A new multi-cell cellular configuration networks is provided for analysis of handover initiation probability, which is based on multi-beam base-station antenna splitting in the elevation-radiating plane. The sum of th...A new multi-cell cellular configuration networks is provided for analysis of handover initiation probability, which is based on multi-beam base-station antenna splitting in the elevation-radiating plane. The sum of the received signal power in the mobile station, including both desired and interference signal power, has been introduced into the handover initiation algorithm. Along with the idea, we present three models of handover initiation algorithm with the shadowing process of Gaussian distribution. The formulation of handover initiation probability of those algorithms is also analyzed. The validity of the presented models has been checked through the comparison with simulation results. The results present the performance characteristics of handover initiation vary with cluster number and base-station antenna elevation angle.展开更多
Connexins and pannexins are two protein families that play an important role in cellular communication. Pannexin 1 (PANX1), one of the members of pannexin family, is a channel protein. It is glycosylated and forms thr...Connexins and pannexins are two protein families that play an important role in cellular communication. Pannexin 1 (PANX1), one of the members of pannexin family, is a channel protein. It is glycosylated and forms three species, GLY0, GLY1, and GLY2. Here, we describe four independent families in which mutations in PANX1 cause familial or sporadic female infertility via a phenotype that we term “oocyte death.” The mutations, which are associated with oocyte death, alter the PANX1 glycosylation pattern, influence the subcellular localization of PANX1 in cultured cells, and result in aberrant PANX1 channel activity, ATP release in oocytes, and mutant PANX1 GLY1. Overexpression of a patient-derived mutation in mice causes infertility, recapitulating the human oocyte death phenotype. Our findings demonstrate the critical role of PANX1 in human oocyte development, provide a genetic explanation for a subtype of infertility, and suggest a potential target for therapeutic intervention for this disease.展开更多
文摘A new multi-cell cellular configuration networks is provided for analysis of handover initiation probability, which is based on multi-beam base-station antenna splitting in the elevation-radiating plane. The sum of the received signal power in the mobile station, including both desired and interference signal power, has been introduced into the handover initiation algorithm. Along with the idea, we present three models of handover initiation algorithm with the shadowing process of Gaussian distribution. The formulation of handover initiation probability of those algorithms is also analyzed. The validity of the presented models has been checked through the comparison with simulation results. The results present the performance characteristics of handover initiation vary with cluster number and base-station antenna elevation angle.
文摘Connexins and pannexins are two protein families that play an important role in cellular communication. Pannexin 1 (PANX1), one of the members of pannexin family, is a channel protein. It is glycosylated and forms three species, GLY0, GLY1, and GLY2. Here, we describe four independent families in which mutations in PANX1 cause familial or sporadic female infertility via a phenotype that we term “oocyte death.” The mutations, which are associated with oocyte death, alter the PANX1 glycosylation pattern, influence the subcellular localization of PANX1 in cultured cells, and result in aberrant PANX1 channel activity, ATP release in oocytes, and mutant PANX1 GLY1. Overexpression of a patient-derived mutation in mice causes infertility, recapitulating the human oocyte death phenotype. Our findings demonstrate the critical role of PANX1 in human oocyte development, provide a genetic explanation for a subtype of infertility, and suggest a potential target for therapeutic intervention for this disease.
