123rc/medical_text huggingface dataset:
Excretion of thromboxane A2 and prostacyclin metabolites before and after exercise testing in patients with and without signs of ischemic heart disease. We addressed the hypothesis that platelets are not activated in association with effort-induced myocardial ischemia in stable coronary disease. Seventy-two patients undergoing a diagnostic bicycle exercise test were stratified according to the development of chest pain (yes/no, 33/39) and of exercise-induced ST-segment depression of at least 200 microV in the electrocardiogram (yes/no, 12/60). Noninvasive indexes of platelet activation and of platelet/vessel wall interaction (urinary excretion of the 2,3-dinor-metabolites of thromboxane A2 [Tx-M] and prostacyclin [PGI-M], respectively) were analyzed in samples collected in the basal state and after the test. Basal Tx-M and PGI-M did not differ in patients with (236 +/- 35 and 131 +/- 22 pg/mg creatinine, respectively) and without (185 +/- 16 and 101 +/- 13 pg/mg creatinine, respectively) chest pain, or in those with (178 +/- 45 and 162 +/- 41 pg/mg, respectively) and without (216 +/- 22 and 104 +/- 11 pg/mg, respectively) ST-segment depression during the test. Patients without chest pain or without ST-segment depression moderately increased (p less than 0.05) their urinary Tx-M (by 21% and 13%, respectively) and PGI-M (by 28% and 23%, respectively) after exercise. No significant increases were observed in those developing chest pain or ST depression during exercise. These data indicate that effort-induced myocardial ischemia is not associated with an increase in platelet activation or platelet/vessel wall interaction in patients with stable coronary disease.
Intraoperative management of severe endobronchial hemorrhage Endobronchial hemorrhage due to pulmonary artery perforation by a Swan-Ganz catheter developed during coronary artery bypass grafting while weaning from cardiopulmonary bypass. After reinstitution of cardio-pulmonary bypass with pulmonary artery venting, bleeding was localized to the right lower lobe bronchus using fiberoptic bronchoscopy. A Fogarty embolectomy catheter was inflated in the bronchus to tamponade successfully only the right lower lobe. This case illustrates a method of distal bronchial blockade for maximal retention of pulmonary function and avoidance of pulmonary resection.
Restricted heterogeneity of T lymphocytes in combined immunodeficiency with hypereosinophilia (Omenn's syndrome). We report the immunological characteristics of five patients with Omenn's syndrome, a rare inherited immunodeficiency also known as combined immunodeficiency with hypereosinophilia. The syndrome is characterized by T cell infiltration of skin, gut, liver, and spleen leading to diffuse erythroderma, protracted diarrhea, failure to thrive, and hepatosplenomegaly. Blood T cells as well as those infiltrating the skin and gut were found to express activation markers and were partially activated by mitogens but not by antigens. Although the lesions resembled those in graft-versus-host disease, the blood T cells were shown by DNA haplotype analysis using probes revealing variable number of tandem repeats to belong to the patients as well as the T cells infiltrating the gut and skin in one patient. A given T cell subset (TCR alpha beta+, CD4+/CD8+, or TCR gamma delta+) was predominant in each patient, with a specific distribution in the skin lesions. Moreover, the study of T cell receptor beta, gamma, and delta gene rearrangements in four patients revealed oligoclonality involving C beta 1, C beta 2, or different V gamma J gamma or V delta J delta genes. This indicates that restricted heterogeneity of the T cell repertoire, previously reported in one case, is a major feature of this syndrome. The occurrence of alymphocytosis-type severe combined immunodeficiency in the brother of one of the patients suggests that the restricted heterogeneity of T cell receptor gene usage in Omenn's syndrome may arise from leakiness, within the context of a genetically determined faulty T cell differentiation.
Methodological problems in evaluation of cardiovascular effects of stress in humans. Cardiovascular effects of stress in humans are often assessed by application of physical or emotional stimuli in a laboratory environment. Although this method provides important information, these procedures have several limitations. First, blood pressure and heart rate responses to laboratory stressors are characterized by a limited within-subject reproducibility. Second, there is poor correlation between blood pressure and heart rate responses to different stressors, which implies that individual reaction to stress may be estimated differently according to the test used. Finally, these responses bear only a limited relation to 24-hour or daytime blood pressure variability, that is, they reflect to only a limited extent the tendency of blood pressure to vary during daily activities. If assessed by techniques that allow blood pressure to be continuously recorded for 24 hours in ambulatory subjects, blood pressure variability represents a possible approach to observation of cardiovascular reactivity away from an artificial laboratory environment. However, whether blood pressure variability should be expressed as a percentage or in absolute values is controversial. Furthermore, although naturally occurring stress may markedly increase blood pressure, 24-hour blood pressure variations also depend on factors that are not related to emotional stimuli. Thus, the study of cardiovascular responses to stress in humans encounters several problems, regardless of the method used.
Biohistory of slavery and blood pressure differences in blacks today. A hypothesis. Genetic factors are known to play an important role in the variations in blood pressure levels. However, genetic factors that explain the higher average blood pressure levels of western hemisphere blacks when compared with African blacks have not been seriously considered. Because the genetic makeup of a population is largely determined by biological and ecological forces in the past, an examination of the biohistory of blacks, specifically the slavery era, was conducted. An overview of the salient findings of that investigation is included in this article. The published historical evidence on the transatlantic slave trade and New World slavery (from the 16th century to the 19th century) reveals that conditions existed for "natural selection," and therefore, genetic changes were virtually inevitable in the slave populations. During this period of history, mortality was extremely high, and fertility (or reproductive success) was so low among the survivors that most plantation societies in the western hemisphere depended on a constant importation of captives (over 12 million) from Africa for the viability of the plantation communities. Because the major causes of death were salt-depletive diseases such as diarrhea, fevers, and vomiting, it is argued that individuals with an enhanced genetic-based ability to conserve salt had a distinct survival advantage over others and were, therefore, more likely to bequeath their genotype to subsequent generations of Western hemisphere blacks. Thus, it is predicted that blacks in the Americas have a greater frequency of individuals with an enhanced genetic-based ability to conserve salt than African blacks.
Anemia after traumatic spinal cord injury. The incidence and natural history of anemia in patients with spinal cord injuries (SCI) were investigated in a prospective study of 68 patients consecutively admitted to a regional acute SCI unit. Fifty had SCI and 18 had spine injuries (SI) without neurologic deficit. Thirty-six of 41 males (88%) and six of nine females (67%) with SCI were anemic on at least one occasion. In the first two weeks after injury, in females and in males, there was no significant difference in mean hemoglobin level between SI and SCI patients. At six weeks, no male with SI was anemic, and males with SCI had significantly lower mean hemoglobin levels than those with SI (121.6 g/L vs 145.4 g/L, p less than .001). Identified early causes of anemia were blood loss due to bony soft tissue or visceral injury, gastrointestinal bleeding, and surgery. In the postacute phase (more than six weeks after injury), anemia occurred in 25 of 41 male and three of nine female SCI patients, and its occurrence was associated with the presence of an identified chronic disease, especially urinary tract infection.
Heterotopic liver transplantation for fulminant Wilson's disease. Wilson's disease may present with severe acute hepatocellular failure. The only effective treatment for fulminant Wilson's disease is liver transplantation, which may lead to reversal of the underlying disease. Some patients with cirrhosis who are too ill to undergo orthotopic liver transplantation have been treated with heterotopic liver transplantation. However, use of heterotopic liver transplantation for fulminant hepatocellular failure has not been successful. This case study involves a patient in whom a heterotopic liver transplant was successfully used for treatment of Wilson's disease presenting with fulminant hepatocellular failure.
Effect of antiarrhythmic therapy on mortality in survivors of myocardial infarction with asymptomatic complex ventricular arrhythmias: Basel Antiarrhythmic Study of Infarct Survival (BASIS) In view of the high risk of sudden cardiac death and the prognostic importance of complex ventricular ectopic activity, the effects of prophylactic antiarrhythmic treatment were investigated prospectively in patients with persisting asymptomatic complex arrhythmias after myocardial infarction. End points were total mortality and arrhythmic events (sudden death, sustained ventricular tachycardia and ventricular fibrillation). Of 1,220 consecutively screened survivors of myocardial infarction, 312 had Lown class 3 or 4b arrhythmia on 24 h electrocardiographic recordings before hospital discharge and consented to the study. They were randomized to individualized antiarrhythmic treatment (Group 1, n = 100), treatment with low dose amiodarone, 200 mg/day (Group 2, n = 98) or no antiarrhythmic therapy (Group 3 [control group], n = 114). During the 1 year follow-up period, 10 patients in Group 1 died, as did 5 in Group 2 and 15 in Group 3. On the basis of an intention to treat analysis, the probability of survival of patients given amiodarone was significantly greater than that of control patients (p less than 0.05). In addition, arrhythmic events were significantly reduced by amiodarone (p less than 0.01). These effects were less marked and not significant for individually treated patients (Group 1). These findings suggest that low dose amiodarone decreases mortality in the 1st year after myocardial infarction in patients at high risk of sudden death.
Putative mechanisms of cytoprotective effect of certain antacids and sucralfate. An investigation of cytoprotective activity of certain antacids and inert particles was carried out by treating ethanol-induced gastric mucosal damage in rats in order to clarify possible mechanisms by which aluminum-containing antacids act. Al(OH)3 inhibited gastric mucosal damage in a dose-related and time-dependent manner. Neither aluminum ions themselves nor the particle size of the Al(OH)3 complex were responsible for the observed cytoprotection, since neither AlCl3, chemically inert Al2O3*C, nor sea sand showed protective effects. Hyperosmolality in the gastric lumen was not a deciding factor in inducing cytoprotection. Silicic acid and titanium dioxide, with superficial charge similar to Al(OH)3 proved to be effective in inhibiting gastric hemorrhagic lesions and releasing PGE2, suggesting that the surface charge of Al(OH)3 may be important in its cytoprotective properties. The same may also be valid for sucralfate. Since antacid-induced cytoprotection was only partly reduced by pretreatment with indomethacin, it is likely that additional mechanisms and mediators other than prostaglandins, such as nonprotein sulfhydryls, also are involved in gastric cytoprotection arising from aluminum-containing antacids.
Transesophageal echocardiography is superior to transthoracic echocardiography in the diagnosis of sinus venosus atrial septal defect. The purpose of this study was to compare transthoracic and transesophageal echocardiography in the diagnosis of various types of atrial septal defects. Forty-one adult patients with the clinical diagnosis of atrial septal defect were studied by transthoracic and transesophageal echocardiography (30 women, 11 men; 18 to 81 years of age). Transthoracic echocardiography demonstrated the atrial septal defect in 33 patients (secundum type in 28, primum type in 3 and sinus venosus type in 2). Transesophageal echocardiography demonstrated the defect in all 41 patients. Thus, in 8 (20%) of 41 patients the atrial septal defect was demonstrated by transesophageal and not by transthoracic echocardiography. Six of the eight had a sinus venosus type atrial septal defect; the other two patients had a secundum atrial septal defect (one of these two had a technically poor transthoracic echocardiogram and the other had a small atrial septal defect). Transthoracic echocardiography, therefore, failed to demonstrate the sinus venosus defect in six (75%) of eight patients. An anomalous venous connection associated with the sinus venosus defect was visualized by transesophageal echocardiography in seven of the eight patients but was not seen on transthoracic echocardiography in any patient. Sinus venosus type atrial septal defects are frequently not visualized in adults by conventional transthoracic echocardiography. Transesophageal echocardiography is recommended when an atrial septal defect is clinically suspected but cannot be visualized by transthoracic echocardiography.
Noninvasive assessment of cerebral collateral blood supply through the ophthalmic artery. We assessed the potential of 2-MHz pulsed-wave transorbital Doppler ultrasonography to delineate the role of the ophthalmic artery as a source of collateral cerebral blood supply by comparing oculopneumoplethysmography, transorbital Doppler ultrasonography, periorbital continuous-wave Doppler ultrasonography, and transcranial Doppler ultrasonography in 25 patients with unilateral internal carotid artery occlusion and five controls with 10 normal internal carotid arteries. Systolic ophthalmic artery blood velocity was reduced ipsilateral to an internal carotid artery occlusion (38.2 +/- 10.2 cm/sec) compared with the contralateral and control velocities (46.0 +/- 10.3 and 47.5 +/- 6.8 cm/sec, respectively; p less than 0.05). Ophthalmic systolic pressure measured by oculopneumoplethysmography was 94.7 +/- 13.2 mm Hg ipsilateral to an internal carotid artery occlusion compared with 108.4 +/- 15.3 mm Hg on the contralateral side (p less than 0.01). Transorbital and periorbital Doppler ultrasonography detected reversed ophthalmic artery blood flow ipsilateral to an internal carotid artery occlusion in 44.0% and 40.0% of the patients, respectively. Systolic middle cerebral artery blood velocity was 55.2 +/- 22.3 cm/sec ipsilateral to an internal carotid artery occlusion compared with 79.4 +/- 23.5 cm/sec on the contralateral side (p less than 0.05) and 101.2 +/- 18.9 cm/sec in the controls (p less than 0.05). Reversed ophthalmic artery blood flow was associated with a low middle cerebral artery blood velocity and lack of major intracerebral collaterals. Transorbital Doppler ultrasonography permits noninvasive evaluation of the ophthalmic artery.
Retroperitoneal mobilization of the vas deferens in the complex vasovasostomy. Anatomic distances along retroperitoneal, inguinal, and infrainguinal segments of the vas deferens were measured in 14 formalin fixed cadavers and in 15 recently postmortem males. There were no significant differences in segment lengths between the two groups nor between the right and left vasa. Data from the recent postmortem group reveals a mean length of 5.83 +/- .65 cm to be gained from retroperitoneal mobilization of the vas deferens. This information is important to surgical decisions in cases of microsurgical repair of obstructive azoospermia resulting from damage to the inguinal segment of the vas deferens. Data on other vasal segment lengths is beneficial for planning repair in other complex cases of obstructive azoospermia as well.
Sequential magnetic resonance imaging following stereotactic radiofrequency ventralis lateralis thalamotomy. Serial postoperative magnetic resonance (MR) studies were obtained in 21 patients who underwent somatotopically placed stereotactic radiofrequency (rf) ventralis lateralis thalamotomy for the control of movement disorders. The MR studies were reviewed to determine the MR characteristics of early-phase (less than or equal to 7 days) and late-phase (8 days to 5 months) lesions. Surgery was performed for the control of parkinsonian tremor (14 cases), intention tremor (six cases), and essential tremor (one case). Single rf lesions were made with an electrode (1.6 mm in diameter, 3 mm in tip length) heated to 78 degrees C for 60 seconds. On MR images of the lesions, three distinct concentric zones were identified, described as follows (from the center outward). Zone 1 gives increased signal on long-relaxation time (TR) (T2-weighted) MR images in early- and late-phase lesions and decreased signal on short-TR (T1-weighted) MR images in early-phase lesions only. Zone 2 gives decreased signal on long-TR (T2-weighted) images in early- and late-phase lesions; it gives isointense signal on short-TR (T1-weighted) images in early-phase lesions only. Zone 3 gives increased signal on long-TR (T2-weighted) images in early-phase lesions only and decreased signal on short-TR (T1-weighted) MR images in early-phase lesions only. It is considered that in early-phase lesions, Zone 2, with a mean diameter of 7.3 mm on axial long-TR (T2-weighted) imaging, represents an area of hemorrhagic coagulation necrosis. In late-phase lesions, Zone 2, with a mean diameter of 5.0 mm on axial long-TR (T2-weighted) imaging, represents hemosiderin deposition. Zone 3 likely represents edema, and this zone disappears between the early and late periods. From regression analysis, lesion size began to stabilize at approximately 7 months with a mature lesion diameter of 3.3 mm. Long-term follow-up monitoring (median 16 months) showed good tremor control. Based on clinical and radiological findings, the authors conclude that forms of hemoglobin are suitable markers to assess the size of rf lesions. Serial MR imaging provides a noninvasive means of studying the evolution of rf thalamotomy lesions.
Prehospital care: the future of emergency medical services. Most prehospital interventions, both pharmacologic and procedural, have been accepted without clear demonstrations of their abilities to impact patient outcomes or without clear indications that withholding or delaying the intervention pending arrival at a definitive emergency department will adversely affect the patient. Interventions that have the benefit of supportive research have been applied equally to urban and nonurban emergency medical services environments. In selecting interventions, inadequate consideration has been given to the differences in emergency medical services personnel training, frequencies of their exposure to patients, frequencies of skill use, and availabilities of effective continuing education programs in the urban and nonurban environments. These issues are discussed, and the necessary focus of the future of emergency medical services in urban, suburban, and rural environments is predicted.
Myocardial infarct size-limiting effect of ischemic preconditioning was not attenuated by oxygen free-radical scavengers in the rabbit. BACKGROUND. The limiting effect of ischemic preconditioning on infarct size has been reported in canine hearts, which contain considerable amounts of xanthine oxidase, a free radical-producing enzyme. Furthermore, a recent study suggested that free radicals generated during preconditioning may contribute to the cardioprotective effect of preconditioning. The present study examined 1) whether preconditioning limits infarct size in rabbits, which, like humans, lack myocardial xanthine oxidase and 2) whether the cardioprotective effect of PC is mediated by free radicals. METHODS AND RESULTS. A branch of the circumflex coronary artery in rabbits was occluded for 30 minutes and then reperfused for 72 hours. Myocardial infarct size and area at risk were determined by histology and fluorescent particles, respectively. Five groups were studied: an untreated control group, a preconditioned group (PC group), a high-dose superoxide dismutase (SOD)-treated preconditioned group (high-dose SOD-PC group), a low-dose SOD-treated preconditioned group (low-dose SOD-PC group), and a SOD-plus-catalase-treated preconditioned group (SOD/CAT-PC group). Preconditioning was performed with four episodes of 5 minutes of ischemia and 5 minutes of reperfusion. The free radical scavengers (30,000 units/kg SOD for high-dose SOD-PC group, 15,000 units/kg SOD for low-dose SOD-PC group, and 30,000 units/kg SOD plus 55,000 units/kg catalase for SOD/CAT-PC group) were infused intravenously over 60 minutes starting 20 minutes before preconditioning. Infarct size as the percentage of area at risk was 45.1 +/- 3.5% (mean +/- SEM) in the control group (n = 11), 13.3 +/- 3.0% in the PC group (n = 12), 9.7 +/- 1.8% in the high-dose SOD-PC group (n = 8), 11.9 +/- 2.2% in the low-dose SOD-PC group (n = 6), and 9.6 +/- 2.3% in the SOD/CAT-PC group (n = 6) (p less than 0.05 versus control for the last four values). The differences in infarct size as the percent of area at risk among the PC, high-dose SOD-PC, low-dose SOD-PC, and SOD/CAT-PC groups were not significant. CONCLUSION. Ischemic preconditioning delays ischemic myocardial necrosis regardless of myocardial xanthine oxidase content. Free radicals are unlikely to have a major role in the mechanism of the preconditioning in rabbits.
Decreased toxicity of polymorphonuclear neutrophils toward hepatocytes isolated from rats with acute inflammatory reaction. We have recently demonstrated that polymorphonuclear neutrophils were toxic to hepatocytes through a protease-mediated mechanism. Since synthesis of antiproteases is markedly increased during acute inflammatory reaction, the aim of this work was to investigate the toxicity of neutrophils against normal vs. inflammatory rat hepatocytes. Acute inflammatory reaction was induced by subcutaneous injection of turpentine 24 hr before the experiments. Hepatocytes from normal and turpentine-treated rats were isolated by collagenase digestion. They were incubated with human neutrophils stimulated by 1 mg/ml opsonized zymosan. Cytotoxicity was quantified by the percentage of alanine aminotransferase activity released by hepatocytes in culture medium after an 18-hr incubation period. By comparison to normal hepatocytes, inflammatory hepatocytes were more resistant to the toxicity of neutrophils. At a neutrophil/hepatocyte ratio of 20:1, the alanine aminotransferase activity releases were 53.7% +/- 5.4% (mean +/- 1 S.E.) and 27.4% +/- 4.8% for normal and inflammatory hepatocytes, respectively. Similarly, inflammatory hepatocytes were found to be less sensitive than normal hepatocytes to the toxic effect of purified neutrophil cathepsin G. In contrast, both types of hepatocytes exhibited the same sensitivity to H2O2 generated by a system consisting of glucose and glucose oxidase. Two arguments suggested that the resistance of inflammatory hepatocytes to protease toxicity was explained by an increased production of antiproteases by these cells: (a) when tested against cathepsin G and porcine pancreatic elastase activities, the protease inhibitory capacity of conditioned medium from inflammatory hepatocytes was higher than that of conditioned medium from normal hepatocytes; (b) conditioned medium from inflammatory hepatocytes markedly reduced the toxicity of stimulated neutrophils as that of cathepsin G.