gebhart/patrepeval huggingface dataset:
[The roles of cytokine in organ-specific tumor metastasis]. (1993)

The production of cytokines by tumor cells has been suggested as the molecular perturbation responsible for the development of malignant tumors. The behavior of tumor cells in animals is presumed to be affected by these factors, which include such hematopoietic cytokines as GM-CSF, IL-1, and IL-6. Here, we report findings demonstrating that GM-CSF is produced by many murine transplantable tumors with metastatic ability in the lungs, and IL-6 and/or IL-1 are produced by the tumors metastatic in the liver. We discuss the notion that the particular organ or organs in which tumor cells metastasize may be associated with the type of cytokines produced by the tumors. Metastatic spread requires interactions of tumor cells with components of the extracellular matrix of host tissues or with other cells, almost all of which depend on cell surface determinants such as cell adhesion molecules. We also discuss the possibility that the expression and adhesive potentials of adhesive protein (CD44) may be regulated by the cytokine (GM-CSF) excreted from the tumor cells. We then emphasize the possibility that both gene expression of cytokines and adhesive proteins play a critical role in tumor metastasis and in determining organ specificity in metastasis.
Fatigue Testing of Suture Anchors (2002)

In a porcine tibia model, we subjected widely used anchor-suture combinations to a fatigue-testing protocol. The Ethibond No. 2 suture was the weakest part of the anchor-suture combinations when they were loaded to failure by a single pull. Under cyclic-loading conditions, fixation strength was decreased compared with single-pull tests. The suture/anchor interface was identified as the weakest link in the Mitek GII/No. 2 combination and in the Zimmer Statak 3.5/No. 2 combination. In most cases the suture was worn through at the eyelet. Threading the GII anchor with a No. 5 suture and use of larger anchors in combination with No. 2 sutures increased the fatigue strength. Suture breakage at the knot was the predominant failure mode for biodegradable anchors inserted into cortical bone. The highest fatigue strength was seen for the Super Anchor/No. 5 combination when the anchor was inserted in cortical bone. Fatigue testing is crucial for evaluation of suture anchors and should be performed along with single-pull testing. The mechanical performance of a suture anchor threaded with a defined suture depends on several key factors: the pullout strength of the anchor, the tensile strength of the suture, and the interaction of anchor and suture at the eyelet (suture/anchor interface).
Preganglionic and Postganglionic Neurons Responsible for Cerebral Vasodilation Mediated by Nitric Oxide in Anesthetized Dogs (2000)

The authors performed investigations to functionally determine the route of efferent innervation in vivo responsible for cerebral vasodilation mediated by nitric oxide (NO). In anesthetized beagles, electrical stimulation of the pterygopalatine ganglion vasodilated ipsilateral cerebral arteries such as the middle cerebral and posterior communicating arteries. Intravenous injections of NG-nitro-L-arginine (L-NA) markedly inhibited the response to nerve stimulation, and the effect was reversed by L-arginine. Stimulation of the proximal portion of the greater superficial petrosal nerve, upstream of the pterygopalatine ganglion, also produced cerebral vasodilation, which was abolished by L-NA and restored by L-arginine. Treatment with hexamethonium abolished the response to stimulation of the petrosal nerve but did not affect the response to pterygopalatine ganglion stimulation. Destruction of the pterygopalatine ganglion by cauterization constricted the cerebral arteries. Postganglionic denervation abolished the vasodilation, lacrimation, and nasal secretion induced on the ipsilateral side by stimulation of the pterygopalatine ganglion and petrosal nerve. The vasodilator response was suppressed by L-NA but unaffected by atropine, whereas lacrimation and nasal secretion were abolished solely by atropine. It is concluded that postganglionic neurons from the pterygopalatine ganglion play crucial roles in cerebral vasodilation mediated by NO from the nerve, and preganglionic neurons, possibly from the superior salivatory nucleus through the greater superficial petrosal nerve, innervate the pterygopalatine ganglion. Tonic discharges from the vasomotor center participate significantly in the maintenance of cerebral vasodilation.
A real-time articulated human motion tracking using tri-axis inertial/magnetic sensors package (2004)

A basic requirement in virtual environments is the tracking of objects, especially humans. A real time motion-tracking system was presented and evaluated in this paper. System sensors were built using tri-axis microelectromechanical accelerometers, rate gyros, and magnetometers. A Kalman-based fusion algorithm was applied to obtain dynamic orientations and further positions of segments of the subject's body. The system with the proposed algorithm was evaluated via dynamically measuring Euler orientation and comparing with other two conventional methods. An arm motion experiment was demonstrated using the developed system and algorithm. The results validated the effectiveness of the proposed method.
Improving the representation of legal case texts with information extraction methods (2001)

The prohibitive cost of assigning indices to textual cases is a major obstacle for the practical use of AI and Law systems supporting reasoning and arguing with cases. While progress has been made toward extracting certain facts from well-structured case texts or classifying case abstracts under Key Number concepts, these methods still do not suffice for the complexity of indexing concepts in CBR systems.
Purification and characterization of recA protein from salmonella typhimurium. (1983)

recA protein was purified to homogeneity from Salmonella typhimurium TA98 strain after induction of the cells by nalidixic acid. The purification was monitored with a radioimmune assay and involved a specific elution of the protein by ATP from a single-stranded DNA-cellulose column. From 240 liters of cell culture we obtained 40 mg of recA protein which was more than 98% pure. This protein exhibited the same molecular weight as measured on sodium dodecyl sulfate-polyacrylamide gel and the same isoelectric point as the Escherichia coli recA protein purified by a similar procedure. In addition, the S. typhimurium recA protein is endowed with a single-stranded DNA-dependent ATPase activity and cleaves the phage lambda repressor in vitro at the same rate as E. coli recA protein and with the same qualitative requirements. However, peptide mapping with the Staphylococcus aureus V8 protease and cross-reaction with heterologous antibodies show that these two proteins are slightly different.
High-performance interconnects: an integration overview (2001)

The Information Revolution and enabling era of silicon ultralarge-scale integration (ULSI) have spawned an ever-increasing level of functional integration on-chip, driving a need for greater circuit density and higher performance. While traditional transistor scaling has thus far met this challenge, interconnect scaling has become the performance-limiting factor for new designs. The increasing influence of interconnect parasitics on crosstalk noise and R(L)C delay as well as electromigration and power dissipation concerns have stimulated the introduction of low-resistivity copper and low-permittivity (k) dielectrics to provide performance and reliability enhancement. Integration of these new materials into integrated circuit fabrication is a formidable task, requiring material, process, design, and packaging innovations. Additionally, entirely new technologies such as RF and optical interconnects may be required to address future global routing needs and sustain performance improvement.
Anti‐VEGF Aptamer (Pegaptanib) Therapy for Ocular Vascular Diseases (2006)

Vascular endothelial growth factor (VEGF) is a central regulator of both physiological and pathological angiogenesis. Pegaptanib, a 28-nucleotide RNA aptamer specific for the VEGF(165) isoform, binds to it in the extracellular space, leaving other isoforms unaffected, and inhibits such key VEGF actions as promotion of endothelial cell proliferation and survival, and vascular permeability. Pegaptanib already has been examined as a treatment for two diseases associated with ocular neovascularization, age-related macular degeneration (AMD) and diabetic macular edema (DME). Preclinical studies have shown that VEGF(165) alone mediates pathological ocular neovascularization and that its inactivation by pegaptanib inhibits the choroidal neovascularization observed in patients with neovascular AMD. In contrast, physiological vascularization, which is supported by the VEGF(121) isoform, is unaffected by this inactivation of VEGF(165). In addition, animal model studies have shown that intravitreous injection of pegaptanib can inhibit the breakdown of the blood-retinal barrier characteristic of diabetes and even can reverse this damage to some degree. These preclinical findings formed the basis for randomized controlled trials examining the efficacy of pegaptanib as a therapy for AMD and DME. The VEGF Inhibition Study in Ocular Neovascularization (VISION) trial comprising two replicate, pivotal phase 3 studies, demonstrated that intravitreous injection of pegaptanib resulted in significant clinical benefit, compared with sham injection, for all prespecified clinical end points, irrespective of patient demographics or angiographic subtype, and led to pegaptanib's approval as a treatment for AMD. A phase 2 trial has provided support for the efficacy of intravitreous pegaptanib in the treatment of DME.
Space/time trade-offs in hash coding with allowable errors (1970)

In this paper trade-offs among certain computational factors in hash coding are analyzed. The paradigm problem considered is that of testing a series of messages one-by-one for membership in a given set of messages. Two new hash-coding methods are examined and compared with a particular conventional hash-coding method. The computational factors considered are the size of the hash area (space), the time required to identify a message as a nonmember of the given set (reject time), and an allowable error frequency. The new methods are intended to reduce the amount of space required to contain the hash-coded information from that associated with conventional methods. The reduction in space is accomplished by exploiting the possibility that a small fraction of errors of commission may be tolerable in some applications, in particular, applications in which a large amount of data is involved and a core resident hash area is consequently not feasible using conventional methods. In such applications, it is envisaged that overall performance could be improved by using a smaller core resident hash area in conjunction with the new methods and, when necessary, by using some secondary and perhaps time-consuming test to “catch” the small fraction of errors associated with the new methods. An example is discussed which illustrates possible areas of application for the new methods. Analysis of the paradigm problem demonstrates that allowing a small number of test messages to be falsely identified as members of the given set will permit a much smaller hash area to be used without increasing reject time.
Solution stability in linear programming relaxations (2009)

We propose a new method to quantify the solution stability of a large class of combinatorial optimization problems arising in machine learning. As practical example we apply the method to correlation clustering, clustering aggregation, modularity clustering, and relative performance significance clustering. Our method is extensively motivated by the idea of linear programming relaxations. We prove that when a relaxation is used to solve the original clustering problem, then the solution stability calculated by our method is conservative, that is, it never overestimates the solution stability of the true, unrelaxed problem. We also demonstrate how our method can be used to compute the entire path of optimal solutions as the optimization problem is increasingly perturbed. Experimentally, our method is shown to perform well on a number of benchmark problems.
Genome-wide analysis of gene expression in human hepatocellular carcinomas using cDNA microarray: identification of genes involved in viral carcinogenesis and tumor progression. (2001)

To disclose detailed genetic mechanisms in hepatocellular carcinoma (HCC) with a view toward development of novel therapeutic targets, we analyzed expression profiles of 20 primary HCCs and their corresponding noncancerous tissues by means of cDNA microarrays consisting of 23,040 genes. Up-regulation of mitosis-promoting genes was observed in the majority of the tumors examined. Some genes showed expression patterns in hepatitis B virus-positive HCCs that were different from those in hepatitis C virus-positive HCCs; most of them encoded enzymes that metabolize carcinogens and/or anticancer agents. Furthermore, we identified a number of genes associated with malignant histological type or invasive phenotype. Accumulation of such data will make it possible to define the nature of individual tumors, to provide clues for identifying new therapeutic targets, and ultimately to optimize treatment of each patient.
Knockdown of SOX18 inhibits the proliferation, migration and invasion of hepatocellular carcinoma cells (2015)

Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world. Recent studies have demonstrated that SOX18 is highly expressed in various types of cancer. In the present study, we found that SOX18 mRNA was overexpressed in HCC compared with non-tumorous tissues. We aimed to explore the effects of SOX18 siRNA on the proliferation, invasion and migration of two HCC cell lines, MHCC97H and HepG2, which overexpress SOX18. We found that SOX18 siRNA significantly inhibited the proliferation and induced cell cycle arrest at the G0/G1 phase. Results of the Transwell assay showed that the migration and invasion of the HCC cells were markedly impaired in the SOX18-knockdown cells. Gene set enrichment analysis (GSEA) showed that KEGG focal adhesion and chemokine signaling pathways were correlated with SOX18 expression. Furthermore, the mRNA and protein levels of RhoA, PDGFB, IGF1R, CCL2, CCL3 and CCL5 were decreased in the SOX18-knockdown cells. Importantly, we demonstrated that upregulation of SOX18 was associated with a poor outcome in HCC patients. These results indicate that SOX18 may serve as a prognostic factor and a promising therapeutic strategy for HCC.
High‐Frequency Intracerebral EEG Activity (100–500 Hz) Following Interictal Spikes (2006)

Thus high-frequency EEG activity can be recorded with macroelectrodes in humans and may provide insights on neuronal mechanisms related to human epilepsy. This activity undergoes consistent modifications after EEG spikes. We propose that the reduction in high frequencies reflects a postspike depression in neuronal activity that is more pronounced in the region of spike generation. This depression is almost always seen in hippocampus but less in amygdala.
Efficient Discrimination between Different Densities of Target Antigen by Tetracycline-Regulatable T Bodies (1999)

Engineered T cells expressing chimeric T cell receptors (chTCRs) are of interest for cancer gene therapy but many "cancer antigens" are thought to be unsuitable targets because they are expressed at low levels on normal tissues. We therefore sought to determine whether engineered T cells expressing variable surface densities of a high-affinity chTCR could discriminate different concentrations of the targeted antigen. We plotted the relationship between chTCR density and the concentration of target antigen using Jurkat T cells expressing a hapten-binding chTCR whose expression could be modulated by tetracycline. Our analysis reveals that there is a dynamic equilibrium between cell surface density of the chTCR and the antigen density that optimally triggers T cell activation. At a fixed density of target antigen, optimal T cell activation can be achieved only within a certain range of chTCR densities, while excessive TCR signaling triggers apoptosis of the engineered T cells. Our results show that T cells can be engineered to discriminate different antigen densities and that the T cell response to a fixed concentration of antigen can be optimized by tuning the cell surface density of TCRs.
How to present information on wrist-worn point-light displays (2014)

In the last years there has been an emerging trend towards wearable devices, such as wristwatches, and wristbands. Common wrist-worn devices often present information visually and in an abstract way. However, little research has been done on the question of how these displays should present information in daily life. In this work we built a point-light bracelet to explore this question. In a user study participants designed light patterns for a hands-on scenario: physical activity feedback. Afterwards, we investigated how the participants experienced the light patterns in their daily life. From the study results we derive implications for the design of light patterns on a wrist-worn display, e.g. how and when to use the light parameters colour and brightness.
Comparative clonal analysis of human immunodeficiency virus type 1 (HIV-1)-specific CD4+ and CD8+ cytolytic T lymphocytes isolated from seronegative humans immunized with candidate HIV-1 vaccines. (1992)

The lysis of infected host cells by virus-specific cytolytic T lymphocytes (CTL) is an important factor in host resistance to viral infection. An optimal vaccine against human immunodeficiency virus type 1 (HIV-1) would elicit virus-specific CTL as well as neutralizing antibodies. The induction by a vaccine of HIV-1-specific CD8+ CTL in humans has not been previously reported. In this study, CTL responses were evaluated in HIV-1-seronegative human volunteers participating in a phase I acquired immune deficiency syndrome (AIDS) vaccine trial involving a novel vaccine regimen. Volunteers received an initial immunization with a live recombinant vaccinia virus vector carrying the HIV-1 env gene and a subsequent boost with purified env protein. An exceptionally strong env-specific CTL response was detected in one of two vaccine recipients, while modest but significant env-specific CTL activity was present in the second vaccinee. Cloning of the responding CTL gave both CD4+ and CD8+ env-specific CTL clones, permitting a detailed comparison of critical functional properties of these two types of CTL. In particular, the potential antiviral effects of these CTL were evaluated in an in vitro system involving HIV-1 infection of cultures of normal autologous CD4+ lymphoblasts. At extremely low effector-to-target ratios, vaccine-induced CD8+ CTL clones lysed productively infected cells present within these cultures. When tested for lytic activity against target cells expressing the HIV-1 env gene, CD8+ CTL were 3-10-fold more active on a per cell basis than CD4+ CTL. However, when tested against autologous CD4+ lymphoblasts acutely infected with HIV-1, CD4+ clones lysed a much higher fraction of the target cell population than did CD8+ CTL. CD4+ CTL were shown to recognize not only the infected cells within these acutely infected cultures but also noninfected CD4+ T cells that had passively taken up gp120 shed from infected cells and/or free virions. These results were confirmed in studies in which CD4+ lymphoblasts were exposed to recombinant gp120 and used as targets for gp120-specific CD4+ and CD8+ CTL clones. gp120-pulsed, noninfected targets were lysed in an antigen-specific fashion by CD4+ but not CD8+ CTL clones. Taken together, these observations demonstrate that in an in vitro HIV-1 infection, sufficient amounts of gp120 antigen are produced and shed by infected cells to enable uptake by cells that are not yet infected, resulting in the lysis of these noninfected cells by gp120-specific, CD4+ CTL.(ABSTRACT TRUNCATED AT 400 WORDS)
Intratracheal gene delivery to the mouse airway: characterization of plasmid DNA expression and pharmacokinetics. (1995)

Intratracheal administration of plasmid DNA resulted in gene expression in mouse airways in the absence of any enhancing agent. Administration of plasmid DNA encoding the chloramphenicol acetyltransferase gene (CAT) in sterile water lead to CAT transgene expression that peaked between 1 and 3 days and was detected up to 28 days after DNA administration. Transgene expression was independent of mouse gender, age and strain. Levels of expression from DNA in various isotonic solutions did not differ from levels obtained with DNA administered in water, suggesting that transfection is not dependent on damage to airway cells caused by a hypo-osmotic delivery vehicle. Pharmacokinetic studies using radiolabeled plasmid DNA showed that DNA was rapidly degraded, while higher levels of radioactivity were retained for longer duration following administration of cationic liposome-DNA complexes in the airway. Southern blot and PCR analysis confirmed that DNA complexed with DOTMA-DOPE was retained in the airways for a longer period. However, cationic liposomes DOTMA-DOPE (1:1) or DOTAP complexed with DNA, did not enhance expression over DNA alone. These results suggest that 'naked' plasmid DNA should be included as a control in all studies on intratracheal gene delivery using nonviral systems.
Vascular Calcification (2004)

Vascular calcification, long thought to result from passive degeneration, involves a complex, regulated process of biomineralization resembling osteogenesis. Evidence indicates that proteins controlling bone mineralization are also involved in the regulation of vascular calcification. Artery wall cells grown in culture are induced to become osteogenic by inflammatory and atherogenic stimuli. Furthermore, osteoclast-like cells are found in calcified atherosclerotic plaques, and active resorption of ectopic vascular calcification has been demonstrated. In general, soft tissue calcification arises in areas of chronic inflammation, possibly functioning as a barrier limiting the spread of the inflammatory stimulus. Atherosclerotic calcification may be one example of this process, in which oxidized lipids are the inflammatory stimulus. Calcification is widely used as a clinical indicator of atherosclerosis. It progresses nonlinearly with time, following a sigmoid-shaped curve. The relationship between calcification and clinical events likely relates to mechanical instability introduced by calcified plaque at its interface with softer, noncalcified plaque. In general, as calcification proceeds, interface surface area increases initially, but eventually decreases as plaques coalesce. This phenomenon may account for reports of less calcification in unstable plaque. Vascular calcification is exacerbated in certain clinical entities, including diabetes, menopause, and osteoporosis. Mechanisms linking them must be considered in clinical decisions. For example, treatments for osteoporosis may have unanticipated effects on vascular calcification; the converse also applies. Further understanding of processes governing vascular calcification may yield new therapeutic options for vascular disease.
Charge-Pump Phase-Lock Loops (1980)

Phase/frequency detectors deliver output in the form of three-state, digital logic. Charge pumps are utilized to convert the timed logic levels into analog quantities for controlling the locked oscillators. This paper analyzes typical charge-pump circuits, identifies salient features, and provides equations and graphs for the design engineer.