Multifunctional two-dimensional perovskite based solar cells for photodetectors and resistive switching.

The escalating interest in low-dimensional perovskites stems from their tunable optoelectronic traits and robust stability. The pursuit of multifaceted optoelectronic devices holds substantial importance for energy-efficient and space-constrained systems. This investigation showcases the realization of multifunctional two-dimensional perovskite solar cells, incorporating transient light detection and resistive switching functions within a single device, achievable by facile external bias adjustments. Serving as a photodetector, the device exhibits commendable self-powered photodetection attributes, including an exceptionally low dark current density of 1 nA mm-2, a remarkable specific detectivity of 7.67 × 1012 Jones, a swift response time of 0.60 µs, and an expansive linear dynamic range of 72 dB. As a memristor, it showcases enduring performance across 4 × 102 cycles, a substantial on/off ratio of 106, and a rapid operation time of less than 1 µs. This endeavor unveils a pioneering avenue for advancing high-performance, air-stable multifunctional two-dimensional perovskite electronics.

Plant-Derived Molecule 4-Methylumbelliferone Suppresses FcεRI-Mediated Mast Cell Activation and Allergic Inflammation.

Mast cells (MCs) are an important treatment target for high-affinity IgE Fc receptor (FcεRI)-mediated allergic diseases. The plant-derived molecule 4-methylumbelliferone (4-MU) has beneficial effects in animal models of inflammation and autoimmunity diseases. The aim of this study was to examine 4-MU effects on MC activation and probe the underlying molecular mechanism(s). We sensitized rat basophilic leukemia cells (RBLs) and mouse bone marrow-derived mast cells (BMMCs) with anti-dinitrophenol (DNP) immunoglobulin (Ig)E antibodies, stimulated them with exposure to DNP-human serum albumin (HSA), and then treated stimulated cells with 4-MU. Signaling-protein expression was determined by immunoblotting. In vivo allergic responses were examined in IgE-mediated passive cutaneous anaphylaxis (PCA) and ovalbumin (OVA)-induced active systemic anaphylaxis (ASA) mouse models. 4-MU inhibited ß-hexosaminidase activity and histamine release dose-dependently in FcεRI-activated RBLs and BMMCs. Additionally, 4-MU reduced cytomorphological elongation and F-actin reorganization while down-regulating IgE/Ag-induced phosphorylation of SYK, NF-κB p65, ERK1/2, p38, and JNK. Moreover, 4-MU attenuated the PCA allergic reaction (i.e., less ear thickening and dye extravasation). Similarly, we found that 4-MU decreased body temperature, serum histamine, and IL4 secretion in OVA-challenged ASA model mice. In conclusion, 4-MU had a suppressing effect on MC activation both in vitro and in vivo and thus may represent a new strategy for treating IgE-mediated allergic conditions.

Chromosome-level assembly of Dermatophagoides farinae genome and transcriptome reveals two novel allergens Der f 37 and Der f 39.

Accurate house dust mite (HDM) genome and transcriptome data would promote our understanding of HDM allergens. We sought to assemble chromosome-level genome and precise transcriptome profiling of Dermatophagoides farinae and identify novel allergens. In this study, genetic material extracted from HDM bodies and eggs were sequenced. Short-reads from next generation sequencing (NGS) and long-reads from PacBio/Nanopore sequencing were used to construct the D. farinae nuclear genome, transcriptome, and mitochondrial genome. The candidate homologs were screened through aligning our assembled transcriptome data with amino acid sequences in the WHO/IUIS database. Our results showed that compared with the D. farinae draft genome, bacterial DNA content in the presently developed sequencing reads was dramatically reduced (from 22.9888% to 1.5585%), genome size was corrected (from 53.55 Mb to 58.77 Mb), and the contig N50 was increased (from 8.54 kb to 9365.49 kb). The assembled genome has 10 contigs with minimal microbial contamination, 33 canonical allergens and 2 novel allergens. Eight homologs (≥50% homology) were cloned; 2 bound HDM allergic-sera and were identified as allergens (Der f 37 and Der f 39). In conclusion, a chromosome-level genome, transcriptome and mitochondrial genome of D. farinae was generated to support allergen identification and development of diagnostics and immunotherapeutic vaccines.

FAK inhibitor PF-431396 suppresses IgE-mediated mast cell activation and allergic inflammation in mice.

Mast cells (MCs) initiate and maintain allergic inflammation. Upon being stimulated with immunoglobulin (Ig)E and antigen (Ag), MCs exhibit FcεRI (high-affinity IgE) receptor-mediated degranulation, cytokine secretion, and increased focal adhesion kinase (FAK) activity. The aims of this study were to examine mechanisms of FAK regulation in IgE-mediated MC activation and the effects of FAK inhibition on MC-mediated allergic responses. FAK activity was manipulated with short hairpin RNA (shRNA) knockdown, FAK overexpression, and the FAK inhibitor PF-431396 (PF). Gene expression and kinase activation were analyzed with quantitative molecular biology assays. PF effects were tested in the passive cutaneous anaphylaxis (PCA), active systemic anaphylaxis (ASA), and allergic conjunctivitis (AC) mouse models. Our results showed that FAK overexpression increased IgE-mediated degranulation and reduced the dexamethasone inhibitory effect on MCs activation. The FAK inhibitor PF diminished MC release of ß-hexosaminidase (ß-hex), histamine, and inflammatory cytokines, via a mechanism that involves MAPK and NF-κB signaling pathways. CaMKII was identified as a robust FAK-associating protein. Inhibition of CaMKII activation by KN-93 suppressed FAK activity and its downstream pathway. PF attenuated inflammatory responses in our PCA and ASA models, and relieved signs of allergic disease in AC model mice. In conclusions, MC degranulation and production of inflammatory mediators in allergic disease may be consequent to FcεRI crosslinking inducing CaMKII-mediated activation of FAK activity. FAK inhibition may represent a new MC-suppressing treatment strategy for the treatment of allergic diseases.

Inhibition of c-Fos expression attenuates IgE-mediated mast cell activation and allergic inflammation by counteracting an inhibitory AP1/Egr1/IL-4 axis.

BACKGROUND: Activator protein-1 (AP1), a c-Fos-JUN transcription factor complex, mediates many cytobiological processes. c-Fos has been implicated in immunoglobulin (Ig)E activation of mast cells (MCs) via high-affinity IgE Fc receptor (FcεRI) binding. This study examined c-Fos involvement in MC activation and tested the effects of the c-Fos/AP1 inhibitor T-5224 on MCs activation and allergic responses. METHODS: In vitro studies were conducted with two MC model systems: rat basophilic leukemia cells (RBLs) and mouse bone marrow derived mast cells (BMMCs). MC degranulation and effector functions were examined with ß-hexosaminidase release and cytokine secretion assays. c-Fos/AP1 was inhibited with T-5224. c-Fos activity was suppressed with short hairpin RNA targeting c-Fos (shFos). In vivo immune responses were evaluated in passive cutaneous anaphylaxis (PCA) and ovalbumin-induced active systemic anaphylaxis (ASA) models, as well as in an oxazolone (OXA)-induced model of atopic dermatitis, a common allergic disease. RESULTS: c-Fos expression was elevated transcriptionally and translationally in IgE-stimulated MCs. c-Fos binding of the Egr1 (early growth response 1) promoter upregulated Egr1 transcription, leading to production of interleukin (IL)4. T-5224 reduced FcεRI-mediated MC degranulation (evidenced by ß-hexosaminidase activity and histamine levels) and diminished EGR1 and IL4 expression. T-5224 attenuated IgE-mediated allergic responses in PCA and ASA models, and it suppressed MC-mediated atopic dermatitis in mice. CONCLUSION: IgE binding can activate MCs via a c-Fos/Egr1/IL-4 axis. T-5224 suppresses MC activation in vitro and in vivo and thus represents a promising potential strategy for targeting MC activation to treat allergic diseases.

Ribonuclease T2 from Aspergillus fumigatus promotes T helper type 2 responses through M2 polarization of macrophages.

Allergic bronchopulmonary aspergillosis (ABPA) is an allergic immunological response to Aspergillus fumigatus (Af) exposure, which induces a strong T helper 2 (Th2) response via mechanisms that have yet to be elucidated. The aim of the present study was to investigate the hypothesis that T2 ribonuclease from Af (Af RNASET2) induces M2­type macrophage polarization to produce a T helper 2 (Th2) immune response. Recombinant Af RNASET2 (rAf RNASET2) was expressed and purified in a prokaryotic pET system and BALB/c mice were immunized with rAf RNASET2 for in vivo analyses. Expression levels of M2 polarization factors were evaluated in RAW264.7 macrophages treated with rAf RNASET2 in vitro using flow cytometry, reverse transcription­quantitative PCR, and western blot analysis. The results predicted that the mature Af RNASET2 protein (382 amino acids; GenBank no. MN593022) contained two conserved amino acid sequence (CAS) domains, termed CAS­1 and CAS­2, which are also characteristic of the RNASET2 family proteins. The protein expression levels of the Th2­related cytokines interleukin (IL)­4, IL­10, and IL­13 were upregulated in mice immunized with rAf RNASET2. RAW264.7 macrophages treated with rAf RNASET2 showed increased mRNA expression levels of M2 factors [arginase 1, Il­10, and Il­13]; however, there was no difference in cells treated with rAf RNASET2 that had been inactivated with a ribonuclease inhibitor (RNasin). The protein expression levels of IL­10 in macrophage culture supernatant were also increased following stimulation with rAf RNASET2. In addition, rAf RNASET2 upregulated the expression of phosphorylated mitogen activated protein kinases (MAPKs) in RAW264.7 cells, whereas MAPK inhibitors attenuated rAf RNASET2­induced IL­10 expression in RAW264.7 cells. In conclusion, the present study reveals that high rAf RNASET2 activity is required for rAf RNASET2­induced M2 polarization of macrophages and suggests an important immune regulatory role for Af RNASET2 in ABPA pathogenesis.

The antipsychotic drug pimozide inhibits IgE-mediated mast cell degranulation and migration.

BACKGROUND: Mast cells (MCs) mediate a key role in allergic diseases. Detailed studies of how the neuroleptic drug pimozide affects MC activity are lacking. The aim of this study was to investigate pimozide inhibition of immunoglobulin E (IgE)-mediated MC activation and MC-mediated allergic responses. METHOD: MCs were stimulated with anti-dinitrophenyl (DNP) IgE antibodies and DNP-horse serum albumin (HSA) antigen (Ag), and anti-allergic pimozide effects were detected by measuring ß-hexosaminidase levels. Morphological changes were observed histologically. In vivo pimozide effects were assessed in passive cutaneous anaphylaxis (PCA) and ovalbumin (OVA)-sensitized active systemic anaphylaxis mouse (ASA) model experiments. Levels of phosphorylated (p-) SYK (spleen tyrosine kinase) and MAPKs (mitogen-activated protein kinases) were detected in western blots. RESULTS: We found that pimozide inhibited MC degranulation, reduced MC release of ß-hexosaminidase dose-dependently in activated RBL-2H3 (IC50: 13.52 µM) and bone marrow derived MC (BMMC) (IC50: 42.42 µM), and reduced MC morphological changes. The IgE/Ag-induced migration effect was suppressed by pimozide treatment dose-dependently. Pimozide down-regulated IgE/Ag-induced phosphorylation of SYK and MAPKs in activated MCs. Moreover, pimozide attenuated allergic reactions in PCA and ASA model mice, and decreased MC populations among splenic cells. CONCLUSIONS: The antipsychotic drug pimozide can suppress IgE-mediated MC activation in vitro and in vivo and should be considered for repurposing to suppress MC-mediated diseases.

Identification of Der f 23 as a new major allergen of Dermatophagoides farinae.

House dust mites (HDM) are common allergen sources worldwide. At present, 32 of the 37 internationally recognized HDM allergen groups have been identified in Dermatophagoides farinae. The present study study describes the identification of the first known D. farinae Group 23 allergen (Der f 23). Recombinant Der f 23 protein (rDer f 23) was cloned, expressed and purified. The open reading frame of rDer f 23 was 525 base pairs and encoded a 174­amino acid protein (GenBank accession no., KU166910.1). ELISAs indicated that 72/129 HDM allergic serum samples (55.8%) had specific immunoglobulin E (sIgE) binding activity to rDer f 23. Additionally, 3/10 patients with HDM allergies (30%) exhibited positive skin prick test reactions to rDer f 23. IgE western blot analysis data suggested that only 4/11 HDM allergic sera had a positive sIgE binding result. Sequence homology analysis revealed an extra P2 region (Ser56­Thr117) in Der f 23 that was not present in the D. pteronyssinus homolog, which may affect sIgE binding. Der f 23ΔP2 demonstrated binding with HDM allergic sera, whereas the P2 peptide alone did not. The sIgE binding ability of Der f 23 ΔP2 (Der f 23 with a truncated P2 region) was more marked compared with that of Der f 23 in an IgE ELISA. These data indicate that P2 region in Der f 23 attenuates IgE binding ability. In conclusion, the results of the present study indicate that Der f 23 is a major HDM allergen with predominantly conformational sIgE binding epitopes. The allergenic identification of Der f 23 and its inclusion in World Health Organization/International Union of Immunological Societies database contributes to the theoretical basis underlying the diagnosis and treatment of HDM allergic diseases.

SMG-1 inhibition by miR-192/-215 causes epithelial-mesenchymal transition in gastric carcinogenesis via activation of Wnt signaling.

SMG-1,a member of the phosphoinositide kinase-like kinase family, functioned as a tumor suppressor gene. However, the role of SMG-1 in GC remain uncharacterized. In this study, regulation of SMG-1 by miR-192 and-215, along with the biological effects of this modulation, were studied in GC. We used gene microarrays to screening and luciferase reporter assays were to verify the potential targets of miR-192 and-215. Tissue microarrays analyses were applied to measure the levels of SMG-1 in GC tissues. Western blot assays were used to assess the signaling pathway of SMG-1 regulated by miR-192 and-215 in GC. SMG-1 was significantly downregulated in GC tissues.The proliferative and invasive properties of GC cells were decreased by inhibition of miR-192 and-215, whereas an SMG-1siRNA rescued the inhibitory effects. Finally, SMG-1 inhibition by miR-192 and-215 primed Wnt signaling and induced EMT. Wnt signaling pathway proteins were decreased markedly by inhibitors of miR-192 and-215, while SMG-1 siRNA reversed the inhibition apparently. Meanwhile, miR-192 and-215 inhitibtors increased E-cadherin expression and decreased N-cadherin and cotransfection of SMG-1 siRNA reversed these effects. In summary, these findings illustrate that SMG-1 is suppressed by miR-192 and-215 and functions as a tumor suppressor in GC by inactivating Wnt signaling and suppressing EMT.

Piezotronic effect tuned AlGaN/GaN high electron mobility transistor.

The piezotronic effect utilizes strain-induced piezoelectric polarization charges to tune the carrier transportation across the interface/junction. We fabricated a high-performance AlGaN/GaN high electron mobility transistor (HEMT), and the transport property was proven to be enhanced by applying an external stress for the first time. The enhanced source-drain current was also observed at any gate voltage and the maximum enhancement of the saturation current was up to 21% with 15 N applied stress (0.18 GPa at center) at -1 V gate voltage. The physical mechanism of HEMT with/without external compressive stress conditions was carefully illustrated and further confirmed by a self-consistent solution of the Schrödinger-Poisson equations. This study proves the cause-and-effect relationship between the piezoelectric polarization effect and 2D electron gas formation, which provides a tunable solution to enhance the device performance. The strain tuned HEMT has potential applications in human-machine interface and the security control of the power system.

Functional properties of peripheral CD8+ T cells in patients with repeated implantation failure.

CD8+ T cells are the main candidates to recognize and respond to fetal HLA-C at the fetal-maternal interface, but data on the amount of peripheral CD8+ T cells and their functions during the window of implantation in recurrent implantation failure (RIF) patients are limited. Peripheral blood was obtained from 56 women with RIF and 16 fertile women in the mid-luteal phase of the menstrual cycle, and the CD8+ T cells were determined by FACS analysis. No statistical differences in the proportion of peripheral CD8+ T cells were observed among the women with RIF and the control group. However, the levels of IFN-γ+ and TNF-α+ CD8+ T cells in the RIF group were significantly higher than those in the control group. The cytolytic activity and regulatory proportion of CD8+ T cells in RIF were similar to that in the control group. Our data indicated that the elevated expression levels of IFN-γ and TNF-α in peripheral CD8+ T cells may contribute to an impaired immune tolerance in women with RIF.

MiRNA-194 activates the Wnt/ß-catenin signaling pathway in gastric cancer by targeting the negative Wnt regulator, SUFU.

Emerging evidence has shown that miRNA-194 is aberrantly upregulated in gastric cancer (GC); however, the biological mechanisms underlying its involvement are largely unknown. Wnt/ß-catenin signaling has been implicated in gastric tumorigenesis; we therefore hypothesized that miRNA-194 promotes gastric carcinogenesis by activating Wnt/ß-catenin signaling. MiRNA-194 was found to be overexpressed in GC cell lines and 43 paired GC tissues. Overexpression of miRNA-194 promoted cell proliferation and migration, while inhibition of miRNA-194 blocked these processes. Inhibition of miRNA-194 decreased tumor volumes in nude mice. Furthermore, miRNA-194 inhibitors promoted cytoplasmic localization of ß-catenin, leading to repression of Wnt signaling. We also discovered that SUFU, a known negative regulator of Hedgehog and Wnt signaling, was a target of miRNA-194. Anti-SUFU siRNAs rescued the inhibitory effects of miRNA-194 antagonists on cell proliferation and migration and on colony formation. We also found that SUFU expression was downregulated in GC tissues and cell lines and negatively correlated with miRNA-194 expression in primary GC tissues. Moreover, SUFU expression was negatively correlated with tumor stage, supporting its potential as a diagnostic or prognostic marker in GC. Taken together, these findings suggest that miRNA-194 is oncogenic and promotes GC cell proliferation and migration by activating Wnt signaling, at least in part, via suppression of SUFU.

Tuning carrier lifetime in InGaN/GaN LEDs via strain compensation for high-speed visible light communication.

In recent years, visible light communication (VLC) technology has attracted intensive attention due to its huge potential in superior processing ability and fast data transmission. The transmission rate relies on the modulation bandwidth, which is predominantly determined by the minority-carrier lifetime in III-group nitride semiconductors. In this paper, the carrier dynamic process under a stress field was studied for the first time, and the carrier recombination lifetime was calculated within the framework of quantum perturbation theory. Owing to the intrinsic strain due to the lattice mismatch between InGaN and GaN, the wave functions for the holes and electrons are misaligned in an InGaN/GaN device. By applying an external strain that "cancels" the internal strain, the overlap between the wave functions can be maximized so that the lifetime of the carrier is greatly reduced. As a result, the maximum speed of a single chip was increased from 54 MHz up to 117 MHz in a blue LED chip under 0.14% compressive strain. Finally, a bandwidth contour plot depending on the stress and operating wavelength was calculated to guide VLC chip design and stress optimization.

Freestanding Flag-Type Triboelectric Nanogenerator for Harvesting High-Altitude Wind Energy from Arbitrary Directions.

Wind energy at a high altitude is far more stable and stronger than that near the ground, but it is out of reach of the wind turbine. Herein, we develop an innovative freestanding woven triboelectric nanogenerator flag (WTENG-flag) that can harvest high-altitude wind energy from arbitrary directions. The wind-driven fluttering of the woven unit leads to the current generation by a coupled effect of contact electrification and electrostatic induction. Systematic study is conducted to optimize the structure/material parameters of the WTENG-flag to improve the power output. This 2D WTENG-flag can also be stacked in parallel connections in many layers for a linearly increased output. Finally, a self-powered high-altitude platform with temperature/humidity sensing/telecommunicating capability is demonstrated with the WTENG-flag as a power source. Due to the light weight, low cost, and easy scale-up, this WTENG-flag has great potential for applications in weather/environmental sensing/monitoring systems.

Wearable Self-Charging Power Textile Based on Flexible Yarn Supercapacitors and Fabric Nanogenerators.

A novel and scalable self-charging power textile is realized by combining yarn supercapacitors and fabric triboelectric nanogenerators as energy-harvesting devices.

Integrated miRNA profiling and bioinformatics analyses reveal potential causative miRNAs in gastric adenocarcinoma.

Gastric cancer (GC) is one of the leading causes of cancer-related deaths throughout China and worldwide. The discovery of microRNAs (miRNAs) has provided a new opportunity for developing diagnostic biomarkers and effective therapeutic targets in GC. By performing microarray analyses of benign and malignant gastric epithelial cell lines (HFE145, NCI-N87, MKN28, RF1, KATO III and RF48), 16 significantly dysregulated miRNAs were found. 11 of these were validated by real-time qRT-PCR. Based on miRWalk online database scans, 703 potential mRNA targets of the 16 miRNAs were identified. Bioinformatic analyses suggested that these dysregulated miRNAs and their predicted targets were principally involved in tumor pathogenesis, MAPK signaling, and apoptosis. Finally, miRNA-gene network analyses identified miRNA-125b as a crucial miRNA in GC development. Taken together, these results develop a comprehensive expression and functional profile of differentially expressed miRNAs related to gastric oncogenesis. This profile may serve as a potential tool for biomarker and therapeutic target identification in GC patients.

Piezo-Phototronic Effect Controlled Dual-Channel Visible light Communication (PVLC) Using InGaN/GaN Multiquantum Well Nanopillars.

Visible light communication (VLC) simultaneously provides illumination and communication via light emitting diodes (LEDs). Keeping a low bit error rate is essential to communication quality, and holding a stable brightness level is pivotal for illumination function. For the first time, a piezo-phototronic effect controlled visible light communication (PVLC) system based on InGaN/GaN multiquantum wells nanopillars is demonstrated, in which the information is coded by mechanical straining. This approach of force coding is also instrumental to avoid LED blinks, which has less impact on illumination and is much safer to eyes than electrical on/off VLC. The two-channel transmission mode of the system here shows great superiority in error self-validation and error self-elimination in comparison to VLC. This two-channel PVLC system provides a suitable way to carry out noncontact, reliable communication under complex circumstances.

Piezotronic Effect in Polarity-Controlled GaN Nanowires.

Using high-quality and polarity-controlled GaN nanowires (NWs), we studied the piezotronic effect in crystal orientation defined wurtzite structures. By applying a normal compressive force on c-plane GaN NWs with an atomic force microscopy tip, the Schottky barrier between the Pt tip and GaN can be effectively tuned by the piezotronic effect. In contrast, the normal compressive force cannot change the electron transport characteristics in m-plane GaN NWs whose piezoelectric polarization axis is turned in the transverse direction. This observation provided solid evidence for clarifying the difference between the piezotronic effect and the piezoresistive effect. We further demonstrated a high sensitivity of the m-plane GaN piezotronic transistor to collect the transverse force. The integration of c-plane GaN and m-plane GaN indicates an overall response to an external force in any direction.

Use of Ferritin Expression, Regulated by Neural Cell-Specific Promoters in Human Adipose Tissue-Derived Mesenchymal Stem Cells, to Monitor Differentiation with Magnetic Resonance Imaging In Vitro.

The purpose of this study was to establish a method for monitoring the neural differentiation of stem cells using ferritin transgene expression, under the control of a neural-differentiation-inducible promoter, and magnetic resonance imaging (MRI). Human adipose tissue-derived mesenchymal stem cells (hADMSCs) were transduced with a lentivirus containing the human ferritin heavy chain 1 (FTH1) gene coupled to one of three neural cell-specific promoters: human synapsin 1 promoter (SYN1p, for neurons), human glial fibrillary acidic protein promoter (GFAPp, for astrocytes), and human myelin basic protein promoter (MBPp, for oligodendrocytes). Three groups of neural-differentiation-inducible ferritin-expressing (NDIFE) hADMSCs were established: SYN1p-FTH1, GFAPp-FTH1, and MBPp-FTH1. The proliferation rate of the NDIFE hADMSCs was evaluated using a Cell Counting Kit-8 assay. Ferritin expression was assessed with western blotting and immunofluorescent staining before and after the induction of differentiation in NDIFE hADMSCs. The intracellular iron content was measured with Prussian blue iron staining and inductively coupled plasma mass spectrometry. R2 relaxation rates were measured with MRI in vitro. The proliferation rates of control and NDIFE hADMSCs did not differ significantly (P > 0.05). SYN1p-FTH1, GFAPp-FTH1, and MBPp-FTH1 hADMSCs expressed specific markers of neurons, astrocytes, and oligodendrocytes, respectively, after neural differentiation. Neural differentiation increased ferritin expression twofold, the intracellular iron content threefold, and the R2 relaxation rate two- to threefold in NDIFE hADMSCs, resulting in notable hypointensity in T2-weighted images (P < 0.05). These results were cross-validated. Thus, a link between neural differentiation and MRI signals (R2 relaxation rate) was established in hADMSCs. The use of MRI and neural-differentiation-inducible ferritin expression is a viable method for monitoring the neural differentiation of hADMSCs.