921 research outputs found

    Bumpy Fruit of Papaya as Related to Boron Deficiency

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    Externally deformed papaya fruits with "bumpy" skin surfaces have been present in the papaya industry for many years. A relationship between bumpy fruit and boron deficiency has been established in other studies. Studies relating to boron have not been reported under the "rocky" Hawaiian soil conditions. Since studies on boron nutrition under Hawaiian soil conditions have not been reported, this study has two objectives. The first is to determine if there are differences in boron tissue levels between affected and unaffected trees under field conditions. The second is to determine the application rate of boron at which the milky exudate can be eliminated

    Use of Potassium Nitrate on Mango Flowering

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    Review of the authors' experiments in Hawaii suggested that potassium nitrate did not induce flowering but probably stimulated growth of terminal buds, and flowering was determined by the condition of those buds or the environmental conditions at the time. Genotypic differences in response to the treatment were noted

    Optimizing Germination of Papaya Seeds

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    Field germination of papaya seeds can be greatly improved by soaking them before planting in an aqueous solution of potassium nitrate (KNO3). Germination percentage of both fresh and dried seeds can be increased with this method. The time to germination after the soaking treatment is reduced, and maximum germination is achieved sooner than when untreated seeds are planted

    Magneto-Optical Studies of Exciton Effects in Layer-Type Semiconductors

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    Both experimental and theoretical works were performed with particular reference to a layer-type semiconductor, GaSe, for a coherent treatment of the exciton-like and the oscillatory Landau-like spectra appearing in a form of their combination in semiconductors in magnetic fields. The interband magneto-absorption and the Faraday rotation were measured in pulsed magnetic fields up to ~200 kOe at low temperatures. The theoretical analysis was based mainly on the exact solution for an extremely anisotropic semiconductor in the magnetic field of arbitrary intensity. The exciton effects are discussed in terms of the energy spectrum, the spectral intensity, and the spectral width by the use of the band parameters deduced from the experimental results

    Novel method to rescue a lethal phenotype through integration of target gene onto the X-chromosome.

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    The loss-of-function mutations of serine protease inhibitor, Kazal type 1 (SPINK1) gene are associated with human chronic pancreatitis, but the underlying mechanisms remain unknown. We previously reported that mice lacking Spink3, the murine homologue of human SPINK1, die perinatally due to massive pancreatic acinar cell death, precluding investigation of the effects of SPINK1 deficiency. To circumvent perinatal lethality, we have developed a novel method to integrate human SPINK1 gene on the X chromosome using Cre-loxP technology and thus generated transgenic mice termed "X-SPINK1". Consistent with the fact that one of the two X chromosomes is randomly inactivated, X-SPINK1 mice exhibit mosaic pattern of SPINK1 expression. Crossing of X-SPINK1 mice with Spink3+/- mice rescued perinatal lethality, but the resulting Spink3-/-;XXSPINK1 mice developed spontaneous pancreatitis characterized by chronic inflammation and fibrosis. The results show that mice lacking a gene essential for cell survival can be rescued by expressing this gene on the X chromosome. The Spink3-/-;XXSPINK1 mice, in which this method has been applied to partially restore SPINK1 function, present a novel genetic model of chronic pancreatitis

    Quasiparticles and Energy Scaling in Bi2_2Sr2_2Can1_{n-1}Cun_nO2n+4_{2n+4} (n\it{n}=1-3): Angle-Resolved Photoemission Spectroscopy

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    Angle-resolved photoemission spectroscopy (ARPES) has been performed on the single- to triple-layered Bi-family high-{\it Tc_c} superconductors (Bi2_2Sr2_2Can1_{n-1}Cun_nO2n+4_{2n+4}, n\it{n}=1-3). We found a sharp quasiparticle peak as well as a pseudogap at the Fermi level in the triple-layered compound. Comparison among three compounds has revealed a universal rule that the characteristic energies of superconducting and pseudogap behaviors are scaled with the maximum {\it Tc_c}.Comment: 4 pages, 4 figure

    Deficiency in Lyst function leads to accumulation of secreted proteases and reduced retinal adhesion.

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    Chediak-Higashi syndrome, caused by mutations in the Lysosome Trafficking Regulator (Lyst) gene, is a recessive hypopigmentation disorder characterized by albinism, neuropathies, neurodegeneration, and defective immune responses, with enlargement of lysosomes and lysosome-related organelles. Although recent studies have suggested that Lyst mutations impair the regulation of sizes of lysosome and lysosome-related organelle, the underlying pathogenic mechanism of Chediak-Higashi syndrome is still unclear. Here we show striking evidence that deficiency in LYST protein function leads to accumulation of photoreceptor outer segment phagosomes in retinal pigment epithelial cells, and reduces adhesion between photoreceptor outer segment and retinal pigment epithelial cells in a mouse model of Chediak-Higashi syndrome. In addition, we observe elevated levels of cathepsins, matrix metallopeptidase (MMP) 3 and oxidative stress markers in the retinal pigment epithelium of Lyst mutants. Previous reports showed that impaired degradation of photoreceptor outer segment phagosomes causes elevated oxidative stress, which could consequently lead to increases of cysteine cathepsins and MMPs in the extracellular matrix. Taken together, we conclude that the loss of LYST function causes accumulation of phagosomes in the retinal pigment epithelium and elevation of several extracellular matrix-remodeling proteases through oxidative stress, which may, in turn, reduce retinal adhesion. Our work reveals previously unreported pathogenic events in the retinal pigment epithelium caused by Lyst deficiency. The same pathogenic events may be conserved in other professional phagocytic cells, such as macrophages in the immune system, contributing to overall Chediak-Higashi syndrome pathology
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