Influence of psychological intervention on patients undergoing spinal anesthesia: a randomized trial.

OBJECTIVE: The aim of this study is to evaluate the effects of positive intervention on the anxiety and the physiological and psychological aspects among preoperative and post-surgical patients with spinal anesthesia. PATIENTS AND METHODS: A randomized trial was conducted with an intervention group (n=58) and a control group (n=59). In the intervention group, the patients were well-informed of the details during spinal anesthesia. Multiple methods were performed to control anxiety before surgery, and nurses were not allowed to discuss the condition during surgery. Anesthesiologists were invited to visit patients to avoid excessive anxiety. RESULTS: The intervention group showed lower scores of State-Trait Anxiety Inventory (STAI) (p<0.05) than the control group 24 hours post-operation. Physiological indices such as systolic blood pressure, low frequency (LF) power, high frequency (HF) power and ration of LF/HF showed better surgery recovery (p<0.05) than the control group. The length of post-anesthesia care unit stay was also significantly shortened in the intervention group (p=0.001) compared with the control group. Positive intervention may alleviate the anxiety in surgical patients receiving spinal anesthesia and improve the physiological and psychological outcomes clinically. CONCLUSIONS: Our results provide evidence indicating that proper intervention can be promoted clinically to improve the satisfaction and quality of life of patients undergoing spinal anesthesia.

LncRNA SNHG1 attenuates neuropathic pain following spinal cord injury by regulating CDK4 level.

OBJECTIVE: Neuropathic pain (NP) is one of the most intractable complications of spinal cord injury (SCI). This study aims to explore the role of long non-coding RNA (lncRNA) SNHG1 in influencing SCI-induced NP. MATERIALS AND METHODS: After establishment of the spinal nerve ligation (SNL) model in rats, spinal tissues were extracted. SNHG1 level in rat spinal tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The role of SNHG1 in the development of NP was explored by assessing paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) in model rats. The interaction between SNHG1 and CDK4 was explored by Luciferase assay and RIP (RNA-Binding Protein Immunoprecipitation). Enzyme-linked immunosorbent assay (ELISA) and qRT-PCR were conducted to determine inflammatory factor levels in rat spinal tissues. RESULTS: SNHG1 was upregulated in rats undergoing SNL. Knockdown of SNHG1 alleviated the development of NP and overexpression of SNHG1 was capable of inducing NP symptoms in uninjured rats. SNHG1 induced NP by directly regulating CDK4 level. CONCLUSIONS: SNHG1 is a novel target in the treatment of NP associated with neuroinflammation.

E2F1-induced upregulation of lncRNA HCG18 stimulates proliferation and migration in gastric cancer by binding to miR-197-3p.

OBJECTIVE: LncRNA HCG18 is considered to be an oncogene in many types of tumors. The aim of this study was to explore the role of lncRNA HCG18 in gastric cancer (GC). PATIENTS AND METHODS: HCG18 levels in GC tissues were detected. Potential biological influences of HCG18 on GC cell phenotypes were examined by Cell Counting Kit-8 (CCK-8), wound healing and transwell assay. Subsequently, bioinformatics analysis, Chromatin immunoprecipitation (ChIP), Luciferase assay and rescue experiments were conducted to identify the regulatory network of HCG18 in GC. RESULTS: It was found that HCG18 was upregulated in GC samples, and the knockdown of HCG18 inhibited proliferative and migratory abilities in GC. The transcription factor E2F1 could directly bind to the promoter region of HCG18 and thus activate its transcription. In addition, HCG18 sponged miR-197-3p to stimulate the malignant development of GC. CONCLUSIONS: HCG18 is upregulated in GC samples by E2F1 induction, which stimulates proliferative and migratory abilities in GC by binding to miR-197-3p.

Targeted regulation of miR-195 on MAP2K1 for suppressing ADM drug resistance in prostate cancer cells.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Targeted regulation of miR-195 on MAP2K1 for suppressing ADM drug resistance in prostate cancer cells, by J.-Y. Zhang, Y.-N. Li, X. Mu, Z.-L. Pan, W.-B. Liu, published in Eur Rev Med Pharmacol Sci 2018; 22 (24): 8599-8608-DOI: 10.26355/eurrev_201812_16623-PMID: 30575899" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16623.

Long-range interactions of the ground state muonium with atoms.

The scaling relations for the dispersion coefficients of long-range interactions between the Mu(1s)-Mu(1s, 2s, or 2p) systems and the H(1s)-H(1s, 2s, or 2p) systems are obtained using analytical properties of hydrogenic wavefunctions, which allows us to obtain the dispersion coefficients for Mu(1s)-Mu(1s, 2s, or 2p) systems from the corresponding H(1s)-H(1s, 2s, or 2p) systems. Additionally, the dispersion coefficients of long-range interactions of Mu(1s) with the ground-state H, noble gas atoms He, Ne, Ar, Kr, and Xe, alkali-metal atoms Li, Na, K, and Rb, alkaline-earth atoms Be, Mg, Ca, and Sr, and Cu, Ag, F, and Cl atoms are calculated.

Long noncoding RNA ILF3-AS1 regulates myocardial infarction via the miR-212-3p/SIRT1 axis and PI3K/Akt signaling pathway.

OBJECTIVE: Myocardial infarction (MI) is a serious cardiac disease due to its high incidence and mortality worldwide. Long noncoding RNAs (lncRNAs) have been found to play an essential role in the pathological progress of various cardiovascular diseases. ILF3-AS1 is a newly identified lncRNA, and many studies have demonstrated that ILF3-AS1 affects the development of various malignancies. However, the biological function of ILF3-AS1 and its underlying mechanism in MI are still unknown. In the present study, the function of ILF3-AS1 and the possible mechanisms against hypoxia-induced apoptosis in H9c2 cells were investigated. MATERIALS AND METHODS: H9c2 cells were exposed to hypoxia (1% O2) to mimic the in vitro model of MI. The levels of lncRNA ILF3-AS1 and microRNA miR-212-3p were measured by real-time PCR (RT-PCR). Transfection was performed to upregulate the levels of ILF3-AS1 and miR-212-3p. Western blot assays were carried out to measure protein expression. The relationship between ILF3-AS1 and miR-212-3p was verified by Dual-Luciferase reporter assay. RESULTS: We found that ILF3-AS1 was downregulated by hypoxia. Overexpression of ILF3-AS1 resulted in the relief of hypoxia-induced damage to H9c2 cells by rescuing cell viability, migration, and invasion and suppressing apoptosis, while downregulation of ILF3-AS1 had the opposite effects. Moreover, ILF3-AS1 could negatively regulate miR-212-3p expression, and upregulation of ILF3-AS1 could alleviate hypoxic injury via downregulation of miR-212-3p. Moreover, miR-212-3p negatively regulated SIRT1 expression. Further investigations revealed that ILF3-AS1 activated PI3K/Akt signaling and that application of the PI3K inhibitor LY294002 could abrogate the protective effects of ILF3-AS1 against hypoxia. CONCLUSIONS: In summary, we concluded that ILF3-AS1 provides protection against hypoxia-induced injury via the PI3K/Akt pathway, which may provide clues for the treatment of patients with MI.

The efficacy and safety of immune checkpoint inhibitors in non-small cell lung cancer patients of different age groups: a meta-analysis.

BACKGROUND: Age is closely related to the efficacy of treatment for non-small cell lung cancer (NSCLC) patients. Latest clinical trials have proved the better overall survival (OS) for the use of immune checkpoint inhibitors verse chemotherapy in NSCLC patients. However, we had no clear idea of the efficacy of them in elderly patients. So we conducted a meta-analysis to compare the efficacy of immune checkpoint inhibitors for NSCLC patients of different age groups and summarized overall treatment-related adverse events. MATERIALS AND METHODS: PubMed, EMBASE, Web of Science and the Cochrane Library were searched for all clinical trials in NSCLC until 30th of April 2019. Eligible studies included randomized controlled trials (RCTs) comparing immune checkpoint inhibitors with chemotherapy in NSCLC patients. The hazard ratio (HRs) and 95% confidence intervals (CIs) of OS, progression-free survival or adverse events (AEs) were used. RESULTS: A total of 4994 patients from 8 RCTs were included. Immune checkpoint inhibitors significantly prolonged the OS (HR, 0.73; 95% CI, 0.61-0.89) versus chemotherapy in NSCLC patients who were less than 65 years old. Also, they prolonged the OS (HR, 0.74; 95% CI, 0.59-0.93) in NSCLC patients who were more than 65 years old. However, there was no statistical significance of OS (HR, 0.87; 95% CI, 0.57-1.30) among NSCLC patients who were more than 75 years old. It also showed that the single use of immune checkpoint inhibitors had fewer all-grade AEs. CONCLUSION: Regardless of the NSCLC patients who were less or more than 65 years, immune checkpoint inhibitors could achieve better OS than chemotherapy. But there was no significant difference when NSCLC patients who were more than 75 years old. Older patient should be offered immune therapies if it is possible and the mechanism in old age treatment should be further studied.

Systematic review: exosomal microRNAs associated with pancreatic cancer for early detection and prognosis.

OBJECTIVE: Pancreatic cancer (PC) is one of the most common malignant tumors of the digestive system with a high degree of malignancy. Currently, there have been many studies on exosomal microRNAs (miRNAs) discovery in pancreatic cancer. This systematic review aimed to give an overview about known exosomal miRNAs and discuss their diagnostic performance, as well as prognostic value in PC. MATERIALS AND METHODS: PubMed and Web of Science were used for systematic literature research for this review. This literature research was mainly to identify studies that performed plasmatic and serological testing for exosomal miRNAs in pancreatic cancer patients and controls. Two independent reviewers separately extracted data on study characteristics and results. RESULTS: In total, nine prior studies were included in this review. Of which, eleven different single exosomal miRNAs and three exosomal miRNA panels were reported. CONCLUSIONS: When single exosomal miRNA was used as a diagnostic tool, the specificity is generally high, but the sensitivity is commonly low. When multiple of exosomal miRNAs were used simultaneously, higher sensitivities can be obtained at relatively reasonable specificity levels with certain miRNA combinations. Developing a combination of miRNA markers may be a promising approach for early detection of pancreatic cancer.

MicroRNA-577 promotes the sensitivity of chronic myeloid leukemia cells to imatinib by targeting NUP160.

OBJECTIVE: To explore the effect of microRNA-577 on the drug sensitivity of chronic myeloid leukemia (CML) and the underlying mechanism. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of microRNA-577 in peripheral blood of patients with chronic myeloid leukemia. Meanwhile, the expression of microRNA-577 was detected in CML cell line after imatinib treatment. Cell counting kit-8 (CCK-8) and flow cytometry assay were applied to verify the effect of microRNA-577 on cell proliferation and cycle. NUP160 was identified as a target gene of microRNA-577 by dual-luciferase reporter gene assay. Cell reverse test was performed to figure out whether microRNA-577 can enhance the sensitivity of CML to imatinib. RESULTS: QRT-PCR results revealed that microRNA-577 level was notably decreased in peripheral blood of patients with CML, and microRNA-577 could inhibit the proliferation and cycle of CML cells. In addition, the result of dual-luciferase reporting assay indicated that microRNA-577 had a binding relationship with NUP160, and up-regulation of microRNA-577 in CML cell lines reduced the expression of NUP160, and vice versa. Lastly, cell reverse experiments confirmed that microRNA-577 can alleviate the resistance of CML to imatinib. CONCLUSIONS: We found that microRNA-577 promotes the sensitivity of chronic myeloid leukemia cells to imatinib by down-regulating the expression of NUP160.

MicroRNA-765 targets MTUS1 to promote the progression of osteosarcoma via mediating ERK/EMT pathway.

OBJECTIVE: Previous studies have shown that microRNA-765 (miR-765) is involved in certain biological behaviors of human cancers. However, abnormal expression and function of miR-765 have not been reported in osteosarcoma (OS). PATIENTS AND METHODS: Changes in the expression of miR-765 and MTUS1 (Microtubule-associated tumor suppressor 1) were examined via Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. The function of miR-765 was investigated through Cell Counting Kit-8 (CCK-8) and transwell assays in OS. The target of miR-765 was identified using a Dual-Luciferase reporter assay. RESULTS: MiR-765 was upregulated in OS tissues. And upregulation of miR-765 promoted cell proliferation, migration and invasion in OS. In addition, MTUS1 was confirmed as a direct target gene of miR-765. Moreover, miR-765 promoted the progression of OS through targeting MTUS1. Furthermore, miR-765 was involved in tumorigenesis of OS through activating extracellular-signal-regulated kinase/ epithelial-mesenchymal transition (ERK/EMT) pathway. CONCLUSIONS: MiR-765 targets MTUS1 to promote the progression of OS via mediating the ERK/EMT pathway. Therefore, miR-765 may be used as a novel biomarker for the diagnosis of OS.

MicroRNA-425-5p promotes the development of prostate cancer via targeting forkhead box J3.

OBJECTIVE: MicroRNAs (miRNAs) have critical roles in the progression of prostate cancer (PCa) and have the potential to be used as prognosis biomarkers. In this study, we aimed to investigate the role of miR-425-5p in the progression of PCa. PATIENTS AND METHODS: miR-425-5p expression in PCa tumor tissues and cell lines was measured by Quantitative Real-time PCR (RT-qPCR). Effects of miR-425-5p expression on PCa cell proliferation, colony formation, cell migration, and cell invasion were measured. RESULTS: We found miR-425-5p expression was elevated in both PCa tissues and cell lines. Importantly, we found overexpression of miR-425-5p promoted proliferation, colony formation, migration and invasion of PCa cell lines in vitro. Forkhead box J3 (FOXJ3) was validated as a downstream target of miR-425-5p. Finally, we found the stimulation effects of miR-425-5p on PCa cell behaviors were fulfilled through directly regulating the expression of FOXJ3, which validated FOXJ3 as a functional target of miR-425-5p in PCa. CONCLUSIONS: Taken together, our results demonstrated miR-425-5p may contribute the malignancy progression of PCa in a mechanism involving FOXJ3, implicating miR-425-5p may be developed as therapeutic target for PCa in the future.

Targeted regulation of miR-195 on MAP2K1 for suppressing ADM drug resistance in prostate cancer cells.

OBJECTIVE: Extra-cellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway participates in cell proliferation, cycle and apoptosis. MAPK kinase 1 (MAP2K1) activates the ERK/MAPK pathway. The down-regulation of miR-195 is correlated with the onset and drug resistance of prostate cancer. Bioinformatics analysis identified complementary binding sites between miR-195 and MAP2K1. This study aimed to investigate the effect of miR-195 on the proliferation, apoptosis and adriamycin (ADM) resistance of prostate cancer cells. MATERIALS AND METHODS: Dual-Luciferase reporter gene assay confirmed targeted regulation between miR-195 and MAP2K1. ADM resistant cell line DU145/ADM and PC-3/ADM were generated for comparing the miR-195 and MAP2K1 expression. Apoptosis was measured by flow cytometry and caspase-3 activity was quantified. Cultured cells were treated with miR-195 mimic, followed by quantitative real-time PCR (qRT-PCR) was used for MAP2K1 expression. Western blot measured MAP2K1, ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2) expression, and flow cytometry quantified cell apoptosis, followed by EdU staining for cell proliferation. RESULTS: Targeted regulation existed between miR-195 and MAP2K1 mRNA. Drug-resistant cells had lower miR-195 than parental cells, whilst MAP2K1 expression was higher. Under ADM treatment with IC50 concentration, drug resistant cells showed lower apoptosis. The transfection of miR-195 decreased MAP2K1 expression and p-ERK1/2, elevated cell apoptosis and suppressed EdU positive rate or cell proliferation. CONCLUSIONS: The down-regulation of miR-195 is correlated with ADM resistance of prostate cancer cells. The over-expression of miR-195 weakens cancer cell proliferation, facilitates cell apoptosis and decreases ADM resistance via targeted inhibition on MAP2K1 expression and ERK/MAPK signal pathway.

A combination of mRNA expression profile and miRNA expression profile identifies detection biomarkers in different tumor stages of laryngeal squamous cell carcinoma.

OBJECTIVE: This study was conducted to investigate microRNA (miRNA) target regulations during the disease progression in laryngeal squamous cell carcinoma (LSCC) and identify biomarkers in different tumor stages. MATERIALS AND METHODS: The mRNA dataset GSE59102 and miRNA dataset GSE70289 were used in this study. After pretreatment, differentially expressed genes/miRNAs (DEGs/DEMs) in different tumor stages (beginning vs. margin, advanced vs. margin, and beginning vs. advanced) were selected on the basis of their limma package. Then, the enrichment analysis for these DEGs was conducted using ClueGO. Protein-protein interaction (PPI) network analysis was performed on the basis of the BioGRID database. After prediction of target genes of DEMs according to three validated miRNA databases, an integrated miRNA target network and its pathways were drawn using the multiMiR package. RESULTS: Numerous DEGs were identified in different tumor stages of LSCC (beginning vs. margin, advanced vs. margin, and beginning vs. advanced), and a set of 18 DEMs was identified. Cell cycle was the most significantly enriched pathway of the DEGs. Four hub nodes (MCM2, EGFR, CDK2, and CDK1) were highlighted in the PPI network. In the integrated miRNA target network, 2 miRNAs were predominant: hsa-miR-331-3p (2 predicted targets, E2F1 and TNFRSF10B) and has-miR-375 (1 predicted target, TNNI3). These genes were tied up with cell cycle or apoptosis pathway. CONCLUSIONS: Several genes and miRNAs might be used as markers for LSCC in different tumor stages (e.g., MCM2, EGFR, CDK1, CDK2, hsa-miR-331-3p, hsa-miR-375). They might function through the involvement of the cell cycle pathway.

Octreotide protects doxorubicin-induced cardiac toxicity via regulating oxidative stress.

OBJECTIVE: To explore the role of octreotide in doxorubicin-induced (DOX) cardiac toxicity in rats, and to investigate its underlying mechanism. MATERIALS AND METHODS: A total of 24 male Sprague Dawley (SD) rats were randomly assigned into 3 groups, including: the control group (NS group), the DOX-induced cardiac toxicity group (DOX group) and the OCT pretreatment + DOX-induced cardiac toxicity group (OCT group). Each group had 8 experimental SD rats. Electrocardiogram was performed in each rat before and after animal procedure, respectively. The serum and heart samples of each rat were collected 10 days after the surgical procedure. Cardiomyocyte apoptosis in the myocardial ischemic area of rats was determined by hematoxylin and eosin (HE) staining and Terminal Deoxynucleotidyl Transferase dUTP Nick-end Labeling (TUNEL) staining. DOX-induced oxidative stress was evaluated by detecting the activities of SOD (superoxide dismutase), MDA (malondialdehyde), GSH (glutathione), T-AOC (total antioxidant capacity) and CAT (catalase). The expression levels of nuclear factor E2 related factor-2 (Nrf2), heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO1) were detected by Western blot and immunohistochemistry. RESULTS: Compared with the NS group, heart rate and voltage of QRS wave were both significantly reduced in the DOX group, whereas Q-T interval was significantly prolonged (p < 0.05). Arrhythmia was even found in some rats of the DOX group. However, rats in the OCT group had significantly higher heart rate and voltage of QRS wave, as well as shorter Q-T interval when compared with those of the DOX group (p < 0.05). The levels of plasma CK-MB and LDH were remarkably lower in the OCT group than those of the DOX group. The activities of SOD, GSH, CAT and T-AOC in cardiac homogenate of the OCT group were higher than those of the DOX group. However, MDA activity and ROS level in cardiac homogenate were remarkably reduced in the OCT group when compared with those of the DOX group (p < 0.05). Cardiac pathological lesions were alleviated by OCT pretreatment. Moreover, the expression levels of Nrf2, HO-1 and NQO1 were significantly upregulated in the OCT group than those of the DOX group. CONCLUSIONS: Octreotide improves the anti-oxidant capacity of cardiomyocytes via activating the Nrf2 pathway, thereby protecting doxorubicin-induced cardiac toxicity in rats.

Low expression of microRNA-21 inhibits trophoblast cell infiltration through targeting PTEN.

OBJECTIVE: We investigate whether microRNA-21 could increase the infiltration ability of trophoblast cells via regulating PTEN expression, thus participating in the occurrence and development of preeclampsia. PATIENTS AND METHODS: MicroRNA-21 expression in the placenta tissues of preeclampsia women and normal pregnant women was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The effects of microRNA-21 on cell proliferation and infiltration were examined by cell counting kit-8 (CCK-8) and transwell assay, respectively. The dual-luciferase reporter gene assay was used to determine the binding relationship between microRNA-21 and PTEN. Western blot was performed to detect PTEN and microRNA-21 in trophoblasts. RESULTS: QRT-PCR results showed that the microRNA-21 expression was significantly lower in the placenta of the preeclampsia women than those of normal pregnant women. Overexpression of microRNA-21 in HTR-8/SVneo cells had no effect on cell proliferation, but enhanced cell infiltration ability. Inhibition of microRNA-21 in trophoblasts showed the opposite effects. The results of luciferase activity assay and Western blot showed that microRNA-21 could target PTEN and downregulate its expression. Overexpression of PTEN in HTR-8/SVneo cells partially reversed the enhanced invasive ability induced by microRNA-21 overexpression. CONCLUSIONS: Low expression of microRNA-21 attenuated cell infiltration of trophoblasts via direct regulating PTEN expression.

FAL1 regulates endothelial cell proliferation in diabetic arteriosclerosis through PTEN/AKT pathway.

OBJECTIVE: This study aims to investigate the role of FAL1 in the occurrence and progression of diabetic arteriosclerosis and its underlying mechanism. PATIENTS AND METHODS: FAL1 expression in coronary artery disease (CAD) tissues, normal artery tissues, and tumor necrosis factor-α (TNF-α)-induced endothelial cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The regulatory effects of FAL1 on cell proliferation, migration, and cell cycle were examined by cell counting kit-8 (CCK-8) assay, transwell assay, and flow cytometry, respectively. Western blot was used to detect protein expressions of proliferation-related gene PCNA (proliferating cell nuclear antigen), cell cycle-related genes cyclin D1, PTEN (phosphatase and tensin homolog deleted on chromosome ten) and AKT (protein kinase B) in HUVECs. Subsequently, rescue experiments were performed to assess whether PTEN/AKT signaling pathway is activated during the process of FAL1-regulated proliferation and migration of HUVECs. RESULTS: FAL1 was highly expressed in CAD tissues and TNF-α-induced endothelial cells compared with that of controls. Overexpression of FAL1 in HUVECs promoted cell cycle, proliferation, and migration. FAL1 activated PTEN/AKT pathway in HUVECs, which was partially reversed by PTEN overexpression. CONCLUSIONS: Highly expressed FAL1 can promote proliferation and migration of endothelial cells through activating PTEN/AKT signaling pathway.

Curcumin attenuates IR-induced myocardial injury by activating SIRT3.

OBJECTIVE: Ischemia-reperfusion (IR) injury remains an unresolved and complicated situation in clinical practice. In this study, H9c2 cardiomyocytes were subjected to curcumin (Cur) treatment in the absence or presence of the silent information regulator 3 (SIRT3) inhibitor 3-TYP and were then subjected to IR. MATERIALS AND METHODS: H9c2 cells and male Sprague-Dawley (SD) rats were cultured. MTT assay was performed to assess H9c2 cell viability. Cellular apoptosis was analyzed by TUNEL assay. The expressions of Bcl-2, Bax, SIRT3, and AcSOD2 were measured by Western-blotting. The activities of SOD, GSH-Px, and MDA were determined using commercially available kits. The myocardial infarct size was evaluated using TTC staining. RESULTS: Cur significantly increased H9c2 cell viability, decreased the cell apoptotic index, and altered several biochemical parameters, including upregulation of the anti-apoptotic protein Bcl-2, downregulation of the proapoptotic protein Bax and AcSOD2, activation of SIRT3, increase in SOD and GSH-Px activity, and decrease in MDA content. In isolated rat hearts, Cur significantly improved cardiac function, decreased infarct size, and lowered lactate dehydrogenase levels. These protective effects induced by Cur were reversed by treatment with the SIRT3 inhibitor 3-TYP. CONCLUSIONS: These results demonstrate that Cur protects cardiomyocytes and that rat hearts were exposed to IRI by activating SIRT3.

Tannerella forsythia and coating color on the tongue dorsum, and fatty food liking associate with fat accumulation and insulin resistance in adult catch-up fat.

BACKGROUND/OBJECTIVES: We aimed to determine the alteration of Tannerella forsythia and coating color on the dorsal tongue, and fatty food liking in catch-up fat in adult (CUFA), as well as the probable associations between fat accumulation, insulin resistance (IR) and these changes. SUBJECTS/METHODS: T. forsythia on the tongue dorsum, fatty food liking, fat accumulation and insulin sensitivity were investigated in CUFA humans and rats, and tongue-coating color was observed in CUFA individuals. We further determined the changes of fatty food liking, fat accumulation and IR in T. forsythia-infected rodents by oral lavage. RESULTS: Increases in fat accumulation, IR, percentage of subjects with yellow tongue coating and that with T. forsythia detected were observed in CUFA individuals. Additionally, the fat ranking scores were significantly lower and the hedonic ratings of low-fat options of sampled food were lower, while the ratings of high-fat options were remarkably higher in CUFA subjects. Additionally, T. forsythia level elevated in CUFA rats, and fatty food liking, fat accumulation and IR increased in CUFA and T. forsythia-infected animals, with the increases in T. forsythia infection and fatty food liking preceding the occurrence of fat accumulation and IR. CONCLUSIONS: T. forsythia and yellow coating on the dorsal tongue and fatty food liking associate fat accumulation and IR in CUFA. Moreover, we tentatively put forward that T. forsythia, which is very important in yellow tongue-coating microbiota, and its consequent increases in fatty food liking, might be crucial in the development of fat accumulation and IR in CUFA.

MiR-630 promotes epithelial ovarian cancer proliferation and invasion via targeting KLF6.

OBJECTIVE: MicroRNAs play critical roles in post-translational gene expression. The current study was to investigate the effects of miR-630 in epithelial ovarian cancer. PATIENTS AND METHODS: Thirty epithelial ovarian cancer tissue and thirty normal ovarian tissue samples were collected and were detected miR-630 expression level with qRT-PCR. MiR-630 mimics, inhibitors and negative controls were transfected into SKOV3 and Cell Counting Kit-8 (CCK-8) assay, and transwell experiment were performed to detect the proliferation rate and migration, respectively. The luciferase reporter assay was utilized to identify miR-630's target gene. Balb/c nude mice were utilized to verify the effect of miR-630 in vivo. RESULTS: QRT-PCR showed a significantly high miR-630 expression in epithelial ovarian cancer relative to normal ovarian tissue. The miR-630 overexpression promoted epithelial ovarian cancer cell SKOV3 proliferation and migration. Krüppel-like factor 6 (KLF6) was predicted as the target of miR-630. In vivo study also verified that miR-630 overexpression stimulated ovarian cancer growth. CONCLUSIONS: We propose that targeting miR-630 might be a promising therapeutic approach for ovarian cancer.

Outbreak of enteric microsporidiosis of hatchery-bred juvenile groupers, Epinephelus spp., associated with a new intranuclear microporidian in China.

A new enteric microsporidian was found to be associated with the mass mortality of hatchery-bred juvenile groupers, Epinephelus spp., in China. The outbreak usually occurred during the rainy season between May and November when water temperature ranged from 26 to 30 °C and salinity from 28 to 34 ppt, although this microsporidian can be detected year round. External clinical signs included severe emaciation, white faeces syndrome, anorexia, sinking to the bottom of culture ponds and mass mortality (up to 90%). Upon necropsy, severe intestinal oedema and thin and transparent intestinal wall could be observed. The mature spores are tiny, measuring 1.3-1.5 (1.35 ± 0.13) × 1.6-2.4 (2.16 ± 0.31) µm and can be found in the cytoplasm and the nucleoplasm of most enteric epithelial cells of host. Epidemiological investigation showed that this species was distributed throughout most of the culture area of grouper fingerlings in Fujian, Guangdong, Hainan and Guangxi provinces in China, with maximum prevalence of 95%. Molecular analysis based on the partial small subunit rRNA sequence (1045 bp) placed this species within the Enterocytozoonidae, but sequence identities to other species were below 90%. The exact taxonomic position warrants study of the ultrastructural characteristics of the developmental stages.