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Biomedical subjects

L H Bouwman

Publications and source records attributed to L H Bouwman.

4 recordsLinked to original sources
PubMed2006

Current status and prospects of clinical proteomics studies on detection of colorectal cancer: hopes and fears.

Colorectal adenocarcinoma (CRC) is the third most common type of cancer and the fourth most frequent cause of death due to cancer worldwide. Given the natural history of CRC, early diagnosis appears to be the most appropriate tool to reduce disease-related mortality. A field of recent interest is clinical proteomics, which was reported to lead to high sensitivity and specificities for early detection of several solid tumors. This emerging field uses mass spectrometry-based protein profiles/patterns of easy accessible body fluids to distinguish cancer from non-cancer patients. These discrepancies may be a result of: (1) proteins being abnormally produced or shed and added to the serum proteome, (2) proteins clipped or modified as a consequence of the disease process, or (3) proteins subtracted from the proteome owing to disease-related proteolytic degradation pathways. Therefore, protein pattern diagnostics would provide easy and reliable tools for detection of cancer. This paper focuses on the current status of clinical proteomics research in oncology and in colorectal cancer especially, and will reflect on pitfalls and fears in this relatively new area of clinical medicine, which are reproducibility issues and pre-analytical factors, statistical issues, and identification and nature of discriminating proteins/peptides.

Adenocarcinoma↗
PubMed2006

[Basal cell naevus syndrome as the cause of a chronic foot ulcer].

A 46-year-old man presented to the surgery outpatient clinic with an ulcer on top of his left foot. He had previously been diagnosed with basal cell naevus syndrome but had withdrawn from follow-up. His foot showed a deep ulcerating defect accompanied by profound necrosis extending to the metatarsophalangeal joints. There was a nodular skin defect over the first metatarsophalangeal joint, which was shown by histopathology to be a basal cell carcinoma, and the ulcer was bordered by a raised wall. Further physical examination revealed more than 200 dermal lesions which were identified by the dermatologist who was called in for consultation as basal cell carcinomas; multiple depressions due to abnormal local keratinisation were also seen on the palms of the hands and the soles of the feet. These findings led to a diagnosis of 'basal cell naevus syndrome'. The patient was treated by amputation of the lower leg followed by excision and curettage of the remaining basal cell carcinomas. At the time of the last follow-up, the patient was being checked periodically in the dermatology outpatient clinic. Basal cell naevus syndrome is a rare autosomal dominant hereditary disease. The prevalence is estimated to be between 1 in 57,000 and 1 in 164,000. Basal cell naevus syndrome is generally caused by a mutation in the 'patched homolog' (PTCH)-I gene, located on chromosome 9q22.3. Although the syndrome affects multiple organ systems, the most characteristic of this disorder is the appearance of multiple basal cell carcinomas.

Amputation, Surgical↗
PubMed2001

Human IgA activates the complement system via the mannan-binding lectin pathway.

The recently identified lectin pathway of the complement system, initiated by binding of mannan-binding lectin (MBL) to its ligands, is a key component of innate immunity. MBL-deficient individuals show an increased susceptibility for infections, especially of the mucosal system. We examined whether IgA, an important mediator of mucosal immunity, activates the complement system via the lectin pathway. Our results indicate a dose-dependent binding of MBL to polymeric, but not monomeric IgA coated in microtiter plates. This interaction involves the carbohydrate recognition domain of MBL, because it was calcium dependent and inhibited by mannose and by mAb against this domain of MBL. Binding of MBL to IgA induces complement activation, as demonstrated by a dose-dependent deposition of C4 and C3 upon addition of a complement source. The MBL concentrations required for IgA-induced C4 and C3 activation are well below the normal MBL plasma concentrations. In line with these experiments, serum from individuals having mutations in the MBL gene showed significantly less activation of C4 by IgA and mannan than serum from wild-type individuals. We conclude that MBL binding to IgA results in complement activation, which is proposed to lead to a synergistic action of MBL and IgA in antimicrobial defense. Furthermore, our results may explain glomerular complement deposition in IgA nephropathy.

Antibodies, Monoclonal↗