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Objectives: The aim of this study was to evaluate the effectiveness and safety of acupuncture for the treatment of post-stroke cognitive impairment (PSCI). Methods: The Cochrane Library, Embase, Medline, China National Knowledge Infrastructure (CNKI), Chinese Science and Technology Periodical (VIP), Wanfang, and Chinese Biological Medicine (CBM) databases were electronically searched from their inception to 10 April 2019. The Montreal Cognitive Assessment (MoCA) scale and Mini-Mental State Examination (MMSE) scale were used as outcomes to assess effectiveness with respect to cognitive function. Assessment of risk of bias (ROB) and Grading of Recommendations Assessment, Development, and Evaluation (GRADE) assessment were performed by two reviewers independently. Data were analyzed using Review Manager (RevMan) 5.3. Results: A total of 28 trials with 2144 participants were included in the qualitative synthesis and meta-analysis. Four of the 28 trials (14%) were assessed as being at overall low ROB, 24 of the 28 trials (86%) were assessed as having overall high ROB. The quality of evidence for both MoCA and MMSE were deemed to be very low by the GRADE criteria. Results indicated that acupuncture groups may be benefiting more than non-acupuncture groups with respect to variation of MoCA scores (merged mean difference (MMD): 2.66, 95% confidence interval (CI): 2.18 to 3.13, p < 0.00001; heterogeneity: χ2 = 35.52, p = 0.0007, I2 = 63%), and the heterogeneity decreased in both subgroup analysis and sensitivity analysis. In addition, acupuncture groups might be benefiting more than non-acupuncture groups in terms of changes in MMSE score (MMD = 2.97, 95% CI = 2.13 to 3.80, p < 0.00001; heterogeneity: χ2 = 269.75; p < 0.00001; I2 = 92%), and the heterogeneity decreased in subgroup analysis. Only one RCT addressed adverse events, and the symptoms were mild and did not affect treatment and evaluation. Conclusion: Acupuncture could be effective and safe for PSCI. Nevertheless, the results should be interpreted cautiously due to the high ROB of included trials and very low quality of evidence for assessed outcomes.

Background/Aims A strong correlation between depression and irritable bowel syndrome with diarrhea (IBS-D) has been identified. The aim of this study is to identify the correlations among depression, structural factors, gastrointestinal (GI) and extra-GI symptoms, and efficacy of neuromodulators in patients with IBS-D. Methods Patients meeting the Rome III Diagnostic Criteria for IBS-D were enrolled. The intestinal symptoms and psychological states were evaluated using IBS-specific symptom questionnaires and Hamilton Depression Rating Scale. Results In total, 410 patients with IBS-D were enrolled, 28.8% (118/410) had comorbid depression. Patients with depression did not readily experience improvement in abdominal pain/discomfort after defecation, and had a higher prevalence of passing mucus, overlapping functional dyspepsia, and extra-GI symptoms. The structural factor “mental disorders” significantly correlated with main bowel symptom score and degree of pre-defecation abdominal pain/discomfort. No structural factor significantly correlated with bowel movements or stool form. Patients who had passing mucus, overlapping functional dyspepsia and extra-GI painful symptoms have higher score of “anxiety/somatization.” Patients with sexual dysfunction have higher score of “retardation symptoms.” In total, 28.3% of patients with IBS-D were prescribed neuromodulators. Baseline scores of “anxiety/somatization” and “retardation symptoms” positively correlated with improvement of diarrhea after paroxetine, and “sleep disturbances” positively correlated with improvement of abdominal pain/discomfort and diarrhea after mirtazapine. Conclusions Comorbid depression and higher scores of structural factors might aggravate GI and extra-GI symptoms other than bowel movements and stool form. Structural factors of Hamilton Depression Rating Scale correlated with efficacy of paroxetine and mirtazapine in patients with IBS-D. (J Neurogastroenterol Motil 2020;26:505-513)

Background Acupuncture has been widely used for acute low back pain (LBP), yet there remains continued controversy regarding its efficacy. Therefore, we aimed to critically evaluate the evidence for acupuncture as an effective treatment for acute LBP. Methods English and Chinese databases were searched for randomized controlled trials (RCTs) that involved acupuncture for acute LBP published up to May 2020. Data on the outcomes of pain intensity, functional status, and analgesic use were extracted. The meta-analysis was performed using the Cochrane Collaboration's RevMan 5.3, and pooled data were expressed as mean differences (MD) with 95% confidence intervals (CIs). Results Of the 13 eligible RCTs identified, 11 RCTs (involving 707 patients) provided moderate-quality evidence that acupuncture has a statistically significant association with improvements in VAS (visual analog scale) score [MD: -1.75 (95% CI: -2.39, -1.12)]. Two studies indicated that acupuncture did not influence the RMDQ (Roland-Morris Disability Questionnaire) scores more than the control treatment [MD: -2.34 (95% CI: -5.34, 0.67)]. Three studies suggested that acupuncture influenced the ODI (Oswestry Disability Index) scores more than the control treatment [MD: -12.84 (95% CI: -23.94, -1.74)]. Two studies suggested that acupuncture influenced the number of pills more than the control treatment [MD: -3.19 (95% CI: -3.45, -2.92)]. Conclusions Acupuncture treatment of acute LBP was associated with modest improvements in the VAS score, ODI score, and the number of pills, but not the RMDQ score. Our findings should be considered with caution due to the low power original studies. High-quality trials are needed to assess further the role of acupuncture in the treatment of acute LBP.

Benzyl isothiocyanate (BITC) has been reported to exhibit antitumor properties in various cancer types; however, the underlying mechanisms of its action remain unclear. In the present study, the efficacy of BITC on murine mammary carcinoma cells was evaluated in vitro and in vivo, revealing a potential mechanism for its action. In vivo bioluminescence imaging indicated dynamic inhibition of murine mammary carcinoma cell growth and metastasis by BITC. A terminal deoxynucleotidyl transferase‑mediated dUTP nick end labeling assay demonstrated that BITC also induced apoptosis. BITC further exhibited antitumorigenic activity in 4T1‑Luc cells in vitro via the inhibition of cell proliferation, induction of apoptosis and cell cycle arrest, and inhibition of cell migration and invasion. Furthermore, the activity of key molecules of the adenomatous polyposis coli (APC)/β‑catenin complex was altered following treatment with BITC, which suggested a potential role for the APC/β‑catenin complex in the BITC‑mediated induction of apoptosis and inhibition of metastasis in murine mammary carcinoma. BITC upregulated the activity of glycogen synthase kinase‑3β and APC proteins, whereas it downregulated β‑catenin expression. The inhibition of metastasis was accompanied with the downregulation of vimentin and upregulation of E‑cadherin. Conversely, BITC did not exhibit toxicity or side effects in the normal mammary epithelial cell line MCF‑10A. The present study indicated that BITC exhibited anticancer properties due to the induction of breast cancer cell apoptosis and inhibition of breast cancer cell metastasis mediated by the Wnt/β‑catenin signaling pathway.

Background: Aberrant expression of caveolin-1 (CAV-1) is involved in the pathogenesis of hepatocellular carcinoma (HCC); however, the results have been inconsistent due to the small size of sample in the individual study. Methods: We performed a meta-analysis and evaluated the association of CAV-1 protein overexpression and clinicopathological significance by using Review Manager 5.2. Pooled ORs and HR with corresponding CIs were calculated. Results: Nine studies were included in the meta-analysis with 810 HCC and 172 cirrhosis patients. CAV-1 protein overexpression was correlated with the risk of cirrhosis; OR was 3.25, p=0.01. Furthermore, the rate of CAV-1 protein overexpression was significantly higher in HCC with cirrhosis than HCC without cirrhosis, suggesting that the CAV-1 protein overexpression likely initiated carcinogenesis in liver with cirrhosis and subsequently contributed to the progression of HCC. In addition, CAV-1 protein overexpression was strongly associated with poor differentiated HCC and invasion; ORs were 2.61 and 2.71, respectively. CAV-1 protein overexpression was strongly correlated with poor overall survival in patients with HCC; HR was 0.4, p=0.03. Conclusions: In summary, CAV-1 protein overexpression is at risk for liver cirrhosis and HCC derived from cirrhosis, and CAV-1 is also a promising prognostic predictor in HCC.

Background Opposing needling has an obvious curative effect in the treatment of post-stroke hemiplegia; however, the mechanism of the opposing needling in the treatment of post-stroke hemiplegia is still not clear. The purpose of this study is to investigate the effect of opposing needling on the excitability of primary motor cortex (M1) of healthy participants and patients with post-stroke hemiplegia, which may provide insight into the mechanisms of opposing needling in treating post-stroke hemiplegia. Methods This will be a single-blind, randomised, sham-controlled trial in which 80 healthy participants and 40 patients with post-stroke hemiplegia will be recruited. Healthy participants will be randomised 1:1:1:1 to the 2-Hz, 50-Hz, 100-Hz, and sham electroacupuncture groups. Patients with post-stroke hemiplegia will be randomised 1:1 to the opposing needling or conventional treatment groups. The M1 will be located in all groups by using neuroimaging-based navigation. The stimulator coil of transcranial magnetic stimulation (TMS) will be moved over the left and right M1 in order to identify the TMS hotspot, followed by a recording of resting motor thresholds (RMTs) and motor-evoked potentials (MEPs) of the thenar muscles induced by TMS before and after the intervention. The primary outcome measure will be the percent change in the RMTs of the thenar muscles at baseline and after the intervention. The secondary outcome measures will be the amplitude (μV) and latency (ms) of the MEPs of the thenar muscles at baseline and after the intervention. Discussion The aim of this trial is to explore the effect of opposing needling on the excitability of M1 of healthy participants and patients with post-stroke hemiplegia. Trial registration Chinese Clinical Trial Registry ChiCTR1900028138. Registered on 13 December 2019.

PURPOSE To evaluate the efficacy and safety of combined microwave ablation (MWA) and osteoplasty as a palliative therapy for painful bone metastases. MATERIALS AND METHODS As an extension of a previous limited single-center study, a retrospective review was conducted for 147 patients (77 male, 70 female) with painful bone metastases who underwent MWA combined with osteoplasty. In total, 102 (69.4%), 41 (27.9%), and 4 (2.7%) patients had spinal metastases, extraspinal metastases, and both, respectively. Treatment efficacy was determined by comparing visual analog scale (VAS) scores, daily morphine equivalent opioid consumption, and Oswestry disability index (ODI) scores before treatment and during the follow-up period (mean follow-up, 9.8 months; range 3-16). RESULTS The mean VAS score significantly declined from 6.4 ± 2.3 before treatment to 3.2 ± 2.1, 1.9 ± 1.6, 1.8 ± 1.6, 1.8 ± 1.6, and 1.9 ± 1.6 at 24 hours, 1 week, 4 weeks, 12 weeks, and 24 weeks after treatment, respectively (P < .01). Furthermore, the mean daily morphine equivalent opioid consumption was significantly reduced from 81.5 ± 32.8 mg before treatment to 40.0 ± 20.6, 32.4 ± 10.2, 26.4 ± 10.0, 21.5 ± 8.3, and 19.3 ± 7.4 mg. The mean ODI score also declined after treatment (P < .0001). Major complications occurred in 4 of 147 patients, with 1 pathologic fracture, 1 nerve injury, and 2 mild skin infections. Minor cement leakages were observed at 69 sites (32.8%). CONCLUSIONS MWA combined with osteoplasty is an effective and safe treatment for painful bone metastases.

The aim of the present study was to establish a cell model of Alzheimer's disease (AD) and investigate the neurotoxic effects of β-amyloid (Aβ) on the cytoskeleton. PC12 cells were cultured and treated with Aβ25‑35, and cell survival was analyzed with the MTT assay. Cell apoptosis was visualized using 4',6-diamidino-2-phenylindole staining and the terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. Immunocytochemistry and phalloidin staining were used to label the cytoskeleton of PC12 cells. Aβ25-35 was found to induce PC12 cell apoptosis in a dose-dependent manner (P

Synapses are key structures in neural networks, and are involved in learning and memory in the central nervous system. Investigating synaptogenesis and synaptic aging is important in understanding neural development and neural degeneration in diseases such as Alzheimer disease and Parkinson's disease. Our previous study found that synaptogenesis and synaptic maturation were harmonized with brain development and maturation. However, synaptic damage and loss in the aging cerebellum are not well understood. This study was designed to investigate the occurrence of synaptic aging in the cerebellum by observing the ultrastructural changes of dendritic spines and synapses in cerebellar Purkinje cells of aging mice. Immunocytochemistry, DiI diolistic assays, and transmission electron microscopy were used to visualize the morphological characteristics of synaptic buttons, dendritic spines and synapses of Purkinje cells in mice at various ages. With synaptic aging in the cerebellum, dendritic spines and synaptic buttons were lost, and the synaptic ultrastructure was altered, including a reduction in the number of synaptic vesicles and mitochondria in presynaptic termini and smaller thin specialized zones in pre- and post-synaptic membranes. These findings confirm that synaptic morphology and function is disrupted in aging synapses, which may be an important pathological cause of neurodegenerative diseases.

AIM To analyze predictors of healthcare-seeking behavior among Chinese patients with irritable bowel syndrome (IBS) and their satisfaction with medical care. METHODS Participating patients met IBS Rome III criteria (excluding those with organic diseases) and were enrolled in an IBS database in a tertiary university hospital. Participants completed IBS questionnaires in face-to-face interviews. The questionnaires covered intestinal and extra-intestinal symptoms, medical consultations, colonoscopy, medications, and self-reported response to medications during the whole disease course and in the past year. Univariate associations and multivariate logistic regression were used to identify predictors for frequent healthcare-seeking behavior (≥ 3 times/year), frequent colonoscopies (≥ 2 times/year), long-term medications, and poor satisfaction with medical care. RESULTS In total, 516 patients (293 males, 223 females) were included. Participants’ average age was 43.2 ± 11.8 years. Before study enrollment, 55.2% had received medical consultations for IBS symptoms. Ordinary abdominal pain/discomfort (non-defecation) was an independent predictor for healthcare-seeking behavior (OR = 2.07, 95%CI: 1.31-3.27). Frequent colonoscopies were reported by 14.7% of patients (3.1 ± 1.4 times per year). Sensation of incomplete evacuation was an independent predictor for frequent colonoscopies (OR = 2.76, 95%CI: 1.35-5.67). During the whole disease course, 89% of patients took medications for IBS symptoms, and 14.7% reported they were satisfied with medical care. Patients with anxiety were more likely to report dissatisfaction with medical care (OR = 2.08, 95%CI: 1.20-3.59). In the past year, patients with severe (OR = 1.74, 95%CI: 1.06-2.82) and persistent (OR = 1.66, 95%CI: 1.01-2.72) IBS symptoms sought medical care more frequently. CONCLUSION Chinese patients with IBS present high rates of frequent healthcare-seeking behavior, colonoscopies, and medications, and low satisfaction with medical care. Intestinal symptoms are major predictors for healthcare-seeking behavior.

Background Hemiplegia after stroke is one of the main dysfunctions in stroke patients. Acupuncture had been widely used for poststroke spastic hemiplegia (PSSH), but the efficiency was unclear. This study aimed to examine the efficiency and safety of acupuncture for individuals with PSSH. Methods We searched nine databases from their inception to 27th July 2019. Randomized controlled trials (RCTs) of acupuncture for the treatment of PSSH met the screening criteria. The quality of methodology was evaluated by Cochrane's risk of bias tool. RevMan 5.3 was used to perform the meta-analysis. The primary outcome was the Fugl-Myer Assessment (FMA) score, and the secondary outcomes were the Ashworth Scale for Spasticity (ASS) and Barthel Index (BI) scores. To evaluated the safety of acupuncture therapy, researchers scanned the full text to collect adverse events. Results Researchers retrieved 2452 articles in total, after screening, thirty-eight studies with 2628 participants of were included. In this meta-analysis, twenty-seven trials revealed that acupuncture therapy was associated with an increase in FMA scores compared with rehabilitation training (RT) (MD: 8.43, 95% CI, 6.57 to 10.28, p Conclusions This review discovered that acupuncture might be a safe and effective adjuvant therapy for individuals with PSSH. Nevertheless, there were methodological limitations in the included RCTs, and well-designed and large-scale studies should be carried out to confirm our results.

Alzheimer's disease (AD) is a progressive neurodegenerative disease, characterized by cognitive impairment. However, the pathogenesis of AD are very complicated, and the theories of Aβ and neurofibrillary tangles cannot explain all pathological alterations and clinical symptoms. Here, we used three-dimensional (3D) neural organoids culture derived from mouse induced pluripotent stem cells (iPSCs) to investigate the pathological mechanisms of AD. In this study, AD cerebral organoids were generated by overexpressing familial AD mutations (APP and PS1 genes) in mouse induced pluripotent stem cells, so that the early pathogenesis of AD could be investigated well with protein and cellular phenotype analyses. The results showed that AD cerebral organoids appeared some AD pathological alterations, and high levels of Aβ and p-Tau were induced as well. Furthermore, the number of GFAP-positive astrocytes and glutamatergic excitatory neurons increased significantly, but the number of GABAergic interneurons decreased. In conclusion, we suggest that cerebral organoids are a suitable AD model for scientific study, and that will provide us a novel insight into the understanding of the pathogenesis of AD.

The objective of this study is to understand the impairment of learning and memory in mouse after chronic nitrite exposure. The animal model of nitrite exposure in mouse was created with the daily intubation of nitrite in adult healthy male mice for 3 months. Furthermore, the mouse's learning and memory abilities were tested with Morris water maze, and the expression of Synaptophysin and γ-Synuclein was visualized with immunocytochemistry and Western blot. Our results showed that nitrite exposure significantly prolonged the escape latency period (ELP) and decreased the values of the frequency across platform (FAP) as well as the accumulative time in target quadrant (ATITQ) compared to control, in dose-dependent manner. In addition, after nitrite exposure, synaptophysin (SYN) positive buttons in the visual cortex was reduced, in contrast the increase of γ-synuclein positive cells. The results above were supported by Western blot as well. We conclude that nitrite exposure could lead to a decline in mice's learning and memory. The overexpression of γ-synuclein contributed to the synaptic loss, which is most likely the cause of learning and memory impairment. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1720-1730, 2016.

The available findings concerning the association between branched-chain amino acids (BCAAs)—particularly leucine—and insulin resistance are conflicting. BCAAs have been proposed to elicit different or even opposite effects, depending on the prevalence of catabolic and anabolic states. We tested the hypothesis that leucine supplementation may exert different effects at different stages of insulin resistance, to provide mechanistic insights into the role of leucine in the progression of insulin resistance. Male Sprague-Dawley rats were fed a normal chow diet, high-fat diet (HFD), HFD supplemented with 1.5% leucine, or HFD with a 20% calorie restriction for 24 or 32 weeks. Leucine supplementation led to abnormal catabolism of BCAA and the incompletely oxidized lipid species that contributed to mitochondrial dysfunction in skeletal muscle in HFD-fed rats in the early stage of insulin resistance (24 weeks). However, leucine supplementation induced no remarkable alternations in BCAA catabolism, but did enhance mitochondrial biogenesis with a concomitant improvement in lipid oxidation and mitochondrial function during the hyperglycaemia stage (32 weeks). These findings suggest that leucine trigger different effects on metabolic signatures at different stages of insulin resistance, and the overall metabolic status of the organisms should be carefully considered to potentiate the benefits of leucine.

Myocardial ischemia/reperfusion (IR) injury is one of the most prevalent cardiovascular diseases, known for its high mortality and morbidity worldwide. Based on pre-existing evidence, LGALS3 has been found to be closely associated with cardiac diseases. Hence, the objective of our study is to explore the potential function of KCNQ1OT1/microRNA-204-5p (miR-204-5p)/ LGALS3 axis on myocardial IR injury and the underlying mechanism. A myocardial IR injury mouse model was established in vivo and an in vitro cardiomyocyte model was induced by hypoxia/Reoxygenation exposure. Next, gain- and loss-of-function experiments were employed in order to measure the viability and apoptosis of cardiomyocytes and the area of ischemic infarct by CCK-8, TUNEL staining and Evans blue/TTC double staining. LGALS3 was found to be highly expressed in myocardial IR injury. The downregulation of LGALS3 resulted in the alleviation of myocardial IR injury in mouse models. In addition, KCNQ1OT1 could promote the LGALS3 expression by binding to miR-204-5p, which led to aggravated myocardial IR injury. In conclusion, KCNQ1OT1 binds to miR-204-5p to exacerbate myocardial IR injury in mice through the up-regulation of LGALS3, providing a novel insight for myocardial IR injury treatment.

Background: Sustained Inflations (SI) and Intermittent Positive Pressure Ventilation (IPPV) are two interventions to prevent Bronchopulmonary dysplasia (BPD). The aim of this study is to assess the effect of these two interventions. Methods: The databases of PubMed, EMBASE, and Cochrane Central Register of Controlled Trials (CENTRAL) will be comprehensively searched from inception to September 2019. All RCTs and quasi-RCTs which compare the efficacy of SI vs IPPV among preterm infants are eligible. We will assess the methodological quality using the Cochrane Handbook version 5.1.0. A meta-analysis will be performed using RevMan 5.3 software and the results will be presented using risk ratios (RRs) and 95% confidence intervals (CIs). Conclusions: This study will provide strong evidence for assessing the effect of SI and IPPV on BPD or death among preterm infants. PROSPERO registration number: CRD42019135816.