State (hydrodynamics) Identification In The Lower St. Johns River Using The Ensemble Kalman Filter

This thesis presents a method, Ensemble Kalman Filter (EnKF), applied to a highresolution, shallow water equations model (DG ADCIRC-2DDI) of the Lower St. Johns River with observation data at four gauging stations. EnKF, a sequential data assimilation method for non-linear problems, is developed for tidal flow simulation for estimation of state variables, i.e., water levels and depth-integrated currents for overland unstructured finite element meshes. The shallow water equations model is combined with observation data, which provides the basis of the EnKF applications. In this thesis, EnKF is incorporated into DG ADCIRC-2DDI code to estimate the state variables. Upon its development, DG ADCIRC-2DDI with EnKF is first validated by implementing to a low-resolution, shallow water equations model of a quarter annular harbor with synthetic observation data at six gauging stations. Second, DG ADCIRC-2DDI with EnKF is implemented to a high-resolution, shallow water equations model of the Lower St. Johns River with real observation data at four gauging stations. Third, four different experiments are performed by applying DG ADCIRC-2DDI with EnKF to the Lower St. Johns River

FGF-10 Stimulates Limb Regeneration Ability in Xenopus laevis

AbstractBy reciprocal transplantation experiments with regenerative and nonregenerative Xenopus limbs, we recently demonstrated that the regenerative capacity of a Xenopus limb depends on mesenchymal tissue and we suggested that fgf-10 is likely to be involved in this capacity (Yokoyama et al., 2000, Dev. Biol. 219, 18–29). However, the data obtained in that study are not conclusive evidence that FGF-10 is responsible for the regenerative capacity. We therefore investigated the role of FGF-10 in regenerative capacity by directly introducing FGF-10 protein into nonregenerative Xenopus limb stumps. Exogenously applied FGF-10 successfully stimulated the regenerative capacity, resulting in the reinduction of all gene expressions (including shh, msx-1, and fgf-10) that we examined and the regeneration of well-patterned limb structures. We report here for the first time that a certain molecule activates the regenerative capacity of Xenopus limb, and this finding suggests that FGF-10 could be a key molecule in possible regeneration of nonregenerative limbs in higher vertebrates

ハンドウタイソウチセイゾウヨウノデンシサイクロトロンキョウメイヲモチイタエッチングショリシツニオケルマイクロハデンパントキンイツプラズマセイセイニカンスルケンキュウ

博士（工学）東京農工大

Multiple Digit Formation inXenopusLimb Bud Recombinants

AbstractWe prepared recombinant limb buds ofXenopustadpoles by grafting a mesenchyme mass of the hindlimb bud. TheXenopusrecombinant limb buds with dissociated and reaggregated mesenchyme developed more than 30 digits with cartilage segmentation, while those with undissociated mesenchyme developed a limb with normal cartilage pattern. Before the formation of multiple digits, a patchy expression pattern offgf-8,an AER marker, was observed in the distal region of recombinant limb buds.shh,a ZPA (zone of polarizing activity) marker, was expressed broadly in the distal region of recombinants. Recombinant limb buds with the reaggregated mesenchyme of anterior halves formed anterior digits with claws, and those with the mesenchyme of posterior halves formed posterior digits without claws. The temporal and spatial changes in the potency of multiple digit formation are discussed with reference to the regenerative capacity ofXenopuslimb buds

Glial Cell Lineage Expression of Mutant Ataxin-1 and Huntingtin Induces Developmental and Late-Onset Neuronal Pathologies in Drosophila Models

In several neurodegenerative disorders, toxic effects of glial cells on neurons are implicated. However the generality of the non-cell autonomous pathologies derived from glial cells has not been established, and the specificity among different neurodegenerative disorders remains unknown.We newly generated Drosophila models expressing human mutant huntingtin (hHtt103Q) or ataxin-1 (hAtx1-82Q) in the glial cell lineage at different stages of differentiation, and analyzed their morphological and behavioral phenotypes. To express hHtt103Q and hAtx1-82Q, we used 2 different Gal4 drivers, gcm-Gal4 and repo-Gal4. Gcm-Gal4 is known to be a neuroglioblast/glioblast-specific driver whose effect is limited to development. Repo-Gal4 is known to be a pan-glial driver and the expression starts at glioblasts and continues after terminal differentiation. Gcm-Gal4-induced hHtt103Q was more toxic than repo-Gal4-induced hHtt103Q from the aspects of development, locomotive activity and survival of flies. When hAtx1-82Q was expressed by gcm- or repo-Gal4 driver, no fly became adult. Interestingly, the head and brain sizes were markedly reduced in a part of pupae expressing hAtx1-82Q under the control of gcm-Gal4, and these pupae showed extreme destruction of the brain structure. The other pupae expressing hAtx1-82Q also showed brain shrinkage and abnormal connections of neurons. These results suggested that expression of polyQ proteins in neuroglioblasts provided a remarkable effect on the developmental and adult brains, and that glial cell lineage expression of hAtx1-82Q was more toxic than that of hHtt103Q in our assays.All these studies suggested that the non-cell autonomous effect of glial cells might be a common pathology shared by multiple neurodegenerative disorders. In addition, the fly models would be available for analyzing molecular pathologies and developing novel therapeutics against the non-cell autonomous polyQ pathology. In conclusion, our novel fly models have extended the non-cell autonomous pathology hypothesis as well as the developmental effect hypothesis to multiple polyQ diseases. The two pathologies might be generally shared in neurodegeneration

Characterization of L-Arginine Oxidase Made from L-Glutamate Oxidase

　L‒Glutamate oxidase (LGOX) from Streptomyces sp. X‒119‒6 has strict substrate specificity toward L‒glutamate. Recently, we solved the X‒ray crystal structure of LGOX and this revealed that Arg305 in the active site is the key residue involved in substrate recognition. Therefore, we created 19 mutant enzymes of R305X‒LGOX by saturation mutagenesis. One of them R305D‒LGOX, Arg305 substituted with Asp exhibited oxidase activity for L‒Arg. Optimum pH of R305D‒LGOX mutant enzyme was pH 8.5. Interestingly, the activity of R305D‒LGOX toward L‒Arg was inhibited by phosphate. And furthermore, the substrate specificity of R305D‒LGOX was affected by using buffer. The results of inhibition analysis suggest, that phosphate is a competitive inhibitor of R305D‒LGOX when L‒Arg is used as substrate. Kinetic analysis of R305D‒LGOX showed that Km value and kcat value of R305D‒LGOX toward l-Arg were 0.68 mM and 6.7 s-1 respectively. In this study, we showed that R305D‒LGOX mutant enzyme is a novel l-arginine oxidase and useful for l-arginine biosensor

White Patchy Materials Formed in a Scoriacious Road-cut Profile on Miyake Island(Plant Production Science Soil Science)

Sulfurous gas, sulfur or sulfates are frequently contained in volcanic ejecta. We found white patchy materials (WPM) in a road-cut profile on Miyake Island, Japan. The layer containing WPM consists of scoria deposit in 1874. The major materials we identified in the WPM were CaSO_4・2H_2O and amorphous silica according to X-ray diffraction and energy dispersive X-ray analyses. A possible process for crystallization of CaSO_4・2H_2O in the WPM is the dissolution of CaSO_4・2H_2O contained in the overlying 2000 ash and its re-precipitation on the surface of the scoriacious road-cut profile. Emission of sulfur dioxide gas, converted to sulfuric acid in water, has been so abundant since the 2000 eruption that we further examined reaction products between crushed scoria and dilute H_2SO_4 (0.1-2.5mol L^). CaSO_4・2H_2O was also identified in the reaction products as well as alunogen, iron sulfate, etc. Because alunogen is highly soluble in water, CaSO_4・2H_2O was the major crystalline product after rinsing with water

Luteal blood flow in patients undergoing GnRH agonist long protocol

<p>Abstract</p> <p>Background</p> <p>Blood flow in the corpus luteum (CL) is closely related to luteal function. It is unclear how luteal blood flow is regulated. Standardized ovarian-stimulation protocol with a gonadotropin-releasing hormone agonist (GnRHa long protocol) causes luteal phase defect because it drastically suppresses serum LH levels. Examining luteal blood flow in the patient undergoing GnRHa long protocol may be useful to know whether luteal blood flow is regulated by LH.</p> <p>Methods</p> <p>Twenty-four infertile women undergoing GnRHa long protocol were divided into 3 groups dependent on luteal supports; 9 women were given ethinylestradiol plus norgestrel (Planovar) orally throughout the luteal phase (control group); 8 women were given HCG 2,000 IU on days 2 and 4 day after ovulation induction in addition to Planovar (HCG group); 7 women were given vitamin E (600 mg/day) orally throughout the luteal phase in addition to Planovar (vitamin E group). Blood flow impedance was measured in each CL during the mid-luteal phase by transvaginal color-pulsed-Doppler-ultrasonography and was expressed as a CL-resistance index (CL-RI).</p> <p>Results</p> <p>Serum LH levels were remarkably suppressed in all the groups. CL-RI in the control group was more than the cutoff value (0.51), and only 2 out of 9 women had CL-RI values < 0.51. Treatments with HCG or vitamin E significantly improved the CL-RI to less than 0.51. Seven of the 8 women in the HCG group and all of the women in the vitamin E group had CL-RI < 0.51.</p> <p>Conclusion</p> <p>Patients undergoing GnRHa long protocol had high luteal blood flow impedance with very low serum LH levels. HCG administration improved luteal blood flow impedance. This suggests that luteal blood flow is regulated by LH.</p