gebhart/patrepeval huggingface dataset:
Novel reconfigurable fundamental/harmonic matching network for enhancing the efficiency of power amplifiers (2010)

This paper presents a novel tunable matching network scheme suitable for the design of electronically reconfigurable microwave circuits. These circuits enable the development of high performance and frequency agile RF front-end modules for multi-band and multi-carrier radios in cognitive wireless networks. In this paper, the tunable matching network includes a harmonic tuning feature essential to the design of high efficiency power amplifiers (HEPA). Two different types of electronic tunable devices, namely MEMS switches and semiconductors varactors, are used in the realization of the reconfigurable matching networks proof of concepts prototypes designed to operate in the band spanning from 1.8GHz to 2.7GHz. Both prototypes revealed a broad impedance tuning range (|Γ|> 0.85) along with low insertion loss (IL<1.3dB for high |Γ|). The varactor-based matching network was used to modulate the load impedance of a 10Watt HEPA operating in Class F−1. The control of the load impedance versus the input signal power allowed for significant efficiency improvement compared to conventional Class F−1 PA which attained about 18% at 6 dB back-off.
Src Kinase Mediates the Regulation of Phospholipase C-γ Activity by Glycosphingolipids (2003)

Glucosylceramide-based glycosphingolipids have been previously demonstrated to regulate negatively the formation of inositol 1,4,5-trisphosphate by phospholipase C-gamma1. In the present study, the depletion of endogenous glucosylceramide by D-t-EtDO-P4 in cultured ECV304 cells induced autophosphorylation of Src kinase at tyrosine residue 418 within the catalytic loop and dephosphorylation of Src kinase at tyrosine residues 529 within the carboxyl-terminal regulatory region. Phosphotransferase activities of Src kinase were also induced in the glucosylceramide-depleted cells. c-Src kinase activity and phosphorylations at Src Tyr-418 and epidermal growth factor (EGF) receptor Tyr-1068 were significantly enhanced by bradykinin in response to 100 nm D-t-EtDO-P4 compared with control cells. The phosphorylation and dephosphorylation on Tyr-418 and Tyr-529 residues of c-Src were reversed by treatment of 4-amino-5-(4-chlorophenyl)-7-t-butyl(pyrazolo)[3,4-d]pyrimidine (PP2), an inhibitor of Src kinase, in control cells. Glucosylceramide-depleted cells resisted treatment with PP2, and both phosphorylation of Tyr-418 and dephosphorylation of Tyr-529 induced by depletion of glucosylceramide were maintained. Compared with untreated cells, tyrosine phosphorylation of phospholipase C-gamma1 was enhanced by EGF stimulation in glucosylceramide-depleted cells, associated with enhanced tyrosine phosphorylation of the EGF receptor at Tyr-1068 and Tyr-1086 stimulated by EGF. The Src inhibitor, PP2, significantly blocked EGF-induced tyrosine phosphorylation of phospholipase C-gamma1 in control cells, whereas in glucosylceramide-depleted cells, suppression of Src kinase activity by PP2 toward EGF-induced tyrosine phosphorylation of phospholipase C-gamma1 was less significant. Thus the activation of Src kinase by depletion of glucosylceramide-based glycosphingolipids in cultured ECV304 cells is a critical up-stream event in the activation of phospholipase C-gamma1.
The Transcriptional Activator Hepatocyte Nuclear Factor 6 Regulates Liver Gene Expression (1996)

The hepatocyte nuclear factor 3(alpha) (HNF-3(alpha)), -3(beta), and -3(gamma) proteins share homology in the winged-helix/fork head DNA binding domain and mediate hepatocyte-enriched transcription of numerous genes whose expression is necessary for organ function. In this work, we identify a liver-enriched transcription factor, HNF-6, which recognizes the -138 to -126 region of the HNF-3(beta) promoter and binds the original HNF-3 site of the transthyretin promoter (-94 to -106). We show that HNF-6 and HNF-3 possess different DNA binding specificities by competition and methylation interference studies and are immunologically distinct. Site-directed mutagenesis of the HNF-6 sites in the HNF-3(beta) and transthyretin promoters diminishes reporter gene expression, suggesting that HNF-6 activates transcription of these promoters. Using the HNF-6 binding sequence DHWATTGAYTWWD (where W = A or T, Y = T or C, H is not G, and D is not C) determined by sequence comparison and methylation interference, we predicted that HNF-6 will bind to 22 additional hepatocyte-enriched genes. Of these potential target genes, we selected seven of the HNF-6 binding sequences and demonstrated that they bind the HNF-6 protein. These include promoter sequences from alpha-2 urinary globulin, alpha-1 antitrypsin, cytochrome P-450 2C13, L-type 6-phosphofructo-2-kinase, mouse major urinary protein, tryptophan oxygenase, and alpha-fetoprotein genes. HNF-6 binding activity was also found in the intestinal epithelial cell line HT29, and potential HNF-6 binding sites were present in intestinal sucrase isomaltase, cdx-2 homeodomain protein, and intestinal fatty acid binding protein promoter regions. These studies suggest that HNF-6 may regulate hepatocyte-specific genes and may play a role in epithelial cell differentiation of gut endoderm via regulation of HNF-3(beta).
Albumin turnover: FcRn-mediated recycling saves as much albumin from degradation as the liver produces (2005)

It is now understood that the nonclassical major histocompatibility complex-I molecule FcRn binds albumin and retrieves it from an intracellular degradative fate. Whether FcRn in the liver modulates albumin turnover through effects on biosynthesis and production is not known. Thus we quantified the appearance of biosynthetically labeled albumin in plasma after an intravenous bolus injection of [(3)H]leucine in FcRn-deficient mice. The production rates for both albumin (FcRn substrate) and transferrin (nonsubstrate) are increased by approximately 20% in FcRn-deficient mice compared with normal mice, likely compensating for the lowered plasma oncotic pressure caused by hypoalbuminemia in FcRn-deficient mice. Determining the magnitude of FcRn-mediated effects on albumin turnover, we then measured the steady-state plasma concentrations of biosynthetically labeled albumin and transferrin during [(3)H]leucine infusion. The concentration of albumin was approximately 40% lower in FcRn-deficient mice compared with normal mice. Furthermore, the approximately 40% lower plasma albumin concentration in FcRn-deficient mice along with the approximately 20% increase in albumin production indicate, by the mass-balance equation, that albumin degradation in FcRn-deficient mice is twice that of normal mice. These studies of biosynthetically labeled, and thus native, albumin support our previous finding that FcRn protects albumin from degradation. Permitting quantification of the magnitude of FcRn-mediated recycling, they further indicate that FcRn has extraordinary capacity: the amount of albumin saved from degradation by FcRn-mediated recycling is the same as that produced by the liver.
Proteinase-activated receptors: structural requirements for activity, receptor cross-reactivity, and receptor selectivity of receptor-activating peptides (1997)

We have used three distinct bioassay systems (rat aorta (RA) relaxation; rat gastric longitudinal muscle (LM) contraction; human embryonic kidney 293 (HEK293) cell calcium signal) to evaluate the activity and receptor selectivity of analogues of the receptor-activating peptides derived either from the thrombin receptor (TRAPs, based on the human receptor sequence, SFLLRNPNDK...) or the proteinase-activated receptor 2 (PAR2APs, based on the rat receptor sequence SLIGRL...). Our main focus was on the activation of PAR2 by PAR2APs and the cross-activation of PAR2 by the TRAPs. In the RA and LM assay systems, PAR2APs that were either N-acetylated (N-acetyl-SLIGRL-NH2) or had a reverse N-terminal sequence (LSIGRL-NH2) were inactive, either as agonists or antagonists. An alanine substitution at position 3 of the PAR2AP (SLAGRL-NH2) led to a dramatic reduction of biological activity, as did substitution of threonine for serine at position 1 (TLIGRL-NH2). However, alanine substitution at PAR2AP position 4 caused only a modest reduction in activity, resulting in a peptide (SLIARL-NH2) with a potency equivalent to that of the human PAR2AP, SLIGKV-NH2. The order of potency of the PAR2APs in the RA, LM, and HEK assay systems was SLIGRL-NH2 > SLIARL-NH2 > SLIGKV-NH2 > TLIGRL-NH2 > SLAGRL-NH2. In HEK cells, none of the PAR2APs activated the thrombin receptor (PAR1). However, in the HEK cell assay, the TRAP, SFLLR-NH2, activated or desensitized both PAR1 and PAR2 receptors, whereas the xenopus TRAP, TFRIFD-NH2, activated or desensitized selectively PAR1 but not PAR2. By constructing human-xenopus hybrid peptides, we found that the TRAPs, TFLLR-NH2, and SFLLFD-NH2 selectively activated the thrombin receptor in HEK cells without activating or desensitizing PAR2. In contrast, the TRAPs SFLLRD-NH2 and AFLLR-NH2 activated or desensitized both PAR1 and PAR2. The order of potency for the TRAPs in all bioassay systems was SFLLR-NH2 approximately equal to SFLLRD-NH2 approximately equal to TFLLR-NH2 > SFLLFD-NH2 > TFRIFD-NH2. We conclude that the N-terminal domain of the PAR2AP as well as positon 3 plays important roles for PAR2 activation. In contrast, the first and fifth amino acids in the TRAP motif, SFLLR-NH2, do not play a unique role in activating the thrombin receptor, but if appropriately modified can abrogate the ability of this peptide to cross-desensitize or activate PAR2, so as to be selective for PAR1. The PAR1- and PAR2-selective peptides that we have synthesized will be of use for the evaluation of the roles of the PAR1 and PAR2 receptor systems in vivo.
Beugung im inhomogenen Primärstrahlwellenfeld. I. Prinzip einer Phasenmessung von Elektronenbeungungsinterferenzen (1969)

In addition to the amplitude information, phase information can also be obtained from a generalized diffraction experiment (in spite of the inability of the detector to observe phases directly) on condition that the primary ray can be controlled in a defined way. A single diffraction pattern suffices for the determination of the phases except in the case of a centre of symmetry in real space, and the combination of at least two patterns removes this ambiguity.
Infections in the male genital tract and reactive oxygen species (1999)

In the male genital tract, reactive oxygen species (ROS) are generated by spermatozoa and leukocytes including neutrophils and macrophages. ROS are involved in the regulation of sperm functions such as capacitation and the acrosome reaction. Infections lead to an excessive ROS production, resulting in an 'oxidative burst' from neutrophils/macrophages as a first-line defence mechanism. This is modulated by several cytokines and the pro-oxidant mechanisms of bacteria and viruses. At the site of an infection, the degree of activation of leukocytes, i.e. the amount of ROS produced, and the available antioxidative systems determine whether spermatozoa are damaged or not. During an infection, an imbalance of pro- and antioxidants favouring the former results in oxidative stress which impairs the sperm functions mentioned, as well as motility and fertilization. ROS produced during infections of the testis and epididymis are especially harmful to spermatozoa due to the longer contact time and the lack of antioxidant protection. In the final ejaculate, only very high numbers of ROS-producing leukocytes are detrimental to sperm functions. An infectious injury involving ROS in the prostate gland, seminal vesicles or epididymis could impair sperm functions indirectly. Pro- and antioxidative properties of therapeutics are currently receiving more attention as part of anti-infectious therapies. At present, there are many unresolved questions concerning the exact role of ROS during infections of the male genital tract because of the difficulty of specifically assessing the site of generation and the short-lived effects of ROS. New techniques may enable specific studies to fill this gap in the near future.
Determining the optimum extended instruction-set architecture for application specific reconfigurable VLIW CPUs (poster abstract) (2000)

No abstract available.
II. Pulmonary Neoplasms (1970)

Of 86 dogs trained to smoke through a tracheostoma, 12 dogs (group F) smoked filler-tip, 24 (group H) and 38 (group h) smoked non-filter cigarettes, and 12 (group l), half as many non…filter cigarettes.. Eight dogs (group N) never smokedm By day 875, none of the N dogs, 2 F dogs, 2 L dogs, 12 H dogs, and 12 h dogs had died, and the remaining N, F, L, and H dogs were killede Noninvasive bronchiolo-alveolar tumors were found in dogs of all five groups. Invasive bronchiolo-alveolar tumors were found only in H and h dogs: in two of 12 group h and group H dogs, respectively, which died, and eight of 12 group H dogs which were killed., One extended to and four into the pleura. Early invasive squamous cell carcinoma was found in bronchi of two of group H dogs which were killed.
Solid Lithium‐Silicon Electrode (1976)

Results of a preliminary investigation into the use of a solid Li--Si electrode in a high-temperature fused salt secondary battery are reported. A series of measurements was made to characterize the voltage plateaus and to identify the alloy compositions corresponding to each. Entropy calculations were also made by measuring the variations in the potential of the alloy electrode vs. pure liquid Li at temperatures between 360 and 440/sup 0/C. It is concluded that the Li--Si electrode is promising as an excellent anode material for high-energy-density batteries.
TGFβSignaling in Tumor Initiation, Epithelial-to-Mesenchymal Transition, and Metastasis (2015)

Retaining the delicate balance in cell signaling activity is a prerequisite for the maintenance of physiological tissue homeostasis. Transforming growth factor-beta (TGFβ) signaling is an essential pathway that plays crucial roles during embryonic development as well as in adult tissues. Aberrant TGFβ signaling activity regulates tumor progression in a cancer cell-autonomous or non-cell-autonomous fashion and these effects may be tumor suppressing or tumor promoting depending on the cellular context. The fundamental role of this pathway in promoting cancer progression in multiple stages of the metastatic process, including epithelial-to-mesenchymal transition (EMT), is also becoming increasingly clear. In this review, we discuss the latest advances in the effort to unravel the inherent complexity of TGFβ signaling and its role in cancer progression and metastasis. These findings provide important insights into designing personalized therapeutic strategies against advanced cancers.
Functional Evaluation of Complete Sciatic, Peroneal, and Posterior Tibial Nerve Lesions in the Rat (1989)

Quantification of peripheral nerve regeneration in animal studies of nerve injury and repair by histologic, morphologic, and electrophysiologic parameters has been controversial because such studies may not necessarily correlate with actual nerve function. This study modifies the previously described sciatic functional index (SFI), tibial functional index (TFI), and peroneal functional index (PFI) based on multiple linear regression analysis of factors derived from measurements of walking tracks in rats with defined nerve injuries. The factors that contributed to these formulas were print-length factor (PLF), toe-spread factor (TSF), and intermediary toe-spread factor (ITF). It was shown that animals with selective nerve injuries gave walking tracks that were consistent, predictable, and based on known neuromuscular deficits. The new formula for sciatic functional index was compared with previously described indices. The sciatic functional index, tibial functional index, and peroneal functional index offer the peripheral nerve investigator a noninvasive quantitative assessment of hindlimb motor function in the rat with selective hindlimb nerve injury.
Integrity of Cell‐Free Plasma DNA in Patients with Lung Cancer and Nonmalignant Lung Disease (2008)

In several papers an increased quantity of cell-free plasma DNA as well as the presence of long DNA fragments in cell-free plasma and serum has been described. We isolated cell-free DNA from plasma, serum, and bronchial lavage supernatants from 33 lung cancer patients and 27 patients with a benign lung disease. The DNA was amplified by real-time PCR, and the quantity as well as the DNA integrity was determined. We did not find significant differences between the patient populations. Our results led us to conclude that this method is not useful in a diagnostic setting and is not able to differentiate between lung cancer patients and patients with a benign lung disease.
Miniaturization of inductively coupled plasma sources (1999)

The scaling laws associated with the miniaturization of planar inductively coupled plasmas (ICPs) are investigated. The applications for miniature ICPs include microelectromechanical systems (MEMS) for chemical analysis and micro ion propulsion systems. Langmuir probe and microwave interferometry measurements of three ICPs with spiral-shaped coil diameters of 5, 10, and 15 mm show that electron density typically falls in the range of 10/sup 16/-10/sup 17/ m/sup -3/. The electron density is about an order of magnitude lower than large-scale ICPs as a result of the large surface-to-volume ratio of small discharges. The measured electron temperature is higher than predicted by a simple "global model" unless the plasma dimensions are determined more precisely by subtracting the sheath width from the chamber dimensions. Since the sheath width does not scale with the plasma size, the sheath width may ultimately limit the minimum size of ICPs. Plasma initiation power is determined to have a minimum at a gas pressure for which the electron collision frequency equals the frequency of the RF power supply. Small scale ICPs operating at 460 MHz can therefore be started most easily at /spl sim/1 torr. The design of the coil is critical to miniature ICP performance. Unlike large-scale ICPs that operate efficiently using a broad range of coil shapes, the miniature coil must be carefully designed and constructed to minimize parasitic resistance.
Cipher Systems: The Protection of Communications (1982)

Some early cipher systems -- More recent mechanical cryptographic devices -- A theoretical approach to cryptography -- Practical security -- Linear shift registers -- Non-linear algorithms -- Some block cipher systems -- Applying cipher systems -- Speech security systems -- Public key cryptography.
Giantin, a novel conserved Golgi membrane protein containing a cytoplasmic domain of at least 350 kDa. (1993)

The Golgi complex consists of a series of stacked cisternae in most eukaryotes. Morphological studies indicate the existence of intercisternal cross-bridge structures that may mediate stacking, but their identity is unknown. We have identified a 400-kDa protein, giantin, that is localized to the Golgi complex because its staining in double immunofluorescence experiments was coincident with that of galactosyltransferase, both in untreated cells and in cells treated with agents that disrupt Golgi structure. A monoclonal antibody against giantin yielded Golgi staining in one avian and all mammalian cell types tested, indicating that giantin is a conserved protein. Giantin exhibited reduced mobility on nonreducing sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was recovered in membrane fractions after differential centrifugation or sucrose flotation, and was not released from membranes by carbonate extraction. Thus, giantin appears to be an integral component of the Golgi membrane with a disulfide-linked lumenal domain. Strikingly, the majority of the polypeptide chain is cytoplasmically disposed, because large (up to 350 kDa) proteolytic fragments of giantin could be released from intact Golgi vesicles. This feature, a large contiguous cytoplasmic domain, is present in the calcium-release channel of muscle that cross-bridges the sarcoplasmic reticulum and transverse tubule membranes. Therefore, giantin's localization, conservation, and physical properties suggest that it may participate in forming the intercisternal cross-bridges of the Golgi complex.
Pharmacology of epidermal growth factor inhibitors (2007)

Research into the molecular bases of malignant diseases has yielded the development of many novel agents with potential antitumor activity. Evidence for a causative role for the epidermal growth factor receptor (EGFR), which is now regarded as an excellent target for cancer chemotherapy in human cancer, leads to the development of EGFR inhibitors. Two classes of anti-EGFR agents are currently in clinical use: monoclonal antibodies directed at the extracellular domain of the receptor, and the low-molecular-weight receptor tyrosine kinase inhibitors acting intracellularly by competing with adenosine triphosphate for binding to the tyrosine kinase portion of the EGFR. The effect on the receptor interferes with key biological functions including cell cycle arrest, potentiation of apoptosis, inhibition of angiogenesis and cell invasion and metastasis. Cetuximab, a monoclonal antibody, and the receptor tyrosine kinase inhibitors gefitinib and erlotinib are currently approved for the treatment of patients with cancer. New agents with clinical activity are entering the clinic, and new combinatorial approaches are being explored with the aim of improving the potency and pharmacokinetics of EGFR inhibition, to increase the synergistic activity in combination with chemotherapy and overcome resistance to the EGFR inhibitors.
Optical duobinary transmission systemwith no receiver sensitivity degradation (1995)

This Letter proposes a novel optical duobinary transmission system with no receiver sensitivity degradation. The transmitter yields a narrowband optical signal, and the receiver configuration is as simple as a binary IM-DD receiver. The feasibility of the proposed system is experimentally confirmed at 2.5, 5 and 10 Gbit/s.
Hypocalcemia Complicating Deferoxamine Therapy in an Infant with Parenteral Nutrition-Associated Aluminum Overload (1989)

Aluminum (Al) contaminates total parenteral nutrition (TPN) solutions given to infants, and high levels of Al have been demonstrated in their bone, serum, and urine. However, it is uncertain whether Al at current levels of contamination of TPN solutions is harmful to bone. We report an 8-month-old infant who developed osteopenic bone disease while receiving TPN, which did not respond to large amounts of calcium, phosphate, and vitamin D2. Serum and urine Al levels were greatly elevated and fell after a short course of deferoxamine. However, shortly after treatment began, serum calcium levels fell in the absence of hypercalciuria. We postulate that chelation of Al from this patient's bone permitted increased bone calcium uptake. This would suggest that Al at current levels of contamination of TPN solutions may impair bone calcium uptake and thus contribute to the pathogenesis or exacerbation of TPN-related osteopenia.