gebhart/patrepeval huggingface dataset:
Terahertz generation using plasmonic photoconductive gratings (2012)

A photoconductive terahertz emitter based on plasmonic contact electrode gratings is presented and experimentally demonstrated. The nanoscale grating enables ultrafast and high quantum efficiency operation simultaneously, by reducing the photo-generated carrier transport path to the photoconductor contact electrodes. The presented photoconductor eliminates the need for a short-carrier lifetime semiconductor, which limits the efficiency of conventional photoconductive terahertz emitters. Additionally, the photo-absorbing active area of the plasmonic photoconductive terahertz emitter can be increased without a significant increase in the capacitive loading to the terahertz radiating antenna, enabling high quantum-efficiency operation at high pump power levels by preventing the carrier screening effect and thermal breakdown. A plasmonic photoconductive terahertz emitter prototype based on the presented scheme is implemented and integrated with dipole antenna arrays on a semi-insulating In 0.53 Ga 0.47 As substrate. Emitted terahertz radiation is characterized in a terahertz time-domain spectroscopy setup, measuring a terahertz pulse width of 590Â¬â€ fs full-width at half maximum in response to 150Â¬â€ fs pump pulses at 925Â¬â€ nm.
The retinoblastoma protein binds to RIZ, a zinc-finger protein that shares an epitope with the adenovirus E1A protein. (1995)

The retinoblastoma protein (Rb) is a target of viral oncoproteins. To explore the hypothesis that viral proteins may be structural mimics of cellular proteins, we have searched cDNA libraries for Rb-binding proteins. We report here the cloning of a cDNA for the protein RIZ from rat and human cells. RIZ is a 250-kDa nuclear protein containing eight zinc-finger motifs. It contains an Rb-binding motif that shares an antigenic epitope with the C terminus of E1A. A domain is conserved between RIZ and the PRDI-BF1/Blimp-1 differentiation factor. Other motifs of RIZ include putative GTPase and SH3 (src homology domain 3) domains. RIZ is preferentially expressed in both adult and embryonic rat neuroendocrine tissues. It is also expressed in human retinoblastoma cells and at low levels in all other human cell lines examined. While the function of RIZ is not yet clear, its structure and pattern of expression suggest a role for RIZ in transcriptional regulation during neuronal differentiation and pathogenesis of retinoblastoma.
Synthesis of N-heterocycles via lactam-derived ketene aminal phosphates. Asymmetric synthesis of cyclic amino acids. (1998)

K. C. Nicolaou and K. Namoto, Chem. Commun., 1998, 1757 DOI: 10.1039/A804198I
Inhibitory effects of black tea theaflavin derivatives on 12‐O‐tetradecanoylphorbol‐13‐acetate‐induced inflammation and arachidonic acid metabolism in mouse ears (2006)

Tea has been shown to possess several health beneficial properties primarily due to its polyphenolic content. The major polyphenolic compounds in black tea leaves are theaflavins (TFs) formed by oxidative coupling of catechins in tea leaves during its processing. In this paper, we report the characterization of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear inflammatory model and the inhibitory effects of major black tea TFs derivatives on this inflammation. In addition, the effect on inflammatory biomarkers, such as proinflammatory cytokines and arachidonic acid metabolites, are reported as well. A single topical application of TPA to ears of CD-1 mice induced a time- and dose-dependent increase in edema as well as formation of proinflammatory cytokine proteins interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) in mouse ears. A single topical application of equimolar of black tea constituents (TF, theaflavin-3-gallate, theaflavin-3'-gallate, and theaflavin-3,3'-digallate) strongly inhibited TPA-induced edema of mouse ears. Application of TFs mixture to mouse ears 20 min prior to each TPA application once a day for 4 days inhibited TPA-induced persistent inflammation, as well as TPA-induced increase in IL-1beta and IL-6 protein levels. TFs also inhibited arachidonic acid (AA) metabolism via both cyclooxygenase (COX) and lipoxygenase pathways. This observation was substantiated by decreased amounts of AA metabolites prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) levels. Combined application of TF and sulindac, a nonsteroidal anti-inflammatory drug resulted a significant synergetic anti-inflammatory effect. Oral administration of TFs or the hot water extract of black tea leaves also significantly inhibited TPA-induced edema in mouse ears. In conclusion, proinflammatory cytokines, IL-1beta and IL-6, as well as the intermediated metabolites of AA, PGE2, and LTB4 are good biomarkers for inflammation. Black tea constituents, TF and its derivatives, had strongly anti-inflammatory activity in vivo which may be due to their ability to inhibit AA metabolism via lipoxygenase and COX pathways.
Loss of distal 11q is associated with DNA repair deficiency and reduced sensitivity to ionizing radiation in head and neck squamous cell carcinoma (2007)

About 45% of head and neck squamous cell carcinomas (HNSCC) are characterized by amplification of chromosomal band 11q13. This amplification occurs by a breakage-fusion-bridge (BFB) cycle mechanism. The first step in the BFB cycle involves breakage and loss of distal 11q, from FRA11F (11q14.2) to 11qter. Consequently, numerous genes, including three critical genes involved in the DNA damage response pathway, MRE11A, ATM, and H2AFX are lost in the step preceding 11q13 amplification. We hypothesized that this partial loss of genes on distal 11q may lead to a diminished DNA damage response in HNSCC. Characterization of HNSCC using fluorescence in situ hybridization (FISH) revealed concurrent partial loss of MRE11A, ATM, and H2AFX in all four cell lines with 11q13 amplification and in four of seven cell lines without 11q13 amplification. Quantitative microsatellite analysis and loss of heterozygosity studies confirmed the distal 11q loss. FISH evaluation of a small series of HNSCC, ovarian, and breast cancers confirmed the presence of 11q loss in at least 60% of these tumors. All cell lines with distal 11q loss exhibited a diminished DNA damage response, as measured by a decrease in the size and number of gamma-H2AX foci and increased chromosomal instability following treatment with ionizing radiation. In conclusion, loss of distal 11q results in a defective DNA damage response in HNSCC. Distal 11q loss was also unexpectedly associated with reduced sensitivity to ionizing radiation. Although the literature attributes the poor prognosis in HNSCC to 11q13 gene amplification, our results suggest that distal 11q deletions may be an equally significant factor.
Disruption of EphA2 Receptor Tyrosine Kinase Leads to Increased Susceptibility to Carcinogenesis in Mouse Skin (2006)

EphA2 receptor tyrosine kinase is frequently overexpressed in different human cancers, suggesting that it may promote tumor development and progression. However, evidence also exists that EphA2 may possess antitumorigenic properties, raising a critical question on the role of EphA2 kinase in tumorigenesis in vivo. We report here that deletion of EphA2 in mouse led to markedly enhanced susceptibility to 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA) two-stage skin carcinogenesis. EphA2-null mice developed skin tumors with an increased frequency and shortened latency. Moreover, tumors in homozygous knockout mice grew faster and were twice as likely to show invasive malignant progression. Haploinsufficiency of EphA2 caused an intermediate phenotype in tumor development but had little effects on invasive progression. EphA2 and ephrin-A1 exhibited compartmentalized expression pattern in mouse skin that localized EphA2/ephrin-A1 interactions to the basal layer of epidermis, which was disrupted in tumors. Loss of EphA2 increased tumor cell proliferation, whereas apoptosis was not affected. In vitro, treatment of primary keratinocytes from wild-type mice with ephrin-A1 suppressed cell proliferation and inhibited extracellular signal-regulated kinase 1/2 (ERK1/2) activities. Both effects were abolished in EphA2-null keratinocytes, suggesting that loss of ERK inhibition by EphA2 may be one of the contributing mechanisms for increased tumor susceptibility. Interestingly, despite its tumor suppressive function, EphA2 was overexpressed in skin tumors compared with surrounding normal skin in wild-type mice, similar to the observations in human cancers. EphA2 overexpression may represent a compensatory feedback mechanism during tumorigenesis. Together, these results show that EphA2 is a novel tumor suppressor gene in mammalian skin.
Breath gas aldehydes as biomarkers of lung cancer (2009)

There is experimental evidence that volatile substances in human breath can reflect presence of neoplasma. Volatile aldehydes were determined in exhaled breath of 12 lung cancer patients, 12 smokers and 12 healthy volunteers. Alveolar breath samples were collected under control of expired CO(2). Reactive aldehydes were transformed into stable oximes by means of on-fiber-derivatization (SPME-OFD). Aldehyde concentrations in the ppt and ppb level were determined by means of gas chromatography-mass spectrometry (GC-MS). Exhaled concentrations were corrected for inspired values. Exhaled C(1)-C(10) aldehydes could be detected in all healthy volunteers, smokers and lung cancer patients. Concentrations ranged from 7 pmol/l (161 pptV) for butanal to 71 nmol/l (1,582 ppbV) for formaldehyde. Highest inspired concentrations were found for formaldehyde and acetaldehyde (0-55 nmol/l and 0-13 nmol/l, respectively). Acetaldehyde, propanal, butanal, heptanal and decanal concentrations showed no significant differences for cancer patients, smokers and healthy volunteers. Exhaled pentanal, hexanal, octanal and nonanal concentrations were significantly higher in lung cancer patients than in smokers and healthy controls (p(pentanal) = 0.001; p(hexanal) = 0.006; p(octanal) = 0.014; p(nonanal) = 0.025). Sensitivity and specificity of this method were comparable to the diagnostic certitude of conventional serum markers and CT imaging. Lung cancer patients could be identified by means of exhaled pentanal, hexanal, octanal and nonanal concentrations. Exhaled aldehydes reflect aspects of oxidative stress and tumor-specific tissue composition and metabolism. Noninvasive recognition of lung malignancies may be realized if analytical skills, biochemical knowledge and medical expertise are combined into a joint effort.
Object-oriented programming: Themes and variations (1986)

Many of the ideas behind object-oriented programming have roots going back to SIMULA. The first substantial interactive, display-based implementation was the SMALLTALK language. The object-oriented style has often been advocated for simulation programs, systems programming, graphics, and AI programming. The history of ideas has some additional threads including work on message passing as in ACTORS, and multiple inheritance as in FLAVORS. It is also related to a line of work in AI on the theory of frames and their implementation in knowledge representation languages such as KRL, KEE, FRL, and UNITS.
Analysis by Pulsed-Field Gel Electrophoresis of Candida albicans that Developed Resistance during Antifungal Therapy. (1998)

A patient with myelofibrosis complicated by recurrent candidemia died despite treatment with amphotericin B and fluconazole. Autopsy revealed systemic candidiasis with fungal verrucae in the right ventricle and the root of the pulmonary artery. The strains of Candida albicans isolated from the blood had become resistant to amphotericin B and fluconazole during therapy, as well as to other azole antifungals that had not been used. Pulsed-field gel electrophoresis showed that the resistant isolates had the same genotype as the sensitive strains isolated before treatment, but a chromosomal change in >2.0 Mb-bands was observed after treatment. It was thus proved that these repeatedly isolated C. albicans strains which were causing the continued fungemia in our patient were all the same strain and were acquiring resistance to antifungal agents during the therapy.
Prohexadione-Calcium Controls Vegetative Shoot Growth in Apple (2002)

Abstract Prohexadione-calcium (Phd-Ca) (BAS 125W or 9054 W) applied at petal fall (PF) or within 10 days of PF to apple trees as a single spray or as multiple low-rate sprays reduced the current season's shoot growth. Sprays applied 2 to 3 weeks after PF were less effective. Timing of the initial spray was more important than rate in achieving early growth suppression, but rate was most important for maximum season-long growth control. Reduced shoot growth enhanced spray coverage and reduced dormant pruning time by as much as 23% over control trees. An effective cumulative dose (ECD) of 250 mg·L−1 (based on dilute or tree-row-volume equivalent) active ingredient Phd-Ca applied as a single spray or in several low-rate sprays generally produced season-long control of vigorous shoot growth. However, under some highvigor growing conditions a higher ECD (500 mg·L−1 or greater), applied in multiple low-rate sprays, was required to achieve an acceptable level of growth suppression. When shoots resumed growth in mid-season, a single spray (28 July) at 125 mg·L−1 provided additional suppression of shoot growth. During this 5-year study, there were no adverse effects on fruit quality and little or no effect on fruit size. There was no appreciable carryover effect on the next season's shoot growth or fruit size, and there was no additive effect from successive annual applications.
Soluble E-Selectin and Soluble Tumour Necrosis Factor Receptor (60 kD) Serum Levels in Patients with Psoriasis (1995)

Significantly increased amounts of sE-selectin serum levels were found in psoriatic patients as compared to healthy controls. Moreover, a direct correlation between sE-selectin and PASI scores was observed. On the contrary, sTNF-R (60 kD) serum levels presented no increases. These data suggest that sE-selectin serum levels are a reliable marker of disease activity in psoriatic patients.
The catalytic cycle of β-lactam synthetase observed by x-ray crystallographic snapshots (2002)

The catalytic cycle of the ATP/Mg(2+)-dependent enzyme beta-lactam synthetase (beta-LS) from Streptomyces clavuligerus has been observed through a series of x-ray crystallographic snapshots. Chemistry is initiated by the ordered binding of ATP/Mg(2+) and N(2)-(carboxyethyl)-l-arginine (CEA) to the apoenzyme. The apo and ATP/Mg(2+) structures described here, along with the previously described CEA.alpha,beta-methyleneadenosine 5'-triphosphate (CEA.AMP-CPP)/Mg(2+) structure, illuminate changes in active site geometry that favor adenylation. In addition, an acyladenylate intermediate has been trapped. The substrate analog N(2)-(carboxymethyl)-l-arginine (CMA) was adenylated by ATP in the crystal and represents a close structural analog of the previously proposed CEA-adenylate intermediate. Finally, the structure of the ternary product complex deoxyguanidinoproclavaminic acid (DGPC).AMP/PP(i)/Mg(2+) has been determined. The CMA-AMP/PP(i)/Mg(2+) and DGPC.AMP/PP(i)/Mg(2+) structures reveal interactions in the active site that facilitate beta-lactam formation. All of the ATP-bound structures differ from the previously described CEA.AMP-CPP/Mg(2+) structure in that two Mg(2+) ions are found in the active sites. These Mg(2+) ions play critical roles in both the adenylation and beta-lactamization reactions.
Characteristic wave detection in ECG signal using morphological transform (2005)

The developed MMD method exhibits good potentials for automated ECG signal analysis and cardiovascular arrhythmia recognition.
Defective CTLA-4 cycling pathway in Chediak–Higashi syndrome: A possible mechanism for deregulation of T lymphocyte activation (1999)

Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4, also known as CD152) has been shown to play a major role in the regulation of T cell activation. Its membrane expression is highly regulated by endocytosis and trafficking through the secretory lysosome pathway. Chediak-Higashi syndrome (CHS) is an inherited disorder caused by mutations in the lysosomal trafficking regulator gene, LYST. It results in defective membrane targeting of the proteins present in secretory lysosomes, and it is associated with a variety of features, including a lymphoproliferative syndrome with hemophagocytosis. The murine equivalent of CHS, beige mice, present similar characteristics but do not develop the lymphoproliferative syndrome. We show herein that CTLA-4 is present in enlarged, abnormal vesicles in CHS T cells and is not properly expressed at the cell surface after T cell activation, whereas its surface expression is not impaired. It is therefore proposed that the defective surface expression of CTLA-4 by CHS T cells is involved in the generation of lymphoproliferative disease. This observation may provide insight into the role of CTLA-4 in humans.
The Ig1/2 Domain of MuSK Binds to Muscle Surface and Is Involved in Acetylcholine Receptor Clustering (2008)

The neuromuscular junction, the synapse between motor neurons and muscle cells, serves as an excellent model for studying synapse formation. Agrin is believed to be released by motor neurons to induce postsynaptic differentiation at the neuromuscular junction. MuSK, a receptor tyrosine kinase, appears to be a key component of the agrin receptor complex. However, how agrin activates MuSK remains unclear. To address this question, we characterized the binding of the MuSK extracellular region to the muscle cell surface. The MuSK ectodomain was found to bind to muscle cells in a manner dependent on stimulation with neural agrin. Moreover, the binding was myotube specific and appeared to be mediated by two regions in the MuSK: one region containing the first and second immunoglobin domains and the other containing the cysteine-rich domain. Importantly, recombinant proteins containing the binding activity can block full-length MuSK binding to muscle cells and agrin-induced AChR clustering. These results suggest that the Ig1/2 domain of MuSK is involved in AChR clustering by binding to the muscle surface.
Surgical Treatment of Internal Disc Disruption (1998)

Surgical treatment for internal disc disruption remains controversial in terms of efficacy of spinal fusion and optimal fusion method. The present study was carried out in 56 consecutive patients, with the diagnosis confirmed by computed tomographic (CT) discography, who were operated with one of four different lumbar fusion procedures. Outcomes were determined by postoperative pain questionnaires, independent clinical assessment, and radiographic evaluation. Simultaneous anterior interbody fusion using BAK cage and posterior facet fusion provided the highest rate of fusion (88%) and clinical satisfaction (63%). Pain scores were also significantly lower than facet screw augmented posterolateral fusion, and anterior interbody fusion with fibula allograft, but not significantly different from pedicle screw instrumented posterolateral fusion. Patients who achieved successful lumbar fusion had better clinical outcomes and a better chance of work resumption.
Wearable computing: a first step toward personal imaging (1997)

Miniaturization of components has enabled systems that are wearable and nearly invisible, so that individuals can move about and interact freely, supported by their personal information domain. To explore such new concepts in imaging and lighting, I designed and built the wearable personal imaging system. My invention differed from present-day laptops and personal digital assistants in that I could keep an eye on the screen while walking around and doing other things. Just as computers have come to serve as organizational and personal information repositories, computer clothing, when worn regularly, could become a visual memory prosthetic and perception enhancer.
Effect of Inhibitors of Poly(ADP-Ribose)Polymerase on the Radiation Response of HeLa S3 Cells (1989)

The purpose of this study was to investigate a possible involvement of poly(ADP-ribosyl)ation reactions in hyperthermic cell killing and hyperthermic DNA strand-break induction and repair in HeLa S3 cells. The inhibitors of poly(ADP-ribose) polymerase, 3-aminobenzamide (3AB) and 4-aminobenzamide (4AB), were used as tools in this study. Both inhibitors could sensitize the cells for hyperthermic cell killing equally well, although 3AB is known to be a more effective enzyme inhibitor. The heat sensitization at the level of cell killing could be reversed when the compounds were still present during a 4-h postincubation at 37 degrees C. More heat-induced DNA strand breaks were formed in the presence of 3AB and 4AB. Repair of strand breaks was inhibited during the postincubation at 37 degrees C. Thus the effect of 3AB and 4AB on DNA strand-break repair was different from the cited effect on cell survival. It is concluded that the sensitizing effect of 3AB and 4AB on hyperthermic cell killing is not caused by inhibition of poly(ADP-ribose) polymerase and is also not related to repair of DNA strand breaks.
Therapy of Alzheimer's disease: an update. (2010)

Alzheimer’s disease is a devastating neurodegenerative disorder manifested by deterioration in memory and cognition, impairment in performing activities of daily living, and many behavioral and neuropsychiatric illnesses. The pathological hallmark of Alzheimer’s disease is widespread neuritic plaques which are accumulations of amyloid beta protein and neurofibrillary tangles. Studies report that deficit in cholinergic system is responsible for cognitive decline and memory loss in patients with Alzheimer’s disease. Various pharmacologic approaches are developed for the treatment of Alzheimer’s disease. The leading edge therapies of Alzheimer’s disease are approved drugs; Acetylcholinesterase inhibitors and NMDA receptor antagonist. The experimental therapies are mostly disease modifying and have neuroprotective approaches. Gamma secretase inhibitors aim to reduce amyloid beta formation. Antioxidants, antiinflammatory agents and statins help by preventing oxidation and inflammation. PPAR gamma agonists, estrogen, heavy metal chelators, 5HT6 antagonists and nicotinic receptor agonists are other therapeutic strategies likely to alter the current treatment paradigm of Alzheimer’s disease. The behavioral abnormalities are best treated first by non-pharmacologic interventions. The pharmacological agents used for treatment of Neuropsychiatric illnesses include antipsychotics, antidepressants and mood stabilizers. Treatment of Alzheimer’s disease also includes health maintenance activities and proper nursing care of the patients.

	 

	Key words: Alzheimer’s disease, therapy of Alzheimer’s disease, cholinesterase inhibitors, neuroprotective agents, gamma secretase inhibitors.