Esophageal medication bezoar in a patient receiving enteral feedings and sucralfate.
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Biomedical subjects
Publications and source records attributed to W Anderson.
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We have utilized the 6-day air-pouch model in rats to study the local tissue response to interleukin-1 exposure. Injection of either recombinant human interleukin 1 alpha (rIL-1 alpha) or interleukin 1 beta (rIL-1 beta) directly into preformed air pouches caused a 10- to 100-fold increase in the number of white blood cells present within the pouch. On a weight basis, rIL-1 beta was more active than rIL-1 alpha. Polymorphonuclear neutrophils (PMN) represented the majority of cells entering the pouch following either a single injection or repeated daily injections of rIL-1 alpha or rIL-1 beta. Significant increases in the number of mononuclear cells present were observed only following repeated injections. Repeated injections of rIL-1 beta, but not rIL-1 alpha, also caused the accumulation of large amounts of fluid within preformed pouches and a grossly apparent thickening of the connective-tissue lining of the pouch. Microscopic examination of stained sections of pouch lining tissue indicated a proliferation of the connective-tissue elements of the lining and deposition of large quantities of extracellular collagen within the pouch wall. These findings are entirely consistent with a role for interleukin 1 in the development and perpetuation of inflammatory reactions.
The pseudopeptide [Leu14-psi-CH2NH-Leu13]-bombesin inhibited 125I-GRP binding to membrane preparations of frog cerebrum and peptic cells, rat cerebral cortex and pancreas with IC50's of 44-250 nM (using 180 pM 125I-GRP). It was unable to stimulate amylase release from rat pancreatic acini, but antagonized competitively BB stimulated amylase release with an IC50 of 130 nM. By contrast the pseudopeptide stimulated pepsinogen secretion from frog esophageal peptic cells with an efficacy relative to bombesin of 36%, and with an EC50 of 30 nM. By virtue of its partial agonist activity it inhibited submaximal BB stimulated responses to a level equal to the pseudopeptide alone. Thus [Leu14-psi-CH2NH-Leu13]-BB differentiates certain BB receptors by exhibiting selective intrinsic efficacy.
A 48-yr-old man with chronic myelogenous leukemia and basophilia developed a duodenal ulcer and hemorrhage. Gastric analysis revealed basal hyper-secretion of acid (33.1 mEq/h) and pepsin (44.5 x 10(-4) peptic units/h). Blood, serum, and urine histamine was elevated and serum gastrin was normal. Although acid output was markedly suppressed with ranitidine (50 mg i.v.), pepsin secretion was only inhibited 63% and had returned to basal levels by the sixth hour. Maximal acid output does not suggest a trophic effect of histamine in this patient. The previously reported cases of basophilic leukemia and gastric hypersecretion or duodenal ulcer disease are reviewed.
In order to define the early transient responses of peptic cells to stimulation, we have modified the acidified hemoglobin substrate digestion method for pepsin to provide a very sensitive, linear (10-250 ng/ml), reproducible, inexpensive (less than 3 cents/sample) and simple semi-automated assay. Using a specially designed perifusion chamber, this method was used to accurately measure secretion at 1 min intervals from approximately 3 mg of isolated peptic glands from the esophageal peptic organ of R. catesbeiana, containing approximately 150 micrograms pepsinogen. Responses to carbachol applied for 1, 2 and 4 min could be described in discrete 1 min intervals. Secretion stimulated by carbachol (1-2 min) peaked at 200-300% of basal and upon withdrawal decayed with t1/2 approximately 3 min. Atropine added to continuous carbachol stimulation inhibited secretion with t1/2 approximately 4 min, indicating rapid metabolism of activated messengers.
Eighty subjects were assigned to two conditions in which readings of blood pressure were taken simultaneously by an observer using a Hawkesley Random Zero Sphygmomanometer and by a Pollenex BP-850 Automatic Sphygmomanometer either in its standard form or silenced to stop it bleeping whilst recording blood pressure. Forty subjects were assigned to a comparison group, where simultaneous readings by two observers were taken from one Hawkesley. Analyses performed included correlations, t-tests, and Bland and Altman's (Lancet, 1986, i: 307-310) differences against the mean method. Cues from observer behaviours or the bleeping Pollenex resulted in higher concordance between measures in the standard condition and the Hawkesley comparison condition. However, even in the silent condition the Pollenex proved to be as reliable a monitor of blood pressure as the Hawkesley.
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Bleeding from an induced gastric mucosal wound was monitored for 2 h in a rat model, in which normal hemostasis was disturbed mechanically by perfusing the lesion with saline. The hemorrhage was characterized by continuous bleeding and/or episodes of spontaneous rebleeding, as often seen in patients with gastric hemorrhage. The antifibrinolytic agent, tranexamic acid, significantly reduced total bleeding volume and number of rebleeding episodes, suggesting that plasmin-induced fibrinolysis might aggravate gastric mucosal hemorrhage.
Antibody responses to malarial antigens were determined in 614 serum samples collected from the Wopkaimin population of the Star Mountains of Papua New Guinea. In point prevalence surveys made in 1982-1983, 33.7% of the persons examined were infected with Plasmodium falciparum, P. vivax, or P. malariae. Of these, 72.9% were infected with P. falciparum. In a standard fluorescent antibody test, highest level responses were to P. falciparum, followed by P. malariae, P. vivax, and P. ovale. A strong correlation was found between results of the fluorescent antibody tests and those obtained in an enzyme-linked immunosorbent assay using P. falciparum antigens. The failure of immune responses to eliminate these species of Plasmodium in this highly isolated population is discussed.
In summary, UMC benefitted from the planning process and resulting information systems plan because the Medical Center was better able perform the following tasks: Understand organizational interrelationships; Identify organizational and user needs; Set enterprise-wide priorities; Document information systems needs, priorities, and relationships; Ensure management and user agreement on system direction and sequence prior to system implementation; Maximize opportunities for cost effectiveness and operational efficiency; and Define functional requirements of systems. Essential to the above tasks and resulting benefits were an executive management team at UMC which worked together to plan, and departmental managers who assessed their individual needs in the light of UMC's overall strategy.
The muscarinic receptors coupled to pepsinogen secretion on isolated frog esophageal peptic cells have been characterized using functional and radioligand binding techniques. N-[3H]methylscopolamine [( 3H]NMS) binding to intact cells was complex and indicative of a high affinity, low capacity site and a high capacity uptake site. Binding to the high capacity site was inhibited by atropine with high affinity (IC50, 3 nM) and by imipramine and propranolol with IC50 values of 70 and 270 nM, respectively. After inhibition of uptake by 30 microM propranolol, [3H]NMS bound to a single population of high affinity sites (KD, 125 +/- 16 pM), which exhibited binding site maximum of 2.1 fmol/10(6) cells, equivalent to 1260 sites/cell. Binding to these sites was reversible, stereoselective and inhibited by muscarinic receptor agonists with an order of potency: oxotremorine greater than acetylcholine greater than carbachol greater than bethanechol and by antagonists with an order of potency:atropine greater than 4-diphenylacetoxy-N-methylpiperidine methobromide greater than pirenzepine greater than AF-DX 116 (11-2[2-[[diethylamino) methyl]-1-piperidinyl]acetyl]-5, 11-dihydro-6H-pyrido[2,3-b][1,4]-benzodiazepine-6-one). Pepsinogen secretion was stimulated by the agonists with an order of potency: acetylcholine greater than or equal to carbachol greater than oxotremorine greater than bethanechol. Atropine, pirenzepine and AF-DX 116 competitively inhibited carbachol-stimulated pepsinogen secretion with pA2 values of 9.58, 7.37 and 6.68, respectively, which correlated with their log (inhibition constants) for receptor binding. By contrast, agonists with significant efficacy exhibited EC50 values which were 20 to 90 times lower than their inhibition constants for binding which suggests the possibility of "spare" muscarinic receptors. Our findings indicate that functional muscarinic receptors on peptic cells exhibit similar characteristics to the high affinity sites labeled by [3H]NMS.(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the susceptibility of cyanotic neonatal myocardium to ischemia and the effectiveness of cardioplegia for protection, we induced cyanosis in 2- to 5-day-old lambs (n = 16) by connecting the left atrial appendage to the main pulmonary artery with a 4 mm polytetrafluoroethylene graft, which produced an arterial oxygen tension of 34.1 +/- 1.2 torr. Seven to 10 days after creation of the model, isolated perfused hearts from cyanotic animals were subjected to 2 hours of ischemia with topical cooling or crystalloid cardioplegia (K = 30 mEq/L) for myocardial protection (both at 15 degrees C). Identical studies were performed on hearts from 16 normoxemic neonatal lambs 5 to 14 days old. The overall effect of cyanosis was to produce a significant impairment in recovery of maximum developed pressure (p less than 0.05) after ischemia. The overall effect of cardioplegia was to produce a significant improvement in recovery of maximum developed pressure, developed pressure at V10 (the balloon volume to produce an end-diastolic pressure of 10 mm Hg during the preischemic period), and peak rate of pressure rise at V10 (p less than 0.05). The protective effect of cardioplegia was more prominent in cyanotic hearts than in normoxemic hearts for recovery of maximum of peak rate of pressure rise and peak rate of pressure rise at V10 (p less than 0.05). End-diastolic pressure at V10 and the diastolic stiffness constant at 10 and 20 mm Hg were all significantly higher after ischemia in the cyanotic hearts than in the normoxemic hearts (p less than 0.05). We conclude that in neonatal hearts cyanosis may increase the vulnerability to ischemia and cardioplegia appears to enhance the recovery of systolic but not diastolic function in these hearts.
The Minnesota Department of Health has completed a 2-year feasibility study comparing the completeness and accuracy of information from pathology-based cancer ascertainment with that of the traditional surveillance method based on hospital discharge records. Overall, for incident cancers, the primary site designation of the pathology-based system was correct for 94.5% of the cancers, and the histologic designation was correct for 97.0% of the cancers. For prevalent cancers the accuracy of both site and histology designation was inadequate at 81.0 and 76.8% respectively. Pathology-based ascertainment was more complete than discharge-based surveillance (98.4% vs. 96.6%), which reflected the growing number of cancers diagnosed in hospital outpatient departments and medical clinics. The major limitation of the pathology-based system was the inability to determine from written pathology reports whether the cancer was newly diagnosed. However, when asked, pathologists correctly determined the incidence status for approximately 75% of the cancers. In light of the results of the feasibility study, Minnesota is implementing a pathology-based system as a cost-effective, scientifically valid method to meet the state's current and future needs for cancer surveillance.
Films of certain acrylate-methacrylate copolymers of varying cation (quaternary ammonium) content were cast from three different solvents: acetone, chloroform, and ethanol; their permeability to urea was determined at 30 degrees C. In films containing 66 mole cation mol-1 polymer chain, and cast from acetone, chloroform or ethanol, the permeation rates were 480,900 and 2807 mg h-1, respectively. Differences in permeation rates were however less significant when polymers of cation content lower than 46 mole cation mol-1 polymer chain were used to form films. This observation may relate to differences in the degree of dissociation of the polymer in the different solvents.
To determine possible differences in the cyclic AMP-dependent protein kinases of normal and psoriatic human fibroblasts, the levels of the regulatory subunits (RI and RII, respectively) of protein kinase I and protein kinase II were quantitated by photoaffinity labeling with 8-azido[32P]cAMP. The level of RII was significantly decreased, or was undetectable, in cytosol prepared from fibroblasts from five psoriatic subjects when compared to RII levels found with normal human fibroblasts. The level of cytosolic RI was decreased in fibroblasts from four psoriatic patients and was within the normal range for one diseased patient when compared to RI levels in normal human fibroblasts. The elution profile from a DEAE-cellulose column of protein kinase activity in the soluble fraction from two psoriatic patients also showed a decrease in type I kinase activity and the complete absence of type II kinase activity. Other results indicate that the level of RI in erythrocyte membranes from psoriatic subjects is significantly decreased when compared to that of erythrocyte membranes from eight normal subjects. A significant correlation (P less than 0.001) was observed between the severity of the cutaneous manifestation of the disease and the level of RI in psoriatic erythrocyte membranes. The changes noted in the levels of RI and RII in cell types other than those thought to be specifically involved in the proliferative epidermis disorder of the disease suggest a general protein kinase deficiency.
Blastocysts recovered from control or indomethacin-treated (10 mg/kg s.c. twice daily starting on Day 4.5 of pregnancy) donor rabbits were transferred to the uteri of Day-6 or 6.5 pseudopregnant recipients. The minimal time required to cause an increase in capillary permeability in the endometrium underlying control blastocysts was approximately 9 h. Blastocysts derived from the indomethacin-treated donors were depleted of PGE and PGF (determined by RIA) and were unable to produce any increase in capillary permeability during the same time period, although after 46 h in vivo the diameters of the implantation swellings related to control or indomethacin-treated blastocysts were not different. This suggests that, in the untreated recipients, blastocysts depleted of PGs can become replenished and then release these PGs in a site-directed manner. Indomethacin thus causes a delay rather than a complete inhibition of implantation. Incubation of the indomethacin-treated blastocysts in vitro led to replenishment with PGs, but such replenished blastocysts failed to induce an increase in capillary permeability within the same time-frame as control blastocysts. Evidence is presented that indomethacin is probably not the cyclooxygenase inhibitor of choice, since it interferes with PG uptake and efflux. Such an action could explain the failure of the replenished blastocysts to induce a normal increase in capillary permeability.
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