shukoor65/lab-rag-model huggingface dataset:
Doppler and echocardiographic characteristics of patients having an Austin Flint murmur. BACKGROUND. The purpose of this study was to investigate the genesis of the Austin Flint murmur using Doppler and echocardiographic imaging. METHODS AND RESULTS. A total of 51 patients having significant aortic insufficiency and an anatomically normal mitral valve were evaluated. They were divided into two groups; 30 patients had an audible Austin Flint murmur (AFM+) and 21 did not (AFM-). All patients had a complete M-mode, two-dimensional, and Doppler echocardiographic examination to characterize left ventricular size and function, motion of the mitral valve, transmitral flow velocities, direction of the aortic insufficiency jet, and severity of aortic insufficiency. There was no significant difference in severity of aortic insufficiency between groups. There was, however, a significant difference in direction of the insufficiency jet. In the AFM+ group compared with the AFM- group, for the parasternal long-axis view 24 (80%) versus eight (38%) had their insufficiency jet directed at the mitral valve, for the apical five-chamber view the values were 25 (83%) versus five (24%), and for the apical long-axis view the values were 27 (90%) versus five (24%); for all comparisons p less than 0.01. There was also a greater frequency of localized anterior mitral leaflet distortion by two-dimensional echocardiography (AFM+:23 [77%] versus AFM-:five [24%]; p less than 0.001) and a greater frequency of Doppler striations overlying the aortic insufficiency jet (AFM+:25 [83%] versus AFM-:seven [33%]; p less than 0.001). Regarding transmitral flow velocities, there was no significant difference in filling patterns or absolute velocities during early or late diastole between groups. There was no gradient by Doppler analysis or by hemodynamics (n = 26) across the mitral valve in either group. There also was no difference in the frequency of preclosure of the mitral valve (AFM+:two versus AFM-:three). Systolic function was similar in both groups, but the left ventricular end-diastolic dimension was significantly greater in the AFM+ group (6.8 +/- 0.8 cm) than in the AFM- group (6.2 +/- 0.7 cm, p = 0.008). CONCLUSIONS. The results of this study suggest that the primary factor responsible for the Austin Flint murmur is the presence of an aortic insufficiency jet directed at the anterior mitral leaflet. This, combined with the biphasic pattern of transmitral flow, distorts the shape of the anterior mitral leaflet as it opens and closes during diastole, making it shudder. The leaflet's shuddering sets up vibrations and shock waves that distort the aortic insufficiency jet, causing the observed Doppler striations and probably the sound of the murmur. There is no evidence from this study to support prior theories that have proposed functional mitral stenosis or diastolic mitral regurgitation as the source of the murmur.
Acoustic discrimination of three types of infant cries. The ability of acoustic characteristics, both separately and in linear combination with others, to differentiate among procedural pain-induced, hungry, and fussy crying was explored using audiorecordings of cries from healthy 2 to 4-month-old infants. Fussy cries were less tense than hungry or pain-induced cries and pain-induced cries had significantly stronger second formant amplitudes than fussy or hungry cries. Formants and tenseness were important contributors to a linear combination of acoustic measures, derived from discriminant function analysis, which correctly classified 74% of the procedural pain-induced crying specimens. The inability of this linear combination of acoustic measures to identify correctly approximately one-third of the cry specimens suggests that the discrete acoustic differences among the three situationally defined types of crying is not large.
Morphine-augmented cholescintigraphy: its efficacy in detecting acute cholecystitis Cholescintigrams were performed in 158 patients suspected of having acute cholecystitis after administration of 185 Mbq (5 mCi) of 99mTc-mebrofenin or disofenin. Morphine sulfate, 0.04 mg/kg was given intravenously if there was nonvisualization of the gallbladder at 40-60 min provided that radiotracer was seen within the small bowel. Acute cholecystitis was deemed present if there was nonvisualization of the gallbladder 30 min post-morphine administration; no cystic duct obstruction was present if the gallbladder was demonstrated pre- or post-morphine administration. A final diagnosis was estimated in 51 postoperative patients histologically, the remainder having their final diagnosis gleaned from their medical records. The sensitivity, specificity, positive and negative predictive value of morphine-augmented cholescintigraphy in detecting acute cholecystitis was 94.6, 99.1, 97.2, and 98.3%, respectively. These findings indicate that morphine-augmented cholescintigraphy detects acute cholecystitis with as high a degree of accuracy as conventional hepatobiliary scintigraphy, yet requires only 1.5 hr to establish the diagnosis.
The sleep apnoea syndrome in obesity: risk of sudden death. A total of 34 severely obese men with a history of heavy snoring and excessive daytime sleepiness indicative of obstructive sleep apnoea syndrome (OSAS) were studied prospectively. Their mean age was 46 years, and mean body mass index was 41.6 kg m-2. During a 4-year follow-up, 15% (5/34) of these subjects died (three cases of acute myocardial infarction and two cases of pulmonary oedema), all of them suddenly and unexpectedly, outside hospital. On autopsy the degree of atherosclerosis was found to be moderate in all cases. In 68% (15/22) of the men a pathological apnoea index (mean value 46 +/- 20) confirmed the OSAS diagnosis. Exercise tests and neurological examinations did not reveal any other causes of daytime sleepiness. Mean blood pressure at rest and during exercise was normal, and mean serum lipid and blood glucose levels were normal. Spirometry revealed intrapulmonary restrictive changes that could not be attributed to the heavy thoracic wall. Compliance was reduced to about 50% of reference values, and the mean pCO2 level (5.8 kPa) was close to the upper reference limit. Blood tests suggested that high alcohol consumption may be an important factor contributing to OSAS. These results demonstrate that morbidly obese men with a history of OSAS have a high risk of sudden cardiovascular death, despite the absence of other conventional risk factors.
Pathologic changes associated with androgen deprivation therapy for prostate cancer. Prostate glands exposed to androgen deprivation with leuprolide +/- flutamide were evaluated for pathologic changes which might be related to therapy. Comparing pretreatment and posttreatment tissue by visual discrimination using light microscopic study revealed treatment-related alterations in the size and distribution of neoplastic glands in 60% of cases. Quantitative measurements documented glandular changes in an even greater percentage of cases. Although distinctive, the histologic pattern was not specific for leuprolide/flutamide. The absence of appreciable degeneration and necrosis in tumor cells suggests that this type of androgen deprivation may act through suppression rather than ablation of prostatic cancers. The relationship between treatment-related histologic effects and initial tumor grade and clinical stage as well as expression of prostate-specific antigen was studied. Accurate histologic assessment of leuprolide/flutamide-treated prostate glands should not be a problem so long as specimens are thoroughly examined and drug-related variations in tumor morphologic features are appreciated.
Defective Fc receptor-mediated clearance in patients with primary biliary cirrhosis. Fc receptor-mediated clearance of immunoglobulin G-coated autologous erythrocytes was studied in patients with primary biliary cirrhosis (n = 14), alcoholic liver cirrhosis (n = 5) and healthy reference individuals (n = 14). The mean half-life of the sensitized erythrocytes was significantly prolonged in patients with primary biliary cirrhosis (85 +/- 25 minutes; P less than 0.001) compared with the corresponding value in patients with alcoholic cirrhosis (16 +/- 2 minutes) and healthy reference individuals (20 +/- 5 minutes), respectively. No correlation between clearance rate and age, liver histopathology, or serum levels of bilirubin, aminotransferases, immunoglobulin G, immunoglobulin A, and Clq binding or C3-containing immune complexes was found. The results presented here indicate a profound disturbance of Fc receptor-mediated immune clearance function in patients with primary biliary cirrhosis.
Competitive control of myosin expression: hypertrophy vs. hyperthyroidism. The competition between two opposing influences on the phenotypic expression of skeletal muscle myosin were studied to determine which was the dominant regulator. Experimental hyperthyroidism, which induces fast myosin expression, was produced by subcutaneous implantation of a 40-day constant-time-release triiodothyronine pellet. Compensatory hypertrophy, which induces slow myosin expression, was produced by surgical removal of a synergistic hindlimb muscle. Hyperthyroidism increased the percentage of type II fibers and the fast myosin isoforms in both the plantaris and soleus muscles. Hypertrophy significantly increased the percentage of type I fibers and the slow myosin type in the plantaris and soleus muscles. However, with the simultaneous introduction of hyperthyroidism and hypertrophy, only the hyperthyroid effects were observed. Hyperthyroidism and not physiological demand was found to be the dominant regulator of skeletal muscle myosin expression.
Effect of ketanserin on intraoperative blood loss during total hip arthroplasty in elderly patients under general anaesthesia. We have studied the effect of ketanserin, a selective serotonin S2-receptor antagonist, on surgical bleeding in a double-blind, placebo-controlled study in elderly patients undergoing total hip arthroplasty. One group of patients (n = 9) received ketanserin 10 mg i.v. followed by an infusion of 0.075 mg kg-1 h-1. The second group (n = 8) received placebo. Both groups were comparable with regard to age, height and body weight. Mean intraoperative blood loss was 454 ml with ketanserin and 894 ml with placebo (P = 0.004; Wilcoxon two-sample test). Mean duration of the operation was less with ketanserin (112 min) than with placebo (134 min) (P = 0.004), but rate of blood loss was also less with ketanserin (4.1 vs 6.7 ml min-1; P = 0.03). In the ketanserin group, mean arterial pressures tended to be less than in the placebo group. Reductions in central venous pressure were similar in both groups. There were no complications in relation to the use of ketanserin.
Clinical follow-up and immunogenetic studies of 32 patients with eosinophilia-myalgia syndrome 31 patients with L-tryptophan-associated eosinophilia-myalgia syndrome (EMS) that developed during the United States outbreak in 1989 were followed up prospectively at a university hospital outpatient rheumatology clinic for 16 to 24 months from the onset of their illness. Another patient with EMS associated with L-tryptophan in 1988 was followed up for 30 months. 93% of the 28 survivors from the 1989 cohort continue to have symptoms affecting 1-4 organ systems (median 3) and 3 have died, so the disorder produces considerable morbidity and mortality. The chronic sequelae most often associated with long-term disability are sclerodermatous skin thickening (54%), sensorimotor polyneuropathy (61%), proximal myopathy (36%), and severe episodic myalgias (64%). Thrombocytopenia developed in 1 patient. HLA-class II typing revealed a non-significant trend towards an association with HLA-DR4. Early therapy with corticosteroids did not seem to prevent the development of chronic manifestations.
Growth hormone treatment of growth failure secondary to total body irradiation and bone marrow transplantation. Growth hormone was given to 13 children (nine boys, four girls) with acute leukaemia who had undergone treatment with cyclophosphamide and total body irradiation before bone marrow transplantation. Mean age at total body irradiation and bone marrow transplantation was 9.0 years (range 3.7-15.8). Endocrinological investigation was carried out at a mean of 2.0 years (range 0.4-4.0) after bone marrow transplantation. Peak serum growth hormone responses to hypoglycaemia were less than 10.0 micrograms/l (less than 20.0 mU/l) in 10, 10.5 micrograms/l (21.0 mU/l) in one, greater than 16.0 micrograms/l (greater than 32.0 mU/l) in two patients. Mean age of the patients at the start of growth hormone treatment was 12.2 years (range 5.8-18.2). The mean time between total body irradiation and bone marrow transplantation and the start of growth hormone treatment was 3.2 years (range, 1.1-5.0). Height velocity SD score (SD) increased from a mean pretreatment value of -1.27 (0.65) to + 0.22 (0.81) in the first year, +0.16 (1.11) in the second year, and +0.42 (0.71) in the third year of treatment. Height SD score (SD) changed only slightly from -1.52 (0.42) to -1.50 (0.47) in the first year, to -1.50 (0.46) in the second year, and -1.74 (0.92) in the third year. Measurement of segmental proportions showed no significant increase in subischial leg length from -0.87 (0.67) to -0.63 (0.65) in the first year, to -0.58 (0.70) in the second year, and -0.80 (1.14) in the third year of treatment.
Sympathetically maintained pain of the digits in porphyria cutanea tarda relieved by i.v. regional guanethidine. A case of a sympathetically maintained pain of the tips of the fingers in a 39-year-old man with porphyria cutanea tarda is presented. Occupational vibrating trauma is the presumed cause. The successful treatment with intravenous regional guanethidine is reported.
Coronary heart disease in rhesus monkeys with diet-induced coronary artery atherosclerosis. Diet-induced coronary artery atherosclerosis develops in rhesus monkeys (Macaca mulatta). The goal of this study was to establish the rhesus monkey as an animal model of coronary heart disease (CHD). From a colony of 160 rhesus monkeys fed an atherogenic diet, we identified 14 monkeys with electrocardiographic and echocardiographic evidence of CHD. When compared with 14 rhesus monkeys matched for age, gender, and dietary history with normal electrocardiograms and echocardiograms, monkeys with CHD had higher arterial blood pressures (mean +/- SEM, 92 +/- 4 mm Hg vs 75 +/- 5 mm Hg, respectively), lower high-density lipoprotein cholesterol concentrations (mean +/- SEM, 1.70 +/- 0.25 mmol/L vs 2.32 +/- 0.28 mmol/L [66 +/- 10 mg/dL vs 90 +/- 11 mg/dl]), and lower A-l apolipoprotein concentrations (mean +/- SEM, 200 +/- 17 mg/dL vs 252 +/- 15 mg/dL). Monkeys with CHD tended to have higher total plasma cholesterol concentrations (mean +/- SEM, 11.6 +/- 1.55 mmol/L vs 9.36 +/- 0.93 mmol/L [450 +/- 60 mg/dL vs 362 +/- 36 mg/dL]) and higher low-density lipoprotein cholesterol concentrations (mean +/- SEM, 8.71 +/- 1.75 mmol/L vs 6.12 +/- 0.90 mmol/L [337 +/- 68 mg/dL vs 237 +/- 35 mg/dl]) than monkeys with normal electrocardiograms and echocardiograms. We conclude that rhesus monkeys, like human beings, develop CHD as a complication of coronary artery atherosclerosis. Furthermore, risk factors for CHD in rhesus monkeys and human beings are similar.
Primary chest wall tumor appearing as frozen shoulder. Review and case presentations. The term frozen shoulder may apply to a primary, common, recognizable entity with a predictable course to a painful stiff condition with periarthritis secondary to trauma, rotator cuff or arthritic source. We studied 140 cases of frozen shoulder, referred to a surgical clinic for manipulation when conservative care was not effective. Investigations showed only 40 cases had "primary" frozen shoulder and among these were 3 patients with a local primary invasive neoplasm mimicking the exact features of the common condition. The attending physician and surgeon should be suspicious of tumor in younger patients with progressive pain among the other features of primary frozen shoulder.
Impaired suppression of plasma norepinephrine during head-down tilt in patients with congestive heart failure. Neurohumoral activation is present in congestive heart failure and may contribute to vasoconstriction in this syndrome. The mechanisms leading to and maintaining neurohumoral activation in long-standing congestive heart failure are as yet undefined. The present study addresses the possibility that baroreceptor-mediated suppression of plasma norepinephrine may be abnormal in patients with long-standing congestive heart failure. Eight normal subjects and 12 patients with long-standing congestive heart failure were studied during 15 minutes of 30 degrees head-down tilt. There were no significant changes in heart rate or arterial blood pressure in either group during these maneuvers. In normal subjects, plasma norepinephrine declined from 257 +/- 38 pg/ml at control to 208 +/- 39 pg/ml during head-down tilt (p less than 0.005). Plasma norepinephrine was elevated in the patients with congestive heart failure, 475 +/- 189 pg/ml, and did not change during head-down tilt. These observations suggest that baroreflex loading maneuvers, which in this study included increased central blood volume and hydrostatic effects on the sinoaortic baroreceptor, do not suppress increased plasma norepinephrine in patients with long-standing congestive heart failure. Impaired baroreflex responsiveness could therefore contribute to either the generation or maintenance of high plasma norepinephrine in this syndrome.
Aprotinin reduces intraoperative and postoperative blood loss in membrane oxygenator cardiopulmonary bypass. To determine whether aprotinin can provide a significant improvement of hemostasis in cardiopulmonary bypass using a membrane oxygenator, we tested this drug in a prospective, randomized, double-blind, placebo-controlled clinical trial. The subjects were 80 male patients undergoing cardiopulmonary bypass for coronary artery bypass grafting. Forty patients received aprotinin and 40 patients served as placebo controls. Aprotinin (4 x 10(6) KIU) was given as a continuous infusion, starting before operation and continuing until after cardiopulmonary bypass; additionally, 2 x 10(6) KIU aprotinin was added to the pump prime. Intraoperative and postoperative bleeding, respectively two thirds and one third of the total perioperative blood loss, were both significantly reduced in the aprotinin-treated group (p less than 0.01). The total average perioperative blood loss, corrected to a hemoglobin concentration of 7 mmol/L, was 550 mL in the aprotinin-treated patients versus 900 mL in the control patients. This reduction in blood loss, furthermore, significantly decreased the amount of postoperative blood transfusions (p less than 0.05) and increased the percentage of patients who did not receive postoperative donor blood from 42% to 68%. Aprotinin increased the activated clotting time significantly during cardiopulmonary bypass, which led to a reduction in heparin usage. The improved hemostasis during operation, despite the prolonged activated clotting time, might even abolish the need for heparin conversion with protamine at the end of cardiopulmonary bypass, thus allowing retransfusion through cardiotomy suction to be continued, which saves the blood that is currently lost with vacuum suction.
Quality assurance for patients with head injuries admitted to a regional trauma unit. The efficacy of trauma systems in reducing preventable deaths has been established but the methods of auditing care are still evolving. Various "audit filters" to identify which patients' charts should be reviewed have been proposed. An analysis of all patients admitted to the Regional Trauma Unit (RTU) over a 19-month period was conducted. Of 729 patients, 135 were identified as having suffered a traumatic intracranial hemorrhage (TICH). On review, neither delay in transfer from the emergency room to the operating room nor increasing time from the incident to the operating room correlated with increasing mortality. In contrast to delay, the Glasgow Coma Scale (GCS) score on admission correlated well with outcome. The charts of patients with anomalous outcomes based on admission GCS score were reviewed, and two possibly preventable deaths were identified. There were 48 patients with TICH who had no operations but there were no deaths attributable to a missed operation. There were 76 patients for whom the GCS score at the referring hospital and the GCS score on admission to the RTU were available. Seven of 19 patients who worsened on transfer declined because of significant pulmonary injuries. Anomalous outcomes based on admission GCS score and declining GCS scores are recommended as quality assurance filters.
Protein kinase C plays a role in the induction of tyrosine phosphorylation of lymphoid microtubule-associated protein-2 kinase. Evidence for a CD3-associated cascade that includes pp56lck and that is defective in HPB-ALL. Ligation of the CD3 receptor induces multiple signal transduction events that modify the activation state of the T cell. We have compared two lines that express biologically active CD3 receptors but differ in their biochemical activation pathways during ligation of this receptor. Jurkat cells respond to anti-CD3 with Ca2+ mobilization, PKC activation, induction of protein tyrosine phosphorylation, and activation of newly characterized lymphoid microtubule associated protein-2 kinase (MAP-2K). MAP-2K itself is a 43-kDa phosphoprotein that requires tyrosine phosphorylation for activation. Although ligation of the CD3 receptor in HPB-ALL could stimulate tyrosine phosphorylation of a 59- kDa substrate, there was no associated induction of [Ca2+]i flux, PKC, or MAP-2K activation. A specific PKC agonist, PMA, which bypasses the CD3 receptor, could, however, activate MAP-2K in HPB-ALL cells. This implies that defective stimulation of PKC by the CD3 receptor is responsible for its failure to activate MAP-2K in HPB-ALL. The defect in PKC activation is likely distal to the CD3 receptor as A1F14- failed to activate MAP-2K in HPB-ALL but was effective in Jurkat cells. The stimulatory effect of PMA on MAP-2K activity in HPB-ALL was accompanied by tyrosine phosphorylation of this kinase which implies that PKC may, in some way, regulate tyrosine phosphorylation of MAP-2K. A candidate for this role is pp56lck which underwent posttranslational modification (seen as mobility change on SDS-PAGE) during anti-CD3 and PMA stimulation in Jurkat or PMA treatment in HPB-ALL. There was, in fact, exact coincidence between induction of PKC activity, posttranslational modification of lck and tyrosine phosphorylation/activation of MAP-2K. Lck kinase activity in an immune complex kinase assay was unchanged during PMA treatment. An alternative explanation is that modification of lck may alter its substrate profile. We therefore looked at the previously documented ability of PKC to dissociate lck from the CD4 receptor and found that PMA could reduce the stoichiometry of the lck interaction with CD4 in HPB-ALL and to a lesser extent in Jurkat cells. These results imply the existence of a kinase cascade that is initiated by PKC and, in the course of which, lck and MAP-2K may interact.
Terminal axon pathology in infantile neuroaxonal dystrophy. In order to clarify the pathogenesis of infantile neuroaxonal dystrophy, ultrastructural studies of the terminal and nonterminal axons of motor and autonomic nerves in muscle and skin, of which structures are much simpler than those of the central nervous system, were performed in 5 patients affected by infantile neuroaxonal dystrophy. The primary lesion was located in the axon terminal; the majority of terminal axons were dystrophic with tubulo-membranous profiles, while there were only a few dystrophic axons in the nonterminal axons. According to these findings, it is logical to consider that interruption of axonal transport at the site of the "turnaround" process is a cause of dystrophic change of the terminal axon in infantile neuroaxonal dystrophy.