gebhart/patrepeval huggingface dataset:
Enzyme immunosorbent assay for Ebola virus antigens in tissues of infected primates (1992)

A sandwich enzyme immunosorbent assay (EIA) using a mixture of mouse monoclonal antibodies for antigen capture and polyclonal hyperimmune rabbit anti-Ebola virus serum for antigen detection was developed and evaluated on the tissues of monkeys naturally or experimentally infected with strains of Ebola viruses. When compared with virus isolation, the antigen detection EIA was both sensitive and specific: 44 of 45 (97.7%) liver homogenates and 38 of 41 (92.7%) spleen homogenates that were culture positive and tested by both techniques were positive for viral antigen, while 85 of 87 (97.7%) culture-negative liver homogenates and 66 of 66 culture-negative spleen homogenates were found to be antigen negative. The assay, initially developed to detect antigens of prototype African strains of Ebola virus, reliably detected related strains of Ebola virus found during two recent outbreaks of Ebola virus infection among imported, quarantined Macaca fascicularis monkeys in the United States. The assay allows economical and rapid testing of large numbers of tissue specimens. Antigen was found in homogenates of spleen and liver and in serum.
An iterative design methodology for user-friendly natural language office information applications (1984)

A six-step, iterative, empirical human factors design methodology was used to develop CAL, a natural language computer application to help computer-naive business professionals manage their personal calendars. Input language is processed by a simple, nonparsing algorithm with limited storage requirements and a quick response time. CAL allows unconstrained English inputs from users with no training (except for a five minute introduction to the keyboard and display) and no manual (except for a two-page overview of the system). In a controlled test of performance, CAL correctly responded to between 86 percent and 97 percent of the storage and retrieval requests it received, according to various criteria. This level of performance could never have been achieved with such a simple processing model were it not for the empirical approach used in the development of the program and its dictionaries. The tools of the engineering psychologist are clearly invaluable in the development of user-friendly software, if that software is to accommodate the unruly language of computer-naive, first-time users. The key is to elicit the cooperation of such users as partners in an iterative, empirical development process.
Targeting the Degradation of Angiotensin II With Recombinant Angiotensin-Converting Enzyme 2 (2009)

Angiotensin (Ang)-converting enzyme 2 (ACE2) cleaves Ang II to form Ang-(1-7). Here we examined whether soluble human recombinant ACE2 (rACE2) can efficiently lower Ang II and increase Ang-(1-7) and whether rACE2 can prevent hypertension caused by Ang II infusion as a result of systemic versus local mechanisms of ACE2 activity amplification. rACE2 was infused via osmotic minipumps for 3 days in conscious mice or acutely in anesthetized mice. rACE2 caused a dose-dependent increase in serum ACE2 activity but had no effect on kidney or cardiac ACE2 activity. After Ang II infusion (40 pmol/min), rACE2 (1 mg/kg per day) resulted in normalization of systolic blood pressure and plasma Ang II. In acute studies, rACE2 (1 mg/kg) prevented the rapid hypertensive effect of Ang II (0.2 mg/kg), and this was associated with both a decrease in Ang II and an increase in Ang-(1-7) in plasma. Moreover, during infusion of Ang II, the effect of rACE2 on blood pressure was unaffected by a specific Ang-(1-7) receptor blocker, A779 (0.2 mg/kg), and infusing supraphysiologic levels of Ang-(1-7) (0.2 mg/kg) had no effect on blood pressure. We conclude that, during Ang II infusion, rACE2 effectively degrades Ang II and, in the process, normalizes blood pressure. The mechanism of rACE2 action results from an increase in systemic, not tissue, ACE2 activity and the lowering of plasma Ang II rather than the attendant increase in Ang-(1-7). Increasing ACE2 activity may provide a new therapeutic target in states of Ang II overactivity by enhancing its degradation, an approach that differs from the current focus on blocking Ang II formation and action.
A non-iterative compact model for carbon nanotube FETs incorporating source exhaustion effects (2009)

Because of high carrier velocities and quasi-ballistic transport properties, carbon-based (nanotube, graphene) field effect transistors (CNFETs) are considered to be potential candidates to replace CMOS in future technology generations . Most prior modeling of CNFETs has involved complex models, such as NEGF , but to properly evaluate these devices in circuits and systems, efficient compact models are required. In this paper, a fully analytical model based on ballistic transport and careful analysis of quantum capacitances is developed. This model requires neither iteration nor numeric integration. The model agrees well with numerical simulation and, in the limit of good contacts, predicts that a new effect, source exhaustion (using up all available carriers in the source), should limit the current. The model has also been integrated into a system level design optimization program which evaluates optimal device parameters based on system-level design objectives. The CNFET is projected to achieve 5× chip-level speed up over PDSOI at 11 nm technology node for a high-performance four-core processor with 1.5M logic gates.
The effect of ketorolac tromethamine in reducing postoperative inflammation: double-mask parallel comparison with dexamethasone. (1989)

Anterior chamber fluorophotometry was done after the oral administration of fluorescein sodium in patients undergoing extracapsular cataract extraction and posterior chamber intraocular lens insertion before and after surgery. The administration of ketorolac solution 0.5% eye drops before and after surgery decreased the breakdown of the blood-aqueous barrier as much as did dexamethasone sodium phosphate solution 0.1% (dexamethasone solution) eye drops at each postoperative time period as measured by fluorophotometry. Slit-lamp observations of postoperative anterior ocular inflammation were not different between treatment groups. Both ketorolac and dexamethasone solutions were well tolerated by patients. No additional corticosteroids were given to any patients during the study. Therefore, ketorolac solution was as effective as dexamethasone solution in suppressing postoperative inflammation after cataract surgery as measured by fluorophotometry and as observed by slit-lamp examinations. This study confirms prior studies that suggest ketorolac ophthalmic solution 0.5% may be effective and safe as a nonsteroidal antiinflammatory agent for topical use after cataract surgery and intraocular lens implantation and as a substitute for topically applied corticosteroids.
Role of the Hepatitis B Virus Posttranscriptional Regulatory Element in Export of Intronless Transcripts (1995)

Hepatitis B virus S transcripts contain a region, known as the posttranscriptional regulatory element (PRE), that activates their transport from the nucleus to the cytoplasm. J. Huang and T. J. Liang (Mol. Cell. Biol. 13:7476-7486, 1993) have shown that this element can partially substitute for the human immunodeficiency virus Rev-response element (RRE) in a reporter plasmid that is dependent on the RRE and Rev protein for expression and concluded that PRE exhibits Rev-RRE-like functions by inhibiting splicing. However, we have obtained additional data which indicate that the PRE functions in a novel manner that is not dependent on inhibition of splicing. Unlike Rev-RRE, the PRE functions independently of splice donor and acceptor sites and can activate cytoplasmic expression of an intronless (so-called prespliced) beta-globin transcript. Conversely, a heterologous intron can substitute for the PRE in increasing cytoplasmic expression of hepatitis B virus S transcripts. In addition, the host nuclear factor, YL2 (p32), which enhances Rev-RRE function has no effect on PRE-dependent gene expression. Since S transcripts are not normally known to be spliced and since RNA splicing and cytoplasmic transport are tightly linked processes in higher eucaryotic cells, we conclude that the PRE functions in cis to allow the export of nuclear transcripts that do not interact efficiently with the splicing pathway and hence are normally not exported well from the nucleus. Such elements are critical for the life cycle of viruses, such as hepatitis B virus, which undergo reverse transcription during replication.
Practice parameters in adults with suspected or known supratentorial nonoptic pathway low-grade glioma (1998)

Gene therapy has many potential applications in neurosurgery. One application involves bone morphogenetic protein-2 (BMP-2), a low-molecular-weight glycoprotein that induces bone formation in vivo. Numerous studies have demonstrated that the BMP-2 protein can enhance spinal fusion. This study was undertaken to determine whether direct injection of an adenoviral construct containing the BMP-2 gene can be used for spinal fusion. Twelve athymic nude rats were used in this study. Recombinant, replication-defective type-5 adenovirus with a universal promoter and BMP-2 gene (Ad-BMP-2) was used. A second adenovirus constructed with a universal promoter and beta-galactosidase (beta-gal) gene (Ad-beta-gal) was used as a control. Seven and one-half microliters of virus was injected percutaneously and paraspinally at the lumbosacral junction in three groups (four animals each): 1) Ad-BMP-2 bilaterally, 2) Ad-BMP-2 on the right, Ad-beta-gal on the left, and 3) Ad-beta-gal bilaterally. Computerized tomography (CT) scans of the lumbosacral spine were obtained at 3, 5, and 12 weeks. At 12 weeks, the animals were killed for histological inspection. Ectopic bone formation was seen both on three-dimensional CT reconstruction and histologically in all rats at sites treated with Ad-BMP-2. Histological analysis revealed bone at different stages of maturity adjacent to the spinous processes, laminae, and transverse processes. This study clearly demonstrated that it is possible to produce in vivo endochondral bone formation by using direct adenoviral construct injection into the paraspinal musculature, which suggests that gene therapy may be useful for spinal fusion in the future.
B7-H3 expression in donor T cells and host cells negatively regulates acute graft-versus-host disease lethality (2015)

Members of the B7 family have been shown to be important for regulating immune responses by providing either positive or negative costimulatory signals. The function of B7-H3 has been controversial. We show that B7-H3 is upregulated in graft-versus-host disease (GVHD) target organs, including the colon, liver, and lung. Infusion of allogeneic donor T cells into B7-H3(-/-) vs wild-type (WT) recipients resulted in increased GVHD lethality associated with increased T-cell proliferation, colonic inflammatory cytokines, and destruction of epithelial barriers. Allogeneic B7-H3(-/-) vs WT donor T cells also had increased T-cell proliferation and GVHD lethality associated with increased proliferation and cytokine secretion in the spleen, intraepithelial lymphocyte inflammatory cytokines, and intestinal permeability. Both resting and activated regulatory T cells (Tregs) lack B7-H3 messenger RNA. Consistent with these data, GVHD was augmented in recipients of B7-H3(-/-) Treg-depleted grafts. In two delayed lymphocyte infusion (DLI) models, T cells lacking B7-H3 are capable of providing graft-versus-leukemia (GVL) effects. We conclude that B7-H3 is responsible for providing a negative costimulatory signal. Our studies provide support for developing and testing new therapies directed toward the B7-H3 pathway, including approaches to augment host B7-H3 early after bone marrow transplantation to prevent GVHD and to develop potent antagonistic antibodies later after transplant to facilitate DLI-mediated GVL without GVHD complications.
「Camp」的美學與政治：與愛德蒙懷特共遊後結構同志主體樂園 (2007)

Critics of poststructuralism have used performative contradiction as a way to undermine the effort of poststructuralism. Performative contradictions are when and where contradictions are observed. The “normal rationality” is to quell out those contradictions to keep meaning and reason in order. However, this thesis starts with a position to rethink the importance of seeing performative contradiction as an art of camp. This thesis writes about camp, and takes camp as a tool to criticize one’s situatedness in one’s socio-cultural positioning in the term “subject-scape.” Through camping, one is enabled to see oneself and the others “otherwise” when there is a conflict between the performatives of the self/others and the social norms. It is argued in the way as it is performed through this writing that by cultivating a sense of camp we “let live” ourselves and others in situations where performative contradictions occur. Since gay people are often thought of as camp and as contradictory to an unquestionable natural plan and thus are excluded as illegitimate subjects in the heteronormative society, it is crucial here to utilize camp to work in their favor. To examine this idea, I read Edmund White’s novels as a pursuit of a camp homosexual identity, which never reaches a totalized and fixed condition as the knowledge/discourse of sexuality dictates or the normal path of a meaningful social life expects. Instead, the gay identity, understood by poststructuralism, is never fixated but remains a performative site that various discursive practices work to speak its truth. As complicated in the process of homographesis proposed by Lee Edelman, the meaning of homosexuality is infinitely deferred and in this unstoppable signifying process, and as a result, multiple meanings become possible and alternative stories are meaningful. And importantly, this status of confusion is not undesirable but is the foundation for celebrating life’s many alternative meanings and richness. The thesis also follows Edmund White to the AIDS epidemic in the 80s, and it is through camp used as a critique that keeps oneself at a critical distance from the constraints of the ideology of heteronormative able-bodiedness so that disabled and aging bodies can mean and be lived otherwise. It is also a critique of the normal society that aims to exclude those ill subjects as if they are from the outside, which is also an attitude that gets translated into denial and frustration when one faces illness and death in life and interpersonal encounters. I draw upon Judith Butler’s writing on ethics in the vein of Emmanuel Levinas to reconsider a community that takes as the undeconstructible a common “vulnerability” that makes us all human. It is argued that the vulnerable subject that lives a precarious life in that at times the life and the body are not fully controllable is also the subject that can love and care for the its other, which leads to a conclusion that what we do for the others is ultimately what we do for ourselves.
GMI-1271, a novel E-selectin antagonist, combined with induction chemotherapy in elderly patients with untreated AML. (2017)

2560 Background: The outcomes for elderly patients (pts) with acute myeloid leukemia (AML) remain poor, therefore newer and less toxic therapies are urgently needed. The binding of E-selectin (E-sel), an adhesion molecule expressed in the bone marrow, to the leukemic cell surface activates survival pathways and promotes chemotherapy resistance. GMI-1271, a novel E-sel antagonist, enhances chemotherapy responses and protects from common toxicities in preclinical models (Becker ASH 2013; Winkler ASH 2013 and 2014). We report interim Phase 2 data for GMI-1271 plus chemotherapy in elderly untreated pts with AML. Methods: Pts ≥ 60 yrs with untreated AML, ECOG 0-2, and adequate renal and hepatic function were eligible. Prior treatment of MDS was allowed. GMI-1271 (10 mg/kg) was given 24 hrs prior, during and 48 hrs post induction with infusional cytarabine and idarubicin (7+3). Safety, tolerability, and anti-leukemia activity were assessed. Two cycles of induction were allowed and responders could receive consolidation with GMI-1271 plus intermediate dose cytarabine. Dose-limiting toxicity (DLT), defined as myelosuppression in the absence of disease or related Grade 3 (Gr) non-hematologic toxicity beyond day 42, was assessed in the first 3 pts. Results: 24 pts have been enrolled to date and 17 are evaluable for response. The median age was 68 years (range, 60-79) with 58% male pts, 50% secondary AML (sAML) pts and 25% with high-risk cytogenetics (by SWOG). The first 3 pts had no DLT, allowing enrollment to proceed. Common Gr 3/4 AEs included febrile neutropenia (47%), pneumonia (20%), pulmonary edema (13%) and non-fatal respiratory failure (13%). 2 pts died of sepsis within 60 days. The remission rate (CR/CRi) was 12/17 (71%). CR/CRi rate was 75% for pts with de novodisease and 67% for pts with sAML. E-sel ligand was expressed at high levels on blasts in the majority of pts. Conclusions: The addition of GMI-1271 to anthracycline-based induction chemotherapy in untreated elderly pts with AML demonstrates a high remission rate with acceptable side effect profile and low induction mortality. This study compares favorably to previous studies (Lancet, ASCO 2016). A randomized trial is being planned. Clinical trial information: NCT02306291.
Domain Inversion Effects in Ti - LiNbO 3 Integrated Optical Devices (1985)

Optical domain inversion effects on the performance of electro-optic devices in Ti-indiffused C-cut LiNbO3 are studied. The C- surface was found to be considerably more immune to domain inversion than the C+ surface under similar diffusion conditions. The extent of domain inversion was found to depend on the diffusion temperature, time, initial Ti film thickness and waveguide width. Lower electro-optically induced phase mod lation was observed in the drive voltage in Mach-Zehnder interferometers fabricated on C-1- substrates compared to that of C- substrates under the same voltage drive. The increase in crosstalk levels and change in the switching behavior of directional couplers attributable to domain inversion are also discussed.
157. Some reactions of 14-hydroxycodeine (1960)

A. C. Currie, J. Gillon, G. T. Newbold and F. S. Spring, J. Chem. Soc., 1960, 773 DOI: 10.1039/JR9600000773
Lovastatin-induced E2F-1 modulation and its effect on prostate cancer cell death (2001)

Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, induces growth arrest in a variety of cancer cell lines. Its mechanism of action, however, has not been completely elucidated. E2F-1 is thought to act as an oncogene and a tumour suppressor, with its action probably dependent upon the cellular context. We have shown in this study that transcriptional regulation and proteasomal degradation of E2F-1 are critical regulatory events in lovastatin-induced cell death. Accompanying this is a reduction in the E2F-1-regulated expression of cell cycle genes such as c-myc, cyclin D1, cyclin A and cyclin B1. Cell cycle analysis demonstrated that the accumulation of apoptotic cells was preceded by a progressive decrease in the S-phase cell population in response to lovastatin. Although expression of E2F-1 was reduced in three prostate cancer cell lines-PC-3, LNCaP and DU-145-the p21 and p27 protein levels were not increased in all the cell lines treated, suggesting that increase in p21 and p27 protein expression per se is not responsible for lovastatin-mediated down-regulation of E2F-1. The subsequent apoptotic death of these cells in the presence of lovastatin can be prevented by forced ectopic expression of E2F-1. Taken together, these facts imply that E2F-1 is the target of an HMG-CoA inhibitor and critical cell death mediator in prostate cancer cells.
Dysregulated Innate Immune Responses in Young Children with Autism Spectrum Disorders: Their Relationship to Gastrointestinal Symptoms and Dietary Intervention (2005)

Our results revealed that there are findings limited to GI(+) ASD PBMCs in both the unrestricted and elimination diet groups. Thus our findings indicate intrinsic defects of innate immune responses in GI(+) ASD children but not in NFH or GI(-) ASD children, suggesting a possible link between GI and behavioral symptoms mediated by innate immune abnormalities.
Radiation-induced lung injury. Assessment, management, and prevention. (2008)

Radiation therapy (RT) is an important treatment modality for multiple thoracic malignancies. Incidental irradiation of the lungs, which are particularly susceptible to injury, is unavoidable and often dose-limiting. The most radiosensitive subunit of the lung is the alveolar/capillary complex, and RT-induced lung injury is often described as diffuse alveolar damage. Reactive oxygen species generated by RT are directly toxic to parenchymal cells and initiate a cascade of molecular events that alter the cytokine milieu of the microenvironment, creating a self-sustaining cycle of inflammation and chronic oxidative stress. Replacement of normal lung parenchyma by fibrosis is the culminating event. Depending on the dose and volume of lung irradiated, acute radiation pneumonitis may develop, characterized by dry cough and dyspnea. Fibrosis of the lung, which can also cause dyspnea, is the late complication. Imaging studies and pulmonary function tests can be used to quantify the extent of lung injury. While strict dose-volume constraints to minimize the risk of injury are difficult to impose, substantial data support some general guidelines. New modalities such as intensity-modulated radiation therapy and stereotactic body radiation therapy provide new treatment options but also pose new challenges in safely delivering thoracic RT.
Generating CTLs against the subdominant Epstein-Barr virus LMP1 antigen for the adoptive immunotherapy of EBV-associated malignancies (2003)

The Epstein-Barr virus (EBV)-encoded LMP1 protein is expressed in EBV-positive Hodgkin disease and is a potential target for cytotoxic T-lymphocyte (CTL) therapy. However, the LMP1-specific CTL frequency is low, and so far the generation of LMP1-specific CTLs has required T-cell cloning. The toxicity of LMP1 has prevented the use of dendritic cells (DCs) for CTL stimulation, and we reasoned that an inactive, nontoxic LMP1 mutant (DeltaLMP1) could be expressed in DCs and would enable the activation and expansion of polyclonal LMP1-specific CTLs. Recombinant adenoviral vectors expressing LMP1 or DeltaLMP1 were tested for their ability to transduce DCs. LMP1 expression was toxic within 48 hours whereas high levels of DeltaLMP1 expression were achieved with minimal toxicity. DeltaLMP1-expressing DCs were able to reactivate and expand LMP1-specific CTLs from 3 healthy EBV-seropositive donors. LMP1-specific T cells were detected by interferon-gamma (IFN-gamma) enzyme-linked immunospot assay (ELISPOT) assays using the HLA-A2-restricted LMP1 peptide, YLQQNWWTL (YLQ). YLQ-specific T cells were undetectable (less than 0.001%) in donor peripheral blood mononuclear cells (PBMCs); however, after stimulation the frequency increased to 0.5% to 3.8%. Lysis of autologous target cells by CTLs was dependent on the level of LMP1 expression. In contrast, the frequency of YLQ-specific CTLs in EBV-specific CTLs reactivated and expanded using lymphoblastoid cell lines was low and no LMP1-specific cytotoxic activity was observed. Thus, DeltaLMP1 expression in DCs is nontoxic and enables the generation of LMP1-specific CTLs for future adoptive immunotherapy protocols for patients with LMP1-positive malignancies such as EBV-positive Hodgkin disease. Targeting LMP1 in these malignancies may improve the efficacy of current adoptive immunotherapy approaches.
Effect of repeated dose of erythromycin on the pharmacokinetics of roflumilast and roflumilast N-oxide (2009)

Co-administration of erythromycin (a moderate CYP3A4 inhibitor) and roflumilast does not require dose adjustment of roflumilast.