gebhart/patrepeval huggingface dataset:
On the resemblance and containment of documents (2002)

Given two documents A and B we define two mathematical notions: their resemblance r(A, B) and their containment c(A, B) that seem to capture well the informal notions of "roughly the same" and "roughly contained." The basic idea is to reduce these issues to set intersection problems that can be easily evaluated by a process of random sampling that can be done independently for each document. Furthermore, the resemblance can be evaluated using a fixed size sample for each document. This paper discusses the mathematical properties of these measures and the efficient implementation of the sampling process using Rabin (1981) fingerprints.
Derivatized Porous Silicon Mirrors: Implantable Optical Components with Slow Resorbability (2000)

The stability of derivatized mesoporous silicon mirrors in simulated human blood plasma has been assessed. The rate at which they are dissolved in-vivo is predicted to be tunable by surface chemistry over timescales of weeks to years, and high reflectivity can be maintained until the bottom of the multilayer stack starts to corrode. Such biodegradable optical components could be utilized to direct and define optical path lengths for therapeutic treatments and minimally-invasive diagnostics.
Studies in vitro on the effects of 1H,2H,4H(5H)-octafluorocyclohexane and 1H,4H(2H)-nonafluorocyclohexane on enzymes and organelles (1969)

A comparison has been made of the effect of 1H,2H,4H(5H)-octafluorocyclohexane, which is highly toxic (LD(50) 17mg./kg. in rats), and of 1H,4H(2H)-nonafluorocyclohexane, which is relatively non-toxic (LD(50)>440mg./kg. in rats), on the respiration of rat liver homogenates and mitochondria in vitro. 1H,2H,4H(5H)-Octafluorocyclohexane strongly inhibited the respiration of both homogenates and mitochondria, but neither compound had any significant effect on glycolysis or on glutamate dehydrogenase or NADH-cytochrome c reductase activity. 1H,2H,4H(5H)-Octafluorocyclohexane, however, caused a very marked inhibition of cytochrome oxidase activity, causing an almost complete lesion in this region of the respiratory chain. 1H,4H(2H)-Nonafluorocyclohexane was without effect in this respect. A marked decrease in turbidity of mitochondrial suspensions at 520nm. was caused by addition of both compounds, the effect being greater with 1H,2H,4H(5H)-octafluorocyclohexane. ATP, Mg(2+) and bovine serum albumin did not reverse these changes. Mitochondrial adenosine triphosphatase activity was increased twofold by the toxic compound, but only slightly by the non-toxic compound. Electron-microscopic examination of mitochondria treated with 1H,2H,4H(5H)-octafluorocyclohexane revealed gross morphological damage, whereas the effect of 1H,4H(2H)-nonafluorocyclohexane appeared to be merely to cause swelling. The results obtained account, to some extent at any rate, for the toxic effects of 1H,2H,4H(5H)-octafluorocyclohexane.
Ocular damage induced by near-ultraviolet laser radiation. (1976)

A quantitative study was conducted of ocular damage thresholds in the rhesus monkey eye from krypton, argon, and nitrogen laser radiation. Corneal and lenticular thresholds are reported for various laser beam parameters. Corneal damage was found to occur following incident energy doses of approximately 60 to 70 Joules per square centimeter (J./cm.2) for pulsewidths ranging from 250 musec to 120 sec. The results are consistent with a photochemical damage mechanism. With certain exposure parameters, cataracts were induced with lower energy doses than required to cause corneal damage. The lenticular thresholds, however, appear to be consistent with a thermal rather than a photochemical mechanism. Corneal and lenticular hazards of near-ultraviolet (near-UV) lasers are discussed in terms of existing safety standards for laser radiation.
Genetic analysis of low lambda 1 chain production in mice. (1986)

Several commonly used strains of laboratory mice from Charles River Laboratories were found to produce extremely low or undetectable levels of serum immunoglobulins bearing lambda 1 light chain (lambda 1 Ig). Individual CF-1, CD-1, and CFW random-bred mice were tested for serum lambda 1 levels, lambda 1-specific anti-NP responses, and genomic polymorphisms at the lambda 1 locus. In all cases, a complete correlation among these parameters was observed. The results indicated that nearly all CFW, greater than 70% of CD-1 but none of the CF-1 mice produced low levels of lambda 1 light chain. The low lambda 1 Ig production is due to a genetic defect either similar or identical to that observed in SJL mice. The data suggest that the lambda 1 locus of CD-1, CFW, and SJL mice are derived from a common ancestor. We also surveyed lambda 1 Ig production in a series of wild mice. Mice producing low lambda 1 Ig were frequently observed. The wild mice with low lambda 1 Ig levels were captured in diverse geographic areas, including Europe, Middle East, Asia, and South America. Preliminary study suggests that the defect in the wild mice is different from that of SJL, CD-1, or CFW mice and implies that other mechanisms regulate lambda 1 Ig production in wild mice.
Elimination of transformer inrush currents by controlled switching. II. Application and performance considerations (2001)

For pt. I see ibid., vol.16, no.2, p.276-80 (2001). Transformer inrush currents are high-magnitude, harmonic-rich currents generated when transformer cores are driven into saturation during energization. These currents have undesirable effects, including potential damage or loss-of-life to the transformer, protective relay misoperation, and reduced power quality on the system. Controlled transformer switching can potentially eliminate these transients if residual core and core flux transients are taken into account in the closing algorithm. This paper explores the practical considerations of core flux transients, performance of control strategies, and the application of circuit breakers to control transformer inrush transients.
Procedures and Practices for The Validation of Bioanalytical Methods Using Dried Blood Spots: A Review (2014)

Dried blood spot (DBS) sampling, the collection of whole blood samples on paper, is an emerging technique used for bioanalytical methods. Several analytical challenges, such as possible effects of spotting volume, hematocrit and spot inhomogeneity are identified for these methods, however, no regulatory-based guidelines for the specific validation of DBS-based assays are available hitherto. To date, 68 validation reports concerning methods for the quantitative determination of drugs in human DBS could be traced in the literature, with large differences in the extensiveness of the reported validations. This review aims to present an overview of these published validations. Additionally, the different challenges of DBS-based assays are discussed and recommendations on how to perform validation tests addressing these challenges are provided.
Redox-Switchable Surface for Controlling Peptide Structure (2011)

A general surface chemistry strategy is described for the development of a new switchable material. The method modulates a surface-immobilized-molecules structure by using two orthogonal "click" reactions based on Huisgen cycloaddition and oxime chemistry, where the oxime linkage is redox active and switchable. We demonstrate this strategy by developing a noninvasive, biocompatible, in situ surface chemistry that is able to modulate the affinity of a cell-adhesive peptide to cell integrin receptors to study dynamic cell adhesion and cell migration in real time and as a new hide-and-reveal strategy for application in new types of smart biofouling biomaterials.
Escherichia coli in chronic inflammatory bowel diseases: An update on adherent invasive Escherichia coli pathogenicity (2014)

Escherichia coli (E. coli), and particularly the adherent invasive E. coli (AIEC) pathotype, has been increasingly implicated in the ethiopathogenesis of Crohn's disease (CD). E. coli strains with similar pathogenic features to AIEC have been associated with other intestinal disorders such as ulcerative colitis, colorectal cancer, and coeliac disease, but AIEC prevalence in these diseases remains largely unexplored. Since AIEC was described one decade ago, substantial progress has been made in deciphering its mechanisms of pathogenicity. However, the molecular bases that characterize the phenotypic properties of this pathotype are still not well resolved. A review of studies focused on E. coli populations in inflammatory bowel disease (IBD) is presented here and we discuss about the putative role of this species on each IBD subtype. Given the relevance of AIEC in CD pathogenesis, we present the latest research findings concerning AIEC host-microbe interactions and pathogenicity. We also review the existing data regarding the prevalence and abundance of AIEC in CD and its association with other intestinal diseases from humans and animals, in order to discuss the AIEC disease- and host-specificity. Finally, we highlight the fact that dietary components frequently found in industrialized countries may enhance AIEC colonization in the gut, which merits further investigation and the implementation of preventative measures.
Synthesis of 1,7-Dideaza-2'-deoxyadenosine and Related Pyrrolo[2,3-b]pyridine 2'-Deoxy-b-D-ribonucleosides: Stereoselective Phase-Transfer Glycpsylation via the Nucleobase Anion (1989)

The synthesis of 1,7-dideaza-2'-deoxyadenosine (11 and related pyrrolo[2,3-blpyridine 2'-deoxy-B-D-ribofuranosides is described.Glycosylation of the anions of the pyrrolo[2,3-blpyridines or with 2-deoxy-3,5-di-0-(p-tolu0y1)-a-D-erythr0-pentofuranosyl chloride (61 has been carried out under phase-transfer conditions (NeCN, solid KOH, TDA-1, 25OC) and was complete within less than 15 min.The reaction was stereoselective and 8-nucleosides were formed exclusively.The position of glycosylation as well as the anomeric configuration were assigned by NOE difference spectroscopy.Compound 1 was extremely stable against acid or base and was not deaminated by adenosine deaminase.
Molecular diagnostics of infectious diseases (1997)

Over the past several years, the development and application of molecular diagnostic techniques has initiated a revolution in the diagnosis and monitoring of infectious diseases. Microbial phenotypic characteristics, such as protein, bacteriophage, and chromatographic profiles, as well as biotyping and susceptibility testing, are used in most routine laboratories for identification and differentiation. Nucleic acid techniques, such as plasmid profiling, various methods for generating restriction fragment length polymorphisms, and the polymerase chain reaction (PCR), are making increasing inroads into clinical laboratories. PCR-based systems to detect the etiologic agents of disease directly from clinical samples, without the need for culture, have been useful in rapid detection of unculturable or fastidious microorganisms. Additionally, sequence analysis of amplified microbial DNA allows for identification and better characterization of the pathogen. Subspecies variation, identified by various techniques, has been shown to be important in the prognosis of certain diseases. Other important advances include the determination of viral load and the direct detection of genes or gene mutations responsible for drug resistance. Increased use of automation and user-friendly software makes these technologies more widely available. In all, the detection of infectious agents at the nucleic acid level represents a true synthesis of clinical chemistry and clinical microbiology techniques.
Conditional Random Fields: An Introduction (2004)

University of Pennsylvania Department of Computer and Information Science Technical Report No. MS-CIS-04-21.
Characterization of the novel brown adipocyte cell line hib 1b adrenergic pathways involved in regulation of uncoupling protein gene expression (1994)

The HIB 1B cell line, derived from a brown fat tumor of a transgenic mouse, is the first established brown adipocyte cell line capable of expressing the brown fat-specific mitochondrial uncoupling protein (UCP). UCP gene expression, which was virtually undetectable under basic conditions, was stimulated by acute catecholamine or cyclic AMP treatment to levels comparable to primary cultures of brown adipocytes. Elevation of UCP mRNA levels following stimulation was very rapid but transient, decreasing after about 4 hours with a half-life between 9 and 13 hours. Immunoblotting showed the presence of UCP in HIB 1B mitochondria, but expression was much lower than observed in BAT or primary cultures of brown adipocytes. Upon transfection of HIB 1B cells with a reporter gene containing the UCP promoter, the activity of the transgene was regulatable by cAMP and norepinephrine. Investigation of the possible adrenergic receptors involved in UCP stimulation showed that specific beta 3-adrenergic agonists were much less effective than nonspecific beta-adrenergic agonists and that mRNA levels of the atypical, fat-specific beta 3-adrenoceptor were lower than those observed in brown adipocytes differentiated in primary culture. From pharmacological evidence we conclude that beta 3-adrenergic receptors account for approximately 30-40% of catecholamine induced UCP gene stimulation, whereas about 60-70% is stimulated via the classical beta 1/2 adrenergic pathway. We conclude that HIB 1B cells represent a functional system for the study of mechanisms related to brown adipose thermogenesis.
Factors Contributing to Dehydration in Nursing Homes: Inadequate Staffing and Lack of Professional Supervision (1999)

When staffing is inadequate and supervision is poor, residents with moderate to severe dysphagia, severe cognitive and functional impairment, aphasia or inability to speak English, and a lack of family or friends to assist them at mealtime are at great risk for dehydration. Adequate fluid intake can be achieved by simple interventions such as offering residents preferred liquids systematically and by having an adequate number of supervised staff help them to drink while properly positioned.
In Vitro and In Vivo Efficacy of CD38 Directed Therapy with Daratumumab In the Treatment of Multiple Myeloma (2010)

Abstract Abstract 3058 Daratumumab (DARA) is a fully human antibody against CD38, a membrane-associated antigen, which is considered to be a highly relevant target for the treatment of hematological malignancies such as multiple myeloma (MM) and chronic lymphocytic leukemia (CLL). DARA has the ability to effectively kill target cells by CDC, ADCC and by induction of apoptosis. While CD38 is frequently overexpressed on MM cells, it has a variable degree of expression on the malignant CLL cells. To gain detailed insight into the potential therapeutic power of DARA in tumors with different CD38 expression levels, we now investigated the correlation between the level of CD38 expression and DARA-induced kill by CDC and ADCC. To this end, we first used the human MM cell lines L363 and UM9, expressing low and intermediate CD38 levels, respectively. While both cell lines could be lysed via ADCC, they were not susceptible to killing via CDC. To delineate a possible correlation between CD38 expression and induction of CDC, we lentivirally transduced the CD38 gene into L363 and UM9 cells to generate cell lines ranging in CD38 expression from 50,000 to 800,000 molecules per cell. Hereby we covered the range of CD38 expression found in CLL and MM patients. The L363 and UM9 cell lines were also transduced with the luciferase-GFP marker genes to enable their in vivo quantitative monitoring by bioluminescence imaging (BLI). In CDC assays, up to 95% lysis of CD38-transduced L363 and UM9 cells was achieved and showed an excellent correlation with the level of CD38 expression (r2=0.90). In ADCC assays, however, killing already reached maximum levels at DARA concentrations as low as 1 ng/ml at the lowest CD38 expression levels tested. These in vitro assays indicated that cell killing via CDC is enhanced with increasing CD38 expression levels, while CDC resistant, low CD38-expressing tumors could be targeted by DARA via ADCC. To explore this in an in vivo setting, we used a newly developed MM model in Rag2−/−gc−/− mice and we inoculated the mice with nontransduced, CD38low, UM9 cells, which can be lysed by ADCC but not by CDC. Treatment of the mice with DARA one day after tumor inoculation completely prevented the outgrowth of these UM9 cells; treatment of established UM9 tumours at week 3 resulted in a significant delay in tumor growth. These results confirmed that the CDC resistant UM9 could be readily targeted by DARA in vivo, possibly via ADCC mediated by monocytes in this model. In vivo experiments with variants that express high levels of CD38 are in progress. Taken together, these in vitro and in vivo data underscore the potency of DARA as a novel antibody for CD38-targeted therapy in hematological malignancies, and warrant further exploration in clinical trials. Disclosures: de Weers: Genmab bv: Employment. Parren:Genmab: Employment.
The relationship of socioeconomic status, race, and modifiable risk factors to outcomes in patients with systemic lupus erythematosus (1997)

Disease activity and health status were most strongly associated with potentially modifiable psychosocial factors such as self-efficacy for disease management. Cumulative organ damage was most highly associated with clinical factors such as age and duration of disease. None of the outcomes measured were associated with race. These results suggest that education and counseling, coordinated with medical care, might improve outcomes in patients with SLE.
Mutations affecting the development of the embryonic zebrafish brain (1996)

In a large scale mutagenesis screen for embryonic mutants in zebrafish, we have identified 63 mutations in 24 loci affecting the morphogenesis of the zebrafish brain. The expression of marker genes and the integrity of the axonal scaffold have been studied to investigate abnormalities in regionalization, neurogenesis and axonogenesis in the brain. Mutants can be broadly classified into two groups, one affecting regionalization along the anterior-posterior or dorsal-ventral axis, and the other affecting general features of brain morphology. The first group includes one locus that is required to generate the anlage of the midbrain-hindbrain boundary region at the beginning of somitogenesis. Four loci were identified that affect dorsal-ventral patterning of the brain, including the previously described cyclops locus. Mutant embryos of this class show a reduction of ventral neuroectodermal structures and variable fusion of the eyes. The second group includes a large class of mutations affecting the formation of brain ventricles. Analysis of this class reveals the requirement of a functional cardiovascular system for ventricle enlargement during embryogenesis. Mutations in one locus lead to the formation of supernumerary primary neurons, a phenotype reminiscent of neurogenic mutants in Drosophila. Other mutant phenotypes described here range from abnormalities in the fasciculation and outgrowth of axons to defects in the diameter of the neural tube. The identified loci establish the genetic foundation for a further analysis of the development of the zebrafish embryonic brain.
Allergic Eosinophil-rich Inflammation Develops in Lungs and Airways of B Cell–deficient Mice (1997)

Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease. To validate this paradigm we examined homozygous mutant C57BL/6 mice, which are B cell deficient, lacking all Ig. Mice were immunized intraperitoneally with 10 micrograms ovalbumin (OVA) plus alum, followed by daily (day 14-20) 30 min exposures to OVA aerosol (OVA/OVA group). Three control groups were run: OVA intraperitoneally plus saline (SAL) aerosol (OVA/SAL group); saline intraperitoneally plus saline aerosol; saline intraperitoneally plus OVA aerosol (n = 6-7). Lung and large airway tissues obtained 24 h after the last OVA or SAL exposure were examined by light microscopy and transmission electron microscopy (TEM). The Ig-deficient mice receiving OVA/ OVA treatment had swollen and discolored lungs and exhibited marked eosinophilia both in large airway subepithelial tissue (49.2 +/- 12.0 cells/mm basement membrane [BM] versus OVA/ SAL control 1.2 +/- 0.3 cells/mm BM; P < 0.001), and perivascularly and peribronchially in the lung (49.3 +/- 9.0 cells/unit area versus OVA/SAL control 2.6 +/- 0.6 cells/unit area; P < 0.001). The eosinophilia extended to the regional lymph nodes. TEM confirmed the subepithelial and perivascular localization of eosinophils. Mucus cells in large airway epithelium increased from 1.5 +/- 0.8 (OVA/SAL mice) to 39.5 +/- 5.7 cells/mm BM in OVA/OVA treated mice (P < 0.001). OVA/SAL mice never differed from the other control groups. Corresponding experiments in wild-type mice (n = 6-7 in each group) showed qualitatively similar but less pronounced eosinophil and mucus cell changes. Macrophages and CD4+ T cells increased in lungs of all OVA/OVA-treated mice. Mast cell number did not differ but degranulation was detected only in OVA/OVA-treated wild-type mice. Immunization to OVA followed by OVA challenges thus cause eosinophil-rich inflammation in airways and lungs of mice without involvement of B cells and Ig.
Primary structure of a human arginine-rich nuclear protein that colocalizes with spliceosome components. (1991)

The cDNA for a 54-kDa nuclear protein (p54) has been cloned from a human hepatoma expression library. Contained within p54 is an arginine/serine-rich region similar to segments of several proteins that participate in pre-mRNA splicing including the 70-kDa component of U1 small nuclear and "suppressor-of-white-apricot" proteins. The arginine/serine-rich region is dominated by a series of 8-amino acid imperfect repetitive motifs (consensus sequence, Arg-Arg-Ser-Arg-Ser-Arg-Ser-Arg). Antibodies raised against synthetic peptides of p54 react with an approximately 70-kDa protein on immunoblots of HeLa cell and rat liver nuclear proteins. This apparent discrepancy in mass is also observed when p54 mRNA is translated in vitro. Indirect immunofluorescence studies in HeLa cells show that p54 is distributed throughout the nucleus in a speckled pattern, with an additional diffuse labeling of the nucleus excluding the nucleoli. Double immunofluorescence experiments indicate that these punctate regions are coincident with the speckles seen in cells stained with antibodies against several constituents of the pre-mRNA splicing machinery. Sedimentation analysis of HeLa cell extracts on sucrose gradients showed that p54 migrates at 4-6 S, indicating that the protein is not a tightly associated component of snRNPs. Although the function of p54 is not yet known, our structure and immunolocalization data suggest that this protein may have a role in pre-mRNA processing.