gebhart/patrepeval huggingface dataset:
Oxygen radicals induce human endothelial cells to express GMP-140 and bind neutrophils. (1991)

The initial step in extravasation of neutrophils (polymorphonuclear leukocytes [PMNs]) to the extravascular space is adherence to the endothelium. We examined the effect of oxidants on this process by treating human endothelial cells with H2O2, t-butylhydroperoxide, or menadione. This resulted in a surface adhesive for PMN between 1 and 4 h after exposure. The oxidants needed to be present only for a brief period at the initiation of the assay. Adhesion was an endothelial cell-dependent process that did not require an active response from the PMN. The adhesive molecule was not platelet-activating factor, which mediates PMN adherence when endothelial cells are briefly exposed to higher concentrations of H2O2 (Lewis, M. S., R. E. Whatley, P. Cain, T. M. McIntyre, S. M. Prescott, and G. A. Zimmerman. 1988. J. Clin. Invest. 82:2045-2055), nor was it ELAM-1, an adhesive glycoprotein induced by cytokines. Oxidant-induced adhesion did not require protein synthesis, was inhibited by antioxidants, and, when peroxides were the oxidants, was inhibited by intracellular iron chelators. Granule membrane protein-140 (GMP-140) is a membrane-associated glycoprotein that can be translocated from its intracellular storage pool to the surface of endothelial cells where it acts as a ligand for PMN adhesion (Geng, J.-G., M. P. Bevilacqua, K. L. Moore, T. M. McIntyre, S. M. Prescott, J. M. Kim, G. A. Bliss, G. A. Zimmerman, and R. P. McEver. 1990. Nature (Lond). 343:757-760). We found that endothelial cells exposed to oxidants expressed GMP-140 on their surface, and that an mAb against GMP-140 or solubilized GMP-140 completely blocked PMN adherence to oxidant-treated endothelial cells. Thus, exposure of endothelial cells to oxygen radicals induces the prolonged expression of GMP-140 on the cell surface, which results in enhanced PMN adherence.
Passive haptics significantly enhances virtual environments (2001)

BRENT EDWARD INSKO: Passive Haptics Significantly Enhances Virtual Environments (Under the direction of Frederick P. Brooks, Jr.) One of the most disconcertingly unnatural properties of most virtual environments (VEs) is the ability of the user to pass through objects. I hypothesize that passive haptics, augmenting a high-fidelity visual virtual environment with low-fidelity physical objects, will markedly improve both sense of presence and spatial knowledge training transfer. The low-fidelity physical models can be constructed from cheap, easy- to-assemble materials such as styrofoam, plywood, and particle board.
Efficient Compression of Multi-View Video Exploiting Inter-View Dependencies Based on H.264/MPEG4-AVC (2006)

Efficient multi-view coding requires coding algorithms that exploit temporal, as well as inter-view dependencies between adjacent cameras. Based on a spatiotemporal analysis on the multi-view data set, we present a coding scheme utilizing an H.264/MPEG4-AVC codec. To handle the specific requirements of multi-view datasets, namely temporal and inter-view correlation, two main features of the coder are used: hierarchical B pictures for temporal dependencies and an adapted prediction scheme to exploit inter-view dependencies. Both features are set up in the H.264/MPEG4-AVC configuration file, such that coding and decoding is purely based on standardized software. Additionally, picture reordering before coding to optimize coding efficiency and inverse reordering after decoding to obtain individual views are applied. Finally, coding results are shown for the proposed multi-view coder and compared to simulcast anchor and simulcast hierarchical B picture coding
Regulation of an Endogenous Locus Using a Panel of Designed Zinc Finger Proteins Targeted to Accessible Chromatin Regions (2001)

We have mapped conserved regions of enhanced DNase I accessibility within the endogenous chromosomal locus of vascular endothelial growth factor A (VEGF-A). Synthetic zinc finger protein (ZFP) transcription factors were designed to target DNA sequences contained within the DNase I-hypersensitive regions. These ZFPs, when fused to either VP16 or p65 transcriptional activation domains, were able to activate expression of the VEGF-A gene as assayed by mRNA accumulation and VEGF-A protein secretion through a range exceeding that induced by hypoxic stress. Importantly, multiple splice variants of VEGF-A mRNA with defined physiological functions were induced by a single engineered ZFP transcription factor. We present evidence for an enhanced activation of VEGF-A gene transcription by ZFP transcription factors fused to VP16 and p65 targeted to two distinct chromosomal sites >500 base pairs upstream or downstream of the transcription start site. Our strategy provides a novel approach for dissecting the requirements for gene regulation at a distance without altering the DNA sequence of the endogenous target locus.
Integrins regulate the apoptotic response to DNA damage through modulation of p53 (2002)

p53 mediates apoptosis of cells after DNA damage including tumor cells after radiation or chemotherapy. Survival of isolated cancer cells after therapy leads to recurrence of therapy-resistant tumors. We now show that for some melanoma, sarcoma, or fibroblastic cell types that survive without integrin-mediated adhesion, apoptosis in response to DNA damage requires cell adhesion. This effect correlates with rapid changes in levels of p14/p19 Arf and its downstream component, p53. Killing of nonadherent cells is increased by treatment with antiintegrin antibodies or by increasing levels of p53 or Arf. Consistent with low p53 levels, suspended cells show chromosomal instability after irradiation. Thus, loss of normal adhesion in susceptible tumor cells during genotoxic stress may play a role in therapy resistance and promote survival of cells with aberrant DNA.
Wideband Active and Passive Antenna Solutions for Handheld Terminals (2007)

This thesis presents solutions and studies related to the design of wideband antennas for wireless handheld terminal applications. A method of electrically shortening the terminal chassis length to obtain resonance at high frequencies has been proposed and evaluated, thereby increasing the antennas impedance bandwidth. No significant effect on the lower frequency band in a dual-band antenna prototype has been observed, making the method suitable for multi-band applications. The chassis has further been utilized as a zero-thickness 0.9 - 2.7 GHz high efficiency antenna by inserting a notch in the chassis center, and a feasibility study for typical phones has been performed. Additionally, the effect of talk position on the chassis wave-mode has been investigated, where the standard equivalent circuit model for terminal antennas has been modified to include the presence of the users head. The model has been used to explain measured and simulated effects concerning frequency detuning, efficiency reduction and bandwidth enhancements when the terminal is placed in talk position. The use of a hands-free earpiece cord is currently mandatory for FM radio reception as the cord is utilized as antenna. However, there is currently a market driven demand for removing the cord requirement since many modern phones are equipped with speakers and Bluetooth headsets. In this thesis, an active ferrite loop antenna is proposed as an internal replacement/complement with a performance of -23 dB (G/T degradation) compared to a full-size lossless dipole in urban environments. Also, a modification to the cord is suggested for DVB H reception. Complex matching networks have been investigated to increase the bandwidth of dual band PIFA antennas, and a printed dual band dipole has been integrated with a modified Marchand balun for dual resonance at two separate frequency bands, thus covering the commercial cellular bands 824-960 and 1710-2170 MHz with a single antenna.
MicroRNA-31 functions as an oncogenic microRNA in mouse and human lung cancer cells by repressing specific tumor suppressors (2010)

MicroRNAs (miRNAs) regulate gene expression. It has been suggested that obtaining miRNA expression profiles can improve classification, diagnostic, and prognostic information in oncology. Here, we sought to comprehensively identify the miRNAs that are overexpressed in lung cancer by conducting miRNA microarray expression profiling on normal lung versus adjacent lung cancers from transgenic mice. We found that miR-136, miR-376a, and miR-31 were each prominently overexpressed in murine lung cancers. Real-time RT-PCR and in situ hybridization (ISH) assays confirmed these miRNA expression profiles in paired normal-malignant lung tissues from mice and humans. Engineered knockdown of miR-31, but not other highlighted miRNAs, substantially repressed lung cancer cell growth and tumorigenicity in a dose-dependent manner. Using a bioinformatics approach, we identified miR-31 target mRNAs and independently confirmed them as direct targets in human and mouse lung cancer cell lines. These targets included the tumor-suppressive genes large tumor suppressor 2 (LATS2) and PP2A regulatory subunit B alpha isoform (PPP2R2A), and expression of each was augmented by miR-31 knockdown. Their engineered repression antagonized miR-31-mediated growth inhibition. Notably, miR-31 and these target mRNAs were inversely expressed in mouse and human lung cancers, underscoring their biologic relevance. The clinical relevance of miR-31 expression was further independently and comprehensively validated using an array containing normal and malignant human lung tissues. Together, these findings revealed that miR-31 acts as an oncogenic miRNA (oncomir) in lung cancer by targeting specific tumor suppressors for repression.
TAR RNA-binding protein is an inhibitor of the interferon-induced protein kinase PKR. (1994)

A cDNA encoding a double-stranded-RNA (dsRNA)-binding protein was isolated by screening a HeLa cell cDNA expression library for proteins that bind the HIV-1 Rev-responsive-element RNA. The cDNA encoded a protein that was identical to TRBP, the previously reported cellular protein that binds the transactivation response element (TAR) RNA of human immunodeficiency virus type 1. TRBP inhibited phosphorylation of the interferon-induced ribosome-associated protein kinase PKR and of the eukaryotic translation initiation factor eIF-2 alpha in a transient-expression system in which the translation of a reporter gene was inhibited by the localized activation of PKR. TRBP expression in HeLa cells complemented the growth and protein-synthesis defect of a vaccinia virus mutant lacking the expression of the dsRNA-binding protein E3L. These results implicate TRBP as a cellular regulatory protein that binds RNAs containing specific secondary structure(s) to mediate the inhibition of PKR activation and stimulate translation in a localized manner.
The effect of sacral neuromodulation on pudendal nerve function and female sexual function (2014)

Women with refractory overactive bladder and non-obstructive urinary retention have abnormal pudendal nerve function, which showed a non-significant trend toward improvement after SNM. Sexually active women undergoing sacral neuromodulation experienced improvement in sexual function. Quality of life improved due to improvement in urinary and colorectal function.
Picosecond optical breakdown: Tissue effects and reduction of collateral damage (1989)

The effects of picosecond laser-induced optical breakdown on tissue were investigated using high-intensity 40 ps Nd:YAG laser pulses at 1.06 microns. Tissue damage was evaluated using the corneal endothelium in vitro as a model system. Systematic studies were performed to determine the scaling of the tissue damage and damage range with pulse energy. For suprathreshold lesions, the radius of the damage zone varies as the cube root of the pulse energy, in agreement with simple physical scaling laws. A minimum damage range of less than 100 microns was observed for pulse energies of 8 muJ. Damage morphology was investigated by scanning electron microscopy. Three different damage patterns were observed; cell damage, cell removal, and rupture of Descemet's membrane. Different irradiation geometries were used to study damage mediated by either the shock wave or the cavitation bubble. Comparative studies using 10 ns pulses demonstrated that picosecond pulses yielded a significant reduction in collateral tissue damage.
A new nude mouse model for postmenopausal breast cancer using MCF-7 cells transfected with the human aromatase gene. (1994)

MCF-7 cells transfected with human placental aromatase gene (MCF-7Ca cells) or cells transfected with plasmid vector only (MCF-7Cc cells) were inoculated into nude mice with Matrigel. Tumors formed from both MCF-7Ca and MCF-7Cc cells grew faster in intact mice than in ovariectomized mice, suggesting that the tumors maintained their responsiveness to estrogen stimulation and that their growth was supported by ovarian estrogen. Injections of androstenedione (0.1 mg/mouse/day) to provide the substrate for aromatization to ovariectomized mice bearing MCF-7Ca tumors accelerated their growth but did not affect growth of MCF-7Cc tumors. This result indicates that local production of estrogen by intratumoral aromatase was sufficient to stimulate tumor growth. When ovariectomized mice with MCF-7Ca tumors supplemented with androstenedione were treated with aromatase inhibitors 4-hydroxyandrostenedione (1 mg/mouse/day, s.c.) or CGS 16949A (0.5 mg/mouse/day, s.c.), or with the antiestrogen tamoxifen (10 micrograms/mouse/day, s.c.), tumor growth was significantly inhibited. Tumor aromatase activity measured at the end of treatment was also inhibited by 4-hydroxyandrostenedione when the mice were sacrificed 4 h after the last injection. The tumors of this mouse model are dependent for their growth on estrogens from an endogenous nonovarian source. Thus, it simulates the situation in the postmenopausal breast cancer patient and could be used to evaluate the effect of aromatase inhibitors and antiestrogens.
Effect of laser pulse repetition rate and pulse duration on mast cell number and degranulation (1996)

Increase in mast cell number is not pulsing frequency dependent, whereas degranulation is.
The Role of Mesenchymal Stem Cells in Skin Wound Healing (2015)

Mesenchymal stem cells (MSCs) could differentiate into various types of tissues. These cells serve as a backup for the regeneration and repair of tissues or cells after injury. A skin wound is defined as an injury to the skin that needs to be restored. All types of cells in skin especially mesenchymal stem cells play important role in wound healing process. In particular, paracrine signaling of MSC regulates the cellular responses at the wound site leading to reduction of inflammation, stimulation of angiogenesis and induction of cell migration and proliferation. Because of these abilities, MSCs are one of the most common stem cells for cell therapy in wound healing. This review focuses on the role of MSCs on wound healing process. In addition, major phases of wound repair and challenges of cell therapy are discussed.
RNA interference using boranophosphate siRNAs: structure-activity relationships (2004)

In RNA interference (RNAi), short double-stranded RNA (known as siRNA) inhibits expression from homologous genes. Clinical or pre-clinical use of siRNAs is likely to require stabilizing modifications because of the prevalence of intracellular and extracellular nucleases. In order to examine the effect of modification on siRNA efficacy and stability, we developed a new method for synthesizing stereoregular boranophosphate siRNAs. This work demonstrates that boranophosphate siRNAs are consistently more effective than siRNAs with the widely used phosphorothioate modification. Furthermore, boranophosphate siRNAs are frequently more active than native siRNA if the center of the antisense strand is not modified. Boranophosphate modification also increases siRNA potency. The finding that boranophosphate siRNAs are at least ten times more nuclease resistant than unmodified siRNAs may explain some of the positive effects of boranophosphate modification. The biochemical properties of boranophosphate siRNAs make them promising candidates for an RNAi-based therapeutic.
The Endoplasmic Reticulum—Gateway of the Secretory Pathway (1999)

In the mid to late 1960s, the discovery that eukaryotic secreted proteins are first segregated in the lumen of the endoplasmic reticulum (ER) before traveling within membranous structures to reach the cell surface placed the ER at the start point of a newly recognized metabolic pathway now known as
Different responses of rat liver adenosine metabolizing enzymes during in vivo and in vitro treatment with interferon‐α2b (1998)

Interferon-alpha 2b (IFN-alpha 2b) can exert antiproliferative activity in both normal and malignant liver tissue. To study mechanisms of its antiproliferative action, the activity of the enzymes of adenosine metabolism were investigated. We studied 5'-nucleotidase (an adenosine-producing enzyme) and adenosine deaminase (involved in adenosine degradation). Female Wistar rats (3 weeks old) were treated with IFN-alpha 2b for 48 h, as were adult rats (3 months old) and adult rats subjected to partial hepatectomy. During IFN-alpha 2b administration, the activity of 5'-nucleotidase increased in the liver of 3-week-old rats, proportionately more than in adult rats, but the greatest increase was seen in partially hepatectomised rats. The activity of adenosine deaminase decreased in the liver of 3-week-old rats, did not change significantly in 3-month-old rats, but was significantly lower in partially hepatectomised rats. As high adenosine concentrations are toxic for mammalian cells, especially during proliferation, the progressive increase of adenosine production, together with the progressive decrease of its degradation, could be one of the mechanisms of IFN-alpha 2b-induced antiproliferative activity. In vitro studies were performed using collagenase-isolated hepatocytes. They were exposed to IFN-alpha 2b, a cAMP analogue, or both. The incubation of hepatocytes with IFN-alpha 2b did not significantly change the activity of both enzymes, whereas incubation with the cAMP analogue decreased 5'-nucleotidase activity and increased adenosine deaminase activity. The mechanism of IFN-alpha 2b-induced alteration in adenosine metabolism is therefore unclear.
Platelet storage in synthetic media lacking glucose and bicarbonate (1991)

The goal of these studies was to develop a cost-effective medium for the storage at 22 +/- 2 degrees C of platelets for transfusion. Platelet concentrates were prepared from platelet-rich plasma in a standard fashion and resuspended in 55 mL of medium. Residual plasma was 14.4 +/- 4.3 percent of the final suspending solution. The use of a simple solution containing electrolytes and citrate, but no glucose or bicarbonate, was associated with a drop in pH to the range of 6.0 to 6.6, as a result of the production of lactic acid from the platelet glycogen and glucose present in residual plasma. When 25 mM (25 mmol/L) sodium phosphate was included as a buffer, the drop in pH was retarded, but the range throughout storage was still 6.5 to 6.8. Nonetheless, platelets stored for 5 days in this phosphate-containing medium showed satisfactory maintenance of many in vitro variables. However, there was a 10 to 35 percent reduction of in vivo recovery after isotopic labeling. There was no significant reduction in subsequent mean cell life. Because of the in vivo abnormalities, these media are not recommended for use at the present time. However, the results are encouraging and suggest that further research may lead to a satisfactory, cost-effective medium.
Role of tumor necrosis factor in the pathogenesis of intravascular coagulopathy of sepsis: potential new therapeutic implications. (1991)

Tumor necrosis factor (TNF) induced by bacterial lipopolysaccharide (LPS) was shown to have an important role in precipitation of septic shock and disseminated intravascular clotting (DIC). At the endothelial level TNF down-regulates thrombomodulin (thus preventing protein C formation) and inhibits the production of tissue plasminogen activator (t-PA), thus impairing anticoagulant mechanisms. On the other hand, TNF up-regulates the production of procoagulant factors such as t-PA inhibitor (PAI), tissue factor and platelet activating factor (PAF). These effects create an imbalance between procoagulant and anticoagulant mechanisms, in favor of the former. TNF also activates polymorphonuclears (PMNs), and increases their chemotaxis and adherence to endothelial surfaces by up-regulation of specific endothelial (ELAM-1) and PMN (CDw18) adherence proteins. The damage inflicted by activated PMN to the endothelial cell promotes tissue factor exposure and PAI release, with initiation of the characteristic explosive coagulation process of DIC, facilitated by the dissociation between pro- and anticoagulant mechanisms induced by TNF. These newly discovered mechanisms precipitating septic shock and DIC enable consideration of new treatments for this condition as anti-TNF antibodies or TNF inhibitors, anti-ELAM-1 antibodies anti-tissue factor antibodies, administration of activated factor C, etc. These therapeutic approaches may revolutionize the treatment of septic shock and DIC in the next decade.
An unexpectedly high excision capacity for mispaired 5-hydroxymethyluracil in human cell extracts (2000)

The oxidation of thymine in DNA can generate a base pair between 5-hydroxymethyluracil (HmU) and adenine, whereas the oxidation and deamination of 5-methylcytosine (5mC) in DNA can generate a base pair between HmU and guanine. Using synthetic oligonucleotides containing HmU at a defined site, HmU-DNA glycosylase activities in HeLa cell and human fibroblast cell extracts have been observed. An HmU-DNA glycosylase activity that removes HmU mispaired with guanine has been measured. Surprisingly, the HmU:G excision activity is 60 times greater than the corresponding HmU:A activity, even though the expected rate of formation of the HmU:A base pair exceeds that of the HmU:G base pair by a factor of 10(7). The HmU:G mispair would arise from the 5mC:G base pair, and, if unrepaired, would give rise to a transition mutation. The observation of an unexpectedly high HmU:G glycosylase activity suggests that human cells may encounter the HmU:G mispair much more frequently than expected. The conversion of 5mC to HmU must be considered as a potential pathway for the generation of 5mC to T transition mutations, which are often found in human tumors.
An Internal Ribosome Entry Segment Promotes Translation of the Simian Immunodeficiency Virus Genomic RNA (2000)

The retroviral genomic RNA is the messenger for the synthesis of the group-specific antigen (gag) and polymerase precursors of the major structural proteins and enzymes of the virion. The 5'-untranslated leader of the simian immunodeficiency virus (SIV) genomic RNA is formed of highly structured domains involved in key steps of the viral life cycle. Thus, the presence of stable RNA structures between the 5'-cap and the gag start codon are thought to strongly inhibit scanning of a 43 S preinitiation ribosomal complex. This prompted us to look for an alternative to the canonical ribosome scanning. By using a standard bicistronic assay in the rabbit reticulocyte lysate, we show that the SIVmac 5'-leader contains an internal ribosome entry segment (IRES) and that gene expression driven by this IRES is stimulated upon cleavage of eukaryotic initiation factor 4G. Deletion analysis revealed that the sequence between the major splice donor and the gag AUG codon is required for IRES activity. DNA transfection and viral transduction experiments in both NIH-3T3 and COS-7 cells confirmed that translation driven by the SIV leader is IRES-dependent and thus insensitive to the immunosuppressant rapamycin. Identification of an IRES in SIV is of particular interest for the understanding of lentivirus replication and also for the design of novel lentiviral vectors suitable for gene transfer.