tbuckley/cabot-search huggingface dataset:
Abstract 114: Chest Compression Release Velocity Does Not Affect Net Forward Flow but Does Affect Hydrodynamic Power in the Inferior Vena Cava
Authors: Joshua W Lampe, Josiah D Garcia, Tai Yin, George Bratinov, Christopher L Kaufman, Lance B Becker
Journal: Circulation (2012)

Introduction: Research has suggested that chest compression (CC) release velocity or waveform impacts CPR effectiveness. However, a detailed investigation of the impact of changes in CC waveform on...
Abstract 4568: Surgical Management of Complete Atrioventricular Septal Defect: Associations with Surgical Technique, Age and Trisomy 21
Authors: Andrew M Atz, John Hawkins, Minmin Lu, Meryl Cohen, James Jaggers, Brian W McCrindle, Renee Margossian, Ralph Mosca, Steven Colan, Ron Lacro, L LuAnn Minich
Journal: Circulation (2008)

Background: Surgical strategies vary for repair of complete atrioventricular septal defect (AVSD). The impact of age, surgical technique and trisomy 21 on contemporary outcomes is poorly defined. Methods: From 6/04 to 2/06, 124 children with primary repair of complete AVSD were studied in a Pediatric Heart Network sponsored observational study. Demographic, procedural, and outcome data were obtained within 28 days of surgery and 6 months later. Results: Median age at repair was 115 days (9 – 396 days). Type of surgical repair was single patch (19%), double patch (71%), and single ASD patch with primary VSD closure (10%). Repair types varied significantly across centers (p=0.002) but there were no differences noted in residual atrial or ventricular septal defects or degree of mitral regurgitation (MR) by repair type within 28 days. Median intensive care unit (ICU) stay was 4 days, length of ventilation 2 days, total hospital stay 7 days; there were no differences by presence of trisomy 21(80% of cohort). A patch margin VSD was detected by echo within 28 days in 43% and at 6 months in 14% (p&lt;0.05). A VSD &gt; 3mm was seen in 6% at discharge and 1% at 6 months. At least moderate MR was present in 26% early and 22% at 6 months. Hospital mortality was 3/124 (2.4%); one within 30 days (0.8%). Overall survival at 6 months was 96% (119/124). Pleural effusion was the most common reported postoperative complication (20%). Earlier age at surgery was associated with longer time on ventilator (p=0.02), longer ICU stay (p=0.03) and use of circulatory arrest (p=0.01). Older age was associated with longer duration of aortic cross clamp time (p=0.05). Age at repair was not associated with residual abnormalities including residual VSD and moderate or greater MR at 6 months. . Conclusions: Contemporary outcomes following repair of complete AVSD are excellent regardless of repair type or presence of trisomy 21. Although a residual VSD may be detected by echo in 43%, most are trivial and resolve by 6 months. Earlier age at surgery is associated with increased resource utilization but has no influence on incidence of residual VSD or significant MR.
Infection in the preterm infant
Authors: William McGuire, Linda Clerihew, Peter W Fowlie
Journal: BMJ (2004)

Systemic infection in preterm infants has two categories with distinct aetiologies and outcomes.

Early onset infection —acquired in the intrapartum period and presenting in the first 48-72 hours after birth.

Late onset infection —usually acquired in hospital and clinically evident more than 72 hours after birth (usually after the first week of life).

### Incidence

Early onset systemic infection includes bacteraemia, pneumonia, meningitis, and urinary tract infection. Although rare, early onset infection is a serious complication of preterm birth. In North America the incidence of bacteraemia proved by culture in very low birthweight (< 1500 g) infants is 1.5% of live births. The principal pathogens responsible are Group B streptococci and Escherichia coli . Congenital listeriosis (caused by spread of Listeria monocytogenes across the placenta after the mother has eaten infected food) is rare in North America and the United Kingdom but more common in some areas in Europe.

In many developed countries the incidence of Group B streptococcal infection has fallen in the past decade, perhaps because of the greater use of intrapartum antibiotic treatment for women with specific risk factors. During this period, however, there has been a rise in the incidence of infection with Gram negative coliforms Microbiological surveillance should be continued to identify changes in the epidemiology of early onset infection, particularly antibiotic resistance.

View this table:

Micro-organisms causing early onset infection in very low birthweight infants*



### Presentation and treatment

Most infants with early onset systemic infection will present with signs of sepsis, such as respiratory distress or fever, in the first 12 hours after birth. Presentation can be delayed, and microbiological diagnosis may be difficult, especially if the mother has received intrapartum antibiotics. As it is difficult to rule out systemic infection …
Adaption to Hyperoxia
Authors: Gloria D. Massaro, Donald Massaro
Journal: Journal of Clinical Investigation (1974)

We studied the influence of prolonged exposure to hyperoxia (O(2) > 98%) on protein synthesis and on the ultrastructure of the granular pneumocyte. To study protein synthesis, as indicated by l-[U-(14)C]-leucine incorporation into protein, lung slices were incubated with radioactive leucine and a surface-active fraction was obtained by ultracentrifugation of lung homogenates. We found that, following an initial depression in protein synthesis after 48 h of hyperoxia, protein synthesis in rats exposed to oxygen for 96 h rose to greater than control levels. This increase in protein synthesis was noted in whole lung protein and in protein present in the surface-active fraction. Stereologic ultrastructural analysis of granular pneumocytes revealed that the lamellar bodies occupy the same percentage of cytoplasmic volume in oxygen-exposed and control rats after 96 h; a previous study had shown lamellar bodies of oxygen-exposed rats to occupy less volume than those of control rats after 48 h of exposure at which time protein synthesis was also depressed. After 96 h of exposure there is a greater amount of rough endoplasmic reticulum in the granular pneumocytes of oxygen-exposed rats. These studies show that after 96 h of hyperoxia the lung has recovered its ability to synthesize protein including protein in the surface-active fraction and that these biochemical changes are associated with consistent ultrastructural alterations in the granular pneumocyte.
Abstract 13965: Are TAPSE and S' Reliable Measures of Right Ventricular Performance?
Authors: Karima Addetia, Roberto M Lang, Amit R Patel, Victor Mor-Avi, Kirk T Spencer
Journal: Circulation (2013)

Introduction: According to recent recommendations, both tricuspid annular systolic excursion (TAPSE) and tissue-Doppler-derived tricuspid lateral annular systolic velocity (S’) are reliable methods...
Globalisation and health
Authors: K. Lee, D. Bradley, M. Ahern, T. McMichael, C. Butler, D. Legge, J. N Rao, R. G A Feachem, J. Woodcock, A. Porter, R. Saracci, M. Cuttini, J. Macq
Journal: BMJ (2002)

Editor—We live in extraordinary times, but not for the reasons that Feachem celebrates in his eulogy on globalisation as “mostly good for your health.”1 An informed, inclusive discussion of globalisation's merits and demerits, including its impacts on human health, is needed, given the increasingly polarised nature of this debate. The mass demonstrations of anti-capitalist protesters at major international meetings, most recently at the G8 summit in Genoa, Italy, communicate the angst felt by many for the human, social, and environmental consequences of the kind of globalisation we are experiencing today. But the violence that has accompanied these demonstrations has undermined and confused the protestors' message.

For the health community, a fuller review of the evidence begins with a disentangling of globalisation as a complex web of cause and effect.2 Both sides of the debate have abused the term as a catch all to explain many natural and human induced changes. Defining globalisation as openness does not capture the multiple, often contradictory, forces at play. Globalisation can also be defined as processes that are changing the ways in which people interact across boundaries, notably physical (such as the nation-state), temporal (such as instantaneous communication via email), and cognitive (such as cultural identity). The result is a redefining of human societies across many spheres—economic, political, cultural, technological and so on. As such, globalisation affects the health of different people in very different ways. How good or bad globalisation happens to be for you will be influenced by socioeconomic status, sex, education, age, geographical location, and other factors.

We are only beginning to understand these interconnections, but existing evidence about the adverse health impacts of globalisation cannot be readily dismissed.3 The role of global environmental change on diseases such as malaria, dengue fever, and cholera has been well documented. The alarming rise of tobacco related diseases has followed recent global economic policies.4 The claim that globalisation will ultimately bring greater wealth, and thus better health, is open to challenge. What is needed is a comprehensive examination of the data bearing on each of the many components of globalisation, an assessment of the risks and benefits of each component, and innovative policy responses enabling us to act appropriately when choices are possible, and to adapt to changes that are inevitable.5 To do otherwise will reinforce a simplistic debate that is not only widely divided already, but will ultimately fail to benefit the health of all people.
Abstract 15841: Contact Force-Time Integral Predicts Radiofrequency Lesion Size and Incidence of Steam Pop in the Canine Beating Heart
Authors: Atsushi Ikeda, Hiroshi Nakagawa, Hendrik Lambert, Dipen C Shah, Tushar Sharma, Jan V Pitha, Ralph Lazzara, Warren M Jackman
Journal: Circulation (2012)

Introduction: During radiofrequency (RF) ablation at constant power, the lesion size and incidence of steam pop increase strikingly with increasing contact force (CF) and RF application time. An RF...
Abstract 9624: Suppressive Effects of Irbesartan on Inflammation and Apoptosis in Atherosclerotic Plaques of Apoe-/- Mice: Molecular Imaging with 14C-FDG and 99mTc-annexin A5
Authors: Yan Zhao, Songji Zhao, Yuji Kuge, Ayahisa Watanabe, Keita Fukao, Yoshikazu Tanaka, Toru Nakano, Hiroshi Takemoto, Nagara Tamaki
Journal: Circulation (2011)

Background: Although irbesartan, an angiotensin II subtype 1 receptor blocker, reportedly can suppress the progression of atherosclerosis, the mechanisms of the therapeutic effects remain unclear. ...
Changes in regulatory T-cells in responding and non-responding patients with indolent B-cell or mantle cell lymphomas during treatment with lenalidomide, dexamethasone, and rituximab.
Authors: N. Aqui, L. Leinbach, E. A. Chong, T. Ahmadi, J. Svoboda, A. Gordon, L. H. Downs, S. Nasta, S. J. Schuster
Journal: Journal of Clinical Oncology (2010)

8085 Background: Lenalidomide may enhance anti-tumor immune responses by inhibiting regulatory T-cells (Tregs) and by augmenting NK-cell mediated antibody-dependent cytotoxicity. These immunologic effects may synergize when lenalidomide is combined with rituximab. Methods: We are conducting a single center, open label phase II trial of lenalidomide, dexamethasone, and rituximab in patients (pts) with indolent B-cell or mantle cell lymphomas refractory to rituximab, defined as failure to respond to or progression within 6 months of rituximab monotherapy, prior rituximab-chemotherapy, or rituximab maintenance. The regimen consists of two 28-day treatment cycles of lenalidomide 10 mg daily and dexamethasone 8 mg once weekly (Part 1). During cycle 3, all pts receive rituximab 375 mg/m2 weekly for 4 doses (Part 2). Lenalidomide-dexamethasone therapy is continued during and after rituximab until disease progression. Peripheral blood is collected for assessment of immune parameters by flow cytometry at enrollment, after Part 1 (end of cycle 2) and after Part 2 (3 months from 1st dose of rituximab). Results: 25 pts are enrolled on study; 11 pts have completed immune assessment. Pts with a CR or PR were analyzed as responders (N=7); pts with stable/progressive disease as nonresponders (N=4). After Part 1, Tregs (CD4+FOXP3+) remained relatively unchanged in responders (median +0.06-fold change, range: -0.98, +0.68) and increased in non-responders (median +1.2-fold change, range: -0.48, +3.49). After Part 2, Tregs decreased in responders (median -0.35-fold change, range: -0.58, +0.15) and further increased in non-responders (median +2.1-fold change, range: -0.25, +2.4). Between Parts 1 and 2, the difference in fold change in Tregs for responders vs non-responders was statistically significant (mean -0.26 vs +1.6-fold change, respectively; p=0.003). Conclusions: Based on these preliminary findings, there is a significant change in Tregs during therapy with lenalidomide, dexamethasone and rituximab. Non-responding pts appear to have an increase in Tregs, while responding pts exhibit either no change or a decline with therapy. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Celgene Celgene Celgene
Reversal of immunoparalysis by recombinant human granulocyte-macrophage colony-stimulating factor in patients with severe sepsis
Authors: Axel Nierhaus, Barbara Montag, Nicole Timmler, Daniel P. Frings, Kai Gutensohn, Roman Jung, Claus G. Schneider, Werner Pothmann, Anne K. Brassel, Jochen Schulte am Esch
Journal: Intensive Care Medicine (2003)
Abstract 17184: Depression Recognition and 1-Year Survival in Acute Myocardial Infarction Patients
Authors: Kim G Smolderen, Donna M Buchanan, Kensey Gosch, Mary Whooley, Paul S Chan, Viola Vaccarino, Susmita Parashar, Amit Shah, Michael Ho, John A Spertus
Journal: Circulation (2011)

Background: Depression among acute myocardial infarction (AMI) patients is prevalent and associated with an adverse prognosis. Although depression often remains undetected in AMI patients, there is still debate about the importance of screening for depression at the time of AMI. Defining the prognostic importance of unrecognized depression may support better efforts to increase its recognition. Methods: In the prospective TRIUMPH study, 4062 AMI patients from 24 US hospitals completed the Patient Health Questionnaire-9 (PHQ-9) during their index AMI admission. Depression was defined by a PHQ-9 score of ≥10. Depression was considered to be recognized by the treating team if it was documented in the patient's chart (discharge depression diagnosis, discharge anti-depressants, referrals for counseling). Follow-up interview data on use of anti-depressants and/or counseling was collected at 1 and 6 months. One-year mortality was compared between: (1) recognized depressed; (2) unrecognized depressed; and (3) non-depressed (PHQ-9&lt;10; reference) patients, adjusting for demographics, AMI severity, and clinical factors. Sensitivity analysis additionally adjusted for follow-up depression treatment. Results: Although 759 (19%) patients were depressed, only 231 (30%) were recognized. As compared with non-depressed patients, recognized depressed AMI patients had similar 1-year mortality rates (6.7% vs. 6.1%, adjusted HR=1.12, 95%CI 0.63-2.00), whereas those with unrecognized depression had increased mortality (10.8% vs. 6.1%, HR=1.92, 95%CI 1.39-2.64). Recognized vs. unrecognized depressed patients received more depression treatment after discharge (70% vs. 24%), but this did not attenuate the increased hazard for the unrecognized patients. Conclusion: AMI patients with recognized depression had similar survival compared with non-depressed patients, but patients with unrecognized depression had worse survival. These findings raise the possibility that recognizing depression during AMI care may be crucial to better risk-stratify depressed AMI patients so that more aggressive cardiac treatments can be considered to reduce their elevated mortality risk.
Pathology of Coronary Heart Disease
Authors: B L SEGAL
Journal: JAMA (1963)

The distribution of coronary atherosclerosis in patients with ischemic heart disease is extensive, and involves at least two major coronary arteries. Thrombosis, occlusion by atheromatous debris and, infrequently, internal hemorrhage may produce final closure of the coronary artery. The anatomy of the coronary vessels, localization of occlusion, recanalization, the extent of intercoronary anastomoses and the physiological demands of the myocardium all affect the ultimate clinical expression of the basic occlusive process.
Abstract 2617: Importance of Atrial Surface Area and Refractory Period in Sustaining Atrial Fibrillation: Testing the Critical Mass Hypothesis in vivo
Authors: Anson M Lee, Abdulhameed Aziz, Kal L Clark, Richard B Schuessler, Ralph J Damiano
Journal: Circulation (2009)

Purpose: The critical mass hypothesis for atrial fibrillation (AF) was proposed in 1914; however, there are no studies precisely defining the relationship between atrial surface area and AF in an i...
Differential diagnosis of tardive dyskinesia: an overview
Authors: R P Granacher
Journal: American Journal of Psychiatry (1981)

The author states that most psychiatrists should be able easily to recognize tardive dyskinesia. However, this disorder is a subset of a large variety of abnormal involuntary movements, some of which may resemble tardive dyskinesia. Others have serious implications if they are misdiagnosed as tardive dyskinesia. The author describes the characteristic features of a wide variety of abnormal involuntary movements, including parkinsonism, the dystonias, choreas and choreoathetosis, tremors, tics, stereotypies and mannerisms, oral-facial dyskinesias, and disorders with varied or complex manifestations. He emphasizes the differential diagnosis of tardive dyskinesia.
Abstract 15894: Poor Bioavailability of Ethyl Ester Omega-3's on a Low-Fat Diet is Dramatically Improved With a Free Fatty Acid Formulation
Authors: Michael H Davidson, Judith Johnson, Michael W Rooney, Douglas F Kling
Journal: Circulation (2011)

Background: Ethyl esters (EE) of omega-3's require significant pancreatic lipase hydrolysis to be converted into a free fatty acid for intestinal absorption. Previous human trials have demonstrated...
Abstract 5209: Oxidative Stress Uncouples eNOS in a BH4-independent Manner via the Formation of Protein Thiol-radicals
Authors: Chun-An Chen, Lawrence J Druhan, Tse-Yao Wang, Yeong-Renn Chen, Jay L Zweier
Journal: Circulation (2009)

Imbalance of nitric oxide (NO) and superoxide (·O 2 − ) production in the endothelium contributes to many cardiovascular diseases, including hypertension, atherosclerosis, and heart failure. Under conditions of oxidative stress, NO synthase (NOS) can switch from NO to ·O 2 − generation. We have demonstrated that endothelial NOS (eNOS) is reversibly S-glutathiolated in vivo and in vitro , in response to oxidative stress. This redox modification of eNOS leads to uncoupling, with decreased eNOS-derived NO and increased ·O 2 − . There are several proposed mechanisms that can lead to protein S-glutathiolation: thiol-disulfide exchange with GSSG; formation of thiyl radicals, sulphenic acid, or protein-S-nitrosothiols, which in turn react with GSH. Here we demonstrate the oxidant induced formation of an eNOS protein thiyl radical using immunoblotting, immunostaining, and mass spectrometry. BH 4 -free eNOS was used to self generate ·O 2 − , which in turn can modify sulfhydryl groups to form protein radicals. We trapped these short lived protein radicals with the spin trap DMPO. Immunoblotting using an anti-DMPO antibody, demonstrated the formation of eNOS protein radicals, which were abolished by SOD and L-NAME, and were Ca 2+ /CaM sensitive, indicating that protein radical formation is due to ·O 2 − generation from the eNOS heme domain. With BH 4 reconstituted eNOS, which will only generate NO, formation of the eNOS protein radical is completely inhibited. Furthermore, in endothelial cells treated with menadione to trigger cellular ·O 2 − generation, formation of eNOS protein radical as visualized with confocal microscopy was increased compared to control, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody. Using mass spectrometric analysis, we identified Cys908 as the only residue involved in protein radical formation. Of note, we have also demonstrated the oxidant-induced S-glutathiolation of Cys908. Thus, eNOS protein radical formation provides the groundwork for a mechanism of ·O 2 − -directed regulation of eNOS, involving S-glutathiolation; defining a unique pathway for the redox regulation of cardiovascular function. This research has received full or partial funding support from the American Heart Association, Great Rivers Affiliate (Delaware, Kentucky, Ohio, Pennsylvania &amp; West Virginia).
Abstract 2419: The Presence of Q Waves, QRS Fragmentation or QRS Duration Does Not Correlate with Scar Volume in Patients with Ischemic Cardiomyopathy.
Authors: Mary G Carey, Andrew J Luisi, Sunil Baldwa, Joshua M Thomas, John M Canty, James A Fallavollita
Journal: Circulation (2007)

Background. Recent studies have suggested that scar volume is one of the predictors of ICD utilization. We hypothesized that noninvasive ECG predictors of myocardial scar (number of leads with Q waves and/or fragmented QRS complexes, fQRS) would correlate with infarct size and could predict patients with a depressed ejection fraction that would be the most likely to benefit from imaging scar volume. Methods. Patients with ischemic cardiomyopathy eligible for an ICD for the primary prevention of sudden death underwent PET imaging (n=78). Scar volume (% LV) was quantified from 18 FDG uptake during insulin stimulation and 13 N-ammonia flow using a validated algorithm (MyoPC, Ottawa Heart Institute). Pathologic Q waves and fQRS (RSR morphology or notching in R or S waves) on the 12-lead ECG were assessed by consensus of three blinded readers. Results. Subjects were 67 ± 12 years of age and 87% male. Average ejection fraction was 28 ± 10%. Myocardial scar encompassed 17.1 ± 7.3% of the left ventricle, with a very wide range among subjects (1.9 to 34.4%). In patients with a QRS duration &lt;120 msec (n=47), there was very poor correlation between scar volume and the number of leads with Q waves, fQRS or both (R 2 =0.01– 0.06, Table ). Furthermore, patients with a wide QRS (&gt;120 msec) did not have an increase in scar volume (Table ). Conclusions. These results indicate that 1.) The volume of scar varies widely in patients with ischemic cardiomyopathy that are eligible to receive an ICD for primary prevention and 2.) Infarct volume is independent of electrocardiographic indices of scar. Thus, imaging is necessary to stratify risk for SCD as a function of scar volume.