[Assessment of teleradiology patients in a major regional hospital]. / Charakterisierung teleradiologisch untersuchter Patienten an einem Krankenhaus der Schwerpunktversorgung.

PURPOSE: To evaluate teleradiology examinations regarding the most frequently requested exams and examined body regions. Additionally, the frequency of pathological changes depending on the examined region and clinical situation as well as the time profile for requesting teleradiology (daytime, day of the week) were analyzed. MATERIALS AND METHODS: A retrospective analysis of all consecutive teleradiology exams in 2018 that were reported in the radiology department of a major regional hospital and scanned in three referring primary health care institutions regarding clinical history, working diagnosis and requested body region was performed. Additionally, the date and time of the examination were analyzed. RESULTS: A total of 1207 CT (computer tomography) scans that were reported as part of the teleradiology agreement were included. The most frequently requested examination was a cranial CT (77.9%) with 14.6% pathological findings, followed by abdominal CT (14%) with 63.9% pathological changes, spine/extremities (8.8%) with 50% pathological changes and CT of the chest (7.9%) with 53.7% abnormal scans. Most teleradiology requests were referred on weekends between 8 am and 4 pm, followed by 4 pm to 6 pm on weekdays. The smallest number of scans was requested between 2 am and 4 am. CONCLUSION: Most teleradiology CT requests focus on brain examinations, followed by abdominal CT, CT of the spine and extremities and CT chest. Most cranial CTs do not show an acute pathology, while abdominal CTs had the highest rate of pathological findings.

Ketamine inhibits transcription factors activator protein 1 and nuclear factor-kappaB, interleukin-8 production, as well as CD11b and CD16 expression: studies in human leukocytes and leukocytic cell lines.

BACKGROUND: Recent data indicate that ketamine exerts antiinflammatory actions. However, little is known about the signaling mechanisms involved in ketamine-induced immune modulation. In this study, we investigated the effects of ketamine on lipopolysaccharide-induced activation of transcription factors activator protein 1 (AP-1) and nuclear factor-kappaB (NF-kappaB) in human leukocyte-like cell lines and in human blood neutrophils. METHODS: Electric mobility shift assays were used to investigate ketamine's effects on nuclear binding activity of both transcription factors in U937 cells, and a whole blood flow cytometric technique was used for AP-1 and NF-kappaB determination in leukocytes. Cell lines with different expression patterns of opioid and N-methyl-D-aspartate receptors were used for reverse transcription-polymerase chain reaction to investigate receptors involved in ketamine signaling. Ketamine's effect on interleukin-8 production was assessed in a whole blood assay. RESULTS: Ketamine inhibited both transcription factors in a concentration-dependent manner. These effects did not depend on opiate or N-methyl-D-aspartate receptors. Ketamine also reduced interleukin-8 production in whole blood and expression of CD11b and CD16 on neutrophils. CONCLUSION: The immunoinhibitory effects of ketamine are at least in part caused by inhibition of transcription factors NF-kappaB and AP-1, which regulate production of proinflammatory mediators. However, signaling mechanisms different from those present in the central nervous system are responsible for ketamine-mediated immunomodulation.

A comprehensive study of survival, tissue damage, and neurological dysfunction in a murine model of cardiopulmonary resuscitation after potassium-induced cardiac arrest.

There are only few strategic and therapeutic options to improve the functional outcome of patients after cardiac arrest and resuscitation (CPR). The pathophysiology of reperfusion injury after global ischemia is not completely understood. We present here a murine model of cardiac arrest and resuscitation that allows an analysis of the pathophysiology of reperfusion injury, especially focusing on survival, tissue damage, and functional neurological parameters. Under systemic hemodynamic monitoring, male C57BL/6J mice were subjected to 3 min of a potassium-induced cardiac arrest. After resuscitation under controlled conditions, mice were observed and neurologically scored for 72 h post-CPR. As a control, sham-treated animals were provided. In addition, blood samples were drawn and organs were removed for a histological analysis. Here, global I/R led to functional and histological reperfusion damage. The overall mortality up to day 3 post-CPR was 54%. Resuscitated animals developed marked functional neurologic deficits, as assessed by Rotarod and elevated plus-maze testing. Histological examinations and blood analyses of CPR animals revealed significant leukocyte tissue infiltration and morphological damage of brain, lung, and kidneys. In summary, mice undergoing CPR after cardiac arrest present distinct neurological deficits, marked organ damage, and a 54% mortality rate. Our highly standardized and reproducible model of mice resuscitation provides a means for a better understanding of the post-CPR pathophysiology and thus opens new perspectives to develop relevant therapeutic approaches to minimize global I/R injury.

Protective role of the inhibitor of apoptosis protein, survivin, in toxin-induced acute renal failure.

Acute renal failure (ARF) is a major worldwide cause of morbidity and mortality, lacking specific targeted, effective therapies. Renal tubular cell apoptosis has been recognized to play a critical role in the pathogenesis of ARF, yet few studies have evaluated whether intervention in apoptotic pathways can ameliorate the deterioration in renal function associated with ARF. Using transgenic mice with diminished levels of the inhibitor of apoptosis protein, survivin, we show that survivin is required to protect the kidney from apoptosis, to suppress renal expression of p53, and to ameliorate renal dysfunction in two models of ARF. Gene delivery of survivin to wild-type mice and mice with 50% levels of survivin, prior to or at the time of induction of ARF, interferes with the deterioration of renal function and preserves the integrity of the kidneys and the renal tubular cells by inhibiting activation of apoptotic pathways in the kidneys and suppressing expression of p53. These results encourage further evaluation of survivin, its active structural domains, and other inhibitors of apoptosis proteins, for preventing and/or treating acute renal failure.

Indicators of erythrocyte damage after microwave warming of packed red blood cells.

BACKGROUND: Localized overheating of packed red blood cells (PRBCs) after microwave warming with consequent damage to erythrocytes has been reported. We therefore compared possible cellular markers of erythrocyte damage, as measured by flow cytometry, with laboratory indicators of hemolysis to evaluate the effects of microwave warming on PRBCs. METHODS: PRBC samples were warmed to room temperature or to 37, 42, 47, 52, or 57 degrees C in a water bath. Flow cytometry was performed after fluorescein labeling using antibodies to spectrin, Ca(2+)-ATPase, and Na(+)-K(+)-ATPase. The forward-to-sideward scatter (FSC/SSC) ratio and antibody binding were evaluated. Plasma free hemoglobin (FHb) and alpha-hydroxybutyrate dehydrogenase (HBDH) were measured immediately after heating and after 48 h. In addition, all measurements were made before and after the heating of PRBCs to 35 degrees C by a microwave blood warmer. RESULTS: Analysis of 15000 erythrocytes showed a decrease in the FSC/SSC ratio and antibody binding above 47 degrees C [at 37 degrees C, median (SD) of 94.2 (7.4) with 0.07 (0.05)% fluorescein-positive; at 52 degrees C, median (SD) of 177.0 (19.0) with 18.5 (6.4)% positively gated; P <0.001]. FHb [room temperature, 0.3 (0.2) g/L] was increased 2-fold at 37 and 42 degrees C, 4-fold at 47 degrees C, and 25-fold at 52 degrees C. HBDH increased in parallel. Hemolysis markers showed an additional twofold increase 48 h after heating to 42 and 47 degrees C. Microwave heating to 35 degrees C did not produce significant changes of any marker. CONCLUSIONS: All markers of cellular damage were altered after heating to >47 degrees C, and a substantial part of hemolysis was delayed. The methodology can be used for future testing of other blood warming devices.