gebhart/patrepeval huggingface dataset:
Plasticity of marrow-derived stem cells (2003)

Bone marrow (BM) contains hematopoietic stem cells (HSCs), which differentiate into every type of mature blood cell; endothelial cell progenitors; and marrow stromal cells, also called mesenchymal stem cells (MSCs), which can differentiate into mature cells of multiple mesenchymal tissues including fat, bone, and cartilage. Recent findings indicate that adult BM also contains cells that can differentiate into additional mature, nonhematopoietic cells of multiple tissues including epithelial cells of the liver, kidney, lung, skin, gastrointestinal (GI) tract, and myocytes of heart and skeletal muscle. Experimental results obtained in vitro and in vivo are the subject of this review. The emphasis is on how these experiments were performed and under what conditions differentiation from bone marrow to epithelial and neural cells occurs. Questions arise regarding whether tissue injury is necessary for this differentiation and the mechanisms by which it occurs. We also consider which bone marrow subpopulations are capable of this differentiation. Only after we have a better understanding of the mechanisms involved and of the cells required for this differentiation will we be able to fully harness adult stem cell plasticity for clinical purposes.
Micromechanical resonators for oscillators and filters (2002)

Fully monolithic, high-Q, micromechanical signal processors are described. A completely monolithic high-Q oscillator, fabricated via a combined CMOS plus surface micromachining technology, is detailed, for which the oscillation frequency is controlled by a polysilicon micromechanical resonator to achieve high stability. The operation and performance of mechanical resonators are modelled, with emphasis on circuit and noise modelling. Micromechanical filter design is described, and a prototype two-resonator bandpass filter is demonstrated. An integrated micro-oven that stabilizes the resonance frequency against temperature variations using only 2 mW of power is reviewed. Brownian motion and mass loading phenomena are shown to have a greater influence on short-term stability and dynamic range in this micro-scale. Scaling strategies are proposed to alleviate potential limitations due to Brownian noise.
Terrain-based navigation: Trajectory recovery from LiDAR data (2008)

The need for complementary technologies to support navigation in GPS-challenged environment is rapidly growing in both outdoor and indoor environments. Remote sensing/mapping sensor performance continues to advance resulting in better spatial and temporal resolution of the acquired geospatial data, which, combined with the increasing hardware performance, can be available real-time or near real-time, and thus could be utilized in forming or improving the navigation solution. Terrain-based navigation has been used for a number of years to navigate airborne platforms, but the continuous exchange of precise geolocation information between the imaging and navigation modules to improve the overall error calibration is a novel idea, which should significantly increase the systempsilas fault tolerance in a variety of situations. The typical navigation solutions for airborne mapping systems are currently based on a GPS or integrated GPS/IMU systems, supporting usually a single imaging sensor, with no feedback between the sensory data processing filters. Most of the research in terrain-based navigation proposes the use of optical measurements from airborne imagery, although the concept of exploring LiDAR-based terrain navigation has also been reported. This paper is concerned with obtaining navigation data from LiDAR, and investigates the feasibility of the airborne trajectory recovery method based on LiDAR data using reference terrain surface models. If GPS signals are lost, the coordinates of LiDAR points can still be computed using the inertial-only solution, however, with errors growing in time. If reference surface data exists, they can be used to recover the LiDAR sensor trajectory by surface matching as long as the IMU drift is under a certain threshold. To assess the performance of the proposed method both simulated LiDAR data were used and an analysis oF the feasibility of the method is provided.
Cell-lab on a chip: a CMOS-based microsystem for culturing and monitoring cells (2005)

We describe a MEMS-on-CMOS microsystem to encage, culture, and monitor cells. The system was designed to perform long-term measurements on arrays of single electrically active cells. A MEMS process flow was developed for the fabrication of closeable microvials to contain each cell, a custom bio-amplifier CMOS chip was designed, fabricated, and tested, and the fabrication of the MEMS structures on this chip was demonstrated. In addition, bovine aortic smooth muscle cells were plated on the surface, and over the course of a week they adhered, formed processes, and reproduced, verifying the compatibility of the materials used with the cell culture.
Energy-efficiency and storage flexibility in the blue file system (2004)

A fundamental vision driving pervasive computing research is access to personal and shared data anywhere at anytime. In many ways, this vision is close to being realized. Wireless networks such as 802.11 offer connectivity to small, mobile devices. Portable storage, such as mobile disks and USB keychains, let users carry several gigabytes of data in their pockets. Yet, at least three substantial barriers to pervasive data access remain. First, power-hungry network and storage devices tax the limited battery capacity of mobile computers. Second, the danger of viewing stale data or making inconsistent updates grows as objects are replicated across more computers and portable storage devices. Third, mobile data access performance can suffer due to variable storage access times caused by dynamic power management, mobility, and use of heterogeneous storage devices. To overcome these barriers, we have built a new distributed file system called BlueFS. Compared to the Coda file system, BlueFS reduces file system energy usage by up to 55% and provides up to 3 times faster access to data replicated on portable storage. 1
Fibroblast cell interactions with human melanoma cells affect tumor cell growth as a function of tumor progression. (1991)

It is known from a variety of experimental systems that the ability of tumor cells to grow locally and metastasize can be affected by the presence of adjacent normal tissues and cells, particularly mesenchymally derived stromal cells such as fibroblasts. However, the comparative influence of such normal cell-tumor cell interactions on tumor behavior has not been thoroughly investigated from the perspective of different stages of tumor progression. To address this question we assessed the influence of normal dermal fibroblasts on the growth of human melanoma cells obtained from different stages of tumor progression. We found that the in vitro growth of most (4 out of 5) melanoma cell lines derived from early-stage radial growth phase or vertical growth phase metastatically incompetent primary lesions is repressed by coculture with normal dermal fibroblasts, suggesting that negative homeostatic growth controls are still operative on melanoma cells from early stages of disease. On the other hand, 9 out of 11 melanoma cell lines derived from advanced metastatically competent vertical growth phase primary lesions, or from distant metastases, were found to be consistently stimulated to grow in the presence of dermal fibroblasts. Evidence was obtained to show that this discriminatory fibroblastic influence is mediated by soluble inhibitory and stimulatory growth factor(s). Taken together, these results indicate that fibroblast-derived signals can have antithetical growth effects on metastatic versus metastatically incompetent tumor subpopulations. This resultant conversion in responsiveness to host tissue environmental factors may confer upon small numbers of metastatically competent cells a growth advantage, allowing them to escape local growth constraints both in the primary tumor site and at distant ectopic tissue sites.
Cephalosporins to carbapenems: 1-oxygenated carbapenems and carbapenams (1990)

The photo "Wolff" rearrangement of readily available 2-diazoceph-3-em oxides (1) directly affords carbapen-2-ems, allowing a facile entry into a ring system previously accessible only by total synthesis, lengthly semisynthesis or fermentation. The chirality of the cephalosporin is accurately translated into the corresponding carbapenem. The resulting 1-oxocarbapenems (2) were selectively transformed through reduction into 1-oxygenated carbapenems and carbapenams (3 and 4, respectively). On microbiological screening, a carbapenem (3c) was found to possess a broad spectrum of activity. An interesting antibacterial profile was discovered for a carbapenam (26).
Frame-rate up-conversion using transmitted true motion vectors (2002)

In this paper, we present a video frame-rate up-conversion scheme that uses transmitted true motion vectors for motion-compensated interpolation. In a past work, we demonstrated that a neighborhood-relaxation motion tracker can provide more accurate true motion information than a conventional minimal-residue block-matching algorithm. Although the technique to estimate the true motion vectors is a novelty in its own right, the strength of this technique can be further demonstrated through various spatio-temporal interpolation applications. In this work, we focus on the particular problem of frame-rate up-conversion. In the proposed scheme, the true motion field is derived by the encoder and transmitted by normal means (e.g., MPEG or H.263 encoding). Then, it is recovered by the decoder and is used not only for motion compensated predictions but also used to reconstruct missing data. It is shown that the use of our neighborhood-relaxation motion estimation provides a method of constructing high quality image sequences in a practical manner.
Mutation profiling of mismatch repair-deficient colorectal cncers using an in silico genome scan to identify coding microsatellites. (2002)

Human colorectal, endometrial, and gastric cancers with defective DNA mismatch repair (MMR) have microsatellite instability, a unique molecular alteration characterized by widespread frameshift mutations of repetitive DNA sequences. We developed "Kangaroo," a bioinformatics program for searches in nucleotide and protein sequence databases, and performed an in silico genome scan for DNA coding microsatellites that may have novel mutations in MMR-deficient cancers. Examination of 29 previously untested coding polyadenines revealed widespread mutations in MMR-deficient colorectal cancers, with the highest frequencies in ERCC5, CASP8AP2, p72, RAD50, CDC25, RECQL1, CBF2, RACK7, GRK4, and DNAPK (range, 10-33%). This algorithm allows comprehensive mutation profiling of MMR-deficient cancers, an important step in understanding the pathogenesis of these neoplasms.
Nonrandom gene organization: structural arrangements of specific pre-mRNA transcription and splicing with SC-35 domains. (1995)

This work demonstrates a highly nonrandom distribution of specific genes relative to nuclear domains enriched in splicing factors and poly(A)+ RNA, and provides evidence for the direct involvement of these in pre-mRNA metabolism. As investigated in hundreds of diploid fibroblasts, human collagen I alpha 1 and beta-actin DNA/RNA showed a very high degree of spatial association with SC-35 domains, whereas three nontranscribed genes, myosin heavy chain, neurotensin, and albumin, showed no such preferential association. Collagen I alpha 1 RNA accumulates within the more central region of the domain, whereas beta-actin RNA localizes at the periphery. A novel approach revealed that collagen RNA tracks are polarized, with the entire gene at one end, on the edge of the domain, and the RNA extending into the domain. Intron 26 is spliced within the RNA track at the domain periphery. Transcriptional inhibition studies show both the structure of the domain and the gene's relationship to it are not dependent upon the continued presence of accumulated collagen RNA, and that domains remaining after inhibition are not just storage sites. Results support a model reconciling light and electron microscopic observations which proposes that transcription of some specific genes occurs at the border of domains, which may also function in the assembly or distribution of RNA metabolic components. In contrast to the apparently random dispersal of total undefined hnRNA synthesis through interdomain space, transcription and splicing for some genes occurs preferentially at specific sites, and a high degree of individual pre-mRNA metabolism is compartmentalized with discrete SC-35 domains.
Different dynamics of IL-15R activation following IL-15 cis- or trans-presentation. (2010)

Interleukin (IL)-15 is a cytokine critical for the homeostasis and the function of NK cells, NK-T cells, and memory CD8+ T cells. IL-15 signals are delivered through the IL-15Rβ and the common γ (γ(c)) receptor chains. The third receptor chain, IL-15Rα, confers specificity and high affinity for the cytokine. While IL-15 can activate with high affinity the trimeric receptor expressed by a target cell (cis-presentation), IL-15Rα is also known to trans-present IL-15 with high affinity to target cells expressing the IL-15Rβ/γ(c) complex. In order to compare the IL-15 cis- and trans-presentation processes, and using a T cell line expressing both IL-15Rα/β/γ(c) and IL-15Rβ/γ(c), we analyzed cell surface receptor chain down-modulation, cytokine internalization and signaling responses induced either with IL-15 (cis-presentation) or with RLI, a protein resulting from fusion between IL-15 and an extended IL-15Rα sushi domain, that mimics trans-presentation. Whereas IL-15 bound with high affinity to IL-15Rα/β/γ(c), RLI bound with a similar high affinity to IL-15Rβ/γ(c). The kinetics of cell surface IL-15R down-modulation were slower following RLI treatment than after IL-15 treatment, as were the kinetics of RLI internalization, which was slower than that of IL-15. IL-15 and RLI dose-dependently induced the activation of similar signaling pathways. However, the kinetics and duration of these activations were markedly different, RLI-induced signaling, being slower, but more prolonged than that induced by IL-15, although the final proliferative responses at 48 h were similar. These findings collectively indicate that IL-15 cis- and trans-presentation mechanisms lead to different dynamics of receptor activation and signal transduction, with cis-presentation inducing fast and transient responses, and trans-presentation inducing slower, more persistent ones. They provide clues for a better understanding of how IL-15 action is controlled, and how it plays a key role in the coordination between innate and adaptative immunity.
NTRK2 activation cooperates with PTEN deficiency in T-ALL through activation of both the PI3K–AKT and JAK–STAT3 pathways (2016)

Loss of PTEN, a negative regulator of the phosphoinositide 3-kinase signaling pathway, is a frequent event in T-cell acute lymphoblastic leukemia, suggesting the importance of phosphoinositide 3-kinase activity in this disease. Indeed, hyperactivation of the phosphoinositide 3-kinase pathway is associated with the disease aggressiveness, poor prognosis and resistance to current therapies. To identify a molecular pathway capable of cooperating with PTEN deficiency to drive oncogenic transformation of leukocytes, we performed an unbiased transformation screen with a library of tyrosine kinases. We found that activation of NTRK2 is able to confer a full growth phenotype of Ba/F3 cells in an IL3-independent manner in the PTEN-null setting. NTRK2 activation cooperates with PTEN deficiency through engaging both phosphoinositide3-kinase/AKT and JAK/STAT3 pathway activation in leukocytes. Notably, pharmacological inhibition demonstrated that p110α and p110δ are the major isoforms mediating the phosphoinositide 3-kinase/AKT signaling driven by NTRK2 activation in PTEN-deficient leukemia cells. Furthermore, combined inhibition of phosphoinositide 3-kinase and STAT3 significantly suppressed proliferation of PTEN-mutant T-cell acute lymphoblastic leukemia both in culture and in mouse xenografts. Together, our data suggest that a unique conjunction of PTEN deficiency and NTRK2 activation in T-cell acute lymphoblastic leukemia, and combined pharmacologic inhibition of phosphoinositide 3-kinase and STAT3 signaling may serve as an effective and durable therapeutic strategy for T-cell acute lymphoblastic leukemia.
GM‐CSF triggers a rapid, glucose dependent extracellular acidification by TF‐1 cells: Evidence for sodium/proton antiporter and PKC mediated activation of acid production (1993)

The extracellular acidification rate of the human bone marrow cell line, TF-1, increases rapidly in response to a bolus of recombinant granulocyte-macrophage colony stimulating factor (GM-CSF). Extracellular acidification rates were measured using a silicon microphysiometer. This instrument contains micro-flow chambers equipped with potentiometric sensors to monitor pH. The cells are immobilized in a fibrin clot sandwiched between two porous polycarbonate membranes. The membranes are part of a disposable plastic "cell capsule" that fits into the microphysiometer flow chamber. The GM-CSF activated acidification burst is dose dependent and can be neutralized by pretreating the cytokine with anti-GM-CSF antibody. The acidification burst can be resolved kinetically into at least two components. A rapid component of the burst is due to activation of the sodium/proton antiporter as evidenced by its elimination in sodium-free medium and in the presence of amiloride. A slower component of the GM-CSF response is a consequence of increased glycolytic metabolism as demonstrated by its dependence on D-glucose as a medium nutrient. Okadaic acid (a phospho-serine/threonine phosphatase inhibitor), phorbol 12-myristate 13-acetate (PMA, a protein kinase C (PKC) activator), and ionomycin (a calcium ionophore) all produce metabolic bursts in TF-1 cells similar to the GM-CSF response. Pretreatment of TF-1 cells with PMA for 18 h resulted in loss of the GM-CSF acidification response. Although this treatment is reported to destroy protein kinase activity, we demonstrate here that it also down-regulates expression of high-affinity GM-CSF receptors on the surface of TF-1 cells. In addition, GM-CSF driven TF-1 cell proliferation was decreased after the 18 h PMA treatment. Short-term treatment with PMA (1-2 h) again resulted in loss of the GM-CSF acidification response, but without a decrease in expression of high-affinity GM-CSF receptors. Evidence for involvement of PKC in GM-CSF signal transduction was obtained using calphostin C, a specific inhibitor of PKC, which inhibited the GM-CSF metabolic burst at a subtoxic concentration. Genistein and herbimycin A, tyrosine kinase inhibitors, both inhibited the GM-CSF response of TF-1 cells, but only at levels high enough to also inhibit stimulation by PMA. These results indicate that GM-CSF activated extracellular acidification of TF-1 cells is caused by increases in sodium/proton antiporter activity and glycolysis, through protein kinase signalling pathways which can be both activated and down-regulated by PMA.
Asymmetric synthesis of (+)- or (-)-2-methyloctanal via the metalloenamines of chiral alkoxy amines (1978)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTAsymmetric synthesis of (+)- or (-)-2-methyloctanal via the metalloenamines of chiral alkoxy aminesA. I. Meyers, Graham S. Poindexter, and Zdenek BrichCite this: J. Org. Chem. 1978, 43, 5, 892–898Publication Date (Print):March 1, 1978Publication History Published online1 May 2002Published inissue 1 March 1978https://pubs.acs.org/doi/10.1021/jo00399a021https://doi.org/10.1021/jo00399a021research-articleACS PublicationsRequest reuse permissionsArticle Views859Altmetric-Citations96LEARN 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
Activation of the gadd153 promoter by genotoxic agents: a rapid and specific response to DNA damage. (1992)

Accumulation of gadd153 mRNA is strongly stimulated in mammalian cells by treatments which arrest growth or damage DNA (A. J. Fornace, Jr. et al., Mol. Cell. Biol., 9: 4196-4203, 1989). In previous studies, we demonstrated that the increased expression of gadd153 following treatment with several DNA-damaging agents was mediated transcriptionally (J. D. Luethy et al., J. Biol. Chem., 265: 16521-16526, 1990). To better define the specificity of this response, we have established a sensitive reporter system in which we have stably integrated a chimeric gene containing the gadd153 promoter linked to the coding region of the chloramphenicol acetyltransferase (CAT) gene into the genome of HeLa cells. Transcriptional activation from the gadd153 promoter was monitored by determining levels of CAT activity in cellular lysates prepared from gadd153CAT/HeLa cells treated with a variety of agents. The gadd153 promoter was strongly activated by a broad spectrum of genotoxic agents including UV-mimetic agents, DNA-cross-linking and alkylating agents, DNA intercalators, and topoisomerase inhibitors. Of the DNA-damaging agents tested, only X-irradiation and bleomycin treatments failed to induce gadd153 promoter activity. Agents which inhibit replication and cell division and agents which otherwise result in cytotoxicity or growth arrest also had little influence on gadd153 promoter activity. Expression of the gadd153CAT chimeric gene in xeroderma pigmentosum Group A cells, which are deficient in nucleotide excision DNA repair of pyrimidine dimers, was maximally induced at UV doses at least 6-fold lower than those required for similar induction in repair-proficient HeLa cells. However, the methyl methanesulfonate-induced gadd153 promoter activities were similar in both cell lines. Novobiocin pretreatment inhibited both UV- and methyl methanesulfonate-induced gadd153CAT expression. Collectively, these data indicate that: (a) the gadd153 promoter is activated rapidly and specifically by DNA damage; (b) the altered DNA structure is the inducing signal for the activation of the signal transduction pathway responsible for enhanced gadd153 expression; and (c) regulation of gadd153 by growth arrest is distinct from that of DNA damage. Thus, the gadd153CAT/HeLa cells are a useful model for examining the molecular mechanisms associated with the response to DNA damage and provide a reporter system for the screening of potential genotoxic agents.