Background
The aim of this study was to investigate the prevalence of epidemiologic and physician‐diagnosed pollen‐induced AR (PiAR) in the grasslands of northern China and to study the impact of the ...intensity and time of pollen exposure on PiAR prevalence.
Methods
A multistage, clustered and proportionately stratified random sampling with a field interviewer‐administered survey study was performed together with skin prick tests (SPT) and measurements of the daily pollen count.
Results
A total of 6043 subjects completed the study, with a proportion of 32.4% epidemiologic AR and 18.5% PiAR. The prevalence was higher in males than females (19.6% vs 17.4%, P = .024), but no difference between the two major residential and ethnic groups (Han and Mongolian) was observed. Subjects from urban areas showed higher prevalence of PiAR than rural areas (23.1% vs 14.0%, P < .001). Most PiAR patients were sensitized to two or more pollens (79.4%) with artemisia, chenopodium, and humulus scandens being the most common pollen types, which were similarly found as the top three sensitizing pollen allergens by SPT. There were significant regional differences in the prevalence of epidemiologic AR (from 18.6% to 52.9%) and PiAR (from 10.5% to 31.4%) among the six areas investigated. PiAR symptoms were positively associated with pollen counts, temperature, and precipitation (P < .05), but negatively with wind speed and pressure P < .05).
Conclusion
Pollen‐induced AR (PiAR) prevalence in the investigated region is extremely high due to high seasonal pollen exposure, which was influenced by local environmental and climate conditions.
Due to the poor self-regeneration of brain tissue, stem cell transplantation therapy is purported to enable the replacement of lost neurons after traumatic brain injury (TBI). The main challenge of ...brain regeneration is whether the transplanted cells can survive and carry out neuronal functions in the lesion area. The brain is a complex neuronal network consisting of various types of cells that significantly influence on each other, and the survival of the implanted stem cells in brain is critically influenced by the surrounding cells. Although stem cell-based therapy is developing rapidly, most previous studies just focus on apply single type of stem cells as cell source. Here, we found that co-culturing human umbilical cord mesenchymal stem cells (hUC-MSCs) directly with the activated astrocytes benefited to the proliferation and neuron differentiation of hUC-MSCs in vitro. In this study, hUC-MSCs and the activated astrocytes were seeded in RADA16-BDNF peptide scaffold (R-B-SPH scaffold), a specifical self-assembling peptide hydrogel, in which the environment promoted the differentiation of typical neuron-like cells with neurites extending in three-dimensional directions. Moreover, the results showed co-culture of hUC-MSCs and activated astrocytes promoted more BDNF secretion which may benefit to both neural differentiation of ectogenic hUC-MSCs and endogenic neurogenesis. In order to promote migration of the transplanted hUC-MSCs to the host brain, the hUC-MSCs were forced with CXC chemokine receptor 4 (CXCR4). We found that the moderate-sized lesion cavity, but not the large cavity caused by TBI was repaired via the transplantation of hUC-MSCs
and activated astrocytes embedded in R-B-SPH scaffolds. The functional neural repair for TBI demonstrated in this study is mainly due to the transplantation system of double cells, hUC-MSCs and activated astrocytes. We believe that this novel cell transplantation system offers a promising treatment option for cell replacement therapy for TBI.
In this reach, we specifically linked RGIDKRHWNSQ, a functional peptide derived from BDNF, to the C-terminal of RADARADARADARADA (RADA16) to structure a functional self-assembling peptide hydrogel scaffold, RADA16-BDNF (R-B-SPH scaffold) for the better transplantation of the double cell unit. Also, the novel scaffold was used as cell-carrier for transplantation double cell unit (hUC-MSCs/astrocyte) for treating traumatic brain injury. The results of this study showing that R-B-SPH scaffold was pliancy and flexibility to fit the brain lesion cavity and promotes the outgrowth of axons and dendrites of the neurons derived from hUC-MSCs in vitro and in vivo, indicating the 3D R-B-SPH scaffold provided a suitable microenvironment for hUC-MSC survival, proliferation and differentiation. Also, our results showing the double-cells transplantation system (hUC-MSCs/astrocyte) may be a novel cell-based therapeutic strategy for neuroregeneration after TBI with potential value for clinical application.
Background
Metastasis-related in colon cancer 1 (MACC1) is highly expressed in a variety of solid tumours, but its role in pancreatic cancer (PC) remains unknown. Interferon gamma (IFN-γ) affecting ...MACC1 expression was explored as the potential mechanism following its intervention.
Methods
Expressions of MACC1 treated with IFN-γ gradient were confirmed by quantitative real-time PCR (qRT-PCR) and western blot (WB). Proliferation, migration, and invasion abilities of PC cells treated with IFN-γ were analysed by CCK8, EDU, colony formation, Transwell (with or without matrix gel) and wound-healing assays. Expression of antisense long non-coding RNA of MACC1, MACC1-AS1, and proteins of AKT/mTOR pathway, (pho-)AKT, and (pho-)mTOR was also assessed by qRT-PCR and WB. SiRNA kit and lentiviral fluid were conducted for transient expression of MACC1 and stable expression of MACC1-AS1, respectively. Rescue assays of cells overexpressing MACC1-AS1 and of cells silencing MACC1 were performed and cellular properties and proteins were assessed by the above-mentioned assays as well.
Results
IFN-γ inhibited MACC1 expression in a time- and dose-dependent manner; 100 ng/mL IFN-γ generally caused downregulation of most significant (
p
≤ 0.05). In vitro experiments revealed that IFN-γ decreased cellular proliferation, migration, and invasion abilities and downregulated the expression of pho-AKT and pho-mTOR (
p
≤ 0.05). Conversely, overexpression of MACC1-AS1 upregulated pho-AKT and pho-mTOR proteins, and reversed cellular properties (
p
≤ 0.05). Rescue assays alleviated the above changes of pho-AKT/ mTOR and cellular properties.
Conclusion
IFN-γ affected PC properties by MACC1-AS1/MACC1 axis via AKT/mTOR signaling pathway, which provides novel insight for candidate targets for treating PC.
Summary
Background
CD8+ T cells are important effectors of cell‐mediated immunity; however, their contribution to the pathogenesis of CRS is unclear.
Objective
This study aimed to characterize the ...cytokine‐producing features and cytotoxic activity of CD8+ T cells, and their correlation with inflammation patterns in CRS with nasal polyps.
Methods
The expression of IFN‐γ, IL‐4, IL‐5, IL‐17A, forkhead box P3 (FOXP3), perforin, and granzyme B in CD8+ T cells was studied by means of flow cytometry, immunohistochemistry, and immunofluorescence. The expression of CD8+ T‐cell subset relevant chemokines and chemokine receptors was detected by means of real‐time RT‐PCR or ELISA. The cytotoxic activity of sorted CD8+ T cells was defined by anti‐CD3‐redirected killing assay.
Results
Compared with controls, elevated percentages of total CD8+ T cells and cytotoxic T lymphocyte (Tc) 1 (IFN‐γ+), Tc2 (IL‐4+), and Tc17 (IL‐17A+) cell subset, and decreased percentages of FOXP3+CD8+ regulatory T cells, were found in both eosinophilic and non‐eosinophilic polyps with a Tc2‐skewed and Tc1/Tc17‐dominated response in eosinophilic and non‐eosinophilic polyps, respectively. Nasal CD8+ T cells were found to produce similar or even higher levels of IFN‐γ and IL‐4 compared with CD4+ T cells. Tc1 and Tc17, and Tc2 (IL‐4+ and IL‐5+) cell subset percentages positively correlated with neutrophil and eosinophil counts in sinonasal mucosa, respectively. Strikingly, the expression of perforin and granzyme B and cytotoxic activity were significantly reduced in nasal CD8+ T cells compared with their counterparts in peripheral blood. The expression of CXCL16, CCL17, and CCL20 positively correlated with Tc1, Tc2, and Tc17 cell subset number in sinonasal mucosa, respectively.
Conclusion and Clinical Relevance
CD8+ T cells have low cytotoxic activity; nevertheless, they are a significant and previously underappreciated source of inflammatory cytokine production in polyps. Different Tc cell subset domination may contribute to distinctly biased granulocyte inflammation in eosinophilic and non‐eosinophilic polyps.
•Hollow SnO2/α-Fe2O3 core–shell nanofibers were synthesized by electrospun and hydrothermal.•Glacial acetic acid could adjust the nucleation site and density of α-FeOOH nanorods on SnO2.•SnO2/α-Fe2O3 ...nanofibers exhibited better gas sensing performance than α-Fe2O3 and SnO2 fibers.
One dimensional hierarchically hollow SnO2/α-Fe2O3 core–shell nanofibers were synthesized by using electrospun SnO2 hollow nanofibers as core followed by the hydrothermal growth and calcination of α-FeOOH nanorods on the outer surface of SnO2 nanofibers. The control experiments indicated that glacial acetic acid introduced in the hydrothermal solution could adjust the nucleation site and density of α-FeOOH nanorods as well as prevent the formation of urchin-like α-FeOOH byproduct. The growth process of α-FeOOH nanorods on SnO2 hollow nanofibers was also investigated. The hierarchical SnO2/α-Fe2O3 hollow nanofibers were then fabricated as gas sensors for the investigation of gas sensing applications. By comparison of sensing properties, the response values of the sensors fabricated with hierarchical SnO2/α-Fe2O3 core–shell nanofibers toward 100ppm acetone and ethanol could reach to be 30.363 and 20.370, respectively, exhibiting much better performance than those using urchin-like α-Fe2O3 nanostructures and pure SnO2 nanofibers. Meanwhile, the sensors based on hierarchical SnO2/α-Fe2O3 nanofibers also had shorter response and recovery times than those of α-Fe2O3 nanostructures. The synergetic effect of the composite of α-Fe2O3 and SnO2 together with unique hollow core–shell architectures are main contribution for the enhanced gas sensing properties.
Macro-autophagy is associated with drug resistance in various cancers and can function as an adaptive response to maintain cell survival under metabolic stresses, including androgen deprivation. ...Androgen deprivation or treatment with androgen receptor (AR) signaling inhibitor (ARSI), Enzalutamide (MDV-3100, ENZA) or bicalutamide induced autophagy in androgen-dependent and in castration-resistant CaP (castration-resistant prostate cancer (CRPC)) cell lines. The autophagic cascade triggered by AR blockage, correlated with the increased light chain 3-II/I ratio and ATG-5 expression. Autophagy was observed in a subpopulation of C4-2B cells that developed insensitivity to ENZA after sustained exposure in culture. Using flow cytometry and clonogenic assays, we showed that inhibiting autophagy with clomipramine (CMI), chloroquine or metformin increased apoptosis and significantly impaired cell viability. This autophagic process was mediated by AMP-dependent protein kinase (AMPK) activation and the suppression of mammalian target of rapamycin (mTOR) through Raptor phosphorylation (Serine 792). Furthermore, small interfering RNA targeting AMPK significantly inhibited autophagy and promoted cell death in CaP cells acutely or chronically exposed to ENZA or androgen deprivation, suggesting that autophagy is an important survival mechanism in CRPC. Lastly, in vivo studies with mice orthotopically implanted with ENZA-resistant cells demonstrated that the combination of ENZA and autophagy modulators, CMI or metformin significantly reduced tumor growth when compared with control groups (P<0.005). In conclusion, autophagy is as an important mechanism of resistance to ARSI in CRPC. Antiandrogen-induced autophagy is mediated through the activation of AMPK pathway and the suppression of mTOR pathway. Blocking autophagy pharmacologically or genetically significantly impairs prostate cancer cell survival in vitro and in vivo, implying the therapeutics potential of autophagy inhibitors in the antiandrogen-resistance setting.
Using 6.32 fb–1 of electron-positron collision data recorded by the BESIII detector at center-of-mass energies between 4.178 and 4.226 GeV, we present the first search for the decay $D^{+}_{s}$ → ...a0(980)0e+νe, a0(980)0 → π0η, which could proceed via a0(980) – f0(980) mixing. No significant signal is observed. An upper limit of 1.2 × 10–4 at the 90% confidence level is set on the product of the branching fractions of $D^{+}_{s}$ → a0(980)0e+νe and a0(980)0 → π0η decays.
A
bstract
Using (27
.
12 ± 0
.
14) × 10
8
ψ
(3686) events collected by the BESIII detector at the center-of-mass energy of
s
= 3
.
686 GeV, we search for the first time for two nonleptonic hyperon ...decays that change strangeness by two units, Ω
−
→ Σ
0
π
−
and Ω
−
→
nK
−
. No significant signal is observed. The upper limits on their decay branching fractions are determined to be
B
(Ω
−
→ Σ
0
π
−
)
<
5
.
4 × 10
−
4
and
B
(Ω
−
→
nK
−
)
<
2
.
4 × 10
−
4
at the 90% confidence level.
The decays ψ2(3823 ) → γχc0,1,2, π+π− J/ψ, π0π0J/ψ , ηJ/ψ, and π0J/ψ are searched for using the reaction e+e− → π+π− ψ2 (3823) in a 19 fb−1 data sample collected at center-of-mass energies between ...4.1 and 4.7 GeV with the BESIII detector. The process ψ2(3823) → γχc1 is observed in a 9 fb−1 data sample in the center-of-mass energy range 4.3–4.7 GeV, which confirms a previous observation but with a higher significance of 11.8 σ , and evidence for ψ2(3823) → γχc2 is found with a significance of 3.2 σ for the first time. The branching-fraction ratio ... is determined. No significant ψ2 (3823) signals are observed for any of the other decay channels. Upper limits of branching-fraction ratios for ψ2(3823 ) → π+π− J/ψ , π0π0 J/ψ, ηJ/ψ , π0 J/ψ, γ χc0 relative to ψ2 (3823) → γχc1 are reported. The process e+e− → π0π0ψ2 (3823) is also searched for, and we find evidence for the process with a significance of 4.3 σ . The average cross-section ratio σ (e+e− → π0π0ψ2 (3823)) σ (e+e− → π+π− ψ2 (3823)) is also determined. (ProQuest: ... denotes formula omited.).
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