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1.  Epithelial Cell Innate Response to Candida albicans 
Advances in Dental Research  2011;23(1):50-55.
With the advent of treatments and diseases such as AIDS resulting in increasing numbers of patients with suppressed immune systems, fungal diseases are an escalating problem. Candida albicans is the most common of these fungal pathogens, causing infections in many of these patients. It is therefore important to understand how immunity to this fungus is regulated and how it might be manipulated. Although work has been done to identify the receptors, fungal moieties, and responses involved in anti-Candida immunity, most studies have investigated interactions with myeloid or lymphoid cells. Given that the first site of contact of C. albicans with its host is the mucosal epithelial surface, recent studies have begun to focus on interactions of C. albicans with this site. The results are startling yet in retrospect obvious, indicating that epithelial cells play an important role in these interactions, initiating responses and even providing a level of protection. These findings have obvious implications, not just for fungal pathogens, but also for identifying how host organisms can distinguish between commensal and pathogenic microbes. This review highlights some of these recent findings and discusses their importance in the wider context of infection and immunity.
doi:10.1177/0022034511399285
PMCID: PMC3144045  PMID: 21441481
HIV/AIDS; mycology; innate immunity; oral epithelium; fungal pathogens
4.  The role of nitric oxide in experimental murine sepsis due to pyrogenic exotoxin A-producing Streptococcus pyogenes. 
Infection and Immunity  1997;65(5):1767-1772.
Nitric oxide (NO) produced by inducible NO synthase (iNOS) mediates hypotension in endotoxemia. In this study, NO induction by a toxin-producing Streptococcus pyogenes isolate, H250, and by recombinant streptococcal pyrogenic exotoxin A (rSPEA) has been examined, both in vitro and in vivo. Streptococcal supernatants, but not rSPEA, induce production of nitrite by murine macrophages when both are coincubated with gamma interferon. Intraperitoneal injection of rSPEA did not cause significant production of NO. However, an elevated level of nitrate in serum was detected in a model of streptococcal fasciitis due to live H250. iNOS was localized to Kupffer cells, hepatocytes, and renal tubular cells by immunostaining. Administration of a NOS inhibitor, N(G)-monomethyl-L-arginine (L-NMMA), reduced peak concentrations of nitrate in serum but did not affect survival. NO is induced by H250, both in vitro and in vivo, mainly via SPEA-independent mechanisms. In this model, iNOS is expressed predominantly in the liver. Furthermore, in this model L-NMMA is not protective.
PMCID: PMC175214  PMID: 9125560
5.  Resuscitation of the newborn. 
British Medical Journal  1980;280(6214):646-647.
PMCID: PMC1600734  PMID: 7370623
6.  Driving after anaesthetics. 
British Medical Journal  1979;1(6175):1425.
PMCID: PMC1598903  PMID: 445114
7.  Cardiopulmonary bypass in hereditary spherocytosis: a case report 
Thorax  1971;26(1):131-132.
A cardiopulmonary bypass procedure in a patient with hereditary spherocytosis is described. Details of in vitro tests carried out prior to surgery are given.
PMCID: PMC472250  PMID: 5101263

Results 1-7 (7)