tbuckley/cabot-search huggingface dataset:
Tendon neuroplastic training: changing the way we think about tendon rehabilitation: a narrative review
Authors: Ebonie Rio, Dawson Kidgell, G Lorimer Moseley, Jamie Gaida, Sean Docking, Craig Purdam, Jill Cook
Journal: British Journal of Sports Medicine (2015)

Tendinopathy can be resistant to treatment and often recurs, implying that current treatment approaches are suboptimal. Rehabilitation programmes that have been successful in terms of pain reduction and return to sport outcomes usually include strength training. Muscle activation can induce analgesia, improving self-efficacy associated with reducing one's own pain. Furthermore, strength training is beneficial for tendon matrix structure, muscle properties and limb biomechanics. However, current tendon rehabilitation may not adequately address the corticospinal control of the muscle, which may result in altered control of muscle recruitment and the consequent tendon load, and this may contribute to recalcitrance or symptom recurrence. Outcomes of interest include the effect of strength training on tendon pain, corticospinal excitability and short interval cortical inhibition. The aims of this concept paper are to: (1) review what is known about changes to the primary motor cortex and motor control in tendinopathy, (2) identify the parameters shown to induce neuroplasticity in strength training and (3) align these principles with tendon rehabilitation loading protocols to introduce a combination approach termed as tendon neuroplastic training. Strength training is a powerful modulator of the central nervous system. In particular, corticospinal inputs are essential for motor unit recruitment and activation; however, specific strength training parameters are important for neuroplasticity. Strength training that is externally paced and akin to a skilled movement task has been shown to not only reduce tendon pain, but modulate excitatory and inhibitory control of the muscle and therefore, potentially tendon load. An improved understanding of the methods that maximise the opportunity for neuroplasticity may be an important progression in how we prescribe exercise-based rehabilitation in tendinopathy for pain modulation and potentially restoration of the corticospinal control of the muscle-tendon complex.
WITHDRAWN: Factors affecting formation of microemulsions containing modified coconut oil
Authors: Sirikarn Pengon, Chutima Limmatvapirat, Sontaya Limmatvapirat
Journal: Asian Journal of Pharmaceutical Sciences (2015)

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.
Induced abortion can predispose to tetanus
Authors: S. Akhter, C. Edwards, J. Ikimalo, S. Panezai
Journal: BMJ (1995)

wellbeing but is potentially counterproductive to promotion ofbreast feeding.I suggest the following amendments to the author's key messages: * First assess whether the heel prick is really necessary * Minimise the discomfort of the procedure by asking the parent (or member of staff) to cuddle and soothe the baby * If the mother is breastfeeding encourage her to put the baby to the breast before the procedure starts and allow the baby to suckle during the procedure Lastly, before drug manufacturers seize a new opportunity to market prepacked phials of sterile sucrose solution, complete with dropper, could I urge the authors to consider mounting a study to answer their own query-namely, "whether simply cuddling a crying infant after heel prick is as effective in reducing crying as 50% sucrose."It may be that going back to the basics is all that is needed.CORALJEPSON
Antiviral therapy for chronic hepatitis B viral infection in adults: A systematic review and meta‐analysis
Authors: Anna S.F. Lok, Brian J. McMahon, Robert S. Brown, John B. Wong, Ahmed T. Ahmed, Wigdan Farah, Jehad Almasri, Fares Alahdab, Khalid Benkhadra, Mohamed A. Mouchli, Siddharth Singh, Essa A. Mohamed, Abd Moain Abu Dabrh, Larry J. Prokop, Zhen Wang, Mohammad Hassan Murad, Khaled Mohammed
Journal: Hepatology (2015)

Chronic hepatitis B viral (HBV) infection remains a significant global health problem. Evidence-based guidelines are needed to help providers determine when treatment should be initiated, which medication is most appropriate, and when treatment can safely be stopped. The American Association for the Study of Liver Diseases HBV guideline methodology and writing committees developed a protocol a priori for this systematic review. We searched multiple databases for randomized controlled trials and controlled observational studies that enrolled adults ≥18 years old diagnosed with chronic HBV infection who received antiviral therapy. Data extraction was done by pairs of independent reviewers. We included 73 studies, of which 59 (15 randomized controlled trials and 44 observational studies) reported clinical outcomes. Moderate-quality evidence supported the effectiveness of antiviral therapy in patients with immune active chronic HBV infection in reducing the risk of cirrhosis, decompensated liver disease, and hepatocellular carcinoma. In immune tolerant patients, moderate-quality evidence supports improved intermediate outcomes with antiviral therapy. Only very low-quality evidence informed the questions about discontinuing versus continuing antiviral therapy in hepatitis B e antigen-positive patients who seroconverted from hepatitis B e antigen to hepatitis B e antibody and about the safety of entecavir versus tenofovir. Noncomparative and indirect evidence was available for questions about stopping versus continuing antiviral therapy in hepatitis B e antigen-negative patients, monotherapy versus adding a second agent in patients with persistent viremia during treatment, and the effectiveness of antivirals in compensated cirrhosis with low-level viremia.Most of the current literature focuses on the immune active phases of chronic HBV infection; decision-making in other commonly encountered and challenging clinical settings depends on indirect evidence.
WITHDRAWN: Improved pharmacokinetic and cytotoxicity characteristics of imatinib by utilizing nanostructured lipid carriers
Authors: Kyu Bong Woo, Biki Gupta, Pathak Shiva, Bijay Kumar Poudel, Nguyen Hanh Thuy, Raj Kumar Tapa, Han-Gon Choi, Jee-Heon Jeong, Jong Oh Kim, Chul Soon Yong
Journal: Asian Journal of Pharmaceutical Sciences (2015)

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.
Diagnosing myocardial infarction
Authors: S. Goodacre, F. Morris, S. Campbell, D. Quinney, S. Capewell, C. E Palffy
Journal: BMJ (2001)

Risk of adverse birth outcomes near landfill sitesEvidence suggests that it is probably safe for fetuses to develop near landfill sites Editor-Elliott et al report a large geographical study of adverse birth outcomes in populations living near landfill sites. 1 They conclude that there are small excess risks of congenital anomalies and low birth weight in such populations.Although they advise caution when interpreting their results, the study is nevertheless hailed by the press and by environmental groups as evidence that living near such sites is hazardous to health. 2 The concerns felt by parents, often with no opportunity to move elsewhere, are fuelled, and perhaps on no grounds.Scientists contribute to the media generated intrigue in subtle ways.For example, the description of the paper in an editorial by McNamee and Dolk as a report "on the risks to fetuses associated with residence" when "a study of the statistical association between reported anomalies and residence" would have been more accurate and less sensationalist. 3 Health authorities are left to pick up the pieces when a story breaks, with no advance warning, about a landfill site in their area.Another interpretation of the results of Elliott et al is that this essentially negative study goes some way to reassuring other scientists who have been studying this question that it is probably safe for fetuses to develop near such sites.Any scientist who has any experience of multivariate epidemiological analysis would have to admit that such small and inconsistent excesses and deficits, even though significant, could well be attributable to inadequately adjusted social deprivation, to name but one of many important confounders.The fact that there was no increase after the landfill sites became operational, and a significant deficit of anomalies around landfill sites in Scotland, must leave even the most determined author feeling uneasy about suggesting a causal association.Epidemiological techniques used in this study are blunt instruments unlikely to detect subtle or unidentified effects.Perhaps it is time for epidemiologists to admit that their tools are inadequate to answer this question.Other scientists should take this forward by developing better techniques to identify any putative agents in the gas emissions, leachates, and soil that may be of sufficiently high concentrations to affect human health.Many of these landfill sites are unattractive and foul smelling, attracting seagulls and peppering the landscape with rubbish.More imaginative long term wastemanagement solutions are long overdue.
Abstract 9922: The Induction of YAP Expression Following Arterial Injury is Crucial for Smooth Muscle Phenotypic Modulation and Neointima Formation
Authors: Xiaobo Wang, Guoqing Hu, Yong Wang, Jiliang Zhou
Journal: Circulation (2012)

Rationale: Abnormal proliferation and migration of vascular smooth muscle cells (SMCs) are the key events in the progression of neointimal formation in response to vascular injury. Previous studies have shown that YAP is a potent oncogene promoting cell migration and proliferation, while the role of YAP in vascular diseases remain unknown. Objective: The goal of this study is to investigate the functional role of YAP in smooth muscle phenotypic modulation in vitro and in vivo. Methods and Results: In vitro in cell culture and in vivo in both mouse and rat arterial injury models YAP expression is significantly induced and correlated with the vascular SMC synthetic phenotype. YAP is also highly expressed in human carotid atherosclerotic plaque and localized in the majority of SMCs. Over-expression of YAP promotes SMC migration and proliferation while attenuating smooth muscle contractile gene expression. Conversely, knocking-down endogenous YAP in SMCs up-regulates smooth muscle gene expression but attenuates SMC proliferation and migration. Consistent with this, knocking-down YAP expression in a rat carotid balloon injury model attenuates injury-induced smooth muscle dedifferentiation and neointima formation. Furthermore, carotid artery ligation in mice with genetic deletion of YAP specifically in SMCs leads to increase smooth muscle-specific gene expression and reduction of neointima formation. Conclusion: YAP plays a novel integrative role in smooth muscle phenotypic modulation by inhibiting smooth muscle-specific gene expression while promoting smooth muscle proliferation and migration in vitro and in vivo. Blocking the induction of YAP would be a potential therapeutic approach for ameliorating vascular occlusive diseases.
Population Level Purifying Selection and Gene Expression Shape Subgenome Evolution in Maize
Authors: Saurabh D. Pophaly, Aurélien Tellier
Journal: Molecular Biology and Evolution (2015)

The maize ancestor experienced a recent whole-genome duplication (WGD) followed by gene erosion which generated two subgenomes, the dominant subgenome (maize1) experiencing fewer deletions than maize2. We take advantage of available extensive polymorphism and gene expression data in maize to study purifying selection and gene expression divergence between WGD retained paralog pairs. We first report a strong correlation in nucleotide diversity between duplicate pairs, except for upstream regions. We then show that maize1 genes are under stronger purifying selection than maize2. WGD retained genes have higher gene dosage and biased Gene Ontologies consistent with previous studies. The relative gene expression of paralogs across tissues demonstrates that 98% of duplicate pairs have either subfunctionalized in a tissuewise manner or have diverged consistently in their expression thereby preventing functional complementation. Tissuewise subfunctionalization seems to be a hallmark of transcription factors, whereas consistent repression occurs for macromolecular complexes. We show that dominant gene expression is a strong determinant of the strength of purifying selection, explaining the inferred stronger negative selection on maize1 genes. We propose a novel expression-based classification of duplicates which is more robust to explain observed polymorphism patterns than the subgenome location. Finally, upstream regions of repressed genes exhibit an enrichment in transposable elements which indicates a possible mechanism for expression divergence.
Agents that Release Histamine from Mast Cells
Authors: D Lagunoff, T W Martin, G Read
Journal: The Annual Review of Pharmacology and Toxicology (1983)

A fully differentiated mast cell, packed with 500 to 1000 granules, poised for secretion, wants only the appropriate stimulus to release the contained histamine, heparin, and hydrolytic enzymes into the connective tissue. Since the major storage site of histamine in mammalian tissues was located in the mast cell by Riley & West (1), the cell has been a major focus in the study of histamine release. The literature is abundant and there is no dearth of reviews (2-7) and books (8-10) on the mast cell and its histamine-releasing activities. We concentrate in this review on agents of more or less known structure capable of releasing histamine, and attempt to collect information on a range of agents and to evaluate succinctly the available information on their modes of action. The behavior of mast cells in response to a few agents has been studied in considerable detail, and we stress these as archetypes. The important category of IgE-mediated release has recently been reviewed in this series (11) and elsewhere (12, 13) and will not be considered here. Under usual conditions, virtually all of the histamine stored in mast cells is located in the cells' secretory granules (14, 15, 16). These granules in the rat consist of a matrix of heparin and a limited number of proteins (17) of which only two, both mast cell proteases, have been characterized substan­ tially (18, 19). Histamine and several acid hydrolases are weakly associated with the matrix by ionic bonding (20, 21); some unbound histamine may
Human Migration and Leishmaniasis—On the Move
Authors: Lola V. Stamm
Journal: JAMA Dermatology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Dermatology journal
Oxidative Modifications of Protein Tyrosyl Residues Are Increased in Plasma of Human Subjects with Interstitial Lung Disease
Authors: Subramaniam Pennathur, Anuradha Vivekanandan-Giri, Morgan L. Locy, Tejaswini Kulkarni, Degui Zhi, Lixia Zeng, Jaeman Byun, Joao A. de Andrade, Victor J. Thannickal
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Interstitial lung diseases (ILDs) are associated with oxidative stress. Plasma biomarkers that are directly linked to oxidative stress responses in this disease have not been identified. Stable oxidation products of tyrosine residues in proteins may reflect the oxidative microenvironment in the lung or a systemic inflammatory state.To determine if levels of protein tyrosine oxidation are elevated in plasma of patients with ILD compared with an age- and sex-matched healthy control cohort.Three tyrosine oxidation products (3-chlorotyrosine, 3-nitrotyrosine, and o,o'-dityrosine) were quantified by tandem mass spectrometry in cellular models, a mouse model of injury-induced fibrosis, and in plasma of healthy control subjects and patients with ILD (n = 42 in each group).Plasma levels of 3-chlorotyrosine, 3-nitrotyrosine, and o,o'-dityrosine were markedly elevated in patients with ILD compared with control subjects with receiver operating characteristic curves separating these groups of 0.872, 0.893, and 0.997, respectively. In a murine model of lung fibrosis, levels of all three oxidative tyrosine modifications were increased in plasma and lung tissue. Cellular models support a critical role for a heme peroxidase and enzymatic sources of reactive oxygen species in the generation of these oxidized products.We demonstrate an increase in oxidized tyrosine moieties within proteins in the circulating plasma of patients with ILD. These data support the potential for development of oxidative stress-related biomarkers in early diagnosis, prognostication, and/or in evaluating responsiveness to emerging therapies for ILD.
Single-copy transduction and expression of human gamma-globin in K562 erythroleukemia cells using recombinant adeno-associated virus vectors: the effect of mutations in NF-E2 and GATA-1 binding motifs within the hypersensitivity site 2 enhancer [published erratum appears in Blood 1995 Feb 1;85(3):862]
Authors: JL Miller, CE Walsh, PA Ney, RJ Samulski, AW Nienhuis
Journal: Blood (1993)
Early modulation of pro-inflammatory microglia by minocycline loaded nanoparticles confers long lasting protection after spinal cord injury
Authors: Simonetta Papa, Ilaria Caron, Eugenio Erba, Nicolò Panini, Massimiliano De Paola, Alessandro Mariani, Claudio Colombo, Raffaele Ferrari, Diego Pozzer, Elisa R. Zanier, Francesca Pischiutta, Jacopo Lucchetti, Andrea Bassi, Gianluca Valentini, Giulio Simonutti, Filippo Rossi, Davide Moscatelli, Gianluigi Forloni, Pietro Veglianese
Journal: Biomaterials (2015)
cAMP-independent effects of GLP-1 on β cells
Authors: Jelena Kolic, Patrick E. MacDonald
Journal: Journal of Clinical Investigation (2015)

The ability of glucose to stimulate insulin secretion from the pancreatic islets of Langerhans is enhanced by the intestinal hormone glucagon-like peptide 1 (GLP-1), which is secreted from the gut in response to nutrient ingestion. This action, called the incretin effect, accounts for as much as half of the postprandial insulin response and is exploited therapeutically for diabetes treatment through the use of incretin mimetic drugs and inhibitors of dipeptidyl peptidase 4, which degrades GLP-1. Despite a prominent role for incretin mimetics in diabetes treatment, several key questions remain about GLP-1–induced insulin secretion. Most studies have examined the effects of GLP-1 at concentrations several orders of magnitude higher than those found in vivo; therefore, one might question the physiological (and perhaps even pharmacological) relevance of pathways identified in these studies and whether other important mechanisms might have been obscured. In this issue of the JCI, Shigeto and colleagues demonstrate that physiological GLP-1 does indeed amplify the insulin secretory response. Intriguingly, while much of this response is PKA dependent, as might be expected, the use of picomolar GLP-1 reveals a new and important mechanism that contributes to GLP-1–induced insulin secretion.
Methylphenidate for ADHD
Authors: Mina Fazel
Journal: BMJ (2015)

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Cholinergic System in Behavior: The Search for Mechanisms of Action
Authors: R W Russell
Journal: The Annual Review of Pharmacology and Toxicology (1982)

. . . any theory of behavior is at present, and must be for some time to come, a  theory. This is because neuroanatomy and physiology have not yet developed to a point such that they yield principles which may be employed as postulates in a system of behavior theory . . .  (1). Some 40 years ago this statement by an internationally respected behavioral scientist recognized the importance of events intervening between changes in the environment, stimuli (S), and an organism'S (0) responses (R) to them. Relations between S � R are dependent upon intervening events and are influenced by them. R cannot be predicted solely on information about S; understanding the characteristics of 0 is essential, even when the simplest of Rs are involved. Although advances in concepts and technologies have enabled very significant strides in knowledge about the biochemical, electro­ physiological, and morphological properties of living organisms, there re­ main challenging questions about relations between the molecular events of these properties and the molar characteristics which constitute a fourth property of organisms, the behavioral property (2). The present review is concerned with examining speculative ideas and hypqtheses about .mechanisms of action by which the cholinergic neuro­ transmitter system may be involved in the behavior of living organisms as they cope with changes in their external and internal environments. Because most of the cholinergic receptors within the mammalian central nervous system (eNS) appear to be muscarinic (3), emphasis in this review will be