gebhart/patrepeval huggingface dataset:
T lymphocytes in skin lesions of psoriasis and mycosis fungoides express B7-1: a ligand for CD28 (1994)

The activation of T cells requires two distinct signals. One signal involves interaction of the antigen-specific T-cell receptor with major histocompatibility complex molecules plus antigenic peptide; a second signal, which is antigen nonspecific, is the interaction of CD28 with its natural ligands B7-1 and B7-2/B70. CD28 is expressed on 80% of T cells, is upregulated after activation, and binds to B7 gene-family members, found on antigen-presenting cells. Because of our interest in the immunologic basis of benign and malignant T-cell-mediated disorders of the skin, we investigated the cellular distribution of CD28 and B7 family members in lesions of psoriasis and mycosis fungoides. By immunostaining cryostat sections of skin, CD28 was found to be expressed on virtually all lymphocytes in the epidermis and dermis of both skin diseases. Surprisingly, B7-1 was also found to be expressed on virtually all lymphocytes in the epidermis and dermis of both skin diseases. B7-1 expression was confirmed on CD3+ T lymphocytes using flow cytometry of single cell suspensions of fresh, unfixed psoriatic lesional tissue. To exclude the possibility that this result was caused by a second reagent contaminating the monoclonal antibody (MoAb) preparation, two different lots were used, and the MoAb was absorbed onto Chinese hamster ovary (CHO) transfectants expressing B7-1, or vector-only transfected CHO cells. These procedures confirmed that a B7-1-like epitope was being recognized on psoriatic lesional T cells. In contrast to B7-1 expression on lymphocytes, B7-3, as defined by anti-BB-1 MoAb reactivity, was found primarily on epidermal keratinocytes in both skin diseases and was not found on T cells. These results indicate that within two common skin disorders, lesional T cells accumulate in the dermis and epidermis, which express B7-1. Such expression may permit self-costimulation involving the CD28-mediated activation pathway, and thereby contribute to the ongoing T-cell proliferation present in these chronic, benign, and malignant skin diseases.
Luminal epithelial antigen (LEA.135) expression correlates with tumor progression for transitional carcinoma of the bladder. (1997)

Luminal epithelial antigen (LEA.135) expression has been shown to have prognostic significance in breast carcinoma, however its relationship to tumor progression in other forms of malignancy is unknown. This study evaluates LEA.135 expression in bladder transitional cell carcinoma (TCC) and compares the findings with tumor stage and grade, and polyclonal Ki-67 derived cell cycle activity. LEA.135 expression was evaluated by immunohistochemical staining using the streptavidin-biotin method. Staining distribution was graded 0 to 4 and the results were compared with World Health Organisation tumor grade, UICC TNM stage and fraction of actively cycling cells showing positive pKi-67 immunohistochemical staining. In normal bladder epithelium, LEA.135 staining was confined to the luminal surface of superficial epithelium. In lower grade, superficial TCC LEA.135 overexpression was noted and there was a progressive loss of expression in tumors of higher grade (p = 0.0001) and advanced stage (p = 0.0001). No LEA.135 staining was seen in carcinoma-in-situ. Loss of LEA.135 expression correlates with tumor progression for bladder TCC.
Anti-minK Antisense Decreases the Amplitude of the Rapidly Activating Cardiac Delayed Rectifier K + Current (1995)

The rapidly and slowly activating delayed rectifier K+ currents (IKr and IKs, respectively), which have different physiological properties have been identified in cardiac cells from several species, including humans. Although expression of the minimal K+ channel protein (minK) cDNA in some systems results in a current resembling IKs, the role of this gene product in channel function remains controversial. In atrial tumor myocytes (AT-1 cells), no IKs is recorded, but minK mRNA is detected, raising the possibility that expression of the minK gene serves an as-yet-unidentified function. In these experiments, AT-1 cells were exposed to antisense oligonucleotides targeting the 5' translation start site of the minK cDNA cloned from an AT-1 library. Cell size, IKr, and L-type and T-type Ca2+ currents were measured 24 to 48 hours after exposure and compared with data in cells exposed to the corresponding sense oligonucleotide or grown in medium only. Antisense oligonucleotide significantly reduced IKr compared with sense and medium-only control cells in 0 of 2 experiments (n = 3 to 6 cells per treatment in each experiment) at 50 nmol/L, 1 of 2 at 250 nmol/L, 6 of 6 at 1000 nmol/L, and 2 of 2 at 10,000 nmol/L. At 1000 nmol/L, maximum tail current in antisense-exposed cells was 2.5 +/- 0.1 pA/pF (mean +/- SEM, n = 28, 6 separate experiment), 6.6 +/- 0.4 pA/pF in sense-exposed cells (n = 27), 5.4 +/- 0.6 pA/pF in medium-only cells (n = 21), and 5.8 +/- 0.7 pA/pF in cells exposed to a random oligonucleotide (n = 9).(ABSTRACT TRUNCATED AT 250 WORDS)
Adsorption of divalent cations to a variety of phosphatidylcholine bilayers (1981)

We have determined the degree of binding of divalent cations to several kinds of phosphatidylcholine (PC) bilayers. This has been done by measuring the electrostatic interbilayer repuslive force that results when multilamellar lattices are exposed to Me2+Cl2 solutions. Divalent cations bind to dipalmitoylphosphatidylcholine in the sequence Ca2+ approximately equal to Cd2+ approximately equal to Mn2+ greater than Ca2+ approximately equal to Mg2+ greater than Ba2+. Among the different synthetic lipids, preference for Ca2+ is in the sequence DOPC less than DLPC less than DMPC approximately equal to DPPC approximately equal to DSPC. The density of bound charge is proportional to the density of polar groups on the bilayer surface. Phosphatidylcholines with mixed hydrocarbon chains, such as egg PC or 1:1 mixtures of synthetic PC's, form two distinct lamellar phases in CaCl2 solutions. In all cases the electrostatic force between bilayers decays exponentially with their separation but more slowly than expected from ionic double-layer theory. We suggest that the electric fields from opposing surfaces perturb the zwitterionic charge-binding polar groups and continuously modify their ion binding affinities as the bilayers approach.
Effects of leukotriene D4 on mucociliary and respiratory function in allergic and nonallergic sheep (1985)

We determined the effect of aerosol challenge with leukotriene D4 (LTD4) on specific lung resistance (sRL) and tracheal mucous velocity (TMV) in conscious sheep with (allergic) and without (nonallergic) Ascaris suum hypersensitivity. In allergic sheep LTD4 in concentrations of 50, 100, and 150 micrograms/ml produced dose-dependent increases in mean sRL by 44 (P = NS), 154 (P less than 0.05), and 233% (P less than 0.05), respectively. The increase in sRL produced by 150 micrograms/ml LTD4 was prevented by FPL 55712, an antagonist of slow-reacting substance of anaphylaxis. In nonallergic sheep 150 micrograms/ml LTD4 failed to elicit a significant change in sRL. In contrast to the changes in airway mechanics, concentrations of LTD4 as low as 25 micrograms/ml produced significant decreases in TMV in allergic sheep. The maximum decrease in TMV at this dose occurred 2 h after challenge; with larger doses of LTD4 (100 and 150 micrograms/ml) the maximum effect was observed 3 h after challenge. Furthermore, 150 micrograms/ml LTD4 reduced TMV in nonallergic sheep (mean decrease 43%, P less than 0.05). FPL 55712 only had a minor effect on the LTD4-induced decreases in TMV. We conclude that allergic sheep exhibit greater airway responsiveness to inhaled LTD4 than nonallergic sheep but that this difference is not evident for the concomitant changes in mucociliary transport. This suggests that the allergic state is associated with an increased responsiveness to LTD4 in tissues controlling airway caliber but not in those contributing to mucociliary function.
Development of a Signal Processing Library for Extraction of SpO2, HR, HRV, and RR from Photoplethysmographic Waveforms (2006)

"Non-invasive remote physiological monitoring of soldiers on the battlefield has the potential to provide fast, accurate status assessments that are key to improving the survivability of critical injuries. The development of WPIâ€™s wearable wireless pulse oximeter, designed for field-based applications, has allowed for the optimization of important hardware features such as physical size and power management. However, software-based digital signal processing (DSP) methods are still required to perform physiological assessments. This research evaluated DSP methods that were capable of providing arterial oxygen saturation (SpO2), heart rate (HR), heart rate variability (HRV), and respiration rate (RR) measurements derived from data acquired using a single optical sensor. In vivo experiments were conducted to evaluate the accuracies of the processing methods across ranges of physiological conditions. Of the algorithms assessed, 13 SpO2 methods, 1 HR method, 6 HRV indices, and 4 RR methods were identified that provided clinically acceptable measurement accuracies and could potentially be employed in a wearable pulse oximeter."
The Delineation of Peptides Able to Mimic Assembled Epitopes (2007)

Present methods allow a detailed study of the immune system's recognition of sequential epitopes. The results so far suggest that peptides homologous with these epitopes may not fulfil the early promise of synthetic vaccines. A procedure is described which now allows the study and evaluation of assembled epitopes. Using a monoclonal antibody which had been shown both to strongly neutralize foot-and-mouth disease virus, and to bind to a discontinuous epitope, peptides mimicking this epitope were determined a priori. An iterative procedure based on the progressive identification of amino acids in a random mixture of antibody-binding octapeptides was used. Strongly binding peptides consisted of the two elements W-Q-M (Trp-Gln-Met) and H-S (His-Ser) separated by a spacer. It was also shown that element W-Q-M was best composed of D-isomers, and the element H-S of L-isomers. Comparison of the sequence of these peptides with that of the immunologically important coat protein of the virus leads to the prediction that the epitope recognized by this monoclonal antibody consists of the residues occurring at positions 29-30, 54-55 and 88. Application of this general approach will answer questions about the nature of discontinuous epitopes and the stereochemical requirements for antigen-antibody interactions, as well as defining useful peptide immunogens.
Inhibition of B16 melanoma experimental metastasis by interferon‐γ through direct inhibition of cell proliferation and activation of antitumour host mechanisms (2002)

Interferon-gamma (IFN-gamma) has pleiotropic activities other than its antivirus action, including cell growth inhibition, natural killer (NK) cell and cytotoxic T lymphocyte (CTL) activation, and angiogenesis inhibitory activity, and these activities are supposed to be involved in its antitumour activity. However, it has not been completely elucidated which activity is mainly involved in the tumour suppression in vivo. In this study, we analysed inhibitory mechanisms of endogenous IFN-gamma against B16 melanoma experimental metastasis. After intravenous injection of tumour cells, tumour deposits in the lungs and liver were increased and life span was shorter in IFN-gamma(-/-) mice, indicating important roles for IFN-gamma in antitumour mechanisms. Interestingly, tumour deposits were not increased in IFN-gamma receptor (R)(-/-) mice. Furthermore, only low levels of cell-mediated immunity against the tumour and activation of NK cells were observed, indicating that antimetastatic effects of IFN-gamma is not mediated by host cells. The survival period of B16 melanoma-bearing IFN-gamma R(-/-) mice was, however, shorter than wild-type mice. These observations suggest that IFN-gamma prevents B16 melanoma experimental metastasis by directly inhibiting the cell growth, although antitumour host functions may also be involved in a later phase.
Association of estrogen replacement therapy with the risk of osteoarthritis of the hip in elderly white women. Study of Osteoporotic Fractures Research Group. (1996)

Postmenopausal estrogen replacement therapy may protect against OA of the hip in elderly white women.
New advances in non-fullerene acceptor based organic solar cells (2015)

Non-fullerene organic molecules are alternative and competitive acceptor materials for high-efficiency organic solar cells.
Metal-organic chemical vapor deposition of aluminum oxide thin films via pyrolysis of dimethylaluminum isopropoxide (2010)

Metal-organic chemical vapor deposited aluminum oxide films were produced via pyrolysis of dimethylaluminum isopropoxide in a high vacuum reaction chamber in the 417–659 °C temperature range. Deposited films contained aluminum, oxygen, and carbon, and the carbon-to-aluminum ratio increased with increased deposition temperature. Aluminum-carbon bonding was observed in films deposited at 659 °C by x-ray photoelectron spectroscopy, but not in films deposited at 417 °C. The apparent activation energy in the surface reaction controlled regime was 91 kJ/mol. The O/Al and C/Al ratios in the deposited films were greater and less than, respectively, the ratios predicted by the stoichiometry of the precursor. Flux analysis of the deposition process suggested that the observed film stoichiometries could be explained by the participation of oxygen-containing background gases present in the reactor at its base pressure.
Pathogenesis of innate immunity and adaptive immunity in the mouse model of experimental autoimmune uveitis (2015)

Experimental autoimmune uveitis, a well-established model for human uveitis, is similar to human uveitis in many pathological features. Studies concerning the mechanisms of experimental autoimmune uveitis would cast a light on the pathogenesis of human uveitis as well as the search for more effective therapeutic agents. The cellular components of innate immunity include natural killer cells, gamma delta T lymphocytes, antigen-presenting dendritic cells, phagocytic macrophages, and granulocytes. It is believed that T cells are central in the generation of human uveitis. It has already become clear that CD4(+) effecter cells that predominantly produce interleukin-17 (the so-called Th17 cells) may play an important role in uveitis. In addition, the occurrence and recurrence of uveitis depends on a complex interplay between the elements of innate and adaptive immunity.
The measurement of the properties of materials (1986)

This review covers approximately 15 years of development in the techniques used to measure dielectric properties of materials over the frequency range 1 MHz to 1500 GHz. An introductory section summarizes the broad development trends and is followed by short sections which deal with developments at a more detailed level. The approaches described include time- and frequency-domain methods; reflection, transmission, and resonant methods, guided and free-space methods; discrete-frequency and broad-band methods, especially Fourier Transform Spectroscopy. Measurements on magnetic materials are also briefly discussed.
Restoration of dopaminergic function by grafting of fetal rat substantia nigra to the caudate nucleus: Long‐term behavioral, biochemical, and histochemical studies (1980)

Motor deficits produced in rats by unilateral substantia nigra lesions have been found to be reduced by grafts of fetal rat substantia nigra to the dopamine denervated caudate nucleus. In the present study these grafts were examined behaviorally, histochemically, and biochemically over six to 10-month periods. The grafts were found to survive in a healthy condition and contain catecholaminergic cells and fibers after eight to ten months. Concentrations of dopamine in adjoining parts of the caudate nucleus were increased when examined six months after grafting. Apomorphine induced rotation was reduced by the grafts, and these reductions persisted for at least six months. Although signs of aging were observed in the brains of the host animals when sacrificed eight to ten months after grafting, the grafts remained healthy and showed no signs of aging or deterioration. It is concluded that substantia nigra grafts can become permanent, functional constituents of the brains of host animals with prior substantia nigra lesions.
The pineal gland: anatomy, physiology, and clinical significance (1985)

Since the discovery of melatonin approximately 25 years ago, there has been intense study regarding the details of the structure and function of the pineal gland. This work is reviewed, with particular emphasis on those aspects of importance to human physiology and disease.
TNF-α inhibits asbestos-induced cytotoxicity via a NF-κB-dependent pathway, a possible mechanism for asbestos-induced oncogenesis (2006)

Asbestos is the main cause of human malignant mesothelioma (MM). In vivo, macrophages phagocytize asbestos and, in response, release TNF-alpha and other cytokines that contribute to carcinogenesis through unknown mechanisms. In vitro, asbestos does not induce transformation of primary human mesothelial cells (HM); instead, asbestos is very cytotoxic to HM, causing extensive cell death. This finding raised an apparent paradox: How can asbestos cause MM if HM exposed to asbestos die? We found that asbestos induced the secretion of TNF-alpha and the expression of TNF-alpha receptor I in HM. Treatment of HM with TNF-alpha significantly reduced asbestos cytotoxicity. Through numerous technical approaches, including chemical inhibitors and small interfering RNA strategies, we demonstrate that, in HM, TNF-alpha activates NF-kappaB and that NF-kappaB activation leads to HM survival and resistance to the cytotoxic effects of asbestos. Our data show a critical role for TNF-alpha and NF-kappaB signaling in mediating HM responses to asbestos. TNF-alpha signaling through NF-kappaB-dependent mechanisms increases the percent of HM that survives asbestos exposure, thus increasing the pool of asbestos-damaged HM that are susceptible to malignant transformation. Cytogenetics supported this hypothesis, showing only rare, aberrant metaphases in HM exposed to asbestos and an increased mitotic rate with fewer irregular metaphases in HM exposed to both TNF-alpha and asbestos. Our findings provide a mechanistic rationale for the paradoxical inability of asbestos to transform HM in vitro, elucidate and underscore the role of TNF-alpha in asbestos pathogenesis in humans, and identify potential molecular targets for anti-MM prevention and therapy.
The structure and function of CD26 in the T‐cell immune response (1998)

CD26 is a widely distributed 110 kD cell-surface glycoprotein with known dipeptidyl-peptidase IV (DPP-IV) activity in its extracellular domain. This ecto-enzyme is capable of cleaving amino terminal dipeptides from polypeptides with either L-proline or L-alanine in the penultimate position. On human T cells, CD26 expression appears late in thymic differentiation and is preferentially restricted to the CD4+ helper/memory population, and CD26 can deliver a potent co-stimulatory T-cell activation signal. The cDNA sequence of CD26 predicts a type II membrane protein with only 6 amino acids in its cytoplasmic region, suggesting that, in addition to DPP-IV enzyme activity, other signal-inducing molecules may be associated with CD26. Considerable evidence exists that CD26 interacts, presumably in its extracellular domain, with both CD45, a protein tyrosine phosphatase, and adenosine deaminase (ADA), each of which is capable of functioning in a signal transduction pathway. In addition, CD26 is the receptor for ADA, and ADA on the cell surface is involved in an important immunoregulatory mechanism by which released ADA binds to the cell-surface ADA. This multifunctional molecule may be involved in cell migration and the HIV-1-associated loss of CD4+ cells through the process of programmed cell death. Thus, CD26 appears to play a key role in a number of aspects of lymphocyte function.
Film Uniformity in Atomic Layer Deposition (2006)

Abstract The sources of non‐uniformity in thin films produced using atomic layer deposition (ALD) have been investigated by reviewing the mechanical hardware of ALD reactors, precursors, and the by‐products of surface reactions. The most common causes of non‐uniformity are overlapping pulses, thermal self‐decomposition of precursors, and non‐uniform gas distribution. Less studied, however, are the consequences of downstream surface reactions of gaseous by‐products. In particular, titanium nitride films have been found to be significantly less uniform than those of transition metal oxides deposited from metal halides. The influence of reaction by‐products on the TiN film growth has been studied by comparing the deposition in the cross‐flow and showerhead style reactors. Finally, the sources of non‐uniformity in plasma enhanced (PE) ALD are illustrated by studying the TiN deposition process.
Molecular Diagnostics and Predictors in Thyroid Cancer (2009)

Testing for cancer-specific mutations in thyroid FNA samples and surgically removed tumor tissues increases diagnostic accuracy of FNA cytology and offers better prognostication of thyroid cancer.
Angiogenic Switch in Multiple Myeloma (2004)

Angiogenesis is the hallmark of cancer. Growing evidence indicates that an imbalance between pro- and anti-angiogenic molecules triggers the angiogenic switch during tumor progression. Several molecules, able to affect vascular formation and function, are now beginning to be elucidated. Recent data indicate that angiogenesis also occurs in hematological malignancies. In multiple myeloma it has been demonstrated that patients with active disease have an increase in bone marrow angiogenesis correlated with the progression of disease and an adverse prognosis. The pathophysiology of myeloma-induced angiogenesis is complex and involves either the direct production of angiogenic molecules by myeloma cells or their induction in the microenvironment. In this review we have focalized our attention on the main factors involved in the angiogenic switch that occurs in MM patients.
The plasminogen activation system in human colon cancer: messenger RNA for the inhibitor PAI-1 is located in endothelial cells in the tumor stroma. (1991)

Fourteen human colon adenocarcinomas were examined by in situ hybridization for the presence of mRNA for plasminogen activator inhibitor type 1 (PAI-1). All specimens contained PAI-1 mRNA in endothelial cells of some vessels in the stroma immediately surrounding the invasive tumor glands, in granulation tissue, and in some capillaries located under the free luminal surface of carcinomatous epithelium. In addition, a limited number of stromal cells in the cancerous areas located at the periphery of newly formed capillary networks, and presumably representing sprouting endothelial cells, contained PAI-1 mRNA. Cancer cells were devoid of detectable PAI-1 mRNA in all cases. PAI-1 mRNA was not seen in three biopsies of normal colon. Together with previous findings of urokinase-type plasminogen activator and its mRNA being located in fibroblast-like cells in the tumor stroma and mRNA for the urokinase receptor in the cancer cells at invasive foci, these results indicate a complex cooperativity among several cell types in regulation of plasminogen activation in colon cancer. A possible role of PAI-1 in protecting the extracellular matrix in the tumor tissue against degradation and a role in tumor-induced angiogenesis are discussed.