189 research outputs found
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 CsCuBr
The field induced magnetic phase transitions of CsCuBr were
investigated by means of magnetization process and neutron scattering
experiments. This system undergoes magnetic phase transition at Ne\'{e}l
temperature K at zero field, and exhibits the magnetization
plateau at approximately one third of the saturation magnetization for the
field directions and . 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 at
zero field. With increasing magnetic field parallel to the c-axis, the ordering
vector increases continuously and is locked at
in the plateau field range . 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
Spatial transcriptomics combined with single-cell RNA-sequencing unravels the complex inflammatory cell network in atopic dermatitis
BackgroundAtopic dermatitis (AD) is the most common chronic inflammatory skin disease with complex pathogenesis for which the cellular and molecular crosstalk in AD skin has not been fully understood.MethodsSkin tissues examined for spatial gene expression were derived from the upper arm of 6 healthy control (HC) donors and 7 AD patients (lesion and nonlesion). We performed spatial transcriptomics sequencing to characterize the cellular infiltrate in lesional skin. For single‐cell analysis, we analyzed the single‐cell data from suction blister material from AD lesions and HC skin at the antecubital fossa skin (4 ADs and 5 HCs) and full‐thickness skin biopsies (4 ADs and 2 HCs). The multiple proximity extension assays were performed in the serum samples from 36 AD patients and 28 HCs.ResultsThe single‐cell analysis identified unique clusters of fibroblasts, dendritic cells, and macrophages in the lesional AD skin. Spatial transcriptomics analysis showed the upregulation of COL6A5, COL4A1, TNC, and CCL19 in COL18A1‐expressing fibroblasts in the leukocyte‐infiltrated areas in AD skin. CCR7‐expressing dendritic cells (DCs) showed a similar distribution in the lesions. Additionally, M2 macrophages expressed CCL13 and CCL18 in this area. Ligand–receptor interaction analysis of the spatial transcriptome identified neighboring infiltration and interaction between activated COL18A1‐expressing fibroblasts, CCL13‐ and CCL18‐expressing M2 macrophages, CCR7‐ and LAMP3‐expressing DCs, and T cells. As observed in skin lesions, serum levels of TNC and CCL18 were significantly elevated in AD, and correlated with clinical disease severity.ConclusionIn this study, we show the unknown cellular crosstalk in leukocyte‐infiltrated area in lesional skin. Our findings provide a comprehensive in‐depth knowledge of the nature of AD skin lesions to guide the development of better treatments
Household laundry detergents disrupt barrier integrity and induce inflammation in mouse and human skin
BackgroundEpithelial barrier impairment is associated with many skin and mucosal inflammatory disorders. Laundry detergents have been demonstrated to affect epithelial barrier function in vitro using air–liquid interface cultures of human epithelial cells.MethodsBack skin of C57BL/6 mice was treated with two household laundry detergents at several dilutions. Barrier function was assessed by electric impedance spectroscopy (EIS) and transepidermal water loss (TEWL) measurements after the 4 h of treatments with detergents. RNA sequencing (RNA‐seq) and targeted multiplex proteomics analyses in skin biopsy samples were performed. The 6‐h treatment effect of laundry detergent and sodium dodecyl sulfate (SDS) was investigated on ex vivo human skin.ResultsDetergent‐treated skin showed a significant EIS reduction and TEWL increase compared to untreated skin, with a relatively higher sensitivity and dose–response in EIS. The RNA‐seq showed the reduction of the expression of several genes essential for skin barrier integrity, such as tight junctions and adherens junction proteins. In contrast, keratinization, lipid metabolic processes, and epidermal cell differentiation were upregulated. Proteomics analysis showed that the detergents treatment generally downregulated cell adhesion‐related proteins, such as epithelial cell adhesion molecule and contactin‐1, and upregulated proinflammatory proteins, such as interleukin 6 and interleukin 1 beta. Both detergent and SDS led to a significant decrease in EIS values in the ex vivo human skin model.ConclusionThe present study demonstrated that laundry detergents and its main component, SDS impaired the epidermal barrier in vivo and ex vivo human skin. Daily detergent exposure may cause skin barrier disruption and may contribute to the development of atopic diseases
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
No major tumorigenic role for β-catenin in serrated as opposed to conventional colorectal adenomas
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