The problem of finding correspondence between a particular neuronal organization and a specific function of the human brain remains a central question of neuroscience. It is sometimes thought that language and music are two sides of the same intellectual coin, but research on brain‐damaged patients has shown that the loss of verbal functions (aphasia) is not necessarily accompanied by a loss of musical abilities (amusia). Amusia without aphasia has also been described. This double dissociation indicates functional autonomy in these mental processes. Yet verbal and musical impairments often occur together. The global picture that emerges from studies of music and its neural substrate is by no means clear and much depends on which subjects and which aspect of musical abilities are investigated.
An illustration of these concepts is provided by the case of the French composer Maurice Ravel, who suffered from a progressive cerebral disease of uncertain aetiology, with prominent involvement of the left hemisphere. As a result, Ravel experienced aphasia and apraxia and became unable to compose. The available facts favour a clinical diagnosis of primary progressive aphasia (PPA), with the possibility of an overlap with corticobasal degeneration (CBD).
In view of Ravel’s clinical history, we propose that two of his final compositions, the Bolero and the Concerto for the Left Hand, include certain patterns characteristic of right‐hemisphere musical abilities and may show the influence of disease on the creative process.
Parkinson's disease (PD) is a major worldwide public health problem with a prevalence that is expected to increase dramatically in the coming decades. Because administrative data are useful for epidemiologic and health service studies, we aimed to define procedural algorithms to identify PD patients (on a regional basis) using these data. We built two a priori algorithms, respecting privacy laws, with increasing theoretical specificity for PD including: (1) a hospital discharge diagnosis of PD; (2) PD-specific exemption; (3) a minimum of two separate prescriptions of an antiparkinsonian drug. The two algorithms differed for drugs included. Sensitivities were tested on an opportunistic sample of 319 PD patients from the databases of 5 regional movement disorders clinics. The estimated prevalence of PD in the sample population from Tuscany was 0.49 % for algorithm 1 and 0.28 % for algorithm 2. Algorithm 1 correctly identified 291 PD patients (sensitivity 91.2 %), and algorithm 2 identified 242 PD patients (sensitivity 75.9 %). We developed two reproducible algorithms demonstrating increasing theoretical specificity with good sensitivity in identifying PD patients based on an evaluation of administrative data. This may represent a low-cost strategy to reliably follow up a large number of PD patients as a whole for evaluating the effects of therapies, disease progression and prevalence.
Educational initiatives will be organized directly to the healthcare professionals involved in the contrast media administration, to promote an appropriate use of the contrast media.
During 14 years of post-marketing surveillance, only few SRA concerning CM-induced ADRs were sent to CRFVC probably due to underreporting. We aim to improve monitoring activity on CM-induced ADRs especially in hospitals. Most reported ADR and CM were in line with current body of literature.
A loss in cholesterol 7a-hydroxylase activity [cholesterol 7a-monooxygenase; cholesterol,NADPH:oxygen oxidoreductase (7a-hydroxylating), EC 1.14.13.17] was seen when rat liver microsomes were incubated in the presence of Ca2+, Mg2+, or Mn2+. The loss in enzyme activity was complete within only 5 min of incubation with Ca2+ and Mn2+, whereas Mg2+ required 10 to 15 min of incubation with microsomes to produce a similar inhibition. This effect of metal ions could be blocked if the incubations were carried out in phosphate buffer. Similarly, preincubation of microsomes in the presence of NaF completely prevented the loss in enzyme activity due to Ca2+ and Mg2+ ions, but only partially the loss due to Mn2+. These results suggest metal ion activation of an endogenous microsomal phosphatase, which in turn may inactivate cholesterol 7at-hydroxylase through its dephosphorylation. Further, a dialyzable microsomal factor appears to be essential for stabilizing the enzyme, because dialysis of a microsomal suspension results in a considerable loss of enzyme activity.Bile acid biosynthesis is believed to be critically regulated by alterations in the level of cholesterol 7a-hydroxylase activity [cholesterol 7a-monooxygenase; cholesterol, NADPH :.oxygen oxidoreductase (7a-hydroxylating), EC 1.14.13.17]. Our recent studies have indicated that short-term rapid changes in the activity of this enzyme may involve the process of phosphorylation/dephosphorylation, with the active enzyme being phosphorylated (1). This observation has been recently confirmed (2). Briefly, incubation of rat liver microsomes with Escherichia coli alkaline phosphatase results in a loss of cholesterol 7a-hydroxylase activity in proportion to the amount of phosphatase added. Much of this loss could be recovered by removal of phosphatase followed by the addition of ATP, Mg2+, and a cytosolic protein fraction. Later experiments, however, revealed that a major part of the enzyme activity could be recovered without the cytosolic protein and could even be improved if Mg2+ was omitted. The latter observation suggested that Mg2+ and some other bivalent cations may have a role in modulating cholesterol 7a-hydroxylase activity. The results of our recent experiments described here are consistent with this notion. These results are typical of a series of experiments and have been consistently reproducible.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.