gebhart/patrepeval huggingface dataset:
Integration of Rac-dependent Regulation of Cyclin D1 Transcription through a Nuclear Factor-κB-dependent Pathway (1999)

The small GTP-binding protein Rac1, a member of the Ras superfamily, plays a fundamental role in cytoskeleton reorganization, cellular transformation, the induction of DNA synthesis, and superoxide production. Cyclin D1 abundance is rate-limiting in normal G(1) phase progression, and the abundance of cyclin D1 is induced by activating mutations of both Ras and Rac1. Nuclear factor-kappaB (NF-kappaB) proteins consist of cytoplasmic hetero- or homodimeric Rel-related proteins complexed to a member of the IkappaB family of inhibitor proteins. In the current studies, activating mutants of Rac1 (Rac(Leu-61), Rac(Val-12)) induced cyclin D1 expression and the cyclin D1 promoter in NIH 3T3 cells. Induction of cyclin D1 by Rac1 required both an NF-kappaB and an ATF-2 binding site. Inhibiting NF-kappaB by overexpression of an NF-kappaB trans-dominant inhibitor (nonphosphorylatable IkappaBalpha) reduced cyclin D1 promoter activation by the Rac1 mutants, placing NF-kappaB in a pathway of Rac1 activation of cyclin D1. Specific amino acid mutations in the amino-terminal effector domain of Rac(Leu-61) had comparable effects on NF-kappaB transcriptional activity and activation of the cyclin D1 promoter. The NF-kappaB factors Rel A (p65) and NF-kappaB(1) (p50) induced the cyclin D1 promoter, requiring both the NF-kappaB binding site and the ATF-2 site. Stable overexpression of Rac(Leu-61) increased binding of Rel A and NF-kappaB(1) to the cyclin D1 promoter NF-kappaB site. Activation of Rac1 in NIH 3T3 cells induces both NF-kappaB binding and activity and enhances expression of cyclin D1 through an NF-kappaB and ATF-2 site in the proximal promoter, suggesting a critical role for NF-kappaB in cell cycle regulation through cyclin D1 and Rac1.
Generation of Fertile Cloned Rats by Regulating Oocyte Activation (2003)

International audience
REVIEWS (1990)

Return to Eden: A Journey Through the Promised Landscape of Amagalyuagba. By David H. Turner. Toronto Studies in Religion, vol. 9. New York: Peter Lang. 1989. Pp. 299.
Reversal of Azidothymidine-Induced Bone Marrow Suppression by 2′,3′-Dideoxythymidine as Studied by Hemopoietic Clonal Culture (1990)

The hematological toxicity of the antiviral drug azidothymidine (AZT) was studied in vitro by measuring the cell growth of hematopoietic progenitor cells obtained from normal bone marrow. AZT inhibited the growth of granulocyte-macrophage (CFU-GM) and early and late erythroid (BFU-E and CFU-E) progenitors in a dose-dependent manner. The hemopoietic inhibition of AZT was significantly reduced by the addition of 2',3'-dideoxythymidine (2',3'-ddT). The results suggest that 2',3'-ddT may be of potential value in reducing AZT toxicity.
Collaborative wideband sensing for cognitive radios (2008)

Cognitive radio (CR) has recently emerged as a promising technology to revolutionize spectrum utilization in wireless communications. In a CR network, secondary users continuously sense the spectral environment and adapt transmission parameters to opportunistically use the available spectrum. A fundamental problem for CRs is spectrum sensing; secondary users need to reliably detect weak primary signals of possibly different types over a targeted wide frequency band in order to identify spectral holes for opportunistic communications. Conceptually and practically, there is growing awareness that collaboration among several CRs can achieve considerable performance gains. This article provides an overview of the challenges and possible solutions for the design of collaborative wideband sensing in CR networks. It is argued that collaborative spectrum sensing can make use of signal processing gains at the physical layer to mitigate strict requirements on the radio frequency front-end and to exploit spatial diversity through network cooperation to significantly improve sensing reliability.
Antibody Therapeutics in Oncology (2016)

One of the newer classes of targeted cancer therapeutics is monoclonal antibodies. Monoclonal antibody therapeutics are a successful and rapidly expanding drug class due to their high specificity, activity, favourable pharmacokinetics, and standardized manufacturing processes. Antibodies are capable of recruiting the immune system to attack cancer cells through complement-dependent cytotoxicity or antibody dependent cellular cytotoxicity. In an ideal scenario the initial tumor cell destruction induced by administration of a therapeutic antibody can result in uptake of tumor associated antigens by antigen-presenting cells, establishing a prolonged memory effect. Mechanisms of direct tumor cell killing by antibodies include antibody recognition of cell surface bound enzymes to neutralize enzyme activity and signaling, or induction of receptor agonist or antagonist activity. Both approaches result in cellular apoptosis. In another and very direct approach, antibodies are used to deliver drugs to target cells and cause cell death. Such antibody drug conjugates (ADCs) direct cytotoxic compounds to tumor cells, after selective binding to cell surface antigens, internalization, and intracellular drug release. Efficacy and safety of ADCs for cancer therapy has recently been greatly advanced based on innovative approaches for site-specific drug conjugation to the antibody structure. This technology enabled rational optimization of function and pharmacokinetics of the resulting conjugates, and is now beginning to yield therapeutics with defined, uniform molecular characteristics, and unprecedented promise to advance cancer treatment.
Sequential clinico-histological studies in psoriasis following methotrexate therapy. (2012)

Ten cases of psoriasis were studied to see the pattern of histological resolution and to evaluate clinico-histological correlation in psoriasis following weekly methotrexate therapy. Five sequential biopsies were taken in each patient. Scaling was first to regress followed by induration and erythema in 18, 26 and 35 days, respectively. Uniform granular layer appeared in 4 days, stratum corneum became orthokeratotic in 7 days, mitotic activity got restricted to basal layer in 7 days and rete ridges elongation was reduced to half in 11 days. Mild acanthosis, cellular infiltrate and vascular dilatation pesisted even after full clinical regression. Interestingly, 5 out of 10 biopsies revealed increase in cellular infiltrate and oedema after first methotrexate pulse.
Proinflammatory pathways in cervicogenic headache. (2000)

Cervicogenic headache (CEH) is a relatively common form of headache arising from the neck structures. The pathophysiology probably results from various local pain-producing factors such as intervertebral dysfunction, with a no less important role played by the frequent coexistence of a history of head traumas. This report represents a series of pathophysiological studies in CEH patients and the results achieved by pharmacological treatment of the disease. Interleukin-1 beta (IL-1 beta) and Tumour Necrosis Factor alpha (TNF-alpha) exert their multifunctional biological effects by promoting and increasing the molecular events of cellular inflammation. We found that the cytokine pattern of CEH patients is--similar to cluster headache--biased towards an inflammatory status. Higher levels of both IL-1 beta and TNF-alpha were detected in the sera of CEH patients than the levels in patients with migraine without aura and in healthy subjects. There were also differences between the spontaneous and mechanically worsened pain phases of CEH. Nitric oxide (NO) synthase is also activated in cervicogenic headache. No change in NO metabolites levels has been observed after NO donor administration. This behaviour is clearly different from that observed in migraine and tension headache patients. We conclude that the high degree of cytokine and NO production in CH may depend on the differing pathophysiological mechanisms at work in CEH than in other forms of headache.
Structure and function of tight junctions. Role in intestinal barrier. (1999)

The tight junctions are narrow belts that circumferentially surround the upper part of the lateral surfaces of the adjacent epithelial cells to create fusion points or "kisses". They are involved in maintaining the cellular polarity and in the establishment of compositionally distinct fluid compartments in the body. Tight junctions are formed by many specific proteins and are connected with the cytoskeleton. In contrast to what might be expected, the intestinal tight junctions are highly dynamic areas and their permeability can change in response to both external and intracellular stimuli. In fact, the tight junctions play an important role in the regulation of the passive transepithelial movement of molecules. A number of signalling molecules have been implicated in the regulation of tight junction function, including Ca++, protein kinase C, G proteins, phospholipase A2 and C. In many intestinal and systemic diseases, changes in intestinal permeability are related to alteration of tight junctions as an expression of intestinal barrier damage. Moreover, permeability of the tight junctions can be modified by bacterial toxins, cytokines, hormones and drugs. A better understanding of tight junction structure, biogenesis and regulation mechanisms should throw further light on the intestinal barrier functions and suggest innovative therapeutic strategies.
Reduction of blood trauma in roller pumps for long‐term perfusion (1985)

Abstract As part of an attempt to develop a roller pump for long‐term (2 weeks) cardiac assist, factors generating blood trauma in roller pumps were re‐examined. Fresh human blood was pumped for 4 hr in a simple closed circulatory loop. Samples drawn at regular intervals were examined for plasma hemoglobin, lactate dehydrogenase, platelet function, and activation of coagulation factors. Experiments were performed in which tubing diameters were varied (polyvinyl chloride, 1/2‐ and 3/8‐inch internal diameters), roller diameters were varied (3/4, 1 1/8, and 1 3/4 inches), and roller occlusion was varied from total occlusion to 0.020‐inch underocclusion. The results showed more hemolysis when the roller diameters and the tubing diameters were smaller and when the rollers were more occlusive. Changes in platelet function and activation of coagulation factors were observed, but were not correlated with occlusion. These results suggest that when roller pumps are used for long‐term cardiac support, the diameter of the rollers should be as large as possible, the tubing diameter should be as large as practical, and the occlusion setting should be as open as possible while still maintaining required flow rates. New techniques for setting occlusion are suggested .
Oxidative para-Triflation of Acetanilides (2013)

Direct triflation of acetanilide derivatives with silver triflate has been accomplished under mild iodine(III)-mediated oxidative conditions. The reaction shows excellent regioselectivity for the para position and tolerates a range of ortho and meta substituents on the aromatic ring. This method is also compatible with the preparation of arylnonaflates in synthetically useful yields.
Optimised KD-trees for fast image descriptor matching (2008)

In this paper, we look at improving the KD-tree for a specific usage: indexing a large number of SIFT and other types of image descriptors. We have extended priority search, to priority search among multiple trees. By creating multiple KD-trees from the same data set and simultaneously searching among these trees, we have improved the KD-treepsilas search performance significantly.We have also exploited the structure in SIFT descriptors (or structure in any data set) to reduce the time spent in backtracking. By using Principal Component Analysis to align the principal axes of the data with the coordinate axes, we have further increased the KD-treepsilas search performance.
Group II Metabotropic Glutamate Receptor Stimulation Triggers Production and Release of Alzheimer's Amyloid β42from Isolated Intact Nerve Terminals (2010)

Aberrant accumulation of amyloid beta (Abeta) oligomers may underlie the cognitive failure of Alzheimer's disease (AD). All species of Abeta peptides are produced physiologically during normal brain activity. Therefore, elucidation of mechanisms that interconnect excitatory glutamatergic neurotransmission, synaptic amyloid precursor protein (APP) processing and production of its metabolite, Abeta, may reveal synapse-specific strategies for suppressing the pathological accumulation of Abeta oligomers and fibrils that characterize AD. To study synaptic APP processing, we used isolated intact nerve terminals (cortical synaptoneurosomes) from TgCRND8 mice, which express a human APP with familial AD mutations. Potassium chloride depolarization caused sustained release from synaptoneurosomes of Abeta(42) as well as Abeta(40), and appeared to coactivate alpha-, beta- and gamma-secretases, which are known to generate a family of released peptides, including Abeta(40) and Abeta(42). Stimulation of postsynaptic group I metabotropic glutamate receptor (mGluRs) with DHPG (3,5-dihydroxyphenylglycine) induced a rapid accumulation of APP C-terminal fragments (CTFs) in the synaptoneurosomes, a family of membrane-bound intermediates generated from APP metabolized by alpha- and beta-secretases. Following stimulation with the group II mGluR agonist DCG-IV, levels of APP CTFs in the synaptoneurosomes initially increased but then returned to baseline by 10 min after stimulation. This APP CTF degradation phase was accompanied by sustained accumulation of Abeta(42) in the releasate, which was blocked by the group II mGluR antagonist LY341495. These data suggest that group II mGluR may trigger synaptic activation of all three secretases and that suppression of group II mGluR signaling may be a therapeutic strategy for selectively reducing synaptic generation of Abeta(42).
Waveform inverstion of marine reflection seismograms for P impedance and Poisson's ratio (1996)

The estimation of the elastic properties of the crust from surface seismic recordings is of great importance for an understanding of the lithology and the detection of mineral resources. Although in marine reflection experiments only P waves are recorded, information on shear properties of the medium is contained in the reflection amplitudes recorded at different distances from the source. Being able to estimate both dilatational and shear properties gives stronger constraints on the lithology. It is therefore desirable to recover both types of elastic parameters from multi-offset seismograms. In the real-data example presented here, the amplitude of the reflections cannot be explained by one parameter related to the dilatational properties (P impedance) only, when trying to minimize the least-squares fit between synthetic and real multi-offset seismograms. When adding an additional parameter related to the shear properties (Poisson's ratio), the fit between synthetic and real seismograms improves. Synthetic-waveform-fitting experiments underline the possibility of recovering Poisson's ration when the P-impedance model is well known from fitting waveforms recorded at small offsets. In the real-data example, the resulting models for P impedance and Poisson's ratio are anticorrelated in most depth regions, but are correlated in particular depth region, indicating a sudden change in lithology.
Intrinsic Cooperation between p16INK4a and p21Waf1/Cip1 in the Onset of Cellular Senescence and Tumor Suppression In vivo (2010)

Although the p16(INK4a) and p21Waf1/Cip1 cyclin-dependent kinase (CDK) inhibitors are known to play key roles in cellular senescence in vitro, their roles in senescence remain rather poorly understood in vivo. This situation is partly due to the possibility of compensatory effect(s) between p16INK4a and p21Waf1/Cip1 or to the upregulation of functionally related CDK inhibitors. To directly address the cooperative roles of p16INK4a and p21Waf1/Cip1 in senescence in vivo, we generated a mouse line simply lacking both p16INK4a and p21Waf1/Cip1 genes [double-knockout (DKO)]. Mouse embryonic fibroblasts (MEF) derived from DKO mice displayed no evidence of cellular senescence when cultured serially in vitro. Moreover, DKO MEFs readily escaped Ras-induced senescence and overrode contact inhibition in culture. This was not the case in MEFs lacking either p16INK4a or p21Waf1/Cip1, indicating that p16(INK4a) and p21Waf1/Cip1 play cooperative roles in cellular senescence and contact inhibition in vitro. Notably, we found the DKO mice to be extremely susceptible to 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate-induced skin carcinogenesis that involves oncogenic mutation of the H-ras gene. Mechanistic investigations suggested that the high incidence of cancer in DKO mice likely reflected a cooperative effect of increased benign skin tumor formation caused by p21Waf1/Cip1 loss, with increased malignant conversion of benign skin tumors caused by p16(INK4a) loss. Our findings establish an intrinsic cooperation between p16INK4a and p21Waf1/Cip1 in the onset of cellular senescence and tumor suppression in vivo.
Cancer stem cells: implications for the progression and treatment of metastatic disease (2007)

Metastasis is the major cause of death for cancer patients with solid tumours, due mainly to the ineffectiveness of current therapies once metastases begin to form. Further insight into the biology of metastasis is therefore essential in order to gain a greater understanding of this process and ultimately to develop better cancer therapies. Metastasis is an inefficient process, such that very few cells that leave a tumour successfully form macrometastases in distant sites. This suggests that only a small subset of cells can successfully navigate the metastatic cascade and eventually re-initiate tumour growth to form life-threatening metastases. Recently, there has been growing support for the cancer stem cell (CSC) hypothesis which stipulates that primary tumours are initiated and maintained by a small subpopulation of cancer cells that possess "stem-like" characteristics. Classical properties of normal stem cells are strikingly reminiscent of the observed experimental and clinical behaviour of metastatic cancer cells, including an unlimited capacity for self renewal; the requirement for a specific 'niche' or microenvironment to grow; use of the stromal cell-derived factor 1 (SDF-1)/chemokine receptor 4 (CXCR4) axis for migration; enhanced resistance to apoptosis and an increased capacity for drug resistance. Therefore, in addition to playing a role in primary tumour formation, we believe that CSCs are also key players in the metastatic process. We will review the current evidence supporting this idea and discuss the potential implications of the CSC hypothesis with regards to experimental investigation and treatment of metastatic disease.
Fibrinolytic Enhancement in Diabetic Microangiopathy with Defibrotide (1992)

Skin microcirculation was evaluated in 117 patients with diabetic microangiopathy over a period of six months. They were divided into two groups. Group 1 (64 patients) was treated with oral defibrotide, a new profibrinolytic drug, in association with diet and oral antidiabetic drugs. Group 2 (53 patients) was treated only with diet and antidiabetic agents. The microcirculation was studied by means of laser-Doppler flowmetry transcutaneous partial pressure of oxygen and carbon dioxide pressure measurements, and evaluation of capillary filtration. After six months, patients in group 1 improved their microcirculatory parameters in association with an improvement in signs and symptoms. Moreover, 30 patients in group 1 and 36 in group 2 were followed up for eighteen months, and the authors observed that the deterioration of the microcirculatory parameters was significantly slowed in diabetics treated with defibrotide. A decrease in plasma fibrinogen during defibrotide treatment was observed in all treated patients in association with an increased fibrinolytic activity. In conclusion, it appears that defibrotide, enhancing fibrinolysis, improved the microcirculation in diabetics, preventing further, progressive deterioration.
Emissions of Ammonia, Hydrogen Sulfide, and Odor before, during, and after Slurry Removal from a Deep-Pit Swine Finisher (2006)

It is a common practice in the midwestern United States to raise swine in buildings with under-floor slurry storage systems designed to store manure for up to one year. These so-called "deep-pit" systems are a concentrated source for the emissions of ammonia (NH3), hydrogen sulfide (H2S), and odors. As part of a larger six-state research effort (U.S. Department of Agriculture-Initiative for Future Agriculture and Food Systems Project, "Aerial Pollutant Emissions from Confined Animal Buildings"), realtime NH3 and H2S with incremental odor emission data were collected for two annual slurry removal events. For this study, two 1000-head deep-pit swine finishing facilities in central Iowa were monitored with one-year storage of slurry maintained in a 2.4 m-deep concrete pit (or holding tank) below the animal-occupied zone. Results show that the H2S emission, measured during four independent slurry removal events over two years, increased by an average of 61.9 times relative to the before-removal H2S emission levels. This increase persisted during the agitation process of the slurry that on average occurred over an 8-hr time period. At the conclusion of slurry agitation, the H2S emission decreased by an average of 10.4 times the before-removal emission level. NH3 emission during agitation increased by an average of 4.6 times the before-removal emission level and increased by an average of 1.5 times the before-removal emission level after slurry removal was completed. Odor emission increased by a factor of 3.4 times the before-removal odor emission level and decreased after the slurry-removal event by a factor of 5.6 times the before-removal emission level. The results indicate that maintaining an adequate barn ventilation rate regardless of animal comfort demand is essential to keeping gas levels inside the barn below hazardous levels.
Statistical Analysis of Accepted Manuscripts in Journal of Oral and Maxillofacial Surgery from 2004 to 2008 (2009)

Objective:To evaluate and analyze the academic value and characteristics of published articles from Journal of Oral and Maxillofacial Surgery (JOMS).Methods:With the application of literature metrology,the information publication of 5 volumes 22 issues of JOMS from 2004 to 2008 was analyzed.Results:The total number of articles published from 2004 to 2008 in JOMS was 641,the average grant-supported paper ratio was 0.30,90.80% of the articles contributed by more than one author.Contributing authors distributed in 28 provinces and regions all over the mainland.There are 18 first authors whose accepted manuscripts were over 3,make a total of 63 (9.83%).The total number of citations were 6083,the citation rate was 93.92%.70.43% of the citations were from abroad.Conclusion:JOMS is dedicated to the dissemination of new knowledge and information on sciences relevant to oral and maxillofacial region in health and disease.