Impact of cirrhosis-related complications on posttransplant survival in patients with acute-on-chronic liver failure.

BACKGROUND: Acute-on-chronic liver failure (ACLF) is a life-threatening syndrome defined as acute decompensation in patients with chronic liver disease. Liver transplantation (LT) is the most effective treatment. We aimed to assess the impact of cirrhosis-related complications pre-LT on the posttransplant prognosis of patients with ACLF. METHODS: This was an observational cohort study conducted between January 2018 and December 2020. Clinical characteristics, cirrhosis-related complications at LT and patient survival post-LT were collected. All liver recipients with ACLF were followed for 1 year post-LT. RESULTS: A total of 212 LT recipients with ACLF were enrolled, including 75 (35.4%) patients with ACLF-1, 64 (30.2%) with ACLF-2, and 73 (34.4%) with ACLF-3. The median waiting time for LT was 11 (4-24) days. The most prevalent cirrhosis-related complication was ascites (78.8%), followed by hepatic encephalopathy (57.1%), bacterial infections (48.1%), hepatorenal syndrome (22.2%) and gastrointestinal bleeding (11.3%). Survival analyses showed that patients with complications at LT had a significantly lower survival probability at both 3 months and 1 year after LT than those without complications (all P < 0.05). A simplified model was developed by assigning one point to each complication: transplantation for ACLF with cirrhosis-related complication (TACC) model. Risk stratification of TACC model identified 3 strata (≥ 4, = 3, and ≤ 2) with high, median and low risk of death after LT (P < 0.001). Moreover, the TACC model showed a comparable ability for predicting the outcome post-LT to the other four prognostic models (chronic liver failure-consortium ACLF score, Chinese Group on the Study of Severe Hepatitis B-ACLF score, model for end-stage liver disease score and Child-Turcotte-Pugh score). CONCLUSIONS: The presence of cirrhosis-related complications pre-LT increases the risk of death post-LT in patients with ACLF. The TACC model based on the number of cirrhosis-related complications pre-LT could stratify posttransplant survival, which might help to determine transplant timing for ACLF.

Effects of Lateral Size, Thickness, and Stabilizer Concentration on the Cytotoxicity of Defect-Free Graphene Nanosheets: Implications for Biological Applications.

In this work, we apply liquid cascade centrifugation to highly concentrated graphene dispersions produced by liquid-phase exfoliation in water with an insoluble bis-pyrene stabilizer to obtain fractions containing nanosheets with different lateral size distributions. The concentration, stability, size, thickness, and the cytotoxicity profile are studied as a function of the initial stabilizer concentration for each fraction. Our results show that there is a critical initial amount of stabilizer (0.4 mg/mL) above which the dispersions show reduced concentration, stability, and biocompatibility, no matter the lateral size of the flakes.

Revealing Spatial Patterns of Cultural Ecosystem Services in Four Agricultural Landscapes: A Case Study from Hangzhou, China.

Monitoring and mapping agricultural cultural ecosystem services (CES) is essential, especially in areas with a sharp contradiction between agricultural land protection and urban development. Despite research assessing CES increasing exponentially in recent years, our knowledge of the CES of agricultural landscapes is still inadequate. This study used four types of agricultural landscapes in Hangzhou, China, as the study area, analyzed their CES spatial patterns, and explored their societal preferences by integrating the multi-sourced datasets, clustering algorithms, and Maxent model. The results indicated that hot spots of agricultural CES correspond to river valley plains, which were also easily vulnerable to urbanization. Moreover, we found that the CES level of paddy field and dry farmland were higher than tea garden and orchard. Based on the above spatial patterns of supply, demand, and flow of CES, we identified four groups of agricultural land by cluster analysis, distinguishing between significant, unimportant, little used, and potential CES. Further, our results showed that natural and human factors could explain societal preferences. This study can provide a valuable basis for stakeholders to develop balanced strategies by the aforementioned results.

Curcumin inhibits the invasion and metastasis of triple negative breast cancer via Hedgehog/Gli1 signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: In traditional Chinese medicine, there is a long history that curcuma longa L is used to treat distending pain of chest and belly, arthralgia of shoulder and arm aggravated by cold. Traditional Chinese medicine holds that breast cancer is caused by cold congelation, stagnation of qi and blood stasis. It is usually treated with some pungent and warm Chinese herbs, such as Curcuma longaL and Curcuma zedoaria (Christm.) Rosc, which are effective in promoting blood circulation for removing blood stasis, activating qi-flowing and relieving pain. Curcumin, a polyphenolic compound, is the main pharmacological component extracted from the rhizome of Curcuma longa L. Modern pharmacological studies have found that curcumin has many kinds of pharmacological activities of anti-inflammatory, anti-tumor, anti-angiogenesis, anti-metastasis and anti-multidrug resistance. AIM OF THE STUDY: To explore the mechanism of curcumin and Glioma-associated oncogene homolod-1 (Gli1) on invasion and metastasis of triple negative breast cancer (TNBC) cells through the Hedgehog (Hh)/Gli signaling pathway. MATERIAL AND METHODS: The effect of curcumin on TNBC cells was detected by colony formation, wound healing and transwell assay. Breast cancer stem cells (BCSCs) were cultured in serum-free medium and its stemness was detected by flow cytometry and subcutaneous xenografted tumor assay. The formation of mammospheres was used to detect the effect of curcumin and GANT61 (Gli inhibitor)on the formation ability of BCSCs. Gli1 overexpressed was conducted in MDA-MB-231 cells by lentivirus vector HBLV-h-Gli1-3xflag-ZsGreen-PURO. RT-qPCR and Western blot were detected the mRNA and protein level of genes of Hh pathway, Epithelial-mesenchymal transition (EMT) and stemness. The nuclear localization and expression of Gli1 was observed by laser confocal microscope scanning. Co-IP was investigated the key genes interacted with Gli1. RESULTS: The abilities of proliferation, invasion, migration and the formation of mammospheres in TNBC cells were inhibited by curcumin. Furthermore, curcumin reduced the invasion and migration abilities in stable Gli1-overexpressing MDA-MB-231 cell. Moreover, curcumin down-regulated the expression of genes related Hh pathway, EMT and stemness in MDA-MB-231 mammospheres. Observation of laser confocal microscope showed that Gli1 were expressed mainly in nucleus in MDA-MB-231 adherent cells and completely in nucleus in BCSCs, which was significantly reduced in the nucleus and cytoplasm after curcumin treatment. Besides, our results suggested that vimentin was interacted with Gli1. CONCLUSIONS: Curcumin can inhibit the proliferation and metastasis of TNBC cells, EMT and characteristics of BCSC by Hedgehog/Gli1 pathway.

Roles of mesenchymal stem cells and exosomes in interstitial cystitis/bladder pain syndrome.

Interstitial cystitis/bladder pain syndrome (IC/BPS) is characterized by several symptoms of higher sensitivity of the lower urinary tract, such as bladder pain/discomfort, urgency, urinary frequency, pelvic pain and nocturia. Although the pathophysiology of IC/BPS is not fully understood, the hypothesis suggests that mast cell activation, glycosaminoglycan (GAG) layer defects, urothelium permeability disruption, inflammation, autoimmune disorder and infection are potential mechanisms. Mesenchymal stem cells (MSCs) have been proven to protect against tissue injury in IC/BPS by migrating into bladders, differentiating into key bladder cells, inhibiting mast cell accumulation and cellular apoptosis, inhibiting inflammation and oxidative stress, alleviating collagen fibre accumulation and enhancing tissue regeneration in bladder tissues. In addition, MSCs can protect against tissue injury in IC/BPS by secreting various soluble factors, including exosomes and other soluble factors, with antiapoptotic, anti-inflammatory, angiogenic and immunomodulatory properties in a cell-to-cell independent manner. In this review, we comprehensively summarized the current potential pathophysiological mechanisms and standard treatments of IC/BPS, and we discussed the potential mechanisms and therapeutic effects of MSCs and MSC-derived exosomes in alleviating tissue injury in IC/BPS models.

Curcumin Administered in Combination with Glu-GNPs Induces Radiosensitivity in Transplanted Tumor MDA-MB-231-luc Cells in Nude Mice.

Curcumin is a type of plant polyphenol extracted from Curcuma longa L. rhizome, which demonstrates antitumor activity in breast cancer cells in vitro. To investigate the combined effect and possible mechanism of curcumin and glucose-gold nanoparticles (Glu-GNPs), the radiosensitivity of breast carcinoma xenografts was assessed in nude mice. MDA-MB-231 cells labeled with firefly luciferase were inoculated into the mammary fatty pads of nude mice to establish a transplantation tumor model of human breast cancer. The tumor-bearing mice were treated with different drugs (curcumin, Glu-GNPs, and cisplatin) for 3 weeks prior to radiotherapy. The body weights and tumor volumes of the mice were measured in regular intervals. Tumor bioluminescence intensity was determined in real-time using an in vivo bioluminescence imaging system to monitor tumor growth. Transplanted tumor tissue samples were taken for hematoxylin and eosin (HE) staining, and the expression of VEGF, HSP90, HIF-1α, and MMP9 was evaluated via reverse transcription-quantitative PCR or immunohistochemistry. The results revealed that the breast tumor-bearing nude mouse model was successfully established, as evidenced by a stable expression of luciferase. Curcumin inhibited the growth of tumors without causing significant weight loss in mice. Furthermore, additive inhibition was demonstrated when curcumin was administered in combination with Glu-GNPs and irradiation. Tumor bioluminescence intensity was decreased in the model group following curcumin, Glu-GNPs, and irradiation treatment. HE staining demonstrated that transplanted tumors were malignant, with necrotic tissue exhibited centrally. It was concluded that curcumin administered in combination with Glu-GNPs and X-ray irradiation could reduce the protein expression of VEGF, HSP90, HIF-1α, and MMP9 in tumor tissue when compared with the model group. Curcumin and Glu-GNPs administered with X-ray irradiation significantly inhibited tumor growth and induced radiosensitivity, which may be associated with the inhibition of angiogenesis in tumor tissue.

Regulation of autophagy protects against liver injury in liver surgery-induced ischaemia/reperfusion.

Transient ischaemia and reperfusion in liver tissue induce hepatic ischaemia/reperfusion (I/R) tissue injury and a profound inflammatory response in vivo. Hepatic I/R can be classified into warm I/R and cold I/R and is characterized by three main types of cell death, apoptosis, necrosis and autophagy, in rodents or patients following I/R. Warm I/R is observed in patients or animal models undergoing liver resection, haemorrhagic shock, trauma, cardiac arrest or hepatic sinusoidal obstruction syndrome when vascular occlusion inhibits normal blood perfusion in liver tissue. Cold I/R is a condition that affects only patients who have undergone liver transplantation (LT) and is caused by donated liver graft preservation in a hypothermic environment prior to entering a warm reperfusion phase. Under stress conditions, autophagy plays a critical role in promoting cell survival and maintaining liver homeostasis by generating new adenosine triphosphate (ATP) and organelle components after the degradation of macromolecules and organelles in liver tissue. This role of autophagy may contribute to the protection of hepatic I/R-induced liver injury; however, a considerable amount of evidence has shown that autophagy inhibition also protects against hepatic I/R injury by inhibiting autophagic cell death under specific circumstances. In this review, we comprehensively discuss current strategies and underlying mechanisms of autophagy regulation that alleviates I/R injury after liver resection and LT. Directed autophagy regulation can maintain liver homeostasis and improve liver function in individuals undergoing warm or cold I/R. In this way, autophagy regulation can contribute to improving the prognosis of patients undergoing liver resection or LT.

Rational synthesis of novel "giant" CuInTeSe/CdS core/shell quantum dots for optoelectronics.

"Giant" core/shell quantum dots (g-QDs) are promising candidates for emerging optoelectronic technologies thanks to their facile structure/composition-tunable optoelectronic properties and outstanding photo-physical/chemical stability. Here, we synthesized a new type of CuInTeSe (CITS)/CdS g-QDs and regulated their optoelectronic properties by controlling the shell thickness. Through increasing the shell thickness, as-prepared g-QDs exhibited tunable red-shifted emission (from 900 to 1200 nm) and prolonged photoluminescence (PL) lifetimes (up to ∼14.0 µs), indicating a formed band structure showing efficient charge separation and transfer, which is further testified by theoretical calculations and ultrafast time-resolved transient absorption (TA) spectroscopy. These CITS/CdS g-QDs with various shell thicknesses can be employed to fabricate photoelectrochemical (PEC) cells, exhibiting improved photoresponse and stability as compared to the bare CITS QD-based devices. The results indicate that the rational design and engineering of g-QDs is very promising for future QD-based optoelectronic technologies.

Melatonin and its protective role in attenuating warm or cold hepatic ischaemia/reperfusion injury.

Although the liver is the only organ with regenerative capacity, various injury factors induce irreversible liver dysfunction and end-stage liver disease. Liver resection and liver transplantation (LT) are effective treatments for individuals with liver failure, liver cirrhosis and liver cancers. The remnant or transplanted liver tissues will undergo hepatic ischaemia/reperfusion (IR), which leads to oxidative stress, inflammation, immune injury and liver damage. Moreover, systemic ischaemia induced by trauma, stroke, myocardial ischaemia, haemorrhagic shock and other injury factors also induces liver ischaemia/reperfusion injury (IRI) in individuals. Hepatic IRI can be divided into warm IRI, which is induced by liver surgery and systemic ischaemia, and cold IRI, which is induced by LT. Multiple studies have shown that melatonin (MT) acts as an endogenous free radical scavenger with antioxidant capacity and is also able to attenuate hepatic IRI via its anti-inflammatory and antiapoptotic capacities. In this review, we discuss the potential mechanisms and current strategies of MT administration in liver surgery for protecting against warm or cold hepatic IRI. We highlight strategies to improve the efficacy and safety of MT for attenuating hepatic IRI in different conditions. After the potential mechanisms underlying the interactions between MT and other important cellular processes during hepatic IR are clarified, more opportunities will be available to use MT to treat liver diseases in the future.

Induction therapy with mesenchymal stromal cells in kidney transplantation: a meta-analysis.

OBJECTIVE: The aim of this meta-analysis was to evaluate the therapeutic effects of mesenchymal stromal cells (MSCs) versus traditional regimens for induction therapy in kidney transplantation (KT), especially the safety of MSC infusion, practicability of MSCs as induction therapy agents, and posttransplant complications. METHODS: PubMed, Embase, EBSCO, Ovid, and the Cochrane Library were searched for prospective clinical trials that compared MSCs with traditional regimens for induction therapy in KT. RESULTS: Four trials were included, including a total of 197 patients. The pooled results revealed that MSC therapy had a lower 1-year infection rate than did the traditional therapies (RR = 0.65, 95% CI: 0.46-0.9, P = 0.01). There were no significant differences between the two protocols regarding the 1-year acute rejection (AR) rate (RR = 0.77, 95% CI: 0.41-1.45, P = 0.42), 1-year graft survival rate (RR = 0.99, 95% CI: 0.95-1.03, P = 0.74), delayed graft function (DGF) rate (RR = 0.54, 95% CI: 0.21-1.38, P = 0.2) and renal graft function at 1 month (MD = -1.56, 95% CI: - 14.2-11.08, p = 0.81), 3 months (MD = 0.15, 95% CI: - 5.63-5.93, p = 0.96), 6 months (MD = - 1.95, 95% CI: - 9.87-5.97, p = 0.63), and 12 months (MD = - 1.13, 95% CI: - 7.16-4.89, p = 0.71) postsurgery. Subgroup analysis demonstrated that the 1-year AR rate, 1-year graft survival rate, DGF rate, and renal graft function at 12 months postsurgery did not significantly differ between the low-dose calcineurin inhibitor (CNI) group and the standard-dose CNI group, indicating the potential benefits of successful CNI sparing in combination with MSC treatment. Moreover, when MSCs were applied as an alternative therapy rather than an additional therapy or allogeneic MSCs were utilized instead of autologous MSCs, all of the outcomes mentioned above were comparable. CONCLUSION: Induction therapy with MSCs is safe and has similar immune response modulation effects to those of traditional regimens in the short term in KT recipients. However, regarding the long-term effects, as suggested by the 1-year infection rate and the potential of CNI sparing, MSC therapy has significant advantages. However, these advantages should be further verified in more well-designed, multicenter randomized controlled trials (RCTs) with large sample sizes and long follow-up periods.

Hippo/TEAD4 signaling pathway as a potential target for the treatment of breast cancer.

Breast cancer is the most common type of cancer among women worldwide. The Hippo signaling pathway is strongly associated with cell proliferation, migration, invasion, metastasis and resistance to breast cancer treatment. The upstream factors involved in the Hippo signaling pathway, including mammalian Ste20 kinases 1/2, large tumor suppressor kinases 1/2 and transcription coactivator Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ), have been extensively studied as they are considered therapeutic targets for breast cancer. Recently, it has been suggested that the transcriptional enhancer factor domain (TEAD) family of transcription factors, particularly TEAD4, plays an important role in breast cancer. TEADs interact with YAP/TAZ to act as transcription factors. Notably, recent studies have demonstrated that TEAD4 may also function in a YAP/TAZ-independent manner and serve as a prognostic marker for breast cancer. The present review summarizes the current research on the effect of the aberrant activation of the Hippo signaling pathway on breast cancer progression. Furthermore, the latest advances on the role of the TEAD family in breast cancer are highlighted, and the role of TEAD4 as a potential target for therapeutic intervention in breast cancer is discussed.

Combination of mesenchymal stromal cells and machine perfusion is a novel strategy for organ preservation in solid organ transplantation.

Organ preservation is a prerequisite for an urgent increase in the availability of organs for solid organ transplantation (SOT). An increasing amount of expanded criteria donor (ECD) organs are used clinically. Currently, the paradigm of organ preservation is shifting from simple reduction of cellular metabolic activity to maximal simulation of an ex vivo physiological microenvironment. An ideal organ preservation technique should not only preserve isolated organs but also offer the possibility of rehabilitation and evaluation of organ function prior to transplantation. Based on the fact that mesenchymal stromal cells (MSCs) possess strong regeneration properties, the combination of MSCs with machine perfusion (MP) is expected to be superior to conventional preservation methods. In recent years, several studies have attempted to use this strategy for SOT showing promising outcomes. With better organ function during ex vivo preservation and the potential of utilization of organs previously deemed untransplantable, this strategy is meaningful for patients with organ failure to help overcome organ shortage in the field of SOT.

Genetic modification by overexpression of target gene in mesenchymal stromal cell for treating liver diseases.

Different hepatoxic factors cause irreversible liver injury, leading to liver failure, cirrhosis, and cancer in mammals. Liver transplantation is the only effective strategy, which can improve the prognosis of patients with end-stage liver diseases, but it is limited by liver donor shortage, expensive costs, liver graft rejection and dysfunction, and recurring liver failure. Recently, mesenchymal stromal cells (MSCs) isolated from various tissues are regarded as the main stem cell type with therapeutic effects in liver diseases because of their hepatogenic differentiation, anti-inflammatory, immuoregulatory, anti-apoptotic, antifibrotic, and antitumor capacities. To further improve the therapeutic effects of MSCs, multiple studies showed that genetically engineered MSCs have increased regenerative capacities and are able to more effectively inhibit cell death. Moreover, they are able to secrete therapeutic proteins for attenuating liver injury in liver diseases. In this review, we mainly focus on gene overexpression for reprogramming MSCs to increase their therapeutic effects in treating various liver diseases. We described the potential mechanisms of MSCs with gene overexpression in attenuating liver injury, and we recommend further expansion of experiments to discover more gene targets and optimized gene delivery methods for MSC-based regenerative medicine. We also discussed the potential hurdles in genetic engineering MSCs. In conclusion, we highlight that we need to overcome all scientific hurdles before genetically modified MSC therapy can be translated into clinical practices for patients with liver diseases.

Dispersant-assisted liquid-phase exfoliation of 2D materials beyond graphene.

The extensive research on liquid-phase exfoliation (LPE) performed in the last 10 years has enabled a low cost and mass scalable approach to the successful production of a range of solution-processed 2-dimensional (2D) materials suitable for many applications, from composites to energy storage and printed electronics. However, direct LPE requires the use of specific solvents, which are typically toxic and expensive. Dispersant-assisted LPE allows us to overcome this problem by enabling production of solution processed 2D materials in a wider range of solvents, including water. This approach is based on the inclusion of an additive, typically an amphiphilic molecule, designed to interact with both the nanosheet and the solvent, enabling exfoliation and stabilization at the same time. This method has been extensively used for the LPE of graphene and has been discussed in many reviews, whilst little attention has been given to dispersant-assisted LPE of 2D materials beyond graphene. Considering the increasing number of 2D materials and their potential in many applications, from nanomedicine to energy storage and catalysis, this review focuses on the dispersant-assisted LPE of transition metal dichalcogenides (TMDs), hexagonal boron nitride (h-BN) and less studied 2D materials. We first provide an introduction to the fundamentals of LPE and the type of dispersants that have been used for the production of graphene, we then discuss each class of 2D material, providing an overview on the concentration and properties of the nanosheets obtained. Finally, a perspective is given on some of the challenges that need to be addressed in this field of research.

Serum ammonia is a strong prognostic factor for patients with acute-on-chronic liver failure.

Ammonia is thought to be central to the pathogenesis of hepatic encephalopathy (HE), but its prognostic role in acute-on-chronic liver failure (ACLF) is still unknown. We aimed to determine the association between serum ammonia level and short-term prognosis in ACLF. Furthermore, we performed an in-depth evaluation of the independent effect of serum ammonia level on the short-term prognosis of hepatitis B virus (HBV) reactivation-induced ACLF patients. We identified 174 patients as part of prospective observational studies in patients with ACLF. Plasma ammonia levels were measured on admission, and several prognostic scores were used to determine the prognostic effect of ammonia. The 28-day patient survival was determined. Receiver operating characteristic analysis was used to identify the cut-off points for ammonia values, and multivariable analysis was performed using the Cox proportional hazard regression model. Plasma ammonia was significantly higher in nonsurvivors (83.53 ± 43.78 versus 67.13 ± 41.77 µmol/L, P = 0.013), and ACLF patients with hyperammonemia had significantly higher 28-day mortality than those without hyperammonemia. Ammonia was also closely related to ACLF grade (P < 0.001) and organ failure, including liver (P = 0.048), coagulation (P < 0.001) and brain (P < 0.001). HBV reactivation serves as the main precipitating factor in the ACLF population. Subgroup analysis showed that ammonia is also a strong prognostic factor in the HBV reactivation-induced ACLF population. Ammonia level is closely correlated with failure of other organs and is an independent risk factor for mortality in ACLF and the special population defined as HBV reactivation-related ACLF. Based on the results from our study, we measured serum ammonia in the population with ACLF, which strongly indicates their prognosis. It serves as an important biomarker and a therapeutic target.

Mesenchymal stem cell-based cell-free strategies: safe and effective treatments for liver injury.

Various hepatoxic factors, such as viruses, drugs, lipid deposition, and autoimmune responses, induce acute or chronic liver injury, and 3.5% of all worldwide deaths result from liver cirrhosis, liver failure, or hepatocellular carcinoma. Liver transplantation is currently limited by few liver donors, expensive surgical costs, and severe immune rejection. Cell therapy, including hepatocyte transplantation and stem cell transplantation, has recently become an attractive option to reduce the overall need for liver transplantation and reduce the wait time for patients. Recent studies showed that mesenchymal stem cell (MSC) administration was a promising therapeutic approach for promoting liver regeneration and repairing liver injury by the migration of cells into liver sites, hepatogenic differentiation, immunoregulation, and paracrine mechanisms. MSCs secrete a large number of molecules into the extracellular space, and soluble proteins, free nucleic acids, lipids, and extracellular vesicles (EVs) effectively repair tissue injury in response to fluctuations in physiological states or pathological conditions. Cell-free-based therapies avoid the potential tumorigenicity, rejection of cells, emboli formation, undesired differentiation, and infection transmission of MSC transplantation. In this review, we focus on the potential mechanisms of MSC-based cell-free strategies for attenuating liver injury in various liver diseases. Secretome-mediated paracrine effects participate in the regulation of the hepatic immune microenvironment and promotion of hepatic epithelial repair. We look forward to completely reversing liver injury through an MSC-based cell-free strategy in regenerative medicine in the near future.

Fluorescence Lifetime-Tunable Water-Resistant Perovskite Quantum Dots for Multidimensional Encryption.

Using temporal dimension in optical multiplexing is a promising method to increase the security of data encryption. However, adjusting the fluorescence lifetime of light-emitting material often results in inevitable changes in their fluorescence spectra, which is unfavorable for confidential information protection. Here, we report the preparation of various perovskite quantum dot/polymer nanospheres (PQD/polymer) with tunable and long fluorescence lifetimes but identical fluorescence spectra, which are ideal multidimensional data encryption materials. This new data encryption strategy utilizes the water sensitivity of perovskite and achieves spatial dimension encryption of information using different water stabilities between uncoated perovskite quantum dots and PQD/polymer. The fluorescence lifetime of PQD/polymer is used as the coding element to achieve temporal dimension data encryption, and the data are decrypted by fluorescence lifetime imaging microscopy and time-gated luminescence imaging techniques. This study shows the potential of PQD/polymer as a new class of materials for advanced data encryption.

Autophagy regulation is an effective strategy to improve the prognosis of chemically induced acute liver injury based on experimental studies.

Acute liver injury (ALI) induced by chemicals in current experimental studies is characterized by inflammation, oxidative stress and necrosis, which can greatly influence the long-term outcome and lead to liver failure. In liver cells, different autophagy forms envelop cytoplasm components, including proteins, endoplasmic reticulum (ER), mitochondria and lipids, and they effectively participate in breaking down the cargo enclosed inside lysosomes to replenish cellular energy and contents. In general, autophagy serves as a cell survival mechanism in stressful microenvironments, but it also serves as a destructive mechanism that results in cell death in vitro and in vivo. In experimental animals, multiple chemicals are used to mimic ALI in patients to clarify the potential pathological mechanisms and develop effective strategies in the clinic. In this review, we summarize related publications about autophagy modulation to attenuate chemically induced ALI in vitro and in vivo. We also analysed the underlying mechanisms of autophagy regulators and genetic modifications to clarify how to control autophagy to protect against chemically induced ALI in animal models. We anticipate that selectively controlling the dual effects of hepatic autophagy will help to protect against ALI in various animals, but the detailed mechanisms and effects should be determined further in future studies. In this way, we are more confident that modulating autophagy in liver regeneration can improve the prognosis of ALI.