gebhart/patrepeval huggingface dataset:
Induction of DNA Double-Strand Breaks by Electroporation of Restriction Enzymes into Mammalian Cells (2003)

The introduction of restriction endonucleases into mammalian cells in culture provides a unique method for introducing double-strand breaks (DSBs) into the DNA of the host cell. Restriction enzymes recognize, bind, and cleave specific DNA sequences to produce a DNA DSB in the absence of other types of DNA damage. Not only is the DSB the only lesion produced in DNA, but the type of break (i.e., whether it has blunt ends or cohesive ends with 3′- or 5′-overhangs), the nucleotide sequences at the break site, and in certain instances, the precise chromosomal location of the induced break are also known. Once inside a cell, restriction enzymes are extremely efficient inducers of DSBs as measured by pulsed-field gel electrophoresis () and neutral filter elution (). Consequently, the introduction of restriction enzymes into cells has been used to investigate the biological consequences of DSBs in the genome at the molecular, cytogenetic, and cellular level. At the molecular level, the rejoining of DSBs with known end structure has been investigated (), and although it is not possible to determine the frequency of faithfully repaired DSBs, Phillips and Morgan () were able to describe unambiguously illegitimate recombination events occurring within the chromosome. At the cellular level, restriction enzyme-induced DSBs lead to mutations (,), chromosome rearrangements (, , , ), gene amplification () and cell killing (,). Interestingly, restriction enzymes do not induce delayed chromosomal instability, suggesting that DSBs are not the signal responsible for initiating this process ().
Project Summary of the NREL Amorphous Silicon Team (2003)

The Amorphous Silicon Team at NREL has improved the properties of many materials, increased solar cell device performance, and improved the fundamental understanding of thin-film silicon based materials and devices since the last NCPV Program Review Meeting. In this paper we present a summary of the work of the team since that last meeting.
Leveraging 3D Technology for Improved Reliability (2007)

Aggressive technology scaling over the years has helped improve processor performance but has caused a reduc- tion in processor reliability. Shrinking transistor sizes and lower supply voltages have increased the vulnerability of computer systems towards transient faults. An increase in within-die and die-to-die parameter variations has also led to a greater number of dynamic timing errors. A potential solution to mitigate the impact of such errors is redundancy via an in-order checker processor. Emerging 3D chip technology promises increased pro- cessor performance as well as reduced power consump- tion because of shorter on-chip wires. In this paper, we leverage the snap-on functionality provided by 3D inte- gration and propose implementing the redundant checker processor on a second die. This allows manufacturers to easily create a family of reliable processors without sig- nificantly impacting the cost or performance for customers that care less about reliability. We comprehensively eval- uate design choices for this second die, including the ef- fects of L2 cache organization, deep pipelining, and fre- quency. An interesting feature made possible by 3D inte- gration is the incorporation of heterogeneous process tech- nologies within a single chip. We evaluate the possibility of providing redundancy with an older process technology, an unexplored and especially compelling application of die heterogeneity. We show that with the most pessimistic as- sumptions, the overhead of the second die can be as high as either a 7 °C temperature increase or a 8% performance loss. However, with the use of an older process, this over- head can be reduced to a 3 °C temperature increase or a 4% performance loss, while also providing higher error re- silience. Keywords: reliability, redundant multi-threading, 3D die-stacking, parameter variation, soft errors, dynamic timing errors, power-efficient microarchitecture, on-chip temperature.
A novel gene which is up-regulated during colon epithelial cell differentiation and down-regulated in colorectal neoplasms. (1997)

To identify new molecular markers for differentiation of normal and neoplastic colon epithelium, we have studied changes in gene expression during the in vitro differentiation of the HT29-D4 colon carcinoma cell line. Using a modified differential display procedure, we cloned a novel cDNA, designated differentiation-related gene 1 (Drg1). Drg1 mRNA has a length of approximately 3 kb and is induced approximately 20-fold during in vitro differentiation of the colon carcinoma cell lines HT29-D4 and Caco-2. The absence of Drg1 induction in growth-inhibited A431 epidermoid carcinoma cells indicates that Drg1 up-regulation in colon carcinoma cells is not a result of decreased proliferation. The Drg1 cDNA contains an open-reading frame of 1182 bp that encodes a protein with a predicted molecular weight of 43 kd. Drg1 mRNA is expressed most prominently in placental membranes and prostate, kidney, small intestine, and ovary tissues. Compared to normal colon mucosa, Drg1 mRNA expression is decreased in colon adenomas and adenocarcinomas. An antiserum raised against recombinant Drg1 protein detected a band of the expected size in Western blots. Immunohistochemistry showed that in normal colon Drg1 protein is expressed in the cytoplasm and basolateral membranes of surface epithelial cells that border the gut lumen, indicating that Drg1 protein is expressed late during differentiation, just before apoptosis and shedding of cells into the colon lumen.
Immunization of allogeneic bone marrow transplant recipients with tumor cell vaccines enhances graft-versus-tumor activity without exacerbating graft-versus-host disease (2000)

Allogeneic bone marrow transplantation (BMT) induces 2 closely associated immune responses: graft-versus-tumor (GVT) activity and graft-versus-host disease (GVHD). We have previously shown that pretransplant immunization of allogeneic BMT donors with a recipient-derived tumor cell vaccine increases both GVT activity and lethal GVHD because of the priming of donor T cells against putative minor histocompatibility antigens (mHAgs) on the tumor vaccine cells. The work reported here tested the hypothesis that tumor cell vaccination after BMT would produce an increase in GVT activity without exacerbating GVHD. C3H.SW donor bone marrow and splenocytes were transplanted into major histocompatibility complex-matched, mHAg-mismatched C57BL/6 recipients. One month after BMT, recipients were immunized against either a C57BL/6 myeloid leukemia (C1498) or fibrosarcoma (205). Immunized recipients had a significant increase in survival and protection against tumor growth in both tumor models, and significant tumor protection was seen even in recipients with preexisting micrometastatic cancer before immunization. Alloreactivity appeared to contribute to the in vitro anti-tumor cytolytic activity, but in vivo immunity was tumor specific, and no exacerbation of GVHD was observed. Although the immunodominant mHAg B6(dom1) was shown to be expressed by all B6 tumors tested and was largely responsible for the alloreactivity resulting from tumor immunization of donors, the in vitro alloreactivity of immune recipients was more restricted and was not mediated by recognition of B6(dom1). In conclusion, post-transplant tumor immunization of allogeneic BMT recipients against either a leukemia or a solid tumor can increase GVT activity and survival without exacerbating GVHD.
The International Classification System and the Progression of Age-Related Macular Degeneration (2009)

Overall, progression from earlier stages of AMD to either of the two forms of advanced AMD were reflected accurately by the IC grading in the vast majority of cases.
Quassinoid synthesis. 2. Preparation of a tetracyclic intermediate having the bruceantin tetrahydrofuran ring (1987)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTQuassinoid synthesis. 2. Preparation of a tetracyclic intermediate having the bruceantin tetrahydrofuran ringSean M. Kerwin, Axel G. Paul, and Clayton H. HeathcockCite this: J. Org. Chem. 1987, 52, 9, 1686–1695Publication Date (Print):May 1, 1987Publication History Published online1 May 2002Published inissue 1 May 1987https://pubs.acs.org/doi/10.1021/jo00385a008https://doi.org/10.1021/jo00385a008research-articleACS PublicationsRequest reuse permissionsArticle Views1253Altmetric-Citations33LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Effect of Recombinant Human Bone Morphogenetic Protein‐2/Absorbable Collagen Sponge (rhBMP‐2/ACS) on Healing in 3‐Wall Intrabony Defects in Dogs (2002)

Surgical implantation of rhBMP-2/ACS may be used safely to support regeneration of alveolar bone in intrabony periodontal defects in dogs without aberrant events such as root resorption or ankylosis complicating the regenerative procedure. rhBMP-2/ACS does not appear to have a significant effect on cementum regeneration and formation of a functional periodontal ligament in this model.
Increased cortical porosity in type 2 diabetic postmenopausal women with fragility fractures (2012)

The primary goal of this study was to assess peripheral bone microarchitecture and strength in postmenopausal women with type 2 diabetes with fragility fractures (DMFx) and to compare them with postmenopausal women with type 2 diabetics without fractures (DM). Secondary goals were to assess differences in nondiabetic postmenopausal women with fragility fractures (Fx) and nondiabetic postmenopausal women without fragility fractures (Co), and in DM and Co women. Eighty women (mean age 61.3 ± 5.7 years) were recruited into these four groups (DMFx, DM, Fx, and Co; n = 20 per group). Participants underwent dual-energy X-ray absorptiometry (DXA) and high-resolution peripheral quantitative computed tomography (HR-pQCT) of the ultradistal and distal radius and tibia. In the HR-pQCT images volumetric bone mineral density and cortical and trabecular structure measures, including cortical porosity, were calculated. Bone strength was estimated using micro-finite element analysis (µFEA). Differential strength estimates were obtained with and without open cortical pores. At the ultradistal and distal tibia, DMFx had greater intracortical pore volume (+52.6%, p = 0.009; +95.4%, p = 0.020), relative porosity (+58.1%, p = 0.005; +87.9%, p = 0.011) and endocortical bone surface (+10.9%, p = 0.031; +11.5%, p = 0.019) than DM. At the distal radius DMFx had 4.7-fold greater relative porosity (p < 0.0001) than DM. At the ultradistal radius, intracortical pore volume was significantly higher in DMFx than DM (+67.8%, p = 0.018). DMFx also displayed larger trabecular heterogeneity (ultradistal radius: +36.8%, p = 0.035), and lower total and cortical BMD (ultradistal tibia: -12.6%, p = 0.031; -6.8%, p = 0.011) than DM. DMFx exhibited significantly higher pore-related deficits in stiffness, failure load, and cortical load fraction at the ultradistal and distal tibia, and the distal radius than DM. Comparing nondiabetic Fx and Co, we only found a nonsignificant trend with increase in pore volume (+38.9%, p = 0.060) at the ultradistal radius. The results of our study suggest that severe deficits in cortical bone quality are responsible for fragility fractures in postmenopausal diabetic women.
Regulation and Function of Insulin-Like Growth Factor-Binding Protein-1 (1993)

Insulin-like growth factor-binding protein (IGFBP)-1 is one of six homologous proteins that specifically bind and modulate the mitogenic and metabolic actions of insulin-like growth factor (IGF)-I and IGF-II. Of the six IGFBP, IGFBP-1 is the only one that displays rapid dynamic regulation in vivo, with serum levels varying 10-fold or more in relation to meals. The complementary cDNA for IGFBP-1 was first reported in 1988. The predicted 234-amino acid sequence has a molecular mass of 25.3 kDa. The N-terminal and C-terminal regions are highly homologous among rat, human, and bovine sequences, and contain 18 conserved cysteines which are postulated to provide a framework for ligand binding. The 65-residue midregion is less homologous and does not contain cysteines, but does include a Pro-Glu-Ser-Thr (PEST) domain that is typical of rapidly metabolized proteins. The gene for IGFBP-1 has been localized to human chromosome region 7p12-p14, where it is contiguous with the gene for IGFBP-3. IGFBP-1 mRNA and protein expression have been identified in human liver and uterine decidua, and in nonhuman kidney. In vitro and in vivo studies indicate that insulin is the primary regulator of IGFBP-1 expression in these tissues, and that the primary effect of insulin is rapid inhibition of transcription. On the other hand, cortisol, glucagon, and cAMP stimulate IGFBP-1 production. Limited data also show a potent stimulatory effect of phorbol esters. A detailed review of IGFBP-1 levels and physiology in vivo and in vitro is presented. The function of IGFBP-1 is not completely defined. However, several studies demonstrate that IGFBP-1 inhibits IGF binding to cell surface receptors and thereby inhibits IGF-mediated mitogenic and cell metabolic actions. Furthermore, IGFBP-1 regulation by insulin and glucoregulatory hormones in vitro and limited in vivo data are consistent with a role for IGFBP-1 in glucose counterregulation.
Infant mortality statistics from the 1999 period linked birth/infant death data set. (2002)

In general, mortality rates were lowest for infants born to Chinese and Japanese mothers (2.9 and 3.4 per 1,000, respectively). Infants of Cuban, Central and South American, Mexican, and non-Hispanic white mothers had low rates, while rates were higher for infants of Puerto Rican and highest for non-Hispanic black mothers (13.9). Filipino mothers also had low rates. Rates were high for infants of Hawaiian and American Indian mothers. Infant mortality rates were higher for those infants whose mothers had no prenatal care, were teenagers, had 9-11 years of education, were unmarried, or smoked during pregnancy. Infant mortality was also higher for male infants, multiple births, and infants born preterm or at low birthweight. The three leading causes of infant death--Congenital malformations, low birthweight, and Sudden infant death syndrome (SIDS)--taken together accounted for 45 percent all infant deaths in the United States in 1999. Cause-specific mortality rates varied considerably by race and Hispanic origin. For infants of black mothers, the infant mortality rate for low birthweight was four times that for white mothers. For infants of American Indian mothers, the SIDS rate was 2.4 times that for non-Hispanic white mothers. SIDS rates for infants of Hispanic and Asian or Pacific Islander mothers, were 40-50 percent lower than those for non-Hispanic white mothers.
Trimmomatic: a flexible trimmer for Illumina sequence data (2014)

Supplementary data are available at Bioinformatics online.
Identification of mutator genes and mutational pathways in Escherichia coli using a multicopy cloning approach (2004)

We searched for genes that create mutator phenotypes when put on to a multicopy plasmid in Escherichia coli. In many cases, this will result in overexpression of the gene in question. We constructed a random shotgun library with E. coli genomic fragments between 3 and 5 kbp in length on a multicopy plasmid vector that was transformed into E. coli to screen for frameshift mutators. We identified a total of 115 independent genomic fragments that covered 17 regions on the E. coli chromosome. Further studies identified 12 genes not previously known as causing mutator phenotypes when overproduced. A striking finding is that overproduction of the multidrug resistance transcription regulator, EmrR, results in a large increase in frameshift and base substitution mutagenesis. This suggests a link between multidrug resistance and mutagenesis. Other identified genes include those encoding DNA helicases (UvrD, RecG, RecQ), truncated forms of the DNA mismatch repair protein (MutS) and a primosomal component (DnaT), a negative modulator of initiation of replication/GATC-binding protein (SeqA), a stationary phase regulator AppY, a transcriptional regulator PaaX and three putative open reading frames, ycgW, yfjY and yjiD, encoding hypothetical proteins. In addition, we found three genes encoding proteins that were previously known to cause mutator effects under overexpression conditions: error-prone polymerase IV (DinB), DNA methylase (Dam) and sigma S factor (RpoS). This genomic strategy offers an approach to identify novel mutator effects resulting from the multicopy cloning (MCC) of specific genes and therefore complementing the conventional gene inactivation approach to finding mutators.
Epinephrine-induced potentially lethal arrhythmia during arthroscopic shoulder surgery: a case report. (1999)

Arthroscopic shoulder surgery performed on a healthy female could have resulted in a fatal outcome when the epinephrine present in the arthroscopic irrigating solution contributed to the onset of ventricular tachycardia requiring defibrillation during surgery. During this procedure, the shoulder was infiltrated with 30 mL of a 1:100,000 solution of epinephrine into the subacromial space and glenhumeral joint. Subsequently, instrumentation of the glenhumeral joint by the orthopedic surgeon with a standard arthroscopy trocar resulted in a 0.5-cm size lesion to the posterior humeral cortex. Minutes after the start of the surgical procedure, the patient displayed an abrupt onset of ventricular tachycardia and hypertension. These signs and symptoms suggested an intraosseous infusion of both infiltrated and irrigation solution containing epinephrine through the lesion in the humeral cortex. Approximately 800 mL of a .01 mg/mL concentration of irrigation solution containing epinephrine was used. A diagnosis of epinephrine-induced ventricular tachycardia was made. The arthroscopic irrigating solution was immediately discontinued and lidocaine, 100 mg intravenously, was administered; however, the patient's cardiac rhythm degenerated into a sustained ventricular tachycardia that was unresponsive to pharmacologic intervention. A full code was called; the surgeon, anesthesia team, and operating room personnel succesfully provided advanced cardiac life support and cardioverted the patient back into a sinus rhythm with no untoward effects.
Irinotecan plus Fluorouracil and Leucovorin for Metastatic Colorectal Cancer (2000)

Weekly treatment with irinotecan plus fluorouracil and leucovorin is superior to a widely used regimen of fluorouracil and leucovorin for metastatic colorectal cancer in terms of progression-free survival and overall survival.
Ordered Interstrand and Intrastrand DNA Transfer During Reverse Transcription (1988)

Retroviruses contain two copies of the plus stranded viral RNA genome. As a means of determining whether both of these RNA's are used in the reverse transcription reaction, cells were infected with heterozygous virus particles that varied in nucleotide sequence at two separate locations at the RNA termini. The DNA proviruses formed from a single cycle of reverse transcription were then examined. Of the 12 proviruses that were characterized, all exhibited long terminal repeats (LTR's) that would be expected to arise only if both RNA templates were used for the generation of minus strand DNA. In contrast, only a single minus strand DNA appeared to be used as template for the plus strand DNA in the generation of fully double-stranded viral DNA. These results indicate that the first strand transfer step in reverse transcription is an intermolecular event while that of the second transfer is intramolecular. Thus, retroviruses contain two functionally active RNA's, and both may be required for the generation of a single linear DNA molecule. Formation of heterozygotes during retrovirus infection would be expected to result in the efficient generation of LTR recombinants.
Characterization of two cis-acting DNA elements involved in the androgen regulation of the probasin gene. (1993)

The location and sequence of androgen responsive elements (AREs) in the 5'-flanking DNA of the androgen-regulated rat probasin (PB) gene were determined. The DNA- and steroid-binding domains of the rat androgen receptor [glutathione-S-transferase (GST)-AR1] and the DNA-binding domain and hinge region alone (GST-AR2) were expressed in Escherichia coli as isopropyl-B-D-thioglactopyranoside-induced fusion proteins with GST and purified using glutathione affinity chromatography. Band shift assays indicated that the AR1 peptide was at least five times more effective than AR2 in binding to PB 5'-flanking DNA (-426 to +28), although both gave qualitatively similar patterns and were displaced by anti-AR antibodies. DNase I footprinting experiments revealed two putative AREs: one between positions -236 and -223 (ARE-1) and the other between -140 and -117 (ARE-2). Hormonal regulation of PB was determined by cotransfecting reporter constructions containing the PB 5'-flanking region (-426 to +28) linked to the bacterial chloramphenicol acetyl transferase (CAT) gene with androgen, glucocorticoid, or progesterone receptor expression vectors into human prostatic carcinoma cells (PC-3). PB-CAT gene expression was more effectively induced by androgens than by glucocorticoids or progestins. Both 5'- and 3'-deletion mapping of the PB 5'-flanking DNA revealed that ARE-1 and ARE-2 were required for androgen regulation. A single base mutation in either ARE resulted in a more than 95% loss of androgen induction of CAT. In comparable transfection experiments, the PB hormone-responsive elements showed a greater induction by androgens than did mouse mammary tumor virus or tyrosine aminotransferase elements. Thus, the preferential androgen regulation of the PB gene involves the participation of two different cis-acting DNA elements that bind AR.
Overlapping section coverage in multisection imaging (1993)

A method is proposed in which the section position for two-dimensional Fourier transform multisection imaging is advanced from one phase-encoding step to the next, so that information is sampled continuously over the total volume under observation. This "ramp scan" technique allows reconstruction of images from any arbitrary position within the sampled volume. The imaging properties depend strongly on the order of distribution of phase-encoding steps to the different section positions. In practice, images are reconstructed at each nominal position of a multisection experiment, plus at each position halfway between sections. The volume under study is thus represented by overlapping sections. The gaps between sections that arise in conventional multisection imaging--even with optimized pulse shapes--are thus avoided. This approach is applicable not only to conventional spin-echo imaging but to other techniques such as RARE (rapid acquisition with relaxation enhancement) and gradient-echo and echo-planar imaging.