Many reports have been made on gallbladder dysfunction after gastric surgery. We reported that the gallbladder contractions were abolished after antrectomy. Our hypothesis is that preservation of the neural connection along gastric vessels maintains normal gallbladder function during fasting after antrectomy. Six dogs underwent antrectomy with preservation of the extrinsic nerves and six other dogs underwent conventional antrectomy with dissection of the extrinsic nerves and vessels. Laparotomy alone was performed on another six control dogs. Motor activities of the gallbladder and upper gastrointestinal tract were recorded by strain gauges in conscious dogs. Motilin and CCK-OP were used for pharmacological interventions. In conventional antrectomy, the amplitudes of the cyclic motor activity of the gallbladder and the stomach during fasting were significantly reduced, while this activity was maintained in dogs when extrinsic nerves were preserved. The coordination of the motor activity among the gallbladder, stomach and the duodenum was not impaired in the dogs when extrinsic nerves were preserved. The contractions of the gallbladder induced by exogenous motilin were reduced significantly in conventional antrectomy. Therefore, the preserved neural connection along the gastric vessels maintains normal gallbladder function in the fasting state even after distal gastrectomy.
In this paper, we propose an SRAM macro that realizes 0.5V operation by combining a device technique with simple design architecture. Regarding the device technique, we utilize asymmetric halo implant MOSFETs, which enables to enhance both the static noise margin and write margin of SRAM, simultaneously. As for the design technique, dynamic body-bias scheme which operates body bias dynamically is introduced to overcome the speed degradation due to lower supply voltage. Showing measured data fabricated on 45nm CMOS technology, we demonstrate a plausible scenario for achieving 0.5V operating SoC products.
Abstract. Gicerin, an Ig-superfamily cell adhesion molecule, has homophilic adhesion activity, thus leading to the formation of gicerin aggregates. Gicerin is highly expressed in various embryonic tissues, and it contributes to development through its adhesive activities. In contrast, the expression of the protein is limited to the muscular tissues and endothelial cells in the mature animals. In the liver, gicerin is constitutively expressed in sinusoidal endothelial cells. Interestingly, an overexpression of gicerin is found in a variety of tumors and may play a role in tumorigenesis. Previously, up-regulated expression of the gicerin protein was found in some sporadic cases of chicken colorectal adenocarcinomas and their hepatic metastasized lesions. In the present study, gicerin cDNA was introduced into endogenous gicerin negative ACL-15 cells, a rat colon adenocarcinoma cell line. The cells were subsequently evaluated for changes in their metastatic potentials in order to elucidate the possible role of gicerin in the hepatic metastasis of colorectal adenocarcinomas. The stable overexpression of gicerin in the cells enhanced the self-aggregation and migratory activities on the protein compared with the mock-transfectants. In addition, the gicerintransfectants had enhanced metastatic potential to the liver compared with mock-transfected cells after implantation into the ileocolic vein of the cognate rats. These results suggest that gicerin might promote the interaction of tumor cells with a hepatic endothelium, thus leading to the hepatic metastasis of colon adenocarcinomas.
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