Using teach-back in patient education to improve patient satisfaction and the clarity of magnetic resonance imaging.

OBJECTIVE: To explore the effects of using the teach-back method prior to contrast-enhanced magnetic resonance imaging (MRI) on patients' knowledge and satisfaction as well as the clarity of the resulting scans. METHODS: A total of 254 patients who underwent contrast-enhanced MRI examination from July 4, 2022 to September 19, 2022 were enrolled and assigned to the intervention and control groups. Patients in the intervention group received education using the teach-back method, while those in the control group were given routine health education. A questionnaire that included patients' knowledge of contrast-enhanced MRI examination was answered before and after patient education. Data on patient satisfaction with nursing services were also collected. The clarity of the MRI images of all patients was assessed. RESULTS: The scores of knowledge related to MRI after receiving education were significantly higher than those before receiving education (P < 0.001), and there were no significant differences between the intervention and control groups (11.27 ± 9.74 vs. 12.07 ± 8.71, P = 0.498). The score of satisfaction with nursing service in the teach-back group was significantly higher than that in the control group (39.82 ± 0.86 vs. 38.59 ± 3.73, P < 0.001), as was the image clarity score (96.4 ± 0.5 vs. 95.0 ± 0.4, P = 0.039). CONCLUSION: Teach-back improves patient satisfaction and contrast-enhanced MRI clarity. PRACTICE IMPLICATIONS: Including teach-back in patient education improves patient satisfaction and contrast-enhanced MRI clarity.

Effect of Electroacupuncture Stimulation on Proliferation and Differentiation of Endogenous Neural Stem Cells in Rats with Spinal Cord Injury.

The aim of this work was to investigate the effects of electroacupuncture (EA) stimulation on the proliferation and differentiation of endogenous neural stem cells (NSCs) in rats with spinal cord injury (SCI). One hundred rats were included and randomly divided into the sham-operation (SO) group, model (MO) group, EA group, and preacupuncture stimulation (PAS) group, with 25 rats in each group. All the rats in the SO group had their spinal cord of thoracic segment T10 exposed but without SCI. In the remaining three groups, the modified Allen's weight dropping method was adopted to make SCI models. Those in the SO group and the MO group did not receive any treatment. Those in the EA group were treated with EA after the modelling was completed, which stopped when the samples were collected at each time point. The spinal cord tissue of rats was subjected to immunohistochemical staining and real-time quantitative polymerase chain reaction (PCR) to detect the expressions of neurofilament nestin and glial fibrillary acidic protein (GFAP). The Basso-Beattie-Bresnahan (BBB) score of the MO group was much lower than that of the SO group on the 3rd, 7th, and 14th days after surgery (P < 0.05). The BBB scores of the EA group and PAS group were notably higher than that of the MO group (P < 0.05). The number of nestin-, GFAP-, and MAP-2-positive cells was significantly increased in rat tissues after spinal cord injury. On the 3rd, 7th, and 14th days postoperatively, the numbers of nestin-positive cells in the EA and PAS groups were considerably higher than those in the MO group (P < 0.01). However, the numbers of GFAP-positive cells in the EA and PAS groups were considerably decreased compared with those in the MO group (P < 0.01). The positive rate of MAP-2 in the model group was significantly increased compared to that in the sham-operation group (P < 0.001). The positive rates of MAP-2 in the EA group and PAS group were significantly higher than those in the MO group (P < 0.01). After spinal cord injury, EA could activate the proliferation of endogenous NSCs and promote their differentiation into neuronal cells. Consequently, injuries were repaired, and functions were rehabilitated.

Electroacupuncture-Regulated miR-34a-3p/PDCD6 Axis Promotes Post-Spinal Cord Injury Recovery in Both In Vitro and In Vivo Settings.

Electroacupuncture (EA) could enhance neuroregeneration and posttraumatic conditions; however, the underlying regulatory mechanisms remain ambiguous. PDCD6 (programmed cell death 6) is an established proapoptotic regulator which is responsible for motoneuronal death. However, its potential regulatory role in post-spinal cord injury (SCI) regeneration has remained largely unknown. Further investigations are warranted to clarify the involvement of PDCD6 post-SCI recovery and the underlying mechanisms. In our study, based on bioinformatics prediction, we found that miR-34a-3p might be an upstream regulator miRNA for PDCD6, which was subsequently validated through combined utilization of the qRT-PCR, western blot, and dual-luciferase reporter system. Our in vitro results showed that miR-34a-3p might promote the in vitro differentiation of neural stem cell (NSC) through suppressing PDCD6 and regulating other important neural markers such as fibroblast growth factor receptor 1 (FGFR1), MAP1/2 (MAP kinase kinases 1/2), myelin basic protein (MBP), ßIII-tubulin Class III ß-tubulin (ßIII tubulin), and glial fibrillary acidic protein (GFAP). Notably, in the post-SCI rat model, exogenous miR-34a-3p agomir obviously inhibited the expression of PDCD6 at the protein level and promoted neuronal proliferation, motoneurons regeneration, and axonal myelination. The restorations at cellular level might contribute to the improved hindlimbs functions of post-SCI rats, which was manifested by the Basso-Beattie-Bresnahan (BBB) locomotor test. The impact of miR-34a-3p was further promoted by EA treatment in vivo. Conclusively, this paper argues that a miR-34a-3p/PDCD6 axis might be a candidate therapeutic target for treating SCI and that the therapeutic effect of EA is driven through this pathway.

The Mechanism of miR-141 Regulating the Proliferation and Metastasis of Liver Cancer Cells by Targeting STAT4.

BACKGROUND: In recent years, it has been reported that miRNA can be used as one of the markers of tumor diagnosis, treatment, and prognosis (including liver cancer), and it plays an important role in tumorigenesis. However, there are still very few studies on the mechanism and role of miR-141 in liver cancer. METHODS: qRT-PCR was used to test the expressions of miR-141 and STAT4 in collected liver cancer tissues and adjacent tissues, cultured liver cancer cell lines MHCC97H, Hep3B, and Huh7, and normal human liver cells HL7702. After processing the results of the qRT-PCR experiment, liver cancer cell MHCC97H which has the lowest expression level was decided to be taken as the research object. miR-NC, miR-141 mimics, si-NC, si-STAT4, miR-141 mimics and pcDNA-NC, and miR-141 mimics and pcDNA-STAT4 were transfected into MHCC97H cells, respectively. The MTT assay was used to detect the proliferation of each group of cells, and the Transwell test was used to detect the effect of miR-141 on cell proliferation, migration, and invasion. The interaction between miR-141 and STAT4 was verified by the dual-luciferase reporter experiment, and the expression level of Cyclin D1 and MMP2 was detected by the western blot. RESULTS: Compared with normal cell HL7702, the expression level of miR-141 in liver cancer cell lines was relatively low (P < 0.05) and the expression level of STAT4 in liver cancer cell lines was relatively high (P < 0.05) after testing the expression level of STAT4; transfecting miR-141 mimics or Si-SLBP can inhibit cell proliferation, migration, and invasion; dual-luciferase reporter experiments confirmed that miR-141 can specifically bind to the 3'UTR of STAT4; cotransfection of miR-141 mimics and pcDNA-STAT4 can antagonize the effects of miR-141 mimics on cell proliferation, migration, and invasion. CONCLUSION: miR-141 can target the STAT4 gene expression to inhibit the proliferation, migration, and invasion of liver cancer cells.

Strategies for poverty alleviation supply chain with government subsidies and misreporting behavior in China.

In the poverty alleviation supply chain, subsidies for enterprises or farmers are widely implemented as part of government policy. However, subsidy fraud often occurs, such as misreporting cost information to secure subsidies. Inspired by this, our study aims to explore the optimal decision-making problem of the three-level (government + enterprises + farmers) poverty alleviation supply chain under asymmetric cost information. Four-stage models are constructed to capture the interactions among these three players. Additionally, numerical examples are used to analyze the implications of key parameters, such as cost coefficient and punitive measures coefficient, on supply chain members' optimal decision and profit. Our findings demonstrate that both the enterprise and the farmer can obtain maximum profit from the misreporting behavior. Unfortunately, this behavior always damages the profit of other participants and weakens the efficiency of subsidy policy. Moreover, to mitigate the negative implication of misreporting behavior, the government can establish punitive measures to curtail misreporting. Our work provides important policy implications for governments and enterprises. To ensure that more consumers have access to poverty alleviation products, government organizations should prioritize such projects. In addition, the provision of public facilities and technical guidance should be more effective and prompt to share enterprises' and farmers' costs. We further recommend that subsidy policies be formulated according to recipients' performance in poverty alleviation projects, with corresponding supervision and punitive measures. Finally, in cooperating with farmers in poverty alleviation, enterprises should maximize their interests and reduce costs through technological innovation and channel sharing.

NF-κB 1-induced LINC00665 regulates inflammation and apoptosis of neurons caused by spinal cord injury by targeting miR-34a-5p.

Background: Spinal cord injury (SCI) has high disability rate and low cure rate, which frustrates the patients and brings a heavy burden to their families. This study aimed to explore whether NF-κB1 could induce the expression of LINC00665 and form a feedback loop with miR-34a-5p to regulate inflammation and apoptosis of neurons. Results: Basso, Beattie, and Bresnahan (BBB) scoring was decreased, damage for spinal cord tissue was aggravated and neuron number was decreased in SCI rats. The levels of TNF-α, IL-1ß and IL-6 in serum and the expression of LINC00665 and NF-κB1 in spinal cord tissues were all increased in SCI rats. After LPS induction, PC12 cell viability was decreased. The expression of LINC00665 and NF-κB1 in LPS-induced PC12 cells was increased, which was partially reversed by BAY11-7082 (NF-κB inhibitor). Inhibition of LINC00665 improved cell viability, suppressed apoptosis and inflammation and down-regulated the NF-κB1 expression in LPS-induced PC12 cells. Furthermore, miR-34a-5p expression was decreased in LPS-induced PC12 cells, which could be promoted by inhibition of LINC00665. miR-34a-5p inhibitor restrained the effect of inhibition of LINC00665 on NF-κB1 expression in LPS-induced PC12 cells. Conclusion: inhibition of LINC00665 improved cell viability, suppressed apoptosis and inflammation in LPS-induced PC12 cells, and the NF-κB1/LINC00665/miR-34a-5ploop might be a useful therapeutic target in SCI treatment.

Exploration of potential therapeutic targets for stroke based on the GEO database.

BACKGROUND: This study aimed to analyze non-coding RNA sequencing results, screen differentially expressed long non-coding RNAs (lncRNAs), and predict lncRNA target genes. It further clarifies the potential functions of lncRNAs, thus exploring potential biomarkers and therapeutic targets for stroke. METHODS: LncRNA sequencing data of blood samples from stroke patients and healthy subjects (GSE102541 and GSE140275) were downloaded from the Gene Expression Omnibus (GEO) database. This study used R software and related R packages to conduct a batch correction and differential analysis of sequencing results. It also screened differentially expressed lncRNAs and visualized the correlations between significantly different lncRNAs. Target genes of differential lncRNAs were predicted by the StarBase database. Gene ontology (GO) functional enrichment analysis of related target genes was performed using the DAVID database. Principal component analysis was performed based on the expression levels of lncRNAs with the most significant differences in stroke blood samples. RESULTS: A total of 239 differentially expressed lncRNAs were screened out in this study, of which 146 were upregulated and 93 were downregulated. According to |log2FC| values from highest to lowest, the top 10 lncRNAs with the most significant differences were selected. The upregulated lncRNAs were LINC02334, TARID, MRGPRF-AS1, CAI2, LINC00189, TUG1, and RNF5P1. The downregulated lncRNAs included AC005180.2, ADAMTS9-AS1, and AC036108.3. TARID was strongly correlated with MRGPRF-AS1. Meanwhile, LINC02334 was strongly correlated with TUG1. CAI2, LINC00189, and RNF5P1 were at the core of the correlation network and may therefore be the critical lncRNAs in stroke pathogenesis. GO functional enrichment results indicated that genes were significantly enriched in muscle contraction, RNA polymerase II promoter transcription regulation, muscle structure composition, focal adhesion, endothelial cell chemotaxis, actin, actin cytoskeleton, actin filament binding, blood lipid regulation, smooth muscle contraction regulation, skeletal muscle cell differentiation, and other functions. Principal component analysis showed that the 10 lncRNAs with significant differences could significantly distinguish stroke blood samples from healthy control blood samples, and could characterize the essential characteristics of stroke. CONCLUSIONS: LINC02334, TARID, MRGPRF-AS1, CAI2, LINC00189, TUG1, RNF5P1, AC005180.2, ADAMTS9-AS1, and AC036108.3 play an essential role in the pathogenesis of stroke, and may be potential therapeutic targets.

TRPV1, Targeted by miR-338-3p, Induces Neuropathic Pain by Interacting with NECAB2.

A variety of studies have proposed that transient receptor potential vanilloid 1 (TRPV1) is involved in the progression of multiple diseases, including neuropathic pain. Although increased expression of TRPV1 in chronic constriction injury was described earlier, the underlying regulatory mechanisms of TRPV1 in neuropathic pain remain largely unknown. In our study, we constructed a chronic constriction injury (CCI) rat model to deeply analyze the mechanisms underlying TRPV1. RT-qPCR-indicated TRPV1 mRNA and protein expression were extremely upregulated in CCI rat dorsal spinal cord tissues. Then, TRPV1 was corroborated to interact with N-terminal EF-hand Ca2+-binding protein 2 (NECAB2). The mRNA and protein levels of NECAB2 were increased in CCI tissues. Moreover, TRPV1 and NECAB2 together regulated nociceptive procession-associated protein metabotropic glutamate receptor 5 (mGluR5), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and Ca2+ in isolated microglia of CCI rats. Moreover, TRPV1 upregulation apparently increased mechanical allodynia and thermal hyperalgesia as well as the expression of inflammation-associated genes (COX-2, TNF-α, and IL-6). In addition, downregulation of NECAB2 significantly decreased mechanical allodynia and thermal hyperalgesia as well as the expression of COX-2, TNF-α, and IL-6. Furthermore, TRPV1 was confirmed to be a downstream target of miR-338-3p. TRPV1 overexpression abolished the inhibitory effect by miR-338-3p elevation on neuropathic pain development. In summary, this study proved TRPV1, targeted by miR-338-3p, induced neuropathic pain by interacting with NECAB2, which provides a potential therapeutic target for neuropathic pain treatment.

[Efficacy differences between different position in patients treated with electroacupuncture for lumbar herniated disc].

OBJECTIVE: To observe the clinical efficacy differences between modified lateral position and prone position in patients treated with electroacupuncture (EA) for lumbar herniated disc (LHD). METHODS: Seventy-six patients with LHD were randomly divided into a lateral position group and a prone position group, 38 cases in each one. The acupoint selection and treatment method were identical in the two groups except the position. Mingmen (GV 4), Yaoyangguan (GV 3), Dachangshu (BL 25), Xiaochangshu (BL 27), Zhibian (BL 54) and Huantiao (GB 30) were selected. EA was given three times a week, ten times were taken as one course and totally 20 times were given. The visual analogue scale (VAS) and Japanese orthopaedic association (JOA) scale were taken as efficacy criteria, which were evaluated before and after treatment as well as one month after treatment. RESULTS: After treatment, VAS and JOA were significantly improved in the two groups (lateral position group:JOA 10.60±2.60 vs 18.92±3.87, VAS 8.13±0.99 vs 2.34±0.81; prone position group:JOA 10.94±2.06 vs 17.02±3.96, VAS 8.02±1.05 vs 2.86±0.96, all P<0.01); the VAS and JOA in the lateral position group were higher than those in the prone position group (both P<0.05). One month after treatment, VAS and JOA were significantly improved in the two groups (all P<0.01), which was more significant in the lateral position group (both P<0.05). CONCLUSIONS: The treatment position could influence the efficacy of EA for LHD, and lateral position pre-sents certain advantages to prone position group.