bluuebunny/crossref_metadata_2025_split huggingface dataset:
Incidence of Iron Deficiency, with and without Anaemia, in Women in General Practice
Authors: McFarlane D. B. , Pinkerton P. H. , Dagg J. H. , Goldberg A. 
Published: March 2008

SUMMARYThe incidence of iron deficiency anaemia in 500 women in an urban general practice was found to be 8.2 per cent, 9.7 per cent in 402 ‘patients’ and 2 per cent in 98 symptomless volunteers (‘subjects’). Iron deficiency anaemia was diagnosed when the haemoglobin was less than 12 g. per 100 ml. and the saturation of the total iron binding capacity of the serum was less than 16 per cent.Women who had a haemoglobin of more than 12g. per 100 ml. but who had a saturation of the total iron binding capacity of less than 16 per cent, were considered to be ‘iron deficient without anaemia’. This state was found in 22.2 per cent of ‘patients’ and 16.3 per cent of ‘subjects’.There was no decrease in the incidence of iron deficiency following the menopause; indeed, iron deficiency with and without anaemia was slightly more common over the age of 40 years. While a higher incidence was seen in widows than in married or single women, this difference was not significant, nor were the differences in the social classes or ABO, blood groups.
Sequence of Events Terminating in Death of Leucocytes
Authors: Aune Janet M. , Gantner G. E. , Wade N. J. 
Published: March 2008

SUMMARYCellular damage in human granulocytes was evident by light microscopy after 24 hours of 30° C. incubation in unfortified whole blood. Injury was indicated by the cell's inability to accommodate neutral red and the simultaneous loss of motility. Cellular death was delimited to this loss of physiological integrity.Biochemical changes which occurred intracellularly during incubation were correlated with changes in the surrounding milieu: plasma glucose diminished first, and after this was depleted there was histochemical evidence of decreased cytoplasmic glycogen. It appears by analogy, therefore, that after the glucose was utilized, intracellular glycogen may have been used for energy metabolism enabling the cell to function an additional 10–15 hours. When nutrient deficiency produced structural disintegration, the cell was unable to maintain itself and death followed.
Biological Half‐Life of Transfused Antihaemophilic Globulin (Factor VIII) In Normal Man
Authors: Pool Judith G. , Cohen Theodore , Creger William P. 
Published: March 2008

SUMMARYThe biological half‐life of anti‐haemophilic globulin (Factor VIII) was determined in two normal subjects. Using plasmapheresis, approximately 25 bags of plasma were collected from each over a 9‐week period. From these plasma donations, cryoprecipitates were prepared and stored in the freezer. At the time of the study their pre‐infusion Factor‐VIII levels were carefully determined and then the pooled solutions of the cryoprecipitates rapidly administered and the post‐infusion Factor‐VIII levels determined serially. Although fluctuations in level interfered with the establishment of a smooth curve, the approximate half‐life time was 2+ hours for each subject. It was concluded that the biological half‐life for Factor VIII in the normal is no longer than, and possibly shorter than, that for the haemophilic subject and that this observation supports the hypothesis that haemophilia is a disease of inadequate synthesis of Factor VIII rather than of accelerated destruction.
Hereditary Elliptocytosis in Iceland
Authors: Jensson Ó. , Jonasson Th. , ÓLafsson Ó. 
Published: March 2008

SUMMARYAn Icelandic family with 50 elliptocytic individuals is surveyed. Pedigree studies indicate strongly that affected members of the family are descendants of a common ancestor. The hereditary pattern is typical for a dominant, autosomal gene with full penetrance. A high incidence (over 57 per cent) of signs and/or symptoms of haemolysis is found among the affected at one time or another. No haptoglobin was detected in 80 per cent of affected individuals investigated. The age distribution of the affected at the time of diagnosis shows an increased incidence of anaemia with increasing age. In three affected individuals splenectomy has been performed with satisfactory results.The variation in the grades of haemolysis and the high incidence of haemolysis found in the affected family members are discussed.
Lysis of P.N.H. Cells in Solutions of Low Ionic Strength
Authors: Stratton F. , Evans D. I. K. 
Published: March 2008

SUMMARYA test to detect P.N.H. red cells when exposed to fresh serum in a sucrose‐veronal‐albumin buffer solution of low ionic strength, pH 7.6, is described.The serological findings suggest that the basis of the test is another example of the peculiar sensitivity of P.N.H. cells to complement in the presence of antibody.
Intravascular Haemolysis with Experimentally Produced Vascular Thrombi
Authors: Brain M. C. , Esterly J. R. , Beck E. A. 
Published: March 2008

SUMMARYStudies are presented on the haemoglobinaemia observed during intravascular coagulation in rabbits due to thrombin infusion or endotoxin injection.The haemoglobinaemia was unrelated to the type or amount of thrombin, but was closely correlated to the degree and extent of fibrin thrombi in the renal glomeruli and in the small vessels of other organs, an effect potentiated by thorotrast.The haemoglobinaemia was not dependent on the presence of the spleen or the kidneys, or on circulating granulocytes, but could be prevented by heparin.The haemoglobinaemia was associated with the appearance of fragmented red cells in the circulation.It is suggested that the haemoglobinaemia is due to intravascular destruction of red cells at the site of fibrin thrombi, and that changes in the red cell may also enhance thrombosis.
The Effect of Iron Stores on Ferrokinetics in Polycythaemia
Authors: Ellis L. D. , Westerman M. P. , Balcerzak S. P. 
Published: March 2008

SUMMARYThe ferrokinetic data of patients with primary polycythaemia are those of patients with depleted iron stores. Differences in iron kinetics between polycythaemia vera and secondary polycythaemia are related to the variation in the quantity of iron stores and do not appear to be inherent to the type of polycythaemia. If ferrokinetic studies are to be used to evaluate or classify polycythaemia, storage iron must be assessed.
Experiments on the Nature of the Prothrombin‐Converting Principle: Alteration of Proaccelerin Thrombin
Authors: Prentice C. R. M. , Ratnoff O. D. , Breckenridge R. T. 
Published: March 2008

SUMMARYAn incubation mixture of activated Stuart factor, calcium, phospholipid and proaccelerin caused the generation of thrombin from prothrombin. The activity of this prothrombin‐ converting principle was measured by the rate at which it converted prothrombin to thrombin. In the absence of thrombin in the incubation mixture, a lag phase, following addition of the prothrombin‐converting principle to prothrombin, was observed before thrombin formation occurred. But when a trace of thrombin was added to the incubation mixture, it converted the principle into an active form, causing the immediate formation of thrombin from prothrombin without any delay. It was demonstrated that thrombin had this action upon the prothrombin‐converting principle by changing proaccelerin into a more active form.Thrombin‐treated proaccelerin would not convert prothrombin to thrombin in the absence of activated Stuart factor, indicating that it is not, by itself, the prothrombin‐converting principle.By purification of the thrombin preparation, and the use of hirudin, it was shown that the action of thrombin on proaccelerin was due to thrombin itself and not to activated Stuart factor or other contaminating substances in the thrombin preparation.
Desferrioxamine Chelatable Iron in Haemolytic, Megaloblastic and Sideroblastic Anaemias*
Authors: Karabus C. D. , Fielding J. 
Published: March 2008

SUMMARYThe chelation of body iron by desferrioxamine methanesulphonate in patients with haemolytic anaemias of varying types, in megaloblastic and in sideroblastic anaemias was measured by the differential ferrioxamine test. Thirty‐five out of 44 patients studied had chelation values above the normal range, sometimes exceeding those found in untreated haemochromatosis.In the haemolytic anaemias, the amount of chelation increased with the severity of the anaemia. In the megaloblastic anaemias, specific therapy reduced the amount of iron chelated by desferrioxamine at the same time as normal erythropoiesis was re‐established.Concepts of labile iron and metabolically active iron are compared with desferrioxamine chelatable iron. These findings suggest that in addition to storage iron (ferritin‐haemosiderin) chelated with difficulty, there is a compartment of readily chelatable iron derived from haem catabolism, possibly sited in reticulo‐endothelium. A model of intracellular iron transport in reticulo‐endothelial cells is proposed which provides a primary pathway of metabolically active, highly chelatable iron derived from haemoglobin catabolism, and a secondary pathway to intracellular ferritin.
VII. CHANGES IN LYMPHOCYTES AND TRANSITIONAL CELLS IN THE BONE MARROW DURING PROLONGED REBOUND
Authors: Jones Hilary B. , Jones J. J. , Yoffey J. M. 
Published: March 2008

SUMMARYThe bone marrow has been studied by a quantitative technique in 48 guinea‐pigs from the 8th to 12th days of rebound following 7 days of hypoxia at a simulated altitude of 17,000 feet. On the 8th and 9th days of rebound there is a highly significant increase in the small lymphocytes, which form nearly 70 per cent of all the nucleated cells of the marrow. This increase is associated with a fall in the transitional lymphocytes and also of the myeloid cells. The significance of these changes is discussed.
VIII. EFFECT OF HYPOXIA AND POST‐HYPOXIC POLYCYTHAEMIA (REBOUND) ON MOUSE MARROW AND SPLEEN
Authors: Turner M. S. , Hurst J. M. , Yoffey J. M. 
Published: March 2008

SUMMARYQuantitative marrow changes,59Fe incorporation into erythrocytes and spleen weight variations have been studied in mice during primary hypoxia and rebound. The pattern of the mouse response to hypoxia is similar to that already described in the guinea‐pig. The possible involvement of the lymphocyte in erythropoiesis whether as stem cell or otherwise is suggested by the fact that its accumulation in the marrow seems to be inversely related to erythropoietic activity. The effect of hypoxia on the stem cell compartment is discussed.
Leucocyte Folate in Vitamin B12 and Folate Deficiency and in Leukaemia
Authors: Hoffbrand A. V. , Newcombe Beverley F. A. 
Published: March 2008

SUMMARYLeucocyte folate concentrations were measured in 24 normal subjects, in 32 patients with subnormal serum folate concentrations and normal serum B12 concentrations associated with chronic gastro‐intestinal disease, in seven patients with leukaemia, and in 10 patients with untreated pernicious anaemia.In the normal subjects, the leucocyte folate levels ranged from 60 to 123 ng./ml. of packed leucocytes. Among the patients with subnormal serum folate concentrations, leucocyte folate concentrations were normal in seven or eight patients with entirely normoblastic haemopoiesis, but were subnormal in all eight patients whose marrows showed normoblastic erythropoiesis and giant metamyelocytes, in all eight patients with obvious megaloblastic changes, and in all eight patients with overt megaloblastic anaemia due to folate deficiency.Leucocyte folate was raised in six of the seven patients with leukaemia including patients with acute and chronic myeloid leukaemia, myelomonocytic leukaemia and chronic lymphatic leukaemia.Of the 10 patients with untreated pernicious anaemia, three had raised, three had normal, and four subnormal leucocyte folate. The changes in leucocyte folate produced by B12 therapy in four of the pernicious anaemia patients are described.
Erythroid Aplasia in Riboflavin‐Deficient Baboons and its Relation to Marasmus and Kwashiorkor
Authors: Kondi Athena , Foy H. , Mbaya Vertistine 
Published: March 2008

SUMMARYAn erythroid hypoplasia characterized by falls in red cell precursors, haemoglobin, packed cell volume, reticulocytes and sometimes platelets, resembling that which occurs in marasmus and kwashiorkor, has been produced experimentally in baboons on a synthetic riboflavin‐deficient diet. The red cell uptake of59Fe on the 8th and 12th days was 40 per cent lower in the riboflavin‐deprived animals and thus agreed with the low marrow activity estimated cytologically. The haematological abnormalities were accompanied by gross skin changes, falls in serum folate, and sometimes intramuscular and intestinal haemorrhages. Striking macroscopic and histological abnormalities were also present in the adrenals. All the abnormalities disappeared when riboflavin was given, and re‐appeared when it was again omitted from the diet. When prednisone was given to the deprived animals instead of riboflavin, only the erythroid hypoplasia disappeared. Since the diet was adequate in all respects and contained 20 per cent of its kilocalories in the form of animal protein, the abnormalities cannot have been due to protein deficiency. The pair‐fed controls on a similar diet but with added riboflavin developed no abnormalities. It is suggested that as riboflavin is an important co‐enzyme in many vital metabolic processes, its absence may affect marrow activity directly or by disturbing corticosteroid metabolism, as well as being associated with serum protein changes.
Complications and. Treatment of Acquired Aplastic Anaemia
Authors: Vincent P. C. , Gruchy G. C. de 
Published: March 2008

SUMMARYThe clinical and haematological findings in 43 cases of aplastic anaemia are reviewed. Approximately two‐thirds of the cases were considered to be secondary to toxic agents, the commonest of which were chloramphenicol and phenylbutazone, and one‐third were idiopathic. Severe neutropenia and thrombocytopenia were a feature of the series, a neutrophil count of less than 500/cu.mm. and a platelet count of less than 20,000/cu.mm. being found initially in over one‐half of cases. There was an unexplained and marked elevation of the ESR in over 90 per cent of cases. Fifty‐two episodes of infection occurred in 29 patients (67 per cent); 36 of these episodes were serious. Infection was more frequent in young patients and serious infection was more likely in the presence of severe neutropenia. The occurrence of infection, especially serious infection, was usually followed by a fall in neutrophil and platelet counts, and frequently by the onset of serious bleeding. Bleeding phenomena occurred at some stage in all but one patient and in two‐thirds of cases the bleeding was serious. Thrombocytopenia was marked in patients with serious bleeding but equally low platelet counts were found in patients in whom bleeding was not serious. The onset of serious bleeding was more likely in the presence of infection.Administration of corticosteroids or corticotrophin either with or without androgens was followed by a haematological response in about two‐thirds of cases, but in only one‐third was the response sustained; in the remainder it was transient. In those with a sustained response, the haemoglobin and neutrophil values gradually increased and ultimately returned to normal; however, the platelet count returned to normal in less than one‐half of these.The overall mortality rate was 63 per cent, bleeding and infection being the commonest causes of death. The mortality was higher in the idiopathic cases (86 per cent) than in the secondary cases (52 per cent); however, the period of survival in fatal secondary cases was shorter than that in fatal idiopathic cases. The prognosis appeared to be better in patients with secondary aplasia, in patients with an initial haemoglobin value greater than 8 g. per 100 ml., and in patients who remained free of serious bleeding. The outcome showed no relation to sex, age, the initial neutrophil and platelet counts or the cellularity of the bone marrow on admission. Seven of the 16 survivors are considered cured, eight are well but are still thrombo‐cytopenic, and one has developed paroxysmal nocturnal haemoglobinuria 8 years after diagnosis and 6 years after a complete haematological remission. Treatment with corticosteroids is still necessary to control bleeding in three of the eight survivors with thrombocytopenia.
X‐Linked Hypochromic Anaemia of Mice
Authors: Bannerman R. M. , Pinkerton P. H. 
Published: March 2008

SUMMARYAn X‐linked recessive mutant gene (symbol sla) in the mouse causes hypochromic anaemia in hemizygous males and homozygous females; heterozygous carrier females show only slight changes. A detailed assessment of the anaemia is presented here. The red cells show a wide variety of morphological changes, including target cell formation, and the MCV is strikingly reduced. The anaemia and morphological changes tend to regress with increasing age. The anaemia also responds to parenteral iron‐dextran treatment, but not to pyridoxine and other agents.These findings and preliminary results of other investigations suggest that the underlying metabolic disturbance is likely to involve some step in the supply of iron to the erythron. It thus appears that in the mouse an X‐linked locus plays a role in iron metabolism, and this mutant provides an opportunity further to elucidate mechanisms of iron transfer.
Inhibitor of Platelet Aggregation Present in Saliva of the Vampire Bat Desmodus rotundus
Authors: Hawkey Christine 
Published: March 2008

SUMMARYA substance capable of inhibiting ADP‐induced and thrombin‐induced aggregation of human platelets in vitro has been found in saliva of D. rotundus. This substance does not act on ADP directly but probably exerts its effect on the platelet ADP‐binding sites or on the plasma co‐factor involved in this reaction. Partial separation of the aggregation inhibitor from other active substances in the saliva has been carried out using G‐200 Sephadcx.
The Excretion of Methylmalonic Acid and Succinic Acid in Vitamin B12 and Folate Deficiency
Authors: Brozović M. , Hoffbrand A. V. , Dimitriadou A. , Mollin D. L. 
Published: March 2008

SUMMARYThe excretion of methylmalonic acid (MMA) and of succinic acid was measured in 18 control subjects and in 58 patients with vitamin B12 and/or folate deficiency.The 18 control subjects excreted from 0.0 to 3·5 mg. MMA in 24 hours. MMA excretion was raised in 27 of 41 patients (Group I) with conditions associated primarily with B12 deficiency. These 27 patients included 15 patients with Addisonian pernicious anaemia, two patients following total gastrectomy, two patients with anatomical lesions of the small intestine and eight patients following partial gastrectomy, whereas MMA excretion was normal in four patients with atrophic gastritis and in a further 10 patients following partial gastrectomy.In Group I, MMA excretion was raised in all but one of the patients with serum B12 levels less than 100 pg./ml. due to uncomplicated B12 deficiency, but was invariably normal in patients with borderline serum B12 levels (from 100 to 160 pg./ml.). In the patients with serum B12 levels less than 100 pg./ml., with associated iron and/or folate deficiency, the excretion of MMA tended to be lower than in patients with uncomplicated B12 deficiency, and was often normal.MMA excretion was slightly raised in one of 17 patients with megaloblastic anaemia, primarily due to folate deficiency (Group II), although six of them had serum B12 levels less than 100 pg./ml. The patient with a raised MMA excretion needed B12 therapy for a full haematological remission.The 18 control subjects excreted from 2.0 to 12.5 mg. succinic acid in 24 hours. Succinic acid excretion was subnormal in nine and raised in five patients in Group I. These 14 patients all had serum B12 levels less than 100 pg./ml.None of the Group II patients excreted subnormal amounts of succinic acid but three, including two patients with serum B12 levels less than 100 pg./ml., excreted raised amounts of succinic acid.
Epitope recognition patterns of thyroid peroxidase autoantibodies in healthy individuals and patients with Hashimoto's thyroiditis*
Authors: Nielsen Claus H. , Brix Thomas H. , Gardas Andrzej , Banga J. Paul , Hegedüs Laszlo 
Published: March 2008

SummaryObjective  Thyroid peroxidase antibodies (TPOAb) are markers of autoimmune thyroid disease (AITD), including Hashimoto's thyroiditis (HT), but naturally occurring TPOAb are also detectable in healthy, euthyroid individuals. In AITD, circulating TPOAb react mainly with two immunodominant regions (IDR), IDR‐A and IDR‐B. The present study was undertaken in order to compare the epitope recognition pattern of TPOAb in HT patients and healthy subjects.Design  Sera from 21 out of 98 healthy controls were selected on the basis of high TPOAb values, required for determination of TPOAb recognition pattern; as were sera from 92 HT patients.Measurements  Measurement of IDR‐reactivity was possible in 90 patients and 12 controls. IDR‐A‐, IDR‐B‐ and non‐IDR‐A/non‐IDR‐B‐Ab constituted 24 ± 11%, 50 ± 15% and 26 ± 12%, respectively, in the patients. The distribution in the controls was distinctly different, only 12 ± 13% being directed against IDR‐A (P < 0·002) and 66 ± 22% against IDR‐B (P < 0·002). Half of the healthy individuals, vs. none of the HT patients, lacked IDR‐A reactivity completely (P < 0·0001). In HT patients, IDR‐B‐Ab proportions increased slightly with increasing TPOAb levels (P < 0·05), while IDR‐B‐Ab of the controls showed a strong opposite trend (P < 0·0001). Accordingly, the proportion of non‐A/non‐B‐Ab correlated with TPOAb levels in the healthy controls (P < 0·008), and an inverse correlation was seen in HT patients (P < 0·02).Conclusion  The data suggest that TPOAb do not differ only in quantity between HT patients and healthy individuals, but may also follow distinct qualitative patterns. Larger studies are required to confirm this, and to determine whether the propensity to produce antibodies to certain TPO epitopes, for example, IDR‐A, is of pathogenic relevance.
Increased serum visfatin in patients with metabolic syndrome and carotid atherosclerosis
Authors: Zhong Ming , Tan Hong‐wei , Gong Hui‐ping , Wang Shu‐fang , Zhang Yun , Zhang Wei 
Published: March 2008

SummaryObjective  Visfatin is a newly identified adipocytokine and recent studies indicated that visfatin may have potential proinflammatory effect. However, its pathophysiological role in the metabolic syndrome (MetS) is not fully understood. In this study we investigated whether serum visfatin levels is altered in patients with the MetS, and compared the levels of visfatin between patients with and without carotid plaques.Design and method  A total of 139 patients with MetS and 105 controls were included. The patients were further divided into two groups: 40 with carotid plaques and 99 without carotid plaques. Serum visfatin was measured by using enzyme immunoassay method and carotid intimal‐media thickness (IMT) was measured by ultrasound in all subjects.Results  Serum visfatin was elevated in both MetS patients with and without carotid plaques compared to controls (log visfatin: 1·14 ± 0·14 vs. 0·99 ± 0·17 ng/ml vs. 0·93 ± 0·23 ng/ml, P < 0·001 and P < 0·05 vs. control group, respectively), and in patients with carotid plaques more than in patients without carotid plaques (P < 0·001). Multiple stepwise regression analysis revealed that only LDL‐cholesterol correlated with visfatin, and visfatin independently correlated with max IMT in the patients with MetS. A log visfatin > 1·08 ng/ml had 70% sensitivity and 67% specificity for detecting patients with carotid plaques.Conclusions/interpretation  Our results showed that serum visfatin was increased in patients with MetS, especially in those with carotid plaques. Visfatin may be an inflammatory marker of MetS.