shukoor65/lab-rag-model huggingface dataset:
Assessment of energy expenditure by indirect calorimetry in healthy subjects and patients with liver cirrhosis. The reliability of resting energy expenditure (REE) measurements by indirect calorimetry with a ventilated hood was investigated in 50 healthy controls and 10 patients with liver cirrhosis. In each subject basal energy expenditure (BEE) was determined once and REE three times (morning REE1, noon REE2, afternoon REE3). In controls and patients the first 5-minute BEE and first 5-minute REE (controls also second 5-minute REE) were higher than in the remainder of the 30-minute recording. Only the last 20 minutes of recordings were used to calculate BEE (1645 +/- 315, mean +/- SD, in kilocalories per day), REE1 (1880 +/- 365), REE2 (1782 +/- 384), and REE3 (1775 +/- 316) in controls, and in cirrhotics: BEE (1530 +/- 235), REE1 (1714 +/- 267), REE2 (1715 +/- 238), and REE3 (1779 +/- 275). REE was higher than BEE in controls and cirrhotics (p less than 0.05). The REE variation coefficient was 5 +/- 3% in controls and 5 +/- 2% in cirrhotics. No systematic difference between REE1, REE2, and REE3 was found. Energy expenditure predicted by the Harris-Benedict equation differed up to 21% from measured BEE in individual controls; group mean BEE, however, was correctly predicted. In cirrhotics differences between measured and predicted BEE up to 26% occurred, while measured BEE was higher than predicted BEE (p = 0.06). It is concluded that REE can be reliably assessed by indirect calorimetry with a ventilated hood system in controls and patients at any time of the day, when values obtained in the first 10 minutes are deleted.
Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy. BACKGROUND. Left ventricular (LV) midwall geometry has been described conventionally as the sum of the chamber radius and half of the wall thickness; this convention is based on the assumption of uniform transmural thickening during systole. However, theoretical considerations and experimental data indicate that the inner half (inner shell) of the LV wall thickens more than the outer half (outer shell). Thus, an end-diastolic circumferential midwall fiber exhibits a relative migration toward the epicardium during systole. As a result, the conventional method provides an overestimate of the extent of the midwall fiber shortening. METHODS AND RESULTS. We developed an ellipsoidal model with a concentric two-shell geometry (nonuniform thickening) to assess midwall fiber length transients throughout the cardiac cycle. This modified midwall method was used in the analysis of LV cineangiograms from 15 patients with systemic arterial hypertension and 14 normal subjects. Study groups were classified according to LV mass index (LVMI): 14 normal subjects (group I), eight hypertensive patients with a normal LVMI (group II), and seven hypertensive patients with an increased LVMI (group III). There were no significant differences in LV end-diastolic pressure or volume among the three groups; the ejection fraction was slightly greater in group II (70 +/- 5%) than in groups I (65 +/- 8%) and III (66 +/- 4%), but this trend did not achieve statistical significance. Values for endocardial and conventional midwall fractional shortening (FS) were also similar in the three groups. By contrast, FS by the concentric two-shell geometry (modified midwall method) in group III (16 +/- 2%) was significantly less than that seen in groups I and II (21 +/- 4% and 21 +/- 5%, respectively; both p less than 0.05). This difference achieves greater importance when it is recognized that mean systolic circumferential stress was lower in group III (151 +/- 22 g/cm2) than in groups I and II (244 +/- 37 g/cm2 and 213 +/- 38 g/cm2, respectively; both p less than 0.01). The midwall stress-shortening coordinates in six of the seven group III patients were outside the 95% confidence limits for the normal (group I) subjects. Thus, despite a normal ejection fraction, systolic function is subnormal in hypertensive patients with LV hypertrophy. CONCLUSIONS. Chamber dynamics provide an overestimate of myocardial function, especially when LV wall thickness is increased. This is due to a relatively greater contribution of inner shell thickening in pressure-overload hypertrophy.
Impaired potassium-induced dilation in hypertensive rat cerebral arteries does not reflect altered Na+,K(+)-ATPase dilation. We have recently demonstrated that K(+)-induced dilation of cerebral resistance-sized vessels has two independent components, only one of which seemed sodium pump dependent. In our current investigation, potassium-induced dilation of spontaneous tone was compared in cerebral arteries from normotensive Wistar-Kyoto rats and age-matched stroke-prone spontaneously hypertensive rats. Branches of the posterior cerebral artery were cannulated and pressurized, and these vessels developed spontaneous tone. After a 5-minute period in K(+)-free physiological saline solution, K+ was increased in 1-mM increments to a final concentration of 15 mM. In the normotensive arteries, K+ concentrations between 0 and 5 mM K+ resulted in dilations that had a transient (sodium pump-dependent) component, and K+ concentrations in excess of 7 mM produced dilations that lacked a transient (sodium pump-independent) component. Similar branches from the hypertensive rat also responded with transient dilations to K+ (less than 5 mM), and these were significantly greater at 3 mM K+. However, the maintained dilations to K+ (greater than 7 mM), noted in preparations from Wistar-Kyoto rats, were absent in seven of eight preparations. Thus, the impaired dilations, in the hypertensive vessels, to K+ described here is a consequence of altered function of some sodium pump-independent component rather than altered Na+,K(+)-ATPase activity.
Endocarditis due to Trichosporon beigelii: in vitro susceptibility of isolates and review. Infection with Trichosporon beigelii is an uncommon cause of endocarditis. Of the eight cases of T. beigelii endocarditis that have been reported (one herein and seven previously), six involved prosthetic heart valves and two involved native heart valves. The clinical manifestations of this infection included embolization of the superficial femoral artery or of the bifurcation of the posterior tibial and peroneal arteries in three of these patients (two with prosthetic valve and one with native valve endocarditis). In seven of the eight reported cases, blood cultures were positive for the organism. Although clinical isolates of the organism are generally reported to be susceptible to amphotericin B, isolates can vary in their sensitivities to antifungal agents in vitro depending on the methodology used, and clinical response to therapy with antifungal agents in a regimen that includes amphotericin B is generally poor. Only two of six patients who were treated with antifungal agents survived endocarditis caused by T. beigelii and were apparently cured; one of these patients was also managed surgically with valve replacement. Infection with T. beigelii should be considered in the differential diagnosis of endocarditis in immunocompetent patients, particularly those who have a prosthetic heart valve. Rapid, aggressive therapy may be necessary to eradicate this organism.
Triangulation of pedicular instrumentation. A biomechanical analysis. Tensile load-to-failure pullout tests were performed on 54 cadaveric spinal segments. The vertebrae were grouped by adjacent levels and matched for bone mineral density (g/cm2), which was measured by dual-photon absorptiometry. Triangulation of Steffee screws and CD pedicle screws was accomplished by transverse plates specifically designed to increase fixation within the same vertebra before the longitudinal Steffee plate or CD rod was applied. A transverse plate with adjustable length was also tested to accommodate variable interpedicular distances. Comparative pullout load-to-failures were as follows: laminar hook, 809 SE 99.4 N; single CD pedicular screws, 863 SE 108 N; single Steffee pedicular screw, 1245 SE 75.3 N; adjustable transverse plate, 1341 SE 114; triangulated Steffee pedicle screws with a transverse plate, 1701 SE 151 N; and triangulated CD pedicle screws with a transverse plate, 2096 SE 115 N. Three triangulated constructs with pedicle screws and a transverse plate (CD, Steffee, and Kirschner) provided significantly greater fixation than conventional pedicular or laminar hook based instrumentation systems (P less than 0.05). Improved treatment of spinal deformities in the elderly and osteoporotic population is dependent on improving the fixation at the metal-bone interface of spinal implants Particularly in osteoporotic vertebrae, the strength of fixation of two triangulated pedicle screws is better than either laminar hooks or single pedicle screws. The strength of fixation of triangulated pedicle screws connected by a transverse plate is superior to a single pedicle screw because it is dependent on the mass of bone between the screws rather than simply the amount of bone within the screw thread.
Pericardiac extravasation during intravenous digital subtraction angiography: a case report. The authors reported a case, pericardiac extravasation of contract medium during an intravenous angiographic (IV DSA) procedure. To their knowledge this is the first such case in the literature. They suggest modifications of the IV DSA method to avoid this complication.
Remission of hepatitis B-associated membranous glomerulonephritis in human immunodeficiency virus infection. Hepatitis B virus (HBV) infection has been associated with several renal diseases, the most common being membranous glomerulonephritis (MGN). The role of concurrent human immunodeficiency virus (HIV) infection in affecting the course of the renal involvement is largely unknown. We report the case of a HIV-infected adult male with chronic HBV-associated MGN who had complete remission of the nephrotic syndrome associated with spontaneous seroconversion from hepatitis B e antigen (HBeAg)-positive to HBeAg-negative. The present case illustrates that HIV infection does not preclude improvement of chronic HBV infection or an associated membranous nephropathy. Such improvement may be dependent on the ability of the host immune system to clear HBeAg.
Spatial control of gut-specific gene expression during Caenorhabditis elegans development. The nematode Caenorhabditis elegans was transformed with constructs containing upstream deletions of the gut-specific ges-1 carboxylesterase gene. With particular deletions, ges-1 was expressed, not as normally in the gut, but rather in muscle cells of the pharynx (which belong to a sister lineage of the gut) or in body wall muscle and hypodermal cells (which belong to a cousin lineage of the gut). These observations suggest that gut-specific gene expression in C. elegans involves not only gut-specific activators but also multiple repressors that are present in particular nongut lineages.
Hexamethylmelamine chemotherapy for persistent or recurrent epithelial ovarian cancer. The purpose of this study was to determine the activity and toxicity of hexamethylmelamine chemotherapy in patients with persistent or recurrent epithelial ovarian cancer. Forty-nine women received hexamethylmelamine 100 to 150 mg/day for 14 days, repeated at 4-week intervals. All patients had previously received at least one chemotherapy regimen, and 46 (94%) had received cisplatin. Among 25 patients with clinically measurable disease there were three complete and two partial responses, for an objective response rate of 20%. The mean progression-free interval for responders was 38.6 months versus 9.6 months for nonresponders or patients with nonmeasurable disease (p less than 0.001). Thirteen patients are alive, eight with no clinical evidence for disease. Only four patients discontinued therapy because of toxic reactions. Hexamethylmelamine appears to be a well-tolerated drug with activity against ovarian cancer previously treated with cisplatin.
Psychiatric disorders in patients with esophageal disease. Psychiatric disorders have potentially important roles in the manifestations of esophageal disease. A primary causative role for psychiatric factors in the common motility disorders associated with chest pain (esophageal spasm and the nonspecific motor disorders) remains unproven, but psychiatric disorders appear particularly prevalent in this group. In most other esophageal diseases, psychiatric factors interact through recognized psychophysiologic or behavioral mechanisms to affect the clinical presentation. Recognizing the possible levels of interaction has significant therapeutic implications.
Early thrombolytic treatment reduces analgesic requirement in patients with myocardial infarction. The duration and amount of analgesics required were investigated in 67 patients with myocardial infarction treated with intravenous recombinant tissue-type plasminogen activator (rtPA) or placebo in a randomized double-blind trial. Infusion of rtPA (100 mg)/placebo was started within 5 h after the onset of symptoms, and the requirement for analgesics during the following 48 h was recorded. Sixty-seven per cent of the 30 rtPA-treated patients required analgesic treatment for less than 6 h, compared to 38% of the 37 patients in the placebo group (P = 0.04). During the study period, patients in the rtPA group used the equivalent of 5.3 mg (median value) intravenous morphine, which was significantly less than the 11.2 mg used in the placebo group (P = 0.04). In conclusion, the present study suggests that early thrombolysis with intravenous rtPA reduces the amount and duration of analgesic treatment required by patients with myocardial infarction.
Immediate and late inflammatory responses to ragweed antigen challenge of the peripheral airways in allergic asthmatics. Cellular, mediator, and permeability changes. Asthma may represent the clinical manifestations of a unique form of chronic airway inflammation and is often associated with allergy. To better define the components of allergic inflammation in the lung, fluids obtained by bronchoalveolar lavage (BAL) were examined for cells, inflammatory mediators, and markers of airway permeability 5 min and 19 h following instillation of ragweed antigen directly into an airway segment of allergic asthmatic subjects. The 5-min response to antigen challenge (n = 10) was characterized by 17- to 208-fold increases in histamine, prostaglandin D2 (PGD2), and its metabolite, 9 alpha,11 beta-PGF2, thromboxane B2, and 6-keto-PGF1 alpha compared with a saline-challenged segment (0.004 less than p less than 0.017). The increases in most of these mediators were significantly correlated with each other (0.0001 less than p less than or equal to 0.01), and the magnitude of all significant mediator increases was directly correlated with skin test sensitivity to ragweed antigen (0.007 less than or equal to p less than or equal to 0.05). There was also a slight increase in kinins (p = 0.04). Changes in cells and airway permeability were not detected. In contrast, the 19-h response to antigen challenge (n = 9) was characterized by a 13-fold increase in total cells recovered by BAL. Eosinophils, basophils, and lymphocytes were significantly increased and comprised 38, 1, and 9% of total cells, respectively. A neutrophil influx was also observed but was not specific for antigen challenge since a similar change was observed in a sham, saline-challenged site.
Antiischemic and metabolic effects of glutamate during pacing in patients with stable angina pectoris secondary to either coronary artery disease or syndrome X. The effects of glutamate on anginal threshold, cardiac metabolism and hemodynamics were studied in 11 patients with stable angina pectoris, positive stress test results, and pacing-induced myocardial lactate release due to coronary artery disease (CAD) (n = 9) or syndrome X (n = 2). Data were obtained before, during and after 2 identical periods of coronary sinus pacing, the second being preceded by an intravenous injection of monosodium glutamate 1.2 (n = 7) or 2.5 (n = 4) mg/kg body weight. After glutamate administration, pacing time to onset of angina increased from mean +/- standard deviation 103 +/- 53 to 166 +/- 71 seconds (p less than 0.01) and ST-segment depression after pacing decreased from 2.3 +/- 1.0 to 1.6 +/- 1.1 mm (p less than 0.01). Arterial glutamate concentration increased 60% (p less than 0.01) after the low dose and 150% (p less than 0.01) after the high dose of glutamate. Regardless of dose, myocardial glutamate uptake increased by 25% (p less than 0.01). Pacing-induced cardiac release of lactate diminished 50% (p less than 0.05), whereas the releases of xanthine and hypoxanthine were unchanged by glutamate. Arterial free fatty acids decreased 20% (p less than 0.01). Circulating levels and cardiac exchanges of alanine, glucose and citrate were unchanged. Glutamate did not influence heart rate, arterial blood pressure, coronary blood flow, coronary vascular resistance or myocardial oxygen consumption. One patient complained of short-lasting burning sensations after receiving the high glutamate dose. In conclusion, augmented provision of glutamate enhances pacing tolerance in stable angina, presumably by a metabolic improvement of cardiac energy production during ischemia.
Oxygen utilization, carbon dioxide elimination and ventilation during recovery from supine bicycle exercise 6 to 8 weeks after acute myocardial infarction. The pattern of oxygen (O2) consumption (VO2), carbon dioxide (CO2) production (VCO2), ventilatory and metabolic responses during and in recovery from supine bicycle exercise was examined in 18 patients with recent myocardial infarction. An increase in VO2 with increasing work load was accomplished by proportional increases in both cardiac output and the arteriovenous O2 difference. During recovery, however, the arteriovenous O2 difference rapidly decreased below levels at rest, whereas VO2 and cardiac output remained elevated, indicating that VO2 during recovery further depended on relatively high cardiac output. The ratio of VCO2 to VO2 further increased after exercise, suggesting that such cardiac output contributed to the remaining high CO2 flow to the lung and therefore enhanced ventilation. Increased arterial catecholamines during exercise remained elevated for the first 5 minutes of recovery. Arterial lactate during this period continued to increase and resulted in profound metabolic acidosis, causing alveolar hyperventilation after exercise. These results suggest that during recovery from exercise, cardiopulmonary responses remain enhanced because of continuing high cardiac output, resulting in subsequent high CO2 flow to the lung and metabolic acidosis, and that this may be associated with profound fatigue or dyspnea after exercise.
Lipoprotein (a) blood levels in unstable angina pectoris, acute myocardial infarction, and after thrombolytic therapy. Lipoprotein (a) [Lp(a)] appears to be involved in atherogenesis and in vitro studies have suggested that it may interfere with thrombolysis. In this study, Lp(a) serum levels were determined by radioimmunoassay in 124 patients with ischemic heart disease. Of these, 47 had acute myocardial infarction, 13 had unstable angina, and 64 were age-matched patients with stable angina. Of the 60 patients with acute coronary artery disease, 34 received thrombolysis and 26 did not. In addition to Lp(a), serum plasminogen, alpha 2 antiplasmin, fibrinogen, and D-dimer (cross-linked fibrin degradation products) levels were measured. These tests were repeated after 6 hours in patients with myocardial infarction and unstable angina. No significant difference was found for admission Lp(a) levels among patients with myocardial infarction (0.324 +/- 0.047 g/liter), unstable angina (0.435 +/- 0.123 g/liter) and stable angina (0.431 +/- 0.023 g/liter), between patients with myocardial infarction with or without thrombolytic treatment, nor between late and early measurements in patients with unstable angina and acute myocardial infarction. Plasminogen, alpha 2 antiplasmin and fibrinogen values decreased significantly after thrombolytic treatment. The size of this decrease correlated positively with higher Lp(a) blood levels (p less than 0.05). Patients with Lp(a) greater than 0.25 g/liter had a 66% decrease in fibrinogen and a 53% decrease in anti-plasmin, compared with 35 and 32%, respectively, in patients with Lp(a) level less than or equal to 0.25 g/liter (p less than 0.05). Plasminogen levels revealed a similar trend, with a 61% decrease for the higher values and a 45% decrease for the lower values.
Orthotopic liver transplantation, Epstein-Barr virus, cyclosporine, and lymphoproliferative disease: a growing concern. Lymphoproliferative disease (LPD) is a well-recognized complication of both solid organ and bone marrow transplantations. The occurrence of LPD in these settings is related in part to the use of the immunosuppressive agent cyclosporine. We report 12 cases of LPD after orthotopic liver transplantations in 132 pediatric patients. Lymphoproliferative disease occurred as one of three clinical syndromes: (1) lymphadenopathic, (2) systemic, and (3) lymphomatous. Effective management of LPD with excisional therapy or reduction of immunosuppressive medications or both resulted in the survival of 7 of 12 patients. In an alarming and increasing percentage of patients after orthotopic liver transplantation, progressive LPD develops with lethal outcome (5/12 patients). Early recognition of LPD and aggressive intervention may improve outcome in this group.
Coffee, coronary heart disease and mortality in middle-aged Swedish men: findings from the Primary Prevention Study. The effect of coffee consumption on the incidence of coronary heart disease (CHD) was studied prospectively in a population sample of 6765 men aged 51-59 years at baseline during the period 1974-1977, and free of myocardial infarction (MI) prior to the screening. During a 7.1-year follow-up there were 230 non-fatal myocardial infarctions. 169 coronary deaths and 478 deaths from all causes. Among men who were smokers at baseline there was no relationship between either non-fatal MI or death from CHD, and coffee consumption. Among non-smokers, a weak but far from significant trend towards an increasing incidence of CHD in heavy consumers of coffee was observed. There was an inverse relationship between mortality from all causes and coffee consumption.
Dietary lipid predictors of coronary heart disease in men. The Framingham Study. The relationship between dietary lipids and the 16-year incidence of coronary heart disease (CHD) morbidity and mortality was examined in two male cohorts, aged 45 to 55 years (n = 420) and 56 to 65 years (n = 393) from the Framingham Study. Dietary lipids were assessed through a single 24-hour recall at the initiation of follow-up in 1966 to 1969. In the younger cohort, there were significant positive associations between the incidence of CHD and the proportion of dietary energy intake from total fat and monounsaturated fatty acids. The proportion of energy intake from saturated fatty acids had a marginally significant positive association with CHD. The associations remained even after adjustment for cardiovascular disease risk factors, including serum cholesterol level, suggesting that their effects are at least partially independent of other established risk factors. In contrast to the younger cohort, none of the dietary lipids were associated with CHD in the older cohort. Dietary intervention for the prevention of CHD in younger men is supported by these findings.
Pill-esophagitis caused by nonsteroidal antiinflammatory drugs. A case of meclofenamate-induced pill-esophagitis is reported, and the relevant literature is reviewed. The role of posture, amount of fluid chaser, esophageal obstruction or dysmotility, drug formulation, physical and chemical properties of the drug, and concomitant ingestion of alcohol, as well as the diagnosis and management of such cases, are discussed.