Supramolecular polymers with dual energy storage mechanism for high-performance supercapacitors.

In this paper, we prepared the supramolecular polymers (MWCNT-APP-s) with a dual energy storage mechanism as the electrode materials by the coordination of four transition metal ions with the small molecule chelator (APP) and functionalized carbon nanotubes, respectively. Among four MWCNT-APP-s, MWCNT-APP-Fe has the characteristics of moderate micropore/mesopore, significant hydrophobicity, redox property and functional groups. Interestingly, the redox reaction of Fe3+/Fe2+ and -CN-/-CN- transformation give MWCNT-APP-Fe an energy storage basis of pseudocapacitance, while MWCNTs and the micro/mesopore structure in MWCNT-APP-Fe provide a double-layer energy storage platform. As expected, on base of the dual energy storage mechanism, the symmetric supercapacitor assembled with MWCNT-APP-Fe has a higher specific capacity (Cs, 421 F g-1 at 1 mV s-1) as well as a long-lasting stability of 94.8% capacity retention with 99% Coulombic efficiency after 10,000 cycles at 20 mV s-1. More notably, the relevant aqueous Zn2+ hybrid supercapacitor provides a high capacity (Cm) of 191 mAh g-1 at 0.5 A g-1 and a long duration of over 2000 cycles at 50 A g-1, with a capacity retention of 92.4%. In summary, MWCNT-APP-Fe with a dual energy storage mechanism enables a potential application as an electrode material for high-performance supercapacitor.

Fecal fermentation and high-fat diet-induced obesity mouse model confirmed exopolysaccharide from Weissella cibaria PFY06 can ameliorate obesity by regulating the gut microbiota.

Obesity associated with diet and intestinal dysbiosis is a worldwide public health crisis, and exopolysaccharides (EPS) produced by lactic acid bacteria (LAB) have prebiotic potential to ameliorate obesity. Therefore, the present study obtained LAB with the ability to produce high EPS, examined the structure of EPS, and explained its mechanism of alleviating obesity by in vivo and in vitro models. The results showed that Weissella cibaria PFY06 with a high EPS yield was isolated from strawberry juice, and pure polysaccharide (PFY06-EPS) was purified by Sephadex G-100. The structural characteristics of PFY06-EPS showed that the molecular weight was 8.08 × 106 Da and composed of α-(1,6)-D glucosyl residues. An in vitro simulated human colon fermentation test demonstrated that PFY06-EPS increased the abundance of Prevotella and Bacteroides. Cell tests confirmed that PFY06-EPS after fecal fermentation inhibited fat accumulation by promoting the secretion of endogenous gastrointestinal hormones and insulin and inhibiting the secretion of inflammatory factors. Notably, PFY06-EPS reduced weight gain, fat accumulation, inflammatory reactions and insulin resistance in a high-fat diet-induced obesity mouse model and improved glucolipid metabolism. PFY06-EPS intervention reversed obesity-induced microflora disorders, such as reducing the Firmicutes/Bacteroides ratio and increasing butyrate-producing bacteria (Roseburia and Oscillibacter), and reduced endotoxemia to maintain intestinal barrier integrity. Therefore, in vivo and in vitro models showed that PFY06-EPS had potential as a prebiotic that may play an anti-obesity role by improving the function of the gut microbiota.

MiR-454-3p promotes apoptosis and autophagy of AML cells by targeting ZEB2 and regulating AKT/mTOR pathway.

BACKGROUND: miR-454-3p is considered to have a crucial role in cancer progression, but the potential involvement in acute myeloid leukemia (AML) remains unclear. METHODS: Expression of miR-454-3p and ZEB2 mRNA and protein were quantified in AML cell lines. Cells were transfected with miR-454-3p inhibitor or mimic and cell growth was assessed by colony formation and CCK-8 assays and the cell cycle, apoptosis and autophagy were investigated by Western blotting, flow cytometry, immunofluorescence and 3-methyladenine (3-MA) treatment. RESULTS: miR-454-3p expression was attenuated in AML cells. miR-454-3p overexpression attenuated cell growth and stimulated cell cycle arrest, apoptosis and autophagy. Dual-luciferase reporter assays and bioinformatics analysis showed that AML progression was inhibited when miR-454-3p regulated ZEB2, an effect confirmed by rescue assays. 3-MA reduced the autophagy-inducing effect of ZEB2 knockdown and indicated that autophagy induced apoptosis. miR-454-3p downregulated p-mTOR/p-AKT levels in AML cells. CONCLUSION: The novel role of miR-454-3p as a tumor inhibitor in AML via regulation of the ZEB2/AKT/mTOR axis was demonstrated, indicating miR-454-3p as a potential new molecular target for AML.

DNMT3A R882H mutation promotes acute leukemic cell survival by regulating glycolysis through the NRF2/NQO1 axis.

BACKGROUND: Studies have confirmed that acute myeloid leukemia (AML) cells with DNA methyltransferase 3A Arg882His (DNMT3A R882H) mutation show an increased proliferation capability. However, the associated mechanism is still unclear. Glycolysis is involved in regulating malignant proliferation of cancer cell. Hence, we analyzed whether the DNMT3A R882H mutation interferes with glycolysis and thereby influences AML cell proliferation. METHODS: We generated AML cell line carrying a DNMT3A-R882H mutation and compared it with the wild type (DNMT3A-WT) with regard to glycolysis regulation. Moreover, we analyzed the cell line's proliferation and apoptosis by a CCK-8 assay, western blotting, and flow cytometry. The role of NRF2/NQO1 signaling in regulating glycolysis was investigated by NRF2-knockdown and Brusatol (specific inhibitor of NRF2) treatment. RESULTS: DNMT3A R882H cells had a higher glucose transport capacity compared to WT cells and their viability could be reduced by glucose deprivation. Moreover, daunorubicin had a slight inhibitory effect on glycolysis while glycolysis inhibition re-sensitized mutant cells to daunorubicin. Obviously, DNMT3A R882H mutation activated the NRF2/NQO1 pathway and enhanced the glycolytic activity in mutant cells. CONCLUSION: Taken together, these results suggest a novel mechanism by which a DNMT3A R882H mutation promotes glycolysis via activation of NRF2/NQO1 pathway. A parallel glycolysis inhibition adds to the anticancer effects of daunorubicin which might lead to a novel therapeutic approach for the treatment of AML patients carrying a DNMT3A R882H mutation.

Evaluation of antioxidation, regulation of glycolipid metabolism and potential as food additives of exopolysaccharide from Sporidiobolus pararoseus PFY-Z1.

At present, there are relatively few studies on the production of exopolysaccharide (EPS) by yeasts. Therefore, exploring the properties of EPS produced by yeast can not only enrich the source of EPS, but also play an important role in its future application in the food field. The aim of this study was to explore the biological activities of EPS (named SPZ) from Sporidiobolus pararoseus PFY-Z1, as well as the dynamic changes in physical and chemical properties that occur during simulated gastrointestinal digestion, and the effects of SPZ on microbial metabolites during fecal fermentation in vitro. The results revealed that SPZ had good water solubility index, water-holding capacity, emulsifying ability, coagulated skim milk, antioxidant properties, hypoglycemic activities, and bile acid-binding abilities. Furthermore, the content of reducing sugars increased from 1.20 ± 0.03 to 3.34 ± 0.11 mg/mL after gastrointestinal digestion, and had little effect on antioxidant activities. Moreover, SPZ could promote the production of short-chain fatty acids during fermentation for 48 h, in particular, propionic acid and n-butyric acid increased to 1.89 ± 0.08 and 0.82 ± 0.04 mmol/L, respectively. Besides this, SPZ could inhibit LPS production. In general, this study can help us to better understand the potential bioactivities, and the changes in bio-activities of compounds after digestion of SPZ.

Downregulation of Polo-like kinase 4 induces cell apoptosis and G2/M arrest in acute myeloid leukemia.

BACKGROUND: Polo-like kinase 4 (PLK4) is a crucial regulator for centriole replication and is reported to be aberrantly expressed in various cancers, where it participates to tumorigenesis. However, PLK4 effect in acute myeloid leukemia (AML), is still uncertain. This study investigates the function of PLK4 in AML. METHODS: Quantitative real-time PCR was used to measure the level of PLK4. Centrinone, a selective PLK4 small molecule inhibitor, was used for PLK4 inhibition and explore its effect in AML cells. The cell growth was detected by the CCK8, while the cell cycle and apoptosis were assessed by flow cytometry. The level of proteins associated with apoptosis, cell cycle and endoplasmic reticulum (ER) stress were analyzed by western blotting. RESULTS: PLK4 was overexpressed in AML cells. PLK4 knockdown or its specific inhibition by centrinone induced G2/M phase arrest via suppressing the expression of cyclin B1 and Cdc2 and promoting the level of proapoptotic proteins. Moreover, PLK4 targeting enhanced the level of proteins related to ER stress, such as GRP78, ATF4, ATF6, and CHOP. CONCLUSION: These findings demonstrated that targeting PLK4 can induce apoptosis, G2/M and ER stress in AML cells.

Exploration of the cysteine reactivity of human inducible Hsp70 and cognate Hsc70.

Hsp70s are multifunctional proteins and serve as the central hub of the protein quality control network. Hsp70s are also related to a number of diseases and have been established as drug targets. Human HspA1A (hHsp70) and HspA8 (hHsc70) are the major cytosolic Hsp70s, and they have both overlapping and distinct functions. hHsp70 contains five cysteine residues, and hHsc70 contains four cysteine residues. Previous studies have shown these cysteine residues can undergo different cysteine modifications such as oxidation or reaction with electrophiles to regulate their function, and hHsp70 and hHsc70 have different cysteine reactivity. To address the mechanism of the differences in cysteine reactivity between hHsp70 and hHsc70, we studied the factors that determine this reactivity by Ellman assay for the quantification of accessible free thiols and NMR analysis for the assessment of structural dynamics. We found the lower cysteine reactivity of hHsc70 is probably due to its lower structural dynamics and the stronger inhibition effect of interaction between the α-helical lid subdomain of the substrate-binding domain (SBDα) and the ß-sheet substrate-binding subdomain (SBDß) on cysteine reactivity of hHsc70. We determined that Gly557 in hHsp70 contributes significantly to the higher structural dynamics and cysteine reactivity of hHsp70 SBDα. Exploring the cysteine reactivity of hHsp70 and hHsc70 facilitates an understanding of the effects of redox reactions and electrophiles on their chaperone activity and regulation mechanisms, and how these differences allow them to undertake distinct cellular roles.

Production, characterization and antioxidant activity of exopolysaccharide from Sporidiobolus pararoseus PFY-Z1.

At present, the study on exopolysaccharid is mainly focused on lactic acid bacteria, and the research on exopolysaccharide produced by yeast, especially Sporidiobolus pararoseus, is relatively few. Therefore, the aim of this study was to explore the characterization and antioxidant activities of a novel neutral exopolysaccharide SPZ, which was isolated and purified from S. pararoseus PFY-Z1. The results showed that SPZ was mainly composed of mannose, followed by glucose, with a molecular weight was 24.98 kDa, had O-glycosidic bonds, no crystalline, and no triple helix structure. Based on fourier transform-infrared, high-performance liquid chromatography and nuclear magnetic resonance analyses, SPZ was identified to be a exopolysaccharide with some side chains, presence of α-, ß-pyranose ring and nine sugar residues. Furthermore, the morphology features of SPZ have performed a relatively rough and uneven surface, covered with small pores and fissures. Moreover, SPZ had higher antioxidant activities and the maximum scavenging abilities of ⋅OH, NO2- and reducing power were 28.05 ± 0.73%, 92.76 ± 1.86% and 0.345 ± 0.024, respectively. Hence, SPZ could be used as a potential antioxidant application in the food and pharmaceutical industries.

DNMT3A R882H mutation drives daunorubicin resistance in acute myeloid leukemia via regulating NRF2/NQO1 pathway.

BACKGROUND: DNA methyltransferase 3A (DNMT3A) often mutate on arginine 882 (DNMT3AR882) in acute myeloid leukemia (AML). AML patients with DNMT3A R882 mutation are usually resistant to daunorubicin treatment; however, the associated mechanism is still unclear. Therefore, it is urgent to investigate daunorubicin resistance in AML patients with DNMT3A R882 mutant. METHOD: AML cell lines with DNMT3A-wild type (DNMT3A-WT), and DNMT3A-Arg882His (DNMT3A-R882H) mutation were constructed to investigate the role of DNMT3A R882H mutation on cell proliferation, apoptosis and cells' sensitivity to Danunorubin. Bioinformatics was used to analyze the role of nuclear factor-E2-related factor (NRF2) in AML patients with DNMT3A R882 mutation. The regulatory mechanism of DNMT3A R882H mutation on NRF2 was studied by Bisulfite Sequencing and CO-IP. NRF2 inhibitor Brusatol (Bru) was used to explore the role of NRF2 in  AML cells carried DNMT3A R882H mutation. RESULTS: AML cells with a DNMT3A R882H mutation showed high proliferative and anti-apoptotic activities. In addition, mutant cells were less sensitive to daunorubicin and had a higher NRF2 expression compared with those in WT cells. Furthermore, the NRF2/NQO1 pathway was activated in mutant cells in response to daunorubicin treatment. DNMT3A R882H mutation regulated the expression of NRF2 via influencing protein stability rather than decreasing methylation of NRF2 promoter. Also, NRF2/NQO1 pathway inhibition improved mutant cells' sensitivity to daunorubicin significantly. CONCLUSION: Our findings identified NRF2 as an important player in the regulation of cell apoptosis through which helps mediate chemoresistance to daunorubicin in AML cells with DNMT3A R882H mutation. Targeting NRF2 might be a novel therapeutic approach to treat AML patients with a DNMT3A R882H mutation. Video abstract.

miRNA-222-3p enhances the proliferation and suppresses the apoptosis of acute myeloid leukemia cells by targeting Axin2 and modulating the Wnt/ß-catenin pathway.

MicroRNA (miRNA)-222-3p is overexpressed in numerous tumors, where it acts as an oncogene. Although miRNA-222 is highly expressed in acute myeloid leukemia (AML), its functions and the mechanisms underlying these functions have not yet been fully elucidated. This study aimed to investigate the regulatory roles of miRNA-222-3p in AML and the molecular mechanisms underlying these roles. In this study, we observed that miRNA-222-3p increased the viability and suppressed the apoptosis of AML cells. Axin2 was demonstrated to be a direct target of miRNA-222-3p, which when overexpressed, inhibited Axin2 expression and stimulated the Wnt/ß-catenin pathway. In contrast, upregulation of Axin2 expression levels reduced the viability and enhanced the apoptosis of AML cells. Moreover, it partially reversed the effects of the miRNA-222-3p mimic on the proliferation and apoptosis of, and modulation of the Wnt/ß-catenin pathway in, AML cells. Taken together, this study provides strong evidence that miRNA-222-3p can serve as a molecular target for AML treatment.

RIP1-dependent Apoptosis and Differentiation Regulated by Skp2 and Akt/GSK3ß in Acute Myeloid Leukemia.

Acute myeloid leukemia (AML) is a heterogeneous neoplasm characterized by variations in cytogenetics and molecular abnormalities, which result in variable response to therapy. Receptor-interacting serine/threonine kinase 1 (RIP1)-mediated necroptosis has been reported to have a potential role in the treatment of AML. We obtained Skp2 and RIP1 are significantly overexpressed in AML samples using original published data, and identified that Skp2-depletion in AML cells significantly suppressed RIP1. Functional analysis showed that the inhibition of RIP1 caused by necrostatin-1 (Nec-1) inhibited the proliferation, simultaneously facilitate both the apoptosis and differentiation of AML cells. Mechanistical analysis elucidated that knockdown of Skp2 suppresses RIP1 by transcriptional regulation but not by proteasome degradation. Additionally, Skp2 regulated the function of RIP1 by decreasing K63-linked ubiquitin interaction with RIP1. Moreover, the suppression of Akt/GSK3ß was observed in Skp2 knockdown stable NB4 cells. Also, GSK3ß inactivation via small-molecule inhibitor treatment remarkably decreased RIP1 level. RIP1 regulates differentiation by interacting with RARα, increasing RA signaling targets gene C/EBPα and C/EBPß. In conclusion, our study provides a novel insight into the mechanism of tumorigenesis and the development of AML, for which the Skp2-Akt/GSK3ß-RIP1 pathway can be developed as a promising therapeutic target.

The Effectiveness and Adverse Events of Amitriptyline and Aripiprazole in Very Elderly Patients With BMS.

Burning mouth syndrome (BMS) is defined by chronic oral burning sensations without any corresponding abnormalities. Besides amitriptyline, aripiprazole has been reported as a possible medication to manage BMS. However, especially for elderly patients, the adverse events of these medications would be a problem. The aim of the present study was to investigate the differences in the effectiveness and adverse events of amitriptyline and aripiprazole in very elderly patients with BMS. This is a retrospective comparative study of 80 years old and older patients with BMS who were initially treated with amitriptyline or aripiprazole and who were new outpatients of our department from April 2017 to March 2020. All clinical data, including sex, age, comorbid physical diseases, comorbid psychiatric disorders, the prescribed doses (initial, maximum, and effective dose), prognosis, and adverse events, were collected from their medical charts. Each medication was selected considering their medical history. Amitriptyline was prescribed in 13 patients (11 women, 82.3 ± 2.1 years old) and aripiprazole was prescribed in 27 patients (26 women, 84.2 ± 3.8 years old). There were no significant between-group differences in sex, age, duration of illness, pain intensity, salivation, and psychiatric comorbidity at the first examination. Amitriptyline clinically improved more patients (7 patients, 53.8%) with the effective dose of 10 (7.5, 15.0) mg than aripiprazole (11 patients, 40.7%) of which the effective dose was 1.0 (0.5, 1.5) mg, although there were no significant between-group differences. The adverse events of amitriptyline were found in 9 patients (69.2%) and most patients had constipation (46.2%). For aripiprazole, 7 patients (25.9%) showed adverse events, most of them reported sleep disorder (11.1%). Amitriptyline had significantly longer duration taking medication (p = 0.021) and lower discontinuation (p = 0.043) despite of higher occurrence rate of adverse events (p = 0.015) compared to aripiprazole. These results suggest that both psychopharmacotherapies with a low dose of amitriptyline and aripiprazole are effective for the very elderly patients with BMS. Furthermore, aripiprazole may have some advantages in the adverse events compared to amitriptyline; however, the low dose amitriptyline monotherapy may have more benefit in the effectiveness and tolerability over prudent collaboration with primary physicians.

MiRNA-301b-3p induces proliferation and inhibits apoptosis in AML cells by targeting FOXF2 and regulating Wnt/ß-catenin axis.

BACKGROUND: MiRNA-301b-3p functions as an oncomiRNA or tumor suppressor, and has been reported in various cancer types, including pancreatic, colorectal, oral, hepatocellular and lung cancers. Although the expression of miRNA-301b-3p is upregulated in acute myeloid leukemia (AML), its biological function and precise mechanisms remain unclarified. This study explores the roles of miRNA-301b-3p in AML, with the aim of ascertaining its regulatory action on Wnt/ß-catenin axis by targeting Forkhead box F2 (FOXF2). METHODS: The expression levels of miRNA-301b-3p and FOXF2 were measured by quantitative real-time PCR. The effects of miRNA-301b-3p knockdown and overexpression on cell proliferation were evaluated by CCK8 and cell counting assays, while cell apoptosis was analyzed by flow cytometry. The expression levels of apoptosis-related proteins, including FOXF2, and other targets in Wnt/ß-catenin axis were determined by immunoblotting. Possible interaction between miRNA-301-3p and FOXF2 in AML cells was examined by luciferase reporter assays. RESULTS: MiRNA-301b-3p was dramatically upregulated in AML cells, and showed a negative correlation with FOXF2 expression. Downregulation of miRNA-301b-3p suppressed proliferation and promoted apoptosis in AML cells. MiRNA-301b targeted FOXF2 to regulate Wnt/ß-catenin axis. In the rescue experiments, FOXF2 overexpression partly reversed the effect of miRNA-301b-3p mimic in AML cells. CONCLUSION: The current findings demonstrate that miRNA-301b-3p targets FOXF2 to induce proliferation and inhibit apoptosis in AML cells via regulation of Wnt/ß-catenin axis.

ZFP91 promotes cell proliferation and inhibits cell apoptosis in AML via inhibiting the proteasome-dependent degradation of RIP1.

Acute myeloid leukemia (AML) is a quickly progressive and devastated hematological malignancy with large rate of relapse and the appearance of chemotherapy resistance. Therefore, the identification of new therapeutic targets is urgent. ZFP91 is a hidden oncogene. Nevertheless, how ZFP91 takes part in regulating AML is less clear. Our research aims at investigating the molecular mechanisms and uncovering the effects of ZFP91 on AML. This research demonstrates that ZFP91 boosts AML cell proliferation and stops AML cell apoptosis. Mechanistically, experimental results showed the interaction between ZFP91 and RIP1 and inhibitory effect of ZFP91 on the K48-linked ubiquitination of endogenous RIP1, which is an important molecule in AML. Taken together, our results provide the evidence that targeted inhibition of ZFP91 could be a hopeful measure to treat AML.

PES derivative PESA is a potent tool to globally profile cellular targets of PES.

PES (2-phenylethynesulfonamide, pifithrin-µ, PFTµ) is an electrophilic compound that exhibits anticancer properties, protects against chemotherapy-induced peripheral neuropathy in chemotherapy, and shows immunomodulatory, anti-inflammatory and anti-viral activities. PES generally shows higher cytotoxicity towards tumor cells than non-tumor cells. The mechanism of action of PES is unclear but may involve the covalent modification of proteins as PES has been found to be a covalent inhibitor of Hsp70. We developed a new PES derivative PESA with a terminal alkynyl group to perform click-reaction-assisted activity-based protein profiling (click-reaction ABPP) and used this to screen for cellular targets of PES. We found PES and its derivatives PES-Cl and PESA have comparable ability to undergo a Michael addition reaction with GSH and Hsp70, and showed similar cytotoxicity. By fluorescence imaging and proteomics studies we identified over 300 PESA-attached proteins in DOHH2 cells. Some proteins involved in cancer-related redox processes, such as peroxiredoxin 1 (PRDX1), showed higher frequency and abundance in mass spectrometry detection. Our results suggest that cytotoxicity of PES and its derivatives may be related to attack of protein thiols and cellular GSH resulting in breakdown of cellular redox homeostasis. This study provides a powerful new tool compound within the PES class of bioactive compounds and gives insight into the working mechanisms of PES and its derivatives.

Simultaneous reduction in cadmium and arsenic accumulation in rice (Oryza sativa L.) by iron/iron-manganese modified sepiolite.

It is challenging to reduce the cadmium (Cd) and arsenic (As) contents of brown rice simultaneously due to their converse chemical behaviors in the paddy soil. Clay minerals, such as sepiolite (SEP), have significant advantages in remediating Cd-contaminated soil. Moreover, iron or manganese oxide loaded SEP can improve the As adsorption efficiency. Herein, ferric nitrate modified sepiolite (NIMS) and iron­manganese modified sepiolite (FMS) were prepared to study their effects on Cd and As accumulation in rice using pot experiments. The results showed that NIMS and FMS had a larger specific surface area than SEP. The application of SEP only decreased Cd content (by 45%), while NIMS and FMS treatments reduced both Cd (by 57% and 87%) and As (by 30% and 25%) contents in brown rice compared with the control. The X-ray photoelectron spectroscopy (XPS) analysis results indicated that MnO2 and MnOOH⁎ in FMS enhanced the adsorption and co-precipitation of Cd as well as the oxidation of As(III) to As(V). The NIMS, as well as the FMS application, increased soil pH, decreased the exchangeable Cd and non-specifically and specifically adsorbed As fractions in soil, and reduced the level of Cd in the pore water. Moreover, NIMS and FMS addition limited the transfer of As from the soil to the roots by enhancing its sequestration in the iron plaque. On the other hand, FMS treatment significantly promoted the uptake of Mn by rice (P < 0.05). The results suggested that both NIMS and FMS were promising materials for simultaneous reduction of Cd and As accumulation in rice. Notably, FMS had better performance in reducing the Cd content in rice than that of NIMS.

Clinical Characteristics of Predominantly Unilateral Oral Cenesthopathy With and Without Neurovascular Contact.

Oral cenesthopathy (OC) is characterized by unusual oral discomfort without corresponding evidence, and it has often been categorized as "delusional disorder, somatic type". Regarding possible causative factors of OC, involvement of neurovascular contact (NVC) of the trigeminal nerve, which transmits not only pain but also thermal, tactile, and pressure sensations, has never been observed yet. This study aimed to investigate the relationship between clinical characteristics of unilateral OC and the presence of trigeminal nerve NVC. This is a retrospective comparative study that involved 48 patients having predominantly unilateral OC who visited the Psychosomatic Dentistry Clinic of Tokyo Medical and Dental University between April 2016 and February 2019. Magnetic resonance imaging was performed to assess NVC presence. The Oral Dysesthesia Rating Scale (Oral DRS) was used to assess the various oral sensations and functional impairments besides psychometric questionnaires. Clinical characteristics were retrospectively obtained from the patients' medical charts. NVC was present in 45.8% (22/48) of the patients. There was no significant difference in sex, age, psychiatric history, oral psychosomatic comorbidity, and psychometric questionnaire scores between patients with and without NVC. However, compared to the patients with NVC, the patients without NVC had significantly higher scores for overall subjective severity of OC symptoms (p = 0.008). Moreover, patients having predominantly unilateral OC without NVC showed significantly higher scores in symptom severity and functional impairment of the following parameters: movement (p = 0.030), work (p = 0.004), and social activities (p = 0.010). In addition, compared with the patients with NVC, the patients without NVC showed significantly higher averages of the total symptom severity scale (SSS) and functional impairment scale (FIS) scores in the Oral DRS (p = 0.015 and p = 0.031, respectively). Furthermore, compared with the patients with NVC, the patients without NVC had significantly higher numbers of corresponding symptoms in both the SSS and FIS (p = 0.041 and p = 0.007, respectively). While NVC may be involved in the indescribable subtle OC symptoms, more complex mechanisms may also exist in OC patients without NVC, which yield varying and more unbearable oral symptoms.

Case Report: Iatrogenic Dental Progress of Phantom Bite Syndrome: Rare Cases With the Comorbidity of Psychosis.

Introduction: Phantom bite syndrome (PBS) is considered as the preoccupation with dental occlusion and the continual inability to adapt to changed occlusion. These patients constantly demand occlusal corrections and undergo extensive and excessive dental treatments. We present three cases with PBS-suspected iatrogenic concerns and the attribution to underlying psychosis. Case Presentation: A 70-year-old female demanded orthodontic retreatment and complained of tightness and cramped sensation of teeth in the oral cavity, uncomfortable occlusion, and pain in her neck and legs that she was convinced was induced by orthodontic treatment. However, even earlier than the orthodontic treatment, she had kept doctor shopping for over 35 years, not merely dentists but also psychiatrists, neurologists, and so on; she was diagnosed with bipolar disorder. A 48-year-old female complained of malaligned improper occlusion and demanded occlusal adjustment. These symptoms occurred in the absence of a dental trigger and were worsened by orthodontic treatment. She underwent psychiatric treatment for 15 years with a diagnosis of bipolar disorder. A 38-year-old female, who had a history of schizophrenia for over 20 years, complained of occlusal discomfort and revisited with a complaint of abnormal occlusion due to excessive dental procedures. In the last two cases, requests for dental procedures had reduced owing to the collaboration between the psychiatrists and dentists. All the cases first visited our clinic following a succession of dental visits. They were strongly convinced that occlusal correction was the only solution to their symptoms, including the symptoms of discomfort in other body parts. Their misleading perceptions were uncorrectable, and repeated dental treatments exacerbated their complaints. Moreover, the dentists overlooked the psychotic histories of the patients, while the comorbid psychosis resulted in a strict demand for dental treatment by the patients. Conclusions: The presented PBS cases with psychosis suggest that repeated dental treatments and comorbid psychosis exacerbate PBS. Moreover, their persistent demands reflecting comorbid psychosis led dentists to perform numerous procedures. Early detection of underlying psychosis and the prompt collaboration between psychiatrists and dentists are integral to help prevent complications in PBS cases with psychosis.

[Screening of Amendments for Simultaneous Cd and As Immobilization in Soil].

Simultaneously reducing the availability of Cd and As is difficult owing to converse chemical behaviors of Cd and As in soil. In this study, amendments that can simultaneously immobilize Cd and As in soil were determined by an pure soil culture experiment in which flooding and wetting were performed for 30 d each. The effects of sepiolite (Sep), modified sepiolite (IMS and Sep-FM), steel slag (SS), and iron modified biochar (Fe-Bio) on soil pH, Eh, Cd, and As concentrations in pore water, and Cd and As fractions in soil were investigated. It showed that Sep (1%, 2.5%), IMS (1%, 2.5%), Sep-FM (1%, 2.5%), and SS (1%, 5%) treatments increased soil pH value and decreased Eh value and Cd concentrations in soil solution. In addition, As concentrations in soil solution treated with high doses of IMS (2.5%) and SS (5%) were lower than that of CK treatment during the whole incubation period. However, Fe-bio treatment decreased soil pH and increased Eh value and only decreased Cd and As concentrations in soil solution under wet conditions. Compared with the control, the application of the above amendments promoted the transformation of Cd fraction from exchangeable to reducible, oxidizable, and residual. High application rates of IMS (2.5%), Sep-FM (2.5%), and SS (5%) also reduced available As fraction (non-specifically sorbed and specifically-sorbed As fraction), and increased amorphous and poorly-crystalline hydrated Fe and Al oxide-bound As. On the contrary, Fe-bio treatment increased the fractions of non-specifically sorbed, specifically sorbed and residual As in soil. In short, IMS, Sep-FM, and SS are potential materials for remediation of Cd and As contaminated soil. They can effectively immobilize soil Cd and As and promote their transformation to the fractions that plants are difficult to uptake.

Amelioration of aggregate cytotoxicity by catalytic conversion of protein oligomers into amyloid fibrils.

The aggregation of peptides and proteins into amyloid fibrils is a molecular self-assembly phenomenon associated with both biological function and malfunction, notably in the context of neurodegenerative diseases. Oligomeric species formed early in the aggregation process are generally associated with cytotoxicity. Extrinsic molecules such as peptides have been found to influence amyloid formation kinetics and regulate this cellular process. Here, we use single-molecule FRET and bulk assays combined with global kinetic analysis to study quantitatively the effect of an 8-residue peptide (LQVNIGNR) on fibril formation by the yeast prion protein Ure2. This peptide, which is derived from a segment of the Ure2 prion domain, forms vesicular assemblies that accelerate fibril formation of Ure2 by promoting conformational conversion of oligomeric intermediates into fibrillar species in a catalytic manner. This reduces oligomer longevity and consequently ameliorates cytotoxicity. The LQVNIGNR peptide was found to accelerate fibril formation of unrelated proteins including Tau and α-Synuclein, suggesting a general ability to catalyse fibrillation. This study provides a general strategy for investigating the microscopic mechanism of extrinsic factors on amyloid aggregation. This approach can readily be applied to other amyloid systems and demonstrates that acceleration of oligomer conversion is a promising strategy to reduce amyloid toxicity.