gebhart/patrepeval huggingface dataset:
Flow Measurement at the Pump Head of Centrifugal Pumps: Comparison of Ultrasonic Transit Time and Ultrasonic Doppler Systems (1997)

Determination of blood flow is essential for monitoring rotary blood pumps. However, accurate measurement directly adjacent to the pump housing is difficult because of the highly irregular flow profiles near the fast spinning rotor. Therefore, a specially adapted flow probe based on the ultrasound transit time (USTT) principle was designed to evaluate the flow in centrifugal blood pumps. The probe can be directly mounted at the housing and creates 2 crossed measuring ultrasound beams. The mean value, Qm, of the 2 output signals corresponds to the blood flow and the difference, Qd, correlates to the vorticity of the flow profile in the pump outflow tract. In vitro measurements obtained an accuracy for mean flow values of better than +/-0.6 L/min in extreme working points and for vorticity values even as high as Qd = 3.5 L/min. Because of vorticity, however, the output signal contained considerable noise, and that required the application of a 10 Hz filter. Positioning of the ultrasound (US) beams parallel to the axial direction of the pump was superior to radial positioning. Additional measurement of the flow profile demonstrated that a large vorticity occurred (up to Qd equal to 3.5 L/min), and this vorticity was highly dependent upon the afterload of the pump. In vivo experiments demonstrated the reliability of the method. We concluded that USTT flow measurement can determine blood flow immediately adjacent to the pump housing with sufficient accuracy, and these measurements are superior to those from US-Doppler systems (which cannot handle the vorticity accurately enough) and electromagnetic devices (which lack zero stability).
Thrombin-induced rabbit platelet microbicidal protein is fungicidal in vitro (1993)

Platelet microbicidal protein (PMP) is released from platelets in response to thrombin stimulation. PMP is known to possess in vitro bactericidal activity against Staphylococcus aureus and viridans group streptococci. To determine whether PMP is active against other intravascular pathogens, we evaluated its potential fungicidal activity against strains of Candida species and Cryptococcus neoformans. Anionic resin adsorption and gel electrophoresis confirmed that the fungicidal activity of PMP resided in a small (approximately 8.5-kDa), cationic protein, identical to previous studies of PMP-induced bacterial killing (M.R. Yeaman, S.M. Puentes, D.C. Norman, and A.S. Bayer, Infect. Immun. 60:1202-1209, 1992). When assayed over a 180-min period in vitro, the susceptibilities of these fungi to PMP varied considerably. Generally, Candida albicans strains (mean survival, 33.5% +/- 6.9% [n = 6]) as well as isolates of Candida glabrata (mean survival, 50.8% +/- 2.9% [n = 2]) were the most susceptible to killing by PMP, while Candida guillermondii and Candida parapsilosis were relatively resistant to PMP-induced killing. Compared with C. albicans, C. neoformans was relatively resistant to the fungicidal activity of PMP, with a mean survival among the isolates studied of 77.4% +/- 12.4% (n = 6). Against C. albicans, PMP-induced fungicidal activity was time dependent (range, 0 to 180 min), PMP concentration dependent (range, 10 to 150 U/ml), and inversely related to the fungal inoculum (range, 5 x 10(3) to 1 x 10(5) CFU/ml). Scanning electron microscopy of PMP-exposed C. albicans and C. neoformans cells revealed extensive surface damage and collapse, suggesting that the site of PMP fungicidal action may directly or indirectly involve the fungal cell envelope.
Self-Assembly of Giant Peptide Nanobelts (2009)

Many alkylated peptide amphiphiles have been reported to self-assemble into cylindrical nanofibers with diameters on the order of a few nanometers and micrometer scale lengths; these nanostructures can be highly bioactive and are of great interest in many biomedical applications. We have discovered the sequences for these molecules that can eliminate all curvature from the nanostructures they form in water and generate completely flat nanobelts with giant dimensions relative to previously reported systems. The nanobelts have fairly monodisperse widths on the order of 150 nm and lengths of up to 0.1 mm. The sequences have an alternating sequence with hydrophobic and hydrophilic side chains and variations in monomer concentration generate a "broom" morphology with twisted ribbons that reveals the mechanism through which giant nanobelts form. Interestingly, a variation in pH generates reversibly periodic 2 nm grooves on the surfaces of the nanobelts. With proper functionalization, these nanostructures offer a novel architecture to present epitopes to cells for therapeutic applications.
[Cutaneous cryosurgery in family medicine: dimethyl ether-propane spray versus liquid nitrogen]. (1996)

No clinically relevant differences between the efficacy, tolerance and safety of the two cryogenic agents used in primary care were found. The low freezing of DMEP was sufficient for the cryotherapy of benign lesions.
DNA mismatch repair detected in human cell extracts. (1987)

A system to study mismatch repair in vitro in HeLa cell extracts was developed. Preformed heteroduplex plasmid DNA containing two single base pair mismatches within the SupF gene of Escherichia coli was used as a substrate in a mismatch repair assay. Repair of one or both of the mismatches to the wild-type sequence was measured by transformation of a lac(Am) E. coli strain in which the presence of an active supF gene could be scored. The E. coli strain used was constructed to carry mutations in genes associated with mismatch repair and recombination (mutH, mutU, and recA) so that the processing of the heteroduplex DNA by the bacterium was minimal. Extract reactions were carried out by the incubation of the heteroduplex plasmid DNA in the HeLa cell extracts to which ATP, creatine phosphate, creatine kinase, deoxynucleotides, and a magnesium-containing buffer were added. Under these conditions about 1% of the mismatches were repaired. In the absence of added energy sources or deoxynucleotides, the activity in the extracts was significantly reduced. The addition of either aphidicolin or dideoxynucleotides reduced the mismatch repair activity, but only aphidicolin was effective in blocking DNA polymerization in the extracts. It is concluded that mismatch repair in these extracts is an energy-requiring process that is dependent on an adequate deoxynucleotide concentration. The results also indicate that the process is associated with some type of DNA polymerization, but the different effects of aphidicolin and dideoxynucleotides suggest that the mismatch repair activity in the extracts cannot simply be accounted for by random nick-translation activity alone.
State transition analysis: a rule-based intrusion detection approach (1995)

The paper presents a new approach to representing and detecting computer penetrations in real time. The approach, called state transition analysis, models penetrations as a series of state changes that lead from an initial secure state to a target compromised state. State transition diagrams, the graphical representation of penetrations, identify precisely the requirements for and the compromise of a penetration and present only the critical events that must occur for the successful completion of the penetration. State transition diagrams are written to correspond to the states of an actual computer system, and these diagrams form the basis of a rule based expert system for detecting penetrations, called the state transition analysis tool (STAT). The design and implementation of a Unix specific prototype of this expert system, called USTAT, is also presented. This prototype provides a further illustration of the overall design and functionality of this intrusion detection approach. Lastly, STAT is compared to the functionality of comparable intrusion detection tools.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Luman, a New Member of the CREB/ATF Family, Binds to Herpes Simplex Virus VP16-Associated Host Cellular Factor (1997)

The human host cell factor (HCF) is expressed in a variety of adult and fetal tissues, and its gene is conserved in animals as diverse as mammals and insects. However, its only known function is to stabilize the herpes simplex virus virion transactivator VP16 in a complex with the cellular POU domain protein Oct-1 and cis-acting regulatory elements in promoters of immediate-early viral genes. To identify a cellular function for HCF, we used the yeast two-hybrid system to identify a cellular ligand for HCF. This protein, Luman, appears to be a cyclic AMP response element (CRE)-binding protein/activating transcription factor 1 protein of the basic leucine zipper superfamily. It binds CREs in vitro and activates CRE-containing promoters when transfected into COS7 cells. This activation of transcription was synergistically enhanced by the presence of CCAAT/enhancer-binding protein elements and inhibited by AP-1 elements in the promoter. In addition to a basic DNA binding domain, Luman possesses an unusually long leucine zipper and an acidic amino-terminal activation domain. These features in Luman are also present in what appear to be homologs in the mouse, Drosophila melanogaster, and Caenorhabditis elegans. Luman and VP16 appear to have similar mechanisms for binding HCF, as in vitro each competitively inhibited the binding of the other to HCF. In transfected cells, however, while VP16 strongly inhibited the ability of GAL-Luman to activate transcription from a GAL4 upstream activation sequence-containing promoter, Luman was unable to inhibit the activity of GAL-VP16. Luman appears to be a ubiquitous transcription factor, and its mRNA was detected in all human adult and fetal tissues examined. The possible role of HCF in regulating the function of this ubiquitous transcription factor is discussed.
Increased bronchovascular permeability after allergen exposure in sensitive asthmatics (1987)

To investigate the possibility that an increase in bronchovascular permeability is associated with allergen exposure in sensitive asthmatics we evaluated the amounts of serum proteins in bronchoalveolar lavage (BAL) effluents before and after local challenge with allergen. After exposure of sensitive asthmatic airways (n = 15) to allergen significant increases in total protein compared with controls were observed: 0.08 +/- 0.01 mg/ml in control airways and 0.13 +/- 0.02 mg/ml in challenged airways; P less than 0.05. The greatest changes induced by allergen exposure involved small-molecular-weight proteins (less than 345,000) and an inverse correlation was observed between log molecular weight and percent increase in the concentrations of the specific proteins; r = -0.61. BAL-serum distribution coefficients of serum proteins in airway fluids reflected a greater diffusability of low-molecular-weight proteins immediately after allergen exposure. We also evaluated the movement of serum proteins into lung after local allergen exposure using intravenously administered 99mTc-albumin (n = 10) and found an immediate 3.8-fold increase in amounts of radioactive albumin in allergen exposed airways compared with airways exposed to diluent. Most of the radioactivity was recovered in the first 5 ml of aliquot withdrawn, suggesting a marked increase in the permeability of the bronchial (large airway) vascular-epithelial membrane. An increase in serum proteins was also observed in BAL fluid of asthmatics 2-4 h after aerosol challenge (n = 4), including all proteins in the molecular weight range 45,000-900,000. These studies suggest that allergen exposure in sensitive asthmatics causes an acute increase in bronchovascular permeability to serum proteins.
Preexisting Immunity to Adenovirus in Rhesus Monkeys Fails To Prevent Vector-Induced Toxicity (2002)

In an earlier study we evaluated innate immune responses to a first-generation adenoviral vector infused into the portal vein of rhesus monkeys who had never been exposed to adenovirus previously. In these animals, the systemic administration of E1/E3-deleted adenoviral vectors resulted in immediate activation of innate immunity and serious toxicity caused by targeting of vector to antigen-presenting cells and systemic inflammation. We analyze here how these responses are affected by vector-specific preexisting immunity that was induced by intramuscular immunization 6 months prior to evaluation. Our results show that preexposure to the vector substantially diminishes the transgene expression in most tissues but has little effect on gene transfer. Significantly, preimmunization does not eliminate systemic vector-induced toxicity. These conclusions are based on the presence of clinical features of coagulopathy and elevated levels of proinflammatory cytokine interleukin-6 in the serum of animals treated with vector after intramuscular immunization. Furthermore, preexisting immunity appears to induce a vector-specific inhibitory effect on erythroid progenitor development in the bone marrow that is not found when naive animals are challenged with vector.
Inhibiting Cholesterol Absorption with CP-88,818 (β-Tigogenin Cellobioside; Tiqueside): Studies in Normal and Hyperlipidemic Subjects (1997)

CP-88,818 (beta-tigogenin cellobioside; tiqueside) is a synthetic saponin developed to treat hypercholesterolemia by inhibiting the absorption of biliary and dietary cholesterol. Two studies are reported here: one in patients to assess safety and efficacy, and one in normal volunteers to explore the mechanism of action. The former included 15 hypercholesterolemic outpatients [low-density lipoprotein cholesterol (LDL-C) > or = 160 mg/dl] treated with 1, 2, and 3 g of tiqueside daily (b.i.d.) in a crossover design for three 2-week treatment periods, each separated by a 3-week placebo period. The mechanistic study was conducted with 24 healthy male subjects who were randomized in a parallel group design to either placebo (n = 6) or tiqueside (2 or 4 g/day; n = 9 each) once daily for 3 weeks. All subjects in this study were fed a low-fat, low-cholesterol diet [National Cholesterol Education Program (NCEP) Step 1]. Fecal steroid excretion rates and plasma lipid levels were determined at baseline and after 3 weeks of treatment. Fractional cholesterol absorption was measured before and after treatment by the continuous feeding, dual-isotope method. Tiqueside produced a dose-dependent reduction in plasma LDL cholesterol levels in the hypercholesterolemic patients. In the mechanistic study, it decreased fractional cholesterol absorption rates and increased fecal neutral sterol excretion rates, changes associated with trends toward lower LDL cholesterol levels. Other lipoprotein levels were unaffected, as were fecal fat and bile acid excretion and fat-soluble vitamin absorption. Thus tiqueside dose-dependently inhibits cholesterol absorption in humans, resulting in a reduction in serum LDL cholesterol levels.
A review of the treatment options for Huntington’s disease (2004)

Huntington's disease (HD) is an autosomal dominant, inherited, neuropsychiatric disease which gives rise to progressive motor, cognitive and behavioural symptoms. Its core pathology involves degeneration of the basal ganglia, in particular, the caudate and putamen, and is caused by a single autosomal gene coding for a mutated form of the protein, huntingtin. At the present time, the only treatment options available in HD are symptomatic. There are several substances available today for the treatment of chorea. Other neurological symptoms, such as dystonia, can be treated, but treatment is associated with a high risk of adverse events. Psychiatric symptoms, on the other hand, are often amenable to treatment and relief of these symptoms may provide significant improvement in quality of life.
Colonoscopic Fecal Microbiota Transplant for Recurrent Clostridium difficile Infection in a Child (2012)

1 Department of Pediatrics, Section of Pediatric Gastroenterology, Hepatology, and Nutrition, University of Chicago, Chicago, Illinois, USA 2 Department of Medicine, Section of Gastroenterology, Hepatology, & Nutrition, University of Chicago, Chicago, Illinois, USA Correspondence: Stacy A. Kahn, MD, Department of Pediatrics, Section of Pediatric Gastroenterology, Hepatology, and Nutrition, University of Chicago, 5841 South Maryland Avenue, MC 4065, Chicago, Illinois 60637, USA. E-mail: [email protected]
Δ5-Androstenediol is a natural hormone with androgenic activity in human prostate cancer cells (1998)

It is known that androst-5-ene-3beta,17beta-diol (Adiol), a precursor of testosterone (T), can activate estrogen target genes. The androgenic activity of Adiol itself, however, is poorly understood. Using a transient transfection assay, we here demonstrate in human prostate cancer cells that Adiol can activate androgen receptor (AR) target genes in the presence of AR, and that AR coactivator ARA70 can further enhance this Adiol-induced AR transcriptional activity. In contrast to this finding, an active metabolite of dehydroepiandrosterone, 7-oxo-dehydroepiandrosterone, does not activate AR target gene in the absence or presence of ARA70. Thin layer chromatography analysis reveals that T, dihydrotestosterone, and 17beta-estradiol are undetectable in human prostate cancer DU145 cells after treatment with Adiol. Additionally, a proteolysis assay shows that a distinct ligand-receptor conformational difference exists between T-AR and Adiol-AR. Together, the above findings and the fact that T, but not Adiol, can induce transcriptional activity in a mutant AR (mtAR708), suggest that, without being metabolized into T, Adiol itself may represent a natural hormone with androgenic activity in human prostate cancer cells. Because two potent antiandrogens, hydroxyflutamide (Eulexin), and bicalutamide (casodex), that are widely used for the treatment of prostate cancer, fail to block Adiol-mediated induction of AR transcriptional activity in prostate cancer cells, the effectiveness of so-called "total androgen blockage," a standard treatment for prostate cancer, may need to be reevaluated.
Successful treatment with tocilizumab for refractory scleritis associated with relapsing polychondritis (2017)

"Successful treatment with tocilizumab for refractory scleritis associated with relapsing polychondritis." Scandinavian Journal of Rheumatology, 46(5), pp. 418–419
Structure and promoter activity of the gene for the erythroid transcription factor GATA-1. (1991)

We have cloned the gene for the chicken erythroid transcription factor GATA-1 (formerly Eryf1, NF-E1, or GF-1). The gene is composed of six exons, two of which encode the two finger domains of the protein. Transcription of GATA-1 in chicken embryonic erythroid cells initiates from multiple sites clustered approximately 200 base pairs upstream from the start of protein-coding sequence. A number of sequence motifs for known DNA-binding proteins are found to be protected in DNase I-footprinting experiments by either erythroid or brain nuclear extracts or by both. Notably, a cluster of three GATA-1 sites is protected by the erythroid extract, as well as by purified GATA-1. We find that the upstream region of the gene functions as a powerful promoter when transfected into embryonic erythroid cells. In primary chicken embryo fibroblasts the promoter exhibits lower activity, which is increased when the cells are cotransfected with a second plasmid expressing the GATA-1 cDNA. The results suggest that GATA-1 protein plays an autoregulatory role in its own expression.
Intracellular Localization of Polymerase Chain Reaction (PCR)-Amplified Hepatitis C cDNA (1993)

The cellular distribution of hepatitis C virus was examined in formalin-fixed, paraffin-embedded tissues by in situ localization of the polymerase chain reaction (PCR)-amplified viral cDNA. Of nine liver biopsies studied, five were from patients seropositive for hepatitis C, one was from a seronegative patient who had detectable hepatitis C cDNA by standard reverse transcriptase (RT) PCR, and the remaining three were from patients without evidence of hepatitis C infection. Sequences homologous to viral RNA were rarely identified in the hepatitis C cases by standard RNA-cDNA in situ hybridization, but PCR-amplified viral cDNA was detectable in many hepatocytes in a panlobular distribution and in scattered Kupffer cells in each of the six hepatitis C cases and none of the controls. The pattern was equivalent whether intracellular localization was done by in situ hybridization after the RT and PCR steps or if digoxigenin-labeled nucleotide was incorporated into the amplified product. No signal was evident in the positive biopsies if the RT step was omitted, if "nonsense" primers were used, or if RT in situ PCR was preceded by RNase digestion. The RT in situ PCR technique allows for the rapid detection of any RNA virus, even if it is present in low copy number, and permits direct morphological correlation.
Identities and frequencies of mutations of the otoferlin gene (OTOF) causing DFNB9 deafness in Pakistan (2009)

Mutations in OTOF, encoding otoferlin, cause non-syndromic recessive hearing loss. The goal of our study was to define the identities and frequencies of OTOF mutations in a model population. We screened a cohort of 557 large consanguineous Pakistani families segregating recessive, severe-to-profound, prelingual-onset deafness for linkage to DFNB9. There were 13 families segregating deafness consistent with linkage to markers for DFNB9. We analyzed the genomic nucleotide sequence of OTOF and detected probable pathogenic sequence variants among all 13 families. These include the previously reported nonsense mutation p.R708X and 10 novel variants: 3 nonsense mutations (p.R425X, p.W536X, and p.Y1603X), 1 frameshift (c.1103_1104delinsC), 1 single amino acid deletion (p.E766del) and 5 missense substitutions of conserved residues (p.L573R, p.A1090E, p.E1733K, p.R1856Q and p.R1939W). OTOF mutations thus account for deafness in 13 (2.3%) of 557 Pakistani families. This overall prevalence is similar, but the mutation spectrum is different from those for Western populations. In addition, we demonstrate the existence of an alternative splice isoform of OTOF expressed in the human cochlea. This isoform must be required for human hearing because it encodes a unique alternative C-terminus affected by some DFNB9 mutations.
Primary structure of rabbit C-reactive protein. (1982)

permitted the assignments of amino acid residues that might be involved in the binding of phosphorylcholine.In the presence of infectious diseases and various other pathological conditions there appears in the serum of man a protein not normally detected.This is called C-reactive protein because it has the curious property of precipitating with C-polysaccharide derived from the cell wall of Streptococcus pneumoniae (1).Proteins analogous to CRP' have been isolated from sera of other species (2-5) including an invertebrate, Limuluspolyphemus (6).Like immunoglobulins, CRP mediates in vitro many reactions, enhancing phagocytosis (7) and promoting precipitation of bacterial cells (1) and certain polymers (8).There is, however, no structural homology between CRP and immunoglobulins (9).The occurrence in the rabbit of an acute phase protein analogous to human CRP has been reported by Anderson and McCarty (2).Thus, an animal model exists for the study of the biochemical and physiological role of this protein.The present investigation was initiated to determine the primary