Hematopoietic-Derived Galectin-3 Causes Cellular and Systemic Insulin Resistance.

In obesity, macrophages and other immune cells accumulate in insulin target tissues, promoting a chronic inflammatory state and insulin resistance. Galectin-3 (Gal3), a lectin mainly secreted by macrophages, is elevated in both obese subjects and mice. Administration of Gal3 to mice causes insulin resistance and glucose intolerance, whereas inhibition of Gal3, through either genetic or pharmacologic loss of function, improved insulin sensitivity in obese mice. In vitro treatment with Gal3 directly enhanced macrophage chemotaxis, reduced insulin-stimulated glucose uptake in myocytes and 3T3-L1 adipocytes and impaired insulin-mediated suppression of glucose output in primary mouse hepatocytes. Importantly, we found that Gal3 can bind directly to the insulin receptor (IR) and inhibit downstream IR signaling. These observations elucidate a novel role for Gal3 in hepatocyte, adipocyte, and myocyte insulin resistance, suggesting that Gal3 can link inflammation to decreased insulin sensitivity. Inhibition of Gal3 could be a new approach to treat insulin resistance.

Van der Waals heterostructure polaritons with moiré-induced nonlinearity.

Controlling matter-light interactions with cavities is of fundamental importance in modern science and technology1. This is exemplified in the strong-coupling regime, where matter-light hybrid modes form, with properties that are controllable by optical-wavelength photons2,3. By contrast, matter excitations on the nanometre scale are harder to access. In two-dimensional van der Waals heterostructures, a tunable moiré lattice potential for electronic excitations may form4, enabling the generation of correlated electron gases in the lattice potentials5-9. Excitons confined in moiré lattices have also been reported10,11, but no cooperative effects have been observed and interactions with light have remained perturbative12-15. Here, by integrating MoSe2-WS2 heterobilayers in a microcavity, we establish cooperative coupling between moiré-lattice excitons and microcavity photons up to the temperature of liquid nitrogen, thereby integrating versatile control of both matter and light into one platform. The density dependence of the moiré polaritons reveals strong nonlinearity due to exciton blockade, suppressed exciton energy shift and suppressed excitation-induced dephasing, all of which are consistent with the quantum confined nature of the moiré excitons. Such a moiré polariton system combines strong nonlinearity and microscopic-scale tuning of matter excitations using cavity engineering and long-range light coherence, providing a platform with which to study collective phenomena from tunable arrays of quantum emitters.

Hepatocyte leukotriene B4 receptor 1 promotes NAFLD development in obesity.

BACKGROUND AND AIMS: NAFLD is the most prevalent chronic liver disease worldwide and has emerged as a serious public health issue with no approved treatment. The development of NAFLD is strongly associated with hepatic lipid content, and patients with NAFLD have significantly higher rates of hepatic de novo lipogenesis (DNL) than lean individuals. Leukotriene B4 (LTB4), a metabolite of arachidonic acid, is dramatically increased in obesity and plays important role in proinflammatory cytokine production and insulin resistance. But the role of liver LTB4/LTB4 receptor 1 (Ltb4r1) in lipid metabolism is unclear. APPROACH AND RESULTS: Hepatocyte-specific knockout (HKO) of Ltb4r1 improved hepatic steatosis and systemic insulin resistance in both diet-induced and genetically induced obese mice. The mRNA level of key enzymes involved in DNL and fatty acid esterification decreased in Ltb4r1 HKO obese mice. LTB4/Ltb4r1 directly promoted lipogenesis in HepG2 cells and primary hepatocytes. Mechanically, LTB4/Ltb4r1 promoted lipogenesis by activating the cAMP-protein kinase A (PKA)-inositol-requiring enzyme 1α (IRE1α)-spliced X-box-binding protein 1 (XBP1s) axis in hepatocytes, which in turn promoted the expression of lipogenesis genes regulated by XBP1s. In addition, Ltb4r1 suppression through the Ltb4r1 inhibitor or lentivirus-short hairpin RNA delivery alleviated the fatty liver phenotype in obese mice. CONCLUSIONS: LTB4/Ltb4r1 promotes hepatocyte lipogenesis directly by activating PKA-IRE1α-XBP1s to promote lipogenic gene expression. Inhibition of hepatocyte Ltb4r1 improved hepatic steatosis and insulin resistance. Ltb4r1 is a potential therapeutic target for NAFLD.

Nanoscale Mapping of Morphology of Organic Thin Films.

We determine precise nanoscale information about the morphologies of several organic thin film structures using Fourier plane imaging microscopy (FIM). We used FIM microscopy to detect the orientation of molecular transition dipole moments from an extremely low density of luminescent dye molecules, which we call "morphology sensors". The orientation of the sensor molecules is driven by the local film structure and thus can be used to determine details of the host morphology without influencing it. We use symmetric planar phosphorescent dye molecules as the sensors that are deposited into the bulk of organic film hosts during the growth. We demonstrate morphological mapping with a depth resolution to a few Ångstroms that is limited by the ability to determine thickness during deposition, along with an in-plane resolution limited by optical diffraction. Furthermore, we monitor morphological changes arising from thermal annealing of metastable organic films that are commonly employed in photonic devices.

Inflammation and insulin resistance: New targets encourage new thinking: Galectin-3 and LTB4 are pro-inflammatory molecules that can be targeted to restore insulin sensitivity.

Galectin-3 and LTB4 are pro-inflammatory molecules recently shown to directly cause insulin resistance in mouse and human cells. They are highly expressed in the obese state, and can be targeted both genetically and pharmacologically to improve insulin sensitivity in vivo. This expands on previous research showing that targeting inflammatory cytokines can be insulin sensitizing in animal models. However, translating these potential therapies into the human setting remains challenging. Here we review this latest research, and discuss how balancing their pleiotropic functions, the action of the microbiome, and the ability to identify relevant patient populations are vital considerations for successful anti-inflammatory insulin sensitizing therapy.

Effect of Chronic Pioglitazone Treatment on Hepatic Gene Expression Profile in Obese C57BL/6J Mice.

Pioglitazone, a selective ligand of peroxisome proliferator-activated receptor gamma (PPARγ), is an insulin sensitizer drug that is being used in a number of insulin-resistant conditions, including non-alcoholic fatty liver disease (NAFLD). However, there is a discrepancy between preclinical and clinical data in the literature and the benefits of pioglitazone treatment as well as the precise mechanism of action remain unclear. In the present study, we determined the effect of chronic pioglitazone treatment on hepatic gene expression profile in diet-induced obesity (DIO) C57BL/6J mice in order to understand the mechanisms of NAFLD induced by PPARγ agonists. DIO mice were treated with pioglitazone (25 mg/kg/day) for 38 days, the gene expression profile in liver was evaluated using Affymetrix Mouse GeneChip 1.0 ST array. Pioglitazone treatment resulted in exacerbated hepatic steatosis and increased hepatic triglyceride and free fatty acids concentrations, though significantly increased the glucose infusion rate in hyperinsulinemic-euglycemic clamp test. The differentially expressed genes in liver of pioglitazone treated vs. untreated mice include 260 upregulated and 86 downregulated genes. Gene Ontology based enrichment analysis suggests that inflammation response is transcriptionally downregulated, while lipid metabolism is transcriptionally upregulated. This may underlie the observed aggravating liver steatosis and ameliorated systemic insulin resistance in DIO mice.

[Metformin ameliorates ß-cell dysfunction by regulating inflammation production, ion and hormone homeostasis of pancreas in diabetic KKAy mice].

This study is to evaluate the effects of the metformin (Met) on ß cell function of diabetic KKAy mice. Female diabetic KKAy mice selected by insulin tolerance test (ITT) were divided randomly into two groups. Con group was orally administered by gavage with water, Met group with metformin hydrochloride at a dose of 0.2 g x kg(-1) for about 12 weeks. ITT and glucose tolerance tests (OGTT) were determined. Beta cell function was assessed by hyperglycemic clamp. Pancreatic biochemical indicators were tested. The changes of gene and protein expression in the pancreas and islets were also analyzed by Real-Time-PCR and immunostaining. Met significantly improved glucose intolerance and insulin resistance in KKAy mice. Fasting plasma glucose and insulin levels were also decreased. In addition, Met markedly increased glucose infusion rate (GIR) and elevated the Ist phase and maximum insulin secretion during clamp. It showed that Met decreased TG content and iNOS activities and increased Ca(2+) -Mg(2+)-ATPase activity in pancreas. Islets periphery was improved, and down-regulation of glucagon and up-regulated insulin protein expressions were found after Met treatment. Pancreatic mRNA expressions of inflammation factors including TLR4, NF-κB, JNK, IL-6 and TNF-α were down-regulated, p-NF-κB p65 protein levels also down-regulated by Met. And mRNA expressions of ion homeostasis involved in insulin secretion including SERCA2 and Kir6.2 were up-regulated by Met. Met increased SIRT5 expression level in pancreas of KKAy mice under the hyperglycemic clamp. These results indicated that chronic administration of Met regulated pancreatic inflammation generation, ion and hormone homeostasis and improved ß cell function of diabetic KKAy mice.

[Effect of Mudan Granule on islets beta cell function in monosodium glutamate induced obese mice with insulin resistance: an experimental study].

OBJECTIVE: To study the effect of Mudan Granule (MD) on the glucose metabolism and beta cell function in monosodium glutamate (MSG) induced obese mice with insulin resistance (IR). METHODS: MSG obese mice were induced by subcutaneous injecting MSG (4 g/kg for 7 successive days in neonatal ICR mice). Forty MSG mice with IR features were recruited and divided into four groups according to body weight, fasting blood glucose, triglyceride (TG), total cholesterol (TC), and the percentage of blood glucose decreased within 40 min in the IR test, i.e., the model group (Con), the low dose MD group, the high dose MD group, and the Metformin group (Met). Besides, another 10 ICR mice were recruited as the normal control group (Nor). The water solvent of 2.5 g/kg MD or 5 g/kg MD was respectively administered to mice in the low dose MD group and the high dose MD group. Metformin hydrochloride was given to mice in the Met group at 0.2 g/kg body weight. Equal dose solvent distilled water was administered to mice in the Nor group and the Con group by gastrogavage, once per day. All medication was lasted for 15 weeks. Insulin tolerance test (ITT) and oral glucose tolerance test (OGTT) were performed after 6 weeks of treatment. Beta cell function was assessed by hyperglycemic clamp technique. The morphological changes in the pancreas were evaluated by hematoxylin-eosin (HE) staining. Changes of iNOS, NF-kappaB p65, and p-NF-kappaB p65 in the pancreas were tested. RESULTS: Compared with the Nor group, the blood glucose level, AUC, and fasting blood insulin, ONOO-contents, iNOS activities, and the expression of iNOS, NF-kappaB p65 subunit, pNF-kappaB p65 subunit obviously increased; decreased percentage of blood glucose within 40 min in ITT, glucose infusion rate (GIR), Clamp 1 min insulin, and Max-Insulin obviously decreased in the Con group (P < 0.05, P < 0.01). Compared with the Con group, the aforesaid indices could be improved in the Met group (P < 0.05, P < 0.01). In the low dose MD group, AUC, iNOS activities, and the expression of iNOS and p-NF-kappaB p65 subunit obviously decreased; percentage of blood glucose within 40 min in ITT and GIR obviously increased (P < 0.05, P < 0.01). In the high dose MD group, AUC, ONOO-contents, iNOS activities, and the expression of iNOS, NF-kappaB p65 subunit, and p-NF-KB p65 subunit obviously decreased; percentage of blood glucose within 40 min in ITT, Max-Insulin, and GIR obviously increased (P < 0.05, P < 0.01). CONCLUSION: MD could significantly improve IR and functional disorder of 3 cells in MSG obese mice, which might be associated with lowering inflammatory reaction in the pancreas.

Understanding and Weakening Photon Recycling in Solar Cells to Approach the Radiative Limit.

Photon recycling plays an important role in the light outcoupling of state-of-the-art solar cells and is considered a necessary condition to achieve the radiative limit of open-circuit voltage (VOC) and efficiency. However, due to the impact of photon recycling on bulk and surface radiation of solar cells being overlooked, experimental demonstrations on the accuracy of existing photon recycling models are scarce and some contrary theoretical results also emerge. Here, the relationship between photon recycling and radiation processes, as well as the corresponding VOC losses of solar cells based on the principle of detailed balance is clarified. It is shown that weakening photon recycling is more effective to boost the device performance than enhancing it, promoting the theoretical efficiencies of solar cells, such as perovskite, Si, and GaAs, to 98.5%, 94.9%, and almost 100% of their radiative limit, respectively. Moreover, weakening photon recycling also helps to maintain higher efficiency when the internal radiative efficiency decreases, which benefits higher device stability. This work provides an in-depth understanding of the role of photon recycling in solar cells and helps to push efficiency to a new limit.

Reduced graphene oxide-encaged submicron-silicon anode interfacially stabilized by Al2O3 nanoparticles for efficient lithium-ion batteries.

Silicon-carbon composites have been recognized as some of the most promising anode candidates for advancing new-generation lithium-ion batteries (LIBs). The development of high-efficiency silicon/graphene anodes through a simple and cost-effective preparation route is significant. Herein, by using micron silicon as raw material, we designed a mesoporous composite of silicon/alumina/reduced graphene oxide (Si/Al2O3/RGO) via a two-step ball milling combined annealing process. Commercial Al2O3 nanoparticles are introduced as an interlayer due to the toughening effect, while RGO nanosheets serve as a conductive and elastic coating to protect active submicron silicon particles during lithium alloying/dealloying reactions. Owing to the rational porous structure and dual protection strategy, the core/shell structured Si/Al2O3/RGO composite is efficient for Li+ storage and demonstrates improved electrical conductivity, accelerated charge transfer and electrolyte diffusion, and especially high structural stability upon charge/discharge cycling. As a consequence, Si/Al2O3/RGO yields a high discharge capacity of 852 mA h g-1 under a current density of 500 mA g-1 even after 200 cycles, exhibiting a high capacity retention of ∼85%. Besides, Si/Al2O3/RGO achieves excellent cycling reversibility and superb high-rate capability with a stable specific capacity of 405 mA h g-1 at 3000 mA g-1. Results demonstrate that the Al2O3 interlayer is synergistic with the indispensable RGO nanosheet shells, affording more buffer space for silicon cores to alleviate the mechanical expansion and thus stabilizing active silicon species during charge/discharge cycles. This work provides an alternative low-cost approach to achieving high-capacity silicon/carbon composites for high-performance LIBs.

Trimethylamine N-oxide impairs ß-cell function and glucose tolerance.

ß-Cell dysfunction and ß-cell loss are hallmarks of type 2 diabetes (T2D). Here, we found that trimethylamine N-oxide (TMAO) at a similar concentration to that found in diabetes could directly decrease glucose-stimulated insulin secretion (GSIS) in MIN6 cells and primary islets from mice or humans. Elevation of TMAO levels impairs GSIS, ß-cell proportion, and glucose tolerance in male C57BL/6 J mice. TMAO inhibits calcium transients through NLRP3 inflammasome-related cytokines and induced Serca2 loss, and a Serca2 agonist reversed the effect of TMAO on ß-cell function in vitro and in vivo. Additionally, long-term TMAO exposure promotes ß-cell ER stress, dedifferentiation, and apoptosis and inhibits ß-cell transcriptional identity. Inhibition of TMAO production improves ß-cell GSIS, ß-cell proportion, and glucose tolerance in both male db/db and choline diet-fed mice. These observations identify a role for TMAO in ß-cell dysfunction and maintenance, and inhibition of TMAO could be an approach for the treatment of T2D.

Galectin-3 impairs calcium transients and ß-cell function.

In diabetes, macrophages and inflammation are increased in the islets, along with ß-cell dysfunction. Here, we demonstrate that galectin-3 (Gal3), mainly produced and secreted by macrophages, is elevated in islets from both high-fat diet (HFD)-fed and diabetic db/db mice. Gal3 acutely reduces glucose-stimulated insulin secretion (GSIS) in ß-cell lines and primary islets in mice and humans. Importantly, Gal3 binds to calcium voltage-gated channel auxiliary subunit gamma 1 (CACNG1) and inhibits calcium influx via the cytomembrane and subsequent GSIS. ß-Cell CACNG1 deficiency phenocopies Gal3 treatment. Inhibition of Gal3 through either genetic or pharmacologic loss of function improves GSIS and glucose homeostasis in both HFD-fed and db/db mice. All animal findings are applicable to male mice. Here we show a role of Gal3 in pancreatic ß-cell dysfunction, and Gal3 could be a therapeutic target for the treatment of type 2 diabetes.

Isolating the Oxygen Adsorption Defects on Sputtered Tin Oxide for Efficient Perovskite Solar Cells.

Tin oxide (SnO2) is the most commonly used electron transport material for perovskite solar cells (PSCs). Various techniques have been applied to deposit tin dioxide, including spin-coating, chemical bath deposition, and magnetron sputtering. Among them, magnetron sputtering is one of the most mature industrial deposition techniques. However, PSCs based on magnetron-sputtered tin oxide (sp-SnO2) have a lower open-circuit voltage (Voc) and power conversion efficiency (PCE) than those prepared by the mainstream solution method. This is mainly due to the oxygen-related defects at the sp-SnO2/perovskite interface, and traditional passivation strategies usually have little effect on them. Herein, we successfully isolate the oxygen adsorption (Oads) defects located on the surface of sp-SnO2 from the perovskite layer using a PCBM double-electron transport layer. This isolation strategy effectively suppresses the Shockley-Read-Hall recombination at the sp-SnO2/perovskite interface, which results in an increase in the Voc from 0.93 to 1.15 V and an increase in PCE from 16.66 to 21.65%. To our knowledge, this is the highest PCE achieved using a magnetron-sputtered charge transport layer to date. The unencapsulated devices maintain 92% of their initial PCE after storage in air with a relative humidity of 30-50% after 750 h. We further use the solar cell capacitance simulator (1D-SCAPS) to confirm the effectiveness of the isolation strategy. This work highlights the application prospect of magnetron sputtering in the field of perovskite solar cells and provides a simple yet effective way to tackle the interfacial defect issue.

All-carbon electrode-based fiber-shaped dye-sensitized solar cells.

A novel fiber-shaped dye-sensitized solar cell (DSSC) based on an all-carbon electrode is presented, where low-cost, highly-stable, and biocompatible carbon materials are applied to both the photoanode and the counter electrode. The fibrous carbon-based photoanode has a core-shell structure, with carbon fiber core used as conductive substrate to collect carriers and sensitized porous TiO(2) film as shell to harvest light effectively. The highly catalytic all-carbon counter electrode is made from ink carbon coatings and carbon fiber substrate. Results show that the open circuit voltage can be largely improved through engineering at the carbon fiber/TiO(2) interface. An optimized diameter of the photoanode results in an efficiency of 1.9%. It is the first demonstration of efficient DSSCs based on all-carbon electrodes, and the devices are totally free from TCOs or any other expensive electrode materials. Also, this type of solar cell is significant in obtaining bio-friendly all-carbon photovoltaics suitable for large-scale production.

Flexible and Conductive Polymer Threads for Efficient Fiber-Shaped Supercapacitors via Vapor Copolymerization.

Flexible fiber electrodes are critical for high-performance fiber and wearable electronics. In this work, we presented a highly conductive all-polymer fiber electrode by vapor copolymerization of 2,5-dibromo-3,4-vinyldioxythiophene (DBEDOT) and 2,5-diiodo-3,4-vinyldioxythiophene (DIEDOT) monomers on commonly used polyester threads (PETs) at a temperature as low as 80 °C. The poly(3,4-ethylenedioxythiophene) (PEDOT)-coated PET threads maintain excellent flexibility and show conductivity of 7.93 S cm-1, nearly four times higher than that reported previously via homopolymerization of DBEDOT monomer. A MnO2 active layer was embedded into the PEDOT double layers, and the flexible fiber composite electrode showed a high linear specific capacitance of 157 mF cm-1 and improved stability, retaining 86.5% capacitance after 5000 cycles. Fiber-shaped solid-state supercapacitors (FSSCs) based on the composite electrodes were assembled, and they displayed superior electrochemical performance. This work provides a new approach to realize high-performance and stable wearable electronics.

Doping Mechanism of Perovskite Films with PbCl2 Prepared by Magnetron Sputtering for Enhanced Efficiency of Solar Cells.

The last decade has witnessed a rapid growth of perovskite solar cells extended from mesoporous to planar architecture as well as from solution processing to solvent-free fabrication. The preparation of perovskite films by solvent-free method still presents significant challenges, such as the difficulty of film preparation by multiple evaporation sources in vapor deposition and the immaturity of the sputtered method. Here, we present a planar perovskite solar cell fabricated by solvent-free magnetron sputtering without the assistance of the mesoporous TiO2 layer, and lead chloride (PbCl2) was mechanically milled into the target of methylammonium lead halides (MAPbI3) to improve the quality of perovskite film by regulating the crystallization process with the Cl element. Furthermore, the internal reason for the effect of different PbCl2 doping contents on the trap density of perovskite films was also investigated in detail. These lead to an improved power conversion efficiency of planar heterojunction perovskite solar cells up to 17.10%, which is the highest efficiency recorded for the sputtered perovskite solar cells so far. The stability of resulting solar cells has also been significantly improved by exploring the doping mechanism of perovskite films with PbCl2 in detail, showing great research and application prospect.

Insulin induces insulin receptor degradation in the liver through EphB4.

Insulin signaling is essential for glucose metabolism, and insulin decreases insulin receptor (InsR) levels in a dose-dependent and time-dependent manner. However, the regulatory mechanisms of InsR reduction upon insulin stimulation remain poorly understood. Here, we show that Eph receptor B4 (EphB4), a tyrosine kinase receptor that modulates cell adhesion and migration, can bind directly to InsR, and this interaction is markedly enhanced by insulin. Due to the adaptor protein 2 (Ap2) complex binding motif in EphB4, the interaction of EphB4 and InsR facilitates clathrin-mediated InsR endocytosis and degradation in lysosomes. Hepatic overexpression of EphB4 decreases InsR and increases hepatic and systemic insulin resistance in chow-fed mice, whereas genetic or pharmacological inhibition of EphB4 improve insulin resistance and glucose intolerance in obese mice. These observations elucidate a role for EphB4 in insulin signaling, suggesting that EphB4 might represent a therapeutic target for the treatment of insulin resistance and type 2 diabetes.

Large size, high efficiency fiber-shaped dye-sensitized solar cells.

A high-efficiency dye-sensitized solar cell prototype has been designed and fabricated, in which the working electrode and counter electrode are in direct contact and singly twisted. The cell is sealed in a capillary. In this solar cell configuration, the area ratio between the counter and working electrode is extremely low which allows the independent adjustment of electrolyte volume and the distance between counter electrode and photo-anode. Also it is more easily sealed compared to planar solar cell. The effects of TiO(2) film thickness, twisted pitch of counter electrode and length of device have been investigated. Our results indicate that this novel configuration has demonstrated excellent modularization function, three dimensional light harvesting capacities and the relative independence of incident light angles due to the symmetry structure. The power conversion efficiency of one cell of 9.5 cm in length can reach up to 5.41% at standard test condition (100 mW cm(-2)) and the power output may double under intense diffuse illumination. As far as we know, this is the longest and most efficient fiber-shaped dye-sensitized solar cell consisting of liquid electrolyte. The longer the fiber-shaped solar cell is, the more suitable it is for woven solar power textile if it is encapsulated in transparent flexible plastic capillary.

Paracrine FGFs target skeletal muscle to exert potent anti-hyperglycemic effects.

Several members of the FGF family have been identified as potential regulators of glucose homeostasis. We previously reported that a low threshold of FGF-induced FGF receptor 1c (FGFR1c) dimerization and activity is sufficient to evoke a glucose lowering activity. We therefore reasoned that ligand identity may not matter, and that besides paracrine FGF1 and endocrine FGF21, other cognate paracrine FGFs of FGFR1c might possess such activity. Indeed, via a side-by-side testing of multiple cognate FGFs of FGFR1c in diabetic mice we identified the paracrine FGF4 as a potent anti-hyperglycemic FGF. Importantly, we found that like FGF1, the paracrine FGF4 is also more efficacious than endocrine FGF21 in lowering blood glucose. We show that paracrine FGF4 and FGF1 exert their superior glycemic control by targeting skeletal muscle, which expresses copious FGFR1c but lacks ß-klotho (KLB), an obligatory FGF21 co-receptor. Mechanistically, both FGF4 and FGF1 upregulate GLUT4 cell surface abundance in skeletal muscle in an AMPKα-dependent but insulin-independent manner. Chronic treatment with rFGF4 improves insulin resistance and suppresses adipose macrophage infiltration and inflammation. Notably, unlike FGF1 (a pan-FGFR ligand), FGF4, which has more restricted FGFR1c binding specificity, has no apparent effect on food intake. The potent anti-hyperglycemic and anti-inflammatory properties of FGF4 testify to its promising potential for use in the treatment of T2D and related metabolic disorders.

Ultralong-Range Energy Transport in a Disordered Organic Semiconductor at Room Temperature Via Coherent Exciton-Polariton Propagation.

Amorphous molecular solids are inherently disordered, exhibiting strong exciton localization. Optical microcavities containing such disordered excitonic materials have been theoretically shown to support both propagating and localized exciton-polariton modes. Here, the ultrastrong coupling of a Bloch surface wave photon and molecular excitons in a disordered organic thin film at room temperature is demonstrated, where the major fraction of the polaritons are propagating states. The delocalized exciton-polariton has a group velocity as high as 3 × 107 m s-1 and a lifetime of 500 fs, leading to propagation distances of over 100 µm from the excitation source. The polariton intensity shows a halo-like pattern that is due to self-interference of the polariton mode, from which a coherence length of 20 µm is derived and is correlated with phase breaking by polariton scattering. The demonstration of ultralong-range exciton-polariton transport at room temperature promises new photonic and optoelectronic applications such as efficient energy transfer in disordered condensed matter systems.