PubMed · 9174718
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P G Walfish. 1997. Thyroiditis.. https://pubmed.ncbi.nlm.nih.gov/9174718/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The excretion of nitrate, nitrite, apparent total N-nitroso compounds and volatile nitrosamines was measured in 24 hr urine from 61 Egyptians, divided into 4 groups: controls, Schistosoma haematobium-infected patients and bladder cancer patients with and without a history of schistosomal infection. Urinary nitrate in S. haematobium-infected patients was significantly higher than in the other 3 groups. Nitrite was below the detection limit of the method (</=0.015 microgram/mg creatinine) in all but one of the control samples. S. haematobium infection significantly increased urinary nitrite to 0.9 +/- 1.16 microgram/mg creatinine (mean +/- SD, p = 0. 001). In both bladder cancer groups, nitrite was about 20 times that in S. haematobium-infected patients without bladder cancer. Excretion of apparent total N-nitroso compounds paralleled that of nitrite. Overall, a good correlation was observed between these 2 variables (r = 0.71, p = 0.0001). N-nitrosodimethylamine was present in all the samples analyzed. S. haematobium infection significantly increased urinary N-nitrosodimethylamine level compared with that of controls (4.02 +/- 1.61 and 2.04 +/- 2.97 ng/mg creatinine, respectively, p = 0.01). Among cancer patients, N-nitrosodimethylamine was higher than in controls only in those with schistosomal infection. The presence of N-nitroso compounds and N-nitrosodimethylamine in the urine of S. haematobium-infected patients both before and after the development of cancer, and the observation that these compounds also occur in bladder cancer patients with no history of schistosomal infection, suggest that these compounds might have a role not only in the initiation of the carcinogenic process, but also in its progression.
Studies on the potential role of infectious agents in sudden infant death syndrome (SIDS) have been published over the years in a variety of journals. The aim of this special issue of FEMS Immunology and Medical Microbiology is to bring together a group of the most recent studies from Europe, Australia and Canada which cover epidemiology and laboratory studies examining hypotheses relating to infection and inflammation in SIDS. The articles in this issue examine evidence for the involvement of specific micro-organisms in SIDS and the problems relating to experimental studies on infection in relation to the underlying pathology of these deaths. There is an update on the evidence for the common bacterial hypothesis proposed in 1987 examining risk factors identified in epidemiological studies, particularly how the prone sleeping position could affect bacterial colonisation or induction of toxins. Evidence for induction of inflammatory responses in SIDS infants is reviewed and the relation of these responses to mechanisms proposed as causes of death assessed. Factors found to be associated with reduction of the risk of SIDS (breast feeding and immunisation) are examined in relation to some of the toxigenic bacteria implicated in these deaths. Finally, the high incidence of SIDS in some ethnic groups is examined as a potential model to investigate the contributions of genetic, environmental and cultural differences to susceptibility of infants not only to SIDS but to serious respiratory tract infections.
Neutrophil accumulation at sites of inflammation is mediated by specific groups of cell adhesion molecules including the beta2 (CD18) integrins on leukocytes and the selectins (P- and E-selectin on the endothelium and L-selectin on the leukocyte). This is supported by studies of patients with leukocyte adhesion deficiency syndromes whose leukocytes are genetically deficient in the expression of beta2 integrins or selectin carbohydrate ligands (eg, sialyl-Lewis(x)). However, inherited deficiency or dysfunction of endothelial cell adhesion molecules involved in leukocyte recruitment has not been previously described. In this report we describe a child with recurrent infections and clinical evidence of impaired pus formation reminiscent of a leukocyte adhesion deficiency syndrome, but whose neutrophils were functionally normal and expressed normal levels of CD18, L-selectin, and sialyl-Lewis(x). In contrast, immunohistochemical staining of inflamed tissue from the patient showed the absence of E-selectin from the endothelium, although E-selectin mRNA was present. However, E-selectin protein was expressed as significantly elevated levels of circulating soluble E-selectin were detected, the molecular size of which was consistent with a proteolytically cleaved form of E-selectin. Gene sequencing failed to show evidence of a secreted mutant variant. These data represent, to our knowledge, the first description of a potentially inherited dysfunction of an endothelial cell adhesion molecule involved in leukocyte recruitment and provide additional human evidence of the importance of endothelial selectins in the inflammatory response.