Dino Saban

Dino Saban
University Hospital Essen | UK Essen · Clinic for Neurosurgery

Doctor of Medicine

About

23
Publications
1,122
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212
Citations
Introduction
Cerabral cavernous malformations, Glioblastoma

Publications

Publications (23)
Article
OBJECTIVE The objective of this study was to analyze the impact of medication intake on hemorrhage risk in patients with familial cerebral cavernous malformation (FCCM). METHODS The authors’ institutional database was screened for patients with FCCM who had been admitted to their department between 2003 and 2020. Patients with a complete magnetic...
Article
Background and Purpose: Analyze and compare the natural course of confirmed familial cerebral cavernous malformation (FCCM), assumed FCCM and non-familial multiple cerebral cavernous malformation (CCM) disease over a 5-year period. Methods: Our institutional database was screened for patients with CCM admitted between 2003 and 2020. Patients with...
Article
OBJECTIVE Cavernous spinal cord malformations (SCMs) are believed to have a high rate of bleeding. The risk of intramedullary hemorrhage (IMH) or recurrent IMH and the neurological impact of bleeding events are important for clinical decision-making and could impact current treatment strategies. METHODS The authors screened their institutional dat...
Article
Background This study aimed to assess occurrence and significance of postoperative neuropathic pain in patients with surgically-treated brainstem cavernous malformations (BSCM). Methods Seventy-four BSCM patients surgically treated between 2003 and 2019 were reviewed for the occurrence of postoperative NP and related treatment. We evaluated releva...
Article
BACKGROUND AND PURPOSE: The purpose of this study was to investigate the natural course of cerebral cavernous malformations (CCM) in the pediatric population, with special emphasis on the risk of first and recurrent bleeding over a 5-year period. METHODS: Our institutional database was screened for patients with CCM treated between 2003 and 2020. P...
Article
Full-text available
Background To determine the prevalence of cardiovascular comorbidities and allergic diseases in patients with cavernous malformations of the central nervous system (CCM) compared to normal population. Methods Clinical and MRI data of 1,352 patients with CCM from an observational cross‐sectional single‐institutional study were analyzed and compared...
Article
Background and Purpose This study aims to assess the influence of modifiable cardiovascular risk factors on hemorrhage risk of sporadic cerebral cavernous malformations (CCMs). Methods From 1219 consecutive CCM patients (2003–2018), adult subjects with sporadic CCM and complete magnetic resonance imaging were included. We evaluated presence of int...
Article
Background Cerebral cavernous malformations (CCMs) is the second most common cerebrovascular disease and is classified as familial (20%) and sporadic (80%) forms. Loss of function mutation of three CCM genes results in the familial CCM. Considering the similar clinic presentation of familial and sporadic CCMs, and based on enriched CpG islands in t...
Article
Full-text available
Objective: To estimate health related quality of life (HRQOL) in patients with untreated cavernous malformation of the CNS (CCM). Methods: We performed a cross-sectional observational study on patients with CCM admitted to our department from 01.11.2017-10.01.2020 using standardized interviews (short-form -36 questionnaire, hospital anxiety and...
Article
Full-text available
We previously reported an angiogenic and tumor-suppressor-like function of programmed cell death 10 (PDCD10) in glioblastoma (GBM). However, the underlying mechanism remains to be elucidated. We hypothesized that loss of PDCD10 activates GBM cells and tumor progression via EphB4. To this end, PDCD10 was knocked down in U87 and T98g by lentiviral me...
Article
Objective To determine the role of associated developmental venous anomalies (DVAs) in intracranial hemorrhage (ICH) caused by cerebral cavernous malformations (CCMs). Methods We analyzed patient registry data of 1,219 patients with cavernous malformations treated in our institution between 2003 and 2018. Patients with spinal and familial CCM and...
Article
Full-text available
Purpose Glioblastoma (GBM) is one of the most aggressive and incurable primary brain tumors. Identification of novel therapeutic targets is an urgent priority. Programmed cell death 10 (PDCD10), a ubiquitously expressed apoptotic protein, has shown a dual function in different types of cancers and in chemo-resistance. Recently, we reported that PDC...
Article
Objectives: Intracerebral hematoma (ICH) complicates the course of aneurysmal subarachnoid hemorrhage (SAH). To date, there are no unique guidelines for management of aneurysmal ICH. The aim of this study was to identify risk factors for and impact of aneurysmal ICH with special attention on treatment decisions derived from ICH volume. Patients a...
Article
Prions cause transmissible spongiform encephalopathies for which no treatment exists. Prions consist of PrP(Sc), a misfolded and aggregated form of the cellular prion protein (PrP(C)). We explore the antiprion properties of luminescent conjugated polythiophenes (LCPs) that bind and stabilize ordered protein aggregates. By administering a library of...
Article
Full-text available
Prions cause neurodegeneration in vivo, yet prion-infected cultured cells do not show cytotoxicity. This has hampered mechanistic studies of prion-induced neurodegeneration. Here we report that prion-infected cultured organotypic cerebellar slices (COCS) experienced progressive spongiform neurodegeneration closely reproducing prion disease, with th...
Data
Tga20 COCS were infected with RML and harvested at 35 dpi (passage 1). COCS homogenate was re-transmitted into tga20 COCS at 10 µg ml−1, equivalent to a titer of 10−4, and harvest at 35 dpi (passage 2). Immunoblots of PrPSc in tga20 COCS show an efficient prion replication at both the first and the second passage through COCS. Sc; scrapie-sick wt m...
Data
(A) Histology of NBH and RML treated tga20 COCS at 42 dpi. H&E stainings identified vacuolation selectively in prion infected tissue (arrow). (B) Representative images of Figure 2C. COCS prepared from mice with conditional PrP-ablation in CGCs (PrPΔCGC) showed no prion toxicity at 56 dpi, while control COCS (PrPCGC+) showed prion toxicity. (EPS)
Data
(A) Immunoblot of C57BL/6 COCS exposed to RML-infected (RML) or uninfected (NBH) brain homogenate, cultured for 21 days, treated with various compounds for 14 days, and probed with antibody POM1 to PrP at 35 dpi. Leftmost lane: brain homogenate of a terminally scrapie-sick wt mouse. (B) Misfolded protein assay (MPA) of RML homogenate decadically di...
Data
(A) Tga20 slices exposed to RML or NBH at 45 dpi from Figure 4A. NeuN images represent the slice with the highest and lowest NeuN value quantified in Figure 4A. (B) Images of strongest and weakest PI-positive image from Figure 4A at 42 dpi. (EPS)
Data
Densitometric analysis of PrP band on Figure 4E, normalized to GAPDH. RML infected COCS showed increased density of C2 and decreased density of C1 fragments. While E64d had no significant impact on C1 or C2 fragments, a small decrease was observed in full length PrP. (EPS)
Data
Tga20 slices were exposed to RML or NBH, cultured and analyzed at 42 dpi by TUNEL assay and counterstained with dapi. Sts: staurosporine treatment (48 hrs, 5 µM). (A) Representative TUNEL images. (B) The number of TUNEL+ cells was counted and RML treated samples showed increased TUNEL positivity compared to NBH samples and substantially less than S...
Data
(A) Tga20 slices were treated with calpain inhibitors from 21–42 dpi and analyzed by NeuN morphometry. Uninfected COCS showed no adverse effects of calpain inhibitor treatment. (B) Staurosporine treatment of uninfected tga20 cultures treated with caspase and calpain inhibitors. PI incorporation was assessed after 48 h staurosporine treatment (1 µM)...
Data
This file contains Table S1, which shows the effects of anti-prion compounds reported in this study. The ‘in vitro’ and ‘in vivo’ columns describe the reported abilities of drugs to affect prion replication in prion infected cell lines or mice respectively. ‘PrP interaction’ indicates drugs that are thought to interact physically with PrPC or PrPSc...

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