The introduction of more sensitive solid-phase assays (SPAs) to detect human leukocyte antigen (HLA) antibodies has led to a dramatic SBE-β-CD increase in the number of the patients on the waitlist. This review advocates
the use of the ‘old-fashioned’ CDC to define the degree of sensitization and as the tool for allocation of kidneys to highly sensitized patients.
Recent findings
HLA-antibody screening using CDC is a cumbersome method that needs a high degree of expertise. SPA is easier, more reproducible and accessible to a large number of laboratories. The dogma that donor-specific antibodies (DSAs) are a contraindication for transplantation disappeared. The presence of SPA-DSA is rather a risk factor for complications than a contraindication. The opinion on the clinical relevance
of SPA-DSA differs between the centers.
Summary
A proper designation of highly sensitized patients is crucial since it impacts the allocation. CDC-DSA is generally considered a contraindication for transplantation, whereas SPA-DSA remains controversial. The lack of consensus between centers is partly due to the heterogeneity of the HLA antibodies involved, the lack of standardization in antibody titer, the immunoglobulin (sub) class and the epitopes recognized. Until the issues are resolved, one should be careful to use the information Selleckchem BIX 01294 generated in SPA for the allocation of kidneys and focus on the ‘old CDC’ that has shown to be effective NU7026 research buy in the past.”
“Fetal growth restriction (FGR) is a serious pregnancy complication associated with increased perinatal mortality and morbidity. Although the majority of cases
with FGR result from placental dysfunction, the pathophysiology is incompletely understood. Autophagy is a physiological form of cell degradation exacerbated by nutrient and oxygen restriction, which are both thought to play a role in the aetiology of FGR. We hypothesized that autophagy is present in the normal human placenta and is exaggerated in FGR. Autophagy was assessed in electron micrographs from normal and FGR placentas and by Western blotting for LC3B and LAMP-2. The localization of regulators of autophagy was examined by immunohistochemistry. Culture of BeWo cells was used to investigate whether nutrient and/or oxygen deprivation can induce autophagy in trophoblast. Autophagy predominantly localized to the syncytiotrophoblast layer and autophagosomes were more frequent in FGR. The regulators LAMP-2, LC3B, Beclin-1, ATG 5, ATG9 and ATG16L1 were all present in villous trophoblast. LAMP-2 immunostaining was more punctate in FGR. In BeWo cells, culture in reduced oxygen tension and/or serum depleted conditions led to the appearance of autophagosomes which was associated with changes in LAMP-2 configuration. We conclude that autophagy in human term placenta may be involved in the placental dysfunction present in FGR.