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B Mayhew

Publications and source records attributed to B Mayhew.

17 recordsLinked to original sources
PubMed2000

The application of high density microarray for analysis of mitogenic signaling and cell-cycle in the adrenal.

Angiotensin II (AII) binds to specific G-protein coupled receptors and is mitogenic in adrenal, liver epithelial, and vascular smooth muscle cells. The H295R human adrenocortical cell line, which expresses AII receptors predominantly of the AT1 subclass, proliferates in response to treatment with AII. The induction and maintenance of cellular proliferation involves a precisely coordinated induction of a variety of genes. As the human genome sequencing projects near completion a variety of high throughput technologies have been developed in order to create dynamic displays of genomic responses. One high throughput method, the gridded cDNA microarray has been developed in which immobilised DNA samples are hybridized on glass slides for the identification of global genomic responses. For this purpose high precision robotic microarrayers have been developed at AECOM. The cyclin D1 gene, which encodes the regulatory subunit of the cyclin D1-dependent kinase (CD1K) required for phosphorylation of the retinoblastoma protein (pRB), was induced by AII in H295R cells. Abundance of the cyclin D1 gene is rate-limiting in G1 phase progression of the cell-cycle in a variety of cell types. AII induced cyclin D1 promoter activity through a c-Fos and c-Jun binding sequence at -954 bp. Theabundance of c-Fos within this complex was increased by AII treatment. Analysis of AII signaling in adrenal cells by cDNA microarray demonstrated an induction of the human homologue of Xenopus XPMC2 (HXPMC2). The cDNA for XPMC2 was previously shown to rescue mitotic catastrophe in mutant S. Pombe defective in cdc2 kinase function. Further studies are required to determine the requirement for cyclin D1 and XPMC2H in AII-induced cell-cycle progression and cellular proliferation in the adrenal.

Adrenal Cortex↗
PubMed1994

Measurement of insulin wastage in five Ontario hospitals.

This study was designed to determine the extent of insulin wastage and the extrapolated cost of wastage for Ontario hospitals. The five hospitals in the study were chosen to include differences in patient mix and drug distribution systems. Beginning and ending inventories of all insulin types were taken spanning a six-week period. The quantity of insulin dispensed and wasted during this time period was recorded. Partial vials were measured using a calibrated scale. Wastage was calculated as insulin discarded divided by the amount of insulin used in the time period. Insulin wastage averaged 34.1%. This was equivalent to up to $8,000 a year for the largest hospital surveyed and translates to an estimated cost of $360,000 a year in all Ontario hospitals. Therefore, hospitals should estimate their insulin wastage and seek ways to reduce it. The pharmaceutical industry should be encouraged to develop cost-effective insulin delivery systems.

Data Collection↗
PubMed1979

The production of contact sensitivity by the injection into the footpads of recipients of the lymph node cells from mice 1 day after painting the skin with contact sensitizing agent: requirement for matching at the major histocompatibility complex between donor and recipient mice.

Donor mice were painted on the skin of the abdomen with the contact sensitizing agent, oxazolone. One day later 2-5 x 10(6) cells from the regional lymph nodes were injected into the footpads of recipient mice. Contact sensitivity was detected 6 days later by challenging the ears of the recipients and measuring the increase of thickness at 24 h. Good contact sensitivity was obtained when CBA cells were injected into CBA mice and BALB/c cells injected into BALB/c mice; the injection of BALB/c (H-2d) cells into CBA (H-2k) mice and vice versa failed to give rise to contact sensitivity. Hybrid F1 cells gave intermediate responses. The contact sensitivity caused by the injection of small numbers of lymph node cells into the footpad is interpreted as a mode of active immunization and the present results show that this only occurs when there is genetic matching at the major histocompatibility complex between the donor and the recipient mouse.

Animals↗
PubMed1977

Analysis of the induction phase of contact sensitivity by footpad transfer of regional lymph node cells. Macrophages and radioresistant T-lymphocytes induce immunity.

The skin of CBA mice was painted with the contact sensitizing agent 4-ethoxymethylene-2-phenyloxazolone (oxazolone). One day later the regional lymph node cells were injected into the footpads of normal recipients. The recipients were tested 6 days later for contact sensitivity by challenging the ears with oxazolone and measuring the increase of ear thickness at 24 h. T cells and macrophages in the regional lymph nodes each independently gave rise to contact sensitivity in the recipient following injection into the footpad. This activity of T cells and macrophages was found in lymph nodes taken 1, 3 and 4 days after painting the donors. The role of T cells in the injected population was shown by purifying T cells by nylon-wool filtration and rosetting with sheep red cells coated with antibody and complement (EAC rosetting) and by destroyed T cells with anti-0 serum and complement. The activity of purified T cells resisted 2000 rad in vitro. The activity of cells from T-deprived (B) mice showed that a second cell type was important in the footpad transfer. This cell behaved like a macrophage, and not like a B cell, on EAC rosetting in the presence or absence of divalent cations and on treatment with silica and carrageenan--agents which damage macrophages. Our working hypothesis is that the footpad transfer may be caused independently by macrophages or T cells with oxazolone (probably linked to major histocompatibility complex antigens) on their surface and that these cells act by collaborating with T cells in the recipient which give rise to the effector cells for contact sensitivity.

Animals↗
PubMed1976

Adult thymectomy prevention of the appearance of suppressor T cells which depress contact sensitivity to picryl chloride and reversal of adult thymectomy effect by thymus extract.

Suppressor cells, which depress the passive transfer of contact sensitivity appear in the lymph nodes and spleen of mice injected with picryl sulfonic acid (PSA). These cells produce a soluble suppressor T cell product (s-TCP), and immune lymph node cells incubated in s-TCP fail to transfer contact sensitivity. This paper shows that the appearance of suppressor T cells following the injection of PSA was prevented by adult thymectomy (ATx). ATx also limited the production of s-TCP. However, ATx had no effect on the DNA synthesis which occurs in the lymph nodes of mice injected with PSA. The adverse effect of ATx on suppressor cells was completely reversed by a neonatal thymus graft placed under the renal capsule and partially reversed by grafts given 600 r in vitro and to a limited extent by grafts given 1000 r. The injection of thymus extract also reversed the effect of ATx whereas splenic extract was inactive. It is suggested that the suppressor T cell which depresses contact sensitivity is dependent on the presence of the thymus because it requires a thymus hormone, and not primarily because it belongs to a short-lived population which is rapidly renewed by cells coming from the thymus.

Animals↗
PubMed1975

Control of the immune response. I. Depression of DNA synthesis by immune lymph node cells.

The DNA response in the regional lymph nodes draining the site of immunization with contact sensitizing agents was assessed by measuring the uptake of radioactive iododeoxyuridine. The DNA response in the regional lymph nodes reached a peak on day 3 after immunization and fell to pre-immunization levels by day 6. The hypothesis was tested that lymph node cells from mice immunized with picryl chloride might depress the DNA response to the same antigen. Immune lymph node cells were injected intravenously and the recipient mice were immunized with picryl chloride on the same day. The immune cells depressed the DNA response on day 4 by an average of about 60 per cent. Smaller but significant depression also occurred on day 3. The cells responsible for the depression appeared in the regional lymph nodes 3-4 days after immunization and disappeared by day 21. The transfer of small numbers of immune cells (less than 2-5 X 10(6)) increased the DNA response in recipients 4 days after immunization with picryl chloride. The depression of the DNA response was largely specific. Pooled data from ten experiments showed that cells immunized with 4-ethoxymethylene-phenyl oxazolone ('oxazolone') caused no depression of the DNA response to picryl chloride, although in two of these experiments significant depression of about 21 per cent was seen. Similar results were obtained when immune cells were injected into mice immunized with 'oxazolone'.

Animals↗
PubMedDate not supplied

Induction of cell-mediated immunity in the mouse: circumstantial evidence for highly immunogenic antigen in the regional lymph nodes following skin painting with contact sensitizing agents.

This paper describes an investigation of why contact sensitizing agents cause strong cell-mediated immunity. Contact sensitivity was induced in mice by painting the skin with 4-ethoxymethylene-2-phenyloxazolone (oxazolone), and measured by the increase of ear thickness following challenge six days later. Reactivity was transferred by taking the regional lymph node cells from mice 18 h after immunization and injecting them into the footpads of recipients. This "18-h transfer" has several characteristics. As few as 2 X 10(4) cells were effective. The donor lymph node cells were best taken one to three days after immunization, were less effective on day 4 and virtually inactive by day 7. The recipients developed contact sensitivity when challenged on day 4, but lacked sensitivity when challenged on days 1 and 2 after transfer. The transferred cells were still active after treatment with anti-theta serum and complement. They also resisted 2,000 R in vitro, mitomycin, vinblastine, and inhibitors of protein synthesis such as emetine, cycloheximide and puromycin. The transfer was prevented by treatment with trypsin, freeze-thawing, and heating at 56 C. Plasma membranes were also immunogenic. The evidence suggests that the "18-h transfer" is a special type of active immunization, not due to ordinary free oxazolone, and that the agent is present within the lymph node in a free oxazolone, and that the agent is present within the lymph node in a specially immunogenic location or form.

Animals↗