We introduce bicircular high-harmonic spectroscopy as a new method to probe dynamical symmetries of atoms and molecules and their evolution in time. Our approach is based on combining a circularly ...polarized femtosecond fundamental field of frequency ω with its counterrotating second harmonic 2ω. We demonstrate the ability of bicircular high-harmonic spectroscopy to characterize the orbital angular momentum symmetry of atomic orbitals. We further show that breaking the threefold rotational symmetry of the generating medium-at the level of either the ensemble or that of a single molecule-results in the emission of the otherwise parity-forbidden frequencies 3qω (q∈N), which provide a background-free probe of dynamical molecular symmetries.
Deposition of H2A.Z in chromatin is known to be mediated by a conserved SWR1 chromatin‐remodeling complex in eukaryotes. However, little is known about whether and how the SWR1 complex cooperates ...with other chromatin regulators. Using immunoprecipitation followed by mass spectrometry, we found all known components of the Arabidopsis thaliana SWR1 complex and additionally identified the following three classes of previously uncharacterized plant‐specific SWR1 components: MBD9, a methyl‐CpG‐binding domain‐containing protein; CHR11 and CHR17 (CHR11/17), ISWI chromatin remodelers responsible for nucleosome sliding; and TRA1a and TRA1b, accessory subunits of the conserved NuA4 histone acetyltransferase complex. MBD9 directly interacts with CHR11/17 and the SWR1 catalytic subunit PIE1, and is responsible for the association of CHR11/17 with the SWR1 complex. MBD9, TRA1a, and TRA1b function as canonical components of the SWR1 complex to mediate H2A.Z deposition. CHR11/17 are not only responsible for nucleosome sliding but also involved in H2A.Z deposition. These results indicate that the association of the SWR1 complex with CHR11/17 may facilitate the coupling of H2A.Z deposition with nucleosome sliding, thereby co‐regulating gene expression, development, and flowering time.
Synopsis
Cooperation of the SWR1 remodeler, responsible for histone H2A.Z deposition, with other chromatin regulators is incompletely understood. Here, proteomic identification of plant SWR1 complex components reveals its coupling to nucleosome sliding activities.
Characterization of the Arabidopsis SWR1 complex identifies CHR11, CHR17, TRA1A, TRA1B, and MBD9 as plant‐specific components.
ISWI remodeler catalytic subunits CHR11 and CHR17 associate with the SWR1 complex to couple nucleosome sliding and H2A.Z deposition.
MBD9 bridges CHR11 and CHR17 to the core SWR1 complex.
Together with other SWR1 components, MBD9 and CHR11/17 co‐regulate gene expression, development, and flowering time.
Proteomic analysis of Arabidopsis thaliana SWR1 complex components implicates nucleosome‐sliding ISWI remodeler subunits CHR11 and CHR17 also in histone deposition.
We performed the CH
4
/(Ar–H
2
) plasma post-treatments on ultrananocrystalline diamond films prepared by hot filament chemical vapor deposition. The results show that during the CH
4
/(Ar–H
2
) ...plasma treatment, 3–5 nm diamond grains agglomerate and regrow, and the graphite between the grains transformed into diamond due to the combined action of hydrogen and tantalum atoms in the samples. This produces bigger diamond grains in size of 200 nm with a large number of stacking faults formed during the grain aggregation, and the graphite phase is greatly reduced. Moreover, the electron field emission (EFE) performance of the films is significantly improved after the CH
4
/(Ar–H
2
) plasma treatment. This suggests that the improved EFE performance is not caused by the graphite phase, but by the diamond grains with lots of stacking faults that provide transport channels for electrons. This provides a method for enhancing the EFE properties of diamond films.
Different peak trends of tiny grains carbon film have been observed under the investigations of the Raman spectroscopy and energy loss spectroscopy. Carbon films known in nanocrystalline and ...ultrananocrystalline diamond films are synthesized by employing microwave‐based vapor deposition system. Carbon atoms exhibit several state behaviors depending on the incurred positions of their electrons. Different morphology of tiny grains under different chamber pressure is related to different rate of arriving typical energies at/near substrate surface. Those tiny grains of carbon film, which evolved in graphitic state atoms are converted to structure of smooth elements where elongation of atoms of one‐dimensional arrays is as per exerting surface format forces along opposite poles from their centers. Such tiny grains in the film are the cause of v1 peak under the investigation of the Raman spectrum because of the enhanced propagation of input laser signals through channelized inter‐state electron gaps of elongated graphitic state atoms. Those tiny grains of carbon film, which evolved in fullerene state are the cause of v2 peak. The tiny grains related to v1 peak possess a low intensity as compared with the ones which comprised atoms having state behaviors known in their exceptional hardness. Tiny grains representing v1 peak in the Raman spectrum are also the cause of field emission characteristic of a carbon film. Different peak recordings were made for the Raman at defined positions indicating a different state of carbon atoms for a different phase of deposited tiny grains, which is in line to their energy loss spectroscopy.
Background and Purpose
The interleukin (IL)‐36 pathway is a critical player in the pathogenesis of pustular psoriasis. However, therapies targeting this pathway are limited or unaffordable (e.g. the ...anti‐IL‐36 receptor antibody). AMP‐activated protein kinase (AMPK), a regulator of cellular energy and metabolism, is known to participate in inflammatory diseases. However, its role in IL‐36‐induced skin inflammation remains unclear. Therefore, we sought to investigate the role of AMPK signals in regulating IL‐36‐induced responses in the skin.
Experimental Approach
IL‐36‐stimulated primary normal human epidermal keratinocytes (NHEKs) and IL‐36‐injected (intradermally) BALB/c mice served as the cell and animal models, respectively. Additionally, 5‐aminoimidazole‐4‐carboxamide riboside (AICAR) and A769662 served as AMPK activators.
Key Results
AICAR and A769662 significantly suppressed the IL‐36‐induced IL‐8 (CXCL8) and CCL20 production from NHEKs. IL‐36‐induced IκBζ protein expression was prominently reduced and IKK/IκBα phosphorylation was attenuated by AICAR and A769662. Conversely, AMPKα knockdown increased IκBζ protein expression and IKK/IκBα phosphorylation in IL‐36‐treated NHEKs. Furthermore, AICAR and A769662 enhanced IL‐36‐induced‐IκBζ protein degradation via the proteasome‐dependent but not the lysosome‐dependent pathway. Pretreatment of NHEKs with IL‐36 slightly suppressed the AICAR‐ and A769662‐triggered phosphorylation of AMPK and acetyl‐CoA carboxylase. In the mouse model, topical application of AICAR significantly reduced ear swelling, redness, epidermal thickening, neutrophil infiltration and inflammatory and antimicrobial peptide gene expression.
Conclusion and Implications
AMPK activation suppresses IL‐36‐induced IL‐8 and CCL20 release by regulating IκBζ expression in keratinocytes and reduces IL‐36‐induced skin inflammation in mice, suggesting that AMPK activation is a potential strategy for treating patients with IL‐36‐mediated inflammatory skin disorders.
Infections caused by enterohemorrhagic Escherichia coli (EHEC) can lead to diarrhea with abdominal cramps and sometimes are complicated by severe hemolytic uremic syndrome. EHEC secretes effector ...proteins into host cells through a type III secretion system that is composed of proteins encoded by a chromosomal island, locus for the enterocyte effacement (LEE). EspA is the major component of the filamentous structure connecting the bacteria and the host's cells. Synthesis and secretion of EspA must be carefully controlled since the protein is prone to polymerize. CesAB, CesA2, and EscL have been identified as being able to interact with EspA. Furthermore, the intracellular level of EspA declines when cesAB, cesA2, and escL are individually deleted. Here, we report a LEE gene named l0033, which also affects the intracellular level of EspA. We renamed l0033 as escA since its counterpart in enteropathogenic E. coli has been recently described. Similar to CesAB, EscL, and CesA2, EscA interacts with EspA and enhances the protein stability of EspA. However, EscA is also able to interact with inner membrane-associated EscL, CesA2, and EscN, but not with cytoplasmic CesAB. In terms of gene organizations, escA locates in LEE3. Expression of EscA is faithfully regulated via Mpc, the first gene product of LEE3. Since Mpc is tightly regulated to low level, we suggest that EscA is highly synchronized and critical to the process of escorting EspA to its final destination.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Canine parvovirus type 2 (CPV-2) was first identified in the late 1970s; it causes intestinal hemorrhage with severe bloody diarrhea in kennels and dog shelters worldwide. Since its emergence, CPV-2 ...has been replaced with new genetic variants (CPV-2a, CPV-2b, and CPV-2c). Currently, information about the genotype prevalence of CPV-2 in Vietnam is limited. In the present study, we investigated the genotype prevalence and distribution of CPV-2 in the three regions of Vietnam.
Rectal swabs were collected from 260 dogs with suspected CPV-2 infection from northern, central, and southern Vietnam from November 2016 to February 2018. All samples were identified as parvovirus positive by real-time PCR, and further genotyping was performed using a SimpleProbe® real-time PCR assay.
Of the 260 Vietnamese CPV-2 isolates, 6 isolates (2.31%) were identified as CPV-2a, 251 isolates (96.54%) were identified as CPV-2c and 3 isolates (1.15%) were untypable using the SimpleProbe® real-time PCR assay. In northern Vietnam, the percentages of CPV-2a and CPV-2c were 2.97% (3/101) and 97.3% (98/101), respectively. In central Vietnam, the percentages of CPV-2a and CPV-2c were 1.11% (1/90) and 98.89% (89/90), respectively. In southern Vietnam, the percentages of CPV-2a and CPV-2c were 3.03% (2/66) and 96.97% (64/66), respectively. CPV-2b was not observed in this study. The VP2 genes of CPV-2c in Vietnam are more genetically similar to those of CPV-2c strains in China and Taiwan than to those of prototype CPV-2c strains (FJ222821) or the first Vietnamese CPV-2c (AB120727).
The present study provides evidence that CPV-2c is the most prevalent variant in Vietnam. Phylogenetic analysis demonstrated that the recent Vietnamese CPV-2c isolates share a common evolutionary origin with Asian CPV-2c strains.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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In response to mitochondrial damage, mitochondria activate mitochondrial dynamics to maintain normal functions, and an imbalance in mitochondrial dynamics triggers multiple programmed ...cell death processes. Recent studies have shown that phosphoglycerate mutase 5 (PGAM5) is associated with mitochondrial damage. PGAM5 activates mitochondrial biogenesis and mitophagy to promote a cellular compensatory response when mitochondria are mildly damaged, whereas severe damage to mitochondria leads to PGAM5 inducing excessive mitochondria fission, disruption to mitochondrial movement, and amplification of apoptosis, necroptosis and mitophagic death signals, which eventually evoke cell death. PGAM5 functions mainly through protein-protein interactions and specific Ser/Thr/His protein phosphatase activity. PGAM5 is also regulated by mitochondrial proteases. Detection of PGAM5 and its interacting protein partners should enable a more accurate evaluation of mitochondrial damage and a more precise method for the diagnosis and treatment of diseases.
ABSTRACT
We examine whether stress tests distort banks' risk‐taking decisions. We study a model in which a regulator may choose to rescue banks in the event of concurrent bank failures. Our analysis ...reveals a novel coordination role of stress tests. Disclosure of stress‐test results informs banks of the failure likelihood of other banks, which can reduce welfare by facilitating banks' coordination in risk‐taking. However, conducting stress tests also enables the regulator to more effectively intervene banks, coordinating them preemptively into taking lower risks. We find that, if the regulator has a strong incentive to bail out, stress tests improve welfare, whereas if the regulator's incentive to bail out is weak, stress tests impair welfare.
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