Review of harmful gastrointestinal effects of carrageenan in animal experiments.
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In this article I review the association between exposure to carrageenan and the occurrence of colonic ulcerations and gastrointestinal neoplasms in animal models. Although the International Agency for Research on Cancer in 1982 identified sufficient evidence for the carcinogenicity of degraded carrageenan in animals to regard it as posing a carcinogenic risk to humans, carrageenan is still used widely as a thickener, stabilizer, and texturizer in a variety of processed foods prevalent in the Western diet. I reviewed experimental data pertaining to carrageenan's effects with particular attention to the occurrence of ulcerations and neoplasms in association with exposure to carrageenan. In addition, I reviewed from established sources mechanisms for production of degraded carrageenan from undegraded or native carrageenan and data with regard to carrageenan intake. Review of these data demonstrated that exposure to undegraded as well as to degraded carrageenan was associated with the occurrence of intestinal ulcerations and neoplasms. This association may be attributed to contamination of undegraded carrageenan by components of low molecular weight, spontaneous metabolism of undegraded carrageenan by acid hydrolysis under conditions of normal digestion, or the interactions with intestinal bacteria. Although in 1972, the U.S. Food and Drug Administration considered restricting dietary carrageenan to an average molecular weight > 100,000, this resolution did not prevail, and no subsequent regulation has restricted use. Because of the acknowledged carcinogenic properties of degraded carrageenan in animal models and the cancer-promoting effects of undegraded carrageenan in experimental models, the widespread use of carrageenan in the Western diet should be reconsidered. (+info)
The incidence and pathology of conjunctival ulceration in Behcet's syndrome.
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AIMS: To describe the results of a study of the incidence of conjunctival ulceration and its pathology as a manifestation of Behcet's syndrome. METHODS: The authors reviewed retrospectively medical charts of 152 patients with Behcet's syndrome seen at the uveitis service of Okayama University Hospital from January 1995 to December 1999. Criteria used to diagnose Behcet's syndrome in this study required the presence of oral aphthous ulceration plus any two of three other manifestations-genital ulceration, eye lesions such as iridocyclitis and uveoretinitis, or skin lesions such as erythema nodosum. The presence of conjunctival ulceration was determined in patients with Behcet's syndrome through standardised ophthalmological examinations. A biopsy of the conjunctival ulceration was performed in one patient. The incidence of conjunctival ulceration in patients with Behcet's syndrome was calculated and the clinical and pathological features of this ulceration were examined. RESULTS: Four of 152 patients (2.6%) developed conjunctival ulceration in concordance with exacerbation of their systemic symptoms. Histopathological examinations of a conjunctival biopsy specimen in one patient revealed intraepithelial and perivascular infiltration with neutrophils and lymphocytes, consistent with Behcet's syndrome. The conjunctival ulcerations of the study patients showed good response to topical corticosteroids or topical steroids plus oral colchicine. CONCLUSIONS: Conjunctival ulceration should be noted as an uncommon but possible manifestation of Behcet's syndrome. Accordingly, routine examination of the conjunctiva is recommended in patients with Behcet's syndrome, and Behcet's syndrome should be included in a list of differential diagnoses for patients with conjunctival ulcerations. (+info)
Surgical endovascular stent grafting for a ruptured penetrating atherosclerotic ulcer of the aortic arch.
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Penetrating atherosclerotic ulcer (PAU) is defined as an atherosclerotic lesion in which an ulceration occurs in the diseased aortic intima leading to disruption of the internal elastic lamina. It may cause a pseudoaneurysm formation or transmural aortic rupture. We describe a patient in whom a ruptured PAU in the distal aortic arch was treated successfully by a surgical endovascular stent graft. Through a median sternotomy and under deep hypothermic circulatory arrest, the aorta was transected between the left common carotid and subclavian arteries. A dacron prosthetic graft with self-expanding original Z type stents attached inside of the distal half was inserted through the aortotomy to exclude the PAU. By performing the procedure through a median sternotomy, we could eliminate dissection around the ruptured aortic wall. The stented graft was secured safely in the thoracic aorta to exclude the ruptured ulceration located distal to the left subclavian artery. PAU should be recognized widely as a distinct cardiovascular surgical problem which may lead to intramural hematoma with or without dissection or rupture. (+info)
Alterations in fibroblast alpha1beta1 integrin collagen receptor expression in keloids and hypertrophic scars.
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Keloids and hypertrophic scars are significant symptomatic clinical problems characterized by excess collagen. Although extensive research has focused on fibroblasts and collagen turnover in these aberrant scars, little work has been done on the expression of integrins (cell membrane structures that link cells to extracellular matrix) within these lesions. Integrin-mediated regulation of collagen synthesis has previously been observed in explanted fibroblasts from normal and fibrotic dermis, and integrin alpha1 knockout mice maintain increased collagen synthesis consistent with a role for alpha1beta1 in providing negative feedback on collagen synthesis. These findings suggested the need to evaluate integrin roles in keloids and hypertrophic scars. In this study we examined integrin expression in keloids (n = 11), hypertrophic scars (n = 5), radiation ulcers (n = 2), and normal skin specimens (n = 8). We used a novel approach to analysis by isolating dermal fibroblasts directly from tissue (without explant culture) and determining surface integrin expression by flow cytometry. We found that keloids and hypertrophic scars have marked alterations in fibroblast integrin expression and contain several distinct populations of fibroblasts. One of these populations expresses high levels of alpha1 integrin, and the proportion of these cells is higher in keloids (63% +/- 3.6% SEM) and hypertrophic scars (45% +/- 2.7% SEM) than in normal skin tissues (28% +/- 4.7% SEM). The different populations of fibroblasts defined by integrin expression merge, however, when the cells are serially cultured, suggesting that there may be aspects of the dermal microenvironment that maintain the integrin phenotypic heterogeneity in dermal fibroblasts. (+info)
Rapid detection of herpes simplex virus DNA in genital ulcers by real-time PCR using SYBR green I dye as the detection signal.
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We have evaluated a real-time PCR procedure based on the LightCycler technology for rapid detection of herpes simplex virus (HSV) in genital lesions. Two sets of primers, corresponding to the thymidine kinase and DNA polymerase regions, were used for the amplification reactions in separate capillaries containing the SYBR Green I dye as detection signal. In 28 of 118 samples (24%), HSV was isolated by conventional cell culture. All cell culture-positive samples were also positive by real-time PCR. Six additional cell culture-negative samples were positive by PCR with both sets of primers. Total processing time was less than 3 h. Real-time PCR using SYBR Green I as detection signal is a sensitive procedure for the rapid diagnosis of HSV in genital lesions. (+info)
Selective cyclooxygenase-2 blocker delays healing of esophageal ulcers in rats and inhibits ulceration-triggered c-Met/hepatocyte growth factor receptor induction and extracellular signal-regulated kinase 2 activation.
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Nonsteroidal anti-inflammatory drugs, both nonselective and cyclooxygenase-2 (COX-2) selective, delay gastric ulcer healing. Whether they affect esophageal ulcer healing remains unexplored. We studied the effects of the COX-2 selective inhibitor, celecoxib, on esophageal ulcer healing as well as on the cellular and molecular events involved in the healing process. Esophageal ulcers were induced in rats by focal application of acetic acid. Rats with esophageal ulcers were treated intragastrically with either celecoxib (10 mg/kg, once daily) or vehicle for 2 or 4 days. Esophageal ulceration triggered increases in: esophageal epithelial cell proliferation; expression of COX-2 (but not COX-1); hepatocyte growth factor (HGF) and its receptor, c-Met; and activation of extracellular signal-regulated kinase 2 (ERK2). Treatment with celecoxib significantly delayed esophageal ulcer healing and suppressed ulceration-triggered increases in esophageal epithelial cell proliferation, c-Met mRNA and protein expression, and ERK2 activity. In an ex vivo organ-culture system, exogenous HGF significantly increased ERK2 phosphorylation levels in esophageal mucosa. A structural analog of celecoxib, SC-236, completely prevented this effect. These findings indicate that celecoxib delays esophageal ulcer healing by reducing ulceration-induced esophageal epithelial cell proliferation. These actions are associated with, and likely mediated by, down-regulation of the HGF/c-Met-ERK2 signaling pathway. (+info)
Buruli ulcer in Ghana: results of a national case search.
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A national search for cases of Buruli ulcer in Ghana identified 5,619 patients, with 6,332 clinical lesions at various stages. The overall crude national prevalence rate of active lesions was 20.7 per 100,000, but the rate was 150.8 per 100,000 in the most disease-endemic district. The case search demonstrated widespread disease and gross underreporting compared with the routine reporting system. The epidemiologic information gathered will contribute to the design of control programs for Buruli ulcer. (+info)
Nuclear beta-catenin expression is closely related to ulcerative growth of colorectal carcinoma.
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Although most colorectal cancer develops based on the adenoma-adenocarcinoma sequence, morphologically, colorectal cancer is not a homogeneous disease entity. Generally, there are two distinct morphological types: polypoid and ulcerative colorectal tumours. Previous studies have demonstrated that K-ras codon 12 mutations are preferentially associated with polypoid growth of colorectal cancer; however, little is known about the molecular mechanism that determines ulcerative growth of colorectal cancer. beta-catenin complex plays a critical role both in tumorigenesis and morphogenesis. We examined the differential expression of beta-catenin and its related factors among different types of colorectal cancer in order to determine any relationship with gross tumour morphology. Immunohistochemical staining of beta-catenin, E-cadherin and MMP-7 was performed on 51 tumours, including 26 polypoid tumours and 25 ulcerative tumours. Protein truncation tests and single-strand conformational polymorphism for mutation of the adenomatous polyposis coli tumour suppressor gene, as well as single-strand conformational polymorphism for the mutation of beta-catenin exon 3 were also done. Nuclear expression of beta-catenin was observed in 18 out of 25 (72%) cases of ulcerative colorectal cancer and seven out of 26 (26.9%) cases of polypoid colorectal cancer. A significant relationship of nuclear beta-catenin expression with ulcerative colorectal cancer was found (P<0.001). However, this finding was independent of adenomatous polyposis coli tumour suppressor gene mutation and E-cadherin expression. Together with previous data, we propose that different combinations of genetic alterations may underlie different morphological types of colorectal cancer. These findings should be taken into consideration whenever developing a new genetic diagnosis or therapy for colorectal cancer. (+info)