The MRI unit is a work station where all processes have to be well planned and staff trained to guarantee maximum patient safety, superior quality of imaging and economic needs. For optimal performance trained, experienced and certified personnel, appropriate drugs for the individual patient risk profile and sufficient monitoring equipment are essential.
Arterial blood pressure (BP) is a fundamental cardiovascular variable, is routinely measured in perioperative and intensive care medicine, and has a significant impact on patient management. The clinical reference method for BP monitoring in high-risk surgical patients and critically ill patients is continuous invasive BP measurement using an arterial catheter. A key prerequisite for correct invasive BP monitoring using an arterial catheter is an in-depth understanding of the measurement principle, of BP waveform quality criteria, and of common pitfalls that can falsify BP readings. Here, we describe how to place an arterial catheter, correctly measure BP, and identify and solve common pitfalls. We focus on 5 important steps, namely (1) how to choose the catheter insertion site, (2) how to choose the type of arterial catheter, (3) how to place the arterial catheter, (4) how to level and zero the transducer, and (5) how to check the quality of the BP waveform.
Non-homologous end-joining (NHEJ) of DNA double-strand breaks (DSBs) is mediated by two protein complexes comprising Ku80/Ku70/DNA-PKcs/Artemis and XRCC4/LigaseIV/XLF. Loss of Ku or XRCC4/LigaseIV function compromises the rejoining of radiation-induced DSBs and leads to defective V(D)J recombination. In this study, we sought to define how XRCC4 and Ku80 affect NHEJ of site-directed chromosomal DSBs in murine fibroblasts. We employed a recently developed reporter system based on the rejoining of I-SceI endonuclease-induced DSBs. We found that the frequency of NHEJ was reduced by more than 20-fold in XRCC4−/− compared to XRCC4+/+ cells, while a Ku80 knock-out reduced the rejoining efficiency by only 1.4-fold. In contrast, lack of either XRCC4 or Ku80 increased end degradation and shifted repair towards a mode that used longer terminal microhomologies for rejoining. However, both proteins proved to be essential for the repair of radiation-induced DSBs. The remarkably different phenotype of XRCC4- and Ku80-deficient cells with regard to the repair of enzyme-induced DSBs mirrors the embryonic lethality of XRCC4 knock-out mice as opposed to the viability of the Ku80 knock-out. Thus, I-SceI-induced breaks may resemble DSBs arising during normal DNA metabolism and mouse development. The removal of these breaks likely has different genetic requirements than the repair of radiation-induced DSBs.
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