Extended-donor criteria liver allografts

Extended-donor criteria liver allografts do not meet traditional criteria for transplantation. Although these organs offer immediate expansion of the donor pool, transplantation of extended-donor criteria liver allografts increases potential short- and long-term risk to the recipient. This risk may manifest as impaired allograft function or donor-transmitted disease. Guidelines defining this category of donor, level of acceptable risk, principles of consent, and post-transplantation surveillance have not been defined. This article reviews the utilization, ethical considerations, and outcomes of extended-donor criteria liver allografts.     

Repair of a floating sternum with autologous rib grafts and polylactide bioabsorbable struts in an 18-year-old male

Failed regeneration of costal cartilage after open repair of pectus chest wall deformities can result in a floating sternum. A floating sternum can be repaired by insertion of a rib graft between the rib and sternum, and stabilization with a metal strut. The metal implant is usually removed with a second operation. We report use of bioabsorbable struts to stabilize rib grafts during repair of a floating sternum in an 18-year-old male with a failed open repair of pectus carinatum. He had an uncomplicated peri-operative course. One year later, the sternum had a normal appearance and was sturdy. A second operation for removal of hardware was not necessary.     

Hypothermia abolishes hypoxia-induced hyperpermeability in brain microvessel endothelial cells

The effect of mild (32 degrees C) and deep (22 degrees C) hypothermia on hypoxia-induced hyperpermeability was examined using an in vitro model of brain derived microvascular endothelial cells (BMEC). It was shown that hypoxia-induced hyperpermeability to inulin across the BMEC monolayer was completely abolished at 32 degrees C and 22 degrees C for up to 24 h of hypoxia. During normoxia, no influence of hypothermia on BMEC monolayer permeability was observed. The hypoxia-induced decrease of the cyclic AMP level after 6 h was abolished at 32 degrees C as well as at 22 degrees C of hypoxia. But after 24 h of hypoxia, hypothermia did no longer prevent the hypoxia-induced decrease of the cAMP level, which suggests that the effect of hypothermia on hypoxia-induced hyperpermeability is not caused by maintenance of the cAMP level. Because vascular endothelial growth factor (VEGF) has been shown to be the mediator of hypoxia-induced permeability changes of BMEC via the release of nitric oxide (NO), the effect of hypothermia on the VEGF expression was evaluated. During normoxia, hypothermia did not change the VEGF expression significantly but the hypoxia-induced increase in VEGF mRNA and protein expression was completely abolished at 32 degrees C and 22 degrees C respectively. Accordingly, the hypoxia-induced increase of the cGMP level was depressed by hypothermia, which demonstrates that also the amount of NO released during hypoxia is decreased at lower temperatures. Results suggest that deep as well as mild hypothermia decreased hypoxia-induced hyperpermeability by lowering the expression of the permeability-increasing protein VEGF and with it the release of NO.     

Hardware considerations for MR imaging physics

Since its commercial introduction as a diagnostic tool in 1984, MR imaging has undergone dramatic improvements in all the features that define image quality. This article discusses what a modern MR imaging scanner should look like and how the components of an MR system, especially the magnet, gradient, and RF components must be matched with one another to ensure optimal performance.     

In-vitro-Effekte von Anästhetika auf die Blut-Hirn-Schranke

BACKGROUND: The blood-brain barrier (BBB) forms a selective barrier between blood and brain and regulates the passage of most molecules. Pathological conditions such as ischemia lead to breakdown of the BBB. Vascular endothelial growth factor (VEGF) has been shown to be responsible for hypoxia-induced hyperpermeability of the BBB in vivo as well as in vitro. To eliminate factors which alter the permeability of the BBB in vivo, an in vitro model was used to test the effects of intravenous and volatile anesthetics on the permeability and on VEGF expression during normoxia and hypoxia. METHODS: The in vitro model of the BBB consisted of primary cultures of porcine brain microvascular endothelial cells (BMEC). The permeability was measured by the paracellular passage of [3H]inulin across the BMEC monolayer and the expression of VEGF was determined by northern blot analysis. RESULTS: All intravenous and volatile anesthetics tested (etomidate, ketamine, fentanyl, propofol, midazolam, sodium-gamma-hydroxybutyrate as well as halothane, enflurane, isoflurane, sevoflurane, desflurane) did not alter the permeability of the BBB or the expression of VEGF in vitro. Hypoxia (2 vol%) increased the permeability and the VEGF expression significantly which was not altered in the presence of the anesthetics. CONCLUSION: The in vitro model represents a suitable model of the BBB to investigate direct effects of anesthetics on functions of the BBB independent of hemodynamic factors.     

Differential regulation of neurotrophin expression by mitogens and neurotransmitters in mouse lymphocytes

In this study, we examined the expression of neurotrophins in mouse lymphocytes and the regulation of their expression by mitogens and neurotransmitters. We found that mixed splenocytes as well as T and B lymphocytes expressed mRNA for all the neurotrophins examined. Differential regulation of the neurotrophins was obtained upon stimulation of the cells. Thus, LPS increased the expression of NGF, BDNF and NT-3 in splenocytes and B cells, whereas Con-A increased the mRNA of NT-3 and NT-4 in T cells and NGF expression in splenocytes. The neurotransmitter substance P and the beta-adrenergic agonist, isoproterenol induced an increase in the expression of NGF. Our results suggest an important role for the different neurotrophins in the function of the immune system and point to a bi-directional interaction between neurotrophins and neurotransmitters in this system.     

Augmentation of allergic early-phase reaction by nerve growth factor

The allergic early-phase reaction, a hallmark of allergic bronchial asthma, is caused by allergen and immunoglobulin E-dependent mediator release from mast cells. It was previously shown that nerve growth factor (NGF) contributes to acute airway inflammation. This study further investigates the role of NGF in the allergic early-phase reaction using a well-established mouse model of ovalbumin-induced allergic airway inflammation. Treatment of sensitized and aerosol challenged BALB/c mice with blocking anti-NGF antibodies inhibited allergen-induced early-phase reaction and suppressed airway inflammation. Transgenic mice constitutively overexpressing NGF in the airways (Clara-cell secretory protein promoter [CCSP]-NGF-tg) were employed and compared with wild-type animals. In sensitized and challenged CCSP-NGF-tg mice, early-phase reaction, airway inflammation, as well as percental relative increases in serotonin levels were augmented compared with wild-type mice. These effects were paralleled by increased serotonin levels in the airways, whereas immunoglobulin E levels remained unaffected. Furthermore, CCSP-NGF-tg mice developed an increased reactivity of sensory neurons in response to inhaled capsaicin demonstrating NGF-mediated neuronal plasticity. These data provide evidence for the functional role of NGF in the development of allergic early phase responses in the airways and the lung.