Background. The congenitally corrected transposition of the great arteries (L-TGA) is a very rare congenital heart defect, which often remains undetected for several decades of life. Case Presentation. We report on a 45-year-old man without prior history of heart disease, presenting with cardiac shock related to a first episode of tachycardic atrial fibrillation. The diagnostic work-up identified a L-TGA as the underlying cause for acute heart failure. Discussion. L-TGA is a very rare congenital heart defect, which is characterized by an atrioventricular as well as a ventriculoarterial discordance. By this means, the physiological sequence of pulmonary and systemic circulation is still maintained. On the basis of an ongoing strain of the right ventricle, which has to carry the burden of the systemic blood pressure, after more than four decades without symptoms, acute heart failure was triggered by a tachycardic atrial fibrillation.
Dieser interdisziplinäre Sammelband führt Beiträge zusammen, die sich mit Inszenierungen in Film, Geschichte und Literatur sowie in den darstellenden und bildenden Künsten befassen. Sie spannen eine Richtschnur hinsichtlich derjenigen Elemente, die bei der Inszenierung und ihren Diskursen eine entscheidende Rolle spielen. Die Aufsätze stammen von langjährigen Kolleg:innen und Freund:innen des Romanisten Christopher F. Laferl, den Fragestellungen nach der Inszenierung von Leben, Identität und Geschichte seit vielen Jahren beschäftigen und dem diese Festschrift zugeeignet ist.
We report on 2 critically ill patients with pneumonitis and acute respiratory distress syndrome due to pandemic (H1N1) 2009 influenza A virus who were treated with intravenous zanamivir and had favorable clinical outcomes. Zanamivir given intravenously may be a therapeutic option in patients with critical illness and mechanical ventilation.
C-reactive Protein (CRP) is synthesized in the liver. Synthesis is stimulated via the IL-1ß/IL6 pathway. CRP activates the complement system via C1q and macrophages via Fcγ receptors. Since elevated CRP plasma levels are associated with increased cardiovascular risk, CRP may play a causal role in cardiovascular disease. One approach to transfer these observations into standard medical care would be to generate hepatic CRP synthesis inhibitors and use them in controlled clinical trials. Despite huge pharmacological efforts, the search for CRP synthesis inhibitors proved to be difficult. First, the antisense oligonucleotide RNA technology, although a promising idea, has not yet led to results feasible for clinical practice. Secondly, high throughput screening assays in search for hepatic CRP inhibitors were limited by the fact that primary human hepatocytes do not adequately grow in vitro . Use of genetically engineered hepatoma cells led to the observation that cardiac glycosides are capable of inhibiting CRP synthesis. Because of patent law considerations, however, pharmaceutical companies had limited interest in further pursuing this possible path. Upstream inhibition of IL-1ß and IL-6 by antibodies has shown positive results in cardiovascular clinical trials, but because of side effects none of these antibodies has yet received FDA approval. In contrast, long-term colchicine treatment, though not being a CRP-specific approach, has recently been approved by the FDA. Taken together, there is no compelling evidence until today that hepatic CRP synthesis can specifically, effectively and safely be inhibited in vivo in human medicine. Currently, other avenues appear more promising. Here, we summarize contemporary approaches to inhibit CRP synthesis and potential goals for future clinical trials.
Gene transfer into human CD34+ haematopoietic progenitor cells (HPC) and multi-potent mesenchymal stromal cells (MSC) is an essential tool for numerous in vitro and in vivo applications including therapeutic strategies, such as tissue engineering and gene therapy. Virus based methods may be efficient, but bear risks like tumorigenesis and activation of immune responses. A safer alternative is non-viral gene transfer, which is considered to be less efficient and accomplished with high cell toxicity. The truncated low affinity nerve growth factor receptor (ALNGFR) is a marker gene approved for human in vivo application. Human CD34+ HPC and human MSC were transfected with in vitro-transcribed mRNA for DeltaLNGFR using the method of nucleofection. Transfection efficiency and cell viability were compared to plasmid-based nucleofection. Protein expression was assessed using flow cytometry over a time period of 10 days. Nucleofection of CD34+ HPC and MSC with mRNA resulted in significantly higher transfection efficiencies compared to plasmid transfection. Cell differentiation assays were performed after selecting DeltaLNGFR positive cells using a fluorescent activating cell sorter. Neither cell differentiation of MSC into chondrocytes, adipocytes and osteoblasts, nor differentiation of HPC into burst forming unit erythroid (BFU-E) colony forming unit-granulocyte, erythrocyte, macrophage and megakaryocyte (CFU-GEMM), and CFU-granulocyte-macrophage (GM) was reduced. mRNA based nucleofection is a powerful, highly efficient and non-toxic approach for transient labelling of human progenitor cells or, via transfection of selective proteins, for transient manipulation of stem cell function. It may be useful to transiently manipulate stem cell characteristics and thus combine principles of gene therapy and tissue engineering.
A 73-year-old man was admitted with progressive dyspnea; he also had benign prostatic hyperplasia (BPH). An angio computed tomography scan showed pulmonary embolism with thrombi in both main pulmonary arteries. By duplex ultrasonography, we detected a thrombus in the right vena femoralis superficialis and vena femoralis communis. Simultaneously, we also noticed a large diverticulum on the right side of the urinary bladder and urinary stasis II of the left kidney. We consider the BPH as the trigger for a secondary diverticulum of the urinary bladder. As a result of its large dimensions, mechanical compression of the deep right pelvic veins resulted in thrombosis which finally caused the pulmonary embolism. With respect to the urinary stasis II, surgical excavation of the diverticulum with infravesical desobstruction was planned. The potentially lethal course of large diverticula may require surgery.
