Multiple exposures to low-dose ionizing radiation induced the initiation and progression of pro-atherosclerotic phenotypes in mice and vascular endothelial cell damage.

OBJECTIVE: This study aimed to investigate the effects of low-dose radiation on the abdominal aorta of mice and vascular endothelial cells. METHODS: Wild-type and tumor-bearing mice were exposed to 15 sessions of low-dose irradiation, resulting in cumulative radiation doses of 187.5, 375, and 750 mGy. The effect on the cardiovascular system was assessed. Immunohistochemistry analyzed protein expressions of PAPP-A, CD62, P65, and COX-2 in the abdominal aorta. Microarray technology, Gene Ontology analysis, and pathway enrichment analysis evaluated gene expression changes in endothelial cells exposed to 375 mGy X-ray. Cell viability was assessed using the Cell Counting Kit 8 assay. Immunofluorescence staining measured γ-H2AX levels, and real-time polymerase chain reaction quantified mRNA levels of interleukin-6 (IL-6), ICAM-1, and Cx43. RESULTS: Hematoxylin and eosin staining revealed thickening of the inner membranes and irregular arrangement of smooth muscle cells in the media membrane at 375 and 750 mGy. Inflammation was observed in the inner membranes at 750 mGy, with a clear inflammatory response in the hearts of tumor-bearing mice. Immunohistochemistry indicated increased levels of PAPP-A, P65, and COX-2 post-irradiation. Microarray analysis showed 425 up-regulated and 235 down-regulated genes, associated with processes like endothelial cell-cell adhesion, IL-6, and NF-κB signaling. Cell Counting Kit 8 assay results indicated inhibited viability at 750 mGy in EA.hy926 cells. Immunofluorescence staining demonstrated a dose-dependent increase in γ-H2AX foci. Reverse transcription quantitative PCR results showed increased expression of IL6, ICAM-1, and Cx43 in EA.hy926 cells post 750 mGy X-ray exposure. CONCLUSION: Repeated low-dose ionizing radiation exposures triggered the development of pro-atherosclerotic phenotypes in mice and damage to vascular endothelial cells.

Apoptotic Vesicular Metabolism Contributes to Organelle Assembly and Safeguards Liver Homeostasis and Regeneration.

BACKGROUND & AIMS: Apoptosis generates plenty of membrane-bound nanovesicles, the apoptotic vesicles (apoVs), which show promise for biomedical applications. The liver serves as a significant organ for apoptotic material removal. Whether and how the liver metabolizes apoptotic vesicular products and contributes to liver health and disease is unrecognized. METHODS: apoVs were labeled and traced after intravenous infusion. Apoptosis-deficient mice by Fas mutant (Fasmut) and Caspase-3 knockout (Casp3-/-) were used with apoV replenishment to evaluate the physiological apoV function. Combinations of morphologic, biochemical, cellular, and molecular assays were applied to assess the liver while hepatocyte analysis was performed. Partial hepatectomy and acetaminophen liver failure models were established to investigate liver regeneration and disease recovery. RESULTS: We discovered that the liver is a major metabolic organ of circulatory apoVs, in which apoVs undergo endocytosis by hepatocytes via a sugar recognition system. Moreover, apoVs play an indispensable role to counteract hepatocellular injury and liver impairment in apoptosis-deficient mice upon replenishment. Surprisingly, apoVs form a chimeric organelle complex with the hepatocyte Golgi apparatus through the soluble N-ethylmaleimide-sensitive factor attachment protein receptor machinery, which preserves Golgi integrity, promotes microtubule acetylation by regulating α-tubulin N-acetyltransferase 1, and consequently facilitates hepatocyte cytokinesis for liver recovery. The assembly of the apoV-Golgi complex is further revealed to contribute to liver homeostasis, regeneration, and protection against acute liver failure. CONCLUSIONS: These findings establish a previously unrecognized functional and mechanistic framework that apoptosis through vesicular metabolism safeguards liver homeostasis and regeneration, which holds promise for hepatic disease therapeutics.

Molecular and Aggregate Synergistic Engineering of Aggregation-Induced Emission Luminogens to Manipulate Optical/Electronic Properties for Efficient and Diversified Functions.

The optical/electronic properties of organic luminescent materials can be regulated by molecular structure modification, which not only requires sophisticated and time-consuming synthesis but also is unable to accurately afford the optical properties of materials in the aggregate state. Herein, a facile strategy of molecular and aggregate synergistic engineering is proposed to manipulate the optical/electronic properties of a luminogen, ACIK, in the solid state for efficient and diversified functions. ACIK is facilely synthesized and exhibits three polymorphic states (ACIK-Y, ACIK-R, and ACIK-N) with a large emission difference of 102 nm from yellow to near-infrared (NIR). Their structure-property relationships were investigated by crystallographic analyses and computational studies. ACIK-Y, with the most twisted structure, exhibits an intriguing color-tuned fluorescence between yellow and NIR in the solid state in response to multiple stimuli. Shuttle-like ACIK-R microcrystals exhibit an optical waveguide property with a low optical loss coefficient of 19 dB mm-1. ACIK dots display bright NIR-I emission, large Stokes shift, and strong NIR-II two-photon absorption. ACIK dots show specific lipid droplets-targeting capability and can be successfully applied for two-photon fluorescence imaging of mouse brain vasculature with deep penetration and high spatial resolution. This study will inspire more insights in developing advanced optical/electronic materials based on a single chromophore for practical applications.

Red-grouper nervous necrosis virus B1 protein inhibits fish IFN response by targeting Ser5-phosphorylated RNA polymerase II to promote viral replication.

Nervous necrosis virus (NNV) could infect more than 200 fish species worldwide, with almost 100% mortality in affected larvae and juvenile fish. Among different genotypes of NNV, the red-grouper nervous necrosis virus (RGNNV) genotype is the most widely reported with the highest number of susceptible species. Interferon (IFN) is a crucial antiviral cytokine and RGNNV needs to develop some efficient strategies to resist host IFN-stimulated antiviral immune. Although considerable researches on RGNNV, whether RGNNV B1 protein participates in regulating the host's IFN response remains unknown. Here, we reported that B1 protein acted as a transcript inhibition factor to suppress fish IFN production. We firstly found that ectopic expression of B1 protein significantly decreased IFN and IFN-stimulated genes (ISGs) mRNA levels and IFNφ1 promoter activity induced by polyinosinic:polycytidylic acid [poly (I:C)]. Further studies showed that B1 protein inhibited the IFNφ1 promoter activity stimulated by the key RIG-I-like receptors (RLRs) factors, including MDA5, MAVS, TBK1, IRF3, and IRF7 and decreased their protein levels. Moreover, B1 protein significantly inhibited the activity of constitutively active cytomegalovirus (CMV) promoter, which suggested that B1 protein was a transcription inhibitor. Western blot indicated that B1 protein decreased the Ser5 phosphorylation of RNA polymerase II (RNAP II) C-terminal domain (CTD). Together, our data demonstrated that RGNNV B1 protein was a host transcript antagonist, which intervened RNAP II Ser5-phosphorylation, inhibiting host IFN response and facilitating RGNNV replication.

Recent advances in aggregation-induced emission materials for enhancing solar energy utilization.

Aggregation-induced emission (AIE) materials possessing unique properties in both the solution state and the aggregate state in the aspects of absorption, photoluminescence and heat generation have been well-established for wide applications in the past two decades. In recent years, several emerging applications of AIE materials in solar energy utilization, including luminescent solar concentrators, photosynthesis augmentation and solar steam generation have been reported. This mini-review provides a concise summary of these AIE materials in these aspects.

Apoptotic extracellular vesicles are metabolized regulators nurturing the skin and hair.

Over 300 billion of cells die every day in the human body, producing a large number of endogenous apoptotic extracellular vesicles (apoEVs). Also, allogenic stem cell transplantation, a commonly used therapeutic approach in current clinical practice, generates exogenous apoEVs. It is well known that phagocytic cells engulf and digest apoEVs to maintain the body's homeostasis. In this study, we show that a fraction of exogenous apoEVs is metabolized in the integumentary skin and hair follicles. Mechanistically, apoEVs activate the Wnt/ß-catenin pathway to facilitate their metabolism in a wave-like pattern. The migration of apoEVs is enhanced by treadmill exercise and inhibited by tail suspension, which is associated with the mechanical force-regulated expression of DKK1 in circulation. Furthermore, we show that exogenous apoEVs promote wound healing and hair growth via activation of Wnt/ß-catenin pathway in skin and hair follicle mesenchymal stem cells. This study reveals a previously unrecognized metabolic pathway of apoEVs and opens a new avenue for exploring apoEV-based therapy for skin and hair disorders.

CPT1 Mediated Ionizing Radiation-Induced Intestinal Injury Proliferation via Shifting FAO Metabolism Pathway and Activating the ERK1/2 and JNK Pathway.

The intestinal compensatory proliferative potential is a key influencing factor for susceptibility to radiation-induced intestinal injury. Studies indicated that the carnitine palmitoyltransferase 1 (CPT1) mediated fatty acid ß-oxidation (FAO) plays a crucial role in promoting the survival and proliferation of tumor cells. Here, we aimed to explore the effect of 60Co gamma rays on CPT1 mediated FAO in the radiation-induced intestinal injury models, and investigate the role of CPT1 mediated FAO in the survival and proliferation of intestinal cells after irradiation. We detected the changed of FAO in the plasma and small intestine of Sprague Dawley (SD) rats at 24 h after 60Co gamma irradiation (0, 5 and 10 Gy), using target metabolomics, qRT-PCR, immunohistochemistry (IHC), western blot (WB) and related enzymatic activity kits. We then analyzed the FAO changes in radiation-induced intestinal injury models regardless of ex vivo (mice enteroids), or in vitro (normal human intestinal epithelial cell lines, HIEC-6). HIEC-6 cells were transduced with lentivirus vector GV392 and treated with puromycin for obtaining CPT1 stable knockout cell lines, named CPT1 KO. CPT1 enzymatic activities of HIEC-6 cells and mice enteroids were also inhibited by pharmaceutical inhibitor ST1326 and Etomoxir (ETO), to study the function of CPT1 in the survival and proliferation of HIEC-6 cells after 60Co gamma irradiation. We found that CPT1 mediated FAO was altered in the small intestine of the SD rats after irradiation, especially, the expression level and enzymatic activity of CPT1 were significantly increased. Similarly, the expression levels of CPT1 were also remarkably enhanced in mice enteroids and HIEC-6 cells after irradiation. CPT1 inhibition decreased the proliferation of the HIEC-6 cells and mice enteroids after irradiation partially by reducing the extracellular signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) pathways activation, CPT1 inhibition also reduced the proliferation of mice enteroids after irradiation partially by down-regulating the Wnt/ß-catenin signaling activity. In conclusion, our study indicated that CPT1 plays a crucial role in promoting intestinal epithelial cell proliferation after irradiation.

Molecular cloning, expression and functional analysis of STAT2 in orange-spotted grouper, Epinephelus coioides.

Signal transducer and activator of transcription 2 (STAT2) is an important molecule involved in the type I interferon signaling pathway. To better understand the functions of STAT2 in fish immune response, a STAT2 gene from orange-spotted grouper (Epinephelus coioides) (EcSTAT2) was cloned and characterized in this study. EcSTAT2 encoded a 802-amino acid peptide which shared 99.5% and 91.5% identity with giant grouper (Epinephelus lanceolatus) and leopard coral grouper (Plectropomus leopardus), respectively. Amino acid alignment analysis showed that EcSTAT2 contained five conserved domains, including N-terminal protein interaction domain, coiled coil domain (CCD), DNA binding domain (DBD), Src-homology 2 (SH2) domain, and C-terminal transactivation domain (TAD). Phylogenetic analysis indicated that EcSTAT2 clustered into fish STAT2 group and showed the nearest relationship to giant grouper STAT2. In healthy grouper, EcSTAT2 was distributed in all tissues tested, and the expression of EcSTAT2 was predominantly detected in spleen, kidney and gill. In vitro, EcSTAT2 expression was significantly increased in response to polyinosinic:polycytidylic acid [poly (I:C)] stimulation and red-spotted grouper nervous necrosis virus (RGNNV) infection. Subcellular localization showed that EcSTAT2 was located in the cytoplasm in a punctate manner. EcSTAT2 overexpression significantly inhibited RGNNV replication, as evidenced by the decreased severity of cytopathic effect (CPE) and the reduced expression levels of viral genes and protein. Consistently, knockdown of EcSTAT2 using small interfering RNA (siRNA) promoted RGNNV replication. Furthermore, EcSTAT2 overexpression increased both interferon (IFN) and interferon stimulated genes (ISGs) expression. In addition, EcSTAT2 knockdown decreased the transcription levels of IFN and ISGs. Together, our data demonstrated that EcSTAT2 exerted antiviral activity against RGNNV through up-regulation of host interferon response.

Fluorescent Imaging and Sorting of High-Lipid-Content Strains of Green Algae by Using an Aggregation-Induced Emission Luminogen.

Microalgae-based biofuels are receiving attention at the environmental, economic, and social levels because they are clean, renewable, and quickly produced. The green algae Chlorella vulgaris has been extensively studied in research laboratories and the biofuel industry as a model organism to increase lipid production to be cost-effective in commercial production. In this work, we utilized a lipid-droplet-specific luminogen with aggregation-induced emission (AIE) characteristics to increase the lipid production of C. vulgaris by fluorescent imaging and sorting of those algal cells with large and rich lipid droplets for subculturing. The AIE-active TPA-A enabled real-time monitoring of the size and number of lipid droplets in C. vulgaris during their growth period so that we can identify the best time for harvesting. Furthermore, the algae cells with high lipid content were identified and collected for subculturing by the technique of fluorescence-activated cell sorting (FACS). The lipid production in the generation of two successive selections was almost doubled compared to the generation with natural selection. This work demonstrated that the technologies of AIE and FACS could be applied together to improve the production of a third-generation biofuel.

CPT1 Mediated Ionizing Radiation-Induced Intestinal Injury Proliferation via Shifting FAO Metabolism Pathway and Activating the ERK1/2 and JNK Pathway.

The intestinal compensatory proliferative potential is a key influencing factor for susceptibility to radiation-induced intestinal injury. Studies indicated that the carnitine palmitoyltransferase 1 (CPT1) mediated fatty acid ß-oxidation (FAO) plays a crucial role in promoting the survival and proliferation of tumor cells. Here, we aimed to explore the effect of 60Co gamma rays on CPT1 mediated FAO in the radiation-induced intestinal injury models, and investigate the role of CPT1 mediated FAO in the survival and proliferation of intestinal cells after irradiation. We detected the changed of FAO in the plasma and small intestine of Sprague Dawley (SD) rats at 24 h after 60Co gamma irradiation (0, 5 and 10 Gy), using target metabolomics, qRT-PCR, immunohistochemistry (IHC), western blot (WB) and related enzymatic activity kits. We then analyzed the FAO changes in radiation-induced intestinal injury models regardless of ex vivo (mice enteroids), or in vitro (normal human intestinal epithelial cell lines, HIEC-6). HIEC-6 cells were transduced with lentivirus vector GV392 and treated with puromycin for obtaining CPT1 stable knockout cell lines, named CPT1 KO. CPT1 enzymatic activities of HIEC-6 cells and mice enteroids were also inhibited by pharmaceutical inhibitor ST1326 and Etomoxir (ETO), to study the function of CPT1 in the survival and proliferation of HIEC-6 cells after 60Co gamma irradiation. We found that CPT1 mediated FAO was altered in the small intestine of the SD rats after irradiation, especially, the expression level and enzymatic activity of CPT1 were significantly increased. Similarly, the expression levels of CPT1 were also remarkably enhanced in mice enteroids and HIEC-6 cells after irradiation. CPT1 inhibition decreased the proliferation of the HIEC-6 cells and mice enteroids after irradiation partially by reducing the extracellular signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) pathways activation, CPT1 inhibition also reduced the proliferation of mice enteroids after irradiation partially by down-regulating the Wnt/ß-catenin signaling activity. In conclusion, our study indicated that CPT1 plays a crucial role in promoting intestinal epithelial cell proliferation after irradiation.

Precise and long-term tracking of mitochondria in neurons using a bioconjugatable and photostable AIE luminogen.

Tracking mitochondrial movement in neurons is an attractive but challenging research field as dysregulation of mitochondrial motion is associated with multiple neurological diseases. To realize accurate and long-term tracking of mitochondria in neurons, we elaborately designed a novel aggregation-induced emission (AIE)-active luminogen, TPAP-C5-yne, where we selected a cationic pyridinium moiety to target mitochondria and employed an activated alkyne terminus to achieve long-term tracking through bioconjugation with amines on mitochondria. For the first time, we successfully achieved the accurate analysis of the motion of a single mitochondrion in live primary hippocampal neurons and the long-term tracking of mitochondria for up to a week in live neurons. Therefore, this new AIEgen can be used as a potential tool to study the transport of mitochondria in live neurons.

Logistic role of carnitine shuttle system on radiation-induced L-carnitine and acylcarnitines alteration.

PURPOSE: With the development of radiation metabolomics, a large number of radiation-related metabolic biomarkers have been identified and validated. The L-carnitine and acylcarnitines have the potential to be the new promising candidate indicators of radiation exposure. This review summarizes the effect of carnitine shuttle system on the profile of acylcarnitines and correlates the radiation effects on upstream regulators of carnitine shuttle system with the change characteristics of L-carnitine and acylcarnitines after irradiation across different animal models as well as a few humans. CONCLUSIONS: Studies report that acylcarnitines were ubiquitously elevated after irradiation, especially the free L-carnitine and short-chain acylcarnitines (C2-C5). However, the molecular mechanism underlying acylcarnitine alterations after irradiation is not fully investigated, and further studies are needed to explore the biological effect and its mechanism. The activity of the carnitine shuttle system plays a key role in the alteration of L-carnitine and acylcarnitines, and the upstream regulators of the system are known to be affected by irradiation. These evidences indicate that that there is a logistic role of carnitine shuttle system on radiation-induced L-carnitine and acylcarnitines alteration.

Screening of radiation gastrointestinal injury biomarkers in rat plasma by high-coverage targeted lipidomics.

INTRODUCTION: In the event of radiological accidents and cancer radiotherapies in the clinic, the gastrointestinal (GI) system is vulnerable to ionizing radiation and shows GI injury. Accessible biomarkers may provide means to predict, evaluate, and treat GI tissue damage. The current study investigated radiation GI injury biomarkers in rat plasma. MATERIAL AND METHODS: High-coverage targeted lipidomics was employed to profile lipidome perturbations at 72 h after 0, 1, 2, 3, 5, and 8 Gy (60Co γ-rays at 1 Gy/min) total-body irradiation in male rat jejunum. The results were correlated with previous plasma screening outcomes. RESULTS: In total, 93 differential metabolites and 28 linear dose-responsive metabolites were screened in the jejunum. Moreover, 52 lipid species with significant differences both in jejunum and plasma were obtained. Three lipid species with linear dose-response relationship both in jejunum and plasma were put forth, which exhibited good to excellent sensitivity and specificity in triaging different exposure levels. DISCUSSION: The linear dose-effect relationship of lipid metabolites in the jejunum and the triage performance of radiation GI injury biomarkers in plasma were studied for the first time. CONCLUSION: The present study can provide insights into expanded biomarkers of IR-mediated GI injury and minimally invasive assays for evaluation.

Aggregation-Induced Emission (AIE) in Super-resolution Imaging: Cationic AIE Luminogens (AIEgens) for Tunable Organelle-Specific Imaging and Dynamic Tracking in Nanometer Scale.

Organelle-specific imaging and dynamic tracking in ultrahigh resolution is essential for understanding their functions in biological research, but this remains a challenge. Therefore, a facile strategy by utilizing anion-π+ interactions is proposed here to construct an aggregation-induced emission luminogen (AIEgen) of DTPAP-P, not only restricting the intramolecular motions but also blocking their strong π-π interactions. DTPAP-P exhibits a high photoluminescence quantum yield (PLQY) of 35.04% in solids, favorable photostability and biocompatibility, indicating its potential application in super-resolution imaging (SRI) via stimulated emission depletion (STED) nanoscopy. It is also observed that this cationic DTPAP-P can specifically target to mitochondria or nucleus dependent on the cell status, resulting in tunable organelle-specific imaging in nanometer scale. In live cells, mitochondria-specific imaging and their dynamic monitoring (fission and fusion) can be obtained in ultrahigh resolution with a full-width-at-half-maximum (fwhm) value of only 165 nm by STED nanoscopy. This is about one-sixth of the fwhm value in confocal microscopy (1028 nm). However, a migration process occurs for fixed cells from mitochondria to nucleus under light activation (405 nm), leading to nucleus-targeted super-resolution imaging (fwhm= 184 nm). These findings indicate that tunable organelle-specific imaging and dynamic tracking by a single AIEgen at a superior resolution can be achieved in our case here via STED nanoscopy, thus providing an efficient method to further understand organelle's functions and roles in biological research.

Effect of Ultraviolet B Irradiation on Melanin Content Accompanied by the Activation of p62/GATA4-Mediated Premature Senescence in HaCaT Cells.

OBJECTIVE: To explore the effect and mechanism of ultraviolet B (UVB) on melanin synthesis and premature senescence in human immortalized keratinocytes (HaCaT) cells. METHODS: HaCaT cells were irradiated with 0, 20, 50, 80, 100, 150, and 200 mJ/cm2 of UVB. NaOH method was used for melanin content assay, cellular tyrosinase (TYR) activity was determined by 3,4-Dihydroxy-L-phenylalanine (L-DOPA) oxidation to dopachrome, premature senescence was analyzed by senescence-associated beta-galactosidase (SA-ß-gal) staining kit, and the levels of p21, p16, p62, and GATA4 proteins were detected by Western blotting. Premature senescence was inhibited by the inhibitors of ataxia telangiectasia mutated (ATM) or ataxia telangiectasia and Rad3-related (ATR), and the p53 signaling pathway was activated by Nutlin-3. The mRNA levels of senescence-associated secretory phenotype (SASP) factors including tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor A (VEGF-A), and interleukin-8 (IL-8) were measured by real-time quantitative polymerase chain reaction in HaCaT cells after 80 mJ/cm2 of UVB irradiation. RESULTS: The melanin level increased significantly with the elevation of irradiation dose (F = 28.19, 43.82, 143.60, P < .05), reaching the peak at the dose of 80 mJ/cm2. The tyrosinase activity increased significantly (F = 84.50, P < .05), the percentage of premature senescence increased (F = 16.31, P < .05), the levels of p62 decreased, and the level of GATA4 increased obviously with the increase of UVB dose after irradiation. The UVB-induced promotion of GATA4 level was significantly inhibited by being treated with ATM or ATR inhibitor. However, this did not occur in the Nutlin-3-treated group. The mRNA and protein expression of TNF-α increased significantly at 72 h at 80 mJ/cm2 of UVB irradiation. CONCLUSIONS: Melanin contents increased first and decreased afterward with the increasing of UVB irradiation. The decrease of p62-mediated selective autophagy was accompanied by the accumulation of GATA4 after different doses of UVB irradiation. Activation of this p62/GATA4 pathway depends on the ATM and ATR but is independent of p53, and the SASP factor was activated in HaCaT cells at 80 mJ/cm2 of UVB irradiation.

Enhancement of Acylcarnitine Levels in Small Intestine of Abdominal Irradiation Rats Might Relate to Fatty Acid ß-Oxidation Pathway Disequilibration.

OBJECTIVE: This study aims to analyze the alteration of carnitine profile in the small intestine of abdominal irradiation-induced intestinal injury rats and explore the possible reason for the altered carnitine profile. METHODS: The abdomens of 15 male Sprague Dawley (SD) rats were irradiated with 0, 10, and 15 Gy of 60Co gamma rays. The carnitine profile in the small intestine and plasma samples of SD rats at 72 h after abdominal irradiated with 0 Gy or 10 Gy of 60Co gamma rays were measured by targeted metabolomics. The changes of fatty acid ß-oxidation (FAO), including the expression of carnitine palmitoyltransferase 1 (CPT1) and acyl-CoA dehydrogenases, were analyzed in the small intestine samples of SD rats after exposed to 0, 10, and 15 Gy groups. RESULTS: There were eleven acylcarnitines in the small intestine and fourteen acylcarnitines in the plasma of the rat model significantly enhanced, respectively (P < .05). The expression level and activity of CPT1 in the small intestine were remarkably increased (P < .05), and the activity of acyl-CoA dehydrogenase in the small intestine was noticeably reduced (P < .01) after abdominal irradiation. CONCLUSION: The enhanced acylcarnitine levels in the small intestine of abdominal irradiation rats might relate to the FAO pathway disequilibration.

Aggregation-induced emission luminogens for augmented photosynthesis.

Photosynthesis is promising in sequestrating carbon dioxide and providing food and biofuel. Recent findings have shown that luminescent materials could shift the wavelength of light to a more usable range for augmented photosynthesis. Among them, aggregation-induced emission luminogens (AIEgens) have advantages of efficient light conversion, high biocompatibility, large Stokes' shift, and so on. In this perspective, emerging reports of augmented photosynthesis with luminescent materials, especially the AIEgens are included. We emphasized the spectra shift characteristics, material formation, and sustainable development based on augmented photosynthesis.

A smartphone-based electroporation system with highly robust and low-voltage silicon nanopillar chips.

In this work, a novel smartphone-based electroporation (EP) system integrated with 3D scalable and robust gold-coated silicon-nanopillar Electroporation (Au-Si NP-EP) chip using projection photolithography is developed, for the first time, for both EP and electric cell lysing (ECL) at low voltages. Au-SiNP-EP chip consists of silicon nanopillars fabricated by using ASML stepper, Deep Reactive Ion Etching (DRIE) process and coated with a gold microelectrode. The silicon nanopillars were optimized based on theoretical analysis and numerical simulations to enhance the electrical field intensity and mechanical strength. The fabricated Au-SiNP-EP chips are tested with both permeable (Acridine Orange (AO) and impermeable (Propidium Iodide (PI)) molecules for HeLa cells at different volts (1-8 V) and pulse duration (1-9 µs). The fabricated chip achieved an optimized EP efficiency of 84.3% and cell viability of 81.4% at a much smaller voltage (4.5V) than reported planar electroporation (PEP) devices (8-100V). Compared with nanostructures-based devices (2-20 V), our devices show both higher mechanical strength and fabrication yield. Besides, a smartphone app integrated with a low-cost open-source portable Arduino-based system is developed to provide optimized electrical protocols for both EP and ECL. The electric cell lysing with ECL efficiency of 97.0% at 7 V and pulse duration of 9 ms has been successfully demonstrated. The experimental results show that the proposed smartphone-based EP system with Au-SiNP EP chips is promising for various applications, including intracellular delivery of various biomolecules, drugs, and release of DNA/RNA molecules from biological cells.

Augmenting photosynthesis through facile AIEgen-chloroplast conjugation and efficient solar energy utilization.

Photosynthesis is regarded as the foundation for sustaining life on our planet. Light-harvesting is the initial step that activates the subsequent photochemical reactions. In the photosystems, chloroplast is the basic light-driven metabolic factory of higher plant cells. However, there is an incomplete match between the solar radiation spectrum and absorption profile of chloroplasts. It is hard for the photosynthetic pigments to fully utilize the sunlight energy. Here, we designed two new aggregation-induced emission (AIE) molecules with activated alkyl groups (TPE-PPO and TPA-TPO). Via a facile metal-free "Click" reaction, we realized the substantial manipulation of live chloroplasts with the AIE luminogens (AIEgens). Owing to the matched photophysical properties, the AIEgens could harvest harmful ultraviolet radiation (HUVR) and photosynthetically inefficient radiation (PIR), and further convert them into photosynthetically active radiation (PAR) for chloroplast absorption. As a result, the conjugated AIEgen-chloroplast exhibited better capability of water splitting and electron separation. It promoted the generation of adenosine triphosphate (ATP), which is an important product of photosynthesis. This work provides an effective strategy for improving plant photosynthesis.

Fibrillar Collagen Quantification With Curvelet Transform Based Computational Methods.

Quantification of fibrillar collagen organization has given new insight into the possible role of collagen topology in many diseases and has also identified candidate image-based bio-markers in breast cancer and pancreatic cancer. We have been developing collagen quantification tools based on the curvelet transform (CT) algorithm and have demonstrated this to be a powerful multiscale image representation method due to its unique features in collagen image denoising and fiber edge enhancement. In this paper, we present our CT-based collagen quantification software platform with a focus on new features and also giving a detailed description of curvelet-based fiber representation. These new features include C++-based code optimization for fast individual fiber tracking, Java-based synthetic fiber generator module for method validation, automatic tumor boundary generation for fiber relative quantification, parallel computing for large-scale batch mode processing, region-of-interest analysis for user-specified quantification, and pre- and post-processing modules for individual fiber visualization. We present a validation of the tracking of individual fibers and fiber orientations by using synthesized fibers generated by the synthetic fiber generator. In addition, we provide a comparison of the fiber orientation calculation on pancreatic tissue images between our tool and three other quantitative approaches. Lastly, we demonstrate the use of our software tool for the automatic tumor boundary creation and the relative alignment quantification of collagen fibers in human breast cancer pathology images, as well as the alignment quantification of in vivo mouse xenograft breast cancer images.