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Three-dimensional (3D) culture of mesenchymal stem cells has become an important research and development topic. However, comprehensive analysis of human dental pulp-derived mesenchymal stem cells (DPSCs) in 3D-spheroid culture remains unexplored. Thus, we evaluated the cellular characteristics, multipotent differentiation, gene expression, and related-signal transduction pathways of DPSCs in 3D-spheroid culture via magnetic levitation (3DM), compared with 2D-monolayer (2D) and 3D-aggregate (3D) cultures. The gross morphology and cellular ultrastructure were observed in the 2D, 3D, and 3DM experimental groups using scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Surface markers and trilineage differentiation were evaluated using flow cytometry and staining analysis. Quantitative reverse transcription-polymerase chain reaction and immunofluorescence staining (IF) were performed to investigate the expression of differentiation and stemness markers. Signaling transduction pathways were evaluated using western blot analysis. The morphology of cell aggregates and spheroids was largely influenced by the types of cell culture plates and initial cell seeding density. SEM and TEM experiments confirmed that the solid and firm structure of spheroids was quickly formed in the 3DM-medium without damaging cells. In addition, these three groups all expressed multilineage differentiation capabilities and surface marker expression. The trilineage differentiation capacities of the 3DM-group were significantly superior to the 2D and 3D-groups. The osteogenesis, angiogenesis, adipogenesis, and stemness-related genes were significantly enhanced in the 3D and 3DM-groups. The IF analysis showed that the extracellular matrix expression, osteogenesis, and angiogenesis proteins of the 3DM-group were significantly higher than those in the 2D and 3D-groups. Finally, 3DM-culture significantly activated the MAPK and NF-kB signaling transduction pathways and ameliorated the apoptosis effects of 3D-culture. This study confirmed that 3DM-spheroids efficiently enhanced the therapeutic efficiency of DPSCs.

Obesity is associated with an increased risk of an iron deficiency; however, a synergistic relationship between iron and lipid homeostasis was also observed. The aim of this study was to investigate the effects of pharmacological doses of iron supplementation on omega 3 (n-3) and omega 6 (n-6) polyunsaturated fatty acids (PUFAs). Sprague-Dawley (SD) rats were fed a normal diet or a 50% high-fat diet (HFD) without or with pharmacological doses of ferric citrate (0.25, 1, or 2 g ferric iron per kg diet) for 12 weeks, and erythrocyte profiles of n-3 and n-6 PUFAs were quantitated. Ferric citrate supplementation showed dose-related effects on liver inflammation, liver iron accumulation, and increasing circulating levels of iron, erythrocyte degradation biomarkers LVV-hemorphin-7, malondialdehyde (MDA), and insulin. Obese rats supplemented with 2 g ferric iron per kg diet also had decreased levels of eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and total n-3 PUFAs compared to rats fed a normal diet or HFD alone. A western blotting analysis revealed that iron-mediated downregulation of n-3 PUFA-converting enzymes (Δ5 and Δ6 desaturases) only occurred at high dosages (≥1 g ferric iron per kg diet). A Spearman correlation analysis showed that total liver iron and serum LVV-hemorphin-7 and MDA were negatively correlated with n-3 PUFAs and their converting enzymes (Δ5 and Δ6 desaturases) (all p 1 g of ferric iron per kg diet) exhibited decreased n-3 PUFA levels via downregulation of expressions of Δ5 and Δ6 desaturase enzymes.

IgA nephropathy (IgAN), the most common primary glomerular disorder, has a relatively poor prognosis yet lacks a pathogenesis-based treatment. Compound K (CK) is a major absorbable intestinal bacterial metabolite of ginsenosides, which are bioactive components of ginseng. The present study revealed promising therapeutic effects of CK in two complementary IgAN models: a passively induced one developed by repeated injections of IgA immune complexes and a spontaneously occurring model of spontaneous grouped ddY mice. The potential mechanism for CK includes 1) inhibiting the activation of NLRP3 inflammasome in renal tissues, macrophages and bone marrow–derived dendritic cells, 2) enhancing the induction of autophagy through increased SIRT1 expression, and 3) eliciting autophagy-mediated NLRP3 inflammasome inhibition. The results support CK as a drug candidate for IgAN.

Background:Mesenchymal stem cell (MSC)-based tissue engineering plays a major role in regenerative medicine. However, the efficiency of MSC transplantation and survival of engrafted stem cells remain challenging. Melatonin can regulate MSC biology. However, its function in the osteogenic differentiation of dental pulp-derived MSCs (DPSCs) remains unclear. We investigated the effects and mechanisms of melatonin preconditioning on the osteogenic differentiation and bone regeneration capacities of DPSCs.Methods:The biological effects and signaling mechanisms of melatonin with different concentrations on DPSCs were evaluated using a proliferation assay, the quantitative alkaline phosphatase (ALP) activity, Alizarin red staining, a real-time polymerase chain reaction, and a western blot in vitro cell culture model. The in vivo bone regeneration capacities were assessed among empty control, MBCP, MBCP+DPSCs, and MBCP+DPSCs+melatonin preconditioning in four-created calvarial bone defects by using micro–computed tomographic, histological, histomorphometric, and immunofluorescence analyses after 4 and 8 weeks of healing.Results:In vitro experiments revealed that melatonin (1, 10, and 100 μM) significantly and concentration-dependently promoted proliferation, surface marker expression (CD 146), ALP activity and extracellular calcium deposition, and osteogenic gene expression of DPSCs (p < 0.05). Melatonin activated the phosphorylation of RUNX-2 and OCN and inhibited COX-2/NF-κB phosphorylation. Furthermore, the phosphorylation of mitogen-activated protein kinase (MAPK) P38/ERK signaling was significantly increased in DPSCs treated with 100 μM melatonin, and their inhibitors significantly decreased osteogenic differentiation. In vivo experiments demonstrated that bone defects implanted with MBCP bone-grafting materials and melatonin-preconditioned melatonin exhibited significantly greater bone volume fraction, trabecular bone structural modeling, new bone formation, and osteogenesis-related protein expression than the other three groups at 4 and 8 weeks postoperatively (p < 0.05).Conclusions:These results suggest that melatonin promotes the proliferation and osteogenic differentiation of DPSCs by regulating COX-2/NF-κB and p38/ERK MAPK signaling pathways. Preconditioning DPSCs with melatonin before transplantation can efficiently enhance MSC function and regenerative capacities.

Background Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion of trinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HD involve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinase ataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM is involved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays a critical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expanded mutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effective component of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HD remains unclear and warrants further investigation. Methods This study used the R6/2 transgenic mouse model of HD and performed behavioral tests, survival rate, histological analyses, and immunoblot assays. Results The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK and reduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density and lifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2 protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions Thus, the oral administration of CK reduced the disease progression and markedly enhanced lifespan in the transgenic mouse model (R6/2) of HD.

Oral squamous cell carcinoma (OSCC) accounts for 5.8% of all malignancies in Taiwan, and the incidence of OSCC is on the rise. OSCC is also a common malignancy worldwide, and the five-year survival rate remains poor. Therefore, new and effective treatments are needed to control OSCC. In the present study, we prepared ginsenoside M1 (20-O-beta-d-glucopyranosyl-20(S)-protopanaxadiol), a major deglycosylated metabolite of ginsenoside, through the biotransformation of Panax notoginseng leaves by the fungus SP-LSL-002. We investigated the anti-OSCC activity and associated mechanisms of ginsenoside M1 in vitro and in vivo. We demonstrated that ginsenoside M1 dose-dependently inhibited the viability of human OSCC SAS and OEC-M1 cells. To gain further insight into the mode of action of ginsenoside M1, we demonstrated that ginsenoside M1 increased the expression levels of Bak, Bad, and p53 and induced apoptotic DNA breaks, G1 phase arrest, PI/Annexin V double-positive staining, and caspase-3/9 activation. In addition, we demonstrated that ginsenoside M1 dose-dependently inhibited the colony formation and migration ability of SAS and OEC-M1 cells and reduced the expression of metastasis-related protein vimentin. Furthermore, oral administration or subcutaneous injection of ginsenoside M1 significantly reduced tumor growth in SAS xenograft mice. These results indicate that ginsenoside M1 can be translated into a potential therapeutic against OSCC.

Formaldehyde is a reactive carbonyl species (RCS) that is produced naturally in the human body via metabolic and epigenetic biochemical processes, yet in high concentrations is highly toxic to the environment as well as to living organisms. Therefore, we designed two ratiometric electrochemical molecular redox probes, Formaldehyde oxidative latent probe (FOLP) and dihydroxy-formaldehyde oxidative latent probe (HFOLP), for the selective profiling of endogenous formaldehyde. FOLP and HFOLP each underwent the aza-Cope reaction with formaldehyde followed by hydrolysis to eliminate unmask redox reporter N-alkylated aminoferrocene (AAF) to monitor their response current. The FOLP and HFOLP sensors showed broad dynamic ranges of 0.12–1000 μM and 0.09–3 mM for formaldehyde with detection limits of 48.2 nM and 31.6 μM, respectively. Also, since formaldehyde is the byproduct of biochemical reactions for detecting creatinine and creatinine is an important biomarker for chronic kidney disease (CKD), we tested the FOLP probe for its ability to monitor creatinine. It successfully did so, and this ability was used to develop an electrochemical platform for the quantification of creatinine; it showed a dynamic range of 3.25–200 μM and a limit of detection (1.3 μM). In addition, the FOLP-based assay platform delivered a reliable analytical performance for the quantification of formaldehyde in human whole blood and of creatinine in saliva, and also for the real-time monitoring of endogenous formaldehyde secretion in HeLa cells. Moreover, the concentrations determined using our method were found to be consistent with those determined using formaldehyde and creatinine fluorometric assay kits.

This study was motivated by clinical observations that dysmetabolic iron overload syndrome (DIOS) and an androgen deficiency are common features observed in obese adult men; however, the molecular mechanism underlying the effects of DIOS on androgen deficiency remains to be elucidated. We established a DIOS animal model by feeding Sprague-Dawley rats an iron/fat-enriched diet (50% fat plus 0.25, 1, or 2 g ferric iron per kg diet) for 12 weeks to induce iron dysfunction (indicated by decreased tissue iron efflux) in obese rats. Obese rats fed an iron/fat-enriched diet showed decreased levels of testicular total Testosterone (T) and iron exporter ferroportin but increased levels of testicular iron and hepcidin, and these effects were more evident with a >1 g ferric iron per kg diet. A western blot analysis showed that an iron/fat-enriched diet triggered testicular endoplasmic reticular (ER) stress but decreased mitochondrion biogenesis proteins (PGC1α and TFAM) and T-converting proteins (StAR, CYP11A, and 17β-HSD). TUNEL staining showed that >1 g ferric iron induced apoptosis mainly in germ cells and Leydig's cells. Uncontrolled testicular iron efflux may cause mitochondrial-ER dysfunction and affect T biosynthesis. Future study targeting the testicular hepcidin–ferroportin axis may offer a therapeutic tool to alleviate testicular iron retention and mitochondrial-ER stress in Leydig's cells.

The literature suggests a bidirectional relationship between testosterone (T) and iron, but mechanisms underlying this relationship remain unclear. We investigated effects of iron on advanced glycation end products (AGEs) in obesity-related androgen deficiency. In total, 111 men were recruited, and iron biomarkers and N(ɛ)-(carboxymethyl)lysine (CML) were measured. In an animal study, rats were fed a 50% high-fat diet (HFD) with (0.25, 1, and 2 g ferric iron/kg diet) or without ferric citrate for 12 weeks. Obese rats supplemented with &gt, 1 g iron/kg diet had decreased testicular total T compared to HFD alone. Immunohistochemical staining showed that &gt, 1 g of ferric iron increased iron and AGE retention in testicular interstitial tissues, which is associated with increased expression of the receptor for AGEs (RAGE), tumor necrosis factor-α, and nitric oxide. Compared with normal weight, overweight/obese men had lower T levels and higher rates of hypogonadism (19% vs. 11.3%) and iron overload (29.8% vs.15.9%). A correlation analysis showed serum total T was positively correlated with transferrin saturation (r = 0.242, p = 0.007) and cathepsin D (r = 0.330, p = 0.001), but negatively correlated with red blood cell aggregation (r = −0.419, p&lt, 0.0001) and CML (r = −0.209, p &lt, 0.05). In conclusion, AGEs may partially explain the underlying relationship between dysregulated iron and T deficiency.

The bone regeneration efficiency of bone marrow mesenchymal stem cells (BMSCs) and dental pulp mesenchymal stem cells (DPSCs) combined with xenografts in the craniofacial region remains unclear. Accordingly, this study commenced by comparing the cell morphology, cell proliferation, trilineage differentiation, mineral synthesis, and osteogenic gene expression of BMSCs and DPSCs in vitro. Four experimental groups (empty control, Bio-Oss only, Bio-Oss+BMSCs, and Bio-Oss+DPSCs) were then designed and implanted in rabbit calvarial defects. The BMSCs and DPSCs showed a similar morphology, proliferative ability, surface marker profile, and trilineage-differentiation potential in vitro. However, the BMSCs exhibited a higher mineral deposition and expression levels of osteogenic marker genes, including alkaline phosphatase (ALP), runt related transcription factor 2 (RUNX2), and osteocalcin (OCN). In the in vivo studies, the bone volume density in both MSC groups was significantly greater than that in the empty control or Bio-Oss only group. Moreover, the new bone formation and Collagen I / osteoprotegerin protein expressions of the scaffold+MSC groups were higher than those of the Bio-Oss only group. Finally, the Bio-Oss+BMSC and Bio-Oss+DPSC groups had a similar bone mineral density, new bone formation, and osteogenesis-related protein expression. Overall, the DPSCs seeded on Bio-Oss matched the bone regeneration efficacy of BMSCs in vivo and hence appear to be a promising strategy for craniofacial defect repair in future clinical applications.

Chinese herbal medicines used in combination have long-term been shown to be mild remedies with "integrated effects." However, our study provides the first demonstration that M1, an active metabolite of ginsenoside, exerted its dramatic therapeutic effects on accelerated and severe lupus nephritis (ASLN) mice, featuring acute renal function impairment, heavy proteinuria, high serum levels of anti-dsDNA, and high-grade, diffuse proliferative renal lesions. In the present study, NZB/WF1 mice were given injections of lipopolysaccharide to induce the ASLN model. M1 (30 mg/kg) was then administered to the mice by gavage daily, and the mice were sacrificed on week 3 and week 5 after the induction of disease. To identify the potential mechanism of action for the pure compound, levels of NLRP3 inflammasome activation in bone marrow-derived dendritic cells (BMDCs), podocytes and macrophages, and antigen-specific T cell activation in BMDCs were determined in addition to mechanistic experiments in vivo. Treatment with M1 dramatically improved renal function, albuminuria and renal lesions and reduced serum levels of anti-dsDNA in the ASLN mice. These beneficial effects with M1 treatment involved the following cellular and molecular mechanistic events: [1] inhibition of NLRP3 inflammasome associated with autophagy induction, [2] modulation of T help cell activation, and [3] induction of regulatory T cell differentiation. M1 improved the ASLN mice by blunting NLRP3 inflammasome activation and differentially regulating T cell functions, and the results support M1 as a new therapeutic candidate for LN patients with a status of abrupt transformation of lower-grade (mesangial) to higher-grade (diffuse proliferative) nephritis.

Monascus species have been used in Chinese fermented foods such as Anka pork, and rice wine because of its bioactive substances including pigment, and monacolin K. In this study, the effect of light and temperature on red pigment, total polyphenols, DPPH radical scavenging, reducing ability and monacolin K of Monascus ruber BCRC31535 in rice solid culture was conducted. No obvious difference was observed by the DPPH radical scavenging assay whatever the cultural condition of light and temperature was performed. However, the results revealed that the red pigment, total polyphenols, reducing ability and monacolin K were the highest in the darkness at 30°C. Blue light and red light remarkably declined these secondary metabolites and antioxidant capacity, probably resulting from the induction of oxidative stress. By contrast, blue light can stimulate the production of red pigment and monacolin K at 20°C while red light can improve the reducing ability. Nevertheless, total polyphenols were not affected by light at the low temperature. Taking together, the temperature was also the interference factor in the solid-state culture of M. ruber BCRC31535, which influenced the light on the yield of secondary metabolites.

Leucine aminopeptidase (LAP) is an essential proteolytic enzyme and potential biomarker for liver malignancy. Overexpression of LAP is directly linked with some fatal physiological and pathological disorders. In this regard, we have designed an activity based electrochemical substrate leucine-benzyl ferrocene carbamate (Leu-FC) for selective profiling of LAP activity in live cells. In practice, LAP instantaneously hydrolyze the Leu residue of the substrate Leu-FC to eliminate the unmasked electrochemical reporter amino ferrocene via predefined self-immolative cascade. The electrochemical signal is distinctly specific for LAP and free of other electroactive biological interference. The substrate Leu-FC empowered sensor displayed broad dynamic range with admirable detection limits. On top of this, the probe Leu-FC was employed in real-time active profiling of cellular LAP activity in HepG2 cells and effect of LAP inhibitor. In extent, the substrate Leu-FC can effectively monitor cisplatin induced overexpression of LAP activity in HepG2 cells in presence and absence of bestatin. The sensor showcased an excellent reliability towards monitoring cellular LAP activity in HepG2 cells. Unlike the traditional antibody-based immunoassays, our approach is capable of monitoring in-situ activity of LAP in live cells.

Graphene oxide has been extensively investigated as an electron acceptor due to its exceptional electronic and optical properties. Here we report an unusual ultrafast electron transfer occurring in the nanocomposites of Au nanocluster (Au NC)–graphene oxide (GO) in which GO acts as an electron donor. An ultrafast electron transfer is corroborated from the excited states of graphene oxide into the highest occupied molecular orbital (HOMO) of Au NCs. It is found that the electron transfer rate is significantly higher in Au10–GO nanocomposites (4.17 × 1012 s−1) than that in Au25–GO (0.49 × 1012 s−1) due to a larger energy difference and smaller sized ligands. This finding suggests that graphene oxide–Au nanocluster nanocomposites can be very useful to construct novel nanostructures with enhanced visible light photovoltaic, photonic and photo-catalytic activities.

The behaviors of cat-anionic vesicles composed of dioctadecyldimethylammonium bromide (DODAB) and dihexadecyl phosphate (DHP) with varying lipid composition were investigated through the measurements of size, zeta potential and fluorescence polarization, morphological observations, determination of thermotropic phase behavior, cell viability assay, and examination of entrapment efficiency and colloid stability. DODAB is miscible with DHP in the bilayer domain, which expresses a non-ideal mixing characteristic. The DODAB-rich vesicles show a smaller particle size, higher positive zeta potential, lower main transition temperature, less angular structure, better storage stability, and higher encapsulation efficiency than the DHP-rich ones. Introduction of DODAB into DHP vesicles enhances the membrane fluidity in the ripple and liquid crystalline phases. The membrane fluidity of mixed DODAB-DHP vesicles with the near charge might have a significant effect on the survival of nontransformed human skin fibroblast Hs68 cells. The degree of the cytotoxicity of Hs68 cells is dominated mainly by the charge nature of DODAB-DHP vesicles with varying lipid composition. The results gathered provide necessary information for future drug/gene delivery applications.

cope Diabetes is associated with increased risks of anemia and activation of advanced glycation end products (AGEs) and the receptor for AGEs (RAGE). However, the effects of pharmacological doses of iron supplementation on AGE metabolism are less clear. The aim was to investigate the effect of ferric citrate supplementation on AGE metabolism. Methods and results Diabetes was induced in overnight starved rats by intraperitoneal injections of 40 mg/kg streptozotocin and 120 mg/kg nicotinamide. Diabetic rats were fed a standard diet or pharmacological doses of ferric citrate (0.5, 1, 2, and 3 g of ferric iron/kg diet) for 10 weeks. Ferric citrate supplementation showed a dose-related effect on the hepatic steatosis score, malondialdehyde, cathepsin D, and glyoxalase I. A Western blot analysis revealed that >1 g of ferric iron suppressed hepatic AGE receptor 1 and high-mobility group-box 1 expressions but increased heme oxygenase-1 and RAGE expressions. Further analysis showed that high doses of ferric iron triggered sterol regulatory element-binding protein 1c, p38-mitogen-activated protein kinase, and nuclear factor-κB protein expressions. Conclusions Overall, the present results suggest a dose-related effect of ferric citrate supplementation on AGE metabolism, and this effect was more evident at high iron doses (>1 g of ferric iron/kg diet). This article is protected by copyright. All rights reserved

Fluorescent Au25 nanoclusters recently have drawn considerable research interest due to their unique properties and potential applications. Despite significant advances in their synthesis methods and application development, the origin of the fluorescence and underlying mechanism still remain unclear. In this work we investigate the fluorescence dynamics in BSA-protected Au25 nanoclusters by time-resolved photoluminescence and transient absorption techniques covering picosecond to microsecond time scales. We demonstrate here that the red fluorescence consists of both prompt fluorescence and thermally activated delayed fluorescence, and the latter is more dominant. A small energy gap of 30 meV between the triplet and the singlet states was determined from our temperature-dependent time-resolved fluorescence measurement. Moreover, we elucidate that the absorption band at 2.34 eV corresponds to the HOMO–LUMO transition in this system due to the interaction between Au25 NCs and BSA. We also show that an effec...

cope : Obesity is associated with elevated serum ferritin and increased macrophage activation and infiltration; however, the causal mechanisms underlying this relationship remain undefined. Methods and results : Serum ferritin and soluble P-selectin glycoprotein ligand (sPSGL)-1 level were higher in obese adolescents and patients with moderate nonalcoholic fatty liver disease (NAFLD) compared with controls (all p < 0.05). Multivariate linear regression revealed that serum ferritin was independently associated with sPSGL-1 (B = 0.249, 95% confidence interval: 0.011–0.487, p = 0.041) after adjustment for covariates. The messenger (m) RNA expression of GRP78/Bip, ferritin, and PSGL-1 in leukocytes was greater in patients with NAFLD than in controls. An animal study showed that a tunicamycin injection (an endoplasmic reticulum [ER] stress inducer) triggered serum sPSGL-1 and ferritin elevation (all p < 0.01). An in vitro study revealed that serum ferritin and apoferritin induced tumor necrosis factor-α and sPSGL-1 secretion (all p < 0.01). A wound healing assay showed that PSGL-1 blocking inhibited apoferritin-mediated macrophage migration. GRP78/Bip knockdown by the endotoxin EGF-SubA completely inhibited apoferritin-mediated macrophage migration and PSGL-1 expression at the protein and mRNA levels (all p < 0.05). Conclusion : ER stress-associated mechanisms are required for apoferritin/ferritin-mediated macrophage migration via the PSGL-1-dependent pathway. This article is protected by copyright. All rights reserved

Linoleic acid (LA) improves insulin resistance and prevents diabetes. To investigate whether linoleic acid could protect against streptozotocin (STZ)-induced cell death, rat RIN-m5F cells were exposed to STZ. SL and SO groups consisted of cells treated with STZ and then LA or oleic acid (OA) respectively. STZ treatment decreased the mitochondrial membrane potential in the STZ, SO, and SL groups. Cells of the SL group had more intact mitochondria. Increased mRNA expression of mitochondrial DNA (mtDNA) and nuclear DNA (nDNA), as well as of the mitochondrial biogenesis regulators peroxisome proliferator activated receptor gamma coactivator-1alpha (PGC-1alpha), and mitochondrial transcription factor A (Tfam), were found in the LA group. The insulin content was significantly decreased in all three groups. These results suggest that the effects of LA on cell viability after STZ damage occur through maintenance of mitochondrial structure and increased mitochondrial biogenesis.

Carbon nanodots (CNDs) have emerged as fascinating materials with exceptional electronic and optical properties, and thus they offer many promising applications in photovoltaics and photocatalysis. In this paper we investigate electron transfer in nanocomposites of CNDs–graphene oxide (GO), –multi-walled carbon nanotubes (MWNTs) and –TiO2 nanoparticles without linker molecules, using steady state and time-resolved spectroscopy. Significant fluorescence quenching was observed in the CND–GO system, and it is attributed to the ultrafast electron transfer from CNDs to GO with a time constant of 400 fs. In comparison, carbon nanotubes result in static quenching of fluorescence in CNDs. No charge transfer was observed in both CND–MWNT and CND–TiO2 nanocomposites. This finding suggests that the CND–GO nanocomposite can be an excellent candidate for hot carrier solar cells due to the effective carrier extraction, broad spectral absorption, weak electron–phonon scattering, and thus a slow cooling rate for hot carriers.

The near-infrared emission, matching the biological window, is conducive to biological applications. To date, most of the reported carbon nanodots emit the blue to green fluorescence and few of carbon nanodots emit the near-infrared with relatively lower efficiency. Here, we report an approach to generate or to enhance the near-infrared luminescence from the green luminescent carbon nanodots. Experiments reveal that the near-infrared emission is significantly enhanced by thermally assisted growth in vacuum, which is attributed to the formation of the larger nano-domains from the small carbon clusters at elevated temperatures.