gebhart/patrepeval huggingface dataset:
The p38 subunit of the aminoacyl-tRNA synthetase complex is a Parkin substrate: linking protein biosynthesis and neurodegeneration (2003)

Parkinson's disease (PD) is a severe neurological disorder, characterized by the progressive degeneration of the dopaminergic nigrostriatal pathway and the presence of Lewy bodies (LBs). The discovery of genes responsible for familial forms of the disease has provided insights into its pathogenesis. Mutations in the parkin gene, which encodes an E3 ubiquitin-protein ligase involved in the ubiquitylation and proteasomal degradation of specific protein substrates, have been found in nearly 50% of patients with autosomal-recessive early-onset parkinsonism. The abnormal accumulation of substrates due to loss of Parkin function may be the cause of neurodegeneration in parkin-related parkinsonism. Here, we demonstrate that Parkin interacts with, ubiquitylates and promotes the degradation of p38, a key structural component of the mammalian aminoacyl-tRNA synthetase complex. We found that the ubiquitylation of p38 is abrogated by truncated variants of Parkin lacking essential functional domains, but not by the pathogenic Lys161Asn point mutant. Expression of p38 in COS7 cells resulted in the formation of aggresome-like inclusions in which Parkin was systematically sequestered. In the human dopaminergic neuroblastoma-derived SH-SY5Y cell line, Parkin promoted the formation of ubiquitylated p38-positive inclusions. Moreover, the overexpression of p38 in SH-SY5Y cells caused significant cell death against which Parkin provided protection. Analysis of p38 expression in the human adult midbrain revealed strong immunoreactivity in normal dopaminergic neurons and the labeling of LBs in idiopathic PD. This suggests that p38 plays a role in the pathogenesis of PD, opening the way for a detailed examination of its potential non-canonical role in neurodegeneration.
Work in progress: nuclear magnetic resonance study of a paramagnetic nitroxide contrast agent for enhancement of renal structures in experimental animals. (1983)

A piperidinyl nitroxide stable free radical derivative, TES, was tested as an NMR contrast enhancer of renal structures in normal animals and animals with experimentally induced unilateral renal ischemia, renal vascular congestion, and hydronephrosis. Physiologic measurements indicated that TES is rapidly excreted in the urine with a clearance rate equal to the glomerular filtration rate. Because the compound is strongly paramagnetic, it increases the observable NMR intensity within the kidneys and urine in relatively low doses (0.04 to 0.9 g/kg). TES-enhanced spin echo renal images clearly demonstrated the presence of disease and functional abnormalities in diseased kidneys. These abnormalities were either not evident or only indirectly suggested on nonenhanced NMR images.
Studies of Heterocyclic Compounds. II. : Synthesis of 2-Furylvinyl-benzenes and Studies of Polarography (1968)

2-[2-(2-Furyl)vinyl]nitrobenzene, 3-[2-(2-furyl)vinyl]nitrobenzene, 4-[2-(2-furyl)vinylene]nitrobenzene, 4-[2-(5-bromo-2-furyl)viny]nitrobenzene, and 4-[2-(5-methyl-2-furyl)vinyl]nitrobenzene were prepared by the Wittig reaction. Stereoisomers of 5-bromo and 5-methyl derivatives were obtained during their synthesis, and their fractionation and isolation were effected. Polarographic measurements of these compounds were carried out.
The conversion of thyroxine to triiodothyronine in the lung: comparison of activity of type I iodothyronine 5' deiodinase in lung cancer with peripheral lung tissues. (2004)

1. Conversion of T4 to T3 occurs also in the lung. 2. The activity of DI is statistically significantly lower, in lung cancer than in peripheral lung tissue (13.3 +/- 9.5 vs 22.20 +/- 13.4 pmol/min/mg protein) respectively, p < 0.001. 3. DII activity in lung is present and similar in peripheral lung and lung cancer tissue. 4. There is a non-significant trend for correlation of DI activity and grade of differentiation (G1-G3) of tumour tissue and stage of lung cancer. Abbreviations' list: T3--triiodothyronine, T4--thyroxine, FT4--free thyroxine, rT3--revers triiodothyronine TSII--Thyroid Stimulating Hormone Type I lodothyronine 5'deiodinase = type I 5'deiodinase = 5'DI = DI Type II Iodothyronine 5'deiodinase = typeII 5'deiodinase = 5'DII = DII E.S.S.--Euthyroid Sick Syndrome, hDII = human type II iodothyronine deiodinase HDII-b, hDII-c = two novel splice variants SCC--Squamous Cell Cancer, A--adenocarcinoma, BMI--Body Mass Index BSA--Bovine Standard Albumin, DTT-1,4 Dithio-L-treitol, PTU--Propylothiouracil TCA--Tricholoroacetic Acid, TNM--Tumour Nodule Metastases (class.) G1-G3-grade of differentiation, COPD--Chronic Obstructive Pulmonary Disease.
Separation of horse dander allergen proteins by two‐dimensional electrophoresis (1998)

The aim of this work was to identify which proteins in horse dander extracts are allergens and to characterise them. Two-dimensional PAGE showed that horse dander preparations are composed of up to 50 proteins, all having acidic isoelectric points in the pH range 3-4.5. Immunoblots of two-dimensional PAGE were used to compare the reactivity of the proteins with IgE from 23 allergic patients. Patient sera were divided into two main groups recognising either allergens of 18.5 kDa or proteins of 27-29 and 31 kDa. The proteins of 27-29 kDa and 31 kDa were all N-glycosylated and their glycan chains seem to play a role in the binding of IgE from allergic patients. The sugar composition of their carbohydrate moiety was determined and lectin-binding experiments indicated presence of terminal sialic acid linked alpha-(2-->6) to galactose, galactose linked beta-(1-->4) to N-acetylglucosamine, and possibly presence of sialic acid linked alpha-(2-->3) to galactose. The 27-29-kDa glycoproteins had heterogeneous isoelectric points, most probably due to different degrees of sialylation in their oligosaccharide chains. The two 18.5-kDa allergens exhibited slightly different isoelectric points and their N-terminal sequences were identical, showing that they most likely were isoforms of the same protein. Sequence analyses revealed that their N-terminal sequences are similar to proteins belonging to the lipocalin family. We named the two 18.5-kDa proteins Equ c 2.0101 and Equ c 2.0102, according to International Allergen Nomenclature recommendations [King, T. P., Hoffman, D., Lowenstein, H., Marsh, D. G., Platts-Mills, T. A. E. & Thomas, W. (1995) J. Allergy Clin. Immunol. 96, 5-14]. The N-terminal of the allergens of 27-29 kDa were blocked and their sequences were not determined. Their amino acid compositions were determined and comparison with acidic mammalian proteins in the Swiss-Prot database revealed high scores with lipocalin proteins. This suggests that the glycosylated horse dander allergens belong to the lipocalin family, like Equ c 2.0101 and Equ c 2.0102.
Diffusion PDEs on vector-valued images (2002)

In this article, we propose a local and geometric point of view of vector image filtering using diffusion PDEs. It allows us to analyze proposed methods of vector data regularization, as well as propose a new vector PDE, well adapted for image restoration. This equation, whose key feature is the use of a local vector geometry, combines the advantages of diffusion PDEs for noise removing but also uses vector shock filters to enhance blurred edges. The extension to norm constrained vector fields can be the start for other well-known constrained problems, as optical flow computation, orientation analysis, and tensor image restoration.
Tyrosine 706 and 807 phosphorylation site mutants in the murine colony-stimulating factor-1 receptor are unaffected in their ability to bind or phosphorylate phosphatidylinositol-3 kinase but show differential defects in their ability to induce early response gene transcription. (1991)

The receptor for colony-stimulating factor-1 (CSF-1) is a receptor protein-tyrosine kinase. To study the possible function of CSF-1 receptor autophosphorylation, two autophosphorylation sites, Tyr-706, located in the kinase insert, and Tyr-807, a residue conserved in all protein-tyrosine kinases, were changed independently to either phenylalanine or glycine. Wild-type and mutant receptors were stably expressed in Rat-2 cells. In response to CSF-1, cells expressing Phe- or Gly-706 mutant receptors showed increased growth rate and altered cell morphology. Both the Phe- and Gly-706 mutant receptors associated with and phosphorylated phosphatidylinositol-3 kinase at levels comparable with those of wild-type receptors. However, these mutant receptors differed subtly from each other and from the wild-type receptor in their ability to induce different aspects of the response to CSF-1. The Phe-706 mutant receptor was most strongly affected in its ability to increase growth rate or elevate the levels of c-fos and NGF1A mRNAs, whereas the Gly-706 mutant receptor was most markedly affected in its ability to induce a change in cell morphology or increase the levels of c-jun and NGF1A mRNAs. These findings indicate that Tyr-706 itself, or this region of the receptor, may be important for interaction of the CSF-1 receptor with different signalling pathways. Gly-807 mutant receptors lacked protein-tyrosine kinase activity, failed to respond to CSF-1, and were defective in biosynthetic processing. Phe-807 mutant receptors had 40 to 60% reduced protein-tyrosine kinase activity in vitro. Although cells expressing Phe-807 receptors were able to respond to CSF-1, the changes in growth rate and cell morphology were significantly less than seen with wild-type receptors, and the induction of early response genes was also slightly lower than for the wild-type receptor. In contrast, Phe-807 receptors were equivalent to wild-type receptors when tested for their ability to interact with phosphatidylinositol-3 kinase. These findings indicate that phosphorylation of Tyr-807 may be important for full activation of the receptor.
Gene transfer of a soluble receptor of VEGF inhibits the growth of experimental eyelid malignant melanoma. (2000)

Adenovirus-mediated gene transfer of a soluble form of VEGF receptor (flt-1) gene inhibited the growth of the experimental eyelid malignant melanoma. This method may be useful as an antiangiogenic therapy for eyelid malignant melanoma.
The Stability of Cyclodextrin Complexes in Solution (1997)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe Stability of Cyclodextrin Complexes in SolutionKenneth A. ConnorsView Author Information School of Pharmacy, University of Wisconsin, 425 North Charter Street, Madison, Wisconsin 53706 Cite this: Chem. Rev. 1997, 97, 5, 1325–1358Publication Date (Web):August 5, 1997Publication History Received15 November 1996Revised26 January 1997Published online5 August 1997Published inissue 1 August 1997https://pubs.acs.org/doi/10.1021/cr960371rhttps://doi.org/10.1021/cr960371rresearch-articleACS PublicationsCopyright © 1997 American Chemical SocietyRequest reuse permissionsArticle Views14509Altmetric-Citations1857LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose SUBJECTS:Cavities,Molecular mechanics,Molecules,Solvents,Stability Get e-Alerts
Immunization with the receptor–binding domain of SARS-CoV-2 elicits antibodies cross-neutralizing SARS-CoV-2 and SARS-CoV without antibody-dependent enhancement (2020)

Abstract Recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the ongoing coronavirus disease 2019 (COVID-19) pandemic. Currently, there is no vaccine available for preventing SARS-CoV-2 infection. Like closely related severe acute respiratory syndrome coronavirus (SARS-CoV), SARS-CoV-2 also uses its receptor-binding domain (RBD) on the spike (S) protein to engage the host receptor, human angiotensin-converting enzyme 2 (ACE2), facilitating subsequent viral entry. Here we report the immunogenicity and vaccine potential of SARS-CoV-2 RBD (SARS2-RBD)-based recombinant proteins. Immunization with SARS2-RBD recombinant proteins potently induced a multi-functional antibody response in mice. The resulting antisera could efficiently block the interaction between SARS2-RBD and ACE2, inhibit S-mediated cell-cell fusion, and neutralize both SARS-CoV-2 pseudovirus entry and authentic SARS-CoV-2 infection. In addition, the anti-RBD sera also exhibited cross binding, ACE2-blockade, and neutralization effects towards SARS-CoV. More importantly, we found that the anti-RBD sera did not promote antibody-dependent enhancement of either SARS-CoV-2 pseudovirus entry or authentic virus infection of Fc receptor-bearing cells. These findings provide a solid foundation for developing RBD-based subunit vaccines for SARS-CoV2.
Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men. (1995)

Oral oxandrolone decreased SQ abdominal fat more than TE or weight loss alone and also tended to produce favorable changes in visceral fat. TE and ASND injections given every 2 weeks had similar effects to weight loss alone on regional body fat. Most of the beneficial effects observed on metabolic and cardiovascular risk factors were due to weight loss per se. These results suggest that SQ and visceral abdominal fat can be independently modulated by androgens and that at least some anabolic steroids are capable of influencing abdominal fat.
A Plasminogen-Activating Protease Specifically Controls the Development of Primary Pneumonic Plague (2007)

Primary pneumonic plague is transmitted easily, progresses rapidly, and causes high mortality, but the mechanisms by which Yersinia pestis overwhelms the lungs are largely unknown. We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination during pneumonic plague than during bubonic plague. Experiments manipulating its temporal expression showed that Pla allows Y. pestis to replicate rapidly in the airways, causing a lethal fulminant pneumonia; if unexpressed, inflammation is aborted, and lung repair is activated. Inhibition of Pla expression prolonged the survival of animals with the disease, offering a therapeutic option to extend the period during which antibiotics are effective.
Performance tuning of InGaZnO thin-film transistors with a SnInGaZnO electron barrier layer (2013)

Indium gallium zinc oxide (InGaZnO) thin-film transistors (TFTs) with a co-sputtered tin indium gallium zinc oxide (SnInGaZnO) electron barrier layer (EBL) are fabricated. The effect of the SnInGaZnO layer thickness on device characteristics is investigated. With stacking a 250-nm-thick SnInGaZnO EBL in the source/drain region, it introduces an additional potential barrier of around 0.14 V to the channel carriers. Experimental results show that the turn-off voltage of TFTs increases from −0.5 V to about 0 V, the on/off current ratio increases from 1.9 × 105 to 1.9 × 106, and the subthreshold swing decreases from 0.13 V/dec to 0.073 V/dec.
Brain macrophages: neurotoxic or neurotrophic effector cells? (1994)

The development of the central nervous system and various pathological contexts imply remodeling or alteration of neuronal networks associated with tissue recruitment of mononuclear phagocytes. Purification and culture of brain macrophages have provided a tool for investigating the functions of these cells. We discuss different mechanisms whereby macrophages could directly influence the survival of neurons and the growth of their processes.
A compressed sensing receiver for bursty communication with UWB Impulse Radio (2009)

We propose a novel receiver for ultra-wideband impulse-radio communication in bursty applications like wireless sensor networks. It is based on the principle of compressed sensing, and exploits the sparsity of the transmitted signal to achieve reliable demodulation. Instead of a full-fledged high-rate A/D, a modest number of projections of the received signal are acquired using analog correlators, and a joint decoding of the time of arrival and the data bits is performed from these under-sampled measurements via an efficient quadratic program. The receiver does not use wideband analog delay lines, and is robust to large timing uncertainty, hence the transmitter need not waste power on explicit training headers for timing synchronization. Moreover, the receiver can operate in a regime of heavy inter-symbol interference (ISI), and allows a very high baud rate (close to the Nyquist rate). Its performance is shown to remain close to the maximum likelihood receiver under every scenario of under-sampling, timing uncertainty, ISI, and delay spread.
Differentiation of mesenchymal stem cells into dopaminergic neuron-like cells in vitro. (2005)

MSCs can differentiate into dopaminergic neuron-like cells and are a new cell source for the treatment of neurodegeneration diseases and have a great potential for wide application.
Focal cooling rapidly terminates experimental neocortical seizures (2001)

The efficacy of surgical resection for epilepsy is considerably lower for neocortical epilepsy than for temporal lobe epilepsy. We have explored focal cooling with a thermoelectric (Peltier) device as a potential therapy for neocortical epilepsy. After creating a cranial window in anesthetized rats, we induced seizures by injecting artificial cerebrospinal fluid containing 4-aminopyridine (4-AP), a potassium channel blocker. Within 30 minutes of 4-AP injection, animals developed recurrent seizures (duration 85.7 +/- 26.2 seconds; n = 10 rats) that persisted for 2 hours. When a small Peltier device cooled the exposed cortical surface to 20-25 degrees C at seizure onset, the seizure duration was reduced to 8.4 +/- 5.0 seconds (n = 10 rats; p < 0.001). When the Peltier device was placed close to the cortical surface, but not allowed to make physical contact, there was no effect on seizure duration (104.3 +/- 20.7 seconds; p > 0.05 compared to control). Interestingly, the duration of uncooled seizures was reduced after we allowed the cortex to rewarm from prior cooling. Histological examination of the cortex after cooling has shown no evidence of acute or delayed neuronal injury, and blood pressure and temperature remained stable. It may be possible to use Peltier devices for cortical mapping or, when seizure detection algorithms improve, for chronic seizure control.
The human UDP‐N‐Acetylglucosamine:α‐6‐d‐Mannoside‐β‐1,2‐N‐Acetylglucosaminyltransferase II Gene (MGAT2) (1995)

UDP‐GlcNAc:α‐6–D‐mannoside [GlcNAc to Manα1–6] β‐1,2‐ N ‐acetylglucosaminyltransferase II (GlcNAc‐T II, EC 2.4.1.143) is a Golgi enzyme catalyzing an essential step in the conversion of oligo‐mannbse to complex N‐glycans. A 1.2‐kb probe from a rat liver cDNA encoding GlcNAc‐T II was used to screen a human genomic DNA library in λEMBL3. Southern analysis of restriction endonuclease digests of positive phage clones identified two hybridizing fragments (3.0 and 3.5 kb) which were sub‐cloned into pBlueScript. The inserts of the resulting plasmids (pHG30 and pHG36) are over‐lapping clones containing 5.5 kb of genomic DNA. The pHG30 insert (3.0 kb) contains a 1341‐bp open reading frame encoding a 447‐amino‐acid protein, 250 bp of G+C‐rich 5′‐upstream sequence and 1.4kb of 3′‐downstream sequence. The pHG36 insert (3.5 kb) contains 2.75 kb of 5′‐upstream sequence and 750 bp of the 5′‐end of the open reading frame. The protein sequence showed the domain structure typical of all previously cloned glycosyltransferases, i.e. a short 9‐residue putative cytoplasmic N‐terminal domain, a 20‐residue hydrophobic non‐cleavable putative signal‐anchor domain and a 418‐residue C‐terminal catalytic domain. Northern analysis of human tissues showed a major message at 3 kb and minor signals at 2 and 4.5 kb. There is no sequence similarity to any previously cloned glycosyltransferases including human UDP‐GlcNAc:α‐3‐ d ‐mannoside [GlcNAc to Manα;1–3] β‐1,2‐ N ‐acetylglucosaminyltransferase I (GlcNAc‐T I) which has 445 amino acids with a 418‐residue C‐terminal catalytic domain. The human GlcNAc‐T I and II genes ( MGAT1 and MGAT2 ) map to chromosome bands 5q35 and 14q21, respectively, by fluorescence in situ hybridization. The entire coding regions of human GlcNAc‐T I and II are each on a single exon. There is 92% identity between the amino acid sequences of the catalytic domains of human and rat GlcNAc‐T II. Southern analysis of restriction enzyme digests of human genomic DNA indicates that there is only a single copy of the MGAT2 gene. The full‐length coding region of GlcNAc‐T II has been expressed in the baculovirus/Sf9 insect cell system, the recombinant enzyme has been purified to near homogeneity with a specific activity of about 20 μmol · min ‐1 · mg ‐1 · and the product synthesized by the recombinant enzyme has been identified by high‐resolution 1 H‐NMR spectroscopy and mass spectrometry.
Immunological detection of an analogue of the erythroid protein 4.1 in endothelial cells (1986)

Endothelial cells (EC) of arterial and venous origin were investigated by indirect immunofluorescence and immunoautoradiography for the presence of red cell membrane 4.1-like protein. By immunofluorescence, EC exhibited a relatively uniform fluorescent staining sometimes of a reticular pattern, distributed over the entire cell. All controls were negative. Immunoblot analysis of EC revealed a cross reactive band of a molecular weight comparable to that of the erythrocyte band 4.1. These findings indicate that endothelial cells of arterial and venous origin express a polypeptide immunologically related to the erythrocyte protein 4.1, which may play an important role in membrane-cytoskeleton interactions.
Hematopoietic Stem Cell Gene Therapy with a Lentiviral Vector in X-Linked Adrenoleukodystrophy (2009)

X-linked adrenoleukodystrophy (ALD) is a severe brain demyelinating disease in boys that is caused by a deficiency in ALD protein, an adenosine triphosphate-binding cassette transporter encoded by the ABCD1 gene. ALD progression can be halted by allogeneic hematopoietic cell transplantation (HCT). We initiated a gene therapy trial in two ALD patients for whom there were no matched donors. Autologous CD34+ cells were removed from the patients, genetically corrected ex vivo with a lentiviral vector encoding wild-type ABCD1, and then re-infused into the patients after they had received myeloablative treatment. Over a span of 24 to 30 months of follow-up, we detected polyclonal reconstitution, with 9 to 14% of granulocytes, monocytes, and T and B lymphocytes expressing the ALD protein. These results strongly suggest that hematopoietic stem cells were transduced in the patients. Beginning 14 to 16 months after infusion of the genetically corrected cells, progressive cerebral demyelination in the two patients stopped, a clinical outcome comparable to that achieved by allogeneic HCT. Thus, lentiviral-mediated gene therapy of hematopoietic stem cells can provide clinical benefits in ALD.