Search

Rechtsmedizin : Organ der Deutschen Gesellschaft für Rechtsmedizin 31(5), 457-462 (2021). doi:10.1007/s00194-021-00460-1 special issue: "COVID-19", Published by Springer, Berlin ; Heidelberg

Intraokulare Infektionen durch Abiotrophia defectiva sind sehr selten. Hier berichten wir von einer 57-jährigen Patientin, welche sich 3 Monate nach erfolgter komplikationsloser Kataraktoperation mit Implantation eines Glaukom-Gelstents am rechten Auge mit einer Abiotrophia-defectiva-assoziierten Endophthalmitis bei uns vorstellte. Die Patientin klagte zuvor über eine Rötung im Bereich der nasal oberen Bindehaut des rechten Auges sowie über Schmerzen 2 Wochen vor Auftreten der Endophthalmitis. Eine 2‑wöchige topische Steroidtherapie ohne Antibiotikaschutz brachte eine kurzfristige Besserung. Die Patientin stellte sich nun bei uns mit einem Hypopyon, einer akuten Visusverschlechterung und starken periokulären Schmerzen seit dem frühen Morgen vor. Der Gelstent hatte spontan die Konjunktiva perforiert. Es erfolgte die unmittelbare Therapie mit lokaler und systemischer Antibiose. Sechs Stunden danach wurde eine Pars-plana-Vitrektomie mit intraokularer Gabe von Antibiotika durchgeführt. Durch eine zeitnahe Therapie konnte in diesem Fall ein relativ benigner Verlauf erreicht werden. Im klinischen Alltag sollte bei Patienten, die sich nach glaukomchirurgischen Eingriffen mit akuter Visusverschlechterung und Schmerzen präsentieren, dringend an eine mögliche spontane Bindehautperforation und Late-onset-Endophthalmitis gedacht werden. Zudem ist zu empfehlen, dass eine unklare Konjunktivitis nach Glaukomchirurgie immer antibiotisch abgedeckt und engmaschiger kontrolliert werden sollte.

Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft 117(12), 1229-1233 (2020). doi:10.1007/s00347-020-01077-7 special issue: "Mikrochirurgische Operationstechniken aus ophthalmopathologischer Sicht", Published by Springer, Berlin

Myocardial necrosis triggers inflammatory changes and a complex cytokine cascade that are only incompletely understood. The chemokine receptor CCR1 mediates inflammatory recruitment in response to several ligands released by activated platelets and up-regulated after myocardial infarction (MI). Here, we assess the effect of CCR1 on remodelling after MI using Ccr1-deficient (Ccr1(-)(/-)) mice. MI was induced in Ccr1(-/-) or wild-type mice by proximal ligation of the left anterior descending (LAD). Mice were sacrificed and analysed at day 1, 4, 7, 14 and 21 after MI. While initial infarct areas and areas at risk did not differ between groups, infarct size increased to 20.6+/-8.4% of the left ventricle (LV) in wild-type mice by day 21 but remained at 11.2+/-1.2% of LV (P

BioMed research international 2015, 863845 (2015). doi:10.1155/2015/863845, Published by Hindawi, New York [u.a.]

Purpose To investigate the reliability of partial coherence laser interferometry for optical biometry in highly myopic eyes. Methods Axial length measurements by the IOLMaster (Carl Zeiss Meditec, Germany) with signal-to-noise ratio (SNR) ≥2 were performed in 52 consecutive myopic subjects with axial length ≥26.5 mm and 45 emmetropic patients before cataract surgery. Axial length measurements and SNR were analyzed and compared among the two study groups. Results Axial length measurements were feasible in 46 of 52 (88.5%) highly myopic eyes and in 41 of 45 (91.1%) eyes with normal axial length. To achieve two reliable axial length values with SNR ≥2, a mean number of 2.06±0.25 measurements was necessary in myopic eyes and 2.10±0.37 in emmetropic counterparts. Mean SNR after two measurements was 4.98±2.44 in myopic eyes versus 5.56±2.32 in control eyes. Even though successful measurement was independent of preoperative visual acuity, patients with visual acuity better than 20/63 showed significantly higher SNR values. Conclusions Partial coherence laser interferometry shows satisfying feasibility and good signal quality for axial length determination in highly myopic eyes with stable retinal condition and clear media.

Objective— Although junctional adhesion molecule (JAM)-C has been implicated in the control of inflammatory leukocyte recruitment, its role in neointima formation after arterial injury has not been elucidated. Methods and Results— In apolipoprotein E–deficient ( Apoe −/− ) mice fed an atherogenic diet, antibody blockade of JAM-C significantly reduced neointimal hyperplasia after wire injury of carotid arteries without altering medial area and decreased neointimal macrophage but not smooth muscle cell (SMC) content. An increased expression of JAM-C was detected in colocalization with luminal SMCs 1 day after injury and neointimal SMCs after 3 weeks. Blocking JAM-C inhibited monocytic cell arrest and leukocyte adhesion to carotid arteries perfused ex vivo and in vivo. Furthermore, monocyte adhesion to activated coronary artery SMCs under flow conditions in vitro was diminished by blocking JAM-C. Conclusions— Our data provide the first evidence for a crucial role of JAM-C in accelerated lesion formation and leukocyte recruitment in atherosclerosis-prone mice.

Background—Although activation of the complement system has been implicated in the progression of human atherosclerosis, its function during arterial remodeling after injury has not been investigated. Here, we examined the contribution of the complement cascade to neointima formation in apolipoprotein E–deficient mice using a C1-esterase inhibitor (C1-inhibitor).Methods and Results—Apolipoprotein E–deficient mice fed an atherogenic diet were subjected to wire-induced endothelial denudation of the carotid artery and treated with C1-inhibitor (Berinert; 15 IU IV) or vehicle perioperatively and subsequently every 2 days. The effectiveness of C1-inhibitor treatment was confirmed by measurement of plasma C1-inhibitor activity. A significant reduction in serum triglyceride levels was observed in C1-inhibitor–treated mice, whereas cholesterol levels did not differ. After 3 weeks, neointimal area was significantly reduced in C1-inhibitor–treated mice versus controls, whereas medial area was unaltered. This was associated with a significant decrease in neointimal and medial macrophage and CD3+T-cell content. Expression of C3 mRNA was significantly reduced in plaques of C1-inhibitor–treated mice 10 days after injury, as assessed by reverse-transcription polymerase chain reaction. The peak in serum C3 levels after injury was markedly downregulated by C1-inhibitor, as evidenced by ELISA. Immunohistochemistry revealed strong expression of C3 and C3c, which colocalized to plaque macrophages and was reduced in C1-inhibitor–treated mice. C1-inhibitor impaired monocyte arrest on activated endothelium and platelets under flow conditions in vitro and leukocyte recruitment to carotid arteries 1 day after injury in vivo.Conclusions—C1-inhibitor limits neointimal plaque formation and inflammation. This may involve blockade of complement activation, inhibition of leukocyte recruitment, and reduced triglyceride levels, thus providing a multimodal approach to treat arterial disease.

The CXC ligand (CXCL)12/CXC receptor (CXCR)4 chemokine–receptor axis controls hematopoiesis, organ development, and angiogenesis, but its role in the inflammatory pathogenesis of atherosclerosis is unknown. Here we show that interference with Cxcl12/Cxcr4 by a small-molecule antagonist, genetic Cxcr4 deficiency, or lentiviral transduction with Cxcr4 degrakine in bone marrow chimeras aggravated diet-induced atherosclerosis in apolipoprotein E-deficient ( Apoe −/− ) or LDL receptor–deficient ( Ldlr −/− ) mice. Chronic blockade of Cxcr4 caused leukocytosis and an expansion of neutrophils and increased neutrophil content in plaques, associated with apoptosis and a proinflammatory phenotype. Whereas circulating neutrophils were recruited to atherosclerotic lesions, depletion of neutrophils reduced plaque formation and prevented its exacerbation after blocking Cxcr4. Disrupting Cxcl12/Cxcr4 thus promotes lesion formation through deranged neutrophil homeostasis, indicating that Cxcl12/Cxcr4 controls the important contribution of neutrophils to atherogenesis in mice

A 62-year-old man presented with mild left hemiparesis, headache, and blurred vision of his right eye. Ten days before, he had undergone thromboendarterectomy because of subtotal stenosis of his right internal carotid artery. MRI revealed confluent white matter edema together with focal hemorrhage consistent with cerebral hyperperfusion syndrome (CHS; figure 1). Likewise, funduscopy showed small retinal hemorrhages confined to the right eye (figure 2). Under careful blood pressure control, symptoms and brain edema fully resolved within weeks. CHS occurs in around 3% of patients undergoing carotid thromboendarterectomy and can induce severe neurologic deficits.1 Rarely, hyperperfusion also involves the ipsilateral eye.2