tbuckley/cabot-search huggingface dataset:
Book Review Neonatal–Perinatal Medicine: Diseases of the Fetus and Infant Seventh edition. Edited by Avroy A. Fanaroff and Richard J. Martin. 1732 pp. in two volumes, illustrated. St. Louis, Mosby, 2001. $199. 0-323-00929-8
Authors: Max Perlman
Journal: New England Journal of Medicine (2002)
Acute angle closure glaucoma associated with nebulised ipratropium bromide and salbutamol.
Authors: D. M. Humphreys
Journal: BMJ (1992)

fragments on breaking in the manner described, glasses annually attests to the limited life of most covered that the manufacturers had made a Certainly the base, the thickest part, does fragment pub glasses.commercial decision to stop marketing diazoxide when a glass breaks, but this is not so with the thin Tempering will never completely eliminate tablets.When we asked how such a decision could si'de wall, which either remains intact or breaks inj'uries due to glass, but it substantially reduces be made without consultation we were informed into pieces with "razor blade" edges.the risk of breakage.As De Grave states in the that consultation, with endocrinologists had taken Interestingly, the French claim only that their conclusion of a paper cited by Grimes, "In fact, place.We have not yet been able to locate those glass is three times stronger than a normal, stress toughening has provided an opportunity for the consulted.free glass; we dispute this figure, let alone Shepherd production of high resistance tumblers, dishes,We invite other would be users of the drug and colleagues' claim that it is six times stronger.plates, bowls, casseroles, etc, of great variety of to write to the suppliers, Allen and Hanburys Breaking a used tempered glass does not present a shapes, and colours which are now normally used Limited, Stockley Park West, Uxbridge, Middle- problem to an assailant, and the same jagged by everyone."' sex UB 11 IBT, requesting that the drug once more shards characteristic of normal glassware on J P SHEPHERD be supplied as tablets.breakage are produced.
Impairment of epithelial transport but not of barrier function in idiopathic pouchitis after ulcerative colitis
Authors: A J Kroesen
Journal: Gut (2002)

Little is known of the permeability of ileoanal pouches. Hence the aim of the present study was to determine changes in permeability and mucosal function after ileo-pouchanal anastomosis (IPAA) in patients with ulcerative colitis.Biopsies were taken from 43 patients (male:female ratio 28:15; mean age 35.2 (12.5) years) prior to colectomy (ileum prior to pouch), prior to closure of ileostomy (deviation), and after closure of ileostomy (intact pouch) in the case of pouchitis, and from 14 healthy controls. Tissues were mounted in a miniaturised Ussing chamber. Epithelial and subepithelial resistance was determined by transmural impedance analysis. Active Na(+)-glucose cotransport was measured as change in short circuit current after stepwise addition of glucose, and active Cl(-) secretion was measured after stimulation with theophylline and prostaglandin E(2).Neither epithelial resistance nor mannitol fluxes were significantly altered compared with intact controls, indicating no barrier defect in pouchitis. Subepithelial resistances of intact pouches and pouchitis were increased compared with deviation (18.2 (1.6) and 24.3 (1.5) v. 13.6 (1.0) Omegaxcm(2)) consistent with an adaptive thickening of the subepithelial layer. In contrast, active Cl(-) secretion of pouchitis tissues was reduced versus intact pouch and controls (1.4 (0.3) v. 4.3 (0.7) and 4.6 (0.7) micromol/h/cm(2)), and Na(+)-glucose cotransport of pouchitis was reduced compared with intact pouch and controls (1.8 (0.5) v. 4.2 (0.8) and 8.8 (1.3) micromol/h/cm(2)).Ileal mucosa in pouchitis and terminal ileum prior to IPAA exhibit impaired secretory and absorptive transport functions whereas the epithelial barrier function remains unchanged. This differs from findings in ulcerative colitis. Thus the hypothesis that pouchitis represents a remanifestation of ulcerative colitis has to be questioned.
Abstract C63: Structure of the Skp1‐Fbx4 complex reveals a new class of the SCF ubiquitin ligase
Authors: Yunfeng Li, Bing Hao
Journal: Cancer Research (2009)

Abstract Ubiquitin-mediated proteolysis governs the levels of many cellular proteins via a triple-enzyme cascade, involving ubiquitin-activating (E1), conjugating (E2) and ligating (E3) activities. The E3 ligases recruit both E2 and specific substrates and catalyze the final step in ubiquitination reaction. SCF complexes are the largest family of E3 ubiquitin-protein ligases that consist of Cul1, Rbx1, Skp1 and a member of the F-box protein family. F-box proteins are the substrate-recognition components of SCF; they interact with Skp1 through the N-terminal ∼40-residue F box motif, to recruit substrates through their variable C-terminal protein-protein interaction domains, including WD40 repeats (Fbxw subfamily), leucine-rich repeats (LRRs; Fbxl subfamily) and other different or unknown domains (Fbxo subfamily). Fbx4, which is the F-box protein responsible for the recognition of cell-cycle regulator cyclin D1 and telomeric DNA-binding protein Pin2, belongs to the Fbxo family that lack recognizable protein-protein interaction motif in their C-terminus. Reduced Fbx4 expression appears to be responsible, at least in part, for overexpression of cyclin D1 in human cancers. On the other hand, overexpression of Fbx4 in human cells promotes degradation of endogenous Pin2 and results in progressive telomere elongation. In order to define the fundamental structural properties of Fbx4, we have determined the crystal structure of the human Fbx4 protein in complex with Skp1 by single-wavelength anomalous dispersion method. The structure of the binary complex reveals that Skp1 and the F-box domain of Fbx4 retain the same overall fold as in other Fbxl and Fbxw structures determined, and that binding of the F box to Skp1 is very similar to that in other Skp1-F box complexes. Interestingly, the C-terminal domain of Fbx4 is projected away from Skp1 and F box, to adopt an α/β fold with a seven-stranded β sheet surrounded by seven α helices, which is distinct from LRR (in Fbxl) and WD40 (in Fbxw), reinforcing the notion that Fbx4 represents a new family of substrate-recognition subunits in SCF E3s. Moreover, mutagenesis experiments have revealed a potential substrate-binding site in Fbx4 C-terminal domain. Taken together, our structural and biochemical data provide a framework for understanding the molecular mechanism of substrate recognition by the SCFFbx4 ubiquitin ligase. Citation Information: Cancer Res 2009;69(23 Suppl):C63.
G20210A Prothrombin Gene Polymorphism and Prothrombin Activity in Subjects With or Without Angiographically Documented Coronary Artery Disease
Authors: Carla Russo, Domenico Girelli, Oliviero Olivieri, Patrizia Guarini, Franco Manzato, Francesca Pizzolo, Barbara Zaia, Alessandro Mazzucco, Roberto Corrocher
Journal: Circulation (2001)

Background —G20210A prothrombin mutation has been associated with high prothrombin levels and an increased risk of venous thrombosis. The role of this common polymorphism, as well as that of prothrombin levels, in determining the risk of arterial disease is still somewhat controversial. Methods and Results —We determined the prevalence of the G20210A mutation and prothrombin activity in 660 individuals, of whom 436 had angiographically documented severe coronary artery disease (CAD patients) and 224 had normal coronary angiography (CAD-free control subjects). Heterozygosity for the 20210A allele was found in 5.3% of the CAD patients versus 3.1% of the CAD-free subjects ( P =0.21). Similarly, no statistically significant difference was found between CAD patients with or without previous myocardial infarction (4.5% versus 5.3%, respectively; P =0.73). The genotype-phenotype correlation study showed a significant influence of the 20210A allele on prothrombin activity, with higher levels in carriers compared with noncarriers (153.2% versus 122.2%, respectively; P &lt;0.001). Prothrombin activity was significantly higher in CAD patients than in CAD-free subjects (132.8% versus 123.3%, respectively; P &lt;0.005). By multiple logistic regression, prothrombin activity in the upper tertile of the control distribution was significantly associated with CAD compared with prothrombin activity in the lower tertile (adjusted odds ratio 1.86, 95% CI 1.01 to 3.4). Conclusions —In a population with a clear-cut definition of the phenotype, the G20210A prothrombin mutation was not significantly associated, per se, with either angiographically documented CAD or myocardial infarction, whereas it significantly influenced prothrombin activity. In our population, high prothrombin activity itself was independently associated with CAD but not with the presence or absence of previous myocardial infarction.
Whistleblowers' concerns are ignored in care sector, report says
Authors: J. Wise
Journal: BMJ (2011)

Whistleblowers’ concerns in the care sector were either ignored or denied by management in 40% of cases, according to a report by Public Concern at Work—the independent whistleblowing advice line.

The charity looked at its database of over 19 000 calls received between 2002 and 2010. More than 15% of all the calls came from the care sector, the highest percentage of calls from any sector. In care, 55% of calls were about abuse. The most common concerns were about physical abuse, lack of dignity, neglect, conduct of staff, verbal abuse, and drugs administered incorrectly or not at all.

In more than half of all cases …
Author's reply to letters on death in heat waves
Authors: W. R Keatinge
Journal: BMJ (2004)

EDITOR—Although air movement alone will not always prevent heat stroke in air close to body temperature if the air is saturated1 or if sweating is impaired—for example, by drugs with anticholinergic actions2—air movement is an essential component in preventing heat stroke. Recent advice specifically related to heat stress in Britain over the next decade included not only a fan but moistening of clothing, open windows, light clothing, and avoidance of physical exertion.3

Moistening …
643 EXPRESSION OF HEPATITIS C VIRUS (HCV) RECEPTORS IN GRAFTS FROM HCV-INFECTED LIVER TRANSPLANT RECIPIENTS
Authors: G. Crespo, L. Mensa, M. Gastinger, R. Miquel, S. Perez del Pulgar, S. Emerson, R.H. Purcell, X. Forns
Journal: Journal of Hepatology (2010)
Lehrbuch der klinischen Allergie
Authors: Max Samter
Journal: JAMA (1967)

Clinical Textbook of Allergy is an offspring of Hansen's monumental Allergie . While its ancestry is apparent—particularly in chapters written by the same authors for both volumes—it has acquired a character of its own. It is far less encyclopedic, moderately dogmatic, and well adapted to the needs of practitioners.  The editors have attracted a host of capable writers and have edited lightly; they have created a cohesive and pleasant volume. One might argue whether the arrangement of the material, according to routes of exposure, is the most practical arrangement, but as in most disciplines which are in transition, we move along by trial and error. As in other textbooks on allergy, the philosophers engage in teleological debate; and there is no unanimity amongst practicing allergists about time-tested techniques. On the philosophical side the late Prausnitz and the historian Schadewaldt present allergy as a defense mechanism, although their essay ends with Kallos'
Active modulation of electrical coupling between cardiac cells of the dog. A mechanism for transient and steady state variations in conduction velocity.
Authors: M S Spach, J M Kootsey, J D Sloan
Journal: Circulation Research (1982)

Propagation velocities of action potentials were measured simultaneously along the longitudinal and transverse axes of cardiac fibers in ventricular muscle. The anisotropic distribution of propagation velocities was found to be altered transiently and in the steady state by the rate and pattern of stimulation and by ouabain. The relative amount of velocity change varied with the direction of propagation and was greatest in the direction perpendicular to the long fiber axis. None of the variables usually associated with the membrane ionic mechanism of depolarization--resting potential, Vmax, and taufoot--showed enough variation to account for the observed changes in velocity. A simplified anisotropic propagation model representing the internal current pathway as an alternating sequence of cytoplasmic and junctional resistance is presented, taking into account the larger contribution to the internal resistance made by the cell couplings in the transverse direction than in the longitudinal direction. On the basis of this model, it was concluded that the observed changes in velocity were due to changes in cell coupling. Both transient and steady state velocity changes were found to correspond to changes in the action potential duration, suggesting that there is a common factor, such as the internal calcium and/or sodium concentrations, linking the control of the action potential duration and the coupling resistance between cardiac cells.
Bone Marrow Transplantation in Man
Authors: MARTIN J. CLINE
Journal: Annals of Internal Medicine (1975)

Bone marrow transplantation is emerging as a viable therapeutic approach to a number of diseases that are usually or uniformly fatal. We review here recent experiences in bone marrow transplantation in man at UCLA and in various other institutions throughout the world. We examine marrow transplantation in immunodeficiency diseases, acute leukemia, and aplastic anemia and consider the problems of infection in the transplant recipients. The applications of tissue typing to marrow transplantation and immunologic manipulations, which may influence engraftment and graft-versus-host disease, are also reported.
INFLAMMATION IS INCREASED IN NON-CALCIFIED / MIXED LEFT MAIN CORONARY PLAQUES AND IS MODIFIABLE BY STATINS: A MULTI-CENTER PET-CT STUDY
Authors: Sharath Subramanian, Gergana Marincheva-Savcheva, Hector Medina, Pal Maurovich-Horvat, Amr Abdelbaky, Jayanthi Vijayakumar, Robin Mogg, Sudha Shankar, James Rudd, Zahi Fayad, Tom Brady, Udo Hoffmann, Ahmed Tawakol
Journal: Journal of the American College of Cardiology (2012)
Hyperinsulinemia and Autonomic Nervous System Dysfunction in Obesity
Authors: Michele Emdin, Amalia Gastaldelli, Elza Muscelli, Alberto Macerata, Andrea Natali, Stefania Camastra, Ele Ferrannini
Journal: Circulation (2001)

Because hyperinsulinemia acutely stimulates adrenergic activity, it has been postulated that chronic hyperinsulinemia may lead to enhanced sympathetic tone and cardiovascular risk.In 21 obese (body mass index, 35+/-1 kg/m(2)) and 17 lean subjects, we measured resting cardiac output (by 2-dimensional echocardiography), plasma concentrations and timed (diurnal versus nocturnal) urinary excretion of catecholamines, and 24-hour heart rate variability (by spectral analysis of ECG). In the obese versus lean subjects, cardiac output was increased by 22% (P:<0.03), and the nocturnal drop in urinary norepinephrine output was blunted (P:=0.01). Spectral power in the low-frequency range was depressed throughout 24 hours (P:<0.04). During the afternoon and early night, ie, the postprandial phase, high-frequency power was lower, heart rate was higher; and the ratio of low to high frequency, an index of sympathovagal balance, was increased in direct proportion to the degree of hyperinsulinemia independent of body mass index (partial r=0.43, P:=0.01). In 9 obese subjects who lost 10% to 18% of their body weight, cardiac output decreased and low-frequency power returned toward normal (P:<0.05).In free-living subjects with uncomplicated obesity, chronic hyperinsulinemia is associated with a high-output, low-resistance hemodynamic state, persistent baroreflex downregulation, and episodic (postprandial) sympathetic dominance. Reversal of these changes by weight loss suggests a causal role for insulin.
STUDIES ON LYMPHOID ACTIVITY
Authors: James B. Murphy, Waro Nakahara, Ernest Sturm
Journal: The Journal of Experimental Medicine (1921)

It has been shown that resistance to transplanted cancer follows stimulation of the lymphoid tissue when the stimulation is induced by either heat or small doses of x-rays. In this paper we have attempted to determine whether the degree of immunity had a quantitative relation to the amount of the stimulation. Fortunately, the two methods at our disposal give stimulation of markedly different characters. The small dose of x-rays gives a sluggish lymphoid cell reaction of short duration with a definite latent period between the treatment and the evidence of marked stimulation, while after heat a short period of depression is followed by a sharp stimulation continuing over a much longer period. The cancer inoculation into groups of mice made immediately after exposure to x-rays shows little resistance, while the inoculation made at the height of the stimulation phase shows a definite increase in the immunity. Animals inoculated with cancer immediately after the heat treatment exhibit a pronounced immunity, but not so marked as that shown when the inoculation is made at the height of the stimulation. The amount of resistance shown when the cancer inoculation is made at the height of the moderately stimulating effect following exposure to x-rays, is much less than that seen when the inoculation is made at the height of the heat effect when the degree of stimulation is much greater. When the lymphocytosis sets in after the tumor graft is established only a slight effect is noted. All these results together are taken to indicate that the degree of immunity is dependent on the amount of lymphoid stimulation existing either at the time of or following soon after the cancer inoculation.
Pelvic Hypoplasia After Radiation Therapy
Authors: Jan Stauss, Leonard P. Connolly, Laura A. Drubach, S Ted Treves
Journal: Clinical Nuclear Medicine (2003)

Skeletal scintigraphy showed a disproportionately small pelvis in a 15-year-old girl with a slipped capital femoral epiphysis and a history of therapeutic pelvic irradiation at the age of 18 months. This case illustrates the hypoplasia of flat bones and the predisposition to physeal injury that can result from radiation damage to chondroblasts of the growing skeleton.
Novel mouse model for studying role of ER-nongenomic actions in breast cancer.
Authors: R Rajhans, V Cortez, SS Nair, RR Tekmal, R Kumar, RK Vadlamudi
Journal: Cancer Research (2009)

Abstract Abstract #601 Back ground: Estradiol (E2) and estrogen receptor (ER) signaling play a key role in development and progression of breast cancer. ER signaling is complex, involves coregulatory proteins and the status of ER coregulators in tumor cells plays an important role in hormonal responsiveness and tumor progression. In addition, ER also participates in non-genomic signaling events in the cytoplasm, however the significance of non-genomic signaling in mammary tumorigenesis remain unknown. PELP1/MNAR is novel ER coregulator that participates in ER genomic and non-genomic actions. PELP1 expression is deregulated in breast tumors and in a subset of tumors PELP1 is predominantly localized in the cytoplasm. Since PELP1 cytoplamsic localization promotes excessive activation of Src and AKT pathways, we hypothesized that PELP1 mediated excessive activation of ER-nongenomic functions may play a role tumorigenesis. To test this, we have generated MMTV-PELP1cyto TG model that uniquely express PELP1 in the cytoplasm of mammary glands that mimics the pathological situation of PELP1 localization seen breast cancer.&amp;#x2028; Methods: As a means of targeting the expression of the PELP1 transgene to the mammary gland, we placed the PELP1cyto cDNA under the control of the MMTV promoter. PELP1 transgene integration was verified by PCR and expression levels by Western and IHC in each founder line. Whole-mount preparations and IHC analysis was performed using Tg and age controlled wild type littermates from different developmental stages. Total protein extracts of mammary gland were used for western blot analysis of nongenomic signaling components.&amp;#x2028; Results: Preliminary analysis of mammary gland from PELP-cyto mice showed hyperplasia, increased proliferation as analyzed by PCNA staining. Mammary tumors were observed as early as 32 weeks. No spontaneous mammary tumors were found in the wild type cohort. Pathological analysis revealed that these tumor masses represent full blown mammary adenocarcinomas. Mammary tumors showed excessive activation of nongenomic signaling including activation of Src and AKT pathways. A clear induction of aromatase expression was found in PELP1 tumors compared with the wild-type that showed no aromatase expression in the mammary gland.&amp;#x2028; Discussion: We have established and characterized a transgenic mouse model that mimics deregulated ER-nongenomic signaling. Our results suggest that PELP1 is a proto-oncogene and demonstrates its in vivo tumorigenic potential. PELP1 driven tumors are ER+ve, express aromatase, thus provide an interesting in vivo model for studying ER-mediated tumorigenesis and to study effect of local E2 on ER-mediated tumorigenesis. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 601.
Benefits and Safety of Long-Term Fenofibrate Therapy in People With Type 2 Diabetes and Renal Impairment
Authors: Ru-Dee Ting, Anthony C. Keech, Paul L. Drury, Mark W. Donoghoe, John Hedley, Alicia J. Jenkins, Timothy M.E. Davis, Seppo Lehto, David Celermajer, R. John Simes, Kushwin Rajamani, Kim Stanton
Journal: Diabetes Care (2011)

Diabetic patients with moderate renal impairment (estimated glomerular filtration rate [eGFR] 30-59 mL/min/1.73 m(2)) are at particular cardiovascular risk. Fenofibrate's safety in these patients is an issue because it may elevate plasma creatinine. Furthermore, guidelines regarding fenofibrate dosing in renal impairment vary internationally. We investigated fenofibrate's effects on cardiovascular and end-stage renal disease (ESRD) events, according to eGFR, in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study.Type 2 diabetic patients (aged 50-75 years) with eGFR ≥30 mL/min/1.73 m(2) were randomly allocated to a fixed dose of fenofibrate (200 mg daily) (n = 4,895) or placebo (n = 4,900) for 5 years. Baseline renal function (Modification of Diet in Renal Disease equation) was grouped by eGFR (30-59, 60-89, and ≥90 mL/min/1.73 m(2)). The prespecified outcome was total cardiovascular events (composite of cardiovascular death, myocardial infarction, stroke, and coronary/carotid revascularization). Serious adverse events and instances of ESRD (plasma creatinine >400 μmol/L, dialysis, renal transplant, or renal death) were recorded. Analysis was by intention to treat.Overall, fenofibrate reduced total cardiovascular events, compared with placebo (hazard ratio 0.89 [95% CI 0.80-0.99]; P = 0.035). This benefit was not statistically different across eGFR groupings (P = 0.2 for interaction) (eGFR 30-59 mL/min/1.73 m(2): 0.68 [0.47-0.97], P = 0.035; eGFR ≥90 mL/min/1.73 m(2): 0.85 [0.70-1.02], P = 0.08). ESRD rates were similar between treatment arms, without adverse safety signals of fenofibrate use in renal impairment.Patients with type 2 diabetes and moderate renal impairment benefit from long-term fenofibrate, without excess drug-related safety concerns compared with those with no or mild renal impairment. Fenofibrate treatment should not be contraindicated in moderate renal impairment, suggesting that current guidelines may be too restrictive.
Conversion of Polycythemia Vera to Chronic Di Guglielmo's Syndrome
Authors: Philip Eastman
Journal: JAMA (1968)

A patient with polycythemia vera was treated with sodium phosphate P 32. The polycythemia vera converted to chronic Di Guglielmo's syndrome, with dwarfed binucleate megakaryocytes, and the patient died of acute myeloid leukemia.