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Sparganosis is a severe parasitic infection caused by the larvae of Spirometra mansoni, also called "sparganum." In human hosts, the Spirometra mansoni larva commonly targets the subcutaneous tissue or muscle. Sometimes it can also migrate into the brain, resulting in cerebral sparganosis, mainly characterized by focal neurological symptoms such as seizures and radiological "wandering lesions" on magnetic resonance images (MRIs). Clinical cases of cerebral sparganosis have been reported worldwide, mainly in Asian countries, but also in North America, South America and Australia. Only two cases have been previously reported in Europe. A 29-year-old male from Bolivia, who lived in Spain, presented to our service for seizures and a multicystic brain lesion, initially suspected to be a dysembryoplastic neuroepithelial tumor (DNET). He underwent gross total resection of the mixed solid/cystic lesion. Pathology revealed gliosis, multiple interconnected cystic cavities with fibrous walls, inflammatory cell infiltration and no necrotizing granulomatous reaction. Inside the cavities, a parasitic form was identified as the larva of the cestode Spirometra mansoni. At 1-year follow-up, the patient had no deficits and was seizure free. Clinicians should be alerted to the possible existence of this rare entity in Europe, especially in patients from endemic areas with a possible infection history as well as "wandering lesions" on the MRI.

The prediction of the series of complexes [Au(3)Cl(3)M(2)] with M = Li, Na, K, Rb and Cs, has been achieved at the ab initio level of theory. All geometries were fully optimized at the MP2 level of theory; the central Au(3) cluster is capped by chlorine atoms and the alkaline metals lie above and below the plane of the central ring; aurophilic interactions were found on the metal cluster, and also a strong aromatic character coming from the delocalized d-electrons of the Au atoms according to nuclear independent chemical shift calculations. On the other hand, the chemical hardness parameter was used to test the stability of the series of complexes, and the Fukui indexes of electrophilic and nucleophilic attack were employed to explore possible sites where chemical reactivity may play a role.

Dystrophin Dp71 has been implicated with cognitive impairment shown by Duchenne muscular dystrophy patients. To study Dp71 neural role, we used PC12 cell line, since these cells differentiate into sympathetic like neurons when stimulated with nerve growth factor Previously in undiferentiated PC12 cells, it was demonstrated that dystrophin Dp71f is a key component of the beta1-integrin adhesion complex that confers proper complex assembly. Since integrin based mediated adhesion is important during neuronal differentiation, it was important to know if dystrophin Dp71f was a structural component of the beta1-integrin adhesion complex in neurites of nerve growth factor stimulated PC12 cells. In the present work, by performing immunofluorescence assays, we determined the association of dystrophin Dp71f with some components of the beta1-integrin adhesion complex such as beta1-integrin subunit, talin, alpha-actinin and vinculin in neurites of nerve growth factor stimulated PC12 cells seeded onto the extracellular matrix protein laminin. The association was stronger in neural growth cones suggesting that dystrophin Dp71f is important for the function that the beta1-integrin complex has during neurite outgrowth.

Aromatic rings can suffer severe distortions upon substituting transition metal centers with certain kinds of organometallic compounds. This property is very interesting because aromaticity can remain despite the deformation. Theoretical calculations at the density functional theory level were carried out on two such structures containing vanadium and iron centres [(C5H5-V-H)(2)C6H6 and (CpFe)(2)C6(CH3)(6)] in order to analyze the nature of the bonds as well as the magnitude of the prevalent aromaticity and how this depends on the electronic characteristics around each metal atom. The analysis of aromaticity was carried out on the basis of known methods, such as HOMA and FLU, with consistent results. The results also show features that suggest a possible catalytic behavior of the species under study.

A theoretical study of a sandwich compound with a metal monolayer sheet between two aromatic ligands is presented. A full geometry optimization of the [Au(3)Cl(3)Tr(2)](2+) (1) compound, which is a triangular gold(I) monolayer sheet capped by chlorines and bounded to two cycloheptatrienyl (Tr) ligands was carried out using perturbation theory at the MP2 computational level and DFT. Compound (1) is in agreement with the 18-electron rule, the bonding nature in the complex may be interpreted from the donation interaction coming from the Tr rings to the Au array, and from the back-donation from the latter to the former. NICS calculations show a strong aromatic character in the gold monolayer sheet and Tr ligands; calculations done with HOMA, also report the same aromatic behavior on the cycloheptatrienyl fragments giving us an insight on the stability of (1). The Au -Au bond lengths indicate that an intramolecular aurophilic interaction among the Au(I) cations plays an important role in the bonding of the central metal sheet.

In this work, we tested whether L-type Ca(2+ )channels are involved in the increase of caffeine-evoked tension in frog slow muscle fibers. Simultaneous net Ca(2+) fluxes and changes in muscle tension were measured in the presence of caffeine. Isometric tension was recorded by a mechanoelectrical transducer, and net fluxes of Ca(2+) were measured noninvasively using ion-selective vibrating microelectrodes. We show that the timing of changes in net fluxes and muscle tension coincided, suggesting interdependence of the two processes. The effects of Ca(2+)channel blockers (verapamil and gadolinium) were explored using 6 mM: caffeine; both significantly reduced the action of caffeine on tension and on calcium fluxes. Both caffeine-evoked Ca(2+) leak and muscle tension were reduced by 75% in the presence of 100 microM: GdCl(3), which also caused a 92% inhibition of net Ca(2+) fluxes in the steady-state condition. Application of 10 microM: verapamil to the bath led to 30% and 52% reductions in the Ca(2+)leak caused by the presence of caffeine for the peak and steady-state values of net Ca(2+) fluxes, respectively. Verapamil (10 microM): caused a 30% reduction in the maximum values of caffeine-evoked muscle tension. Gd(3+)was a more potent inhibitor than verapamil. In conclusion, L-type Ca(2+) channels appear to play the initial role of trigger in the rather complex mechanism of slow fiber contraction, the latter process being mediated by both positive Ca(2+)-induced Ca(2+ )release and negative (Ca(2+) removal from cytosol) feedback loops.