gebhart/patrepeval huggingface dataset:
DNA alkali-labile sites induced by incorporation of 5-aza-2'-deoxycytidine into DNA of mouse leukemia L1210 cells. (1985)

The effects of 5-aza-2'-deoxycytidine on DNA in mouse L1210 leukemia cells were investigated using the alkaline elution technique. By comparing the DNA elution rate at pH 12.1 and 12.6, it was found that the drug produced DNA alkali-labile lesions. Alkali-labile sites were present only in DNA strands that were synthesized in the presence of the drug. They persisted for at least 48 h after drug treatment, and only after 72 h did the number of alkali-labile sites decline, thus suggesting a slow repair process. The production of alkali-labile sites was found to be concentration dependent and observable at concentrations which were effective in inhibiting the clonogenic viability of L1210 cells and which are attainable in vivo. 5-Aza-2'-deoxycytidine did not cause other DNA lesions such as DNA double-strand breaks or DNA-protein cross-links. Two hypotheses were considered to explain the origin of alkali-labile lesions in DNA that has incorporated 5-aza-2'-deoxycytidine: (a) the production of apyrimidinic sites by a glycosylase that recognizes and removes aza-cytosine from DNA and (b) the alkali-catalyzed decomposition of azacytosine residues to ring-opened products which could lead to alkali-induced DNA strand scission through a beta-elimination mechanism. The second hypothesis was considered to be the more probable and suggests that the alkali lability may be a means by which one could determine the extent of substitution and precise location of azacytosine residues or their ring-opened products in DNA.
Occurrence of NKX3.1 C154T polymorphism in men with and without prostate cancer and studies of its effect on protein function. (2002)

NKX3.1, a member of the NK class of homeodomain proteins, is expressed primarily in the adult prostate and has growth suppression and differentiating effects in prostate epithelial cells. A C-->T polymorphism at nucleotide 154 (NKX3.1 C154T) is present in approximately 11% of healthy men with equal distribution among whites and blacks. In a cohort of 1253 prostate cancer patients and age-matched controls, the presence of the polymorphism was associated with a 1.8-fold risk of having stage C or D prostate cancer or Gleason score > or =7 (confidence interval, 1.01-3.22). The NKX3.1 C154T polymorphism codes for a variant protein that contains an arginine-to-cysteine substitution at amino acid 52 (R52C) adjacent to a protein kinase C phosphorylation site at serine 48. Substitution of cysteine for arginine 52 or of alanine for serine 48 (S48A) reduced phosphorylation at serine 48 in vitro and in vivo. Phosphorylation of wild-type NKX3.1, but not of NKX3.1 R52C or NKX3.1 S48A, diminished binding in vitro to a high-affinity DNA binding sequence. NKX3.1 also serves as a transcriptional coactivator of serum response factor. Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate to phosphorylate NKX3.1 had no effect on NKX3.1 coactivation of serum response factor. Neither the R52C nor the S48A substitution affected serum response factor coactivation by NKX3.1 We conclude that the polymorphic NKX3.1 allele codes for a variant protein with altered DNA binding activity that may affect prostate cancer risk.
Retro-retinoids in regulated cell growth and death. (1996)

Vitamin A serves as a prohormone from which three classes of active metabolites are derived: the aldehydes, the carboxylic acids, and the retro-retinoids. Although these three classes are united under the rubric of signal transduction, they act by different molecular mechanisms: the 11-cis-retinaldehydes combine with opsin to form the universal visual pigments and the retinoic acids form ligands for transcription factors, whereas the retro-retinoids, as shown here, intersect with signal transduction at a cytoplasmic or membrane site. The retro-retinoid, anhydroretinol (AR), has long been known to act as a growth inhibitor in lymphocytes, whereas 14-hydroxy-4,14-retro-retinol (14-HRR) is required for normal lymphocyte proliferation. A mutually reversible relationship exists between these two retro-retinoids as one can reverse the effects of the other when given in pharmacological doses. The common explanation for reversible inhibition is competition for a shared receptor. We now provide evidence that when AR is given to T cells unmitigated by 14-HRR, rapid cell death can occur. The circumstances are closely related to nonclassical forms of apoptosis: within 2 h of AR administration the T cells undergo widespread morphological changes, notably surface blebbing and ballooning and, inevitably, bursting. In contrast, nuclear changes are comparatively mild, as indicated by absence of chromatin condensation and overt DNA cleavage to discrete nucleosomal fragments, although DNA nicks are readily discernible by terminal deoxynucleotidyl transferase assay. What further distinguishes the AR-induced form of apoptosis from classical ones is a lack of requirements of messenger RNA and protein synthesis, suggesting that the events leading to cell death are primarily initiated and play themselves out in the cytoplasm. This view is further reinforced by the finding that herbimycin A can prevent the onset of programmed cell death. The importance of our findings is that they strongly suggest a second messenger role for vitamin A metabolites in the cytoplasmic realm that has not been seen previously. These findings are entirely compatible with a general notion that in a cell requiring multiple coordinated signals for survival, the provision of an unbalanced signal can initiate programmed cell death. Collectively, our data also challenge the paradigm that retinoids (outside vision) solely mediate their function via the steroid/ retinoic acid receptor family of nuclear transcription factors. Instead, a mode of action in the cytoplasmic realm akin to one attributed to other small lipophilic second messenger molecules, such as diacyl glycerol or ceramide, may apply to retro-retinoids.
Galectin-1 exerts immunomodulatory and protective effects on concanavalin a-induced hepatitis in mice (2000)

Galectin-1, an endogenous lectin with immunomodulatory activities, induces selective, Fas-independent apoptosis of activated T cells. The aim of the present study was to evaluate the effect galectin-1 exerts on concanavalin A (Con A)-induced hepatitis, a T-cell-dependent model of liver injury. Con A administration resulted in liver injury, as shown by the increased transaminase plasma levels and liver DNA fragmentation, and caused spleen T-cell activation, which was associated with a strong increment in liver infiltrating T helper cells. Moreover, Con A injection leads to a marked increase in plasma tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) levels. Galectin-1 pretreatment dose-dependently prevented both liver injury and T-helper cell liver infiltration induced by Con A. In vivo and in vitro experiments indicated that the protective effects of galectin-1 depend on the selective elimination of Con A-activated T cells. In addition, galectin-1 almost completely prevented the Con A-induced increase in plasma TNF-alpha and IFN-gamma, an effect that was, at least in part, independent on the elimination of activated T helper cells, because galectin-1 prevented lipopolysaccharide (LPS)-induced release of TNF-alpha and IFN-gamma also from macrophages in vitro, without affecting their viability. The present study suggests that galectin-1 is potentially useful in the treatment of T-cell-mediated human liver disorders.
NF-kB Activation in Microglia Induces Motor Neuron Death in Amyotrophic lateral sclerosis (2013)

ALS is a fatal neurodegenerative disease that affects motor neurons (MNs) resulting in severe muscle atrophy and paralysis. Despite the fact that about 5,600 people are diagnosed with ALS in the US each year, there is no cure. One of the most striking pathological hallmarks observed in patients and rodent models of ALS is neuroinflammation, characterized by activation of microglia, the resident immune cells of the central nervous system. Genetic approaches to globally eliminate single inflammatory genes in ALS mouse models have largely failed, highlighting the complexity of this inflammatory process. Nuclear Factor-kappa B (NF-κB) regulates many pro-inflammatory mediators found in areas of MN death in ALS, and this pathway is activated in the spinal cords of ALS patients. Therefore, the purpose of this study is to determine the role of NF-κB, a master regulator of inflammation, in ALS. By immunoblot and immunohistochemical analyses, we determined NF-kB activation increases with disease progression in ALS mice and occurs predominantly in microglia. To determine the role of NF-kB activation in microglial-mediated MN death, we utilized an in vitro co-culture model in which 61% of MNs die when co-cultured with ALS microglia after 72 hours. NF-kB inhibition in ALS microglia fully rescued MNs from microglial-mediated death in vitro. Remarkably, conditional inhibition of NF-kB in microglia in vivo extends survival in the ALS mice by delaying disease progression by 51%, one of the longest extensions reported in this severe model. NF-kB inhibition in microglia leads to marked reduction in prototypic inflammatory markers such as CD68, CD86 and iNOS, suggesting that NF-kB regulates microglial conversion to a pro-inflammatory, neurotoxic state in ALS. Furthermore, we show that constitutive activation of NF-kB selectively in microglia in wild-type mice promoted a similar microglial activation state observed in ALS mice. Strikingly, microglia isolated from these constitutively active NF-kB mice rapidly induced 48% MN death in vitro. These data provide a cellular and molecular mechanism by which microglia induce MN death in ALS and suggest a novel therapeutic target to modulate microglial activation and slow the progression of ALS and other neurodegenerative diseases by which microglial activation plays a role.
The conservative treatment of phimosis in boys (1996)

Treatment with 0.05% betamethasone cream is a simple and safe method for the treatment of phimosis in boys older than 3 years. An early operation is necessary in cases of genuine phimosis when 1 month of treatment with topical steroids has failed. We strongly support the saying, "The fortunate foreskin of an infant boy will usually be left well alone by everyone but its owner'.
Complex System Fault Diagnostic Method Based on Convolutional Neural Network (2019)

As a branch of machine learning, deep learning is characterized by multi-level learning to obtain different abstraction levels of raw data, thus improving the accuracy of the tasks such as classification and prediction. It brings a new idea of the complex system fault diagnostics and prognostics. Combining the characteristics of complex system test data and the advantages of deep learning, a fault diagnostics method based on convolutional neural network is proposed, including preprocessing, model training and optimization. Then a complex system fault diagnostic algorithm platform based-on deep learning method is realized. The simulation method of an aero-engine gas path test proves that the proposed method has good feasibility and effect, can fully utilize the advantages of deep learning, and is more suitable for characterizing the complex and varied characteristics hidden inside the complex system data. It can provide the technical support for the design, test and management of the complex system, and improve the safety and effectively reduce the life cycle costs of the complex system.
语音分析初探(上)——区别性特征及其相互关系 (1981)

一区别性特征的概念1.1 分解语言为最小单位在测验语言的可懂度的一次典型实验中,一个说英语的说话人念出一些孤立的根词(如 bill,put,fig 等),而一个说英语的听话人努力去正确地听懂这些词,对于听者,这种情况,在某种意义上要比正常的语言交际简单些,因为他所对付的样品词不能分解为更短的有意义的实体,也不曾被组合成更高的单位。这样,对这个听者来说,既没有把句子分解为词的问题,也没有把词分解为语法成分的问题。他不用说出句中诸词的相互关
Optimal design of electromechanical actuators for active loads (1998)

The proliferation of electromechanical actuation promises reduced maintenance requirements and cost, improved efficiency and reliability, and more environmentally friendly operation. Within this paper, the issue of optimal component selection for actuator design is addressed. Optimality is defined as an engineering trade-off concerning power transfer to the load, efficiency, and torque demand. An equivalent circuit for the actuator/active load system is developed and represented in the phasor domain. Sinusoidal steady-state techniques are employed for system analysis and definition of the conditions for optimality in applications where load force and velocity profiles are known. The actuator application of thrust vector control on the Space Shuttle main engine is specifically addressed.
Effect of Calcination Temperature of Unsupported NiMo Catalysts on the Hydrodesulfurization of Dibenzothiophene (2014)

The effects of NiMo catalyst calcination temperature (250, 350, 450, 550, and 650 °C) on catalytic hydrodesulfurization of dibenzothiophene (DBT) were studied. The physiochemical properties of the unsupported NiMo catalysts were characterized by various techniques, including N2 adsorption–desorption, X-ray diffraction (XRD), Fourier-transform infrared spectroscopy (FT-IR), scanning electron microscopy (SEM), and high-resolution transmission electron microscopy (HRTEM). XRD and FT-IR results showed that increasing the calcination temperature brought about a phase change of the NiMo catalyst precursors from ammonium nickel molybdate to nickel molybdate. The agglomeration of precursor particles and MoS2 nanoclusters changed with various calcination temperatures as revealed by SEM and HRTEM, respectively. DBT catalytic results showed that the NiMo catalyst calcined at 350 °C exhibited higher activity than other NiMo catalysts, and the selectivity of bicyclohexane was much preferred at a reaction temperature of 320 °C over NiMo catalysts endowed with the phase of ammonium nickel molybdate. The high hydrogenation ability might be due to the efficient formation of the “Ni-Mo-S” phase and will be attractive for industrial applications.
Complement C2 Receptor Inhibitor Trispanning and the β-Chain of C4 Share a Binding Site for Complement C2 (2002)

Complement C2 receptor inhibitor trispanning (CRIT) of the Schistosoma parasite binds human C2 via the C2a segment. The receptor in vivo functions as C2 decoy receptor by directly competing with C4b for binding to C2. As a result, CRIT is able to limit the extent of classical pathway (CP) C3 convertase formation. We report that the CRIT-extracellular domain 1 (ed1) peptide inhibits CP-mediated complement activation with an ICH(50) of approximately 0.1 microM, the C-terminal 11 aa of CRIT-ed1, named H17, even more effectively. The beta-chain region F222-Y232 of C4 shares 55% identity and 73% similarity with H17. Peptides based on this region also inhibit CP in a dose-dependent manner. As further evidence of C2 binding we showed CRIT-ed1 peptides and homologous C4 beta-chain peptides to inhibit complement in C2 hemolytic assays. We have predicted C4 beta-c F222-Y232 as a C2 binding site which we have termed the CRIT-ed1 domain, and the sequence [F/H]EVKX(4/5)P as a consensus C2-binding sequence. Anti-CRIT-ed1 cross-reacts with the C4 beta-chain and F222EVKITPGKPY232 appears to be the key epitope recognized by this Ab. Furthermore, anti-CRIT-ed1 was found to inhibit CP activation in a total hemolytic assay. We believe that Schistosoma CRIT-ed1, as well as C4 beta-chain peptides based on the CRIT-ed1 domain, function as interface peptides. These peptides, based on C2-binding sequences in CRIT, or C4, competitively inhibit the binding of C2 to C4b and thus limit the activation of C. The C4 peptides, unlike CRIT-ed1, did not inhibit the cleavage of C2 by C1s.
An overview of the quiet short-haul research aircraft program (1978)

An overview of the Quiet Short Haul Research Aircraft (QSRA) Program is presented, with special emphasis on its propulsion and acoustic aspects. A description of the NASA technical participation in the program including wind tunnel testing, engine ground tests, and advanced aircraft simulation is given. The aircraft and its systems are described and, measured performance, where available, is compared to program goals. Preliminary data indicate that additional research and development are needed in some areas of which acoustics is an example. Some of these additional research areas and potential experiments using the QSRA to develop the technology are discussed. The concept of the QSRA as a national flight research facility is explained.
Gerhardt (1964)

Charles Frédéric Gerhardt (Strasbourg; 21 August 1816–19 August 1856), whose father was Swiss and descended from a family of brewers in the Palatinate, studied in Karlsruhe (1831–3) under Walchner, and under Erdmann, with whom he boarded, in Leipzig (1833). Friedrich August Walchner (Meersburg, Baden, 2 September 1799-Karlsruhe, 17 February 1865) was professor of mineralogy and geology at Karlsruhe; his publications are mostly minera-logical, but he investigated racemic acid.1 Gerhardt's father, who had lost most of his money in speculation, set up a white-lead factory in 1834 and wished Charles to join him; but the two quarrelled and Charles entered a lancer regiment at Hagenau. He was reprimanded for studying after lights-out, but his colonel gave permission for this. A friend (doubtfully identified with Liebig) paid 2000 francs on loan for Gerhardt's release. In 1835 Gerhardt published his first paper (in German) on the formulae of the natural silicates,2 which Berzelius noticed favourably in his Jahres-Bericht. In 1836 Gerhardt worked for six months with Liebig in Giessen. In 1837 he returned to Strasbourg to work in Persoz' laboratory, but was not satisfied, as no organic analyses were made.
Protein expression in Pichia pastoris: recent achievements and perspectives for heterologous protein production (2014)

Pichia pastoris is an established protein expression host mainly applied for the production of biopharmaceuticals and industrial enzymes. This methylotrophic yeast is a distinguished production system for its growth to very high cell densities, for the available strong and tightly regulated promoters, and for the options to produce gram amounts of recombinant protein per litre of culture both intracellularly and in secretory fashion. However, not every protein of interest is produced in or secreted by P. pastoris to such high titres. Frequently, protein yields are clearly lower, particularly if complex proteins are expressed that are hetero-oligomers, membrane-attached or prone to proteolytic degradation. The last few years have been particularly fruitful because of numerous activities in improving the expression of such complex proteins with a focus on either protein engineering or on engineering the protein expression host P. pastoris. This review refers to established tools in protein expression in P. pastoris and highlights novel developments in the areas of expression vector design, host strain engineering and screening for high-level expression strains. Breakthroughs in membrane protein expression are discussed alongside numerous commercial applications of P. pastoris derived proteins.
ENHANCEMENT OF THE SEDIMENTATION RATES OF FIBROUS SUSPENSIONS (1991)

The settling of suspensions of slender rod-like particles with large aspect ratios was studied. The novel technique of enhancement of sedimentation rates by the addition of buoyant particle promoters was applied to such suspensions. The settling rates could be increased by many times by this simple technique. Sedimentation velocity increases of between 5 to 7 times have been observed for fibrous suspensions of concentrations of about 0.5%. A statistical analysis of the experimental data was performed to establish a correlation for the enhancement in settling velocities. The sediment volume was unaffected by the presence of buoyant particles. The buoyant parjticles were found to adsorb some surfactants onto their surfaces.
Angiogenic Activity as a Marker of Neoplastic and Preneoplastic Lesions of the Human Bladder (1980)

Angiogenic activity has been assessed in biopsy specimens from 49 patients with transitional cell carcinoma, benign prostatic hypertrophy and vesicoureteral reflux. Over 95% of the specimens containing malignant and premalignant transitional epithelium stimulated capillary proliferation on rabbit iris. In contrast, less than 10% of normal tissues had this effect. Sixty-one per cent of specimens with inflammatory round cells were angiogenic but this was reduced to 10% by preincubation with rabbit antihuman lymphocyte serum. Cystitis cystica also induced capillary proliferation even if incubated with the antilymphocyte serum. Angiogenic capacity may be an early marker of preneoplastic and neoplastic lesions of the human bladder.
A Data-Augmented 3D Morphable Model of the Ear (2018)

Morphable models are useful shape priors for biometric recognition tasks. Here we present an iterative process of refinement for a 3D Morphable Model (3DMM) of the human ear that employs data augmentation. The process employs the following stages 1) landmark-based 3DMM fitting; 2) 3D template deformation to overcome noisy over-fitting; 3) 3D mesh editing, to improve the fit to manual 2D landmarks. These processes are wrapped in an iterative procedure that is able to bootstrap a weak, approximate model into a significantly better model. Evaluations using several performance metrics verify the improvement of our model using the proposed algorithm. We use this new 3DMM model-booting algorithm to generate a refined 3D morphable model of the human ear, and we make this new model and our augmented training dataset public.
Translation of the sequence AGG-AGG yields 50% ribosomal frameshift. (1988)

We have inserted the sequence 5'-AAG-GAGGU-3', which is complementary to the 3' terminus of Escherichia coli 16S rRNA, in a reading frame and analyzed its effect on the accuracy and overall rate of translation in vivo. Translation over the sequence yields a 50% ribosomal frameshift if the reading phase is A-AGG-AGG-U. The other two possible frames do not give shifts. The introduction of a UAA stop codon before (UAA-AGG-AGG-U) but not after (A-AGG-AGG-UAA) the AGG codons abolishes the frameshift. The change in the reading phase occurs exclusively to the +1 direction. Efficient frameshifting is also induced by the sequence A-AGA-AGA-U. The arginine codons AGG and AGA are read by minor tRNA. Suppression of frameshifting takes place when a gene for minor tRNA(Arg) is introduced on a multicopy plasmid. We suggest that frameshifting during translation of the A-AGG-AGG-U sequence is due to the erroneous decoding of the tandem AGG codons and arises by depletion of tRNA(Arg). The complementarity of tandem AGG codons to the 3' terminus of 16S rRNA is a coincidence and apparently not related to the shift. Replacing the AGG-AGG sequence by the optimal arginine codons CGU-CGU does not increase the overall rate of translation.
High levels of inflammatory chemokines and cytokines in joint fluid and synovial tissue throughout the course of antibiotic‐refractory lyme arthritis (2007)

Patients with antibiotic-refractory Lyme arthritis have high synovial fluid levels of proinflammatory chemokines and cytokines, especially CXCL9 and IFNgamma, throughout the illness. Thus, even when antibiotic treatment reduces or completely clears the infection in these patients, the inflammatory response in synovium persists.
Localization Algorithm Based on SVM-Data Fusion in Wireless Sensor Networks (2009)

This positioning process of the wireless sensor network (WSN) nodes is interfered by multipath, multiple access, especially NLOS transmission effect, Basing on TOA/TDOA positioning technology, the article brings forward TOA/TDOA measurement data model, and improves on a location algorithm which bases on least square support vector machine (LS-SVM). On one network with uniformly distributed nodes, node localization experiments show that SVM data fusion location algorithm can effectively reduce the effect of distance estimation error on positioning accuracy, minish coverage loop holes and network cost.