On pseudomodular matroids and adjoints

AbstractThere are two concepts of duality in combinatorial geometry. A set theoretical one, generalizing the structure of two orthocomplementary vector spaces, and a lattice theoretical concept of an adjoint, that mimics duality between points and hyperplanes. The latter — usually called polarity — seems to make sense almost only in the linear case. In fact the only non-linear combinatorial geometries known to admit an adjoint were of rank 3. Moreover, N.E. Mnëv conjectured that in higher ranks there would exist no non-linear oriented matroid that has an oriented adjoint. At least with unoriented matroids this is not true. In this paper we present a class of rank-4 matroids with adjoint including a non-linear example

Prostaglandin D2-supplemented “functional eicosanoid testing and typing” assay with peripheral blood leukocytes as a new tool in the diagnosis of systemic mast cell activation disease: an explorative diagnostic study

Background: Systemic mast cell activation disease (MCAD) is characterized by an enhanced release of mast cell-derived mediators, including eicosanoids, which induce a broad spectrum of clinical symptoms. Accordingly, the diagnostic algorithm of MCAD presupposes the proof of increased mast cell mediator release, but only a few mediators are currently established as routine laboratory parameters. We thus initiated an explorative study to evaluate in vitro typing of individual eicosanoid pattern of peripheral blood leukocytes (PBLs) as a new diagnostic tool in MCAD. Methods: Using the “functional eicosanoid testing and typing” (FET) assay, we investigated the balance (i.e. the complex pattern of formation, release and mutual interaction) of prostaglandin E2 (PGE2) and peptido-leukotrienes (pLT) release from PBLs of 22 MCAD patients and 20 healthy individuals. FET algorithms thereby consider both basal and arachidonic acid (AA)-, acetylsalicylic acid (ASA)-, and substance P (SP)-triggered release of PGE2 and pLT. The FET assay was further supplemented by analyzing prostaglandin D2 (PGD2), as mast cell-specific eicosanoid. Results: We observed marked PGE2-pLT imbalances for PBLs of MCAD patients, as indicated by a markedly enhanced mean FET value of 1.75 ± 0.356 (range: 1.14–2.36), compared to 0.53 ± 0.119 (range: 0.36-0.75) for healthy individuals. In addition, mean PGD2 release from PBLs of MCAD patients was significantly, 6.6-fold higher than from PBLs of healthy individuals (946 ± 302.2 pg/ml versus 142 ± 47.8 pg/ml; P < 0.001). In contrast to healthy individuals, PGD2 release from PBLs of MCAD patients was markedly triggered by SP (mean: 1896 ± 389.7 pg/ml; P < 0.001), whereas AA and ASA caused individually varying effects on both PGD2 and pLT release. Conclusions: The new in-vitro FET assay, supplemented with analysis of PGD2, demonstrated that the individual patterns of eicosanoid release from PBLs can unambiguously distinguish MCAD patients from healthy individuals. Notably, in our analyses, the FET value and both basal and triggered PGD2 levels were not significantly affected by MCAD-specific medication. Thus, this approach may serve as an in-vitro diagnostic tool to estimate mast cell activity and to support individualized therapeutic decision processes for patients suffering from MCAD

Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options

Mast cell activation disease comprises disorders characterized by accumulation of genetically altered mast cells and/or abnormal release of these cells' mediators, affecting functions in potentially every organ system, often without causing abnormalities in routine laboratory or radiologic testing. In most cases of mast cell activation disease, diagnosis is possible by relatively non-invasive investigation. Effective therapy often consists simply of antihistamines and mast cell membrane-stabilising compounds supplemented with medications targeted at specific symptoms and complications. Mast cell activation disease is now appreciated to likely be considerably prevalent and thus should be considered routinely in the differential diagnosis of patients with chronic multisystem polymorbidity or patients in whom a definitively diagnosed major illness does not well account for the entirety of the patient's presentation

Effective chemical virus inactivation of patient serum compatible with accurate serodiagnosis of infections.

OBJECTIVES Highly pathogenic viruses such as EBOV are a threat to routine laboratory workers. Inactivation procedures with Triton X-100 0.1% and/or heat are currently recommended, but have unknown effects on the accuracy of serological testing. Furthermore, virus inactivation by Triton X-100 0.1% was shown to be ineffective in serum. This study aimed to demonstrate virus inactivation in serum by Triton X-100 1% and maintained accuracy of serological testing. METHODS A panel of 19 serological tests was run on patient serum samples after treatment with Triton X-100 1%, 0.1%, and 0.1% + heat inactivation at 60°C for 1 h. Mean differences between measurements (bias) were calculated applying the Bland-Altman method. To determine effectiveness of virus inactivation, herpes simplex virus 1 (HSV-1) was spiked into medium containing 90% or 1% serum, and treated with Triton X-100 0.1% or 1%. Infectious titres were then determined on Vero cells. RESULTS Serological measurements showed good agreement between controls and samples treated with Triton X-100 0.1% and 1%, with an estimated bias of 0.6 ± 9.2% (n = 258) and -0.1 ± 18.6% (n = 174), respectively. Discordant qualitative results were rare. Conversely, heat inactivation alone and combined with Triton X-100 0.1% triggered a bias of 17.5 ± 66.4% (n = 200) and 37.9 ± 79.8% (n = 160), respectively. Triton X-100 1% completely inactivated HSV-1 in 1% and 90% serum while Triton X-100 0.1% failed to do so in 90% serum. CONCLUSIONS Unlike heat inactivation, Triton X-100 1% enabled accurate serological testing and completely inactivated HSV-1 in serum. This simple method could allow safe routine serological diagnostics in high-risk patients

Adenosine-induced Asystole during AVM Embolization:A Case Series

BACKGROUND: Adenosine induced cardiac standstill has been used intraoperatively for both aneurysm and arteriovenous malformation (AVM) surgery and embolization. We sought to report the results of adenosine induced cardiac standstill as an adjunct to endovascular embolization of brain AVMs. MATERIAL AND METHODS: We retrospectively identified patients in our prospectively maintained database to identify all patients since January 2007 in whom adenosine was used to induce cardiac standstill during the embolization of a brain AVM. We recorded demographic data, clinical presentation, Spetzler Martin grade, rupture status, therapeutic intervention and number of embolization sessions, angiographic and clinical results, clinical and radiological outcomes and follow-up information. RESULTS: We identified 47 patients (22 female, 47%) with average age 42 ± 17 years (range 6–77 years) who had undergone AVM embolization procedures using adjunctive circulatory standstill with adenosine. In total there were 4 Spetzler Martin grade 1 (9%), 9 grade 2 (18%), 15 grade 3 (32%), 8 grade 4 (18%), and 11 grade 5 (23%) lesions. Of the AVMs six were ruptured or had previously ruptured. The average number of embolization procedures per patient was 5.7 ± 7.6 (range 1–37) with an average of 2.6 ± 2.2 (range 1–14) embolization procedures using adenosine. Overall morbidity was 17% (n = 8/47) and mortality 2.1% (n = 1/47), with permanent morbidity seen in 10.6% (n = 5/47) postembolization. Angiographic follow-up was available for 32 patients with no residual shunt seen in 26 (81%) and residual shunts seen in 6 patients (19%). The angiographic follow-up is still pending in 14 patients. At last follow-up 93.5% of patients were mRS ≤2 (n = 43/46). CONCLUSION: Adenosine induced cardiac standstill represents a viable treatment strategy in high flow AVMs or AV shunts that carries a low risk of mortality and permanent neurological deficits

On adjoints and dual matroids

SIGLETIB Hannover: RO 3476(49) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman