tbuckley/cabot-search huggingface dataset:
Nutrient Deficiencies After Gastric Bypass Surgery
Authors: Edward Saltzman, J. Philip Karl
Journal: Annual Review of Nutrition (2013)

Bariatric surgery, and in particular, gastric bypass, is an increasingly utilized and successful approach for long-term treatment of obesity and amelioration of comorbidities. Nutrient deficiencies after surgery are common and have multiple causes. Preoperative factors include obesity, which appears to be associated with risk for several nutrient deficiencies, and preoperative weight loss. Postoperatively, reduced food intake, suboptimal dietary quality, altered digestion and absorption, and nonadherence with supplementation regimens contribute to risk of deficiency. The most common clinically relevant micronutrient deficiencies after gastric bypass include thiamine, vitamin B₁₂, vitamin D, iron, and copper. Reports of deficiencies of many other nutrients, some with severe clinical manifestations, are relatively sporadic. Diet and multivitamin use are unlikely to consistently prevent deficiency, thus supplementation with additional specific nutrients is often needed. Though optimal supplement regimens are not yet defined, most micronutrient deficiencies after gastric bypass currently can be prevented or treated by appropriate supplementation.
In vitro studies of the rabbit immune system. V. Suppressor T cells activated by concanavalin A block the proliferation, not the induction of antierythrocyte plaque-forming cells.
Authors: D Redelman, C B Scott, H W Sheppard, S Sell
Journal: The Journal of Experimental Medicine (1976)

The late B-cell proliferative phase of the in vitro antibody response by rabbit spleen cells is highly susceptible to suppression by activated T cells. The in vitro antisheep erythrocyte plaque-forming cell (PFC) response by spleen cells from normal or primed rabbits can be suppressed by adding concanavalin A (Con A), Con A-prestimulated peripheral blood or spleen lymphocytes, or supernates from Con A-prestimulated peripheral blood lymphocytes. The suppression is not mediated by a direct interaction of Con A with responding cells as shown by the effectiveness of prestimulated cells. Primed spleen cultures remain sensitive to Con A suppression as late as 72 h after initiation, and the addition of Con A after 24-72 h rapidly stops the increase in the number of PFC. T cells are required for Con A addition to be effective but the suppression can be induced at a time when T-helper cells are no longer necessary. Further, the suppressive effect of Con A addition is abrogated by specific antisera to rabbit T cells. We propose that Con A activates suppressor T cells which then exert their effects on proliferating PFC or their immediate precursor B cells. The early inductive or recruitment phase of the response is probably not blocked by suppressor cells. Also, there is an apparent relationship between the number of proliferating B cells and the number of suppressor cells required. Finally, the difficulties in inducing a stimulatory effect by Con A and the prolonged period that Con A addition is suppressive suggests that the rabbit has relatively more and/or longer-lived suppressor cells than the mouse and may be a particularly useful species for studying suppressive phenomena and their mechanisms.
The independent effects of oxygen radical scavengers on canine infarct size. Reduction by superoxide dismutase but not catalase.
Authors: S W Werns, M J Shea, E M Driscoll, C Cohen, G D Abrams, B Pitt, B R Lucchesi
Journal: Circulation Research (1985)

Previous studies demonstrated a significant reduction of ultimate infarct size in the canine heart by the combined administration of superoxide dismutase plus catalase. This study was performed to assess the independent effects of each enzyme on ultimate infarct size due to ischemia/reperfusion. Dogs received 2-hour infusions of superoxide dismutase, catalase, or albumin (controls) via the left atrium beginning 15 minutes before and ending 15 minutes after a 90-minute occlusion of the left circumflex coronary artery. The dogs were killed 6 hours after reperfusion. After histochemical staining, infarct and risk area masses were calculated by gravimetric and planimetric analysis. Infarct size expressed as a percentage of the area at risk was: superoxide dismutase, 19 +/- 5; catalase, 30 +/- 5; and controls, 40 +/- 3. Infarct size in the superoxide dismutase group, but not the catalase group, was significantly less than in controls (P less than 0.05). No significant differences in hemodynamics or area at risk were observed that could explain the differences in infarct size. The results indicate that superoxide dismutase alone protects reperfused ischemic myocardium as well as does the combination of superoxide dismutase and catalase. The beneficial effect of superoxide dismutase and insignificant effect of catalase suggest that tissue damage during ischemia and reperfusion may be mediated largely by superoxide anion but not by hydrogen peroxide.
Particulate matter, science and EU policy
Authors: I. Annesi-Maesano, F. Forastiere, N. Kunzli, B. Brunekref
Journal: European Respiratory Journal (2007)

Several new research findings regarding the health effects of airborne particulate matter (PM) (usually studied by the size of the particles, e.g. PM10, particles with a 50% cut-off aerodynamic diameter of 10 μm, and PM2.5, particles with a 50% cut-off aerodynamic diameter of 2.5 μm) have been presented at two important scientific meetings held in September 2006: the Conference of the European Respiratory Society (ERS), in Munich, and the joint Conference of the International Society for Environmental Epidemiology (ISEE) and the International Society for Exposure Analysis (ISEA) in Paris. This is not surprising, since: 1) the health effects of air pollution are among the largest environmental problems worldwide 1; 2) several scientific questions are still open; and 3) common research efforts from the epidemiological, toxicological and clinical worlds are under way.

A brief review of the evidence follows. The initial suggestion that mortality increases due to long-term, low-level exposure to PM was provided by the Harvard Six Cities study 2. These findings were confirmed in the long-term follow-up (1982–1998) of the American Cancer Society (ACS) II cohort, consisting of ∼500,000 adults from metropolitan areas throughout the USA 3, 4. In the latter study, each 10 μg·m−3 elevation in PM2.5 was associated with approximately a 6, 9 and 14% increased risk of all-cause, cardiopulmonary and lung cancer mortality, respectively. A recent report from Los Angeles 5, which included a large proportion of the ACS II cohort from that area, has indicated that a more refined method for assessing exposure produces a higher risk estimate of mortality increase (17% increase; 95% confidence interval 5–30%) for an increase of 10 μg·m−3 in PM2.5. Well-conducted cohort studies in Europe, which have estimated air pollution exposure at individual residences, confirm the findings from the USA …
GPs working in singlehanded practices earn most
Authors: Adrian O’Dowd
Journal: BMJ (2008)

GPs working singlehandedly earn an average of £132 010 (€168 240; $265 100)—about £26 000 more than doctors who work with six or more partners, official data show.⇓



Overall GPs’ average pay has doubled in real terms in the past 20 years, according to newly published figures from the NHS Information Centre.

The figures also show that doctors’ earnings rise as GPs get older until the age of 60, with an average earning of £117 820 for GPs in the 50-59 age group.

The statistics, from the NHS Information Centre, look at the changes in family doctors’ pay as well as how …
Clinical Niche Sought for Platelet-Boosting Drugs
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1996)

Clinical Niche Sought for Platelet-Boosting DrugsAlthough two pharmaceutical giants and a third, smaller drug company, are vying over who will develop thrombopoietins (TPO) first, the role of these platelet-boosting drugs in the clinical arena is far from defined.At least one expert believes that role may be somewhat limited, or possibly, one that is "not even conceived of today.
Remarkable Tumor Response to Crizotinib in a 14-Year-Old Girl With <i>ALK</i>-Positive Non–Small-Cell Lung Cancer
Authors: Su-Jung Kim, Dong-Wan Kim, Tae Min Kim, Se-Hoon Lee, Dae Seog Heo, Yung-Jue Bang
Journal: Journal of Clinical Oncology (2012)

Remarkable Tumor Response to Crizotinib in a 14-Year-Old Girl With ALK-Positive Non-Small-Cell Lung CancerCase Report A 14-year-old girl presented in July 2010 with weight loss (12 kg over 6 months), intermittent fever, night sweats, mild sputum, and cough.She was initially treated for pneumonia in a community hospital.Because her symptoms did not improve despite the treatment for pneumonia, she underwent a chest computed tomography (CT) scan, which showed enlargement of multiple lymph nodes and a lung mass in the left lower lobe and interlobular septal thickening in the left lung.Enlargement of multiple lymph nodes was observed on chest and abdominal CT at the mediastinum, in both the supraclavicular and retroperitoneal areas, around the B A Fig 1.
FGF Signaling Emerged Concomitantly with the Origin of Eumetazoans
Authors: Stéphanie Bertrand, Thomas Iwema, Hector Escriva
Journal: Molecular Biology and Evolution (2013)

Complex metazoan bodies require cell-to-cell communication for development, a process often mediated by signaling molecules binding to specific receptors. Relatively few signaling pathways have been recruited during evolution to build multicellular animals from unicellular zygotes. Of these few signaling pathways, one of particular importance is the receptor tyrosine kinase (RTK) pathway. In metazoans, fibroblast growth factors (FGFs) bind to receptors in the RTK family, but the origin of the FGF gene family has so far remained a mystery. Here we show that extant bona fide FGFs most likely originated from proteins bearing an FGF-like domain that arose in a choanoflagellate/metazoan ancestor. We found orthologous genes closely related to FGF in choanoflagellates as well as in many metazoans such as sponges, acoels, protostomes, or nonvertebrate deuterostomes. We also show that these genes have a common evolutionary history with Retinitis Pigmentosa 1 (RP1). Even if some metazoan signaling pathways emerged long before multicellularity, we show that FGFs, like their receptors, originated in a eumetazoan ancestor.
Retinoblastoma: Saving Life with Vision
Authors: David H. Abramson
Journal: Annual Review of Medicine (2014)

Retinoblastoma has gone from &gt;95% mortality to &gt;95% survival in the past 100 years. Once enucleation techniques were perfected, the majority of children survived, but without the eye (or vision in that eye). Over the past 100 years, progressively better techniques have been developed for salvaging vision without sacrificing patient survival. Presently, 99% of children treated at our center survive their cancer, &gt;99% retain at least one eye, and &gt;90% retain normal vision in at least one eye. The introduction of ophthalmic artery chemosurgery has been the most dramatic, non-radiation-based mode to maximally preserve vision.
Testicular Cancer Risk in First- and Second-Generation Immigrants to Denmark
Authors: Charlotte Myrup, Tine Westergaard, Tine Schnack, Anna Oudin, Christian Ritz, Jan Wohlfahrt, Mads Melbye
Journal: JNCI Journal of the National Cancer Institute (2007)

Immigrant studies offer insights into the relative importance of environment and genes in disease etiology. There is considerable variation in testicular cancer incidence worldwide. We investigated testicular cancer risk in first- and second-generation immigrants to Denmark, a high-incidence country, to evaluate the relative influence of genes and environment and the potential timing of action of environmental factor(s).A cohort of 2.1 million men who were born since 1930 and lived in Denmark between 1968 and 2003 was established based on information in the Danish Civil Registration System, which included their immigration histories. Cancer histories were obtained from the Danish Cancer Registry. Testicular cancer risk was estimated as rate ratios (RRs) with 95% confidence intervals (CIs) based on log-linear Poisson regression.Overall, 4216 testicular cancer cases occurred during 43 million person-years of follow-up in 2.1 million men. These included 166 cases among 344,444 direct immigrants to Denmark and 13 cases among 56,189 men born in Denmark to immigrant parents. These first- and second-generation immigrants had RRs of testicular cancer of 0.37 (95% CI = 0.31 to 0.43) and 0.88 (95% CI = 0.51 to 1.53), respectively, compared with men born in Denmark of parents born in Denmark. The rate in first-generation immigrants was not modified by age at immigration or duration of stay and reflected that in the country of origin.The testicular cancer risk in first-generation immigrants was lower than that in native-born Danes and reflected that in the countries of origin, whereas the risk in second-generation immigrants was similar to that in natives of Denmark. Together these findings argue for a substantial influence of environmental factors limited to the period early in life, most probably to the period in utero.
Government should investigate trusts that charge NHS patients for treatment, says Labour
Authors: A. O'Dowd
Journal: BMJ (2012)

The government should investigate several trusts that are charging patients for treatment even though they are not private patients, the Labour Party has said.

A squeeze on funding is leading increasing numbers of NHS trusts to offer patients the option of “self funding” certain treatments and procedures, including in vitro fertilisation. The Labour Party said that the practice breaks the principle of the NHS being free at the point of delivery.

However, the trusts involved have said that the practice was not new and was being introduced as a result of commissioning decisions being made by primary care trusts regarding what should and should not be funded, rather than an issue of hospital practice.

An investigation by the Sunday Times published on 8 July found that several trusts were inviting patients to pay for certain treatments that they would otherwise have to wait a long time for or be refused, because their local primary care trust would not fund them.

The trusts involved are Homerton University Hospital NHS Foundation Trust in London; Epsom and St Helier University Hospitals NHS Trust in Surrey; University Hospitals …
Herpes simplex encephalitis
Authors: M. Sabah, J. Mulcahy, A. Zeman
Journal: BMJ (2012)

#### How common is herpes simplex encephalitis?

The wife of a previously healthy 40 year old man requested a domiciliary visit from their general practitioner for her husband, who had been in bed for a few days with “bad flu,” fever, and headache. She was worried that he was becoming quite confused and unable to recall recent events. The GP finds the patient is febrile, agitated, and disoriented in time and place. Concerned about encephalitis, he sends the patient immediately to hospital. There a CT scan shows an area of decreased attenuation in the right temporal lobe and a lumbar puncture a raised lymphocyte count, both suggesting herpes simplex encephalitis. Aciclovir treatment is immediately started.

Herpes simplex encephalitis is a severe viral infection of the central nervous system that is usually localised to the temporal and frontal lobes in adults . Typically, it causes a flu-like illness with headache and fever …
FRI0077 Relative efficiencies of joint counts and laboratory tests are no higher than patient-reported measures to document superior results in the guepard tight-control versus espoir routine care cohorts:
Authors: I. Castrejon, T. Pincus, M. Soubrier, Y.C. Lin, M. Dougados
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> A single “gold standard” measure such as blood pressure or serum glucose is not available in rheumatoid arthritis (RA) for diagnosis and monitoring of all individual patients. A Core Data Set of 7 measures has been developed for RA, with 3 measures from a physician - tender (TJC) and swollen joint count (SJC), assessor global (DOCGL); 1 laboratory test - erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP); 3 from a patient questionnaire - function (HAQ-FN), pain (PAIN), and patient global estimate (PATGL), all 7 measures, including patient-reported measures, have similar relative efficiencies to distinguish active from control treatment in reported clinical trials of methotrexate, leflunomide, adalimumab, abatacept, and certolizumab<sup>1</sup>. <h3>Objectives</h3> To analyze standardized response means (SRM) and relative efficiencies of each of the 7 RA core data set measures in the treat-to-target GUEPARD clinical trial versus the routine care ESPOIR cohort. <h3>Methods</h3> Post-hoc analyses were performed on 2 databases of patients with RA: 65 patients from GUEPARD with tight control, and 130 matched patients from ESPOIR with routine care<sup>2</sup>. Each of the 7 RA Core set measures was computed in each patient at baseline and 6 months later, and changes in the two cohorts were compared using Student’s t tests. Standardized response mean (SRM) and relative efficiencies with TJC as the referent measure were computed.<sup>3</sup> <h3>Results</h3> Baseline demographic and clinical characteristics did not differ between the 2 groups, other than disease duration (5.6 months in GUEPARD tight control versus 3.5 months in ESPOIR routine care groups) and higher use of glucocorticoids, biological agents, and mean glucocorticoid dose in the GUEPARD tight control trial. Substantial improvement was seen in both groups, but was significantly greater in GUEPARD tight control for all RA Core Data set measures other than ESR and CRP. The highest SRMs of &gt;4 were observed for pain, and patient and physician global estimates (Table) compared to 1-3 for TJC, SJC, and HAQ function, and &lt;0.2 for ESR and CRP. <h3>Conclusions</h3> Patient self-report measures document better results in GUEPARD tight control versus ESPOIR routine care as efficiently as TJC and SJC, and more efficiently than laboratory tests. <h3>References</h3> Pincus T, Amara I, Segurado OG, Bergman M, Koch GG. J Rheumatol 2008;35:201-5. Soubrier M, Lukas C, Sibilia J, et al. Ann Rheum Dis 2011;70(4):611-5. Wells G, Li T, Maxwell L, Maclean R, Tugwell P. Ann Rheum Dis 2008;67:260-5. <h3>Disclosure of Interest</h3> None Declared
Effect of aluminium hydroxide on serum ionised calcium, immunoreactive parathyroid hormone, and aluminium in chronic renal failure.
Authors: C K Biswas, R S Arze, J M Ramos, M K Ward, J H Dewar, D N Kerr, D H Kenward
Journal: BMJ (1982)

According to the Bricker-Slatopolsky theory, secretion of parathyroid hormone (PTH) is switched on in chronic renal failure by hypocalcaemia due to phosphate retention. In an attempt to reverse this process 20 patients in preterminal renal failure (plasma creatinine 569 +/- 195 mumol/l) were given aluminium hydroxide, 3.8 g daily. They were studied for four weeks and all measurements were made at the start and weekly, except measurements of serum aluminium concentration, which were made at the start and at the end of the fourth week. Mean serum phosphate fell from 1.89 to 1.47 mmol/l (5.9 to 4.6 mg/100), mean serum calcium rose from 2.07 to 2.24 mmol/l (8.3 to 9.0 mg/100 ml), and serum ionised calcium rose from 1.07 to 1.20 mmol/l (4.3 to 4.8 mg/100 ml), but serum immunoreactive PTH did not fall. Thirteen patients had initial serum immunoreactive PTH concentrations at or near to normal and 11 were taking beta-blockers but even in those with neither explanation, PTH concentrations did not fall. Serum aluminium concentrations rose from 0.4 to 1.02 mumol/l (10.9 to 27.4 microgram/l). Aluminium hydroxide corrects serum phosphate, total calcium, and ionised calcium at the price of a rise in serum aluminium concentration; in this study it did not affect serum immunoreactive PTH. The Bricker-Slatopolsky theory still needs verification in studies of patients with chronic renal failure.
Molecular Alterations in Prostate Carcinomas that Associate with <i>In vivo</i> Exposure to Chemotherapy: Identification of a Cytoprotective Mechanism Involving Growth Differentiation Factor 15
Authors: Chung-Ying Huang, Tomasz M. Beer, Celestia S. Higano, Lawrence D. True, Robert Vessella, Paul H. Lange, Mark Garzotto, Peter S. Nelson
Journal: Clinical Cancer Research (2007)

Abstract Purpose: To identify molecular alterations associating with in vivo exposure of prostate carcinoma to chemotherapy and assess functional roles modulating tumor response and resistance. Experimental Design: Patients with high-risk localized prostate cancer (tumor-node-metastasis ≥ T2b or prostate-specific antigen ≥ 15 ng/mL or Gleason glade ≥ 4+3) were enrolled into a phase II clinical trial of neoadjuvant chemotherapy with docetaxel and mitoxantrone followed by prostatectomy. Pretreatment prostate tissue was acquired by needle biopsy and posttreatment tissue was acquired by prostatectomy. Prostate epithelium was captured by microdissection, and transcript levels were quantitated by cDNA microarray hybridization. Gene expression changes associated with chemotherapy were determined by a random variance t test. Several were verified by quantitative reverse transcription PCR. In vitro analyses determining the influence of growth differentiation factor 15 (GDF15) on chemotherapy resistance were done. Results: Gene expression changes after chemotherapy were measured in 31 patients who completed four cycles of neoadjuvant chemotherapy. After excluding genes shown previously to be influenced by the radical prostatectomy procedure, we identified 51 genes with significant transcript level alterations following chemotherapy. This group included several cytokines, including GDF15, chemokine (C-X-C motif) ligand 10, and interleukin receptor 1β. Overexpression of GDF15 or exposure of prostate cancer cell lines to exogenous recombinant GDF15 conferred resistance to docetaxel and mitoxantrone. Conclusions: Consistent molecular alterations were identified in prostate cancer cells exposed to docetaxel and mitoxantrone chemotherapy. These alterations include transcripts encoding cytokines known to be regulated through the nuclear factor-κB pathway. Chemotherapy-induced cytokines and growth factors, such as GDF15, contribute to tumor cell therapy resistance and may serve as targets to improve responses.