tbuckley/cabot-search huggingface dataset:
The Medical Management of Hormone-Secreting Tumors of the Pituitary
Authors: J A H Wass, G M Besser
Journal: Annual Review of Medicine (1983)

A great deal of knowledge is now available about the hypothalamic control of anterior pituitary function. This puts the medical treatment of pituitary tumors on a sound scientific footing. In addition, medical treatment may decrease the size of these tumors in some cases, as well as improve other pituitary functions.
The infarcted myocardium Simply dead tissue, or a lively target for therapeutic interventions
Authors: J Cleutjens
Journal: Cardiovascular Research (1999)

Time for primary review 32 days. 

It has been known for many years that infarction of the heart induces prominent alterations of cardiac structure. The most apparent is the scarring of the infarct. Structural changes after infarction are, however, not limited to the infarcted area, but also extend into the non-infarcted myocardium. Changes in the non-infarcted myocardium include hypertrophy of the cardiomyocytes, growth of the capillary network, and an increase in interstitial collagen.

Cardiac structure is a major determinant of function, which is depressed after myocardial infarction (MI). After infarction, both short term and long term compensatory or regulatory mechanisms are activated. Often these mechanisms also affect cardiac structure. Although activation of these compensatory mechanisms may be beneficial early after infarction, they may have adverse effects, when activation is continued for a longer time. Indeed, pharmacological treatments that block the long term activation of these compensatory mechanisms, like angiotensin converting enzyme inhibitors (ACEI) that block the renin—angiotensin system (RAS), have been shown to improve cardiac function after infarction.

Although we know that cardiac function and structure are closely related and do indeed both change after infarction, it is largely unknown what the exact structural component is that causes the reduction in cardiac function after infarction. Also it is not clear which structural component should be targeted for effective pharmacotherapy after infarction.

In this review we attempt to clarify the structural alterations after infarction. We and others have focused for many years on the potential importance of changes in the vital non-infarcted myocardium and, indeed, found several alterations in cardiac structure after infarction and effects thereon of drugs that improved cardiac function. However, recent data in animal studies and humans point to the importance of the infarct itself as a potential target for intervention. The infarct appears to be more than … 

* Corresponding author. Tel.: +31-43-387-6631; fax: +31-43-387-6613 jcl{at}lpat.azm.nl
Family-centred care: the ‘captive mother’ revisited
Authors: Linda Shields
Journal: Journal of the Royal Society of Medicine (2015)

In 1969, Sir Roy Meadow published a paper in which he described the ‘captive mother’ as one who, admitted with her child, would be stuck in a hospital ward with a child with whom she would not normally spend much of her day. He argued that school-aged children would normally spend most of their time outside the home, under the influence of people other than their parents. A busy mother, whose job as housewife and carer of other children was jeopardised by having to stay away from the home, was caused great inconvenience and trouble, and it was unrealistic and put too much unnecessary pressure on the mother (and the family) to insist that she stay with the child. While mothers’ roles have changed, the ‘captive mother’ still resonates in relation to admission of children, and in particular in relation to family-centred care. It is time to rethink family-centred care.
European protocols for the diagnosis and initial treatment of interstitial lung disease in children
Authors: Andrew Bush, Steve Cunningham, Jacques de Blic, Angelo Barbato, Annick Clement, Ralph Epaud, Meike Hengst, Nural Kiper, Andrew G Nicholson, Martin Wetzke, Deborah Snijders, Nicolaus Schwerk, Matthias Griese
Journal: Thorax (2015)

Interstitial lung disease in children (chILD) is rare, and most centres will only see a few cases/year. There are numerous possible underlying diagnoses, with specific and non-specific treatment possibilities. The chILD-EU collaboration has brought together centres from across Europe to advance understanding of these considerations, and as part of this process, has created standard operating procedures and protocols for the investigation of chILD. Where established consensus documents exist already, for example, for the performance of bronchoalveolar lavage and processing of lung biopsies, these have been adopted. This manuscript reports our proposals for a staged investigation of chILD, starting from when the condition is suspected to defining the diagnosis, using pathways dependent on the clinical condition and the degree of illness of the child. These include the performance of genetic testing, echocardiography, high-resolution CT, bronchoscopy when appropriate and the definitive investigation of lung biopsy, in order to establish a precise diagnosis. Since no randomised controlled trials of treatment have ever been performed, we also report a Delphi consensus process to try to harmonise treatment protocols such as the use of intravenous and oral corticosteroids, and add-on therapies such as hydroxychloroquine and azithromycin. The aim is not to dictate to clinicians when a therapeutic trial should be performed, but to offer the possibility to collaborators of having a unified approach when a decision to treat has been made.
Opportunities to improve antimicrobial use in paediatric intensive care units: a nationwide survey in Spain
Authors: J.R. Paño-Pardo, C. Schüffelmann-Gutiérrez, L. Escosa-García, M. Laplaza-González, F. Moreno-Ramos, R. Gómez-Gil, J.D. López, I. Jordán, C. Téllez, P. de la Oliva
Journal: Clinical Microbiology and Infection (2015)
Patient-physician discordance in global assessment in early spondyloarthritis and its change over time: the DESIR cohort
Authors: Carole Desthieux, Anna Molto, Benjamin Granger, Alain Saraux, Bruno Fautrel, Laure Gossec
Journal: Annals of the Rheumatic Diseases (2015)

To assess patient-physician discordance in global assessment of disease activity in early axial spondyloarthritis (axSpA) over time and determinants of discordance.DESIR (Devenir des Spondyloarthropathies Indifférenciées Récentes) is a French, multicentre, longitudinal cohort of patients with early inflammatory back pain suggestive of axSpA. Patient global assessment (PGA) and physician global assessment (PhGA) were rated with a 0-10 numerical rating scale, every 6 months during 2 years then at 3 years. Discordance was defined by the absolute difference |PGA-PhGA|≥3 (range 0-10) and was analysed at each visit. Determinants of (PGA-PhGA) were assessed at the visit level by a generalised linear mixed model.A total of 702 patients were analysed at baseline (401 with complete data over 3 years): mean age 33.8±8.6 years, 379 (54.0%) female, mean symptom duration 18.1±10.5 months. Mean PGA values were always higher than mean PhGA values with a mean absolute difference of 1.8 points. At baseline, 202 (28.8%) patients had discordance mainly by PGA>PhGA; over 3 years the frequency of discordance was stable (range 25.5-28.8%). Discordance was not stable at the patient level, 118 (29.4%) patients were discordant once and 88 (22.0%) twice, and only 92 (22.9%) more than twice. Determinants of (PGA-PhGA) were spine pain (β=0.24, p<0.001) and fatigue (β=0.13, p<0.001).Discordance concerned a quarter of patients with early axSpA. Over 3 years of follow-up, discordance did not decrease (no 'reference shift'). Discordance was not a stable trait, indicating discordance is not a patient characteristic.
Effect of Altered Nutritional States on Insulin Receptors
Authors: M Adamo, D LeRoith, J Simon, J Roth
Journal: Annual Review of Nutrition (1988)

The objective of this review is to provide an overview of intermittent fasting regimens, summarize the evidence on the health benefits of intermittent fasting, and discuss physiological mechanisms by which intermittent fasting might lead to improved ...Read More
Red Blood Cell Dysfunction Induced by High-Fat Diet
Authors: Dusten Unruh, Ramprasad Srinivasan, Tyler Benson, Stephen Haigh, Danielle Coyle, Neil Batra, Ryan Keil, Robert Sturm, Victor Blanco, Mary Palascak, Robert S. Franco, Wilson Tong, Tapan Chatterjee, David Y. Hui, W. Sean Davidson, Bruce J. Aronow, Theodosia Kalfa, David Manka, Abigail Peairs, Andra Blomkalns, David J. Fulton, Julia E. Brittain, Neal L. Weintraub, Vladimir Y. Bogdanov
Journal: Circulation (2015)

High-fat diet (HFD) promotes endothelial dysfunction and proinflammatory monocyte activation, which contribute to atherosclerosis in obesity. We investigated whether HFD also induces the dysfunction of red blood cells (RBCs), which serve as a reservoir for chemokines via binding to Duffy antigen receptor for chemokines (DARC).A 60% HFD for 12 weeks, which produced only minor changes in lipid profile in C57/BL6 mice, markedly augmented the levels of monocyte chemoattractant protein-1 bound to RBCs, which in turn stimulated macrophage migration through an endothelial monolayer. Levels of RBC-bound KC were also increased by HFD. These effects of HFD were abolished in DARC(-/-) mice. In RBCs from HFD-fed wild-type and DARC(-/-) mice, levels of membrane cholesterol and phosphatidylserine externalization were increased, fostering RBC-macrophage inflammatory interactions and promoting macrophage phagocytosis in vitro. When labeled ex vivo and injected into wild-type mice, RBCs from HFD-fed mice exhibited ≈3-fold increase in splenic uptake. Finally, RBCs from HFD-fed mice induced increased macrophage adhesion to the endothelium when they were incubated with isolated aortic segments, indicating endothelial activation.RBC dysfunction, analogous to endothelial dysfunction, occurs early during diet-induced obesity and may serve as a mediator of atherosclerosis. These findings may have implications for the pathogenesis of atherosclerosis in obesity, a worldwide epidemic.
Cytomegalovirus (CMV) in the Compromised Host(s)
Authors: R F Betts, J B Hanshaw
Journal: Annual Review of Medicine (1977)

Cytomegalovirus (CMV) in the Compromised Host(s), Page 1 of 1 < Previous page | Next page > /docserver/preview/fulltext/med/28/1/annurev.me.28.020177.000535-1.gif
Mitomycin C skin toxicity studies in mice: reduced ulceration and altered pharmacokinetics with topical dimethyl sulfoxide.
Authors: R T Dorr, M J Soble, J D Liddil, J H Keller
Journal: Journal of Clinical Oncology (1986)

A series of toxicologic and pharmacokinetic studies were performed in BALB/c mice administered intradermal (ID) mitomycin C (MMC) at doses of .015 to 0.25 mg. Dose-dependent skin ulcers were produced at clinically relevant MMC dose levels of .05 and .075 mg (3.6 to 10.7 mg/m2). These doses produced peak ulcers of 0.15 to 0.22 cm2, respectively, one to five days after injection. The integrated ulcer area X time values (area under the curve [AUC] ulceration) were 0.89 and 3.11 cm2 X d. A large number of local pharmacologic adjuvants were found to be ineffective at reducing MMC ulceration after proximal ID injection. These included diphenhydramine, catalase, heparin, hyaluronidase, hydrocortisone, cysteine, N-acetylcysteine, lidocaine, vitamin E, and superoxide dismutase. Also, neither topical heating nor cooling of skin reduced MMC ulcerations. In contrast, a single topical application of a 100% dimethyl sulfoxide (DMSO) solution completely prevented 0.025 mg MMC-induced skin ulceration and significantly reduced .075 mg MMC ulceration (P less than .05 by multiple range tests). Topical DMSO also altered the disposition of ID MMC in mouse skin but not in plasma. Unexpectedly, the DMSO applications slowed MMC elimination from the skin. DMSO significantly increased the AUC for MMC in skin from 0.89 to 2.25 ng/h/mL of tissue (P less than .05). DMSO did not alter the degree of protein binding in skin tissue nor the in vitro chemical stability of MMC in skin tissue homogenates. These results show that experimental MMC-induced skin ulcers in mice can be ameliorated with an immediate application of topical DMSO. This effect is not due to enhanced systemic drug uptake, but may be due to reduced reactivity of MMC with target cellular nucleophiles.
Preterm labour: summary of NICE guidance
Authors: Grammati Sarri, Melanie Davies, Maryam Gholitabar, Jane E Norman
Journal: BMJ (2015)

#### What you need to know Preterm birth is the single biggest cause of neonatal mortality and morbidity in the UK, affecting over 52 000 babies (around 7.3% of live births) in England and Wales in 2012.1 About 75% of women delivering preterm do so after preterm labour,2 which is sometimes preceded by preterm prelabour membrane rupture.2 A "cause" for preterm labour is not always found, but it may be associated with infection. In other cases, preterm birth may result from elective delivery. Babies born preterm have high rates of mortality, with the risk of mortality being inversely proportional to gestational age at birth.3 Babies who survive have increased rates of disability.3 This article summarises the most recent recommendations on the prevention, diagnosis, and management of preterm labour from the National Institute for Health and Care Excellence (NICE).4 #### What's new in this guidance
Atlas of Human Cross-Sectional Anatomy
Journal: Thorax (1996)

Lung disease induced by drug addictionIn their editorial on the pulmonary con- sequences ofillicit drug use (November 1995; 50:1125-7) Benson and Bentley draw at- tention to barotrauma as a complication of cocaine inhalation.Pneumothorax, pneumomediastinum, and pneumopericardium have also been described, however, in association with the use of marijuana,12 a drug that is more widely used in England and Australia than cocaine.The mechanism of injury is thought to be by coughing while breath- holding in inspiration, or by performance of a Valsalva manoeuvre.The latter has been recognised as a cause of spontaneous pneumo- mediastinum since the 17th century.3We have found it rewarding to seek a history of illicit drug use in young adult patients presenting with spontaneous pneumothorax.
Sleepwalking Into Infertility: The Need for a Public Health Approach Toward Advanced Maternal Age
Authors: Marie-Eve Lemoine, Vardit Ravitsky
Journal: The American Journal of Bioethics (2015)

In Western countries today, a growing number of women delay motherhood until their late 30s and even 40s, as they invest time in pursuing education and career goals before starting a family. This social trend results from greater gender equality and expanded opportunities for women and is influenced by the availability of contraception and assisted reproductive technologies (ART). However, advanced maternal age is associated with increased health risks, including infertility. While individual medical solutions such as ART and elective egg freezing can promote reproductive autonomy, they entail significant risks and limitations. We thus argue that women should be better informed regarding the risks of advanced maternal age and ART, and that these individual solutions need to be supplemented by a public health approach, including policy measures that provide women with the opportunity to start a family earlier in life without sacrificing personal career goals.
Cachectin: Its Impact on Metabolism and Nutritional Status
Authors: L L Moldawer, S F Lowry, A Cerami
Journal: Annual Review of Nutrition (1988)

The objective of this review is to provide an overview of intermittent fasting regimens, summarize the evidence on the health benefits of intermittent fasting, and discuss physiological mechanisms by which intermittent fasting might lead to improved ...Read More
Conflicts of interest in medical publishing: it's all about trustworthiness
Authors: P. Gjersvik
Journal: British Journal of Dermatology (2015)

Openness and transparency are vital for the trustworthiness of scientific journals and researchers. The term 'conflict of interest' should be defined broadly. Both financial and nonfinancial conflicts of interest may influence the reporting and evaluation of medical research. This should not hinder scientific cooperation between academic and industry-affiliated researchers. In the name of transparency, scientific journals should disclose the identity of a paper's peer reviewers and publish more information on the authors.
Brain metastases and testicular tumors: need for aggressive therapy.
Authors: S G Lester, J G Morphis, N B Hornback, S D Williams, L H Einhorn
Journal: Journal of Clinical Oncology (1984)

In late 1974, the combination of cisplatin, vinblastine, and bleomycin (PVB) became the standard chemotherapeutic regimen for treatment of disseminated nonseminomatous germ cell testicular tumors (NSGCT) at Indiana University Hospital. A retrospective analysis of the treatment records of all patients with brain metastases from NSGCTs treated at the Indiana University Radiation Oncology Department from 1975 through 1982 was undertaken. These 22 patients were divided into four groups. Group 1 (n = 5) consisted of those patients who presented initially with brain metastases and had no prior systemic treatment. Group 2 (n = 4) were referred to Indiana University after failing systemic therapy other than PVB chemotherapy. Group 3 (n = 5) consisted of those patients who after achieving a complete response with PVB developed a relapse confined to the brain. Group 4 (n = 8) consisted of those patients who were initially treated with PVB and eventually developed progressive disease and brain metastases. The survival by group is 80%, 0%, 60%, and 0%, respectively, with the overall survival for the entire group being 31.8%. All patients currently alive have a range of follow-up of 22 to 96 months from diagnosis and 12 to 83 months from whole brain irradiation (WBRT). Group 1 was treated with PVB +/- doxorubicin plus WBRT. Group 3 was treated with surgical excision, when feasible, followed by WBRT and platinum-containing chemotherapy. Group 2 and 4 were usually treated with palliative intent WBRT. The CNS is a site of sanctuary from PVB. Patients with brain metastases who may achieve a complete response should be treated with curative intent and receive aggressive WBRT (5,000 rad/25 fractions) with concomitant chemotherapy.
Oral cladribine as primary therapy for patients with B-cell chronic lymphocytic leukemia.
Authors: G Juliusson, I Christiansen, M M Hansen, S Johnson, E Kimby, A Elmhorn-Rosenborg, J Liliemark
Journal: Journal of Clinical Oncology (1996)

PURPOSE Purine analogs have wide potential indications in the treatment of hematologic malignancies, but intravenous administration has been required. We previously established that the oral bioavailability of cladribine is 50%. Our aim was to evaluate the efficacy and toxicity of oral cladribine to previously untreated patients with chronic lymphocytic leukemia (CLL). PATIENTS AND METHODS Sixty-three patients with symptomatic but previously untreated CLL received cladribine solution 10 mg/m2/d orally for 5 consecutive days in monthly courses. RESULTS Complete remission (CR) was achieved in 24 patients (38%), and 23 patients (37%) had a partial response (PR). Most patients, including those in whom there was no remission (NR) achieved normal blood lymphocyte counts. Failure to meet response criteria was mostly due to thrombocytopenia. The median response duration was not reached at 2 years. The median survival time among 13 deceased patients was 322 days, whereas the median observation time of surviving patients is 760 days. The overall survival rate at 2 years is 82%. Response rate was associated with clinical stage. Grade III to IV infectious toxicity occurred in one third of patients. CONCLUSION Orally administered cladribine is an effective and feasible therapy for CLL, and produces durable remissions in three quarters of the patients. However, significant toxicity may occur and further studies are required to assess long-term effects and quality-of-life aspects.
Domestic mite sensitization in German patients—Including Chortoglyphus arcuatus and Gohieria fusca
Authors: H. Müsken, J.T. Franz, U. Schlensog, A. Heutelbeck, T. Schulz, C. Junghans, P. Tucholla, P. Hallier, K.C. Bergmann
Journal: Journal of Allergy and Clinical Immunology (2003)
Biology of Myasthenia Gravis
Authors: J Lindstrom, P Dau
Journal: The Annual Review of Pharmacology and Toxicology (1980)

The chronic muscular weakness and fatigability characteristic of myas­ thenia gravis (MG) results from defective neuromuscular transmission caused by an autoimmune response to acetylcholine receptors (AChR) in skeletal muscle. The initial direct evidence for this long held suspicion (1) was the observation that rabbits immunized with purified AChR developed MG-like weakness (2). Subsequent studies of experimental autoimmune myasthenia gravis (EAMG) have substantially illuminated the complex pathological mechanisms by which the aberrant autoimmune response to AChR in MG impairs neuromuscular transmission. Neither the cause of the autoimmune response in MG nor a cure is known. However, knowledge of the pathological mechanisms is being used to improve both diagnosis and therapy. Because it is the binding of antibodies to parts of the AChR molecule that begins the pathology at the endplate, and because properties of the AChR molecule are as critical as properties of the immune system in determining the ultimate effects of this antibody binding, we first briefly review AChR structure, function, and metabolism. The structure of AChR from electric organs is best understood, the metabolism of AChR in noninnervated mus­ cle cells is best understood, and AChR function has been best studied in intact muscle cells. We take the point of view that AChR structure, metabo-
Molecular and Ionic Mimicry of Toxic Metals
Authors: T W Clarkson
Journal: The Annual Review of Pharmacology and Toxicology (1993)

The landmark review by Wetterhahn-Jennette (1) laid the foundation for this review. A recent review on mechanisms of metal transport (2) has also been an important literature resource. Wetterhahn-Jennette pointed out the structural similarities of many oxyanions and explained the toxicities of several metals in terms of oxyanions competing with endogenous oxyanions, phosphate, and sulfate in transport, enzymatic and receptor-mediated processes. She also introduced the term   to describe the competition between many divalent endogenous and toxic metal ions in biological systems, such competition giving a mechanistic insight into the toxic action of certain metals. The term   has been mainly confined to the field of immunology. In the context of this review, the term roolecular mimicry is restricted to those examples in which a toxic metal forms a complex with an endogenous ligand such that the resulting compound mimics the behavior of a normal substrate. An example to be discussed in some detail is the reaction of the methylmercury cation with the amino acid cysteine to form a compound that mimics the amino acid methionine and thus gains entry into the cell on an amino acid carrier. This review updates the literature on both oxyanion and divalent metal competition and introduces a new extension of molecular and ionic mimicry to complexes formed by mercury that are structurally similar to and biologi­ cally mimic endogenous molecules. This review is not intended to be an exhaustive account of all the literature but gives examples that illustrate the role of molecular and ionic mimicry in the action of the toxic metals.