tbuckley/cabot-search huggingface dataset:
Is there an association between tendinopathy and diabetes mellitus? A systematic review with meta-analysis
Authors: Tom A Ranger, Andrea M Y Wong, Jill L Cook, Jamie E Gaida
Journal: British Journal of Sports Medicine (2015)

Background Musculoskeletal symptoms limit adherence to exercise interventions for individuals with type 2 diabetes. People with diabetes may be susceptible to tendinopathy due to chronically elevated blood glucose levels. Therefore, we aimed to investigate this potential association by systematically reviewing and meta-analysing case–control, cross-sectional, and studies that considered both of these conditions. Methods Nine medical databases and hand searching methods were used without year limits to identify all relevant English language articles that considered diabetes and tendinopathy. Two authors applied exclusion criteria and one author extracted data with verification by a second author. Meta-analysis was conducted using a random effects model. Results were expressed as odds ratio (OR), mean difference or standardised mean difference with a confidence intervals (95% CI). Heterogeneity was assessed by I 2 . Findings 31 studies were included in the final analysis of which 26 recruited people with diabetes and five recruited people with tendinopathy. Tendinopathy was more prevalent in people with diabetes (17 studies, OR 3·67, 95% CI 2·71 to 4·97), diabetes was more prevalent in people with tendinopathy (5 studies, OR 1·28, 95% CI 1·10 to 1·49), people with diabetes and tendinopathy had a longer duration of diabetes than people with diabetes only (6 studies, mean difference 5·26 years, 95% CI 4·15 to 6·36) and people with diabetes had thicker tendons than controls (9 studies, standardised mean difference 0·79 95% CI 0·47 to 1·12). Interpretation These findings provide strong evidence that diabetes is associated with higher risk of tendinopathy. This is clinically relevant as tendinopathy may affect adherence to exercise interventions for diabetes.
Intracardiac Thrombi and Systemic Thromboembolism: Detection, Incidence, and Treatment
Authors: J H Chesebro, M Ezekowitz, L Badimon, V Fuster
Journal: Annual Review of Medicine (1985)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Sustained Activation of Wnt/β-Catenin Signaling Drives AKI to CKD Progression
Authors: Liangxiang Xiao, Dong Zhou, Roderick J. Tan, Haiyan Fu, Lili Zhou, Fan Fan Hou, Youhua Liu
Journal: Journal of the American Society of Nephrology (2015)

AKI is increasingly recognized as a major risk factor for progression to CKD. However, the factors governing AKI to CKD progression are poorly understood. In this study, we investigated this issue using moderate (20 minutes) and severe (30 minutes) ischemia/reperfusion injury (IRI) in mice. Moderate IRI led to acute kidney failure and transient Wnt/ β -catenin activation, which was followed by the restoration of kidney morphology and function. However, severe IRI resulted in sustained and exaggerated Wnt/ β -catenin activation, which was accompanied by development of renal fibrotic lesions characterized by interstitial myofibroblast activation and excessive extracellular matrix deposition. To assess the role of sustained Wnt/ β -catenin signaling in mediating AKI to CKD progression, we manipulated this signaling by overexpression of Wnt ligand or pharmacologic inhibition of β -catenin. In vivo , overexpression of Wnt1 at 5 days after IRI induced β -catenin activation and accelerated AKI to CKD progression. Conversely, blockade of Wnt/ β -catenin by small molecule inhibitor ICG-001 at this point hindered AKI to CKD progression. In vitro , Wnt ligands induced renal interstitial fibroblast activation and promoted fibronectin expression. However, activated fibroblasts readily reverted to a quiescent phenotype after Wnt ligands were removed, suggesting that fibroblast activation requires persistent Wnt signaling. These results indicate that sustained, but not transient, activation of Wnt/ β -catenin signaling has a decisive role in driving AKI to CKD progression.
Emergence of Nonobstructive Coronary Artery Disease
Authors: Carl J. Pepine, Keith C. Ferdinand, Leslee J. Shaw, Kelly Ann Light-McGroary, Rashmee U. Shah, Martha Gulati, Claire Duvernoy, Mary Norine Walsh, C. Noel Bairey Merz
Journal: Journal of the American College of Cardiology (2015)

Recognition of ischemic heart disease (IHD) is often delayed or deferred in women. Thus, many at risk for adverse outcomes are not provided specific diagnostic, preventive, and/or treatment strategies. This lack of recognition is related to sex-specific IHD pathophysiology that differs from traditional models using data from men with flow-limiting coronary artery disease (CAD) obstructions. Symptomatic women are less likely to have obstructive CAD than men with similar symptoms, and tend to have coronary microvascular dysfunction, plaque erosion, and thrombus formation. Emerging data document that more extensive, nonobstructive CAD involvement, hypertension, and diabetes are associated with major adverse events similar to those with obstructive CAD. A central emerging paradigm is the concept of nonobstructive CAD as a cause of IHD and related adverse outcomes among women. This position paper summarizes currently available knowledge and gaps in that knowledge, and recommends management options that could be useful until additional evidence emerges.
Restenosis After Coronary Balloon Angioplasty
Authors: R A Lange, E D Flores, L D Hillis
Journal: Annual Review of Medicine (1991)

A recurrence of stenosis (restenosis) following successful coronary angioplasty continues to be a frequent problem limiting the long-term efficacy of the procedure. An overexuberant reparative response to the arterial injury induced by balloon dilatation leads to intimal hyperplasia, the major mechanism responsible for restenosis. Although none has yet been proven effective, agents designed to prevent this hyperplastic response are under investigation.
Recent Advances in Malarial Immunity
Authors: D W Taylor, W A Siddiqui
Journal: Annual Review of Medicine (1982)

Malaria is one of the world's most severe health problems for inhabitants of tropical and subtropical areas. The morbidity and mortality resulting from this infectious disease severely hamper economic progress in these regions. Between 1956 and 1962, a large-scale malaria eradication program was undertaken by the World Health Organization (1). Application of malaria control methods in certain countries of Asia, North Africa, Central and South America, and parts of Europe reduced the prevalence of malaria from an estimated 300 million cases in 1940 to 90 million cases in 1975. In addition, the eradication program has eliminated malaria from large parts of the Americas and Australia, and almost completely from Europe and the Asiatic portions of the USSR. The overwhelming success and impact of this control program was so impressive that by 1961 scientific research and training of workers in the field of malaria had rapidly declined. Since then, however, the initial momentum of success has been replaced by a gradual, unrelenting battle with the disease that has now undergone a sudden resur­ gence in many parts of the world, especially in Asia and Africa.
Biosynthesis and Function of Enzymes with Covalently Bound Flavin
Authors: K. F. Decker
Journal: Annual Review of Nutrition (1993)

Biosynthesis and Function of Enzymes with Covalently Bound Flavin, Page 1 of 1 < Previous page | Next page > /docserver/preview/fulltext/nutr/13/1/annurev.nu.13.070193.000313-1.gif
Pathogenesis of Acute Pancreatitis
Authors: Michael L. Steer, Jacopo Meldolesi
Journal: Annual Review of Medicine (1988)

Recent studies using experimental models of acute pancreatitis suggest that events blocking evoked secretion of digestive enzymes from acinar cells may play an important role in the pathogenesis of this disease. Under these conditions, digestive enzymes become co-localized with lysosomal hydrolases within large intracellular vacuoles, where activation of trypsin by the lysosomal enzyme cathepsin B could initiate the cascade activation of the other pancreatic zymogens. Development of acute pancreatitis might, therefore, be initiated by events occurring within acinar cells rather than in the ductal system or the interstitium of the gland.
Macromolecular Adducts: Biomarkers for Toxicity and Carcinogenesis
Authors: L W Chang, S M Hsia, P C Chan, L L Hsieh
Journal: The Annual Review of Pharmacology and Toxicology (1994)

Due to the massive data sets available for drug candidates, modern drug discovery has advanced to the big data era. Central to this shift is the development of artificial intelligence approaches to implementing innovative modeling based on the dynamic, ...Read More
Genital Warts, Papillomaviruses, and Genital Malignancies
Authors: K V Shah, J Buscema
Journal: Annual Review of Medicine (1988)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
WITHDRAWN: Modified delivery of axitinib loaded nanohybrid liposomal nanoparticles for hypoxic tumor growth
Authors: Ju Yeon Choi, Ramasamya Thiruganesh, Tran Tuan Hiep, Raj Kumar Thapa, Dong Shik Kim, Han-Gon Choi, Jee-Heon Jeong, Chul Soon Yong, Jong Oh Kim
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.
DRUGS AND PORPHYRIN METABOLISM
Authors: M. WEATHERALL
Journal: Pharmacological Reviews (1954)

One or two ways in which porphyrin metabolism might be disturbed, such as disturbances of the formation and breakdown of myoglobin or of the cytochromes, have not been mentioned, because there is little or no evidence whether drugs affect them. Most of the known disturbances of porphyrin metabolism involve either haemopoiesis or liver function. Lead poisoning is clearly in the first category, poisoning by Sedormid and other substances containing allyl groups in the second. The mild porphyrinuria produced by aromatic amines and nitro-compounds may be due to abnormal haemoglobin breakdown, but seems more likely to be comparable to the effect of lead. The dyshaemopoietic porphyrinurias can be conceived simply as due to blockage at one or more stages of the normal synthesis of iron-protoporphyrin, so that intermediaries or products of diverted metabolism such as coproporphyrin appear in excess. Details about the stage of blockage have still to be worked out. The porphyrinurias associated with changes in the liver are less comprehensible. They may involve abnormal formation or destruction of iron-porphyrin compounds which are synthesized by a mechanism different from the haemopoietic one, and so susceptible to damage by different agents; or they may arise through some as yet undetermined influence of the liver on haemopoiesis, for example, in synthesizing, excreting or failing to excrete some essential intermediary metabolite. The particular porphyrins which appear in the urine are not diagnostic of the site of the disturbance; porphobilinogen and uroporphyrin appear after Sedormid and after the combination of phenylhydrazine, lead and light and coproporphyrin appears both when the liver is diseased, and after interference with haemopoiesis by lead. The isomeric type is also not diagnostic. There is a connexion between coproporphyrin I excretion and increased haemopoiesis and coproporphyrin III excretion and obstructed haemopoiesis, but with the uroporphyrinurias and in liver disease there is a notable variability in the isomer type in any particular condition. The most promising developments now appear to be in the study of isolated tissue systems or homogenates, in the further investigation of precursors and the conditions under which they form free porphyrins, and in examining in more detail the actions of drugs on the tissue porphyrins as well as on the porphyrins excreted by experimental animals.
Serology, virulence, antimicrobial susceptibility and molecular characteristics of clinical Vibrio parahaemolyticus strains circulating in southeastern China from 2009 to 2013
Authors: Y. Chen, X. Chen, F. Yu, M. Wu, R. Wang, S. Zheng, D. Han, Q. Yang, H. Kong, F. Zhou, J. Zhu, H. Yao, W. Zhou, L. Li
Journal: Clinical Microbiology and Infection (2015)
Abstract 2436: Understanding the molecular mechanism of targeted kinase inhibitor resistance mediated by the FGFR1 gatekeeper mutation
Authors: Christal D. Sohl, Molly Ryan, BeiBei Luo, Kathleen Frey, Karen S. Anderson
Journal: Cancer Research (2015)

Abstract Human fibroblast growth factor receptors (FGFRs) can serve as drivers of oncogenesis and are a target of several inhibitors in clinical trials. Unfortunately, resistance severely hampers the long-term success of tyrosine kinase inhibitors (TKIs), with mutations at the gatekeeper residue often serving as an early means of resistance to cancer therapy, resulting in tumor progression. Here we show the first crystal structures of the FGFR1 gatekeeper mutation, V561M FGFR1, and use kinetic and structural methods to explore the mechanisms of the catalytic activation we observe for this mutation. We show that while the FGFR1 gatekeeper mutation confers resistance to two inhibitors currently in clinical trials, the extent of change in efficacy differ, indicating two unique resistance profiles. We show that some affinity for one inhibitor is maintained by the V561M mutation due to a flexible linker that allows multiple binding conformations. This is the first example showing the same inhibitor binding in unique ways to the WT and gatekeeper mutant forms of FGFR, highlighting some regions of drug design flexibility both within the binding pocket and in the linker of the inhibitor. Identifying this flexibility in the context of the structural features of an active conformation of V561M FGFR1, the form most kinase inhibitors target, will provide critical insights for designing future inhibitors effective against the FGFR gatekeeper mutations. Citation Format: Christal D. Sohl, Molly Ryan, BeiBei Luo, Kathleen Frey, Karen S. Anderson. Understanding the molecular mechanism of targeted kinase inhibitor resistance mediated by the FGFR1 gatekeeper mutation. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2436. doi:10.1158/1538-7445.AM2015-2436
Molecular Mechanism of the Two-Component Suicidal Weapon of<i>Neocapritermes taracua</i>Old Workers
Authors: Thomas Bourguignon, Jan Šobotník, Jana Brabcová, David Sillam-Dussès, Aleš Buček, Jana Krasulová, Blahoslava Vytisková, Zuzana Demianová, Michael Mareš, Yves Roisin, Heiko Vogel
Journal: Molecular Biology and Evolution (2015)

In termites, as in many social insects, some individuals specialize in colony defense, developing diverse weaponry. As workers of the termite Neocapritermes taracua (Termitidae: Termitinae) age, their efficiency to perform general tasks decreases, while they accumulate defensive secretions and increase their readiness to fight. This defensive mechanism involves self-sacrifice through body rupture during which an enzyme, stored as blue crystals in dorsal pouches, converts precursors produced by the labial glands into highly toxic compounds. Here, we identify both components of this activated defense system and describe the molecular basis responsible for the toxicity of N. taracua worker autothysis. The blue crystals are formed almost exclusively by a specific protein named BP76. By matching N. taracua transcriptome databases with amino acid sequences, we identified BP76 to be a laccase. Following autothysis, the series of hydroquinone precursors produced by labial glands get mixed with BP76, resulting in the conversion of relatively harmless hydroquinones into toxic benzoquinone analogues. Neocapritermes taracua workers therefore rely on a two-component activated defense system, consisting of two separately stored secretions that can react only after suicidal body rupture, which produces a sticky and toxic cocktail harmful to opponents.
Low-dose versus high-dose fish oil for pain reduction and function improvement in patients with knee osteoarthritis
Authors: Yan Chen, Yong-Can Huang, William W Lu
Journal: Annals of the Rheumatic Diseases (2015)

Osteoarthritis (OA) is one of the leading generators of musculoskeletal pain and the main cause of disability.1 It has been considered an inflammatory disease with low grade inflammation affecting the synovium, cartilage and subchondral bone.2 To date, there is no disease-modifying OA drug.3 A few studies have evaluated the efficacy of fish oil in the treatment of OA;4 nevertheless, the effectiveness and precise benefits of fish oil intake in patients with OA are still far from well understood. We read with deep interest a recent article published in this journal by Hill et al , who found significant improvement of OA pain and function after treatment by fish oil, and suggested that the low-dose fish oil group had much better improvement in pain and function at 2 years in comparison to the high-dose one.5 The authors are congratulated for the excellent findings and we really appreciate the work performed by them; nevertheless, some worthwhile issues need …
Alcohol stimulates macrophage activation through caspase-dependent hepatocyte derived release of CD40L containing extracellular vesicles
Authors: Vikas K. Verma, Haiyang Li, Ruisi Wang, Petra Hirsova, Malek Mushref, Yaming Liu, Sheng Cao, Patricia C. Contreras, Harmeet Malhi, Patrick S. Kamath, Gregory J. Gores, Vijay H. Shah
Journal: Journal of Hepatology (2015)
Optimal Dosing for Targeted Therapies in Oncology: Drug Development Cases Leading by Example
Authors: Jeffrey R. Sachs, Kapil Mayawala, Satvik Gadamsetty, Soonmo Peter Kang, Dinesh P. de Alwis
Journal: Clinical Cancer Research (2015)

Abstract One of the key objectives of oncology first-in-human trials has often been to establish the maximum tolerated dose (MTD). However, targeted therapies might not exhibit dose-limiting toxicities (DLT) at doses significantly higher than sufficiently active doses, and there is frequently a limited ability to objectively quantify adverse events. Thus, while MTD-based determination of recommended phase II dose may have yielded appropriate dosing for some cytotoxics, targeted therapeutics (including monoclonal antibodies and/or immunotherapies) sometimes need alternative or complementary strategies to help identify dose ranges for a randomized dose-ranging study. One complementary strategy is to define a biologically efficacious dose (BED) using an “effect marker.” An effect marker could be a target engagement, pharmacodynamic, or disease progression marker (change in tumor size for solid tumors or bone marrow blast count for some hematologic tumors). Although the concept of BED has been discussed extensively, we review specific examples in which the approach influenced oncology clinical development. Data extracted from the literature and the examples support improving dose selection strategies to benefit patients, providers, and the biopharmaceutical industry. Although the examples illustrate key contributions of effect markers in dose selection, no one-size-fits-all approach to dosing can be justified. Higher-than-optimal dosing can increase toxicity in later trials (and in clinical use), which can have a negative impact on efficacy (via lower adherence or direct sequelae of toxicities). Proper dose selection in oncology should follow a multifactorial decision process leading to a randomized, dose-ranging study instead of a single phase II dose. Clin Cancer Res; 22(6); 1318–24. ©2015 AACR.
Successful Treatment in a Patient with Neuroendocrine Tumor Who Developed Everolimus-Associated Interstitial Pneumonia
Authors: Satoshi Tamaru, Toshiro Mizuno, Akihiko Sawaki, Keiki Nagaharu, Haruna Sakaguchi, Hiroyasu Oda, Mikiya Ishihara, Yumiko Sugawara, Yoshiki Yamashita, Naoyuki Katayama
Journal: Annals of Oncology (2014)
Vasopressin Function in the Syndrome of Inappropriate Antidiuresis
Authors: R Zerbe, L Stropes, G Robertson
Journal: Annual Review of Medicine (1980)

In 1938 Winkler & Crankshaw (1) described a group of patients who had hypochloremia and excessive urinary excretion of chloride despite appar­ ently normal kidneys and adrenal glands at autopsy. Subsequently other investigators reported patients with hyponatremia and urinary sodium wasting (2-5). In 1957, Schwartz et al (6) described similar findings in association with impaired urinary dilution in two patients with broncho­ genic carcinoma. They concluded from indirect evidence that the syndrome was due to inappropriate secretion of the antidiuretic hormone, arginine vasopressin. It is now recognized that the syndrome of inappropriate anti­ diuresis (SIAD) occurs in a great variety of malignant and nonmalignant diseases, most commonly those involving the central nervous system and lungs (Table 1) (7-51). The pathophysiology of this syndrome has been well delineated and reviewed elsewhere (7,8). Briefly, Schwartz and Bartter originally deduced from earlier studies of the effect of exogenous antidiuretic hormone in normal humans (52) that the syndrome resulted from inappropriate secre­ tion of antidiuretic hormone in the face of excessive water intake. This constellation of defects results in hyponatremia due to dilution and exces­ sive urinary excretion of sodium caused by the water retention. Hence, the cardinal features of SIAD as defined by Bartter & Schwartz (7) are (a) hyponatremia with corresponding hypoosmolality of the plasma, (b) osmo­ lality of the urine greater than that appropriate for concomitant plasma
Fistulizing Epstein-Barr virus-positive plasmablastic lymphoma in an HIV-positive man
Authors: J. Rangel, R. Novoa, C. Morrison, D. Frank, C. Kovarik
Journal: British Journal of Dermatology (2015)

Plasmablastic lymphoma (PBL) is an unusual subtype of non‐Hodgkin lymphoma recently classified as a diffuse immunoblastic lymphoma with a plasma‐cell immunophenotype. Originally described in the oral cavity of HIV‐positive patients, it has also been recognized to occur rarely at other sites. We describe a previously unreported fistulizing presentation of Epstein–Barr virus (EBV)‐positive PBL, reviewing its association with HIV‐1 infection and its importance as an AIDS‐defining malignancy.
P-346 Non-interventional study in elderly patients with metastatic colorectal cancer treated with first line bevacizumab combined to chemotherapy in real life: The CASSIOPEE Study - Interim analysis on patients' characteristics
Authors: E. François, S. Kim, G. Deplanque, D. Smith, S. Gourgou, F. Rollot-Trad, S. Gally, A. Berthier, L. Mineur
Journal: Annals of Oncology (2015)
Role of Immune Therapies for Myeloma
Authors: Jacalyn Rosenblatt, David Avigan
Journal: Journal of the National Comprehensive Cancer Network (2015)

Immune therapy has emerged as a promising area of cancer therapeutics based on its potential for tumor selectivity and targeting of chemotherapy-resistant clones. Allogeneic transplantation produces durable remissions in a subset of patients, albeit at the cost of graft- versus-host disease. Recent years have witnessed efforts to induce more selective immune responses via dendritic cell vaccines, autologous and engineered T-cell therapy, and immune checkpoint blockade. Optimizing these immunotherapeutic approaches, understanding how to best use them in combination, and determining how to integrate them with standard anti-myeloma therapy could provide the potential to alter the natural history of this disease.