Rabies post-exposure prophylaxis in the emergency department: A monocentric retrospective observational study.

Background: Emergency departments (ED) are frequently visited after suspected rabies exposure (SRE) and the potential need for rabies post-exposure prophylaxis (R-PEP). However, data on the number of visits, patients' demographics, travel history and the medical treatment is still rare. Therefore, the aim of this study was to assess the number of R-PEP and the appropriateness of medical management including wound treatment, vaccination regime and immunoglobulin application following SRE in a university hospital ED.

[Invasive Streptococcal infections - an interdisciplinary challenge].

History And Clinical Findings:  We report on a 34-year-old female patient and a 50-year-old male patient, both of whom were admitted to our emergency department with severe septic conditions.

Medical Examinations:  Both patients were resuscitated and exhibited clinical as well as laboratory evidence of a severe bacterial infection.

Diagnosis:  Both patients had an invasive infection with Group A Streptococcus.

[Motives of patients presenting independently at the emergency department-a prospective monocentric observational study].

Background: In the ongoing professional, societal, and political discussion, the hypothesis is repeatedly put forward that a large portion of patients who independently visit the emergency department could also be treated in other care settings such as by a general practitioner, the statutory medical on-call service, or in emergency clinics. Various reasons are cited for why these alternative care settings are not utilized in these cases.

Objectives: This study investigates the motives of patients who presented independently at the emergency department, as well as the socio-demographic parameters of this study cohort.

[Vasculitis oft the skin after cocaine use].

History And Clinical Findings: A 20-years-old patient presented himself to our emergency room with extensive and extremely painful purpura with necrotizing spots and blisters, especially on the lower extremities, but also on the arms, trunk and ears. There was a pre-existing use of cocaine.

Medical Examinations: Laboratory tests showed increased signs of inflammation as well as an increase in proteinase 3- and myeloperoxidase-ANCA (Anti-neutrophil cytoplasmatic antibody).

Medical and cardio-vascular emergency department visits during the COVID-19 pandemic in 2020: is there a collateral damage? A retrospective routine data analysis.

Background: In this retrospective routine data analysis, we investigate the number of emergency department (ED) consultations during the COVID-19 pandemic of 2020 in Germany compared to the previous year with a special focus on numbers of myocardial infarction and acute heart failure.

Methods: Aggregated case numbers for the two consecutive years 2019 and 2020 were obtained from 24 university hospitals and 9 non-university hospitals in Germany and assessed by age, gender, triage scores, disposition, care level and by ICD-10 codes including the tracer diagnoses myocardial infarction (I21) and heart failure (I50).

Results: A total of 2,216,627 ED consultations were analyzed, of which 1,178,470 occurred in 2019 and 1,038,157 in 2020.

[COVID-19 in GP Practice and Emergency Rooms - Update 2021].

COVID-19 continues to pose major challenges for GP practice and emergency rooms across Germany. Even if there is now a certain routine, the optimal treatment of patients is still difficult. This article provides an overview of the aspects of caring for COVID-19 patients in GP practice and emergency rooms and the changes since the beginning of the pandemic.

[COVID-19 in GP Practice and Emergency Rooms].

COVID-19 challenges GP practice and emergency rooms across Germany. In addition to hygiene, the correct assignment of patients to outpatient, inpatient or intensive care management is difficult. This article provides an overview of aspects of initial care, management and risk assessment in COVID-19 patients.

[Prevention of "contrast-induced" acute kidney injury - practical considerations].

Acute kidney injury (AKI) episodes after iodine radiocontrast application are decreasing since non-ionic agents are routinely used. Retrospective studies (in total comprising more than 100 000 patients) DO NOT show increased AKI rates after CT scans with the application of radiocontrast (vs. uncontrasted CT scans).

Double-stranded DNA induces a prothrombotic phenotype in the vascular endothelium.

Double-stranded DNA (dsDNA) constitutes a potent activator of innate immunity, given its ability to bind intracellular pattern recognition receptors during viral infections or sterile tissue damage. While effects of dsDNA in immune cells have been extensively studied, dsDNA signalling and its pathophysiological implications in non-immune cells, such as the vascular endothelium, remain poorly understood. The aim of this study was to characterize prothrombotic effects of dsDNA in vascular endothelial cells.

Arterial thrombosis in the context of HCV-associated vascular disease can be prevented by protein C.

Hepatitis C virus (HCV) infection is a major problem worldwide. HCV is not limited to liver disease but is frequently complicated by immune-mediated extrahepatic manifestations such as glomerulonephritis or vasculitis. A fatal complication of HCV-associated vascular disease is thrombosis.

BK virus infection activates the TNFα/TNF receptor system in Polyomavirus-associated nephropathy.

Polyomavirus-associated nephropathy due to BK virus infection (BKVAN) is recognized as an important cause of significant kidney transplant dysfunction often leading to renal graft loss. The activation of innate immune defense mechanisms during BKVAN is still poorly understood and an altered regulation of inflammatory mediators by resident kidney cells upon viral infection can be expected to contribute to the onset and progression of disease. TNFα interacting with its receptors, TNF receptor 1 (TNFR1) and TNF receptor 2 (TNFR2), is largely accepted to be involved in viral responses, exhibiting both proinflammatory and immunosuppressive effects.

LL37 inhibits the inflammatory endothelial response induced by viral or endogenous DNA.

In viral infection, morbidity and mortality often result from extrahepatic disease manifestations such as vasculitis. We hereby show that human microvascular endothelial cells express viral receptors of the innate immune system which are induced upon ligand engagement. Furthermore, stimulation of endothelial cells with the synthetic analog of viral DNA, poly (dA:dT), human DNA and hepatitis B virus-containing immunoprecipitates from a patient with polyarteritis nodosa induces an inflammatory response including the upregulation of adhesion molecules, which is mediated exclusively by TLR9 and involves an IRF3-dependent pathway.

The tyrosine phosphatase SHP-1 regulates hypoxia inducible factor-1α (HIF-1α) protein levels in endothelial cells under hypoxia.

Introduction: The tyrosine phosphatase SHP-1 negatively influences endothelial function, such as VEGF signaling and reactive oxygen species (ROS) formation, and has been shown to influence angiogenesis during tissue ischemia. In ischemic tissues, hypoxia induced angiogenesis is crucial for restoring oxygen supply. However, the exact mechanism how SHP-1 affects endothelial function during ischemia or hypoxia remains unclear.

Hepatitis C virus induced endothelial inflammatory response depends on the functional expression of TNFα receptor subtype 2.

In hepatitis C virus (HCV) infection, morbidity and mortality often result from extrahepatic disease manifestations. We provide evidence for a role of receptors of the innate immune system in virally induced inflammation of the endothelium in vitro and in vivo. Corresponding to the in vitro finding of an HCV-dependent induction of proinflammatory mediators in endothelial cells, mice treated with poly (I:C) exhibit a significant reduction in leukocyte rolling velocity, an increase in leukocyte adhesion to the vessel wall and an increased extravasation of leukocytes.

Viral nucleic acid recognition in human nonimmune cells: in vitro systems.

The innate immune system detects viral infections through a variety of receptors that sense the virus via their nucleic acid genome and evokes initial antiviral responses. Nonimmune cells possess pathogen-recognition mechanisms that enable them to respond to virus by the expression of RNA or DNA recognition receptors, thereby initiating the first steps in the host-pathogen interaction and inducing the production of pro-inflammatory and antiviral mediators. To better understand the activation of innate-immune defense mechanisms by nonimmune cells, we describe an experimental procedure that mimics viral infection, using four human nonimmune cell culture models under stimulation with synthetic analogues of RNA and DNA virus.

Renal lipidosis in patients enrolled in a methadone substitution program.

Kidney biopsies often show accumulation of lipids or lipidlike material. Evidence has been provided that lipids can directly initiate and contribute to the progression of glomerular and tubulointerstitial lesions. In this study we describe a renal lipidosis occurring in patients with a positive history of narcotic abuse who were enrolled in a methadone substitution program.

The endothelial tyrosine phosphatase SHP-1 plays an important role for vascular haemostasis in TNFα -induced inflammation in vivo.

Introduction: Inflammation and endothelium-derived superoxides are important pathomechanisms in atherothrombotic diseases. We could previously show that the tyrosine phosphatase SHP-1 acts as a negative regulator in endothelial superoxide production. In this study we investigated the influence of SHP-1 on platelet-endothelium interaction and arterial thrombosis in TNFα -induced endothelial inflammation in vivo.

PAR-1 mediates the thrombin-induced mesothelial cell overproduction of VEGF and PAI-1.

Purpose: Thrombin mediates an excess in the production of neoangiogenetic (VEGF) and profibrotic (PAI-1) factors in human peritoneal mesothelial cells (HMC). The mechanisms leading to this overproduction have not been elucidated so far; in the context of peritoneal dialysis it can result in impaired peritoneal membrane function.

Objectives: This study was performed to evaluate the presence of the thrombin receptor protease-activated receptor-1 (PAR-1) in HMC and to characterize its function in the thrombin-dependent effects mentioned above.

Prothrombotic effects of tumor necrosis factor alpha in vivo are amplified by the absence of TNF-alpha receptor subtype 1 and require TNF-alpha receptor subtype 2.

Introduction: Elevated serum levels of the proinflammatory cytokine tumor necrosis factor alpha (TNFα) correlate with an increased risk for atherothrombotic events and TNFα is known to induce prothrombotic molecules in endothelial cells. Based on the preexisting evidence for the impact of TNFα in the pathogenesis of autoimmune disorders and their known association with an acquired hypercoagulability, we investigated the effects of TNFα and the role of the TNF receptor subtypes TNFR1 and TNFR2 for arteriolar thrombosis in vivo.

Methods: Arteriolar thrombosis and platelet-rolling in vivo were investigated in wildtype, TNFR1-/-, TNFR2-/- and TNFR1-/R2-/- C57BL/6 mice using intravital microscopy in the dorsal skinfold chamber microcirculation model.

Hydrogen sulfide-releasing aspirin derivative ACS14 exerts strong antithrombotic effects in vitro and in vivo.

Objective: Hydrogen sulfide (H(2)S)-releasing NSAIDs exert potent anti-inflammatory effects beyond classical cyclooxygenase inhibition. Here, we compared the platelet inhibitory effects of the H(2)S-releasing aspirin derivative ACS14 with its mother compound aspirin to analyze additional effects on platelets.

Methods And Results: In platelets of mice fed with ACS14 for 6 days (50 mg/kg per day), not only arachidonic acid-induced platelet aggregation but also ADP-dependent aggregation was decreased, an effect that was not observed with an equimolar dose of aspirin (23 mg/kg per day).

TNFα enhances TLR3-dependent effects on MMP-9 expression in human mesangial cells.

The role of MMPs (matrix metalloproteinases) in kidney diseases has been widely accepted, where they can regulate inflammatory response because of their effects on both recruitment and survival of inflammatory cells. TNFα (tumour necrosis factor α) has also been implicated in the pathogenesis of inflammatory kidney diseases, including forms of glomerulonephritis associated with viral diseases. Previously, we established the functional linkage between viral receptors of the innate immune system, the TLRs (Toll-like receptors) and control of MMP activity in human MC (mesangial cells).

Response of VEGF to activation of viral receptors and TNFα in human mesangial cells.

Vascular endothelial growth factor (VEGF) plays an important role in glomerular homeostasis as well as in the pathogenesis of kidney diseases as glomerulonephritis (GN) and diabetic nephropathy. Mesangial cells (MC), which are an integral part of the functional glomerular filtration barrier in that providing structural support, can behave like inflammatory cells and produce mediators as chemokines and growth factors; they are known to express viral receptors, with TLR3 having been attributed relevance in viral disease-associated GN. Experiments were performed on human MC in cell culture.