Interface Regulation for Efficient and Stable Perovskite Solar Cells through Potassium Citrate Molecules.

Efficiency and stability are key factors determining the final cost of electricity that perovskite solar cells (PSCs) generate. To date, effective strategy to progress in achieving efficient and stable PSCs is still a difficult problem that researchers continue to explore. Here, we report a useful way to improve the quality of SnO2 film by introducing potassium citrate (PC) into SnO2 nanoparticles solution. PC passivates interface defects between perovskite and SnO2 layers via the interactions of functional groups (K+, -COO-) in PC with undersaturated Pb and I ions in perovskite and Sn4+ in SnO2. The resultant photovoltaic (PV) device achieves a champion power conversion efficiency (PCE) of 22.79%. The introduction of PC interface also significantly suppress the degradation of PSCs, by which 87.6% of initial PCE is maintained after 2850 hours storage in ambient environment. Moreover, the devices retained 95.5% of initial PCE under 1-sun continuous illumination for 1000 hours.

The location of estrogen receptor variant ER-α36 is associated with the invasion of glioblastoma.

Glioblastoma (GBM) is the most common central nervous system tumor and is associated with poor outcomes. There have been no significant improvements in GBM mortality in recent decades. ER-α36 is a variant of ER-α66 that may be involved in carcinoma growth and proliferation via genomic and nongenomic mechanisms. This variant might play an essential role in tamoxifen resistance of several tumors. Previously, our laboratory found that ER-α36 is expressed in GBM and participates in proliferation; nevertheless, the role of ER-α36 in GBM invasion remains unknown. This study aimed to determine the effects of the ER-α36 modulator SNG162 on GBM growth and invasion. U251 cells, U87cells, and U87-36KD cells with knockdown of ER-α36 expression were cultured under the two-dimensional and the three-dimensional (3D) environments. GBM cells growth was examined by cell counting, flow cytometry, western blot, and MTT assays. Invasiveness was measured using confocal microscopy in the 3D environment. Growth of U87 cells with downregulated EGFR and ER-α36 expression was significantly reduced after treatment with 1 µM, 3 µM, and 5 µM of SNG162; growth inhibition in U251 cells was more potent than in U87 cells, although the expression level of ER-α36 in U251 cells was lower than in U87 cells. We found that 1 µM SNG162 suppressed E2-induced MAPK/ERK pathway activation in U87 cells. We also showed that SNG162 inhibited U87 cells invasion; however, it did not significantly affect U251 and U87-36KD cells invasion using the 3D culture method. Finally, we determined that ER-α36 was expressed in the nucleus of invading GBM cells, and SNG162 significantly inhibited the expression of ER-α36 in these cells. SNG162 inhibited the expression of EGFR on cell membranes of non-invasive GBM cells. These results suggest that SNG162 could be a therapeutic agent for GBM by targeting ER-α36.

Psoas Hematoma After Posterior Lumbar Interbody fusion: A Case Report and Literature Review.

Introduction: This article introduced the management of a case with severe left lower extremity pain and forced hip flexion after posterior lumbar interbody fusion and a final diagnosis of left psoas hematoma. Materials and methods: Here we reported a case of a 65-year-old female received posterior lumbar interbody fusion (PLIF) for L4-L5 spondylolisthesis and L4 instability. On the postoperative day one, the hemoglobin level decreased from 108 g/L to 78 g/L. Meanwhile, the patient presented low back pain and inner thigh radiating pain (VAS pain scale = 8). The pain was so severe that it could be barely relieved by keeping left hip in flexion position. On the postoperative day 6, the pain was still severe even after taking mecobalamin, ankylosaurus, dehydrant agents and central pain relievers(VAS pain scale = 9). Computed Tomography indicated a left intramuscular hematoma image extending down to the left iliac fossa. Active hemorrhage of lumbar segmental arterial was detected by B-ultrasound. The patient then received vascular embolization under angiography on the postoperative day 7. Results: The pain in the low back and inner thigh were significantly relieved after the procedure (VAS3-4). On the postoperative day nineteen, the left hip can be fully extended, but the patient was still not able to stand on left leg without a walking stick. On the postoperative day 27, she was able to walk independently. Discussion: The main reason for the complication was the second conical dilation channel slipped and entered the lateral side of the vertebral body along the transverse process. After timely embolization, pain was significantly relieved and muscle strength was improved. Conclusions: Angiographic embolization is an effective treatment for psoas hematoma after posterior lumbar interbody fusion.

Voluntarily wheel running inhibits the growth of CRPC xenograft by inhibiting HMGB1 in mice.

INTRODUCTION: Exercise has been proved to reduce the risk of recurrence and mortality of cancer. Emerging evidence indicated that exercise may regulate both systematical and local metabolism, immunity and other ways. Although the role of exercise in inhibiting castration-resistant prostate cancer is well established, the underlying mechanism remains unclear. METHOD: Twenty C57BL/6 male mice were used to construct CRPC xenograft models and randomly divided into exercise group (n = 10) and control group (n = 10). After exercised with voluntarily wheel running for 21 days, the mice were sacrificed and the tumor tissues and serum were collected. TUNEL staining was used to detect the apoptosis of tumor cells. The expression of PI3K signal pathway and apoptosis related proteins were detected by Western blot. The expression of AR and HMGB1 were examined by Western blot and Immunohistochemical staining. IFN-γ, TNF-α, TGF-ß, IL-4, IL-6, IL-10 in serum was examined using ELISA kits. RESULTS: Voluntarily wheel running inhibited the growth of CRPC xenografts, inhibited the proliferation of tumor cells and promoted the apoptosis of tumor cells. HMGB1 levels in serum and tumor tissues were significantly reduced after exercise, which enhanced local immunity by inducing more leukocyte infiltration and inhibited systemic inflammatory response by regulating cytokines. CONCLUSION: Voluntary wheel running can down-regulate the expression of HMGB1 in serum and transplanted tumor tissues, inhibit proliferation and promote apoptosis of tumor cells, enhance immune cell infiltration and systemic inflammatory response, and regulate local anti-tumor effects in tumor microenvironment.

Wearable biosensors for human fatigue diagnosis: A review.

Fatigue causes deleterious effects to physical and mental health of human being and may cause loss of lives. Therefore, the adverse effects of fatigue on individuals and the society are massive. With the ever-increasing frequency of overtraining among modern military and sports personnel, timely, portable and accurate fatigue diagnosis is essential to avoid fatigue-induced accidents. However, traditional detection methods require complex sample preparation and blood sampling processes, which cannot meet the timeliness and portability of fatigue diagnosis. With the development of flexible materials and biosensing technology, wearable biosensors have attracted increased attention to the researchers. Wearable biosensors collect biomarkers from noninvasive biofluids, such as sweat, saliva, and tears, followed by biosensing with the help of biosensing modules continuously and quantitatively. The detection signal can then be transmitted through wireless communication modules that constitute a method for real-time understanding of abnormality. Recent developments of wearable biosensors are focused on miniaturized wearable electrochemistry and optical biosensors for metabolites detection, of which, few have exhibited satisfactory results in medical diagnosis. However, detection performance limits the wide-range applicability of wearable fatigue diagnosis. In this article, the application of wearable biosensors in fatigue diagnosis has been discussed. In fact, exploration of the composition of different biofluids and their potential toward fatigue diagnosis have been discussed here for the very first time. Moreover, discussions regarding the current bottlenecks in wearable fatigue biosensors and the latest advancements in biochemical reaction and data communication modules have been incorporated herein. Finally, the main challenges and opportunities were discussed for wearable fatigue diagnosis in the future.

Morphology modulation of artificial muscles by thermodynamic-twist coupling.

Human muscles can grow and change their length with body development; therefore, artificial muscles that modulate their morphology according to changing needs are needed. In this paper, we report a strategy to transform an artificial muscle into a new muscle with a different morphology by thermodynamic-twist coupling, and illustrate its structural evolution during actuation. The muscle length can be continuously modulated over a large temperature range, and actuation occurs by continuously changing the temperature. This strategy is applicable to different actuation modes, including tensile elongation, tensile contraction and torsional rotation. This is realized by twist insertion into a fibre to produce torsional stress. Fibre annealing causes partial thermodynamic relaxation of the spiral molecular chains, which serves as internal tethering and inhibits fibre twist release, thus producing a self-supporting artificial muscle that actuates under heating. At a sufficiently high temperature, further relaxation of the spiral molecular chains occurs, resulting in a new muscle with a different length. A structural study provides an understanding of the thermodynamic-twist coupling. This work provides a new design strategy for intelligent materials.

Perylene Monoimide Phosphorus Salt Interfacial Modified Crystallization for Highly Efficient and Stable Perovskite Solar Cells.

Reducing the interfacial defects of perovskite films is key to improving the performance of perovskite solar cells (PSCs). In this study, two kinds of perylene monoimide (PMI) derivative phosphonium bromide salts were designed and used as a multifunctional interface-modified layer in PSCs. These two molecules are inserted between SnO2 and perovskite to produce a bidirectional passivation effect. The interaction with SnO2 reduces the oxygen vacancy on the surface of SnO2 and tunes the energy level of the electron transport layer, making more matches with the perovskite layer. The modified layer can promote the growth of perovskite crystals and reduce the interfacial defects of the perovskite film. Furthermore, the power conversion efficiency (PCE) of PSCs increased from 19.49 to 22.85%, and the open-circuit voltage (VOC) increased from 1.06 to 1.14 V. At the same time, the PCE of the SnO2/PMI-TPP-based device remained 88% of the initial PCE after 240 h of continuous illumination. In addition, these two PMI derivatives with a quasi-planar structure can improve the flexibility of flexible PSCs. This study provided a new strategy for the interfacial modification of PSCs and a new insight into the application of flexible PSCs.

Apigenin ameliorates non-eosinophilic inflammation, dysregulated immune homeostasis and mitochondria-mediated airway epithelial cell apoptosis in chronic obese asthma via the ROS-ASK1-MAPK pathway.

BACKGROUND: Obese asthma is one of the important asthma phenotypes that have received wide attention in recent years. Excessive oxidative stress and different inflammatory endotypes may be important reasons for the complex symptoms, frequent aggravation, and resistance to traditional treatments of obese asthma. Apigenin (API), is a flavonoid natural small molecule compound with good anti-inflammatory and antioxidant activity in various diseases and proved to have the potential efficacy to combat obese asthma. METHODS: In vivo, this study fed C57BL/6 J mice with high-fat diets(HFD)for 12 weeks and then stimulated them with OVA for 6 weeks to establish a model of chronic obese asthma, while different doses of oral API or dexamethasone were used for therapeutic interventions. In vitro, this study used HDM to stimulate human bronchial cells (HBEs) to establish the model and intervened with API or Selonsertib (SEL). RESULTS: This study clarified that OVAinduced a type of mixed granulocytic asthma with elevated neutrophils and eosinophils in obese male mice fed with long-term HFD, which also exhibited mixed TH17/TH1/TH2 inflammation. Apigenin effectively suppressed this complex inflammation and acted as a regulator of immune homeostasis. Meanwhile, apigenin reduced AHR, inflammatory cell infiltration, airway epithelial cell apoptosis, airway collagen deposition, and lung oxidative stress via the ROS-ASK1-MAPK pathway in an obese asthma mouse model. In vitro, this study found that apigenin altered the binding status of TRAF6 to ASK1, inhibited ASK1 phosphorylation, and protected against ubiquitin-dependent degradation of ASK1, suggesting that ROS-activated ASK1 may be an important target for apigenin to exert anti-inflammatory and anti-apoptotic effects. To further verify the intervention mechanism, this study clarified that apigenin improved cell viability and mitochondrial function and inhibited apoptosis by interfering with the ROS-ASK1-MAPK pathway. CONCLUSIONS: This study demonstrates for the first time the therapeutic effect of apigenin in chronic obese asthma and further clarifies its potential therapeutic targets. In addition, this study clarifies the specificity of chronic obese asthma and provides new options for its treatment.

Nuclear access of DNlg3 c-terminal fragment and its function in regulating innate immune response genes.

Neuroligins (NLGNs) are one of the autism susceptibility genes, however, the mechanism that how dysfunction of NLGNs leads to Autism remains unclear. More and more studies have shown that the transcriptome alteration may be one of the important factors to generate Autism. Therefore, we are very concerned about whether Neuroligins would affect transcriptional regulation, which may at last lead to Autism. As a single-transmembrane receptor, proteolytic cleavage is one of the most important posttranslational modifications of NLGN proteins. In this study, we demonstrated the existence of DNlg3 C-terminal fragment. Studies in the S2 cells and HEK293T cells showed the evidence for nuclear access of the DNlg3 C-terminal fragment. Then we identified the possible targets of DNlg3 C-terminal fragment after its nuclear access by RNA-seq. The bioinformatics analysis indicated the transcriptome alteration between dnlg3 null flies and wild type flies focused on genes for the innate immune responses. These results were consistent with the infection hypotheses for autism. Our study revealed the nuclear access ability of DNlg3 c-terminal fragment and its possible function in transcriptional regulation of the innate immune response genes. This work provides the new links between synaptic adhesion molecule NLGNs and immune activation, which may help us to get a deeper understanding on the relationship between NLGNs and Autism.

Identification of prognostic values of the transcription factor-CpG-gene triplets in lung adenocarcinoma: A narrative review.

OBJECTIVE: Abnormal DNA methylation can regulate carcinogenesis in lung adenocarcinoma (LUAD), while transcription factors (TFs) mediate methylation in a site-specific manner to affect downstream transcriptional regulation and tumor progression. Therefore, this study aimed to explore the TF-methylation-gene regulatory relationships that influence LUAD prognosis. METHODS: Differential analyses of methylation sites and genes were generated by integrating transcriptome and methylome profiles from public databases. Through target gene identification, motif enrichment in the promoter region, and TF prediction, TF-methylation and methylation-gene relation pairs were obtained. Then, the prognostic TF-methylation-gene network was constructed using univariate Cox regression analysis. Prognostic models were constructed based on the key regulatory axes. Finally, Kaplan-Meier curves were created to evaluate the model efficacy and the relationship between candidate genes and prognosis. RESULTS: A total of 1878 differential expressed genes and 1233 differential methylation sites were screened between LUAD and normal samples. Then 10 TFs were predicted to bind 144 enriched motifs. After integrating TF-methylation and methylation-gene relations, a prognostic TF-methylation-gene network containing 4 TFs, 111 methylation sites, and 177 genes was constructed. In this network, ERG-cg27071152-MTURN and FOXM1-cg19212949-PTPR regulatory axes were selected to construct the prognostic models, which showed robust abilities in predicting 1-, 3-, and 5-year survival probabilities. Finally, ERG and MTURN were downregulated in LUAD samples, whereas FOXM1 and PTPR were upregulated. Their expression levels were related to LUAD prognosis. CONCLUSION: ERG-cg27071152-MTURN and FOXM1-cg19212949-PTPR regulatory axes were proposed as potential biomarkers for predicting the prognosis of LUAD.

Effect of one-time high load exercise on skeletal muscle injury in rats of different genders: oxidative stress and mitochondrial responses.

PURPOSE: To evaluate the impact of one-time high load exercise on skeletal muscle injury and analysis its mechanism in different genders. METHODS: Twenty-four male and 24 female rats were divided randomly into four groups respectively: control, 0 h, 6 h, and 24 h after exercise. The activities of creatine kinase (CK), lactate dehydrogenase (LDH), and myohemoglobin (MYO) in serum, the expression level of oxidative stress markers, mitochondrial respiratory chain complex enzyme, and the apoptosis related protein in quadriceps were detected. RESULTS: The results showed that the activities of CK, LDH and MYO in serum increased immediately after exercise and restored faster in female rats. More obvious structural disorder and apoptosis in male rats were showed. Malondialdehyde (MDA) and superoxide dismutase (SOD) were increased while catalase (CAT) and glutathione (GSH) were decreased in male rats. SOD, CAT and GSH were increased in female rats. Mitochondrial complex enzyme activity was decreased in males and increased in females. CONCLUSIONS: The skeletal muscle injury in both genders of rat could be induced by one-time high load exercise due to the mitochondrial respiratory enzyme dysfunction and oxidative stress, which was relatively mild and recovered quicker in female rats.

Intravenous lidocaine simultaneously infused with sufentanil to accelerate gastrointestinal function recovery in patients after thoracolumbar surgery: a prospective, randomized, double-blind controlled study.

PURPOSE: Postoperative gastrointestinal dysfunction is one of the common complications of surgery, especially after surgery for a thoracolumbar spinal fracture. Intravenous lidocaine is a potential method to improve postoperative gastrointestinal function in surgical patients, reduce opioid use and shorten hospital stays. The purpose of this study is to explore the effect of intravenous lidocaine on the recovery of gastrointestinal function in patients after thoracolumbar surgery. METHODS: In this study, 48 eligible patients undergoing elective thoracolumbar spine fractures resection and internal fixation surgery were enrolled to receive intravenous injections of lidocaine in different concentrations during the perioperative period. Patients were randomly divided into three groups: control group (group A), low concentration of lidocaine group (group B) and high concentration of lidocaine group (group C), 16 patients in each group. First postoperative exhaust time, numbers of bowel sound at preoperative and postoperative 3, 6, 12, 24 h, pain scores at postoperative 0, 3, 6, 12, 24, 48 h, total sufentanil use in PACU and perioperative periods, postoperative hospital stay and analgesic remedy within postoperative 48 h were recorded and compared. The primary endpoints include: the time of first flatus passage after the operation, the number of bowel sounds per minute counted with stethoscope at 30 min before anesthesia induction and at 3, 6, 12 and 24 h postoperative. The secondary endpoints included: the pain scores at PACU (after entering into PACU), 3, 6, 12, 24 and 48 h postoperative, the amount of sufentanil administrated by intravenous push during operation and the numbers of patients needed rescuing sufentanil in PACU, and the numbers of patients needed administration of gastric motility drugs or non-steroidal analgesics at ward within 48 h postoperation, length of hospital stay (from the first day after surgery to discharge from hospital) and the incidence of adverse reactions. RESULTS: Compared with group A, the first postoperative exhaust time in group B and C occurred much earlier (23.3 ± 11.0 h vs. 16.0 ± 6.6 h, 16.6 ± 5.1 h, P < 0.05). Compared with preoperation, the numbers of bowel sound significantly increased at 24 h postoperatively in group B, while group B at 6 h and group C at 6 and 24 h postoperatively had significantly more active bowel sounds compared to group A (P < 0.05). There were no remarkable differences in VAS scores within 12 h postoperatively among three groups, and however, significantly lower VAS scores were found at 12, 24 and 48 h postoperatively in group C when comparing to Group A (p < 0.05). There was no statistical significance in the incidence of postoperative flatulence and nausea and vomiting, the number of patients needed rescuing sufentanil in PACU, the length of postoperative hospital stay and the number of patients requiring non-steroidal analgesics at ward within 48 h postoperation. CONCLUSIONS: Intravenous lidocaine infusion together with patient-controlled analgesia of sufentanil expedited the early recovery of gastrointestinal function and improved analgesic quality of sefentanyl in patients undergoing thoracolumbar surgeries.

TMT-Based Quantitative Proteomic Analysis Reveals Downregulation of ITGAL and Syk by the Effects of Cycloastragenol in OVA-Induced Asthmatic Mice.

Background: Cycloastragenol (CAG) has been reported to alleviate airway inflammation in ovalbumin- (OVA-) induced asthmatic mice. However, its specific mechanisms remain unclear. Objective: This study is aimed at investigating the effects of CAG on asthma, comparing its efficacy with dexamethasone (DEX), and elucidating the mechanism of CAG's regulation. Methods: The asthma mouse model was induced by OVA. CAG at the optimal dose of 125 mg/kg was given every day from day 0 for 20-day prevention or from day 14 for a 7-day treatment. We observed the preventive and therapeutic effects of CAG in asthmatic mice by evaluating the airway inflammation, AHR, and mucus secretion. Lung proteins were used for TMT-based quantitative proteomic analysis to enunciate its regulatory mechanisms. Results: The early administration of 125 mg/kg CAG before asthma happened prevented asthmatic mice from AHR, airway inflammation, and mucus hypersecretion, returning to nearly the original baseline. Alternatively, the administration of CAG during asthma also had the same therapeutic effects as DEX. The proteomic analysis revealed that the therapeutical effects of CAG were associated with 248 differentially expressed proteins and 3 enriched KEGG pathways. We then focused on 3 differentially expressed proteins (ITGAL, Syk, and Vav1) and demonstrated that CAG treatment downregulated ITGAL, Syk, and Vav1 by quantitative real-time PCR, western blot analysis, and immunohistochemical staining. Conclusion: These findings suggest that CAG exerts preventive and protective effects on asthma by inhibiting ITGAL, Syk, and the downstream target Vav1.

Experimental pathogenicity and comparative genome analysis of high- and low-virulence strains of rabbit-origin Pasteurella multocida.

Pasteurella multocida, the causative pathogen of rabbit pasteurellosis, causes significant economic losses in the commercial rabbit industry. However, the associated pathogenic mechanism of P. multocida remains unclear. The aim of this study is to compare the genomes and pathogenicity of high- and low-virulence strains of P. multocida to advance the current understanding of rabbit pasteurellosis. The high-virulence strain rapidly proliferates in the lung and spleen of infected mice within approximately 9 h, maintaining a high bacterial load until host death. Meanwhile, the low-virulence strain only proliferates in mouse organs for a short time, with the bacterial load beginning to decrease 13 h post-infection. Moreover, the expressions of inflammatory cytokines MCP-1, TNF-α, and IL-1ß are upregulated in all infected mouse lung and spleen tissue, however, the high-virulence strain induced significantly higher expression than the low-virulence strain. Histopathological analysis revealed greater inflammation and tissue lesions in the lung and spleen of mice infected with the high-virulence strain. Two pathogenicity-associated regions unique to the genome of the high-virulence strain harbor approximately 199 genes, including functional genes related to virulence factors, such as lipopolysaccharide biosynthesis, iron acquisition, biosynthesis of outer membrane proteins, and adhesion. These two genomic regions are shared by three previously sequenced, highly virulent P. multocida strains in rabbits. In conclusion, the increased pathogenicity of high-virulence P. multocida may be due to the presence of virulence-associated genes in two unique genomic regions, resulting in strong proliferative activity, significant inflammation, and pathological lesions in the mouse model. These findings provide important insights regarding the pathogenic mechanism underlying rabbit pasteurellosis.

Design and synthesis of DNA hydrogel based on EXPAR and CRISPR/Cas14a for ultrasensitive detection of creatine kinase MB.

Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas systems exhibit significant potential in developing biosensing technology due to their collateral cleavage capabilities. Herein, we introduced the collateral cleavage activity of CRISPR/Cas14a to activate DNA hydrogel for ultrasensitive detection of the myocardial infarction biomarker creatine kinase MB (CK-MB). In this strategy, the designed CRISPR/Cas14a system can be activated by introducing complementary DNA (cDNA) derived from competitive dissociation and exponential amplification (EXPAR), which is positively correlated with creatine kinase isoenzyme (CK-MB) concentration. Then the activated Cas14a protein can be utilized to indiscriminately cleave the DNA hydrogel cross-linker strand, leading to the degradation of the gel matrix and thus releasing the pre-encapsulated PtNPs/Cu-TCPP(Fe). PtNPs/Cu-TCPP(Fe) can trigger the TMB reaction, leading to an increase in absorbance value at 450 nm, thus enabling the quantitative detection of CK-MB. The proposed strategy combines CRISPR/Cas14a with DNA hydrogel for the first time, improving the programmability of DNA hydrogel and providing a reliable, sensitive, and versatile detection platform for trace non-nucleic acid targets.

Recent progress and research trend of anti-cataract pharmacology therapy: A bibliometric analysis and literature review.

Cataract is the leading cause of blindness worldwide. Cataract phacoemulsification combined with intraocular lens implantation causes great burden to global healthcare, especially for low- and middle-income countries. Such burden would be significantly relieved if cataracts can effectively be treated or delayed by non-surgical means. Excitingly, novel drugs have been developed to treat cataracts in recent decades. For example, oxysterols are found to be able to innovatively reverse lens clouding, novel nanotechnology-loaded drugs improve anti-cataract pharmacological effect, and traditional Chinese medicine demonstrates promising therapeutic effects against cataracts. In the present review, we performed bibliometric analysis to provide an overview perspective regarding the research status, hot topics, and academic trends in the field of anti-cataract pharmacology therapy. We further reviewed the curative effects and molecular mechanisms of anti-cataract drugs such as lanosterol, metformin, resveratrol and curcumin, and prospected the possibility of their clinical application in future.

The regulatory role of exosomes in venous thromboembolism.

Exosomes are nanoscale endocytic vesicles, 30-150 nm in diameter, secreted by most cells. They mainly originate from multivesicular bodies formed by intracellular invagination of lysosomal microparticles, and released into the extracellular matrix after fusion of multivesicular bodies with cell membrane. Studies have shown that exosomes contain a variety of active molecules, such as proteins, lipids and RNAs (such as mRNA, miRNA, lncRNA, circRNA, etc.), which regulate the behavior of recipient cells and serve as circulating biomarkers of diseases, including thrombosis. Therefore, exosome research is important for the diagnosis, treatment, therapeutic monitoring, and prognosis of thrombosis in that it can reveal the counts, surface marker expression, protein, and miRNA cargo involved. Recent studies have shown that exosomes can be used as therapeutic vectors for tissue regeneration and as alternative vectors for drug delivery. In this review, we summarize the physiological and biochemical characteristics, isolation, and identification of exosomes. Moreover, we focus on the role of exosomes in thrombosis, specifically venous thromboembolism, and their potential clinical applications, including as biomarkers and therapeutic vectors for thrombosis.

Protective effect of low-dose radiation on doxorubicin-induced brain injury in mice.

BACKGROUND: To investigate the protective effect of low-dose radiation (LDR) on brain injury in mice induced by doxorubicin (DOX). METHODS: Sixty female BALB/C mice were randomly divided into the control (CTR) group, low-dose radiation (LDR) group, doxorubicin treatment (DOX) group and low-dose radiation before doxorubicin treatment (COM) group. After 72 h of exposure to 75 mGy, the mice were intraperitoneally injected with 7.5 mg/kg of doxorubicin and sacrificed 5 days later. Neuron-specific enolase (NSE), lactate dehydrogenase (LDH), adenosine triphosphate (ATP), neurotransmitters, inflammatory mediators, apoptosis- and oxidative stress-related mediators as well as mitochondrial dysfunction were examined. RESULTS: Compared to the DOX group, the concentrations of DA, 5-HT, EPI and GABA in the COM group were significantly decreased, and the number of TUNEL-positive cells was decreased. In addition, the expression of proapoptotic proteins was downregulated in the COM group compared to the DOX group. Low-dose radiation in advance reduced reactive oxygen species and activated the SOD antioxidant defense system as indicated by significantly reduced GSH expression, increased GSSG expression, increased GPx expression and activation of the Nrf2 redox pathway. After low-dose radiation, the expression levels of ATP5f1, NDUFV1 and CYC1 were close to normal, and the mitochondrial respiratory control rate (RCR) and activity of respiratory chain complex enzymes also tended to be normal. Low-dose radiation upregulated the expression levels of IL-2 and IL-4 but downregulated the expression levels of IL-10 and TGF-ß. CONCLUSION: LDR has a protective effect on brain injury in mice treated with DOX. The mechanism is related to LDR alleviating mitochondrial dysfunction and oxidative stress, which promotes the production of antioxidant damage proteins, thus exerting an adaptive protective effect on cells.

Gomisin A enhances the antitumor effect of paclitaxel by suppressing oxidative stress in ovarian cancer.

Gomisin A (GA) is an effective component of Schisandra. The crude extracts of Schisandra chinensis and its active ingredients have been shown to inhibit multidrug resistance in tumour cells. Reactive oxygen species (ROS) have different roles in cancer and may contribute to therapy resistance. The human ovarian cancer (OC) cell lines SKOV3 and A2780, and a mouse model of OC, were used in the present study. MTT assay, colony formation assay, flow cytometry, western blot analysis, and haematoxylin and eosin (H&E) staining were performed to determine the antitumor effect of GA and paclitaxel (PTX) in vitro and in vivo. The ROS inhibitor N­acetyl cysteine (NAC) was used to assess the mechanism underlying the chemosensitizing effects of GA. Notably, the proliferation of OC cells was inhibited by PTX, which could be enhanced by the ROS inhibitor NAC or GA. Treatment with NAC + PTX or GA + PTX enhanced the cell cycle arrest, but not apoptosis, induced by PTX. Moreover, the molecular mechanism underlying this effect may be that GA decreases the levels of ROS in ovarian cancer cells and inhibits cell cycle progression by downregulating the expression of the cell cycle proteins cyclin­dependent kinase 4 and cyclin B1. In conclusion, the combination of PTX and the ROS inhibitor GA may be a novel strategy in OC chemotherapy.