gebhart/patrepeval huggingface dataset:
Spatial control of sheet and film forming processes (1987)

Abstract The general problem of controlling both machine and cross‐directional properties on sheet and film forming processes is treated. A flexible class of linear dynamic‐stochastic models capable of characterizing the process and disturbance dynamics in these systems is suggested. Procedures are presented for identifying these models from data collected from common scanning type sensors. Linear‐Quadratic‐Gaussian (LQG) control theory is used to design multivariable controllers capable of jointly controlling the machine and cross‐directional property variations using both lumped and spatially distributed actuators.
TMPRSS2:ERG Fusion-Associated Deletions Provide Insight into the Heterogeneity of Prostate Cancer (2006)

Prostate cancer is a common and clinically heterogeneous disease with marked variability in progression. The recent identification of gene fusions of the 5'-untranslated region of TMPRSS2 (21q22.3) with the ETS transcription factor family members, either ERG (21q22.2), ETV1 (7p21.2), or ETV4 (17q21), suggests a mechanism for overexpression of the ETS genes in the majority of prostate cancers. In the current study using fluorescence in situ hybridization (FISH), we identified the TMPRSS2:ERG rearrangements in 49.2% of 118 primary prostate cancers and 41.2% of 18 hormone-naive lymph node metastases. The FISH assay detected intronic deletions between ERG and TMPRSS2 resulting in TMPRSS2:ERG fusion in 60.3% (35 of 58) of the primary TMPRSS2:ERG prostate cancers and 42.9% (3 of 7) of the TMPRSS2:ERG hormone-naive lymph node metastases. A significant association was observed between TMPRSS2:ERG rearranged tumors through deletions and higher tumor stage and the presence of metastatic disease involving pelvic lymph nodes. Using 100K oligonucleotide single nucleotide polymorphism arrays, a homogeneous deletion site between ERG and TMPRSS2 on chromosome 21q22.2-3 was identified with two distinct subclasses distinguished by the start point of the deletion at either 38.765 or 38.911 Mb. This study confirms that TMPRSS2:ERG is fused in approximately half of the prostate cancers through deletion of genomic DNA between ERG and TMPRSS2. The deletion as cause of TMPRSS2:ERG fusion is associated with clinical features for prostate cancer progression compared with tumors that lack the TMPRSS2:ERG rearrangement.
FMS-Like Tyrosine Kinase 3–Internal Tandem Duplication Tyrosine Kinase Inhibitors Display a Nonoverlapping Profile of Resistance Mutations In vitro (2009)

FMS-like tyrosine kinase 3 (FLT3) inhibitors have shown activity in the treatment of acute myelogenous leukemia (AML). Secondary mutations in target kinases can cause clinical resistance to therapeutic kinase inhibition. We have previously shown that sensitivity toward tyrosine kinase inhibitors varies between different activating FLT3 mutations. We therefore intended to determine whether different FLT3 inhibitors would produce distinct profiles of secondary, FLT3 resistance mutations. Using a cell-based screening approach, we generated FLT3-internal tandem duplication (ITD)-expressing cell lines resistant to the FLT3 inhibitors SU5614, PKC412, and sorafenib. Interestingly, the profile of resistance mutations emerging with SU5614 was limited to exchanges in the second part of the kinase domain (TK2) with exchanges of D835 predominating. In contrast, PKC412 exclusively produced mutations within tyrosine kinase domain 1 (TK1) at position N676. A mutation at N676 recently has been reported in a case of PKC412-resistant AML. TK1 mutations exhibited a differential response to SU5614, sorafenib, and sunitinib but strongly impaired response to PKC412. TK2 exchanges identified with SU5614 were sensitive to PKC412, sunitinib, or sorafenib, with the exception of Y842D, which caused a strong resistance to sorafenib. Of note, sorafenib also produced a highly distinct profile of resistance mutations with no overlap to SU5614 or PKC412, including F691L in TK1 and exchanges at position Y842 of TK2. Thus, different FLT3 kinase inhibitors generate distinct, nonoverlapping resistance profiles. This is in contrast to Bcr-Abl kinase inhibitors such as imatinib, nilotinib, and dasatinib, which display overlapping resistance profiles. Therefore, combinations of FLT3 inhibitors may be useful to prevent FLT3 resistance mutations in the setting of FLT3-ITD-positive AML.
Altered poly(ADP-ribose) metabolism in family members of patients with systemic lupus erythematosus. (1994)

To determine whether the previously detected decrease in poly(ADP-ribose) synthesis in systemic lupus erythematosus (SLE) is familial.Poly(ADP-ribose) metabolism was studied in the peripheral blood lymphocytes of members of 3 families with lupus and in healthy controls.Synthesis, as determined by the incorporation of 3H NAD into acid precipitable counts was 30% of normal in the patients with SLE (p < 0.001) and 70% of normal in the unaffected family members (p < 0.05). Family members also had increased prevalence of antinuclear antibodies but the presence of these antibodies did not correlate with abnormalities in poly(ADP-ribose) metabolism.The healthy biologic relatives of patients with SLE have a decrease in poly(ADP-ribose) synthesis similar to, but less marked than, their affected relatives. Poly(ADP-ribose) polymerase activity appears to be an inherited trait and abnormalities in it may be one of the susceptibility factors for SLE. If this is the case, then further investigation of this gene and its regulation is warranted.
Diagnosis of typhus infection with Rickettsia tsutsugamushi by polymerase chain reaction (1992)

Two sets of oligonucleotide primers were used to amplify the genomic DNA of Rickettsia tsutsugamushi, the causative agent of scrub typhus (tsutsugamushi disease), by the polymerase chain reaction. Each set of primers amplified 538-bp and 109-bp products, representing part of a gene encoding a possible major 58-kDa immunogenic protein, from whole genomic DNA extracted from R. tsutsugamushi strains Karp, Kato, Gilliam, Kuroki and Kawasaki. No amplification was observed from R. sibirica, R. rickettsii, mouse and human genomic DNA. DNA amplification was observed from crude lysates of peripheral whole blood, tissue homogenates and paraffin-embedded skin biopsy sections obtained from patients with scrub typhus disease. Southern blot analysis demonstrated the specificity of the amplified DNA fragments following hybridisation with a DNA probe generated from R. tsutsugamushi strain Karp. By means of this procedure, a rapid and sensitive diagnosis of scrub typhus disease can be made during the acute stage of this infection.
Optical heterodyne detection of an atmospherically distorted signal wave front (1967)

The effect of atmospheric distortion of an optical wave front on the performance of an optical heterodyne detection system is examined theoretically. With the distortion measured by the phase and log-amplitude structure functions, an exact expression is derived relating the distortion to the detector signal-to-noise ratio. It is shown that because of distortion there is a limit to the achievable signal-to-noise ratio no matter bow large the detector collection aperture is. The minimum aperture diameter which will (nearly) achieve this limit, called the efficiency saturation dimension r <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">0</inf> , is obtained in terms of the phase and log-amplitude structure fractions. Using the current theory for propagation in a turbulent medium, an expression for r <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">0</inf> is obtained for a receiver in the atmosphere looking at a source above the atmosphere. The expression is in terms of the wavelength, the receiver altitude, and the zenith angle of the receiver line-of-sight.
Pandemic influenza A(H1N1)v in New Zealand: the experience from April to August 2009 (2009)

Following the detection of imported cases of pandemic influenza A(H1N1)v on 25 April 2009, New Zealand implemented containment measures that appeared to slow establishment of the pandemic during May. The pandemic accelerated markedly in June, reaching a peak within four to six weeks, and has been declining since mid-July. By 23 August there had been 3,179 recorded cases (97.8% reported as confirmed), including 972 hospitalisations, 114 intensive care admissions, and 16 deaths. Influenza-like illness (ILI) surveillance in general practice suggests that 7.5% (95% CI: 3.4-11.2) of the population of New Zealand had symptomatic infection, giving a case fatality ratio of 0.005%. Hospitalisations were markedly higher for Māori (age standardised relative risk (RR)=3.0, 95% CI: 2.9-3.2) and Pacific peoples (RR=6.7, 95% CI: 6.2-7.1) compared with Europeans and others. The apparent decline of the pandemic (shown by all surveillance systems) cannot be fully explained. New Zealand remains in the middle of its traditional influenza season, the influenza A(H1N1)v virus appears relatively infectious, and we estimate that only about 11% of the population have been infected by this novel agent.
A Programmable System of Functional Electrical Stimulation (FES) (2007)

The development of a novel system intended to perform functional electrical stimulation (FES) is presented. A virtual instrument developed in Labview communicates with a PC through USB and controls the hardware compound of analog and digital circuits. The block diagram of the hardware and the main characteristics of the virtual instrument are presented, as well the results of the electrical safety tests and the errors associated to the programmed and real values of the amplitude, pulse width and frequency of the output current. The results point the equipment can be used in the therapy of paraplegic patients maintaining safety limits reported in the literature.
A genome-wide scan for common genetic variants with a large influence on warfarin maintenance dose (2008)

Warfarin dosing is correlated with polymorphisms in vitamin K epoxide reductase complex 1 (VKORC1) and the cytochrome P450 2C9 (CYP2C9) genes. Recently, the FDA revised warfarin labeling to raise physician awareness about these genetic effects. Randomized clinical trials are underway to test genetically based dosing algorithms. It is thus important to determine whether common single nucleotide polymorphisms (SNPs) in other gene(s) have a large effect on warfarin dosing. A retrospective genome-wide association study was designed to identify polymorphisms that could explain a large fraction of the dose variance. White patients from an index warfarin population (n = 181) and 2 independent replication patient populations (n = 374) were studied. From the approximately 550 000 polymorphisms tested, the most significant independent effect was associated with VKORC1 polymorphisms (P = 6.2 x 10(-13)) in the index patients. CYP2C9 (rs1057910 CYP2C9*3) and rs4917639) was associated with dose at moderate significance levels (P approximately 10(-4)). Replication polymorphisms (355 SNPs) from the index study did not show any significant effects in the replication patient sets. We conclude that common SNPs with large effects on warfarin dose are unlikely to be discovered outside of the CYP2C9 and VKORC1 genes. Randomized clinical trials that account for these 2 genes should therefore produce results that are definitive and broadly applicable.
Speech synthesis by phonological structure matching (1999)

This paper presents a new technique for speech synthesis by unit selection. The technique works by specifying the synthesis target and the speech database as phonological trees, and using a selection algorithm which finds the largest parts of trees in the database which match parts of the target tree. The technique avoids many of the errors made by prosody generation modules by incorporating their operation in the selection implicitly. A technique for using signal processing only when it is needed most is also described. The technique produces better quality speech than previous approaches and is also significantly faster.
Peroxisomes in Dermatology. Part I (2001)

Background: Peroxisomes are small cellular organelles that were almost ignored for years because they were believed to play only a minor role in cellular functions. However, it is now known that peroxisomes play an important role in regulating cellular proliferation and differentiation as well as in the modulation of inflammatory mediators. In addition, peroxisomes have broad effects on the metabolism of lipids, hormones, and xenobiotics. Through their effects on lipid metabolism, peroxisomes also affect cellular membranes and adipocyte formation, as well as insulin sensitivity, and peroxisomes play a role in aging and tumorigenesis through their effects on oxidative stress. Objective: To review genetically determined peroxisomal disorders, especially those that particularly affect the skin, and some recent information on the specific genetic defects that lead to some of these disorders. In addition, we present some of the emerging knowledge of peroxisomal proliferator activator receptors (PPARs) and how ligands for mese receptors modulate different peroxisomal functions. We also present information on how the discovery of PPARs, and the broad and diverse group of ligands that activate these members of the superfamily of nuclear binding transcription factors, has led to development of new drugs that modulate the function of peroxisomes. Conclusion: PPAR expression and ligand modulation within the skin have shown potential uses for these ligands in a number of inflammatory cutaneous disorders, including acne vulgaris, cutaneous disorders with barrier dysfunction, cutaneous effects of aging, and poor wound healing associated with altered signal transduction, as well as for side effects induced by the metabolic dysregulation of other drugs.
Vision-based active sensor using a flexible beam (2001)

Proposes a vision-based active sensing system, termed vision-based active antenna. This is composed of a camera, a flexible beam whose force-deformation characteristic is known, and an actuator for rotating the beam. The camera observes the beam deformation, including the contact information, while the beam is in contact with an object. By solving a set of equations based on the information acquired through the camera, the sensor can detect the contact location, the contact force, and the stiffness of the object, even though the contact point is hidden by occlusion. For two particular versions, we show some experimental results to verify the basic idea.
Mutational analysis and molecular modeling of the N-terminal kringle-containing domain of hepatocyte growth factor identifies amino acid side chains important for interaction with the c-Metreceptor (1994)

The hepatocyte growth factor receptor (HGFr) transduces a wide range of biological signals, including mitogenesis, motogenesis and morphogenesis. We recently localized a region within the N-terminal 175 amino acids of hepatocyte growth factor (HGF), termed HGF/NK1, that is necessary and sufficient for binding to the HGFr. HGF/NK1 contains an as-yet structurally undefined N-terminal region followed by the first of four HGF kringles. We have used a combination of molecular modeling and mutagenesis to dissect the function of this region of HGF. Two mutation-sensitive patches on the proposed surface regions of HGF kringle one (K1) were identified. The first patch consists of residues E159, S161, E195 and R197, all of which are predicted to be close to each other in the tertiary structure of K1. The second patch, lying on the opposite side of the kringle, consists of residues D171 and Q173. Mutational analysis of the N-terminal region of HGF identified residue D117 which also appeared to influence receptor binding. We also investigated the properties of a naturally occurring HGF variant (delta 5-HGF) that arises from an alternatively spliced transcript and therefore lacks five residues within K1. Our data suggest that in wild-type HGF, F162 is crucial in maintaining the hydrophobic core of the kringle. In delta 5-HGF, the loss of this residue is compensated for by a functional substitution of F162 with Y167, which is predicted to occupy the delta 5-HGF K1 core. Comparison of the models of wild-type and delta 5 kringles reveals that the positions of the presumed receptor binding determinants remain unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Sur l'acide dinitro‐4,5‐anthranilique (1951)

Abstract La synthèse der l'acide dinitro‐4,5‐anthranilique est décrite. Dans ce composé; le groupe nitro situé en 4 est mobile et se laisse remplacer directement par un groupe amino, anilino ou méthoxyle; dans le diazoïque correspondant, au contraire, c'est le groupe nitro situé en 5 qui est mobile et est remplacé facilement par un groupe hydroxyle ou un atome de chlore.
Tumor MicroRNA Expression Profiling Identifies Circulating MicroRNAs for Early Breast Cancer Detection (2015)

Circulating miRNAs reflect the presence of breast tumors. The identification of deregulated miRNAs in plasma of patients with breast cancer supports the use of circulating miRNAs as a method for early breast cancer detection.
Convergent Syntheses of Oral THF 1.BETA.-Methylcarbapenems. (1999)

Convergent syntheses of oral THF 1beta-methylcarbapenems 4 (OCA-983) and 5 starting from M2-phosphate 1 were developed. Reaction of the M2-phosphate 1 with THF thiols containing a requisite prodrug side chain, 9 and 10, gave the desired oral THF 1beta-methylcarbapenems 4 and 5, respectively, in 46% and 42% overall yields.
Interaction of Farnesylated PRL-2, a Protein-tyrosine Phosphatase, with the β-Subunit of Geranylgeranyltransferase II (2001)

Protein of regenerating liver (PRL)-1, -2, and -3 comprise a subgroup of closely related protein-tyrosine phosphatases featuring a C-terminal prenylation motif conforming to either the consensus sequence for farnesylation, CAAX, or geranylgeranylation, CCXX. Yeast two-hybrid screening for PRL-2-interacting proteins identified the beta-subunit of Rab geranylgeranyltransferase II (betaGGT II). The specific interaction of betaGGT II with PRL-2 but not with PRL-1 or -3 occurred in yeast and HeLa cells. Chimeric PRL-1/-2 molecules were tested for their interaction with betaGGT II, and revealed that the C-terminal region of PRL-2 is required for interaction, possibly the PRL variable region immediately preceeding the CAAX box. Additionally, PRL-2 prenylation is prequisite for betaGGT II binding. As prenylated PRL-2 is localized to the early endosome, we propose that this is where the interaction occurs. PRL-2 is not a substrate for betaGGT II, as isoprenoid analysis showed that PRL-2 was solely farnesylated in vivo. Co-expression of the alpha-subunit (alpha) of GGT II, betaGGT II, and PRL-2 resulted in alpha/betaGGT II heterodimer formation and prevented PRL-2 binding. Expression of PRL-2 alone inhibited the endogenous alpha/betaGGT II activity in HeLa cells. Together, these results indicate that the binding of alphaGGT II and PRL-2 to betaGGT II is mutually exclusive, and suggest that PRL-2 may function as a regulator of GGT II activity.
Polarization-sensitive optical coherence tomography for photoelasticity testing of glass/epoxy composites (2003)

We measure the spatial distribution of the mechanical stress induced inside translucent glass/epoxy composites by means of polarizationsensitive optical coherence tomography. The Stokes parameters determined from two orthogonal polarization components of the backscattered light allow the internal stress to be identified in terms of its magnitude and principal direction based on a birefringence light scattering model of glass/epoxy composites. Measurement examples show the particular case of stress concentration near a through hole and the internal structural damages caused by excessive tensile loading.
Increased protein kinase C alpha expression in human colonic Caco-2 cells after insertion of human Ha-ras or polyoma virus middle T oncogenes. (1993)

The proteins encoded by ras and src protooncogenes are frequently activated in a constitutive state in human colorectal cancers. To investigate the mechanism(s) whereby oncogenic p21ras and pp60c-src contribute to malignant transformation of intestine, human colonic Caco-2 cells transfected with an activated (Val 12) human Ha-ras gene (Caco-2-T cells) or Py-MT oncogene, a constitutive activator of pp60c-src tyrosine kinase activity (Caco-2-MT cells), were analyzed for tumorigenicity, protein kinase C (PKC) isoform expression, and PKC activity. As compared with control vector Caco-2-H cells, Caco-2-T and Caco-2-MT cells displayed: (a) an enhanced tumorigenicity in nude mice; (b) a 4-fold increase in the level of PKC-alpha mRNA which was not due to enhanced mRNA stability and was mediated through a PKC-independent pathway since it persisted after PKC depletion; (c) increased PKC-alpha immunoreactive protein content (3-fold), total PKC catalytic activity (3.5-fold), and total cell number of [3H]phorbol-12,13-dibutyrate binding sites (4-fold); and (d) a 1.7-fold higher membrane-bound/total PKC activity ratio together with 1.8- and 1.5-fold increases in [3H]arachidonate- and [3H]myristate-labeled diacylglycerol levels. In conclusion, the tumorigenic progression induced by oncogenic p21ras or the Py-MT/pp60c-src complex in Caco-2 cells is associated with increased PKC-alpha gene transcription and PKC-alpha expression as well as with constitutive PKC activation. These results provide the first evidence that the PKC-alpha gene is a target for the signaling pathways of oncogenically activated p21ras and pp60c-src in human colonic cells. They raise the possibility that PKC-alpha is an effector of these oncoproteins for activation of Caco-2 cell tumorigenic potential.
COMPETITIVE ELECTRICITY MARKETS IN NEW YORK STATE: EMPIRICAL IMPACTS OF INDUSTRY RESTRUCTURING (1996)

The analysis finds that if high industrial prices for electricity induce industrial customers to leave the regulated grid for self-generation or contracts with IPPs, this raises rates for those remaining on the system and reduces quantities purchased. It is assumed that lower industrial sector rates, such as those associated with a competitive electricity industry, will effectively eliminate defections. A switch to a more efficient two-part tariff, which can be expected to occur in a competitive electricity market, has the effect of increasing sales of electricity in all sectors while still raising needed revenues. Such a price structure is also found to lower the average price of electricity in each sector. An efficient two-part tariff is also likely to shift revenue responsibilities to immobile residential and commercial customers. This would occur because industrial customers shift demand by defection in response to average price changes, but residential and commercial demand is inelastic to customer charges. If prices are efficient, strandable cost allocations only have a minor effect on electricity demand because strandable cost payments are raised via a customer charge. If strandable costs are recovered by a wires charge (e.g. higher prices),however, there will be negative demand effects. Strandable costs significantly affect the average price of electricity and the average monthly bill in either case. Their allocation is important for equity reasons, as is the method of collection in determining the levels of sales. Removing strandable costs lowers the average price of electricity in each sector and increases demand. Lowering strandable costs is the only option which clearly benefits all sectors. •