tbuckley/cabot-search huggingface dataset:
Reperfusion-induced arrhythmias and oxygen-derived free radicals. Studies with "anti-free radical" interventions and a free radical-generating system in the isolated perfused rat heart.
Authors: M Bernier, D J Hearse, A S Manning
Journal: Circulation Research (1986)

We have assessed, whether six agents, that either inhibit free radical formation or scavenge free radicals once they are produced, can reduce the incidence of reperfusion-induced arrhythmias, whether a free radical-generating system (FeCl3 X adenosine diphosphate) can increase the incidence of reperfusion-induced arrhythmias, and whether "anti-free radical" interventions can reduce reperfusion rhythm disturbances caused by the addition of FeCl3 X adenosine diphosphate. With the isolated, perfused rat heart (n = 15 in each group), inclusion of L-methionine (1 and 10 mM), superoxide dismutase (2.5 X 10(4) and 1 X 10(5) U/liter), catalase (5 X 10(4), 5 X 10(5), and 1 X 10(6) U/liter), mannitol (50 mM), glutathione (10 microM), or desferrioxamine (150 microM) significantly reduced the incidence of reperfusion-induced ventricular fibrillation and, in many cases, the incidence of reperfusion-induced ventricular tachycardia. The mean duration of sinus rhythm during reperfusion was also increased significantly. Perfusion of hearts with boiled superoxide dismutase (1 X 10(5) U/liter) or boiled catalase (1 X 10(6) U/liter) did not decrease arrhythmias. Conversely, under conditions where, in the control group, the incidence of reperfusion arrhythmias was lowered by increasing perfusate potassium to 6.5 mM, the addition of the free radical-generating system FeCl3 X adenosine diphosphate (0.1 microM X 1 microM) to the perfusion fluid increased dramatically the incidence of reperfusion-induced ventricular fibrillation and tachycardia. Simultaneous perfusion with FeCl3 X adenosine diphosphate and superoxide dismutase (1 X 10(5) U/liter), catalase (1 X 10(6) U/liter), mannitol (50 mM), methionine (10 mM), or desferrioxamine (150 microM) again reduced the incidence of reperfusion-induced arrhythmias and increased the duration of normal sinus rhythm during the reperfusion phase. Thus, addition of six "anti-free radical" interventions reduced the incidence of reperfusion-induced arrhythmias, addition of a free radical-generating system increased the incidence of reperfusion-induced arrhythmias, and simultaneous perfusion of the hearts with FeCl3 X adenosine diphosphate and "anti-free radical" interventions again reduced reperfusion rhythm disturbances. These results are further evidence supporting the hypothesis that oxygen-derived free radicals play an important role in the genesis of reperfusion-induced arrhythmias.
Moving to Fingolimod From Natalizumab in Multiple Sclerosis—Reply
Authors: Mikael Cohen, Christine Lebrun
Journal: JAMA Neurology (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
Morphological development of the pulmonary vascular bed in experimental pulmonic stenosis.
Authors: D L Levin, M A Heymann, A M Rudolph
Journal: Circulation (1979)

The main pulmonary trunk was banded in four fetal sheep at 63--69 days of gestation. The fetuses were killed after they had developed progressive pulmonary stenosis at 98, 123, 134 and 135 days of gestation. The right lung of each animal was perfused with glutaraldehyde and serial sections followed microscopically. The medial width/external diameter ratios for fifth generation resistance vessels were significantly less (0.13) than those from six normal control lungs (0.16, p less than 0.001). In addition, the number of resistance vessels per cm2 lung tissue in the lungs of the animals with experimental pulmonic stenosis was less than in normal controls. The altered in utero hemodynamics with severe pulmonic stenosis results in thin-walled pulmonary arterial vessels. This may be caused by an increased blood oxygen tension of the blood perfusing the pulmonary circulation via reversed flow through the ductus arteriosus, or altered pulmonary arterial pressure characteristics in the pulmonary vessels distal to the obstructed pulmonary trunk.
Genome-wide scan for type 1 diabetic nephropathy in the Finnish population reveals suggestive linkage to a single locus on chromosome 3q
Authors: A.-M. Osterholm, B. He, J. Pitkaniemi, L. Albinsson, T. Berg, C. Sarti, J. Tuomilehto, K. Tryggvason
Journal: Kidney International (2006)
Suprasternal Transaortic Coronary Arteriography
Authors: WILLIAM M. LEMMON, J. STAUFFER LEHMAN, RANDAL A. BOYER
Journal: Circulation (1959)

Opacification of the coronary arteries has been accomplished by direct needle puncture of the ascending portion of the thoracic aorta via a suprasternal approach and injection of highly-concentrated radiopaque medium. Experience with 35 attempts in 31 patients at such coronary opacification is described. The electrocardiographic observations, the reactions, and the complications incident to the study are discussed. Thirteen of the 31 patients had some type of intrapericardial cardiac surgery subsequent to this procedure, and the surgical observations regarding the status of the coronary arteries are compared with the coronary arteriographic findings.
Physical exercise enhances hepatic insulin signaling and inhibits phosphoenolpyruvate carboxykinase activity in diabetes-prone Psammomys obesus
Authors: Yuval Heled, Yair Shapiro, Yoav Shani, Daniel S Moran, Lea Langzam, Varda Barash, Sanford R Sampson, Joseph Meyerovitch
Journal: Metabolism (2004)
Surreptitious Insulin Administration in Adolescents With Insulin-Dependent Diabetes Mellitus
Authors: Donald P. Orr
Journal: JAMA (1986)

Six adolescents, 12 to 15 years old, with insulin-dependent diabetes mellitus were discovered to be secretively taking extra insulin, not with the intent of improving metabolic control. Large discrepancies between reported and observed insulin requirements were noted. Psychosocial problems antedated the discovery of surreptitious insulin administration in all. Psychological testing and psychiatric evaluation revealed a variety of psychiatric conditions; depression was common. In two patients surreptitious insulin administration was believed to represent suicidal behavior. In others, it appeared to represent symptom substitution when use of other health-threatening behaviors such as recurrent ketoacidosis was made increasingly difficult through appropriate intervention. Surreptitious insulin administration may be one symptom of serious underlying psychiatric dysfunction in adolescents with insulin-dependent diabetes.
Increased hypoxic stress decreases AMP hydrolysis in rabbit heart
Authors: L Gustafson
Journal: Cardiovascular Research (1999)

Objective: AMP conversion to adenosine by cytosolic 5′-nucleotidase (5NT) or to IMP by AMP deaminase determines the degree of nucleotide degradation, and thus ATP resynthesis, during reoxygenation. To elucidate the regulation of AMP hydrolysis during ischemia, data from 31P NMR spectroscopy and biochemical analyses were integrated via a mathematical model. Since 5NT is downregulated during severe underperfusion (5% flow), we tested 5NT regulation during less severe underperfusion (10% flow) and then made the perfusate hypoxic to see if the greater stress reactivated 5NT. Methods:31P NMR spectra and coronary venous effluents were obtained from Langendorff-perfused rabbit hearts subjected to two 30-min periods of underperfusion (10% flow); the second period with or without additional hypoxia (30% O2). Data were analyzed with a mathematical model describing the kinetics of myocardial energetics and metabolism. Results: A single 30-min period of 10% flow causes downregulation of AMP hydrolysis and the data from the second period of underperfusion are best described by lower 5NT activity, even in the presence of extra hypoxia. Thirty percent less purines appear in the venous effluent than predicted by the phosphoenergetics (PCr and ATP) when IMP is not allowed to accumulate by the model, however the model indicates that a constant accumulation of IMP via AMP deaminase could explain the discrepancy between expected and measured purines in the venous effluent. Conclusions: While AMP hydrolysis to adenosine is prominent in early ischemia and acts to preserve cellular energy potential, during a second ischemic period, nucleotides are conserved by the stable inhibition of AMP hydrolysis. Furthermore, during 10% flow conditions, nucleotides are conserved, possibly via an IMP-accumulatory pathway.
The maternal immune response to fetal platelet GPIbα causes frequent miscarriage in mice that can be prevented by intravenous IgG and anti-FcRn therapies
Authors: Conglei Li, Siavash Piran, Pingguo Chen, Sean Lang, Alessandro Zarpellon, Joseph W. Jin, Guangheng Zhu, Adili Reheman, Dianne E. van der Wal, Elisa K. Simpson, Ran Ni, Peter L. Gross, Jerry Ware, Zaverio M. Ruggeri, John Freedman, Heyu Ni
Journal: Journal of Clinical Investigation (2011)

Fetal and neonatal immune thrombocytopenia (FNIT) is a severe bleeding disorder caused by maternal antibody–mediated destruction of fetal/neonatal platelets. It is the most common cause of severe thrombocytopenia in neonates, but the frequency of FNIT-related miscarriage is unknown, and the mechanism(s) underlying fetal mortality have not been explored. Furthermore, although platelet αIIbβ3 integrin and GPIbα are the major antibody targets in immune thrombocytopenia, the reported incidence of anti-GPIbα–mediated FNIT is rare. Here, we developed mouse models of FNIT mediated by antibodies specific for GPIbα and β3 integrin and compared their pathogenesis. We found, unexpectedly, that miscarriage occurred in the majority of pregnancies in our model of anti-GPIbα–mediated FNIT, which was far more frequent than in anti-β3–mediated FNIT. Dams with anti-GPIbα antibodies exhibited extensive fibrin deposition and apoptosis/necrosis in their placentas, which severely impaired placental function. Furthermore, anti-GPIbα (but not anti-β3) antiserum activated platelets and enhanced fibrin formation in vitro and thrombus formation in vivo. Importantly, treatment with either intravenous IgG or a monoclonal antibody specific for the neonatal Fc receptor efficiently prevented anti-GPIbα–mediated FNIT. Thus, the maternal immune response to fetal GPIbα causes what we believe to be a previously unidentified, nonclassical FNIT (i.e., spontaneous miscarriage but not neonatal bleeding) in mice. These results suggest that a similar pathology may have masked the severity and frequency of human anti-GPIbα–mediated FNIT, but also point to possible therapeutic interventions.
Mutations in GATA2 are associated with the autosomal dominant and sporadic monocytopenia and mycobacterial infection (MonoMAC) syndrome
Authors: Amy P. Hsu, Elizabeth P. Sampaio, Javed Khan, Katherine R. Calvo, Jacob E. Lemieux, Smita Y. Patel, David M. Frucht, Donald C. Vinh, Roger D. Auth, Alexandra F. Freeman, Kenneth N. Olivier, Gulbu Uzel, Christa S. Zerbe, Christine Spalding, Stefania Pittaluga, Mark Raffeld, Douglas B. Kuhns, Li Ding, Michelle L. Paulson, Beatriz E. Marciano, Juan C. Gea-Banacloche, Jordan S. Orange, Jennifer Cuellar-Rodriguez, Dennis D. Hickstein, Steven M. Holland
Journal: Blood (2011)
Studying clonal dynamics in response to cancer therapy using high-complexity barcoding
Authors: Hyo-eun C Bhang, David A Ruddy, Viveksagar Krishnamurthy Radhakrishna, Justina X Caushi, Rui Zhao, Matthew M Hims, Angad P Singh, Iris Kao, Daniel Rakiec, Pamela Shaw, Marissa Balak, Alina Raza, Elizabeth Ackley, Nicholas Keen, Michael R Schlabach, Michael Palmer, Rebecca J Leary, Derek Y Chiang, William R Sellers, Franziska Michor, Vesselina G Cooke, Joshua M Korn, Frank Stegmeier
Journal: Nature Medicine (2015)
Familial hypertrophic cardiomyopathy is a genetically heterogeneous disease.
Authors: S D Solomon, J A Jarcho, W McKenna, A Geisterfer-Lowrance, R Germain, R Salerni, J G Seidman, C E Seidman
Journal: Journal of Clinical Investigation (1990)

We demonstrate that familial hypertrophic cardiomyopathy (FHC), an autosomal dominant disorder of heart muscle, is a genetically heterogeneous disease. The locus responsible for FHC in members of one large kindred was recently mapped to chromosome 14q11-12 (FHC-1). We have characterized three additional unrelated families in which the gene for FHC segregates as an autosomal dominant trait to determine if these disease loci also map to FHC-1. All family members were clinically studied by physical examination, electrocardiogram, and two-dimensional echocardiography. Genetic studies were performed using DNA probes which are derived from loci that are closely linked to FHC-1. In one family the genetic defect maps to the previously identified FHC-1 locus. However, the loci responsible for FHC in two other families were not linked to FHC-1. We conclude that FHC can be caused by defects in at least two loci and is a genetically heterogeneous disorder.
Hemodynamic response–guided therapy for prevention of variceal rebleeding: An uncontrolled pilot study
Authors: Antonio González, Salvador Augustin, Mercedes Pérez, Joan Dot, Esteban Saperas, Alejandro Tomasello, Antoni Segarra, Josep Ramón Armengol, Joan Ramón Malagelada, Rafael Esteban, Jaime Guardia, Joan Genescà
Journal: Hepatology (2006)

The clinical usefulness of assessing hemodynamic response to drug therapy in the prophylaxis of variceal rebleeding is unknown. An open-labeled, uncontrolled pilot trial was performed to evaluate the feasibility and efficacy of using the hemodynamic response to pharmacological treatment to guide therapy in this setting. Fifty patients with acute variceal bleeding underwent a hepatic venous pressure gradient (HVPG) measurement 5 days after the episode. Nadolol and nitrates were initiated, and a second HVPG was measured 15 days later. Responder patients (≥20% decrease in HVPG from baseline) were maintained on drugs, partial responders (≥10% and <20%) had banding ligation added to the drugs, and nonresponders (<10%) received a transjugular intrahepatic portal-systemic shunt (TIPS). Mean follow-up was 22 months. Eight patients (16%) did not receive the second HVPG, 6 of them because of early variceal rebleeding. Of the other 42 patients, 24 were classified as responders (57%); 10 as partial responders (24%), who had banding added; and 8 as nonresponders (19%), who received a TIPS. Patients with cirrhosis of viral etiology compared to alcoholic cirrhosis tended to present more early rebleedings, less response to drugs and needed more TIPS. Variceal rebleeding occurred in 22% of all patients but only in 12% of patients whose hemodynamic response was assessed. The 3 therapeutic groups were not different. In conclusion, using hemodynamic response to pharmacological treatment to guide therapy in secondary prophylaxis to prevent variceal bleeding is feasible and effectively protects patients from rebleeding. In this context, viral cirrhosis seems to present a worse outcome than alcoholic cirrhosis. (HEPATOLOGY 2006;44:806–812.)
Subcellular location and properties of bactericidal factors from human neutrophils.
Authors: J E Gabay, J M Heiple, Z A Cohn, C F Nathan
Journal: The Journal of Experimental Medicine (1986)

We examined the subcellular location of bactericidal factors (BF) in human neutrophils, using an efficient fractionation scheme. Nitrogen bomb cavitates of DIFP-treated PMN were centrifuged through discontinuous Percoll gradients, each fraction extracted with 0.05 M glycine, pH 2.0, and tested for the killing of Escherichia coli. greater than 90% of BF coisolated with the azurophil granules. After lysis of azurophils, 98% of azurophil-derived BF (ADBF) sedimented with the membrane. ADBF activity was solubilized from azurophil membrane with either acid or nonionic detergent (Triton X-100, Triton X-114). Bactericidal activity was linear with respect to protein concentration over the range 0.3-30 micrograms/ml. 0.1-0.3 microgram/ml ADBF killed 10(5) E. coli within 30 min at 37 degrees C. At 1.4 micrograms/ml, 50% of 2 X 10(5) bacteria were killed within 5 min. ADBF was effective between pH 5-8, with peak activity at pH 5.5. Glucose (20 mM), EDTA (1-25 mM), and physiologic concentrations of NaCl or KCl had little or no inhibitory effect on ADBF. ADBF killed both Gram-positive and Gram-negative virulent clinical isolates, including listeria, staphylococci, beta-hemolytic streptococci, and Pseudomonas aeruginosa. Thus, under these conditions of cell disruption, fractionation, extraction, and assay, almost all BF in human PMN appeared to be localized to the membrane of azurophilic granules as a highly potent, broad-spectrum, rapidly acting protein(s) effective in physiologic medium. Some of these properties appear to distinguish ADBF from previously described PMN bactericidal proteins.
Non-cryopreserved peripheral blood stem cells autotransplants for hematological malignancies can be performed entirely on an outpatient basis
Authors: Guillermo J. Ruiz-Argüelles, Alejandro Ruiz-Argüelles, Beatriz Pérez-Romano, Antonio Marín-López, José Luis Delgado-Lamas
Journal: American Journal of Hematology (1998)

We have prospectively performed peripheral blood stem cell autotransplants in six patients with hematological malignancies on an entirely outpatient basis. Patients were conditioned with high-dose melphalan and received a median of 4.2 × 108/kg non-cryopreserved, non-purged mononuclear cells, containing a median of 3.9 × 106/kg CD34 + cells. The median time to achieve > 500 granulocytes/μl was 21 days, with a range of 16 to 40, whereas the median time to achieve > 20,000 platelets/μl was 38 days, with a range of 21 to 48. Only three patients were transfused with platelets whereas packed red blood cells were transfused in two. All patients survived 60 days after the autograft and three are alive at 450, 690, and 1,950 days after the autotransplant. One patient was given an allogeneic bone marrow transplant when relapsing after the autotransplant. One patient had to be admitted to the hospital on day +10 because of fever. A median of 6,500.00 USD per patient was calculated as the total cost of each outpatient autotransplant. Since outpatient autologous transplants with non-frozen PBSC are feasible, restrictions to PBSC autotransplant programs may be overcome and costs may be diminished. Am. J. Hematol. 58:161–164, 1998. © 1998 Wiley-Liss, Inc.
Unexpected Readmissions to the Coronary-Care Unit during Recovery from Acute Myocardial Infarction
Authors: Daniel E. Singer, Albert G. Mulley, George E. Thibault, G. Octo Barnett
Journal: New England Journal of Medicine (1981)

Because it is difficult to predict the course in a patient recovering from acute myocardial infarction who is stable enough to leave the coronary-care unit (CCU), we studied such patients in order to identify those at risk of complications. Over two years of study, 485 of 536 consecutive patients admitted with myocardial infarction survived their first stay in the CCU. Complications serious enough to warrant readmission developed in 61 (13%). Readmissions occurred early: half were within 2.7 days of initial transfer from the unit. The subsequent course was severely complicated: 16 readmitted patients (26%) died in the hospital. Physicians were not able to identify clearly these high-risk patients during their first stay in the CCU. Several previously cited indicators of poor prognosis did not help identify those later readmitted, but recurrent ischemic pain that occurred for the first time after 24 hours in the CCU did. The absence of rales on admission, coupled with absence of recurrent chest pain, was indicative of a subgroup with a favorable short-term prognosis.
Effect of Coronary Artery Disease on Parasympathetic Cardiovascular Reflexes in NIDDM Patients
Authors: K E Juhani Airaksinen, M Juhani Koistinen, Markku J Ikäheimo, Heikki Pirttiaho, Heikki V Huikuri, Juha T Takkunen
Journal: Diabetes Care (1990)

To evaluate the effect of coronary artery disease on parasympathetic cardiac reflexes in patients with non-insulin-dependent diabetes mellitus (NIDDM), we studied standard cardiovascular reflexes in 27 NIDDM patients with coronary artery disease (group 1) and in 21 NIDDM patients with no signs of coronary artery disease (group 2). Groups did not differ with respect to age, duration of diabetes, or presence of retinopathy. The mean +/- SD heart-rate variation in deep breathing was lower in group 1 than in group 2 (11.6 +/- 6.5 vs. 17.1 +/- 9.0 beats/min, P less than 0.05). Heart-rate variation was more often abnormally low (less than or equal to 10 beats/min) in group 1 than in group 2 (48 vs. 19%, P less than 0.05). Thus, the presence of coronary artery disease appears to modify cardiac parasympathetic reflexes in patients with diabetes mellitus and must be kept in mind when interpreting test results.
Does drop in T and A's pose new issue of adenotonsillar hypertrophy?
Authors: William A. Check
Journal: JAMA (1982)

The A he dramatic trend over the last two decades of treating otitis media and pharyngotonsillitis conservatively—with antimicrobial agents and tympanostomy tubes rather than surgical removal of the tonsils and adenoids—may be causing an increasing incidence of airway obstruction from adenotonsillar hypertrophy. At the recent meeting of the southern section of the Triological Society in Atlanta, Kenneth M. Grundfast, MD, chairman of the Department of Otorhinolaryngology at Children's Hospital National Medical Center, Washington, DC, and Donald J. Wittich, Jr, MD, of the Head and Neck Surgery Service at Walter Reed Army Medical Center, Washington, DC, described 13 cases that they had seen in the last year of acute or chronic upper airway obstruction in children due to adenotonsillar hypertrophy. (In fact, Grundfast told<i>JAMA</i>MEDICAL NEWS, since preparing the report, he has seen two additional cases.) The 13 children ranged in age from 15 months to 10 years. Nine had
ON THE USE OF STRYCHNINE IN THE CURARE-AIDED METRAZOL TREATMENT OF PSYCHOSES
Authors: MARCEL HEIMAN
Journal: American Journal of Psychiatry (1943)

1. A modification of the metrazol treatment is described. The material consisted of 30 female patients who received strychnine simultaneously with curare intravenously in amounts of 1/120 gr. to 1/30 gr. preceding the injection of metrazol. 2. Strychnine reduces the metrazol requirement, the maximum average dosage being only 23.5 per cent higher than the initial average dosage, compared to 62.7 per cent increase without its use. It is assumed that strychnine sensitizes the central nervous system to metrazol. 3. Strychnine has a beneficial action upon the respiration which is impaired centrally due to the effect of the metrazol convulsion and which is impaired peripherally due to the effect of curare. This action is assumed to be due to the excitatory effect of strychnine upon the respiratory center and to the action of strychnine on the peripheral nerves. 4. It is concluded that strychnine might be of value by virtue of its sensitizing effect in metrazol as well as in other shock therapies.