miR-34c inhibits PDGF-BB-induced HAVSMCs phenotypic transformation and proliferation via PDGFR-ß/SIRT1 pathway.

The purpose of this study was to explore the effect of miR-34c on PDGF-BB-induced HAVSMCs phenotypic transformation and proliferation via PDGFR-ß/SIRT1 pathway, so as to find a new method for early diagnosis and treatment of cardiovascular disease. HA-VSMCs were treated with platelet-derived growth factor-BB (PDGF-BB) at 0 h, 12 h, 24 h, 48 h or 36 h to explore the optimal time for phenotypic transformation of VSMCs. And then, PDGF-BB-induced HA-VSMCs were transfected with miR-34c mimics/mimics NC and pcDNA3.1-PDGFR-ß/pcDNA3.1-NC to observe cell biological behaviour. CCK8 was used to detect cell proliferation activity. Transwell chamber assay was used to detect cell invasion. Early apoptosis was analyzed by flow cytometry. The expression of α-SMA and Smemb was detected by immunofluorescence staining. The expressions of PDGFR-ß, IRF9, Acetyl-NF-κB/p65, Acetyl-p53 and CyclinD1 were analyzed by Western blot analysis. The expression of miR-34a, miR-34b and miR-34c was detected by RT-PCR, and the targeting relationship between miR-34c and PDGFR-ß was detected by luciferase reporting assay. The results indicated the proliferation and migration of PDGF-BB-induced HA-VSMCs significantly increased, and apoptosis significantly decreased. Besides, α-SMA decreased significantly, while Smemb increased significantly. Furthermore, expressions of PDGFR-ß, IRF9, Acetyl-NF-κB/p65, Acetyl-p53 and CyclinD1 increased significantly, and SIRT1 decreased significantly. Experimental results showed that, miR-34c mimics significantly inhibited cell proliferation and migration, and promoted cell apoptosis, and miR-34c inhibitor had the opposite effects. MiR-34c mimics significantly increased α-SMA expression and decreased Smemb expression, while the opposite effects were reflected after transfection with miR-34c inhibitor. Moreover, miR-34c mimics significantly decreased the expressions of PDGFR-ß, IRF9, Acetyl-NF-κB/p65, Acetyl-p53 and CyclinD1, and significantly increased the expression of SIRT1, while miR-34c inhibitor had the opposite effects. Luciferase assay confirmed that PDGFR-ß was a potential target of miR-34c. Subsequently, PDGF-BB-induced HA-VSMCs were co-transfected with miR-34c mimics and pcDNA3.1-PDGFR-ß. The results indicated that PDGFR-ß reversed the biological function of miR-34c mimic. The results revealed the potential application value of miR-34c as a marker molecule of phenotypic transformation, providing a potential target for improving phenotypic transformation.

Oral health in patients with dementia: A meta-analysis of comparative and observational studies.

OBJECTIVE: Poor oral health is common in dementia, but findings of epidemiological studies have been inconsistent. This meta-analysis examined oral health in patients with dementia diagnosed according to standardized diagnostic criteria. METHODS: Six international databases (PubMed, EMBASE, PsycINFO, Medline, Cochrane Library, and Web of Science) were searched from their commencement date until 8 November 2018. Oral health was measured by the Remaining Teeth (RT) and Decayed, Missing, and Filled Teeth (DMFT) Index. The mean differences (MD) and 95% confidence intervals (CI) of DMFT Index total and component scores were calculated using a random-effect model. RESULTS: Twenty-four studies were included for analyses. The pooled DMFT Index was 23.48 (95% CI: 22.34, 24.62), while the pooled score for each component was 2.38 (95% CI: 1.56, 3.20) in decayed teeth (DT), 18.39 (95% CI: 15.92, 20.87) in missing teeth (MT), 2.29 (95% CI: 0.62, 3.95) in filled teeth (FT), and 11.59 (95% CI: 9.14, 14.05) in RT. Compared to controls, people with dementia had significantly a higher DMFT Index total score (MD = 3.80, 95% CI: 2.21, 5.39, p < 0.00,001), and significantly lower number of RT (MD = -3.15, 95% CI: -4.23, -2.06, p < 0.00,001). Subgroup analyses revealed that higher DMFT Index score was significantly associated with year of survey (>2010), study design (case-control study), percentage of females (≤54.3), and the Mini Mental State Examination score (≤18.2). Higher MT score was significantly associated with study design (cross-sectional study), and lower FT score was significantly associated with year of survey (>2010). CONCLUSIONS: Oral health was significantly poorer in people with dementia compared with controls. Regular screening and effective treatment should be implemented for this population.

The Prevalence of Burnout and its Associations with Demographic Correlates and Quality of Life among Psychiatric Nurses in China.

This study examined the prevalence of burnout and its association with quality of life (QOL) among psychiatric nurses in China.Ten psychiatric hospitals were included. Burnout and QOL were measured using standardized instruments. Altogether, 1449 nurses completed the assessment. The mean scores of emotional exhaustion (EE), depersonalization (DP) and personal accomplishment (PA) were 11.87 (SD = 6.72), 6.98 (SD = 5.71) and 22.06 (SD = 8.67), respectively. Of the participants, 59.8% (95% CI: 57-62%) experienced burnout; with 23.3% (95% CI: 21-25%) in EE, 14.6% (95% CI: 13-16%) in DP and 45.1% (95% CI: 43-48%) in PA. Psychiatric nurses who reported burnout had lower QOL in social (F (1, 1448) = 86.20, P < 0.001), physical (F (1, 1448) = 170.46, P < 0.001), psychological (F (1, 1448) = 205.63, P < 0.001), and environmental (F (1, 1448) = 120.24, P < 0.001) domains. Multiple logistic regression analysis revealed that alcohol users (P = 0.04; OR = 1.29, 95%CI: 1.01-1.64 in model 1 and P = 0.03; OR = 1.32, 95%CI: 1.04-1.69 in model 2) were significantly more susceptible to burnout, while senior nurses (P = 0.007; OR = 0.70, 95%CI: 0.53-0.91) and nurses with longer work experience (P = 0.02; OR = 0.70, 95%CI: 0.53-0.91) were less likely to develop burnout. Burnout is common in psychiatric nurses in China. In light of its negative impact on health and QOL, there is an urgent need for regular screening as well as effective preventive measures and interventions to reduce burnout within this at-risk occupational group.

Prevalence of Poor Sleep Quality in Nursing Staff: A Meta-Analysis of Observational Studies.

Objective: Poor sleep quality is common in nursing staff. This meta-analysis aimed to examine the pooled prevalence of poor sleep quality in nursing staff. Methods: A systematic search in PubMed, EMBASE, PsycINFO, and Web of Science databases was performed. Studies that reported sleep quality measured by the Pittsburgh Sleep Quality Index (PSQI) were synthesized using a random-effects model. Results: Fifty-three studies were analyzed. The pooled prevalence of poor sleep quality was 61.0% (95% CI: 55.8-66.1%). The pooled total PSQI score was 7.13 ± 0.18 (95% CI: 6.78-7.50). The pooled component scores were 1.47 ± 0.20 (95% CI of mean score: 1.08-1.85) in sleep latency, 0.91 ± 0.15 (95% CI of mean score: 0.61-1.21) in sleep duration, 1.59 ± 0.13 (95% CI of mean score: 1.35-1.84) in overall sleep disturbances, 0.33 ± 0.18 (95% CI of mean score: 0-0.67) in sleeping medication, 1.21 ± 1.20 (95% CI of mean score: 0.83-1.60) in daytime dysfunction, 1.39 ± 0.14 (95% CI of mean score: 1.11-1.67) in subjective sleep quality, and 0.66 ± 0.11 (95% CI of mean score: 0.44-0.87) in habitual sleep efficiency. Subgroup and meta-regression analyses found that PSQI cutoff values, mean age, body mass index (BMI), sample size, study quality, and work experience moderated the prevalence of poor sleep quality. Conclusions: Poor sleep quality appears to be common in nursing staff. Considering its negative impact on health, effective measures should be taken to improve poor sleep quality in this population. Longitudinal studies should be conducted to examine the contributing factors of nurses' poor sleep quality.

Prevalence of burnout in mental health nurses in China: A meta-analysis of observational studies.

OBJECTIVE: Burnout is common in mental health nurses because of work-related stress. Burnout has a negative impact on nurses' health and work performance. The prevalence of high burnout in mental health nurses has been inconclusive across studies. This meta-analysis aimed to estimate the pooled prevalence of high burnout in mental health nurses in China. METHODS: Electronic databases (PubMed, EMBASE, PsycINFO, Web of Science, CNKI, WanFang and SinoMed) were independently and systematically searched from their commencement date up to 14 May 2018. Studies that reported the prevalence of any of the 3 burnout dimensions (high Emotional Exhaustion (EE), Depersonalization (DP), and low Personal Accomplishment (PA)) as measured by the Maslach Burnout Inventory (MBI) were included and analyzed using the random-effects model. RESULTS: A total of 19 studies were included in this meta-analysis. The pooled prevalence of high EE was 28.1% (95% CI: 20.4-35.8%), DP was 25.4% (18.1-32.6%) and low PA was 39.7% (28.3-51.1%). Subgroup analyses found that short working experience, use of MBI-Human Services Survey (HSS), and younger age had moderating effects on prevalence of high burnout. CONCLUSIONS: Burnout is common in mental health nurses in China. Considering its negative impact on health and work performance, regular screening, preventive measures and effective interventions should be implemented.

[Expression of Translocator Protein in Early Brain Injury After Subarachnoid Hemorrhage in Mice].

OBJECTIVE: To evaluate the expression of translocator protein (TSPO) in brain tissue within 72 h after subarachnoid hemorrhage (SAH) in mice. METHODS: Forty-four C57BL/6J mice were randomly divided into two groups, 17 in the Sham group and 27 in the SAH group. SAH mice model was performed by endovascular perforation as previously described with slight modifications. Sham group mice were performed by the same method but without piercing the blood vessels. Before and 6 h, 24 h, 48 h, 72 h after modeling, the two groups were scored with modified Garcia score for neurological function. At 6 h, 24 h, 48 h, 72 h after modeling, the mice were sacrificed. Sham group mice were sacrificed at 24 h after modeling. The expression of TSPO in brain tissue was evaluated by Western blot, positron emission tomography-computed tomography (PET-CT) and immunofluorescence staining. Fluorescent double staining was used to assess the relationship of TSPO and microglia. RESULTS: The neurological function scores of the SAH group mice decreased with time and then increased. The expression of TSPO in the brain tissue increased first and then decreased with time, and there was a negative correlation between them (r=-0.615 6, P < 0.01). PET-CT showed that the tracer intake of mouse brain tissue after SAH was higher than that of Sham group, and the difference was statistically significant (P < 0.05). Immunofluorescence staining showed that TSPO increased in the parietal cortex and basal cortex of the SAH group. And fluorescent double staining suggested that TSPO colocalized with Iba-1 which was a specific marker of microglia. CONCLUSIONS: In the early brain injury after SAH, the expression of TSPO in brain is widely increased, and the expression level increases first and then decreases. TSPO could participate in the activation of microglia and regulate the occurrence and development of brain injury after SAH.

The effect of miR-21 on SWOZ2 glioma cells and its biological mechanism.

PURPOSE: To investigate the role of micro RNA-21 (miR- 21) in human glioma cells and its potential disease-causing mechanism. METHODS: jetPRIME was used to transfect the miR-21- mimics and its negative control into SWOZ2 human glioma cells. Real-time fluorescence quantitative PCR assay was used to measure differences in the expression of miR-21 in SWOZ2 glioma cells, SWOZ2-miR-21-mimics cells, and control cells. Cell counting kit-8 assay was used to measure the activity of SWOZ2 glioma cells and SWOZ2-miR-21- mimics cells, and Western blot was used to measure PTEN, p-Akt, and P-glycoprotein (P-gp). RESULTS: The level of miR-21 in SWOZ2-miR-21-mimics cells was significantly higher than in SWOZ2 cells and the negative control group. Compared with SWOZ2 cells, the expression of PTEN protein in SWOZ2-miR-21 cells decreased significantly, and the expression of p-Akt and P-gp protein were significantly increased. Compared with SWOZ2 cells and the negative control group, the proliferation rate of SWOZ2-miR-21-mimics cells was significantly increased (p<0.05).The rate of apoptosis as determined by flow cytometry showed that the number of apoptotic SWOZ2-miR-21- mimics cells decreased significantly (p<0.05). Transwell assay found that the invasive ability of SWOZ2-miR-21-mimics cells increased significantly, suggesting that miR-21 can mediate the biological functions of SWOZ2 cells by inhibiting the expression of PTEN. CONCLUSION: miR-21 may regulate the proliferation and apoptosis of human glioma cells by downregulating the expression of the PTEN protein, and miR-21 may represent a potential therapeutic target for the treatment of glioma.

Effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is correlated with obesity, but specific therapeutic interventions are lacking. Adiponectin is an adipokine with anti-inflammatory activity and is considered a hepatic protector. We aimed to investigate effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD. MATERIALS AND METHODS: Sixteen male SD rats were fed a high-fat diet for 8 weeks (HFD1 group) or 16 weeks (HFD2 group) to induce NAFLD, and these rats were compared with rats on a normal diet for 8 weeks (NC1 group) or 16 weeks (NC2 group). Another group of 8 rats was fed an HFD for 8 weeks and then switched to a low-fat diet (DIET group) until the 16th week. The expression of hepatic adiponectin and its receptors was detected by western blotting, immunohistochemistry and RT-qPCR. RESULTS: The NAFLD activity score (NAS) in the HFD groups increased from 3.2 ± 0.45 (8th week) to 6.2 ± 0.84 (16th week) (P < 0.001), reflecting the progression in the NAFLD histology. In contrast to the HFD2 group, the low-fat diet ameliorated the steatosis, ballooning degeneration and inflammation. Dietary intervention augmented the expression of adiponectin and its receptors, which was down-regulated in the HFD2 group. CONCLUSIONS: The NAFLD rat model was successfully developed by feeding the animals a high-fat diet. Adiponectin may play a role in the pathogenesis of NAFLD, especially in the progression from steatosis to NASH. The low-fat diet alleviated the histological lesions associated with NAFLD by up-regulating the expression of adiponectin and its receptors.

[The Role of Cancer-associated Fibroblasts in Invasive Behavior of Pituitary Adenoma].

OBJECTIVE: To determine the role of cancer associated fibroblasts (CAFs) in the invasive behavior of pituitary adenoma. METHODS: Pituitary adenoma tissues were divided into invasive group (IPA) and non-invasive group (nIPA) according to pre-operative MRI and observations during surgery. Those tissues were cultured and CAFs were identified through a smooth muscle actin (α-SMA). The migratory and invasive ability of CAFs was tested with transwell migration and invasion assay. The expressions of α-SMA and matrix metalloproteinase (MMP)-9 from CAFs were determined by immunocytochemistry and Western blot. RESULTS: All cultured CAFs expressed α-SMA. No significant difference in migratory ability of CAFs was found between the IPA and nIPA tissues; however, CAFs from the IPA tissues had stronger invasive ability than those from the nIPA tissues (P= 0. 010). Higher levels of MMP-9 expression were found in group IPA as compared with nIPA (P=0. 025). No significant difference in the expression of α-SMA was found between the two groups. CONCLUSION: CAFs may promote invasive behavior by secreting more MMP-9, which may play a part in the invasive behavior of pituitary adenomas.

ODF3B affects the proliferation and apoptosis of glioma via the JAK/STAT pathway.

The pathogenesis of glioma has remained unclear. In this study, it was found that high expression of the outer dense fibers of sperm tail 3B (ODF3B) in gliomas was positively correlated with the grade of glioma. The higher the grade, the worse the prognosis. ODF3B is closely related to the growth and apoptosis of glioma. In terms of mechanism, ODF3B was found to affect the proliferation and apoptosis of glioma through the JAK1 and JAK2/STAT3 pathways. ODF3B was also found to affect the growth and apoptosis of glioma in vivo. We conclude that ODF3B affects glioma proliferation and apoptosis via the JAK/STAT pathway and is a potential therapeutic target.

[Expression pattern of inflammatory cytokines at various inflammatory levels of adamantinomatous craniopharyngioma].

OBJECTIVE: To explore the expression pattern of inflammatory cytokines at various inflammatory levels of adamantinomatous craniopharyngioma by cytokine antibody array. METHODS: The inflammatory levels of adamantinomatous craniopharyngioma were evaluated on the basis of the number of inflammatory cells at the interface of tumor and normal tissues. And the expression of inflammatory cytokines was examined at various inflammatory levels of adamantinomatous craniopharyngioma by inflammatory cytokine antibody array and the results were verified by Western blot. RESULTS: Compared with the mild inflammatory group, the levels of inflammatory cytokines of severe inflammatory group markedly increased, including pro-inflammatory cytokines, chemokines and cytokine receptors. CONCLUSION: Antibody array demonstrates a significant change in cytokine profiles in adamantinomatous craniopharyngioma with severe inflammation, as compared with those with mild inflammation.

Protein Disulfide Isomerase A2 Is Correlated with Immune Infiltrates and Is a Novel Prognostic Biomarker in Glioma Patients.

OBJECTIVE: Protein disulfide isomerase A2 (PDIA2), a member of the protein disulfide isomerase family, plays a key role in the folding of nascent proteins in the endoplasmic reticulum by forming disulfide bonds, together with enzymes such as thiol isomerase, oxidase, and reductase. This study investigated the clinical significance and potential functions of PDIA2 in glioma. METHODS: The expression of PDIA2 in gliomas was explored using The Cancer Genome Atlas and Gene Expression Omnibus databases. We analyzed the clinical characteristics of glioma patients and the prognostic and diagnostic value of PDIA2 expression. Kaplan-Meier and Cox regression analyses were used to examine the effect of PDIA2 expression on overall survival, progression-free interval, and disease-specific survival. Furthermore, we performed Gene Set Enrichment Analysis and immune infiltration analysis to investigate the functions of PDIA2. PDIA2 mRNA and protein expression was evaluated in cell lines and glioma tissues. RESULTS: PDIA2 was expressed at low levels in glioma patients. Kaplan-Meier survival analysis showed that glioma patients with low PDIA2 levels had a worse prognosis than those with high PDIA2 levels. Receiver operating characteristic curve analysis indicated the diagnostic and prognostic ability of PDIA2 (area under the curve = 0.918). Pathways associated with PD1, PI3K/AKT, cancer immunotherapy via PD1 blockade, Fceri-mediated NF-kB activation, FOXM1, and DNA repair were enriched in glioma patients with low levels of PDIA2. PDIA2 expression levels were negatively correlated with immune cell infiltrate levels. CONCLUSION: PDIA2 levels are significantly downregulated in glioma. PDIA2 expression may be a potential biomarker for the diagnosis and prognosis of glioma patients.

HOXA11-AS aggravates microglia-induced neuroinflammation after traumatic brain injury.

Long noncoding RNAs (lncRNAs) participate in many pathophysiological processes after traumatic brain injury by mediating neuroinflammation and apoptosis. Homeobox A11 antisense RNA (HOXA11-AS) is a member of the lncRNA family that has been reported to participate in many inflammatory reactions; however, its role in traumatic brain injury remains unclear. In this study, we established rat models of traumatic brain injury using a weight-drop hitting device and injected LV-HOXA11-AS into the right lateral ventricle 2 weeks before modeling. The results revealed that overexpression of HOXA11-AS aggravated neurological deficits in traumatic brain injury rats, increased brain edema and apoptosis, promoted the secretion of proinflammatory factors interleukin-1ß, interleukin-6, and tumor necrosis factor α, and promoted the activation of astrocytes and microglia. Microglia were treated with 100 ng/mL lipopolysaccharide for 24 hours to establish in vitro cell models, and then transfected with pcDNA-HOXA11-AS, miR-124-3p mimic, or sh-MDK. The results revealed that HOXA11-AS inhibited miR-124-3p expression and boosted MDK expression and TLR4-nuclear factor-κB pathway activation. Furthermore, lipopolysaccharide enhanced potent microglia-induced inflammatory responses in astrocytes. Forced overexpression of miR-124-3p or downregulating MDK repressed microglial activation and the inflammatory response of astrocytes. However, the miR-124-3p-mediated anti-inflammatory effects were reversed by HOXA11-AS. These findings suggest that HOXA11-AS can aggravate neuroinflammation after traumatic brain injury by modulating the miR-124-3p-MDK axis. This study was approved by the Animal Protection and Use Committee of Southwest Medical University (approval No. SMU-2019-042) on February 4, 2019.

Malignant Solitary Fibrous Tumor of the Right Cerebellum: A Case Report.

Solitary fibrous tumor is a very rare mesenchymal tumor that occurs mostly in the pleura, and there are few reported cases of a presence in the central nervous system, particularly in the cerebellum. In 2016, the WHO classified solitary fibrous tumors into grade I. In this article, we present a case of malignant solitary fibrous tumor recurring 8 years after surgery in a 63-year-old male. Magnetic resonance imaging showed low to intermediate mixed signal intensity on T1W1. Immunohistochemical staining positivity for Vimentin, CD99, CD34 and Bcl-2, it is consistent with the immunohistochemical characteristics of solitary fibrous tumor. We resected the patient's tumor, and the patient was followed up for 3 months with no signs of recurrence. Solitary fibrous tumors are very rare in the central nervous system. Immunohistochemical staining positivity for CD34 and Bcl-2 is strongly expressed in most solitary fibrous tumor. Surgical resection is the preferred treatment. Due to the small number of cases, the biological behavior and prognosis of this tumor need to be further explored.

Rosiglitazone alleviates lipopolysaccharide-induced inflammation in RAW264.7 cells via inhibition of NF-κB and in a PPARγ-dependent manner.

Rosiglitazone is a synthetic peroxisome proliferator-activated receptor (PPAR)γ agonist widely used for the treatment of type 2 diabetes. Recent studies have demonstrated that rosiglitazone displays anti-inflammatory effects. The present study aimed to investigate whether rosiglitazone alleviates decreases in RAW264.7 cell viability resulting from lipopolysaccharide (LPS)-induced inflammation, as well as exploring the underlying mechanism. A macrophage inflammatory injury model was established by treating RAW264.7 cells with 100 ng/ml LPS. Cells were divided into LPS and rosiglitazone groups with different concentrations. Cell viability was assessed by performing an MTT assay. The expression of inflammatory cytokines was detected by conducting enzyme-linked immunosorbent assays and reverse transcription-quantitative PCR. Nitric oxidesecretion was assessed using the Griess reagent system. The expression levels of key nuclear factor-κB pathway-associated proteins were detected via western blotting. Rosiglitazone alleviated LPS-induced decrease in RAW264.7 cell viability and inhibited inflammatory cytokine expression in a concentration-dependent manner. Rosiglitazone significantly inhibited LPS-induced upregulation of p65 phosphorylation levels and downregulated IκBα expression levels. However, rosiglitazone-mediated inhibitory effects were reversed by PPARγ knockdown. The results of the present study demonstrated that rosiglitazone significantly inhibited LPS-induced inflammatory responses in RAW264.7 macrophage cells, which was dependent on PPARγ activation and NF-κB suppression.

Extracranial multiorgan metastasis from primary glioblastoma: A case report.

BACKGROUND: Glioblastoma has a high degree of malignancy and poor prognosis. It is common to have in situ recurrence and intracranial metastasis, while extracranial metastasis is rare, and extracranial multiorgan metastasis is extremely rare. We report a case of glioblastoma with extracranial multiorgan metastasis, which will strengthen clinicians' attention to the extracranial metastasis of glioblastoma and its treatment. CASE SUMMARY: A male patient visited our hospital for treatment of dizziness and headache. Magnetic resonance imaging of the brain revealed a space-occupying lesion in the right temporoparietal occipital region. Chest computed tomography and abdominal ultrasound were normal, and no space-occupying lesions were observed in other organs of the body. The patient underwent surgery and diagnosed with glioblastoma. Postoperative concurrent radiotherapy and chemotherapy were completed. During the follow-up, the tumor was found to have metastasized to the scalp and neck, and a second tumor resection was performed. Postoperative follow-up revealed extracranial metastases to multiple extracranial organs including skull, scalp, ribs, spine, liver and lung. His family members refused further treatment, and requested only symptomatic treatment such as pain relief, and the patient died of systemic multiple organ failure. Survival time from diagnosis to death was 13 mo and from extracranial metastasis to death was 6 mo. CONCLUSION: Glioblastoma extracranial metastasis is extremely rare, clinicians should always pay attention to its existence. The mechanism of glioblastoma extracranial metastasis is still unclear, and genetic and molecular studies are required.

A Hybrid Glioma Tumor Cell Lysate Immunotherapy Vaccine Demonstrates Good Clinical Efficacy in the Rat Model.

BACKGROUND: Conventional immunotherapy for glioma is not only expensive but also demonstrates less-than-desired clinical efficacy. In this study, we evaluated the immunotherapeutic efficacy of a tumor cell lysate-based hybrid glioma vaccine developed using a molecular-based approach. METHODS: First, the ability of the autologous (9L-cell lysate) and allogeneic (C6-cell lysate) vaccines against glioma, individually and in combination, to activate Fischer344 rat dendritic cells (DCs) was determined. Next, the activated DCs were co-cultured with T lymphocytes and screened for the optimal DC-to-T-cell ratio. The in vitro efficacy of the DC/T-cell vaccine formulations subjected to different immunogen treatments and co-cultured with glioma cells was evaluated based on glioma cell viability and monocyte chemoattractant protein (MCP)-2 and interferon (IFN)-γ secretion. Subsequently, the efficacy of the 9L + C6 hybrid vaccine was evaluated in 32 glioma rat models, randomly allocated to the following five treatment groups: blank control, tumor, vaccine treatment, thymosin treatment, and vaccine + thymosin treatment (combined treatment). Changes in survival duration, intracranial tumor volume, peripheral blood immune-cell (CD4+ T, CD8+ T, and natural killer [NK] cell) count, and serum cytokine (interleukin [IL]-2, IL-10) levels were assessed in these groups. RESULTS: The hybrid vaccine demonstrated the highest glioma cell apoptosis and the lowest cell viability and promoted MCP-2 and IFN-γ secretion in vitro. The vaccine treatment and combined treatment groups demonstrated longer survival duration, lower intracranial tumor volume, and higher immune cell glioma tissue infiltration and IL-2 secretion than the untreated tumor group, indicating the vaccine's good in vivo efficacy. Thymosin treatment had minimal effect in enhancing anti-glioma immunity. CONCLUSION: We demonstrated the feasibility of combining autologous and allogeneic tumor cell lysates to stimulate specific host cell immune response against glioma cells. The good clinical efficacy of our developed glioma hybrid vaccine in rat models suggests its potential clinical application.

Botulinum toxin A treatment for post-herpetic neuralgia: A systematic review and meta-analysis.

The present meta-analysis study aimed to investigate the safety and efficacy of local administration of botulinum toxin (BTX-A) vs. lidocaine in the treatment of post-herpetic neuralgia. A systematic search of the Cochrane Library, PubMed, Embase, Chinese National Knowledge Infrastructure, Wanfang, Chongqing VIP Information Co. and Chinese Biomedical Literature Database was performed to identify randomized controlled trials (RCTs) comparing BTX-A and lidocaine in the treatment of post-herpetic neuralgia. The primary outcomes were Visual Analogue Scale (VAS) pain scores at 1, 2 and 3 months after treatment and the effective rate. Secondary outcomes were scores on the McGill pain questionnaire and adverse event rate. A total of 7 RCTs comprising 752 patients were included. The VAS pain score was significantly lower at 1 month [mean difference (MD)=-2.31; 95% CI: -3.06, -1.56; P<0.00001)], 2 months (MD=-2.18; 95% CI: -2.24, -2.11; P<0.00001) and 3 months (MD=-1.93; 95% CI: -3.05, -0.82; P=0.0007) after treatment, the effective rate was significantly higher (odds ratio=2.9; 95% CI: 1.71, 4.13; P<0.0001) and scores on the McGill pain questionnaire were significantly lower (MD=-10.93; 95% CI: -21.02, -0.83; Z=2.12; P=0.03) in patients who received BTX-A for post-herpetic neuralgia compared to those who received lidocaine. There was no difference in the adverse event rate between treatments. In conclusion, BTX-A has potential as a safe and effective treatment option for post-herpetic neuralgia. Further large and well-designed RCTs are required to confirm this conclusion.

Gender Difference in the Prevalence of Insomnia: A Meta-Analysis of Observational Studies.

Objective: Insomnia is a major health challenge in the general population, but the results of the gender differences in the epidemiology of insomnia have been mixed. This is a meta-analysis to examine the gender difference in the prevalence of insomnia among the general population. Methods:Two reviewers independently searched relevant publications in PubMed, EMBASE, PsycINFO, Web of Science from their inception to 16 April 2019. Studies that reported the gender-based prevalence of insomnia according to the international diagnostic criteria were included for analyses using the random-effects model. Results:Eventually 13 articles were included in the meta-analysis. The pooled prevalence of insomnia in the general population was 22.0% [n = 22,980, 95% confidence interval (CI): 17.0-28.0%], and females had a significantly higher prevalence of insomnia compared with males (OR = 1.58, 95% CI: 1.35, 1.85, Z = 5.63, p < 0.0001). Subgroup analyses showed that greater gender difference was associated with the use of case-control study design and consecutive sampling method. Meta-regression analyses also revealed that higher proportion of females and better study quality were significantly associated with greater gender difference. Conclusions:This meta-analysis found that the prevalence of insomnia in females was significantly higher than males in the included studies. Due to the negative effects of insomnia on health, regular screening, and effective interventions should be implemented in the general population particularly for females.