Hazards with both determining and utilizing oxygen consumption measurements in the management of critically ill patients.
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Biomedical subjects
Publications and source records attributed to R S Fishman.
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OBJECTIVE: To review the work of David Ferrier (1843-1928), the British pioneer in the localization of function in the cerebral cortex. In his experiments on monkeys, Ferrier mistakenly located the center for vision in the angular gyrus of the parietal lobe. What led him to this error? DATA SOURCES: Ferrier included details of his technique and many of his original laboratory observations in his published papers and books; these published works have allowed a reconstruction of his thought processes as he struggled to assess vision in untrained animals. CONCLUSIONS: The occipital lobe lesions produced by Ferrier did not yield vision defects that were gross enough to be detected by observing a monkey's random behavior. On the other hand, the posterior parietal lesions produced by Ferrier did change a monkey's behavior in ways in which Ferrier misinterpreted as being due to induced blindness. Ferrier had probably induced visual neglect and a disinclination in the monkey to move its body, as well as actual vision disturbances in guiding voluntary limb movements.
David Ferrier and Hermann Munk, both pioneers in early brain research, engaged in a running controversy regarding the primary vision center in the brain. Both misinterpreted their experimental observations, but in different ways. Ferrier placed vision in the parietal lobe, Munk in the occipital lobe, However, Munk also felt he had observed a 'psychic blindness' in his animals, which was in reality only a central scotoma or other primary vision defect, and not the impairment of higher visual capacities that he proposed. Munk's concept has been repeatedly cited as the experimental correlate of visual agnosia, but is inherently fallacious.
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To determine how diet modulates short-term exercise capacity, skeletal muscle pH and bioenergetic state were examined by 31P-magnetic resonance spectroscopy in nine healthy volunteers. Subjects performed incremental quadriceps exercise to exhaustion after 5 days of high-carbohydrate (HCHO) or high-fat (HFAT) diet randomly assigned in crossover fashion and separated by a 2.5-day period of ad libitum mixed diet. Simultaneous measurements were made of pulmonary gas exchange, minute ventilation, and quadriceps muscle pH and phosphorylation potential. At rest and peak exercise, respiratory exchange ratio and minute ventilation were higher after HCHO than after HFAT (P < 0.05), reflecting greater CHO utilization. Peak O2 consumption (VO2) was not increased after HCHO (P > 0.05), but exercise duration was (339 +/- 34 s for HCHO vs. 308 +/- 25 s for HFAT; P < 0.05). HCHO was associated with a blunted early fall of phosphocreatine (PCr)/Pi vs. VO2 (-4.1 +/- 0.7 x 10(-2) min/ml for HCHO vs. -5.6 +/- 1.2 x 10(-2) min/ml for HFAT; P < 0.05). On both study days, the slope of PCr/Pi vs. VO2, before and after the PCr threshold, was correlated with exercise time. The results suggest that a diet rich in CHO improves exercise efficiency through beneficial effects on intracellular phosphorylation potential.
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Over the past 15 years evaluation of the patient with exertional complaints has changed from a simple qualitative estimate of overall fitness to a detailed assessment of cardiovascular and pulmonary pathophysiology. By quantifying exercise impairment and identifying the physiological limit to exercise, CPEx can help direct and evaluate the efficacy of medical and surgical interventions. Although no clear consensus has emerged, an objective determination of the etiology of exercise intolerance may also help identify the patient at increased risk for postthoracotomy complications.
In the hepatocyte endoplasmic reticulum, a substrate transporter could provide a means of regulating hydrolysis of glucose-6-phosphate by specifically modulating access of the substrate to the hydrolase. Several characteristics of the cerebral microsomal enzyme suggest that such an hypothesis is untenable in the brain. These are: (a) the inability of the enzyme in either untreated or detergent-disrupted brain microsomes to distinguish between glucose-6-phosphate and mannose-6-phosphate; (b) the close agreement of the apparent Km values for either substrate in intact or disrupted microsomal preparations; (c) the constancy of the latency toward both substrates over a wide concentration range; (d) the inability of nonpenetrating, covalently-linking reagents [e.g., 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)] to affect the accessibility of the hydrolase to its substrate; (e) the absence of a putative transporter polypeptide, such as that of the liver, in experiments where tritiated H2DIDS, polyacrylamide gel electrophoresis, and radioautography are applied to brain microsomes.
Von Hippel-Lindau disease is a hereditary neoplastic disorder that is most commonly manifested as vascular tumors of the retina and cerebellum. Although visceral involvement is uncommon and is almost always clinically silent, we have encountered three closely related patients with extensive symptomatic pancreatic involvement. One patient had pronounced exocrine pancreatic insufficiency.
A 63-year-old man presented with fever, splenomegaly, steatorrhea, diarrhea, and weight loss. A tissue diagnosis of systemic mastocytosis was made. This case is unusual in that diarrhea and steatorrhea were present in the absence of skin lesions and because fever was a prominent symptom. Thus, systemic mastocytosis should be included in the differential diagnosis of intestinal malabsorption even when the skin shows no abnormalities. The gastrointestinal manifestations of systemic mastocytosis are reviewed.
Crohn's colitis has recently been shown to predispose the patient to cancer of the colon. Unfortunately, many of the manifestations of colonic malignancy, such as polypoid intraluminal masses and strictures, can be simulated roentgenographically by Crohn's colitis. We present five patients in whom this diagnostic difficulty arose. As established by total or subtotal colectomy, none proved to have malignancy; instead, pronounced transmural inflammation and, in two cases, multiple large pseudopolyps were found to account for the roentgenographically indeterminate lesions. These findings exemplify the difficulty in roentgenographic diagnosis of colonic mass lesions in patients with Chrohn's colitis.
Of 38 patients with presumed or proven pituitary adenomas, 24 first presented with ocular complaints. Of these, ten patients had a physician-caused delay in the formulation of the correct diagnosis. Reasons for the physician-caused delay in diagnosis include inadequate history evaluation, failure to perform adequate testing, provide follow-up examination, and recognize typical signs of pituitary adenomas.
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