tbuckley/cabot-search huggingface dataset:
Abstract 59: Assessing Capabilities and Attitudes among Paramedics during CPR on Manikins with Different Chest Stiffness
Authors: Silje Odegaard, Jo Kramer-Johansen, Allan Bromley, Helge Myklebust, Jon Nysaether, Lars Wik, Petter Andreas Steen
Journal: Circulation (2006)

Introduction: We have recently shown that quality of CPR performed by professionals is substandard even with automated feedback on actual performance. We hypothesized that inadequate chest compress...
Abstract 3679: Kynurenine is a Novel Vasodilator in Human Septic Shock
Authors: Dechaboon Changsirivathanathamrong, Yutang Wang, Clive Woolfe, Dorrilyn Rajbhandari, David S Celermajer, Roland Stocker
Journal: Circulation (2008)

Kynurenine is produced when the enzyme indoleamine 2,3-dioxygenase (IDO) metabolises the essential amino acid tryptophan. IDO expression is induced in endothelial cells of resistance vessels when mice are infected with malaria (a model of systemic inflammation). These mice become hypotensive and treatment with 1-methyl-tryptophan, an IDO inhibitor, restores normal blood pressure. In vitro vessel function studies have shown that kynurenine acts as an endothelium-independent relaxant. Kynurenine contributes to the hypotension in human septic shock. Patients admitted to ICU with a diagnosis of septic shock (sepsis with hypotension not responsive to fluids) had serum levels of kynurenine and tryptophan measured throughout the course of their illness. Systemic IDO activity was inferred from the kynurenine/tryptophan ratio and was correlated with the degree of hypotension assessed as each patient’s inotrope requirements. The kynurenine/tryptophan ratio changed in parallel with the inotrope requirements in our c...
Abstract 297: Caveolae and Mitochondria: a Subcellular Symbiotic Relationship that Facilitates Cardiac Myocyte Function
Authors: Hemal H Patel, Brian P Head, Edward J Lesnefsky, Michelle Jennings, Jason N Peart, John P Headrick, Emily R Rothstein, Ingrid R Niesman, David M Roth, Marilyn G Farquhar, Robert S Balaban, Paul A Insel
Journal: Circulation (2007)

Caveolae, membrane microdomains composed of lipids and various proteins, including the protein caveolin (Cav), are involved in trafficking and compartmentation of signaling molecules. The possible relationship between caveolae and intracellular organelles is poorly defined. Here, we used whole hearts and cardiac myocytes (CM) and sought to determine whether caveolae and mitochondria associate and if this association has a functional consequence. Electron microscopy of CM revealed close apposition of subsarcolemmal mitochondria and caveolae. Subsarcolemmal mitochondria have greater expression of Cavs-1 and -3 relative to interfibrillar mitochondria and expression of Cav-3 in mitochondria was confirmed by immunoelectron microscopy. Immunoblotting of sucrose density gradient fractions prepared from CM, which facilitates the isolation of caveolae from other cellular membranes, detected enrichment of multiple enzymes that can serve as antioxidants (heme oxygenase-1, eNOS, cytochrome P450 reductase, and Cu-Zn and Mn superoxide dismutase) in caveolin-enriched buoyant fractions. Hearts of aged animals (24+ months), which have mitochondrial dysfunction, showed a 48% reduction in Cav-3 expression (p&lt;0.01) relative to young animals (6 months). Adenoviral overexpression of Cav-3 in CM resulted in increased formation of caveolae and reduced generation of superoxide (as assessed by dihydroethidium staining) in response to hypoxia/reperfusion stress compared to control and LacZ- treated CM. Cav-3 overexpressing myocytes had endogenously elevated levels of phosphorylated Akt and glycogen synthase kinaseβ, two downstream mediators of cardiac protection. The close apposition of caveolae and mitochondria, the enrichment of redox-enzymes in caveolae, the ability of increased Cav expression to form caveolae and attenuate free radical generation and loss of Cav expression with age suggest that caveolae are microdomains that may serve as “antioxidant sinks” for free radicals produced by adjacent mitochondria in CM. The close association of caveolae and mitochondria may thus represent an important symbiotic subcellular organization that helps promote function and limit oxidative damage in the heart.
A Pilot Study Of Rituximab In Patients With Moderate Aplastic Anemia, Diamond-Blackfan Anemia and Pure Red Cell Aplasia
Authors: Sabrina Martyr, Arun Balakumuran, Aldemar Montero, Cynthia E. Dunbar, Elizabeth M. Kang, Phillip Scheinberg, Barbara Weinstein, Xin Tian, Neal S. Young, Adrian Wiestner
Journal: Blood (2013)
Abstract 13341: Improving Lifestyle Exercise in Cardiac Patients: Results of the SystemCHANGE Trial
Authors: Shirley M Moore, Jacqueline M Charvat, Farrokh Alemi, Nahida Gordon, Paul Ribisl, Michael Rocco
Journal: Circulation (2011)

Assisting individuals to adopt and maintain lifestyle exercise after a cardiac event remains challenging. The purpose of this 3- group, randomized controlled trial was to test two theoretically-dis...
Evaluation of three prognostic indexes in follicular lymphoma
Authors: R. Sidhu, D. Lebrun, H. Feilotter, T. Baetz
Journal: Journal of Clinical Oncology (2005)

6595 Background: Three validated prognostic models have been proposed for use in patients with follicular lymphoma (FL), the International Non-Hodgkin’s Lymphoma Prognostic Index (IPI), the ILI model from the Italian intergroup, and recently the FLIPI model from the French International Lymphoma Prognostic Index. The aim of this study was to apply these three models to a group of FL patients to determine the concordance between them and their usefulness in predicting clinical outcome, including rate of transformation. Methods: The IPI index (age >60 years, extranodal involvement ≥2 sites, elevated lactate dehydrogenase (LDH), ECOG performance status ≥2, stage ≥3), the ILI index (age >60, extranodal involvement ≥ 2 sites, elevated LDH, male sex, B symptoms and erythrocyte sedimentation rate ≥ 30) and the FLIPI index (age > 60, stage ≥ 3, elevated LDH, number of nodal sites > 4, hemoglobin < 120 g/L), respectively were calculated and applied to 100 patients diagnosed with FL (grade I-III) between 1994 and 2001. Overall survival (OS) and progression free survival (PFS) were calculated for each prognostic group (low, intermediate and high risk) by the Kaplan-Meier method. Results: The median follow-up of our series was 31 months (mo) (range 1–340). Median OS was 24 mo (range 1–226). The median PFS was 41 mo (range 4–145). Concordance between the three indexes was 40%. The index that best predicted mortality was the ILI (p=0.027). The distribution of patients and mean overall survival according to risk group were similar for each index. Patients who went on to transform to aggressive NHL were rarely classified as high risk at diagnosis of FL by any index. Conclusions: Although the concordance between the three models was low, each is useful for classifying FL patients into risk groups and in predicting outcome in this group of patients. Transformation was not well predicted by any of the models. This information will be combined with cytogenetic, immunohistochemical, and DNA microarray data from frozen tumor tissue (currently proceeding) to develop a combined molecular and clinical prognostic index. A combined index may help select appropriate treatment for individual patients. No significant financial relationships to disclose.
Abstract 3334: Comparison of Medical Treatment and Coronary Revascularization in Patients with Moderate Coronary Lesions and Borderline Fractional Flow Reserve Measurements
Authors: Javier Courtis, Olivier F Bertrand, Eric Larose, Can M Nguyen, Jean-Pierre Déry, Onil Gleeton, Louis Roy, Guy Proulx, Gerald Barbeau, Bernard Noël, Robert DelaRochellière, Josep Rodés-Cabau
Journal: Circulation (2007)

Background. There is little information available regarding deferral of revascularization in cases of fractional flow reserve (FFR) measurements in the borderline range (between 0.75 to 0.80). The objectives of this study were to evaluate the clinical outcomes of patients with moderate coronary lesions and FFR measurements between 0.75 and 0.80, comparing those who underwent coronary revascularization (CR) to those who had medical treatment (MT), and to determine the predictive factors of major adverse cardiac events (MACE) at follow-up. Methods. A total of 107 consecutive patients (mean age 62 ± 10 years) with at least one moderate coronary lesion (mean percent diameter stenosis 47 ± 12%) evaluated by coronary pressure wire with FFR measurement between 0.75 and 0.80 (mean 0.77 ± 0.02) were included in the study. Maximal hyperemia was obtained by intracoronary administration of adenosine (mean dose 215 ± 84 μg). MACE (coronary revascularization, myocardial infarction, cardiac death) and the presence of angina were evaluated at follow-up. Results. A total of 63 patients (59%) underwent CR and 44 patients (41%) had MT, with no clinical differences between groups. At a mean follow-up of 13 ± 7 months, MACE related to the coronary lesion evaluated by FFR were higher in the MT group compared to CR group (23% vs 5%, difference 18%, 95% CI 5%–30%, p=0.005). FFR measurement in an artery supplying a territory with previous myocardial infarction was the only predictive factor of MACE in the MT group (odds ratio 14.1, 95% CI 1.3–39, p=0.03). The presence of angina at follow-up was more frequent in the MT group compared to the CR group (41% vs 9%, difference 32%, 95% CI 11%–49%, p&lt;0.001). Conclusions. In patients with moderate coronary lesions and FFR measurements in the “grey zone” range deferral of revascularization was associated with a higher rate of cardiac events and a higher prevalence of angina at follow-up, especially in those with previous myocardial infarction in the territory evaluated by FFR. These results suggest that a FFR cut-off point of 0.80 rather than 0.75 might be more appropriate for deferring coronary revascularization in these cases.
Abstract 309: TLR4 Gene Silencing Attenuates Atherosclerosis Progression via Inhibition of PI3-kinase/Akt/NF-κB Signaling Pathway in Apolipoprotein E Knockout Mice
Authors: Ying Wang, Li Hang Qi, Cheng Zhang, Shi Fang Ding, Mei Ni, Yun Zhang
Journal: Circulation (2007)

TLR4 activation induces the expression of IL-6 which may initiate or aggravate atherosclerotic lesions. The purpose of this study was to test the hypothesis that TLR4 gene silencing may attenuate atherosclerosis progression through inhibiting the expression of IL-6 induced by endotoxin.TLR4 knockdown ECV304 cell line (ECV304-TLR4) was constructed and cells were divided into four groups: control group (with fresh serum-free medium in ECV304 cells), LPS group (with LPS in ECV304 cells), LPS + LY294002 group (pretreatment with LY294002 and then adding LPS in ECV304 cells) and LPS + RNAi group (treatment with LPS in ECV304-TLR4). Cells were collected and the protein expression of P-AKT, AKT, P65, Iκ-α and IL-6 were assayed. Fifty-four apoE−/− mice were equally divided into two groups: group 1 received adenoviral RNAi vector containing TLR4 and group 2 received adenoviral RNAi vector containing scrambled siRNA as a negative control at the end of week 6. All mice were fed a high-fat diet and received celiac injections of LPS (1mg/kg, twice per week) for 10 weeks and were then sacrificed. Levels of serum lipids and IL-6 were measured. Plaque contents were evaluated by immunohistochemistry and the vulnerability index (VI) was calculated as:VI = (macrophage + lipid)/(SMC + collagen) contents. The results showed that TLR4 protein expression in vitro was significantly inhibited in ECV304-TLR4. Compared with control cells (0.67 ± 0.002), the NF-κB binding activity reached the maximum at 30min stimulation of LPS (1.89 ± 0.04),which was inhibited by RNAi (0.96 ± 0.04) (P  P   0.05). Plaque Area, lipid content and serum lipid levels between the two groups showed no significant difference. In conclusion, TLR4 gene silencing significantly reduces the expression of IL-6 and attenuates atherosclerosis progression probably through the inhibition of PI3-kinase/Akt/NF-κB signaling pathway.
Abstract 9423: Acute Illness is a Risk Factor for Impaired Respiratory Function during Nurse-administered Procedural Sedation and Analgesia in the Cardiac Catheterization Laboratory
Authors: Aaron Conway, Karen Page, John Rolley, Paul Fulbrook
Journal: Circulation (2012)

Introduction Impaired respiratory function (IRF) during procedural sedation and analgesia (PSA) poses considerable risk to patient safety as it can lead to inadequate oxygenation and ventilation. Risk factors that can be screened prior to the procedure have not been identified for the cardiac catheterization laboratory (CCL). Methods A matched case-control design was used. Clinical information from two hospitals, one public and one private, was abstracted from 573 medical records of those undergoing procedures in a CCL. IRF was defined as SpO2&lt;95% or less than 8 respirations per minute. To control for potential intra-procedural confounders, those who also received nurse-administered PSA were matched based on the type of procedure as well as age and gender. Factors with significance p &lt;0.10 on univariate analyses were entered into a backward stepwise conditional logistic regression model. Results Nurses administered PSA during 252 procedures (44%). IRF occurred during 8.3% (95%CI=4.9%-11.7%) of these procedures (n=21). The 21 cases were matched with 113 controls. According to the regression model, with each additional indicator of acute illness, patients were nearly two times more likely than their controls to experience impaired respiratory function during nurse-administered PSA in the CCL (Table). Indicators of acute illness included emergency admission, transfer from critical care unit and requiring respiratory or haemodynamic support in the lead up to the procedure. Conclusion The finding that patients with acute illness were most likely to have IRF during PSA has considerable face validity as it is probable these patients had underlying conditions impacting on their cardiopulmonary function. This significant risk needs to be addressed in practice. Nurses should be proactive when managing this group of patients, recognising the increased likelihood for respiratory impairment and applying intensive respiratory monitoring.
Screening for breast and cervical cancer as a common cause for litigation
Authors: R. M Wilson
Journal: BMJ (2000)

A delay in the diagnosis of cancer is now one of the commonest reasons for medical litigation. Increasingly women in whom breast or cervical cancers are diagnosed after a “normal” screening test are alleging negligence through a delay in diagnosis and are seeking compensation through the legal system. Medical staff involved in providing screening are highly concerned about this situation.1 How has it arisen?

The enthusiasm of the health service to promote screening has perhaps given women unrealistic expectations. Women may falsely believe that screening prevents cancer rather than detects it earlier. There is also a perception that cancers arising after a normal screening examination must have been “missed” and that the delays in diagnosis have prognostic significance.

Population screening is different from health care, which manages individuals with symptoms; most people who are screened are free from disease, and an acceptable balance between the sensitivity and specificity of the screening test must take this …
Abstract 5693: Detection of a Founder Effect in LQT1 in Five Apparently Unrelated Families in a Regional Inherited Arrhythmia Clinic
Authors: Christopher Gray, George J Klein, Raymond Yee, Allan C Skanes, Lorne J Gula, Jorge Wong, Andrew D Krahn
Journal: Circulation (2008)

The Inherited Arrhythmia Clinic follows families with inherited arrhythmia syndromes from a population of 1.5 million people. Patients referred for evaluation of Long QT Syndrome (LQTS) underwent resting and standing ECGs, and 3 forms of exercise. Patients with findings consistent with LQTS underwent genetic testing, with assessment of all 1 st degreerelatives. A proband from each of 5 unrelated families was found to have an identical disease causing transmembrane mutation in KCNQ1, suggesting a founder effect (Exon 6, 797 T&gt;C). Systematic screening of 1 st degree relative of affected individuals was performed. 31 patients (age 42±24yrs (range 4 – 89 years), 18 female) were identified from the 5 families, including the 5 probands. All affected individuals were offered beta-blockers. 18 affected family members and 13 unaffected 1 st degree relatives were identified. Several family members had malignant presentations including sudden death and unexplained drowning. One proband had torsades de pointes during an exercise test. Other family members were asymptomatic until their 8 th and 9 th decades when they developed cardiac ischemia and had further QT prolongation, torsades de pointes and cardiac arrest. Sudden death occurred in a deaf child; both of the child’s consanguineous parents were gene positive for the KCNQ1 mutation (Jervell and Lange-Nielsen Syndrome). There was no identifiable common relative after pedigree construction of the previous 4 –7 generations. Affected patients typically had borderline QT prolongation at rest with dramatic prolongation with exercise (Table ). Genetic testing in this LQTS population suggests a founder effect for the five families with the descendants clustering in our geographical region. The observations highlight the utility of genetic testing when used in conjunction with a specialized clinic setting.
Pyridoxine supplements may help patients with carpal tunnel syndrome
Authors: P. J Lewis
Journal: BMJ (1995)

EDITOR,—The standard treatment offered for the carpal tunnel syndrome is still a splint, a local injection of corticosteroid, or surgical decompression.1 Awareness of a simple and effective nutritional intervention—supplementation with pyridoxine (vitamin B-6)—remains low despite overwhelming evidence of its efficacy.

Vitamin B-6 deficiency is a common finding in the carpal tunnel syndrome, and the total …
Congressional Autism Hearings Continue
Authors: B Vastag
Journal: JAMA (2001)

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Debate on cot death
Authors: J L Emery
Journal: BMJ (2000)

Editor—Green's article is obviously intended to stir up the cot death establishment.1 When cot death was introduced as a registerable cause of death, largely under the influence of forensic pathologists Bernard Knight of Cardiff and Francis Camps of London, some of us working in paediatric pathology were not in favour of this as we knew that it had many different causes.

We have known from the outset that a proportion of the deaths were technically filicide. In the early 1980s, when we publicly gave the figure of 10%, our findings were fiercely contested, but they were confirmed recently.2 The recent studies by Meadows and Southall et al showing parents deliberately and calculatingly harming their infants apply to only a small proportion of the group of cot deaths that could be classified as infanticide.3,4 In our experience of hundreds of confidential inquiries into sudden unexpected deaths the most usual scenario for filicide is for the baby to have been suffocated by an exhausted parent (usually the mother) while trying to quieten his or her crying. These parents usually barely knew what they were doing and did not intend or want to kill their child.

We need to prevent these deaths, not victimise the parents.

Green's advice to “think dirty” needs to be considered against our experience with the care of next infant (CONI) programme. This programme, funded by the Foundation for the Study of Infant Deaths, provides support for families with children born after a cot death. Of 5000 babies from 4182 families in the programme, 44 died (8.8 per 1000 live births), 35 unexpectedly.5 After confidential inquiries 20 were considered to be natural deaths, of which 12 were classified as inevitable because of congenital anomaly or specific diseases and eight as unexplained because there was minimal or no disease. Fourteen were classified as non-natural deaths, including four attributed to overlaying. Ten deaths were not fully investigated (in seven cases the family declined investigation, in two cases no histology was done, and in the last the mother could not be traced). Thus at least 20 of the second deaths in these families were due to natural causes.

We found that before the death that led to enrolment the 4182 families had had 6406 infants, of whom 112 died (17.5 per 1000 live births). The difference between the earlier mortality and that on the programme cannot be explained simply by falling infant mortality over the period. 

What is needed are deeper non-critical confidential inquiries into all unexpected deaths that include interested paediatric pathologists and are followed by systematic support. We do not need to create a pool of parents to which a label of unproved homicide is publicly attached.
Comparison of propranolol, sotalol, and betaxolol in the treatment of neuroleptic-induced akathisia
Authors: B Dupuis, J Catteau, J P Dumon, C Libert, H Petit
Journal: American Journal of Psychiatry (1987)

In earlier open studies, beta-blockers were found to be effective in the treatment of neuroleptic-induced akathisia. In the present study, 16 patients with severe neuroleptic-induced akathisia successively received low doses of three beta-blockers--propranolol, sotalol, and betaxolol. There was rapid and complete improvement in seven of 16 patients (and partial improvement in three patients) treated with betaxolol. The efficacy of propranolol and betaxolol and failure of sotalol in treating neuroleptic-induced akathisia suggest a central mechanism of action.