tbuckley/cabot-search huggingface dataset:
Prehospital Care of Acute Myocardial Infarction
Authors: PAUL N. YU
Journal: Circulation (1972)

It has been estimated recently that half of deaths among the patients with acute myocardial infarction occur before they ever reach the hospital for definitive medical care. One of the major reasons for the high incidence of death was attributed to delays in reaching medical care, involving patients themselves, physicians, transportation, and receiving areas of the hospital. In order to reduce this high mortality substantially we should focus our attention on the prehospital care of this disease, which may include several major approaches. A. To shorten the delay in securing medical care: 1. Public education, with emphasis on the early warning symptoms and signs of acute myocardial infarction, and the need and importance of seeking early medical care, with special attention directed toward the high-risk coronary patients. 2. Professional education. 3. Mechanisms to direct and/or bring patients with suspected or proven acute myocardial infarction promptly to the system of medical care with special emphasis on the utilization of a telephone information center and provision of rapid transportation. B. Establishment of emergency life-support stations for screening, monitoring, and early stabilization of cardiac arrhythmias: 1. Fixed. a. Emergency department of hospitals, preferably with an attached precoronary care area. b. Areas where many employees are working on weekdays. c. Areas where many people move in and out from day to day. d. Areas where there is periodic concentration of mass population. 2. Mobile. a. Mobile coronary care unit. b. Mobile intensive care unit. C. Prevention of sudden death: 1. Study of mechanism and clinical environment of sudden death. 2. Development of techniques for early diagnosis and management of acute myocardial infarction prior to inception of symptoms. 3. Identification of individuals prone to sudden death. 4. Preventive measures directed toward the individuals prone to sudden death. a. Effective control of risk factors. b. Intermittent or periodic electrocardiographic monitoring in these individuals. c. Long-term antiarrhythmic therapy for these individuals. d. Possibility of implanting an automatic defibrillator in patients with previous myocardial infarction or in those recovered from ventricular fibrillation. 5. Early administration of antiarrhythmic drugs in patients with suspected or proven acute myocardial infarction.
Use of Cardiac Rehabilitation by Medicare Beneficiaries After Myocardial Infarction or Coronary Bypass Surgery
Authors: Jose A. Suaya, Donald S. Shepard, Sharon-Lise T. Normand, Philip A. Ades, Jeffrey Prottas, William B. Stason
Journal: Circulation (2007)

Cardiac rehabilitation (CR) is effective in prolonging survival and reducing disability in patients with coronary heart disease. However, national use patterns and predictors of CR use have not been evaluated thoroughly.Using Medicare claims, we analyzed outpatient (phase II) CR use after hospitalizations for acute myocardial infarctions or coronary artery bypass graft surgery in 267,427 fee-for-service beneficiaries aged > or = 65 years who survived for at least 30 days after hospital discharge. We used multivariable analyses to identify predictors of CR use and to quantify geographic variations in its use. We obtained unadjusted, adjusted-smoothed, and standardized rates of CR use by state. Overall, CR was used in 13.9% of patients hospitalized for acute myocardial infarction and 31.0% of patients who underwent coronary artery bypass graft surgery. Older individuals, women, nonwhites, and patients with comorbidities (including congestive heart failure, previous stroke, diabetes mellitus, or cancer) were significantly less likely to receive CR. Coronary artery bypass graft surgery during the index hospitalization, higher median household income, higher level of education, and shorter distance to the nearest CR facility were important predictors of higher CR use. Adjusted CR use varied 9-fold among states, ranging from 6.6% in Idaho to 53.5% in Nebraska. The highest CR use rates were clustered in the north central states of the United States.CR use is relatively low among Medicare beneficiaries despite convincing evidence of its benefits and recommendations for its use by professional organizations. Use is higher after coronary artery bypass graft surgery than with acute myocardial infarctions not treated with revascularization procedures and varies dramatically by state and region of the United States.
Wornout and Prufrock
Authors: GEORGE F. DONAHOWER
Journal: Annals of Internal Medicine (1973)

Letters, Comments, and Corrections1 February 1973Wornout and PrufrockGEORGE F. DONAHOWER, M.D.GEORGE F. DONAHOWER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-2-315_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: "The Wardsong of J. Alvin Wornout" by Doctor McAvoy is a masterpiece! His rendition is true, not only to the experience of everyone who has served as an intern and resident, but is true also, I think, to T. S. Eliot's style and intent in his "Love Song." Thank you for departing from your usual "straight" format to bring us this talented colleague's medical version.... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1973Volume 78, Issue 2Page: 315-315 ePublished: 1 December 2008 Issue Published: 1 February 1973 PDF downloadLoading ...
Trends of Antibiotic Use In the United States
Authors: Jules Cooper
Journal: JAMA (1974)

<h3>To the Editor.—</h3> In my opinion, on the basis of my personal experience since before the advent of the antibiotic era, the highly questionable "formidable force" of "patient pressure," which you emphasize, was not, and is not, the primary cause of the frightful and very obvious misuse of antibiotics. Rather, and equally obvious, I believe it was our own widespread and glaring ineptitude involving abusive overuse of these drugs that originally spawned the boomerang of "patient pressure." The patient is not to blame, and we must not further compound and expand the problem by seeking to make him the whipping boy while whitewashing the doctor, who is really culpable. I have not, for some 20 years, found it necessary or desirable to give injectable penicillin except in certain cases of venereal disease or in the relatively rare cases in which it was definitively indicated. I have prescribed oral penicillin and
Intranasal Lidocaine for Treatment of Migraine-Reply
Authors: Morris Maizels
Journal: JAMA (1996)

In Reply.  —Dr Diamond raises concerns about the toxicity of lidocaine. Blood levels of lidocaine greater than 26 μmol/L (5 μg/mL), which occasionally develop in patients receiving intravenous infusions of lidocaine administered at 2 to 4 mg per minute, may be associated with central nervous system toxicity. The bioavailability of intranasal lidocaine is 0.05 to 0.48 with a mean of 0.26. 1 The maximum dose used in our study was 80 mg (2 mL of a 4% solution), yielding a level well below that which might cause concern of toxicity. One patient (outside the study) who claimed to use a nasal spray of lidocaine every 2 hours had a level of 0.043 μmol/L (0.01 μg/mL) determined immediately after her last dose.  Our patients were not evaluated for the presence of nasal abnormalities, as Dr Lane suggests. In a study of intranasal lidocaine as a prognostic aid for preoperative assessment of facial pain
Metabolism of L-Thyroxine by Phagocytosing Human Leukocytes
Authors: Kenneth A. Woeber, Sidney H. Ingbar
Journal: Journal of Clinical Investigation (1973)

Intact normal human leukocytes deiodinated L-thyroxine (T(4)) with the generation of inorganic iodide, chromatographically immobile origin material, and small quantities of L-triiodothyronine (T(3)). When phagocytosis was induced in the leukocytes through the addition of zymosan particles that had been opsonized by coating with plasma, T(4)-deiodination was greatly stimulated. In addition to the stimulation of T(4)-deiodination, the accumulation by the leukocytes of undegraded T(4) was increased. Anoxia, which has previously been shown not to interfere with phagocytosis, did not prevent the increased cellular accumulation of T(4) that phagocytosis induced, but virtually abolished T(4)-deiodination. On the other hand, calcium, which has previously been shown to be required for optimal phagocytosis, was required for the increase in both the cellular accumulation and deiodination of T(4) that phagocytosis induced. Phospholipase-C, which has previously been shown to induce a metabolic burst that mimics that induced by phagocytosis, did not increase the cellular accumulation or deiodination of T(4). On the other hand, colchicine, which has previously been shown to depress the metabolic burst that accompanies phagocytosis, did not prevent the increase in either the cellular accumulation or deiodination of T(4) that phagocytosis induced. Thus, increased accumulation of T(4) by the leukocytes during phagocytosis appears to be the primary factor responsible for the stimulation of deiodination that phagocytosis induces. The increased accumulation of T(4) did not appear to be owing to engulfment of suspending medium surrounding the particles or to binding of T(4) to the particles themselves. In addition to the enhanced cellular accumulation, other factors related to the metabolic burst that accompanies phagocytosis might also be involved in the stimulation of T(4)-deiodination. In leukocytes from two patients with chronic granulomatous disease, a disorder in which phagocytosis appears to occur normally but in which the metabolic burst and attendant increase in hydrogen peroxide generation do not occur, stimulation of T(4)-deiodination was either greatly diminished or totally lacking. In myeloperoxidase-deficient leukocytes, on the other hand, stimulation of T(4)-deiodination was at least as great as that in normal cells. Thus, we conclude that the primary factor responsible for the increased deiodination of T(4) that phagocytosis induces is the enhanced cellular uptake of hormone. The increased generation of hydrogen peroxide that accompanies phagocytosis may be necessary for the enhanced deiodination of the accumulated T(4), but the latter reaction does not require the mediation of myeloperoxidase.
Neuropsychological Sequelae of Cardiac Arrest
Authors: Risto O. Roine
Journal: JAMA (1993)

Prospective and community-based studies on the cognitive outcome of out-of-hospital cardiac arrest have not been published. We studied prospectively the neuropsychological sequelae of cardiac arrest and evaluated the effects of nimodipine on them.Placebo-controlled, randomized, double-blind trial of nimodipine compared with placebo in out-of-hospital ventricular fibrillation.Urban area of 500,000 inhabitants served by the physician-manned Advanced Life Support Unit of Helsinki.A total of 155 successfully resuscitated consecutive patients out of 677 resuscitation attempts during 2 1/2 years. Sixty-eight survivors were examined by a neuropsychologist and a neurologist.Neuropsychological outcome 3 months and 1 year after cardiac arrest.Nimodipine or placebo at a dosage of 10 micrograms/kg as an intravenous injection immediately after restoration of spontaneous circulation, followed by an infusion of 0.5 micrograms/kg per minute for 24 hours.Three months after cardiac arrest, 41 (60%) of 68 patients were found to have moderate to severe cognitive deficits. At 12 months, 26 (48%) of 54 survivors still had moderate to severe deficits, and the Symptom Check List 90--Revised score indicated the presence of depression in 22 patients (45%) and severe depression in 12 patients (24%).Moderate to severe neuropsychological sequelae of out-of-hospital cardiac arrest are still present in approximately one half of the survivors at 1 year and may be permanent. There seems to be no excess of increased disability in the subgroup of patients with delayed advanced life support. Nimodipine failed to show any effect on the cognitive functions tested.
Efficient Gene Therapy for Parkinson's Disease Using Astrocytes as Hosts for Localized Neurotrophic Factor Delivery
Authors: Anja Drinkut, Yuliya Tereshchenko, Jörg B Schulz, Mathias Bähr, Sebastian Kügler
Journal: Molecular Therapy (2011)

Current gene therapy approaches for Parkinson's disease (PD) deliver neurotrophic factors like glial cell line-derived neurotrophic factor (GDNF) or neurturin via neuronal transgene expression. Since these potent signaling-inducing neurotrophic factors can be distributed through long-distance neuronal projections to unaffected brain sites, this mode of delivery may eventually cause side effects. To explore a localized and thus potentially safer alternative for gene therapy of PD, we expressed GDNF exclusively in astrocytes and evaluated the efficacy of this approach in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rat 6-hydroxy-dopamine (6-OHDA) models of PD. In terms of protection of dopaminergic cell bodies and projections, dopamine (DA) synthesis and behaviour, astrocyte-derived GDNF demonstrated the same efficacy as neuron-derived GDNF. In terms of safety, unilateral striatal GDNF expression in astrocytes did not result in delivery of bio-active GDNF to the contralateral hemispheres (potential off-target sites) as happened when GDNF was expressed in neurons. Thus, astrocytic GDNF expression represents a localized but efficient alternative to current gene therapeutic strategies for the treatment of PD, especially if viral vectors with enhanced tissue penetration are considered. Astrocytic neurotrophic factor expression may open new venues for neurotrophic factor-based gene therapy targeting severe diseases of the brain. Current gene therapy approaches for Parkinson's disease (PD) deliver neurotrophic factors like glial cell line-derived neurotrophic factor (GDNF) or neurturin via neuronal transgene expression. Since these potent signaling-inducing neurotrophic factors can be distributed through long-distance neuronal projections to unaffected brain sites, this mode of delivery may eventually cause side effects. To explore a localized and thus potentially safer alternative for gene therapy of PD, we expressed GDNF exclusively in astrocytes and evaluated the efficacy of this approach in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rat 6-hydroxy-dopamine (6-OHDA) models of PD. In terms of protection of dopaminergic cell bodies and projections, dopamine (DA) synthesis and behaviour, astrocyte-derived GDNF demonstrated the same efficacy as neuron-derived GDNF. In terms of safety, unilateral striatal GDNF expression in astrocytes did not result in delivery of bio-active GDNF to the contralateral hemispheres (potential off-target sites) as happened when GDNF was expressed in neurons. Thus, astrocytic GDNF expression represents a localized but efficient alternative to current gene therapeutic strategies for the treatment of PD, especially if viral vectors with enhanced tissue penetration are considered. Astrocytic neurotrophic factor expression may open new venues for neurotrophic factor-based gene therapy targeting severe diseases of the brain.
A prion protein epitope selective for the pathologically misfolded conformation
Authors: Eustache Paramithiotis, Marc Pinard, Trebor Lawton, Sylvie LaBoissiere, Valerie L Leathers, Wen-Quan Zou, Lisa A Estey, Julie Lamontagne, Marty T Lehto, Leslie H Kondejewski, Gregory P Francoeur, Maria Papadopoulos, Ashkan Haghighat, Stephen J Spatz, Mark Head, Robert Will, James Ironside, Katherine O'Rourke, Quentin Tonelli, Harry C Ledebur, Avi Chakrabartty, Neil R Cashman
Journal: Nature Medicine (2003)
Induction of specific transplantation immune reactions using anti-idiotypic antibodies.
Authors: H Frischknecht, H Binz, H Wigzell
Journal: The Journal of Experimental Medicine (1978)

B and T lymphocytes with reactivity against major histocompatibility antigens are known to express this immune potential via a display on the outer surface of antigen-specific, idiotypic receptors. Here, we show that anti-idiotypic antibodies directed against such receptors may serve as specific triggering agents of the idiotype-positive lymphocytes in the physical absence of foreign histocompatibility antigens. This was shown in vitro using normal or immune spleen T cells where anti-idiotypic antibodies would lead to the selective proliferation and development of antigen-specific cytolytic T cells as determined by short-time 51Cr release assays. Furthermore, purified anti-idiotypic antibodies in adjuvant administered in vivo to normal syngeneic animals could be shown to lead to production of high titers of specific alloantibodies. The present experiments were in most cases carried out using auto-anti-idiotypic antibodies as triggering agents. The present results thus lend further support to the concept that idiotype-anti-idiotype reactions may be normal parts of conventional immune processes with either stimulatory or inhibitory consequences, depending upon the prevailing conditions.
Abstract LB-13: The role of p38/MAPK14 in Sonic Hedgehog-driven CGNP proliferation
Authors: Guldal G. Cemile, Lori Mainwaring, Susana Parathath, Anna M. Kenney
Journal: Cancer Research (2010)

Abstract Development of the cerbellum occurs primarily postnatally and is marked by a rapid proliferation of cerebellar granule neuron precursors (CGNPs). This proliferation requires the activity of the mitogen Sonic Hedgehog (Shh). The rapid proliferation stage of CGNPs has led to speculation that they are the cells of origin for some classes of medulloblastoma, the most common solid pediatric tumor. Since MAP kinases play important roles in many aspects of development, proliferation, and cancer we investigated if any of the three major classes of MAP kinases were involved in Shh-driven CGNP proliferation. We have previously shown that p42/p44 ERK MAP kinases are not involved in Shh signaling in CGNP proliferation. We have also shown that JNK/SAP kinases are not involved in Shh-driven proliferation. However, p38/MAPK14 is induced and activated in proliferating CGNPs compared to CGNPs that exit the cell cycle and differentiate in the absence of Shh. Other known pathway components upstream and downstream of MAPK14, such as ASK1, MKK3 and ATF-2, are also activated in the presence of Shh. Antioxidants such as lipoic acid and n-acetyl-cysteine that relieve oxidative stress reduced Shh-induced activation of MAPK14 and caused a marked decrease in CGNP proliferation measured by Ki67 and BrdU staining. We are currently investigating the role of oxidative stress and MAPK14 in CGNP proliferation by over-expressing and knocking down MAPK14 in CGNPs under oxidative stress conditions. Preliminary data suggests that knocking down MAPK14 reduces CGNP proliferation. Elucidating the role of MAPK14 pathway in CGNP proliferation will not only help us understand normal cerebellum development but may also lead to possible therapies for diseases where constitutive Shh signaling has been shown to play a role such as some classes of medulloblastoma and Gorlin's syndrome. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-13.
Female Fecundity as a Function of Age
Authors: D. Schwartz, M. J. Mayaux
Journal: New England Journal of Medicine (1982)

Fecundity has been reported to decline in women over 30 years of age. It is not known whether the decrease in fecundity is biologic or simply the consequence of diminished sexual activity. Artificial insemination with donor semen (AID) offers an opportunity to control certain variables in the study of female fecundity over time. 2193 nulliparous women who were receiving AID from 1973-80 at the Centres d'Etude et de Conservation du Sperme Humain (CECOS) and whose husbands were totally sterile were studied. The women were divided into 4 age groups: 25 years old or younger (n=371), 26-30 (n=1079), 31-35 (n=599), and 35 or older (n=144). At the end of the study period, the women were categorized into 4 groups, depending on the outcome: success (all pregnancies occurring during the study period), lost to follow-up (if the result of the last AID cycle was unknown), open case (result of last AID cycle was known but the next insemination procedure had not yet taken place), and dropout (discontinued treatment). The cumulative success rates were calculated ater 12 cycles with the life table technique adapted to AID as if there were no dropouts (theoretical cumulative rates). The Mantel-Haenzel test was used to compare the curves obtained from the cumulative rate as a function of the number of treatment cycles for the various age groups. The 4 curves differed significantly (chi-square=15.72, with 3 degrees of freedom; p0.01). The curves for the 2 age groups under 30 were very similar. Overall, the study shows that a decrease in fecundability (conception rate per cycle) as a function of a woman's age is slight but significant after 30 years of age and marked after 35 years. The probability of success of AID for 12 cycles declined to 61% (from 73% for those under 31 years old) for the 31-35 age group (p0.03) and to 54% (from 74% for those under 31 years old) for those over 35 (p0.001). 2 major problems encountered in studying variations in fecundity as a function of a woman's age are: 1) the need to separate the effect of the woman's age from associated variables such as coital pattern and husband's age, and 2) the woman's age itself, which could result in bias, since time introduces a type of selection. AID may provide the best means of minimizing the effects of associated variables and sources of bias.
Association Between Early Stage Colon Neoplasms and False-negative Results From the Fecal Immunochemical Test
Authors: Han–Mo Chiu, Yi–Chia Lee, Chia–Hung Tu, Chien–Chuan Chen, Ping–Huei Tseng, Jin–Tung Liang, Chia–Tung Shun, Jaw–Town Lin, Ming–Shiang Wu
Journal: Clinical Gastroenterology and Hepatology (2013)