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Retinoblastoma (RB) is an intraocular malignancy that mainly occurs in infants and young children under 5 years of age. Circular RNA hsa_circ_0000034 (circ_0000034) was reported to be upregulated in RB tissues. Nevertheless, the function and mechanism of circ_0000034 in RB are unclear. Expression of circ_0000034, microRNA-361-3p (miR-361-3p), and a disintegrin and metalloproteinase 19 (ADAM19) was examined via quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, migration, invasion, and apoptosis were determined though Cell Counting Kit-8 (CCK-8), transwell, or flow cytometry assays. Caspase-3 activity was detected using a caspase-3 activity assay kit. Some protein levels were examined using Western blot analysis. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, or RNA pull-down assay were performed to verify the relationship between circ_0000034 or ADAM19 and miR-361-3p. The function of circ_0000034 in vivo was confirmed via animal experiment. We verified that circ_0000034 expression was elevated in RB tissues and cells. Circ_0000034 silencing reduced RB growth in vivo, repressed viability, migration, invasion, and EMT, and induced apoptosis of RB cells in vitro. Circ_0000034 acted as a sponge for miR-361-3p, which targeted ADAM19 in RB cells. Furthermore, the inhibition of miR-361-3p restored circ_0000034 knockdown-mediated impacts on viability, migration, invasion, apoptosis, and EMT of RB cells. Moreover, ADAM19 overexpression abolished the influence of miR-361-3p mimic on viability, migration, invasion, apoptosis, and EMT of RB cells. Circ_0000034 expedited RB progression through upregulating ADAM19 via sponging miR-361-3p, which indicated that circ_0000034 might a target for RB therapy.

Cardiovascular and cerebrovascular diseases continue to be significant public health problems, with high mortality and morbidity rates worldwide. Inflammation and ROS are believed to be the hallmarks of these diseases, but conventional therapies targeting inflammation and ROS have had limited success due to their limited pharmacokinetics, low bioavailability, shorter half-life, and notable side effects. Over the last decade, nanomedicine has rapidly evolved with diverse applications in diagnostics, drug delivery, and treatment of various diseases, including cardiovascular and cerebrovascular diseases. Nanomaterials such as nanozymes have gained success with remarkable therapeutic efficacy due to their stability, formulations, enzyme-mimetic activities, and ability to deliver more than one drug. Moreover, nanozymes can uphold a constant rate of drug release, maintaining a low frequency of dosing to reduce the side effects of drugs. Due to their multifunctional nature, they can be used as targeted delivery vehicles to the damaged brain, arterial, and other tissues to mitigate inflammation and ROS while promoting blood-brain barrier protection, ischemic stroke neurovascular recovery, and neuronal cell survival. In this review article, we have explored the mechanisms and different types of nanozyme-based targeted therapies for several cardiovascular and cerebrovascular diseases, including myocardial infarction, atherosclerosis, and ischemic stroke. We have discussed their enzyme-mimetic catalytic activities, immune-modulatory effects, ROS scavenging abilities, and anti-inflammatory properties. We have also discussed the challenges that slow down the clinical and translational success of these nanozyme-based therapies. Continuing work with integrated and multidisciplinary approaches, these nanozymes may offer potential solutions for cardiovascular and cerebrovascular diseases. Highlights Nanozymes offer high stability, low cost, and tunable activity. They mimic various enzymes, enabling diverse applications in biomedicine, including cardiac and cerebrovascular diseases. Recent advances focus on improving catalytic efficiency and substrate specificity through rational design involving size, shape, composition, and surface modification. Metal-based and carbon-based nanozymes have shown robust catalytic performance and biocompatibility. Nanozymes are explored by reducing oxidative stress, scavenging reactive oxygen species, and helping to control inflammation in damaged heart and brain tissues. Key challenges in treating cardiac and brain diseases include improving treatment specificity, understanding underlying mechanisms, and ensuring long-term safety and compatibility for real-world use. Graphical Abstract This photo abstract shows the cardiovascular and cerebrovascular disease applications of nanozymes (NEs). The classification of nanozymes includes carbon-based nanozymes, metal-based nanozymes, and other nanozymes. Nanozymes work by scavenging ROS, anti-inflammatory and immunomodulatory, as well as targeted delivery and controlled release. It is used in cardiovascular diseases (arteriosclerosis, myocardial infarction, thrombosis) and cerebrovascular disease (ischemic stroke, hemorrhagic stroke, nerve repair). Challenges include toxicity, large-scale production, and regulatory issues, and future directions include optimal design, clinical trials, and interdisciplinary collaboration. Nanozymes show great potential in the treatment of cardiovascular and cerebrovascular diseases by mimicking the activity of natural enzymes, effectively clearing ROS, regulating inflammation, and promoting tissue repair.

A phosphorus-containing bio-based epoxy resin（EADI）was synthesized from itaconic acid（IA）and 9,10-dihydro-9-oxa-10-phosphaphenanthrene 10-oxide（DOPO）.As a matrix,its cured epoxy network with methyl hexahydrophthalic anhydride（MHHPA）as the curing agent showed comparable glass-transition temperature and mechanical properties to diglycidyl ether in a bisphenol A（DGEBA）system as well as good flame retardancy with UL94 V-0 grade during a vertical burning test.As a reactive flame retardant,its flame-resistant effect on DGEBA/MHHPA system as well as its influence on the curing behavior and the thermal and mechanical properties of the modified epoxy resin were investigated.Results showed that after the introduction of EADI,not only were the flame retardancy determined by vertical burning test,LOI measurement,and thermogravimetric analysis significantly improved,but also the curing reactivity,glass transition temperature（T g）,initial degradation temperature for 5%weight loss（T d（5%））,and flexural modulus of the cured system improved as well.EADI has great potential to be used as a green flame retardant in epoxy resin systems.

To study the structure and distribution characteristics of the phytoplankton community in the Huaihe River Basin, Yangtze River Basin, and Taihu Lake Basin in Jiangsu Province, 126 sampling sites were set up in 35 rivers in the region, and samples were collected during the wet season (August–September) in 2023. Based on the monitoring results of phytoplankton, the study selected 20 candidate indicators and conducted range screening, discriminative ability analysis, and correlation analysis. Finally, seven core indicators were determined to construct the Phytoplankton Biological Integrity Index (P-IBI) evaluation system. The rating standards were determined by the ratio method, and the phytoplankton integrity of Jiangsu Province was evaluated. The differences were analyzed. As the results showed, the overall health status of rivers in Jiangsu Province was general. From the point of view of the basin scope, the Huaihe River Basin and the Yangtze River Basin were in sub-healthy state, and the Taihu Lake Basin was general. There were significant differences in the phytoplankton density community structure in the Yangtze River, Huaihe River, and Taihu Lake Basins. Phytoplankton integrity was positively correlated with total nitrogen and nitrate nitrogen, but not with other environmental factors. Nitrogen is the main factor affecting the integrity of river phytoplankton in Jiangsu Province.

Assessing the impact of varied rainfall patterns on soil and water loss within a hilly watershed over an extended temporal scope holds paramount importance in comprehending regional runoff and sediment traits. This study utilized continuous rainfall and sediment data spanning from 2013 to 2021, and the K-means clustering method was employed to analyze rainfall types. Subsequently, the rain-type characteristics underwent further analysis through LSD, and a multiple linear regression equation was formulated. The result showed that: within the Qiaotou small basin, rainfall, maximum rainfall intensity within 30 min (I30), and rainfall erosivity exhibited notable effects on sediment yield and loss. The water-sediment attributes of 305 rainfall events were characterized by rainfall below 100 mm, I30 of less than 35 mm/h, a runoff coefficient below 0.5, and sediment content under 0.6 g/L. According to the characteristics of different rainfall types and the degree of influence on water and sediment in small watersheds, 305 rainfall events in the basin were divided into three types by the K-means clustering analysis method: A (heavy rainfall, moderate rain), B (small rainfall, light rain), and C (medium rainfall, heavy rain). The most frequent rain type observed was B, followed by C, while A had the lowest frequency. Despite the lower intensity of B-type rainfall, it holds significant regional importance. Conversely, C-type rainfall, although intense and short, serves as the primary source of sediment production. The multiple regression equation effectively models both sediment yield modulus and flood peak discharge, exhibiting an R2 coefficient exceeding 0.80, signifying significance. This equation enables the quantitative calculation of pertinent indicators. Sediment yield modulus primarily relies on sediment concentration, runoff depth, and rainfall, while peak discharge is significantly influenced by runoff depth, sediment concentration, and I30. Furthermore, the efficacy of various soil and water conservation measures for flow and sediment reduction correlates with I30. Overall, the impact of different measures on reducing flow and sediment increases with a higher I30, accompanied by a reduced fluctuation range.

Autophagy is crucial for cell survival, development, division, and homeostasis. The mammalian target of rapamycin (mTOR), which is the foremost negative controller of autophagy, plays a key role in many endogenous processes. The present study investigated whether rapamycin can ameliorate surgery—induced cognitive deficits by inhibiting mTOR and activating autophagy in the hippocampus. Both adult and aged C57BL/6J mice received an intraperitoneal injection of rapamycin (10 mg/kg/day) for 5 days per week for one and a half months. Mice were then subjected to partial hepatectomy under general anesthesia. Behavioral performance was assessed on postoperative days 3, 7, and 14. Hippocampal autophagy-related (Atg)-5, phosphorylated mTOR, and phosphorylated p70S6K were examined at each time point. Brain derived neurotrophic factor (BDNF), synaptophysin, and tau hyperphosphorylation (T396) in the hippocampus were also examined. Surgical trauma and anesthesia exacerbated spatial learning and memory impairment in aged mice on postoperative days 3 and 7. Following partial hepatectomy, the levels of phosphorylated mTOR, phosphorylated 70S6K, and phosphorylated tau were all increased in the hippocampus. A corresponding decline in BDNF and synaptophysin were observed. Rapamycin treatment restored autophagy function, attenuated phosphorylation of tau protein, and increased BDNF and synaptophysin expression in the hippocampus of surgical mice. Furthermore, surgery and anesthesia induced spatial learning and memory impairments were also reversed by rapamycin treatment. Autophagy impairments and mTOR hyperactivation were detected along with surgery—induced behavioral deficits. Inhibiting the mTOR signaling pathway with rapamycin successfully ameliorated surgery-related cognitive impairments by sustaining autophagic degradation, inhibiting tau hyperphosphorylation, and increasing synaptophysin and BDNF expression.

Background/Aims: TREM2 plays a crucial role in modulating microglial function through interaction with DAP12, the adapter for TREM2. Emerging evidence has demonstrated that TREM2 could suppress neuroinflammatory responses by repression of microglia-mediated cytokine production. This study investigated the potential role of TREM2 in surgery-induced cognitive deficits and neuroinflammatory responses in wild-type (WT) and APPswe/PS1dE9 mice. Methods: Adult APPswe/PS1dE9 transgenic male mice (a classic transgenic model of Alzheimer’s disease, 3 months old) and their age-matched WT mice received intracerebral lentiviral particles encoding the mouse TREM2 gene and then were subjected to partial hepatectomy at 1 month after the lentiviral particle injection. The behavioral changes were evaluated with an open-field test and Morris water maze test on postoperative days 3, 7, and 14. Hippocampal TREM2, DAP12, and interleukin (IL)-1β were measured at each time point. Ionized calcium-binding adapter molecule 1 (Iba-1), microglial M2 phenotype marker Arg1, synaptophysin, tau hyperphosphorylation (T396), and glycogen synthase kinase-3β (GSK-3β) were also examined in the hippocampus. Results: Surgical trauma induced an exacerbated cognitive impairment and enhanced hippocampal IL-1β expression in the transgenic mice on postoperative days 3 and 7. A corresponding decline in the levels of TREM2 was also found on postoperative days 3, 7, and 14. Overexpression of TREM2 downregulated the levels of IL-1β, ameliorated T396 expression, inhibited the activity of GSK-3β, and improved sickness behavior. Increased Arg1 expression and a high level of synaptophysin were also observed in the transgenic mice following TREM2 overexpression. Conclusion: The downregulation of TREM2 exacerbated surgery-induced cognitive deficits and exaggerated neuroinflammatory responses in this rodent model. Overexpression of TREM2 potentially attenuated these effects by decreasing the associated production of proinflammatory cytokines, inhibiting tau hyperphosphorylation, and enhancing synaptophysin expression.

The PANI/Mesoporous MnO2 composites were prepared through a simple one step method and we introduced the KI-H2SO4 solution as the electrolyte of PANI/MnO2 composites creatively. The characterization of structure, morphology, and composition are obtained by X-ray diffraction, Fourier transform infrared spectroscopy, thermal gravity analysis, Raman spectra, and scanning electron microscope. The electrochemical performances were investigated by constant-current charge–discharge, the voltammetry curve, and alternating current (AC) impedance technique. The specific capacitance of composites is 1405 F/g, which is almost 10 times larger than MnO2 (158 F/g). We also find that the iodide concentration is closely related to the specific capacitance. Therefore, we explored the specific capacitance at different iodide concentration (0.05, 0.1, 0.2, 0.5, and 1 M), the results indicated that the specific capacitance reached a maximum value (1580 F/g) at 0.5 mol/L. Additionally, the PANI/Mesoporous MnO2 composites not only exhibited a good ratio discharge property (857 F/g) at high current density, but also revealed an excellent cycling stability after 500 cycles, which retained 90% of the original specific capacitance.

Sprague-Dawley adult male rats (12-14 weeks old) were exposed to 14-day CUS and then subjected to partial hepatectomy 24 h after the last stress session. The rats were pretreated with an antagonist of the glucocorticoids (GCs) receptor RU486 (30 mg/kg, i.p.) 1 h prior to stress exposure. The behavioral changes were evaluated with open field test and elevated plus-maze test. The hippocampal cytokines interleukin (IL)-1β and IL-6 were measured on postoperative days 1, 3 and 7. Ionized calcium binding adaptor protein (Iba)-1, microglial M2 phenotype marker Arg1, brain derived neurotrophic factor (BDNF) and CD200 were also examined at each time point. CUS exacerbated surgery-induced sickness behavior. Exposure to CUS alone failed to alter the levels of pro-inflammatory cytokines in the brain. However, CUS exaggerated surgery-induced pro-inflammatory cytokines expression (e.g. IL-1β and IL-6) and upregulated the levels of Iba-1 on postoperative days 1 and 3. An additional significant decreased BDNF, CD200 and a lower level of Arg1 were also observed in the stressed rats following surgical procedure. Pretreatment with RU486 blunted the potentiating effects of CUS on surgery-induced sickness behavior and neuroinflammatory responses. Chronic unpredictable stress enhanced surgery-induced sickness behavior and neuroinflammatory responses. Stress-induced GCs played a pivotal role in enhancing surgery-induced neuroinflammatory processes by modulation of microglia functions.