gebhart/patrepeval huggingface dataset:
Transcript Profiles in Sugar Beet Genotypes Uncover Timing and Strength of Defense Reactions toCercospora beticolaInfection (2011)

Cercospora leaf spot disease, caused by the fungus Cercospora beticola, is the most destructive foliar disease of sugar beet (Beta vulgaris) worldwide. Despite the great agronomical importance of this disease, little is known about its underlying molecular processes. Technical resources are scarce for analyzing this important crop species. We developed a sugar beet microarray with 44,000 oligonucleotides that represent 17,277 cDNAs. During the four stages of C. beticola-B. vulgaris interactions, we profiled the transcriptional responses of three genotypes: susceptible, polygenic partial resistance, and monogenic resistant. Similar genes were induced in all three genotypes during infection but with striking differences in timing. The monogenic resistant genotype displayed strong defense responses at 1 day postinoculation (dpi). The other genotypes displayed defense responses in a later phase (15 dpi) of the infection cycle. The partially resistant genotype displayed a strong defense response in the late phase of the infection cycle. Furthermore, the partially resistant genotype expressed pathogen-related transcripts that the susceptible genotype lacked. These results indicate that resistance was achieved by the ability to mount an early defense response, and partial resistance was determined by additional defense and signaling transcripts that allowed effective defense in the late phase of the infection cycle.
[Therapeutic effect of hypoxia-inducible factor-1alpha on focal cerebral ischemia: experiment with rats]. (2006)

HIF-1alpha gene had definite therapeutic effect on focal cerebral ischemia in adult rats, which settles a foundation for next HIF-1alpha gene study and clinic application.
Modeling and bonding-free fabrication of flexible fluidic microactuators with a bending motion (2013)

Flexible fluidic actuators recently attracted the interest of the microsystem community, especially for soft robotic applications including minimally invasive surgery. These actuators, based on a well-known actuator design where a void is surrounded by an asymmetric elastic structure, can achieve large bending strokes when pressurized. Miniaturized versions of these actuators typically fail due to poor bonding of constituting components, and further, there is little theoretical understanding of these devices. This paper presents a new actuator design which does not require any bonding and provides new insights into the modeling of these actuators. The newly developed production process of the actuators is based on out-of-plane high aspect ratio micromolding, which enables high-throughput bonding-free fabrication. Furthermore, a mathematical model based on Euler-Bernoulli's beam equation with a deformable cross section is developed that shows good agreement with validation experiments on prototypes. These theoretical insights greatly facilitate the design and optimization of flexible bending actuators. © 2013 IOP Publishing Ltd.
p53 accumulates but is functionally impaired when DNA synthesis is blocked (2001)

p53 is required for the induction of a G 1 and/or G 2 irreversible arrest after γ irradiation (IR), whereas blocked DNA replication causes a p53-independent S-phase arrest. We have examined the response to p53 when DNA synthesis is blocked by hydroxyurea (HU) or aphidicolin or when DNA is damaged by γ IR. Similarly to γ IR, blocked DNA synthesis induces high levels of phosphorylated nuclear p53. Surprisingly, several (but not all) p53 transcriptional targets that are rapidly induced by γ IR are weakly or not induced when DNA replication is blocked. Moreover, the p53 response to γ IR is inhibited by pretreatment of cells with HU or aphidicolin, suggesting that blocked DNA replication prevents p53 from being fully active as a transcription factor. HU-induced stabilization of p53 neither requires functional ATM (ataxia telangiectasia mutated), nor interferes with the γ IR-dependent activation of the ATM kinase. Thus, stalled replication forks activate kinases that modify and stabilize p53, yet act downstream of ATM to impair p53 transcriptional activity. The ramifications of this novel regulation of p53 are discussed.
Catheter-based ultrasound applicators for selective thermal ablation: progress towards MRI-guided applications in prostate (2004)

High-temperature thermal therapy is emerging as a feasible treatment option for prostate cancer and benign prostatic hyperplasia. Previous investigations have demonstrated distinct advantages of catheter-based ultrasound technology over other heating modalities for thermal ablation therapies, with significant potential for better spatial control and faster heating times. The purpose of this study was to develop ultrasound devices and techniques specifically for treating prostate cancer in conjunction with magnetic resonance thermal imaging (MRTI) to monitor and control treatment progression. Directional transurethral applicators have been designed with arrays of sectored tubular (90 degrees active acoustic sector) or with narrow planar transducer segments and integrated with a flexible delivery catheter with a cooling balloon. This applicator can be rotated within the prostatic urethra to target specific regions during treatment. MRI compatible catheter-cooled interstitial ultrasound applicators with 180 degrees active acoustic sectors were developed specifically to treat the prostate. These applicators may be implanted through the perineum into the posterior portion of the prostate, with their heating energy directed away from the rectum. Both heating strategies were evaluated via biothermal simulations and in vivo experiments within canine prostate (n = 3). During the in vivo studies, MRTI was used to monitor treatment temperatures, cytotoxic thermal doses (t43 > 240 min) and corresponding maximum temperature thresholds (Tmax > 52 degrees C) within three imaging planes simultaneously. Urethral and endorectal cooling was employed with both treatment strategies to provide further protection of the urethral mucosa and rectum from thermal damage. Results using the transurethral applicators demonstrated that narrow zones of coagulation (approximately 30 degrees sector for planar, approximately 90 degrees for tubular), extending up to 20 mm from the urethra to the periphery of the prostate gland, could be produced within 10-15 min. Further, rotation of the applicator during treatment could be used to destroy larger regions in the prostate. Experiments using multiple interstitial directional applicators (approximately 180 degrees active sectors), implanted within the posterior margin of the prostate with the energy directed away from the rectum, produced contiguous zones of thermal coagulation which extended from the posterior prostate toward the anterior-lateral periphery of the gland. Both transurethral and interstitial treatment strategies demonstrated significant potential for thermal ablation of localized prostate cancer, particularly when MRTI is used to guide and assess treatment.
Potentiation of photodynamic therapy of cancer by complement: the effect of γ-inulin (2006)

Host response elicited by photodynamic therapy (PDT) of cancerous lesions is a critical contributor to the clinical outcome, and complement system has emerged as its important element. Amplification of complement action was shown to improve tumour PDT response. In search of a clinically relevant complement activator for use as a PDT adjuvant, this study focused on gamma-inulin and examined its effects on PDT response of mouse tumours. Intralesional gamma-inulin (0.1 mg mouse(-1)) delivered immediately after PDT rivaled zymosan (potent classical complement activator) in delaying the recurrence of B16BL6 melanomas. This effect of gamma-inulin was further enhanced by IFN-gamma pretreatment. Tumour C3 protein levels, already elevated after individual PDT or gamma-inulin treatments, increased much higher after their combination. With fibrosarcomas MCA205 and FsaR, adjuvant gamma-inulin proved highly effective in reducing recurrence rates following PDT using four different photosensitisers (BPD, ce6, Photofrin, and mTHPC). At 3 days after PDT plus gamma-inulin treatment, over 50% of cells found at the tumour site were CTLs engaged in killing specific targets via perforin-granzyme pathway. This study demonstrates that gamma-inulin is highly effective PDT adjuvant and suggests that by amplifying the activation of complement system, this agent potentiates the development of CTL-mediated immunity against PDT-treated tumours.
Phase II randomized study of ISIS 3521 and ISIS 5132 in patients with locally advanced or metastatic colorectal cancer: a National Cancer Institute of Canada clinical trials group study. (2002)

Neither ISIS 5132 nor ISIS 3521given in the dose and schedule studied induced objective responses in untreated colorectal cancer patients.
Codon repeats in genes associated with human diseases: fewer repeats in the genes of nonhuman primates and nucleotide substitutions concentrated at the sites of reiteration. (1996)

Five human diseases are due to an excessive number of CAG repeats in the coding regions of five different genes. We have analyzed the repeat regions in four of these genes from nonhuman primates, which are not known to suffer from the diseases. These primates have CAG repeats at the same sites as in human alleles, and there is similar polymorphism of repeat number, but this number is smaller than in the human genes. In some of the genes, the segment of poly(CAG) has expanded in nonhuman primates, but the process has advanced further in the human lineage than in other primate lineages, thereby predisposing to diseases of CAG reiteration. Adjacent to stretches of homogeneous present-day codon repeats, previously existing codons of the same kind have undergone nucleotide substitutions with high frequency. Where these lead to amino acid substitutions, the effect will be to reduce the length of the original homopolymeric stretch in the protein.
Pretreatment with the nitric oxide donor SNAP or nerve transection blocks humoral preconditioning by remote limb ischemia or intra-arterial adenosine (2010)

We have previously shown that remote ischemic preconditioning (rIPC) by transient limb ischemia leads to the release of a circulating factor(s) that induces potent myocardial protection. Intra-arterial injection of adenosine into a limb also leads to cardioprotection, but the mechanism of its signal transduction is poorly understood. Eleven groups of rabbits received saline control or rIPC or adenosine administration with additional pretreatment with the nitric oxide (NO) synthase blocker N(G)-nitro-l-arginine methyl ester, the NO donor S-nitroso-N-acetylpenicillamine, its non-NO-donating derivative N-acetylpenicillamine, or femoral nerve section. Blood was then drawn from each animal, and the dialysate of the plasma was used to perfuse a naïve heart from an untreated donor. Infarct size was measured after 30 min of global ischemia and 120 min reperfusion. When compared with that of the control, mean infarct size was significantly smaller in groups treated with rIPC alone (P < 0.01) and intra-arterial adenosine (P < 0.01). Pretreatment with N(G)-nitro-l-arginine methyl ester or N-acetylpenicillamine did not affect the level of protection induced by rIPC (P = not significant, compared with rIPC alone) or intra-arterial adenosine (P = not significant, compared with intra-arterial adenosine alone), but prior femoral nerve transection or pretreatment with S-nitroso-N-acetylpenicillamine abolished the cardioprotective effect of intra-arterial adenosine and rIPC. Intra-arterial adenosine, like rIPC, releases a blood-borne cardioprotective factor(s) that is dependent on an intact femoral nerve and is inhibited by pretreatment with a NO donor. These results may be important when designing or assessing the results of clinical trials of adenosine or rIPC cardioprotection, where NO donors are used as part of therapy.
Living Polymerization Methods (1991)

Living polymerization techniques can be used to achieve a high degree of control over polymer chain architecture. Examples of the type of polymers that can be synthesized include block copolymers, comb-shaped polymers, multiarmed polymers, ladder polymers, and cyclic polymers. This control of structure, in turn, results in polymers with widely diverse physical properties, even though they are made from readily available low-cost monomers.
Research progress and prospect of circular RNA in multiple myeloma (2023)

Circular RNAs (circRNAs) are a novel type of covalently closed RNAs recently found to be involved in several physiological and pathological processes. A series of studies have proved that cyclic RNAs are related with the genesis and development of tumors, for example circ_0007841 and PVT1. Some circRNAs are strictly related to advanced clinical stage and poor prognosis, including circPTK2, circ-RNF217, circ-AFF2, circ-MYBL2, circ_0069767, circ-CDYL, circ_0000142, circRNA_101237 and exo-circMYC. In addition, circRNAs are involved in drug resistance and complications, they are circ-CCT3, Circ-007841, ciRS-7,circPVT1, circ_0001821, Exo-circ-G042080 and circCHEK1_246aa. Therefore, we propose that circRNAs can be considered as potential diagnostic and prognostic markers, which can induce chemoresistance, and might indicate novel therapeutic targets for multiple myeloma. Targeting cyclic RNA therapy will bring spring to the treatment of multiple myeloma.
Comb-referenced laser distance interferometer for industrial nanotechnology (2016)

A prototype laser distance interferometer is demonstrated by incorporating the frequency comb of a femtosecond laser for mass-production of optoelectronic devices such as flat panel displays and solar cell devices. This comb-referenced interferometer uses four different wavelengths simultaneously to enable absolute distance measurement with the capability of comprehensive evaluation of the measurement stability and uncertainty. The measurement result reveals that the stability reaches 3.4 nm for a 3.8 m distance at 1.0 s averaging, which further reduces to 0.57 nm at 100 s averaging with a fractional stability of 1.5 × 10(-10). The uncertainty is estimated to be in a 10(-8) level when distance is measured in air due to the inevitable ambiguity in estimating the refractive index, but it can be enhanced to a 10(-10) level in vacuum.
Quick atmospheric correction code: algorithm description and recent upgrades (2012)

The quick atmospheric correction (QUAC) code performs atmospheric correction on multi- and hyperspectral imagery spanning all or part of the visible and near infrared-short wave infrared spectral range, ∼ 400−2500 nm. It utilizes an in-scene approach, requiring only approximate specification of sensor band locations (i.e., central wavelengths) and their radiometric calibration; no additional metadata is required. Because QUAC does not involve first principles radiative-transfer calculations, it is significantly faster than physics-based methods; however, it is also more approximate. We present a detailed description of the QUAC algorithm, highlighting recent accuracy improvements. Example results for several multi-and hyperspectral data sets are presented, and comparisons are made to more rigorous correction approaches.
1,1-Bis(3′-indolyl)-1-(p-substituted phenyl)methanes inhibit ovarian cancer cell growth through peroxisome proliferator–activated receptor–dependent and independent pathways (2006)

1,1-Bis(3'-indolyl)-1-(p-t-butylphenyl)methane (DIM-C-pPhtBu) is a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, and treatment of SKOV3 ovarian cancer cells with this compound (5 micromol/L) inhibits cell proliferation, whereas up to 15 micromol/L rosiglitazone had no effect on cell growth. DIM-C-pPhtBu also inhibits G0-G1 to S phase cell cycle progression and this is linked, in part, to PPARgamma-dependent induction of the cyclin-dependent kinase inhibitor p21. DIM-C-pPhtBu induces PPARgamma-independent down-regulation of cyclin D1 and we therefore further investigated activation of receptor-independent pathways. DIM-C-pPhtBu also induced apoptosis in SKOV3 cells and this was related to induction of glucose-related protein 78, which is typically up-regulated as part of the unfolded protein response during endoplasmic reticulum (ER) stress. Activation of ER stress was also observed in other ovarian cancer cell lines treated with DIM-C-pPhtBu. In addition, DIM-C-pPhtBu induced CCAAT/enhancer binding protein homologous protein through both ER stress and c-jun NH2-terminal kinase-dependent pathways, and CCAAT/enhancer binding protein homologous protein activated death receptor 5 and the extrinsic pathway of apoptosis. These results show that DIM-C-pPhtBu inhibits growth and induces apoptosis in ovarian cancer cells through both PPARgamma-dependent and PPARgamma-independent pathways, and this complex mechanism of action will be advantageous for future clinical development of these compounds for treatment of ovarian cancer.
Transforming Growth Factor- β1 Induces Phenotypic Modulation of Human Lung Fibroblasts to Myofibroblast Through a c-Jun-NH2-Terminal Kinase-Dependent Pathway (2001)

Myofibroblasts play an important role in the fibrogenic process of pulmonary fibrosis. Transforming growth factor (TGF)-beta is well known to induce the phenotypic modulation of fibroblasts to myofibroblasts; however, the intracellular signal regulating induction of the myofibroblastic phenotype of human lung fibroblasts (HLF) has not been determined. In the present study, we examined the role of the mitogen-activated protein kinase (MAPK) superfamily in inducing the phenotypic modulation of HLF to myofibroblasts characterized by alpha-smooth-muscle actin expression, in order to clarify this issue. The results showed that: (1) TGF-beta1 caused the phenotypic modulation of HLF to myofibroblasts in a dose- and a time-dependent manner; (2) TGF-beta1 induced increases in c-Jun-NH2- terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (Erk) phosphorylation and activity; (3) the inhibitors CEP-1347, SB 203580, and PD 98059 attenuated TGF-beta1-induced JNK, p38 MAPK, and Erk activity, respectively; and (4) CEP-1347, but not SB 203580 or PD 98059, attenuated the TGF-beta1-induced phenotypic modulation of HLF to myofibroblasts in a dose-dependent manner. These results indicate that TGF-beta1 is capable of inducing the myofibroblastic phenotype of HLF, and that JNK regulates the phenotypic modulation of TGF-beta1-stimulated HLF to myofibroblasts.
MicroRNAs modulate the chemosensitivity of tumor cells (2008)

MicroRNAs are strongly implicated in such processes as development, carcinogenesis, cell survival, and apoptosis. It is likely, therefore, that they can also modulate sensitivity and resistance to anticancer drugs in substantial ways. To test this hypothesis, we studied the pharmacologic roles of three microRNAs previously implicated in cancer biology (let-7i, mir-16, and mir-21) and also used in silico methods to test pharmacologic microRNA effects more broadly. In the experimental system, we increased the expression of individual microRNAs by transfecting their precursors (which are active) or suppressed the expression by transfection of antisense oligomers. In three NCI-60 human cancer cell lines, a panel of 60 lines used for anticancer drug discovery, we assessed the growth-inhibitory potencies of 14 structurally diverse compounds with known anticancer activities. Changing the cellular levels of let-7i, mir-16, and mir-21 affected the potencies of a number of the anticancer agents by up to 4-fold. The effect was most prominent with mir-21, with 10 of 28 cell-compound pairs showing significant shifts in growth-inhibitory activity. Varying mir-21 levels changed potencies in opposite directions depending on compound class; indicating that different mechanisms determine toxic and protective effects. In silico comparison of drug potencies with microRNA expression profiles across the entire NCI-60 panel revealed that approximately 30 microRNAs, including mir-21, show highly significant correlations with numerous anticancer agents. Ten of those microRNAs have already been implicated in cancer biology. Our results support a substantial role for microRNAs in anticancer drug response, suggesting novel potential approaches to the improvement of chemotherapy.
Tumor necrosis factor receptor p75 mediates cell-specific activation of nuclear factor kappa B and induction of human cytomegalovirus enhancer. (1994)

The functional role of human tumor necrosis factor receptor (TNFR) p75 was studied by the use of TNFR p75-specific agonistic antibodies. Human SW480T adenocarcinoma cells, stably transfected with a reporter construct containing beta-galactosidase under the control of human cytomegalovirus immediate early enhancer, were stimulated with anti-TNFR p75 polyclonal antiserum or monoclonal antibodies followed by measurement of beta-galactosidase activity and analysis by electrophoretic mobility shift assays. It was found that cross-linking of TNFR p75 led to strong induction of the human cytomegalovirus enhancer as well as activation of nuclear factor-kappa B (NF-kappa B). Stimulation of TNFR p75 also mediated activation of NF-kappa B in human KYM-1 rhabdomyosarcoma cells but not in other cell types such as U937 and HL-60 monocytic cells or in Eahy 926 endothelial cells. NF-kappa B activation induced by TNFR p75 was delayed approximately 15 min compared with NF-kappa B activation induced by TNFR p55, indicating that the two TNFRs activate NF-kappa B through different signaling pathways. The data presented in this study identify intracellular responses mediated by TNFR p75 which have not been reported previously and suggest that TNFR p75-induced activation of NF-kappa B is strictly cell type-specific.
The Classification of Autism, Asperger's Syndrome, and Pervasive Developmental Disorder (2000)

The current classification of the pervasive developmental disorders (PDDs) as conceptualized in both the DSM-IV and ICD-10 is deeply unsatisfying to many parents, front-line clinicians, and academic researchers. Is the diagnostic validity of the various disorders simply lacking empirical data for full substantiation, or does the overall conceptualization of the category have more fundamental problems, not reflecting the "true" nature of the phenomena? This paper argues the latter hypothesis. I review the historical development of the classification of PDD, summarize recent empirical data on issues of reliability and validity, and suggest a new approach to classification and understanding.
Active Object Localization with Deep Reinforcement Learning (2015)

We present an active detection model for localizing objects in scenes. The model is class-specific and allows an agent to focus attention on candidate regions for identifying the correct location of a target object. This agent learns to deform a bounding box using simple transformation actions, with the goal of determining the most specific location of target objects following top-down reasoning. The proposed localization agent is trained using deep reinforcement learning, and evaluated on the Pascal VOC 2007 dataset. We show that agents guided by the proposed model are able to localize a single instance of an object after analyzing only between 11 and 25 regions in an image, and obtain the best detection results among systems that do not use object proposals for object localization.