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Biomedical subjects

J Beard

Publications and source records attributed to J Beard.

At least 73 records · Page 4Linked to original sources
PubMed1988

High-dose intravenous immunoglobulin and splenectomy for the treatment of HIV-related immune thrombocytopenia in patients with severe haemophilia.

Four patients with severe haemophilia A and one patient with severe Christmas disease developed severe immune thrombocytopenia (platelet count less than 20 x 10(9)/l). All five patients were HIV-antibody positive and one was HIV-antigen positive. Four patients were treated initially with prednisolone, but with only a transient platelet response in three and no response in the fourth. All patients were treated with high dose intravenous immunoglobulin (0.4 g/kg daily for 5 d) resulting in a rise in platelet count in all cases (range 138-300 x 10(9)/l) and then proceeded to splenectomy. Three remain in complete remission after 6-14 months, and one showed a good response with platelet counts ranging from 103 to 187 x 10(9)/l. The fifth patients achieved a normal platelet count for 3 months post-splenectomy, but suffered a relapse with platelet counts ranging from 25 to 108 x 10(9)/l over the next 3 years. However, following a severe Varicella infection 10 months ago, during which he developed a marked transient thrombocytosis, he has also maintained a normal platelet count.

Adolescent↗
PubMed1988

Norepinephrine turnover in iron deficiency at three environmental temperatures.

Iron-deficient anemic rats had a significant elevation in urinary norepinephrine (NE) after 7 days at 30 and 24 degrees C, but not at 10 degrees C, compared with control animals. NE turnover studies were performed to examine sympathetic nervous system activity in a tissue-specific fashion. NE content in myocardium decreased by nearly 50% in hypertrophied iron-deficient hearts at all three temperatures, whereas fractional turnover rates were compensatorily increased. In contrast, interscapular brown adipose tissue NE turnover was significantly reduced to 30% of normal in iron-deficient animals at both 30 and 10 degrees C. Serum triiodothyronine concentrations were similar to controls at 30 degrees C but were decreased at lower temperatures. Serum tetraiodothyronine concentrations were lower in iron-deficient animals at all three environmental temperatures. We conclude that increased sympathetic nervous system activity compensatory to temperatures below thermoneutrality is less well controlled in iron-deficient animals than in controls, and at a low environmental temperature this may possibly explain the poor thermoregulatory capacity of iron-deficient animals. A generalized hypernoradrenergic state is not supported by our NE turnover study and does not explain the elevated urine NE concentrations.

Adipose Tissue↗
PubMed1988

Primary polycythaemia, essential thrombocythaemia and myelofibrosis--three facets of a single disease process?

Primary polycythaemia (PP), idiopathic myelofibrosis (MF), essential thrombocythaemia (ET) and chronic granulocytic or myeloid leukaemia (CGL) are clonal disorders of the pluripotent haemopoietic stem cells. We have studied granulocyte, megakaryocyte and erythroid progenitors from the peripheral blood of 7 patients with PP, 9 with ET, 19 with MF and 6 with CGL in order to characterise similarities and differences at the committed progenitor cell level. Spontaneous megakaryocytic and erythrocytic growth was characteristic of MF, PP and ET but was not seen in CGL. Circulating erythroid (BFU-E) and granulocyte/macrophage (CFU-GM) progenitors were markedly increased in MF and CGL, less raised in ET and closest to normal in PP. Erythropoietin-independent erythroid bursts (EIBFU-E) grew from the blood of patients with MF, PP and ET but spontaneous growth of megakaryocytes occurred in only MF and ET. These results suggest a progression of increasing abnormality from PP, where EIBFU-E occurred with relatively normal numbers of circulating progenitors, to ET where both EIBFU-E and megakaryocyte precursors regularly occur with elevated numbers of progenitors, to MF where spontaneous BFU-E, CFU-Mk and CFU-GM occur at high levels.

Colony-Forming Units Assay↗
PubMed1987

Feed efficiency and norepinephrine turnover in iron deficiency.

Norepinephrine turnover and energetic efficiency studies were conducted in three groups of male Sprague-Dawley rats placed on low iron diets for 5 weeks on weaning. Iron-deficient rats had significant anemia (hematocrit less than 20%) and growth retardation relative to pair-fed and ad libitum fed controls who received the same diet plus weekly iron dextran injections. Energetic efficiency over a 7-day period was nearly 30% less in anemic animals. This was associated with significantly higher rates of norepinephrine turnover in brown adipose tissue (110%) and heart (330%) with significant hypertrophy in both tissues. There was no difference in body composition in ad libitum groups. Plasma triiodothyronine and thyroxine were reduced by 37% in iron deficients compared to controls. Thus 39% increase in caloric requirements in iron deficiency is associated with increased sympathetic and perhaps thermogenic activity in brown adipocytes.

Adipose Tissue↗
PubMed1984

Effect of iron-deficiency anemia on hormone levels and thermoregulation during cold exposure.

When exposed to an ambient temperature of 4 degrees C, iron-deficient anemic rats become hypothermic. This lesion is related more to anemia than to tissue iron deficiency, since exchange transfusion to hematocrits over 25 restored normal thermoregulatory performance. Likewise poor cold responses were induced in control rats by transfusion to low hematocrits. Cold sensitivity in all anemic animals was paralleled by poor thyroid responses: there was a significant positive correlation between hematocrit and percent rise in triiodothyronine (r = 0.63) and thyroxine (r = 0.53) during 6 h at 4 degrees C. Basal levels of thyroid-stimulating hormone (TSH) were similar in control and iron-deficient animals: after cold exposure, TSH rose to higher levels in those animals with hematocrits over 25 than in those with lower hematocrits. Diminished O2 delivery to tissues responsible for heat production is probably a major component of the cold sensitivity of anemic rats. The novel finding that thyroid hormone responses are compromised by anemia implies effects on hormonal regulation that may also contribute to this functional lesion.

Anemia, Hypochromic↗
PubMed1977

The subunit structure of rabbit skeletal-muscle phosphofructokinase and the amino acid sequence of the tryptic peptide containing the highly reactive thiol group.

1. The single highly reactive (class I) thiol group per 80000-mol.wt. subunit of skeletal-muscle phosphofructokinase was specifically carboxymethylated with iodo[2-14C]acetate, and after denaturation the remaining thiol groups were carboxymethylated with bromo[2-3H]acetate. After tryptic digestion and peptide 'mapping' it was found that the 14C radioactivity was in a spot that did not contain significant amounts of 3H radioactivity, so it is concluded that there is not a second, 'buried' cysteine residue within a sequence identical with that of the class-I cysteine peptide. 2. The total number of tryptic peptides as well as the number of those containing cysteine, histidine or tryptophan were inconsistent with the smallest polypeptide chain of phosphofructokinase (mol.wt. about 80000) being composed of two identical amino acid sequences. 3. The amino acid sequence of the tryptic peptide containing the class-I thiol group was shown to be Cys-Lys-Asp-Phe-Arg. This sequence is compared with part of the sequence containing the highly reactive thiol group of phosphorylase.

Amino Acid Sequence↗
PubMed1977

In vivo immune responses of mice during carcinogenesis by ultraviolet irradiation.

In these experiments, we tested in various in vivo assays the immune responses of inbred C3H/HeN(MTV-) (C3H-) mice during carcinogenesis by chronic exposure to UV irradiation. Although the UV-treated mice were unable to reject syngeneic UV-induced tumor transplants, they rejected H-2-incompatible tumor allografts and H-2-compatible skin allografts. The primary hemagglutinin response to sheep red blood cells was normal in these mice, as were the induction of a local graft-versus-host reaction with lymphoid cells from UV-irradiated donors and the induction of an inflammatory response to dimethyl sulfoxide in the footpads of UV-treated mice. An early transient depression of two reactions in UV-irradiated mice occurred: delayed hypersensitivity to dinitrochlorobenzene measured by footpad swelling and the graft-versus-host reaction in UV-irradiated recipients measured by the use of the popliteal lymph node weight gain assay. Both of these reactions returned to a normal level before the development of primary tumors. We conclude that the inability of UV-irradiated mice to reject syngeneic and autochthonous UV-induced tumors was not due to a generalized immunosuppressive effect of chronic UV irradiation.

Animals↗
PubMed1903

The Germ-Cells.

Explore the source record for details and available documents.

Journal Article↗
PubMedDate not supplied

Interactions of iron deficiency, anemia, and thyroid hormone levels in response of rats to cold exposure.

We have earlier shown that iron-deficient rats have increased urinary norepinephrine (NE) excretion. They also have an exaggerated rise in urinary NE when placed in the cold, a stimulus known to cause increased NE excretion in normal rats. Nonetheless, they fall to maintain body temperature. We have now examined the thyroidal response to cold in iron-deficient rats. As others have shown, control rats had a rise in plasma levels of thyroxine (T4) and triiodothyronine (T3) soon after entering the cold environment (4 degree C); they also maintained a rectal temperature above 36 degree C. In the iron-deficient rats, basal levels of T3 and T4 were normal, but there was little or no increase after 6 hr in the cold, and, as before, body temperatures fell. Injections of T3, 10 microgram/kg, 15 min before cold exposure improved the ability of iron-deficient rats to maintain body temperature, but they still did not do as well as the controls. We conclude that the inability of iron-deficient rats to increase T3 levels after cold exposure is one factor in their poor resistance to cold. The defect could involve inability to augment thyroid secretion, imparied ability to convert T4 to T3 in peripheral tissues, or both. Preliminary data suggest that anemia is an important and perhaps critical factor in the cold sensitivity of iron deficiency. Transfusing iron-deficient rats from their usual hematocrit of 15-20 to one of 30 restores cold resistance to normal. Transfusion also allows a more normal thyroid response, with a rise in T3 and T4 levels, so thyroid hormones may be a factor in the improvement produced by transfusion.

Anemia, Hypochromic↗