Volcanic stratigraphy of Hannah Point, Livingston Island, South Shetland Islands, Antarctica

The Upper Cretaceous volcanic succession of Hannah Point is the best exposure of the Antarctic Peninsula Volcanic Group on L ivingston Island. The aim of the present paper is to contribute to the characterisation of the stratigr a p hy and petrogr a p hy of this little studied succession, and briefly discuss some aspects of the eru p t ive style of its volcanism. The succession is about 470 m thick and is here subdivided into five lithostratigraphic units (A to E from base to top). Unit A, approximately 120 m thick, is mainly composed of polymict clast-supported volcaniclastic breccias and also includes a dacitic lava laye r. Interstratified in the breccias of this unit, there is a thin laminated devitrified layer which shows some degree of welding. Unit B, approx imately 70 m thick, is almost entirely composed of volcaniclastic breccias, and includes a volcaniclastic conglomerate laye r. Breccias in this unit can be subdivided into two distinct types; polymict clast-supported breccias, and monomict matrix-supported breccias rich in juvenile components and displaying incipient welding. Unit C, about 65 m thick, is mainly composed of basaltic lavas, which are interlayered with minor vo lcaniclastic breccias. Unit D, approximately 65 m thick, is lithologically similar to unit B, composed of an alternation of polymict clasts upported breccias and matrix-supported breccias, and includes a volcaniclastic conglomerate laye r. Unit E, about 150 m thick, is mainly formed of thick andesitic lava layers. Minor basaltic dykes and a few normal faults cut the succession, and the contact betwe e n units A and B can be interpreted both as an unconformity or a fault. The matrix-supported breccias included in the succession of Hannah Point have high contents of juvenile components and incipient welding, which suggest that part of the succession is the result of pyroclastic fragmentation and emplacement from pyroclastic flows. In contrast, the polymict clast-supported breccias suggest reworking of previous deposits and deposition from cool mass flows. The lavas indicate eff u s ive volcanic eruptions, and the absence of features indicative of subaqueous volcanism suggests that at least these portions of the succession were emplaced in a subaerial environment .

A unique role for Kv3 voltage-gated potassium channels in starburst amacrine cell signaling in mouse retina

Direction-selective retinal ganglion cells show an increased activity evoked by light stimuli moving in the preferred direction. This selectivity is governed by direction-selective inhibition from starburst amacrine cells occurring during stimulus movement in the opposite or null direction. To understand the intrinsic membrane properties of starburst cells responsible for direction-selective GABA release, we performed whole-cell recordings from starburst cells in mouse retina. Voltage-clamp recordings revealed prominent voltage-dependent K+ currents. The currents were mostly blocked by 1 mm TEA, activated rapidly at voltages more positive than -20 mV, and deactivated quickly, properties reminiscent of the currents carried by the Kv3 subfamily of K+ channels. Immunoblots confirmed the presence of Kv3.1 and Kv3.2 proteins in retina and immunohistochemistry revealed their expression in starburst cell somata and dendrites. The Kv3-like current in starburst cells was absent in Kv3.1-Kv3.2 knock-out mice. Current-clamp recordings showed that the fast activation of the Kv3 channels provides a voltage-dependent shunt that limits depolarization of the soma to potentials more positive than -20 mV. This provides a mechanism likely to contribute to the electrical isolation of individual starburst cell dendrites, a property thought essential for direction selectivity. This function of Kv3 channels differs from that in other neurons where they facilitate high-frequency repetitive firing. Moreover, we found a gradient in the intensity of Kv3.1b immunolabeling favoring proximal regions of starburst cells. We hypothesize that this Kv3 channel gradient contributes to the preference for centrifugal signal flow in dendrites underlying direction-selective GABA release from starburst amacrine cells.

The univalent Bloch-Landau constant, harmonic symmetry and conformal glueing

By modifying a domain first suggested by Ruth Goodman in 1935 and by exploiting the explicit solution by Fedorov of the Polyá-Chebotarev problem in the case of four symmetrically placed points, an improved upper bound for the univalent Bloch-Landau constant is obtained. The domain that leads to this improved bound takes the form of a disk from which some arcs are removed in such a way that the resulting simply connected domain is harmonically symmetric in each arc with respect to the origin. The existence of domains of this type is established, using techniques from conformal welding, and some general properties of harmonically symmetric arcs in this setting are established.

A Novel Missense Mutation, I890T, in the Pore Region of Cardiac Sodium Channel Causes Brugada Syndrome

Brugada syndrome (BrS) is a life-threatening, inherited arrhythmogenic syndrome associated with autosomal dominant mutations in SCN5A, the gene encoding the cardiac Na₊ channel alpha subunit (Naᵥ1.5). The aim of this work was to characterize the functional alterations caused by a novel SCN5A mutation, I890T, and thus establish whether this mutation is associated with BrS. The mutation was identified by direct sequencing of SCN5A from the proband’s DNA. Wild-type (WT) or I890T Naᵥ1.5 channels were heterologously expressed in human embryonic kidney cells. Sodium currents were studied using standard whole cell patch-clamp protocols and immunodetection experiments were performed using an antibody against human Naᵥ1.5 channel. A marked decrease in current density was observed in cells expressing the I890T channel (from -52.0 ± 6.5 pA/pF, n=15 to 35.9 ± 3.4 pA/pF, n = 22, at -20 mV, WT and I890T, respectively). Moreover, a positive shift of the activation curve was identified (V½ =-32.0 ± 0.3 mV, n = 18, and -27.3 ± 0.3 mV, n = 22, WT and I890T, respectively). No changes between WT and I890T currents were observed in steady-state inactivation, time course of inactivation, slow inactivation or recovery from inactivation parameters. Cell surface protein biotinylation analyses confirmed that Nav1.5 channel membrane expression levels were similar in WT and I890T cells. In summary, our data reveal that the I890T mutation, located within the pore of Nav1.5, causes an evident loss-of-function of the channel. Thus, the BrS phenotype observed in the proband is most likely due to this mutation