gebhart/patrepeval huggingface dataset:
On-Demand Routing in Multi-hop Wireless Mobile Ad Hoc Networks (2001)

This thesis introduces a deep reactive-ion-etch (DRIE) CMOS-MEMS process which incorporates bulk Si into microstructures using backside etch. The resultant microstructures are flat and have no release holes. Electrically isolated silicon is obtained using a silicon undercut. This process is suitable for applications that require large mass and flat surfaces such as inertial sensors and micromirrors. 
A technique for vertical-axis sensing and actuation using comb-finger sidewall capacitance is developed. For vertical-axis sensing, this technique has small parasitic capacitance compared to the counterparts that have an electrode on the substrate. For vertical actuation, this technique has a very large gap to substrate set by the process, so that the actuation range is not limited. A unique curled comb drive design demonstrates a maximum 62 μm out-of-plane displacement for a micro-mirror scanning. 
Several thin-film and DRIE devices are fabricated and characterized. A 0.5 mm by 0.5 mm microstage moves 0.3 μm vertically at 14 V d.c. Thin-film and DRIE z-axis accelerometers (both are about 0.5 mm by 0.6 mm) have noise floors of 6 mg/Hz1/2 and 0.5 mg/Hz1/2, respectively. The noise floor of a lateral-axis gyroscope is improved from 0.8°/s/Hz 1/2 for the thin-film CMOS-MEMS process to 0.02°/s/Hz 1/2 for the DRIE CMOS-MEMS process. 
Solutions for improving the gyroscopes' performance and yield are proposed, including a new process flow for independently controlling silicon undercut and a vertical-axis electrostatic force cancellation technique for compensating the off-axis motion. 
The electrostatic micromirror rotates 5° at 18 V d.c. The thermally actuated micromirror rotates 17° at 12 mA current and has been installed into an endoscopic optical coherence tomography imaging system for in vivo imaging of biological tissue. Transverse and axial resolutions of roughly 20 μm and 10 μm, respectively, are achieved. Cross-sectional images of 500 x 1000 pixels covering an area of 2.9 x 2.8 mm2 are acquired at 5 frames/s.
Inhibition of Protein Kinases Sensitizes Human Tumor Cells to Ionizing Radiation (1992)

Protein kinase C (PKC) is activated rapidly and transiently following ionizing radiation exposure and is postulated to activate downstream nuclear signal transducers. Inhibition of this enzyme attenuates radiation-mediated expression of the c-jun and Egr-1/zif-268 genes which are associated with cellular proliferation. To investigate further the role of PKC in the radiation response of human tumor cell lines, two human squamous cell carcinoma cell lines, SQ-20B and JSQ-3, were exposed to graded doses of X rays in the presence of staurosporine, sangivamycin, or H7, all PKC inhibitors. The protein kinase inhibitors staurosporine and sangivamycin produced dose-dependent cytotoxicity in cells of the SQ-20B and JSQ-3 cell lines while H7 did not. Nontoxic concentrations of sangivamycin (10 nM) and staurosporine (1 nM), added to cell cultures from 1 to 7 h before X irradiation, enhanced cell killing by radiation in both cell lines. Maximal sensitization of killing occurred when inhibitors were added 1 h prior to irradiation. The enhanced radiation-induced cell killing was not due to any measurable alteration in the induction or rejoining of DNA single- or double-strand breaks as determined by alkaline and neutral filter elution assays. These data suggest that protein kinase activity is important for cell survival following radiation exposure, although the specific role of PKC in radiation responses is unknown.
[Pharyngeal muscles and sleep obstructive apnea syndrome]. (1999)

An analysis of the way the pharyngeal musculature modulates the caliber of the pharynx is important to better understand and treat obstructive sleep apnea syndromes. The caliber of the pharynx at the soft palate depends on the action of the tensor veli, the palatoglossus, the palatopharyngeus and the uvula muscles. At the ligual level, the action of the genioglossus and the geniohyoideus predominate. These different muscle groups contract in co-ordination before the diaphragm contracts. Their activity is diminished and disorganized during sleep. These muscles appears to have a histological composition adapted to short-duration intense contractions making them vulnerable to fatigue. In apneic patients, these muscles are solicited constantly. Muscular lesions related to overwork have been suggested. The histological composition of these muscles is modified in apneic patients compared with non-apneic subjects (increased number of type IIa fibres), the expression of an adaptive process. The degree of adaptation varies depending of the pharyngeal level considered. Similar to their reflex stimulation, the response of these pharyngeal muscles to increased resistance is probably greater at the soft palate level. Greater solicitation of palatine muscles associated with their greater vulnerability to fatigue could explain why obstruction is particularly important at this level. A study of the mechanical and histological properties of the pharyngeal musculature is required for a better understanding of the occlusive mechanisms of the upper airways and must be undertaken before initiating therapeutic stimulation of these muscles.
The Vulnerable Neonatal Brain (2011)

Preterm infants (<30 weeks' gestation) often have neurodevelopmental difficulties in childhood. In two recent studies, researchers examined early
The use of cystatin C to inhibit epithelial–mesenchymal transition and morphological transformation stimulated by transforming growth factor-β (2005)

Our findings show that TGF-beta stimulation of initiating metastatic events, including decreased cell polarization, reduced cell-cell contact, and elevated cell invasion and migration, are prevented by CystC treatment. Our findings also suggest that the future development of CystC or its peptide mimetics hold the potential to improve the therapeutic response of human breast cancers regulated by TGF-beta.
Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products (1992)

Mature circulating polymorphonuclear cells (PMN) have the shortest half-life among leukocytes and undergo rapid programmed cell death in vitro. In this study, we have examined the possibility that inflammatory signals (cytokines and bacterial products) can regulate PMN survival. PMN in culture were found to rapidly die, with percentages of survival at 24, 48, 72, and 96 hours of 97.3% +/- 1.9%, 36.8% +/- 5.3%, 14.5% +/- 3.1%, and 4.2% +/- 2.9%, respectively (mean +/- SE of 20 different donors). PMN incubated with interleukin-1 beta (IL-1 beta), tumor necrosis factor, granulocyte-macrophage colony-stimulating factor (CSF), granulocyte-CSF, and interferon-gamma (IFN-gamma), but not with prototypic chemoattractants (fMLP, recombinant C5a, and IL-8), showed a marked increase in survival, with values ranging at 72 hours of incubation from 89.5% +/- 5.8% for IL-1 beta to 47.6% +/- 6.4% for IFN-gamma. The calculated half-life was 35 hours for untreated and 115 hours for IL-1-treated PMN. PMN activated with lipopolysaccharide (LPS) or inactivated streptococci also showed a longer survival compared with untreated cells (94.4% +/- 3.2% and 95.5% +/- 2.4%, respectively, at 72 hours). PMN surviving in response to LPS or IL-1 beta retained the capacity to produce superoxide anion when treated with phorbol esters or fMLP. All inducers of PMN survival protect these cells from programmed cell death because they reduced cells with morphologic features of apoptosis and the fragmentation of DNA in multiples of 180 bp. Thus, certain cytokines and bacterial products can prolong PMN survival by interfering with the physiologic process of apoptosis. Prolongation of survival may be important for the regulation of host resistance and inflammation, and may represent a crucial permissive step for certain cytokines and microbial products that activate gene expression and function in PMN.
Early fumonisin B1 toxicity in relation to disrupted sphingolipid metabolism in male BALB/c mice (1998)

Fumonisin B1 is a mycotoxin produced by Fusarium moniliforme, a common fungus in corn. It is known to cause a variety of diseases, including hepatic and renal degeneration in many species of laboratory and domestic animals. The known biochemical events in fumonisin B1 toxicity involve inhibition of ceramide synthase leading to disruption of sphingolipid metabolism. The effect of fumonisin B1 on ceramide and more complex sphingolipids in mice is not known. Groups of five male BALB/c mice each were injected with fumonisin B1 subcutaneously at doses of 0, 0.25, 0.75, 2.25, and 6.75 mg/kg body weight daily for 5 days. This protocol has been shown to produce a dose-dependent increase in apoptosis in liver and kidney of these animals. In the present study, liver, kidney, and brain were sampled and analyzed for free sphingoid bases and complex sphingolipids one day after the last treatment. A dose-related accumulation of free sphinganine and sphingosine was observed in liver and kidney, but not brain. The maximal increase in free sphinganine in kidney was 10-fold greater than in liver. Total phospholipids increased only in liver, whereas ceramide levels were not consistently altered in liver, kidney, or brain. In liver and kidney, fumonisin B1 treatment increased the sphinganine-containing complex sphingolipids, but no effect was observed on sphingosine-containing complex sphingolipids. No changes in complex sphingolipids were observed in brain. In liver, there was a close correlation between the extent of free sphinganine accumulation, and apoptosis and hepatopathy. This correlation was also evident in kidney but to a lessor extent. Nonetheless, the apoptosis and nephropathy occurred with little or no change in the levels of ceramide or more complex sphingolipids.
Detection of moving cast shadows for object segmentation (1999)

To prevent moving shadows being misclassified as moving objects or parts of moving objects, this paper presents an explicit method for detection of moving cast shadows on a dominating scene background. Those shadows are generated by objects moving between a light source and the background. Moving cast shadows cause a frame difference between two succeeding images of a monocular video image sequence. For shadow detection, these frame differences are detected and classified into regions covered and regions uncovered by a moving shadow. The detection and classification assume plane background and a nonnegligible size and intensity of the light sources. A cast shadow is detected by temporal integration of the covered background regions while subtracting the uncovered background regions. The shadow detection method is integrated into an algorithm for two-dimensional (2-D) shape estimation of moving objects from the informative part of the description of the international standard ISO/MPEG-4. The extended segmentation algorithm compensates first apparent camera motion. Then, a spatially adaptive relaxation scheme estimates a change detection mask for two consecutive images. An object mask is derived from the change detection mask by elimination of changes due to background uncovered by moving objects and by elimination of changes due to background covered or uncovered by moving cast shadows. Results obtained with MPEG-4 test sequences and additional sequences show that the accuracy of object segmentation is substantially improved in presence of moving cast shadows. Objects and shadows are detected and tracked separately.
Two mechanisms of the enhanced antibody-dependent cellular cytotoxicity (ADCC) efficacy of non-fucosylated therapeutic antibodies in human blood (2009)

Our results demonstrate that removal of fucosylated antibody ingredients from antibody therapeutics elicits high ADCC in human blood by two mechanisms: namely, by evading the inhibitory effects both of plasma IgG on FcgammaRIIIa binding (effector side interaction) and of fucosylated antibodies on antigen binding (target side interaction).
Cell-mediated amplification and down regulation of cytotoxic immune response against autologous human cancer. (1987)

The cytotoxic host immune response toward autologous human cancer may be regulated by the immunoregulatory network. Here we show that helper T cells, cloned from peripheral blood lymphocytes that were sensitized in vitro against an autologous human malignant paraganglioma, proliferated against and made interleukin 2 when cocultured with the tumor-associated antigen in the presence of autologous accessory cells. Furthermore, the helper cell clones amplified cytotoxic immune response by peripheral blood lymphocytes against the paraganglioma cells in coculture with the blood lymphocytes and the paraganglioma cells. An autologous T cell line bearing suppressor phenotype, established from a lymph node that had been infiltrated with the paraganglioma tumor cells, in contrast to the helper cells, selectively suppressed the cytotoxic immune response by the blood lymphocytes against the paraganglioma cells in identical coculture. These results, therefore, demonstrate the existence of cell-mediated immunologic regulations of the cytotoxic immune response (concurrent amplification and suppression in the same host) against an autologous human tumor.
1.544-Mbits/s Transmission of TV Signals by Interframe Coding System (1976)

As a powerful tool for economizing on the digital transmission of videotelephone signals, interframe coding techniques have drawn increasing attention, and various interframe coding schemes have been proposed recently. However, many problems remain to be studied in establishing technical feasibility for these techniques and schemes. This concise paper reports on field trial in which a 1.544-Mbits/s digital transmission of videotelephone signals was conducted over Nippon Telegraph and Telephone Public Corporation's (NTT's) PCM100M digital repeatered line between Tokyo and Yokohama, Japan. The experimental interframe codec is based on the well-understood conditional picture element replenishment algorithm. The object of the field trial was to demonstrate, not the validity of the algorithm itself, but the technical feasibility of the interframe coding system as an entity. Experimental results are satisfactory enough to assure us of the system's practicality in the near future.
Testosterone‐mediated neuroprotection through the androgen receptor in human primary neurons (2001)

Estrogen is an active neuroprotectant and is presently investigated as a potential therapy against Alzheimer's disease for women. To determine if male hormones could also be neuroprotective, we investigated the effect of testosterone, methyltestosterone, and epitestosterone at physiological concentrations on primary cultures of human neurons induced to undergo apoptosis by serum deprivation. Serum deprivation significantly induces neuronal apoptosis in a protracted fashion. As expected, physiological concentrations of 17-beta-estradiol and transcriptionally inactive 17-alpha-estradiol protect neurons against apoptosis. Similar to 17-beta-estradiol, physiological concentrations of testosterone are also neuroprotective. Androgen receptors are present at 8 +/- 2 fmol/mg protein in the neuron cultures. The non-aromatizable androgen, mibolerone, is also neuroprotective and aromatase inhibitor, 4-androsten-4-OL-3,17-dione, does not prevent testosterone-mediated neuroprotection. In contrast, anti-androgen, flutamide, eliminates testosterone-mediated neuroprotection. Testosterone analog, methyltestosterone, showed androgen receptor-dependent neuroprotection that was delayed in time indicating that a metabolite may be the active agent. The endogenous anti-androgen, epitestosterone, also showed a slight neuroprotective effect but not through the androgen receptor. These results indicate that androgens induce neuroprotection directly through the androgen receptor. These data suggest that androgens may also be of therapeutic value against Alzheimer's disease in aging males.
High-performance (<tex>$\text{EOT} &lt; 0.4\text{nm}$</tex>, Jg∼10−7 A/cm2) ALD-deposited Ru\SrTiO<inf>3</inf> stack for next generations DRAM pillar capacitor (2018)

We demonstrate the fabrication of strontium titanate (STO) based metal-insulator-metal (MIM) capacitors with very-high dielectric constant (k~118) and low leakage of 10 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">-7</sup> A/cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> at ±1V for a ~11nm thick dielectric using Ru as bottom electrode (BE) and top electrode (TE). The k enhancement is attributed to the formation of an ultrathin cubic SrRuO <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">3</sub> phase at the Ru\STO bottom interface, acting as a template optimizing the STO crystal quality from the interface to the bulk. This interface quality is evidenced by the same k~118 extracted from STO thickness series and relating to the bulk-k value. This achievement opens up an alternative integration roadmap for DRAM capacitors, moving from the current cup-shape to a denser pillar-shape design.
Studies of the role of factor Va in the factor Xa-catalyzed activation of prothrombin, fragment 1.2-prethrombin-2, and dansyl-L-glutamyl-glycyl-L-arginine-meizothrombin in the absence of phospholipid. (1990)

In order to specifically evaluate the role of Factor Va in the prothrombinase complex, studies of the activation of prothrombin, Fragment 1.2-prethrombin-2, and active-site-blocked meizothrombin were carried out, both in the absence of phospholipid and at concentrations of substrates and Factor Va sufficient to approach saturation in all components. Km values were independent of Factor Va concentrations, whereas kcat (apparent) values approached saturation with respect to Factor Va concentrations. The three respective substrates exhibited the following parameters of kinetics (Km, microM; kcat, s-1 at saturating [Factor Va]): prothrombin (9.0 +/- 0.4; 31 +/- 1); Fragment 1.2-prethrombin-2 (5.4 +/- 0.4; 13 +/- 2); and meizothrombin (3.6 +/- 0.3; 51 +/- 5). Models of kinetics were constructed to interpret the results, and two of these were formally consistent with experimental results. Both models indicated that the variation of kcat(app) with concentrations of Factor Va reflects the formation of a Factor Va-Factor Xa binary complex. Analysis of kinetics indicated Kd values for this interaction of 1.3 +/- 0.1, 3.0 +/- 0.5, and 1.0 +/- 0.1 microM for the three respective substrates. The models differed in the interpretation of Km. One indicated that Km reflects a binary interaction between Factor Xa and prothrombin, whereas the other indicated a binary interaction between Factor Va and prothrombin. Both indicated that two of the three possible binary interactions between the three components would be reflected in Km and kcat values but not the third. To distinguish these models, the binary interactions were studied by extrinsic fluorescence (Va.Xa), light-scattering (Factor Va.prothrombin), and competition kinetics (Xa.II). The first two interactions were detected and were characterized by Kd values of 2.7 +/- 0.1 microM (Va.Xa) and 8.8 +/- 0.8 microM (Factor Va.prothrombin). No active-site-dependent interaction between prothrombin and Factor Xa could be detected in the absence of Factor Va. The results of these studies suggest that Factor Va interacts with both Factor Xa and prothrombin and effectively presents one to the other in the formation of a ternary enzyme-substrate-cofactor complex. In addition, a comparison of the parameters of kinetics of conversion of prothrombin and its intermediates indicates that meizothrombin is the major intermediate of prothrombin activation in the absence, as well as in the presence of phospholipid.
Immediate-early genes of murine cytomegalovirus: location, transcripts, and translation products (1987)

Cloned genomic fragments from the region (0.769 to 0.818 map units) coding for immediate-early (IE) transcripts of murine cytomegalovirus (MCMV) were used to analyze the physical organization of this region, the direction of transcription, and the proteins synthesized in vitro. Three IE transcription units could be identified. From IE coding region 1 (ie1; 0.781 to 0.796 map units) a dominant 2.75-kilobase (kb) RNA was transcribed from right to left on the prototype arrangement of the MCMV genome which directed the synthesis of an 89,000-molecular-weight polypeptide (89K polypeptide), the major IE protein. This phosphoprotein (pp89) has been shown to be active in the regulation of transcription. Upstream of ie1 and separated by the MCMV enhancer sequence was a second IE coding region, ie2, which was mapped at 0.803 to 0.817 map units. From ie2 a 1.75-kb RNA of moderate abundance was transcribed in the direction opposite to that of the ie1 RNA. After hybrid selection of the ie2 transcript, a 43,000-molecular-weight translation product was detected. A third coding region, ie3, was located directly downstream of ie1 (0.773 to 0.781 map units). The series of RNAs with low abundance, terminating in ie3, probably used the ie1 transcription start site and ranged from 1.0 to 5.1 kb in size. The 5.1-kb RNA apparently represents the nonspliced transcript from both coding regions ie1 and ie3. A 15K polypeptide was translated in vitro from RNA that was hybrid selected by ie3 sequences. Immunoprecipitation with monoclonal antibody revealed that 31K to 67K polypeptides were related to pp89. Some of these proteins were translated from RNAs that were smaller than 2.75 kb. Polypeptides related to pp89 were also synthesized in vivo. Because polypeptides unrelated to pp89 that were translated from RNA that was selected by ie2 and ie3 sequences were not immunoprecipitated by murine antisera, we assumed that the amount of these proteins synthesized in vivo during infection was probably very low.