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Biomedical subjects

R Woodman

Publications and source records attributed to R Woodman.

At least 19 recordsLinked to original sources
PubMed2002

Identification of a novel HLA-B*07 allele--HLA-B*0726.

We describe here, the identification of a novel HLA-B*07 allele named HLA-B*0726. This allele was found in a Caucasian individual serologically typed as HLA-B7, B35. Novel DNA probe patterns for the HLA-B*07 allele were found using HLA-B specific reverse sequence-specific oligonucleotide probe (SSOP) and sequence-specific primer (SSP) typing. DNA sequencing demonstrated the presence of a new HLA-B*07 sequence variant encoding a single nucleotide substitution from a G to a T at nucleotide 539 in exon 3. This results in an amino acid substitution from arginine to leucine at residue 156 in exon 3.

Alleles↗
PubMed2002

Successful treatment of post-transplant lymphoproliferative disorder in autologous blood stem cell transplant recipients.

We report three cases of post-transplant lymphoproliferative disorder (PTLD) in the context of autologous stem cell transplantation (ASCT) for multiple myeloma (MM) and non-Hodgkin's lymphoma. The first two cases received ASCT for MM, one with a CD34-selected autograft and the other with an unmanipulated autograft. Both these cases of PTLD achieved a complete response following treatment with IVIG, gancyclovir, solumedrol and interferon (IFN). The third case received ASCT with an unmanipulated autograft for relapsed angioimmunoblastic lymphoma. He also achieved a complete response but only after rituximab was added to IVIG, gancyclovir, solumedrol and IFN. None of these patients experienced a relapse of their PTLD with follow-up ranging from 1.5 to 5 years. These cases highlight the importance of considering PTLD in the differential diagnosis of lymphadenopathy and fever post ASCT. They also demonstrate the possibility of durable complete remission of post-ASCT PTLD following antiviral and immune modulating therapy.

Adult↗
PubMed2001

Regulation of leukocyte adhesion to heart by the tripeptides feG and feG(NH2).

The role of the D-isomeric form of the salivary gland tripeptide FEG (feG) and its carboxyl-amidated derivative, feG(NH2), in regulating leukocyte adherence to nonfixed atrial slices from Sprague-Dawley rats was examined under static conditions. Optimal binding of the leukocytes was seen if the leukocytes were treated with platelet activating factor (PAF; 10(-9)M). The increased adherence of PAF-treated peripheral blood leukocytes was totally inhibited by both feG and feG(NH2) (10-9M), as well as by antibodies against CD18 and CD49d. In contrast, the binding of peritoneal leukocytes was blocked only by CD49d antibody. Circulating leukocytes obtained from lipopolysaccharide (LPS) treated (2 mg/kg ip) rats did not bind to atrial slices obtained from normal hearts, but readily bound to atrial slices obtained from LPS-treated rats. This leukocyte binding was inhibited by in vivo feG treatment (100 microg/kg ip, 24 h before harvest) or by treating the isolated cells with feG (10(-9)M). The amidated peptide feG(NH2) reduced neutrophil accumulation in the atrium elicited by ip injection of LPS, whereas feG was ineffective. The reduction in neutrophil infiltration into the myocardium by feG(NH2) and the prevention of leukocyte interaction with myocytes seen with both feG and feG(NH2) probably results in hindered leukocyte migration in the inflamed heart, resulting in less tissue damage. The inhibition by these tripeptides on neutrophil adhesion to myocytes suggests that salivary glands hormones regulate the severity of cardiac inflammation.

Animals↗