Production Of Anemia Research Articles

Exploring the role of the endogenous opiate system in the pathogenesis of anemia in an opiate receptor knock-out model of Restless Legs Syndrome

Restless Legs Syndrome (RLS) is characterized by bothersome leg discomfort accompanied by an urge to move to obtain relief and symptoms are worse at night and on lying down. There is at least partial and temporary relief with activity. It is also an opioid responsive disorder, often accompanied by iron deficiency with or without anemia, and inflammation may be a precipitating factor in some cases. We created two in-vivo opiate receptor knock out mouse models of RLS – a triple opiate receptor knock-out mouse and a mu opiate receptor knock-out mouse. Both sets of animals were restless during the sleep period as is also true of RLS. Both of our knockout models showed statistically significantly decreased Hemoglobin and Hematocrit indicating anemia and both models showed statistically significant decreases in serum iron suggestive of either iron deficiency anemia or inflammatory anemia. The rest of the hematologic studies were not consistent enough to determine which of these two types of anemia was present in either model. An additional experiment in normal wild type mice showed a statistically significant decrease in serum iron when an opiate receptor blocker was used. To our knowledge this is the first demonstration that deficiency of endogenous opioids might play a role in the production of anemia. Our hypothesis is that an intact endogenous opiate system is necessary for red cell homeostasis. The presence of opioid receptors both on red blood cells and on various immunologically based white blood cells suggest mechanisms by which deficiency in the endogenous opiate system could cause anemia of either the iron deficiency or inflammatory types. The administration of opioid agonists or antagonists to iron deficient cultures of red blood cell precursors is a next step in determining the role of the endogenous opiate system in the maintenance of red cell homeostasis and in the possible prevention of iron deficiency or inflammatory anemia where iron dysregulation is key.

Low Serum Retinol Concentration Explain Higher Hepcidin Levels In Mexican Older Adults

BackgroundElevated hepcidin levels have been linked to anemia of inflammation (AI). Retinol deficiency has shown to modulate hepcidin expression in animals; however, no studies have explored low serum retinol (LSR) concentration in older adults (OA) and their possible association with hepcidin concentrations. Anemia affect 27% of Mexican OA and inflammation may play a role in the production of anemia in this population. Understanding the mechanisms that play a role in the control hepcidin secretion is an important goal in the prevention of AI.AimTo explore if low serum retinol is associated with higher serum hepcidin concentrations in Mexican older adults (≥60years).MethodsMexican OA were participants in a crossectional study to identify the main causes of anemia. They were recruited in August 2015. Fasting serum samples were collected in 535 OA. Serum retinol (SR) was measured by HPLC and LSR was defined if SR<20μg/dL. Hepcidin (ng/mL) was measured using a commercial ELISA kit. Due to skewed distribution of hepcidin, a quantil regression model was used to associate the LSR and hepcidin, adjusting by sex, age, BMI, ferritin, transferrin receptor, vitamin B12 status, IL‐6, C reactive protein, Alpha‐1‐acid glycoprotein, diabetes, hypertension, tertil of socioeconomic status, sarcopenia and functional disability.ResultsMean age was 71.5y for male and 70.7y for female. LSR was present in 3.2% of OA. Mexican OA with low serum retinol had 12.2 ng/mL higher hepcidin levels than OA with normal serum retinol levels (p=0.03). Hepcidin adjusted median (by confounders) were (median±EE): 19.4± 1.0 ng/mL in OA with normal serum retinol and 31.9±5.7 ng/mL in OA with LSR. Sarcopenic OA had higher hepcidin levels (coef: 7.5 ng/mL, p=0.03) than OA non‐sarcopenic.ConclusionsLSR levels in OA explain their higher hepcidin concentrations. Retinol concentrations affects iron homeostasis but the mechanism is unclear. This data document for the first time that in humans, low serum retinol concentration is inversely associated with hepcidin concentrations. Further longitudinal studies are needed to understand the role of serum hepcidin and Retinol in the development of AI in OA.Support or Funding InformationCONACYT‐FONSEC SSA/IMSS/ISSSTE SALUD 2014‐1, S0008‐2014‐1‐000000000234157

Lead and its Effects on Cytochromes P450

Background: The adverse effects of lead on heme biosynthesis and production of anemia are well known. Lead may disrupt the normal activity of other hemoproteins, such as cytochromes P450 (CYP) which are responsible for drug metabolism. While data in animals suggest a decrease in CYP function with lead exposure, there is little data in humans. Methods: After IRB approval, consented patients with asymptomatic, low to moderate level (10 mg/dl to 44 mg/ dl) lead poisoning were assessed for CYP1A2 and CYP2D6 activity at diagnosis, 1 month, 2 months and after lead level was less than 10 mg/dl. Low doses of caffeine (CYP1A2 activity) and dextromethorphan (DM) (CYP2D6 activity) were administered and urine collected for 12-24 hours at each visit. Lead levels, free erythrocyte protoporphyrin, and iron studies were performed as well. A mixed linear model was used to analyze the data. CYP2D6 genotyping was performed using PCR techniques. Results: Eleven out of the sixteen eligible children (7 males, 4 Caucasian, average age: 33 months) completed the study. Average time to complete the study was 20 months. Seven had lead levels between 10-25 mcg/dl. Eight had elevated EPP. None had low iron levels. A random intercepts mixed linear model was fit to the data. No statistical significance was found for CYP1A2 or CYP2D6 metabolic ratio related to the lead level, change in lead level or time. Discussion: Lead was found to have no effect on the CYP drug metabolizing enzymes at low blood lead levels. Lead has been shown to effect multiple sites on the hemoglobin synthesis pathway resulting in elevated EPP at lead levels >10 mg/dl. However, threshold for decreased hemoglobin levels in children is judged to be approximately 40 μg/dL. Thus, cytochromes may not be affected until higher lead levels are seen. The size of the study limits generalizability. Conclusion: Based on this study, no changes in drug treatment for children with low blood lead levels are necessary. However, further studies may be needed to assess the effect from higher blood lead levels.

Antioxidant status of erythrocytes and their response to oxidative challenge in humans with argemone oil poisoning

Oxidative damage of biomolecules and antioxidant status in erythrocytes of humans from an outbreak of argemone oil (AO) poisoning in Kannauj (India) and AO intoxicated experimental animals was investigated. Erythrocytes of the dropsy patients and AO treated rats were found to be more susceptible to 2,2′-azobis (2-amidinopropane) dihydrochloride (AAPH) induced peroxidative stress. Significant decrease in RBC glutathione (GSH) levels (46, 63%) with concomitant enhancement in oxidized glutathione (172, 154%) levels was noticed in patients and AO intoxicated animals. Further, depletion of glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G-6-PDH) and glutathione- S-transferase (GST) (42–52%) was observed in dropsy patients. Oxidation of erythrocyte membrane lipids and proteins was increased (120–144%) in patients and AO treated animals (112–137%) along with 8-OHdG levels in whole blood (180%) of dropsy patients. A significant reduction in α-tocopherol content (68%) was noticed in erythrocytes of dropsy patients and hepatic, plasma and RBCs of AO treated rats (59–70%) thereby indicating the diminished antioxidant potential to scavenge free radicals or the limited transport of α-tocopherol from liver to RBCs leading to enhanced oxidation of lipids and proteins in erythrocytes. These studies implicate an important role of erythrocyte degradation in production of anemia and breathlessness in epidemic dropsy.

Bone Marrow Response to Acute and Chronic Trypanosoma congolense Infection in Multimammate Rats (Mastomys coucha)

The femoral bone marrow of multimammate rats (n=90), aged 3–8 weeks, experimentally infected with different doses of Trypanosoma congolense was examined by light and electron microscopy. Some animals died from trypanosomosis, but groups of 10 were killed at 4–8, 9–16, 20–24, 30, 40, 50 and 60 days post-infection (dpi). In the acute stage of infection (4–8 dpi) the bone marrow invariably showed a striking increase in erythropoiesis, characterized by an increase in the number of mitotic figures and erythroblastic islands and by a marked decrease in the myeloid:erythroid cell ratio. Later in the infection, erythropoietic activity decreased, while erythrophagocytosis, granulopoiesis, megakaryopoiesis and plasma cell population increased. In chronic infection (16–60 dpi), erythropoietic activity decreased, while intra- and extra-vascular erythrophagocytosis greatly increased. There was also an increase in the bone marrow stroma cells. Excessive erythrophagocytosis by these cells led to the formation of myelin figures and cytoplasmic telephagolysosomes. Degeneration and necrosis of neutrophils lining the adluminal surfaces of the blood sinuses were observed. It is concluded that in the acute stage of the infection, the bone marrow is responsive to the anaemia and that in the chronic stage, dyserythropoiesis and increased erythrophagocytosis by the expanded and activated cells of the mononuclear phagocytic system play an important role in the production of anaemia.

Folic acid and folates: the feasibility for nutritional enhancement in plant foods

In mammalian and plant cells the folates play a key role in the methylation cycle and in the DNA biosynthesis cycle (in the de novo biosynthesis of purines and pyrimidines). Deficiency of folate in the diet is likely to result in a reduction in the capacity to synthesise DNA and maintain the usual rate of cell division. This most evidently results in the production of anaemia from folate deficiency due to a reduction in the biosynthesis of cells in the bone marrow. In addition it has been shown that high levels of plasma homocysteine occur which is an important risk factor in cardiovascular disease. Furthermore it has been shown that reduced maternal folate status is associated with the progressive increase in neural tube defects in infants. There is good evidence for folate deficiency in a considerable number of the population in developed countries, even where folate supplementation of foods is practised, and for a level of intake in excess of the recommended dietary allowance. This paper reviews the principal routes of folate biosynthesis in plants and the potential for increasing the levels of natural folates through conventional plant breeding and biotechnological means. The effect of the major food preservation processes on the levels of folates in plants is also reviewed. The current information about the bioavailability of folates from plant food sources, and how this might be improved, is also summarised. The important health benefits that would arise from increasing folate intake in the diet provide a strong incentive for considering how this might be achieved. © 2000 Society of Chemical Industry

Chronic anemia in pregnant ewes: maternal and fetal effects

To examine maternal and fetal responses to a sustained reduction in maternal hematocrit during days 110-138 of ovine gestation, 22 ewes and their singleton fetuses were instrumented. By repetitive exchange transfusions, the hematocrit in 12 ewes was decreased from 28.1 +/- 0.8 (baseline, day 110) to 14.0 +/- 0.7% (day 117) and maintained at that level. Anemic ewes demonstrated a transient increase in heart rate from 99 +/- 4 to 116 +/- 4 beats/min and a sustained increase in cardiac output from 117 +/- 8 to 153 +/- 11 ml.min-1.kg-1 compared with control animals. Uterine blood flow steadily increased in control animals from 868 +/- 100 (day 110) to 1,410 +/- 177 ml/min (day 138) but failed to increase in the anemic ewes. Uterine oxygen delivery fell from 83 +/- 10 to 39 +/- 4 ml/min with production of anemia and remained low in the anemic ewes. Arterial PO2 and oxygen content in the fetuses of anemic ewes fell transiently below control values (19.9 +/- 0.8 vs. 23.4 +/- 1.0 mmHg and 5.3 +/- 0.3 vs. 6.8 +/- 0.4 ml/dl, respectively) but did not persist. Fetal weights at 138 days gestation were lower in the anemic group (2,596 +/- 329 vs. 4,313 +/- 132 g). We conclude that chronic maternal anemia results in a decreased uterine blood flow as well as decreased uterine oxygen delivery. The fetus responds with decreased growth but does not develop sustained hypoxia or acidosis.

Peripheral vascular responses during acute anemia.

Peripheral vascular responses during acute anemia were studied in 19 anesthetized dogs. In one study (n = 9) hindlimb weight and venous pressures were measured prior to and during acute anemia produced by isovolemic dextran-for-blood exchange. In another series of five control and five anemic dogs (hematocrit = 14 +/- 1% (mean +/- SE)), flow to the limb was occluded and arterial and venous pressure changes in the occluded limb were measured as an index of neurally mediated alterations in limb vasomotor tone. Following reduction of the hematocrit to 14 +/- 0.3%, hindlimb weight decreased by an average of 10.0 g (P less than 0.01) at 15 min and 12.8 g (P less than 0.01) at 30 min of anemia. The decrease in limb weight was associated with a rise (P less than 0.01) in limb venous pressure. There was also a relatively greater degree of vasomotor tone in the occluded hindlimb of anemic dogs as compared with control animals. Although both arterial and venous pressure decreased in an occluded hindlimb following the production of anemia, the decreases in vascular pressures were significantly less than those observed in control experiments. It was not possible to distinguish between tone changes in arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone. arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone. arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone.

T cell chronic lymphocytic leukemia: presence in bone marrow and peripheral blood of cells that suppress erythropoiesis in vitro

The pathogenesis of the anemia associated with malignancy was investigated in a patient with T cell chronic lymphocytic leukemia. The plasma clot culture system was used as a measure in vitro of erythropoiesis. The patient's peripheral blood and marrow T lymphocytes obtained both before and after transfusion therapy suppressed erythroid colony formation by normal human bone marrow cells. Pretreatment of the patient's bone marrow T cells by antithymocyte globulin (ATG) and complement reversed this suppression. In addition, pretreatment of the patient's marrow cells with ATG and complement markedly augmented erythropoiesis in vitro. The expression of erythroid activity caused by the selective destruction of the suppressor T lymphocytes in the patient's bone marrow with ATG and the suppression of normal erythropoiesis by the patient's bone marrow and peripheral blood lymphocytes suggest that interaction between the malignant T cell and the erythropoietin-responsive stem cell is important in production of anemia in this patient.

T Cell Chronic Lymphocytic Leukemia: Presence in Bone Marrow and Peripheral Blood of Cells That Suppress Erythropoiesis In Vitro

The pathogenesis of the anemia associated with malignancy was investigated in a patient with T cell chronic lymphocytic leukemia. The plasma clot culture system was used as a measure in vitro of erythropoiesis. The patient's peripheral blood and marrow T lymphocytes obtained both before and after transfusion therapy suppressed erythroid colony formation by normal human bone marrow cells. Pretreatment of the patient's bone marrow T cells by antithymocyte globulin (ATG) and complement reversed this suppression. In addition, pretreatment of the patient's marrow cells with ATG and complement markedly augmented erythropoiesis in vitro. The expression of erythroid activity caused by the selective destruction of the suppressor T lymphocytes in the patient's bone marrow with ATG and the suppression of normal erythropoiesis by the patient's bone marrow and peripheral blood lymphocytes suggest that interaction between the malignant T cell and the erythropoietin-responsive stem cell is important in production of anemia in this patient.

Postresectional Anemia

The incidence of anemia after total gastrectomy has not received sufficient clinical emphasis. During a follow-up period averaging 32 months, postresectional anemia developed in seven of ten patients without evidence of malignant neoplasm; all but one of these patients had received parenterally administered cyanocobalamin. Despite low levels of circulating erythrocytes and proportionately increased erythropoietin levels, reticulocytosis was not evident. This observation suggests an uncharacterized failure of marrow erythyroid precursors. Multiple deficits in intake of constituents necessary for the production of erythrocytes were demonstrated. With the possible exception of iron, malabsorption of these constituents is not an important factor in the production of anemia. Postresectional anemia is multicausal, but is primarily nutritional. As total gastrectomy becomes more commonly employed in the treatment of nonmalignant conditions, recognition of the frequency and causes of postresectional anemia should assist both diagnostic anticipation and therapy.

Prolonged Immunization

Summary Rabbit anti-mouse erythrocyte sera from each of 7 courses of immunization were studied with 9 immunologic techniques, namely, agglutinin titrations with antiglobulin serum, in serum-albumin medium, with papain treated cells, and in saline medium; hemolysin and complement fixation titrations; determination of combining ability with fluorescein and I125 labeled sera; and production of anemia in mice. Formalinized erythrocytes can be used successfully to study certain immunologic reactions. In vitro reactions, except for complement fixation and coating with fluorescent antibodies, did come near their peak levels in 2-course sera; after 4 or more courses, titers of all in vitro reactions were essentially parallel to the base line. Whether these tests are demonstrating different reactions of the same antibody or reactions of different antibodies requires further investigation. On the other hand, the anemia producing ability showed marked decrease in sera collected after more than 3 courses of immunization. Our studies permit the conclusion that no in vitro reaction has yet been found to serve as a reliable indicator of the in vivo potency of a rabbit anti-mouse erythrocyte serum.

CARDIOVASCULAR REACTIVITY IN ANEMIC DOGS.

Cardiovascular responses to the intravenous administration of adrenaline were measured as a means of assessing cardiovascular reactivity in intact anaesthetized dogs, before and at 3 hours and 3 days after the rapid production of anaemia by a dextran-for-blood exchange. Three types of experiments were carried out. In experiments A and B, 2.0 and 5.0 μg/kg of adrenaline (respectively) were injected intravenously before and at both periods after exchange, and the changes in arterial blood pressure were assessed. In experiment B the changes in the arterial plasma concentration of potassium and sodium were also measured. In experiment C, several cardiovascular parameters, including cardiac output (Fick method), arterial pressure, and heart rate, were measured before and at the end of a 15-minute infusion of adrenaline in a dose of 0.2 μg/kg minute. In all three experiments, evidence of a reduced cardiovascular response to adrenaline was found when the dogs were anaemic; and in experiment B the adrenaline-induced hyperkalaemia and hyponatraemia were found to be significantly reduced during anaemia.The mechanism of the hyporeactivity to adrenaline during anaemia is not clear, but may include changes in blood volume, electrolyte disturbances, and severe anoxia.

THE HUMORAL REGULATION OF ERYTHROPOIESIS AND METABOLISM DURING RECOVERY FROM THE RAPID PRODUCTION OF ANAEMIA IN THE DOG.

The levels of erythropoietin and metabolic stimulating factor(s) were assayed in the plasma of dogs at 1 and 3 hours and at 2, 3, 4, 6–7, and 8–9 days after the rapid production of anaemia by dextran-for-blood exchange. The assay results were considered in relation to the reticulocyte response and oxygen consumption of the anaemic dogs over this same period.An increase in erythropoietin was first detected at 2 days and reached a maximum by 4 days after exchange. The level of erythropoietin was falling by 6–7 days and reached control levels by 8–9 days. An increase in reticulocyte level in anaemic dogs did not occur until 3–4 days and was maximal at 8–9 days.The metabolic stimulating activity of the plasma tended to parallel the changes in level of erythropoietin except at 3 hours when there was a considerable increase in metabolic activity although there was a normal level of erythropoietin. Protein-bound iodine in plasma was decreased following dextran-for-blood exchange. The oxygen consumption of the anaemic dog was below control levels at 1 and 3 hours, but subsequently above control levels at 4 to 9 days.The changes in erythropoietin and metabolic stimulating factor were somewhat similar to the change in level of a cardiotonic agent previously found in the blood of dogs during recovery from anaemia.

The circulatory adjustments to posthemorrhagic anemia in dogs.

Several measures of cardiovascular function were made in nine dogs before, during, and after the production of anemia by daily venesections. Stress is laid on the time sequence of the various changes in the circulation and their relation to each other. From the results obtained it was concluded that the elevated cardiac output observed in anemia was not the result of an increase in right atrial pressure or a decrease in tissue oxygen tension, per se. It is suggested that the increased cardiac output may be due to a slowly elaborated or slow-acting humoral agent produced as a result of tissue anoxia.

The influence of some hormonal, dietary, and tumor factors on liver catalase activity in rats.

Liver catalase activity can be reduced by the administration of cortisone or stilboestrol and by the production of anemia, as well as by the presence of a tumor in the host. All of these factors cause a disturbance of body growth. However, interference with growth produced by adrenalectomy or low protein diet is not associated with loss of liver catalase activity. The loss of liver catalase activity in tumor-bearing rats is associated frequently with an increase in liver size. But rats with large tumors may have small livers and still demonstrate the drop in catalase activity. It is suggested that the loss of liver catalase activity in tumor-bearing rats is not due to body growth disturbance or liver hypertrophy, and is produced in excess of such nonspecific factors as adrenal stimulation.

International Recommendations on Radiological Protection

HomeRadiologyVol. 56, No. 3 PreviousNext EditorialInternational Recommendations on Radiological ProtectionRevised by the International Commission on Radiological Protection at the Sixth International Congress of Radiology, London, July 1950Published Online:Mar 1 1951https://doi.org/10.1148/56.3.431MoreSectionsPDF ToolsImage ViewerAdd to favoritesCiteTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinked In AbstractIntroductionDevelopments in nuclear physics and their practical applications since the last International Congress have greatly increased the number and scope of potential hazards. At the same time biological research has led to an extension of our knowledge of the dangers associated with ionizing radiations. This increase of biological knowledge has not only brought a realization of the importance of certain effects, particularly carcinogenic and genetic effects, but has also provided more information as to the permissible levels of radiation. The International Commission on Radiological Protection has therefore adopted new radiation safety standards with more rigid criteria. Such standards must, in view of the still limited experience of the effects of radiation, be kept continually under review.It appears that the effects to be considered are :1. Superficial injuries.2. General effects on the body, particularly the blood and blood forming organs, e.g., production of anemia and leukemias.3. The induction of malignant tumors.4. Other deleterious effects including cataract, obesity, impaired fertility, and reduction of life span.5. Genetic effects.While it is still fundamental to express whole body exposure in terms of a single number, it is not practicable, in general, in view of the complexity of circumstances now arising, to express the maximum permissible hazards in terms of a single parameter. It is, for example, highly desirable to derive values of maximum permissible concentrations of radioactive materials, in the air or in drinking water, taking into account the metabolism of the materials concerned, and assuming standard anatomical, physiological, and chemical data. Furthermore, the pre-viously accepted value of 1 r per week for maximum permissible exposure to external radiation itself needs revision in the light of the nature of the radiations to which workers are now exposed. There is the added difficulty that the roentgen is not an acceptable unit of dose for all ionizing radiations. Accordingly the following recommendations are based on considerations of the equivalent energy absorbed in tissue coupled with the appropriate relative biological efficiency.While the values proposed for maximum permissible exposures are such as to involve a risk which is small compared to the other hazards of life, nevertheless in view of the unsatisfactory nature of much of the evidence on which our judgments must be based, coupled with the knowledge that certain radiation effects are irreversible and cumulative, it is strongly recommended that every effort be made to reduce exposures to all types of ionizing radiations to the lowest possible level.Exposure to External RadiationArticle HistoryPublished in print: Mar 1951 FiguresReferencesRelatedDetailsCited ByRadiation Protection of a Pregnant Worker, the Embryo and Fetus: Historical Changes in ICRP Recommendations and Current IssuesNobuyukiHAMADA2017 | Japanese Journal of Health Physics, Vol. 52, No. 3Individual response to ionizing radiationNicolasForay, MichelBourguignon, NobuyukiHamada2016 | Mutation Research/Reviews in Mutation Research, Vol. 770Interim Report of the JHPS Expert Committee on Radiation Protection of the Lens of the Eye (I)KeiichiAKAHANE, TakeshiIIMOTO, TakeshiICHIJI, SatoshiIWAI, HiroyukiOHGUCHI, KazukoOHNO, ChiyoYAMAUCHI-KAWAURA, HideoTATSUZAKI, NorioTSUJIMURA, NobuyukiHAMADA, YukiFUJIMICHI, YutakaHOTTA, TadashiYAMASAKI, SumiYOKOYAMA2014 | Japanese Journal of Health Physics, Vol. 49, No. 3Why the concept of hormesis has not been incorporated into mainstream radiation health theory: Radiation perspectiveArthur C.Upton2000 | Human and Ecological Risk Assessment: An International Journal, Vol. 6, No. 2Annex D List of the commission's publications1991 | Annals of the ICRP, Vol. 21, No. 1-3Issues and Reviews in TeratologyWilliam J.Schull, Julia K.Bailey1984Publications of the commission1977 | Annals of the ICRP, Vol. 1, No. 3Radiation protection standards (Part 2)Lauriston S.Taylor, Harold O.Wyckoff1972 | C R C Critical Reviews in Environmental Control, Vol. 2, No. 1-4Radiation DosimetryC.C.Wang, L.L.Robbins1956Konstitution Allergische Krankheiten Krankheiten der Knochen, Gelenke und Muskeln Krankheiten Aus Äusseren Physikalischen Ursachen Ernährungskrankheiten Vitamine und VitaminkrankheitenGerhardSchubert, GünterHöhne1954Künstliche Radioaktive IsotopeGerhardSchubert, GünterHöhne1953Recommended Articles RSNA Education Exhibits RSNA Case Collection Vol. 56, No. 3 Metrics Altmetric Score PDF download

Production of Anemia in Swine Fed Purified Diets and Sul-fasuxidine.

SummaryPigs maintained on a diet in which purified casein was substituted for crude casein and to which 2 per cent sulfasuxidine was added developed anemia which responded partially to purified liver extract and completely to pteroylglutamic acid. This anemia resembles that which has been produced in pigs given a folic acid antagonist.Pigs maintained on a diet containing crude casein and to which 2 per cent sulfasuxidine was added developed less pronounced anemia which disappeared spontaneously.

Production of anemia in a pig which responded to purified liver extract.

Abstract One pig maintained on a diet in which purified casein (Borden's Labco vitamin-free) was substituted for crude casein (Sheffield new process) and to which 2 per cent sulfasuxidine was added failed to grow normally and developed partial alopecia and a normocytic anemia. Following treatment with a highly purified antipernicious anemia liver extract, body hair growth was resumed, and following a definite although not marked reticulocytosis the blood returned to normal. The anemia was accompanied by normal erythrocyte protoporphyrin, normal plasma iron, and an elevated serum copper level. Four animals maintained on a diet in which crude casein was used in place of the purified casein and to which sulfasuxidine was added grew well, maintained normal coats, and failed to develop anemia.

Production of Anemia by Tetanus Toxin

SummarySmall sublethal doses of tetanus toxin produce a typical secondary anemia—low red cell count, reduced hemoglobin index, increased sedimentation rate. Injection of antitoxin produced a prompt return to normal, the red cell count rose rapidly as a result of large numbers of reticulocytes pouring into the system.The severe anemia following the administration of toxin and the prompt recovery following that of antitoxin may serve as a simple early diagnostic test of possible tetanus intoxication in wounded.