The dual King relation Yamamoto, Yasuhiro
Physics letters. B,
03/2023, Letnik:
838
Journal Article
Recenzirano
Odprti dostop
We introduce a new linear relation in the isotope shifts of atomic spectroscopy. While the famous King relation is the linear relation among the different transitions, the new one is the linear ...relation among the different isotope pairs. Since we obtain this relation by exchanging the roles of the electronic and the nuclear factors in the original relation, we call it the dual King relation. This relation shows us similar information to the original King relation without including new fit parameters when we measure the isotope shifts of many transitions. In the dual King relation, the fit coefficients consist of the nuclear factors. Then, the fit results give us constraints to the ratios of the isotope dependence independent of the electron wave functions. This helps us to test the origin of unknown higher order isotope shifts. We show that the dual King relation can also be employed to constrain the weakly interacting light new boson at the same level as the original King relation.
Flavor anomalies from asymptotically safe gravity Kowalska, Kamila; Sessolo, Enrico Maria; Yamamoto, Yasuhiro
European physical journal. C, Particles and fields,
04/2021, Letnik:
81, Številka:
4
Journal Article
Recenzirano
Odprti dostop
We use the framework of asymptotically safe quantum gravity to derive predictions for scalar leptoquark solutions to the
b
→
s
and
b
→
c
flavor anomalies. The presence of an interactive UV fixed ...point in the system of gauge and Yukawa couplings imposes a set of boundary conditions at the Planck scale, which allows one to determine low-energy values of the leptoquark Yukawa matrix elements. As a consequence, the allowed leptoquark mass range can be significantly narrowed down. We find that a consistent gravity-driven solution to the
b
→
s
anomalies predicts a leptoquark with the mass of 4–7
TeV
, entirely within the reach of a future hadron-hadron collider with
s
=
100
TeV
. Conversely, in the case of the
b
→
c
anomalies the asymptotically safe gravity framework predicts a leptoquark mass at the edge of the current LHC bounds. Complementary signatures appear in flavor observables, namely the (semi)leptonic decays of
B
and
D
mesons and kaons.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
•Effects of defects, surface roughness and HIP on the fatigue strength of a Ti6Al4V by AM were studied.•HIP improved fatigue strength to the level of ideal fatigue limit if surface roughness is ...removed.•Evaluating method for the effective size √areaeffmax of irregularly shaped defects was proposed.•AM fatigue design method was proposed with the √area parameter model and the statistics of extremes.
The additive manufacturing (AM) is expected to be a promising manufacturing process for high strength or hard steels such as Ti-6Al-4V for the aerospace industry components having complex shapes. However, disadvantage or challenge of AM is presence of defects which are inevitably contained in the manufacturing process. This paper focuses on the effects of defects, surface roughness and Hot Isostatic Pressing (HIP) process on the fatigue strength of a Ti-6Al-4V manufactured by AM. Defects were mostly gas pores and those made by lack of fusion. Many defects which were formed at subsurface were eliminated by HIP and eventually HIP improved fatigue strength drastically to the level of the ideal fatigue limit to be expected from the hardness. Surface roughness had strong detrimental influence on fatigue strength. The method for estimating the effective size √areaeffmax of irregularly shaped defects and interacting adjacent defects was proposed from the viewpoint of fracture mechanics.
We revisit the stellar cooling limits on the light scalar boson whose coupling to the Standard Model particles is described by its mixing with the Higgs boson. Strong constraints have been obtained ...from the electron-nucleus bremsstrahlung process (Ne→NeS) and the resonant plasma effect in the medium. We find that the bremsstrahlung contribution from the electron and nucleus scattering is of similar magnitude to the plasma mixing effect including the off-resonant mixing. The constraints on the scalar coupling are found to be about three orders of magnitude weaker than the previous evaluations because of the missing factor of the electron-nucleon mass ratio. For white dwarfs, the stellar cooling constraint is even more suppressed due to the Pauli blocking effect. We obtain limits on the Higgs-scalar mixing angle of 10−10–10−9, which are given by white dwarfs or red giants up to the luminosity limits, in the region where the scalar mass is lighter than about 10 keV.
Cyclooxygenases (COXs) oxidize arachidonic acid to prostaglandin (PG) G
2
and H
2
followed by PG synthases that generates PGs and thromboxane (TX) A
2
. COXs are divided into COX-1 and COX-2. In the ...central nervous system, COX-1 is constitutively expressed in neurons, astrocytes, and microglial cells. COX-2 is upregulated in these cells under pathophysiological conditions. In hippocampal long-term potentiation, COX-2, PGE synthase, and PGE
2
are induced in post-synaptic neurons. PGE
2
acts pre-synaptic EP2 receptor, generates cAMP, stimulates protein kinase A, modulates voltage-dependent calcium channel, facilitates glutamatergic synaptic transmission, and potentiates long-term plasticity. PGD
2
, PGE
2
, and PGI
2
exhibit neuroprotective effects via Gs-coupled DP1, EP2/EP4, and IP receptors, respectively. COX-2, PGD
2
, PGE
2
, PGF
2α
, and TXA
2
are elevated in stroke. COX-2 inhibitors exhibit neuroprotective effects in vivo and in vitro models of stroke, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, epilepsy, and schizophrenia, suggesting neurotoxicities of COX products. PGE
2
, PGF
2α
, and TXA
2
can contribute to the neurodegeneration via EP1, FP, and TP receptors, respectively, which are coupled with Gq, stimulate phospholipase C and cleave phosphatidylinositol diphosphate to produce inositol triphosphate and diacylglycerol. Inositol triphosphate binds to inositol triphosphate receptor in endoplasmic reticulum, releases calcium, and results in increasing intracellular calcium concentrations. Diacylglycerol activates calcium-dependent protein kinases. PGE
2
disrupts Ca
2+
homeostasis by impairing Na
+
-Ca
2+
exchange via EP1, resulting in the excess Ca
2+
accumulation. Neither PGE
2
, PGF
2α
, nor TXA
2
causes neuronal cell death by itself, suggesting that they might enhance the ischemia-induced neurodegeneration. Alternatively, PGE
2
is non-enzymatically dehydrated to a cyclopentenone PGA
2
, which induces neuronal cell death. Although PGD
2
induces neuronal apoptosis after a lag time, neither DP1 nor DP2 is involved in the neurotoxicity. As well as PGE
2
, PGD
2
is non-enzymatically dehydrated to a cyclopentenone 15-deoxy-Δ
12,14
-PGJ
2
, which induces neuronal apoptosis without a lag time. However, neurotoxicities of these cyclopentenones are independent of their receptors. The COX-2 inhibitor inhibits both the anchorage-dependent and anchorage-independent growth of glioma cell lines regardless of COX-2 expression, suggesting that some COX-2-independent mechanisms underlie the antineoplastic effect of the inhibitor. PGE
2
attenuates this antineoplastic effect, suggesting that the predominant mechanism is COX-dependent. COX-2 or EP1 inhibitors show anti-neoplastic effects. Thus, our review presents evidences for pathophysiological roles of cyclooxygenases and prostaglandins in the central nervous system.
Probing new intra-atomic force with isotope shifts Mikami, Kyoko; Tanaka, Minoru; Yamamoto, Yasuhiro
European physical journal. C, Particles and fields,
12/2017, Letnik:
77, Številka:
12
Journal Article
Recenzirano
Odprti dostop
In the development of atomic clocks, some atomic transition frequencies are measured with remarkable precision. These measured spectra may include the effects of a new force mediated by a weakly ...interacting boson. Such effects might be distilled out from possible violation of a linear relation in isotope shifts between two transitions, as known as King’s linearity, with relatively suppressed theoretical uncertainties. We discuss the experimental sensitivity to a new force in the test of the linearity as well as the linearity violation owing to higher-order effects within the Standard Model. The sensitivity to new physics is limited by such effects. We have found that, for
Yb
+
, the higher-order effect is in the reach of future experiments. The sensitivity to a heavy mediator is also discussed. It is analytically clarified that the sensitivity becomes weaker than that in the literature. Our numerical results of the sensitivity are compared with other weak force search experiments.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The Atomiki anomaly can be interpreted as a new light vector boson. If such a new particle exists, it could be a mediator between the Standard Model sector and the dark sector including the dark ...matter. We discussed some simple effective models with these particles. In the models, the secluded dark matter models are good candidates to satisfy the thermal relic abundance. In particular, we found that the dark matter self-interaction can be large enough to solve the small scale structure puzzles if the dark matter is a
fermion.
Abstract
Autophagy regulates primary cilia formation, but the underlying mechanism is not fully understood. In this study, we identify NIMA-related kinase 9 (NEK9) as a GABARAPs-interacting protein ...and find that NEK9 and its LC3-interacting region (LIR) are required for primary cilia formation. Mutation in the LIR of NEK9 in mice also impairs in vivo cilia formation in the kidneys. Mechanistically, NEK9 interacts with MYH9 (also known as myosin IIA), which has been implicated in inhibiting ciliogenesis through stabilization of the actin network. MYH9 accumulates in NEK9 LIR mutant cells and mice, and depletion of MYH9 restores ciliogenesis in NEK9 LIR mutant cells. These results suggest that NEK9 regulates ciliogenesis by acting as an autophagy adaptor for MYH9. Given that the LIR in NEK9 is conserved only in land vertebrates, the acquisition of the autophagic regulation of the NEK9–MYH9 axis in ciliogenesis may have possible adaptive implications for terrestrial life.
Proteases are classified into six distinct classes (cysteine, serine, threonine, aspartic, glutamic, and metalloproteases) on the basis of catalytic mechanism. The cellular control of protein quality ...senses misfolded or damaged proteins principally by selective ubiquitin-proteasome pathway and non-selective autophagy-lysosome pathway. The two pathways do not only maintain cell homeostasis physiologically, but also mediate necrosis and apoptosis pathologically. Proteasomes are threonine proteases, whereas cathepsins are lysosomal aspartic proteases. Calpains are non-lysosomal cysteine proteases and calcium-dependent papain-like enzyme. Calpains and cathepsins are involved in the neuronal necrosis, which are accidental cell death. Necrosis is featured by the disruption of plasma membranes and lysosomes, the loss of ATP and ribosomes, the lysis of cell and nucleus, and the caspase-independent DNA fragmentation. On the other hand, caspases are cysteine endoproteases and mediate neuronal cell death such as apoptosis and pyroptosis, which are programmed cell death. In the central nervous system, necroptosis, ferroptosis and autophagic cell death are also classified into programmed cell death. Neuronal apoptosis is characterized by cell shrinkage, plasma membrane blebbing, karyorrhexis, chromatin condensation, and DNA fragmentation. Necroptosis and pyroptosis are necrotic and lytic forms of programmed cell death, respectively. Although autophagy is involved in cell survival, it fails to maintain cellular homeostasis, resulting in autophagic cell death. Ferroptosis is induced by reactive oxygen species in excitotoxicity of glutamate and ischemia-reperfusion. Apoptosis and pyroptosis are dependent on caspase-3 and caspase-1, respectively. Autophagic cell death and necroptosis are dependent on calpain and cathepsin, respectively, but independent of caspase. Although apoptosis has been defined by the absence of morphological features of necrosis, the two deaths are both parts of a continuum. The intracellular proteases do not only maintain cell homeostasis but also regulate neuronal maturation during the development of embryonic brain. Furthermore, neurodegenerative diseases are caused by the impairment of quality control mechanisms for a proper folding and function of protein.
Suppression of ubiquitin proteasome pathway (UPP) and stimulation of caspase-3 are involved in neurodegeneration. Can UPP activators and caspase-3 inhibitors ameliorate neurodegeneration? Here, we ...found a novel neuronal cell death accompanied with UPP activation and caspase-3 inhibition. Recently, plasmalemmal neuron-specific enolase (NSE) has been identified as one of membrane targets of 15-deoxy-Δ
12,14
-prostaglandin J
2
(15d-PGJ
2
). 15d-PGJ
2
induces neuronal apoptosis via activating caspase-3 and inactivating UPP, whereas the anti-NSE antibody inactivated caspase-3, activated UPP, and caused neuronal cell death. The anti-NSE antibody activated caspase-1 (pyroptosis marker), but not condense chromatin (apoptosis marker). The anti-NSE antibody declined intracellular level of ATP, which is not altered in pyroptosis. The intracellular level of calcium is elevated in necrosis and pyroptosis, but its chelator did not ameliorate the neurotoxicity of anti-NSE. Thiol antioxidants such as
N
-acetyl cysteine and glutathione reduced the neurotoxicity of 15d-PGJ
2
but enhanced that of the anti-NSE antibody. The anti-NSE antibody incorporated propidium iodide into neurons through the disrupted plasma membrane, which are not observed in ferroptosis and autophagic cell death. Thus, the anti-NSE antibody induced neuronal cell death in a novel fashion distinguished from necrosis, necroptosis, apoptosis, pyroptosis, ferroptosis, and autophagic cell death.
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