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Covalent organic frameworks (COFs) have attracted much attention in energy storage due to their porous network structure, large specific surface area, high crystallinity, and pseudocapacitive ability brought by redox reactions. However, the traditional synthesis method of COFs involves toxic solvents and requires high temperatures and pressure. Therefore, it is necessary to develop simple synthesis methods for large-scale practical application of COFs. This study investigated the synthesis and electrochemical properties of two kinds of COFs, which were synthesized through the reflux heating method and solvothermal method using tri(4-aminophenyl)amine (TAPA) and tris(benzaldehyde) (TFB) as monomers. The results indicate that COFs synthesized by the reflux heating method (Re-COF-TAFB) have better specific surface area, thermal stability, and electrochemical properties compared to those synthesized by the solvothermal method (So-COF-TAFB). Re-COF-TAFB has a specific capacitance of 248 F·g−1 at 0.1 A·g−1 and a capacitance retention rate of 104.13% after 10,000 charge and discharge cycles. This paper contributes to understanding COFs' synthesis methods and their impact on material properties. Reflux heating is highlighted as an efficient technique for developing high-performance COF-based supercapacitors. [ABSTRACT FROM AUTHOR]

NAD-dependent deacetylase Sirt2 is involved in mammalian metabolic activities, matching energy demand with energy production and expenditure, and is relevant to a variety of metabolic diseases. Here, we constructed Sirt2 knockout and adeno-associated virus overexpression mice and found that deletion of hepatic Sirt2 accelerated primary obesity and insulin resistance in mice with concomitant hepatic metabolic dysfunction. However, the key targets of Sirt2 are unknown. We identified the M2 isoform of pyruvate kinase (PKM2) as a key Sirt2 target involved in glycolysis in metabolic stress. Through yeast two-hybrid and mass spectrometry combined with multi-omics analysis, we identified candidate acetylation modification targets of Sirt2 on PKM2 lysine 135 (K135). The Sirt2-mediated deacetylation-ubiquitination switch of PKM2 regulated the development of glycolysis. Here, we found that Sirt2 deficiency led to impaired glucose tolerance and insulin resistance and induced primary obesity. Sirt2 severely disrupted liver function in mice under metabolic stress, exacerbated the metabolic burden on the liver, and affected glucose metabolism. Sirt2 underwent acetylation modification of lysine 135 of PKM2 through a histidine 187 enzyme active site-dependent effect and reduced ubiquitination of the K48 ubiquitin chain of PKM2. Our findings reveal that the hepatic glucose metabolism links nutrient state to whole-body energetics through the rhythmic regulation of Sirt2. [ABSTRACT FROM AUTHOR]

Hypothermia is an essential environmental factor in gastrointestinal diseases, but the main molecular mechanisms of pathogenesis remain unclear. The current study sought to better understand how chronic cold stress affects gut damage and its underlying mechanisms. In this work, to establish chronic cold stress (CS)-induced intestinal injury model, mice were subjected to continuous cold exposure (4 °C) for 3 h per day for 3 weeks. Our results indicated that CS led to gut injury via inducing changes of heat shock proteins 70 (HSP70) and apoptosis-related (caspases-3, Bax and Bcl-2) proteins; enhancing expression of intestinal tight-related (ZO-1 and occludin) proteins; promoting releases of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), high mobility group box 1 (HMGB1), interleukin1β (IL-1β), IL-18 and IL-6 inflammatory mediators in the ileum; and altering gut microbial diversity. Furthermore, persistent cold exposure resulted in the cleavage of pyroptosis-related Gasdermin D (GSDMD) protein by regulating the NLRP3/ASC/caspase-1 and caspase-11 pathway, and activation of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, which are strongly associated with changes in gut microbiota diversity. Taken together, these investigations provide new insights into the increased risk of intestinal disorders at extremely low temperatures and establish a theoretical foundation for the advancement of novel pharmaceutical interventions targeting cold-related ailments. [ABSTRACT FROM AUTHOR]

Covalent organic frameworks (COFs) with reversible redox units and a conjugated molecular skeleton possess novel photoelectrochemical properties. In this work, tris(4-aminophenyl)amine and 4,4-biphenyldiformaldehyde were chosen to synthesize TABP-COF electrochromic film with triphenylamine (TPA) active unit by a solvothermal method in a Teflon-lined reactor. The growth process and reaction time optimization of the TABP-COF were studied. TABP-COF shows a self-assembly growth process from an array of nanosheets to nanospheres. Owing to the redox characteristics of TPA, the TABP-COF film exhibits reversible electrochromic behavior. With a solvothermal reaction time of 72 h, the TABP-COF-3 film exhibits the best electrochromic properties, including contrast of 0.483 and response time of 7.3 s/13.6 s. Considering the abundance of redox-active units that can be chosen, COF materials with different redox units and color changes can be designed for a variety of applications in the field of electrochromic materials. [ABSTRACT FROM AUTHOR]

Supercapacitors have been widely studied as a typical representative of new energy storage systems. As a type of novel crystalline porous material, covalent triazine frameworks (CTFs) have attracted enormous attention owing to their high nitrogen content and unique triazine ring structure, which give them high chemical and thermal stability. In this paper, 2,4,6‐tris(4‐aldophenyl)‐1,3,5‐triazine (TFPT) and 2,4,6‐tris(4‐aminophenyl)‐1,3,5‐triazine (TAPT) were used to synthesize TPT‐CTFs by Schiff base reaction. TPT‐CTFs exhibit regular nanosheets structure and high crystallinity. The specific capacitance of TPT‐CTFs is 110 F/g at current density of 0.1 A/g. After 10,000 cycles of charge and discharge, the capacitance retention rate is high as 105%, due to the high crystallinity support and expandable channels of TPT‐CTFs. In addition, the simple and convenient one‐pot hydrothermal synthesis used in this paper, avoids harsh conditions of common ampoule methods for synthesis of CTFs materials. [ABSTRACT FROM AUTHOR]

Cold is a factor affecting health in humans and animals. The liver, a major metabolic center, is highly susceptible to ambient air temperature. Recent studies have shown that endoplasmic reticulum (ER) stress is associated with the liver, and regulates the occurrence and development of liver injury and autophagy. However, the mechanism underlying the relationship between cold exposure and ER stress in the liver is not well understood. In this study, we investigated the effect of ER stress on liver autophagy and its mechanism under cold exposure. AML12 cells were treated with Tg to construct an ER stress model, and the level of autophagy increased. To further explore the mechanism through which ER stress regulates autophagy, we knocked down SIRT2 with shRNA in Tg‐treated AML12 cells. Knockdown of SIRT2 significantly increased ER stress and autophagy, increased FoxO1 acetylation, and promoted its entry into the nucleus. To further verify the results of in vitro experiments, we exposed mice to 4°C for 3 h per day for 3 weeks to exacerbate the burden on the liver after cold exposure. Cold exposure damaged the structure and function of the liver and promoted the inflammatory response. It also activated ER stress and promoted autophagy. In addition, cold exposure inhibited the expression of SIRT2, promoted FoxO1 acetylation, and enhanced the interaction with autophagy. Our findings indicated that cold exposure induces liver damage, ER stress, and autophagy through the SIRT2/FoxO1 pathway. These findings suggest that SIRT2 may be a potential target for regulating health under cold exposure. [ABSTRACT FROM AUTHOR]

Melatonin is an important molecule in both animals and plants, regulating circadian rhythms and stress responses. Therefore, the improvement of melatonin accumulation not only strengthens the function of melatonin but also improves stress resistance in crops. Although melatonin biosynthetic enzymes have been identified through reverse genetics previously, an investigation of melatonin level‐related genes through forward genetics in plants has yet to be performed. In this study, a genome‐wide association study using cassava natural population of 298 genetic resources identified melatonin accumulation 1 (MA1), which regulates the natural variation of melatonin levels in cassava. We found that MA1 encodes type 2C protein phosphatase 1 (PP2C1), which serves as a negative regulator of melatonin levels in cassava. MePP2C1 physically interacts with MeRAV1/2 and MeWRKY20 and dephosphorylates them at serine (S) 35 residue, S34 residue, and S176 residue, respectively, thereby hindering their transcriptional activation on downstream melatonin biosynthetic genes. Notably, MePP2C1 interacts with phytomelatonin receptor MePMTR1 and dephosphorylates it at S11 residue, repressing its binding to melatonin. In summary, this study demonstrates that MePP2C1 as MA1 plays dual roles in negatively regulating both melatonin accumulation and signaling, extending the understanding of the molecular mechanism underlying melatonin accumulation and signaling through forward genetics in plants. [ABSTRACT FROM AUTHOR]

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Ambient air temperature is a key factor affecting human health. Long-term exposure to a cold environment can cause various diseases, while the impact on the intestine, the organ which has the largest contact area with the external environment, cannot be ignored. In this study, we investigated the effect of chronic cold exposure on the colon and its preliminary mechanism of action. Mice were exposed to 4°C for 3 hours a day for 10 days. We found that cold exposure damaged the morphology and structure of the colon, destroyed the tight junctions of the colonic epithelial tissue, and promoted inflammation of the colon. At the same time, cold exposure also activated the unfolded protein response (UPR) in the colon and promoted apoptosis in intestinal epithelial cells. Chronic cold exposure induced oxidative stress in vivo , but also significantly enhanced the response of the Nrf2 pathway that promotes an anti-oxidant effect. Furthermore, we demonstrated that chronic cold exposure promoted p65 acetylation to aggravate the inflammatory response by inhibiting SIRT1. Similar results were observed following SIRT1 knock-down by shRNA in Caco-2 cells treated with Thapsigargin (Tg). Knock-down of SIRT1 promoted nuclear localization of Nrf2, and increased the level of Nrf2 acetylation. Taken together, our study indicates that cold exposure may aggravate endoplasmic reticulum stress and damage epithelial tight junctions in the colon by inhibiting SIRT1, which promotes nuclear localization of Nrf2 and induces an anti-oxidant response to maintain intestinal homeostasis. These findings suggest that SIRT1 is a potential target for regulating intestinal health under cold exposure conditions. [ABSTRACT FROM AUTHOR]

Pigs are susceptible to low temperature conditions, and cold stress causes metabolic changes in the body to increase heat production as an adaption to adverse environments. To characterize and validate different metabolites in piglet livers at different cold exposure times, sixteen 30-day-old male weaned piglets with similar weights were randomly divided into four groups: the normal temperature group (24 ± 2°C, NT) and cold exposure (4 ± 2°C) 2-h group (CS2), 6-h group (CS6), and 12-h group (CS12). At the end of the experiment, the liver samples were analyzed using systemic non-targeted metabolomics. Eight known differentially abundant metabolites (farnesyl pyrophosphate, isocitrate, triethanolamine, phenylethylamine, deoxynosine, citric acid, maltotriose, and epinephrine) were observed between the CS groups and the control group in positive and negative ion modes. The eight main differentially abundant metabolites involved in seven metabolite classifications. Metabolic pathways and enrichment analyses revealed that the pathways involved three KEGG pathway classifications. Most of the pathways were related to amino acid or energy metabolism. Moreover, the metabolic pathways were not identical under different cold exposure times, with those following 2 and 6 h of cold exposure more related to carbohydrates and energy production and those following 12 h of cold exposure more related to the metabolism connected with epinephrine. Thus, under different cold exposure times, the metabolite profiles and metabolic pathways differed. [ABSTRACT FROM AUTHOR]

Melatonin is widely involved in plant disease resistance through modulation of immune responses. Pathogenesis‐related (PR) proteins play important roles in plant immune responses. However, the direct association between melatonin biosynthetic enzyme and PR protein remains elusive in plants. In this study, we found that N‐acetylserotonin O‐methyltransferase 2 (MeASMT2) physically interacted with MePR1 in vitro and in vivo, thereby promoting the anti‐bacterial activity of MePR1 against Xanthomonas axonopodis pv. manihotis (Xam). Consistently, MeASMT2 improved the effect of MePR1 on positively regulating cassava disease resistance. In addition, we found that type 2C protein phosphatase 1 (MePP2C1) interacted with MeASMT2 to interfere with MePR1‐MeASMT2 interaction, so as to inhibiting the effect of MeASMT2 and MePR1 on positively regulating cassava disease resistance. In contrast to the increased transcripts of MeASMT2 and MePR1 in response to Xam infection, the transcript of MePP2C1 was decreased upon Xam infection. Therefore, disease activated MeASMT2 was released from disease inhibited MePP2C1, so as to improving the anti‐bacterial activity of MePR1, resulting in improved immune response. In summary, this study illustrates the dynamic modulation of the MePP2C1‐MeASMT2‐MePR1 module on cassava defense response against cassava bacterial blight (CBB), extending the understanding of the correlation between melatonin biosynthetic enzyme and PR in plants. [ABSTRACT FROM AUTHOR]

The application of traditional electrode materials for high‐performance capacitive deionization (CDI) has been persistently limited by their low charge‐storage capacities, excessive co‐ion expulsion and slow salt removal rates. Here we report a bottom‐up approach to the preparation of a two‐dimensional (2D) Ti3C2Tx MXene‐polydopamine heterostructure having ordered in‐plane mesochannels (denoted as mPDA/MXene). Interfacial self‐assembly of mesoporous polydopamine (mPDA) monolayers on MXene nanosheets leads to the mPDA/MXene heterostructure, which exhibits several unique features: (1) MXene undergoes reversible ion intercalation/deintercalation and possesses high conductivity; (2) mPDA layers establish redox capacitive characteristics and Na+ selectivity, and also help to prevent self‐stacking and oxidation of MXene; (3) in‐plane mesochannels enable the smooth transport of ions at the internal spaces of this stacked 2D material. When applied as an electrode material for CDI, mPDA/MXene nanosheets exhibit top‐level CDI performance and cycling stability compared to those of the so far reported 2D materials. Our study opens an avenue for the rational construction of MXene‐organic hybrid heterostructures, and further motivates the development of high‐performance CDI electrode materials. [ABSTRACT FROM AUTHOR]

The application of traditional electrode materials for high‐performance capacitive deionization (CDI) has been persistently limited by their low charge‐storage capacities, excessive co‐ion expulsion and slow salt removal rates. Here we report a bottom‐up approach to the preparation of a two‐dimensional (2D) Ti3C2Tx MXene‐polydopamine heterostructure having ordered in‐plane mesochannels (denoted as mPDA/MXene). Interfacial self‐assembly of mesoporous polydopamine (mPDA) monolayers on MXene nanosheets leads to the mPDA/MXene heterostructure, which exhibits several unique features: (1) MXene undergoes reversible ion intercalation/deintercalation and possesses high conductivity; (2) mPDA layers establish redox capacitive characteristics and Na+ selectivity, and also help to prevent self‐stacking and oxidation of MXene; (3) in‐plane mesochannels enable the smooth transport of ions at the internal spaces of this stacked 2D material. When applied as an electrode material for CDI, mPDA/MXene nanosheets exhibit top‐level CDI performance and cycling stability compared to those of the so far reported 2D materials. Our study opens an avenue for the rational construction of MXene‐organic hybrid heterostructures, and further motivates the development of high‐performance CDI electrode materials. [ABSTRACT FROM AUTHOR]

Stimulating photosensitizers (PS) by Cerenkov radiation (CR) can overcome the light penetration limitation in traditional photodynamic therapy. However, separate injection of radiopharmaceuticals and PS cannot guarantee their efficient interaction in tumor areas, while co‐delivery of radionuclides and PS face the problem of nonnegligible phototoxicity in normal tissues. Here, we describe a 131I‐labeled smart photosensitizer, composed of pyropheophorbide‐a (photosensitizer), a diisopropylamino group (pH‐sensitive group), an 131I‐labeled tyrosine group (CR donor), and polyethylene glycol, which can self‐assemble into nanoparticles (131I‐sPS NPs). The 131I‐sPS NPs showed low phototoxicity in normal tissues due to aggregation‐caused quenching effect, but could self‐produce reactive oxygen species in tumor sites upon disassembly. Upon intravenous injection, 131I‐sPS NPs showed great tumor inhibition capability in subcutaneous 4T1‐tumor‐bearing Balb/c mice and orthotopic VX2 liver tumor bearing rabbits. We believed 131I‐sPS NPs could expand the application of CR and provide an effective strategy for deep tumor theranostics. [ABSTRACT FROM AUTHOR]

Stimulating photosensitizers (PS) by Cerenkov radiation (CR) can overcome the light penetration limitation in traditional photodynamic therapy. However, separate injection of radiopharmaceuticals and PS cannot guarantee their efficient interaction in tumor areas, while co‐delivery of radionuclides and PS face the problem of nonnegligible phototoxicity in normal tissues. Here, we describe a 131I‐labeled smart photosensitizer, composed of pyropheophorbide‐a (photosensitizer), a diisopropylamino group (pH‐sensitive group), an 131I‐labeled tyrosine group (CR donor), and polyethylene glycol, which can self‐assemble into nanoparticles (131I‐sPS NPs). The 131I‐sPS NPs showed low phototoxicity in normal tissues due to aggregation‐caused quenching effect, but could self‐produce reactive oxygen species in tumor sites upon disassembly. Upon intravenous injection, 131I‐sPS NPs showed great tumor inhibition capability in subcutaneous 4T1‐tumor‐bearing Balb/c mice and orthotopic VX2 liver tumor bearing rabbits. We believed 131I‐sPS NPs could expand the application of CR and provide an effective strategy for deep tumor theranostics. [ABSTRACT FROM AUTHOR]

Procyanidin B2 (PB2), a naturally occurring flavonoid abundant in a wide range of fruits, has been shown to exert antioxidant, anti‐inflammatory and anticancer properties. However, the role of PB2 in the prevention of cold stimulation (CS)‐induced liver injury. The present study was undertaken to determine the effects of PB2 on liver injury induced by cold stimulation and its potential molecular mechanisms. The present study results showed that treatment with PB2 significantly reduced CS‐induced liver injury by alleviating histopathological changes and serum levels of alanine transaminase and aspartate transaminase. Moreover, treatment with PB2 inhibited secretion of inflammatory cytokines and oxidative stress in cold‐stimulated mice. PB2 reduced cold stimulation‐induced inflammation by inhibiting TLR4/NF‐κB and Txnip/NLRP3 signalling. Treatment with PB2 reduced oxidative stress by activating Nrf‐2/Keap1, AMPK/GSK3β signalling pathways and autophagy. Furthermore, simultaneous application of Shh pathway inhibitor cyclopamine proved that PB2 targets the Hh pathway. More importantly, co‐treatment with PB2 and cyclopamine showed better efficacy than monotherapy. In conclusion, our findings provide new evidence that PB2 has protective potential against CS‐induced liver injury, which might be closely linked to the inhibition of Shh signalling pathway. [ABSTRACT FROM AUTHOR]

SUMMARY: Heat shock protein 90 (HSP90) is involved in plant growth and various stress responses via regulating protein homeostasis. Autophagy keeps cellular homeostasis by recycling the components of cellular cytoplasmic constituents. Although they have similar effects on cellular protein homeostasis, the direct association between HSP90 and autophagy signaling remains unclear in plants, especially in tropical crops. In this study, the correlation between HSP90 and autophagy signaling was systematically analyzed by protein–protein interaction in cassava, one of the most important economy fruit in tropic. In addition, their effects on plant disease response and underlying mechanisms in cassava were investigated by functional genomics and genetic phenotype assay. The potential MeHSP90.9‐MeSGT1‐MeRAR1 chaperone complex interacts with MeATGs and subsequently triggers autophagy signaling, conferring improved disease resistance to cassava bacterial blight (CBB). On the contrary, HSP90 inhibitor and autophagy inhibitor decreased disease resistance against CBB in cassava, and autophagy may be involved in the potential MeHSP90.9‐MeSGT1‐MeRAR1 chaperone complex‐mediated multiple immune responses. This study highlights the precise modulation of autophagy signaling by potential MeHSP90.9‐MeSGT1‐MeRAR1 chaperone complex in autophagy‐mediated disease resistance to CBB. [ABSTRACT FROM AUTHOR]

The preventive and therapeutic mechanisms of CDBE on osteoporosis were studied by observing the serum bone‐related biochemical indicators, bone trabecular micro‐structure and intestinal flora in ovariectomized osteoporosis model mice, in order to provide a scientific theoretical basis for the further study on the effect of CDBE on osteoporosis, and the prevention and treatment of osteoporosis with clinical traditional Chinese medicines. The components in CDBE were detected by UHPLC‐MS. A mouse osteoporosis model was established by the bilateral ovariectomy in female ICR mice. The biochemical indicators related to osteoporosis were detected, the right proximal tibia was scanned by Micro‐CT, the intestinal microflora in the colon contents were examined, and the changes of microflora were taken as the main target to evaluate the effect of CDBE on the intestinal microflora in the model mice. A total of 16 compounds were obtained by the combined application of UHPLC‐MS. CDBE could significantly increase the contents of E2, Ca2+, CT, HyP, OCN, FOXP3, P1NP and CTX‐II, in the model mice. CDBE could significantly improve the trabecular micro‐structure, Tb.N, Tb.Sp, SMI and Conn.D. CDBE could make the intestinal flora of osteoporosis model mice tend to healthy mice in species and quantity. CDBE can improve the symptoms of postmenopausal osteoporosis in mice, with a positive effect on the intestinal flora of postmenopausal mice. Its mechanism of regulating the symptoms of osteoporosis may be related to the regulation of bone‐related biochemical indicators in the serum of mice. Practical applications: This research has a positive impact on the development of functional food with anti‐osteoporosis in the future. [ABSTRACT FROM AUTHOR]

Melatonin is an important indole amine hormone in animals and plants. The enzymes that catalyse melatonin synthesis positively regulate plant stress responses through modulation of the accumulation of reactive oxygen species (ROS). However, the relationship between melatonin biosynthetic enzymes and ROS-scavenging enzymes has not been characterized. In this study, we demonstrate that two enzymes of the melatonin synthesis pathway in Manihot esculenta (MeTDC2 and MeASMT2) directly interact with ascorbate peroxidase (MeAPX2) in both in vitro and in vivo experiments. Notably, in the presence of MeTDC2 and MeASMT2, MeAPX2 showed significantly higher activity and antioxidant capacity than the purified MeAPX2 protein alone. These findings indicate that MeTDC2–MeAPX2 and MeASMT2–MeAPX2 interactions both activate APX activity and increase antioxidant capacity. In addition, the combination of MeTDC2, MeASMT2, and MeAPX2 conferred improved resistance to hydrogen peroxide in Escherichia coli. Moreover, this combination also positively regulates oxidative stress tolerance in cassava. Taken together, these findings not only reveal a direct interaction between MeTDC2, MeASMT2, and MeAPX2, but also highlight the importance of this interaction in regulating redox homoeostasis and stress tolerance in cassava. [ABSTRACT FROM AUTHOR]

The Zi goose is native to North‐east China and is noted for its high egg production. Alpha enolase (ENO1) is a glycolytic enzyme which functions as a plasminogen receptor in follicular granulosa cells (FGCs), with several studies showing that FGCs can support follicular development. By transfecting the ENO1 interfering plasmid (shRNA) into FGCs, ENO1 expression in these cells was downregulated, suggesting the successful knock‐down of ENO1 in these cells. In this knock‐down model, we detected 13 metabolites from FGCs using LC/MS. When compared with the non‐coding shRNA (NC) group, the lower level metabolites were (R)‐(+)‐citronellic acid, altretamine, 3‐hydroxycaproic acid, heptadecanoic acid, cholecalciferol vitamin D3, indole, benzoic acid, capric acid, caffeic acid, azelaic acid, 3,4‐dihydroxyhydrocinnamic acid and cholic acid, while oleic acid was detected at high levels. To further examine the results of metabolomics, six key metabolites were verified by gas chromatography‐mass spectrometry (GC‐MS). We found that vitamin D3, indole, benzoic acid, capric acid and cholic acid were significantly downregulated in the shRNA group, while oleic acid was significantly upregulated. This observation was consistent with the metabolomics data. Through these studies, we found that decreased ENO1 levels altered certain metabolite levels in FGCs. [ABSTRACT FROM AUTHOR]

Nanoparticles with effective tumor accumulation and efficient renal clearance have attracted significant interests for clinical applications. We prepared 2.5 nm tyrosine based carbon dots (TCDs) with phenolic hydroxyl groups on the surface for directly 125I labeling. The 125I labeled polyethylene glycol (PEG) functionalized TCDs (125I-TCDPEGs) showed excellent radiochemical stability both in vitro and in vivo. Due to the enhanced permeability and retention effect, these 125I-TCDPEGs demonstrated a tumor accumulation around 4%–5% of the injected dose per gram (ID/g) for U87MG, 4T1, HepG2 and MCF7 tumor-bearing mice at 1 h post-injection. Meanwhile, the 125I-TCDPEGs also could be fast renally excreted, with less than 0.6% ID/g left in the liver and spleen within 24 h. These radioactive carbon dots not only can be used for cellular fluorescence imaging due to their intrinsic optical property, but are also effective single photon emission computed tomography (SPECT) imaging agents for tumor. Together with their excellent biocompatibility and stability, we anticipate these 125I-TCDPEGs of great potential for early tumor diagnosis in clinic. What's more, our TCDPEGs are also proved to be feasible carriers for other iodine isotopes such as 127I and 131I for different biomedical application. [ABSTRACT FROM AUTHOR]

A ratiometric two-photon fluorescent probe for SO2 derivatives was first proposed based on acedan–merocyanine dyads via a TP-FRET strategy. It was successfully applied to visualization of the fluctuations of enzymatically generated SO2 derivatives in the mitochondria of HepG2 cells and rat liver tissues using two-photon fluorescence microscopy imaging. [ABSTRACT FROM AUTHOR]

During cold stress, liver cells undergo apoptotic injury as a result of oxidative stress. Heat shock 70 kDa protein (Hsp70) is a protein involved in modulating a variety of physiological processes, including stress responses, proliferation, and apoptosis. In addition, Hsp70 regulates apoptotic signaling pathways in different manners, promoting or suppressing apoptosis. In this study, we investigated the effects of Hsp70 overexpression on hydrogen peroxide (HO)-induced apoptosis of Buffalo rat liver (BRL) cells and the underlying mechanisms of these effects. Our results show that in comparison with the control group, Hsp70 overexpression displayed increased protein levels of Bcl-2, and decreased cytochrome c (Cyt c), cleaved caspase 3, and cleaved caspase 8, but no apparent differences were found in levels of Bax. Furthermore, Hsp70 overexpression significantly suppresses the amount of apoptotic cells. Such findings indicate that overexpression of Hsp70 inhibits HO-mediated activation of caspase 8 and caspase 3, upregulates the expression of Bcl-2 which is a known anti-apoptotic protein, and decreases the release of Cyt c from the mitochondria into the cytoplasm, collectively decreasing cell apoptosis. [ABSTRACT FROM AUTHOR]