Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lateral X-ray pictures of the skull in certain several and chronic disorders of the blood as thalassaemia, congenital haemolytic anaemia, sickle cell anaemia and iron deficiency disease show frequently changes of the outlines of the cranial bones. They consist of a double contour of the outer cranial border and on the interior side below the sagittal sutura of a band-like shadow or of multiple stripes and lines running parallel to the carnial vault. They concern the parietal bones and may extend from the bregma till to the lamda or occupy only a part of this distance. The roentgenological features are due to the enlargement of the crainal bones, the bulging out of both parietal bondes, the sometimes enlarged and deepened borders of the sulcus sagittalis superior and particularly to the furrow and depression on the skull above the sagittal suture caused by the protruding parietal bones on both sides. As these different abnormal structures must be passed by the picturing X-ray, effects of superposition and interference are produced. Longitudinal ridges or bony edges which could explain the roentgenological findings could not be established. Since the peculiar alterations of the cranial bones are mainly found in the mentioned blood disorders, where they are caused by the overgrowing red marrow, they also display the same roentgenological features. These features are, therefore, a characteristic sign of these diseases.
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PMID:[Double contours and companion shadows in the skull associated with anaemias (author's transl)]. 15 80

A 1-month-old Jersey calf died of oxalate nephropathy. The calf had access to antifreeze (ethylene glycol) 3 days prior to death. Since ethylene glycol toxicosis had not been reported in cattle, the effects or oral administration of ethylene glycol were studied in 7 calves and 3 cows. The toxic dose ranged from 2 to 10 ml of ethylene glycol per kg of body weight. Clinical signs were increased respiration, staggering gait, paraparesis, depression and later, recumbency and death. Hemoglobinuria and epistaxis were seen at doses of 10mg/kg of body weight. Azotemia, hypocalcemia and neutrophilia were constant findings whereas acidosis, plasma hyperosmolality and hemolytic anemia were seen in the animals receiving the higher doses. A diagnosis of ethylene glycol toxicosis must be based upon a history of ingestion and the presence of calcium oxalate crystals in body tissues (especially the kidney and brain).
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PMID:Ethylene glycol toxicosis in cattle. 47 24

A 4-year-old boy had hemolytic uremic syndrome (HUS) associated with depression of serum C3 level, a B-hemolytic streptococcal throat infection, and an elevated level of antistreptolysin O titer. In addition to the characteristic histologic changes associated with this syndrome, substantial infiltration of polymorphonuclear leukocytes and nodular deposits of C3 globulin were seen in the glomeruli of the first biopsy specimen. Two months after clinical remission, he had a recurrence of hemolytic anemia, thrombocytopenia, and acute renal failure. The serum C3 concentration had decreased again, and serum C3NeF was detected in the serum. The typical changes associated with HUS were still present on electron microscopy. Bilateral nephrectomy and renal transplantation were done because of the development of uncontrollable severe hypertension and increasing azotemia. This patient had three manifestations of HUS, but because of several differences, such as hypocomplementemia, serum C3NeF, a recurrence, and persistent glomerular deposits of C3 globulin, he appears to have had a different form of the syndrome.
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PMID:Hemolytic uremic syndrome with hypocomplementemia, serum C3NeF, and glomerular deposits of C3. 57 89

Three Rhmod siblings were found to have identical Rh: w1, w2, -3, -4, w5 (see article) phenotypes. All had stomatocytic hemolytic anemia. On quantitative hemagglutination studies, as well as on hand tests, all Rh antigens were not equally depressed. Rh17 (Hr0, 'not D') and Rh29 (RH, 'total Rh') were both normal. Rh5 (hr", e) was only slightly depressed. Rh25 (LW) had 50% of the expression expected in normal Rh:-1 cells. Rh1 (Rh0, D), Rh13 (RhA), Rh14 (RhB), Rh15 (RhC), and Rh16 (RhD), were severely depressed. Rh2 (rh', C) was depressed, while Rh7 (rhi, Ce) was absent. Both Rh19 (hrS) and Rh31 (hrB) were depressed. Rh12 (rhG, G) was distinctly depressed, scoring considerably less than rGrG red cells. The unrelated parents, the child of the proposita, and some siblings of each parent showed lessened depression of Rh antigens without displaying the consistent pattern that might be expected from a presumed single suppressor gene. Absence of a consistent pattern may have resulted from differing Rh genotypes, but a frequently observed depression involved Rh14, Rh15, and Rh16 (RhB, RhC, and RhD) without an effect on either Rh1 (RH3 or D) or Rh13 (RhA).
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PMID:Rhmod, a second kindred (Craig). 81 11

Rates of glucose, glycine, and folic (pteroylglutamic) acid absorption were determined for a 30 cm jejunal segment in vivo, with a double-lumen tube perfusion system, in 10 Zambian African women with a mean haemoglobin concentration of 5-1 (3-5-9-2) g/dl. In four the anaemia was megaloblastic (due to folate deficiency) and in six hypochromic. Perfusion solutions contained (1) glucose 200 mmol/1, (2) glycine 100 mmol/1, and (3) folic acid 250 mug/1. D-xylose absorption after a 25 g oral load was determined in them, and also in 18 additional patients (11 had megaloblastic and seven either hypochromic or haemolytic anaemia). Xylose absorption tests were significantly impaired in the patients with megaloblastic compared with hypochromic or haemolytic anaemia (P less than 0-001); those with untreated megaloblastic anaemia had a greater abnormality than those who had started treatment. Mean glucose, glycine, and folic acid absorption rates were similar to those in controls, and the rates in patients with megaloblastic and hypochromic anaemia were not significantly different. Correlation between glucose absorption rate and xylose excretion was, however, significantly (P less than 0-02). If more patients had been studied it seems likely therefore that a significant impairment of glucose absorption rate in the presence of megaloblastic anaemia would also have been demonstrated. In this investigation anaemia per se did not affect glucose, glycine, or folic acid absorption rates or xylose absorption, but xylose absorption was reduced in patients with megaloblastic anaemia. That abnormality was probably related to folate deficiency, and the underlying mechanism seems to be different from that causing impairment of monosaccharide absorption in patients with systemic bacterial infections. Mean glycine and folic acid absorption rates were not altered by megaloblastic anaemia, indicating that folate deficiency does not cause a general depression of absorption.
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PMID:Absorption of xylose, glucose, glycine, and folic (pteroylglutamic) acid in Zambian Africans with anaemia. 97 99

A patient with a biochemically "new" type of congenital erythropoietic porphyria has been studied under various therapeutic trials. Splenectomy had no demonstrable effect on porphyrin excretion or clinical picture. Vitamin E caused a moderate fall in porphyrin excretion, however, there was no significant improvement in light tolerance and tendency to hemolysis. Beta-carotene reduced skin photosensitivity appreciably, while total porphyrin excretion remained unchanged and the tendency to develop hemolytic anemia showed only slight improvement. Red cell transfusion caused a rapid, dramatic fall in prophyrin excretion (in 4-5 days) and a transient increase in light tolerance, while the distribution of the different porphyrins excreted remained unchanged. These observations indicate that all or nearly the abnormal porphyrins excreted are of erythropoietic origin, and that the overwhelming part of the porphyrins originate from an abnormal population of shortlived red cells. Findings on fluorescence microscopy of blood and bone marrow support this view. Meticulous protection against light of the shorter wavelengths caused a similar rise in hemoglobin level as produced by red cell transfusion, however, in this instance the total excretion of porphyrins did not fall. It is suggested that the inhibitory effect of transfusion on erythropoiesis (and thereby porphyrin excretion) might be due partly to a depression of erythropoietin formation, partly to the presence of an erythropoiesis inhibiting factor (chalone) in the transfused red cells.
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PMID:The effect of various therapeutic trials on the prophyrin excretion in a case of congenital erythropoietic prophyria. 113 Jan 87

1. The hemolytic effect of L-sorbose on canine erythrocytes characterized by inherited high Na, K-ATPase activity and a high potassium concentration (HK RBCs) was compared with that on normal canine erythrocytes (LK RBCs). 2. Dogs having HK RBCs (HK dogs) revealed no clinical and hematological changes after administration of L-sorbose, whereas normal dogs (LK dogs) developed severe hemolytic anemia associated with hemoglobinuria and marked decreases of erythrocyte ATP concentrations. 3. In vitro, L-sorbose induced hemolysis in LK RBCs along with the depression of both ATP and lactate formation in these cells, but not in HK RBCs. The inhibition of glycolysis by L-sorbose in LK RBCs, however, was not observed when glucose-6-phosphate was used as a substrate instead of glucose. 4. These results suggest that the disparity of susceptibility to sorbose-induced hemolysis may be due to the difference in erythrocyte metabolism between HK and LK RBCs, especially the high activity of hexokinase in HK cells, which was 2-fold greater than that in LK RBCs.
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PMID:L-sorbose does not cause hemolysis in dog erythrocytes with inherited high Na, K-ATPase activity. 135 45

Severe anemia was found in a 4-month-old heifer, which was admitted with a 1-day history of anorexia, signs of depression, and recumbency. A diagnosis of immune-mediated hemolytic anemia (IHA) was made on the basis of a Coomb's titer of 1:128 and decreased resistance to osmotic stress, as determined by an RBC fragility test. Anaplasmosis and leptospirosis were ruled out as possible causes of the IHA. Other causes of hemolytic anemia, including intoxication by copper, water, Brassica spp, or drugs were ruled out. Therefore the IHA was considered idiopathic. Treatment consisted of supportive therapy, oxytetracycline, and dexamethasone. After 60 days of treatment, CBC, Coomb's test result, and RBC fragility were within normal limits.
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PMID:Idiopathic immune-mediated hemolytic anemia in a calf. 164 56

A transplantable mononuclear cell leukemia (MCL) was established from spontaneous MCL in an F344 rat. In this work, we paid special attention to a nodular tumor, named MCL-YSK, developed at the subcutaneous transplant site. MCL-YSK was serially passaged in subcutaneous tissue of syngeneic rats up to the 19th generation. Transplants from MCL-YSK grew into nodules 3 cm in diameter and 11.3 g in weight 9 weeks after subcutaneous implantation. Neoplastic cells forming the nodules had azurophilic cytoplasmic granules, which ultrastructurally appeared to be lysosomes. The cells reacted positively for acid phosphatase and nonspecific esterase, but not for alkaline phosphatase, alpha-1 antitrypsin and lysozyme, nor reacted with anti-rat monocyte/macrophage monoclonal antibody and anti-rat CD-8 monoclonal antibody. They possessed Fc-receptor. Leukemic cells first appeared in the peripheral blood 6 weeks after transplantation when subcutaneous nodules reached an average diameter of one cm. Subsequently, leukemic changes progressed in recipients as MCL-YSK grew larger. The recipients died during the period from 8 to 12 weeks after transplantation, showing anemia, depression, splenohepatomegaly and lymph node enlargement. Diffuse or focal proliferation of sprinkled tumor cells was present in many organs. Hematologic changes suggestive of hemolytic anemia, elevated plasma enzymes and decreased drug-metabolizing enzymes, indicative of hepatic malfunction, were seen in transplant recipients. MCL-YSK was easily transplanted into athymic nude mice. The transplanted mice showed leukemic changes similar to those observed in rats with transplanted MCL-YSK.
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PMID:Transplantable mononuclear cell leukemia in F344 rat with particular reference to nodular tumor developing at the transplant site. 183 99

The B19 strain of parvovirus causes several distinct and important clinical diseases in humans. Aplastic crisis in patients with chronic hemolytic anemia, persistent bone marrow depression in immunocompromised individuals, and hydrops fetalis all result from direct infection of hematopoietic cells by the virus. Erythema infectiosum, arthritis, and purpuric vasculitis are postinfectious manifestations of B19 parvovirus infection.
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PMID:Human parvovirus infections. 215 61


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