Modeling photometric variations due to a global inhomogeneity on an obliquely rotating star: application to lightcurves of white dwarfs

We develop a general framework to compute photometric variations induced by the oblique rotation of a star with an axisymmetric inhomogeneous surface. We apply the framework to compute lightcurves of white dwarfs adopting two simple models of their surface inhomogeneity. Depending on the surface model and the location of the observer, the resulting lightcurve exhibits a departure from a purely sinusoidal curve that are observed for a fraction of white dwarfs. As a specific example, we fit our model to the observed phase-folded lightcurve of a fast-spinning white dwarf ZTF J190132.9+145808.7 (with the rotation period of 419s). We find that the size and obliquity angle of the spot responsible for the photometric variation are \dts \approx 60^\circ and \thetaS \approx 60^\circ or $90^\circ$, respectively, implying an interesting constraint on the surface distribution of the magnetic field on white dwarfs.Comment: 25 pages, 9 figures, accepted for publication in PAS

Effects of glycosylation on swimming ability and flagellar polymorphic transformation in Pseudomonas syringae pv. tabaci 6605

The role of flagellin glycosylation on motility was investigated in Pseudomonas syringae pv. tabaci. The swimming activity of glycosylation-defective mutants was prominently decreased in a highly viscous medium. The mutants showed differences in polymorphic transitions and in the bundle formation of flagella, indicating that glycosylation stabilizes the filament structure and lubricates the rotation of the bundle.</p

Senescence-accelerated mice (SAMP1/TA-1) treated repeatedly with lipopolysaccharide develop a condition that resembles hemophagocytic lymphohistiocytosis

Hemophagocytic lymphohistiocytosis is a life-threatening systemic hyperinflammatory disorder with primary and secondary forms. Primary hemophagocytic lymphohistiocytosis is associated with inherited defects in various genes that affect the immunological cytolytic pathway. Secondary hemophagocytic lymphohistiocytosis is not inherited, but complicates various medical conditions including infections, autoinflammatory/autoimmune diseases, and malignancies. When senescence-accelerated mice (SAMP1/TA-1) with latent deterioration of immunological function and senescence-resistant control mice (SAMR1) were treated repeatedly with lipopolysaccharide, SAMP1/TA-1 mice displayed the clinicopathological features of hemophagocytic lymphohistiocytosis such as hepatosplenomegaly, pancytopenia, hypofibrinogenemia, hyperferritinemia, and hemophagocytosis. SAMR1 mice showed no features of hemophagocytic lymphohistiocytosis. Lipopolysaccharide induced upregulation of proinflammatory cytokines such as interleukin-1β, interleukin-6, tumor necrosis factor-α, and interferon-γ, and interferon-γ-inducible chemokines such as c-x-c motif chemokine ligands 9 and 10 in the liver and spleen in both SAMP1/TA-1 and SAMR1 mice. However, upregulation of proinflammatory cytokines and interferon-γ-inducible chemokines in the liver persisted for longer in SAMP1/TA-1 mice than in SAMR1 mice. In addition, the magnitude of upregulation of interferon-γ in the liver and spleen after lipopolysaccharide treatment was greater in SAMP1/TA-1 mice than in SAMR1 mice. Furthermore, lipopolysaccharide treatment led to a prolonged increase in the proportion of peritoneal M1 macrophages and simultaneously to a decrease in the proportion of M2 macrophages in SAMP1/TA-1 mice compared with SAMR1 mice. Lipopolysaccharide appeared to induce a hyperinflammatory reaction and prolonged inflammation in SAMP1/TA-1 mice, resulting in features of secondary hemophagocytic lymphohistiocytosis. Thus, SAMP1/TA-1 mice represent a useful mouse model to investigate the pathogenesis of bacterial infection-associated secondary hemophagocytic lymphohistiocytosis

Study of human Wharton’s duct structure and its relationship with salivary flow

Of all major salivary glands, the human submandibular gland secretes the largest amount of saliva. Along with the sublingual duct, the main duct (Wharton’s duct) is known to open into the sublingual caruncula; however, reports regarding this common opening structure are scarce and details unclear. The structure of Wharton’s duct opening is quite different from that of parotid duct (Stensen’s duct) opening in its overall size and diameter despite what is commonly noted in text books. About 85% of sialolith occurrences in humans is in the submandibular gland and duct, which causes local pain during swallowing in most cases. The details of Wharton’s duct’s inner structure is relatively unknown, and further investigation is necessary to understand its special characteristics and clinical applications. In this study, we observed the inner structure of the ducts’ common opening area by scanning electron microscopy and confirmed a large number of blood vessels present in the connective tissue layer just under the epithelium. In addition, we confirmed the presence of smooth muscle in the same area using smooth muscle actin antibody. These structural findings suggest that Wharton’s duct itself is likely responsible for the regulation of salivary flow

Calpain-dependent disruption of nucleo-cytoplasmic transport in ALS motor neurons

Nuclear dysfunction in motor neurons has been hypothesized to be a principal cause of amyotrophic lateral sclerosis (ALS) pathogenesis. Here, we investigated the mechanism by which the nuclear pore complex (NPC) is disrupted in dying motor neurons in a mechanistic ALS mouse model (adenosine deaminase acting on RNA 2 (ADAR2) conditional knockout (AR2) mice) and in ALS patients. We showed that nucleoporins (Nups) that constituted the NPC were cleaved by activated calpain via a Ca2+-permeable AMPA receptor-mediated mechanism in dying motor neurons lacking ADAR2 expression in AR2 mice. In these neurons, nucleo-cytoplasmic transport was disrupted, and the level of the transcript elongation enzyme RNA polymerase II phosphorylated at Ser2 was significantly decreased. Analogous changes were observed in motor neurons lacking ADAR2 immunoreactivity in sporadic ALS patients. Therefore, calpain-dependent NPC disruption may participate in ALS pathogenesis, and inhibiting Ca2+-mediated cell death signals may be a therapeutic strategy for ALS.UTokyo Research掲載「核と細胞質間の分子輸送経路の破綻が筋萎縮性側索硬化症に関与」 URI: http://www.u-tokyo.ac.jp/ja/utokyo-research/research-news/disruption-of-molecule-transport-pathway-between-nucleus-and-cytoplasm-involved-in-als.htmlUTokyo Research "Disruption of molecule transport pathway between nucleus and cytoplasm involved in ALS" URI: http://www.u-tokyo.ac.jp/en/utokyo-research/research-news/disruption-of-molecule-transport-pathway-between-nucleus-and-cytoplasm-involved-in-als.htm

Mechanical Properties and Histological Evaluation of Bone Grafting Materials Containing Different Ratios of Calcium Phosphate Cement and Porous β-tricalcium Phosphate Granules

Article信州医学雑誌 66(2): 139-150(2018)journal articl

Short-Term Effects of Acupuncture on Open-Angle Glaucoma in Retrobulbar Circulation: Additional Therapy to Standard Medication

Background. The relation between glaucoma and retrobulbar circulation in the prognosis has been indicated. Purpose. To investigate the effects of acupuncture on retrobulbar circulation in open-angle glaucoma (OAG) patients. Methods. Eleven OAG patients (20 eyes with OAG) who were treated by topical antiglaucoma medications for at least 3 months were enrolled. Acupuncture was performed once at acupoints BL2, M-HN9, ST2, ST36, SP6, KI3, LR3, GB20, BL18, and BL23 bilaterally. Retrobulbar circulation was measured with color Doppler imaging, and intraocular pressure (IOP) was also measured at rest and one hour after rest or before and after acupuncture. Results. The Δ value of the resistive index in the short posterior ciliary artery (P < .01) and the Δ value of IOP (P < .01) were decreased significantly by acupuncture compared with no acupuncture treatment. Conclusions. Acupuncture can improve the retrobulbar circulation and IOP, which may indicate the efficacy of acupuncture for OAG

Characterizing the flagellar filament and the role of motility in bacterial prey-penetration by Bdellovibrio bacteriovorus

The predatory bacterium Bdellovibrio bacteriovorus swims rapidly by rotation of a single, polar flagellum comprised of a helical filament of flagellin monomers, contained within a membrane sheath and powered by a basal motor complex. Bdellovibrio collides with, enters and replicates within bacterial prey, a process previously suggested to firstly require flagellar motility and then flagellar shedding upon prey entry. Here we show that flagella are not always shed upon prey entry and we study the six fliC flagellin genes of B. bacteriovorus, finding them all conserved and expressed in genome strain HD100 and the widely studied lab strain 109J. Individual inactivation of five of the fliC genes gave mutant Bdellovibrio that still made flagella, and which were motile and predatory. Inactivation of the sixth fliC gene abolished normal flagellar synthesis and motility, but a disordered flagellar sheath was still seen. We find that this non-motile mutant was still able to predate when directly applied to lawns of YFP-labelled prey bacteria, showing that flagellar motility is not essential for prey entry but important for efficient encounters with prey in liquid environments

Transgenic rescue of hemolytic anemia due to red blood cell pyruvate kinase deficiency

Background and Objectives Red blood cell pyruvate kinase (R-PK) deficiency is the most common glycolytic enzyme defect associated with hereditary non-spherocytic hemolytic anemia. Cases with the most severe deficiency die in the peri- or neonatal period and no specific therapy exists at present. To test whether the targeted overexpression of the normal R-PK gene in erythroid cells could reduce hemolysis in R-PK mutant mice, we performed a genetic rescue study using human R-PK transgenic mice.Design and Methods Human R-PK promoter driven with human μLCR of the human β-globin locus was used for the erythroid-specific expression of human R-PK in murine erythrocytes. The transgenic lines were mated with homozygous R-PK mutant mice and subsequently back-crossed. Mutant homozygotes with the μLCR-R-PK transgene were examined for any therapeutic effects of transgene expression.Results Two PK transgenic lines, hRPK_lo and hRPK_hi, were obtained. R-PK activity of the transgenic mice reached as high as three times that of the animals with the endogenous PK gene. Overexpression of human R-PK in the homozygous mutant mice successfully reduced hemolytic anemia. Improvements of hemolysis were evaluated by hemoglobin concentration, reticulocyte count, and spleen weight, which showed significant correlations with the levels of expression of the transgene. Recovery from metabolic disturbance in mutant red blood cells was shown as normalized concentrations of the glycolytic intermediates upstream of PK. In addition, there was a remarkable negative correlation between R-PK activity and the number of TUNEL-positive erythroid progenitors in the spleen.Interpretation and Conclusions These results indicate that overexpression of the wild-type PK gene in mutant erythroid cells ameliorates both erythroid apoptosis and the shortened red blood cell lifespan observed in PK mutant mice. It is likely that the level of transgene expression required to achieve evident therapeutic effects should be equivalent to or more than that of the endogenous PK gene. This gene-addition strategy may be suitable for clinical application if there is a high level of transgene expression of R-PK in erythroid progenitors/red blood cells