Evaluation of a microbiological screening and acceptance procedure for cryopreserved skin allografts based on 14 day cultures

Viable donor skin is still considered the gold standard for the temporary covering of burns. Since 1985, the Brussels military skin bank supplies cryopreserved viable cadaveric skin for therapeutic use. Unfortunately, viable skin can not be sterilised, which increases the risk of disease transmission. On the other hand, every effort should be made to ensure that the largest possible part of the donated skin is processed into high-performance grafts. Cryopreserved skin allografts that fail bacterial or fungal screening are reworked into ‘sterile’ non-viable glycerolised skin allografts. The transposition of the European Human Cell and Tissue Directives into Belgian Law has prompted us to install a pragmatic microbiological screening and acceptance procedure, which is based on 14 day enrichment broth cultures of finished product samples and treats the complex issues of ‘acceptable bioburden’ and ‘absence of objectionable organisms’. In this paper we evaluate this procedure applied on 148 skin donations. An incubation time of 14 days allowed for the detection of an additional 16.9% (25/148) of contaminated skin compared to our classic 3 day incubation protocol and consequently increased the share of non-viable glycerolised skin with 8.4%. Importantly, 24% of these slow-growing microorganisms were considered to be potentially pathogenic. In addition, we raise the issue of ‘representative sampling’ of heterogeneously contaminated skin. In summary, we feel that our present microbiological testing and acceptance procedure assures adequate patient safety and skin availability. The question remains, however, whether the supposed increased safety of our skin grafts outweighs the reduced overall clinical performance and the increase in work load and costs

Insulin biosynthesis and glycolysis in the beta cell

info:eu-repo/semantics/publishe

The stimulus secretion coupling of glucose induced insulin release. XV. Participation of cations in the recognition of glucose by the β cell

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Glucose-induced insulin biosynthesis :a model for different types of inhibition

info:eu-repo/semantics/nonPublishe

The stimulus secretion coupling of glucose induced insulin release. XIV. Glucose regulation of insular biosynthetic activity

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Studies on the glucoreceptor mechanism in the pancreatic B-cell

info:eu-repo/semantics/publishedComm. 8th Congress of the International Diabetes Federation - Bruxelles, 18.7.197

Metabolic, cationic and pharmacological influences on insulin biosynthesis

info:eu-repo/semantics/publishedComm. 8th Annual Meeting European Association for the Study of Diabetes - Madrid, 6.9.1972

Hyperplasia of "pancreatic polypeptide"-cells in the pancreas of juvenile diabetics

The cellular composition of the pancreatic islets of juvenile diabetics was studied, using recently developed immunocytochemical methods. B-cells were identified only in juvenile diabetics with a disease of short duration. In chronic juvenile diabetics, the islets which are classically viewed as "atrophic", were shown to be composed of glucagon- and of somatostatin-cells. Another type of islets which commonly occurs in the pancreas of juvenile diabetics, i. e. the ribbon-like type first described by Cecil in 1911, appeared to be composed almost exclusively of "pancreatic polypeptide" (HPP)-cells. It is suggested that hyperplasia of the HPP-cells in the pancreas of juvenile diabetics results from an atypical type of islet regeneration induced by a severe and prolonged injury to the pancreatic endocrine tissue. © 1977 Springer-Verlag.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Endocytosis of low density lipoprotein by human pancreatic beta cells and uptake in lipid-storing vesicles which increase with age

Studies with I(125)-labeled low-density lipoproteins (LDLs) have shown the presence of high-affinity LDL receptors on insulin-producing beta cells but not on neighboring alpha cells. By using gold-labeled lipoproteins, we demonstrate receptor-mediated endocytosis of LDLs and very low-density lipoproteins in rat and human beta cells. Specific for human beta cells is the fusion of LDL-containing endocytotic vesicles with lipid-storing vesicles (LSVs; diameter, 0.6-3.6 microm), which are absent in rodent beta cells. LSVs also occur in human pancreatic alpha and duct cells, but these sequester little gold-labeled LDL. In humans 50 years old, LSV surface area in beta cells (11 +/- 2% of cytoplasmic surface area) is fourfold higher than in alpha and duct cells and 10-fold higher than in beta cells at younger ages (P < 0.001); the mean LSV diameter in these beta cells (1.8 +/- 0.04 microm) is larger than at younger ages (1.1 +/- 0.2 microm; P < 0.005). Oil red O staining on pancreatic sections confirms that neutral lipids accumulate in beta cells of older donors. We conclude that human beta cells can incorporate LDL and very low-density lipoprotein material in LSVs. The marked increase in the LSV area of aging human beta cells raises the question whether it is caused by prolonged exposure to high lipoprotein levels such as occurs in Western populations and whether it is causally related to the higher risk for type 2 diabetes with aging.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe