35 research outputs found
Positive flow-spines and contact 3-manifolds, II
This paper corresponds to Section 8 of arXiv:1912.05774v3 [math.GT]. The
contents until Section 7 are published in Annali di Matematica Pura ed
Applicata as a separate paper. In that paper, it is proved that for any
positive flow-spine P of a closed, oriented 3-manifold M, there exists a unique
contact structure supported by P up to isotopy. In particular, this defines a
map from the set of isotopy classes of positive flow-spines of M to the set of
isotopy classes of contact structures on M. In this paper, we show that this
map is surjective. As a corollary, we show that any flow-spine can be deformed
to a positive flow-spine by applying first and second regular moves
successively.Comment: 17 pages and 22 figures. This paper covers Section 8 of the preprint
arXiv:1912.05774v3 [math.GT]. The part until Section 7 is covered in
arXiv:1912.05774v4 [math.GT] as a separate pape
Positive flow-spines and contact 3-manifolds
We say that a contact structure on a closed, connected, oriented, smooth
3-manifold is supported by a flow-spine if it has a contact form whose Reeb
flow is a flow of the flow-spine. We then define a map from the set of positive
flow-spines to the set of contact 3-manifolds up to contactomorphism by sending
a positive flow-spine to the supported contact 3-manifold and show that this
map is well-defined and surjective. We also determine the contact 3-manifolds
supported by positive flow-spines with up to 3 vertices. As an application, we
introduce the complexity for contact 3-manifolds and determine the contact
3-manifolds with complexity up to 3.Comment: 73 pages, 78 figures. The last subsection was remove
Pseudotachylytes from Langhovde and Skarvsnes in the Lützow-Holm Complex, East Antarctica, and their conditions of formation
The Tenth Symposium on Polar Science/Ordinary sessions: [OG] Polar Geosciences, Wed. 4 Dec. / Entrance Hall (1st floor), National Institute of Polar Researc
Geological field survey in the regions of L*tzow-Holm Bay, Prince Olav Coast and Enderby Land, 2018-2019 (JARE-60)
The Tenth Symposium on Polar Science/Ordinary sessions: [OG] Polar Geosciences, Wed. 4 Dec. / 3F Seminar room, National Institute of Polar Researc
Calcium sparks enhance the tissue fluidity within epithelial layers and promote apical extrusion of transformed cells
In vertebrates, newly emerging transformed cells are often apically extruded from epithelial layers through cell competition with surrounding normal epithelial cells. However, the underlying molecular mechanism remains elusive. Here, using phospho-SILAC screening, we show that phosphorylation of AHNAK2 is elevated in normal cells neighboring RasV12 cells soon after the induction of RasV12 expression, which is mediated by calcium-dependent protein kinase C. In addition, transient upsurges of intracellular calcium, which we call calcium sparks, frequently occur in normal cells neighboring RasV12 cells, which are mediated by mechanosensitive calcium channel TRPC1 upon membrane stretching. Calcium sparks then enhance cell movements of both normal and RasV12 cells through phosphorylation of AHNAK2 and promote apical extrusion. Moreover, comparable calcium sparks positively regulate apical extrusion of RasV12-transformed cells in zebrafish larvae as well. Hence, calcium sparks play a crucial role in the elimination of transformed cells at the early phase of cell competition
Brown adipose tissue dysfunction promotes heart failure via a trimethylamine N-oxide-dependent mechanism.
Low body temperature predicts a poor outcome in patients with heart failure, but the underlying pathological mechanisms and implications are largely unknown. Brown adipose tissue (BAT) was initially characterised as a thermogenic organ, and recent studies have suggested it plays a crucial role in maintaining systemic metabolic health. While these reports suggest a potential link between BAT and heart failure, the potential role of BAT dysfunction in heart failure has not been investigated. Here, we demonstrate that alteration of BAT function contributes to development of heart failure through disorientation in choline metabolism. Thoracic aortic constriction (TAC) or myocardial infarction (MI) reduced the thermogenic capacity of BAT in mice, leading to significant reduction of body temperature with cold exposure. BAT became hypoxic with TAC or MI, and hypoxic stress induced apoptosis of brown adipocytes. Enhancement of BAT function improved thermogenesis and cardiac function in TAC mice. Conversely, systolic function was impaired in a mouse model of genetic BAT dysfunction, in association with a low survival rate after TAC. Metabolomic analysis showed that reduced BAT thermogenesis was associated with elevation of plasma trimethylamine N-oxide (TMAO) levels. Administration of TMAO to mice led to significant reduction of phosphocreatine and ATP levels in cardiac tissue via suppression of mitochondrial complex IV activity. Genetic or pharmacological inhibition of flavin-containing monooxygenase reduced the plasma TMAO level in mice, and improved cardiac dysfunction in animals with left ventricular pressure overload. In patients with dilated cardiomyopathy, body temperature was low along with elevation of plasma choline and TMAO levels. These results suggest that maintenance of BAT homeostasis and reducing TMAO production could be potential next-generation therapies for heart failure.We thank Kaori Yoshida, Keiko Uchiyama, Satomi Kawai, Naomi Hatanaka, Yoko Sawaguchi, Runa Washio,
Takako Ichihashi, Nanako Koike, Keiko Uchiyama, Masaaki Nameta (Niigata University), Kaori Igarashi, Kaori
Saitoh, Keiko Endo, Hiroko Maki, Ayano Ueno, Maki Ohishi, Sanae Yamanaka, Noriko Kagata (Keio University)
for their excellent technical assistance, C. Ronald Kahn (Joslin Diabetes Center and Harvard Medical School)
for providing the BAT cell line, Evan Rosen (Harvard Medical School) for providing us Ucp-Cre mice, Kosuke
Morikawa (Kyoto University), Tomitake Tsukihara (University of Hyogo) and Shinya Yoshikawa (University of
Hyogo) for their professional opinions and suggestions. Tis work was supported by a Grant-in-Aid for Scientifc Research (A) (20H00533) from MEXT, AMED under Grant Numbers JP20ek0210114, and AMED-CREST
under Grant Number JP20gm1110012, and Moonshot Research and Development Program (21zf0127003s0201),
MEXT Supported Program for the Strategic Research Foundation at Private Universities Japan, Private University
Research Branding Project, and Leading Initiative for Excellent Young Researchers, and grants from the Takeda
Medical Research Foundation, the Vehicle Racing Commemorative Foundation, Ono Medical Research Foundation, and the Suzuken Memorial Foundation (to T.M.). Support was also provided by a Grants-in-Aid for Young
Scientists (Start-up) (26893080), and grants from the Uehara Memorial Foundation, Kowa Life Science Foundation, Manpei Suzuki Diabetes Foundation, SENSHIN Medical Research Foundation, ONO Medical Research
Foundation, Tsukada Grant for Niigata University Medical Research, Te Nakajima Foundation, SUZUKEN
memorial foundation, HOKUTO Corporation, Mochida Memorial Foundation for Medical & Pharmaceutical
Research, Grants-in-Aid for Encouragement of Young Scientists (A) (16H06244), Daiichi Sankyo Foundation of
Life Science, AMED Project for Elucidating and Controlling Mechanisms of Aging and Longevity under Grant
Number JP17gm5010002, JP18gm5010002, JP19gm5010002, JP20gm5010002, JP21gm5010002, Astellas Foundation for Research on Metabolic Disorders, Research grant from Naito Foundation, Te Japan Geriatrics Society
(to I.S.); by a Grant-in-Aid for Scientifc Research (C) (19K08974), Yujin Memorial Grant, Sakakibara Memorial
Research Grant from Te Japan Research Promotion Society for Cardiovascular Diseases, TERUMO Life Science Foundation, Kanae Foundation (to Y.Y.), JST ERATO (JPMJER1902), AMED-CREST (JP20gm1010009),
the Takeda Science Foundation, the Food Science Institute Foundation (to S.F.), and by a grant from Bourbon
(to T.M., I.S. and Y.Y.).S