ARVs and ARTs: medicoscapes and the unequal place-making for biomedical treatments in sub-Saharan Africa.

Asking why some diseases gain global attention whereas others are neglected, we present two case studies that demonstrate the unequal treatment and financing options available for HIV/AIDS versus infertility treatments. We track three key phenomena central to understanding the unequal public attention given to certain ailments: peace and security, subordination of the social to the biological, and a "global" quality. Existing concepts such as global assemblages or therapeutic citizenship are quite limited when it comes to bodily conditions that result in social suffering and do not satisfy the conditions of advocacy. Since it is not enough to observe "flowing" and "moving," we propose the concept of medicoscapes, to acknowledge that such activities simultaneously entail channeling and carving out. Medicoscapes enhance the analysis of linkages between different health conditions regardless of whether they are biological or social and how they interconnect places, sites, and people.

Music perception in cochlear implant users: an event-related potential study.

OBJECTIVE: Compare the processing of music-syntactic irregularities and physical oddballs between cochlear implant (CI) users and matched controls. METHODS: Musical chord sequences were presented, some of which contained functionally irregular chords, or a chord with an instrumental timbre that deviated from the standard timbre. RESULTS: In both controls and CI users, functionally irregular chords elicited early (around 200 ms) and late (around 500 ms) negative electric brain responses (early right anterior negativity,ERAN and N5). Amplitudes of effects depended on the degree of music-syntactic irregularity in both groups; effects elicited in CI users were distinctly smaller than in controls. Physically deviant chords elicited a timbre-mismatch negativity (MMN) and a P3 in both groups, again with smaller amplitudes in CI users. CONCLUSIONS: ERAN and N5 (as well as timbre-MMN and P3), can be elicited in CI users. Although amplitudes of effects were considerably smaller in the CI group, the presence of MMN and ERAN indicates that neural mechanisms of both physical and music-syntactic irregularity-detection were active in this group.

Attenuation of the P2Y receptor-mediated control of neuronal Ca2+ channels in PC12 cells by antithrombotic drugs.

1. In PC12 cells, adenine nucleotides inhibit voltage-activated Ca(2+) currents and adenylyl cyclase activity, and the latter effect was reported to involve P2Y(12) receptors. To investigate whether these two effects are mediated by one P2Y receptor subtype, we used the antithrombotic agents 2-methylthio-AMP (2-MeSAMP) and N(6)-(2-methyl-thioethyl)-2-(3,3,3-trifluoropropylthio)-beta,gamma-dichloromethylene-ATP (AR-C69931MX). 2. ADP reduced A(2A) receptor-dependent cyclic AMP synthesis with half maximal effects at 0.1-0.17 micro M. In the presence of 30 micro M 2-MeSAMP or 100 nM AR-C69931MX, concentration response curves were shifted to the right by factors of 39 and 30, indicative of pA(2) values of 6.1 and 8.5, respectively. 3. The inhibition of Ca(2+) currents by ADP was attenuated by 10-1000 nM AR-C69931MX and by 3-300 micro M 2-MeSAMP. ADP reinhibited Ca(2+) currents after removal of 2-MeSAMP within less than 15 s, but required 2 min to do so after removal of AR-C69931MX. 4. ADP inhibited Ca(2+) currents with half maximal effects at 5-20 micro M. AR-C69931MX (10-100 nM) displaced concentration response curves to the right, and the resulting Schild plot showed a slope of 1.09 and an estimated pK(B) value of 8.7. Similarly, 10-100 micro M 2-MeSAMP also caused rightward shifts resulting in a Schild plot with a slope of 0.95 and an estimated pK(B) of 5.4. 5. The inhibition of Ca(2+) currents by 2-methylthio-ADP and ADPbetaS was also antagonized by AR-C69931MX, which (at 30 nM) caused a rightward shift of the concentration response curve for ADPbetaS by a factor of 3.8, indicative of a pA(2) value of 8.1. 6. These results show that antithrombotic drugs antagonize the inhibition of neuronal Ca(2+) channels by adenine nucleotides, which suggests that this effect is mediated by P2Y(12) receptors.