Summary
Background
Recent studies suggest that Staphylococcus aureus enterotoxin sensitization is a risk factor for asthma. However, there is a paucity of epidemiologic evidence on adult‐onset asthma ...in community‐based populations.
Objective
We sought to evaluate the epidemiology and the clinical significance of staphylococcal enterotoxin sensitization in community‐based adult populations.
Methods
The present analyses were performed using the baseline data set of Korean adult population surveys, consisting of 1080 adults (mean age = 60.2 years) recruited from an urban and a rural community. Questionnaires, methacholine challenge tests, and allergen skin tests were performed for defining clinical phenotypes. Sera were analysed for total IgE and enterotoxin‐specific IgE using ImmunoCAP.
Results
Staphylococcal enterotoxin sensitization (≥ 0.35 kU/L) had a prevalence of 27.0%. Risk factors were identified as male sex, current smoking, advanced age (≥ 61 years), and inhalant allergen sensitization. Current asthma was mostly adult onset (≥ 18 years old) and showed independent associations with high enterotoxin‐specific IgE levels in multivariate logistic regression tests. In multivariate linear regressions, staphylococcal enterotoxin‐specific IgE level was identified as the major determinant factor for total IgE level.
Conclusions and Clinical Relevance
Staphylococcal enterotoxin sensitization was independently associated with adult‐onset asthma in adult community populations. Strong correlations between the enterotoxin‐specific IgE and total IgE levels support the clinical significance. The present findings warrant further studies for the precise roles of staphylococcal enterotoxin sensitization in the asthma pathogenesis.
Metastasis is a life-threatening feature of cancer and is primarily responsible for cancer patient mortality. Cross talk between tumor cells and endothelium is important for tumor progression and ...metastasis. However, very little is known about the mechanisms by which endothelial cells (ECs) that are close to tumor cells, respond to the tumor cells during tumor progression and metastasis. In this study, we exploited the use of EC-specific signal transducer activator of transcription 3 (STAT3) knockout mice to investigate the role of STAT3 in ECs in tumor progression and metastasis. We found that the loss of STAT3 in ECs did not affect primary Lewis lung carcinoma (LLC) tumor growth, but it reduced in vivo LLC metastasis in experimental and spontaneous metastasis models. Mechanistically, STAT3 activation upregulated cell adhesion molecule expression, including E-selectin and P-selectin, in murine endothelial MS-1 cells treated with tumor cell-conditioned media in vitro and in pre-metastatic lungs of tumor-bearing mice in vivo. We also found that both E-selectin and P-selectin were, at least in part, responsible for STAT3-induced adhesion and invasion of LLC cells through an EC monolayer. However, tumor cell-conditioned media from B16F10 melanoma cells did not activate STAT3 in MS-1 cells. As a result, EC STAT3 knockout did not affect B16F10 melanoma cell metastasis. In addition, various human cancer cells activated STAT3 in human ECs (HUVECs), resulting in increased cell adhesion molecule expression. Collectively, our findings demonstrate that STAT3 activation in ECs promotes tumor metastasis through the induction of cell adhesion molecules, demonstrating a role for ECs in response to tumor cells during tumor metastasis.
Background
Although expression of peptidyl‐prolyl cis/trans isomerase NIMA‐interacting 1 (PIN1) was reported in bone tissue, the precise role of PIN1 in periodontal tissue and cells remain unclear.
...Material & Methods
To elucidate the roles of PIN1 in periodontal tissue, its expression in periodontal tissue and cells, and effects on in vitro 4 osteoblast differentiation and the underlying signaling mechanisms were evaluated.
Results
PIN1 was expressed in mouse periodontal tissues including periodontal ligament cells (PDLCs), cementoblasts and osteoblasts at the developing root formation stage (postnatal, PN14) and functional stage of tooth (PN28). Treatment of PIN1 inhibitor juglone, and gene silencing by RNA interference promoted osteoblast differentiation in PDLCs and cementoblasts, whereas the overexpression of PIN1 inhibited. Moreover, osteogenic medium‐induced activation of AMPK, mTOR, Akt, ERK, p38 and NF‐jB pathways were enhanced by PIN1 siRNA, but attenuated by PIN1 overexpression. Runx2 expressions were induced by PIN1 siRNA, but downregulated by PIN1 overexpression.
Conclusion
In summary, this study is the first to demonstrate that PIN1 is expressed in developing periodontal tissue, and in vitro PDLCs and cementoblasts. PIN1 inhibition stimulates osteoblast differentiation, and thus may play an important role in periodontal regeneration.
B-flavor tagging at Belle II Akopov, N.; Banerjee, Sw; Bauer, M. ...
The European physical journal. C, Particles and fields,
04/2022, Letnik:
82, Številka:
4
Journal Article
Recenzirano
Odprti dostop
We report on new flavor tagging algorithms developed to determine the quark-flavor content of bottom (
) mesons at Belle II. The algorithms provide essential inputs for measurements of quark-flavor ...mixing and charge-parity violation. We validate and evaluate the performance of the algorithms using hadronic
decays with flavor-specific final states reconstructed in a data set corresponding to an integrated luminosity of 62.8 fb
-
1
, collected at the
resonance with the Belle II detector at the SuperKEKB collider. We measure the total effective tagging efficiency to be
ε
eff
=
(
30.0
±
1.2
(
stat
)
±
0.4
(
syst
)
)
%
for a category-based algorithm and
ε
eff
=
(
28.8
±
1.2
(
stat
)
±
0.4
(
syst
)
)
%
for a deep-learning-based algorithm.
Retinal neuronal abnormalities occur before vascular changes in diabetic retinopathy. Accumulating experimental evidence suggests that neurons control vascular pathology in diabetic and other ...neovascular retinal diseases. Therefore, normalizing neuronal activity in diabetes may prevent vascular pathology. We investigated whether fibroblast growth factor 21 (FGF21) prevented retinal neuronal dysfunction in insulin-deficient diabetic mice. We found that in diabetic neural retina, photoreceptor rather than inner retinal function was most affected and administration of the long-acting FGF21 analog PF-05231023 restored the retinal neuronal functional deficits detected by electroretinography. PF-05231023 administration protected against diabetes-induced disorganization of photoreceptor segments seen in retinal cross section with immunohistochemistry and attenuated the reduction in the thickness of photoreceptor segments measured by optical coherence tomography. PF-05231023, independent of its downstream metabolic modulator adiponectin, reduced inflammatory marker interleukin-1β (IL-1β) mRNA levels. PF-05231023 activated the AKT-nuclear factor erythroid 2-related factor 2 pathway and reduced IL-1β expression in stressed photoreceptors. PF-05231023 administration did not change retinal expression of vascular endothelial growth factor A, suggesting a novel therapeutic approach for the prevention of early diabetic retinopathy by protecting photoreceptor function in diabetes.
The tightly structured neural retina has a unique vascular network comprised of three interconnected plexuses in the inner retina (and choroid for outer retina), which provide oxygen and nutrients to ...neurons to maintain normal function. Clinical and experimental evidence suggests that neuronal metabolic needs control both normal retinal vascular development and pathological aberrant vascular growth. Particularly, photoreceptors, with the highest density of mitochondria in the body, regulate retinal vascular development by modulating angiogenic and inflammatory factors. Photoreceptor metabolic dysfunction, oxidative stress, and inflammation may cause adaptive but ultimately pathological retinal vascular responses, leading to blindness. Here we focus on the factors involved in neurovascular interactions, which are potential therapeutic targets to decrease energy demand and/or to increase energy production for neovascular retinal disorders.
Detection of female premutation (PM) carriers of fragile X syndrome may be important in that a PM allele from the mother can expand to a full mutation (FM) when transmitted to the fetus. Although the ...PM carrier frequency might be different in varying populations, there is a little data on the Korean population. Furthermore, the risks of expansion to FM have not been studied in Korean PM carriers. In this retrospective study, we estimated the female PM carrier frequency and the risks of expansion to FM in Korean diagnostic samples collected for FMR1 gene testing. Of 10,241 pre‐conceptional or pregnant women, 13 PM 1 in 788; 95% confidence interval (CI), 1/1 250–1/455 and 75 intermediate allele carriers (1 in 137; 95% CI, 1/172–1/110) were identified. In 26 prenatal diagnoses cases, the PM allele was transmitted to the fetus in 13 pregnancies (50%), and five of these expanded to FM. All of the maternal alleles exceeding 70 repeats expanded to FM. In conclusion, the PM frequency in Korean diagnostic samples was lower than that reported in Western populations, while the risk for FM expansion in alleles exceeding 70 repeats might be higher than expected based upon previous reports.
We present the first measurements of the absolute branching fractions of Ξc+ decays into Ξ−π+π+ and pK−π+ final states. Our analysis is based on a data set of (772±11)×106 BB¯ pairs collected at the ...ϒ(4S) resonance with the Belle detector at the KEKB e+e− collider. We measure the absolute branching fraction of B¯0→Λ¯c−Ξc+ with the Ξc+ recoiling against Λ¯c− in B¯0 decays resulting in B(B¯0→Λ¯c−Ξc+)=1.16±0.42(stat.)±0.15(syst.)×10−3. We then measure the product branching fractions B(B¯0→Λ¯c−Ξc+)B(Ξc+→Ξ−π+π+) and B(B¯0→Λ¯c−Ξc+)B(Ξc+→pK−π+). Dividing these product branching fractions by B¯0→Λ¯c−Ξc+ yields B(Ξc+→Ξ−π+π+)=2.86±1.21(stat.)±0.38(syst.)% and B(Ξc+→pK−π+)=0.45±0.21(stat.)±0.07(syst.)%. Our result for B(Ξc+→Ξ−π+π+) can be combined with Ξc+ branching fractions measured relative to Ξc+→Ξ−π+π+ to set the absolute scale for many Ξc+ branching fractions.
Summary Background For all countries, information on pathogens causing healthcare-associated infections is important in order to develop proper strategies for preventing and treating nosocomial ...infections. Aim To assess the change in frequencies and antimicrobial resistance of pathogens causing device-associated infections (DAIs) in intensive care units (ICUs) in South Korea between July 2006 and June 2014. Methods Data from the Korean Nosocomial Infections Surveillance System (KONIS) were analysed, including three major DAI types in ICUs. Findings The frequency of Gram-negative bacteria gradually increased for central line-associated bloodstream infection (CLABSI) and ventilator-associated pneumonia (VAP) (from 24.6% to 32.6% and from 52.8% to 73.5%, respectively). By contrast, the frequency of Gram-positive bacteria decreased from 58.6% to 49.2% for CLABSI, and from 44.3% to 23.8% for VAP ( P < 0.001). Staphylococcus aureus was the most frequent causative pathogen in CLABSI throughout the surveillance period, but for VAP was replaced as the most frequent pathogen by Acinetobacter baumannii as of 2010. Candida albicans was the most frequent pathogen for catheter-associated urinary tract infection. The meticillin resistance rate in S. aureus decreased from 95% to 90.2% ( P < 0.001); amikacin resistance in Klebsiella pneumoniae and Escherichia coli decreased from 43.8% to 14.7% and from 15.0% to 1.8%, respectively ( P < 0.001); imipenem resistance in A. baumannii increased from 52.9% to 89.8% ( P < 0.001). Conclusion The proportion of Gram-negative bacteria as nosocomial pathogens for CLABSI and VAP has increased. The prevalence of A. baumannii causing DAIs in Korean ICUs has increased rapidly, as has the rate of carbapenem resistance in these bacteria.
The light‐sensitive photoreceptors in the retina are extremely metabolically demanding and have the highest density of mitochondria of any cell in the body. Both physiological and pathological ...retinal vascular growth and regression are controlled by photoreceptor energy demands. It is critical to understand the energy demands of photoreceptors and fuel sources supplying them to understand neurovascular diseases. Retinas are very rich in lipids, which are continuously recycled as lipid‐rich photoreceptor outer segments are shed and reformed and dietary intake of lipids modulates retinal lipid composition. Lipids (as well as glucose) are fuel substrates for photoreceptor mitochondria. Dyslipidemia contributes to the development and progression of retinal dysfunction in many eye diseases. Here, we review photoreceptor energy demands with a focus on lipid metabolism in retinal neurovascular disorders.
In the growing field of lipid metabolism in retinopathies, this review provides insights on the possible implication of lipid metabolism, energy demands and fuel source in the retina, but also systemic dyslipidemia on neovascular retinopathy.
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