Effectiveness of Mindfulness-Based Stress Reduction on Mental Health and Psychological Quality of Life among University Students: A GRADE-Assessed Systematic Review.

Background: Psychological distress is a progressive health problem that has been linked to decreased quality of life among university students. This meta-analysis reviews existing randomized controlled trials (RCTs) that have examined the effects of mindfulness-based stress reduction (MBSR) on the relief of psychosomatic stress-related outcomes and quality of life among university students. Methods: The PubMed, EMBASE, Web of Science, PsycINFO (formerly PsychLit), Ovid MEDLINE, ERIC, Scopus, Google Scholar, ProQuest, and Cochrane Library databases were searched in November 2023 to identify the RCTs for analysis. Data on pathology (anxiety, depression, and perceived stress), physical capacity (sleep quality and physical health), and well-being (mindfulness, self-kindness, social function, and subjective well-being) were analyzed. Results: Of the 276 articles retrieved, 29 met the inclusion criteria. Compared with control therapies, the pooled results suggested that MBSR had significant effects, reducing anxiety (SMD = -0.29; 95% CI: -0.49 to -0.09), depression (SMD = -0.32; 95% CI: -0.62 to -0.02), and perceived stress (SMD = -0.41; 95% CI: -0.60 to -0.29) and improving mindfulness (SMD = 0.34; 95% CI: 0.08 to 0.59), self-kindness (SMD = 0.57; 95% CI: 0.30 to 1.12), and physical health (SMD = -0.59; 95% CI: -1.14 to -0.04). No significant differences were observed in sleep quality (SMD = -0.20; 95% CI: -0.06 to 0.20), social function (SMD = -0.71; 95% CI: -2.40 to 0.97), or subjective well-being (SMD = 0.07; 95% CI: -0.18 to 0.32). The quality of the evidence regarding sleep quality and physical health outcomes was low. Conclusions: MBSR therapy appears to be potentially useful in relieving functional emotional disorders. However, additional evidence-based large-sample trials are required to definitively determine the forms of mindfulness-based therapy that may be effective in this context and ensure that the benefits obtained are ongoing. Future studies should investigate more personalized approaches involving interventions that are tailored to various barriers and students' clinical characteristics. To optimize the effects of such interventions, they should be developed and evaluated using various designs such as the multiphase optimization strategy, which allows for the identification and tailoring of the most valuable intervention components.

LncBIRC3-OT promotes the malignant progression of glioma by interacting with RELA to upregulate stanniocalcin-1 expression.

Glioma is the most common malignant intracranial tumor, accounting for 80 % of all malignant brain tumors. Growing evidence suggests that lncRNAs are involved in the growth, angiogenesis, metastasis, and therapeutic resistance in a variety of tumors, including glioma. In this study, lncBIRC3-OT (NONHSAT159592.1), which is highly expressed in glioma, was screened by RNA-seq method and verified by quantitative reverse transcription polymerase chain reaction. Subsequently, we knocked down the endogenous expression of lncBIRC3-OT in U87 and U251 cells and found that down-regulated lncBIRC3-OT inhibited cell proliferation, colony formation, migration, and invasion. Mechanically, lncBIRC3-OT could guide RELA protein to the stanniocalcin-1 (STC1) promoter, initiate STC1 transcription, and ultimately promote the progression of glioma. Together, these findings suggest that lncBIRC3-OT is an important regulator promoting glioma progression, and may be a promising therapeutic target for glioma.

Sequencing and Bioinformatics analysis of lncRNA/circRNA-miRNA-mRNA in Glioblastoma multiforme.

Evidence suggests that non-coding RNAs have a role in glioblastoma multiforme (GBM), although the regulatory mechanisms controlled by competing endogenous RNAs (ceRNAs) in GBM are still poorly understood and infrequently described. This research extensively analyzed circRNA, lncRNA, miRNA, and mRNA expression changes in GBM patients. RNA-sequencing analyses were conducted to investigate differentially expressed genes (DEGs), lncRNAs (DELs), miRNAs (DEMs), and circRNAs (DECs) in the GBM. In this study, researchers found that GBM patients and healthy controls differed in the presence of 1224 DECs, 1406 DELs, 229 DEMs, and 2740 DEGs. PPI network analysis demonstrated that CEACAM5, CXCL17, FAM83A, TMPRSS4, and GGPRC5A were hub genes and enriched in modules. Then a ceRNA network was constructed with 8 circRNA, 7 lncRNAs, 16 miRNAs, and 17 mRNAs. Overall, the ceRNA interaction axes that were found may prove to be pivotal therapeutic targets for treating GBM.

Correction to: EIF4A3-induced circular RNA MMP9 (circMMP9) acts as a sponge of miR-124 and promotes glioblastoma multiforme cell tumorigenesis.

An amendment to this paper has been published and can be accessed via the original article.

Insulin-like growth factor-1 enhances neuroprotective effects of neural stem cell exosomes after spinal cord injury via an miR-219a-2-3p/YY1 mechanism.

Spinal cord injury (SCI) remains the most common cause of paralysis, and there are no effective therapies for SCI patients. Neural stem cell (NSC)-derived exosomes can attenuate apoptosis and neuroinflammation after traumatic spinal cord injury, but the mechanisms underlying these effects remain unclear. Here, we examined the efficacy of miRNAs isolated from exosomes as treatments for SCI and characterized their mechanisms of action. Furthermore, we evaluated the effects of exosomes formed in the presence of insulin growth factor-1 (IFG-1, IGF-Exo), which promotes neural proliferation and regeneration, as well as normal exosomes (Nor-Exo) and compared control and H2O2-treated groups both invitro and invivo. Using microRNA sequencing and qRT-PCR, we identified miR-219a-2-3p, levels of which were higher in the IGF-Exo than Nor-Exo group and played crucial anti-inflammatory and anti-apoptosis roles. Additional experiments revealed that IGF-Exo inhibits YY1 expression through up-regulation of miR-219a-2-3p. This in turn inhibits the NF-κB pathway, partly inhibiting neuroinflammation and promoting the neuroprotective effects after SCI.

EIF4A3-induced circular RNA MMP9 (circMMP9) acts as a sponge of miR-124 and promotes glioblastoma multiforme cell tumorigenesis.

BACKGROUND: Circular RNAs (circRNAs) have been found to play critical roles in the development and progression of various cancers. However, little is known about the effects of the circular RNA network on glioblastoma multiforme (GBM). METHODS: A microarray was used to screen circRNA expression in GBM. Quantitative real-time PCR was used to detect the expression of circMMP9. GBM cells were transfected with a circMMP9 overexpression vector or siRNA, and cell proliferation, migration and invasion, as well as tumorigenesis in nude mice, were assessed to examine the effect of circMMP9 in GBM. Biotin-coupled miRNA capture, fluorescence in situ hybridization and luciferase reporter assays were conducted to confirm the relationship between circMMP9 and miR-124. RESULTS: In this study, we screened differentially expressed circRNAs and identified circMMP9 in GBM. We found that circMMP9 acted as an oncogene, was upregulated in GBM and promoted the proliferation, migration and invasion abilities of GBM cells. Next, we verified that circMMP9 served as a sponge that directly targeted miR-124; circMMP9 accelerated GBM cell proliferation, migration and invasion by targeting miR-124. Furthermore, we found that cyclin-dependent kinase 4 (CDK4) and aurora kinase A (AURKA) were involved in circMMP9/miR-124 axis-induced GBM tumorigenesis. Finally, we found that eukaryotic initiation factor 4A3 (eIF4A3), which binds to the MMP9 mRNA transcript, induced circMMP9 cyclization and increased circMMP9 expression in GBM. CONCLUSIONS: Our findings indicate that eIF4A3-induced circMMP9 is an important underlying mechanism in GBM cell proliferation, invasion and metastasis through modulation of the miR-124 signaling pathway, which could provide pivotal potential therapeutic targets for the treatment of GBM.

Clinical Benefits of Acupuncture for the Reduction of Hormone Therapy-Related Side Effects in Breast Cancer Patients: A Systematic Review.

IMPORTANCE: Acupuncture can help reduce unpleasant side effects associated with endocrine therapy for breast cancer. Nevertheless, comprehensive evaluation of current evidence from randomized controlled trials(RCTs) is lacking. OBJECTIVE: To estimate the efficacy of acupuncture for the reduction of hormone therapy-related side effects in breast cancer patients. EVIDENCE REVIEW: RCTs of acupuncture in breast cancer patients that examined reductions in hormone therapy-related side effects were retrieved from PubMed, EMBASE, Web of Science, Ovid MEDLINE, and Cochrane Library databases through April 2016. The quality of the included studies was evaluated according to the 5.2 Cochrane Handbook standards, and CONSORT and STRICTA (Revised Standards for Reporting Interventions in Clinical Trials of Acupuncture) statements. INTERVENTION: Interventions included conventional acupuncture treatment compared with no treatment, placebo, or conventional pharmaceutical medication. Major outcome measures were the alleviation of frequency and symptoms and the presence of hormone therapy-related side effects. Findings/Results. A total of 17 RCTs, including a total of 810 breast cancer patients were examined. The methodological quality of the trials was relatively rigorous in terms of randomization, blinding, and sources of bias. Compared with control therapies, the pooled results suggested that acupuncture had moderate effects in improving stiffness. No significant differences were observed in hot flashes, fatigue, pain, gastrointestinal symptoms, Kupperman index, general well-being, physical well-being, tumor necrosis factor (TNF), and interleukin (IL). CONCLUSIONS: Acupuncture therapy appears to be potentially useful in relieving functional stiffness. However, further large-sample trials with evidence-based design are still needed to confirm these findings.

CircNT5E Acts as a Sponge of miR-422a to Promote Glioblastoma Tumorigenesis.

Circular RNA and long noncoding RNA function as efficient miRNA sponges that regulate gene expression in eukaryotes. However, the sponges of functional miRNAs in glioblastoma remain largely unknown. Here, we identify a subset of circRNAs and lncRNAs that are specifically increased in miR-422a-downregulated glioblastoma tissues. We characterized a novel circRNA derived from NT5E, named circNT5E, that is regulated by ADARB2 binding to sites flanking circRNA-forming introns. We hypothesized that circNT5E may serve as a sponge against miR-422a in glioblastoma tumorigenesis. circNT5E controlled multiple pathologic processes, including cell proliferation, migration, and invasion. circNT5E directly bound miR-422a and inhibited miR-422a activity. Furthermore, circNT5E was observed to sponge other miRNAs, exhibiting tumor suppressor-like features in glioblastoma. Taken together, these findings highlight a novel oncogenic function of circRNA in glioblastoma tumorigenesis.Significance: Microarray profiling of circRNA/lncRNA/mRNA in glioblastoma identifies circNT5E as an oncogenic circular RNA and a sponge of miR-422a. Cancer Res; 78(17); 4812-25. ©2018 AACR.

Hypothermia-Modulating Matrix Elasticity of Injured Brain Promoted Neural Lineage Specification of Mesenchymal Stem Cells.

Both chemical and physical microenvironments appear to be important for lineage specification of umbilical cord mesenchymal stem cells (UCMSCs). However, physical factors such as the elastic modulus in traumatic brain injury (TBI) are seldom studied. Intracranial hypertension and cerebral edema after TBI may change the brain's physical microenvironment, which inhibits neural lineage specification of transplanted UCMSCs. The purpose of this study is to investigate the potential regulatory effect of mild hypothermia on the elastic modulus of the injured brain. First, we found that more UCMSCs grown on gels mimicking the elastic modulus of the brain (0.5 kPa) differentiated into neural cells, which were verified with the formation of branched cells and the expression of neural markers. Then, UCMSCs were transplanted into TBI rats, and we observed that mild hypothermia resulted in the differentiation of more neurons and astrocytes from transplanted UCMSCs. To demonstrate that more neural specification of UCMSCs was due to the regulation of the elastic modulus, we monitored intracranial pressure and cerebral edema. The results showed that mild hypothermia significantly reduced intracranial pressure and brain water content, indicating modulation of the elastic modulus by mild hypothermia. An examination with atomic force microscopy (AFM) in a cell injury model in vitro further verified hypothermia-regulated elastic modulus. In this study, we found a novel role of mild hypothermia in modulating the elastic modulus of the injured brain, resulting in the promotion of neural lineage specification of UCMSCs, which suggested that the combination of mild hypothermia had more advantages in cell-based therapy after TBI.

Establishment of an ideal time window model in hypothermic-targeted temperature management after traumatic brain injury in rats.

Although hypothermic-targeted temperature management (HTTM) holds great potential for the treatment of traumatic brain injury (TBI), translation of the efficacy of hypothermia from animal models to TBI patientshas no entire consistency. This study aimed to find an ideal time window model in experimental rats which was more in accordance with clinical practice through the delayed HTTM intervention. Sprague-Dawley rats were subjected to unilateral cortical contusion injury and received therapeutic hypothermia at 15mins, 2 h, 4 h respectively after TBI. The neurological function was evaluated with the modified neurological severity score and Morris water maze test. The brain edema and morphological changes were measured with the water content and H&E staining. Brain sections were immunostained with antibodies against DCX (a neuroblast marker) and GFAP (an astrocyte marker). The apoptosis levels in the ipsilateral hippocampi and cortex were examined with antibodies against the apoptotic proteins Bcl-2, Bax, and cleaved caspase-3 by the immunofluorescence and western blotting. The results indicated that each hypothermia therapy group could improve neurobehavioral and cognitive function, alleviate brain edema and reduce inflammation. Furthermore, we observed that therapeutic hypothermia increased DCX expression, decreased GFAP expression, upregulated Bcl-2 expression and downregulated Bax and cleaved Caspase-3 expression. The above results suggested that HTTM at 2h or even at 4h post-injury revealed beneficial brain protection similarly, despite the best effect at 15min post-injury. These findings may provide relatively ideal time window models, further making the following experimental results more credible and persuasive.

MiR-422a acts as a tumor suppressor in glioblastoma by targeting PIK3CA.

Although surgical treatment, chemotherapy, and radiotherapy have improved the overall survival rate in glioblastoma multiforme (GBM), further intensive research of GBM's molecular mechanism is still needed. In this study, we observed that miR-422a was downregulated in GBM tissues and cell lines by quantitative real-time polymerase chain reaction (PCR) and primer extension assay. Overexpression of miR-422a significantly reduced the cell proliferation, migration, and invasion of GBM cells. Functional study indicated that miR-422a inhibited cell proliferation, invasion, and migration by targeting PIK3CA, an important member of PI3K/Akt signal pathway. These results demonstrate that the miR-422a/PIK3CA axis may constitute a potential target for GBM therapy.

[The effect of inhibition of hyperplasia on spinal cord reactive astrocytes by mild hypothermia].

OBJECTIVE: To observe changes in the morphology and activity of astrocytes in spinal cord at different temperatures after scratches treatment, and to investigate the effect of mild hypothermia on hyperplasia of reactive astrocytes. METHODS: Spinal cord astrocytes were cultured from the neonatal SD rat, and reactive astrocytes were prepared by scratches treatment. Mild hypothermia choose 33℃, cell cul-ture 48 h. Cells were divided into control group、scratches group、mild hypothermia group and scratch+mild hypothermia group. Cell mor-phology of each group were observed in 0 h、6 h、12 h、24 h、48 h、3 d、5 d、7 d. Nestin positive rate were detected by using immunofluorescence staining method. Cell activity were observed by methyl thiazolyl tetrazolium salt (MTT) assay. The degree of apoptosis was observed by using PI staining method. RESULTS: Compared with control group and mild hypothermia group, cell body in both scratches group and scratch+mild hypothermia group was hypertrophy, the protrusion around was increased and extend, the cytoplasm was enrich, and the growth rate was signif-icantly increased. Compared with scratches group, scratch+mild hypothermia group cells grew slowly, the protrusion around was decreased, and cells of the scratched area ingrowth significantly slowly. Nestin and PI positive rate of cells were also significantly lower. All the results had statistically significant differences (P<0.01). CONCLUSIONS: After scratch injury, astrocytes were activated to be reactive astrocytes and hyper-plasia. Mild hypothermia significantly inhibited spinal cord reactive astrocytes overgrowth and restrain astrocytes apoptosis.

The PTTG1-targeting miRNAs miR-329, miR-300, miR-381, and miR-655 inhibit pituitary tumor cell tumorigenesis and are involved in a p53/PTTG1 regulation feedback loop.

Deregulation of the pituitary tumor transforming gene (PTTG1), a newly discovered oncogene, is a hallmark of various malignancies, including pituitary tumors. However, the mechanisms regulating PTTG1 expression are still needed to be explored. MicroRNAs (miRNAs) are a novel class of small RNA molecules that act as posttranscriptional regulators of gene expression and can play a significant role in tumor development. Here, we identified a series of miRNAs, namely, miR-329, miR-300, miR-381 and miR-655, which could target PTTG1 messenger RNA and inhibit its expression. Interestingly, all four miRNAs significantly that are downregulated in pituitary tumors were mapped to the 14q32.31 locus, which acts as a tumor suppressor in several cancers. Functional studies show that the PTTG1-targeting miRNAs inhibit proliferation, migration and invasion but induce apoptosis in GH3 and MMQ cells. Furthermore, overexpression of a PTTG1 expression vector lacking the 3'UTR partially reverses the tumor suppressive effects of these miRNAs. Next, we identified the promoter region of PTTG1-targeting miRNAs with binding sites for p53. In our hands, p53 transcriptionally activated the expression of these miRNAs in pituitary tumor cells. Finally, we found that PTTG1 could inhibit p53 transcriptional activity to the four miRNAs. These data indicate the existence of a feedback loop between PTTG1 targeting miRNAs, PTTG1 and p53 that promotes pituitary tumorigenesis. Together, these findings suggest that these PTTG1-targeting miRNAs are important players in the regulation of pituitary tumorigenesis and that these miRNAs may serve as valuable therapeutic targets for cancer treatment.

Tai chi chuan exercise for patients with breast cancer: a systematic review and meta-analysis.

Objective. Tai Chi Chuan (TCC) is a form of aerobic exercise that may be an effective therapy for improving psychosomatic capacity among breast cancer survivors. This meta-analysis analyzed the available randomized controlled trials (RCTs) on the effects of TCC in relieving treatment-related side effects and quality of life in women with breast cancer. Methods. RCTs were searched in PubMed, Embase, Web of Science, and Cochrane Library through April 2014. Data were analyzed on pathology (pain, interleukin-6, and insulin-like growth factor 1), physical capacity (handgrip, limb physical fitness, and BMI), and well-being (physical, social, emotional, and general quality of life). Results. Nine RCTs, including a total of 322 breast cancer patients, were examined. Compared with control therapies, the pooled results suggested that TCC showed significant effects in improving handgrip dynamometer strength, limb elbow flexion (elbow extension, abduction, and horizontal adduction). No significant differences were observed in pain, interleukin-6, insulin-like growth factor, BMI, physical well-being, social or emotional well-being, or general health-related quality of life. Conclusion. The short-term effects of TCC may have potential benefits in upper limb functional mobility in patients with breast cancer. Additional randomized controlled trials with longer follow-up are needed to provide more reliable evidence.

MicroRNA-873 (miRNA-873) inhibits glioblastoma tumorigenesis and metastasis by suppressing the expression of IGF2BP1.

Glioblastoma multiforme (GBM) is known as a highly malignant brain tumor with a poor prognosis, despite intensive research and clinical efforts. In this study, we observed that microRNA-873 (miR-873) was expressed at low levels in GBM and that the overexpression of miR-873 dramatically reduced the cell proliferation, migration, and invasion of GBM cells. Our further investigations of the inhibition mechanism indicated that miR-873 negatively affected the carcinogenesis and metastasis of GBM by down-regulating the expression of IGF2BP1, which stabilizes the mRNA transcripts of its target genes. These results demonstrate that miR-873 may constitute a potential target for GBM therapy.

Baicalin attenuates alzheimer-like pathological changes and memory deficits induced by amyloid ß1-42 protein.

Baicalin is one bioactive flavone with anti-inflammatory and neuroprotective activities. The neuroprotective effects of baicalin on pathological changes and behavioral deficits were explored in a mouse model of amyloid ß (Aß)(1-42) protein-induced Alzheimer's disease (AD). Mice received a bilateral injection of Aß(1-42) protein into the hippocampus, then they were treated with baicalin (30, 50 and 100 mg/kg body weight, orally) or Tween 80. The therapeutic effects of baicalin were monitored by Morris water maze trial and probe test. Then mice were sacrificed for immunohistochemistry and western blot analysis. After a relatively short-term treatment of 14 days, 100 mg/kg of baicalin significantly ameliorated memory impairment in the Morris water maze test and probe test, and also attenuated glial cell activations and increase of TNF-α and IL-6 expressions induced by Aß(1-42) protein. These results suggest that baicalin ameliorated Aß(1-42) protein-related pathology and cognitive dysfunction via its anti-neuroinflammatory activity, and may be a potential candidate for the treatment of AD.

USF-1 inhibition protects against oxygen-and-glucose-deprivation-induced apoptosis via the downregulation of miR-132 in HepG2 cells.

Upstream stimulatory factor 1 (USF-1) is an important transcription factor that participates in glucose metabolism and tumorigenesis. The aim of the current study was to explore the regulatory mechanism of USF-1 in HepG2 cells exposed to oxygen and glucose deprivation (OGD). After the establishment of the OGD model in HepG2 cells, we determined that the cells treated with OGD exhibited a high apoptotic rate and that the introduction of siRNA against USF-1 protected the cells from OGD-induced apoptosis. The miRNA microarray results demonstrated that a set of miRNAs were deregulated in the cells transfected with USF-1 siRNA, and the set of downregulated miRNAs included a novel miRNA, miR-132. Further analyses indicated that miR-132 overexpression inhibits the protective roles of USF-1 siRNA in OGD-induced apoptosis. We also identified several binding sites for USF-1 in the miR-132 promoter. The silencing of USF-1 resulted in a reduction in miR-132 expression, and USF-1 overexpression increased the expression of this miRNA. Our study indicated that the silencing of USF-1 plays protective roles in OGD-induced apoptosis through the downregulation of miR-132, which indicates that the silencing of USF-1 may be a therapeutic strategy for the promotion of cancer cell survival under OGD conditions.

[Protective effect of oxiracetam on traumatic brain injury in rats].

OBJECTIVE: To study the role of oxiracetam on traumatic brain injury in rats. METHODS: Thirty Wistar rats were randomly divided into 3 groups: sham operation group, model group and treatment group. Feeney method were used to establish traumatic brain injury (TBI) model in rats in model and treatment group, and rats in sham group were only broached without hydraumatic fitted. Rats in treatment group were successive administration for 21 days with oxiracetam (100 mg/kg, ig). Neurologic impairment scores were undertook after operation of 1 d, 4 d, 7 d, 14 d and 21 d, and Morris water maze test were proceeded during 15 to 19 days after operation. Average escape latency, searching time in target quadrant and number of crossing target platform in rats were recorded. RESULTS: Neurologic impairment scores of rats in treatment group were significantly less than those of model group after operation of 7, 14 and 21 d (P < 0.05). Average escape latency of model group were significantly higher than those of sham operation group and treatment group (P < 0.05, P < 0.01). Searching time in target quadrant and number of crossing target platform of model group were lower than those of sham operation and treatment group (P < 0.05)). CONCLUSION: Oxiracetam could decrease neural injury and increase ability of learning, memory and space cognition in traumatic brain injury rats.