Electroreductive Ring-Opening Carboxylation of 1,3-Oxazolidin-2-ones with CO2 for Accessing ß-Amino Acids.

Electrocarboxylation of the C(sp3)-O bond in 1,3-oxazolidin-2-ones with CO2 to achieve ß-amino acids is developed. The C-O bond in substrates can be selectively cleaved via the single electron transfer on the surface of a cathode or through a CO2• - intermediate under additive-free conditions. A great diversity of ß-amino acids can be obtained in a moderate to excellent yield and readily converted to various biologically active compounds.

The stigma of patients with chronic insomnia: a clinical study.

BACKGROUND: The objective of this study was to explore the stigma and related influencing factors in individuals with chronic insomnia disorder (CID). METHODS: A total of 70 CID patients and 70 healthy controls (CON) were enrolled in the study. All subjects completed the assessments of sleep, emotion, and cognition. Their stigma and life quality were measured using the Chronic Stigma Scale and the 36-Item Short-Form Health Survey (SF-36). RESULTS: The ratio of individuals with stigma was significantly different between CID and CON groups (C2 = 35.6, p < 0.001). Compared with the CON group, the CID group had higher scores for total stigma (U = 662.0, p < 0.001), internalized stigma (U = 593.0, p < 0.001), enacted stigma (U = 1568.0, p < 0.001), PSQI (U = 2485.0, p < 0.001) and HAMD-17 (U = 69.5, p < 0.001) as well as lower scores for MoCA-C (U = 3997.5, p < 0.001) and most items of SF-36. Partial correlation analysis showed that different items of the Chronic Stigma Scale were positively correlated with illness duration, PSQI and HAMD-17 scores, while negatively correlated with one or more items of the SF-36. Multivariate regression analysis showed that illness duration and the Mental Health domain of the SF-36 were independent risk factors for one or more items of stigma in CID patients. CONCLUSION: Patients with CID have an increased risk of stigma. Moreover, illness duration and Mental Health may be primary factors related to stigma.

Decreased Serum Exosomal miR-152-3p Contributes to the Progression of Acute Ischemic Stroke.

BACKGROUND: The current study aims to investigate the expression and potential role of exosome-derived miR-152-3p in acute ischemic stroke (AIS) patients. METHODS: Exosomes were isolated from AIS patients and healthy controls. The level of exosome miR-152-3p was examined using RT-PCR. Receiver operating characteristic (ROC) curves were used to assess exosome miR-152-3p as a biomarker, and the area under the curve (AUC) was reported. RESULTS: Our data showed that the expression of serum exosome miR-152-3p in patients with AIS was significantly lower than in healthy controls. In contrast to those with NIHSS score < 7, the level of exosome miR-152-3p was significantly reduced in AIS patients with NIHSS score ≥ 7, indicating that the decrease of exosome miR-152-3p level is significantly related to the severity of endothelial injury. Moreover, the lowest level of exosome miR-152-3p was found in large-artery atherosclerosis (LAA) patients compared to that in small-vessel occlusion (SAA), cardioembolism (CE) and stroke of undetermined etiology (SUE) group. In addition, exosome miR-152-3p level was significantly lower in acute phase than in chronic phase. ROC curve showed that the AUC of exosome miR-152-3p level was 0.935, which indicated that exosome miR-152-3p level could distinguish AIS patients from non-healthy controls. CONCLUSIONS: In summary, exosome miR-152-3p is a risk factor of cerebral infarction. Enhancing the expression of exosome miR-152-3p in the circulating system may be a promising strategy for the prevention and treatment of AIS.

Downregulation of miR-205 in migrating epithelial tongue facilitates skin wound re-epithelialization by derepressing ITGA5.

Keratinocyte migration is essential for re-epithelialization during skin wound healing, but the molecular mechanisms regulating this cellular response remain to be completely clarified. Here we show that keratinocyte-specific miR-205 is significantly downregulated in the leading edge of the migrating epithelial tongue after skin injury in mice. In HaCaT keratinocytes, miR-205 could be downregulated by TGF-ß1 stimulation. And similar to the effect of TGF-ß1, miR-205 knockdown could promote keratinocyte migration in wound scratch model in vitro. Furthermore, topical inhibition of miR-205 by administrating Pluronic gel containing antagomir-205 could accelerate re-epithelialization in mouse skin wound model in vivo. Moreover, we identified integrin alpha 5 (ITGA5) as one key functional miR-205 target in the re-epithelialization process and epidermal downregulation of miR-205 may desilence ITGA5 to promote keratinocyte migration. And knockdown of ITGA5 would abolish the pro-migratory effects of miR-205 inhibition in vitro. What's more, we found dysregulation of miR-205 and its target ITGA5 in epidermis of clinical chronic wound samples with persistence of high level miR-205 and absence of ITGA5. Our findings indicate that downregulation of miR-205 in the leading migrating keratinocytes is critical for re-epithelialization and miR-205 may be a potential therapeutic target for chronic wounds.

Cell Density-Dependent Upregulation of PDCD4 in Keratinocytes and Its Implications for Epidermal Homeostasis and Repair.

Programmed cell death 4 (PDCD4) is one multi-functional tumor suppressor inhibiting neoplastic transformation and tumor invasion. The role of PDCD4 in tumorigenesis has attracted more attention and has been systematically elucidated in cutaneous tumors. However, the normal biological function of PDCD4 in skin is still unclear. In this study, for the first time, we find that tumor suppressor PDCD4 is uniquely induced in a cell density-dependent manner in keratinocytes. To determine the potential role of PDCD4 in keratinocyte cell biology, we show that knockdown of PDCD4 by siRNAs can promote cell proliferation in lower cell density and partially impair contact inhibition in confluent HaCaT cells, indicating that PDCD4 serves as an important regulator of keratinocytes proliferation and contact inhibition in vitro. Further, knockdown of PDCD4 can induce upregulation of cyclin D1, one key regulator of the cell cycle. Furthermore, the expression patterns of PDCD4 in normal skin, different hair cycles and the process of wound healing are described in detail in vivo, which suggest a steady-state regulatory role of PDCD4 in epidermal homeostasis and wound healing. These findings provide a novel molecular mechanism for keratinocytes' biology and indicate that PDCD4 plays a role in epidermal homeostasis.

Non-cultured dermal-derived mesenchymal cells attenuate sepsis induced by cecal ligation and puncture in mice.

Sepsis remains a threat to critically ill patients and carries a high morbidity and mortality. Cell-based therapies have risen in prominence in recent years. Dermal-derived mesenchymal cells (DMCs) are attractive as one of the abundant sources from which to isolate mesenchymal cells for therapeutic applications and can be easily accessed with minimal harm to the donor. In this study, we described for the first time the use of non-cultured DMCs for treating sepsis in a cecal ligation and puncture (CLP) mouse model and investigated their immunomodulatory effects. We found that non-cultured DMCs administration provides a beneficial effect to improve survival in CLP-induced sepsis. This effect is partly mediated by the ability of DMCs to home to sites of injury, to reduce the inflammatory response, to inhibit apoptosis, and to stimulate macrophage migration and phagocytosis. Our further findings suggest that DMCs treatment modulates the beneficial cytoprotective effects exhibited during sepsis, at least in part, by altering miRNA expression. These discoveries provide important evidence that non-cultured DMCs therapy has a specific anti-inflammatory effect on sepsis, and provide the basis for the development of a new therapeutic strategy for managing clinical sepsis.

The predictive effect of overexpressed miR-34a on good survival of cancer patients: a systematic review and meta-analysis.

BACKGROUND: MicroRNA-34a (miR-34a) is a potential prognostic factor for survival in patients with several types of cancer according to previous clinical researches. We conducted a systematic review and meta-analysis to summarize the significance of increased miR-34a expression in the prognosis of patients' overall survival. MATERIALS AND METHODS: The present systematic review and meta-analysis of 15 researches included 2,597 patients. Overexpression of miR-34a may predict good overall survival ([OS], HR =0.76, 95% confidence interval: 0.55-1.06, P=0.105), but the effect was not significant enough. Subgroup analysis results showed miR-34a was an ideal predictor for digestive system cancer (OS, HR =0.50, 95% confidence interval: 0.25-0.99, P=0.048). The predictive effects of elevated expression of miR-34a on the OS of untreated and treated patients were not of obvious differences. CONCLUSION: This systematic review and meta-analysis showed that miR-34a has a predictive effect on overall survival of patients with digestive system cancer.

miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2.

BACKGROUND: MiR-198 has been considered as an inhibitor of cell proliferation, invasion, migration and a promoter of apoptosis in most cancer cells, while its effect on non-cancer cells is poorly understood. METHODS: The effect of miR-198 transfection on HaCaT cell proliferation was firstly detected using Cell Count Kit-8 and the cell cycle progression was analyzed by flow cytometry. Using bioinformatics analyses and luciferase assay, a new target of miR-198 was searched and identified. Then, the effect of the new target gene of miR-198 on cell proliferation and cell cycle was also detected. RESULTS: Here we showed that miR-198 directly bound to the 3'-UTR of CCND2 mRNA, which was a key regulator in cell cycle progression. Overexpressed miR-198 repressed CCND2 expression at mRNA and protein levels and subsequently led to cell proliferation inhibition and cell cycle arrest in the G1 phase. Transfection ofSiCCND2 in HaCaT cells showed similar inhibitory effects on cell proliferation and cell cycle progression. CONCLUSION: In conclusion, we have identified that miR-198 inhibited HaCaT cell proliferation by directly targeting CCND2.

Small molecular neutral microcrystalline iridium(III) complexes as promising molecular oxygen sensors.

Small molecular neutral Ir(III) complexes have been demonstrated to be promising self-inclusive microcrystalline thin-film oxygen sensors with relatively high sensitivity (Ksv = 6.41), good stability, and linear Stern-Volmer behavior (R(2) = 0.9979).

Hyperplasia of pericytes is one of the main characteristics of microvascular architecture in malignant glioma.

OBJECTIVES: To investigate the role of pericytes in constructing the malformed microvessels (MVs) and participating microvascular architecture heterogeneity of glioma. METHODS: Forty human glioma tissue samples (WHO grade II-IV) were included in present study. Observation of blood vessel patterns, quantitative analysis of endothelial cells (ECs)- and pericyte-labeled MVs and comparison between malignant grades based on single- or double-immunohistochemical staining. The MV number density (MVND), microvascular pericyte number density (MPND), and microvascular pericyte area density (MPAD) were calculated. The expression of PDGFß was also scored after immunostaining. RESULTS: In grade II glioma, most of tumor MVs were the thin-wall CD34+ vessels with near normal morphology. In addition to thin-wall CD34+ MVs, more thick-wall MVs were found in grade III glioma, which often showed α-SMA positive. Most of MVs in grade IV glioma were in the form of plexus, curled cell cords and glomeruloid microvascular proliferation while the α-SMA+ cells were the main components. The MVs usually showed disordered arrangement, loose connection and active cell proliferation as shown by Ki67 and α-SMA coexpression. With the increase of glioma grades, the α-SMA+ MVND, CD34+ MVND and MPND were significantly augmented although the increase of CD34+ MVND but not MPAD was statistically insignificant between grade III and IV. It was interesting that some vessel-like structures only consist of α-SMA+ cells, assuming the guiding role of pericytes in angiogenesis. The expression level of PDGFß was upregulated and directly correlated with the MPND in different glioma grades. CONCLUSION: Hyperplasia of pericytes was one of the significant characteristics of malignant glioma and locally proliferated pericytes were the main constituent of MVs in high grade glioma. The pathological characteristics of pericytes could be used as indexes of malignant grades of glioma.

Elevated expression of miR-210 predicts poor survival of cancer patients: a systematic review and meta-analysis.

BACKGROUND: MiRNAs are important regulators of different biological processes, including tumorigenesis. MiR-210 is a potential prognostic factor for survival in patients with cancer according to previous clinical researches. We conducted a systematic review and meta-analysis to summarize the significance of increased miR-210 expression in the prognosis of indicated cancers. METHODOLOGY/PRINCIPAL FINDINGS: The present systematic review and meta-analysis of 16 researches included 1809 patients with 7 different types of cancers from 7 countries, and aimed to explore the association between miR-210 expression and the survival of cancer patients. Over-expression of miR-210 may predict poor overall survival (OS, HR = 1.33, 95% CI: 0.85-2.09, P = 0.210), but the effect was not significant. While the predictive effect on disease-free survival (DFS, HR = 1.89, 95% CI: 1.30-2.74, P = 0.001), progression-free survival (PFS, HR = 1.20, 95% CI: 1.05-1.38, P = 0.007) and relapse-free survival(RFS, HR = 4.42, 95% CI: 2.14-9.15, P = 0.000) for patients with breast cancer, primary head and neck squamous cell carcinoma (HNSCC), renal cancer, soft-tissue sarcoma, pediatric osteosarcoma, bladder cancer or glioblastoma was certain. Subgroup analysis showed the limited predictive effect of over-expressed miR-210 on breast cancer OS (HR = 1.63, 95% CI: 0.47-5.67, P = 0.443), breast cancer DFS (HR = 2.03, 95% CI: 0.90-4.57, P = 0.088), sarcoma OS (HR = 1.24, 95% CI: 0.20-7.89, P = 0.818) and renal cancer OS (HR = 1.16, 95% CI: 0.27-4.94, P = 0.842). CONCLUSIONS/SIGNIFICANCE: This systematic review and meta-analysis suggests that miR-210 has a predictive effect on survival of patients with studied cancer types as indexed by disease-free survival, progression-free survival and relapse-free survival. While the predictive effect on overall survival, breast cancer overall survival, breast cancer disease-free survival, sarcoma overall survival and renal cancer overall survival was not statistically significant.

P53-participated cellular and molecular responses to irradiation are cell differentiation-determined in murine intestinal epithelium.

AIM: Cells respond differently to DNA damaging agents, which may related to cell context and differentiation status. The aim of present study was to observe the cellular and molecular responses of cells in different differentiation status to ionizing irradiation (IR). METHODS: Crypt-villus unit of murine small intestine was adopted as a cell differentiation model. DNA damage responses (DDRs) of crypt and villus were observed 1-24 h after 12 Gy IR using gene expression microarray analysis, immunohistochemical staining, Western blotting and Electrophoretic Mobility Shift Assay. RESULTS: Microarray analysis revealed that most differentially expressed genes were related to p53 signaling pathway in crypt 4h after IR and in both crypt and villus 24h after IR. In crypt stem cells/progenitor cells, H2AX was phosphorylated and dephosphorylated quickly, Ki67 attenuated, cell apoptosis enhanced, phosphorylated P53 increased and translocated into nuclear with the ability to bind p53-specific sequence. In upper crypt (transit amplifying cells) and crypt-villus junction, cells kept survive and proliferate as indicated by retained Ki67 expression, suppressed p53 activation, and rare apoptosis. CONCLUSIONS: DDRs varied with cell differentiation status and cell function in small intestinal epithelium. P53 signaling pathway could be an important regulatory mechanism of DDRs.

Therapeutic anti-tumor effect of exogenous apoptin driven by human survivin gene promoter in a lentiviral construct.

INTRODUCTION: The aim of this study was to construct a lentivirus vector with survivin promoter (pSur)-driven apoptin and test its efficiency in suppressing the growth of tumor cells. MATERIAL AND METHODS: Expression cassettes with different fragments of survivin gene promoter (pSur, 161 bp, 272 bp, 990 bp) driving 6XHis-tagged apoptin were constructed to generate recombinant lentivirus, of which the inhibitory effect on tumor cells was compared. The activity of different pSur in 293FT, and 272 bp pSur in primary bone marrow mesenchymal stem cells (BMSCs), SW480, Hela and MCF-7 was examined by Western blot. Their ability to induce apoptosis in SW480 cells was determined by annexin-V staining. The inhibitory effect of letivirus containing different pSur-driven apoptin on nude mice-xenografted SW480 cells was assessed by tumor size and pathological observation. RESULTS: The 272 bp and 990 bp pSur displayed comparable effects in terms of promoter activity, cell apoptosis/necrosis and G1 phase arrest in vitro, and growth of xenograft tumor in vivo. When lentivirus containing 272 bp pSur was tested, it drove high apoptin expression in tumor cells (SW480, Hela and MCF-7) and weak expression in primary bone marrow mesenchymal stem cells. Xenograft to nude mice using infected Sw480 cells showed that lentiviruses possessing 272 bp and 990 bp pSur were able to significantly induce tumor cell death, focal necrosis, and tumor growth lag. CONCLUSIONS: The data indicated that pSur-apoptin expression cassette in lentivirus vector ensures specific suppression of tumor cells, and may be applicable to monitor malignant transformation of transplanted cells.

Iridium(III) complexes with enhanced film amorphism as guests for efficient orange solution-processed single-layer PhOLEDs with low efficiency roll-off.

By introducing a phenyl substituent into the meta-site of the phenyl segment of the 2-phenylbenzothiazole ligand, two novel orange iridium(III) complexes, namely, (3Phbt)2Ir(acac) and (3OMePhbt)2Ir(acac), have been synthesized. Compared with their parent compound (bt)2Ir(acac), both of them possess much enhanced thermostability and film amorphism, making them suitable candidates as guests for high performance solution-processed phosphorescent organic light-emitting diodes (PhOLEDs). However, (4Phbt)2Ir(acac) bearing para-phenyl possesses worse processability relative to (bt)2Ir(acac) due to spontaneous crystallization stemming from the intense intermolecular interactions. Single-layer solution-processed PhOLEDs with (3Phbt)2Ir(acac) and (3OMePhbt)2Ir(acac) as guests show peak current efficiency of 17.2 cd A(-1) and 15.2 cd A(-1), and maximum brightness of 28,270 cd m(-2) and 27,900 cd m(-2), respectively. Both are greatly improved compared to the devices employing (bt)2Ir(acac) (10.2 cd A(-1) and 14,350 cd m(-2)) and (4Phbt)2Ir(acac) (5.0 cd A(-1) and 13,790 cd m(-2)) as phosphors. Moreover, quite low efficiency roll-off is acquired in these devices at high luminance. The much improved electroluminescence performances of these objective complexes could be mainly attributed to the presence of a rigid phenyl on the appropriate substitution site of the cyclometallate ligand, which leads to improved thermostability with compatible alleviated intermolecular interactions, and consequently enhanced film amorphism.

miR-21 regulates skin wound healing by targeting multiple aspects of the healing process.

With the clarification of the important roles of microRNAs (miRNAs) in diverse physiologic and pathologic processes, the effects of miRNAs in wound healing have attracted more attention recently. However, the global pattern of miRNA expression in wound tissue is still unknown. In the present study, we depicted the miRNA profile and identified at least 54 miRNAs, including miR-21, changed for more than twofold at the stage of granulation formation during wound healing. These miRNAs were closely related to the major events of wound healing, including cell migration and proliferation, angiogenesis, and matrix remolding. Furthermore, we found that miR-21 was up-regulated after skin injury, mainly in activated and migrating epithelial cells of epidermis and mesenchymal cells of dermis. Locally antagonizing miR-21 by directly injecting antagomir to wound edge caused significant delay of wound closure with impaired collagen deposition. Unexpectedly, we found wounds treated with miR-21 antagomir had an obvious defect in wound contraction at an early stage of wound healing. The significant role of miR-21 in wound contraction was further confirmed by in vivo gain-of-function and in vitro loss-of-function experiments. In conclusion, the present study has for the first time depicted miRNA profiling of wound healing and demonstrated the involvement of miR-21 in regulating the wound contraction and collagen deposition. These results suggest that miR-21 may be a new medical target in skin wound manipulation.

Different roles of TGF-ß in the multi-lineage differentiation of stem cells.

Stem cells are a population of cells that has infinite or long-term self-renewal ability and can produce various kinds of descendent cells. Transforming growth factor ß (TGF-ß) family is a superfamily of growth factors, including TGF-ß1, TGF-ß2 and TGF-ß3, bone morphogenetic proteins, activin/inhibin, and some other cytokines such as nodal, which plays very important roles in regulating a wide variety of biological processes, such as cell growth, differentiation, cell death. TGF-ß, a pleiotropic cytokine, has been proved to be differentially involved in the regulation of multi-lineage differentiation of stem cells, through the Smad pathway, non-Smad pathways including mitogen-activated protein kinase pathways, phosphatidylinositol-3-kinase/AKT pathways and Rho-like GTPase signaling pathways, and their cross-talks. For instance, it is generally known that TGF-ß promotes the differentiation of stem cells into smooth muscle cells, immature cardiomyocytes, chondrocytes, neurocytes, hepatic stellate cells, Th17 cells, and dendritic cells. However, TGF-ß inhibits the differentiation of stem cells into myotubes, adipocytes, endothelial cells, and natural killer cells. Additionally, TGF-ß can provide competence for early stages of osteoblastic differentiation, but at late stages TGF-ß acts as an inhibitor. The three mammalian isoforms (TGF-ß1, 2 and 3) have distinct but overlapping effects on hematopoiesis. Understanding the mechanisms underlying the regulatory effect of TGF-ß in the stem cell multi-lineage differentiation is of importance in stem cell biology, and will facilitate both basic research and clinical applications of stem cells. In this article, we discuss the current status and progress in our understanding of different mechanisms by which TGF-ß controls multi-lineage differentiation of stem cells.

A highly selective sulfur-free iridium(III)-complex-based phosphorescent chemidosimeter for detection of mercury(II) ions.

A neutral phosphorescent coordination compound bearing a benzimidazole ligand, Ir(pbi)(2)(acac) (Hpbi = 1,2-diphenyl-1H-benzo[d]imidazole; Hacac = acetylacetone), is demonstrated to be the first example of a sulfur-free iridium complex for the detection of Hg(2+) cations with high selectivity and sensitivity. Ir(pbi)(2)(acac) shows a multisignaling response towards mercury(II) ions through UV-vis absorption, phosphorescence and electrochemistry measurements. Upon addition of Hg(2+) ions, solutions of this complex change from yellow to colorless, which could be observed easily by the naked eye, while its phosphorescence turns from bright green (λ(PLmax) = 520 nm) into faint skyblue (λ(PLmax) = 476 nm), and the detection limit is calculated to be 2.4 × 10(-7) mol L(-1). (1)H NMR spectroscopic titration as well as ESI-MS results indicate that the decomposition of Ir(pbi)(2)(acac) in the presence of Hg(2+) through rupture of Ir-O bonds is responsible for the significant variations in both optical and electrochemical signals.

TGF-ß-induced miR-21 negatively regulates the antiproliferative activity but has no effect on EMT of TGF-ß in HaCaT cells.

The transforming growth factor-ß (TGF-ß) signaling pathway plays important roles in maintaining normal tissue homeostasis, and is tightly controlled by a network of biomolecules. MicroRNAs (miRNAs) are small noncoding RNAs of ∼22 nucleotides that regulate gene expression at posttranscriptional levels. Increasing evidence points to the important role of miRNAs in TGF-ß signaling. OncomicroRNA miR-21 has been established as a key regulator of mesenchymal phenotype transition induced by TGF-ß. However, the effects of miR-21 on epithelial biology involved in TGF-ß signaling pathway such as cytostatic program and epithelial to mesenchymal transition (EMT) processes are unclear. Here we show that miR-21 is upregulated after TGF-ß exposure in both growth inhibition and EMT models of HaCaT keratinocytes. To determine the potential roles of miR-21 in TGF-ß-induced growth-arrest and EMT models, we showed that ectopic expression of miR-21 overcame TGF-ß' growth-inhibitory effect and the knockdown of miR-21 potentialized this effect, but perturbation of miR-21 levels had little effect on EMT. Moreover, TGFBR2, PTEN, PDCD4, and TAp63 were identified as targets of miR-21 in HaCaT cells. And among them, TGFBR2, PTEN, and TAp63 were associated with TGF-ß-induced cytostatic program. Thus, our results suggest that miR-21 regulates the ability of epithelial cells to respond to TGF-ß, with potential impact on epithelium homeostasis, wound-healing and tumorigenesis.

Mesenchymal stromal cells for cell therapy: besides supporting hematopoiesis.

Mesenchymal stromal cells (MSC) have attracted the attention of scientists and clinicians due to their self-renewal, capacity for multipotent differentiation, and immunomodulatory properties. Some essential problems remain to be solved before the clinical application of MSC. Platelet lysate (PL) has recently been used as a substitute for FBS in MSC amplification in vitro to achieve clinically applicable numbers of MSC. In addition to promising trials in regenerative medicine, such as in the treatment of major bone defects and myocardial infarction, MSC have shown therapeutic effect other than direct hematopoiesis support in hematopoietic reconstruction. It has been confirmed that MSC promote hematopoietic cell engraftment and immune recovery after allogeneic hematopoietic stem cell transplantation, probably through the provision of cytokines, matrix proteins, and cell-to-cell contacts. Their suppressive effects on immune cells, including T cells, B cells, NK cells and DC cells, suggest MSCs as a novel therapy for GVHD and other autoimmune disorders. These cells thus present as promising candidates for cellular therapy in the fields of regenerative medicine, allogeneic hematopoietic stem cell transplantation, and autoimmune disorders.

Fine tuning of emission color of iridium(III) complexes from yellow to red via substituent effect on 2-phenylbenzothiazole ligands: synthesis, photophysical, electrochemical and DFT study.

Four novel iridium(III) complexes bearing biphenyl (7a-7c) or fluorenyl (7d) modified benzothiazole cyclometallate ligands are synthesized. In comparison with the yellow parent complex, bis(2-phenylbenzothiozolato-N,C(2')) iridium(III) (acetylacetonate) [(pbt)(2)Ir(acac)] (λ(PLmax) = 557 nm, φ(PL) = 0.26), 7a-7d show 20-43 nm bathochromic shifted orange or red phosphorescence in solution, with maximum photoluminescence (PL) quantum yield of 0.62, and PL lifetime of 1.8-2.0 µs. Meanwhile, the resulting complexes also exhibit intense orange or red phosphorescence of λ(PLmax) = 588-611 nm in solid films. The complex 7c with two tert-butyl substituents possesses the highest phosphorescent efficiency both in dilute solution and thin solid films, therefore may be a prospective candidate for both doping and host emitting electrophosphorescent material. Furthermore, despite the observation of severe oxygen quenching for 7a-7d in solution, 7a and 7c even show efficient emission intensity quenching by oxygen in their solid state due to the existence of void channels in crystals; consequently, they are promising molecular oxygen sensor reagents. Electrochemical measurement and DFT calculation results suggest that all these chelates own declined LUMOs of 0.1 eV relative to that of (pbt)(2)Ir(acac) owing to the contribution of the phenyl substituents; whereas only 7d shows a more destabilized HOMO (∼0.1 eV) compared with the parent chelate.