floating point sums over processing elements. The initial results suggest that the parallel processors have the potential for performing large scale plasma simulations.
[Autologous skeletal myoblast transplantation for cardiac insufficiency. First clinical case]. (2001)

The authors report the first intramyocardial transplantation of autologous skeletal myoblasts in a patient with severe ischaemic cardiac failure. The encouraging result after eight months' follow-up underlines the potential of this new approach.
Costimulatory Pathways in Multiple Sclerosis: Distinctive Expression of PD-1 and PD-L1 in Patients with Different Patterns of Disease (2009)

T lymphocytes costimulatory molecules, including CD80, CD86, CD28, CTLA4, PD-1, PD-L1, and B7-H3, are associated with the preferential production of pro- or anti-inflammatory cytokines. We analyzed the expression of these molecules and myelin basic protein (MBP)-specific IL-10 and IFN-gamma production in patients with multiple sclerosis (MS) with relapsing-remitting acute (AMS, n = 40) or stable (SMS, n = 38). Twenty-two patients successfully undergoing therapy with glatimer acetate (n = 12) or IFNbeta (n = 10) were also analyzed. MBP-specific and PD-1-expressing T lymphocytes, PD-L1-expressing CD19(+) cells, and PD-L1(+)/IL-10(+)/CD14(+) and CD19(+) cells were significantly augmented in SMS patients. Additionally, MBP-specific and annexin V-expressing CD4(+) and CD8(+) (apoptotic) T lymphocytes were augmented and pAkt-positive (proliferating) cells were decreased in SMS compared with AMS patients. PD-1 ligation resulted in the increase of pAkt(+) lymphocytes in AMS patients alone. B7-H3 expression and IFN-gamma production were comparable in all individuals but the PD-L1(+)/IL-10(+) over B7-H3(+)/IFN-gamma(+) ratio was significantly lower in AMS compared with SMS patients. Finally, PD-L1 expression on immune cells was reduced in treated patients, suggesting that therapy-induced disease remission is not associated with the modulation of the expression of this molecule. The PD-1/PD-L1 pathway plays an important role in modulating immune functions in MS patients; monitoring and targeting these proteins could offer diagnostic and therapeutic advantages.
Expression and Mutation of the Tumor Suppressor Gene p53 in AIDS-Associated Kaposi's Sarcoma (1997)

Alteration of the p53 gene is the most frequent event reported in human cancer, and p53 mutations have been observed in various neoplasms, including certain forms of skin cancer. Therefore, we postulated that p53 may also be involved in Kaposi's sarcoma associated with AIDS (AIDS-KS). Expression of the p53 gene was examined in freshly isolated tumor biopsy specimens from 15 patients with AIDS-KS. p53 mRNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) in both the AIDS-KS tumors and in normal skin control samples. p53 protein was detected in 4 of the 15 AIDS-KS specimens by immunohistochemical staining. Single-strand conformation polymorphism analysis PCR-products (PCR-SSCP) was used for detection of mutations of the p53 gene. One of the p53 positive AIDS-KS samples showed mobilized shifts in exon 6 suggestive of a mutation. Sequencing data showed the mutation to be located in codon 210. We examined other mechanisms that could stabilize p53 protein. SV40 large T antigen and adenovirus E1B protein were not found in the AIDS-KS specimens. MDM2, a p53-binding protein, was also detected in five of the AIDS-KS specimens, two of which also contained p53-positive cells. These observations suggest that the tumor suppressor gene p53 may be involved in the pathogenesis of AIDS-KS.
PTEN Autoregulates Its Expression by Stabilization of p53 in a Phosphatase-Independent Manner (2006)

PTEN (phosphatase and tensin homologue, deleted on chromosome 10) is a tumor suppressor with dual phosphatase activity and mutations of its gene, PTEN, have been associated with many sporadic cancers and heritable neoplasia syndromes, including Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome. However, accumulating evidence now shows that PTEN may have novel functions other than as a phosphatase. In the present study, we show that PTEN is able to autoregulate its expression through the stabilization of another tumor suppressor p53. We further show that PTEN enhances p53 transactivation, a relationship that requires the interaction between PTEN and p53 and is PTEN phosphatase independent. We show that cell lines from Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome patients with germ line PTEN promoter mutations in the vicinity of the p53-binding motifs have altered p53 regulation. This seems to be due to reduced PTEN stability and decreased PTEN-p53 interactions. Our data provide clues to better understand the regulation of PTEN expression and the possible mechanisms of the pathogenesis of the subset of Cowden syndrome individuals with germ line promoter variation and who lack mutations in the PTEN coding region and splice sites. Importantly, this mechanism also holds for those sporadic tumors that lack intragenic mutations but have hemizygous deletion of PTEN, which includes the promoter region as manifested by loss-of-heterozygosity of 10q markers. The importance of our observations is underlined by the broad spectrum of neoplasias that harbor somatic PTEN or p53 alterations, or both.
Glasgow Coma Scale (1979)

CATHY JONES, R.N., M.S.N., is a clinical nurse specialist in neurosurgery at the University of Texas Medical Branch, Galveston. She is a faculty member, University of Texas School of Nursing.
The similarity laws for the maintenance field and the absorbed power per electron in low-pressure surface wave produced plasmas and their extension to HF plasmas in general (1988)

This paper presents a theoretical analysis of high-frequency, diffusion-controlled discharges in which the ionization is provided by direct electron impact with gas atoms within the discharge volume. The theoretical formulation uses the electron Boltzmann equation along with two-moment, hydrodynamic-type equations for the electrons and the ions. The treatment followed covers a wide range of applied field frequencies, ω/2π, from ω ≪ νc to ω ≫ νc, where νc is the electron-neutral collision frequency for momentum transfer; it is, however, limited to situations for which ω ≫ τ−1, where τ is the characteristic electron energy relaxation time by collisions. It is shown that, under steady-state conditions, the maintenance field and the average absorbed power per electron are practically independent of the field configuration and essentially determined by the gas pressure, the configuration and the dimensions of the discharge vessel, and ω, and not by the applied HF power level. Both the maintenance field and the average absorbed power per electron are shown to obey similarity laws as a function of the discharge operating parameters.
Data clustering using evidence accumulation (2003)

We explore the idea of evidence accumulation for combining the results of multiple clusterings. Initially, n d-dimensional data is decomposed into a large number of compact clusters; the K-means algorithm performs this decomposition, with several clusterings obtained by N random initializations of the K-means. Taking the co-occurrences of pairs of patterns in the same cluster as votes for their association, the data partitions are mapped into a co-association matrix of patterns. This n/spl times/n matrix represents a new similarity measure between patterns. The final clusters are obtained by applying a MST-based clustering algorithm on this matrix. Results on both synthetic and real data show the ability of the method to identify arbitrary shaped clusters in multidimensional data.
Defeasible logic programming: an argumentative approach (2004)

The work reported here introduces Defeasible Logic Programming (DeLP), a formalism that combines results of Logic Programming and Defeasible Argumentation. DeLP provides the possibility of representing information in the form of weak rules in a declarative manner, and a defeasible argumentation inference mechanism for warranting the entailed conclusions. In DeLP an argumentation formalism will be used for deciding between contradictory goals. Queries will be supported by arguments that could be defeated by other arguments. A query $q$ will succeed when there is an argument ${\mathcal A}$ for $q$ that is warranted, i.e. the argument ${\mathcal A}$ that supports $q$ is found undefeated by a warrant procedure that implements a dialectical analysis. The defeasible argumentation basis of DeLP allows to build applications that deal with incomplete and contradictory information in dynamic domains. Thus, the resulting approach is suitable for representing agent's knowledge and for providing an argumentation based reasoning mechanism to agents.
Quinolone resistance by mutations in chromosomal gyrase genes. Just the tip of the iceberg? (1998)

Quinolones are, currently, a widely used group of antibacterial agents. 1 The targets of these compounds are bacterial topoisomerases. 2An ample body of evidence has supported the conventional wisdom that clinical bacterial isolates develop high-level resistance to quinolones by acquiring mutations in the gyrA gene 3-6 that encodes for the synthesis of the GyrA subunit of bacterial topoisomerase II.Mutations in the gyrB gene 4,7 that encodes the synthesis of the GyrB subunit of bacterial topoisomerase II, and in the chromosomal genes involved in the uptake or efflux of drugs 8-10 should only have a secondary role in quinolone resistance.It was also generally accepted that wild-type alleles of gyrA and gyrB are dominant over the mutant, resistance-encoding ones, 11,12 so that it was considered that plasmid-encoded quinolone resistance would be unlikely if not impossible. 11,13,14However, several publications in the last few years indicate that the genetic landscape of quinolone resistance is more complicated than previously thought.
Reversible Inhibitory Effects of Interferon‐γ and Tumour Necrosis Factor‐α on Oligodendroglial Lineage Cell Proliferation and Differentiation In Vitro (1996)

We have investigated the effects of the two prominent inflammatory cytokines, interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha), on oligodendroglial lineage cell development and survival. Purified oligodendrocytes and oligodendrocyte precursors obtained from neonatal rat brain primary cultures were subcultured in a defined, serum-free medium and exposed to IFN-gamma (1-100 U/ml, TNF-alpha (25-100 ng/ml) or both (100 U/ml and 50 ng/ml respectively) from day 1 to day 3 or from day 3 to day 6. While cell survival was not affected in any of the conditions tested, IFN-gamma dose-dependently inhibited [3H]thymidine or bromodeoxyuridine incorporation (by up to 50%) and the reduction of the tetrazolium salt 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT; by up to 33%). TNF-alpha synergized with IFN-gamma, but was ineffective by itself. Moreover, IFN-gamma totally antagonized the induction by basic fibroblast growth factor and platelet-derived growth factor of the proliferation of the oligodendroglial lineage cell population under study. IFN-gamma also blocked the differentiation of oligodendrocyte precursors, as evidenced by cell morphology, immunostaining for early and late differentiation markers (galactocerebroside and myelin basic protein respectively) and activity of ceramide galactosyl transferase. Again, the effect of IFN-gamma was potentiated by TNF-alpha, which was ineffective when tested alone. The inhibitory activity of IFN-gamma was rapidly reversible: 3 days after removal of the cytokine, administered from day 1 to day 3, complete recovery of cll proliferation and differentiation could be documented. The cytokine-induced arrest in the expression of differentiation antigens was accompanied by perturbations in the expression of the corresponding mRNAs, revealed by a semiquantitative reverse transcription-polymerase chain reaction method. In particular, the message for myelin basic protein (and, in the case of treatment from days 3 to 6, also that for myelin associated glycoprotein) was decreased in cultures exposed to IFN-gamma, and further depressed in cultures treated with IFN-gamma and TNF-alpha, while TNF-alpha alone was ineffective. The above observations may help explain the role of IFN-gamma and TNF-alpha in the pathogenesis of inflammatory demyelinating diseases, in which increases in the levels of these substances have been described. In particular, in the case of multiple sclerosis, our results may bear on the problem of defective remyelination and are consistent with the frequent relapsing-remitting course of the disease.
Breakout: the evolving threat of drug-resistant disease (1996)

A study of drug-resistant disease cites indiscriminate antibiotic usage, global ecosystem disruption, and short-sighted approaches to disease control as direct causes of emerging resistant diseases.