gebhart/patrepeval huggingface dataset:
Heat capacity of hydration in zeolites (2007)

Dehydration of zeolites is a critical factor in their stability, effectiveness as storage media for thermal energy, and influence on the thermal evolution of radioactive waste repositories. Prediction of the hydration states of zeolites as a function of temperature, pressure, and water activity is often hampered by limited data on the heat capacity changes associated with (de)hydration reactions. This property is often assumed to be temperature invariant based on statistical-mechanical reasoning. To test this assumption, heat capacities of homologous hydrated and dehydrated zeolites (analcime, natrolite, wairakite) were measured by differential scanning calorimetry from 130 to 600 K that were subsequently used to calculate the heat capacity of hydration. Simultaneous monitoring of sample mass was used to discard data for hydrated phases affected by thermal effects associated with dehydration at elevated temperature. All three phases exhibited marked variations in the heat capacity of hydration with temperature. This behavior appears to be related to second-order phase transitions involving the water molecules. In wairakite, a second-order phase transition associated with a change in framework symmetry from monoclinic to tetragonal only occurs in the hydrated form, and leads to a prominent peak in the temperature dependence of the heat capacity of hydration. Above the transition temperature, the heat capacity of hydration becomes negligible. Neglecting the temperature dependence of the heat capacity of hydration in zeolites can have a significant effect on thermodynamic properties of dehydration reactions regressed from equilibrium observations at elevated temperatures
Typing of Field Isolates of Infectious Bronchitis Virus Based on the Sequence of the Hypervariable Region in the S1 Gene (2003)

A universal primer set was developed that amplifies a region covering hypervariable region (HVR) 1 and HVR 2 in the S1 gene of the infectious bronchitis virus (IBV). The universality of this primer set was confirmed by testing the reference strains of different serotypes or variants of the IBV present in the United States. An approximately 450-bp region containing HVR 1 and HVR 2 of 7 untyped field isolates obtained in 1999 and 2000 was amplified. Direct sequencing followed by phylogenetic analysis on that region allowed us to type those field isolates that were not typable by reverse transcriptase-polymerase chain reaction (RT-PCR) and restriction fragment length polymorphism (RFLP). Furthermore, it was found that typing by phylogenetic analysis of that region correlates with virus neutralization results. Together with RT-PCR and RFLP, this method will serve as a fast typing method for IBV diagnosis.
Dexamethasone Concentration Gradients Along Scala Tympani After Application to the Round Window Membrane (2008)

The existence of substantial basal-apical concentration gradients of Dex-P in ST perilymph were demonstrated experimentally. If the variability in peak concentration and gradient is also present under clinical conditions, this may contribute to the heterogeneity of outcome that is observed after intratympanic application of glucocorticoids for various inner ear diseases.
Identification of Glycosylated 38-kDa Connective Tissue Growth Factor (IGFBP-Related Protein 2) and Proteolytic Fragments in Human Biological Fluids, and Up-Regulation of IGFBP-rP2 Expression by TGF-β in Hs578T Human Breast Cancer Cells (1998)

Connective Tissue Growth Factor (CTGF) is a cysteine-rich peptide involved in human atherosclerosis and fibrotic disorders such as scleroderma. CTGF has considerable N-terminal sequence similarity with the insulin-like growth factor binding proteins (IGFBPs), including preservation of cysteines, and has been postulated to be a member of the IGFBP superfamily. Indeed, recent studies have shown that baculovirus generated CTGF, a secreted 38-kDa protein, binds IGFs in a specific manner, leading to the provisional renaming of CTGF as IGFBP-8 (or IGFBP-rP2). With immunoprecipitation and immunoblotting, using polyclonal anti-IGFBP-rP2 antibody generated against recombinant human IGFBP-rP2bac, IGFBP-rP2 can be identified in the serum-free conditioned media of Hs578T human breast cancer cells, as well as in various human biological fluids, such as normal sera, pregnancy sera, and cerebrospinal, amniotic, follicular and peritoneal fluids. Glycosylation studies with endoglycosidase F reveal that endogenous human IGFBP-rP2 is a secreted, glycosylated, approximately 32-38-kDa protein with 2-8-kDa of N-linked sugars and a 30-kDa core. There are 18- and 24-kDa proteins that appear to be IGFBP-rP2 degradation products. In Hs578T human breast cancer cells, transforming growth factor (TGF)-beta 2, a potent growth inhibitor for these cells, upregulates IGFBP-rP2 mRNA and protein levels. Expression of Hs578T IGFBP-rP2 is significantly increased by TGF-beta 2 treatment in a dose-dependent manner, with 2.5- and 6-fold increases in mRNA and protein levels, respectively, at a TGF-beta 2 concentration of 10 ng/ml. Our studies indicate that IGFBP-rP2 appears to be an important endocrine factor, and one of the critical downstream effectors of the critical downstream effectors of TGF-beta, similar to the role of IGFBP-3 in TGF-beta-induced growth inhibition in human breast cancer cells.
Depletion of extrinsic pathway inhibitor (EPI) sensitizes rabbits to disseminated intravascular coagulation induced with tissue factor: evidence supporting a physiologic role for EPI as a natural anticoagulant. (1991)

Although in vitro experiments have established that extrinsic pathway inhibitor (EPI) is the only known plasma inhibitor of factor VIIa-tissue factor (TF) catalytic activity of potential physiologic significance, evidence of its function in vivo has been lacking. TF-induced intravascular coagulation may occur in patients despite normal plasma levels of EPI and, in our earlier studies, normal plasma EPI levels did not protect rabbits from intravascular coagulation induced by an infusion of purified TF (1 microgram/kg). Studies have now been carried out in which plasma EPI levels were reduced in rabbits to below 20% of the initial level by injection of anti-rabbit EPI IgG. Infusion into such animals of purified rabbit TF apoprotein (0.25 microgram/kg) reconstituted into phospholipid vesicles induced substantial disseminated intravascular coagulation. Infusion of control saline or phospholipid vesicles not containing TF was without significant effect as was infusion of TF (0.25 microgram/kg) into animals injected with nonimmune goat IgG. These data establish that EPI can dampen TF-induced intravascular coagulation in rabbits. They support the hypothesis that EPI plays a significant role in regulating coagulation resulting from the exposure of blood to trace concentrations of TF during the illnesses and minor injuries of normal existence.
APOEɛ4 influences the pathological phenotype of Alzheimer's disease by favouring cerebrovascular over parenchymal accumulation of Aβ protein (2003)

The relative amounts of amyloid beta-protein (A beta) in cerebral blood vessels and parenchyma vary considerably amongst patients with Alzheimer's disease (AD). Although several mechanisms have been proposed to explain this variability, the underlying genetic and environmental determinants are still unclear, as are the functional consequences. Polymorphisms in APOE, the gene for apolipoprotein E (ApoE), influence the risk of developing AD and of deposition of A beta within the brain. We examined the relationship between the APOE genotype and the relative extent of accumulation of A beta as plaques within the cerebral parenchyma and in cortical blood vessels in the form of cerebral amyloid angiopathy (CAA), in autopsy brain tissue from 125 AD cases and from 53 elderly, neurologically normal controls of which 19 had CAA without other neuropathological features of AD. In the AD cases, we also assessed whether the severity of CAA was related to the age of onset and duration of dementia, risk factors for atherosclerotic vascular disease, and histologically demonstrable cerebral infarcts or foci of haemorrhage. The APOE genotype was determined by a standard polymerase chain reaction-based method. Paraffin sections of frontal, temporal and parietal lobes were immunolabelled for A beta and the parenchymal A beta load (total A beta minus vessel-associated A beta) was quantified by computer-assisted image analysis. CAA severity was scored for cortical and leptomeningeal vessels. The relevant clinical data were obtained from the database of the South West Brain Bank. In AD, we found the severity of CAA to be strongly associated with the number of epsilon 4 alleles (P < 0.0001) but the parenchymal A beta load to be independent of APOE genotype. Cases with severe CAA had a lower parenchymal A beta load than had those with moderate CAA (P = 0.003). Neither the severity of CAA nor the parenchymal A beta load correlated with age of onset, duration of disease or age at death, and the severity of CAA also did not correlate with the presence of cerebral infarcts or foci of haemorrhage. These findings indicate that possession of the APOE epsilon 4 allele favours vascular over parenchymal accumulation of A beta in AD. This may influence the pathogenesis of neurodegeneration in epsilon 4-associated AD.
Nanostructured Materials Designed for Cell Binding and Transduction (2001)

The surface-functionalization of shell cross-linked (SCK) nanoparticles with the oligomeric peptide sequence YGRKKRRQRRR, the protein transduction domain (PTD) from the human immunodeficiency virus TAT protein, is described, and the cell binding interactions these nanobioconjugates exhibit are demonstrated. A convergent synthetic strategy was employed, whereby the SCK nanoparticles and the PTD were prepared independently and then coupled together during immobilization of the PTD component on a solid support. The SCK nanoparticles were prepared by the micellization of amphiphilic block copolymers of poly(epsilon-caprolactone-b-acrylic acid), followed by amidation-based cross-linking of the acrylic acid residues located within the micellar corona. The PTD sequence was constructed upon a solid support, from C-terminus to N-terminus, followed by extension with four glycine residues, leaving the amino chain end for subsequent coupling with remaining acrylic acid functionalities present on the surface of the SCK. Finally, cleavage from the solid support was performed, which also facilitated deprotection of the peptide side chain functionalities as well as hydrolysis of the poly(epsilon-caprolactone) segments composing the SCK core domain, to yield PTD-derivatized nanocage structures (PTD-nanocage). Covalent labeling of the SCK precursor with fluorescein-5-thiosemicarbazide provided fluorescently tagged PTD-nanocage nanobioconjugates to allow for their detection by fluorescence microscopy. The fluorescent PTD-nanocage bioconjugates were found to interact with CHO cells and HeLa cells, whereas the analogous structure lacking the PTD component did not. CHO cells bound with fluorescent PTD-nanocage bioconjugates were analyzed using flow cytometry and fluorescence activated cell sorting (FACS). Fluorescence confocal microscopy of isolated bioconjugate-bound CHO cells indicated that the bioconjugated nanoparticles were primarily located near the cell periphery; however, transduction of the nanoparticle into the cells also occurred.
Fabrication technology of ultrafine SiO2 masks and Si nanowires using oxidation of vertical sidewalls of a poly-Si layer (1999)

A fabrication technology of the vertical ultrafine SiO2 wall masks using oxidation of sidewalls of a polycrystalline silicon (poly-Si) layer and Si nanowires utilizing the SiO2 wall masks have been developed. To obtain the vertical SiO2 wall mask, an optimum electron cyclotron resonance (ECR) plasma etching and a suitable wet etching of the poly-Si layer after the sidewall oxidation has been achieved. The vertical ultrafine SiO2 wall masks 10 nm wide and 90 nm high with 33 nm in space have been successfully fabricated for the first time. The dimensions of width and space become essentially smaller than the size of an electron beam resist pattern. The height is sufficient for ECR plasma etching. Si nanowires 10 nm wide and 18 nm thick have been precisely obtained by the ECR plasma etching of the thinned silicon-on-insulator layer using the vertical ultrafine SiO2 wall masks. The fabrication technology using the vertical ultrafine SiO2 wall masks has remarkable merits of fineness, scalability, and wide applicability. It can be utilized for fabricating various designed nanostructures.
Cell-mediated suppression of HIV-specific cytotoxic T lymphocytes. (1989)

CTL specific for HIV have been described in lungs of infected patients at early stages of HIV disease. In order to characterize the evolution over time of HIV-specific CTL, we have analyzed the cytotoxic function and the cell surface phenotype of the alveolar lymphocytes from 41 patients at various stages of HIV disease. We demonstrated a progressive decline of alveolar anti-HIV CTL activity and detected Ts cells from the lungs of patients with advanced HIV disease. These alveolar T cells strongly suppressed the effector phase of anti-HIV CTL lysis. They lacked a marked specificity of function because they also block anti-HLA CTL response and were not restricted by the HLA-class-I transplantation Ag. They displayed the CD3, CD8, and HNK1 markers, were CD4 and CD16 negative, and lacked NK activity. The presence of Ts cells at late stages of HIV disease could thus partly explain the inefficiency of host defenses against HIV.
Epidermal growth factor (EGF), transforming growth factor‐α (TGF‐α), and basic fibroblast growth factor (bFGF) differentially influence neural precursor cells of mouse embryonic mesencephalon (1995)

Growth factors are key elements in the process of neural cell differentiation. We examined the effects of classical mitogens on neural precursor cells, by culturing mouse cells of the embryonic (13.5 days postcoitum) mesencephalon and treating them with epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and transforming growth factor-beta (TGF-beta). Our initial results show that EGF, TGF-alpha, or bFGF, but not NGF or TGF-beta, induced general proliferation of the cultured cells, followed by formation of colonies. Combinations of these three growth factors suggest that most cells with the capacity to form colonies responded to EGF, TGF-alpha, or bFGF. The number of colonies increased significantly when EGF, but not TGF-alpha, was used in combination with bFGF. Furthermore, a population responding only to EGF + bFGF was detected in the dorsal mesencephalon. The colony-forming activity of bFGF was dependent on insulin, but bFGF and insulin cooperation was indirect since we could not observe colony formation in subcultures of cells derived from colonies, even in the presence of insulin. Cells obtained from our colonies displayed neuronal and glial morphology and expressed markers of both neurons and astrocytes; nestin, a marker of neural precursor cells, was also expressed in the majority of colonies. Growth factors also influenced neuronal maturation; the best neurite outgrowth was obtained from cells derived from bFGF-induced colonies cultured in the presence of EGF + bFGF. These data indicate the existence of neural precursor cells in the embryonic mesencephalon that respond differentially to growth factors.
Humoral and Cellular Immune Responses to Synthetic Peptides of the Leishmania donovani Kinetoplastid Membrane Protein‐11 (1998)

Native kinetoplastid membrane protein-11 (KMP-11), purified from crude extracts of Leishmania donovani parasites, activates T cells from individuals who have recovered from visceral leishmaniasis. In this work we used three 38-mer peptides spanning the amino acid sequence of the L. donovani KMP-11 as solid-phase ligands in enzyme-linked immunosorbent assays (ELISAs) and as stimulating antigens in lymphoproliferative assays in order to evaluate humoral and cellular immune responses to well-defined sequences of the protein. Antibody reactivity against the three peptides was measured in plasma from 63 Sudanese visceral leishmaniasis patients (VL) and the percentage of patients with anti-KMP-11 antibodies in ELISA were 37% (KMP-11-1), 30% (KMP-11-2) and 58% (KMP-11-3). The fraction of VL patients with measurable antibody reactivity in one or more of the three ELISAs was 79%. Cross-reactivity to the KMP-11 peptides was detected in plasma from Sudanese patients suffering from Leishmania major infections and in plasma from Sudanese and Danish patients infected with Plasmodium falciparum. In lymphoproliferative assays, 10 of 17 PBMC isolates from donors previously infected with L. donovani showed a response to one or more of the three KMP-11 peptides.
Evaluation of Reinforced Concrete Beam Specimens with Acoustic Emission and Cyclic Load Test Methods (2009)

First Name is required invalid characters Last Name is required invalid characters Email Address is required Invalid Email Address Invalid Email Address
Diagnosis and Differentiation ofMycoplasma hyopneumoniaeandMycoplasma hyorhinisInfections in Pigs by PCR Amplification of the p36 and p46 Genes (2000)

The genome of Mycoplasma hyopneumoniae encodes several immunodominant proteins, including a cytosolic protein (p36), three membranous proteins (p46, p65, and p74), and an adhesin (p97). Cross-reactions with M. flocculare and M. hyorhinis reduce the specificity of conventional serological detection methods. However, certain antigenic determinants of the p36 and p46 proteins have been shown to be specific for M. hyopneumoniae. In the present study, pairs of oligonucleotide primers were designed to permit PCR amplification of entire p36 and p46 genes and of internal fragments of these genes. Specific amplicons could be obtained with as low as 0.5 to 50 pg of extracted chromosomal DNA. No amplification product was obtained when testing p36 and p46 primer pairs with genomic DNA or RNA from other mycoplasma species, bacteria, and viruses commonly associated with respiratory diseases in pigs. By using the single p36-PCR method, a positive reaction was demonstrated in 100% (30 of 30) of lungs from pigs that developed typical lesions associated with an M. hyopneumoniae infection, and no false-positive results were detected when 62 apparently normal lungs were tested. On the other hand, with the single p46-PCR method a sensitivity of 86.6% (26 of 30) and a specificity of 96.7% (60 of 62) were obtained in comparison with the necropsy findings. A mixed infection with M. hyorhinis was diagnosed in 13.3% (4 of 30) of the cases by using species-specific primers for the heterologous p37 gene. The sensitivity of the single p36-PCR method for the detection of M. hyopneumoniae, when tested on tracheobronchial swabs, was 100% (20 positive samples), with a specificity of 93.3% (14 of 15 negative samples), compared to the necropsy findings. Both expected amplicons were obtained with 86.6% (26 of 30) positive lungs when p36 and p46 primers were used simultaneously (multiplex PCR) to further increase the specificity of the PCR assay.
Retinoids and Wound Healing (2006)

BACKGROUND Retinoids are widely used in dermatology and may play a role in wound healing. The exact role of retinoids in wounds is confusing and controversial, however. Systemic retinoids are presumed to be detrimental to wound healing; however, this standard is based on isolated reports. OBJECTIVE The objective was to provide a critical review of the available literature regarding the role of both topical and systemic retinoids in various aspects of wound healing. CONCLUSIONS Pretreatment with retinoids likely promotes wound healing after facial resurfacing procedures and full- or partial-thickness wounds. While the evidence is mixed regarding the effects of retinoids applied to fresh and healing wounds, the majority of the evidence available shows favorable wound-healing properties in this setting. The medical–legal standard regarding the avoidance of facial resurfacing and surgical procedures in patients on or recently completing a course of systemic retinoids was likely prematurely established.
Chemical structure of two fragments of human serum albumin and their location in the albumin molecule (1975)

1. 'Inhibitor fragment' isolated from human serum albumin degraded by rabbit cathepsin D is composed of one peptide chain with two intrachain disulphide bonds. There are two kinds of inhibitor molecules having different N-terminal amino acids: one is threonine and the other glutamine. 2. Fragment F1, isolated from inhibitor degraded by trypsin, is composed of two chains linked by a disulphide bond. There are three kinds of fragment F1. All have one alpha chain in common, which has an intrachain disulphide bond. They differ by the nature of the chain, which is linked to the alpha chain by a disulphide bond. The epsilon chain is present in trace amounts. The two other chains, beta and gamma, differ by their C-terminal amino acid, which is respectively arginine and lysine. 3. Inhibitor is composed of the last 92 or 89 residues of the human albumin molecule and fragment F1 is composed of two parts of this C-terminal portion of the albumin molecule.
Activation of Microglia Acidifies Lysosomes and Leads to Degradation of Alzheimer Amyloid Fibrils (2007)

Microglia are the main immune cells of the brain, and under some circumstances they can play an important role in removal of fibrillar Alzheimer amyloid beta peptide (fAbeta). Primary mouse microglia can internalize fAbeta, but they do not degrade it efficiently. We compared the level of lysosomal proteases in microglia and J774 macrophages, which can degrade fAbeta efficiently, and we found that microglia actually contain higher levels of many lysosomal proteases than macrophages. However, the microglial lysosomes are less acidic (average pH of approximately 6), reducing the activity of lysosomal enzymes in the cells. Proinflammatory treatments with macrophage colony-stimulating factor (MCSF) or interleukin-6 acidify the lysosomes of microglia and enable them to degrade fAbeta. After treatment with MCSF, the pH of microglial lysosomes is similar to J774 macrophages (pH of approximately 5), and the MCSF-induced acidification can be partially reversed upon treatment with an inhibitor of protein kinase A or with an anion transport inhibitor. Microglia also degrade fAbeta if lysosomes are acidified by an ammonia pulse-wash or by treatment with forskolin, which activates protein kinase A. Our results indicate that regulated lysosomal acidification can potentiate fAbeta degradation by microglia.