tbuckley/cabot-search huggingface dataset:
Distribution of carbon flux within fatty acid utilization during myocardial ischemia and reperfusion.
Authors: S H Nellis, A J Liedtke, B Renstrom
Journal: Circulation Research (1991)

Twenty-nine intact, working pig hearts were extracorporeally perfused and divided into two study groups (16 Aerobic and 13 Ischemic/Reflow hearts). Step function, equilibrium labeling with [14C]palmitate was used to develop uptake and washout curves of radioactive fatty acid products contained in coronary effluent during either aerobic perfusion or reperfusion after ischemia (60% reduction in left anterior descending coronary flow for 30 minutes). Left anterior descending control flows were slightly overperfused in Aerobic hearts (18% higher than in Ischemic/Reflow hearts); otherwise, circumflex and right coronary flows, left ventricular pressure, and serum fatty acids and blood sugar levels were comparable between groups. As expected in Ischemic/Reflow hearts, recovery of regional systolic shortening and myocardial oxygen consumption in reperfusion was only modestly impaired (-20% and -19%, respectively, not significant and p less than 0.011 compared with preischemic values, not significant from Aerobic hearts). The only significant metabolized product to be released from labeled fatty acid utilization in either group was 14CO2. A smaller fatty acid pool also was measured and accounted for by that contained in the coronary intravascular volume. We could determine no significant back diffusion of fatty acids from myocardium in either perfusion condition. Uptake time constants of the early phase of 14CO2 production also were virtually identical in both groups (19.9 +/- 3.2 versus 16.7 +/- 3.2 minutes in Aerobic and Ischemic/Reflow hearts, respectively) and strongly correlated with hemodynamics as described by heart rate. In washout studies, tissue radioactivity in the aqueous soluble and fatty acid pools declined in both study groups, and counts in complex lipids and cholesterol/cholesteryl esters remained steady, whereas those in triacylglycerols varied. Washout of 14CO2 in both groups never reached background radioactivity over a 40-minute sampling after cessation of isotope infusion into the perfusate, suggesting slow release of trapped substrate from intracellular pools, which then proceeded to fatty acid oxidation. In conclusion, these experiments have demonstrated very similar findings with respect to fatty acid uptake, storage, and release characteristics between aerobic and reperfused myocardium. We found no differences in preferred substrate utilization and oxidation as a result of reversible ischemia followed by reflow.
Osteolysis of the Mandible and Maxilla
Authors: Edito C. Cabal
Journal: JAMA (1978)

<h3>History</h3> A 30-year-old man had a history of intermittent pain for the past four years in the area of previous molar teeth extractions. An oroantral fistula subsequently developed, and he began losing teeth from his mandible. He had periods of remissions and exacerbations concurrent with various treatment procedures during the next three years. There was no history of metabolic disease or exposure to radiation. Roentgenograms of the mandible are shown in Fig 1. Skeletal survey did not disclose any other bone abnormality. <h3>Diagnosis</h3> Osteolysis of the mandible and maxilla secondary to chronic actinomycosis infection. <h3>Comment</h3> Figure 1 shows extensive osteolysis and thinning of the mandible, with pathological fracture of the body of the right side. Maxillary osteolysis is also present, but of lesser degree. Actinomycetes are normal flora of the mouth, but at times may be the cause of infection. There are three species implicated in human infection:<i>Actinomyces</i>
Buccal cell carbohydrates are altered during critical illness.
Authors: K D Weinmeister, A R Dal Nogare
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

Cell-surface carbohydrates mediate the adherence of many pathogenic bacteria to epithelial cells. Because gram-negative bacteria adhere especially well to respiratory epithelial cells obtained from severely ill patients, we compared respiratory epithelial cell-surface carbohydrate levels of normal subjects with those of critically ill patients. Lectins were used to quantitate the amount of mannose, galactose, fucose, and sialic acid on buccal and tracheal cells. Fifteen critically ill patients, 20 normal subjects, and 10 minimally ill hospitalized patients were studied. The severely ill patients' buccal cells had decreased amounts of sialic acid and galactose. No differences were found between the normal and critically ill patients' tracheal-cell carbohydrates. The results obtained with a sialic acid-specific lectin were confirmed by direct measurement of buccal-cell sialic acid. We conclude that severely ill patients have decreased amounts of galactose and sialic acid on their upper-airway epithelial cells, and that loss of these two monosaccharides may explain the high prevalence of gram-negative bacterial colonization and pneumonia in the critically ill.
Measuring the outcome of perinatal care.
Authors: K L Dodd
Journal: BMJ (1993)

tions to alter medical practice.These have included the suggestion that neonatal intensive care should be stopped and telling surgeons not to do certain operations on children.The auditor should have confined the report to aspects of structure and process without reporting on areas of clinical judgment, medical guidelines, or protocols.We share the concerns of our colleagues about the dangers of protocols.If similar audits are usefully to be conducted across Britain we advocate thorough research into the local situation and medical practices and full medical consultation.
Isolated granulocytic sarcoma of the head and neck preceding acute myeloid leukemia
Authors: Oguz Dikbas, Metin Isik, Tugrul Purnak, Omer Karadag, Aysegul Uner, Kadri Altundag
Journal: American Journal of Hematology (2004)

Eosinophilia Presenting as Acute Coronary SyndromeTo the Editor: Cardiovascular involvement in eosinophilia includes eosinophilic myocarditis, Lo¨ffler's endocarditis, and venous thromboembolism [1].Coronary vasculitis in major coronary artery with thrombus formation presenting as acute coronary syndrome was rarely reported. CASE REPORTA 27-year-old male was admitted with a 4-day history of exacerbating cough and dyspnea.He had had bronchial asthma for 2 years.Laboratory data showed a white blood cell count of 11.0 Â 10 9 /l, eosinophils 0.5 Â 10 9 /l, and C reactive protein 8.39 mg/dl.He was treated for acute asthma attack and bronchitis.However, his dyspnea deteriorated.CXR showed progressive enlargement of cardiac shadow and pulmonary edema.Coronary angiography revealed a total occlusion of the mid-left anterior descending coronary artery (LAD), and a large amount of thrombi in the left circumflex coronary artery.Antithrombin III, protein C, protein S, anti-nuclear antibody, and anti-cardiolipin antibody were normal.Percutaneous coronary intervention was unsuccessful.Ten days after admission, whole blood test showed eosinophilia (13.7 Â 10 9 /l).Endomyocardial biopsy disclosed eosinophilic endocarditis with mural thrombus (Fig. 1).Except for IgE of 4,497 IU/ml, the survey of the causes of eosinophilia was negative.There is no evidence of systemic vasculitis.Heart function deteriorated in spite of steroid therapy.He received orthotopic heart transplantation 6 months later.The pathology of the recipient's explanted heart revealed organized thrombus with recanalization within the original lumen of LAD.No evidence of atherosclerosis was found within coronary arteries.This case has two uncommon features.First, the initial eosinophil count only mildly elevated.We overlooked the diagnosis of eosinophilia until we rechecked the total eosinophil count again and performed the endomyocardial biopsy.Although the degree of organ damage usually correlates with the total eosinophil count [1], this case alerts us to re-examine the blood and the tissue involved when there is a clinical suspicion.The second uncommon feature is the presentation of acute coronary syndrome.Coronary involvement in eosinophilia usually limits to distal coronary arteries [2], as shown in patients with Churg-Strauss syndrome [3].Coronary vasculitis in major coronary artery with thrombus formation presenting as acute coronary syndrome, as in this case, was rarely reported in patients with eosinophilia.Eosinophils exert destructive effect on cardiomyocytes and endothelium by releasing eosinophil granule proteins, which in turn interfere with cell membrane permeability, mitochondria respiration, and intrinsic coagulation system [4].This case alerts us that, in patients with acute coronary syndrome, a past history of asthma, and a mildly elevated eosinophil count, eosinophilia with coronary thrombosis should be taken into account.
Association of single nucleotide polymorphisms in the thrombopoietin‐receptor gene, but not the thrombopoietin gene, with differences in platelet count
Authors: She Min Zeng, Jeffrey C. Murray, John A. Widness, Ronald G. Strauss, Jerome Yankowitz
Journal: American Journal of Hematology (2004)

Abstract Little is known about the mechanisms explaining the wide variation in platelet counts (PLT) and other hematologic parameters in humans. We previously showed that the sex‐based difference in hematocrit was associated with nucleotide variation in the erythropoietin receptor gene (EPOR). We sought to identify new polymorphisms of the human thrombopoietin (TPO) and thrombopoietin receptor (TPOR) genes to determine any associations with blood PLT counts. We screened TPO and TPOR for polymorphisms using single‐strand conformation polymorphism (SSCP) and DNA sequencing. Association of polymorphisms was studied in 304 normal subjects with low or high PLT counts. Distribution of allelic frequency was analyzed by the Chi‐square statistic. Single nucleotide polymorphisms (SNPs) with two alleles were found in TPO and TPOR. The TPO SNP was a G to A transition at nucleotide 5753, and the TPOR SNP was a C to A transversion at position 550 in the 5′‐promoter area. The allelic frequencies were 0.54 for G and 0.46 for A of TPO, and 0.62 for C and 0.38 for A of TPOR in a Caucasian population. The frequency of the TPOR allele “C” was significantly higher in subjects with high PLT count (&gt;258 k/mm 3 ) versus low PLT count (&lt;224 k/mm 3 ) and in males with high PLT count (&gt;258 k/mm 3 ) versus males with low PLT count (&lt;212 k/mm 3 ). In contrast, the frequency of the TPO alleles was not related to blood PLT counts. An association of TPO and TPOR allele distribution to red and white blood cell parameters was seen. These new SNPs found for the human TPO and TPOR genes help explain variations in blood PLT counts and may be useful in patient studies related to the roles of TPO and/or TPOR in disease. Am. J. Hematol. 77:12–21, 2004. © 2004 Wiley‐Liss, Inc.
Sudden Death During Treatment With Phenothiazine Derivatives
Authors: Leo E. Hollister
Journal: JAMA (1965)

Six cases of sudden death occurred in otherwise healthy patients following treatment with phenothiazine derivatives in the fairly large doses customarily given to psychiatric patients. In each instance, postmortem findings were inadequate to explain the death. Clinically, the attack begins with a syncopal-seizure episode, followed quickly by cessation of heartbeat and respirations. Resuscitation was temporarily accomplished in one patient, allowing for documentation of irreversible ventricular fibrillation. Compared with past experience with deaths in hospitalized psychiatric patients, this mode of death appears to be definitely associated with drug therapy. The predominant mechanism is probably ventricular fibrillation, though asphyxia during a drug-induced seizure or from aspiration of food is another possibility. The nature of the cardiac disturbance is still unexplained, though recent reports of electrocardiographic abnormalities and pigment deposits in the myocardium in patients on long-term treatment with phenothiazines may be related to this complication.
Scottish death rates published with health warning
Authors: L. Dillner
Journal: BMJ (1994)

Death rates for NHS patients in Scotland were published for the first time by the Scottish Office this week with the warning that only limited comparisons could be made between hospitals. The data published in the Clinical Outcome Indicators Report 1994 looks at 17 measures. Although not all are related to death, the ones most likely to cause a public outcry are mortality within 30 days of admission for acute myocardial infarction, stroke, or fractured neck of femur.

Although the report states that the data do not constitute league tables, the indicators are listed to allow comparisons between the average outcomes of over 20 NHS trusts between 1990 and 1993. For myocardial infarctions, for example, there is a twofold difference between Fife Healthcare NHS Trust, with a mortality rate of nearly 30%, and Western General Hospitals NHS Trust, with a rate of just over 15%. But Dr Robert Kendell, chief medical officer for Scotland, says in his introduction to the report, “It would be wrong to conclude from any one of these clinical outcome indicators that one hospital provides better treatment than another.” Each table carries a footnote:

“Warning: This information should be interpreted strictly in accordance with the general and the specific guidance given in this report.”



FIG 
Deaths occurring within 30 days of admission as percentage of all admissions with acute myocarardial infarction, October 1990 to September 1993



Dr Kendell emphasises that variations in outcomes are as likely to be due to differences in patients themselves rather than in the quality of care between hospitals. No quality of care measures were …
Recombinant Cardiac ATP-Sensitive K <sup>+</sup> Channel Subunits Confer Resistance To Chemical Hypoxia-Reoxygenation Injury
Authors: Aleksandar Jovanović, Sofija Jovanović, Eva Lorenz, Andre Terzic
Journal: Circulation (1998)

Background —Opening of cardiac ATP-sensitive K + (K ATP ) channels has emerged as a promising but still controversial cardioprotective mechanism. Defining K ATP channel function at the level of recombinant channel proteins is a necessary step toward further evaluation of the cardioprotective significance of this ion conductance. Methods and Results —K ATP channel–deficient COS-7 cells were found to be vulnerable to chemical hypoxia-reoxygenation injury that induced significant cytosolic Ca 2+ loading (from 97±3 to 236±11 nmol/L). In these cells, the potassium channel opener pinacidil (10 μmol/L) did not prevent Ca 2+ loading (from 96±3 nmol/L before to 233±12 nmol/L after reoxygenation) or evoked membrane current. Cotransfection with Kir6.2/SUR2A genes, which encode cardiac K ATP channel subunits, resulted in a cellular phenotype that, in the presence of pinacidil (10 μmol/L), expressed K + current and gained resistance to hypoxia-reoxygenation (Ca 2+ concentration from 99±7 to 127±11 nmol/L; P &gt;0.05). Both properties were abolished by the K ATP channel blocker glyburide (1 μmol/L). In COS-7 cells transfected with individual channel subunits Kir6.2 or SUR2A , which alone do not form functional cardiac K ATP channels, pinacidil did not protect against hypoxia-reoxygenation. Conclusions —The fact that transfer of cardiac K ATP channel subunits protected natively K ATP channel–deficient cells provides direct evidence that the cardiac K ATP channel protein complex harbors intrinsic cytoprotective properties. These findings validate the concept that targeting cardiac K ATP channels should be considered a valuable approach to protect the myocardium against injury.
A NEW INSTRUMENT FOR USE IN THE RUBIN TEST
Authors: J. Arthur York
Journal: JAMA (1926)

This instrument is composed of a handle that fits the hand comfortably, and a long, slender shank, which has at its distal end two prongs forming an angle of about 100 degrees with tiring of the hand and without injury to the stopper, which does occur when a clamp is used. This instrument has been received with favor in the gynecologic departments of the Johns Hopkins Hospital, Union Memorial Hospital, and Hospital for the Women of Maryland.
Care of the Premature Infant in Massachusetts
Authors: R. Gerald Rice, Etta Bloom, Vlado A. Getting, Sallie Saunders
Journal: New England Journal of Medicine (1953)

PREMATURITY is recorded as the primary or contributory cause of death on approximately 50 per cent of the death certificates of infants dying under one year of age in Massachusetts. In 1951 more than 1000 infant deaths were recorded as being associated with prematurity.The following study considers the efforts of the Commonwealth of Massachusetts to reduce the number of deaths from this cause. The historical background is presented along with an analysis of the problem based on the available statistics for the year 1951.Historical BackgroundThe physicians of Massachusetts, the Department of Public Health and the people of . . .
Quantification of Absolute Myocardial Perfusion in Patients With Coronary Artery Disease
Authors: Geraint Morton, Amedeo Chiribiri, Masaki Ishida, Shazia T. Hussain, Andreas Schuster, Andreas Indermuehle, Divaka Perera, Juhani Knuuti, Stacey Baker, Erik Hedström, Paul Schleyer, Michael O’Doherty, Sally Barrington, Eike Nagel
Journal: Journal of the American College of Cardiology (2012)
Toxic Dilatation of the Colon in a Case of Amebiasis
Authors: Lawrence D. Wruble, John K. Duckworth, Don D. Duke, Joseph A. Rothschild
Journal: New England Journal of Medicine (1966)

TOXIC megacolon developing during the course of fulminating ulcerative colitis was first described in 1950 by Marshak and Lester.1 Five years later Lumb et al.2 reported 7 cases of "ulcerative colitis with dilatation of the colon." In 1959 Roth and his associates et al.3 coined the term "toxic megacolon." This expression was used to describe extreme dilatation of a segment of the colon or of the entire diseased colon that occurred during a fulminating phase of nonspecific ulcerative colitis. The authors stated that toxic megacolon might not be specific for ulcerative colitis and that it might occur in the violent . . .
Incident Atrial Fibrillation Among Asians, Hispanics, Blacks, and Whites
Authors: Thomas A. Dewland, Jeffrey E. Olgin, Eric Vittinghoff, Gregory M. Marcus
Journal: Circulation (2013)

Background— Because the association between atrial fibrillation (AF) and race has only been rigorously compared in population-based studies that dichotomized participants as white or black, it is unclear whether white race confers elevated AF risk or black race affords AF protection. Methods and Results— The Healthcare Cost and Utilization Project was used to identify patients receiving hospital-based care in California between January 1, 2005 and December 31, 2009. The association between race and incident AF was examined using Cox proportional hazards models. Interaction analyses were performed to elucidate the mechanism underlying the race-AF association. Among 13 967 949 patients, 375 318 incident AF episodes were observed over a median 3.2 (interquartile range 1.8–4.3) years. In multivariable Cox models adjusting for patient demographics and established AF risk factors, blacks (hazard ratio, 0.84; 95% confidence interval, 0.82–0.85; P &lt;0.001), Hispanics (hazard ratio, 0.78; 95% confidence interval, 0.77–0.79; P &lt;0.001), and Asians (hazard ratio, 0.78; 95% confidence interval, 0.77–0.79; P &lt;0.001) each exhibited a lower AF risk compared with whites. AF risk among whites was disproportionately higher in the absence of acquired cardiovascular risk factors and diminished or reversed in the presence of comorbid diseases. Although Hispanics and Asians also had a lower adjusted risk of incident atrial flutter compared with whites, the risk of flutter was significantly higher among blacks. Conclusions— In a large hospital-based cohort, whites have an increased risk of AF whether compared with blacks, Asians, or Hispanics. The heightened AF risk among whites is most pronounced in the absence of cardiovascular comorbidities.
Knee Pain and Disability
Authors: Gabe Mirkin
Journal: JAMA (1984)

Fifteen years ago, patella chondromalacia, or "runner's knee," was a dread disease. A runner would experience pain behind the patella and be treated to no avail with analgesics, steroid injections, and sometimes surgery. He would then think that he would never run again. Nowadays, many cases of knee pain are easily curable with special inserts placed in the shoes. Dr Cailliet has ignored the relationship between footstrike and the knee, but he has written a good book that is easy to understand. He describes the anatomy of the knee as it relates to function. His discussions on injuries to the menisci cover function, pathology, and treatment. Each ligament of the knee is discussed in detail. Arthritis and disorders of the kneecap are covered. Fractures and knee deformities are examined. This is a book that should be owned by every first-year surgical resident. It teaches how muscles, ligaments, and cartilage function
Inhalation therapy education and training programs
Authors: V. J. Collins
Journal: JAMA (1969)

Inhalation therapy is a medical specialty which deals with the testing and treatment of physiologic pulmonary disorders. The responsible physician requires technical assistance. Education of technicians and therapists is out-lined in a curriculum covering a minimum of 18 months. This represents a two-year academic program. A physician is the responsible director and is assisted by a technical supervisor who is registered. Affiliation with colleges is encouraged for teaching the basic sciences. Collegiate courses are preclinical; the applied sciences and the clinical practices must be taught in the hospital setting.
Unhealthy Landscapes: Policy Recommendations on Land Use Change and Infectious Disease Emergence
Authors: Jonathan A. Patz, Peter Daszak, Gary M. Tabor, A. Alonso Aguirre, Mary Pearl, Jon Epstein, Nathan D. Wolfe, A. Marm Kilpatrick, Johannes Foufopoulos, David Molyneux, David J. Bradley
Journal: Environmental Health Perspectives (2004)

Anthropogenic land use changes drive a range of infectious disease outbreaks and emergence events and modify the transmission of endemic infections. These drivers include agricultural encroachment, deforestation, road construction, dam building, irrigation, wetland modification, mining, the concentration or expansion of urban environments, coastal zone degradation, and other activities. These changes in turn cause a cascade of factors that exacerbate infectious disease emergence, such as forest fragmentation, disease introduction, pollution, poverty, and human migration. The Working Group on Land Use Change and Disease Emergence grew out of a special colloquium that convened international experts in infectious diseases, ecology, and environmental health to assess the current state of knowledge and to develop recommendations for addressing these environmental health challenges. The group established a systems model approach and priority lists of infectious diseases affected by ecologic degradation. Policy-relevant levels of the model include specific health risk factors, landscape or habitat change, and institutional (economic and behavioral) levels. The group recommended creating Centers of Excellence in Ecology and Health Research and Training, based at regional universities and/or research institutes with close links to the surrounding communities. The centers' objectives would be 3-fold: a) to provide information to local communities about the links between environmental change and public health; b) to facilitate fully interdisciplinary research from a variety of natural, social, and health sciences and train professionals who can conduct interdisciplinary research; and c) to engage in science-based communication and assessment for policy making toward sustainable health and ecosystems.