gebhart/patrepeval huggingface dataset:
A fullerene–single wall carbon nanotube complex for polymer bulk heterojunction photovoltaic cells (2007)

A novel immobilized fullerene–single wall carbon nanotube (C60–SWCNT) complex was synthesized via a microwave induced functionalization approach. It has been used as a component of the photoactive layer in a bulk heterojunction photovoltaic cell. As compared to a control device with only C60, the addition of SWCNTs resulted in an improvement of both the short circuit current density JSC and the fill factor (FF). This device takes advantage of the electron accepting feature of C60 and the high electron transport capability of SWCNTs. The results indicate that C60 decorated SWCNTs are promising additives for performance enhancement of polymer photovoltaic cells.
IgA nephropathy and IgA vasculitis with nephritis have a shared feature involving galactose-deficient IgA1-oriented pathogenesis (2018)

Galactose-deficient IgA1 has been proposed as an important effector molecule in IgA nephropathy (IgAN). We previously showed that the galactose-deficient IgA1-specific monoclonal antibody KM55 can detect circulating galactose-deficient IgA1 in patients with IgAN, enabling us to study the molecular roles of galactose-deficient IgA1. Herein, we further examined the pathophysiological significance of galactose-deficient IgA1 in glomerular deposits of patients with IgAN by immunohistochemistry using KM55. Immunostaining of galactose-deficient IgA1 with KM55 was performed in paraffin-embedded sections of renal biopsy specimens from 48 patients with IgAN and 49 patients with other renal diseases such as lupus nephritis, HCV-related nephropathy, IgA vasculitis with nephritis (IgA-VN), and membranous nephropathy. Glomerular galactose-deficient IgA1 was specifically detected in IgAN and IgA-VN but not in the other renal diseases. Galactose-deficient IgA1 was localized predominantly in the mesangial region as IgA deposition. However, galactose-deficient IgA1 was not detected in patients with lupus nephritis accompanied by glomerular IgA deposition. Thus, our study strongly suggests that IgAN and IgA-VN have a shared feature regarding galactose-deficient IgA1-oriented pathogenesis.
Targeting Systemically Administered Proteins to Bone by Bisphosphonate Conjugation (2002)

To develop a methodology for bone-specific delivery of proteins, a bone-seeking aminobisphosphonate (aminoBP) was previously conjugated to a model protein, bovine serum albumin (BSA). The conjugates were shown to exhibit a high affinity to bone in vitro and in vivo. This study was conducted to determine whether the systemic delivery of proteins to bone can be increased by aminoBP conjugation. Two model proteins used for this study were BSA and lysozyme (LYZ). For each protein, an unmodified (i.e., control) and aminoBP-conjugated protein were (125)I-labeled and injected into rats, and the organ delivery of the proteins were determined. Intravenous (IV) injection of aminoBP-BSA resulted in a 2.0- to 3.7-fold increased delivery to bones as compared to the control protein in young rats. In osteopenic, ovariectomized rats, aminoBP conjugation enhanced the bone delivery of BSA by 2.2- to 7.5-fold. A 3.7- to 5.6-fold increased delivery was also observed for LYZ after IV injection in normal rats. In addition to IV route of administration, subcutaneous injection was also effective in delivering a higher amount of aminoBP-conjugated proteins to bone. We conclude that conjugating bone-seeking aminoBPs to proteins improved their delivery to mineralized tissues. The proposed targeting approach has the potential to improve the efficacy of recombinant proteins capable of stimulating bone formation by enhancing their localization to bones.
C6 glioma cell-conditioned medium induces neurite outgrowth and survival of rat chromaffin cells in vitro: comparison with the effects of nerve growth factor. (1984)

The effects of medium conditioned by rat C6 glioma cells (C6-CM) on the survival, neurite formation, and catecholamine content of adrenal medullary cells in culture were investigated and compared with the effects of nerve growth factor (NGF). Adrenal medullary cells were isolated from 10-day-old rats and the proportions of surviving and neurite-extending cells were determined after 8 days in culture. In the presence of C6-CM virtually all seeded cells survived and 50% developed neuritic processes. In contrast, NGF did not support survival above control levels (30%) and induced neurite formation from approximately one-third of the surviving cells. C6-CM and NGF had no additive effects on neurite outgrowth. C6-CM-mediated fiber outgrowth was not inhibited by physiological concentrations of glucocorticoids which abolished the NGF-induced neurite formation. Both C6-CM and NGF increased the catecholamine content of the cultures and reduced the relative content of epinephrine. However, in view of its substantial effect on cell survival as compared to NGF, C6-CM caused a reduction of the catecholamine content per cell. We conclude that adrenal medullary cells, like other members of the sensory-sympathetic cell lineage of the neural crest, respond to glial-conditioned medium. This response differs both quantitatively and qualitatively from that mediated by NGF.
Prevalence of Antiretroviral Drug Resistance Mutations in Chronically HIV-Infected, Treatment-Naive Patients: Implications for Routine Resistance Screening before Initiation of Antiretroviral Therapy (2005)

These results demonstrate the persistence of drug resistance mutations in chronically HIV-infected patients and an increasing prevalence of resistance over time, and they support genotyping of virus at baseline for chronically HIV-infected patients.
Targeting Drugs to the Colon: Delivery Systems for Oral Administration (1994)

The oral delivery of drugs to the colon has applications in a variety of therapeutic areas. This review is concerned with the approaches taken to achieve a universal system for delivery. The design of such a system requires the identification and exploitation of a unique feature of the colonic environment. The use of transit times, pH and bacterial enzymes are critically assessed. In addition, the system must provide protection for the drug during transit to the colon. Upper gastro-intestinal physiology and the transit of pharmaceuticals through these regions are reviewed with reference to their relevance in achieving site specificity.
Ab Initio Calculations of Proton Dissociation Energies of Zinc Ligands:  Hypothesis of Imidazolate as Zinc Ligand in Proteins (1999)

Despite intensive studies of zinc's role in proteins and recent growing appreciation of zinc in modern biology, the knowledge of the protonation state of common zinc ligands in proteins remains controversial. Water, the side chains of Glu, Asp, and Cys residues, and even the peptide nitrogen atom are treated as a deprotonated, negatively charged ligand in the zinc complexes in proteins, whereas the side chain of His residue is treated as a neutral ligand in the zinc complexes regardless of the common knowledge that the imidazole nitrogen proton is more acidic than the peptide nitrogen proton. In an attempt to resolve this controversy, we performed large basis set DFT calculations of proton dissociation energies of common zinc ligands in the presence and absence of Zn2+. Herein, we report the results of our calculations revealing that the proton dissociation energies of H2O, MeOH, MeSH, imidazole, and N-methylacetamide are dramatically reduced when they coordinate to Zn2+ and that the proton dissociation energy of the zinc-bound imidazole is 4 kcal/mol lower than that of the zinc-bound N-methylacetamide that is known to be deprotonated according to the X-ray and NMR studies. The result thus suggests further investigations of the possibility of imidazolate as a zinc ligand in proteins.
DNA BREAKAGE CAUSED BY 334‐nm ULTRAVIOLET LIGHT IS ENHANCED BY NATURALLY OCCURRING NUCLEIC ACID COMPONENTS AND NUCLEOTIDE COENZYMES (1984)

Abstract— The induction of breaks in DNA in vitro caused by 334‐nm UV radíation is enhanced by the following compounds (fluence enhancement factors and concentrations used in parentheses): 4‐thiouridine (6.9, 1 m M ), 5‐methylamino‐2‐thiouridine (7.5, 1 m M ), 2‐thiouracil (41.0, 1 m M ), riboflavin (14.4.0.1 m M ), and the oxidized (6.8, 1 m M ) and reduced (3.4, 1 m M ) forms of nicotinamide adenine dinucleotide. Anoxia and diazobicyclo(2.2.2)octane reduce the number of DNA breaks caused by 334‐nm radiation plus 4‐thiouridine by 70 and 76%, respectively.
Cardiopulmonary manifestations of schistosomiasis. (1997)

Three major schistosome species infect hundreds of millions of people worldwide. The majority of these infections are asymptomatic, but significant morbidity and mortality can occur as a consequence of ongoing egg deposition in host tissues. Acutely, transient chest radiographic abnormalities and nonspecific influenza-like symptoms can occur, including cough. The most common chronic pathological sequelae of schistosomiasis are those of portal hypertension with Schistosoma mansoni or S. japonicum, and genitourinary tract obstruction with S. haematobium. In less than 5% of infections, schistosomal egg obstruction of the lung vasculature results in pulmonary hypertension and cor pulmonale. Limited data suggests that cardiopulmonary schistosomiasis is seen most often in S. mansoni infections. Hepatic fibrosis and portal hypertension appear to be a prerequisite to the development of schistosomal cor pulmonale caused by this species. The premortem diagnosis of cardiopulmonary schistosomiasis depends on the detection of viable schistosomal ova in stool or urine along with evidence of characteristic hepatic fibrosis and pulmonary hypertension. Although treatment with praziquantel can effectively eradicate all schistosomal infections with minimal toxicity, cardiopulmonary manifestations are not likely to be reversible given the chronic fibrotic tissue changes that are present.
Protein-Tyrosine Kinases and Adaptor Proteins in Fc&#949;RI-Mediated Signaling in Mast Cells (2003)

Mast cells function as the initiator of the allergic reaction and play a role in the innate immune system. Aggregation of the high affinity IgE receptor (FcepsilonRI) on mast cells triggers degranulation with the release of chemical mediators such as histamine, production of cytokines and leukotrienes. FcepsilonRI signals by activating proximal non-receptor type of protein-tyrosine kinases, Lyn, Syk, Btk and Fyn. Activated tyrosine kinases then phosphorylate their specific substrates which include other enzymes and adaptor proteins and assemble these cytoplasmic signaling molecules for cellular activation. The adaptor proteins have multiple domains that allow binding to effector molecules and therefore act as positive or negative regulators controlling FcepsilonRI signaling. Deletion of the adaptor proteins such as LAT, SLP-76 or Gab2 resulted in decreased FcepsilonRI-mediated anaphylactic reaction in vivo. Functional analysis of adaptor proteins has raised the possibility that they may be new targets for the discovery of anti-allergic drugs.
[Expression and clinical significance of CDC6 and hMSH2 in cervical carcinoma]. (2009)

CDC6 and hMSH2 play an important role in the invasion and metastasis of cervical carcinoma. CDC6 and hMSH2 may be useful for predicting prognosis of cervical carcinoma.
Coupled-mode theory for guided-wave optics (1973)

The problem of propagation and interaction of optical radiation in dielectric waveguides is cast in the coupled-mode formalism. This approach is useful for treating problems involving energy exchange between modes. A derivation of the general theory is followed by application to the specific cases of electrooptic modulation, photoelastic and magnetooptic modulation, and optical filtering. Also treated are nonlinear optical applications such as second-harmonic generation in thin films and phase matching.
Recurrence of endometriosis and its control (2009)

BACKGROUND Although surgery is currently the treatment of choice for managing endometriosis, recurrence poses a formidable challenge. To delay or to eliminate the recurrence is presently an unmet medical need in the management of endometriosis. To this end, proposals to investigate patterns of recurrence, to develop biomarkers for recurrence and to carry out biomarker-based intervention have been made. METHODS Publications pertaining to the recurrence of endometriosis and its related yet unaddressed issues were identified through MEDLINE. The reported recurrence rates, risk factors for recurrence, the effects of post-operative medication and causes of recurrence were reviewed and synthesized. In addition, several poorly explored issues such as time hazard function and mechanisms of recurrence were reviewed. Approaches to the development of biomarkers for recurrence and future intervention are discussed. RESULTS The reported recurrence rate was high, estimated as 21.5% at 2 years and 40-50% at 5 years. Few risk factors for recurrence have been consistently identified, and the evidence on the efficacy of the post-operative use of medication was scanty. The investigation on the patterns of recurrence may provide us with new insight into the possible mechanisms of recurrence and its control. The attempt to identify biomarkers for recurrence has started only very recently. CONCLUSIONS Much research is needed to better understand the patterns of recurrence and risk factors, and to develop biomarkers. One top priority is to develop biomarkers for recurrence, which may provide much needed clues to the possible mechanisms underlying recurrence and would allow the identification of patients with high recurrence risk, and permit for targeted intervention.
Developmentally regulated silencing and reactivation of tobacco chitinase transgene expression (1996)

The tobacco class I chitinase gene CHN48 driven by CaMV 35S RNA expression signals introduced into Nicotiana sylvestris can inactivate its own expression as well as expression of homologous host genes at the mRNA level. Comparison of the silencing of chitinase and β‐1,3‐glucanase transgenes with the same expression signals and breeding experiments with transgenes inserted in different chromosomes showed that chitinase‐gene silencing depends on transcribed sequence hornology and trans‐gene dose. The CHN48 transgene silenced host class I but not class II chitinases suggesting that greater than about 60% identity of sequences encoding the catalytic domain is required for silencing. Although steady‐state mRNA contents were greatly reduced in silent plants, the levels of nascent chitinase transcripts detected in nuclear run‐on experiments were the same in nuclei from high‐expressing and silent plants. This strongly suggests that chitinase‐gene silencing is a post‐transcriptional phenomenon. Silencing and resetting to high‐level expression of chitinase genes is developmentally regulated. Silencing occurs stochastically in 25–100% of seedlings at the 6–10 leaf stage of development and is preceded by a marked, transient increase in transgene‐encoded chitinase. Resetting of silent genes to the high‐expressing state is a non‐stochastic event that occurs in developing seeds 8–11 days after pollination. Experiments with lateral buds and plants regenerated from cultured leaf disks show that once established, competence for silencing can persist in dormant, actively growing, and de novo established shoot meristems. Some plants show a variegated pattern of silencing. Analyses of these patterns indicate that chitinase‐gene silencing is not a clonal event. Thus, it is likely that communication between cells rather than the lineage of the cells is important in stabilizing the silent state. Possible mechanisms for developmentally regulated post‐transcriptional silencing are discussed.
Watching how you drive (1996)

Installing an accident data recorder (ADR)-`black box&apos;-to record vehicle accident information could reduce risks for drivers and help to improve road safety. Two research projects funded under the European Union&apos;s DRIVE (Dedicated Road Infrastructure for Vehicle Safety in Europe) programme are discussed. The first project, DRACO (Driving Accident Coordinating Observer), which began in 1989 under DRIVE 1, examined the specification and design of such a device. It concluded that existing technology could produce a suitable recorder for about £100 in mass production quantities. DRACO was followed by the SAMOVAR (Safety Assessment Monitoring On-Vehicle with Automatic Recording) project which took the ADR concept into a field trial to assess the implications for driver behaviour It is clear that the behaviour of drivers, in terms of their attitude to the handling and control of a vehicle, might be significantly improved by the use of ADRs.
LPS pretreatment reprograms macrophage LPS-stimulated TNF and IL-1 release without protein tyrosine kinase activation (1997)

Pretreatment of macrophages with low-dose endotoxin (LPSp) profoundly alters cytokine release in response to subsequent LPSa activation. These qualitative and quantitative alterations in cytokine release have been termed macrophage reprogramming. Macrophage activation by LPS is thought to occur via a mechanism involving an early protein tyrosine kinase (PTK) phosphorylation step. PTK inhibition with genistein or herbimycin A blocks LPSa-stimulated secretion of tumor necrosis factor (TNF) and interleukin-1 (IL-1). In this study we investigated whether a PTK pathway participates in LPSp pretreatment reprogramming. We show that LPSp pretreatment inhibited TNF and augmented IL-1 release in response to subsequent LPSa stimulation. Blockade of PTK activation pathways during the interval when macrophages were exposed to LPSp prevented mitogen-activated protein kinase phosphorylation, as well as LPSp-stimulated release of TNF and IL-1, but did not block LPSp reprogramming effects. We conclude that LPSp pretreatment reprogramming of macrophage cytokine production does not require PTK activation.
Low-Temperature Materials and Thin Film Transistors for Flexible Electronics (2005)

This paper addresses the low-temperature deposition processes and electronic properties of silicon based thin film semiconductors and dielectrics to enable the fabrication of mechanically flexible electronic devices on plastic substrates. Device quality amorphous hydrogenated silicon (a-Si:H), nanocrystalline silicon (nc-Si), and amorphous silicon nitride (a-SiN/sub x/) films and thin film transistors (TFTs) were made using existing industrial plasma deposition equipment at the process temperatures as low as 75/spl deg/C and 120/spl deg/C. The a-Si:H TFTs fabricated at 120/spl deg/C demonstrate performance similar to their high-temperature counterparts, including the field effect mobility (/spl mu//sub FE/) of 0.8 cm/sup 2/V/sup -1/s/sup -1/, the threshold voltage (V/sub T/) of 4.5 V, and the subthreshold slope of 0.5 V/dec, and can be used in active matrix (AM) displays including organic light emitting diode (OLED) displays. The a-Si:H TFTs fabricated at 75/spl deg/C exhibit /spl mu//sub FE/ of 0.6 cm/sup 2/V/sup -1/s/sup -1/, and V/sub T/ of 4 V. It is shown that further improvement in TFT performance can be achieved by using n/sup +/ nc-Si contact layers and plasma treatments of the interface between the gate dielectric and the channel layer. The results demonstrate that with appropriate process optimization, the large area thin film Si technology suits well the fabrication of electronic devices on low-cost plastic substrates.
A STATISTIC FOR DESCRIBING PULSAR AND CLOCK STABILITIES (1997)

We propose a statistical measure suitable for com- paring the rotational stabilities of pulsars with one another and with terrestrial time scales. By a simple extension of notation long used in the clock community, we call the statisticz(�). Defined in terms of third-order polynomials fitted to sequences of measured time offsets, �z(�) is sensitive to variations in the frequency drift rate of the clock or pulsar. We apply the new sta- tistical formalism to real pulsar data and terrestrial time scales, and show that over the past 10 years these two kinds of data have comparable stabilities.
Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study (1988)

A randomized double-blind study was performed to examine the effect of clofibrate on glucose tolerance in subjects with non-insulin-dependent diabetes mellitus (NIDDM). Clofibrate (1.5 g/day) or placebo was administered to 70 patients and an oral glucose tolerance test (OGTT) was performed before and 12 wk after treatment. Blood glucose levels were significantly improved in clofibrate-treated groups at all time points during OGTT, whereas there was no change in insulin levels. Improvement of fasting glucose levels required 8 wk of clofibrate treatment. Insulin binding to erythrocytes demonstrated no significant change in the clofibrate-treated subjects. These results suggest that clofibrate improves glucose tolerance in NIDDM subjects without a change in insulin receptors and that clofibrate increases insulin sensitivity through an unknown postreceptor mechanism.
Recombinant Tumor Necrosis Factor- Chronically Administered in Rats: Lack of Cachectic Effect (1990)

Recombinant human tumor necrosis factor-alpha (rHuTNF) was injected into rats to test its reported cachectic effects. Rats were subcutaneously injected daily at 1730 hr with either saline or rHuTNF (0.25 mg/kg body wt) for either 5 or 14 days. Daily food intakes were significantly depressed only for the first day and first two days of rHuTNF injection in animals treated for 5 days and 14 days, respectively. There were no significant differences in daily body weights among the groups. Analysis of carcass composition revealed no significant differences in percentage of lipid or protein. Liver and inguinal pad weights were not significantly different. In vitro determination of lipogenesis showed it was enhanced in the inguinal pad and depressed in the liver only after 14 days of treatment. These results demonstrate that although in vivo rHuTNF may specifically alter tissue metabolism, it does not, by itself, result in a sustained cachectic effect.
Constitutive c-myc expression in an IL-3-dependent myeloid cell line suppresses cell cycle arrest and accelerates apoptosis. (1991)

In the murine interleukin 3 (IL-3)-dependent myeloid cell line 32D, down-regulation of c-myc and ornithine decarboxylase (ODC) expression is an immediate response to IL-3 deprivation. This is followed by an accumulation of cells in the G1 phase of the cell cycle, and eventual cell death. However, clones of 32D cells harboring an expression vector which constitutively expresses murine c-myc did not down-regulate ODC transcripts in response to IL-3 withdrawal, and they failed to G1 arrest. Moreover, in contrast to control cultures in which the majority of death occurred following G1 arrest, c-myc clones rapidly initiated a program of cell death characteristic of apoptosis following IL-3 deprivation, and their subsequent loss of viability occurred with accelerated kinetics. The premature induction of apoptosis in cells harboring a deregulated c-myc gene suggests that apoptosis may be an important mechanism in the elimination of hematopoietic cells harboring mutations, such as constitutive c-myc expression, which imbalance normal cell cycle regulatory controls.