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Purpose: Our aim was to determine the utility of Tc-99m-diethylenetriaminepentaacetic acid-galactosyl human serum albumin single-photon-emission computed tomography ( 99m Tc-GSA SPECT/CT) fusion imaging for detecting incomplete portal vein embolization (PVE)., Materials and Methods: Fifty-five candidates underwent PVE. Among them, five underwent second PVE. Detectability of first inadequate PVE using CT and 99m Tc-GSA SPECT/CT fusion imaging was analyzed., Results: Cases of inadequate PVE were detected in three patients using CT and in five using 99m Tc-GSA SPECT/CT fusion imaging. Fusion imaging detected two cases of insufficient PVE in which portal branches were apparently well embolized on CT. Median value for volumetric rate in the embolized liver was 63.3% after the first PVE and 54.7% after the second (P < 0.01). Median functional rate value in embolized liver was 60.1% after the first PVE and 49.4% after the second (P < 0.01). Median value for change of volumetric and functional rates in embolized liver after the second PVE was 7.1 and 10.3%, respectively, and change of functional rate was greater than that of volumetric rate (P < 0.01)., Conclusions: 99m Tc-GSA SPECT/CT fusion imaging was useful for detecting inadequate PVE, and second PVE was effective for increasing volumetric and functional rates.

Ahnak1, a giant 700 kDa protein, has been implicated in Ca(2+) signalling in various cells. Previous work suggested that the interaction between ahnak1 and Cavbeta(2) subunit plays a role in L-type Ca(2+) current (I (CaL)) regulation. Here, we performed structure-function studies with the most C-terminal domain of ahnak1 (188 amino acids) containing a PxxP consensus motif (designated as 188-PSTP) using ventricular cardiomyocytes isolated from rats, wild-type (WT) mice and ahnak1-deficient mice. In vitro binding studies revealed that 188-PSTP conferred high-affinity binding to Cavbeta(2) (K (d) approximately 60 nM). Replacement of proline residues by alanines (188-ASTA) decreased Cavbeta(2) affinity about 20-fold. Both 188-PSTP and 188-ASTA were functional in ahnak1-expressing rat and mouse cardiomyocytes during whole-cell patch clamp. Upon intracellular application, they increased the net Ca(2+) influx by enhancing I (CaL) density and/or increasing I (CaL) inactivation time course without altering voltage dependency. Specifically, 188-ASTA, which failed to affect I (CaL) density, markedly slowed I (CaL) inactivation resulting in a 50-70% increase in transported Ca(2+) during a 0 mV depolarising pulse. Both ahnak1 fragments also slowed current inactivation with Ba(2+) as charge carrier. By contrast, neither 188-PSTP nor 188-ASTA affected any I (CaL) characteristics in ahnak1-deficient mouse cardiomyocytes. Our results indicate that the presence of endogenous ahnak1 is required for tuning the voltage-dependent component of I (CaL) inactivation by ahnak1 fragments. We suggest that ahnak1 modulates the accessibility of molecular determinants in Cavbeta(2) and/or scaffolds selectively different beta-subunit isoforms in the heart.