bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECT OF A SYNTHETIC SULFATED POLYSACCHARIDE (SN‐263)* ON GASTRIC PEPTIC ACTIVITY IN HUMANS
Authors: Sun David C. H. 
Published: December 2006

SummaryThe effect of oral administration of a synthetic sulfated polysaccharide, amylopectin sulfate (SN‐263), on gastric peptic activity was studied in 49 patients with chronic duodenal ulcer. Five dose levels were studied: 100 mg, 200 mg, 300 mg, 500 mg, and 800 mg. A significant depression of gastric peptic activity was observed after oral administration of 200 and 300 mg of SN‐263. This inhibitory action appeared within 15 min and lasted for 45 min. At higher dose levels of 500 and 800 mg, a longer duration of inhibition lasting for 75 min was observed. Oral administration of 100 mg of SN‐263 was ineffective as an anti‐peptic agent. SN‐263 had no effect on the acidities of the gastric contents.When 200 mg of SN‐263 was given at two‐hour intervals, the inhibitory effect of the second administration of SN‐263 on gastric pepsin concentration was similar to that of the first dose. There was no evidence of a cumulative action. The addition of an anticholinergic drug, propanthelie bromide, which will inhibit acid and pepsin secretions at their source, further enhanced the action of SN‐263 as an antipeptic agent. Since SN‐263 exerts no antacid or anticholinergic action, its inhibitory effect on peptic activity must be a direct one.
CARBOHYDRATE HISTOCHEMISTRY OF GASTRIC EPITHELIAL SECRETIONS IN DOG
Authors: Spicer S. S. , Sun D. C. H. 
Published: December 2006

SummaryHistochemical methods specific for carbohydrate constituents distinguish a number of widely different entities in several types of gastric epithelial cells in the dog.The surface gastric epithelium reveals basophilia, indicating mucosubstances rich in both carboxyl groups (presumably sialic acid) and sulfate esters. The carboxyl‐type basophilia predominates in the superficial convolutions, and that attributed to sulfate is found in the foveolar walls. The strong reactivity with both the periodic acid‐Schiff (PAS) and the periodic acid‐para diamine (PAD) methods for vicinal‐hydroxyls indicates presence of hexose‐ or deoxyhexose‐rich mucosubstances in both of these areas. Susceptibility of basophilia to blockage by initial periodate‐meta diamine treatment points to presence of vicinal‐glycols in proximity of the acid groups in surface epithelium mucin. The surface epithelium in the pylorus differs slightly in that its secretion is less strongly basophilic.The mucous neck cells secrete an apparently neutral mucosubstance which differs from the surface epithelium in its lack of both PAD reactivity and basophilia. The parietal cells also form a diastase‐resistant, neutral, carbohydrate‐rich substance. The zymogen cells are abundant, deep in the glands of the cardiac portion and the body of the stomach, but less numerous in the intermediate zone. They contain apical granular secretion apparently rich in sulfated mucosubstances. Lack of reactivity toward vic‐glycol methods, resistance of alcianophilia or azurophilia to a previous periodate‐meta diamine sequence, and resistance of mixed diamine staining to previous periodate oxidation indicate absence of residues with unsubstituted adjacent hydroxyls (e.g., hexose or deoxyhexose), in this acid mucosubstance.The pyloric glands resemble mucous neck cells in their strong PAS staining and lack of PAD reactivity, but differ in that they show a weak staining indicative of sulfomucin.
AUGMENTED HISTAMINE TEST
Authors: Sun David C. H. , Ryan M. L. , Chang P. L. , Keogh R. 
Published: December 2006

Summary(1) The value of and the applications for the augmented histamine test are discussed. Proposals are put forth in reference to the nomenclature of gastric acid and the interpretation of the augmented histamine test for routine clinical purposes.(2) The results of the augmented histamine test in 14 patients with proven gastric ulcer and in 68 subjects with proven duodenal ulcer are presented. The mean acid outputs of men with gastric ulcer (all sites) for basal and histamine‐stimulated secretion were about one‐half that of men with duodenal ulcer. These differences were significant, statistically.(3) Duodenal ulcer patients with complications had a significantly higher maximal acid output to histamine than those without complication. The finding of a maximal acid output greater than 40 mEq/hr is highly suggestive of the presence or the imminence of a complication.(4) We prefer the use of the augmented histamine test as a routine gastric analysis procedure, since it is a quantitative test and, as such, gives reproducible acid output in the same individual, provides an estimate of the parietal cell mass, and gives a positive lead to the diagnosis of Zollinger‐Ellison syndrome.
RELEASE OF THROMBOPLASTIN AFTER THERMAL INJURY*
Authors: Guest M. Mason , Bond Ted P. 
Published: December 2006

SummaryMicrocirculatory flow following a severe burn is hindered by the formation of aggregates of erythrocytes which frequently completely fill the lumena of small arteries, arterioles, and venules. On the arterial side, clusters of cells are often too large to enter branching vessels; large aggregates grow from smaller clusters, and vessels fill with packed, adherent erythrocytes for some distance proximal to divarications. However, if erythrocytes enter capillaries, they move independently of other erythrocytes and are transformed into hollow paraboloids as they are in the absence of trauma to tissue or in the absence of infused thromboplastin.The hypothesis that aggregation of erythrocytes is caused either directly or indirectly by release of thromboplastins from damaged tissue is based upon the following evidence:1) Following a severe burn the observed phenomena in cinephotographic film recorded at conventional film speeds and up to 3200 frames per sec, are similar to those observed following the infusion of thromboplastin.2) Changes in clotting and fibrinolytic components following a severe burn can be duplicated by the infusion of canine thromboplastin. The most pronounced alteration is the shortening of the Stypvin time which is highly dependent upon the concentration of phospholipids.3) Complete fibrinogenolysis results in improvement in microcirculatory flow following a severe burn and following the infusion of thromboplastin, indicating that an altered fibrinogen, or possibly fibrin, is involved in the adherence between erythrocytes in both experimental conditions.
HEMODYNAMIC EFFECTS OF METABOLIC ACIDOSIS IN CHOLERA: IMPLICATIONS FOR FLUID REPLETION IN SEVERE BURNS*
Authors: Enson Y. , Harvey R. M. , Lewis M. L. , Greenough W. B. , Ally K. M. , Panno R. A. 
Published: December 2006

SummaryTo summarize the train of events in cholera as we visualize them: Severe dehydration results in hypovolemia, and cardiac output and all pressures fall. Acidosis causes peripheral venous constriction, thereby reducing the capacity of the venous reservoirs and maintaining, to some extent, venous return to the heart. Fluid administration without correction of acidosis favors a disproportionate venous return to the heart and pulmonary circulation. Alleviation of acidosis during fluid replacement results in a more even distribution of the circulating blood volume and reduces the possibility of engorgement of the pulmonary bed.This mechanism may also explain the occasional appearance of pulmonary congestion in patients with severe burns and metabolic acidosis. Fluid therapy without correction of acidosis in such patients may also favor a disproportionate venous return to the heart and pulmonary circulation. Treatment of the acidosis may be expected to reduce, in these patients as well, the possibility of pulmonary engorgement.In conclusion, these data indicate that the blood pH affects the distribution of the circulating blood volume and thereby influences the volume of blood returning to the heart, and through it, the central blood volume, ventricular filling pressures and cardiac output. We suggest that the site of action is in the peripheral venous bed.
METABOLIC EFFECTS OF TOPICAL SILVER NITRATE THERAPY IN BURNS COVERING MORE THAN FIFTEEN PERCENT OF THE BODY SURFACE*
Authors: Burke J. F. , Bondoc C. C. , Morris P. J. 
Published: December 2006

SummaryElectrolyte and water balance studies have been carried out on 20 patients with total body surface burns ranging from 15 to 85%. All patients were treated with 0.5% aqueous AgNo3 applied directly and continuously to the burn wound. The balance studies showed that the loss of Na through the burn wound was directly related to the square area of burn surface and was constant from day to day. Based on this steady and predictable loss of Na in the uninfected burn, a formula has been derived predicting the daily Na replacement necessary to cover the obligatory loss via the burn wound plus the requirements of normal metabolism. This formula has provided an accurate prediction of daily Na requirements in the treatment of thermal burns of widely varying extent, in patients of widely different ages, as judged by water and electrolyte balance studies.The formula provides a useful guide to the level of Na replacement required. Exact tailoring must be carried out to fit the needs of each patient. The direct monitoring of the accuracy of Na replacement by way of the serum Na level has been found cumbersome but intermittently necessary. In the burn patient in metabolic balance and taking a reasonable diet, the level of urinary excretion of Na has been found to be an accurate prediction of serum Na level. A urinary excretion of 40 mEq of Na per liter or above has uniformly reflected a normal serum Na level. The urinary Na has been used as an indicator of accurate replacement therapy replacing the majority of serum Na determinations.
EARLY FLUID TREATMENT OF SEVERE BURNS: HEMODYNAMIC ALTERATIONS AND THE USE OF DEXTRAN AND BLOOD
Authors: Haynes B. W. 
Published: December 2006

SUMMARYThe early fluid treatment of severe burns at the Medical College of Virginia has emphasized replacement therapy, adequate quantities of electrolyte, water and colloid with the Evans’ Formula as a clinical reference. The use of dextran over a 15‐year‐period has been associated with good clinical response and circulatory maintenance and freedom from reaction. As a rule, the quantities of red cells destroyed during the first 48 hr are sufficiently small as to make the need for red cell replacement unnecessary. Significant red cell transfusion after this period is required commonly.Hemodynamic alterations after severe burns may be divided into three phases. The first phase generally lasts one to two days and is characterized initially by hypotension, which will respond rapidly to plasma volume expansion. Blood pressure becomes normal while blood volume is deficient and cardiac output is low. Total peripheral resistance is increased.A second or intermediate phase occurs after the first or second day and is characterized by maintenance of a normal blood pressure, a progressive increase in plasma volume, and a falling peripheral resistance coincident with a rising cardiac output. Therapeutic support emphasizes fluid and electrolyte maintenance, replacement of red cell deficits, and good nutrition, leading to wound healing and recovery.A third and terminal phase may occur in the extensive burn (4 to 20 days post‐burn) in which the blood pressure falls gradually. Shortly after hypotension occurs, the cardiac output may be normal or elevated, but falls with persistent hypotension. Blood volume expansion and vasoconstrictors may be of only temporary benefit. The control of sepsis may be the crucial point in maintaining circulatory efficiency.
IMMUNOLOGIC SEQUELAE OF THERMAL INJURY*
Authors: Rapaport F. T. , Milgrom F. , Kano K. , Gesner B. , Solowey A. C. , Casson P. , Silverman H. I. , Converse J. M. 
Published: December 2006

Summary1) Thermal injury induces a marked inhibition in the ability of tuberculin‐sensitive guinea pigs to respond to intradermal challenge with tuberculin. The effect is most marked during the first and second weeks after burning, but may persist as long as five weeks.2) Thoracic duct lymph samples obtained from severely burned rats contain a hemagglutinin specific for rat erythrocytes. This hemagglutinating factor has been identified as a 7S gamma globulin, and may constitute an immune response to altered autologous tissues.
BIOCHEMICAL and CLINICAL ASPECTS OF MEGATHROMBOCYTES
Authors: Karpatkin Simon 
Published: December 2006

SummaryHuman platelets have been separated into heavy and light populations by differential centrifugation in specific density media. The heavy‐platelet population has an average volume approximately 2–2.4‐fold that of the light‐platelet population. All eleven enzymes of the Embden‐Meyerhof pathway were examined in both platelet populations. Six of the eleven were found to have a twofold greater content/g wet weight in heavy platelets compared to light platelets. Three of these six: hexokinase, phosphofructokinase, and glyceraldehyde‐3‐P‐dehydroge‐nase were found to be rate‐limiting for glycolysis. The reductive capacity of heavy vs. light platelets was also examined. Heavy platelets contained 1.9‐fold greater GSH, 1.7‐fold greater DPNH, and 1.2‐fold greater TPNH than light platelets. Heavy platelets also contained 1.8‐fold less lipid peroxidation products than light platelets and were 2.4‐fold more resistant to lipid peroxidation catalysed by 0.1 mM FeCl3.Kinetic studies in humans with Se75‐selenomethionine revealed that heavy‐large platelets were young platelets, recently released from the bone marrow, and suggested a transition of heavy‐large platelets to lighter‐smaller platelets.Clinical studies in humans revealed the usefulness of the measurement of the percentage of large platelets (or megathrombocytes) in estimating platelet turnover. An excellent correlation was found between the percentage of megathrombocytes on EDTA peripheral smear (and as determined by volume with Coulter Counter) and the number of megakaryocytes in the bone marrow in all platelet disorders examined with low or normal platelet counts, r=0.70 P < 0.001, except in megaloblastic anemia. In megaloblastic anemia, an increase in the percentage of megathrombocytes was usually found, but in the absence of increased megakaryocyte number. Increased megathrombocyte number (% megathrombocytes X platelet count) could be used to predict compensated thrombocytolytic states: normal platelet counts in the presence of increased platelet turnover. This was detectable in 84 patients. Platelet survival studies with DFP32 were obtained in eight of these patients and found to be exponential and significantly shortened in all eight. Megathrombocyte number was also examined in various clinical disorders (with normal platelet counts) in which increased platelet turnover might be suspected. Significant elevations were noted in SLE (68%), rheumatic heart disease with severe valvular damage (63%), disseminated intravascular coagulation (60%), chronic autoimmune thrombocytopenic purpura “in remission” (55%), and diabetes mellitus with retinopathy (47%).
FACTORS AFFECTING HEMOSTATIC PLUG FORMATION IN AN EXTRACORPOREAL MODEL*
Authors: Didisheim Paul , Pavlovsky Miguel , Kobayashi Itsuro 
Published: December 2006

SUMMARYA model is described for the study of factors affecting hemostasis. It consists of a Teflon extension of the carotid artery of rats. Holes of precise diameter are then produced in the extension with a micromanipulator and the aid of a microscope. The bleeding time of these holes is then recorded.The principal advantage of this method is that it makes possible the production in the “blood vessel” of holes the diameters of which are known with a high degree of accuracy, under known conditions of intravascular pressure.With holes below 75 μ in diameter, prolongation of the coagulation time with heparin did not affect the bleeding time. With increasing hole diameters, or with increasing intravascular pressure, coagulation time did affect the bleeding time. Bleeding time could be predictably modified by increasing or decreasing blood pressure. There is a striking interrelationship of these factors in influencing the bleeding time.Intravenous pyridinolcarbamate (12 mg/kg) significantly prolonged the bleeding time for a 20‐minute period. At a lower dose (8 mg/kg), which was ineffective in prolonging the bleeding time, pyridinolcarbamate partially inhibited the shortening of the bleeding time that follows the administration of epinephrine.Intravenous polyvinylpyrrolidone (PVP), 750 mg/kg, caused a sustained prolongation of the bleeding time, lasting more than three hours.
PLATELET MEMBRANE MUCOPOLYSACCHARIDES: SOME RELEVANT OBSERVATIONS*
Authors: O'Brien John R. 
Published: December 2006

SummaryBiochemical analysis disorganizes the membrane before study; thus there are advantages in studying reactions of intact cells. Alcian blue (AB) causes aggregation of washed red cells–presumably because of membrane staining and a charge effect. Neuraminidase or the presence of plasma prevents this aggregation. AB added to platelets without plasma causes immediate aggregation; added to platelet‐rich plasma at low concentration, it potentiates ADP‐induced aggregation. A higher concentration stains the granules and causes release and delayed aggregation. Aspirin inhibits release induced by ADP but hardly influences that induced by AB. This suggests that aspirin inhibits an early stage of release, since adding AB shows that the later stages are still intact. During release, platelet factor 4, a glycoprotein, is liberated. Thereafter the platelet membrane stains with ruthenium red, but not before. Neuraminidase removes sialic acid. It prevents red cells but not platelets from aggregating with AB, and it exposes platelet factor 3 sites on platelets but not on red cells.These findings are believed to relate to the organization of mucopolysaccharides and glycoproteins in the platelet membrane.
NATURE OF THE PLATELET DEFECT IN THE WISKOTT‐ALDRICH SYNDROME*
Authors: Baldini Mario G. 
Published: December 2006

SummaryThe thrombocytopenia in patients with the Wiskott‐Aldrich syndrome was found to be due to increased platelet destruction caused by an intracorpuscular cell defect. Multiple abnormalities of platelet structure, function, and metabolism were also observed. Platelet adhesiveness to collagen, and platelet aggregation with ADP, collagen, and epinephrine were reduced or absent in the affected patients and partially depressed also in the clinically normal female carrier. Of various biochemical alterations, the decrease in platelet glycogen and in hexokinase activity were most prominent. The latter defect was, however, not rate limiting. Although these platelets were capable of phagocytosis, the typical metabolic reaction to it, with increase in the citric acid cycle activity, did not occur. This reaction was severely depressed also when other aggregating stimuli such as ADP, collagen, and epinephrine were used. Thrombin, on the other hand, could produce both aggregation and stimulation of the citric acid cycle. It is concluded that platelets in the Wiskott‐Aldrich syndrome have a basic defect in energy metabolism. Although there is no intrinsic block in anaerobic and aerobic glycolysis, stimulation of the citric acid cycle does not occur with common aggregating (and degranulating) agents, most probably because a physiologic “regulator” of this metabolic pathway, the energy of which is indispensable for normal platelet aggregation, is lacking or is not made available. Thrombin can either liberate or substitute for such regulator.
IMMUNOTHERAPY OF CHRONIC MYELOCYTIC LEUKEMIA: EFFECTS OF DIFFERENT VACCINATION SCHEDULES*
Authors: Sokal Joseph E. , Aungst C. William , Snyderman Michael , Gomez German 
Published: December 2006

In a clinical trial of immunotherapy in chronic myelocytic leukemia, 62 patients received repeated intradermal injections of BCG‐cultured cell mixtures, while 16 were vaccinated with BCG alone. The lymphoblastoid cell lines used for vaccination were established from blood of patients with advanced myeloid leukemia and were reactive with “specific” primate antisera against myeloid leukemic cells. Both sensitization to target cell antigens and substantial general increases in delayed hypersensitivity responses were recorded among immunized patients. Major immunologic complications (hypersensitivity and “autoimmune” phenomena) were observed in 10 patients. These complications were attributable to the BCG content of vaccines, and their incidence correlated with intensity of immunologic stimulation.Data from cases in which intermittent busulfan therapy was used provided suggestive evidence that immunotherapy (either with BCG‐cell mixtures or with BCG alone) prolonged unmaintained remissions in one‐third of the patients. Among 48 “good‐risk” patients, there was an inverse correlation between intensity of immunologic stimulation and survival. The survival of 18 patients who received the most intensive vaccination schedule was identical to that of controls. Survival of the other 30 patients was significantly better (p = 0.03), with an increase of 2 years in median survival. Survival of 30 poor‐risk patients (24, most intensive vaccination schedule) was identical to that of controls.We conclude that immunologic stimulation may produce worthwhile prolongation of life in CML but that overly aggressive schedules of immunotherapy abrogate this effect. Our experience raises the question whether results in other clinical trials of immunotherapy may have been adversely affected by excessive frequency or dosage of immunologic stimulants.
REVIEW OF CLINICAL CRITERIA OF BRAIN DEATH
Authors: Molinari Gaetano F. 
Published: December 2006

SummaryA spectrum of descriptive definitions of death has been formulated based on a variety of observations using currently available clinical methods. These definitions vary widely in objectivity and some fail to distinguish the inevitability of death or irreversible coma from the fact of death. A hopeless prognosis may be an adequate criterion for termination of artificial resuscitation, but the bioethical issue involved is one of “passive” euthanasia and not brain death. A hopeless prognosis without a pronouncement of death itself would seem inadequate grounds to remove viable organs for transplantation.When organ donation is contemplated, the declaration of death as a past event must be based on cerebral rather than on cardiovascular criteria. At this point in the history of the art and science of medicine, the highest degree of assurance that the brain is dead may be achieved in the shortest possible time, only by using multiple independently measured variables including clinical criteria, electrophysiologic criteria (the EEG), and assessment of cerebral circulation determined either directly or indirectly. As science and technology improve, the degree of objectivity and facility in obtaining objective criteria will also improve.
THE EEG IN DETERMINATION OF BRAIN DEATH
Authors: Bennett Donald R. 
Published: December 2006

SummaryThe values and limitations of electroencephalography in the determination of brain death have been reviewed. Electrocerebral silence per se does not necessarily mean total or irreversible brain dysfunction. In the state of brain death the EEG is always silent; however, ECS does not always mean brain death. Electroencephalography, when properly used, can be a most helpful aid to the physician. Clinical criteria alone for the establishment of brain death may lack specificity, and occasional cases with potentially remediable lesions may be overlooked. The diagnosis of brain death cannot be made by only one test. The physician has to make his decision based on the entire clinical picture and results of the studies that are available to him.