Automated system of dissolution testing with data input through RS-232C interface of a personal computer.
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Biomedical subjects
Publications and source records attributed to Y Yano.
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Bile sample were collected in 17 cases of choledocholithiasis, 28 of malignant obstructive jaundice and 7 of hepatolithiasis and biliary CEA levels were measured by the EIA method. In the malignant obstructive jaundice group, the biliary CEA level was higher than that in the choledocholithiasis group and the bile gave a positive test for CEA more frequently than the serum. As for the hepatolithiasis group, the biliary CEA level was higher than that in the malignant obstructive jaundice group. The EIA method, however, had a possibility that not only CEA but also CEA-related antigens were measured. Therefore, antigen for CEA, NCA and BGP were prepared, and biliary CEA, NCA and BGP levels were measured by the ELISA method. The biliary CEA level (mean +/- S.D.) was 0.086 +/- 0.26 for 21 cases of cholelithiasis, 0.119 +/- 0.24 for 15 of pancreatic carcinoma, and 0.117 +/- 0.016 for 17 cholangiocarcinoma, cholecystic carcinoma, being thus significantly (p less than 0.05) higher in malignant disease. In malignant disease, both biliary NCA and biliary BGP increased, though not so remarkable compared with CEA. Even in controls, the biliary NCA and BGP levels were not negligible.
A modified Langendorff rat heart preparation with an isolated working rat heart was used to establish the presence of opiate receptors in the myocardium and to demonstrate the effects of an opiate agonist on myocardial function in the absence of neuronal and humoral factors. Twenty-five Sprague-Dawley rats weighing 400-500 gm were anesthetized and had their hearts excised and attached to the Langendorff perfusion apparatus. After a 30 min control period, the Krebs-Henseleit Buffer (KHB) perfusion solution was altered by the addition of 0.9% NaCl (S) or morphine sulfate (MS), which resulted in a final concentration of 2 X 10(-4) M or 3 X 10(-4) M MS in the KHB. Temperature, preload, and afterload were kept constant while heart rate (HR), cardiac output (CO), and aortic dP/dtmax were measured. Significant dose-related depression of HR, CO, and less significantly, aortic dP/dtmax were demonstrated. The data suggest that opiate receptors are present in the myocardium and that morphine sulfate directly effects the myocardium causing a significant decrease in HR, CO, and aortic dP/dtmax. These changes are a result of opiate receptor agonism, which seems to be primarily a negative chronotropic effect and might explain the mechanism for the role of endogenous opiates during shock.
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Previous work has demonstrated that a common opiate agonist, morphine sulfate (MS), causes significant depression of myocardial performance when added to the perfusate of a modified Langendorff isolated rat heart preparation. The same model has been used in this study with the addition of higher concentrations of MS to demonstrate that the aforementioned effects occur in a dose-related fashion. In addition, different anesthetics, sodium pentobarbital (P) or chloral hydrate (CH), were compared and demonstrated that there was no significant difference in results. This implies that there is not an anesthetic-morphine interaction occurring. These results suggest opiate agonist depression of myocardial function acts on opiate receptors, causing primarily a chronotropic effect.
We have developed a modified isolated working rat heart model to study the effect of potassium and magnesium cardioplegia given just prior to reperfusion, "terminal cardioplegia," on preservation of aortic flow following a standard ischemic insult. The model incorporates a short-term calcium challenge at the beginning of reperfusion to accentuate ischemic injury. All hearts were given initial potassium cardioplegia and subjected to 30 min of normothermic ischemia. Terminal cardioplegia was given for the 2 min prior to reperfusion. Calcium-challenged hearts were reperfused initially with calcium-enriched reperfusate and then switched to standard reperfusate. Aortic flow prior to and 60 min after ischemia was used to determine functional protection. Hearts recovered 82 +/- 3% of preischemic aortic flow when reperfused with normocalcemic reperfusate. When the initial reperfusate was enriched with calcium, aortic flow was only 43 +/- 4% of control. Hearts given terminal magnesium cardioplegia and then challenged with calcium-enriched reperfusate recovered 79 +/- 4% of control aortic flow. Hearts given terminal potassium cardioplegia recovered only 53 +/- 5% of control aortic flow when challenged with calcium-enriched initial reperfusate. Our results indicate that the recovery of aortic flow is significantly reduced by short-term postischemic calcium challenge. This damage is blocked by terminal magnesium cardioplegia, but not by terminal potassium cardioplegia.
We report an improved method for the synthesis and purification of [11C]methylcholine from the precursors [11C]methyliodide and 2-dimethylaminoethanol (deanol). Preparation time, including purification, is 35 min postbombardment. Forty millicuries of purified injectable [11C]choline were produced with a measured specific activity of greater than 300 Ci/mmol and a radiochemical purity greater than 98%. The decay corrected radiochemical yield for the synthesis and purification was approximately 50%. Residual precursor deanol, which inhibits brain uptake of choline, is removed by a rapid preparative high performance liquid chromatography (HPLC) method using a reverse phase cyano column with a biologically compatible 100% water eluent. Evaporation alone did not completely remove the deanol precursor. Brain uptake of the [11C]choline product was six times greater after HPLC removal of deanol because doses of less than 1 microgram/kg significantly inhibit [14C]choline brain uptake.
A 69-year-old patient with advanced stomach cancer (Borrmann III) was treated with a combination chemotherapy regimen of cis-platinum administered one week after a course of PSK and FT-207. The maximum dosage of CDDP administered was gradually increased step by step from 20 mg/day to 40 mg/day every week. A remarkable decrease of tumor size was observed upon stomach x-ray and endoscopical examination. The cancer marker, serum CEA, determined by RIA also decreased from 59 ng/ml to 3.5 ng/ml. Moreover, no gastrointestinal disturbance was observed during this trial. From the results experienced, in this case, the combination therapy of PSK and FT-207 with CDDP was considered to be one of the most effective antineoplastic therapies available for stomach cancer, suppressing the gastrointestinal disturbances which are usually induced by CDDP administration alone.
Generator produced 68Ga-labeled platelets could be useful for positron emission tomographic (PET) studies of thrombosis or atherosclerosis. To label platelets with 68Ga, we have studied the effects of trace metals in elutions of 68Ga from 68Ge. Studies were conducted on the formation of lipophilic 68Ga complexes 8-hydroxyquinoline, tropolone, and mercaptopyridine-N-oxide (MPO). Parameters such as pH, buffers, concentration of ligand, and stability with time were investigated. High performance liquid chromatography and instant thin layer chromatography were used to quantitate formation of the 68Ga complex. Platelets from human, dog, and rabbit plasma were incubated with the 68Ga complexes and the percent labeling determined. Accumulation of platelets in the catheter scraped aorta of the rabbit was determined by PET imaging, tissue counting, and autoradiography. Gallium-68 MPO gave 40-60% labeling of rabbit platelets with higher accumulation in the scraped aorta compared to the normal.
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An unusual tumor of the trachea was found in a 76-year-old woman. The tumor resembled an adenoid cystic carcinoma in having many cystic spaces, but the fairly uniform tumor cells gradually merged with the myxomatous or hyalinous stroma, and foci of squamous metaplasia and glycogen-rich adenoma-like components were also observed. S-100 protein was demonstrated immunohistochemically in the tumor cells. This tumor was diagnosed as a pleomorphic adenoma (benign mixed tumor) of the trachea.
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