gebhart/patrepeval huggingface dataset:
Critical Care Utilization for the COVID-19 Outbreak in Lombardy, Italy (2020)

On February 20, 2020, a patient in his 30s admitted to the intensive care unit (ICU) in Codogno Hospital (Lodi, Lombardy, Italy) tested positive for a new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19). He had a history of atypical pneumonia that was not responding to treatment, but he was not considered at risk for COVID-19 infection. he positive result was immediately reported to the Lombardy health care system and governmental offices. During the next 24 hours, the number of reported positive cases increased to 36. This situation was considered a serious development for several reasons: the patient ("patient 1") was healthy and young; in less than 24 hours, 36 additional cases were identified, without links to patient 1 or previously identified positive cases already in the country; it was not possible to identify with certainty the source of transmission to patient 1 at the time; and, because patient 1 was in the ICU and there were already 36 cases by day 2, chances were that a cluster of unknown magnitude was present and additional spread was likely.
Production of a Monoclonal Antibody That Recognizes the Lipopolysaccharide of a <i>Campylobacter</i>‐Like Organism (1992)

A monoclonal antibody was produced to a Campylobacter-like organism (RMIT 32A) which was isolated from the terminal ileum of a pig with proliferative enteritis. Isotyping of the antibody revealed that it was an IgG2a with kappa light chains. Immunoblots using the antibody against proteinase-K-treated whole cell lysates of RMIT 32A, a selection of Campylobacter species and other enteric bacteria showed that the antibody was specific for RMIT 32A and was directed against the lipopolysaccharide. This antibody can be used for the specific detection of RMIT 32A.
Skeletal muscle enzyme alterations after sprint and endurance training (1976)

Specifically designed programs of sprint and endurance running were used to determine how different types of training affect enzyme activities in selected energy metabolism pathways. Three types of rat skeletal muscle were studied. After 8 wk of training, small but significant decreases in lactate dehydrogenase activity (15%) were found in the soleus and white vastus lateralis muscles of the sprint animals. Decreased levels of phosphoglucomutase and lactate dehydrogenase (approx. 20%) of the white vastus lateralis muscles of the endurance group were observed at the same time. By 16 wk of training, fumarase activity increased approximately twofold in the white vastus muscles and 45% in the soleus and plantaris muscles of the endurance group. Similarly, increased fumarase activity (42%) was seen in the soleus muscles of the sprint group. In all muscles, phosphoglucomutase and lactate dehydrogenase activities generally were lower in the endurance animals than in the control animals. No significant differences were found between the sprint and endurance groups at either or sixteen weeks of training. These results suggest that similar enzyme adaptations occur over time with both types of training.
Ultrafast 3-D shape measurement with an off-the-shelf DLP projector (2010)

This paper presents a technique that reaches 3-D shape measurement speed beyond the digital-light-processing (DLP) projector's projection speed. In particular, a "solid-state" binary structured pattern is generated with each micro-mirror pixel always being at one status (ON or OFF). By this means, any time segment of projection can represent the whole signal, thus the exposure time can be shorter than the projection time. A sinusoidal fringe pattern is generated by properly defocusing a binary one, and the Fourier fringe analysis means is used for 3-D shape recovery. We have successfully reached 4,000 Hz rate (80 μs exposure time) 3-D shape measurement speed with an off-the-shelf DLP projector.
Regioselective Palladium(II)-Catalyzed Synthesis of Five- or Seven-Membered Ring Lactones and Five-, Six- or Seven-Membered Ring Lactams by Cyclocarbonylation Methodology (1996)

2-Allylphenols react with carbon monoxide and hydrogen in the presence of catalytic quantities of a cationic palladium(II) complex [(PCy3)2Pd(H)(H2O)]+BF4- or palladium acetate and 1,4-bis(diphenylphosphino)butane, affording five- or seven-membered ring lactones (bicyclic, tricyclic, and pentacyclic) as the principal products, often in excellent yields. Use of 2-aminostyrenes as reactants and catalytic quantities of palladium acetate and tricyclohexylphosphine, affords five-membered ring lactams in high yield and selectivity. Bicyclic and tricyclic heterocycles containing six-membered ring lactams can be synthesized from the reaction of 2-allylanilines with CO/H2 using the catalytic system Pd(OAc)2/PPh3, while use of 1,4-bis(diphenylphosphino)butane instead of PPh3 in the latter process results in the formation of the seven-membered lactams benzazepinones in good yield. The regiochemical control depends on the nature of the palladium catalyst, the relative pressures of the gases, and the solvent.
Anti-androgens and the mutated androgen receptor of LNCaP cells: differential effects on binding affinity, heat-shock protein interaction, and transcription activation (1992)

Previous studies from this laboratory have described that LNCaP prostate tumor cells contain an androgen receptor (AR) with a point mutation in the steroid-binding domain (codon 868, Thr to Ala). This defect leads to a change in specificity of the AR. Estrogens, progestagens, and some anti-androgens (e.g., cyproterone acetate, hydroxyflutamide, nilutamide) stimulate LNCaP cell growth rate through the AR. The present studies indicate that not all anti-androgens showed agonistic effects with the mutated receptor. The growth rate of LNCaP cells did not increase with the anti-androgen ICI 176334, nor could this compound increase transcription activation of the reporter gene construct via the mutant receptor in a cotransfection system [HeLa cell cotransfection system with an androgen-regulated reporter gene construct (pG29G-tk-CAT) and the mutant receptor as trans-vector]. Interaction of the AR of LNCaP cells with heat-shock proteins was studied by isolation of the receptor with a specific monoclonal antibody and characterization of associated proteins. Hsp90, hsp70, and hsp56 were found to coprecipitate with the AR. Incubation of the cells at 37 degrees C with androgen (R1881, 10 nM) or the anti-androgen hydroxyflutamide, prior to receptor isolation, resulted in dissociation of the AR-heat-shock protein complex. This dissociation is paralleled by the transformation to a tight nuclear-binding form of the AR. In contrast, ICI 176334 could not induce a release of heat-shock proteins and did not increase nuclear binding, but inhibited the transformation process induced by R1881.(ABSTRACT TRUNCATED AT 250 WORDS)
Regional treatment of epidermal growth factor receptor vIII-expressing neoplastic meningitis with a single-chain immunotoxin, MR-1. (1999)

The incidence of neoplastic meningitis is on the rise. Neoplastic meningitis can result from a direct seeding of the neuraxis by primary brain tumors or by hematogeneous spread of systemic solid tumors. A frequent genetic alteration in primary brain tumors such as gliomas is an in-frame deletion in the epidermal growth factor receptor (EGFR) gene EGFRvIII, which brings together what were normally distant polypeptide sequences in the intact receptor. A novel glycine is formed at the fusion junction, resulting in a unique and tumor-specific target. By using phage display, we have isolated a single-chain antibody specific for the EGFRvIII mutation and expressed it with a modified form of the Pseudomonas exotoxin to form the immunotoxin MR1scFvPE38KDEL (MR-1). The multiple dose toxicity and therapeutic efficacy of MR-1 immunotoxin were tested in an athymic rat model of neoplastic meningitis. The maximally tolerated doses in non-tumor-bearing rats were three doses of 3 microg each. For therapeutic studies, the target was a neoplastic meningitis induced by intrathecal inoculation of the EGFRvIII-expressing human glioma U87MG.deltaEGFR. A dose escalation study compared the survival of three equal doses of 1, 2, and 3 microg of MR-1 immunotoxin with saline or 3 microg of the control immunotoxin specific for the interleukin 2 receptor, anti-Tac. All animals treated with three doses of saline or 3 microg of anti-Tac died, with median survival of 7 and 10 days, respectively. There were 75% (six of eight) long-term survivors in the group treated with three doses of 1 microg and 57% (four of seven) long-term survivors in the groups treated with three doses of either 2 or 3 microg of MR-1 immunotoxin. None of the MR-1 immunotoxin-treated groups reached median survival by the termination of the study at 53 days. Therefore, median survival was estimated to be >53 days, resulting in an estimated increase in median survival of >657% compared with saline and 430% versus anti-Tac. Compartmental therapy with three doses of 2 microg of MR-1 immunotoxin is effective in the treatment of EGFRvIII-expressing neoplastic meningitis. This dose was found to have no clinical or histopathological effects on non-tumor-bearing animals. MR-1 immunotoxin is, therefore, considered specific and safe within its therapeutic window. Phase I clinical trials for tumors invading the intrathecal space that express the EGFRvIII target should be initiated.
Identification and differential regional expression of KOR‐3/ORL‐1 gene splice variants in mouse brain (1998)

KOR‐3, also known as ORL‐1, is a member of the opioid receptor family, encoding the murine receptor for orphanin FQ/nociceptin. In the current studies we have identified five different splice variants of KOR‐3 in mouse brain, three of which have not been previously reported. In addition to variants with a 15 bp deletion at the 3′‐end of the first coding exon (KOR‐3d) and an 81 bp insertion between the second and third coding exons (KOR‐3e), three new variants with insertions of 34 (KOR‐3a), 98 (KOR‐3b), and 139 bp (KOR‐3c) between the first and second coding exons have been obtained. The expression of the three variants in mouse brain varies markedly among brain regions with a distribution which is quite distinct from KOR‐3 itself. Of greatest interest was the presence of high levels of KOR‐3a in the striatum, a region with no demonstrable KOR‐3, and in the cortex. KOR‐3c was seen in the periaqueductal gray and hypothalamus, regions where KOR‐3 predominated. The brainstem had similar levels of KOR‐3, KOR‐3a, and KOR‐3d. In contrast, KOR‐3d was most prominent in the cerebellum. KOR‐3b levels were very low throughout.
Isolation and culture of follicular papillae from murine vibrissae: an introductory approach (1994)

The recent successes in culturing follicular papilla cells have afforded a rapid advance in our understanding of hair biology. Although the experimental manipulation of the papilla is briefly described in the original reports, a detailed description for workers starting in the field is not yet available. In this report we give a brief review of hair biology relevant to the papilla, and illustrate the method we have found successful for isolating and growing papilla cells.
TABLE OF NUCLIDES (1980)

This table presents properties of nuclides, both stable and radioactive, adopted from the 7th edition of the Table of Isotopes. The data are based on experimental results reported in the literature, with the cutoff date varying from January to December, 1977. (The earliest date refers to the lightest nuclides, and vice versa.) Most mass excesses are from the 1977 Atomic Mass Evaluation, with some recent experimental values added. For a few of the very unstable nuclides for which no values were reported in the 1977 Atomic Mass Evaluation, estimates are taken from the tables of W.D. Myers. Natural isotopic abundances and neutron cross sections are taken from compilations by N.E. Holden. For other references, original data, and information on the data measurements, the reader is referred to reference 1.
Role of the SCF/KIT signalling pathway in embryonic stem cells (2011)

Murine embryonic stem (ES) cells are derived from the inner cell mass of the developing embryonic blastocyst. These cells can self renew which allows them to be propagated indefinitely in the laboratory and they can differentiate into cell types derived from all three germ layers. Manipulation of the mouse genome using gene targeting techniques in conjunction with ES cell technology has provided valuable insights into embryonic development and cell lineage specification. KIT is a trans-membrane receptor tyrosine kinase (RTK) that dimerises upon binding to its ligand, stem cell factor (SCF) resulting in the auto-phosphorylation of intracellular kinase domains. This activity is crucial for the transmission of signals from the cell surface to the nucleus. KIT is expressed on stem and progenitor cells of many lineages and defects in the SCF/KIT signaling pathway causes detrimental effects at both the cellular and physiological level. This project aimed to investigate the role of the SCF/KIT signalling pathway during murine ES cell differentiation and survival. To assess the role of SCF/KIT signalling in ES cell proliferation and survival, we knocked out the c-kit gene in mouse ES cells to produce heterozygous (KitW-lacZ/+) and KIT Null (KitW-lacZ/W-lacZ) cell lines. The self renewal and differentiation profile of these cell lines revealed an auxiliary role for SCF/KIT during ES cell self renewal and an absolute role in survival upon in vitro differentiation. This phenotype of apoptosis upon differentiation was recapitulated in wild type E14 ES cells treated with a KIT neutralising antibody (ACK2). Wild type cells that were treated with the JNK inhibitor, SP600125 had a comparable phenotype to KIT null cells indicating that this could be one of the mediators of KIT signalling that has a protective role in the survival of differentiating ES cells. We hypothesised that blocking classical apoptotic pathways might prevent the death on differentiation observed in KIT null cells. However, neither blocking the pro-apoptotic P38 pathway with the chemical inhibitor PD169316 nor over-expressing the pro-survival protein BCL2 in KIT Null cells could prevent their apoptosis upon differentiation phenotype. This strongly suggests that these pathways are not involved in KIT mediated survival of differentiating ES cells. Although compensatory mechanisms are thought to exist for defective KIT signaling in vivo, an absolute role is assigned to KIT during ES cell differentiation. Further analysis of micro array data comparing gene expression from wild type E14 and KIT Null cell lines may reveal the specific mechanisms of KIT mediated survival during differentiation onset.
On fundamental and phenomenological models, structure and mechanical properties of collagen, elastin and glycosaminoglycan complexes (1982)

This paper reviews the structure (from molecular to macroscopic level) of collagen, elastin and glycosaminoglycans, with special reference to their functional properties and to how their behavior can be elucidated from in vitro manipulations of the tissues by biochemical means. Modes to analyse the mechanical behavior are briefly discussed and exemplified by data from reconstituted collagenous "tissue". It is concluded that the basic equation for the "non-linear elasticity" component in Fung's law (and for the reconstituted "tissue" a modification of it) is a powerful tool for analysis of the physiological range of the stress-strain curve. Further, enzymatic "dissection" of one tissue element at a time provides a valuable method for the analysis of tissue element interactions. This approach is illustrated with data from aortic tissue. It is shown that the mechanical properties of the aorta depend on the interaction between elasticity and collagenous elements and that the strength of the tissue is not derived from its collagen fibers per se.
Potentiator ivacaftor abrogates pharmacological correction of ΔF508 CFTR in cystic fibrosis (2014)

Cystic fibrosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR). Newly developed "correctors" such as lumacaftor (VX-809) that improve CFTR maturation and trafficking and "potentiators" such as ivacaftor (VX-770) that enhance channel activity may provide important advances in CF therapy. Although VX-770 has demonstrated substantial clinical efficacy in the small subset of patients with a mutation (G551D) that affects only channel activity, a single compound is not sufficient to treat patients with the more common CFTR mutation, ΔF508. Thus, patients with ΔF508 will likely require treatment with both correctors and potentiators to achieve clinical benefit. However, whereas the effectiveness of acute treatment with this drug combination has been demonstrated in vitro, the impact of chronic therapy has not been established. In studies of human primary airway epithelial cells, we found that both acute and chronic treatment with VX-770 improved CFTR function in cells with the G551D mutation, consistent with clinical studies. In contrast, chronic VX-770 administration caused a dose-dependent reversal of VX-809-mediated CFTR correction in ΔF508 homozygous cultures. This result reflected the destabilization of corrected ΔF508 CFTR by VX-770, markedly increasing its turnover rate. Chronic VX-770 treatment also reduced mature wild-type CFTR levels and function. These findings demonstrate that chronic treatment with CFTR potentiators and correctors may have unexpected effects that cannot be predicted from short-term studies. Combining these drugs to maximize rescue of ΔF508 CFTR may require changes in dosing and/or development of new potentiator compounds that do not interfere with CFTR stability.
File Structure for an On-Line Catalog of One Million Titles (1973)

A description is given of the file organization and design of an on-line catalog suitable for automation of a library of one million books. A method of virtual hash addressing allows rapid search of the indexes to the catalog file. Storage of textual material in a compressed form allows considerable reduction in storage costs.
Conditional Knock-Out of K<sub>ir</sub>4.1 Leads to Glial Membrane Depolarization, Inhibition of Potassium and Glutamate Uptake, and Enhanced Short-Term Synaptic Potentiation (2007)

During neuronal activity, extracellular potassium concentration ([K+]out) becomes elevated and, if uncorrected, causes neuronal depolarization, hyperexcitability, and seizures. Clearance of K+ from the extracellular space, termed K+ spatial buffering, is considered to be an important function of astrocytes. Results from a number of studies suggest that maintenance of [K+]out by astrocytes is mediated by K+ uptake through the inward-rectifying Kir4.1 channels. To study the role of this channel in astrocyte physiology and neuronal excitability, we generated a conditional knock-out (cKO) of Kir4.1 directed to astrocytes via the human glial fibrillary acidic protein promoter gfa2. Kir4.1 cKO mice die prematurely and display severe ataxia and stress-induced seizures. Electrophysiological recordings revealed severe depolarization of both passive astrocytes and complex glia in Kir4.1 cKO hippocampal slices. Complex cell depolarization appears to be a direct consequence of Kir4.1 removal, whereas passive astrocyte depolarization seems to arise from an indirect developmental process. Furthermore, we observed a significant loss of complex glia, suggestive of a role for Kir4.1 in astrocyte development. Kir4.1 cKO passive astrocytes displayed a marked impairment of both K+ and glutamate uptake. Surprisingly, membrane and action potential properties of CA1 pyramidal neurons, as well as basal synaptic transmission in the CA1 stratum radiatum appeared unaffected, whereas spontaneous neuronal activity was reduced in the Kir4.1 cKO. However, high-frequency stimulation revealed greatly elevated posttetanic potentiation and short-term potentiation in Kir4.1 cKO hippocampus. Our findings implicate a role for glial Kir4.1 channel subunit in the modulation of synaptic strength.
Review on Optical Waveguides (2018)

Optical devices are necessary to meet the anticipated future requirements for ultrafast and ultrahigh bandwidth communication and computing. All optical information processing can overcome optoelectronic conversions that limit both the speed and bandwidth and are also power consuming. The building block of an optical device/circuit is the optical waveguide, which enables low-loss light propagation and is thereby used to connect components and devices. This chapter reviews optical waveguides and their classification on the basis of geometry (Non-Planar (Slab/Optical Fiber)/Planar (Buried Channel, Strip-Loaded, Wire, Rib, Diffused, Slot, etc.)), refractive index (Step/Gradient Index), mode propagation (Single/Multimode), and material platform (Glass/Polymer/Semiconductor, etc.). A comparative analysis of waveguides realized in different material platforms along with the propagation loss is also presented.
Human immunodeficiency virus coat protein gp120 inhibits the beta-adrenergic regulation of astroglial and microglial functions. (1993)

The goal of our study was to assess whether the human immunodeficiency virus (HIV) coat protein gp120 induces functional alterations in astrocytes and microglia, known for their reactivity and involvement in most types of brain pathology. We hypothesized that gp120-induced anomalies in glial functions, if present, might be mediated by changes in the levels of intracellular messengers important for signal transduction, such as cAMP. Acute (10 min) exposure of cultured rat cortical astrocytes or microglia to 100 pM gp120 caused only a modest (50-60%), though statistically significant, elevation in cAMP levels, which was antagonized by the beta-adrenergic receptor antagonist propranolol. More importantly, the protein substantially depressed [by 30% (astrocytes) and 50% (microglia)] the large increase in cAMP induced by the beta-adrenergic agonist isoproterenol (10 nM), without affecting that induced by direct adenylate cyclase stimulation by forskolin. Qualitatively similar results were obtained using a glial fibrillary acidic protein (GFAP)-positive human glioma cell line. The depression of the beta-adrenergic response had functional consequences in both astrocytes and microglia. In astrocytes we studied the phosphorylation of the two major cytoskeletal proteins, vimentin and GFAP, which is normally stimulated by isoproterenol, and found that gp120 partially (40-50%) prevented such stimulation. In microglial cells, which are the major producers of inflammatory cytokines within the brain, gp120 partially antagonized the negative beta-adrenergic modulation of lipopolysaccharide (10 ng/ml)-induced production of tumor necrosis factor alpha. Our results suggest that, by interfering with the beta-adrenergic regulation of astrocytes and microglia, gp120 may alter astroglial "reactivity" and upset the delicate cytokine network responsible for the defense against viral and opportunistic infections.