Perilesional enhancement of liver cavernous hemangiomas in magnetic resonance imaging.

OBJECTIVE: To evaluate on magnetic resonance imaging (MRI) the occurrence rate of temporal perilesional parenchymal enhancement (PPE) associated with hepatic hemangiomas in a large consecutive series and to determine which aspects are associated with this observation. MATERIALS AND METHODS: Institutional review board approved this retrospective study. A computerized search of the MRI database was performed for consecutive patients between January 2008 and January 2012. The study population included 513 liver hemangiomas in 224 patients (104 males and 120 females; mean age of 55.2 ± 13.5 years; age range 24-89 years). Two readers independently reviewed the frequency of PPE, size, speed of enhancement and location of each hemangioma. Marginal models with generalized estimating equation were used. Wald test was applied to verify if the model coefficients were significant. RESULTS: 80/513 (15.6%) hemangiomas showed PPE. The incidence of PPE was significantly higher (p < 0.05) in hemangiomas with Type1 speed of enhancement (51/80, 63.8%) than in those with Type2 or Type3. 66/80 (82.5%) hemangiomas with PPE were subcapsular (p < 0.05). Conversely, the majority (280/433, 64.7%) of hemangiomas without PPE were deep in location (p < 0.001). Lesser proportion of hemangiomas with PPE was located in segment IVa (p < 0.05). CONCLUSION: PPE is not uncommonly seen along with hepatic hemangiomas. This appearance is most frequently observed in rapidly enhancing small lesions with a subcapsular location.

A model of zinc dynamics evoked by intense stimulation at the cleft of hippocampal mossy fiber synapses.

Zinc is a transition metal that is particularly abundant in the mossy fibers of the hippocampal CA3 area. Despite the large number of studies about the zinc role in mossy fibers, the action of zinc in synaptic mechanisms is only partly known. The use of computational models can be a useful tool for this study. In a previous work, a model was developed to evaluate zinc dynamics at the mossy fiber synaptic cleft, following weak stimulation, insufficient to evoke zinc entry into postsynaptic neurons. For intense stimulation, cleft zinc effluxes must be considered. Therefore, the initial model was extended to include postsynaptic zinc effluxes based on the Goldman-Hodgkin-Katz current equation combined with Hodgkin and Huxley conductance changes. These effluxes occur through different postsynaptic escape routes, namely L- and N-types voltage-dependent calcium channels and NMDA receptors. For that purpose, various stimulations were assumed to induce high concentrations of cleft free zinc, named as intense (10 µM), very intense (100 µM) and extreme (500 µM). It was observed that the main postsynaptic escape routes of cleft zinc are the L-type calcium channels, followed by the NMDA receptor channels and by N-type calcium channels. However, their relative contribution for cleft zinc clearance was relatively small and decreased for higher amounts of zinc, most likely due to the blockade action of zinc in postsynaptic receptors and channels. Therefore, it can be concluded that the larger the zinc release, the more predominant the zinc uptake process will be in the cleft zinc clearance.

Mycobacterium hassiacum recovers from nitrogen starvation with up-regulation of a novel glucosylglycerate hydrolase and depletion of the accumulated glucosylglycerate.

Some microorganisms accumulate glucosylglycerate (GG) during growth under nitrogen deprivation. However, the molecular mechanisms underlying the role of GG and the regulation of its levels in the nitrogen stress response are elusive. Since GG is required for biosynthesis of mycobacterial methylglucose lipopolysaccharides (MGLP) we examined the molecular mechanisms linking replenishment of assimilable nitrogen to nitrogen-starved M. hassiacum with depletion of GG accumulated during nitrogen deficiency. To probe the involvement of a newly identified glycoside hydrolase in GG depletion, we produced the mycobacterial enzyme recombinantly and confirmed the specific hydrolysis of GG (GG hydrolase, GgH) in vitro. We have also observed a pronounced up-regulation of GgH mRNA in response to the nitrogen shock, which positively correlates with GG depletion in vivo and growth stimulation, implicating GgH in the recovery process. Since GgH orthologs seem to be absent from most slowly-growing mycobacteria including M. tuberculosis, the disclosure of the GgH function allows reconfiguration of the MGLP pathway in rapidly-growing species and accommodation of this possible regulatory step. This new link between GG metabolism, MGLP biosynthesis and recovery from nitrogen stress furthers our knowledge on the mycobacterial strategies to endure a frequent stress faced in some environments and during long-term infection.