tbuckley/cabot-search huggingface dataset:
Autopsies and Preventable Deaths
Authors: F. Michael Gloth
Journal: Annals of Internal Medicine (1989)

Letters and Corrections15 January 1989Autopsies and Preventable DeathsF. Michael Gloth III, MD, William B. Greenough III, MDF. Michael Gloth III, MDSearch for more papers by this author, William B. Greenough III, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-110-2-166 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:In their article on preventable deaths, Dubois and Brook (1) arrive at their conclusions on the basis of what may prove to be an erroneous assumption: that is, that the cause of death determined from the charts reviewed was indeed the true cause. A recent study (2) of more than 2000 autopsy cases collected from 32 university and community hospitals showed major discrepancies (for which appropriate treatment of the patient would likely have resulted in his or her cure or prolonged survival) between premortem diagnoses and those determined at autopsy in more than one third of cases....References1. Dubois R and Brook R. Preventable deaths: who, how often, and why? Ann Intern Med. 1988;109:582-9. LinkGoogle Scholar2. Battle R, Pathak D, and Humble C. Factors influencing discrepancies between premortem and postmortem diagnoses. JAMA. 1987;258:339-44. CrossrefMedlineGoogle Scholar3. Goldman L, Sayson R, and Robbins S. The value of the autopsy in three medical eras. N Engl J Med. 1983;308:1000-5. CrossrefMedlineGoogle Scholar4. Gloth F and Burton J. Discrepancies between clinical and necropsy diagnoses over five years in a chronic care setting. Gerontologist. [Abstract]. 1988;28:280A. Google Scholar1. Dubois R and Brook R. Preventable deaths: who, how often, and why? Ann Intern Med. 1988;109:582-9. LinkGoogle Scholar2. Landefeld C, Chren M, Myers A, Geller R, Robbins S, and Goldman L. Diagnostic yield of the autopsy in a university hospital and a community hospital. N Engl J Med. 1988;318:1249-54. CrossrefMedlineGoogle Scholar3. Battle R, Pathak D, and Humble C. Factors influencing discrepancies between premortem and postmortem diagnoses. JAMA. 1987;258:339-44. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: F. Michael GlothIII, MD; William B. GreenoughIII, MDAffiliations: Johns Hopkins University Baltimore, MD 21224 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 January 1989Volume 110, Issue 2Page: 166-167KeywordsAutopsyChartsPatients ePublished: 1 December 2008 Issue Published: 15 January 1989 PDF downloadLoading ...
Metavinculin Mutations Alter Actin Interaction in Dilated Cardiomyopathy
Authors: Timothy M. Olson, Susanne Illenberger, Nina Y. Kishimoto, Stefan Huttelmaier, Mark T. Keating, Brigitte M. Jockusch
Journal: Circulation (2002)

Background — Vinculin and its isoform metavinculin are protein components of intercalated discs, structures that anchor thin filaments and transmit contractile force between cardiac myocytes. We tested the hypothesis that heritable dysfunction of metavinculin may contribute to the pathogenesis of dilated cardiomyopathy (DCM). Methods and Results — We performed mutational analyses of the metavinculin-specific exon of vinculin in 350 unrelated patients with DCM. One missense mutation (Arg975Trp) and one 3-bp deletion (Leu954del) were identified. These mutations involved conserved amino acids, were absent in 500 control individuals, and significantly altered metavinculin-mediated cross-linking of actin filaments in an in vitro assay. Ultrastructural examination was performed in one patient (Arg975Trp), revealing grossly abnormal intercalated discs. A potential risk-conferring polymorphism (Ala934Val), identified in one DCM patient and one control individual, had a less pronounced effect on actin filament cross-linking. Conclusions — These data provide genetic and functional evidence for vinculin as a DCM gene and suggest that metavinculin plays a critical role in cardiac structure and function. Disruption of force transmission at the thin filament-intercalated disc interface is the likely mechanism by which mutations in metavinculin may lead to DCM.
Physiologic Studies in Mitral Valvular Disease
Authors: A. DRAPER, R. HEIMBECKER, R. DALEY, D. CARROLL, G. MUDD, R. WELLS, W. FALHOLT, E. C. ANDRUS, R. J. BING
Journal: Circulation (1951)

Physiologic findings obtained by cardiac catheterization on 29 patients with mitral valvular disease are discussed. Cardiac outputs, intracardiac pulmonary arterial and pulmonary pressures are determined during rest and exercise. It is shown that the resting cardiac output is reduced in all patients with mitral disease and that exercise results either in a fall or a small increase in the minute volume of circulation. The pulmonary artery and capillary pressures are elevated with rest and rise further with exercise. A clear differentiation by physiologic means between mitral stenosis and mitral insufficiency is difficult. However, in patients with mitral insufficiency the resting cardiac output is lower, the arterial venous oxygen difference is higher and exercise causes a greater fall in the cardiac output. A comparison is made between the physiologic manifestations of mitral disease and myocardial failure: the residual volume of blood of the right ventricle is usually increased in patients with mitral disease and failure and in myocardial failure alone. However, the right ventricular residual volume is normal in mitral disease without evidence of myocardial failure. The pulmonary vascular resistance in mitral disease is usually elevated. It is demonstrated that in a number of patients the pulmonary vascular resistance is not fixed since it decreases during exercise or following valvulotomy of the mitral valve.
Resurgence of Scabies
Authors: Milton Orkin
Journal: JAMA (1971)

This study on the current status of scabies is based upon information obtained from a survey form completed by 86 American and 73 foreign dermatologists, and comprehensive review of the world literature. Although the disease became uncommon in the 1950s, there has been since 1963 and 1964 a progressive increase in scabies in many parts of the world, to epidemic proportions in some areas. The epidemic has not yet involved the United States or Canada, except for sporadic outbreaks and small foci (mainly hippies). The cause of this recent resurgence is not clear; demographic and immunologic considerations seem particularly worthy of further study.
Growth factors and the cardiovascular system: Edited by P Cummins. (Pp 366; 93.95.) Dordrecht: Kluwer, 1993. ISBN 0-7923-2401-3
Authors: J. Pearson
Journal: Cardiovascular Research (1995)

Growth factors and the cardiovascular system: Edited by P Cummins. (Pp 366; £93.95.) Dordrecht: Kluwer, 1993. ISBN 0-7923-2401-3 Get access JD Pearson JD Pearson London, UK Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 29, Issue 1, January 1995, Pages 143–144, https://doi.org/10.1016/S0008-6363(95)90118-3 Published: 01 January 1995
Mentally ill patient chained to tree to highlight shortage of psychiatric beds in India
Authors: S. Bagcchi
Journal: BMJ (2013)

The relatives of a mentally ill patient have chained him to a tree at the entrance of India’s most important medical institute, the All India Institute of Medical Sciences, after failing to get him admitted to the hospital. 

Anil Desai, MP, told the upper house of the Indian parliament1 that the condition of the patient reflected a violation of India’s Mental Healthcare Bill 2013. He has urged the health ministry to respond to the poor treatment of mentally ill patients in India.

The Mental Healthcare Bill 2013, which was introduced at the end of August to the …
Hypercatabolism of Third Complement Component (C3) in Chronic Glomerulonephritis: Role of the Alternate Complement Pathway.
Authors: L. G. Hunsicker
Journal: Annals of Internal Medicine (1972)

Meeting Abstracts1 May 1972Hypercatabolism of Third Complement Component (C3) in Chronic Glomerulonephritis: Role of the Alternate Complement Pathway.L. G. Hunsicker, F.A.C.P., S. Ruddy, M.D., C. B. Carpenter, M.D., J. P. Merrill, F.A.C.P., H. J. Muller-Eberhard, M.D., K. F. Austen, F.A.C.P.L. G. Hunsicker, F.A.C.P.Search for more papers by this author, S. Ruddy, M.D.Search for more papers by this author, C. B. Carpenter, M.D.Search for more papers by this author, J. P. Merrill, F.A.C.P.Search for more papers by this author, H. J. Muller-Eberhard, M.D.Search for more papers by this author, K. F. Austen, F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-76-5-874_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptObservations of circulating factors that destroy the third component of complement (C3) and of circulating split products of C3 suggest the depressions of serum C3 found in membranoproliferative glomerulonephritis are caused by activation with hypercatabolism. Complement (C3) can be activated either by the classical early complement components (Cl, C4, C2) or via the alternate complement pathway, utilizing the C3 proactivator (C3PA). Serum levels of C4 and C3PA have been measured by radial immunodiffusion in 18 patients with chronic hypocomplementemic (low C3) nephritis, to evaluate the participation of the classical and alternate pathways. Levels of C4 were uniformly normal. The C3PA... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Boston, Mass., and La Jolla, Calif. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1972Volume 76, Issue 5Page: 874-874KeywordsGlomerulonephritisNephritis Issue Published: 1 May 1972 PDF DownloadLoading ...
Intravenous versus intracoronary myocardial contrast echocardiography for the evaluation of no-reflow after primary coronary angioplasty
Authors: Jong-Min Song, Jae-Hwan Lee, Young-Hak Kim, Duk-Hyun Kang, Jae-Kwan Song, Myeong-Ki Hong, Seong-Wook Park, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2003)
Elevated HbA1c and Fasting Plasma Glucose in Predicting Diabetes Incidence Among Older Adults
Authors: Kasia J. Lipska, Silvio E. Inzucchi, Peter H. Van Ness, Thomas M. Gill, Alka Kanaya, Elsa S. Strotmeyer, Annemarie Koster, Karen C. Johnson, Bret H. Goodpaster, Tamara Harris, Nathalie De Rekeneire
Journal: Diabetes Care (2013)

To determine which measures-impaired fasting glucose (IFG), elevated HbA1c, or both-best predict incident diabetes in older adults.From the Health, Aging, and Body Composition study, we selected individuals without diabetes, and we defined IFG (100-125 mg/dL) and elevated HbA1c (5.7-6.4%) per American Diabetes Association guidelines. Incident diabetes was based on self-report, use of antihyperglycemic medicines, or HbA1c ≥6.5% during 7 years of follow-up. Logistic regression analyses were adjusted for age, sex, race, site, BMI, smoking, blood pressure, and physical activity. Discrimination and calibration were assessed for models with IFG and with both IFG and elevated HbA1c.Among 1,690 adults (mean age 76.5, 46% men, 32% black), 183 (10.8%) developed diabetes over 7 years. Adjusted odds ratios of diabetes were 6.2 (95% CI 4.4-8.8) in those with IFG (versus those with fasting plasma glucose [FPG] <100 mg/dL) and 11.3 (7.8-16.4) in those with elevated HbA1c (versus those with HbA1c <5.7%). When FPG and HbA1c were considered together, odds ratios were 3.5 (1.9-6.3) in those with IFG only, 8.0 (4.8-13.2) in those with elevated HbA1c only, and 26.2 (16.3-42.1) in those with both IFG and elevated HbA1c (versus those with normal FPG and HbA1c). Addition of elevated HbA1c to the model with IFG resulted in improved discrimination and calibration.Older adults with both IFG and elevated HbA1c have a substantially increased odds of developing diabetes over 7 years. Combined screening with FPG and HbA1c may identify older adults at very high risk for diabetes.
Alterations in muscarinic K+ channel response to acetylcholine and to G protein-mediated activation in atrial myocytes isolated from failing human hearts.
Authors: S Koumi, C E Arentzen, C L Backer, J A Wasserstrom
Journal: Circulation (1994)

BACKGROUND A variety of previous studies have demonstrated reduced diastolic potential and electrical activity in atrial specimens from patients with heart disease. Although K+ channels play a major role in determining resting membrane potential and repolarization of the action potential, little is known about the effects of preexisting heart disease on human atrial K+ channel activity. METHODS AND RESULTS We characterized the inwardly rectifying K+ channel (IKI) and the muscarinic K+ channel [IK(ACh)] in atrial myocytes isolated from patients with heart failure (HF) and compared electrophysiological characteristics with those from donors (control) by the patch-clamp technique. Resting membrane potentials of isolated atrial myocytes from HF were more depolarized (-51.1 +/- 9.7 mV, mean +/- SD, n = 30 patients) than those from donors (-73.0 +/- 7.2 mV, n = 4 patients, P &lt; .001). The action potential duration in HF was longer than that in donors. Although acetylcholine (ACh) shortened the action potential, reduced the overshoot, and hyperpolarized the atrial cell membrane in HF, these effects were attenuated compared with those observed in donors. The whole-cell membrane current slope conductance in HF was small, the reversal potential was more positive, and the sensitivity to ACh was less compared with donors. In single-channel recordings from cell-attached patches, IK1 channel conductance and gating characteristics were the same in HF and donor atria. When ACh was included in the pipette solution, IK(ACh) was activated in both groups. Single-channel slope conductance of IK(ACh) averaged 42 +/- 3 pS (n = 28) in HF and 44 +/- 2 pS (n = 4) in donors, and mean open lifetime was 1.3 +/- 0.3 milliseconds (n = 24) in HF and 1.5 +/- 0.4 milliseconds (n = 4) in donors. These values were virtually identical in the two groups (not significantly different, NS), although both single IK1 and IK(ACh) channel densities were less in HF. Channel open probability of IK(ACh) was also less in HF (4.0 +/- 1.2%, n = 24) than in donors (6.8 +/- 1.1%, n = 3, P &lt; .01). The concentration of ACh at half-maximal activation was 0.11 mumol/L in HF and 0.03 mumol/L in donors. In excised inside-out patches, IK(ACh) from HF required higher concentrations of GTP and GTP gamma S to activate the channel compared with donors. These results suggest a reduced IK(ACh) channel sensitivity to M2 cholinergic receptor-linked G protein (Gi) in HF compared with donors. CONCLUSIONS Atrial myocytes isolated from failing human hearts exhibited a lower resting membrane potential and reduced sensitivity to ACh compared with donor atria. Whole-cell and single-channel measurements suggest that these alterations are caused by reduced IK1 and IK(ACh) channel density and reduced IK(ACh) channel sensitivity to Gi-mediated channel activation in HF.
Rapid Angiographic Progression of Coronary Artery Disease in Patients With Elevated Lipoprotein(a)
Authors: Wolfram Terres, Efstratios Tatsis, Benjamin Pfalzer, F. Ulrich Beil, Ulrike Beisiegel, Christian W. Hamm
Journal: Circulation (1995)

Background The mechanisms underlying rapid angiographic progression of coronary artery disease are still unknown. Intravascular thrombosis with or without plaque rupture may be involved. Methods and Results In a prospective study in 79 patients with coronary artery disease and at least one coronary diameter stenosis ≥50%, possible risk factors for rapid progression were investigated. Quantitative coronary angiography was performed twice at a mean time interval of 66±25 days. Rapid progression of coronary disease defined as (1) an increase &gt;10% in stenosis severity in at least one stenosis ≥50%, (2) occurrence of a new stenosis ≥50%, or (3) occlusion of a formerly patent vessel was found in 21 patients (27%). Between patients with rapid progression and those without, there were no significant differences in sex distribution, age, smoking history, frequency of hypertension or diabetes mellitus, and serum LDL cholesterol, HDL cholesterol, and apolipoprotein B concentrations. In contrast, serum lipoprotein(a) [Lp(a)] concentrations ≥25 mg/dL were found in 14 of 21 patients (67%) with rapid progression of coronary artery disease but in only 19 of 58 (33%) in the group without progression ( P =.007). The respective median Lp(a) concentrations were 66 mg/dL (range, 2 to 139) and 13 mg/dL (range, 2 to 211; P =.01). Conclusions Lp(a) appears to be a risk factor for the rapid angiographic progression of coronary artery disease. The pathophysiological link between Lp(a) and rapid progression may be an interference with thrombolysis through the partial structural homology of Lp(a) with plasminogen.
Heart Cell Transplantation Improves Heart Function in Dilated Cardiomyopathic Hamsters
Authors: K.-J. Yoo, R.-K. Li, R. D. Weisel, D. A. G. Mickle, Z.-Q. Jia, E.-J. Kim, S. Tomita, T. M. Yau
Journal: Circulation (2000)

Little is known about the effect of heart cell transplantation into the dilated cardiomyopathic myocardium. This study was designed to evaluate the effect of heart cell transplantation into dilated cardiomyopathic hamsters.Ventricular heart cells were isolated from 4-week-old BIO 53. 58 hamsters and cultured for 2 weeks before transplantation. The cells were labeled with bromodeoxyuridine (BrdU) before transplantation for identification. Adult hamsters (17 weeks old) were used as recipients. Heart cells (4 x 10(6) cells) or culture medium was transplanted into the left ventricular free wall (transplantation and control groups, respectively, n=12 each). Sham-operated hamsters (n=12) underwent the surgery but not the transplantation. Cyclosporine A was administered subcutaneously to all hamsters daily after the operation. Four weeks after the transplantation, heart function was evaluated with the use of a Langendorff preparation. Histology showed severe focal myocardial necrosis in all groups. BrdU-stained tissue was found at the cell transplantation sites. The transplanted hearts had greater (P:<0. 001) developed pressures at all balloon volumes and improved dP/dt (transplantation 915+/-253 versus control 453+/-120 and sham 530+/-187 mm Hg/s, P:<0.001, balloon volume of 15 microL). No differences in ventricular function were found between control and sham-operated hamsters.The transplanted ventricular heart cells formed cardiac-like tissue in cardiomyopathic myocardium and improved its contractile function.
A PLEA IN BEHALF OF A MEDICAL AID FUND.
Authors: FREDERICK HORNER
Journal: JAMA (1884)

In proof that an urgent necessity exists for an effort to provide for a Medical Aid Fund, it may be stated that for some years past the attention of the profession has been especially directed to this subject, and the facts connected with the origin and history of this movement may be briefly narrated. The Massachusetts Medical Benevolent Society recently held its 25th anniversary, and celebrated it by a dinner. The object of the society, it was stated, is to give financial aid to widows and orphans of medical men. The funds amount to $20,000, and each beneficiary receives $80 per annum. The Mutual Benefit Association of the physicians of Kentucky, Illinois and Indiana, embracing within its fellowship hundreds of our medical brethren, was the next organization of the kind undertaken. Dr. David Keller is deserving all praise for the interest which he has manifested in this successful enterprise. In
Suicide: Accept the possibility of depressive illness
Authors: J Hedges, D Marsh, G B Smith, B L Taylor
Journal: BMJ (1994)

EDITOR, - I feel qualified to comment on the anonymous personal view discussing the right to commit suicide,1 having been similarly thwarted in a serious attempt to take my life. Before this event my suicidal ideation, during periods when life seemed to present unending pressures, seemed a normal thought process, offering the reassurance of a final solution if all others failed. I presumed that being an effective general practitioners, carrying a full practice load, was evidence of sanity,and I could not have accepted that I was suffering major depressive episodes that would benefit from antidepressant treatment.

Adequate antidepressant treatment - made possible by the positive, supportive, non-judgmental attitude of my partners, family, and a …
Beyond single and dual diagnosis in general practice: Editorial's multiple authorship poses difficulties
Authors: J. N Hardy
Journal: BMJ (2003)

EDITOR—In their editorial Wright et al refocus attention on the inextricable links between poverty and poor health.1 They introduce a new term to describe these health problems, “multiple morbidities.”

This is a biomedical construction if ever I heard one, a public health obfuscation. I do not disagree, but the editorial's multiple authorship fails …
VEGF-specific Short Hairpin RNA–expressing Oncolytic Adenovirus Elicits Potent Inhibition of Angiogenesis and Tumor Growth
Authors: Ji Young Yoo, Joo-Hang Kim, Young-Guen Kwon, Eok-Cheon Kim, Nam Kyu Kim, Hye Jin Choi, Chae-Ok Yun
Journal: Molecular Therapy (2007)

RNA interference is being developed to treat cancer. Although highly target specific, its use has been limited by its short duration of expression. To overcome this shortcoming, we constructed an oncolytic adenovirus (Ad)-based short hairpin RNA (shRNA) expression system (Ad-ΔB7-shVEGF) against vascular endothelial growth factor (VEGF), a key mediator in angiogenesis. To demonstrate the VEGF-specific nature of this Ad-based shRNA, replication-incompetent Ad expressing VEGF-specific shRNA (Ad-ΔE1-shVEGF) was also generated. Ad-ΔE1-shVEGF was highly effective in reducing VEGF expression, and elicited an antiangiogenic effect in vitro and in vivo. Similarly, Ad-ΔB7-shVEGF exhibited potent antiangiogenic effects in the matrigel plug assay. Moreover, Ad-ΔB7-shVEGF demonstrated a greater antitumor effect and enhanced survival compared to the cognate control oncolytic Ad, Ad-ΔB7. Ad-ΔB7-shVEGF induced significant reduction in tumor vasculature, verifying the antiangiogenic mechanism. Furthermore, both the duration and magnitude of gene silencing by Ad-ΔB7-shVEGF was greater than Ad-ΔE1-shVEGF. These results suggest that the combined effects of oncolytic viral therapy and cancer cell-specific expression of VEGF-targeted shRNA elicits greater antitumor effect than an oncolytic Ad alone. RNA interference is being developed to treat cancer. Although highly target specific, its use has been limited by its short duration of expression. To overcome this shortcoming, we constructed an oncolytic adenovirus (Ad)-based short hairpin RNA (shRNA) expression system (Ad-ΔB7-shVEGF) against vascular endothelial growth factor (VEGF), a key mediator in angiogenesis. To demonstrate the VEGF-specific nature of this Ad-based shRNA, replication-incompetent Ad expressing VEGF-specific shRNA (Ad-ΔE1-shVEGF) was also generated. Ad-ΔE1-shVEGF was highly effective in reducing VEGF expression, and elicited an antiangiogenic effect in vitro and in vivo. Similarly, Ad-ΔB7-shVEGF exhibited potent antiangiogenic effects in the matrigel plug assay. Moreover, Ad-ΔB7-shVEGF demonstrated a greater antitumor effect and enhanced survival compared to the cognate control oncolytic Ad, Ad-ΔB7. Ad-ΔB7-shVEGF induced significant reduction in tumor vasculature, verifying the antiangiogenic mechanism. Furthermore, both the duration and magnitude of gene silencing by Ad-ΔB7-shVEGF was greater than Ad-ΔE1-shVEGF. These results suggest that the combined effects of oncolytic viral therapy and cancer cell-specific expression of VEGF-targeted shRNA elicits greater antitumor effect than an oncolytic Ad alone.