gebhart/patrepeval huggingface dataset:
A Flexible Kernel for Adaptive Mesh Refinement on GPU (2007)

Abstract We present a flexible GPU kernel for adaptive on‐the‐fly refinement of meshes with arbitrary topology. By simply reserving a small amount of GPU memory to store a set of adaptive refinement patterns, on‐the‐fly refinement is performed by the GPU, without any preprocessing nor additional topology data structure. The level of adaptive refinement can be controlled by specifying a per‐vertex depth‐tag, in addition to usual position, normal, color and texture coordinates. This depth‐tag is used by the kernel to instanciate the correct refinement pattern, which will map a refined connectivity on the input coarse polygon. Finally, the refined patch produced for each triangle can be displaced by the vertex shader, using any kind of geometric refinement, such as Bezier patch smoothing, scalar valued displacement, procedural geometry synthesis or subdivision surfaces. This refinement engine does neither require multipass rendering nor any use of fragment processing nor special preprocess of the input mesh structure. It can be implemented on any GPU with vertex shading capabilities.
Thermally Induced Structural Evolution and Performance of Mesoporous Block Copolymer-Directed Alumina Perovskite Solar Cells (2014)

Structure control in solution-processed hybrid perovskites is crucial to design and fabricate highly efficient solar cells. Here, we utilize in situ grazing incidence wide-angle X-ray scattering and scanning electron microscopy to investigate the structural evolution and film morphologies of methylammonium lead tri-iodide/chloride (CH3NH3PbI(3-x)Cl(x)) in mesoporous block copolymer derived alumina superstructures during thermal annealing. We show the CH3NH3PbI(3-x)Cl(x) material evolution to be characterized by three distinct structures: a crystalline precursor structure not described previously, a 3D perovskite structure, and a mixture of compounds resulting from degradation. Finally, we demonstrate how understanding the processing parameters provides the foundation needed for optimal perovskite film morphology and coverage, leading to enhanced block copolymer-directed perovskite solar cell performance.
Human thymine-DNA glycosylase maps at chromosome 12q22-q24.1: a region of high loss of heterozygosity in gastric cancer. (1997)

Spontaneous hydrolytic deamination of 5-methylcytosine leads to T:G mismatches in double-stranded DNA and comprises a major threat for the integrity of both the DNA primary sequence as well as the epigenetic information stored in the DNA methylation pattern. Failure of the cellular DNA repair machinery to recognize and repair such mismatched nucleotides can lead to a mutator phenotype and subsequent carcinogenesis. A thymine-DNA glycosylase (TDG) has been described that initiates T:G mismatch repair by specifically excising the mismatched T. We have studied the TDG genomic locus and the expression of this enzyme to evaluate its role in cancer development. TDG is highly expressed in thymus and is expressed at lower levels in all human tissues analyzed. The TDG gene has 10 exons covering a region of >25 kb and is located on chromosome 12q22-q24.1. Because gastric tumors have been shown to contain a high percentage of C-->T mutations at CpG sites, we used a microsatellite found in intron 8 of the TDG locus to screen gastric tumor samples for loss of heterozygosity. Although our analysis showed loss of heterozygosity in 10 of 24 samples (42%), none of those tumor samples revealed a mutation in the coding sequence of the remaining TDG allele as analyzed by single-strand conformational polymorphism. Expression of the TDG was not determined because of the limited availability of RNA in these primary tumor samples. At present, we have found no evidence that TDG is central to the development of gastric cancer, limiting the importance of TDG in T:G mismatch repair and subsequent carcinogenesis.
Translation of NRF mRNA Is Mediated by Highly Efficient Internal Ribosome Entry (2000)

The ubiquitous transcription factor NRF (NF-kappaB repressing factor) is a constitutive transcriptional silencer of the multifunctional cytokine interferon-beta. NRF mRNA contains a long 5' untranslated region (5'UTR) predicted to fold into a strong secondary structure. The presence of stable hairpins is known to be incompatible with efficient translation by ribosomal scanning. Using dicistronic reporter gene constructs, we show that the NRF 5'UTR acts as an internal ribosome entry site (IRES) which directs ribosomes to the downstream start codon by a cap-independent mechanism. The relative activity of this IRES in various cell lines is at least 30-fold higher than that of picornaviral IRESs. The NRF 5'UTR also functions as a translational enhancer in the context of monocistronic mRNAs. Our results indicate that the NRF 5'UTR contains a highly potent IRES, which may allow for an alternate mode of translation under physiological conditions in which cap-dependent translation is inhibited.
Construction of a poliovirus type 1/type 2 antigenic hybrid by manipulation of neutralization antigenic site II (1989)

There are three serotypes of poliovirus, poliovirus type 1 (PV-1), PV-2, and PV-3. These viruses each display four distinct neutralization antigenic sites, designated N-AgI, N-AgII, N-AgIIIA, and N-AgIIIB. It has been demonstrated previously that part of N-AgI can be replaced with heterogeneous amino acid sequences, resulting in hybrid viruses expressing heterogeneous antigenic determinants. To study whether hybrid viruses could be constructed by modifying another antigenic site, a part of N-AgII (amino acids 158 to 173 of VP2) of PV-1(Mahoney) was replaced with the equivalent sequence from PV-2(Lansing). The resulting hybrid was viable and expressed both PV-1 and PV-2 antigenic determinants. When inoculated into rabbits, the hybrid induced neutralizing antibodies against both PV-1 and PV-2, showing that amino acids 158 to 173 of VP2 are able to function as an antigenic site independent of the rest of N-AgII. Manipulation of N-AgII represents a useful alternative method for the production of hybrid polioviruses.
Role of the C5a receptor (C5aR) in acute and chronic dextran sulfate-induced models of inflammatory bowel disease (2009)

C5aR exerts detrimental functions in acute colitis, strongly supporting the idea that a C5aR-antagonist might be useful for IBD treatment. However, since the absence of C5aR was no longer protective and in some regards disadvantageous in chronic IBD, future studies should address the efficacy and the possible side effects of a sustained antagonist treatment.
Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice (1990)

Pancreatic islets from SJL/J mice infected with the D variant of encephalomyocarditis virus (EMC-D virus) showed lymphocytic infiltration with moderate to severe destruction of beta cells. Immunohistochemical staining of the islet sections with several monoclonal antibodies, anti-Mac-1, anti-Mac-2, and F4/80 for macrophages, anti-L3T4 for helper/inducer T cells, and anti-Lyt2 for cytotoxic/suppressor T cells revealed that the major population of infiltrating cells at the early stage of viral infection was Mac-2-positive macrophages. In contrast, macrophages detected by anti-Mac-1 and F4/80 monoclonal antibodies were not found at the early stage of viral infection but were found at intermediate and late stages of viral infection. Helper/inducer T cells and cytotoxic/suppressor T cells also infiltrated the islets at intermediate and late stages of viral infection. Short-term treatment of mice with silica prior to viral infection resulted in an enhancement of beta-cell destruction, leading to the development of diabetes. In contrast, long-term treatment of mice with silica resulted in complete prevention of diabetes caused by a low dose of viral infection and a significant decrease in the incidence of diabetes caused by an intermediate or high dose of viral infection. Furthermore, depletion of macrophages by a specific monoclonal antibody (anti-Mac-2) resulted in a much greater decrease in the incidence of diabetes caused by an intermediate dose of viral infection. However, suppression of helper/inducer T cells and cytotoxic/suppressor T cells, by anti-L3T4 and anti-Lyt2 antibodies, respectively, did not alter the incidence of diabetes. On the basis of these data, it is concluded that macrophages, particularly Mac-2-positive macrophages, play a crucial role in the process of pancreatic beta-cell destruction at the early stage of encephalomyocarditis D virus infection in SJL/J mice.
Advanced Public Transportation Systems: The State of the Art Update 2006 (2005)

This report is the latest in a series of State-of-the-Art reports, the last of which was published in December 2000. It contains the results of a high-level scan of the extent and character of the adoption and use of advanced technology in the provision of public transportation services in North America. The objective of this effort was to provide a useful and timely reference on the subject of emerging Transit Intelligent Transportation System (ITS) technological advances and trends, and make the information available to public transportation professionals. The report is intended to provide up to date information on the current deployment status of transit ITS technologies, provide lessons learned based on deployment experiences, and promote understanding of future trends in Advanced Public Transportation Systems (APTS).
Development of a Quantitative Methylation-Specific Polymerase Chain Reaction Method for Monitoring Beta Cell Death in Type 1 Diabetes (2012)

DNA methylation is a mechanism by which cells control gene expression, and cell-specific genes often exhibit unique patterns of DNA methylation. We previously reported that the mouse insulin-2 gene (Ins2) promoter has three potential methylation (CpG) sites, all of which are unmethylated in insulin-producing cells but methylated in other tissues. In this study we examined Ins2 exon 2 and found a similar tissue-specific methylation pattern. These methylation patterns can differentiate between DNA from insulin-producing beta cells and other tissues. We hypothesized that damaged beta cells release their DNA into circulation at the onset of type 1 diabetes mellitus (T1DM) and sought to develop a quantitative methylation-specific polymerase chain reaction (qMSP) assay for circulating beta cell DNA to monitor the loss of beta cells. Methylation-specific primers were designed to interrogate two or more CpG in the same assay. The cloned mouse Ins2 gene was methylated in vitro and used for development of the qMSP assay. We found the qMSP method to be sensitive and specific to differentiate between insulin-producing cells and other tissues with a detection limit of 10 copies in the presence of non-specific genomic DNA background. We also compared different methods for data analysis and found that the Relative Expression Ratio method is the most robust method since it incorporates both a reference value to normalize dayto-day variability as well as PCR reaction efficiencies to normalize between the methylation-specific and bisulfite-specific components of the calculations. The assay was applied in the streptozotocin-treated diabetic mouse model and detected a significant increase in circulating beta cell DNA before the rise in blood glucose level. These results demonstrate that this qMSP assay can be used for monitoring circulating DNA from insulin-producing cells, which will provide the basis for development of assays to detect beta cell destruction in early T1DM.
A Microdissection and Molecular Genotyping Assay to Confirm the Identity of Tissue Floaters in Paraffin-Embedded Tissue Blocks (2003)

Microdissection and genotyping are effective and reliable means to objectively resolve problems of possible floater contamination. Even minute tissue samples provide sufficient DNA template for polymerase chain reaction microsatellite analysis. Because of the potential clinical implications of floaters, we recommend that all suspected floaters that would change a diagnosis from benign to malignant be subjected to genotyping assay to confirm the identity of the floater tissue.
Validation of the ArthroS virtual reality simulator for arthroscopic skills (2014)

The ArthroS™ demonstrated construct validity between novices and experts, but did not demonstrate full face validity. Future improvements should be mainly focused on the development of tactile feedback. It is necessary that a newly presented simulator is validated to prove it actually contributes to proficiency of skills.
Cancer cachexia (1988)

Cancer cachexia describes a syndrome of progressive weight loss, anorexia, and persistent erosion of host body cell mass in response to a malignant growth. Although often associated with preterminal patients bearing disseminated disease, cachexia may be present in the early stages of tumor growth before any signs or symptoms of malignancy. A decline in food intake relative to energy expenditure (which may be increased, normal, or decreased) is the fundamental physiologic derangement leading to cancer-associated weight loss. In addition, abnormalities of host carbohydrate, protein, and fat metabolism lead to continued mobilization and ineffective repletion of host tissue, despite adequate nutritional support. Mediators of cancer anorexia and associated abnormalities are unknown. Cachectin/TNF or other host-derived cytokines (produced as a defense against malignancy) have been implicated as signal molecules in cachexia, based upon similar metabolic derangements produced by these cytokines in other chronic wasting illnesses. Nutritional support is effective in maintaining body weight of cachectic cancer patients, but ineffective in maintaining lean body mass. Although in one study parenteral nutritional support has improved operative morbidity and mortality in cancer patients, it has not yet improved response to chemotherapy or radiation therapy. Because of metabolic derangements seen in cancer cachexia, effective nutritional treatment regimens will probably require manipulation of host intermediary metabolism in addition to feeding. Insulin therapy or exercise are two such methods which appear to preserve host composition by preferential feeding of the host at the expense of the tumor. Future studies which more clearly define the role of signal molecules in producing cancer cachexia syndrome may lead to new treatment strategies, possibly involving modulation of the effects of such molecules on host metabolism.
Gram-negative sepsis: a dilemma of modern medicine (1993)

Gram-negative sepsis is an increasingly common problem, with up to 300,000 cases occurring each year in the United States alone. Despite the ongoing development of new antibiotics, mortality from gram-negative sepsis remains unacceptably high. To stimulate earlier therapeutic intervention by physicians, a new set of broad definitions has been proposed to define the systemic inflammatory response characteristic of sepsis. In this review, the signs and symptoms of this progressive, injurious process are reviewed and its management is discussed, as are the mechanisms by which bacterial endotoxin triggers the biochemical events that lead to such serious complications as shock, adult respiratory distress syndrome, and disseminated intravascular coagulation. These events often occur even when appropriate antimicrobial therapy has been instituted. An increased understanding of the structure of endotoxin and its role in the development of sepsis, together with advances in hybridoma technology, has led to the development of monoclonal antibodies that bind to endotoxin and significantly attenuate its adverse effects. These agents promise to substantially reduce the morbidity and mortality associated with gram-negative sepsis.
Rate of Pregnancy-Related Relapse in Multiple Sclerosis (1998)

In women with multiple sclerosis, the rate of relapse declines during pregnancy, especially in the third trimester, and increases during the first three months post partum before returning to the prepregnancy rate.
Effect of glycosylation inhibitors on N-glycosylpeptides and on invasion of malignant mouse MO4 cells in vitro (1990)

Cell surface glycans are believed to play a role in tumour invasion and metastasis. Yet, we have previously shown that the inhibitors of N-linked glycan processing swainsonine (SW) and 1-deoxynojirimycin (dNM) did not prevent invasion of chick heart fragments by MO4 murine fibrosarcoma cells in organ culture. We now present biochemical evidence that these and other inhibitors of processing were indeed effective in remodeling glycans, including those expressed at the cell surface. After metabolic labeling with tritiated mannose or fucose, glycosylpeptides were obtained by Pronase treatment of material released from intact cells by trypsin. Glycosylpeptides were separated by Biogel P-10 chromatography. With all drugs tested, there was a shift towards lower molecular weight of the glycan chains. There were, however, major quantitative differences between the different drugs and also, for monensin (MON; 0.1 microgram ml-1), between fucose-labeled and mannose-labeled chains. The shift in apparent molecular weight affected mainly fucose-labeled peptides after treatment of MO4 cells with SW (0.4 microgram ml-1). The shift induced by dNM (10 mM) + SW (0.4 microgram ml-1) in both fucosylated and mannosylated chains was much larger than that induced by SW given alone. 1-Deoxymannojirimycin (dMM; 1 mM) had major effects on both mannose and fucose-labeled structures and so did N-methyl-1-deoxynojirimycin (MdNM; 2 mM) and castanospermine (CS; 100 micrograms ml-1). With the latter drugs, incorporation of fucose in complex-type glycosylpeptides was dramatically reduced. The effect of SW on fucose-labeled glycosylpeptides of embryonic chick heart was similar to that observed on MO4 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Co‐occurring conditions associated with FMR1 gene variations: Findings from a national parent survey (2008)

Parents enrolling in a national survey of families of children with fragile X (FX) reported whether each of their children had been diagnosed or treated for developmental delay or eight conditions frequently associated with FX: attention problems, hyperactivity, aggressiveness, self-injury, autism, seizures, anxiety, or depression. This article reports results for 976 full mutation males, 259 full mutation females, 57 premutation males, and 199 premutation females. Co-occurring conditions were frequently reported for all FMR1 gene variations. The number of co-occurring conditions experienced was strongly associated with parent reports of their child's ability to learn, adaptability, and quality of life. Most individuals with the full mutation experienced multiple co-occurring conditions, with a modal number of 4 for males and 2 for females. Most (>80%) full mutation males and females had been diagnosed or treated for attention problems. Premutation males, when compared with a matched group of non-FX males, were more likely to have been diagnosed or treated for developmental delay, attention problems, aggression, seizures, autism, and anxiety. Premutation females were more likely to have been diagnosed or treated for attention problems, anxiety, depression, and developmental delay. Clusters of conditions were identified, seeming to occur in an additive fashion. Self-injury, autism, and seizures rarely occurred in isolation, but were more likely in individuals who also had problems with attention, anxiety, and hyperactivity. The findings provide a reference point for future studies on the prevalence and nature of co-occurring conditions in FX; suggest the possibility that certain conditions cluster together; provide evidence that male and female carriers experience elevated rates of co-occurring conditions compared with matched groups of non-carrier children; and emphasize the importance of including an assessment of co-occurring conditions in any clinical evaluation of individuals with abnormal variation in the FMR1 gene.
Use of a Peptide Mimotope to Guide the Humanization of MRK-16, an Anti-P-glycoprotein Monoclonal Antibody (1999)

A mimotope-guided strategy for engineering antibodies directed against orphan targets or antigens that are difficult to purify was developed and used to humanize the murine MRK-16 monoclonal antibody (mAb). MRK-16 recognizes a conformational epitope of a 170-kDa membrane protein, termed P-glycoprotein (P-gp). Elevated expression of P-gp on tumor cells is associated with resistance to cytotoxic drugs, a major obstacle in chemotherapy. Murine MRK-16 was used to enrich and screen a phage-displayed peptide library to identify reactive mimotopes. One peptide, termed ALR1, was enriched to a greater extent than others and subsequently was expressed as a fusion protein with glutathione S-transferase. ALR1 fusion protein bound MRK-16 specifically and inhibited binding of MRK-16 to cells expressing elevated levels of P-gp. To humanize MRK-16, the murine complementarity determining regions were grafted onto homologous human heavy and light chain variable region frameworks. Framework residues that differed between the murine MRK-16 and the homologous human templates were analyzed and subsequently, five framework positions potentially important for maintaining the specificity and affinity of MRK-16 were identified. A combinatorial library consisting of 32 variants encoding all possible combinations of murine and human residues at the five differing framework positions was expressed in a phage system. In the absence of purified P-gp, ALR1 fusion protein was used as surrogate antigen to screen the antibody library to identify the framework combination that most preserved the binding activity of the mAb. On the basis of the initial screening against the mimotope four antibody variants were selected for further characterization. The binding affinity of these variants for the ALR1 fusion protein correlated with their binding to cells expressing elevated levels of P-gp. Thus, peptide mimotopes which can be identified for virtually any antibody including those that recognize conformational or carbohydrate epitopes, can serve as antigen templates for antibody engineering.
Reversal of Streptozotocin-induced Hyperglycemia by Transplantation of Pseudoislets Consisting of .BETA. Cells Derived from Ductal Cells (2004)

The present study was conducted in an attempt to treat streptozotocin (STZ)-induced hyperglycemia by transplanting beta cells derived from pancreatic ductal cells. Ductal cells obtained from neonatal rats were cultured in vitro. Approximately 70% of the cells were converted to insulin-secreting cells by incubating with betacellulin and activin A. Differentiated cells responded to a depolarizing concentration of potassium, tolbutamide and a high concentration of glucose, and insulin secretion increased by 2.5-, 2.3- and 1.6-fold, respectively. We then prepared pseudoislets using the differentiated cells, which exhibited greatly improved glucose-responsiveness, with a high concentration of glucose inducing a 3-fold increase in insulin secretion. We transplanted these pseudoislets into the portal vein of STZ-treated nude mice. Before transplantation, the plasma glucose concentration was above 400 mg/dl, and after transplantation it was markedly reduced, the effect of which persisted for two weeks. These results indicate that STZ-induced hyperglycemia can be treated by transplanting pseudoislets consisting of beta cells derived from ductal cells.