tbuckley/cabot-search huggingface dataset:
Chronic Hypoxia Increases β <sub>1</sub> -Adrenergic Receptor mRNA and Density but Not Signaling in Neonatal Rat Cardiac Myocytes
Authors: Hong-Tai Li, Norman Y. Honbo, Joel S. Karliner
Journal: Circulation (1996)

Background It is well recognized that the β-adrenergic receptor–adenylylcyclase system is altered during myocardial ischemia/hypoxia. However, there are no data regarding either regulation of β-adrenergic receptors, particularly at the mRNA level, or adenylylcyclase activity in isolated cardiac myocytes exposed to chronic hypoxia. Methods and Results In a chronic hypoxia model in which neonatal rat ventricular myocytes were exposed to a 1% O 2 environment for 72 hours, we investigated (1) β 1 -mRNA and receptor expression and adenylylcyclase activity and (2) β 1 -mRNA and receptor downregulation and adenylylcyclase desensitization induced by prolonged norepinephrine incubation. We found that hypoxia for 72 hours increased myocardial membrane β 1 -adrenergic receptor density by 44%. This increase was not associated with a corresponding decrease in cytosolic β 1 -adrenergic receptors. RNase protection assays demonstrated that hypoxia increased the steady-state levels of β 1 -mRNA by 109%. Adenylylcyclase activity stimulated by isoproterenol, sodium fluoride, guanyl-5′-imidodiphosphate, and forskolin in hypoxic membranes was not altered compared with normoxic controls. Hypoxia for 72 hours also did not affect norepinephrine-induced β 1 -mRNA and receptor downregulation and adenylylcyclase desensitization in response to isoproterenol, guanyl-5′-imidodiphosphate, or forskolin. Conclusions In neonatal rat cardiac myocytes, chronic hypoxia (1) increases β 1 -mRNA and receptor expression but does not alter adenylylcyclase activity stimulated at either the receptor or the postreceptor level and (2) does not affect agonist-induced β 1 -mRNA and receptor downregulation and desensitization of the adenylylcyclase response.
Ambulances and management
Authors: J. Smith
Journal: BMJ (1995)

Research shows how HIV exhausts the bodyA remarkable picture of how HIV attacks the body during the long period of clinical latency is described by two research groups in the US, who used three new experimental drugs that inhibit viral replication.The sci- entists found that, far from being dormant, HIV replicates at a stupendous rate matched only by the ability of the immune system to replace the cells that it attacks.The researchers found that it takes only two days for the drugs-one that inhibits reverse transcriptase and two others that inhibit HIV's protein cleaving enzyme-to halve the amount of virus and cells that pro- duce viruses in a patient who is HIV positive.Within a few weeks, however, the virus makes an equally dramatic comeback, with new and drug resistant strains rising in numbers and once again becoming the engine that drives HIV infection.After sev- eral years the virus wins the struggle, having exhausted the immune defences.
Care of dying patients in hospital Palliative care teams have helped
Authors: M Bennett, D Alison, K Simpson
Journal: BMJ (1994)

EDITOR, - It is disappointing that Mina Mills and colleagues make no comment in their paper on the care of dying patients in hospital about changes that may have led to improvements in the past decade.1 Their study showed a lack of nursing care for dying patients, but whether this poor standard of care was applied to all patients admitted to hospitals in the study …
Economic aspects of tobacco use and taxation policy.
Authors: C. Godfrey, A. Maynard
Journal: BMJ (1988)

Tax levels have important effects on cigarette prices and tax revenues. Over 70p of every pound spent on tobacco goes to the Chancellor of the Exchequer, yielding over 5 billion pounds. But the value of tobacco tax revenues have generally fallen--by 1986 they were 10% lower than at their peak in 1965, and tobacco revenue is becoming a smaller proportion of total tax receipts. The impact of a consistent increase in tobacco taxation is important in terms of reduced consumption (and harm to health) as well as in terms of reduced employment. Revenue may, however, increase in the short term. Finally, if the findings of Townsend and Atkinson et al (see above) still apply then the distributive effects of increased taxation on the poor might be less than is sometimes feared.
Reprocessing flexible gastrointestinal endoscopes after a period of disuse: is it necessary?
Authors: A. Vergis, D. Thomson, P. Pieroni, S. Dhalla
Journal: Endoscopy (2007)

See also: Commentaire de travail de A. S. Vergis et al., pp. 737Endoscopy 2007; 39(08): 847-847DOI: 10.1055/s-0032-1308863
Evidence of Reduced β-Cell Function in Asian Indians With Mild Dysglycemia
Authors: Lisa R. Staimez, Mary Beth Weber, Harish Ranjani, Mohammed K. Ali, Justin B. Echouffo-Tcheugui, Lawrence S. Phillips, Viswanathan Mohan, K.M. Venkat Narayan
Journal: Diabetes Care (2013)

OBJECTIVE To examine β-cell function across a spectrum of glycemia among Asian Indians, a population experiencing type 2 diabetes development at young ages despite low BMI. RESEARCH DESIGN AND METHODS One-thousand two-hundred sixty-four individuals without known diabetes in the Diabetes Community Lifestyle Improvement Program in Chennai, India, had a 75-g oral glucose tolerance test, with glucose and insulin measured at 0, 30, and 120 min. Type 2 diabetes, isolated impaired fasting glucose (iIFG), isolated impaired glucose tolerance (iIGT), combined impaired fasting glucose and impaired glucose tolerance, and normal glucose tolerance (NGT) were defined by American Diabetes Association guidelines. Measures included insulin resistance and sensitivity (homeostasis model assessment of insulin resistance [HOMA-IR], modified Matsuda Index, 1/fasting insulin) and β-cell function (oral disposition index = [Δinsulin0–30/Δglucose0–30] × [1/fasting insulin]). RESULTS Mean age was 44.2 years (SD, 9.3) and BMI 27.4 kg/m2 (SD, 3.8); 341 individuals had NGT, 672 had iIFG, IGT, or IFG plus IGT, and 251 had diabetes. Patterns of insulin resistance or sensitivity were similar across glycemic categories. With mild dysglycemia, the absolute differences in age- and sex-adjusted oral disposition index (NGT vs. iIFG, 38%; NGT vs. iIGT, 32%) were greater than the differences in HOMA-IR (NGT vs. iIFG, 25%; NGT vs. iIGT, 23%; each P &amp;lt; 0.0001). Compared with NGT and adjusted for age, sex, BMI, waist circumference, and family history, the odds of mild dysglycemia were more significant per SD of oral disposition index (iIFG: odds ratio [OR], 0.36; 95% CI, 0.23–0.55; iIGT: OR, 0.37; 95% CI, 0.24–0.56) than per SD of HOMA-IR (iIFG: OR, 1.69; 95% CI, 1.23–2.33; iIGT: OR, 1.53; 95% CI, 1.11–2.11). CONCLUSIONS Asian Indians with mild dysglycemia have reduced β-cell function, regardless of age, adiposity, insulin sensitivity, or family history. Strategies in diabetes prevention should minimize loss of β-cell function.
Molecular and cellular interface between behavior and acute coronary syndromes
Authors: Yori Gidron, Harel Gilutz, Rivka Berger, Mahmoud Huleihel
Journal: Cardiovascular Research (2002)

This review article integrates empirical findings from various scientific disciplines into a proposed psychoneuroimmunological (PNI) model of the acute coronary syndrome (ACS). Our starting point is an existing, mild, atherosclerotic plaque and a dysfunctional endothelium. The ACS is triggered by three stages. (1) Plaque instability: Pro-inflammatory cytokines (IL-1, IL-6, TNF-α) and chemoattractants (MCP-1, IL-8) induce leukocyte chemoattraction to the endothelium, and together with other triggers such as the CD40L–CD40 co-stimulation system activate plaque monocytes (macrophages). The macrophages then produce matrix metalloproteinases that disintegrate extra-cellular plaque matrix, causing coronary plaque instability. Acute stress, hostility, depression and vital exhaustion (VE) have been associated with elevated pro-inflammatory cytokines and leukocyte levels and their recruitment. (2) Extra-plaque factors promoting rupture: Neuro-endocrinological factors (norepinephrine) and cytokines induce vasoconstriction and elevated blood pressure (BP), both provoking a vulnerable plaque to rupture. Hostility/anger and acute stress can lead to vasoconstriction and elevated BP via catecholamines. (3) Superimposed thrombosis at a ruptured site: Increases in coagulation factors and reductions in anticoagulation factors (e.g. protein C) induced by inflammatory factors enhance platelet aggregation, a key stage in thrombosis. Hostility, depression and VE have been positively correlated with platelet aggregation. Thrombosis can lead to severe coronary occlusion, clinically manifested as an ACS. Thus, PNI processes might, at least in part, contribute to the pathogenesis of the ACS. This chain of events may endure due to lack of neuroendocrine-to-immune negative feedback stemming from cortisol resistance. This model has implications for the use of psychological interventions in ACS patients.
Thyroid Function in Addison's Disease
Authors: M. N. Maisey, M. H. Lessof
Journal: BMJ (1969)

Clinical evidence of a thyroid disorder was present in 10 out of 40 patients with Addison9s disease. Though the remaining 30 patients had no clinical evidence of thyroid disease, six (out of 15 tested) had thyroid microsomal antibodies and a considerably impaired response to thyrotrophin. These changes are interpreted as very early indications of developing thyroid failure. When circulating microsomal antibodies are found this seems to indicate the presence of established thyroid disease.
Understanding and Evaluating Research in Applied and Clinical SettingsGeorge A. Morgan, Jeffrey A. Gliner, and Robert J. Harmon, in collaboration with Helena Chmura Kraemer, Nancy L. Leech, and Jerry J. Vaske. Mahwah, NJ, Lawrence Erlbaum Associates, 2005, 367 pp, $110 (hardcover), $39.95 (paper).
Authors: NEAL D. RYAN
Journal: American Journal of Psychiatry (2006)
Gastric and rectal carcinoids
Authors: R. Lambert
Journal: Endoscopy (2010)

The term ”carcinoid” was proposed in 1907 by Siegfried Oberndorfer, for slow-growing tumors in the small bowel, because he considered them to be ”cancer-like” rather than cancerous. In subsequent years this name was applied to tumors of the diffuse endocrine system in the digestive and bronchial mucosae. The term has even been restricted to serotonin-producing tumors resulting in a carcinoid syndrome. The appellation ”carcinoid” is still currently used to denote those tumors that have developed from the disseminated endocrine cells. However, without any accompanying qualification, the term ”carcinoid” is not informative about the management of the lesion; furthermore it is worrying that it carries a connotation that the lesion should always have benign clinical and biological behavior. Therefore, the first step in the history of classification of ”carcinoids” was their designation as tumors of the disseminated endocrine system hosted in the digestive and bronchial mucosae, which are based on enterochromaffin and enterochromaffin-like (ECL) cells. The secretion of serotonin by enterochromaffin cells was confirmed in 1953 and the term ”carcinoid” designated only tumors that had developed from EC cells and produced serotonin and multiple peptides in the rectum and ileum. A further extension of the terminology included tumors of ECL cells which have a potential for secreting histamine.
Patient safety needs closer monitoring, says Healthcare Commission
Authors: Lynn Eaton
Journal: BMJ (2006)

More information is needed on the number of people harmed, or who die, while they are in hospital if a clearer picture of patient safety in the NHS and independent sector is to emerge, the Healthcare Commission has warned.

Almost a quarter (22%) of the 8000 complaints the commission receives each year are related to safety, it says. In the NHS, one in 10 trusts could not reassure the commission they fully met core standards on safety.

“It is frustrating that in 2006 we do not have a clearer idea of how many people die or are harmed in hospitals when this could have been avoided,” said Ian Kennedy, the chairman of the commission, launching its …
Effects of cadmium on nuclear protein kinase C.
Authors: D Beyersmann, C Block, A N Malviya
Journal: Environmental Health Perspectives (1994)

Cadmium is a carcinogen whose genotoxicity is only weak. Besides its tumor-initiating capacity, cadmium may be tumor-promoting, since it interferes with several steps of cellular signal transduction. We have investigated effects of cadmium(II) on protein kinase C (PKC), which is a key enzyme in the control of cellular growth and differentiation. Tumor-promoting phorbol esters cause an activation and translocation of PKC from the cytosol to the plasma membrane and to the nucleus of mammalian cells. In mouse 3T3/10 T 1/2 fibroblasts, cadmium(II) potentiated the effect of phorbol ester on nuclear binding and activation of PKC. Furthermore, in a reconstituted system consisting of rat liver nuclei and rat brain PKC, cadmium stimulated the binding of the enzyme to a 105-kDa protein. We propose a model in which cadmium(II) substitutes for zinc(II) in the regulatory domain of PKC, thus rendering the putative protein-protein binding site exposed. Further work is required to elucidate the potential role of the nuclear PKC binding protein(s) in the control of cell proliferation.
Two Cases of Phaeochromocytoma
Authors: K. V. Crowther
Journal: BMJ (1951)

Phaeochromocytomata are comparatively rare tumours, but the number of cases reported is increasing rapidly owing to clarification of the clinical picture and the diagnostic use of adrenolytic drugs.Two cases are described here.In the first, as a result of radiological investigation, a malformed kidney was thought to be the cause of hypertension.An unsus- pected phaeochromocytoma was present, however, and death occurred shortly after operation.In the second case the diagnosis was correctly made by clinical and biochemical methods, and the tumour was successfully removed.Case 1A man aged 24 was admitted to Cardiff Royal Infirmary complaining of attacks of headache, nausea, and vomiting, with blurring of vision of 16 years' duration.For this period he had suffered from postural giddiness.He had sweated excessively for the past nine years, and had had a dull pain in the right loin for five years.For two years before admission he had complained of dyspnoea and palpitation on moderate exertion.
Wrist watches must be removed before washing hands
Authors: J C Hartley, A D Mackay, G M Scott
Journal: BMJ (1999)

Deprivation and emergency admissions for cancersOther possible explanations for findings need to be explored Editor-The reasons for Pollock and Vickers's findings about the relation between deprivation and emergency admissions for cancers remain speculative. 1To impute the differences in care to failures of primary care seems unfair at this stage.The authors discuss a range of possible explanations, but many other could also be relevant.Day case treatment may require a certain level of facilities at home that are less commonly available in deprived areas.The presence of another adult at home may also be a prerequisite.Single people may be more likely to live in deprived areas; patients from deprived areas may be more likely to have a working partner who cannot afford to take time off work or who has a job where such absences would be unacceptable.Patients with lung cancer due to smoking (more common in areas where smoking is more prevalent) may be less likely to have an operable malignancy because of concomitant disease related to smoking.The authors mention this in their discussion, but limiting the study to inpatient finished consultant episodes with a primary diagnosis of any of the three cancers of interest does not give any information about comorbidity.I hope further research will be carried out to help elucidate the reasons behind the apparently inequitable access and treatment decisions that Pollock and Vickers have found.Both qualitative and quantitative research methods could be used to study patients' and professionals' experiences as patients pass through the system.Perhaps allocation of blame should wait until such results are available.
Impaired function of human T-lymphotropic virus type 1 (HTLV-1)–specific CD8+ T cells in HTLV-1–associated neurologic disease
Authors: Amir H. Sabouri, Koichiro Usuku, Daisuke Hayashi, Shuji Izumo, Yoshiro Ohara, Mitsuhiro Osame, Mineki Saito
Journal: Blood (2008)
Effect of low-density lipoproteins on apolipoprotein AI kinetics in heterozygous familial hypercholesterolemia
Authors: R. Fr[eacute]nais, C. Maugeais, K. Ouguerram, Y. Za[iuml ]r, J.M. Bard, B. Charbonnel, T. Magot, M. Krempf
Journal: Metabolism (2001)
Studies in vivo and in vitro on an abnormality in the metabolism of C3 in a patient with increased susceptibility to infection
Authors: Chester A. Alper, Neil Abramson, Richard B. Johnston, James H. Jandl, Fred S. Rosen
Journal: Journal of Clinical Investigation (1970)

In a patient with increased susceptibility to infection, lowered serum C3 concentration, and continuously circulating C3b, it was shown that purified (125)I-labeled C3 was converted to labeled C3b shortly after intravenous administration. The fractional catabolic rate of C3 was approximately five times normal at 10% of the plasma pool per hr. The synthesis rate and pool distribution of C3 were normal. Despite this evidence of C3 instability in vivo, no accelerated inactivation of C3 was found in vitro. Similarly, no free proteolytic activity could be detected in the patient's serum, and serum concentrations of known protease inhibitors were normal.Complement-mediated functions, which were markedly deficient in the patient's serum, could be restored partially or completely by the addition of a 5-6S heat-labile beta pseudoglobulin from normal serum. The C3 proinactivator, which has these physicochemical characteristics, was also shown to be either absent or nonfunctional in the patient's serum. An unidentified 6S beta pseudoglobulin to which a monospecific antiserum was available was not detectable in the patient's serum. This last protein appeared not to be a complement component, nor was it the C3 inactivator or proinactivator. Finally, the substance or substances necessary for the conversion of C3b to C3c were missing from the patient's serum. The administration of 500 ml of normal plasma to the patient corrected all of his abnormalities partially or completely for as long as 17 days. The changes in C3 were dramatic; serum concentration rose from 8 to 70 mg/100 ml, and C3b could no longer be detected. A second metabolic study during this normalization period showed a decrease in fractional catabolic rate toward normal. The patient's histamine excretion was constantly elevated but increased further after a warm shower and after receiving normal plasma; at both times he had urticaria. These observations were consistent with the endogenous production of C3a and the resulting histamine release from mast cells. The inactivating mechanism for C3a was apparently intact in the patient's serum. The difference in the electrophoretic mobilities of C3b and C3c was shown as well as the electrophoretic heterogeneity of C3c. Suggestive evidence was also presented that the form of C3 with an activated combining site for red cells, previously postulated by others, is a transient C3 conversion product with an electrophoretic mobility slower than that of C3 on agarose electrophoresis.
Heterozygous mutations of the kinesin KIF21A in congenital fibrosis of the extraocular muscles type 1 (CFEOM1)
Authors: Koki Yamada, Caroline Andrews, Wai-Man Chan, Craig A McKeown, Adriano Magli, Teresa de Berardinis, Anat Loewenstein, Moshe Lazar, Michael O'Keefe, Robert Letson, Arnold London, Mark Ruttum, Naomichi Matsumoto, Nakamichi Saito, Lisa Morris, Monte Del Monte, Roger H Johnson, Eiichiro Uyama, Willem A Houtman, Berendina de Vries, Thomas J Carlow, Blaine L Hart, Nicolas Krawiecki, John Shoffner, Marlene C Vogel, James Katowitz, Scott M Goldstein, Alex V Levin, Emin C Sener, Banu T Ozturk, A Nurten Akarsu, Michael C Brodsky, Frank Hanisch, Robert P Cruse, Alina A Zubcov, Richard M Robb, Peter Roggenkäemper, Irene Gottlob, Lionel Kowal, Ravi Battu, Elias I Traboulsi, Piergiorgio Franceschini, Anna Newlin, Joseph L Demer, Elizabeth C Engle
Journal: Nature Genetics (2003)
Impact of Classic and Paradoxical Low Flow on Survival After Aortic Valve Replacement for Severe Aortic Stenosis
Authors: Marie-Annick Clavel, Maxime Berthelot-Richer, Florent Le Ven, Romain Capoulade, Abdellaziz Dahou, Jean G Dumesnil, Patrick Mathieu, Philippe Pibarot
Journal: Journal of the American College of Cardiology (2015)
New Technologies and Directed Agents for Applications of Cancer Imaging
Authors: Mostafa Atri
Journal: Journal of Clinical Oncology (2006)

Molecular imaging represents tissue-specific imaging and quantification of physiologic (functional) and molecular events in tumors utilizing new noninvasive imaging modalities, radioligands, and contrast agents. It combines anatomic, physiologic, and metabolic information in a single imaging session. Molecular imaging relies on the ability to target genes and proteins that are linked directly or indirectly to human disease. New imaging biomarkers are being developed. In addition, functional and molecular imaging can potentially replace anatomic longitudinal studies by assessing treatment response earlier. Vascular targeting agents can be evaluated by imaging of tumor angiogenesis using magnetic resonance imaging (MRI), computed tomography and ultrasound, and positron emission tomography (PET). Targeted contrast agents can accomplish site-directed imaging or therapy by a variety of active and passive mechanisms. Furthermore, there is the possibility of combining different modalities such as ultrasonic imaging and MRI or MRI and PET to increase the flexibility unachievable with either modality alone. However, there is a need to standardize these techniques so that longitudinal evaluation of tumor response to treatment is feasible.
Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs
Authors: Alan D. Guerci, Henry R. Halperin, Rafael Beyar, Charles Beattie, Joshua E. Tsitlik, Edward C. Wurmb, Nisha C. Chandra, Myron L. Weisfeldt
Journal: Journal of the American College of Cardiology (1989)
294 HVPG MEASUREMENT IN CIRRHOTIC HCV CAN BE USED TO PREDICT OUTCOME AND SAFETY OF ANTIVIRAL THERAPY
Authors: T. Reiberger, K. Rutter, A. Ferlitsch, H. Hofer, S. Beinhardt, A.F. Staettermayer, M. Kundi, P. Ferenci, M. Peck-Radosavljevic
Journal: Journal of Hepatology (2010)
A MEMORABLE EVENT
Authors: J. Boyd
Journal: BMJ (1995)

The following story comes from the recently published memoirs of Mr John Boyd, Behind a Surgeon's Mask.

Sir Ian Fraser and I visited BMA House where he was particularly well known, being a past president of that organisation. On our way into this modern looking building Sir Ian was commenting on some of its special features. As we passed through a small courtyard he talked for a short time about a very ordinary looking fish pond which contained some ordinary looking fish. Eventually he spotted something which …
Multiple breakage of a covered esophageal stent
Authors: P. Born
Journal: Endoscopy (2009)

A 59-year-old patient presented with recurrent dysphagia 7 months after successful insertion of an esophageal covered metal stent (Choo-Stent; M.I.Tech Co., Ltd., Seoul, Korea). The stent had been inserted with palliative intent because of an obstructive T4 esophageal squamous cell cancer that was penetrating into the (already stented) trachea. After the esophageal stenting and subsequent chemotherapy the patient had initially made a very good recovery.