SU(3) symmetry breaking in charmed baryon decays Geng, C. Q.; Hsiao, Y. K.; Liu, Chia-Wei ...
The European physical journal. C, Particles and fields,
07/2018, Letnik:
78, Številka:
7
Journal Article
Recenzirano
Odprti dostop
We explore the breaking effects of the
SU
(3) flavor symmetry in the singly Cabibbo-suppressed anti-triplet charmed baryon decays of
B
c
→
B
n
M
, with
B
c
=
(
Ξ
c
0
,
Ξ
c
+
,
Λ
c
+
)
and
B
n
(
M
)
...the baryon (pseudo-scalar) octets. We find that these breaking effects can be used to account for the experimental data on the decay branching ratios of
B
(
Λ
c
+
→
Σ
0
K
+
,
Λ
0
K
+
)
and
R
K
/
π
′
=
B
(
Ξ
c
0
→
Ξ
-
K
+
)
/
B
(
Ξ
c
0
→
Ξ
-
π
+
)
. In addition, we obtain that
B
(
Ξ
c
0
→
Ξ
-
K
+
,
Σ
-
π
+
)
=
(
4.6
±
1.7
,
12.8
±
3.1
)
×
10
-
4
,
B
(
Ξ
c
0
→
p
K
-
,
Σ
+
π
-
)
=
(
3.0
±
1.0
,
5.2
±
1.6
)
×
10
-
4
and
B
(
Ξ
c
+
→
Σ
0
(
+
)
π
+
(
0
)
)
=
(
10.3
±
1.7
)
×
10
-
4
, which all receive significant contributions from the breaking effects, and can be tested by the BESIII and LHCb experiments.
Objective
To systematically assess the prevalence of frailty, including prefrailty, stratified prevalence according to frailty criteria, gender, age, and region, and the risk factors for frailty in ...China.
Design
We conducted a systematic literature review and meta-analysis using articles available in 8 databases including PubMed, Cochrane Library, Web of Science, CINAHL Plus, China Knowledge Resource Integrated Database (CNKI), Wanfang Database, Chinese Biomedical Database (CBM), and Weipu Database (VIP).
Setting
Crosssectional and cohort data from Chinese community.
Participants
Community-dwelling adults aged 65 and older.
Measurements
Two authors independently extracted data based upon predefined criteria. Where data were available we conducted a meta-analysis of frailty parameters using a random-effects model.
Results
We screened 915 different articles, and 14 studies (81258 participants) were ultimately included in this analysis. The prevalence of frailty and prefrailty in individual studies varied from 5.9% to 17.4% and from 26.8% to 62.8%, respectively. The pooled prevalence of frailty and prefrailty were 10% (95% CI: 8% to 12%, I2 = 97.4%, P = 0.000) and 43% (95% CI: 37% to 50%, I2 = 98.0%, P = 0.000), respectively. The pooled frailty prevalence was 8% for the Fried frailty phenotype, 12% for the frail index, and 15% for the FRAIL scale. Age-stratified meta-analyses showed the pooled prevalence of frailty to be 6%, 15%, and 25% for those aged 65–74, 75–84, and ≥85 years old, respectively. The pooled prevalence of frailty was 8% for males and 11% for females. The pooled prevalence of frailty in Mainland China, Taiwan, and Hong Kong was 12%, 8%, and 14%, respectively. The pooled frailty prevalence was 10% in urban areas and 7% in rural areas. After controlling for confounding variables, increasing age (OR = 1.28, 95% CI: 1.2 to 1.36, I
2
= 98.0%, P = 0.000), being female (OR = 1.29, 95% CI: 1.16 to 1.43, I
2
=92.7%, P=0.000), activities of daily living (ADL) disability (OR = 1.72, 95% CI: 1.57 to 1.90, I
2
= 99.7%, P = 0.000), and having three or more chronic diseases (OR = 1.97, 95% CI: 1.78 to 2.18, I
2
= 97.5%, P = 0.000) were associated with frailty.
Conclusions
These findings of this review indicate an overall pooled prevalence of frailty among Chinese community-dwelling older people of 10%. Increasing age, being female, ADL disability, and having three or more chronic diseases were all risk factors for frailty. Further research will be needed to identify additional frailty risk factors in order to better treat and prevent frailty in the community.
A
bstract
We study the semileptonic and non-leptonic charmed baryon decays with SU(3) flavor symmetry, where the charmed baryons can be
B
c
= (Ξ
c
0
, Ξ
c
+
, Λ
c
+
),
B
c
′
= (
Σ
c
(++,+,0)
, Ξ
c
...′ (+,0)
, Ω
c
0
),
B
cc
= (Ξ
cc
+ +
, Ξ
cc
+
, Ω
c
+
) or
B
cc
= Ω
ccc
+ +
. With
B
n
(′)
denoted as the baryon octet (decuplet), we find that the
B
c
→
B
n
′
ℓ
+
ν
ℓ
decays are forbidden, while the Ω
c
0
→ Ω
−
ℓ
+
ν
ℓ
, Ω
cc
+
→ Ω
c
0
ℓ
+
ν
ℓ
, and Ω
ccc
+ +
→ Ω
cc
+
ℓ
+
ν
ℓ
decays are the only existing Cabibbo- allowed modes for
B
c
′
→
B
n
′
ℓ
+
ν
ℓ
,
B
cc
→
B
c
′
ℓ
+
ν
ℓ
, and
B
ccc
→
B
cc
(′)
ℓ
+
ν
ℓ
, respectively. We predict the rarely studied
B
c
→
B
n
(′)
M
decays, such as
ℬ
Ξ
c
0
→
Λ
0
K
¯
0
,
Ξ
c
+
→
Ξ
0
π
+
=
8.3
±
0.9
,
8.0
±
4.1
×
10
−
3
and
ℬ
Λ
c
+
→
Δ
+
+
π
−
,
Ξ
c
0
→
Ω
−
K
+
=
5.5
±
1.3
,
4.8
±
0.5
×
10
−
3
. For the observation, the doubly and triply charmed baryon decays of
Ω
cc
+
→
Ξ
c
+
K
¯
0
,
Ξ
cc
+
+
→
Ξ
c
+
π
+
,
Σ
c
+
+
K
¯
0
,
and
Ω
c
c
c
+
+
→
Ξ
cc
+
+
K
¯
0
,
Ω
cc
+
π
+
,
Ξ
c
+
D
+
are the favored Cabibbo-allowed decays, which are accessible to the BESIII and LHCb experiments.
The E3 ubiquitin ligase adaptor speckle-type POZ protein (SPOP) is frequently dysregulated in prostate adenocarcinoma (PC), via either somatic mutations or mRNA downregulation, suggesting an ...important tumour suppressor function. To examine its physiologic role in the prostate epithelium in vivo, we generated mice with prostate-specific biallelic ablation of Spop. These mice exhibited increased prostate mass, prostate epithelial cell proliferation, and expression of c-MYC protein compared to littermate controls, and eventually developed prostatic intraepithelial neoplasia (PIN). We found that SPOP
can physically interact with c-MYC protein and, upon exogenous expression in vitro, can promote c-MYC ubiquitination and degradation. This effect was attenuated in PC cells by introducing PC-associated SPOP mutants or upon knockdown of SPOP via short-hairpin-RNA, suggesting that SPOP inactivation directly increases c-MYC protein levels. Gene Set Enrichment Analysis revealed enrichment of Myc-induced genes in transcriptomic signatures associated with SPOP
. Likewise, we observed strong inverse correlation between c-MYC activity and SPOP mRNA levels in two independent PC patient cohorts. The core SPOP
;MYC
transcriptomic response, defined by the overlap between the SPOP
and c-MYC transcriptomic programmes, was also associated with inferior clinical outcome in human PCs. Finally, the organoid-forming capacity of Spop-null murine prostate cells was more sensitive to c-MYC inhibition than that of Spop-WT cells, suggesting that c-MYC upregulation functionally contributes to the proliferative phenotype of Spop knock-out prostates. Taken together, our data highlight SPOP as an important regulator of luminal epithelial cell proliferation and c-MYC expression in prostate physiology, identify c-MYC as a novel bona fide SPOP substrate, and help explain the frequent inactivation of SPOP in human PC. We propose SPOP
-induced stabilization of c-MYC protein as a novel mechanism that can increase total c-MYC levels in PC cells, in addition to amplification of c-MYC locus.
MicroRNAs are important epigenetic regulators of protein expression by triggering degradation of target mRNAs and/or inhibiting their translation. Dysregulation of microRNA expression has been ...reported in several cancers, including prostate cancer (PC). We comprehensively characterized the proteomic footprint of a panel of 12 microRNAs that are potently suppressed in metastatic PC (SiM-miRNAs: miR-1, miR-133a, miR-133b, miR-135a, miR-143-3p, miR-145-3p, miR-205, miR-221-3p, miR-221-5p, miR-222-3p, miR-24-1-5p, and miR-31) using reverse-phase proteomic arrays. Re-expression of these SiM-miRNAs in PC cells suppressed cell proliferation and targeted key oncogenic pathways, including cell cycle, apoptosis, Akt/mammalian target of rapamycin signaling, metastasis and the androgen receptor (AR) axis. However, only 12%, at most, of these observed protein expression changes could be explained by predicted direct binding of miRNAs to corresponding mRNAs, suggesting that the majority of these proteomic effects result indirectly. AR and its steroid receptor coactivators (SRCs; SRC-1, -2 and -3) were recurrently affected by these SiM-miRNAs. In agreement, we identified inverse correlations between expression of these SiM-miRNAs and early clinical recurrence, as well as with AR transcriptional activity in human PC tissues. We also identified robust induction of miR-135a by androgen and strong direct binding of AR to the miR-135a locus. As miR-135a potently suppresses AR expression, this results in a negative feedback loop that suppresses AR protein expression in an androgen-dependent manner, while de-repressing AR expression upon androgen deprivation. Our results demonstrate that epigenetic silencing of these SiM-miRNAs can result in increased AR axis activity and cell proliferation, thus contributing to disease progression. We further demonstrate that a negative feedback loop involving miR-135a can restore AR expression under androgen-deprivation conditions, thus contributing to the upregulation of AR protein expression in castration-resistant PC. Finally, our unbiased proteomic profiling demonstrates that the majority of actual protein expression changes induced by SiM-miRNAs cannot be explained based on predicted direct interactions.
ZnxCd1–xS single‐crystal nanoribbons of controlled composition (where 0 ≤ x ≤ 1) can be synthesized by combining laser ablation with thermal evaporation. The nanoribbons (see Figure) exhibit lasing ...emission that can be continuously tuned within the ranges of 340–390 nm and 485–515 nm. These results suggest that ZnxCd1–xS nanoribbon lasers of pre‐selected “tunable” wavelengths between 340 and 515 nm may be achievable by tailoring the value of x.
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