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Biomedical subjects

J G Hudson

Publications and source records attributed to J G Hudson.

7 recordsLinked to original sources
PubMed1999

The effect of high altitude on platelet counts, thrombopoietin and erythropoietin levels in young Bolivian airmen visiting the Andes.

Recognition of thrombosis as a complication of exposure to high altitude has stimulated interest in rheological changes resulting from hypobaric hypoxia. Previous studies of platelet counts at high altitude have yielded conflicting results and have not been studied in conjunction with potential mediating cytokines. We studied the effects of high-altitude exposure on platelet numbers, thrombopoietin (tpo) and erythropoietin (epo) levels in man. A group of 28 volunteers from the Bolivian Airforce stationed at Santa Cruz (600 m altitude) were studied 48 h and 1 week after their ascent to La Paz (3600 m). In addition 105 volunteers based at Santa Cruz for at least 1 year were compared with 175 age- and sex-matched residents at El Alto (4200 m). Platelet counts were measured immediately after sampling and serum samples assayed for tpo and epo. In the ascending group, mean platelet counts were 251 x 10(9), 367 x 10(9) and 398 x10 (9)/l at 600 m and following 48 h and 1 week at 3600 m respectively. Mean tpo levels were 132.5, 76 and 92 pg/ml with epo values of 2.98, 11.6 and 7.9 mIU/ml respectively. In the resident populations mean platelet counts were 271 x 10(9)/l in the low- and 471 x 10(9)/l in the high-altitude groups. Mean tpo and epo levels measured 69.3 pg/ml and 4.5 mIU/ml respectively at 600 m and 58.5 pg/ml and 5.1 mIU/ml at 4200 m. In conclusion we have demonstrated a significant and sustained elevation in platelet numbers within 48 h of ascent to high altitude. Our findings do not support a role for tpo as a mediator of the increased platelet count. However, these data do not discount epo as a potential candidate.

Adaptation, Physiological↗
PubMed1995

In vitro demonstration of a fundamental difference in the proliferation of murine and human bone marrow and lymphocytes following ultraviolet irradiation: relevance to bone marrow transplantation.

Exposure of rodent allogeneic donor marrow and splenocyte grafts to ultraviolet radiation (UVR) has been shown to permit durable engraftment at doses that abolish graft-versus-host disease (GVHD) and graft rejection. We have compared both murine and human alloreactive and mitogen-induced lymphoid responses and bone marrow proliferation in mixed lymphocyte culture (MLC), phytohemagglutinin (PHA)-induced proliferation and colony-forming unit-granulocyte/macrophage (CFU-GM) assays using germicidal UVC (200-290 nm), broadband and narrowband UVB (290-320 nm) and UVA (320-400 nm) sources. Our data show a wavelength and dose-dependent reduction in lymphoid proliferation in the mouse with CFU-GM survival of 50-75% of control at doses required to abolish allogeneic lymphocyte responses for all lamps. In contrast, human lymphocyte responses are more resistant to UVC with CFU-GM proliferation reduced to zero when allostimulation is abolished. Mitogen-induced lymphoid responses show a similar wavelength-dependent sensitivity. Abolition of response in MLC using UV-irradiated stimulator cells was less sensitive than proliferation with UV-irradiated responder cells at all wavelengths in both species. With all sources, murine CFU-GM proliferation is less susceptible to UVR than human marrow at doses required to abolish lymphoid responses.

Animals↗
PubMed1994

A comparison of four ultraviolet sources to alter graft-versus-host responses.

Graft-versus-host disease (GVHD) is a major contributor to the morbidity and mortality associated with allogeneic bone marrow transplantation. Direct ultraviolet B (UVB) irradiation of bone marrow and spleen cell allografts in mice using broadband lamps is known to abolish alloreactive responses which would normally cause GVHD. Using a histoincompatible murine model, we have extended these observations by comparing the physical spectrum of four UV sources (the Philips TUV8W, TL12 and TL01, and the Spectronics XX15B) with in vitro assessment of bone marrow progenitor cell damage and suppression of lymphocyte proliferation and in vivo comparison of the effect on GVHD of the TL12 and XX15B and on the rate of engraftment with the TL12. At doses of uv found to abolish lymphocyte proliferation (2.5, 7, 12 and 1000 J m(-2) with the TUV8W, XX15B, TL12 and TL01 lamps) colony-forming unit granulocyte-macrophage (CFU-GM) proliferation was reduced to 81%, 71%, 79% and 62%, respectively. At an optimal dose found to suppress GVHD (100 J m(-2) integrated radiant energy from 200-320 nm for the TL12 and XX15B) CFU-GM proliferation showed a reduction of 98% with the XX15B and 86% with the TL12. At this radiant energy with the TL12, the rate of bone marrow engraftment was impaired with 72% marrow cellularity at 2 weeks, decreasing to 48% after 200 J m(-2). Our results with this model demonstrate that broadband UVB irradiation of bone marrow permits transplantation across a major histocompatibility barrier. Furthermore we have provided in vitro evidence that narrowband UVB or UVC might potentially be applied to this model.

Animals↗
PubMed1994

Ultraviolet irradiation for the prevention of graft-versus-host disease and graft rejection in bone marrow transplantation.

This review describes an approach to the prevention of graft-versus-host disease (GVHD) and graft rejection following allogeneic BMT that differs from conventional methods. Ultraviolet (UV) irradiation inhibits the proliferative responses of lymphoid cells to mitogens and alloantigens by inactivation of T lymphocytes and dendritic cells, and in animal models this can prevent both GVHD and graft rejection. It is important that the marrow repopulating capacity of haemopoietic stem cells is not damaged by the irradiation process. We have found that polymorphic microsatellite markers are a sensitive way of assessing the impact of UV irradiation on chimerism after BMT in rodents.

Antigen-Presenting Cells↗