gebhart/patrepeval huggingface dataset:
Generation of murine dendritic cells from flt3-ligand–supplemented bone marrow cultures (2000)

Murine dendritic cells (DCs) can be classified into at least 2 subsets, "myeloid-related" (CD11b(bright), CD8alpha(-)) and "lymphoid-related" (CD11b(dull), CD8alpha(+)), but the absolute relationship between the 2 remains unclear. Methods of generating DCs from bone marrow (BM) precursors in vitro typically employ granulocyte-macrophage colony-stimulating factor (GM-CSF) as the principal growth factor, and the resultant DCs exhibit a myeloidlike phenotype. Here we describe a flt3-ligand (FL)-dependent BM culture system that generated DCs with more diverse phenotypic characteristics. Murine BM cells cultured at high density in recombinant human FL for 9 days developed into small lymphoid-sized cells, most of which expressed CD11c, CD86, and major histocompatibility complex (MHC) class II. The CD11c(+) population could be divided into 2 populations on the basis of the level of expression of CD11b, which may represent the putative myeloid- and lymphoid-related subsets. The FL in vitro-derived DCs, when treated with interferon-alpha or lipopolysaccharide during the final 24 hours of culture, expressed an activated phenotype that included up-regulation of MHC class II, CD1d, CD8alpha, CD80, CD86, and CD40. The FL-derived DCs also exhibited potent antigen-processing and antigen-presenting capacity. Neutralizing anti-interleukin-6 (IL-6) antibody, but not anti-GM-CSF, significantly reduced the number of DCs generated in vitro with FL, suggesting that IL-6 has a role in the development of DCs from BM precursors. Stem cell factor, which exhibits some of the same bioactivities as FL, was unable to replace FL to promote DC development in vitro. This culture system will facilitate detailed analysis of murine DC development.
Evidence for linkage of a candidate chromosome 1 region to human systemic lupus erythematosus. (1997)

Genetic susceptibility confers significant risk for systemic lupus erythematosus (SLE). The MHC region and other polymorphic loci have been associated with SLE. Because more compelling evidence for an involvement of a genetic locus includes linkage, we tested a candidate region homologous to a murine SLE susceptibility region in 52 SLE-affected sibpairs from three ethnic groups. We analyzed seven microsatellite markers from the human chromosome 1q31-q42 region corresponding to the telomeric end of mouse chromosome 1, the region where specific manifestations of murine lupus, including glomerulonephritis and IgG antichromatin, have been mapped. Comparing the mean allele sharing in affected sibpairs of each of these seven markers to their expected values of 0.50, only the five markers located at 1q41-q42 showed evidence for linkage (P = 0.0005-0.08). Serum levels of IgG antichromatin also showed evidence for linkage to two of these five markers (P = 0.04), suggesting that this phenotype is conserved between mice and humans. Compared to the expected random distribution, the trend of increased sharing of haplotypes was observed in affected sibpairs from three ethnic groups (P < 0.01). We concluded that this candidate 1q41-q42 region probably contains a susceptibility gene(s) that confers risk for SLE in multiple ethnic groups.
Evidence that SV40 surface tumor antigen originates from the nucleus and cytoplasm. (1991)

Simian virus 40 large T antigen exposed at the cell surface is oligomerized and phosphorylated in a mature fashion. NP40-soluble surface T antigen, prepared from infected cells, sediments mainly as a tetramer and has a nuclear phosphorylation pattern. Since these are modifications that occur over several hours, surface T appears to be a population of older molecules. This is in apparent contradiction to kinetic studies showing that T antigen arrives at the surface in 20 min. We present a model to account for this apparent discrepancy. It postulates that both newly-synthesized and older, mature molecules are transported to the surface. The newly-synthesized molecules are highly unstable and lost rapidly from the surface whereas the mature molecules are stable and accumulate over time. This stability may be due to oligomerization and/or phosphorylation or to an interaction with other surface molecules that act as anchors. Our model further proposes that most of the T antigen in transit to the surface is newly-synthesized protein from the cytoplasm, while the majority of the T antigen at the surface is mature protein from the nucleus.
Molecular and cellular characterisation of highly purified stromal stem cells derived from human bone marrow (2003)

Previous studies have provided evidence for the existence of adult human bone marrow stromal stem cells (BMSSCs) or mesenchymal stem cells. Using a combination of cell separation techniques, we have isolated an almost homogeneous population of BMSSCs from adult human bone marrow. Lacking phenotypic characteristics of leukocytes and mature stromal elements, BMSSCs are non-cycling and constitutively express telomerase activity in vivo. This mesenchymal stem cell population demonstrates extensive proliferation and retains the capacity for differentiation into bone, cartilage and adipose tissue in vitro. In addition, clonal analysis demonstrated that individual BMSSC colonies exhibit a differential capacity to form new bone in vivo. These data are consistent with the existence of a second population of bone marrow stem cells in addition to those for the hematopoietic system. Our novel selection protocol provides a means to generate purified populations of BMSSCs for use in a range of different tissue engineering and gene therapy strategies.
Role of Regulator of G Protein Signaling in Desensitization of the Glucose-Dependent Insulinotropic Peptide Receptor (1998)

The glucose-dependent insulinotropic peptide receptor (GIP-R) is a member of the G protein-coupled receptors. Recent studies have indicated that elevated serum GIP concentrations in type II diabetic patients might induce desensitization of the GIP-R, and this mechanism could contribute to impaired insulin secretion. The cellular and molecular mechanisms governing GIP desensitization are unknown. Here, we report the results of studies on a new family of proteins known as regulators of G protein signaling (RGS) that have been shown to mediate the desensitization process of other receptors. GIP-R and RGS1, -2, -3, and -4 complementary DNAs were cotransfected into human embryonic kidney cells (L293). GIP-stimulated cAMP generation in control cells and in those coexpressing RGS1, -3, and -4 displayed a dose-dependent increase 10 min after GIP treat-ment. In contrast, RGS2 expression inhibited the GIP-induced cAMP response by 50%, a response similar to that of cells desensitized by preincubation with 10 7 M GIP. In TC3 cells, preincubation of GIP attenuated GIP-induced insulin release by 45% at 15 min and by 55% at 30 min. Expression of RGS2 in the TC3 cells significantly decreased GIP-stimulated insulin secretion, whereas glucose-induced insulin release was not affected. RGS2 messenger RNA was identified by Northern blot analysis to be expressed endogenously in TC3 and L293 cells, and its level was significantly induced by GIP treatment in TC3 cells. Moreover, RGS2 bound G s protein in an in vitro system, suggesting that RGS2 attenuated the G s -adenylate cyclase signaling pathway. These results suggest a potential role for RGS2 in modulating GIP-mediated insulin secretion in pancreatic islet cells.
Measurement in vitro of Human Plasma Glycerol with a Hydrogen Peroxide Detecting Microdialysis Enzyme Electrode (1994)

Human plasma glycerol was determined with a microdialysis electrode, containing the enzymes glycerol kinase and glycerol phosphate oxidase held stationary within the electrode. A microdialysis electrode is essentially a conventional microdialysis probe, with a platinum working electrode inserted into the tip of the dialysis fiber and reference and counter electrodes contained in the upper compartment. The linear range of response to glycerol was directly dependent on the concentration of ATP. At 4 mM ATP, the linear range was 0.5-500 microM. A fast response time of 20 s was obtained. Two types of interferences were observed when plasma glycerol was measured: direct oxidation of interferents at the electrode and attenuation of response to glycerol by reaction with hydrogen peroxide and/or poisoning of the platinum electrode. Ascorbate, urate, and acetaminophen were removed from plasma samples by a pretreatment step involving peroxidase and catalase. Any remaining interferent current was reduced by electropolymerizing o-phenylenediamine onto the platinum electrode. Adsorption of plasma proteins on the dialysis fiber was minimal and was not reduced by the preadsorption of human serum albumin. Very good correlation was obtained between the electrode and the standard spectrophotometric technique for the variation in glycerol concentration with time.
TIMING OF WOUND CLOSURE IN SEVERE COMPOUND FRACTURES (1994)

In a consecutive series of 1085 open fractures treated from May 1983 to July 1992, 381 severe compound fractures in 335 patients were managed with the antibiotic bead pouch technique. There were 27 grade I (marked swelling, compartment syndrome), 115 grade II, and 239 grade III open fractures (94 type IIIA, 114 type IIIB, and 31 type IIIC). These fractures were managed with early administration of broad spectrum antibiotics, copious wound irrigation, serial debridements, and external skeletal stabilization. Tobramycin-PMMA beads were placed in the wound, and porous plastic film (Opsite, Smith and Nephew Medical, Limited, Hall, England) covered the soft tissue defect. This dressing was changed every 48 to 72 hours until wound coverage/closure could be obtained. Infection rate, either on an acute or chronic basis, was 2.6% in grade II open fractures and 8.4% in grade III compound fractures. There was no infected wound or bone in the grade I category. Those fractures that did not develop an infection were closed at a mean time of 7.6 days; those that developed an infection were closed at a mean time of 17.9 days. The difference was statistically significant (P < 0.001). When severe open fractures are managed with the antibiotic bead pouch technique, wound closure should be obtained within 1 week to prevent infectious complications.
Reducing crash recoverability to reachability (2016)

Software applications run on a variety of platforms (filesystems, virtual slices, mobile hardware, etc.) that do not provide 100% uptime. As such, these applications may crash at any unfortunate moment losing volatile data and, when re-launched, they must be able to correctly recover from potentially inconsistent states left on persistent storage. From a verification perspective, crash recovery bugs can be particularly frustrating because, even when it has been formally proved for a program that it satisfies a property, the proof is foiled by these external events that crash and restart the program. In this paper we first provide a hierarchical formal model of what it means for a program to be crash recoverable. Our model captures the recoverability of many real world programs, including those in our evaluation which use sophisticated recovery algorithms such as shadow paging and write-ahead logging. Next, we introduce a novel technique capable of automatically proving that a program correctly recovers from a crash via a reduction to reachability. Our technique takes an input control-flow automaton and transforms it into an encoding that blends the capture of snapshots of pre-crash states into a symbolic search for a proof that recovery terminates and every recovered execution simulates some crash-free execution. Our encoding is designed to enable one to apply existing abstraction techniques in order to do the work that is necessary to prove recoverability. We have implemented our technique in a tool called Eleven82, capable of analyzing C programs to detect recoverability bugs or prove their absence. We have applied our tool to benchmark examples drawn from industrial file systems and databases, including GDBM, LevelDB, LMDB, PostgreSQL, SQLite, VMware and ZooKeeper. Within minutes, our tool is able to discover bugs or prove that these fragments are crash recoverable.
Oncogenic NRF2 mutations in squamous cell carcinomas of oesophagus and skin (2009)

Nuclear factor erythroid-related factor 2 (NRF2) encodes a transcription factor that induces expression of cytoprotective proteins upon oxidative stress and oncogenic NRF2 mutations have been found in lung and head/neck cancers that inactivate KEAP1-mediated degradation of NRF2. The aim of this study was to catalogue NRF2 mutations in other human cancers. For this, we analysed 1145 cancer tissues from carcinomas from oesophagus, skin, uterine cervix, lung, larynx, breast, colon, stomach, liver, prostate, urinary bladder, ovary, uterine cervix, and kidney, and meningiomas, multiple myelomas, and acute leukaemias by single-strand conformation polymorphism (SSCP) assay. We detected NRF2 mutations in oesophagus (8/70; 11.4%), skin (1/17; 6.3%), lung (10/125; 8.0%), and larynx (3/23; 13.0%) cancers. Of note, all of the 22 mutations except one were found in squamous cell carcinomas (SCCs) (95.5%). The mutations were observed within or near DLG and ETGE motifs that are important in NRF2 and KEAP1 interaction. All of the oesophageal SCCs and skin SCCs with the NRF2 mutations showed increased NRF2 expression in the nuclei. However, none of the SCCs from oesophagus and skin harboured KEAP1 mutation. Our study demonstrated here that NRF2 mutation occurs not only in lung and head/neck cancers, but also in oesophageal and skin cancers. Our data suggest that the NRF2 mutation plays a role in the development of SCC and is a feature of SCC.
Neuromodulation for the Treatment of Lower Urinary Tract Symptoms (2015)

Neuromodulation therapy incorporates electrical stimulation to target specific nerves that control lower urinary tract symptoms (LUTS). The objectives of this article are to review the mechanism of action, the type of neuromodulation, and the efficacy of neuromodulation mainly according to the results of randomized controlled trials. Neuromodulation includes pelvic floor electrical stimulation (ES) using vaginal, anal and surface electrodes, interferential therapy (IF), magnetic stimulation (MS), percutaneous tibial nerve stimulation, and sacral nerve stimulation (SNS). The former four stimulations are used for external periodic (short-term) stimulation, and SNS are used for internal, chronic (long-term) stimulation. All of these therapies have been reported to be effective for overactive bladder or urgency urinary incontinence. Pelvic floor ES, IF, and MS have also been reported to be effective for stress urinary incontinence. The mechanism of neuromodulation for overactive bladder has been reported to be the reflex inhibition of detrusor contraction by the activation of afferent fibers by three actions, i.e., the activation of hypogastric nerve, the direct inhibition of the pelvic nerve within the sacral cord and the supraspinal inhibition of the detrusor reflex. The mechanism of neuromodulation for stress incontinence is contraction of the pelvic floor muscles through an effect on the muscle fibers as well as through the stimulation of pudendal nerves. Overall, cure and improvement rates of these therapies for urinary incontinence are 30-50, and 60-90% respectively. MS has been considered to be a technique for stimulating nervous system noninvasively. SNS is indicated for patients with refractory overactive bladder and urinary retention.
Protocol implementation on the Nectar Communication Processor (1990)

We have built a high-speed local-area network called Nectar that uses programmable communication processors as host interfaces. In contrast to most protocol engines, our communication processors have a flexible runtime system that supports multiple transport protocols as well as application-specific activities. In particular, we have implemented the TCP/IP protocol suite and Nectar-specific communication protocols on the communication processor. The Nectar network currently has 25 hosts and has been in use for over a year.
Role of the Oral Microflora in Health (2000)

AbstractThe mouth contains both distinct mucosal (lips, cheek, tongue, palate) and, uniquely, non-shedding surfaces (teeth) for microbial colonisation. Each surface harbours a diverse but characteristic microflora, the composition and metabolism of which is dictated by the biological properties of each site. The resident oral microflora develops in an orderly manner via waves of microbial succession (both autogenic and allogenic). Pioneer species (many of which are sIgA protease-producing streptococci) colonise saliva-coated surfaces through specific stereo-chemical, adhesin-receptor interactions. The metabolism of these organisms modifies local environmental conditions, facilitating subsequent attachment and growth by later, and more fastidious, colonisers. Eventually, a stable biofilm community develops, that plays an active role in (a) the normal development of the physiology of the habitat, and (b) the innate host defences (colonisation resistance). Thus, when considering treatment options, clinicians should be aware of the need to maintain the beneficial properties of the resident oral microflora.
Die Überführung der Shikimisäure in Chinasäure (1953)

Abstract Das Eykmansche Dibromid der Shikimisäure hat Chinasäure‐Konfiguration. Es liefert bei der Behandlung mit Silbercarbonat ohne Waldensche Umkehrung das Lacton der 6‐Brom‐chinasäure, welches sich katalytisch zu Chinasäure reduzieren läßt.
No Difference in Cerebral Glucose Metabolism in Patients With Alzheimer Disease and Differing Apolipoprotein E Genotypes (1997)

The APOE epsilon 4 allele does not appear to be associated with specific deficits in brain metabolism in patients with AD despite evidence that the epsilon 4 allele is associated with preclinical alterations. This finding is consistent with previous epidemiologic results that have demonstrated a higher risk for AD in carriers of the epsilon 4 allele, but no change in the rate of progression of AD.
Machining Oxide Thin Films with an Atomic Force Microscope: Pattern and Object Formation on the Nanometer Scale (1992)

An atomic force microscope (AFM) has been used to machine complex patterns and to form free structural objects in thin layers of MoO(3) grown on the surface of MoS(2). The AFM tip can pattern lines with </=10-nanometer resolution and then image the resulting structure without perturbation by controlling the applied load. Distinct MoO(3) structures can also be defined by AFM machining, and furthermore these objects can be manipulated on the MoS(2) substrate surface with the AFM tip. These results suggest application to nanometer-scale diffraction gratings, high-resolution lithography masks, and possibly the assembly of nanostructures with novel properties.
What Is Usability in the Context of the Digital Library and How Can It Be Measured (2005)

This paper reviews how usability has been defined in the context of the digital library, what methods have been applied and their applicability, and proposes an evaluation model and a suite of instruments for evaluating usability for academic digital libraries. The model examines effectiveness, efficiency, satisfaction, and learnability. It is found that there exists an interlocking relationship among effectiveness, efficiency, and satisfaction. It also examines how learnability interacts with these three attributes.
Autologous Bladder Mucosa Graft for Urethral Substitution (1987)

Bladder mucosa was used to construct a neourethra in 32 children. Twenty-five of them had had previous failed surgery for hypospadias and seven had severe congenital defects of the urethra. A satisfactory functional and cosmetic result was achieved in 30 patients.
Premyelinating Oligodendrocytes in Chronic Lesions of Multiple Sclerosis (2002)

Premyelinating oligodendrocytes are present in chronic lesions of multiple sclerosis, so remyelination is not limited by an absence of oligodendrocyte progenitors or their failure to generate oligodendrocytes. Our findings suggest that in the chronic lesions of multiple sclerosis, the axons are not receptive for remyelination. Understanding the cellular interactions between premyelinating oligodendrocytes, axons, and the microenvironment of lesions of multiple sclerosis may lead to effective strategies for enhancing remyelination.
Exosomes: New players in cancer (2017)

The past decade has witnessed an exponential increase in research on exosomes. For many years considered to be extracellular debris, exosomes are now considered important mediators in intercellular communication. The capability of exosomes to transfer proteins, DNA, mRNA, as well as non-coding RNAs has made them an attractive focus of research into the pathogenesis of different diseases, including cancer. Increasing evidence suggests that tumor cells release a large sum of exosomes, which may not only influence proximal tumor cells and stromal cells in local microenvironment, but also can exert systemic effects when participating in blood circulation. In this study, we review the current understanding on this topic. The literature outlines two broad facets of exosomes in cancer: 1) promotion of tumor growth, tumorigenesis, tumor angiogenesis, tumor immune escape, drug resistance, and metastasis and 2) their role as promising biomarkers for cancer diagnosis and even as potential treatment targets for cancer patients.
Penetration of ertapenem into skeletal muscle and subcutaneous adipose tissue in healthy volunteers measured by in vivo microdialysis (2006)

These results support the previously observed clinical efficacy of ertapenem in the treatment of SSSI.
Nonuniform recombination within the human beta-globin gene cluster. (1984)

Population genetic analysis of 15 restriction site polymorphisms demonstrates nonuniform recombination within the human beta-globin gene cluster. These DNA polymorphisms show two clusters of high nonrandom associations, one 5' and another 3' to the beta-globin structural gene, with no significant linkage disequilibrium between the two clusters. The 5'- and 3'-association clusters are 34.6 kilobases (kb) and 19.4 kb long, respectively, and are separated by 9.1 kb of DNA immediately 5' to the beta-globin gene. For each of these three DNA regions, we have observed a relationship between nonrandom associations and physical distance between the polymorphisms. However, this relationship differed for each of these regions. On the assumption that the effective population size (Ne) is 5,000-50,000, we estimate the total recombination rate to be 0.0017%-0.0002% in the 5' cluster, 0.0931%-0.0093% in the 3' cluster, and 0.2912%-0.0219% in the 9.1-kb region between them. The beta cluster thus shows nonuniformity in recombination. Moreover, the recombination rate in the 9.1-kb DNA segment is 3-30 times greater than expected and is thus a hot spot for meiotic recombination.
Sequence of 2,617 nucieotides from the 3′ end of Newcastle disease virus genome RNA and the predicted amino acid sequence of viral NP protein (1986)

DNA fragments complementary to the Newcastle disease virus genome (strain D26) were cloned and sequenced. The sequence of 2,617 nucleotides from the 3' end of the genome was determined and an open reading frame (OP-1) consisting of 1,467 nucleotides, most likely encoding NP protein, was found in this region. This was followed by a second unfinished open reading frame (OP-2) of at least 729 nucleotides which continued beyond the 2,617th nucleotide. Another relatively short (312 nucleotides long) open reading frame (OP-2') was found overlapping with OP-2, but its significance is still unclear. The amino acid sequence deduced from the nucleotide sequence of OP-1 showed a moderate homology to that of the NP protein of Sendai virus in the central portion of the peptide. The leader sequence of 53 nucleotides was also identified. The 5' end of mRNAs synthesized in the infected cells was analyzed and found to be m7GpppA, suggesting that the transcription of viral mRNAs starts with A, but not with G residue.