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Copy numbers of alpha amylase genes (AMY), which encode starch-digesting enzymes, are markedly increased in modern humans and domesticated dogs as an adaptive evolutionary mechanism in response to increased consumption of starch-rich foods acquired either by farming or domestication. In this study, we surveyed total AMY gene copy numbers in 150 domestic pigs (50 pigs of Berkshire breed, 50 of Landrace breed, and 50 of Large White breed) and 51 wild boars (30 Sus scrofa leucomystax and 21 S. s. riukiuanus) to identify whether the gene copy number has changed during the domestication of pigs. The relative copy number of AMY genes was measured using a quantitative polymerase chain reaction (qPCR) and it varied from 2.7 to 10.8 per haploid genome among individuals. However, in the four remaining populations, excluding S. s. riukiuanus, the average copy number was approximately six, and no significant differences were observed between the three selected pig breeds and S. s. leucomystax wild boar. Conversely, S. s. riukiuanus had an average of 7.2 copies. The results indicating six AMY copies per haploid genome were consistent with the porcine genome reference sequence (Sscrofa11.1). These results suggest that there has been no significant increase in the AMY gene copy number during the domestication process of pigs.

Background/Aims: Compared with hemodialysis (HD), hemodiafiltration (HDF) reduces the frequency of episodes of intradialytic hypotension. Intradialytic plasma volume decrease (IPVD) induced by ultrafiltration is a leading cause of the episodes, and hemofiltration might have a preventive effect on IPVD. This study examined whether online HDF (ol-HDF) prevented IPVD compared with HD. Methods: Online HDF of pre-dilution mode (pre-ol-HDF) and post-dilution mode (post-ol-HDF) and HD were performed in 22 patients on maintenance dialysis. In each session, IPVD was calculated by using an intradialytic change in hematocrit, and IPVD in pre-ol-HDF and post-ol-HDF was compared with that in HD in a crossover manner. Results: While the ratios of intradialytic body weight loss to post-dialysis BW (IBWL/BW) in ol-HDF were generally smaller than those in HD, the levels of IPVD and IPVD/IBWL/BW were generally larger than those in HD; the IPVD levels were 0.108 ± 0.058, 0.113 ± 0.053, and 0.101 ± 0.057 (P = 0.67), and those of IPVD/IWL/BW were 2.21 ± 0.97, 2.32 ± 0.91, and 1.98 ± 1.14 (P = 0.21) in pre-ol-HDF, post-ol-HDF, and HD, respectively. Conclusion: Online mode hemofiltration, in either pre-dilution mode or post-dilution mode, performed in combination with hemodialysis has no preventive effect on IPVD.

Abstract Background Intradialytic plasma volume change (IPVC) owing to ultrafiltration is a dominant cause of intradialytic hypotension (IDH). Lower occurrence of IDH in hemodiafiltration (HDF) than in standard hemodialysis (std-HD) indicates that HDF has preventive effect on IPVC. This study examined whether online HDF (ol-HDF) prevented IPVC compared with std-HD. Methods In 115 std-HD, 59 push-pull ol-HDF (pp-ol-HDF), 39 pre-dilution ol-HDF (pre-ol-HDF), and 33 post-dilution ol-HDF (post-ol-HDF) sessions, we calculated IPVC using intradialytic change of hemoglobin (IPVCHb) and also using the change of hematocrit (IPVCHt), and compared them in association with intradialytic body weight loss (IBWL) between the dialysis modes. Results Both IPVCHb and IPVCHt were not different between the modes; in std-HD, pp-ol-HDF, pre-ol-HDF, and post-ol-HDF, IPVCHb were 0.10 ± 0.06, 0.11 ± 0.07, 0.10 ± 0.05, and 0.10 ± 0.06, respectively, and IPVCHt were 0.10 ± 0.07, 0.11 ± 0.07, 0.10 ± 0.06, and 0.10 ± 0.06, respectively. IPVCs divided by relative IBWL to DW (IBWL/DW) were also not different between the modes; in std-HD, pp-ol-HDF, pre-ol-HDF, and post-ol-HDF, IPVCHb/IBWL/DW were 1.9 ± 2.0, 1.7 ± 4.6, 2.1 ± 0.9, and 2.1 ± 1.8, respectively, and IPVCHt/IBWL/DW were 1.9 ± 2.2, 1.9 ± 3.7, 2.1 ± 1.1, and 2.1 ± 2.0, respectively. Conclusion Irrespective of the modes, ol-HDF has the same level of IPVC as std-HD.

Elevation of extracellular Ca(2+) concentration induces intracellular Ca(2+) signaling in parathyroid cells. The response is due to stimulation of the phospholipase C/Ca(2+) pathways, but the direct mechanism responsible for the rise of intracellular Ca(2+) concentration has remained elusive. Here, we describe the electrophysiological property associated with intracellular Ca(2+) signaling in frog parathyroid cells and show that Ca(2+)-activated Cl(-) channels are activated by intracellular Ca(2+) increase through an inositol 1,4,5-trisphophate (IP(3))-independent pathway. High extracellular Ca(2+) induced an outwardly-rectifying conductance in a dose-dependent manner (EC(50) ∼6 mM). The conductance was composed of an instantaneous time-independent component and a slowly activating time-dependent component and displayed a deactivating inward tail current. Extracellular Ca(2+)-induced and Ca(2+) dialysis-induced currents reversed at the equilibrium potential of Cl(-) and were inhibited by niflumic acid (a specific blocker of Ca(2+)-activated Cl(-) channel). Gramicidin-perforated whole-cell recording displayed the shift of the reversal potential in extracellular Ca(2+)-induced current, suggesting the change of intracellular Cl(-) concentration in a few minutes. Extracellular Ca(2+)-induced currents displayed a moderate dependency on guanosine triphosphate (GTP). All blockers for phospholipase C, diacylglycerol (DAG) lipase, monoacylglycerol (MAG) lipase and lipoxygenase inhibited extracellular Ca(2+)-induced current. IP(3) dialysis failed to induce conductance increase, but 2-arachidonoylglycerol (2-AG), arachidonic acid and 12S-hydroperoxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12(S)-HPETE) dialysis increased the conductance identical to extracellular Ca(2+)-induced conductance. These results indicate that high extracellular Ca(2+) raises intracellular Ca(2+) concentration through the DAG lipase/lipoxygenase pathway, resulting in the activation of Cl(-) conductance.