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Background. The revascularization of small vessels using drug-eluting stents remains challenging. The use of the drug-coated balloon is an attractive therapeutic strategy in de novo lesions in small coronary vessels, particularly in the diabetic group. This study aimed to assess the outcomes of DCB-only angioplasty in small vessel disease. Methods. A total of 1198 patients with small vessel disease treated with DCB-only strategy were followed. Patients were divided into the diabetic and nondiabetic groups. Clinical and angiographical follow-up were organized at 12 months. The primary endpoints were target lesion failure and secondary major adverse cardiac events. Results. There was a significantly higher rate of target lesion failure among diabetic patients compared to nondiabetic [17 (3.9%) vs. 11 (1.4%), P = 0.006 ], taken separately, the rate of target lesion revascularization significantly differed between groups with a higher rate observed in the diabetic group [9 (2%) vs. 4 (0.5%), P = 0.014 ]. Diabetes mellitus remained an independent predictor for TLF (HR: 2.712, CI: 1.254–5.864, P = 0.011 ) and target lesion revascularization (HR: 3.698, CI: 1.112–12.298, P = 0.033 ) after adjustment. However, no significant differences were observed between groups regarding the target vessel myocardial infarction (0.6% vs. 0.1%, P = 0.110 ) and MACE [19 (4.4%) vs. 21 (2.7%), P = 0.120 ]. Conclusion. Drug-coated balloon-only treatment achieved lower incidence rates of TLF and MACE. Diabetes is an independent predictor for target lesion failure and target lesion revascularization at one year following DCB treatment in small coronary vessels. We observed no significant differences between groups regarding MACE in one year.

Although drug-eluting stents are the most common interventional devices for patients with coronary disease, drug-coated balloons (DCBs) represent a novel therapeutic alternative in certain scenarios. This prospective, observational all-comers study explored the clinical outcomes of DCB use in patients with coronary lesions. All patients treated with DCBs were enrolled in this study, including patients with in-stent restenosis (ISR) or de novo lesions. The primary outcome was the target lesion revascularization (TLR) rate at one year. We enrolled 2306 patients with 2660 lesions and performed DCB angioplasty in 399 patients (17.3%) with ISR and 1907 patients (82.7%) with de novo lesions. During follow-up (366 ± 46 days), the TLR rate was lower in the de novo lesion group (1.31%) compared to the ISR group (7.02%) [odds ratio (OR) 0.176, 95% confidence interval (CI) 0.101–0.305, p

Background: Preoperative assessment of patients is meaningful to predict survival in patients with malignant tumors. The prognostic nutritional index (PNI) is one of the most significant factors re...

High expression of long intergenic non-protein coding RNA 987 (LINC00987) is strongly associated with low overall survival of osteosarcoma; however, its role in osteosarcoma remains unclear. This study explored the biological function and underlying mechanism of LINC00987 in osteosarcoma. In this study, LINC00987 expression in osteosarcoma cells was analyzed using Cancer Cell Line Encyclopedia and qRT-PCR. The proliferation and migration and invasion in osteosarcoma cells were evaluated using Cell Counting Kit-8 and Transwell assays, respectively. Bioinformatic analysis was used to predict the LINC00987-bound miRNAs and miR-376a-5p-bound mRNAs. Dual-luciferase reporter assays were used to assess the interaction between miR-376a-5p, LINC00987, and forming-binding protein 1 (FNBP1). FNBP1 expression was measured by western blotting. LINC00987 was found to be upregulated in osteosarcoma cells. LINC00987 silencing suppressed proliferation, migration, and invasion of osteosarcoma cells. Additionally, miR-376a-5p expression was downregulated in osteosarcoma cells. miR-376a-5p knockdown reversed the effect of LINC00987 silencing on the biological function of osteosarcoma cell. miR-376a-5p was found to target LINC00987 and FNBP1. FNBP1protein level was increased in osteosarcoma cells; however, it was inhibited by silencing LINC00987 and enhanced by silencing miR-376a-5p. In conclusions, this study suggests LINC00987 silencing inhibits osteosarcoma cell proliferation, migration, and invasion by sponging miR-376a-5p to regulate FNBP1 expression. LINC00987 as a potential therapeutic target for osteosarcoma.

Neonicotinoids (NEOs) are extensively applied in global agricultural production for pest control but have adverse effects on human health. In this study, the concentrations of six NEOs and three characteristic metabolites were investigated by collecting 200 serum samples from an elderly population in China. Results showed that the NEOs and their metabolites were widely detected (89%-98 %) in the serum samples from the osteoporosis (OP) (n = 120) and non-OP (n = 80) population, and their median concentrations ranged from 0.04 ng/mL to 5.99 ng/mL and 0.01 ng/mL to 2.02 ng/mL, respectively. N-desmethyl-acetamiprid (ACE-dm) was the most abundant NEOs in the serum samples. Gender-related differences were found in concentrations of most NEOs and their metabolites in serum, with males having higher target analytes than females. Significantly (p 0.05) positive correlations were observed among most NEO concentrations, suggesting that exposure source of these substances is common or related. However, associations between the concentrations of characteristic metabolites and their corresponding NEOs were insignificant, probably because the exogenous intake are the primary sources of metabolites of NEOs instead of the internal biotransformation. The associations between NEO concentrations (i.e., ACE-dm, dinotefuran, and olefin-imidacloprid) and OP (OR = 2.33-6.92, 95 % CI = 0.37-16.9, p-trend 0.05) indicate that NEO exposure is correlated with increased odds of prevalent OP. This study is the first to document the profiles of NEOs and their metabolites in serum samples collected from an elderly population in South China and examine the relationships between NEO exposure and OP.

In this study, 2-phosphonobutane-1,2,4-tricarboxylic acid (PBTCA) was introduced as a depressant for the flotation separation of apatite from calcite. The micro-flotation test results showed that good floatability of both apatite and calcite were obtained at around pH 8.5 when using sodium oleate (NaOl) as collector. Mixed minerals flotation test results showed that an efficient separation of apatite from calcite was achieved using PBTCA as depressant, which presented a selective depression for the calcite. Zeta potential measurements indicated that the addition of PBTCA prior to NaOl did not interfere the interaction between NaOl and apatite while it decreased NaOl adsorption on calcite surface.

The effect of depressant 2-phosphonobutane-1,2,4-tricarboxylic acid (PBTCA) on the flotation separation of smithsonite from calcite was studied by micro-flotation and electro-kinetic tests. The micro-flotation results showed that good floatability of both smithsonite and calcite were achieved in the presence of sodium oleate. The depressant PBTCA selectively depressed calcite without interfering the floatability of smithsonite. The mixed minerals flotation results showed that efficiency separation of smithsonite from calcite was achieved using PBTCA as the depressant. Zeta potential measurements indicated that NaOl was able to adsorb on the PBTCA pre-treated smithsonite surface, but failed to adsorb on the PBTCA pre-treated calcite surface.

This study was designed to determine whether metaphorical solutions to mental distress problems result in an insightful mental experience and activate the hippocampus and amygdala: areas associated with insight. We recruited 22 healthy university students. Trials presented 75 micro-counseling scenarios while event-related functional magnetic resonance imaging (fMRI) was applied to detect neural responses. Each scenario included a mental distress problem and one of the following solution types: metaphorical, literal, or problem-restatement. The results revealed that, compared with literal solutions or problem-restatement solutions, metaphorical solutions activated two neural networks: one associated with basic metaphorical language processing (i.e., the left inferior frontal gyrus and middle and superior temporal gyri), and a specific network associated with insightful problem solving (i.e., the bilateral hippocampus, amygdala, and fusiform gyrus). Our findings indicate that the use of metaphorical solutions to mental distress problems reliably produces salient neural activities for insight.

A novel method to improve carboxymethyl cellulose (CMC) performance in talc flotation is described in this paper. Micro-flotation results showed that using CMC as the depressant, strong depression on talc floatability was observed when the pulp pH was adjusted from low (4.0) to high (8.5), which improved the separation performance between chalcopyrite and talc. Zeta potential measurements illustrated that talc surface charge was less negative when the pH was regulated from acid to base than the situation that the pulp pH was altered from base to acid. ICP test and XPS results indicated that more magnesium ions were dissolved from the talc lattices at pH 4 and the hydrolyzed species of magnesium cations were adsorbed onto the talc surfaces when the pulp pH was adjusted to 8.5, and thus promoting the CMC adsorption on the talc surfaces, which further decreased its floatability.

backgroundTo analyze and summarize the clinical features and diagnosis and treatment experience on primary intracranial and extracranial communicating leiomyosarcoma to deepen clinicians’understanding of the rare disease.Cases presentationThe clinical data and recurrence of a patient who was diagnosed with primary intracranial and extracranial communicating leiomyosarcoma admitted to the Neurosurgery Department, The Affiliated Ganmei Hospital of Kunming Medical University in May 2015 were retrospectively analyzed. According to the patient data, two successful surgical operations were performed and the surgeries went well, with more than 2-year and 8-month follow-up so far. No obvious complications were found after hospital discharge, and follow-up was continued.ConclusionsSurgical removal is the most important and effective treatment means for primary intracranial and extracranial communicating leiomyosarcoma currently.

Follicular regulatory T cells (Tfr) have critical functions in inflammatory and autoimmune disorders. The main purpose of the current work was to assess Tfr cell frequency in patients with dilated cardiomyopathy (DCM). Flow cytometry showed that, compared with normal controls, DCM cases showed markedly reduced Tfr cell rates and Tfr/Tfh ratios, but significantly increased follicular helper T cell (Tfh) rates. Correlation analysis showed that the Tfr rate in DCM patients was positively correlated with left ventricular ejection fraction (LVEF), and negatively correlated with N-terminal brain natriuretic peptide (NT-proBNP) levels. Lower Foxp3 and higher Bcl-6, ICOS, and PD-1 mRNA expression levels were found in patients with DCM. In addition, plasma interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-21 levels were significantly increased in DCM cases. Moreover, IgG and IgG3 levels were also elevated in individuals with DCM. Correlation analysis showed that the Tfr rate in DCM patients was negatively correlated with IgG and IgG3, while the Tfh rate was positively correlated with IgG and IgG3. Changes in circulating Tfr levels may have a critical immunomodulatory function in DCM and may become a new therapeutic target for DCM.

Background. Relative to nondiabetic patients, percutaneous coronary intervention (PCI) in patients with diabetes mellitus (DM) is associated with inferior clinical outcomes. We aimed to evaluate the outcomes of drug-coated balloon (DCB) in diabetic versus nondiabetic patients. Methods and Results. In this observational, prospective, multicenter study, we compared the outcomes of patients with and without DM after undergoing PCI with DCBs. Target lesion failure (TLF) was analyzed as primary endpoint. Secondary endpoints were the rates of target lesion revascularization (TLR), major adverse cardiovascular events (MACE), cardiac death, myocardial infarction (MI), and any revascularization. Propensity score matching was used to assemble a cohort of patients with similar baseline characteristics. Among 2,306 eligible patients, 578 with DM and 578 without DM had similar propensity scores and were included in the analyses. During follow-up ( 366 ± 46 days), compared with DM patients, patients without DM were associated with a lower yearly incidence of TLF (2.77% vs. 5.36%; OR, 1.991; 95% CI, 1.077 to 3.681; P = 0.025 ) and TLR (1.90% vs. 4.15%; OR, 2.233; 95% CI, 1.083 to 4.602; P = 0.026 ). No significant differences were observed with regards to rates of MACE (OR: 1.580, 95% CI: 0.912-2.735; P = 0.100 ), cardiac death (OR: 1.608, 95% CI: 0.523-4.946; P = 0.403 ), MI (OR: 4.042, 95% CI: 0.855-19.117; P = 0.057 ), and any revascularization (OR: 1.534, 95% CI: 0.983-2.393; P = 0.058 ). Conclusions. Diabetic patients experience higher TLF and TLR rates following DCB angioplasty without substantial increase in the risk of MACE, cardiac death, MI, or revascularization.

Little evidence exists to confirm whether the sensory-related neural activity that occurs when observing others in pain is highly responsive to empathy for pain. From a perspective of intervention, the present study employed placebo manipulation with a transferable paradigm to explore whether the sensory regional activation that occurs when viewing pictures of others in pain could be modulated by the placebo effect. We first performed a screening behavioral experiment for selecting placebo responders and then entered them into a functional magnetic resonance (fMRI) experiment in which they were exposed to the same conditions as before. Participants were informed that it was equally possible to be assigned to the treatment group (placebo manipulation) or the no-treatment group (control); they all, in fact, received treatment and placebo effect would be detected by comparing placebo conditions and no-placebo control condition. Each participant experienced a phase of reinforcing placebo belief with pain in self and a phase of testing transferable placebo effect on empathy for pain. As a result, we found significant activation in sensory areas, including the posterior insula (PI) and the postcentral gyrus, and in the middle cingulate cortex while participants observed pictures of others in pain. More importantly, for the first time, we observed relieved activation in the PI modulated by the placebo effect only associated with pain pictures but not with no-pain pictures. This suggests that sensory activity in the PI might be involved in the processing for empathic pain. This new approach sheds light on research and applications in clinical settings.

Acute myocardial infarction (AMI) induced by ischemia hypoxia severely threatens human life. Cell apoptosis of neurocytes was identified to mediate the pathogenesis, while the potential mechanism was still unclear. Sprague Dawley (SD) rats were used to establish the AMI rat model. Real-time polymerase chain reaction (PCR) and Western blot were performed to detect gene expression in mRNA and protein levels, respectively. A TUNEL assay was carried out to determine cell apoptosis. The relationship between SRY-related HMG-box (SOX7) and miR-128 was verified using luciferase reporter assay. The expression of SOX7 was decreased, while miR-128 was increased in AMI rats and ischemia hypoxia (IH) induced H9c2 cells. Hypoxia induction significantly promoted the expression of interleukin (IL)-33 and soluble ST2 (sST2), and also promoted cell apoptosis. MiR-128 targets SOX7 to regulate its expression. Down-regulated miR-128 reversed the effects of IH on expression of SOX7, sST2 and cell apoptosis, while down-regulated sST2 abolished the effects of miR-128 inhibitor. In addition, overexpressed IL-33 abolished the effects of miR-128 inhibitor that induced by IH on the expression of SOX7 and cell apoptosis. In vivo experiments validated the expression of miR-128 on cell apoptosis. The present study indicated that miR-128 modulated cell apoptosis by targeting SOX7, which was mediated by IL-33/sST2 signaling pathway.

Objective: To determine the underlying mechanism of miR-34b/c in regulating doxorubicin (Dox)-induced myocardial cell injury. Methods: The viability of mouse myocardial cells HL-1 was detected by MTT assay. The apoptosis of HL-1 cells was detected by TUNEL assay. mRNA expressions of ITCH, TNF-α and IL-6 were measured by qRT-PCR. Protein levels of ITCH, NF-κB, TNF-α and IL-6 were measured by western blot. Dual luciferase assay was performed to detect the regulation of miR-34b/c on ITCH. Mouse model of cardiomyopathy was induced by intraperitoneal injection of Dox. Results: Dox reduced HL-1 cell viability and activated NF-κB pathway in HL-1 cells. miR-34b/c expressions were gradually up-regulated and ITCH expression was gradually down-regulated in Dox-treated HL-1 cells. miR-34b/c expression had negative correlation with the mRNA expression of ITCH. Besides, ITCH was a target of miR-34b/c. miR-34b/c mimic reduced cell viability, suppressed ITCH expression, increased TNF-α and IL-6 level, and promoted NF-κB expression in nucleus and cytoplasm of HL-1 cells. Whereas silencing miR-34 protected HL-1 cells through regulating ITCH. Finally, we demonstrated miR-34 antagomir-protected myocardial cells in mouse model of cardiomyopathy. Conclusion: miR-34b/c decreased HL-1 cell viability and promoted the secretion of proinflammatory cytokines in Dox-induced myocardial cells through ITCH/NF-κB pathway.

Cardiac remodeling is a major early event of heart failure, which is regulated by multiple signaling pathways. Here, we demonstrate that TBC1D25 is upregulated during pathological cardiac remodeling. The aim of this study is to determine the role of TBC1D25 in cardiac remodeling and to illustrate the underlying molecular mechanism. Specifically, cardiac remodeling was induced in TBC1D25-KO mice and their wild-type control mice through partial transverse aortic constriction (TAC) of aortic arch. Knockout TBC1D25 exacerbated cardiac hypertrophy, fibrosis and dysfunction. Meanwhile, TBC1D25 overexpression in both H9C2 cells and NRCMs alleviate Angiotensin II-induced cardiomyocyte hypertrophy in vitro. Moreover, TBC1D25 deficiency increases the phosphorylation levels of TAK1 and its downstream molecular (JNK and p38), whereas overexpressed TBC1D25 inhibits phosphorylation of TAK1, JNK and p38. And TAK1 is the key molecule in this process. Furthermore, we demonstrated that TBC1D25 could directly interacts with TAK1 by immunoprecipitation assay and GST pull-down assay, and the interaction needs the amino acids from at least 138 to 226 in the C-terminal region of TBC1D25 and from 1 to 300 in the C-terminal region of TAK1. We conclude that TBC1D25 suppresses pathological cardiac remodeling via regulating TAK1-JNK/p38 signaling pathway, which suggests that TBC1D25 will likely become a promising therapeutic target for heart failure.

The flotation separation of scheelite from calcite using sodium humate (SH) as a potential depressant has been studied through micro-flotation experiments, zeta potential and Fourier transform infrared (FT-IR) spectra measurements. The flotation results indicate SH exhibited selective depression effect on calcite in the presence of sodium oleate, achieving the flotation separation of scheelite from calcite. Zeta potential results indicate that SH strongly absorbed on calcite surface but negligibly on scheelite surface, which prevents the adsorption of sodium oleate on calcite surface. The FT-IR results also show that SH can be adsorb on the surface of calcite. Results shown a higher Ca density on the calcite than on scheelite surface, and that calcite can accommodate the interaction of SH.

Although the effects of cognitive reappraisal in regulating negative emotion are generally well documented, its regulatory effects are usually not very strong because the ordinary reappraisals employed in previous studies were insufficient to overcome the mental set or response bias toward negative situations. In this study, we developed a new strategy employing creative reappraisals that provides an insightful reinterpretation of the negative stimulus. We believe this approach, through adopting a guided (creative) reappraisal rather than self-generation strategy, will greatly improve the emotion regulation effect of reappraisal through activating the neural networks representing the process of deep and structural mental representational change accompanied by the feeling of positive emotion and mental reward. The behavioral results suggested that 1) regarding the transient regulatory effect, creative reappraisal resulted in a positive rating for standardized negative pictures; 2) creative reappraisal had a long-lasting effect in reducing negative affect. In parallel with these behavioral results, the imaging data indicated that 1) creative reappraisal was specifically associated with greater engagement of the amygdala and hippocampus as well as regions in the ventral striatum, and 2) the engagement of the amygdala predicted the transient regulatory effect of creative reappraisal, while the involvement of the hippocampus and the ventral striatum predicted long-term regulatory effects. These findings suggest that the superior regulatory effect of creative reappraisal could be mediated by amygdala-based salient emotional arousal, hippocampus-based new association formation, and striatum-based mental rewarding to lead to a novel and positive experience that could be kept in long-term memory. This research indicates the key role of creative insight in reappraisal and presents a novel and highly efficient reappraisal strategy.

Objective: To detect the changes of gray matter volume (GMV) and their correlation with severity of symptom in patients with post-traumatic stress disorder (PTSD) who were defined with updated DSM-5 diagnostic criteria. Method: 71 participants were assigned into PTSD group (n = 35) or trauma-exposed control (TEC) group (n = 36) with the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Voxel-based morphometry analysis was used to detect alterations in GMV in the PTSD group. Results: We found that the PTSD group had larger GMV in the left middle temporal gyrus (MTG) and in the right dorsal medial prefrontal cortex (dmPFC), and smaller GMV in the region of the right temporal pole (TP) than the TEC group. We also found that PTSD Checklist for DSM-5 (PCL-5) scores correlated positively with the left MTG and right dmPFC GMV, and negatively with left TP GMV. These correlations were consistent with the findings of the between-group comparisons. Conclusions: GMV alterations in the MTG, dmPFC, and TP are detected in the group comparisons and correlated with symptom severity when classifying PTSD individuals according to DSM-5 diagnostic criteria within an earthquake-exposed population.

Cognitive restructuring is an important strategy in cognitive behavioral therapy (CBT). The present study aimed to observe cognitive restructuring in major depressive disorder (MDD) patients using textual micro-counseling dialogue situations. A set of textual micro-counseling dialogues was used to trigger cognitive restructuring in 25 MDD patients and 27 healthy adults. The participants read descriptions ("problems") and explanations ("solutions") for psychologically distressing situations. High-, low-, and zero-restructuring solutions were randomly matched to the problems. The participants evaluated the adaptability and emotional valence of the problems and the insightfulness, adaptability, novelty, and emotional valence of the solutions. Insightfulness ratings for high-restructuring solutions were significantly higher relative to those of low-restructuring solutions in healthy adults, while adaptability ratings for low-restructuring solutions were significantly higher relative to those of high-restructuring solutions in MDD patients. Insightfulness ratings for the solutions were significantly predicted by novelty and adaptability in healthy adults and emotional valence in MDD patients. Lower insightfulness in high-restructuring solutions and higher adaptability in low-restructuring solutions in MDD patients may reflect deficits in cognitive control.

Posttraumatic stress disorder (PTSD) is linked to abnormal amygdala activities. This study measured amygdala functional connectivity using DSM-5 criteria. There were 33 participants in the PTSD group and 33 participants in a trauma-exposed control (TEC) group, who did not have PTSD according to the PTSD checklist of the DSM-5 (PCL-5). Our findings are as follows: (1) In the PTSD group, the amygdala had increased positive connectivity with the medial prefrontal cortex (mPFC) and hippocampus, and decreased positive connectivity with the inferior mPFC and insula. The amygdala had increased negative connectivity with the orbital prefrontal cortex and decreased negative connectivity with the insula in comparison with TEC group. (2) PCL of all participants was correlated with the connectivity between the amygdala and the mPFC, hippocampus, and insula. These regions overlapped with those identified in the between-group comparisons. However, there was no association between PCL of the PTSD group and connectivity in these regions. Abnormal functional connectivity between the amygdala and mPFC subdivisions, hippocampus, and insula reveals their importance in PTSD pathogenesis.

Background/Aims: Myeloid-derived suppressor cells (MDSCs) are increased in inflammatory and autoimmune disorders. This study aims to evaluate the significance of MDSCs in dilated cardiomyopathy (DCM) patients. Methods: In total, 42 newly hospitalized DCM patients and 39 healthy controls were enrolled in the study. The frequencies of circulating CD14+HLA-DR-/low MDSCs were determined by flow cytometry. Then, the functional properties of MDSCs in suppressing T cell proliferation and interferon-gamma (IFN-γ) production were measured in a co-culture model. Then, mRNA expression levels of various important molecules in peripheral blood mononuclear cells were measured by real time polymerase chain reaction. Furthermore, correlation analyses between MDSC frequencies and cardiac function parameters were also performed. Results: The frequencies of circulating CD14+HLA-DR-/low MDSCs were significantly elevated in DCM patients compared with healthy controls. It showed that MDSCs from DCM patients more effectively suppressed T cell proliferation and IFN-γ production compared with those from healthy controls, which was partially mediated by arginase-1 (Arg-1). In addition, the correlation analysis suggested that MDSC frequencies were negatively correlated with left ventricular ejection fraction (LVEF), while positively with N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with DCM. Conclusions: Circulating activated MDSCs might play significant immunomodulatory roles in the pathogenesis of DCM.

Lithium recovery from the density fractions of Baker (namely West Kentucky No. 13) seam coal was investigated in this study. Proximate and elemental analyses showed that lithium contents in the 1.8–2.2 SG and 2.2 SG sink fractions were 185 ppm and 150 ppm, respectively, which are significantly higher than the average content of coal sources (12 ppm) and coal ashes (66 ppm) worldwide. Moreover, due to the high lithium contents and mass distribution, nearly 90% of the lithium present in the Baker coal sample was distributed in the two density fractions. Direct leaching using a HCl solution resulted in less than 10% lithium recovery, which was due to nearly 90% of the lithium being associated with insoluble solids as determined by the results from sequential extraction tests. Calcination of both density fractions under 600 °C for two hours followed by leaching resulted in recovery increases in the range of 70% to 80%. The pyro-metallurgical pretreatment step converted most of the associated lithium minerals to more easy-to-leach forms such as carbonate and metal oxide. Based on mineralogy characterization and leaching test results, it was concluded that the positive effects of calcination on lithium leachability resulted from the dehydration and disintegration of kaolinite as well as dehydroxylation and expansion of muscovite/illite. An analysis of the leaching kinetics revealed that the leaching rate of lithium was controlled by interface transfer and diffusion across the product layer and was negatively impacted when the calcination temperature exceeded 600 °C due to sintering of the kaolinite.

The impacts of calcination on the leaching recovery of rare earth elements (REEs) and other critical metals from a Baker seam coal refuse material were investigated in this study. Acid leaching test results showed that leaching recovery of the REEs, especially the light REEs, was increased significantly from around 24% to 80–90% after calcination under 600–750 °C for two hours. By considering the major element leaching kinetics and the mineralogical changes of the dominant minerals caused by calcination, two mechanisms were proposed for the improved leaching performance: (1) decomposition of difficult-to-dissolve REE-bearing minerals into soluble forms; and (2) liberation of REE-bearing minerals encapsulated in clays after calcination due to the dehydration and disintegration of the layered clay structure. Sequential chemical extraction tests showed that a significant fraction (around 75%) of the REEs in the raw material were present in an insoluble form. After calcination under proper temperatures (600–800 °C), the majority of the insoluble light REEs (LREEs) were converted into soluble forms. Changes in the modes of occurrence of the LREEs and phosphorous based on leaching rate and sequential leaching correlated well as a function of the calcination temperature. This finding in addition to SEM-EDX results tends to indicate the potential that the LREEs occur primarily as rare earth phosphates such as monazite in the untreated coal refuse material. The acid leaching and sequential chemical extraction results show that co-extraction of REEs and other critical metals such as Co, Mn, and Li is possible using a calcination-acid leaching procedure.

Flotation separation of scheelite from calcite is difficult due to the similarities in their surface properties. In this work, the flotation behavior of scheelite and calcite using oxidized paraffin soap(OPS), benzohydroxamic acid(BHA) and the mixed OPS/BHA collectors was investigated through micro-flotation experiments. The flotation results of single mineral experiments demonstrated a higher selectivity for the flotation of scheelite from calcite at pH 9 than individual OPS and BHA when using water glass as depressant. In order to probe the validity of the findings, mixed binary minerals experiments, contact angle and zeta potential experiments were also carried out successfully. Accepted version

Background: The placebo effect in relieving negative emotion arousal is poorly understood.Aims: We examined whether placebo expectation established with noise stimuli could have a transferable anxiolytic effect on negative emotion arousal.Methods: In Experiment 1, noise intensity was surreptitiously lowered during placebo condition in the preconditioning phase to reinforce placebo expectation, and the noise-relieving placebo effect was assessed in the testing phase. In Experiment 2, the same manipulation as in Experiment 1 was administered in the preconditioning phase, but the anxiolytic placebo effect was assessed in the testing phase using negative pictures.Results: Intensity and annoyance by the noise in Experiment 1 were significantly reduced, and unpleasantness in Experiment 2 was also significantly reduced in the placebo condition.Conclusion: Direct noise-relieving placebo effects and transferred anxiolytic placebo effects were found. The present study provides evidence that the placebo effect can be transferred from noise to emotion.

Aim: The aim of this study was to explore whether the circulating frequency and function of myeloid-derived suppressor cells (MDSCs) are altered in patients with acute coronary syndrome (ACS). Methods: The frequency of MDSCs in peripheral blood was determined by flow cytometry, and mRNA expression in purified MDSCs was analyzed by real-time reverse transcription polymerase chain reaction (RT-PCR). The suppressive function of MDSCs isolated from different groups was also determined. The plasma levels of certain cytokines were determined using Bio-Plex Pro™ Human Cytokine Assays. Results: The frequency of circulating CD14+HLA-DR-/low MDSCs; arginase-1 (Arg-1) expression; and plasma levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-33 were markedly increased in ACS patients compared to stable angina (SA) or control patients. Furthermore, MDSCs from ACS patients were more potent suppressors of T-cell proliferation and IFN-γ production than those from the SA or control groups at ratios of 1:4 and 1:2; this effect was partially mediated by Arg-1. In addition, the frequency of MDSCs was positively correlated with plasma levels of IL-6, IL-33, and TNF-α. Conclusions: We observed an increased frequency and suppressive function of MDSCs in ACS patients, a result that may provide insights into the mechanisms involved in ACS.

The IL-33/ST2 signaling pathway plays an important role in coronary artery disease (CHD), however, few studies have explored how variants in IL-33/ST2 genes influence CHD risk. Here, we examined the association between genetic variants in IL-33, ST2, and IL-1RAcP of the IL-33/ST2 axis and the risk of CHD. We conducted a case-controlled study with 1146 CHD cases and 1146 age- and sex-frequency-matched controls. Twenty-eight single nucleotide polymorphisms (SNPs) in IL-33, ST2, and IL-1RAcP were genotyped by Sequenom MassArray and TaqMan assay. Logistic regression was used to analyze these associations. The SNP rs4624606 in IL-1RAcP was nominally associated with CHD risk. The AA genotype was associated with a 1.85-fold increased risk of CHD (95% confidence interval (CI) = 1.01–3.36, p = 0.045) compared to the TT genotype. Further analysis showed that AA carriers also had a higher risk of CHD than TT + TA carriers (odds ratio (OR) = 1.85, 95% CI = 1.85–3.35, p = 0.043). However, no significant association was observed between variants in IL-33/ST2 genes and CHD risk. Further studies are needed to replicate our results in other ethnic groups with larger sample size.

Although long-term depression (LTD) is generally considered as one of the underlying mechanisms of learning and memory, the induction of it in vivo seems difficult. Evidence demonstrates that the total synaptic weight is associated with circadian rhythm, with up-regulation in wakefulness and down-regulation during sleep, suggesting that the induction of LTD may also be affected by it. In this study, we found that in two well-established rat models, low-frequency stimuli (LFS) induced LTD upon daytime anesthesia, but not at night. Upon further study, we found that the induction of LTD could not be blocked at night if we deprived sleep of the rats during the daytime. These results indicate that the induction of LTD is facilitated by daytime or sleep deprivation. Since rats both in the daytime and after sleep deprivation share the same character of high sleep pressure, our results suggest that LTD is actually facilitated by high sleep pressure. Our study also provides a possible explanation why some labs can induce LTD in vivo while others cannot. Sleep pressure should be taken into account as one of the key factors on the induction of LTD in vivo.

With the increasing applications of titanium dioxide nanoparticles (TiO(2) NPs) in industry and daily life, an increasing number of studies showed that TiO(2) NPs may have negative effects on the respiratory or metabolic circle systems of organisms, while very few studies focused on the brain central nervous system (CNS). Synaptic plasticity in hippocampus is believed to be associated with certain high functions of CNS, such as learning and memory. Thus, in this study, we investigated the effects of developmental exposure to TiO(2) NPs on synaptic plasticity in rats' hippocampal dentate gyrus (DG) area using in vivo electrophysiological recordings. The input/output (I/O) functions, paired-pulse reaction (PPR), field excitatory postsynaptic potential, and population spike amplitude were measured. The results showed that the I/O functions, PPR, and long-term potentiation were all attenuated in lactation TiO(2) NPs-exposed offspring rats compared with those in the control group. However, in the pregnancy TiO(2) NPs exposure group, only PPR was attenuated significantly. These findings suggest that developmental exposure to TiO(2) NPs could affect synaptic plasticity in offspring's hippocampal DG area in vivo, which indicates that developmental brains, especially in lactation, are susceptible to TiO(2) NPs exposure. This study reveals the potential toxicity of TiO(2) NPs in CNS. It may give some hints on the security of TiO(2) NPs production and application and shed light on its future toxicological studies.

Our previous study showed that placebo expectations can develop in a transferable manner; for example, a placebo expectation developed within an analgesic experience may lead to reduced anxiety. Considering that activities in such emotion-responsive areas as the amygdala and insula can be detected through functional magnetic resonance imaging (fMRI), we used fMRI to further study the transferable placebo anxiolytic effect. A main-effect analysis showed that activity in the amygdala and insula was reduced in the placebo condition, whereas an interaction analysis showed activity in the two regions was selectively attenuated in the placebo condition when unpleasant pictures were viewed. We also observed greater activity in the subgenual anterior cingulate cortex under placebo conditions when either emotionally negative or neutral pictures were viewed. These data suggest that the anxiety-relieving placebo effect arose from a reward-related response underpinned by the participants' expectations.

Past studies indicate that the placebo expectation established by analgesic treatment significantly relieves pain perception, while ataractic treatment significantly alleviates unpleasant arousal evoked by negative picture processing. But it is unclear whether the placebo effect can be transferred from one domain to the other, namely from pain to emotion. In this study we led participants to believe in the analgesic effect of magnetic treatment equipment (the placebo) by secretly reducing the intensity of pain stimulus. Then, we examined if this placebo could significantly alter participants' negative affect evoked by watching unpleasant pictures. Our results indicated a significant transferable placebo effect that alleviated negative feelings. EEG recordings showed the transferable placebo treatment induced decreased P2 amplitude and increased N2 amplitude, with source location near the posterior cingulate.

The present study compared learning-based placebo effect and cognition-based reappraisal, to reveal the common and unique neural mechanisms between the two emotion regulations. First, the anxiety-relieving effect was tested by conducting a behavioral experiment Next, the participants with the highest placebo or reappraisal effect were selected for the functional magnetic resonance imaging experiments. The results indicated that: (1) they both attenuated activity in the right amygdala and right insula, and (2) placebo effect activated the left subgenual cingulate whereas reappraisal activated the right dorsal prefrontal cortex (PFC) and the left inferior PFC. Our results show that learning-based placebo effect and cognition-based reappraisal have common anxiety-relieving effects. The placebo effect mainly depends on direct pathway subgenual cingulate-amygdala to regulate emotions, whereas the reappraisal may rely on both indirect pathways, such as the dorsal PFC-subgenual cingulate-amygdala, and direct pathways, such as the ventral lateral PFC-amygdala to regulate emotions. (c) 2012 Elsevier Inc. All rights reserved.

Placebo analgesia is one of the most robust and best-studied placebo effects. Recent researches suggest that placebo analgesia activated the µ-opioid receptor signalling in the human brain. However, whether other opioid receptors are involved in the placebo analgesia remains unclear. We have previously evoked placebo responses in mice (Guo et al.2010, 2011) and these mice may serve as a model for investigating placebo analgesia. In the present study, we tried to explore the site of action and types of opioid receptors involved in placebo response. Male Sprague–Dawley rats were trained with 10 mg/kg morphine for 4 d to establish the placebo analgesia model. This placebo analgesia can be blocked by injection of 5 mg/kg dose naloxone or by microinjection with naloxone (1, 3 or 10 µg/rat) into rostral anterior cingulate cortex (rACC). Then, animals were tested after intra-rACC microinjection of d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP, a selective µ-opioid receptor antagonist) or naltrindole (NTI, a highly selective δ-opioid receptor antagonist) or nor-binaltorphimine (nor-BNI, a highly selective κ-opioid receptor antagonist). Our results showed that CTOP, but not NTI or nor-BNI, could reduce the pain threshold in placebo analgesia rats. It may be concluded that rACC is the key brain region involved in placebo analgesia and the opioid placebo analgesia is mediated exclusively through µ-opioid receptor in rat.

This study investigates the effects of operational stress and emotional stress on the cardiovascular response. Eighteen female college students completed two stress tasks: a mirror-tracing task (which represented operational stress) and a speech-preparation task (which represented emotional stress). The intensity of the stress tasks was evaluated. The heart rate and blood pressure of the subjects were also recorded. The results indicated that the stress intensity was not significantly different between two tasks. However, in the mirror-tracing task, high frequency (HF) component of heart rate variability (HRV) and the R-R interval were significantly decreased in comparison to in the baseline. In the speech-preparation task, the R-R interval showed significant reduction and the low frequency LF/HF ratio, as well as the systolic and diastolic blood pressure, was significantly increased, in comparison to in the baseline. These results suggested that different changes of the autonomic nerve tone were induced by two stress tasks with the same subjective intensity. Furthermore, the results indicate that sympathetic and parasympathetic activities do not simply work in an antagonistic manner.

Although the regulatory role of cognitive reappraisal in negative emotional responses is widely recognized, this reappraisal's effect on acute saliva secretory immunoglobulin A (SIgA), as well as the relationships among affective, immunological, and event-related potential (ERP) changes, remains unclear. In this study, we selected only people with low positive coping scores (PCSs) as measured by the Trait Coping Style Questionnaire to avoid confounding by intrinsic coping styles. First, we found that the acute stress of viewing unpleasant pictures consistently decreased SIgA concentration and secretion rate, increased perceptions of unpleasantness and amplitude of late positive potentials (LPPs) between 200-300 ms and 400-1000 ms. After participants used cognitive reappraisal, their SIgA concentration and secretion rate significantly increased and their unpleasantness and LPP amplitudes significantly decreased compared with a control condition. Second, we found a significantly positive correlation between the increases in SIgA and the decreases in unpleasantness and a significantly negative correlation between the increases in SIgA and the increases in LPP across the two groups. This study is the first to demonstrate that cognitive reappraisal reverses the decrease of SIgA. In addition, it revealed strong correlations among affective, SIgA and electrophysiological changes with convergent multilevel evidence.

Associations between “lipid-related” candidate genes, blood lipid concentrations and coronary artery disease (CHD) risk are not clear. We aimed to investigate the effect of three newly identified lipids loci from genome-wide association studies on CHD and blood lipid levels in Chinese Han population. The genotypes of SNPs at three newly identified lipid loci and blood lipids concentrations were examined in 1360 CHD patients and 1360 age- and sex-frequency matched controls from an unrelated Chinese Han population. Allele T of rs16996148 occurred less frequently in CHD patients with the odds ratio (OR) being 0.64 (95% CI 0.50 to 0.81), after adjusting for conventional risk factors and was associated with a 33% decreased CHD risk (P

The placebo effect is a fascinating yet puzzling phenomenon, which has challenged investigators over the past 50 years. In previous studies, the investigators only focused on the placebo effect obtained within a single domain, and pain is the field in which most of the placebo research has been performed. However, recent research by our laboratory (Zhang and Luo in Psychophysiology 46:626-634, 2009; Zhang et al. 2011) showed that, in human subjects, the placebo effect can be transferred from one domain to the other, namely from pain to emotion.The scope of this study was to investigate whether placebo analgesia could affect the depressive behavior in mice.Female C57/BL6 mice were trained to associate the context cue with elevated pain tolerance via a set of procedures. Then the forced swim test and tail suspension test were used to measure the depressive-like behaviors on the test day. Plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone were also detected.Our results showed that the placebo analgesia, which was established by a set of procedures in mice, was transferable and could produce a significant antidepressant effect on depressive test. Plasma levels of corticosterone and ACTH further proved that the placebo analgesia that was established from pain-reducing training not only induced a significant placebo effect on pain, but also decreased significantly the hypothalamus-pituitary-adrenal axis (HPA) response to stress and produced a stress-alleviating effect.These data show that placebo analgesia affects the behavioral despair tests and hormonal secretions in mice.

The vast majority of decision-making research is performed under the assumption of the value maximizing principle. This principle implies that when making decisions, individuals try to optimize outcomes on the basis of cold mathematical equations. However, decisions are emotion-laden rather than cool and analytic when they tap into life-threatening considerations. Using functional magnetic resonance imaging (fMRI), this study investigated the neural mechanisms underlying vital loss decisions. Participants were asked to make a forced choice between two losses across three conditions: both losses are trivial (trivial-trivial), both losses are vital (vital-vital), or one loss is trivial and the other is vital (vital-trivial). Our results revealed that the amygdala was more active and correlated positively with self-reported negative emotion associated with choice during vital-vital loss decisions, when compared to trivial-trivial loss decisions. The rostral anterior cingulate cortex was also more active and correlated positively with self-reported difficulty of choice during vital-vital loss decisions. Compared to the activity observed during trivial-trivial loss decisions, the orbitofrontal cortex and ventral striatum were more active and correlated positively with self-reported positive emotion of choice during vital-trivial loss decisions. Our findings suggest that vital loss decisions involve emotions and cannot be adequately captured by cold computation of minimizing losses. This research will shed light on how people make vital loss decisions.