Circularly Polarized Phosphorescence Energy Transfer Combined with Chirality-Selective Absorption for Modulating Full-Color and White Circularly Polarized Long Afterglow.

Circularly polarized long afterglow (CPLA) attracts great interests in multi-disciplinary fields with significant potentials in optical multiplexing applications, but achieving full-color and white CPLA is still challenging. The present contribution reports the first success in utilizing circularly polarized phosphorescence energy transfer (CPP-ET) combined with chirality-selective absorption (CSA) to construct full-color and white CPLA materials. Blue CPLA with luminescence dissymmetry factor (glum) of 3×10-2 is firstly obtained via the CSA effect of chiral helical polyacetylene and blue ultralong afterglow of inorganic phosphor BP. Significantly, full-color and white CPLA films are prepared by simply blending different fluorophores into the blue-CPLA films via CPP-ET. Benefited from the persistent luminescence of BP, the lifetimes of the fluorophores increase from nanoseconds to minutes, and ultralong full-color CPLA emissions lasting for more than 20 min are realized with glum of 10-3. Also noticeably, chiral optoelectronic devices, multi-dimension information encryption and chiral logic gate are developed based on the full-color tunable CPLA-active materials. The established strategy provides a universal platform for future development of CPLA-active materials with great applications.

A phytomedicine extract exerts an anti-inflammatory response in the lungs by reducing STING-mediated type I interferon release.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is an acute respiratory disease characterized by bilateral chest radiolucency and severe hypoxemia. Quzhou Fructus Aurantii ethyl acetate extract (QFAEE), which is prepared from the traditional Chinese respiratory anti-inflammatory natural herb Quzhou Fructus Arantii, has the potential to alleviate ARDS. In this work, we aimed to investigate the potential and mechanism underlying the action of QFAEE on ARDS and how QFAEE modulates the STING pathway to reduce type I interferon release to alleviate the inflammatory response. METHODS: Lipopolysaccharide (LPS), a potential proinflammatory stimulant capable of causing pulmonary inflammation with edema after nasal drops, was employed to model ARDS in vitro and in vivo. Under QFAEE intervention, the mechanism of action of QFAEE to alleviate ARDS was explored in this study. TREX1-/- mice were sued as a research model for the activation of the congenital STING signaling pathway. The effect of QFAEE on TREX1-/- mice could explain the STING-targeted effect of QFAEE on alleviating the inflammatory response. Our explorations covered several techniques, Western blot, histological assays, immunofluorescence staining, transcriptomic assays and qRT-PCR to determine the potential mechanism of action of QFAEE in antagonizing the inflammatory response in the lungs, as well as the mechanism of action of QFAEE in targeting the STING signaling pathway to regulate the release of type I interferon. RESULTS: QFAEE effectively alleviates ARDS symptoms in LPS-induced ARDS. We revealed that the mechanism underlying LPS-induced ARDS is the STING-TBK1 signaling pathway and further elucidated the molecular mechanism of QFAEE in the prevention and treatment of ARDS. QFAEE reduced the release of type I interferons by inhibiting the STING-TBK1-IRF3 axis, thus alleviating LPS-induced pneumonia and lung cell death in mice. Another key finding is that activation of the STING pathway by activators or targeted knockdown of the TREX1 gene can also induce ARDS. As expected, QFAEE was found to be an effective protective agent in alleviating ARDS and the antagonistic effect of QFAEE on ARDS was achieved by inhibiting the STING signaling pathway. CONCLUSIONS: The main anti-inflammatory effect of QFAEE was achieved by inhibiting the STING signaling pathway and reducing the release of type I interferons. According to this mechanism of effect, QFAEE can effectively alleviate ARDS and can be considered a potential therapeutic agent. In addition, the STING pathway plays an essential role in the development and progression of ARDS, and it is a potential target for ARDS therapy.

Clinical effects and safety of semi-solid feeds in tube-fed patients: a meta-analysis and systematic review.

Background: Enteral nutrition is a very important form of treatment for critically ill patients. This meta-analysis aimed to evaluate the clinical effects and safety of semi-solid feeds in tube-fed patients. Methods: Two researchers searched PubMed, clinical trials, Embase, Cochrane Central Register of Controlled Trials, Web of Science, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang Data, and Weipu databases for randomized controlled trials (RCTs) on the clinical effects and safety of semi-solid feeds in tube-fed patients until 10 October 2023. The quality evaluation tool recommended by the Cochrane Library was used to evaluate the quality of included RCTs. RevMan 5.4 software was used for data analysis. Results: A total of eight RCTs involving 823 tube-fed patients were included in this meta-analysis. A synthesized outcome indicated that semi-solid feeds reduced the incidence of diarrhea (RR = 0.32, 95%CI:0.20-0.50, P < 0.001), vomiting (RR = 0.31, 95%CI:0.15-0.64, P = 0.002), abdominal distension (RR = 0.41, 95%CI:0.22-0.76, P = 0.005), length of intensive care unit (ICU) stay (MD = -3.61, 95%CI: -6.74 to -0.48, P = 0.02), and length of hospital stay (MD = -7.14, 95%CI: -10.31 to -3.97, P < 0.01) in tube-fed patients. Enteric feeding had no effect on the 30-day mortality (RR = 0.55, 95%CI: 0.19-1.56, P = 0.26). No publication bias was detected by the Egger's test results (all P > 0.05). Conclusion: Semi-solid feeds are beneficial in reducing the incidence of diarrhea, abdominal distension, vomiting, and hospital stay. More high-quality studies are needed in the future to verify the effects of semi-solid feeds on mortality.

Cognitive behavioural therapy for depression, quality of life, and cognitive function in the post-stroke period: systematic review and meta-analysis.

The post-stroke period is associated with a lot of sequelae, including depression, decreased quality of life, and decline of cognitive function. Apart from the pharmacotherapy, it is also important to find a non-pharmacological treatment to relieve the sequelae. Cognitive behavioural therapy (CBT) might be a potential candidate, which can be clarified by a systematic review and meta-analysis. The eligible criteria of enrolled studies in the systematic review and meta-analysis were the randomised clinical trials (RCTs) using CBT to treat post-stroke depression, or with the focus on quality of life or cognitive function in the post-stroke period. The endpoint scores of depression, quality of life, and cognitive function scales were the targeted outcome for the final meta-analysis in the random effects model. Ten RCTs with 432 post-stroke patients receiving CBT and 385 controls were included. The meta-analysis results showed significant improvements in depression severity and quality of life. However, no significant difference between CBT and control groups was found in cognitive function. In addition, significant heterogeneity was derived from the meta-analysis. According to the meta-analysis results, CBT might be beneficial for relieving depression severity and improving quality of life. However, cognitive function might not be influenced by CBT. Further studies with a more consistent CBT design with greater sample sizes should be warranted to clarify and confirm the treatment effects of CBT for post-stroke depression and quality of life.

Preparation and Applications of Polydimethylsiloxane-Based Fluorescent Materials.

In the past few years, fluorescent materials have received significant attention due to their fascinating luminescent properties and wide-ranging applications. Polydimethylsiloxane (PDMS) has also attracted the interest of many researchers due to its remarkable performances. The combination of fluorescence and PDMS will undoubtedly produce abundant advanced multifunctional materials. Although numerous achievements have been made in this field, there is still no review to summarize the relevant research. This review summarizes the state-of-the-art achievements made in PDMS-based fluorescent materials (PFMs). First, the preparation of PFM is overviewed following a classification according to the fluorescent sources, including organic fluorescent molecules, perovskite, photoluminescent nanomaterials, and metal complexes. Their applications in sensors, fluorescent probes, multifunctional coatings, and anticounterfeiting are then introduced. Finally, the challenges and development trends in the field of PFMs are presented.

Doxorubicin downregulates autophagy to promote apoptosis-induced dilated cardiomyopathy via regulating the AMPK/mTOR pathway.

The broad-spectrum antineoplastic drug doxorubicin (DOX) has one of the most serious chronic side effects on the heart, dilated cardiomyopathy, but the precise molecular mechanisms underlying disease progression subsequent to long latency periods remain puzzling. Here, we established a model of DOX-induced dilated cardiomyopathy. In a cardiac cytology exploration, we found that differentially expressed genes in the KEGG signaling pathway enrichment provided a novel complex network of mTOR bridging autophagy and oxidative stress. Validation results showed that DOX caused intracellular reactive oxygen species accumulation in cardiomyocytes, disrupted mitochondria, led to imbalanced intracellular energy metabolism, and triggered cardiomyocyte apoptosis. Apoptosis showed a negative correlation with DOX-regulated cardiomyocyte autophagy. To evaluate whether the inhibition of mTOR could upregulate autophagy to protect cardiomyocytes, we used rapamycin to restore autophagy depressed by DOX. Rapamycin increased cardiomyocyte survival by easing the autophagic flux blocked by DOX. In addition, rapamycin reduced oxidative stress, prevented mitochondrial damage, and restored energy metabolic homeostasis in DOX-treated cardiomyocytes. In vivo, we used metformin (Met) which is an AMPK activator to protect cardiac tissue to alleviate DOX-induced dilated cardiomyopathy. In this study, Met significantly attenuated the oxidative stress response of myocardial tissue caused by DOX and activated cardiomyocyte autophagy to maintain cardiomyocyte energy metabolism and reduce cardiomyocyte apoptosis by downregulating mTOR activity. Overall, our study revealed the role of autophagy and apoptosis in DOX-induced dilated cardiomyopathy and demonstrated the potential role of regulation of the AMPK/mTOR axis in the treatment of DOX-induced dilated cardiomyopathy.

Effects of bilateral erector spinae plane block for posterior lumbar spine surgery in elderly patients. / åŒä¾§ç«–è„Šè‚Œå¹³é¢é˜»æ»žåœ¨è€å¹´æ‚£è€ è °æ¤ŽåŽè·¯æ‰‹æœ¯ä¸­çš„åº”ç”¨æ•ˆæžœ.

OBJECTIVES: With the rapid development of aging population, the number of elderly patients undergoing posterior lumbar spine surgery continues to increase. Lumbar spine surgery could cause moderate to severe postoperative pain, and the conventional opioid-based analgesia techniques have many side effects, which are barriers to the recovery after surgery of the elderly. Previous studies have demonstrated that erector spinae plane block (ESPB) could bring about favorable analgesia in spinal surgery. As far as the elderly are concerned, the analgesic and recovery effects of ESPB on posterior lumbar spine surgery are not completely clear. This study aims to observe the effects of bilateral ESPB on elderly patients undergoing posterior lumbar spine surgery, and to improve the anesthesia techniques. METHODS: A total of 70 elderly patients of both sex, who were selected from May 2020 to November 2021, scheduled for elective posterior lumbar spine surgery, and in the age of 60-79 years, with American Society of Anesthesiologists class Ⅱ-Ⅲ, were divided into a ESPB group and a control (C) group using a random number table method, with 35 patients each. Before general anesthesia induction, 20 mL 0.4% ropivacaine was injected to the transverse process of L3 or L4 bilaterally in the ESPB group and only saline in the C group. The score of Numerical Rating Scale (NRS) indicating pain at rest and on movement within 48 h after operation, time of first patient control analgesia (PCA), cumulative consumptions of sufentanil within 48 hours, Leeds Sleep Evaluation Questionnaire (LSEQ) scores on the morning of day 1 and day 2 after operation, Quality of Recovery-15 (QoR-15) scores at 24 and 48 h after operation, full diet intake times, perioperative adverse reactions such as intraoperative hypotension, postoperative dizziness, nausea, vomiting, and constipation were compared between the 2 groups. RESULTS: A total of 70 patients were enrolled and 62 subjects completed the study, including 32 in the ESPB group and 30 in the C group. Compared with the C group, the postoperative NRS scores at rest at 2, 4, 6, and 12 h and on movementat at 2, 4, and 6 h were lower, time of first PCA was later, sufentanil consumptions were significantly decreased during 0-12 h and 12-24 h after operation, LSEQ scores on the morning of day 1 and QoR-15 scores at 24 and 48 h after operation were higher, full diet intakes achieved earlier in the ESPB group (all P<0.05). There were no significant differences in the incidences of intraoperative hypotension, postoperative dizziness, nausea, vomiting, and constipation between the 2 groups (all P>0.05). CONCLUSIONS: Providing favorable analgesic effects with reduced opioids consumption, bilateral ESPB for posterior lumbar spine surgery in the elderly patients could also improve postoperative sleep quality, promote gastrointestinal functional restoration, and enhance recovery with few adverse reactions.

Chiroptical Elastomer Film Constructed by Chiral Helical Substituted Polyacetylene and Polydimethylsiloxane: Multiple Stimuli Responsivity and Chiral Amplification.

Chiral and circularly polarized luminescence (CPL) materials with multiple stimuli responses have become a focus of attention. Meanwhile, elastomers have found substantial applications in a wide variety of fields. However, how to design and construct chiral elastomers, in particular CPL-active elastomers, still remains an academic challenge. In the present study, chiral helical substituted polyacetylene is chemically bonded with polydimethylsiloxane (PDMS) by hydrosilylation to form a chiroptically active elastomer. A CPL-active film was further fabricated by adding achiral fluorophores. Compared with the corresponding chiral helical polymer, the chiral films show much enhanced thermal stability in terms of chiroptical properties. The films also demonstrate reversible tunability in optical activity and CPL property when being subjected to a stretching-restoring process and exposed to a solvent like toluene. Further, noticeable chiral amplification is observed when the chiral PDMS film is superimposed with a pure PDMS film. This interesting finding is proposed to be due to the photoreflectivity of PDMS. This study provides an alternative strategy to exploit novel CPL-active elastomer materials with multiple stimuli responsivity and tunability, which may open up new opportunities for developing novel chiroptical devices.

Metformin enhances neural precursor cells migration and functional recovery after ischemic stroke in mice.

Resident neural precursor cells (NPCs) activation is a promising therapeutic strategy for brain repair. This strategy involves stimulating multiple stages of NPCs development, including proliferation, self-renewal, migration, and differentiation. Metformin, an FDA-approved diabetes drug, has been shown to promote the proliferation and differentiation of NPCs. However, it is still unclear whether metformin promotes the migration of NPCs. EVOS living cell imaging system was used for observing the migration for primary NPCs dynamically in vitro after metformin treatment. For in vivo study, a mouse model of ischemic stroke was established through middle cerebral artery occlusion (MCAO). To label the proliferating cell in subventricular zone, BrdU was injected intraperitoneally into the mice. After co-staining with BrdU and doublecortin (DCX), a marker for NPCs, the migration of Brdu and DCX double positive NPCs was detected along the rostral migratory stream (RMS) and around the infarct area using frozen brain sections. Finally, the rotarod test, corner test and beam walking were performed to evaluate the motor functions of the mice after stroke in different groups. The results showed that metformin enhanced NPCs migration in vivo and in vitro by promoting F-actin assembly and lamellipodia formation. What's more, metformin treatment also significantly reduced the infarct volume and alleviated functional dysfunction after stroke. Mechanistically, metformin promoted NPCs migration via up-regulating the CDC42 expression. Taken together, metformin represents an optimal candidate agent for neural repair that is capable of not only expanding the adult NPC population but also subsequently driving them toward the destination for neuronal differentiation.

Context consistency improves ensemble perception of facial expressions.

Humans have developed the capacity to rapidly extract summary statistics from the facial expressions of a crowd, such as computing the average facial expression. Although dual-task paradigms involving memory and ensemble tasks have recently found that this ensemble coding ability is biased by visual working memory, few studies have examined whether the context-dependent nature of memory itself can influence the perceptual averaging process. In two experiments, participants made forced-choice judgments about mean facial expressions that were paired with task-irrelevant background images, and the background images either matched or mismatched across encoding and response phases. When the backgrounds matched, it was at either the perceptual level (uniformly oriented lines with the same orientation in encoding and response phases, in Experiment 1), or at the summary statistics level (uniformly oriented lines in the response phase that had the same orientation as the mean of randomly oriented lines that were seen in the encoding phase, in Experiment 2). Participants in Experiment 1 showed a higher ensemble precision and better discrimination sensitivity when the backgrounds matched than when they mismatched, which is consistent with the kind of robust contextual memory effect that has been seen in prior research. We further demonstrated that the context-matching facilitation effect occurred at both the perceptual level (Experiment 1) and at the summary statistics level (Experiment 2). These results demonstrate that the effects of visual working memory on perceptual averaging are obligatory, and they highlight the importance of memory-related context dependency in perceptual averaging.

CHMP1A suppresses the growth of renal cell carcinoma cells via regulation of the PI3K/mTOR/p53 signaling pathway.

BACKGROUND: CHMP1A, a member of the ESCRT-III complex family, has been indicated as a brand-new inhibitor gene of tumors. Our previous research has revealed that CHMP1A plays a vital role in the development and progression of renal cell carcinoma (RCC). OBJECTIVE: To investigate the potential target pathway of the regulation of the tumor cell growth by CHMP1A. METHODS: The effect of CHMP1A on mTOR pathway was elucidated by western blotting. The effect of CHMP1A on the expression of p53 was evaluated, and A498 cell growth was assessed by colony formation and MTT assays. The expression of p53 was knocked down by shRNA-p53, and the effect of CHMP1A on mTOR after knockdown of p53 was evaluated. The effect of CHMP1A on apoptosis and its relationship with MDM2 pathway were detected by western blotting and FCM. Finally, the relationship between the regulation of p53 by CHMP1A and the PI3K/mTOR pathway was detected. RESULTS: This study showed that the mTOR pathway was suppressed significantly in CHMP1A-overexpressing A498 and 786-0 cells; moreover, the enhanced expression of p53 and the reduced proliferation were shown in CHMP1A-overexpressing A498 cells. Furthermore, CHMP1A was able to regulate the PI3K/PTEN/mTOR and MDM2/p53 pathways in order to suppress RCC. In addition, CHMP1A regulated Bax and Bcl-2 via MDM2/p53 to induce the apoptosis of tumor cells and upregulated the expression of p53 via the PI3K/mTOR pathway. CONCLUSIONS: The results convey that CHMP1A-related suppression of RCC is closely related to the PI3K/mTOR/p53 pathway.

Traceability of VOCs in tire inner liner by chromatography-mass spectrometry.

Many parts of the vehicle cabin generate volatile organic compounds (VOCs), and some are hazardous and/or odorous to humans. In this study, VOCs in the inner liner of automobile spare tire, including raw rubbers and resins, were detected by gas chromatography-mass spectrometry (GC-MS) coupled with an extracting method of static headspace sampling (SHS). The results demonstrated that the sources of VOCs can be traced back to raw rubbers and resins: alkylphenol resins can release a large amount of 2,4,4-trimethyl-1-pentene and 2,2,4,6,6-pentamethyl-3-heptene; chlorobutyl rubber (CIIR) contained 3-methyl-pentane, and methyl-cyclopentane, and these VOCs are odorous. When alkylphenol resin and natural rubber (NR) with low VOCs were used to replace the corresponding resin and NR in the initial formulation, the total volatile organic compounds (TVOCs) in the inner liner could be reduced. We expected that the information gained from this work could provide a basic reference for the manufacture of environmental-friendly tire products.

The neuroprotection of cerebrolysin after spontaneous intracerebral hemorrhage through regulates necroptosis via Akt/ GSK3ß signaling pathway.

PURPOSE: Spontaneous intracerebral hemorrhage (ICH) is a major cause of death and disability with a huge economic burden worldwide. Cerebrolysin (CBL) has been previously used as a nootropic drug. Necroptosis is a programmed cell death mechanism that plays a vital role in neuronal cell death after ICH. However, the precise role of necroptosis in CBL neuroprotection following ICH has not been confirmed. METHODS: In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model. Mortality, neurological score, brain water content, and neuronal death were evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, Evans blue extravasation, Western blotting, and quantitative real-time polymerase chain reaction (PCR). RESULTS: The results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH. The neuroprotective capacity of CBL is partly dependent on the Akt/GSK3ß signaling pathway. CONCLUSIONS: CBL improves neurological outcomes in mice and reduces neuronal death by protecting against neural necroptosis.

Evidences for the mechanism of Shenmai injection antagonizing doxorubicin-induced cardiotoxicity.

BACKGROUND: Doxorubicin (DOX) is a widely used antitumor drug. However, its clinical application is limited for its serious cardiotoxicity. The mechanism of DOX-induced cardiotoxicity is attributed to the increasing of cell stress in cardiomyocytes, then following autophagic and apoptotic responses. Our previous studies have demonstrated the protective effect of Shenmai injection (SMI) on DOX-induced cardiotoxicity via regulation of inflammatory mediators for releasing cell stress. PURPOSE: To further investigate whether SMI attenuates the DOX-induced cell stress in cardiomyocytes, we explored the mechanism underlying cell stress as related to Jun N-terminal kinase (JNK) activity and the regulation of autophagic flux to determine the mechanism by which SMI antagonizes DOX-induced cardiotoxicity. STUDY DESIGN: The DOX-induced cardiotoxicity model of autophagic cell death was established in vitro to disclose the protected effects of SMI on oxidative stress, autophagic flux and JNK signaling pathway. Then the autophagic mechanism of SMI antagonizing DOX cardiotoxicity was validated in vivo. RESULTS: SMI was able to reduce the DOX-induced cardiomyocyte apoptosis associated with inhibition of activation of the JNK pathway and the accumulation of reactive oxygen species (ROS). Besides, SMI antagonized DOX cardiotoxicity, regulated cardiomyocytes homeostasis by restoring DOX-induced cardiomyocytes autophagy. Under specific circumstances, SMI depressed autophagic process by reducing the Beclin 1-Bcl-2 complex dissociation which was activated by DOX via stimulating the JNK signaling pathway. At the same time, SMI regulated lysosomal pH to restore the autophagic flux which was blocked by DOX in cardiomyocytes. CONCLUSION: SMI regulates cardiomyocytes apoptosis and autophagy by controlling JNK signaling pathway, blocking DOX-induced apoptotic pathway and autophagy formation. SMI was also found to play a key role in restoring autophagic flux for counteracting DOX-damaged cardiomyocyte homeostasis.

The Varying Coherences of Implied Motion Modulates the Subjective Time Perception.

Previous research has demonstrated that duration of implied motion (IM) was dilated, whereas hMT+ activity related to perceptual processes on IM stimuli could be modulated by their motion coherence. Based on these findings, the present study aimed to examine whether subjective time perception of IM stimuli would be influenced by varying coherence levels. A temporal bisection task was used to measure the subjective experience of time, in which photographic stimuli showing a human moving in four directions (left, right, toward, or away from the viewer) were presented as probe stimuli. The varying coherence of these IM stimuli was manipulated by changing the percentage of pictures implying movement in one direction. Participants were required to judge whether the duration of probe stimulus was more similar to the long or short pre-presented standard duration. As predicted, the point of subjective equality was significantly modulated by the varying coherence of the IM stimuli, but not for no-IM stimuli. This finding suggests that coherence level might be a key mediating factor for perceived duration of IM images, and top-down perceptual stream from inferred motion could influence subjective experience of time perception.

Sleep deprivation aggravates brain injury after experimental subarachnoid hemorrhage via TLR4-MyD88 pathway.

Subarachnoid hemorrhage (SAH) is a life-threatening cerebrovascular disease, and most of the SAH patients experience sleep deprivation during their hospital stay. It is well-known that sleep deprivation is one of the key components of developing several neurological disorders, but its effect on brain damage after SAH has not been determined. Therefore, this study was designed to evaluate the effect of sleep deprivation using an experimental SAH model in rats. Induction of sleep deprivation for 24 h aggravated the SAH-induced brain damage, as evidenced by brain edema, neuronal apoptosis and activation of caspase-3. Sleep deprivation also worsened the neurological impairment and cognitive deficits after SAH. The results of immunostaining and western blot showed that sleep deprivation increased the activation of microglial cells. In addition, sleep deprivation differently regulated the expression of anti-inflammatory and pro-inflammatory cytokines. The results of immunofluorescence staining and western blot showed that sleep deprivation markedly increased the activation of Toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein 88 (MyD88). Mechanically, treatment with the TLR4 inhibitor TAK-242 or the MyD88 inhibitor ST2825 significantly attenuated the brain damage and neuroinflammation induced by sleep deprivation after SAH. In conclusion, our results indicate that sleep deprivation aggravates brain damage and neurological dysfunction following experimental SAH in rats. These effects were mediated by the activation of the TLR4-MyD88 cascades and regulation of neuroinflammation.

Dexmedetomidine Resists Intestinal Ischemia-Reperfusion Injury by Inhibiting TLR4/MyD88/NF-κB Signaling.

BACKGROUND: Intestinal ischemia/reperfusion (I/R) is a common clinical problem that occurs during various clinical pathological processes. Dexmedetomidine (DEX), a widely used anesthetic adjuvant agent, can induce protection against intestinal I/R in vivo; however, the underlying mechanism is not fully understood. In the present study, we aimed to investigate the protective effects of DEX and examine whether its mechanism was associated with the TLR4/MyD88/NF-κB signaling pathway. METHODS: Sprague-Dawley rats were pretreated with DEX and then subjected to I/R-induced intestinal injury. In vivo, intestinal histopathological examination and scoring were performed, the levels of serum intestinal fatty acid-binding protein (I-FABP), intestinal tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and expression levels of TLR4, MyD88, and NF-κB in the intestine were determined. In in vitro experiments, the human colon carcinoma cell line (Caco-2) was incubated with DEX before deprivation/reoxygenation (OGD/R) treatment. The cell viability of Caco-2 cells, the levels of lactate dehydrogenase (LDH), TNF-α, and IL-1ß in the supernatant, as well as protein expression of TLR4, MyD88, and NF-κB in Caco-2 cells, were measured. Statistical analysis was performed using SPSS version 21.0. RESULTS: DEX preconditioning significantly reduced the intestinal pathological Chiu's score, serum I-FABP, intestinal TNF-α, IL-1ß levels, and the protein expression of TLR4, MyD88, and NF-κB in the rats with intestinal I/R injury. Similarly, in vitro, DEX pretreatment protected against OGD/R-induced Caco-2 cell damage and inhibited TLR4/MyD88/NF-κB signaling, as evidenced by increased cell viability, decreased LDH activity, reduced TNF-α and IL-1ß levels, as well as downregulated TLR4, MyD88, and NF-κB protein levels. CONCLUSIONS: Our findings suggested that DEX could reduce intestinal I/R injury in rats and OGD/R damage in Caco-2 cells, and this protection might be attributed to antiinflammatory effects and inhibition of the TLR4/MyD88/NF-κB signaling pathway.

The neuroprotection of cerebrolysin after spontaneous intracerebral hemorrhage through regulates necroptosis via Akt/ GSK3B signaling pathway

ABSTRACT Purpose: Spontaneous intracerebral hemorrhage (ICH) is a major cause of death and disability with a huge economic burden worldwide. Cerebrolysin (CBL) has been previously used as a nootropic drug. Necroptosis is a programmed cell death mechanism that plays a vital role in neuronal cell death after ICH. However, the precise role of necroptosis in CBL neuroprotection following ICH has not been confirmed. Methods: In the present study, we aimed to investigate the neuroprotective effects and potential molecular mechanisms of CBL in ICH-induced early brain injury (EBI) by regulating neural necroptosis in the C57BL/6 mice model. Mortality, neurological score, brain water content, and neuronal death were evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, Evans blue extravasation, Western blotting, and quantitative real-time polymerase chain reaction (PCR). Results: The results show that CBL treatment markedly increased the survival rate, neurological score, and neuron survival, and downregulated the protein expression of RIP1 and RIP3, which indicated that CBL-mediated inhibition of necroptosis, and ameliorated neuronal death after ICH. The neuroprotective capacity of CBL is partly dependent on the Akt/GSK3β signaling pathway. Conclusions: CBL improves neurological outcomes in mice and reduces neuronal death by protecting against neural necroptosis.

Nursing care for a patient with right frontoparietal inflammatory granuloma complicated with acute pulmonary embolism: a case report.

Intracranial inflammatory granuloma is a common intracranial occupying lesion. Common postoperative complications include intracranial edema, intracranial infection, hydrocephalus, epilepsy, and cerebrospinal fluid leakage. This report aims to summarize the nursing care of a patient with right frontoparietal inflammatory granuloma complicated with acute pulmonary embolism (APE). Acute pulmonary embolism is a clinical syndrome in which endogenous or exogenous emboli block the main trunk or branches of the pulmonary artery, resulting in disorders of pulmonary and respiratory circulation that seriously threatening the lives of patients. The occurrence and report of pulmonary embolism caused by intracranial inflammatory granuloma are rare. The patient had rapid onset, atypical clinical manifestations, and was in critical condition. Pulmonary embolism can easily lead to death. Nursing care after rapid thrombolysis included observation of coagulation function, prevention of complication, control of infection, improvement of intestinal dysfunction, maintenance and monitoring of sedation, prevention and observation of epilepsy, and prevention of the recurrence of embolism. After early intervention, active treatment and meticulous care, the patient's condition improved, mechanical ventilation was successfully withdrawn, and the patient was ultimately discharged and walked out on his own.

Recent advances, challenges and perspectives in enantioselective release.

Development of chiral drugs has become one of the most important subjects for academic research and pharmaceutical industry. Even though it has been well known that a pair of enantiomers of a chiral drug frequently have different biological and physiological effects, a certain number of chiral drugs are currently still commercialized and used in the form of racemate. In the above context, investigation of enantio-differentiating release and enantioselective effects may lead to alternative use approaches for chiral drugs. In spite of the noticeable advancements, there has been no review paper yet focused on enantioselective release, except the earlier one published by us (Ind. Eng. Chem. Res. 2016, 55, 6037). The present paper reviews the latest advancements made in enantioselective release, with emphasis on the construction of chiral releasing materials. The currently existing difficulty in performing enantioselective release and the emerging issues associated with chiral drugs (and chiral agrochemicals, etc.) are summarized. The issues include: enantioselective effects in chiral carrier-chiral guest compound and chiral carrier-achiral guest compound releasing systems; chiral inversion in release process; chiral pollutants in environment, etc. The review paper might provide new insights into the development and use of chiral drugs.