The Effect of Web-Based Telerehabilitation Programs on Children and Adolescents With Brain Injury: Systematic Review and Meta-Analysis.

BACKGROUND: Acquired brain injury (ABI) in children and adolescents can lead to motor and executive impairments that often require long-term treatment. The implementation of web-based telerehabilitation therapy at home is a method to improve the functional status of patients. Therefore, we performed a systematic review of the effects of web-based telerehabilitation programs on functional outcomes in children and adolescents with brain injury and supplemented the findings with a meta-analysis. OBJECTIVE: This study evaluated the therapeutic effect of web-based telerehabilitation training on children and adolescents with brain injury to determine whether web-based telerehabilitation therapy improved motor function, executive function, physical activity level, lower limb strength, hand and upper limb function, visual processing skills, and occupational functional performance in children and adolescents with brain injury. METHODS: PubMed, Embase, Scopus, Web of Science, and the Cochrane Library were searched for randomized controlled trials on web-based telerehabilitation programs in children and adolescents with brain injury until December 2022, and the risk of bias was evaluated using the Cochrane Collaboration Tool. Relevant data were extracted, and a meta-analysis was performed using RevMan5.3 software. RESULTS: Overall, 17 studies involving 848 patients were included. Web-based telerehabilitation therapy improved the motor function (standardized mean difference [SMD] 0.29, 95% CI 0.01-0.57; P=.04), physical activity level (SMD 0.42, 95% CI 0.11-0.73; P=.007), lower limb strength (SMD 0.52, 95% CI 0.13-0.90; P=.009), and visual processing skills (SMD 0.26, 95% CI 0.02-0.50; P=.04) of children and adolescents with brain injury. It also improved executive function in letter-number sequencing (SMD 1.26, 95% CI 0.26-2.26; P=.01), attention (SMD 0.38, 95% CI 0.09-0.66; P=.009), and symbol search (SMD 1.18, 95% CI 0.43-1.93, P=.002). CONCLUSIONS: Web-based telerehabilitation therapy improved motor function, physical activity level, lower limb strength, letter-number sequencing, attention, and symbol search, which improved the quality of life in children and adolescents with brain injury. Web-based telerehabilitation programs provide great convenience for children and adolescents with ABI who need long-term treatment and allow them to exercise at home for rehabilitation training. The widespread implementation of remote interventions also provides children and adolescents in remote areas with better access to rehabilitation services. This review provides evidence for the effectiveness of web-based telerehabilitation therapy, but there was heterogeneity in some of the results because of different disease types and intervention programs. Future studies can expand the sample size according to disease type and increase follow-up time according to different exercise prescriptions to further refine the long-term effects of this intervention on various functions of children and adolescents with ABI. TRIAL REGISTRATION: PROSPERO CRD42023421917; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=421917.

Voluntary wheel-running improved pulmonary fibrosis by reducing epithelial mesenchymal transformation.

AIMS: Pulmonary fibrosis seriously affects the health and life quality of patients. Exercise has been shown to have anti-inflammatory and antioxidant effects, but its effect on pulmonary fibrosis is unclear. In this study, the effect and mechanism of exercise on pulmonary fibrosis induced by paraquat were detected. MAIN METHODS: Three data sets were retrieved from GEO data. The biological significance of DEGs generation was determined by GO, KEGG, GSEA, and PPI. Thirty male BALB/C mice were randomly divided into control group, model group and exercise group. H&E staining, Masson staining, Immunohistochemistry and Western blot were used to explore the results. The levels of SOD, CAT, MDA, and GSH in lung tissue were analyzed with detection kits. The levels of inflammatory factors in serum and BALF were measured by ELISA. KEY FINDINGS: Compared with the control group, the infiltration of inflammatory cells and fibrotic lesions were increased in the model group. Compared with the model group, voluntary wheel-running reducing the EMT of alveolar epithelial cells, the activation of the Wnt/ß-catenin signaling pathway and the level of oxidative distress. Moreover, compared to model group, the serum IL-4, IL-10 and IFN-γ were increased, while the serum CXCL1 were decreased, while the levels of CXCL1, IL-6, IL-10, TNF-α and IFN-γ in the bronchoalveolar lavage fluid were decreased in exercise group. SIGNIFICANCE: Voluntary wheel-running reduced inflammatory infiltration and upregulated the expression of antioxidative distress proteins, further to improve the degree of EMT, and ultimately alleviated paraquat induced pulmonary fibrosis.

A Pegylated Liposome Loaded with Raddeanin A for Prostate Cancer Therapy.

Introduction: Raddeanin A (RA), a potent triterpenoid extracted from Anemone raddeana Regel, has a moderate therapeutic effect on prostate cancer (PCa), correlating with serious biological toxicity. Therefore, a RA-loaded PEGylated liposome drug delivery system was devised in this study. Methods: Hydrogenated soybean phospholipids (HSPC), 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-Polyethyleneglycol-2000 (sodium salt) (DSPE-PEG2k), cholesterol (CHO), and RA were utilised to prepare a RA-loaded liposome (LRA) drug delivery system via the thin film hydration technique., The drug loading content was confirmed by high performance liquid chromatography. Dynamic light scattering was employed to evaluate the drug's particle size and stability. Methyl tetrazolium, colony formation, and Western blot (WB) were used in vitro to elucidate the inhibitory effect and mechanism of LRA on prostate cancer cells. Finally, xenograft model was used to confirm the tumor-inhibiting efficacy, clarify the mechanism, and determine the biosafety in mice. Results: LRA has stable physicochemical properties and a diameter of 173.5 15.3 nm. LRA inhibited the growth of prostate cancer cells in a dose- and time-dependent manner. LRA can substantially reduce the expression of AR and HMGB1, induce apoptosis, regulate the expression of cell cycle-related proteins in vitro and in vivo. The results of the biosafety tests demonstrated that LRA effectively reduced the adverse effects of RA. Conclusion: As a drug delivery system, LRA could effectively and safely inhibit the progression of prostate cancer.

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.

Prolonged exposure to the herbicide atrazine promotes kidney fibrosis by activating Wnt/ß-catenin signaling in rats.

Exposure to atrazine (ATR), a widely-used herbicide, is a potential harmful to human health due to its long-term environmental persistence and bioaccumulation. The effects of chronic exposure to ATR on renal function in rats were evaluated in this research. Female Sprague-Dawley rats at 4 weeks of age were treated with different concentrations of ATR for 6 months. No significant differences  in terms of renal functions were observed after ATR treatment. In histopathological examination of the kidney, Hematoxylin-Eosin staining indicated the development of degenerative changes in a dose-dependent manner. The results revealed that ATR exposure leads to renal fibrosis and that activation of the Wnt/ß-catenin pathway plays a potential role in ATR-related renal fibrosis. Levels of transforming growth factor (TGF)-ß and TGF-ß1 levels and the reactive oxygen species were significantly upregulated after ATR treatment. In conclusion, long-term exposure to ATR could cause kidney fibrosis, which is the result of epithelial-mesenchymal transition caused by inflammation and oxidative stress.

PPP1R14B is a diagnostic prognostic marker in patients with uterine corpus endometrial carcinoma.

Uterine corpus endometrial carcinoma (UCEC) is one of the most common malignancies of the female genital tract. A recently discovered protein-coding gene, PPP1R14B, can inhibit protein phosphatase 1 (PP1) as well as different PP1 holoenzymes, which are important proteins regulating cell growth, the cell cycle, and apoptosis. However, the association between PPP1R14B expression and UCEC remains undefined. The expression profiles of PPP1R14B in multiple cancers were analysed based on TCGA and GTE databases. Then, PPP1R14B expression in UCEC was investigated by gene differential analysis and single gene correlation analysis. In addition, we performed gene ontology term analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, gene set enrichment analysis, and Kaplan-Meier survival analysis to predict the potential function of PPP1R14B and its role in the prognosis of UCEC patients. Then, a tool for predicting the prognosis of UCEC, namely, a nomogram model, was constructed. PPP1R14B expression was higher in UCEC tumour tissues than in normal tissues. The results revealed that PPP1R14B expression was indeed closely associated with tumour development. The results of Kaplan-Meier plotter data indicated that patients with high PPP1R14b expression had poorer overall survival, disease-specific survival, and progression-free interval than those with low expression. A nomogram based on the results of multifactor Cox regression was generated. PPP1R14B is a key player in UCEC progression, is associated with a range of adverse outcomes, and can serve as a prognostic marker in the clinic.

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.

Efficacy of exercise in patients with pulmonary fibrosis: A systematic review and meta-analysis.

BACKGROUND: Pulmonary fibrosis (PF) is easily caused by a variety of factors, resulting in dyspnea, exertion and movement intolerance. This systematic review aims to synthesize evidence on exercise training during rehabilitation for PF in order to improve patients' exercise capacity, quality of life, and lung function. METHODS: Retrieved from the Cochrane Library, Web of Science, PubMed, Scopus and Embase from inception until April 2022. Participants: patients with PF; Intervention measures: exercise training; Results: exercise ability, quality of life, lung function and cardiopulmonary endurance. Two reviewers independently screen the title, abstract and full text. Finally, quality evaluation and meta-analysis were conducted. RESULTS: In this study, 13 randomized controlled studies from 1468 articles were selected. A total of 456 patients with PF were enrolled. Compared with usual care in the control group, the 6-minute walking distance, predicted forced vital capacity, predicted forced expiratory volume at 1 second and maximal rate of oxygen consumption were increased significantly after exercise training, while there was no significant change in quality of life and predicted diffusing capacity of the lung for carbon monoxide. CONCLUSION: Exercise training can significantly improve the exercise capacity, lung function and cardiopulmonary endurance of patients with PF, but has no effect on the quality of life. Exercise training is an effective rehabilitation strategy for PF.

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.

HMGB1 promotes the development of castration­resistant prostate cancer by regulating androgen receptor activation.

AR signalling pathway reactivation plays a key role in the development of castration­resistant prostate cancer (CRPC). High­mobility group protein B1 (HMGB1) is an important factor involved in the occurrence and development of a variety of tumours by regulating gene transcription. In the present study, the association between HMGB1 and prostate cancer (PCa) and the effects of HMGB1 on androgen receptor (AR) transcription and signalling pathway reactivation in PCa cells in vitro and in vivo were evaluated. A bioinformatics method was used to determine the mRNA expression level of HMGB1 in PCa specimens and its correlation with the mRNA expression of AR. Immunohistochemical staining was used to detect the expression of these proteins in clinical PCa samples. Reporter gene and ChIP assays were performed to determine the activity of AR and the effect of HMGB1 on the ability of AR to bind to the promoters of prostate specific antigen and transmembrane protease, serine 2. A bioluminescence resonance energy transfer assay was employed to observe the direct interaction between HMGB1 and AR protein. Additionally, a castrated nude mouse xenograft tumour model was established to verify the effect of HMGB1 on PCa. The results revealed that HMGB1 expression was significantly increased in PCa specimens, which may have a strong correlation with AR expression. Moreover, HMGB1 could reactivate the AR signalling pathway, directly interact with AR, and promote the development of CRPC in an androgen­independent manner. The results of the present study indicated that HMGB1 promoted the development of CRPC by interacting with AR, which inferred that decreasing the expression of HMGB1 may be a potential effective method for CRPC prevention and treatment.

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.

Efficacy of Endoscopic Intervention plus Growth Inhibitor and Patient Self-Management in the Treatment of Esophagogastric Variceal Bleeding in Cirrhosis.

Objective: To assess the efficacy of endoscopic intervention plus growth inhibitor and patient self-management in the treatment of esophagogastric variceal bleeding. Methods: Between January 2019 and December 2021, 60 patients with esophagogastric variceal bleeding treated in our hospital were assessed for eligibility and randomly recruited. They were concurrently and randomly assigned at a ratio of 1 : 1 to receive either endoscopic intervention plus growth inhibitor (control group) or endoscopic intervention plus growth inhibitor and patient self-management (observation group). The endpoint is clinical efficacy. Results: All eligible patients showed a similar time of hemostasis, success rate of hemostasis, rebleeding rate, and disappearance rate of varicose veins (P > 0.05). Endoscopic intervention plus growth inhibitor and patient self-management were associated with a lower incidence of complication (6.67%, including 1 (3.34%) case of ulcer and 1 (3.34%) case of fever) than endoscopic intervention plus growth inhibitor (26.67%, including 3 (10.00%) cases of ulcer, 2 (6.67%) cases of retrosternal pain, and 3 (10.00%) cases of fever) (P < 0.05). Patients in the observation group had significantly higher life satisfaction scores (25.17 ± 4.28 and 23.68 ± 5.17) than those in the control group (22.13 ± 2.24 and 18.12 ± 3.28) (P < 0.05). A decrease in life satisfaction scores was observed at 6 months after treatment, and the patients given patient self-management showed a higher satisfaction (P < 0.05). Conclusion: Endoscopic intervention plus growth inhibitor and patient self-management yielded remarkable clinical efficacy in the treatment of esophagogastric variceal bleeding as it reduces the incidence of complication and enhances the life satisfaction of patients, and so it is worthy of clinical promotion.

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.

Analysis of the association between KIN17 expression and the clinical features/prognosis of epithelial ovarian cancer, and the effects of KIN17 in SKOV3 cells.

DNA double-strand breaks (DSBs) are an important mechanism of chemotherapy in epithelial ovarian cancer (EOC). Kin17 DNA and RNA binding protein (KIN17) serves a crucial role in DSB repair. In the present study, the association between KIN17 and EOC, and the effects of KIN17 on EOC cells in vitro were evaluated. A bioinformatics method was used to determine the mRNA expression levels of KIN17 in EOC and its association with EOC prognosis including overall survival (OS) and progression free survival (PFS) time. Western blotting and immunohistochemical staining were used to evaluate the expression levels of KIN17 in EOC samples. Kaplan-Meier and Cox regression analyses were utilized to analyze risk factors for the OS of patients with EOC. A Cell Counting Kit-8 assay was performed to explore the roles of KIN17 in SKOV3 cells. Both the transcription and expression of KIN17 were upregulated in EOC tissues. Furthermore, the OS of patients with EOC with high mRNA expression levels of KIN17 was shorter than that of patients with EOC with low expression levels. High KIN17 expression was an independent risk factor for EOC prognosis. Furthermore, KIN17 knockdown inhibited the proliferation of SKOV3 cells, enhanced the sensitivity of the cells to cisplatin and inhibited the migration ability of the cells. These results suggested that KIN17 may act as an ideal candidate for therapy and as a prognostic biomarker of EOC, although the underlying mechanisms require further exploration.

Mesoporous silica nanoparticles combined with AKR1C3 siRNA inhibited the growth of castration-resistant prostate cancer by suppressing androgen synthesis in vitro and in vivo.

Intracrine androgen synthesis plays a critical role in the development of castration-resistant prostate cancer (CRPC). Aldo-keto reductase family 1 member C3 (AKR1C3) is a vital enzyme in the intracrine androgen synthesis pathway. In this study, mesoporous silica nanoparticles (MSNs) were employed to deliver small interfering RNA targeting AKR1C3 (siAKR1C3) to downregulate AKR1C3 expression in CPRC cells. The optimal weight ratio of MSNs/siAKR1C3 was determined by a gel retardation assay. Prostate cancer cells such as VCaP cells, which intracrinally express AKR1C3, and LNCaP-AKR1C3 cells stably transfected with AKR1C3 were used to investigate the antitumour effect of MSNs-siAKR1C3. Fluorescence detection and Western blot analyses were applied to confirm the entrance of MSNs-siAKR1C3 into the cells. A SRB (Sulforhodamine B) assay was employed to assess the cell viability, and a radioimmunoassay was used to measure the androgen concentration. Moreover, real-time PCR (RT-PCR), Western blot analysis and ELISA were used to determine the transcription and expression of prostate-specific antigen (PSA), AKR1C3 and androgen receptor (AR). Meanwhile, a reporter gene assay was performed to determine the AR activity. Additionally, a castrated nude mouse xenograft tumour model was produced to verify the inhibitory effect of MSNs-siAKR1C3 in vivo. The results showed that the optimal weight ratio of MSNs/siAKR1C3 was 140:1, and the complex could effectively enter cells, downregulate AKR1C3 expression, reduce the androgen concentration, inhibit AR activation, and inhibit CRPC development both in vitro and in vivo. These results indicate that decreasing intracrine androgen synthesis and inactivating AR signals by MSNs-siAKR1C3 may be a potential effective method for CRPC treatment.

Ultrasound guided continuous Quadratus Lumborum block hastened recovery in patients undergoing open liver resection: a randomized controlled, open-label trial.

BACKGROUND: Quadratus lumborum (QL) block is increasingly being used as a new abdominal nerve block technique. In some studies of mid and lower abdominal and hip analgesia, continuous QL block achieved favorable outcomes as an alternative to continuous intravenous analgesia with opioids. However, the use of continuous QL block for upper abdominal pain is less well characterized. This study aimed to investigate the effects of continuous anterior QL block (CQLB) on postoperative pain and recovery in patients undergoing open liver resection. METHODS: Sixty-three patients underwent elective open liver resection were randomly divided into continuous anterior QL block (CQLB, n = 32) group and patient-controlled intravenous analgesia (PCIA, n = 31) group. Patients in CQLB group underwent ultrasound-guided anterior QL block at the second lumbar vertebral transverse processes before general anesthesia, followed by postoperative CQLB analgesia. Patients in PCIA group underwent continuous intravenous analgesia postoperatively. Postoperative numerical rating scale (NRS) pain scores upon coughing and at rest, self-administered analgesic counts, rate of rescue analgesic use, time to first out-of-bed activity and anal flatus after surgery, and incidences of analgesic-related adverse effects were recorded. RESULTS: Postoperative NRS pain scores on coughing in CQLB group at different time points and NRS pain score at rest 48 h after surgery were significantly lower than those in PCIA group (P < 0.05). Time to first out-of-bed activity and anal flatus after surgery in CQLB group were significantly earlier than those in PCIA group (P < 0.05). No significant differences of postoperative self-administered analgesic counts, rate of postoperative rescue analgesic usage, or incidences of analgesic-related adverse effects were found between the two groups (P > 0.05). CONCLUSIONS: Ultrasound-guided anterior QL block significantly alleviated the pain during coughing after surgery, shortened the time to first out-of-bed activity and anal flatus, promoting postoperative recovery of the patients undergoing open liver resection. TRIAL REGISTRATION: This study has been registered in April 1, 2018 on Chinese Clinical Trail Registry, the registration number is ChiCTR1800015454 .

Brain-Derived Neurotrophic Factor Precursor in the Hippocampus Regulates Both Depressive and Anxiety-Like Behaviors in Rats.

Depression and anxiety are two affective disorders that greatly threaten the mental health of a large population worldwide. Previous studies have shown that brain-derived neurotrophic factor precursor (proBDNF) is involved in the development of depression. However, it is still elusive whether proBDNF is involved in anxiety, and if so, which brain regions of proBDNF regulate these two affective disorders. The present study aims to investigate the role of proBDNF in the hippocampus in the development of depression and anxiety. Rat models of an anxiety-like phenotype and depression-like phenotype were established by complete Freund's adjuvant intra-plantar injection and chronic restraint stress, respectively. Both rat models developed anxiety-like behaviors as determined by the open field test and elevated plus maze test. However, only rats with depression-like phenotype displayed the lower sucrose consumption in the sucrose preference test and a longer immobility time in the forced swimming test. Sholl analysis showed that the dendritic arborization of granule cells in the hippocampus was decreased in rats with depression-like phenotype but was not changed in rats with anxiety-like phenotype. In addition, synaptophysin was downregulated in the rats with depression-like phenotype but upregulated in the rats with anxiety-like phenotype. In both models, proBDNF was greatly increased in the hippocampus. Intra-hippocampal injection anti-proBDNF antibody greatly ameliorated the anxiety-like and depressive behaviors in the rats. These findings suggest that despite some behavioral and morphological differences between depression and anxiety, hippocampal proBDNF is a common mediator to regulate these two mental disorders.

Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury.

BACKGROUND AND OBJECTIVES: The overall purpose of this study was to investigate the role of cytochrome C oxidase (CcO) in preventing ischemia reperfusion-induced cardiac injury through gaseous signaling molecule pathways. MATERIALS AND METHODS: We used CcO inhibitor, potassium cyanide (KCN) to mimic the pre-treatment of gaseous signaling molecules in a global ischemia/reperfusion (IR) injury model in rats. Intracellular reactive oxygen species (ROS) was determined by measuring mitochondrial H2O2 and mitochondrial complex activity. RESULTS: KCN pre-treatment led to decreased infarction area after IR injury and improved cardiac function. KCN pre-treated group challenged with IR injury was associated with reduced ROS production through inhibition of activity and not downregulation of CcO expression. In addition, KCN pre-treatment was associated with enhanced expression and activity of mitochondrial antioxidase, suggesting the role of CcO in regulating IR injury through oxidative stress. CONCLUSION: KCN pre-treatment reduced the severity of IR injury. The potential mechanism could be increased endogenous anti-oxidase activity and consequently, the enhanced clearance of ROS.

Down-Regulation of miRNA-128 Contributes to Neuropathic Pain Following Spinal Cord Injury via Activation of P38.

BACKGROUND Neuropathic pain (NPP) arises from a lesion or dysfunction of the somatosensory nervous system. Recent studies have demonstrated multiple microRNAs (miRNAs) play key roles in NPP development. This study aimed to investigate the effects of miR-128 on microglial cells. MATERIAL AND METHODS We established a compressive spinal cord injury (SCI) model and collected the spinal cord segment-derived conditioned medium (CM). We then measured the expression of miR-128 in the murine microglial cell line BV2 treated with CM-SCI or CM obtained from control (CM-NC). Furthermore, lentivirus production of miR-128 and scrambled control were transfected into BV2 cells, which were first treated with CM-SCI or CM-NC. Moreover, the effects of miR-128 on cell viability, M1/M2 microglial gene expression, inflammatory cytokines concentration, and the protein expression of P38 and phosphorylated P38 (P-P38) were investigated. RESULTS The expression of miR-128 was downregulated in murine microglial BV2 cells treated with CM-SCI. Overexpression of miR-128 markedly promoted the viability of murine microglial cells. In addition, miR-128 overexpression significantly decreased the expression levels of microglial M1 phenotypic markers CD86 and CD32, and increased the expression levels of M2 phenotypic markers Arg1 and CD206. Furthermore, miR-128 overexpression obviously decreased the concentration of TNF-α, IL-1ß, and IL-6. We found that miR-128 overexpression significantly downregulated the expression levels of P38 andP-P38. CONCLUSIONS Our findings indicate that down-regulation of miR-128 in murine microglial cells may contribute to the development of NPP following SCI via activation of P38. MiR-128 may be a potential intervention target for NPP.