gebhart/patrepeval huggingface dataset:
Hydrogen Bonding in Organometallic Crystals. 1. From Carboxylic Acids and Alcohols to Carbonyl Complexes (1994)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTHydrogen Bonding in Organometallic Crystals. 1. From Carboxylic Acids and Alcohols to Carbonyl ComplexesDario Braga, Fabrizia Grepioni, Piera Sabatino, and Gautam R. DesirajuCite this: Organometallics 1994, 13, 9, 3532–3543Publication Date (Print):September 1, 1994Publication History Published online1 May 2002Published inissue 1 September 1994https://pubs.acs.org/doi/10.1021/om00021a029https://doi.org/10.1021/om00021a029research-articleACS PublicationsRequest reuse permissionsArticle Views329Altmetric-Citations85LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Coarsening phenomenon of Si clusters on artificial nucleation sites (1989)

A coarsening phenomenon of Si clusters is investigated in the process of nucleation and growth. In the early stage of chemical vapor deposition, multiple fine clusters of Si are nucleated on the small portion of an artifical nucleation site. A large cluster emerges among the fine clusters and grows rapidly as the deposition proceeds. As a result, the site is occupied by only one large cluster, while the fine clusters seem to disappear. Such a phenomenon is responsible for the mechanism in which a single nucleus is selected to grow on the site.
ChemInform Abstract: New Method of Synthesis of Vinca Alkaloid Derivatives. (2002)

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
Data from Reprogramming Tumor-Infiltrating Dendritic Cells for CD103&lt;sup&gt;+&lt;/sup&gt;CD8&lt;sup&gt;+&lt;/sup&gt; Mucosal T-cell Differentiation and Breast Cancer Rejection (2023)

&lt;div&gt;Abstract&lt;p&gt;Our studies showed that tumor-infiltrating dendritic cells (DC) in breast cancer drive inflammatory Th2 (iTh2) cells and protumor inflammation. Here, we show that intratumoral delivery of the β-glucan curdlan, a ligand of dectin-1, blocks the generation of iTh2 cells and prevents breast cancer progression &lt;i&gt;in vivo&lt;/i&gt;. Curdlan reprograms tumor-infiltrating DCs via the ligation of dectin-1, enabling the DCs to become resistant to cancer-derived thymic stromal lymphopoietin (TSLP), to produce IL-12p70, and to favor the generation of Th1 cells. DCs activated via dectin-1, but not those activated with TLR-7/8 ligand or poly I:C, induce CD8&lt;sup&gt;+&lt;/sup&gt; T cells to express CD103 (αE integrin), a ligand for cancer cells, E-cadherin. Generation of these mucosal CD8&lt;sup&gt;+&lt;/sup&gt; T cells is regulated by DC-derived integrin αvβ8 and TGF-β activation in a dectin-1–dependent fashion. These CD103&lt;sup&gt;+&lt;/sup&gt;CD8&lt;sup&gt;+&lt;/sup&gt; mucosal T cells accumulate in the tumors, thereby increasing cancer necrosis and inhibiting cancer progression &lt;i&gt;in vivo&lt;/i&gt; in a humanized mouse model of breast cancer. Importantly, CD103&lt;sup&gt;+&lt;/sup&gt;CD8&lt;sup&gt;+&lt;/sup&gt; mucosal T cells elicited by reprogrammed DCs can reject established cancer. Thus, reprogramming tumor-infiltrating DCs represents a new strategy for cancer rejection. &lt;i&gt;Cancer Immunol Res; 2(5); 487–500. ©2014 AACR&lt;/i&gt;.&lt;/p&gt;&lt;/div&gt;
Shear Wave Generation by Remotely Stimulating Aluminum Patches With a Transient Magnetic Field and Its Preliminary Application in Elastography (2020)

The proposed method allows potential application of the cross-correlation approach based elastography in intravascular-based or catheter-based cardiology.
Conformational Flexibility in Crystal Structures of Human 11β-Hydroxysteroid Dehydrogenase Type I Provide Insights into Glucocorticoid Interconversion and Enzyme Regulation (2004)

Human 11beta-hydroxysteroid dehydrogenase type I (11beta-HSD1) is an ER-localized membrane protein that catalyzes the interconversion of cortisone and cortisol. In adipose tissue, excessive cortisol production through 11beta-HSD1 activity has been implicated in the pathogenesis of type II diabetes and obesity. We report here biophysical, kinetic, mutagenesis, and structural data on two ternary complexes of 11beta-HSD1. The combined results reveal flexible active site interactions relevant to glucocorticoid recognition and demonstrate how four 11beta-HSD1 C termini converge to form an as yet uncharacterized tetramerization motif. A C-terminal Pro-Cys motif is localized at the center of the tetramer and forms reversible enzyme disulfides that alter enzyme activity. Conformational flexibility at the tetramerization interface is coupled to structural changes at the enzyme active site suggesting how the central Pro-Cys motif may regulate enzyme activity. Together, the crystallographic and biophysical data provide a structural framework for understanding 11beta-HSD1 activities and will ultimately facilitate the development of specific inhibitors.
A Cryogenic Environment for Microfabricated Surface Electrode Ion Traps. (2020)

Abstract not provided.
JBEI Electronic Laboratory Notebook System (2009)

JBEI is pursuing a novel approach to implement an electronic laboratory notebook (ELN) system.Ease of use, performance and cost are primary factors in the design of the system.Commercially successful, inexpensive software products are combined into a full-featured, hybrid system using integration software developed in-house.Powerful desktop note-taking software on a commodity tablet computer enables scientists to capture and organize notes, sketches, images, documents and other digital data files.All notebook information is periodically copied to a central, web-accessible repository for search and review by other authorized users.Integration with a secure digital timestamping service ensures that intellectual property can be defended in court.Pilot users have exhibited a high level of satisfaction; new users are adopting the system willingly based on peer recommendations.The completed system will facilitate online discovery and scientific collaboration, and will serve as a core component of our GTL knowledgebase.
Psychosocial health in pregnancy and postpartum among women living with - and without HIV and non-pregnant women living with HIV living in Nordic countries – Results from a longitudinal survey study (2022)

A high burden of adverse psychosocial outcomes was observed in both pregnant and non-pregnant women living with HIV compared to pregnant women without HIV. Loneliness and inadequate social support were associated with increased odds of depression in pregnancy and should be a focus in future support interventions.
Efficient parallel verification of Galois field multipliers (2017)

Galois field (GF) arithmetic is used to implement critical arithmetic components in communication and security-related hardware, and verification of such components is of prime importance. Current techniques for formally verifying such components are based on computer algebra methods that proved successful in verification of integer arithmetic circuits. However, these methods are sequential in nature and do not offer any parallelism. This paper presents an algebraic functional verification technique of gate-level GF(2 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">m</sup> ) multipliers, in which verification is performed in bit-parallel fashion. The method is based on extracting a unique polynomial in Galois field of each output bit independently. We demonstrate that this method is able to verify an n-bit GF multiplier in n threads. Experiments performed on pre- and post-synthesized Mastrovito and Montgomery multipliers show high efficiency up to 571 bits.
Abstract 4219: Lysosomal membrane permeabilization, a novel anticancer mechanism induced by pterostilbene (2011)

Abstract Pterostilbene (Pter) (3,5-dimethoxy-4′-hydroxystilbene), a natural dimethylated analog of resveratrol, is a phytoalexin abundant in plants and fruits with a number of potential benefits for human health. Darakchasava, an Indian herbal preparation of Vitis Vinifera, contains Pter and is prescribed as a cardiotonic in ayurvedic and traditional medicine. Furthermore, some observations indicate that Pter can be beneficial in the prevention and treatment of different diseases such as diabetes, dyslipidemia, or cancer. Pter shows higher bioavailability than resveratrol. The substitution of two OH groups (positions 3 and 5) by methyl groups increases the stabilityof the molecule and its resistance to hepatic glucuronidation and sulfonation. Nevertheless, despite these pharmacokinetic advantages, the anticancer potential of Pter is still undefined. Lysosomal membrane permeabilization (LMP) has been postulated as a mechanism leading to cell death. In an initial step LMP causes cytosol acidification and release of cathepsins and other hydrolases from the lysosomal lumen. Ectopic presence of proteases causes the hydrolysis of vital proteins and the activation of other cell death-related proteases such as caspases. Thus linking LMP and cell death type I. In addition, LMP may also induce caspase-independent cell death mechanisms. In fact morphology of cells affected by LMP may be confused with a subapoptotic or necrotis appearance. The aim of our present study was to investigate the mechanisms of cell death activated by Pter in different tumor cells. For this purpose we used a range of Pter concentration between 10uM (below the IC50) and 100uM (an unachievable in vivo concentration). Acridin orange staining was determined by flow cytometry and fluorescence microscopy. Total and cytosolic cathepsin extractions were performed with different digitonin concentration and activity was measured by spectrofluorimetry. Cytosolic pH was evaluated by staining cultured cells with the fluorochrome SNARF. Apoptosis induction was checked through caspase 3 and 7 measurements. The effects observed in the presence of Pter, under in vitro conditions, were concentration and time dependent. An increase in LMP induced an acidification of cytosolic pH, an increase in cathepsin activity and, only at long time exposure, apoptosis stimulation. Our results demonstrate that tumor cell death induction elicited by Pter is preferentially mediated through LMP. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4219. doi:10.1158/1538-7445.AM2011-4219
“FDA-approved carbonic anhydrase inhibitors reduce Amyloid β pathology and improve cognition, by ameliorating cerebrovascular health and glial fitness” (2022)

Abstract Alzheimer’s disease (AD) is a devastating neurodegenerative disorder with no effective cure. Cerebrovascular and neurovascular pathology are early and causal hallmarks of AD, where cerebral amyloid angiopathy (CAA), the deposition of amyloid β (Aβ) at the cerebral vasculature, is present in about 90% of cases. Our previous work has uncovered the protective effect of carbonic anhydrase (CA) inhibition against Aβ-mediated mitochondrial dysfunction, production of reactive oxygen species (ROS) and apoptosis in vascular, glial and neuronal cells in culture. Here, we tested for the first time in a transgenic model of AD and cerebrovascular amyloidosis, the TgSwDI mice, a therapeutic regimen employing the FDA-approved CA inhibitors (CAIs), methazolamide (MTZ) and acetazolamide (ATZ). These drugs are used in humans for glaucoma, high altitude sickness, and other disorders, and can cross the blood-brain barrier. We found that both CAIs were non- toxic, significantly reduced cerebral amyloidosis, vascular, microglial and astrocytic Aβ accumulation, and ameliorated cognition. MTZ and ATZ treatment prevented caspase-3 activation in endothelial cells, microglia and astrocytes, reverted capillary constriction and microhemorrhages, reduced gliosis, and induced glial pro-clearance pathways, which are likely responsible for the reduction of Aβ deposition. Notably, we unveiled a critical new druggable target, revealing that the mitochondrial isozyme CA-VB is specifically upregulated in TgSwDI mouse brains, as well as in human brains of CAA and AD (with CAA) patients. Importantly, Aβ challenge induced CA-VB overexpression in human cerebral endothelial cells, and CA-VB silencing, mimicking CAIs effects, reduced Aβ-mediated endothelial apoptosis. This work paves the way for the application of CAIs in clinical trials for AD and CAA and uncovers CA-VB as a mediator of cerebral amyloid toxicity.
Correlation of Spinal cord and CSF biomarkers to Clinical and Radiological Measures of CNS injury in a Mouse Model of Multiple Sclerosis (P2.198) (2015)

OBJECTIVE: To develop biomarkers relevant to inflammatory, demyelinating CNS injury in the Theiler's encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) model of MS by correlating gene expression in the spinal cord and CSF with MRI and clinical measures of spinal cord injury. BACKGROUND: A major gap in our understanding of MS is a lack of information about the pathogenesis of demyelination and axonal injury that are the pathological hallmarks of the disease. This has led to the lack of availability of useful clinical biomarkers of inflammation and disease. The TMEV-IDD model of MS reproduces both the progressive spastic disability and the pathology of MS, and thus serves as an ideal model to improve our understanding of mechanisms of CNS injury in MS. DESIGN/METHODS: We used gene expression measures of spinal cord tissue and CSF to correlate potential biomarkers to spinal cord injury as measured by MRI (T2 and diffusion tensor imaging) and Rotarod. SJL/J mice with TMEV-IDD with varying levels of clinical disease and anti-TMEV antibodies in the serum were serially imaged using a 9.4T horizontal bore small animal MRI scanner. Mice were then necropsied; blood, CSF, and spinal cord tissue were obtained. Gene expression of a range of host and viral proteins were analyzed by real time RT-PCR for mRNA of tissue, and multiplex bioassay for proteins in the CSF. Correlation was then performed between potential biomarkers and MRI and Rotarod. RESULTS: A number of potential biomarkers, including molecules upregulated in CNS antibody production, were identified using this approach. Many of these potential biomarkers are classified as innate immune molecules. CONCLUSIONS: Correlation of CNS tissue and CSF biomarkers to clinical and MRI measures of disease in the spinal cord in TMEV-IDD represents a sound approach to development of clinically useful biomarkers in MS.
Periwound dopaminergic sprouting is dependent on numbers of wound macrophages (2002)

Injury to many regions of the central nervous system, including the striatum, results in a periwound or 'abortive' sprouting response. In order to directly evaluate whether macrophages play an important role in stimulating periwound sprouting, osteopetrotic (op/op) mice, which when young are deficient in a variety of macrophage subtypes, were given striatal wounds and the degree of dopaminergic sprouting subsequently assessed. Two weeks postinjury, significantly fewer wound macrophages were present in the striata of op/op mice compared with controls (144 +/- 30.1 in op/op mice vs. 416.6 +/- 82.3 in controls, P < 0.005, analysis performed on a section transecting the middle of the wound). Dopamine transporter immunohistochemistry revealed a marked decrease in the intensity of periwound sprouting in the op/op group of animals. Quantification of this effect using [H3]-mazindol autoradiography confirmed that periwound sprouting was reduced significantly in the op/op mice compared with controls (71.4 +/- 21.7 fmol/mg protein in op/op mice vs. 210.7 +/- 27.1 fmol/mg protein in controls, P < 0.0005). In the two groups of animals the magnitude of the sprouting response in individuals was closely correlated with the number of wound macrophages (R = 0.83, R2 = 0.69). Our findings provide strong support for the crucial involvement of macrophages in inducing dopaminergic sprouting after striatal injury.
IL-18 deficiency ameliorates the progression from AKI to CKD (2022)

Inflammation is an important factor in the progression from acute kidney injury (AKI) to chronic kidney disease (CKD). The role of interleukin (IL)-18 in this progression has not been examined. We aimed to clarify whether and how IL-18 limits this progression. In a folic acid induced renal injury mouse model, we studied the time course of kidney injury and renal IL-18 expression. In wild-type mice following injection, renal IL-18 expression increased. In parallel, we characterized other processes, including at day 2, renal tubular necroptosis assessed by receptor-interacting serine/threonine-protein kinase1 (RIPK1) and RIPK3; at day 14, transdifferentiation (assessed by transforming growth factor β1, vimentin and E-cadherin); and at day 30, fibrosis (assessed by collagen 1). In IL-18 knockout mice given folate, compared to wild-type mice, tubular damage and necroptosis, transdifferentiation, and renal fibrosis were attenuated. Importantly, IL-18 deletion decreased numbers of renal M1 macrophages and M1 macrophage cytokine levels at day 14, and reduced M2 macrophages numbers and macrophage cytokine expression at day 30. In HK-2 cells, IL-18 knockdown attenuated necroptosis, transdifferentiating and fibrosis.In patients with tubulointerstitial nephritis, IL-18 protein expression was increased on renal biopsies using immunohistochemistry. We conclude that genetic IL-18 deficiency ameliorates renal tubular damage, necroptosis, cell transdifferentiation, and fibrosis. The renoprotective role of IL-18 deletion in the progression from AKI to fibrosis may be mediated by reducing a switch in predominance from M1 to profibrotic M2 macrophages during the process of kidney repair.
Supplementary Figure 1 from Targeting Protein Synthesis in a Myc/mTOR-Driven Model of Anorexia-Cachexia Syndrome Delays Its Onset and Prolongs Survival (2023)

&lt;p&gt;PDF file - 517K&lt;/p&gt;
LEXCOMM: A low energy, secure and flexible communication protocol for a heterogenous body sensor network (2012)

Body Area Sensor Network(BASN) with application in healthcare domain has garnered significant research interests lately. Despite similarities with Wireless Sensor Network (WSN), BASN has its peculiar design and operational challenges creating interests for focused research. The primary design parameters for BASN are energy consumption, network performance, data heterogeneity and strong security. In our work we have developed a flexible protocol that offers an edge in terms of performances, energy consumption, and security compared to existing systems. This protocol addresses the issues of BASN more precisely and presents a vivid picture on issues of inclusion of security module within BASN protocol. In this paper we describe the protocol and how we address the characteristics of BASN like its heterogeneity to achieve better performance results. We have validated the protocol with real deployment considering selected sensor for patient health monitoring. The protocol has been developed in TinyOS/NesC environment and implemented on Shimmer Motes equipped with health sensors like ECG, EMG, Accelerometer, Temperature and GSR.
An Amphotericin B–Fluorescein Conjugate as a Powerful Probe for Biochemical Studies of the Membrane (2004)

Not only skin deep: A fluorescein–amphotericin B conjugate with a new piperazine linker (see structure) was prepared and used as a probe of the biomembrane and the mechanism of action of amphotericin B both in vivo and in liposomal experiments. The amphotericin B analogue localizes at the membrane of yeast cells but is internalized by mammalian cells. Supporting information for this article is available on the WWW under http://www.wiley-vch.de/contents/jc_2002/2004/z460489_s.pdf or from the author. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Expression of Heterozygous lpr Gene in MRL Mice (1989)

The presence of the homozygous lpr gene (lpr/lpr) in MRL mice has been regarded as mandatory for the development of the early onset of lupus disease, T-cell dysfunction, and polyclonal B-cell activation. Congeneic MRL mice lacking the lpr gene (MRL +/+) display neither the lupus disease nor the immunological abnormalities within the first year of life. In this study we examined the cellular functions of MRL mice heterozygous at the lpr locus. The results indicate that MRL mice heterozygous at the lpr locus display intermediate delayed-type hypersensitivity compared with homozygous lpr/lpr mice on the one hand and congeneic +/+ mice on the other. Furthermore, proliferative responses to concanavalin A, measured by uptake of [3H]thymidine, were significantly lower in MRL mice heterozygous at the lpr locus than in +/+ mice, but significantly higher than in homozygous MRL lpr/lpr mice. Polyclonal B-cell activation, assessed by measurement of frequencies of IgG-secreting spleen cells, a prominent feature in MRL lpr/lpr mice, was significantly lower in lpr/+ mice and totally absent in +/+ mice. Furthermore, spleen cells spontaneously secreting auto-antibodies were found in large numbers in MRL lpr/lpr mice and in considerably lower but still significant numbers in heterozygous MRL +/lpr mice. In contrast, spleen cells from matched MRL +/+ mice did not display any spontaneous autoantibody production. Taken together, these data provide evidence for immunomodulatory properties of the heterozygous lpr gene.