M. B. Pepys

Publication List Details

Period

2001 - 2006

Number

11

Co-Authors

Targeting C-reactive protein for the treatment of cardiovascular disease (2006)

Pepys, M.B., Hirschfield, G.M., Tennent, G.A., Gallimore, J.R., Kahan, M.C., Bellotti, V., ...

Complement-mediated inflammation exacerbates the tissue injury of ischaemic necrosis in heart attacks and strokes, the most common causes of death in developed countries. Large infarct size increases...

Transgenic human C-reactive protein is not proatherogenic in apolipoprotein E-deficient mice (2005)

Hirschfield, G.M., Gallimore, J.R., Kahan, M.C., Hutchinson, W.L., Sabin, C.A., Benson, G.M., ...

The association between circulating concentrations of C-reactive protein (CRP) and future atherothrombotic events has provoked speculation about a possible pathogenetic role of CRP. However, we show...

Inflammation and endothelial function: direct vascular effects of human C-reactive protein on nitric oxide bioavailability (2005)

Clapp, B.R., Hirschfield, G.M., Storry, C., Gallimore, J.R., Stidwill, R.P., Singer, M., ...

Background: Circulating concentrations of the sensitive inflammatory marker C-reactive protein (CRP) predict future cardiovascular events, and CRP is elevated during sepsis and inflammation, when...

Outcome in systemic AL amyloidosis in relation to changes in concentration of circulating free immunoglobulin light chains following chemotherapy (2003)

Lachmann, H.J., Gallimore, R., Gillmore, J.D., Carr-Smith, H.D., Bradwell, A.R., Pepys, M.B., ...

Monoclonal immunoglobulin light chains are deposited as amyloid fibrils in systemic AL (primary) amyloidosis, but the underlying plasma cell dyscrasias are often difficult to detect or...

MHC typing in variant Creutzfeldt-Jakob disease (2003)

Pepys, M.B., Bybee, A., Booth, D.R., Bishop, M.T., Will, R.G., ...

Summary: Identification of factors that cause susceptibility to, and clinical expression of, variant Creutzfeldt-Jakob disease (vCJD) is essential for future management of the disease. We established...

Production of granulocyte colony-stimulating factor in the nonspecific acute phase response enhances host resistance to bacterial infection (2002)

Noursadeghi, M., Bickerstaff, M.C.M., Herbert, J., Moyes, D., Cohen, J., Pepys, M.B.

Mice mounting an acute phase response, induced by sterile inflammation after a single s.c. injection of casein 24 h beforehand, were remarkably protected against lethal infection with Gram-positive...

Misdiagnosis of hereditary amyloidosis as AL (Primary) amyloidosis (2002)

Lachmann, H.J., Booth, D.R., Booth, S.E., Bybee, A., Gilbertson, J.A., Gillmore, J.D., ...

Background: Hereditary, autosomal dominant amyloidosis, caused by mutations in the genes encoding transthyretin, fibrinogen A -chain, lysozyme, or apolipoprotein A-I, is thought to be extremely rare...

Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis (2002)

Pepys, M.B., Herbert, J., Hutchinson, W.L., Tennent, G.A., Lachmann, H.J., Gallimore, J.R., ...

The normal plasma protein serum amyloid P component (SAP) binds to fibrils in all types of amyloid deposits, and contributes to the pathogenesis of amyloidosis. In order to intervene in this process...

Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis (2002)

Pepys, M.B., Herbert, J., Hutchinson, W.L., Tennent, G.A., Lachmann, H.J., Gallimore, J.R., ...

The normal plasma protein serum amyloid P component (SAP) binds to fibrils in all types of amyloid deposits, and contributes to the pathogenesis of amyloidosis. In order to intervene in this process...

Amyloid load and clinical outcome in AA amyloidosis in relation to circulating concentration of serum amyloid A protein (2001)

Gillmore, J.D., Lovat, L.B., Persey, M.R., Pepys, M.B., Hawkins, P.N.

Background: Reactive systemic (AA, secondary) amyloidosis occurs in chronic inflammatory diseases, and most patients present with nephropathy. The amyloid fibrils are derived from the circulating...

Temporary depletion of complement component C3 or genetic deficiency of C1q significantly delays onset of scrapie (2001)

Mabbott, N.A., Bruce, M.E., Botto, M., Walport, M.J., Pepys, M.B.

Following peripheral exposure to transmissible spongiform encephalopathies (TSEs), infectivity usually accumulates in lymphoid tissues before neuroinvasion. The host prion protein (PrPc) is critical...