Incarceration of the Gravid Uterus - a Rare Condition not to be Missed.

BACKGROUND: Incarceration of a gravid uterus (IGU) is a rare manifestation in obstetrics that may be associated with serious complications. CASE: We report on a 29-year-old patient at 34+2 weeks' gestation who presented with HELLP syndrome. IGU had been initially diagnosed in our department at 23+6 weeks' gestation. Urgent cesarean section was performed taking into account the specific characteristics of IGU. A healthy premature child was born. With the prior knowledge of IGU no complications during delivery occurred and mother and child had favorable outcomes. CONCLUSION: IGU is a rare condition in pregnancy that should not be overlooked. Early diagnosis and treatment of IGU can prevent serious complications to the mother and child during pregnancy and delivery. In this report, we discuss the specific peculiarities of an incarcerated uterus that need to be considered in this regard. HINTERGRUND: Ein Uterus incarceratus ist eine seltene Manifestation in der Geburtshilfe, welche mit schwerwiegenden Komplikationen einhergehen kann. FALL: Wir berichten über eine 29-jährige Patientin, die sich mit 34+2 Schwangerschaftswochen (SSW) mit einem HELLP-Syndrom in unserer Klinik vorgestellt hat. Die Erstdiagnose des inkarzerierten Uterus wurde in unserer Klinik mit 23+6 SSW gestellt. Aufgrund unserer Vorkenntnis über diese Diagnose konnte nun die dringend indizierte Sectio caesarea unter Berücksichtigung der spezifischen Merkmale in modifizierter Technik durchgeführt werden. Es wurde ein gesundes Frühgeborenes geboren. Es traten während der Geburt keine Komplikationen auf und Mutter und Kind hatten einen günstigen Verlauf. SCHLUSSFOLGERUNG: Ein Uterus incarceratus ist eine seltene Manifestation in der Schwangerschaft, welche nicht übersehen werden sollte. Eine frühzeitige Diagnose und Behandlung kann schwerwiegende Komplikationen für Mutter und Kind während der Schwangerschaft und unter der Geburt verhindern. Wir diskutieren die spezifischen Besonderheiten eines Uterus incarceratus, die hierbei zu berücksichtigen sind.

Lipopolysaccharide delays demyelination and promotes oligodendrocyte precursor proliferation in the central nervous system.

Systemic infection can influence the course in many diseases of the central nervous system (CNS) such as multiple sclerosis (MS), yet the relationship between infection outside the CNS and potential damage and/or protection within the CNS is still not understood. Activation of microglia is a characteristic feature of most CNS autoimmune disorders, including MS, and both protective and degenerative functions of microglia have been proposed. Hence, we analyzed the effects of a systemic inflammatory reaction induced by peripheral treatment with lipopolysaccharide (LPS) on microglial reaction and cuprizone induced de- and remyelination. We found that LPS administration delayed demyelination, which was linked with inhibition of microglial proliferation and reduced numbers of activated microglia. The phenotype of microglia changed as an increase of Toll-like receptor 4 was found. During remyelination, LPS treatment delayed the onset of myelin protein re-expression, but later there was a beneficial effect via an increase of proliferating oligodendrocyte precursor cells (OPC) and mature oligodendrocytes. Moreover, the expression of ciliary neurotrophic factor was increased in response to LPS, a growth factor known to mediate OPC proliferation. Additional experiments showed that the time window to induce LPS effects was limited and associated with the presence of microglia. In conclusion, LPS delayed demyelination and caused beneficial effects on remyelination via increasing the proliferation of OPC. These differences seem to be an effect of LPS induced microglial modulation and indicate that exposure to certain infectious agents within a given time window may be beneficial in promoting tissue repair.

Beneficial effects of minocycline on cuprizone induced cortical demyelination.

In this study, we investigated the potential of minocycline to influence cuprizone induced demyelination in the grey and white matter. To induce demyelination C57BL/6 mice were fed with cuprizone for up to 6 weeks and were analysed at different timepoints (week 0, 4, 5, 6). Mice treated with minocycline had less demyelination of the cortex and corpus callosum compared with sham treated animals. In the cortex decreased numbers of activated and proliferating microglia were found after 6 weeks of cuprizone feeding, while there were no significant effects for microglial infiltration of the corpus callosum. In addition to the beneficial effects on demyelination, minocycline prevented from motor coordination disturbance as shown in the beam walking test. For astrogliosis and the numbers of OPC and oligodendrocytes no treatment effects were found. In summary, minocycline treatment diminished the course of demyelination in the grey and white matter and prevented disturbances in motor coordination.

Leading your leader.

Learn how one facility developed nurse managers' leadership skills through a questionnaire process and training opportunities.

Effects of fumaric acids on cuprizone induced central nervous system de- and remyelination in the mouse.

BACKGROUND: Fumaric acid esters (FAE) are a group of compounds which are currently under investigation as an oral treatment for relapsing-remitting multiple sclerosis. One of the suggested modes of action is the potential of FAE to exert a neuroprotective effect. METHODOLOGY/PRINCIPAL FINDINGS: We have investigated the impact of monomethylfumarate (MMF) and dimethylfumaric acid (DMF) on de- and remyelination using the toxic cuprizone model where the blood-brain-barrier remains intact and only scattered T-cells and peripheral macrophages are found in the central nervous system (CNS), thus excluding the influence of immunomodulatory effects on peripheral immune cells. FAE showed marginally accelerated remyelination in the corpus callosum compared to controls. However, we found no differences for demyelination and glial reactions in vivo and no cytoprotective effect on oligodendroglial cells in vitro. In contrast, DMF had a significant inhibitory effect on lipopolysaccharide (LPS) induced nitric oxide burst in microglia and induced apoptosis in peripheral blood mononuclear cells (PBMC). CONCLUSIONS: These results contribute to the understanding of the mechanism of action of fumaric acids. Our data suggest that fumarates have no or only little direct protective effects on oligodendrocytes in this toxic model and may act rather indirectly via the modulation of immune cells.