tbuckley/cabot-search huggingface dataset:
Abstract 15761: New Onset Atrial Fibrillation After Transcatheter Aortic Valve Implantation: A Pooled Meta-Analysis
Authors: Arun Kanmanthareddy, Madhu Reddy, Venkata S Koripalli, Avanija Buddam, Nivedita Adabala, Pramod Janga, Trenton Bickel, Cory Gutovitz, Sudharani Bommana, Donita Atkins, Dhanunjaya Lakkireddy
Journal: Circulation (2014)

Introduction: Atrial fibrillation (AF) after cardiac surgery is associated with increased morbidity and mortality. Data comparing the occurrence of AF after transcatheter aortic valve implantation (TAVI) and surgical aortic valve replacement (SAVR) is unknown. Methods: We identified all studies reporting outcomes after TAVI in all available electronic databases. Meta-analysis of all the studies was performed using random effects model to a) evaluate the incidence of AF and b) compare the incidence of AF between TAVI and SAVR. Results: The incidence of AF was reported in 7 studies, 5 prospective observational studies and 2 randomized controlled studies. The cumulative event rate for new onset AF at 30 days after TAVI was 0.1 (95% CI; 0.06 -0.17). Three studies reported incidence of AF after TAVI and SAVR. The odds ratio (OR) of developing new onset AF with TAVI compared to SAVR was 0.3 (95% CI; 0.10 - 0.88) at 30 days. One year outcome of new onset AF was reported in only two studies. Although, the incidence of AF was lower in the TAVI group, this did not reach statistical significance (OR 0.7, 95% CI; 0.46 -1.07). Conclusion: The incidence of new onset AF after TAVI is 10% within the first 30 days. This risk is 70% lower in patients undergoing TAVI compared to SAVR. The impact of AF after TAVI in terms of stroke, mortality and future recurrences of AF are unknown. Further studies are therefore necessary to study these outcomes.
Hodgkin and Reed-Sternberg cells represent an expansion of a single clone originating from a germinal center B-cell with functional immunoglobulin gene rearrangements but defective immunoglobulin transcription
Authors: Theresa Marafioti, Michael Hummel, Hans-Dieter Foss, Helmut Laumen, Petra Korbjuhn, Ioannis Anagnostopoulos, Hetty Lammert, Gudrun Demel, Jan Theil, Thomas Wirth, Harald Stein
Journal: Blood (2000)
HMG-Coa reductase inhibiting statins attenuate the p53 response to DNA damage
Authors: Ulla Stenius, Gerd Pääjärvi, Johan Högberg
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

2960 

HMG-CoA reductase catalyses the formation of mevalonate which is a key step in the biosynthesis in cholesterol. Several studies indicate that drugs inhibiting HMG-CoA reductase, statins, also inhibit growth of cancer cells in vitro and have anticancer effects in animal models. The cytotoxicity of e.g. 5-fluorouracil have been shown to be enhanced by statins. Mechanisms behind these effects have not been well characterized. In the present work the effect of statins on p53 stabilization was studied. It was found that the treatment of HepG2 cells with pravastatin or simvastatin in micromolar concentrations attenuated the induction of p53 by 5-fluorouracil and benzo(a)pyrene (BaP) as indicated in Western blot analysis. A similar effect on the p53 response was also induced by statins in primary rat hepatocytes exposed to diethylnitrosamine. Thus, nuclear staining for p53 was reduced from 9±0.9% to 4.4±0.5% when cells were simultaneously treated with 0.1uM pravastatin. The amount of serine 15 phosphorylated p53 was also reduced. The low p53 response was associated with an attenuated accumulation of the p53 downstream target gene products Mdm2 and p21. Further studies indicated an increased degradation of both Mdm2 and p53 stabilized by 5-fluorouracil, showing decreased half-lives for both proteins. Statins alone have previously been shown to induce p21, but this effect was not induced by the low concentrations of statins (0.1-5 uM) used here. We also examined whether the effect of statins on p53 stabilization was cell cycle dependent and found that simvastatin attenuated the p53 response to DNA damage in G synchronized cells as well as in non-synchronized cells. As the protein level and the degree of phosphorylation of Mdm2 may affect p53 turnover, the effect of statins on Mdm2 protein levels was studied in HepG2 cells. It was found that pravastatin (0.1-5uM) alone increased the level of Mdm2, as determined by the 2A10 antibody in G synchronized cells. Furthermore, an increased fraction of Mdm2 was phosphorylated at a 2A10 epitope. These data indicate that statins can increase Mdm2 levels in hepatocytes and that this effect may attenuate the p53 response in these cells.
A 3 year (2007-2010) tuberculosis treatment analysis in Belfast City Hospital, Northern Ireland
Authors: Izhaq Masih, Anne Breen, Shepherd Richard, Cecelia O'Kane
Journal: European Respiratory Journal (2011)

Introduction: Tuberculosis is on the rise globally. Northern Ireland is facing the enormous task to identify, diagnose and treat tuberculosis. Anti-tuberculosis treatment can be tedious and the side effects can hamper management and outcome.

Objectives: To note the prevalence among local and immigrant patients, ascertain the HIV status and concordance and tolerance of ant-tuberculosis drugs.

Methods: A retrospective clinical notes review, microbiology and biochemistry laboratory record analysis.

Results: In total 92 patients, half were originally from Northern Ireland [Table]; 61% male and 39% female. The mean age was 50 (± 21) years with a bimodal age distribution between immigrants (36±11 years) and local patients (66.5±15.5 years).

View this table:

Table 1





The majority (67%) had pulmonary and 20.5% had lymph node involvement. Rest had skin, bone, peritoneum, and psoas abscess disease. Culture positive were 76% and smear positive 45%. The majority (79%) were fully and 4% were partially sensitive to the treatment. One patient was multi-drug resistant. Four percent had HIV. The commonest side effect was minor GI upset (7%). Hepatitis and arthralgia occurred in 5.5%, minor skin reactions in 3%, and renal impairment, peripheral neuropathy, febrile reaction and retrobulbar neuritis in 2% each. Seven percent of patients received directly observed therapy.

Conclusion: Tuberculosis is increasingly prevalent among the local population. Only 4% were HIV positive. Good drug compliance was observed in two third of patients. Treatment was modified in 24%, no treatment was stopped.
Abstract 5521: TTFields reduce cancer cell clonogenic potential through abnormal chromosome segregation during mitosis
Authors: Rosa S. Schneiderman, Moshe Giladi, Yaara Porat, Mijal Munster, Eilon D. Kirson, Uri Weinberg, Yoram Palti
Journal: Cancer Research (2014)

Abstract TTFields cause mitotic arrest and cell death by the disruption of spindle microtubule arrangement and interference with cytokinesis. Recently it was reported that TTFields application results in reduced clonogenicity of cells surviving treatment. We hypothesized that TTFields can impair chromosome segregation during mitosis thus leading to a long term effect on surviving cancer cells. A2780 human ovarian cancer cells were treated with TTFields for 24, 48 and 72 hours and the cytotoxic effect and clonogenic potential were determined. Abnormal mitotic figures were analyzed using fluorescence microscopy and cell karyotyping was performed using Giemsa staining and SKY analysis. TTFields application led to 36, 52 and 43% cell growth inhibition after 24, 48 and 72 hours, respectively. Clonogenic assays revealed that only 12.9% of cells treated with TTFields for 72 hours maintained their ability to form colonies after 2 weeks. Immunofluorescence images revealed a significant increase in the number of abnormal mitotic figures amongst treated cells. Karyotyping analysis following 24 and 48 hours of TTFields application revealed 38.5% and 53.8% abnormal segregation events, respectively. After 24 hours of treatment, the proportion of cells with reduced and increased chromosomes number was equal, however, following 48 hours of treatment the population with a reduced chromosome number disappeared. These results demonstrate that in addition to their cytotoxic effect leading to mitotic death, TTFields also lead to abnormal chromosome segregation. The surviving aneuploid cells are impaired, providing a possible explanation for the reduced clonogenic potential reported in cancer cells treated with TTFields. Citation Format: Rosa S. Schneiderman, Moshe Giladi, Yaara Porat, Mijal Munster, Eilon D. Kirson, Uri Weinberg, Yoram Palti. TTFields reduce cancer cell clonogenic potential through abnormal chromosome segregation during mitosis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5521. doi:10.1158/1538-7445.AM2014-5521
Abstract 13176: Dissociation of Calmodulin From RyR2 Causes Diastolic Ca2+ leak and Induces Lethal Arrhythmias in Pressure-overload Heart Failure
Authors: Takayoshi Kato, Takeshi Yamamoto, Takako Maeda, Shigehiko Nishimura, Wakako Murakami, Takeshi Suetomi, Makoto Ono, Mamoru Mochizuki, Tetsuro Oda, Shinichi Okuda, Shigeki Kobayashi, Masafumi Yano
Journal: Circulation (2014)

Background:  Calmodulin (CaM) plays a key role in modulating channel gating in ryanodine receptor (RyR2). Here, we investigated the pathogenic role of RyR2 bound CaM in diastolic Ca 2+  leak from sarcoplasmic reticulum and arrhythmogenesis in pressure overload heart failure induced by transverse aortic constriction (TAC).   Methods and results:  Pressure overload to 12 weeks old mice were induced by TAC using a 27 gauge needle. Isolated cardiomyocytes from mice 8 weeks after from TAC operation were used for the present study. LV end-diastolic diameter was significantly enlarged. Lethal arrhythmias such as ventricular tachycardia/fibrillation were frequently observed after infusion of 2 mg/kg epinephrine and 120 mg/kg caffeine in TAC mice (100 %, n=4), but not in Sham mice (0 %, n=5). All following experiments were done under 1 μM of KN93 to avoid the effect of CaMKII. CaM binding to RyR2 was assessed by incorporation of exogenous CaM fluorescently labeled with HiLyte Fluor® in isolated saponin-permeabilised myocytes. The binding affinity of CaM decreased in TAC cells (Kd: 221 nM) compared with Sham cells (Kd: 78 nM). Frequency of the Ca 2+  sparks was measured in isolated saponin-permeabilised myocytes. The Ca 2+  spark frequency ( Events100μm -1 sec -1  by fluo3) was much higher in TAC than in Sham cardiomyocytes {TAC (13 cells, 3 hearts): 13.6±0.8; Sham (14 cells, 3 hearts): 7.5±0.7; p 2+  spark frequency {(18 cells 3 hearts): 9.4±0.5}. Spontaneous Ca 2+  transients were measured during sequential pacing of intact cardiomyocytes from 1 Hz to 5 Hz. Spontaneous Ca 2+  transients were rarely observed in Sham cells (4.9 %), whereas those were observed in 16.8 % of TAC cells. Incorporation of CaM to intact TAC cells using protein delivery kit (BioPORTER®) normalized the frequency of spontaneous Ca 2+  transients (6.2 %).   Conclusions:  In pressure-overloaded heart failure, CaM binding affinity to RyR2 is decreased. Our data suggest that the dissociation of CaM from RyR2 plays a predominant role in the diastolic Ca 2+  leak and arrhythmogenesis. CaM binding affinity to RyR2 might be a novel therapeutic target of lethal arrhythmia in pressure overload heart failure.
Abstract 13876: Cardiovascular Magnetic Resonance Imaging Elucidates Genotype-Phenotype Relationships in Patients with Hypertrophic Cardiomyopathy
Authors: Shahriar Heidary, Matthew T Wheeler, Mihoko V Bennett, Jaehoon Chung, Aleksandra Pavlovic, Marie-Claude Parent, Rajesh Dash, Michael V McConnell, Euan A Ashley, Phillip C Yang
Journal: Circulation (2011)

Shahriar Heidary, 2011 Finalist and Presenting Author
Industry Sponsorship of Continuing Medical EducationIndustry Sponsorship of Continuing Medical Education
Authors: Kurt J Boyce, Jacqueline Parochka, Karen Overstreet
Journal: JAMA (2003)

To the Editor: In his Commentary on the influence of the drug industry on continuing medical education (CME), Dr Relman argued that industry-sponsored medical education and communication companies (MECCs) exist solely for commercial purposes. We disagree, and find nothing in his commentary to support that conclusion. To quote Relman, we believe that “in the absence of evidence to support that assumption, it is an insult to our nation’s leading medical professionals” and to the professionals employed by MECCs to dismiss the value of MECCproduced CME on the basis of innuendo. Among the almost 700 entities accredited by the Accreditation Council for Continuing Medical Education (ACCME) are medical schools, government or military organizations, physician societies, and 94 organizations identified as MECCs. All of these groups carry the same rights and responsibilities implied by the accreditation badge that they earn. There are no different levels of accreditation. Furthermore, not all industry support for CME is funneled through MECCs. Relman quoted a recent Wall Street Journal article that indicated that 60% of all CME is underwritten by industry sources. The ACCME report for 2002 indicates that the external funding (including exhibits) supporting CME activities by organizations they accredit totaled some $933 million. Of those external dollars, 35.2% were generated by MECCs, 31.2% were generated by physician organizations, 17.4% by medical schools, and the balance by other organizations. Many CME courses are underwritten by industry through the licensing of satellite symposia and the selling of exhibit space. The overall enterprise in the case cited by Relman is managed by an MECC. Thus, it appears that medical educators can accept drug industry funds and still provide fair, useful courses on pressing issues. In addition, relative to the response of the Washington Legal Foundation to the ACCME’s proposed new standards, Relman stated, “oddly enough, the WLF [Washington Legal Foundation] brief never mentions MECCs by name or discusses their accreditation.” We do not find this odd at all. As the organization representing MECCs, we have had no discussion of this matter with Washington Legal Foundation. Our own response to the proposed new standards was drafted by our Board of Directors, and it can be found on our Web site (http://www .naamecc.org). We welcome Relman’s contributions to the debate on commercial support of CME, but his identification of MECCs as the major cause of conflict of interest in CME is off target. Through their active participation in the “CME community,” MECCs desire to be part of the solution to this problem. We believe that Relman’s broad condemnation is unjustified and does them a disservice.
Facile Resolution of α-Fetoproteins and Serum Albumins by Immobilized Metal Affinity Chromatography
Authors: Lennart Andersson, Eugene Sulkowski, Jerker Porath
Journal: Cancer Research (1987)

We have explored immobilized metal affinity chromatography as a means of resolving α-fetoprotein from its homologous albumin, a problem perennially encountered in the purification of an α-fetoprotein or its detection.

Human α-fetoprotein and human serum albumin were chromatographed on immobilized iminodiacetic acid charged with either Co2+, Ni2+, Cu2+, or Zn2+. Neither human α-fetoprotein nor human serum albumin displayed any affinity for Co2+ and Zn2+. However, both proteins were bound to Cu2+ and were partially resolved by affinity elution with imidazole. By contrast, human α-fetoprotein and human serum albumin were completely resolved on immobilized Ni2+. Similar results were obtained using bovine α-fetoprotein and bovine serum albumin.

The resolution of an α-fetoprotein from serum albumin should aid the purification of α-fetoprotein from a biological fluid containing overwhelming quantities of albumin, for example, serum. Importantly, the separation of human α-fetoprotein from human serum albumin may improve and help maintain the accuracy of immunoassays for α-fetoprotein, making the chromatography on immobilized Ni2+ a valuable diagnostic tool.
Male Circumcision for HIV Prevention in High HIV Prevalence Settings: What Can Mathematical Modelling Contribute to Informed Decision Making?
Authors: C Hankins, J Hargrove, B Williams, L Abu Raddad, B Auvert, L Bollinger, R Dorrington, A Ghani, R Gray, T Hallett, JG Kahn, N Lohse, N Nagelkerke, T Porco, G Schmid, J Stover, H Weiss, A Welte, P White, R White, Unaids Who Sacema Expert Grp Mod
Journal: PLoS Medicine (2009)

Experts from UNAIDS, WHO, and the South African Centre for Epidemiological Modelling report their review of mathematical models estimating the impact of male circumcision on HIV incidence in high HIV prevalence settings
Treatment of status epilepticus
Authors: Hideo Yamanouchi
Journal: JAMA (1976)

Status epilepticus is defined as epileptic seizure with the duration for over 30 min or clustered seizure without complete recovery of consciousness for 30 min or more. From the management point of view, therapeutic intervention is recommended for prolonged seizures for 5 min or more. Intranasal, buccal or intramuscular administration of midazolam is strongly evidence-based and highly recommended method for the treatment of prolonged seizures before the intravenous access. Diazepam or midazolam is the first choice as initial intravenous treatment. Intravenous bolus administration of fosphenytoin or phenobarbital is the second line treatment. General anesthesia using such as thiopental or propofol is indicated for refractory status epileptic, which should be managed in the intensive care unit.
Abstract 14174: MRI-Based Patient-Specific Virtual Electrophysiology Laboratory for Scar-Related Ventricular Tachycardia
Authors: Hiroshi Ashikaga, Hermenegild Arevalo, Fijoy Vadakkumpadan, Robert C Blake, Ronald D Berger, Hugh Calkins, Natalia A Trayanova, Henry R Halperin
Journal: Circulation (2011)

Hiroshi Ashikaga, 2011 Finalist and Presenting Author
Finding My Father's Hands in Mid-life
Authors: Walt McDonald
Journal: JAMA (2001)

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To transfuse or not to transfuse in upper gastrointestinal hemorrhage? That is the question
Authors: Don C. Rockey
Journal: Hepatology (2014)

Background: The hemoglobin threshold for transfusion of red cells in patients with acute gastrointestinal bleeding is controversial. We compared the efficacy and safety of a restrictive transfusion strategy with those of a liberal transfusion strategy. Methods: We enrolled 921 patients with severe acute upper gastrointestinal bleeding and randomly assigned 461 of them to a restrictive strategy (transfusion when the hemoglobin level fell below 7 g per deciliter) and 460 to a liberal strategy (transfusion when the hemoglobin fell below 9 g per deciliter). Randomization was stratified according to the presence or absence of liver cirrhosis. Results: A total of 225 patients assigned to the restrictive strategy (51%), as compared with 65 assigned to the liberal strategy (15%), did not receive transfusions (P < 0.001). The probability of survival at 6 weeks was higher in the restrictive-strategy group than in the liberal-strategy group (95% vs. 91%; hazard ratio for death with restrictive strategy, 0.55; 95% confidence interval [CI], 0.33 to 0.92; P = 0.02). Further bleeding occurred in 10% of the patients in the restrictive-strategy group as compared with 16% of the patients in the liberal-strategy group (P = 0.01), and adverse events occurred in 40% as compared with 48% (P = 0.02). The probability of survival was slightly higher with the restrictive strategy than with the liberal strategy in the subgroup of patients who had bleeding associated with a peptic ulcer (hazard ratio, 0.70; 95% CI, 0.26 to 1.25) and was significantly higher in the subgroup of patients with cirrhosis and Child–Pugh class A or B disease (hazard ratio, 0.30; 95% CI, 0.11 to 0.85), but not in those with cirrhosis and Child–Pugh class C disease (hazard ratio, 1.04; 95% CI, 0.45 to 2.37). Within the first 5 days, the portal-pressure gradient increased significantly in patients assigned to the liberal strategy (P = 0.03) but not in those assigned to the restrictive strategy. Conclusions: As compared with a liberal transfusion strategy, a restrictive strategy significantly improved outcomes in patients with acute upper gastrointestinal bleeding.
Issues in Statin-Associated MyopathyIssues in Statin-Associated Myopathy
Authors: Join Y. Luh, Bernard M. Karnath
Journal: JAMA (2003)

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