Visualizing the interfacial-layer-based epitaxial growth process toward organic core-shell architectures.

Organic heterostructures (OHTs) with the desired geometry organization on micro/nanoscale have undergone rapid progress in nanoscience and nanotechnology. However, it is a significant challenge to elucidate the epitaxial-growth process for various OHTs composed of organic units with a lattice mismatching ratio of > 3%, which is unimaginable for inorganic heterostructures. Herein, we have demonstrated a vivid visualization of the morphology evolution of epitaxial-growth based on a doped interfacial-layer, which facilitates the comprehensive understanding of the hierarchical self-assembly of core-shell OHT with precise spatial configuration. Significantly, the barcoded OHT with periodic shells obviously illustrate the shell epitaxial-growth from tips to center parts along the seeded rods for forming the core-shell OHT. Furthermore, the diameter, length, and number of periodic shells were modulated by finely tuning the stoichiometric ratio, crystalline time, and temperature, respectively. This epitaxial-growth process could be generalized to organic systems with facile chemical/structural compatibility for forming the desired OHTs.

Precise Synthesis of Organic Cocrystal Alloys with Full-Spectrum Emission Characteristics for the Stepless Color Changing Display.

Organic luminescent materials are indispensable in optoelectronic displays and solid-state luminescence applications. Compared with single-component, multi-component crystalline materials can improve optoelectronic characteristics. This work forms a series of full-spectrum tunable luminescent charge-transfer (CT) cocrystals ranging from 400 to 800 nm through intermolecular collaborative self-assembly. What is even more interesting is that o-TCP-Cor(x) -Pe(1-x) , p-TCP-Cor(x) -Pe(1-x) , and o-TCP-AN(x) -TP(1-x) alloys are prepared based on cocrystals by doping strategies, which correspondingly achieve the stepless color change from blue (CIE [0.22, 0.44]) to green (CIE [0.16, 0.14]), from green (CIE [0.27, 0.56]) to orange (CIE [0.58, 0.42]), from yellow (CIE [0.40, 0.57]) to red (CIE [0.65, 0.35]). The work provides an efficient method for precisely synthesizing new luminescent organic semiconductor materials and lays a solid foundation for developing advanced organic solid-state displays.

Design and Growth of Branched Organic Crystals: Recent Advances and Future Applications.

The rapid development of information technology has resulted in a growing demand for low-dimensional photonic materials. Organic semiconductor materials play an important role in various photonic devices due to their adjustable physicochemical properties, while individual organic crystals do not exhibit the desired performance due to the limitations of their simple structure. Branched organic crystals with inherent multichannel characteristics based on π-conjugated molecules are favorable components in optoelectronics. However, the preparation of branched organic crystals still faces great challenges before they can be applied in integrated optoelectronic devices. In this Review, the development and representative examples of branched organic crystals in terms of molecular design, synthesis, and advanced applications are discussed. We also provide a summary and outlook for the direction of future research on branched organic crystals as excellent candidates in photonic integrated circuits.

Efficient All-Inorganic Perovskite Light-Emitting Diodes with Cesium Tungsten Bronze as a Hole-Transporting Layer.

The realization of high-performance optoelectronic devices requires excellent charge-transporting layers and efficient carrier recombination. Herein, we synthesized cesium tungsten bronze (Cs0.32WO3) nanocrystals and utilized them as the hole-transporting material to fabricate all-inorganic perovskite light-emitting diodes (PeLEDs). Due to the excellent carrier balance characteristics via comparison between the hole-only device and electron-only device, the all-inorganic PeLEDs with CsPbBr3 as the light-emitting layer present the maximum current efficiency of 31.51 cd/A and external quantum efficiency (EQE) of 8.48%, which are self-evidently enhanced compared with the PEDOT:PSS (14.78 cd/A, 4.03%) and WO3 (24.75 cd/A, 6.18%) based devices. Considering the remarkably improved device performance, the proposed HTL of Cs0.32WO3 is promising, acting as a favorable building block for high-efficiency light-emitting devices.

Controlled synthesis of organic single-crystalline nanowires via the synergy approach of the bottom-up/top-down processes.

The controlled fabrication of organic single-crystalline nanowires (OSCNWs) with a uniform diameter in the nanoscale via the bottom-up approach, which is just based on weak intermolecular interaction, is a great challenge. Herein, we utilize the synergy approach of the bottom-up and the top-down processes to fabricate OSCNWs with diameters of 120 ± 10 nm through stepwise evolution processes. Specifically, the evolution processes vary from the self-assembled organic micro-rods with a quadrangular pyramid-like end-structure bounded with {111}s and {11-1}s crystal planes to the "top-down" synthesized organic micro-rods with the flat cross-sectional {002}s plane, to the organic micro-tubes with a wall thickness of ∼115 nm, and finally to the organic nanowires. Notably, the anisotropic etching process caused by the protic solvent molecules (such as ethanol) is crucial for the evolution of the morphology throughout the whole top-down process. Therefore, our demonstration opens a new avenue for the controlled-fabrication of organic nanowires, and also contributes to the development of nanowire-based organic optoelectronics such as organic nanowire lasers.

High performance blue quantum dot light-emitting diodes employing polyethylenimine ethoxylated as the interfacial modifier.

Efficient electron-injection into the emitting layer (EML) plays a pivotal role in the fabrication of high performance blue quantum dot light-emitting diodes (QLEDs). Herein, we reduce the electron-transporting barrier at the ITO/ETL (electron-transporting layer) interface from 0.7 eV to 0.4 eV by spin-coating a polyethylenimine ethoxylated (PEIE) film (8 nm) on the ITO substrate. Meanwhile, the electron-injection barrier was reduced from 0.5 to 0.1 eV at the ETL/QD interface by employing the incorporation of PEIE (0.1 wt%) into a ZnO layer. These above two interfacial modifications jointly decrease the electron barrier and make the electron transportation easier. As a result, the optimized QLEDs with the 460 nm emission peak exhibit a maximum external quantum efficiency (EQE) of 7.85%, which is enhanced by 1.4 fold compared with the reference device (5.68%). It is demonstrated that the facile interfacial modification by the organic polymer PEIE contributes to the fabrication of high-efficiency blue QLEDs.

Polymer as an Additive in the Emitting Layer for High-Performance Quantum Dot Light-Emitting Diodes.

A facile but effective method is proposed to improve the performance of quantum dot light-emitting diodes (QLEDs) by incorporating a polymer, poly(9-vinlycarbazole) (PVK), as an additive into the CdSe/CdS/ZnS quantum dot (QD) emitting layer (EML). It is found that the charge balance of the device with the PVK-added EML was greatly improved. In addition, the film morphology of the hole-transporting layer (HTL) which is adjacent to the EML, is substantially improved. The surface roughness of the HTL is reduced from 5.87 to 1.38 nm, which promises a good contact between the HTL and the EML, resulting in low leakage current. With the improved charge balance and morphology, a maximum external quantum efficiency (EQE) of 16.8% corresponding to the current efficiency of 19.0 cd/A is achievable in the red QLEDs. The EQE is 1.6 times as high as that (10.5%) of the reference QLED, comprising a pure QD EML. This work demonstrates that incorporating some polymer molecules into the QD EML as additives could be a facile route toward high-performance QLEDs.

White-Emissive Self-Assembled Organic Microcrystals.

Organic semiconductor micro-/nanocrystals with regular shapes have been demonstrated for many applications, such as organic field-effect transistors, organic waveguide devices, organic solid-state lasers, and therefore are inherently ideal building blocks for the key circuits in the next generation of miniaturized optoelectronics. In the study, blue-emissive organic molecules of 1,4-bis(2-methylstyryl)benzene (o-MSB) can assemble into rectangular microcrystals at a large scale via the room-temperature solution-exchange method. Because of the Förster resonance energy transfer, the energy of the absorbed photons by the host matrix organic molecules of o-MSB can directly transfer to the dopant organic molecules of tetracene or 1,2:8,9-dibenzopentacene (DBP), which then emit visible photons in different colors from blue to green, and to yellow. More impressively, by modulating the doping molar ratios of DBP to o-MSB, bright white-emissive organic microcrystals with well-preserved rectangular morphology can be successfully achieved with a low doping ratio of 1.5%. These self-assembled organic semiconductor microcrystals with multicolor emissions can be the white-light sources for the integrated optical circuits at micro-/nanoscale.

Pathophysiology of chronic pancreatitis induced by dibutyltin dichloride joint ethanol in mice.

AIM: To search for a new chronic pancreatitis model in mice suitable for investigating the pathophysiological processes leading to pancreatic fibrosis. METHODS: The mice were randomly divided into 2 groups (n = 50), control group and model group. The mice in model group were given ethanol (10%) in drinking water after injection of dibutyltin dichloride (DBTC) (8 mg/kg BW) in tail vein. The mice in control group were injected with only solvent into tail vein (60% ethanol, 20% glycerine and 20% normal saline) and drank common water. At days 1, 7, 14, 28, and 56 after application of DBTC or solvent, 10 mice in one group were killed at each time point respectively. Blood was obtained by inferior vena cava puncture. The activity of amylase, concentration of bilirubin and hyaluronic acid in serum were assayed. The pancreas was taken to observe the pancreatic morphology by HE staining, and to characterize the pancreatic fibrosis by Masson staining. The expression of F4/80, CD3 and fibronectin (FN) were assayed by immuno-histochemistry or Immunofluorescence technique. Collagen type I (COL1A1) in pancreas were detected by Western blot. The expression of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinases-1 (TIMP-1) mRNA in the pancreas was assessed by real time PCR. RESULTS: DBTC induced an acute edematous pancreatitis within 1 d. The dilated acini, scattered acinar cell necrosis, and inflammatory cells were found at day 7. Extensive infiltration with inflammatory cells following deposition of connective tissue was observed at day 14. At day 28, level of pancreatic fibrosis was aggravated. The pancreatic tissue was replaced by an extended interstitial fibrosis at the end of 2 mo. There was significant difference in the level of amylase, bilirubin and hyaluronic acid in serum between control group and model group (P < 0.05). The level of COL1A1 and FN in pancreas increased. The expression of MMP-1 mRNA in pancreas decreased, but TIMP-1 mRNA increased at model group. CONCLUSION: DBTC joint Ethanol drinking can induce chronic pancreatitis in accordance with the pathophysiological modification of human. DBTC joint Ethanol-induced pancreatitis in mice is an effective and handy experimental method. The model is suitable to study the mechanism of pancreatic fibrosis in chronic pancreatitis.

[The roles and mechanisms of p-STAT3 signaling pathway in acute pancreatitis].

OBJECTIVE: To detect the expression ofsignal transducer and activator of transcription 3 (STAT3) in pancreatic tissue of the mouse model of pancreatitis, and to explore its role in the evolution of acute pancreatitis. METHODS: Forty-eight healthy male balb/c mice were randomly divided into 3 groups (n=16):control group (Con) 0.09% NaCl, intraperitoneal injection; mild acute pancreatitis group (MAP) caerulein, intraperitoneal injection; severe acute pancreatitis group (SAP) caerulein plus lipopolysaccharide(LPS), intraperitoneal injection. The mice were sacrificed after 2 h and 6 h after intraperitoneall injection. Serum was isolated for amylase activity. Pancreatic was isolated and weighedto calculate the pancreatic wet weight ratio. Myeloperoxidase (MPO) activity was measured to assess the degree of inflammatory cell infiltration in lung tissue. Using HE staining, the pathological changes of pancreatic and lung were observed under the light microscope. The expression of phosphorylated STAT3 (p-STAT3) was detected by Western blot. RESULTS: Compared with control group, serum amylase activity, pancreatic wet weight ratio and lung MPO activity were significantlyincreased (P<0.05) in MAP and SAP group at each time point, especially SAP group showed higher levels of MPO activity than that in MAP group (P<0.01). The pathological changes of pancreas and lung were observed after modeling in 2 h. Western blot showed the expression of p-STAT3 could be detected in SAP group, the level increased most significantly after modeling 2 h, and decreased slightly after 6 h. The level of p-STAT3 was low in MAP group and negative in Con group at each time point. CONCLUSIONS: The expression of p-STAT3 in MAP and SAP groups are significantly different from that in control group, which indicates that STAT3 isclosely related in acute pancreatitis. Inhibition of STAT3 activity is a potential target to alleviate acute pancreatitis progression.

[Effect of DaChaiHu Decoction on pancreatic fibrosis induced by DBTC combined with alcohol and the mechanism of TGF-beta/Smad signaling pathway].

OBJECTIVE: To investigate the effects of transforming growth factor-ß (TGF-ß) and Smad in chronic pancreatitis (CP) induced by dibutyltin dichloride (DBTC) combined with ethanol, and the effect for prevention and treatment of pancreatic fibrosis by DaChaiHu Decoction (tradeiional Chinese medicine). METHODS: Ninety-six healthy male Kunming mice were randomly divided into control group (Con group), chronic pancreatitis (CP group) group, Dachai Hu decoction treatment group (DCHD group) (n=32). Then the mice were treated with DBTC 8 mg/kg by tail vein injection and fed with 10% ethanol replacing the normal drinking water to replicate mouse CP model. After three days of modeling the mice were randomly divided into CP group and DCHD group. The mice in DCHD group were administered intragastrically with DaChaiHu Decoction (1 g/ml, 6 g/kg·d) at the following 8 weeks. After modeling for 1 week, 2 weeks, 4 weeks and 8 weeks, the mice were anesthetized and sacrificed(n=8). The morphology and the degree of fibrosischanges of pancreatic tissue were detected by HE staining. The protein expressions of type I collagen and TGF beta R I, p-Smad 2/3 and Smad 7 in pancreatic tissue were detected by Western blot assay. The expressions of MMP-1/TIMP-1 mRNA inpancreatic tissue were detected by RT-PCR. RESULTS: Compared with control group, DBTC combined with ethanol induced CP with increased activity of serum amylase and hyaluronic acid level. While in DCHD group, the activity of amylase and hyaluronic acid level were decreased significantly. Compared with control group, the protein expressions of COLA1, TGF beta R I, p-Smad 2/3 in CP Group were elevated,but the expression of Smad 7 was significantly reduced; In DCHD treatment group,the expression of TGF beta R I, p-Smad 2/3 and COLA1 were reduced, and the protein expression of Smad 7 was increased. In 2w and 4w, the level of MMP-1mRNA continued to decrease, while TIMP-1mRNA expression was increased significantly (P<0.01). At each time point of DCHD group, the expression of MMP-1 were markedly increased and TIMP-1 were reduced, compared with those of the CP group (P<0.05). CONCLUSIONS: DaChaiHu Decoction play a role in the prevention and treatment of chronic pancreatitis and the development of fibrosis, the mechanism may related to inhibit the activation of TGF beta/Smad signaling pathway, and regulate the balance between synthesis and degradation of extracellular matrix.

MiR-183 Regulates ITGB1P Expression and Promotes Invasion of Endometrial Stromal Cells.

We applied in the previous study miRNA microarray screening analysis to identify several differentially expressed miRNAs, including miR-183 in normal, eutopic, and ectopic endometrium. Knockdown of miR-183 expression induced the invasiveness and inhibition of apoptosis in endometrial stromal cells. The current study aims to identify the miR-183 targets with relevance to cell functions in endometrial stromal cells, to verify the interaction of miR-183 with its target genes, and to confirm the role of miR-183 in the process of endometriosis. Using microarray analysis, we identified 27 differentially expressed genes (19 were upregulated and 8 downregulated), from which we selected 4 downregulated genes (ITGB1, AMIGO2, VAV3, and PSEN2) based on GO databases for functional analysis and significant pathway analysis. Western blotting analyses showed that integrin ß1 (ITGB1), but not AMIGO2, was affected by miR-183 overexpression, whereas no protein expression of VAV3 and PSEN2 was detected. Luciferase reporter assay verified that ITGB1 is a target gene of miR-183. Moreover, we found that ITGB1 is overexpressed in the endometrium of endometriosis patients. Furthermore, overexpression of ITGB1 rescued the repressive effects of miR-183 on the invasiveness of endometrial stromal cells. These findings, together with the fact that ITGB1 is a critical factor for cell adhesion and invasiveness, suggest that miR-183 may be involved in the development of endometriosis by regulating ITGB1 in endometrial stromal cells.

Shikonin reduces endometriosis by inhibiting RANTES secretion and mononuclear macrophage chemotaxis.

Endometriosis is a common disease in females of reproductive age and has the classic characteristic of mononuclear cell infiltration into lesions. Shikonin is an anti-inflammatory phytocompound obtained from Lithospermum erythrorhizon whose potential therapeutic effects in the treatment of endometriosis remain unclear. The working hypothesis of the present study was that shikonin is capable of inhibiting the development of endometriosis by inhibiting the chemotactic effect. In a murine model of endometriosis, shikonin significantly inhibited the growth of human endometrial tissue implanted into severe combined immunodeficiency (SCID) mice (P<0.05) and no adverse effects were observed. Mouse regulated upon activation normal T-cell expressed and secreted (mRANTES) levels in the peritoneal fluid of the animal endometriosis model were higher than those in normal SCID mice (P<0.05) and decreased significantly following shikonin treatment in a dose-dependent manner (P<0.05). Peritoneal fluid from SCID mice treated with shikonin inhibited the chemotaxis of monocytes; this inhibitory effect was eradicated by mRANTES antibody. In vitro, shikonin significantly inhibited RANTES expression in U937 cells that were cultured alone or co-cultured with human mesothelial and endometrial stromal cells. In addition, shikonin inhibited the RANTES-induced chemotaxis of U937 cells (P<0.05). The results indicate that shikonin inhibits the development of endometriosis by various mechanisms, including the inhibition of RANTES expression and the reduction of mononuclear cell migration to lesions. Therefore, shikonin may be a novel, useful and safe agent for treating endometriosis.

Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis.

Endometriosis is a common gynecological disease, yet its pathogenesis remains poorly understood. Recent studies have demonstrated that the aberrant expression of certain microRNAs (miRNAs) may correlate with the development and progression of endometriosis. In this study, we profiled several differentially expressed miRNAs in the normal, eutopic and ectopic endometrium by miRNA microarray screening analysis, among which, miR-183 was found to be downregulated in the ectopic and eutopic tissues, and the result was further confirmed by real-time PCR (qPCR). Functional analysis indicated that miR-183 plays a promotional role in endometrial stromal cell (ESC) apoptosis and has a negative regulatory impact on the invasive ability of cells, although it has no effect on ESC proliferation. Ovarian steroids (17ß-estradiol and progesterone) and inflammatory factors (tumor necrosis factor-α and interleukin-6) decreased the expression of miR-183 in the ESCs. This regulatory function may further manifest the growth and invasive potential of ESCs by altering the expression of miR-183. These findings suggest that the downregulation of miR-183 expression is involved in the development and progression of endometriosis.

The high level of RANTES in the ectopic milieu recruits macrophages and induces their tolerance in progression of endometriosis.

RANTES (C-C chemokine, regulated on activation, normal T cell expressed and secreted) is involved in progression of endometriosis, but the precise mechanism is understood inadequately. This study is to elucidate the roles of RANTES in macrophage recruitment and tolerance in the endometriotic milieu. The expression of RANTES was analyzed by immunohistochemistry. The cell co-cultures were applied to simulate the endometriotic milieu to investigate the regulation of RANTES secretion and its receptor CCR1 expression. Transwell migration assay was used for chemotaxis of U937 cells (macrophage line) to endometrial stromal cells (ESCs) and/or human pelvic mesothelial cells. The expression of CCR1 was analyzed by RT-PCR and qPCR in transcription and by western blot in translation respectively. Concentrations of RANTES, IL10, and IL12p70 were determined by ELISA. The phenotype of U937 cells and apoptosis of ESCs were analyzed by flow cytometry. We have found that the expression of RANTES is significantly higher in the endometriotic tissue and eutopic endometrium than that of the normal endometrium without endometriosis. The combination of 17ß-estradiol and dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin increases significantly RANTES secretion in the endometriosis-associated cell co-culture which can recruit more macrophages, upregulate CCR1 expression, and induce tolerant phenotype, which inhibits the apoptosis of ESC in the milieu. In conclusion, the higher levels of RANTES in the ectopic milieu facilitate the onset and progression of endometriosis by macrophage recruitment and tolerance that in turn inhibits apoptosis and enhances growth of ESC.

Combination of 17beta-estradiol with the environmental pollutant TCDD is involved in pathogenesis of endometriosis via up-regulating the chemokine I-309-CCR8.

OBJECTIVE: To explore the effects of the combined E(2) with the environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on CCR8-I-309 expression by the endometriotic lesion-associated cells in the pathogenesis of endometriosis. DESIGN: Prospective laboratory study. SETTING: University hospital. PATIENT(S): Chinese women with endometriosis. INTERVENTION(S): The endometriotic tissue and matched eutopic endometrium were collected. Endometrial stromal cells (ESCs), HPMC, and U937 cells were treated with 17beta-E(2) or TCDD. The ESCs were stimulated with I-309. MAIN OUTCOME MEASURE(S): The expression of CCR8 in tissues was analyzed by reverse transcription-polymerase chain reaction and immunohistochemistry. The effect of I-309 on integrin beta1 and alphavbeta3 expression intensity was analyzed by flow cytometry, and the chemotactic activity of I-309 on the ESC was explored by chemotactic assay. Concentration of I-309 in the culture supernatant was quantified by enzyme-linked immunosorbent assay. RESULT(S): CCR8 was overexpressed in the endometriotic tissue. I-309 promoted the expression of integrin beta1. Estradiol and TCDD up-regulated CCR8 expression by ESCs. Estradiol magnified the stimulatory effect of TCDD on I-309 secretion by U937. The interaction of HPMC and U937 cells promoted I-309 secretion. CONCLUSION(S): These findings imply that the combination of 17beta-E(2) with the environmental pollutant TCDD is involved in the pathogenesis of endometriosis via up-regulating the chemokine CCR8-I-309.

Effects of combined 17beta-estradiol with TCDD on secretion of chemokine IL-8 and expression of its receptor CXCR1 in endometriotic focus-associated cells in co-culture.

BACKGROUND: Chemokines play an important role in the pathogenesis of endometriosis. In the present study, the transcription of 18 chemokine receptors in eutopic endometrium and ectopic tissue with endometriosis was first analysed by RT-PCR. Dioxin, an air pollutant, and estrogen are reported to be associated with endometriosis. The regulatory mechanisms of dioxin and estrogen in the expression of CXCR1/IL-8 in the corresponding cells will help in elucidating roles of the chemokine in the aetiology of endometriosis. METHODS AND RESULTS: CXCR1, a type of chemokine receptor, was over-expressed in endometriotic tissue. The high translation of the receptor and its ligand, interleukin (IL-8), in endometriotic tissue was then demonstrated by immunochemistry. Estradiol and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alone inhibited expression of CXCR1, whereas the combination of estradiol with TCDD up-regulated the expression. TCDD promoted IL-8 secretion by human pelvic mesothelial cells (HPMC), and 17beta-estradiol magnified the stimulatory effect. Both 17beta-estradiol and TCDD alone inhibited IL-8 secretion of U937 (a cell line of monocyte), but combination of 17beta-estradiol and TCDD had no further inhibitory effect. The co-culture of endometrial stromal cells (ESC) with HPMC produced more IL-8 than respective or total production of either of the cells alone, and estradiol played a synergistic stimulatory role with TCDD in IL-8 secretion of the co-culture. Interaction of HPMC and the monocytes significantly stimulated IL-8 secretion, suggesting a main resource of IL-8 in peritoneal cavity with endometriosis. TCDD promoted IL-8 secretion by HPMC-U937 co-culture, but exerted a contrary effect for IL-8 secretion when combined with estradiol. CONCLUSION: Estradiol and TCDD in the peritoneal cavity can lead to a persistent and serious inflammation, which gives a new insight into the interactions of estrogen and TCDD in endometriosis.