gebhart/patrepeval huggingface dataset:
Fecal Microbiota Transplantation (FMT) in Multiple Sclerosis (MS) (2011)

Purpose: Recent evidence implicates the GI microbiota in the progression of neurological diseases such as Parkinsons Disease1, Multiple Sclerosis and Myasthenia Gravis2. We report three patients with MS diagnoses who achieved durable symptom reversal with FMT for constipation. Methods: Case study observations on three MS cases Results: Case 1: A 30 yr old male with constipation, vertigo and impaired concentration and a concomitant history of MS and trigeminal neuralgia. Neurological symptoms included severe leg weakness and he required a wheelchair and an indwelling urinary catheter. Previous failed treatments included Mexiletine, Tryptanol and β-interferon. The patient underwent 5 FMT infusions for his constipation, with its complete resolution. Interestingly his MS also progressively improved, regaining the ability to walk and facilitating the removal of his catheter. Initially seen as a ‘remission', the patient remains well 15 yrs post-FMT without relapse. Case 2: A 29 yr old wheelchair-bound male with ‘atypical MS' diagnosis and severe, chronic constipation. He reported parasthesia and leg muscle weakness. The patient received 10 days of FMT infusions which resolved his constipation. He also noted progressive improvement in neurological symptoms, regaining the ability to walk following slow resolution of leg parasthesia. Three years on the patient maintains normal motor, urinary and GI function. Case 3: An 80 yr old female presented with severe chronic constipation, proctalgia fugax and severe muscular weakness resulting in difficulty walking, diagnosed as ‘atypical' MS. She received 5 FMT infusions with rapid improvement of constipation and increased energy levels. At eight months she reported complete resolution of bowel symptoms and neurological improvement, now walking long distances unassisted. Two years post-FMT, the patient was asymptomatic. Conclusion: We report reversal of major neurological symptoms in three patients after FMT for their underlying GI symptoms. As MS can follow a relapsing-remitting course, this unexpected discovery was not reported until considerable time had passed to confirm prolonged remission. It is tempting to speculate that FMT achieved eradication of an occult GI pathogen driving MS symptoms. Our finding that FMT can reverse MS-like symptoms suggests a GI infection underpinning these disorders. It is hoped that such serendipitous findings may encourage a new direction in neurological research.
Molecular Identification of High and Low Affinity Receptors for Nicotinic Acid (2003)

Nicotinic acid has been used clinically for over 40 years in the treatment of dyslipidemia producing a desirable normalization of a range of cardiovascular risk factors, including a marked elevation of high density lipoprotein and a reduction in mortality. The precise mechanism of action of nicotinic acid is unknown, although it is believed that activation of a G(i)-G protein-coupled receptor may contribute. Utilizing available information on the tissue distribution of nicotinic acid receptors, we identified candidate orphan receptors. The selected orphan receptors were screened for responses to nicotinic acid, in an assay for activation of G(i)-G proteins. Here we describe the identification of the G protein-coupled receptor HM74 as a low affinity receptor for nicotinic acid. We then describe the subsequent identification of HM74A in follow-up bioinformatics searches and demonstrate that it acts as a high affinity receptor for nicotinic acid and other compounds with related pharmacology. The discovery of HM74A as a molecular target for nicotinic acid may facilitate the discovery of superior drug molecules to treat dyslipidemia.
Hepcidin in Human Iron Disorders: Diagnostic Implications (2011)

Cell-culture, animal, and human studies have shown that hepcidin is predominantly synthesized by hepatocytes, where its expression is regulated by body iron status, erythropoietic activity, oxygen tension, and inflammatory cytokines. Hepcidin lowers serum iron concentrations by counteracting the function of ferroportin, a major cellular iron exporter present in the membrane of macrophages, hepatocytes, and the basolateral site of enterocytes. Hepcidin is detected in biologic fluids as a 25 amino acid isoform, hepcidin-25, and 2 smaller forms, i.e., hepcidin-22 and -20; however, only hepcidin-25 has been shown to participate in the regulation of iron metabolism. Reliable assays to measure hepcidin in blood and urine by use of immunochemical and mass spectrometry methods have been developed. Results of proof-of-principle studies have highlighted hepcidin as a promising diagnostic tool and therapeutic target for iron disorders. However, before hepcidin measurements can be used in routine clinical practice, efforts will be required to assess the relevance of hepcidin isoform measurements, to harmonize the different assays, to define clinical decision limits, and to increase assay availability for clinical laboratories.
The Entanglement Concept in Polymer Systems (1966)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe Entanglement Concept in Polymer SystemsRoger S. Porter and Julian F. JohnsonCite this: Chem. Rev. 1966, 66, 1, 1–27Publication Date (Print):February 1, 1966Publication History Published online1 May 2002Published inissue 1 February 1966https://doi.org/10.1021/cr60239a001RIGHTS & PERMISSIONSArticle Views3355Altmetric-Citations279LEARN 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 InReddit PDF (2 MB) Get e-Alerts Get e-Alerts
Breast cancer vaccines: maximizing cancer treatment by tapping into host immunity (2005)

Optimizing standard treatment modalities for breast cancer has improved the outlook for women afflicted with it, but the fact that 40% still ultimately die from the disease highlights the need for new therapies. Remarkable advances in molecular immunology and biotechnology have created a unique opportunity for developing active vaccination strategies that engage the patient's own immune system in the fight against breast cancer. Early clinical trials have established the safety and bioactivity of some breast cancer vaccine approaches, with a hint of clinical response. They have also highlighted the importance of elucidating the pharmacodynamic interactions between established therapies for breast cancer, such as tamoxifen, aromatase inhibitors, chemotherapy, the HER-2/neu-specific monoclonal antibody trastuzumab (Herceptin), and breast cancer vaccines. Preclinical studies have simultaneously defined the importance of developing targeted approaches for circumventing established immune tolerance to breast cancer during the vaccination process. The first strategies targeting the negative influence of CD4(+)CD25(+)T regulatory cells and the CTLA-4 signaling pathway are just entering clinical testing in combination with tumor vaccines. Developing the most potent approach for activating antitumor immunity while maintaining the efficacy of standard approaches to breast cancer management will ensure that active immunotherapy is successfully integrated into the standard of care.
High-Resolution Surface-Wave Tomography from Ambient Seismic Noise (2005)

Cross-correlation of 1 month of ambient seismic noise recorded at USArray stations in California yields hundreds of short-period surface-wave group-speed measurements on interstation paths. We used these measurements to construct tomographic images of the principal geological units of California, with low-speed anomalies corresponding to the main sedimentary basins and high-speed anomalies corresponding to the igneous cores of the major mountain ranges. This method can improve the resolution and fidelity of crustal images obtained from surface-wave analyses.
ALGONQUIN: iterating laplace's method to remove multiple types of acoustic distortion for robust speech recognition (2001)

One approach to robust speech recognition is to use a simple speech model to remove the distortion, before applying the speech recognizer. Previous attempts at this approach have relied on unimodal or point estimates of the noise for each utterance. In challenging acoustic environments, e.g., an airport, the spectrum of the noise changes rapidly during an utterance, making a point estimate a poor representation. We show how an iterative form of Laplace’s method can be used to estimate the clean speech, using a time-varying probability model of the log-spectra of the clean speech, noise and channel distortion. We use this method, called ALGONQUIN, to denoise speech features and then feed these features into a large vocabulary speech recognizer whose WER on the clean Wall Street Journal data is 4.9%. When 10 dB of noise consisting of an airplane engine shutting down is added to the data, the recognizer obtains a WER of 28.8%. ALGONQUIN reduces the WER to 12.6%, well below the WER of 25.0% obtained by our spectral subtraction algorithm, and close to the WER of 9.7% obtained by the slow procedure of retraining the recognizer on training data corrupted by the exact same noise. In fact, if ALGONQUIN is used to denoise the noisy training data before the recognizer is retrained, the WER is improved to 8.5%. For 10 dB of additive uniform white noise, our spectral subtraction algorithm reduces the WER from 55.1% to 33.8%. ALGONQUIN reduces the WER to 14.2%. The recognizer trained on noisy data obtains a WER of 14%, whereas the recognizer trained on noisy data denoised by ALGONQUIN obtains a WER of 9.9%.
The anti-CD74 humanized monoclonal antibody, milatuzumab, which targets the invariant chain of MHC II complexes, alters B-cell proliferation, migration, and adhesion molecule expression (2012)

Milatuzumab leads to modestly reduced proliferation, alterations in migration, and adhesion molecule expression preferentially of CD27- naïve B cells. It thus may be a candidate antibody for the autoimmune disease therapy by modifying B cell functions.
Compressive Sensing Reconstruction With Prior Information by Iteratively Reweighted Least-Squares (2009)

<para xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> Iteratively reweighted least-squares (IRLS) algorithms have been successfully used in compressive sensing to reconstruct sparse signals from incomplete linear measurements taken in nonsparse domains. The underlying optimization problem corresponds to finding the vector that solves the <formula formulatype="inline"> <tex Notation="TeX">${\ell _{p}}$</tex></formula> minimization while explaining the measurements, and IRLS allows to easily control the used value of <formula formulatype="inline"><tex Notation="TeX">${p}$</tex></formula>, with effect on the number of required measurements. In this paper, we propose a weighting strategy in the reconstruction method based on IRLS in order to add prior information on the support of the sparse domain. Our simulation results show that the use of prior knowledge about positions of at least some of the nonzero coefficients in the sparse domain leads to a reduction in the number of linear measurements required for unambiguous reconstruction. This reduction occurs for all values of <formula formulatype="inline"><tex Notation="TeX">${p}$</tex> </formula>, so that a further reduction can be achieved by decreasing <formula formulatype="inline"><tex Notation="TeX">${p}$</tex></formula> and using prior information. The proposed weighting scheme also reduces the computational complexity with respect to the IRLS with no prior information, both in terms of number of iterations and computation time. </para>
[6S]‐5‐methyltetrahydrofolate increases plasma folate more effectively than folic acid in women with the homozygous or wild‐type 677C→T polymorphism of methylenetetrahydrofolate reductase (2009)

These data suggest that [6S]-5-MTHF increases plasma folate more effectively than FA irrespective of the 677C-->T mutation of the MTHFR. This natural form of folate could be an alternative to FA supplementation or fortification.
The Cognitive Structure of Emotions (1988)

It has long been clear that the way in which people interpret the world affects our emotional reactions. What has been less clear is exactly how such different interpretations lead to different emotions. This is the central question addressed by The Cognitive Structure of Emotions. Taking a cognitive science perspective, a systematic account is presented of the cognitive structures that underlie a wide range of different emotions. Detailed proposals about the factors that affect intensity are also offered. The authors propose three broad classes of emotions, each corresponding to a different attentional focus. One class consists of reactions to events, one of reactions to the actions of agents, and one of reactions to objects. By basing their analysis of the antecedents of emotions on an analysis of the perceived situational conditions that elicit them, the authors offer the prospect of accounting for variations in the emotions of different individuals, different cultures, and perhaps even different species.
Antibodies that inhibit fusion of human immunodeficiency virus-infected cells bind a 24-amino acid sequence of the viral envelope, gp120. (1988)

Antisera to recombinant human immunodeficiency virus (HIV) proteins containing the entire envelope, gp160, or the central portion of the envelope, PB1, can inhibit fusion of virally infected cells in culture. This fusion inhibition is HIV-variant specific--that is, anti-gp160-IIIB inhibits fusion of isolate HTLV-IIIB-infected cells but not of isolate HTLV-IIIRF-infected cells. Both anti-gp160 and anti-PB1 are completely blocked in fusion inhibition activity by the addition of PB1 protein. A 24-amino acid peptide (RP135, amino acids 307-330) completely blocks fusion inhibition activity of both antisera and also blocks the activity of serum from a chimpanzee infected with HTLV-IIIB. Thus, the principal epitope that elicits fusion-inhibiting antibodies is located in the central portion of gp120.
Cell Entry of Hepatitis C Virus Requires a Set of Co-receptors That Include the CD81 Tetraspanin and the SR-B1 Scavenger Receptor (2003)

Several cell surface molecules have been proposed as receptor candidates, mediating cell entry of hepatitis C virus (HCV) on the basis of their physical association with virions or with soluble HCV E2 glycoproteins. However, due to the lack of infectious HCV particles, evidence that these receptor candidates support infection was missing. Using our recently described infectious HCV pseudotype particles (HCVpp) that display functional E1E2 glycoprotein complexes, here we show that HCV is a pH-dependent virus, implying that its receptor component(s) mediate virion internalization by endocytosis. Expression of the CD81 tetraspanin in non-permissive CD81-negative hepato-carcinoma cells was sufficient to restore susceptibility to HCVpp infection, confirming its critical role as a cell attachment factor. As a cell surface molecule likely to mediate endosomal trafficking, we demonstrate that the human scavenger receptor class B type 1 (SR-B1), a high-density lipoprotein-internalization molecule that we previously proposed as a novel HCV receptor candidate due to its affinity with E2 glycoproteins, is required for infection of CD81-expressing hepatic cells. By receptor competition assays, we found that SR-B1 antibodies that blocked binding of soluble E2 could prevent HCVpp infectivity. Furthermore, we establish that the hyper-variable region 1 of the HCV E2 glycoprotein is a critical determinant mediating entry in SR-B1-positive cells. Finally, by correlating expression of HCV receptors and infectivity, we suggest that, besides CD81 and SR-B1, additional hepatocyte-specific co-factor(s) are necessary for HCV entry.
Pose tracking from natural features on mobile phones (2008)

In this paper we present two techniques for natural feature tracking in real-time on mobile phones. We achieve interactive frame rates of up to 20 Hz for natural feature tracking from textured planar targets on current-generation phones. We use an approach based on heavily modified state-of-the-art feature descriptors, namely SIFT and Ferns. While SIFT is known to be a strong, but computationally expensive feature descriptor, Ferns classification is fast, but requires large amounts of memory. This renders both original designs unsuitable for mobile phones. We give detailed descriptions on how we modified both approaches to make them suitable for mobile phones. We present evaluations on robustness and performance on various devices and finally discuss their appropriateness for augmented reality applications.
HIF-1 regulates hypoxic induction of NHE1 expression and alkalinization of intracellular pH in pulmonary arterial myocytes (2006)

Vascular remodeling resulting from altered pulmonary arterial smooth muscle cell (PASMC) growth is a contributing factor to the pathogenesis of hypoxic pulmonary hypertension. PASMC growth requires an alkaline shift in intracellular pH (pH(i)) and we previously showed that PASMCs isolated from mice exposed to chronic hypoxia exhibited increased Na(+)/H(+) exchanger (NHE) expression and activity, which resulted in increased pH(i). However, the mechanism by which hypoxia caused these changes was unknown. In this study we tested the hypothesis that hypoxia-induced changes in PASMC pH homeostasis are mediated by the transcriptional regulator hypoxia-inducible factor 1 (HIF-1). Consistent with previous results, increased NHE isoform 1 (NHE1) mRNA and protein, enhanced NHE activity, and an alkaline shift in pH(i) were observed in PASMCs isolated from wild-type mice exposed to chronic hypoxia (3 wk at 10% O(2)). In contrast, these changes were absent in PASMCs isolated from chronically hypoxic mice with partial deficiency for HIF-1. Exposure of PASMCs to hypoxia ex vivo (48 h at 4% O(2)) or overexpression of HIF-1 in the absence of hypoxia also increased NHE1 mRNA and protein expression. Our results indicate that full expression of HIF-1 is essential for hypoxic induction of NHE1 expression and changes in PASMC pH homeostasis and suggest a novel mechanism by which HIF-1 mediates pulmonary vascular remodeling during the pathogenesis of hypoxic pulmonary hypertension.
Combination treatment with oncolytic Vaccinia virus and cyclophosphamide results in synergistic antitumor effects in human lung adenocarcinoma bearing mice (2014)

CPA and GLV-1h68 have synergistic antitumor effects on PC14PE6-RFP xenografts. We strongly suppose that in the PC14PE6-RFP model the enhanced tumor growth inhibition achieved by combining GLV-1h68 with CPA is due to an effect on the vasculature rather than an immunosuppressive action of CPA. These results provide evidence to support further preclinical studies of combining GLV-1h68 and CPA in other highly angiogenic tumor models. Moreover, data presented here demonstrate that CPA can be combined successfully with GLV-1h68 based oncolytic virus therapy and therefore might be promising as combination therapy in human clinical trials.
GABAergic neuroactive steroids: a new frontier in bipolar disorders? (2012)

Neurosteroids are synthesized in the brain and modulate brain excitability. There is increasing evidence of their sedative, anesthetic and antiseizure properties, as well as their influence on mood. Currently neurosteroids are classified as pregnane neurosteroids (allopregnanolone and allotetrahydrodeoxycorticosterone), androstane neurosteroids (androstanediol and etiocholanone) or sulfated neurosteroids (pregnenolone sulfate and dehydroepiandrosterone sulfate). Both preclinical and clinical findings indicate that progesterone derivative neurosteroids such as allopregnanolone and allotetrahydrodeoxycorticosterone play a role in mood disorders. Clozapine and olanzapine, which were shown to be effective in stabilizing bipolar disorder, elevate pregnenolone levels in rat hippocampus, cerebral cortex, and serum. In lithium-treated mice, the blood levels of allopregnanolone and pregnenolone were elevated compared to control levels. Women diagnosed with bipolar disorder typically show symptomatic exacerbation in relation to the menstrual cycle, and show vulnerability to the onset or recurrence of mood disorders immediately after giving birth, when the levels of neurosteroid derivatives of progesterone drop. Whereas in women who had recovered from bipolar disorder, the plasma concentration of allopregnanolone was elevated compared to either healthy controls or women with major depressive disorder during the premenstrual period. During depressive episodes, blood level of allopregnanolone is low. Treatment with fluoxetine tends to stabilize the levels of neurosteroids in depression. These findings converge to suggest that these steroids have significant mood-stabilizing effect. This hypothesis is consistent with the observation that a number of anticonvulsants are effective therapies for bipolar disorder, a finding also consistent with the antiseizure properties of neurosteroids. Further exploration of action of neuroactive steroids is likely to open new frontiers in the investigation of the etiology and treatment of mood disorders, particularly bipolar disorders.
Treating activated CD4+ T cells with either of two distinct DNA methyltransferase inhibitors, 5-azacytidine or procainamide, is sufficient to cause a lupus-like disease in syngeneic mice. (1993)

Human antigen-specific CD4+ T cells become autoreactive after treatment with various DNA methylation inhibitors, including 5-azacytidine, procainamide, and hydralazine. This suggests a mechanism that could contribute to the development of some forms of autoimmunity. In this report we have asked whether T cells treated with DNA methylation inhibitors can induce autoimmunity. Murine CD4+ T cells were treated with 5-azacytidine or procainamide and were shown to respond to syngeneic antigen-presenting cells, similar to CD4+ human T cell clones treated with these drugs. Functional characterization demonstrated that cells treated with either drug spontaneously lysed syngeneic macrophages and secreted IL-4, IL-6, and IFN-gamma. Adoptive transfer of 5-azacytidine- or procainamide-treated cells into unirradiated syngeneic recipients induced an immune complex glomerulonephritis and IgG anti-DNA and antihistone antibodies. These experiments demonstrate that T cells treated with either of two distinct DNA methyltransferase inhibitors are sufficient to induce a lupus-like disease. It is possible that the lysis of macrophages, together with the release of cytokines promoting B cell differentiation, contributes to the autoantibody production and immune complex deposition. These results suggest that environmental agents that inhibit DNA methylation could interact with T cells in vivo to produce a lupus-like illness, a mechanism that could have relevance to drug-induced and idiopathic lupus.