tbuckley/cabot-search huggingface dataset:
Abstract 8523: Randomized Trial of Nutraceuticals in Statin-Intolerant Patients Treated with Percutaneous Coronary Intervention
Authors: Francesco Pelliccia, Giuseppe Marazzi, Vincenzo Pasceri, Alessio Arrivi, Gaetano Tanzilli, Enrico Mangieri, Giuseppe Rosano, Giuseppe Mercuro, Carlo Gaudio
Journal: Circulation (2011)

Introduction. Statins have a class I indication after percutaneous coronary intervention (PCI), but can not be used in statin-intolerant patients. Nutraceuticals, i.e. forms of compounds with biological activity derived from foods, that are capable of lowering LDL cholesterol might represent a useful therapeutic alternative. However, there are no data regarding the use of nutraceuticals after PCI. Hypothesis. We performed a randomized, prospective, parallel group, single-blind trial to investigate the efficacy, safety, and tolerability of a nutraceutical-based protocol in statin-intolerant patients treated with PCI. Methods. At time of PCI, we selected 80 patients with stable (70%) or unstable angina (30%) who had previously experienced statin withdrawn because of myalgias (75%), gastrointestinal intolerance (20%) or elevated alanine aminotrasferase (5%). Patients were randomized to receive for 1 year either nutraceutical combined pill (1 capsule/day containing red yeast rice 200 mg, policosanol 10 mg, and berberine 500 mg) or daily placebo. Primary outcomes included reasons for treatment discontinuation and a daily pain severity score, and secondary outcomes included plasma lipids. Results. At entry, 40 patients were randomized to nutraceuticals and 40 to placebo. Clinical features and lipid profiles were similar between groups. During the 1-year trial, 2 patients of the nutraceutical-group stopped the pill due to myalgia (N=1) or gastrointestinal intolerance (N=1). After 1-year treatment, the mean pain severity did not differ significantly between nutraceutical and placebo groups. Similarly, levels of triglyceride, liver enzyme or creatine kinase were similar between groups. Conversely, total cholesterol level (205+31 vs 241+41 mg/dl) and low-density lipoprotein cholesterol (105+31 vs 131+41 mg/dl) were significantly (P=0.001) lower in the nutraceutical-group than in the placebo-group. Conclusions. A combination of nutraceuticals with lipid-lowering biological activity can significantly decrease cholesterol levels without causing clinical or metabolic side effects, thus being a reliable treatment option in statin-intolerant patients treated with PCI.
Development of IgE Antibodies to Human (recombinant DNA), Porcine, and Bovine Insulins in Diabetic Subjects
Authors: Philip Fireman, S Edwin Fineberg, John A Galloway
Journal: Diabetes Care (1982)

Thirty-one previously untreated diabetic individuals received only human insulin (recombinant DNA) for 1 yr with no adverse reactions. The development of serum IgE antibodies to human, porcine, and bovine insulins was assessed by a sepharose radioallergoabsorbent test (RAST). Immunoglobulin (total Ig antibody) binding was assessed by a nonabsorbed species-specific radioimmunoassay. During therapy 2 patients developed IgE antibodies to human insulin as well as increased total Ig binding. The IgE antibodies to human insulin cross-reacted with porcine and bovine insulins, were transient, and were not accompanied by insulin allergy. Ig binding to insulin developed and persisted in 11 of the human insulin-treated diabetics. In comparison, 62 previously untreated diabetic persons received only purified porcine insulin (PPI, &amp;lt; 5 ppm proinsulin, N = 40) or a mixed bovine-porcine insulin (proinsulin &amp;lt; 50 ppm, N = 21). Increased Ig antibody developed in 16 of 21 patients receiving mixed bovineporcine insulin and 25 of 41 PPI-treated patients (P &amp;lt; 0.05). Seven of 41 PPI-treated patients and 4 of 21 mixed bovine-porcine-treated patients developed anti-insulin IgE antibodies, which were transient in 4 and persisted in 6 diabetic patients. IgE antibody levels did not correlate with total Ig antibody. These data suggest that IgE and total Ig antibodies develop less often after human insulin treatment. Also, the immunoregulation mechanisms responsible for anti-insulin IgE antibody synthesis differ from those regulating other Ig that bind to insulins. Since none of the patients in this study have developed clinical manifestations of insulin allergy or resistance, the clinical relevance of the antibody data must remain speculative.
Temporal effects of prolonged hypoxaemia and reoxygenation on systemic, pulmonary and mesenteric perfusion in newborn piglets
Authors: Po-Yin Cheung, Keith J. Barrington, David L. Bigam
Journal: Cardiovascular Research (1998)

Objective: Temporal effects of prolonged hypoxaemia and reoxygenation, on the systemic pulmonary and mesenteric circulations in newborn piglets, were investigated. Methods: Two groups [control (n=5), hypoxaemic (n=7)] of 1–3 day old anaesthetised piglets were instrumented with ultrasound flow probes placed to measure cardiac, hepatic arterial flow and portal venous flow indices, and catheters inserted for measurements of systemic and pulmonary arterial pressures. Hypoxaemia with arterial oxygen saturation 40–50% was maintained for 3 h, followed by reoxygenation with 100% inspired oxygen. Results: Cardiac index was transiently elevated at 30–60 min of hypoxaemia (23% increase from baseline 158±39 ml/kg/min), along with increases in stroke volume but not heart rate. A significant decrease in systemic vascular resistance after 30 min of hypoxaemia was followed by hypotension at 180 min of hypoxaemia. Progressive pulmonary hypertension with significant vasoconstriction was found after 30 min of hypoxaemia. The hypoxaemic mesenteric vasoconstriction was transient with a 37% decrease in portal venous flow index at 15 min of hypoxaemia (29±12 vs. 46±18 ml/kg/min of baseline, p<0.05). The hepatic arterial to total hepatic oxygen delivery ratio increased significantly during hypoxaemia. In contrast to the significant increase in systemic oxygen extraction throughout hypoxaemia, elevation in mesenteric oxygen extraction decreased after 30 min of hypoxaemia associated with modest decreases in oxygen consumption. Following reoxygenation, the pulmonary hypertension was partially reversed. Cardiac index decreased further (130±39 ml/kg/min) with reduced stroke volume, persistent systemic hypotension and decreased systemic oxygen delivery. Conclusions: We demonstrated differential temporal changes in systemic, pulmonary and mesenteric circulatory responses during prolonged hypoxaemia. Cautions need to be taken upon reoxygenation because the neonates are at risk of developing myocardial stunning, persistent pulmonary hypertension and necrotising enterocolitis.
Audi Alteram Partem.
Authors: E. C. Spitzka
Journal: JAMA (1889)

<h3>To the Editor:</h3> —The making of punctures, exploratory and otherwise, through terebrated, instead of trephine openings, as described by Dr. Edmond Souchon, and referred to in your editorial of September 7th, is not new in any sense. It was carried out by me and its results described several years ago.<sup>1</sup>I have never claimed originality for it, as Gibier, if I remember rightly, employed terebration ten years ago, in the course of some inoculation experiments involving the brain. The apparatus used by me was an ordinary watchmaker's drill. Respectfully yours, 712 Lexington Ave., New York, Sept. 7, 1889.
Gateshead dispute was due to antipathy between consultants
Authors: D. Campbell
Journal: BMJ (1998)

A ministerial investigation of gynaecological surgery services at the Queen Elizabeth Hospital, Gateshead, has reported that the hospital's department of gynaecological oncology “provides a safe and effective service,” that “standards of care for women in the region with gynaecological cancers are high,” and that “quality of care is good.”

Health minister Alan Milburn's investigation follows a row within the department that had resulted in seven external reviews in 10 years and has cost the Northern and Yorkshire Region of the NHS an estimated £200000 ($320000).

Mr Milburn was responding to Newcastle MP Jim Cousins after an adjournment debate last year in which “serious concerns” were raised about the unit and a consultant surgeon, John Monaghan (22 November, p 1328). Mr Cousins had claimed that Debi Sinha, a consultant colleague of Mr Monaghan, had been victimised as a “whistleblower” for raising a range of concerns which extended back to the 1980s.

Reviews of the current clinical …
Polyclinics: haven’t we been there before?
Authors: Virginia Berridge
Journal: BMJ (2008)

Cisplatin is a chemotherapeutic agent that is widely used in the treatment of solid tumors. Ototoxicity is a common side effect of cisplatin therapy and often leads to permanent hearing loss. The sensory organs of the avian ear are able to regenerate hair cells after aminoglycoside ototoxicity. This regenerative response is mediated by supporting cells, which serve as precursors to replacement hair cells. Given the antimitotic properties of cisplatin, we examined whether the avian ear was also capable of regeneration after cisplatin ototoxicity. Using cell and organ cultures of the chick cochlea and utricle, we found that cisplatin treatment caused apoptosis of both auditory and vestibular hair cells. Hair cell death in the cochlea occurred in a unique pattern, progressing from the low-frequency (distal) region toward the high-frequency (proximal) region. We also found that cisplatin caused a dose-dependent reduction in the proliferation of cultured supporting cells as well as increased apoptosis in those cells. As a result, we observed no recovery of hair cells after ototoxic injury caused by cisplatin. Finally, we explored the potential for nonmitotic hair cell recovery via activation of Notch pathway signaling. Treatment with the γ-secretase inhibitor <i>N</i>-[<i>N</i>-(3,5-difluorophenacetyl)-l-alanyl]-<i>S</i>-phenylglycine <i>t</i>-butyl ester failed to promote the direct transdifferentiation of supporting cells into hair cells in cisplatin-treated utricles. Taken together, our data show that cisplatin treatment causes maintained changes to inner ear supporting cells and severely impairs the ability of the avian ear to regenerate either via proliferation or by direct transdifferentiation.
Mitral valve prolapse in patients with prior rheumatic fever.
Authors: N J Lembo, L J Dell'Italia, M H Crawford, J F Miller, K L Richards, R A O'Rourke
Journal: Circulation (1988)

It is known that rheumatic heart disease frequently results in isolated mitral regurgitation without concomitant mitral stenosis, especially in countries with a high prevalence of rheumatic fever. However, more recent surgical pathologic data also have demonstrated a high incidence of mitral valve prolapse in cases of rheumatic heart disease, which suggests that rheumatic fever may be a cause of mitral valve prolapse. To determine whether this association of mitral valve prolapse and rheumatic heart disease is present in a stable clinic population, we studied 30 patients who had an apical systolic murmur and a well-documented history of rheumatic fever with dynamic auscultation, two-dimensional echocardiography, and pulsed Doppler examinations. Twenty of the 30 patients (67%) had findings on physical examination consistent with isolated mitral regurgitation and 25 patients (84%) had mitral regurgitation by Doppler examination. Echocardiography demonstrated mitral valve prolapse in 24 patients (80%), whereas only one of the total study group had echocardiographic findings consistent with mitral stenosis. We conclude that (1) the presence of an isolated systolic murmur in patients with a history of rheumatic fever frequently represents pure mitral regurgitation secondary to mitral valve prolapse and (2) postinflammatory changes in valvular tissue resulting from rheumatic fever may be the etiology of mitral valve prolapse in these patients.
Abstract P6-01-03: Decreasing the metastatic potential in Triple Negative Breast Cancer through the miR-17 cluster
Authors: L Jin, B Simone, Y Sano, M Lim, S Zhao, JE Savage, R Baserga, K Camphausen, NL Simone
Journal: Cancer Research (2012)

Abstract Background: In animal models of breast cancer, caloric restriction (CR), or a 25–30% reduction of calories, has decreased tumor initiation and progression. We sought to determine if CR could be used as a novel therapeutic intervention to enhance cytotoxic therapies such as radiation (RT) and alter the molecular profile of triple negative breast cancer (TNBC), which displays a poor prognosis. Methods/Results: In two murine models of TNBC (4T1 which is highly metastatic and 67NR which is locally aggressive), mice with palpable tumors were treated with radiation, caloric restriction (30% intake reduction) or both. 3 times per week measurements revealed significant tumor regression with RT or diet modification, and an even greater regression is observed combining diet modification with RT. Concurrently, many reports have shown that TNBC is most distinct from other breast tumor subtypes due to up-regulation of the miR-17-92 cluster which we have shown by RT-PCR is downregulated with both CR and radiation (RT) and even further decreased with the combination. cDNA arrays done on all conditions revealed that the top 5 statistically significant GO terms with high fold changes were all associated with extracellular matrix and metastases. In silico analysis demonstrated 5 ECM related genes that were targets of the miR-17 cluster: collagen 4 alpha 1 (COL4A1), collagen 4 alpha 3 (COL4A3), laminin alpha 3 (LAMA3), metallopeptidase inhibitor 2 and 3 (TIMP2 and TIMP3) and these were inversely correlated with the miRs. Conclusions: CR, or altering the metabolism of breast cancer, can be combined with RT to decrease progression of TNBC tumors and that the miR-17-92 cluster is also decreased with these conditions. cDNA arrays suggest that extracellular matrix (ECM) proteins play a large role in the mechanism of action of CR and RT combined. Combination therapy with CR and RT can decrease the metastatic potential in TNBC and in part does this through the miR-17-92 cluster by way of controlling ECM. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P6-01-03.
Data on neuraminidase inhibitors were made available
Authors: Zoya Panahloo
Journal: BMJ (2004)

Screening without evidence of efficacy Thyroid ultrasonography is another exampleEditor-I agree with Law's view of screening, that screening of unproved value should not be advocated. 1 As a clinical endocrinologist I often have to deal with patients' anxieties about non-palpable incidental findings on thyroid ultrasonography, often performed for wrong or unjustified reasons.Sometimes patients arrive with already established surgical complications after unnecessary thyroid operations.Although a substantial number of incidental thyroid nodules may be histologically malignant, 2 their clinical importance has never been proved.A recent preliminary study indicates that the progression rate of non-palpable proved thyroid malignant nodules to clinically significant lesions may be very low. 3 Thyroid ultrasonography is an additional example of an often used, often non-efficacious screening modality that may lead to "cascade iatrogenesis." 4
Cross-Sectional Assessment of the Effect of Kidney and Kidney-Pancreas Transplantation on Resting Left Ventricular Energy Metabolism in Type 1 Diabetic-Uremic Patients
Authors: Gianluca Perseghin, Paolo Fiorina, Francesco De Cobelli, Paola Scifo, Antonio Esposito, Tamara Canu, Massimo Danna, Chiara Gremizzi, Antonio Secchi, Livio Luzi, Alessandro Del Maschio
Journal: Journal of the American College of Cardiology (2005)
Mutations induced in the hypoxanthine phosphoribosyl transferase gene by three urban air pollutants: acetaldehyde, benzo[a]pyrene diolepoxide, and ethylene oxide.
Authors: B Lambert, B Andersson, T Bastlova, S M Hou, D Hellgren, A Kolman
Journal: Environmental Health Perspectives (1994)

Provisional mutational spectra at the hypoxanthine phosphoribosyl transferase (HPRT) locus in vitro have been worked out for acetaldehyde (AA) and benzo[a]pyrene diolepoxide (BPDE) in human (T)-lymphocytes and for ethylene oxide (EtO) in human diploid fibroblasts using Southern blotting and polymerase chain reaction (PCR)-based DNA sequencing techniques. The results indicate that large genomic deletions are the predominating hprt mutations caused by AA and EO, whereas BPDE induces point mutations that are mainly GC &gt; TA transversions. The mutational spectra induced by the three agents are clearly different from the background spectrum in human T-cells. Thus, the hprt locus is a useful target for the study of chemical-specific mutational events that may help identify causes of background mutation in human cells in vivo.
Mammography No Benefit in Reducing Deaths From Breast Cancer
Authors: Anita Slomski
Journal: JAMA (2014)

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High dose ascorbic acid in the management of thalassaemia leg ulcers—a pilot study
Authors: A.M. AFIFI, L. ELLIS, R.G. HUNTSMAN, M.I. SAID
Journal: British Journal of Dermatology (1975)

Eight patients with β thalassaemia major suffering from leg ulcers, were treated over an 8‐week period with 3 g ascorbic acid daily in a controlled double‐blind crossover study. The ulcers of all the patients showed a high rate of either complete or partial healing.
Stimulation of endothelial adenosine A1 receptors enhances adhesion of neutrophils in the intact guinea pig coronary system
Authors: S Zahler, B F Becker, P Raschke, E Gerlach
Journal: Cardiovascular Research (1994)

Objective: The primary aim was to determine the action of pathophysiologically relevant adenosine concentrations (0.1-1 μM) on adhesion of neutrophils to coronary endothelium. Further aims were to evaluate the nature and localisation of the adenosine receptor involved, and to assess the effect of endogenous adenosine. Methods: Adhesion was studied in isolated perfused guinea pig hearts by determining the number of cells emerging in the coronary effluent after intracoronary bolus injections of 600 000 neutrophils prepared from guinea pig or human blood. The system was characterised by the use of the proadhesive stimulus thrombin. Results: A 5 min infusion of adenosine (0.1-0.3 μM) or the A1 receptor agonist N6−cyclopentyladenosine (CPA, 0.01 μM) significantly increased adhesion from about 20% (control) to 30%. This effect was prevented by the A1 receptor antagonist dipropyl-8-cyclopentylxanthine (DPCPX, 0.1 μM). It was not diminished by cessation of adenosine infusion 90 s prior to neutrophil injection. At a higher concentration of adenosine (1 μM), adhesion did not seem to be enhanced. However, coinfusion of the A1 receptor antagonist 3,7-dimethyl-l-propargylxanthine (DMPX. 0.1 μM) with 1 μM adenosine unmasked the A1 action, adhesion rising to 39%. Adenosine had a quantitatively identical effect on adhesion of human neutrophils. Total ischaemia of 15 min duration raised adhesion of subsequently applied neutrophils to 35%. This effect was completely blocked by DPCPX, as well as by ischaemic preconditioning (3 × 3 min). Preconditioning raised initial postischaemic coronary effluent adenosine from about 0.8 μM to 1.5 μM. Conclusions: The findings suggest a bimodal participation of adenosine in the development of postischaemic dysfunction by an endothelium dependent modulation of neutrophil adhesion. Stimulation occurs via endothelial A1 receptors at submicromolar adenosine levels, whereas cardio-protection by adenosine may in part relate to the use of pharmacologically high concentrations of adenosine or enhanced endogenous production after preconditioning. Cardiovascular Research 1994;28:1366-1372
Tc-99m MIBI Scintigraphy in Multiple Myeloma
Authors: Jaroslav Bacovsky, Miroslav Myslivecek, Vlastimil Scudla, Pavel Koranda, Eva Buriankova, Jiri Minarik, Tomas Pika, Jana Zapletalova
Journal: Clinical Nuclear Medicine (2010)

Technetium-99m 2 methoxyisobutylisonitrile (Tc-99m MIBI) scintigraphy has been used to identify biologic activity and extent of multiple myeloma (MM) and monoclonal gammopathy of unknown significance (MGUS). The examination could also serve both as a prognostic tool and an examination for monitoring the disease course in MM patients. The purpose of this study was to evaluate the prognostic value of different Tc-99m MIBI uptake patterns.Ninety-nine consecutive patients with newly diagnosed symptomatic MM and 18 patients with MGUS underwent baseline Tc-99m MIBI scintigraphy before applying any kind of therapy. The Tc-99m MIBI scans were classified as showing normal, diffuse, and focal or combined (diffuse and focal) patterns of tracer uptake. To evaluate the prognostic value of different Tc-99m MIBI uptake patterns, overall survival (OS) was chosen as an end point. Median of follow-up period was 84 months. Survival according to patterns of Tc-99m MIBI uptake was calculated using the Kaplan-Meier plots.Statistically significant correlation between the baseline patterns of Tc-99m MIBI uptake and OS was found (P < 0.0001). Focal or combined patterns of Tc-99m MIBI uptake indicated significantly worse prognosis with shorter OS than normal or diffuse tracer patterns.Tc-99m MIBI scintigraphy plays the predictive role in the follow-up of patients with MM. Baseline scintigraphic pattern of Tc-99m MIBI uptake seems to be a useful prognostic indicator of OS in MM patients and Tc-99m MIBI scintigraphy could be used as an additional tool for the initial examination in patients with newly diagnosed MM.
Non-alcoholic steatohepatitis: The role of oxidized low-density lipoproteins
Authors: Sofie M.A. Walenbergh, Ger H. Koek, Veerle Bieghs, Ronit Shiri-Sverdlov
Journal: Journal of Hepatology (2012)

Non-alcoholic steatohepatitis (NASH) is hallmarked by lipid accumulation in the liver (steatosis) along with inflammation (hepatitis). The transition from simple steatosis towards NASH represents a key step in pathogenesis, as it will set the stage for further severe liver damage. Yet, the pathogenesis behind hepatic inflammation is still poorly understood. It is of relevance to better understand the underlying mechanisms involved in NASH in order to apply new knowledge to potential novel therapeutic approaches. In the current review, we propose oxidized cholesterol as a novel risk factor for NASH. Here, we summarize mouse and human studies that provide possible mechanisms for the involvement of oxidized low-density lipoproteins in NASH and consequent potential novel diagnostic tools and treatment strategies for hepatic inflammation.