Biomedical subjects
Publications and source records attributed to C Cooper.
The 8-bromo derivative of cGMP was found to stimulate the ouabain-sensitive uptake of K+ and to reduce the net release of K+ induced by acetylcholine in rat submandibular gland slices incubated in vitro.
Very-low-density lipoprotein (VLDL), labelled in vivo with [9,10-3H]oleate, was taken up rapidly by liver after injection in vivo. Initially, radioactive lipoprotein remnants in the VLDL density range were present in liver as a bound extracellular pool that could be released by perfusion with polyphosphate or heparin. The bound remnant showed a decrease in mean diameter and an increased proportion of cholesteryl ester as a function of time after injection. When VLDL of different mean diameters was injected, it was found that: (1) total uptake by liver was independent of diameter; (2) small VLDL was not taken up more rapidly than large VLDL; and (3) Large VLDL lost no more triacylglycerol before binding than did small VLDL and larger species of mean diameter greater than 40 nm were bound. It is concluded that there is no unique VLDL remnant taken up by liver in vivo. When livers were perfused after binding radioactive VLDL in vivo, the lipoprotein was metabolized, with the production of water-soluble products, and this metabolism was inhibited by chloroquine.
Multicenter clinical trials are often larger and more complex than other methods of clinical inquiry. They tend to involve a number of research or clinical centers and several formal committees. In many of these trials a coordinating center is one of the participating organizational units. This article describes one such coordinating center, that of the Hypertension Detection and Follow-up Program (HDFP). In 1971 the HDFP Coordinating Center was established to assist in planning and implementing this National Heart, Lung, and Blood Institute (NHLBI)-sponsored, multicenter, community-based, randomized, controlled clinical trial. The HDFP Coordinating Center is a large, intricate organization comprised of personnel who perform a wide variety of functions. From 1972 to 1979 it supervised the adherence to a common protocol among the cooperating centers and reported the Program's progress to the various monitoring and review committees, the Steering Committee, and the NHLBI Program Office. The Program screened approximately 159,000 persons ages 30 to 69 years, identifying and following 10,940 hypertensive participants. It has been the responsibility of this Coordinating Center to institute, coordinate, and monitor the data-gathering activities of the study as a whole and to process, store, and analyze the large, multifaceted set of data that were collected.
Computed tomography (CT) is generally superior to plain chest radiographs in differentiating pleural and pulmonary parenchymal lesions. We report a patient with asbestos exposure who had a rare interlobar pleural plaque involving the major fissure. In this patient CT suggested the presence of a lung nodule but the lateral chest radiograph indicated the correct diagnosis.
The inferior pulmonary ligament, a double layer of pleura that tethers the lower lobe of the lung to the mediastinum, is rarely appreciated on plain radiographs but may be involved in pathologic processes. A linear structure on axial computed tomographic (CT) images of the lung bases corresponds to the inferior pulmonary ligament on cadaver sections. Review of 100 CT studies identified at least one inferior pulmonary ligament in 42%. Its presence and configuration did not correlate with patient age or gender. The anatomy and CT appearance of the ligament are discussed.
Radioactive lipoproteins in the very low density lipoprotein (VLDL) density range were taken up by rat liver in vivo. The radioactivity became associated with an intracellular particle of d = 1.11 that did not correspond to lysosomes, endoplasmic reticulum, or plasma membrane as determined by marker enzyme distribution. Radioactive VLDL remnants could be released from these particles by passage through a hydraulic press, hypotonic shock, or sonication. The release of radioactivity from the particles by one of these methods became more complete with increasing time after injection. The injection of colchicine inhibited the breakdown of the VLDL triglyceride and cholesterol ester and caused an accumulation of radioactive material in the d = 1.11 particles. In contrast, injected chloroquine inhibited breakdown of VLDL triglyceride and cholesterol ester and caused an accumulation in lysosomes. We have concluded VLDL remnants are metabolized in liver by an endocytosis-lysosomal digestion pathway and that the d = 1.11 particles are endocytic vesicles. The existence of a releasable pool of VLDL within endocytic vesicles makes it possible to examine the internalized remnant.
The quantitative significance of the conversion in vivo of L-[U-14C]leucine to ketone bodies was determined in rats starved for 3 or 48 h. In animals starved for 3 h, 4.4% of ketone-body carbon is derived from the metabolism of leucine, and in rats starved for 48 h the corresponding value is 2.3%. This conversion occurs rapidly, and the specific radioactivity of ketone bodies in blood is maximal at 2 min after the intravenous injection of labelled leucine for both periods of starvation. The flux of leucine in the blood is 1.01 and 1.04 mumol/min per 100 g body wt. respectively for animals starved for 3 and 48 h. The specific radioactivity of blood ketone bodies was compared at 2 min after the injection of labelled leucine, lysine and phenylalanine. The specific radioactivity was 4-5 fold higher with leucine than with lysine or phenylalanine.
SURPATH is a comprehensive, integrated computer-assisted system for service, research, and management in surgical pathology that has been in use at New England Medical Center (NEMC) since July 1, 1978. Functions of the system include: maintenance of patient-name and diagnostic files; generation, editing, and printing of preliminary and final specimen reports; SNOMED coding and indexing of diagnoses; retrieval and video display or printing of data on individual cases or groups of cases; billing and generation of billing reports; and, calculation of intervals between accession and signout of specimens. Use of the system has greatly facilitated the production of surgical pathology reports; increased the spread with which inquiries about individual specimens can be answered; provided rapid, accurate searches of the diagnostic files; improved timeliness, accuracy, and completeness of billing resulting in increased departmental revenue; reduced intervals between accession and reporting; and, improved the morale of the professional and support staffs.
The Defence Mechanism Inventory (Gleser & Ihilevich, 1969) was validated by examining the 16PF profiles of each group of defenders. These were found to correspond closely to profiles hypothesized on the basis of Freudian theory, and thus suggest that the test may be valid. The ipsative scoring system was thought to limit the clinical usefulness of the five scales and to hinder statistical analyses, and the development of a rating form of the questionnaire was recommended.
UDP-N-acetylgalactosamine--GM3 acetylgalactosaminyltransferase (GM2-synthase) was studied in a Golgi-rich fraction from rat liver. Activity in a cell-free system required the presence of detergents; octyl glucoside was found to be the most effective in stimulating the enzyme. Optimal activity of GM2-synthase was obtained at pH 7.2, in the presence of 0.8% octyl glucoside, 10 mM Mn2+ and 5 mM CDP-choline. The latter was used to counteract the rapid sugar nucleotide hydrolysis caused by a nucleotide pyrophosphatase activity in the Golgi fraction. The apparent Km values for UDP-N-acetylgalactosamine and added GM3 were 0.035 mM and 0.1 mM, respectively. Different results were obtained if endogenous GM3 only was used as the glycolipid acceptor. In this case, the apparent Km value for UDP-N-acetylgalactosamine was 0.18 mM and Co2+ and Fe2+ exceeded Mn2+ in activating GM2-synthase. Under optimal assay conditions and in the presence of added GM3 and 5 mM CDP-choline, the specific activity of the enriched Golgi fraction was measured to be 25-30 nmol X mg protein-1 X h-1; with endogenous GM3 as the sole glycolipid acceptor, V was calculated to be 9 nmol X mg protein-1 X h-1.
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After chronic administration of reserpine, slices of the rat parotid gland incubated in vitro were found to release significantly more K+ and significantly less amylase than similar slices from untreated control animals. The extent of K+ release in the gland slices of the drug-treated animals shows no dependency on external Na+ or Ca++ and is probably enhanced because of a decreased activation of K+ uptake by the Na+-K+ pump. This effect may also involve a defective generation of cyclic GMP, which was found to enhance K+ uptake and, thus, to inhibit K+ release in control slices. The inhibition of amylase release observed after treatment with reserpine most likely results from a deficient level or utilization of the energy or nucleotide sources required for enzyme secretion, because a similar inhibition was observed in control slices after incubation in the absence of the purines inosine and adenine. These results indicate that chronic reserpine administration impairs the stimulus-secretion coupling mechanism in the rat parotid gland and results in abnormal responses from both alpha and beta adrenergic receptors.
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The present study was undertaken to evaluate quantitatively the turnover of serum triacylglycerol (triglyceride) in the starved rat and to determine whether serum triacylglycerol recycled to liver contributes a significant fraction of the total hepatic triacylglycerol turnover. Serum was labelled in vitro with [3H]trioleoylglycerol (glycerol [3H]trioleate) to provide uniform labelling of all lipoprotein species. By using the curves describing disappearance of isotope from serum and its appearance in liver, rate constants for movement of triacylglycerol out of serum (0.29 min-1) and the uptake of serum triacylglycerol by liver (0.22 min-1) were calculated. The total rate of movement (flux) of triacylglycerol in these processes, the product of rate constant and serum pool size, was calculated to be 0.39 and 0.29 mg/min per 100 g body wt. respectively. A model is postulated for whole-body triacylglycerol metabolism consistent with the present data as well as most observations in the literature. From the model it can be predicted that: (1) the entire turnover of liver triacylglycerol in the starved rat can be accounted for on the basis of contributions from serum non-esterified fatty acid and serum triacylglycerol; (2) the entire turnover of the serum triacylglycerol pool can be accounted for quantitatively on the basis of contributions from intestine and liver; (3) the release rate for triacylglycerol from liver should be 0.34 to 0.35 mg/min per 100 g body wt.; (4) triacylglycerol synthesized by liver from non-esterified fatty acid of serum and by intestine can account quantitatively for the irreversible disposal rate of triacylglycerol from serum.
After an intravenous injection of a pulse of [U-14C]palmitate to starved rats, the time-dependent radioactivity profiles were determined in the triacylglycerol (triglyceride) of hepatic microsomal fractions, floating fat, mitochondria and nuclei. The profile of activity in serum gave a value of 0.08 mg/min per 100 g body wt. for the irreversible disposal rate of triacylglycerol from serum. This value, combined with the previously estimated rate of movement of triacylglycerol from serum to liver, and the reported rate from intestine to serum, gave a calculated value of 0.35 mg/min per 100 g body wt. for release rate of triacylglycerol from liver to serum. The rate of release of hepatic triacylglycerol into serum was also measured by the widely used Triton WR-1339 method. The rate obtained with this technique (0.15 mg of triacylglycerol/min per 100 g body wt.) was identical with that reported previously. During the interval from 45 min to 3h after ethanol administration this rate increased to 0.18 mg/min per 100 g body wt. It was concluded that the use of Triton underestimates the true rate of movement of triacylglyerol from liver to serum.