Endovascular Treatment of Anterior Circulation Cerebral Aneurysms by Using Guglielmi Detachable Coils: A 10-Year Single-Center Experience with Special Emphasis on the Use of Three-Dimensional GDC

Purpose:: To analyze the immediate, long-term angiographic and clinical results of endovascular treatment of anterior circulation aneurysms with special regard to the use of three-dimensional Guglielmi detachable coils (3D-GDC). Patients and Methods:: Between 1993 and 2003, 116 patients with 116 anterior circulation aneurysms were treated. 88 patients (75.9%) underwent embolization due to high surgical risk. To analyze the use of 3D-GDC, patients treated before (group 1) and after (group 2) implementation of 3D-GDC in 1999 were compared. Mean duration of angiographic follow-up was 13.9 months. Clinical follow-up was set at hospital discharge and using a questionnaire for long-term follow-up (mean 46.8 months). Results:: Overall, at initial intervention, complete occlusion was achieved in 65 aneurysms (56.0%), neck remnant in 42 (36.2%), and incomplete occlusion in nine (7.8%). Procedure-related permanent morbidity was 4.3% and mortality 2.6%. Recanalization rate at radiologic follow-up was 16.7%. Occlusion success at initial treatment correlated with aneurysm neck size (p = 0.001). Clinical outcome at hospital discharge was dependent on Hunt & Hess grade at presentation (p = 0.01). Subgroup analysis revealed that the use of 3D-GDC produced a higher initial obliteration rate compared to standard coils, but did not reach statistical significance (p = 0.059). Neither aneurysm neck size nor aneurysm dome size nor the use of 3D-GDC significantly influenced recanalization rate. Conclusion:: GDC technology is effective and safe, particularly in case of patients with high surgical risk. Aneurysm neck size was predictive of occlusion rate and Hunt & Hess grade of clinical outcome. Introduction of 3D-GDC probably improved occlusion rate, but did not significantly influence recanalization rat

Wissenschaftliches Reisen

Die Themenklasse 2020/21 möchte mit ihrer Studie einen Grundstein in Richtung nachhaltiger Reisen an der HU legen. Sie hat in ihrer Forschungsarbeit eine wichtige Quelle der CO2-Emissionen, wissenschaftliche (Dienst)-Reisen an der Humboldt-Universität zu Berlin (HU), analysiert. Drei Arbeitsgruppen gingen mit quantitativen sowie qualitativen Methoden zwei Semester lang mehreren Fragestellungen nach: Wie groß ist der CO2-Fußabdruck von wissenschaftlichen (Dienst)-Reisen? Aus welchen Gründen und in welchem Umfang werden Dienstreisen angetreten? Gibt es Einsparungspotenziale bzw. wie kann eine eventuelle Kompensation der CO2-Emissionen gestaltet werden? Mit der Beantwortung dieser Fragen stellt die Forschungsarbeit die Datengrundlage der Auswirkungen von wissenschaftlichem Reisen an der HU bereit und bildet Erklärungsmuster für wissenschaftliche Reisen ab. Ebenso zeigt sie Handlungsoptionen zur Speicherung bzw. Einsparung von CO2-Emissionen durch Dienstreisen an der HU auf. Das Zusammenspiel dieser drei Teilbereiche soll als Basis für einen Wandel hin zu klimabewussterem Reisen und der Implementierung eines CO2-Kompensationssystems an der HU fungieren. Die Themenklasse positioniert sich damit auch nachdrücklich zu den Möglichkeiten und der Verantwortung des Wissenschaftsbetriebes für mehr Nachhaltigkeit

SGLT2 Mediates Glucose Reabsorption in the Early Proximal Tubule

Mutations in the gene encoding for the Na+-glucose co-transporter SGLT2 (SLC5A2) associate with familial renal glucosuria, but the role of SGLT2 in the kidney is incompletely understood. Here, we determined the localization of SGLT2 in the mouse kidney and generated and characterized SGLT2-deficient mice. In wild-type (WT) mice, immunohistochemistry localized SGLT2 to the brush border membrane of the early proximal tubule. Sglt2−/− mice had glucosuria, polyuria, and increased food and fluid intake without differences in plasma glucose concentrations, GFR, or urinary excretion of other proximal tubular substrates (including amino acids) compared with WT mice. SGLT2 deficiency did not associate with volume depletion, suggested by similar body weight, BP, and hematocrit; however, plasma renin concentrations were modestly higher and plasma aldosterone levels were lower in Sglt2−/− mice. Whole-kidney clearance studies showed that fractional glucose reabsorption was significantly lower in Sglt2−/− mice compared with WT mice and varied in Sglt2−/− mice between 10 and 60%, inversely with the amount of filtered glucose. Free-flow micropuncture revealed that for early proximal collections, 78 ± 6% of the filtered glucose was reabsorbed in WT mice compared with no reabsorption in Sglt2−/− mice. For late proximal collections, fractional glucose reabsorption was 93 ± 1% in WT and 21 ± 6% in Sglt2−/− mice, respectively. These results demonstrate that SGLT2 mediates glucose reabsorption in the early proximal tubule and most of the glucose reabsorption by the kidney, overall. This mouse model mimics and explains the glucosuric phenotype of individuals carrying SLC5A2 mutations

Plasticity of DNA methylation in a nerve injury model of pain

<div><p>The response of the peripheral nervous system (PNS) to injury may go together with alterations in epigenetics, a conjecture that has not been subjected to a comprehensive, genome-wide test. Using reduced representation bisulfite sequencing, we report widespread remodeling of DNA methylation in the rat dorsal root ganglion (DRG) occurring within 24 h of peripheral nerve ligation, a neuropathy model of allodynia. Significant (<i>P</i> < 10⁻⁴) cytosine hyper- and hypo-methylation was found at thousands of CpG sites. Remodeling occurred outside of CpG islands. Changes affected genes with known roles in the PNS, yet methylome remodeling also involved genes that were not linked to neuroplasticity by prior evidence. Consistent with emerging models relying on genome-wide methylation and RNA-seq analysis of promoter regions and gene bodies, variation of methylation was not tightly linked with variation of gene expression. Furthermore, approximately 44% of the dynamically changed CpGs were located outside of genes. We compared their positions with the intergenic, tissue-specific differentially methylated CpGs (tDMCs) of an independent experimental set consisting of liver, spleen, L4 control DRG, and muscle. Dynamic changes affected those intergenic CpGs that were different between tissues (<i>P</i> < 10⁻¹⁵) and almost never the invariant portion of the methylome (those CpGs that were identical across all tissues). Our findings—obtained in mixed tissue—show that peripheral nerve injury leads to methylome remodeling in the DRG. Future studies may address which of the cell types found in the DRG, such as specific groups of neurons or non-neuronal cells are affected by which aspect of the observed methylome remodeling.</p></div