tbuckley/cabot-search huggingface dataset:
Book: Caring for Jewish Patients
Authors: Sabina Dosani
Journal: BMJ (2003)

A patient looks down and makes poor eye contact. Could he be embarrassed, worried, or depressed? Caring for Jewish Patients offers an alternative explanation: orthodox Jewish patients may avoid eye contact with a doctor of the opposite sex.​sex.




Figure 1



Joseph Spitzer

Radcliffe Medical Press, £24.95, pp 232 ISBN 1 85775 991 5

Rating: ★★★




Author Joseph Spitzer is an orthodox Jew. He is also a general practitioner in Stamford Hill, north London, home to Europe's largest orthodox Jewish community. Spitzer writes eloquently about his community and with an admirable objectivity. Perhaps it is this mixture of insider insights coupled with the sort of neutrality you might expect from an outsider that makes this book so absorbing and thought provoking.

The Jewish community is more diverse than one might suppose, and alongside the different strands there are levels of religious observance that make generalising impossible. Spitzer's mission is clear: he wants to provide the non-Jewish doctor or nurse with information about his faith to help them understand, engage with, and treat Jewish patients. He does this with remarkable clarity. Readers are taken through a fascinating account of different festivals, rituals, and rites of passage.

Spitzer's text will spare doctors many potential blunders. Most non-Jews are aware of certain Jewish food laws, but most doctors probably don't realise oral medications must also be kosher. For example, Calpol contains glycerine and is therefore non-kosher. Medinol contains glycerine known to be of vegetable origin and is therefore kosher. In contrast with current medical practice, Jewish orthodoxy discourages doctors from telling patients that they are terminally ill. Hope, it is argued, should not be snuffed out prematurely, as this could cause unnecessary suffering.

The text is broken up with case vignettes. Sharon, a Jewish medical graduate, approaches the postgraduate dean and explains that she will not be able to do pre-registration house jobs that involve Friday or Saturday nights on call. Fortunately for Sharon, a job share partner—presumably a non-orthodox Jew—is found.

This book draws attention to connections between religion and health, faith and illness. Those reading it will learn about the impact of different elements of Jewish life and culture on wellbeing, disease, diagnosis, and recovery, and therefore be better placed to treat Jewish patients successfully.
Abstract 15402: Sphingosine 1-phosphate Signaling is Involved in the Pathogenesis of Cardiac Hypertrophy in Response to Pressure Overload and Angiotensin II
Authors: Yuichi Uchino, Ichiro Manabe, Ryozo Nagai
Journal: Circulation (2010)

Molecular mechanisms underlying cardiac remodeling and heart failure are insufficiently understood. Sphingosine 1-phosphate (S1P), a biologically active lysophopholipid, is involved in many critical cellular processes. However, its role in cardiac pathologies is unclear. In the present study, we investigated the involvement of S1P signaling in cardiac hypertrophy in response to pressure overload and angiotensin II. Transverse aortic constriction (TAC) and angiotensin II infusion significantly increased cardiac expression levels of S1P1, the major cardiac receptor subtype for S1P, and sphingosine kinase 1 (SphK1), the key enzyme catalyzing the formation of S1P. Expression levels of S1P1 and SphK1 were increased by angiotensin II in cultured cardiomyocytes and were much higher than those in cardiac fibroblasts, suggesting S1P signaling is primarily activated in cardiomyocytes. S1P and S1P1-selective agonist induced ERK1/2 phosphorylation and cellular hypertrophy in cultured cardiomyocytes. Pharmacological inhibition of the ERK pathway using U0126 reduced S1P-induced cardiomyocyte hypertrophy, and knocking down S1P1 inhibited S1P-induced phosphorylation of ERK1/2, indicating S1P induces hypertrophic responses in cardiomyocytes via S1P1-mediated activation of ERK pathway. Moreover, knocking down S1P1 and SphK1 reduced cardiomyocyte hypertrophy and atrial natriuretic peptide upregulation in response to angiotensin II, suggesting S1P1 pathway is essential for angiotensin II-induced cardiomyocyte hypertrophy. Next we searched for small molecular weight compounds that can potentially inhibit S1P signaling for therapeutic intervention and found LE135, a synthetic retinoid, inhibited angiotensin II-induced S1P1 upregulation and S1P-mediated phosphorylation of ERK1/2. Oral LE135 inhibited TAC-induced S1P1 upregulation in the heart and reduced cardiac hypertrophy and fibrosis in response to pressure overload. LE135 also ameliorated cardiac hypertrophy and fibrosis induced by angiotensin II infusion. These results demonstrate that S1P/S1P1 signaling is an attractive therapeutic target for cardiac hypertrophy and remodeling.
How do HMOs reduce outpatient mental health care costs?
Authors: G S Norquist, K B Wells
Journal: American Journal of Psychiatry (1991)

Because previous studies of differences in utilization of mental health care services have had important limitations, it is not clear if their findings that health maintenance organization (HMO) outpatient mental health care costs less than fee-for-service care are due to less access, less intensive care per user, or selective enrollment of healthier people by HMOs. Therefore, the authors used data from the National Institute of Mental Health Epidemiologic Catchment Area (ECA) study to examine differences in the prevalence of psychiatric disorder and differences in the use of outpatient mental health services for adults enrolled in HMO or fee-for-service health insurance plans.The subjects were an ECA community sample obtained from East Los Angeles and West Los Angeles. This sample included a large number of Hispanic subjects. The subjects were categorized according to their responses to a 5-item battery on insurance as Medicare enrolles, members of private fee-for-service plans, Medicaid enrollees, members of an HMO, and uninsured. The presence or absence of psychiatric disorders was determined by using the NIMH Diagnostic Interview Schedule. Both users and nonusers of mental health services were studied.The HMO and fee-for-service plans had similar prevalence of psychiatric disorder and similar access to specialty mental health care. However, HMO enrollees had significantly fewer visits per user to providers of specialty care.The most likely explanation for lower mental health care costs in HMOs is a less intensive style of care for a comparably sick population.
Comparison of thrombolytic therapy and primary coronary angioplasty with liberal stenting for inferior myocardial infarction with precordial ST-segment depression
Authors: Flavio Ribichini, Giuseppe Steffenino, Antonio Dellavalle, Valeria Ferrero, Antonello Vado, Mauro Feola, Eugenio Uslenghi
Journal: Journal of the American College of Cardiology (1998)
Abstract 13179: Bicuspid Aortic Valve in African Americans is Associated with Smaller Aortic Dimensions Despite Greater Prevalence of Hypertension
Authors: Marion Hofmann Bowman, Sonal Chandra, Jeremy Nicolarsen, Etienne Gayat, Kirk Spencer, Victor Mor-Avi, Roberto Lang
Journal: Circulation (2011)

Bicuspid aortic valve (BAV) is associated with increased risk for aortic dilation, valve dysfunction and acute aortic events. Genetic causes and abnormal hemodynamic flow patterns are considered risk factors. To date, little is known about BAV in African Americans (AAs). The aim of this study was to evaluate the size of the aorta in AAs with BAV, as this may indicate genetic contributions to the susceptibility for aortic disease associated with BAV. By querying our adult ECHO database from 1998-2009 we identified 177 AA or caucasians with complete data set obtained by chart review (race, age, height, weight, hypertension, dyslipidemia, chronic kidney disease, and medication use). The most recent or last pre-surgical study was reviewed for prospective measurements of (i) aortic annulus, sinus of valsalva, sino-tubular junction, and ascending aorta 3 cm distal to the annulus, (ii) LV dimension and ejection fraction, and (iii) severity of aortic stenosis (AS) and aortic regurgitation (AR). Multiple linear re...
Omega-3 Fatty Acids for the Prevention of Recurrent Symptomatic Atrial Fibrillation
Authors: Alejandro Macchia, Hugo Grancelli, Sergio Varini, Daniel Nul, Nicolás Laffaye, Javier Mariani, Daniel Ferrante, Raúl Badra, Julio Figal, Silvina Ramos, Gianni Tognoni, Hernán C. Doval
Journal: Journal of the American College of Cardiology (2012)
Abstract 16817: Overexpression of CARP Exaggerates Cardiac Hypertrophy and Heart Failure by Accumulation of Calcineurin and p53 in Pressure-Overloaded Mice
Authors: Yulin Liao, Ci Chen, Tao Luo, Bing Wu, Zhi Zeng, Jianping Bin, Guofeng Li
Journal: Circulation (2012)

Background:It is known that the muscle ankyrin repeat protein family member Ankrd1/CARP is markedly augmented in cardiac hypertrophy and heart failure (HF). But, its role and the underlying mechanisms the pathogenesis of cardiac hypertrophy and HF remain unclear. Recently CARP was identified as a co-activator of p53, while p53 was demonstrated to play an important role in the progression of HF. We therefore hypothesized that CARP would accelerate HF by activation of p53. Methods and Results: In transverse aortic constriction (TAC) mouse models, cardiac-restricted overexpression of adenoviral CARP (Ad-CARP, myocardial injection) markedly increased heart to body weight ratio (5.81±0.20 mg/g in TAC-Ad-EGFP group, 8.88±1.54 mg/g in Ad-CARP group, P<0.01) and accelerated cardiac dysfunction (left ventricular fractional shortening:35.69%±4.33% in Ad-EGFP group,26.21%±4.16% in Ad-CARP group, P<0.01; lung to body weight ratio: 6.69±1.10mg/g in TAC-Ad-EGFP group, 12.17±3.21 mg/g in Ad-CARP group, P<0.05). In Ad-CA...
Abstract 5257: Inhibition of Myosin Light Chain Phosphatase by Rho Kinase (ROCK) Modulates Arteriolar Tone and Constriction of Coronary Arterioles
Authors: Guangrong Lu, Travis W Hein, Xin Xu, Lih Kuo
Journal: Circulation (2009)

ROCK has been suggested to regulate smooth muscle contraction of conduit artery via multiple pathways including direct myosin light chain (MLC) phosphorylation or inhibition of MLC phosphatase (MLCP) activity. Although recent studies have implicated the involvement of ROCK in pathogenesis of cardiovascular disease, the role and expression of ROCK isoforms (ROCK1 and ROCK2) and their signaling pathway for vasomotor regulation in resistance arterioles remain unclear. Using an isolated and pressurized vessel approach, we found that the resting tone and the endothelin-1 (ET-1)-induced constriction of porcine coronary arterioles (60±4 μ m resting diameter) were preferentially inhibited, in a dose-dependent manner, by a potent ROCK2 inhibitor H-1152 compared to a non-selective ROCK antagonist Y-27632. MLCP inhibitor calyculin A reversed the inhibitory effects of H-1152 and Y-27632, but ROCK inhibition failed to prevent or reverse calyculin A-induced arteriolar constriction. These results indicate that ROCK is involved in the development of basal tone and vasoconstriction to ET-1 and that MLCP is a major target of ROCK. Immunoblotting and immunohistochemical data showed that ROCK2 expression is 2-fold higher than ROCK1 in coronary arterioles with preferential media-layer distribution. Both ROCK1 and ROCK2 were also expressed in cultured porcine coronary arteriolar smooth muscle cells (PCASMC) with ROCK2 as the major isoform. In cultured PCASMC, MLC phosphorylation (ser19) elicited by ET-1, thromboxane analogue (U46619) and 80 mM KCl was sensitive to H-1152, supporting the involvement of ROCK2 in regulating coronary arteriolar tone via MLC phosphorylation. Consistent with our functional data, calyculin A increased MLC phosphorylation (ser19) in PCASMC, but ROCK2 inhibition (by H-1152) failed to reverse such effect. We conclude that ROCK2 is the major isoform mediating the development of basal tone and vasoconstrictor activity in coronary resistance arterioles primarily via regulation of MLCP activity.
Abstract 17843: Comparison of IVUS Findings Using Different Tissue Characterization System; VH-IVUS vs. iMAP-IVUS in Patients with Acute Coronary Syndrome
Authors: Sung-Yun Lee, Joon Hyung Doh, Sang wook Kim, Hyunmin Choe, Sung Uk Kwon
Journal: Circulation (2011)

Background: Two different tissue characterization techniques are available in the real world IUVS-guided percutaneous coronary intervention, VH-IVUS gave clinical implication especially identification of thin-cap fibroatheroma (TCFA) that can predict clinical event. The iMAP-IVUS system is relatively new technology available since last year in Korea. Limited data associated with iMAP-IVUS and no systemized report for comparison of two different systems. Methods: We performed pre-PCI IVUS using both VH-IVUS and iMAP-IVUS system consecutively for 20 patients with acute coronary syndrom treated with stent implantation. We excluded the 4 patients who had lesions with acoustic shadow on grey scale IVUS; because iMAP read the all shadows as necrotic core, then we selected and compared 30 pairs of cross-sectional tissue characterization IVUS images without acoustic shadow. Results: The VH-IVUS interpreted as less fibrotic (10.7 ± 7.9 vs 64.0 ± 5.9 %, p=0.001) when compared to iMAP-fibrotic components and much more fibro-fatty tissue components (64.4 ± 7.0 vs 9.0 ± 1.8 %, p =0.001) when compared to iMAP-lipid pool components for similar cross-sectional pairs. Necrotic core (22.7 ± 6.9 vs 26.9 ± 7.5 %, p =0.342) and calcified (2.1 ± 1.4 vs 6.8 ± 10.9 %, p =0.474) tissue components was similar between two systems. VH-IVUS detected 2 TCFAs but iMAP-IVUS could not fulfill the VH-definition of TCFA. Exact concordant level of cross-sectional IVUS image could not compared in few cases because VH-IVUS images were captured by EKG gating whereas iMAP IVUS by 2 frames/mm interval. Conclusion: Large necrotic core components were detected in two tissue characterization IVUS systems, but there were significant discrepancies in discriminations between fibrotic and lipid tissue components in patients with ACS who had lesions without acoustic shadow. We need more detailed study such as pathology study to verify the accuracy of these tissue characterization system.
Retrospective study of dasatinib in recurrent high-grade glioma (HGG) patients who failed bevacizumab.
Authors: C. Lu-Emerson, A. D. Norden, J. Drappatz, E. C. Quant, A. S. Ciampa, L. M. Doherty, D. C. LaFrankie, P. Y. Wen
Journal: Journal of Clinical Oncology (2010)

e12525 Background: There is no known effective treatment for recurrent high-grade glioma (HGG) after bevacizumab failure. Putative mechanisms of resistance include increased pericyte coverage, mediated partly by platelet-derived growth factor receptors (PDGFR), and an infiltrative tumor growth pattern potentially dependent on src signaling. We explored the efficacy of dasatinib, a PDGFR and src inhibitor, in patients with recurrent HGG after bevacizumab failure. Methods: Adult patients with histologically confirmed HGG who failed bevacizumab therapy were treated with dasatinib 70-100 mg twice daily, either alone (n = 3), in combination with bevacizumab (n = 15), or in combination with another agent (n = 2) until tumor progression or unacceptable toxicity. Results: Twenty patients were treated. Median age was 53 years (range 32-66) and median KPS was 75 (range 40-90). Sixteen patients (80%) had glioblastoma and the other 4 (20%) anaplastic glioma. The median number of prior regimens was 4. Of 19 evaluable patients, none had a complete or partial response. One patient (6%) had stable disease after an 8 week interval. Median progression-free survival (PFS) was 28 days (95% CI 26-35 days) with the longest PFS 110 days. Six month progression free survival (PFS6) was 0%. Median overall survival (OS) was 77 days (95% CI 44-137 days). Treatment was fairly well tolerated although 2 patients sustained grade 4 intracerebral hemorrhages. Conclusions: Dasatinib alone or in conjunction with bevacizumab does not have activity in patients with recurrent, heavily pretreated, HGG. Studies with dasatinib in less heavily pretreated patients before bevacizumab failure may be more effective, although the low CNS penetration of this agent may limit its activity. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Genentech Genentech
Abstract 16159: Differential Expression of Epigenetic Modifying Factors and Enzymes Between Induced Pluripotent Cells, Embryonic Stem Cells and Somatic Cells
Authors: Eneda Hoxha, Erin Lambers, Melissa Thal, Suresh Verma, Prasanna Krishnamurthy, Raj Kishore
Journal: Circulation (2010)

Due to their therapeutic potential in regenerative medicine, iPS cells have been successfully generated via the reprogramming of somatic cells. However, little is known about the molecular and epig...
Abstract 16000: Occurence of Cerebral Microembolic Signals During Pulmonary Vein Isolation: A Comparison of Two Different Ablation Techniques
Authors: Edina Nagy-Balo, Diana Tint, Marcell Clemens, Ildiko Beke, Reka Katalin Kovacs, Laszlo Csiba, Istvan Edes, Zoltan Csanadi
Journal: Circulation (2011)

Pulmonary vein isolation (PVI) techniques have been increasingly used to cure atrial fibrillation (AF). Recently, concerns have been raised that subclinical brain damage may occur due to microembol...
Abstract 9593: Osteoclastogenesis as a Novel Therapeutic Target for Abdominal Aortic Aneurysm
Authors: Dai Yamanouchi, Colin Stair, Stephanie Morgan, K. Craig Kent
Journal: Circulation (2011)

Arterial calcification has been proven to be the result of highly organized processes as seen in bone which relies upon a delicate balance between osteoblasts and osteoclasts. Osteoclast-like cells (OLCs) are derived from the monocyte/macrophage lineage and share features of osteoclasts, including the ability to dissolve extracellular matrix. Although osteoclastogenesis has been reported to occur in calcified arteries, its potential role in the development of abdominal aortic aneurysm (AAA) has yet to be explored. Here, we examined the role of OLCs in the development of AAA. Firstly, we obtained aortic tissues from patients undergoing surgical repair for AAA (N = 5) and aortic occlusive disease (N = 5). Alizarin-Red staining showed calcification in both aneurysmal and occlusive aorta. In contrast, OLCs, recognized as multi-nucleated cells positive for enzymatic TRAP staining, were identified only in aneurysmal aorta (100%, 5 of 5). A time course experiment in mouse calcium chloride-induced AAA (CaCl2 AAA) showed calcium deposition and monocyte/macrophage accumulation starting at 48 hours post-surgery followed by OLC formation, peaking 7 days after CaCl2 injury. Secondly, we administered bisphosphonate (Zoledronic acid, 0.1 mg/kg, once), an inhibitor of osteoclasts, or normal saline as a control, intravenously to mouse after CaCl2 injury (N = 3). Bisphosphonate-treated mice showed a significant reduction in arterial dilation after 7 and 42 days with a mean fold change of 1.08 ± 0.09 vs. 1.62 ± 0.05 (P &lt; 0.01) and 1.24 ± 0.12 vs. 2.26 ± 0.06 (P&lt;0.01), respectively. We also studied the effect of bisphosphonate on “developed aneurysm” by delaying the injection until one week after the injury (N = 5). Bisphosphonate significantly delayed a further expansion of the aneurysm with a percent increase from 7 to 42 days of 11.5% vs. 63.6% (P &lt; 0.01). Finally, mice treated with a neutralizing antibody to RANKL (1mg/kg), a key factor for osteoclast differentiation, showed a significant inhibition at 7 days (N = 3) (1.19 ± 0.06 vs. 1.62 ± 0.05, P &lt; 0.01). In conclusion, we have demonstrated the existence of OLCs in AAA and the inhibitory effect of bisphosphonate and anti-RANKL antibody on aneurysm. These results suggest that OLCs could be a novel therapeutic target for AAA.
A multisite investigation of the reliability of the Scale for the Assessment of Negative Symptoms
Authors: K T Mueser, S L Sayers, N R Schooler, R M Mance, G L Haas
Journal: American Journal of Psychiatry (1994)

The Scale for the Assessment of Negative Symptoms is a widely used instrument for measuring negative symptoms in schizophrenia, but few studies have examined its reliability. This study examined the interrater, internal, and test-retest reliabilities of the scale and its factor structure in the context of a multisite study.Two hundred seven patients with schizophrenia who were participating in the Treatment Strategies in Schizophrenia study were assessed with the Scale for the Assessment of Negative Symptoms following a symptom exacerbation and again 3-6 months later. All assessments were performed by trained psychiatrists who were treating the patients.Interrater reliabilities ranged from low to high for the items on the Scale for the Assessment of Negative Symptoms but were statistically significant in most cases. Most correlations between individual items and subscale total scores were moderate to high, as were coefficient alphas for each subscale, indicating adequate internal consistency. Test-retest correlations were of moderate magnitude. Few differences in reliability statistics between sites were found, although differences in mean scale ratings between sites were present. A factor analysis indicated three factors corresponding to the Affective Flattening or Blunting subscale, the Avolition-Apathy and Anhedonia-Asociality subscales, and the Alogia and Inattention subscales.The results suggest that the Scale for the Assessment of Negative Symptoms has good reliability and is a useful instrument for the measurement of negative symptoms in multisite clinical studies. The internal reliability of the Alogia, Avolition-Apathy, and Inattention subscales could be improved by replacing some items and including additional items.
PREDICTING PEGINTERFERON-alpha AND RIBAVIRIN TREATMENT RESPONSE IN GENOTYPE 1 HCV PATIENTS - SIMPLE NOMOGRAMS TO SUPPORT CLINICIANS
Authors: Alexander J. Thompson, Paul J. Clark, David M. Vock, Ruth Pfeiffer, Hans L. Tillmann, Keyur Patel, Susanna Naggie, F. Fred Poordad, Lisa M. Nyberg, Stephanie Noviello, Lisa Pedicone, Clifford A. Brass, Janice K. Albrecht, David B. Goldstein, John G. McHutchison, Thomas R. O'Brien, Mark S. Sulkowski, Andrew J. Muir
Journal: Hepatology (2011)