RELATIONSHIP BETWEEN UREA DECOMPOSITION AND CELL CLASSES OF RESERVOIR PHYTOPLANKTON IN THE NORTH HAN RIVER SYSTEM

The influence of natural phytoplankton cell classes upon the response of urea decomposition was investigated in four reservoirs in the North Han River System. The decomposition rate of urea was 0.3 to 29.4 μ mol urea・m⁻³・hr.⁻¹ in the light and 0.2 to 14.9 μ mol urea・m⁻³・hr.⁻¹ in the dark. Much higher decomposition rates were observed at the eutrophic stations in Lake Euiam. The urea decomposition in the smaller fraction (25 μm). No differences in the ratios of urea decomposition to chlorophyll-a or photosynthesis among three fractions were observed. This might be mainly due to the difference in the standing crop of phytoplankton. These trends were no different between sampling areas and reservoirs. The greater part of urea decomposition was the phase of CO₂ liberation rate into the water. Eight to 50% of the urea decomposition was incorporated into the particulate phase in the light, but this was much lower in the dark. The results of the present study indicate that urea in reservoirs decomposes by phytoplankton rather than bacteria and the phytoplankton would be competitive to bacteria.Article信州大学理学部付属諏訪臨湖実験所報告 7: 31-40(1991)departmental bulletin pape

A possible role for Ca2+/calmodulin-dependent protein kinase IV during pancreatic acinar stimulus–secretion coupling

AbstractCa2+/calmodulin-dependent protein kinases (CaMKs) are important intracellular mediators in the mediation of stimulus–secretion coupling and excitation–contraction coupling in a wide variety of cell types. We attempted to identify and characterize the functional roles of CaMK in mediating pancreatic enzyme secretion. Immunoprecipitation and immunoblotting studies using a CaMKII or CaMKIV antibody showed that rat pancreatic acini expressed both CaMKII and CaMKIV. Phosphotransferase activities of CaMKs were measured by a radioenzyme assay (REA) using autocamtide II, peptide γ and myosin P-light chain as substrates. Although CaMKII and CaMKIV use autocamtide II as a substrate, peptide γ is more efficiently phosphorylated by CaMKIV than by CaMKII. Intact acini were stimulated with cholecystokinin (CCK)-8, carbachol (CCh) and the high-affinity CCK-A receptor agonist, CCK-OPE, and the cell lysates were used for REA. CCK-8, CCh and CCK-OPE caused a concentration-dependent increase in CaMKs activities. When autocamtide II was used, maximal increases were 1.5–1.8-fold over basal (20.2±2.0 pmol/min/mg protein), with peaks occurring at 20 min after cell stimulation. In separate studies that used peptide γ, CCK-8, CCh and CCK-OPE dose-dependently increased CaMKIV activities. Maximal increases were 1.5–2.4-fold over basal (30.7±3.2 pmol/min/mg protein) with peaks occurring at 20 min after cell stimulation. Peak increases after cell stimulation induced by peptide γ were 1.8–2.8-fold higher than those induced by autocamtide II. CCK-8, CCh and CCK-OPE also significantly increased phosphotransferase activities of myosin light chain kinase (MLCK) substrate (basal: 4.4±0.7 pmol/min/mg protein). However, maximal increases induced by MLCK substrate were less than 10% of those occurring in peptide γ. Characteristics of the phosphotransferase activity were also different between autocamtide II and peptide γ. When autocamtide II was used, elimination of medium Ca2+ in either cell lysates or intact cells resulted in a significant decrease in the activity, whereas it had no or little effect when peptide γ was used. This suggests that Ca2+ influx from the extracellular space is not fully required for CaMKIV activity and Ca2+ is not a prerequisite for phosphotransferase activity once CaMKIV is activated by either intracellular Ca2+ release or intracellular Ca2+ oscillations. The specific CaMKII inhibitor KN-62 (50 μM) had no effect on the CaMKIV activity and pancreatic enzyme secretion elicited by CCK-8, CCh and CCK-OPE. The specific MLCK inhibitor, ML-9 (10 μM), also did not inhibit CCK-8-stimulated pancreatic amylase secretion. In contrast, wide spectrum CaMK inhibitors, K-252a (1 μM) and KT5926 (3 μM), significantly inhibited CaMKIV activities and enzyme secretion evoked by secretagogues. Thus, CaMKIV appears to be an important intracellular mediator during stimulus–secretion coupling of rat pancreatic acinar cells

Magnetization plateaux of S = 1/2 two-dimensional frustrated antiferromagnet Cs2_2CuBr4_4

The field induced magnetic phase transitions of Cs$_2$CuBr$_4$ were investigated by means of magnetization process and neutron scattering experiments. This system undergoes magnetic phase transition at Ne\'{e}l temperature $T_\mathrm{N}=1.4$ K at zero field, and exhibits the magnetization plateau at approximately one third of the saturation magnetization for the field directions $H\parallel b$ and $H\parallel c$. In the present study, additional symptom of the two-third magnetization plateau was found in the field derivative of the magnetization process. The magnetic structure was found to be incommensurate with the ordering vector $\boldsymbol{Q}=(0, 0.575, 0)$ at zero field. With increasing magnetic field parallel to the c-axis, the ordering vector increases continuously and is locked at $\boldsymbol{Q}=(0, 0.662, 0)$ in the plateau field range $13.1 \mathrm{T} < H < 14.4 \mathrm{T}$. This indicates that the collinear \textit{up-up-down} spin structure is stabilized by quantum fluctuation at the magnetization plateau.Comment: 6 pages, 4 Postscript figures, uses iopams.sty and IOPART.CL

Quadrupolar Kondo Effect in Non-Kramers Doublet System PrInAg2

We performed ultrasonic measurement on the rare-earth intermetallic compound PrInAg_2 to examine the quadrupolar Kondo effect associated with the non-Kramers Gamma_3 doublet ground state. The characteristic softening of the elastic constant (c_{11}-c_{12})/2 below 10 K in PrInAg_2 is attributed to a Curie term in quadrupolar susceptibility for the quadrupole O_2^2=J_x^2-J_y^2 of the stable Gamma_3 ground state. (c_{11}-c_{12})/2 turns to a slight increase with the -lnT dependence below 0.1 K, which suggests the quenching of the quadrupolar moment in the quadrupolar Kondo state. Under applied magnetic fields of 10 T and 15 T above 8.7 T corresponding to the Kondo temperature T_K of ~ 0.86 K, the behavior of (c_{11}-c_{12})/2 is described in terms of quadrupolar susceptibility for the stable 4f^2 state.Comment: PDF, 10pages + 5figures, Strongly Correlated Electron

Epithelial barrier hypothesis and the development of allergic and autoimmune diseases

The “epithelial barrier hypothesis” proposes that genetic predisposition to epithelial barrier damage, exposure to various epithelial barrier–damaging agents and chronic periepithelial inflammation are responsible for the development of allergic and autoimmune diseases. Particularly, the introduction of more than 200,000 new chemicals to our daily lives since the 1960s has played a major role in the pandemic increase of these diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defence against external factors. A leaky epithelial barrier initiates the translocation of the microbiome from the surface of affected tissues to interepithelial and even deeper subepithelial areas. In tissues with a defective epithelial barrier, colonization of opportunistic pathogens, decreased microbiota biodiversity, local inflammation, and impaired regeneration and remodelling takes place. A dysregulated immune response against commensals and opportunistic pathogens starts. Migration of inflammatory cells to other tissues and their contribution to tissue injury and inflammation in the affected tissues are key events in the development and exacerbation of many chronic inflammatory diseases. Understanding the underlying factors that affect the integrity of epithelial barriers is essential to find preventive measures or effective treatments to restore its function. The aim of this review is to assess the origins of allergic and autoimmune diseases within the framework of the epithelial barrier hypothesis

β-catenin is a molecular switch that regulates transition of cell-cell adhesion to fusion

When a sperm and an oocyte unite upon fertilization, their cell membranes adhere and fuse, but little is known about the factors regulating sperm-oocyte adhesion. Here we explored the role of β-catenin in sperm-oocyte adhesion. Biochemical analysis revealed that E-cadherin and β-catenin formed a complex in oocytes and also in sperm. Sperm-oocyte adhesion was impaired when β-catenin-deficient oocytes were inseminated with sperm. Furthermore, expression of β-catenin decreased from the sperm head and the site of an oocyte to which a sperm adheres after completion of sperm-oocyte adhesion. UBE1-41, an inhibitor of ubiquitin-activating enzyme 1, inhibited the degradation of β-catenin, and reduced the fusing ability of wild-type (but not β-catenin-deficient) oocytes. These results indicate that β-catenin is not only involved in membrane adhesion, but also in the transition to membrane fusion upon fertilization

Genome-Wide Association Study of Circulating Estradiol, Testosterone, and Sex Hormone-Binding Globulin in Postmenopausal Women

Genome-wide association studies (GWAS) have successfully identified common genetic variants that contribute to breast cancer risk. Discovering additional variants has become difficult, as power to detect variants of weaker effect with present sample sizes is limited. An alternative approach is to look for variants associated with quantitative traits that in turn affect disease risk. As exposure to high circulating estradiol and testosterone, and low sex hormone-binding globulin (SHBG) levels is implicated in breast cancer etiology, we conducted GWAS analyses of plasma estradiol, testosterone, and SHBG to identify new susceptibility alleles. Cancer Genetic Markers of Susceptibility (CGEMS) data from the Nurses’ Health Study (NHS), and Sisters in Breast Cancer Screening data were used to carry out primary meta-analyses among ∼1600 postmenopausal women who were not taking postmenopausal hormones at blood draw. We observed a genome-wide significant association between SHBG levels and rs727428 (joint β = -0.126; joint P = 2.09×10–16), downstream of the SHBG gene. No genome-wide significant associations were observed with estradiol or testosterone levels. Among variants that were suggestively associated with estradiol (P<10–5), several were located at the CYP19A1 gene locus. Overall results were similar in secondary meta-analyses that included ∼900 NHS current postmenopausal hormone users. No variant associated with estradiol, testosterone, or SHBG at P<10–5 was associated with postmenopausal breast cancer risk among CGEMS participants. Our results suggest that the small magnitude of difference in hormone levels associated with common genetic variants is likely insufficient to detectably contribute to breast cancer risk