tbuckley/cabot-search huggingface dataset:
Exercise-induced ST-segment depression in patients without restenosis after coronary angioplasty. Relation to preprocedural impaired left ventricular function.
Authors: J P Beregi, C Bauters, E P McFadden, P Quandalle, M E Bertrand, J M Lablanche
Journal: Circulation (1994)

BACKGROUND ST-segment depression during exercise testing is frequently observed in the absence of restenosis after coronary angioplasty. METHODS AND RESULTS We studied the determinants of this phenomenon in 70 consecutive patients with unstable angina related to a single left anterior descending coronary artery lesion who had successful angioplasty without restenosis (&lt; 50% stenosis by quantitative angiography). We compared preangioplasty clinical, angiographic, and hemodynamic variables in the group with positive (ExT Pos, n = 35; ST depression, 2.3 +/- 0.9 mm) and negative (ExT Neg, n = 35; ST depression, 0.3 +/- 0.5 mm) results on exercise testing at follow-up angiography. At this time, minimal lumen diameter (1.7 +/- 0.4 mm) and mean residual stenosis (34 +/- 11%) in the ExT Pos group were not significantly different from the values (1.9 +/- 0.5 mm, 38 +/- 10%) in the ExT Neg group. Before angioplasty, the ExT Pos group had a lower ejection fraction (63 +/- 8% versus 68 +/- 9%, P &lt; .05), more marked anterior hypokinesis estimated by the extent of anterior wall contraction on quantitative ventriculography (P &lt; .05), and a greater end-systolic volume (30 +/- 11 versus 25 +/- 9 mL/m2, P &lt; .05) than the ExT Neg group. At follow-up angiography, regional anterior wall motion was normal in 68 patients (97%). Anterior hypokinesis before angioplasty was strongly associated (P &lt; .01) with a positive exercise test at control (71% compared with 31% in patients with normal wall motion before angioplasty). CONCLUSIONS In the absence of significant epicardial stenosis after angioplasty, ST-segment depression is strongly associated with the presence of preprocedural regional ventricular dysfunction that has recovered at follow-up angiography.
REGULATION OF THE SECONDARY ANTIBODY RESPONSE IN VITRO
Authors: Charles T. Ambrose
Journal: The Journal of Experimental Medicine (1973)

A material inhibiting antibody synthesis in vitro is produced during the productive phase by rabbit lymph node organ cultures undergoing a secondary response. This antibody inhibitory material (AIM) has been isolated from serum-free medium taken from the cultures and also extracted from lymph node fragments as late as their 4th wk in vitro. AIM inhibits most strikingly the early productive phase of the secondary response in vitro (i.e, during the 2nd wk). AIM isolated from cultures undergoing a given immune response inhibits the same as well as different responses, thus indicating an immunologically nonspecific effect. Ultrafiltration and related studies reveal that the molecular size of AIM is 10,000-50,000 daltons and that it is not antibody. AIM can readily be separated from 7S globulin by use of CM-cellulose. The inhibitory activity of AIM is lost by digestion with ribonuclease. Thus the avoidance of serum with its high levels of ribonucleases may be crucial in the study of this material. The presence in eukaryotic cells of metabolic regulators, governors, etc. has been postulated largely by analogy with microbial systems (27). There is little direct evidence about the chemical nature of these presumed regulators. Our data on the RNase sensitivity of AIM raises the possibility in this lymphoid system of regulation by a species of RNA.
Mutations of Ki-ras and p53 genes in colorectal cancer and their prognostic significance.
Authors: M Morrin, M Kelly, N Barrett, P Delaney
Journal: Gut (1994)

The series of genetic changes leading to malignancy in colorectal cancer is well reported. This includes mutational activation of the proto-oncogene Ki-ras and mutation/deletion of the p53 tumour suppressor gene. The frequency of these mutations was investigated in a panel of 52 colorectal cancer patients using a combination of immunocytochemistry and non-radioactive, digoxigenin-labelled in situ hybridisation. Sixty two per cent (32 of 52) of the study population were positive for p53 overexpression and 36% (19 of 52) positive for Ki-ras mutation. Twenty seven per cent (14 of 52) of the patients expressed both mutations. Mutation of either the p53 or the Ki-ras gene did not correlate with Dukes9s stage, tumour differentiation or 5 year survival rate of the patients. Most of the rectal carcinoma specimens (11 of 15) showed p53 over-expression but the significance of this was not supported statistically. Thus detection of molecular changes is becoming more amenable to incorporation into routine histological carcinoma assessment because of the advent of non-radioactive labelling in in situ hybridisation and antibodies suitable for paraffin wax embedded specimens. The significance of these mutations in disease prognosis, however, remains questionable.
Thyroid Function Within the Normal Range and Risk of Coronary Heart Disease
Authors: Bjørn O. Åsvold, Lars J. Vatten, Trine Bjøro, Douglas C. Bauer, Alexandra Bremner, Anne R. Cappola, Graziano Ceresini, Wendy P. J. den Elzen, Luigi Ferrucci, Oscar H. Franco, Jayne A. Franklyn, Jacobijn Gussekloo, Giorgio Iervasi, Misa Imaizumi, Patricia M. Kearney, Kay-Tee Khaw, Rui M. B. Maciel, Anne. B. Newman, Robin P. Peeters, Bruce M. Psaty, Salman Razvi, José A. Sgarbi, David J. Stott, Stella Trompet, Mark P. J. Vanderpump, Henry Völzke, John P. Walsh, Rudi G. J. Westendorp, Nicolas Rodondi
Journal: JAMA Internal Medicine (2015)

Some experts suggest that serum thyrotropin levels in the upper part of the current reference range should be considered abnormal, an approach that would reclassify many individuals as having mild hypothyroidism. Health hazards associated with such thyrotropin levels are poorly documented, but conflicting evidence suggests that thyrotropin levels in the upper part of the reference range may be associated with an increased risk of coronary heart disease (CHD).
Varicella-zoster virus immunity in dermatological patients on systemic immunosuppressant treatment
Authors: C.B. Hackett, D. Wall, S.F. FitzGerald, S. Rogers, B. Kirby
Journal: British Journal of Dermatology (2011)

Primary varicella infection is caused by varicella-zoster virus (VZV). It is a common childhood infection, which is usually benign but can occasionally cause morbidity and mortality. In immunosuppressed adults, atypical presentation and disseminated disease can occur with significant morbidity and mortality. A VZV vaccine is available.This study was designed to measure the prevalence of immunity to VZV and to determine the predictive value of a self-reported history of varicella infection in a population of dermatological patients receiving systemic immunosuppressant therapy. We sought to assess the need for routine serological testing for varicella-zoster immunity in this cohort.Serological testing for VZV immunity was done on 228 patients receiving systemic immunosuppressive treatment for a dermatological condition. Information regarding a history of previous primary VZV infection was obtained from each patient.Two hundred and twenty-eight patients had VZV serology performed. The mean age of the patients was 49·6 years. The prevalence of VZV seropositivity in this cohort was 98·7%. One hundred and two patients (44·7%) reported having a definite history of primary VZV. The sensitivity of a self-reported history of VZV infection was 45·3% with a specificity of 100%. The positive and negative predictive values of a self-reported history of VZV for serologically confirmed immunity were 100% and 2·3%, respectively.The prevalence of VZV IgG antibodies in our cohort of Irish dermatology patients receiving immunosuppressive therapy is 98·7%. A recalled history of varicella infection is a good predictor of serological immunity. This study has shown that there are VZV-susceptible individuals within our cohort. These patients did not have a clear history of previous infection. We recommend serological testing of patients without a clear history of infection prior to the commencement of immunosuppressive therapy and vaccination of patients with negative serology.
The Politics of Local Tobacco Control
Authors: Bruce Samuels
Journal: JAMA (1991)

Until the nonsmokers' rights movement, tobacco control activity was at the federal or state levels, which is where the tobacco industry dominates. Since the appearance of the nonsmokers' rights movement, progress in tobacco control has occurred primarily at the local level. In response to the success of this movement, the tobacco industry has developed "smokers' rights" groups and other tactics to fight local legislation. Several recent local campaigns in California illustrate these tactics. Tobacco control forces follow many paths, from sitting on the sidelines to making a serious commitment to smoking control legislation. Despite the tobacco industry's superior financial resources, the outcome of proposed local tobacco control legislation appears to depend on how seriously the health advocates mobilize in support of the local legislation. When the health community makes a serious commitment of time and resources, it wins. When it fails to make such a commitment, the tobacco industry prevails, more by default than by its superior financial resources. (<i>JAMA</i>. 1991;266:2110-2117)
A few health insurers monopolise US market
Authors: Janice Hopkins Tanne
Journal: BMJ (2006)

Mergers between health insurance companies have created virtual monopolies that limit consumer choice, do not offer savings on premiums, and give doctors little or no bargaining power, a report from the American Medical Association claims. The past decade has seen more than 400 mergers among health insurance companies and managed care organisations, says the report, which analysed the insurance markets in nearly 300 metropolitan areas.

As of 2005, in 95% of these metropolitan areas, one insurer had at least a 30% market share. In 56% of areas, one insurer had more than half the …
K-<i>ras</i> Codon-Specific Mutations Produce Distinctive Metabolic Phenotypes in Human Fibroblasts
Authors: Pedro Vizan, Laszlo G. Boros, Agnes Figueras, Gabriel Capella, Ramon Mangues, Sara Bassilian, Shu Lim, Wai-Nang P. Lee, Marta Cascante
Journal: Cancer Research (2005)

Abstract Among K-ras mutations, codon 12 mutations have been identified as those conferring a more aggressive phenotype. This aggressiveness is primarily associated with slow proliferation but greatly increased resistance to apoptosis. Using transfected NIH3T3 fibroblasts with a mutated K-ras minigene either at codon 12 (K12) or at codon 13 (K13), and taking advantage of [1,2-13C2]glucose tracer labeling, we show that codon 12 mutant K-ras (K12)-transformed cells exhibit greatly increased glycolysis with only a slight increase in activity along pathways that produce nucleic acid and lipid synthesis precursors in the oxidative branch of the pentose phosphate pathway and via pyruvate dehydrogenase flux. K13 mutants display a modest increase in anaerobic glycolysis associated with a large increase in oxidative pentose phosphate pathway activity and pyruvate dehydrogenase flux. The distinctive differences in metabolic profiles of K12 and K13 codon mutated cells indicate that a strong correlation exists between the flow of glucose carbons towards either increased anaerobic glycolysis, and resistance to apoptosis (K12), or increased macromolecule synthesis, rapid proliferation, and increased sensitivity to apoptosis.
PDGF signaling in pulmonary arterial hypertension
Authors: R. J. Barst
Journal: Journal of Clinical Investigation (2005)

The pathobiology of pulmonary arterial hypertension (PAH) includes endothelial cell dysfunction and proliferation and migration of VSMCs. As PDGF has been implicated in these processes, Schermuly et al. hypothesized that altered PDGF signaling may be involved in the vascular remodeling observed in PAH. To explore this notion further, the authors evaluated the effects of the PDGF receptor inhibitor STI571 in 2 different animal models of pulmonary hypertension. In both models, after development of pulmonary vascular disease, administration of STI571 reversed pulmonary vascular changes. These studies provide preclinical proof of concept for the clinical development of a PDGF inhibitor as a targeted therapy for PAH patients.
Antigenic heterogeneity of gonococcal pili.
Authors: T M Buchanan
Journal: The Journal of Experimental Medicine (1975)

Pili were isolated from two different strains of gonococci (33 and 2686) and demonstrated to be pure by the criteria of electron microscopy and polyacrylamide gel electrophoresis in sodium dodecyl sulfate. Each purified pili preparation was studied for its ability to inhibit; (a) binding of 124-I-labeled purified 2686 pili by antibody to 2686 pili, and (b) binding of 125-I-labeled purified 33 pili by antibody to 33 pili. In each instance progressive inhibition of binding was produced by homologous pili type, but no significant inhibition was observed using comparable weights of the heterologous pili type. These results indicate that the pili of strains 2686 and 33 are antigenically different.
iNKT/CD1d-antitumor immunotherapy significantly increases the efficacy of therapeutic CpG/peptide-based cancer vaccine
Authors: Stéphanie Corgnac, Rachel Perret, Lianjun Zhang, Jean-Pierre Mach, Pedro Romero, Alena Donda
Journal: Journal for ImmunoTherapy of Cancer (2014)

Therapeutic cancer vaccines aim to boost the natural immunity against transformed cancer cells, and a series of adjuvants and co-stimulatory molecules have been proposed to enhance the immune response against weak self-antigens expressed on cancer cells. For instance, a peptide/CpG-based cancer vaccine has been evaluated in several clinical trials and was shown in pre-clinical studies to favor the expansion of effector T versus Tregs cells, resulting in a potent antitumor activity, as compared to other TLR ligands. Alternatively, the adjuvant activity of CD1d-restricted invariant NKT cells (iNKT) on the innate and adaptive immunity is well demonstrated, and several CD1d glycolipid ligands are under pre-clinical and clinical evaluation. Importantly, additive or even synergistic effects have been shown upon combined CD1d/NKT agonists and TLR ligands. The aim of the present study is to combine the activation and tumor targeting of activated iNKT, NK and T cells.Activation and tumor targeting of iNKT cells via recombinant α-galactosylceramide (αGC)-loaded CD1d-anti-HER2 fusion protein (CD1d-antitumor) is combined or not with OVA peptide/CpG vaccine. Circulating and intratumoral NK and H-2Kb/OVA-specific CD8 responses are monitored, as well as the state of activation of dendritic cells (DC) with regard to activation markers and IL-12 secretion. The resulting antitumor therapy is tested against established tumor grafts of B16 melanoma cells expressing human HER2 and ovalbumin.The combined CD1d/iNKT antitumor therapy and CpG/peptide-based immunization leads to optimized expansion of NK and OVA-specific CD8 T cells (CTLs), likely resulting from the maturation of highly pro-inflammatory DCs as seen by a synergistic increase in serum IL-12. The enhanced innate and adaptive immune responses result in higher tumor inhibition that correlates with increased numbers of OVA-specific CTLs at the tumor site. Antibody-mediated depletion experiments further demonstrate that in this context, CTLs rather than NK cells are essential for the enhanced tumor inhibition.Altogether, our study in mice demonstrates that αGC/CD1d-antitumor fusion protein greatly increases the efficacy of a therapeutic CpG-based cancer vaccine, first as an adjuvant during T cell priming and second, as a therapeutic agent to redirect immune responses to the tumor site.
A Self‐Adjuvanting Supramolecular Vaccine Carrying a Folded Protein Antigen
Authors: Gregory A. Hudalla, Justin A. Modica, Ye F. Tian, Jai S. Rudra, Anita S. Chong, Tao Sun, Milan Mrksich, Joel H. Collier
Journal: Advanced Healthcare Materials (2013)

This work illustrates a strategy for the design of molecularly defined immunotherapies, using a blend of supramolecular peptide self-assembly and active site-directed protein capture.
A Controlled Clinical Trial of Bupropion for Attention Deficit Hyperactivity Disorder in Adults
Authors: Timothy E. Wilens, Thomas J. Spencer, Joseph Biederman, Kristine Girard, Robert Doyle, Jefferson Prince, David Polisner, Ramon Solhkhah, Sharyn Comeau, Michael C. Monuteaux, Asha Parekh
Journal: American Journal of Psychiatry (2001)

OBJECTIVE: Despite the increasing recognition of attention deficit hyperactivity disorder (ADHD) in adults, there is a paucity of controlled pharmacological trials demonstrating the effectiveness of compounds used in treatment, particularly nonstimulants. The authors report results from a controlled investigation to determine the anti-ADHD efficacy of bupropion in adult patients with DSM-IV ADHD. METHOD: This was a double-blind, placebo-controlled, randomized, parallel, 6-week trial comparing patients receiving sustained-release bupropion (up to 200 mg b.i.d.) (N=21) to patients receiving placebo (N=19). The authors used standardized structured psychiatric instruments for diagnosis of ADHD. To measure improvement, they used separate assessments of ADHD, depression, and anxiety symptoms at baseline and each weekly visit. RESULTS: Of the 40 subjects (55% male) enrolled in the study, 38 completed the study. Bupropion treatment was associated with a significant change in ADHD symptoms at the week-6 endpoint (42% reduction), which exceeded the effects of placebo (24% reduction). In analyses using a cutoff of 30% or better reduction to denote response, 76% of the subjects receiving bupropion improved, compared to 37% of the subjects receiving placebo. Similarly, in analyses using Clinical Global Impression scale scores, 52% of the subjects receiving bupropion reported being “much improved” to “very improved,” compared to 11% of the subjects receiving placebo. CONCLUSIONS: These results indicate a clinically and statistically significant effect of bupropion in improving ADHD in adults. The results suggest a therapeutic role for bupropion in the armamentarium of agents for ADHD in adults, while further validating the continuity of pharmacological responsivity of ADHD across the lifespan.
Pediatric Obsessive-Compulsive Disorder
Authors: Lisa A. Snider
Journal: JAMA (2000)

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Vascular Inflammation Is Negatively Autoregulated by Interaction Between CCAAT/Enhancer-Binding Protein-δ and Peroxisome Proliferator-Activated Receptor-γ
Authors: Yasunori Takata, Yutaka Kitami, Zhao-Hui Yang, Michitsugu Nakamura, Takafumi Okura, Kunio Hiwada
Journal: Circulation Research (2002)

CCAAT/enhancer-binding proteins (C/EBPs) upregulate transcription of various inflammatory cytokines and acute phase proteins, such as interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and cyclooxygenase-2. Recent studies have demonstrated that peroxisome proliferator-activated receptor (PPAR)-γ is present in atherosclerotic lesions, and negatively regulates expression of these genes. Interestingly, PPAR-γ gene promoter has tandem repeats of C/EBP-binding motif, and C/EBP-δ plays a pivotal role in transactivation of PPAR-γ gene. It has been well known that the interaction between C/EBPs and PPAR-γ plays a central role in maintaining adipocyte differentiation and glucometabolism; however, the relationship between PPAR-γ and C/EBPs in the vessel wall remains unclear. In the present study, we showed that a high level of C/EBP-δ expression induced by inflammation positively regulated transcription and protein expression of PPAR-γ in vascular smooth muscle cells (VSMCs). On the other hand, PPAR-γ ligands troglitazone, pioglitazone, and 15-deoxy-Δ 12,14 -prostaglandin J 2 inhibited IL-1β-induced IL-6 expression at a transcriptional revel in VSMCs. Functional promoter analysis revealed that PPAR-γ ligands inhibited IL-1β-induced transactivation of IL-6 gene via suppression of not only nuclear factor-κB but also C/EBP-DNA binding. Moreover, PPAR-γ ligands suppressed protein expression and transcription of C/EBP-δ through dephosphorylation of signal transducer and activator of transcription 3. These findings strongly suggest that C/EBP-δ is negatively autoregulated via transactivation of PPAR-γ. This feedback mechanism probably downregulates transcription of inflammatory cytokines and acute phase proteins, and modulates inflammatory responses in the early process of atherosclerosis.
Women in their 40s should not be screened for breast cancer, new Canadian guideline says
Authors: A. O'Dowd
Journal: BMJ (2011)

Experts in Canada have recommended that women aged 40 to 49 should not be routinely screened for breast cancer and that the frequency of mammographic screening should be changed from every other year to every two to three years.

The guidance from the Canadian Task Force on Preventive Health Care, published in CMAJ , the journal of the Canadian Medical Association (doi:10.1503/cmaj.110334), also says that women should not be urged to check their breasts for cancer on a regular basis or have their GP carry out an examination, because there was no evidence that doing so reduced mortality rates.

In addition, the guideline, the first on breast cancer issued by the task force since 2001, says that women aged 70 to 74 should be undergoing mammography at the same frequency as women …