Changes in ocular flow induced by hypo- and hypercapnia relate to static visual acuity in humans

We investigated whether the change in ocular blood flow, induced by hypo- and hypercapnia, is related to static visual acuity. Eleven healthy subjects (26±5 years) underwent three treatments. A three-treatment three-period crossover design was used. In the hypocapnia treatment (HYPO), the subjects controlled their minute ventilation (VE) to a target of 25 L/min for 6 min. In the hypercapnia treatment (HYPER), the subjects inspired high-fraction CO2 gas (FICO2 = 4%) for 6 min. In the control treatment (CON), VE was not manipulated. We measured choroidal and retinal blood flow by laser speckle flowmetry as ocular blood flow, and static visual acuity using the Landolt C chart. End-tidal partial pressure of CO2 differed significantly among HYPO, HYPER and CON (21±1, 48±1, and 42±1 mmHg, respectively). Retinal blood flow decreased significantly from the baseline in HYPO (-22±5%), but increased significantly in HYPER (+3±9%) compared to CON. Decimal visual acuity was significantly lower in HYPO than in the CON (0.21±0.1 vs. 0.24±0.1 P<0.05). These results suggest that changes in ocular blood flow induced by changes in arterial CO2 partial pressure influences visual acuity

Cell cycle and chromatin control by nuclear small G protein Ran

Division of Molecular Patholog

染色体末端部位複製過程の機構

金沢大学がん研究所染色体末端部にあるテロメア構造は、3\u27端側の鎖(G-rich鎖)がグアニンとチミンに富んだ繰り返し配列になっており、シトシンとアデニンに富んだ5\u27端側の鎖(C-rich鎖)よりも長く突出している。この領域の複製は特殊な過程を経て行われており、いったんC-rich鎖がnucleaseによって消化され、G-rich鎖が単鎖化する。出芽酵母Saccharomyces cerevisiaeにおいて、この単鎖化したG-rich鎖に結合し、テロメラーゼによる伸長反応とDNA polymeraseによるFill-in反応を制御しているのが、CDC13遺伝子にコードされているタンパク質である。Cdc13タンパク質の機能を解析するために、CDC13と相互作用する因子を2-hybrid法で同定し、そこから分離されたSTM1との相互作用を検討した。タンパクレベルでの直接の相互作用を検討するした。Cdc13のN端側またはC端側をGST(glutathione S-transferase)と融合したタンパク質を大腸菌内で発現させ、glutathione Sepharose beads上に固定し、ウサギreticulocyte抽出液で試験管内で生産したStm1がCdc13のN端側を固定したbeadsと共沈することがわかった。STM1遺伝子を多コピーベクターによって多量に供給することで、CDC13遺伝子の温度感受性変異株cdc13-1の異常伸長したテロメアが正常長に戻り、増殖能も回復する。このことは、遺伝学的機能においても相互作用があることを示している。このSTM1による多コピーサプレッションは、pol1-17やstn1-13の様な他のテロメア異常伸長変異には観察されず、特異的な関係があることが示唆された。研究課題/領域番号:12215051, 研究期間(年度):2000出典：研究課題「染色体末端部位複製過程の機構」課題番号12215051（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-12215051/）を加工して作

Gata6 Promotes GLI3 Repressor Activities in the Limb

Gli3 is a major regulator of Hedgehog signaling during limb development. In the anterior mesenchyme, GLI3 is proteolytically processed into GLI3R, a truncated repressor form that inhibits Hedgehog signaling. Although numerous studies have identified mechanisms that regulate Gli3 function in vitro, it is not completely understood how Gli3 function is regulated in vivo. In this study, we show a novel mechanism of regulation of GLI3R activities in limb buds by Gata6, a member of the GATA transcription factor family. We show that conditional inactivation of Gata6 prior to limb outgrowth by the Tcre deleter causes preaxial polydactyly, the formation of an anterior extra digit, in hindlimbs. A recent study suggested that Gata6 represses Shh transcription in hindlimb buds. However, we found that ectopic Hedgehog signaling precedes ectopic Shh expression. In conjunction, we observed Gata6 and Gli3 genetically interact, and compound heterozygous mutants develop preaxial polydactyly without ectopic Shh expression, indicating an additional prior mechanism to prevent polydactyly. These results support the idea that Gata6 possesses dual roles during limb development: enhancement of Gli3 repressor function to repress Hedgehog signaling in the anterior limb bud, and negative regulation of Shh expression. Our in vitro and in vivo studies identified that GATA6 physically interacts with GLI3R to facilitate nuclear localization of GLI3R and repressor activities of GLI3R. Both the genetic and biochemical data elucidates a novel mechanism by Gata6 to regulate GLI3R activities in the anterior limb progenitor cells to prevent polydactyly and attain proper development of the mammalian autopod

Breaking pairing-based cryptosystems using ηT\eta_T pairing over GF(397)GF(3^{97})

There are many useful cryptographic schemes, such as ID-based encryption, short signature, keyword searchable encryption, attribute-based encryption, functional encryption, that use a bilinear pairing. It is important to estimate the security of such pairing-based cryptosystems in cryptography. The most essential number-theoretic problem in pairing-based cryptosystems is the discrete logarithm problem (DLP) because pairing-based cryptosystems are no longer secure once the underlining DLP is broken. One efficient bilinear pairing is the $\eta_T$ pairing defined over a supersingular elliptic curve $E$ on the finite field $GF(3^n)$ for a positive integer $n$. The embedding degree of the $\eta_T$ pairing is $6$; thus, we can reduce the DLP over $E$ on $GF(3^n)$ to that over the finite field $GF(3^{6n})$. In this paper, for breaking the $\eta_T$ pairing over $GF(3^n)$, we discuss solving the DLP over $GF(3^{6n})$ by using the function field sieve (FFS), which is the asymptotically fastest algorithm for solving a DLP over finite fields of small characteristics. We chose the extension degree $n=97$ because it has been intensively used in benchmarking tests for the implementation of the $\eta_T$ pairing, and the order (923-bit) of $GF(3^{6\cdot 97})$ is substantially larger than the previous world record (676-bit) of solving the DLP by using the FFS. We implemented the FFS for the medium prime case (JL06-FFS), and propose several improvements of the FFS, for example, the lattice sieve for JL06-FFS and the filtering adjusted to the Galois action. Finally, we succeeded in solving the DLP over $GF(3^{6\cdot 97})$. The entire computational time of our improved FFS requires about 148.2 days using 252 CPU cores. Our computational results contribute to the secure use of pairing-based cryptosystems with the $\eta_T$ pairing