Hesperetin derivative 2a inhibits lipopolysaccharide-induced acute liver injury in mice via downregulation of circDcbld2.

Acute liver injury (ALI) is a complex, life-threatening inflammatory liver disease, and persistent liver damage leads to rapid decline and even failure of liver function. However, the pathogenesis of ALI is still not fully understood, and no effective treatment has been discovered. Recent evidence shows that many circular RNAs (circRNAs) are associated with the occurrence of liver diseases. In this study we investigated the mechanisms of occurrence and development of ALI in lipopolysaccharide (LPS)-induced ALI mice. We found that expression of the circular RNA circDcbld2 was significantly elevated in the liver tissues of ALI mice and LPS-treated RAW264.7 cells. Knockdown of circDcbld2 markedly alleviates LPS-induced inflammatory responses in ALI mice and RAW264.7 cells. We designed and synthesized a series of hesperidin derivatives for circDcbld2, and found that hesperetin derivative 2a (HD-2a) at the concentrations of 2, 4, 8 µM effectively inhibited circDcbld2 expression in RAW264.7 cells. Administration of HD-2a (50, 100, 200 mg/kg. i.g., once 24 h in advance) effectively relieved LPS-induced liver dysfunction and inflammatory responses. RNA sequencing analysis revealed that the anti-inflammatory and hepatoprotective effects of HD-2a were mediated through downregulating circDcbld2 and suppressing the JAK2/STAT3 pathway. We conclude that HD-2a downregulates circDcbld2 to inhibit the JAK2/STAT3 pathway, thereby inhibiting the inflammatory responses in ALI. The results suggest that circDcbld2 may be a potential target for the prevention and treatment of ALI, and HD-2a may have potential as a drug for the treatment of ALI.

Circular RNA circUbe2k promotes hepatic fibrosis via sponging miR-149-5p/TGF-ß2 axis.

Abundant regulatory genes and complex circuits involving non-coding RNAs (ncRNAs) monitor the formation and development of hepatic fibrosis (HF). Circular RNAs (circRNAs) are a class of RNAs generated from protein coding genes by back-splicing, playing crucial roles in various pathological processes, including HF. However, little is known about mechanisms of action of circRNAs, let alone in HF. In this study, we found circUbe2k enhanced in CCl4 -induced HF mice and LX-2 cells stimulated with TGF-ß1, regulating the development of HF. Restraining the expression of circUbe2k inhibited α-SMA and Col1α1 expression in CCl4 -induced HF mice and in LX-2 cells stimulated with TGF-ß1. Furthermore, inhibiting circUbe2k expression reduced hepatic stellate cells (HSCs) activation and proliferation in vivo and in vitro. Mechanistically, we demonstrated a direct interaction between circUbe2k and miR-149-5p, which results in the modulation of TGF-ß2 expressions. Together, circUbe2k may act as a "catalyst" of HSCs activation and HF through the circUbe2k/miR-149-5p/TGF-ß2 axis. Our results provide unprecedented evidence for a significant role for circUbe2k to serve as a potential biomarker for HF therapy.

Hesperetin derivative decreases CCl4 -induced hepatic fibrosis by Ptch1-dependent mechanisms.

Hepatic fibrosis (HF), a continuous wound-healing response of the liver to repeated injuries, is characterized by abnormal extracellular matrix (ECM) accumulation. Hepatic stellate cells (HSCs) are considered a major cell type for ECM production. However, recent evidence indicates the lack of effective treatments for HF. Hesperetin, a Traditional Chinese Medicine monomer, has been isolated from the fruit peel of Citrusaurantium L. (Rutaceae). Growing evidence suggests the partial function of hesperetin in HF treatment. A hesperetin derivative (HD) was synthesized in our laboratory to increase the bioavailability and the water solubility of hesperetin. In this study, we detected the functions of HD in a mouse model of CCl4 -induced HF and transforming growth factor-ß1-stimulated HSC-T6 cells, in vivo and in vitro. HD reduced histological damage and CCl4 -induced HF. Moreover, HD interference was associated with the activation of indicators in HSC-T6 cells, showing that HD is involved in HSCs activation in HF. Mechanistically, the Hedgehog pathway is involved in the HD treatment of HF, and HD may attenuate the aberrant expression of patched1. In conclusion, the studies indicate that HD may function as a potential antifibrotic Traditional Chinese Medicine monomer in HF therapy.

miR-324-3p Suppresses Hepatic Stellate Cell Activation and Hepatic Fibrosis Via Regulating SMAD4 Signaling Pathway.

In hepatic fibrosis (HF), hepatic stellate cells (HSCs) form the extracellular matrix (ECM), and the pathological accumulation of ECM in the liver leads to inflammation. Our previous research found that miR-324-3p was down-regulated in culture-activated human HSCs. However, the precise effect of miR-324-3p on HF has not been elucidated. In this study, the HF mouse models were induced through directly injecting carbon tetrachloride (CCl4) into mice; the HF cell models were constructed using TGF-ß1-treated LX-2 cells. Next, real-time-quantitative polymerase chain reaction (RT-qPCR), western blot (WB) and immunohistochemistry (IHC) were applied to assess the expression levels of miR-324-3p, α-smooth muscle actin (α-SMA), Vimentin or SMAD4; hematoxylin and eosin (H&E), Masson' s trichrome and Sirius red staining to evaluate the liver injury; luciferase reporter assay to verify the targeting relationship between miR-324-3p and SMAD4; enzyme-linked immunosorbent assay (ELISA) to determine the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST); and cell counting kit-8 (CCK-8) and flow cytometry to evaluate the effects of miR-324-3p on cell proliferation and cycle/apoptosis, respectively. The experimental results showed a reduction in miR-324-3p level in CCl4-induced HF mice as well as transforming growth factor (TGF)-ß1-activated HSCs. Interestingly, the miR-324-3p level was rescued following the HF recovery process. In HF mice induced by CCl4, miR-324-3p overexpression inhibited liver tissue damage, decreased serum ALT and AST levels, and inhibited fibrosis-related biomarkers (α-SMA, Vimentin) expression, thereby inhibiting HF. Similarly, miR-324-3p overexpression up-regulated α-SMA and Vimentin levels in HF cells, while knockdown of miR-324-3p had the opposite effect. Besides, miR-324-3p played an antifibrotic role through inhibiting the proliferation of hepatocytes. Further experiments confirmed that miR-324-3p targeted and down-regulated SMAD4 expression. SMAD4 was highly expressed in HF cells, and silencing SMAD4 significantly decreased the α-SMA and Vimentin levels in HF cells. Collectively, the miR-324-3p may suppress the activation of HSCs and HF by targeting SMAD4. Therefore, miR-324-3p is identified as a potential and novel therapeutic target for HF.

Self-shedding MOF-nanocarriers modulated CdS/MoSe2 heterojunction activity through in-situ ion exchange: An enhanced split-type photoelectrochemical sensor for deoxynivalenol.

Deoxynivalenol (DON), a mycotoxin produced by Fusarium, poses a significant risk to human health and the environment. Therefore, the development of a highly sensitive and accurate detection method is essential to monitor the pollution situation. In response to this imperative, we have devised an advanced split-type photoelectrochemical (PEC) sensor for DON analysis, which leverages self-shedding MOF-nanocarriers to modulate the photoelectric response ability of PEC substrate. The PEC sensing interface was constructed using CdS/MoSe2 heterostructures, while the self-shedding copper peroxide nanodots@ZIF-8 (CPNs@ZIF-8) served as the Cu2+ source for the in-situ ion exchange reaction, which generated a target-related signal reduction. The constructed PEC sensor exhibited a broad linear range of 0.1 pg mL-1 to 500 ng mL-1 with a low detection limit of 0.038 pg mL-1, demonstrating high stability, selectivity, and proactivity. This work not only introduces innovative ideas for the design of photosensitive materials, but also presents novel sensing strategies for detecting various environmental pollutants.

miR-221/222: promising biomarkers for breast cancer.

MicroRNAs (miRNAs) are small noncoding RNAs of 19-25 nt that can regulate gene expression at a posttranscriptional level. Increasing evidence indicates that miRNAs participate in almost every step of cellular processes and are often aberrantly expressed in human cancer. miR-221 and miR-222 are two highly homologous miRNAs that always act as a gene cluster (miR-221/222) in cellular regulation and have extensively been studied in cancer network. Here, we review the role of miR-221/222 in breast cancer (BCa) development and progression: regulating proliferative signaling pathways, altering telomere and telomerase activity, avoiding cell death from tumor suppressors, autophagy and apoptosis, monitoring angiogenesis, supporting epithelial-mesenchymal transition, and even controlling cell-specific function within microenvironment. We consider that miR-221/222 act as promising biomarkers for BCa and they would offer a new way in molecular targeting cancer treatment.

Systematic expression analysis of genes related to multidrug-resistance in isogenic docetaxel- and adriamycin-resistant breast cancer cell lines.

Docetaxel (Doc) and adriamycin (Adr) are two of the most effective chemotherapeutic agents in the treatment of breast cancer. However, their efficacy is often limited by the emergence of multidrug resistance (MDR). The purpose of this study was to investigate MDR mechanisms through analyzing systematically the expression changes of genes related to MDR in the induction process of isogenic drug resistant MCF-7 cell lines. Isogenic resistant sublines selected at 100 and 200 nM Doc (MCF-7/100 nM Doc and MCF-7/200 nM Doc) or at 500 and 1,500 nM Adr (MCF-7/500 nM Adr and MCF-7/1,500 nM) were developed from human breast cancer parental cell line MCF-7, by exposing MCF-7 to gradually increasing concentrations of Doc or Adr in vitro. Cell growth curve, flow cytometry and MTT cytotoxicity assay were preformed to evaluate the MDR characteristics developed in the sublines. Some key genes on the pathways related to drug resistance (including drug-transporters: MDR1, MRP1 and BCRP; drug metabolizing-enzymes: CYP3A4 and glutathione S-transferases (GST) pi; target genes: topoisomerase II (TopoIIα) and Tubb3; apoptosis genes: Bcl-2 and Bax) were analyzed at RNA and protein expression levels by real time RT-qPCR and western blot, respectively. Compared to MCF-7/S (30.6 h), cell doubling time of MCF-7/Doc (41.6 h) and MCF-7/Adr (33.8 h) were both prolonged, and the cell proportion of resistant sublines in G1/G2 phase increased while that in S-phase decreased. MCF-7/100 nM Doc and MCF-7/200 nM Doc was 22- and 37-fold resistant to Doc, 18- and 32-fold to Adr, respectively. MCF-7/500 nM Adr and MCF-7/1,500 nM Adr was 61- and 274-fold resistant to Adr, three and 12-fold to Doc, respectively. Meantime, they also showed cross-resistance to the other anticancer drugs in different degrees. Compared to MCF-7/S, RT-qPCR and Western blot results revealed that the expression of MDR1, MRP1, BCRP, Tubb3 and Bcl-2 were elevated in both MCF-7/Doc and MCF-7/Adr, and TopoIIα, Bax were down-regulated in both the sublines, while CYP3A4, GST pi were increased only in MCF-7/Doc and MCF-7/Adr respectively. Furthermore, the changes above were dose-dependent. The established MCF-7/Doc or MCF-7/Adr has the typical MDR characteristics, which can be used as the models for resistance mechanism study. The acquired process of MCF-7/S resistance to Doc or Adr is gradual, and is complicated with the various pathways involved in. There are some common resistant mechanisms as well as own drug-specific changes between both the sublines.

Chemical constituents of Arisaema franchetianum tubers.

A novel pyrrolidine alkaloid, (2R*,3S*,5S*)-N,2-dimethyl-3-hydroxy-5-(10-phenyldecyl)pyrrolidine (1), and 17 known compounds were isolated from Arisaema franchetianum Engl. (Araceae) tubers. The 17 compounds were bergenin (2), emodin (3), caffeic acid (4), nobiletin (5), 3-O-ß-d-galactopyranosyl-hederagenin 28-O-ß-d-xylopyranosyl(1 â†’ 6)-ß-d-galactopyranosyl ester (6), coniferin (7), qingyangshengenin (8), methylconiferin (9), syringaresinol 4'-O-ß-d-glucopyranoside (10), gagaminine (11), perlolyrine (12), (S)-1-(1'-hydroxyethyl)-ß-carboline (13), 1-(ß-carboline-1-yl)-3,4,5-trihydroxy-1-pentanone (14), 1-methoxycarbonyl-ß-carboline (15), indolo[2,3-α]carbazole (16), 4-hydroxycinnamic acid methyl ester (17), and methyl 4-[2-hydroxy-2-(4-hydroxy-3-methoxyphenyl)-1-(hydroxymethyl)ethyl] ferulate (18). The inhibitory activities of compound 1 and its N-methyl derivative (1a) against porcine respiratory and reproductive syndrome virus (PRRSV), human leukemic K562 cells, and human breast cancer MCF-7 cells were evaluated. Compounds 1 [50% inhibited concentration (IC(50)) = 12.5 ± 0.6 µM] and 1a (IC(50) = 15.7 ± 0.9 µM) were cytotoxic against K562 cells. Compound 1a also had a weak effect on PRRSV with an IC(50) value of 31.9 ± 6.0 µM [selectivity index (SI) = 18.7].

Renal histopathological manifestations of IgA vasculitis nephritis in children and adults.

BACKGROUND: IgA vasculitis nephritis (IgAVN) is a common form of secondary glomerulonephritis and can occur in patients of any age. Our study was designed to reveal renal histopathological manifestations of children and adults with IgAVN and to explore the potential pathogenesis of IgAVN. METHODS: Sixty-one pediatric and seventy adult patients with IgAVN were enrolled altogether, and all of them underwent kidney biopsies. General information, laboratory parameters, and renal histopathological manifestations of all patients were analyzed. RESULTS: (1) Diabetes, hypertension, and various levels of proteinuria made no difference between children and adults. (2) Global sclerosis and tubular atrophy/interstitial fibrosis occurred more commonly in adults than in children (24.29 % vs 8.20 %, 65.71 % vs 9.84 %, respectively) (P < 0.05). (3) The immunofluorescence deposition of complement C3 was more apparent in adults (P < 0.05). (4) The deposition of IgA, IgG, IgM, and C3 in kidneys was unrelated to the pathological types. (5) The deposition of IgG or IgM was related to the deposition of IgA or C3 in children and adults (P < 0.05). CONCLUSIONS: Chronic kidney injury occurred more commonly in adult IgAVN patients compared to pediatric IgAVN patients. Immunoglobulin and complement deposits in kidneys were independent of the types of renal pathological injury. Additionally, IgG and IgM were probably involved in IgAVN pathogenesis.

Myc-mediated circular RNA circMcph1/miR-370-3p/Irak2 axis is a progressive regulator in hepatic fibrosis.

AIMS: Treating hepatic fibrosis (HF) is a major challenge worldwide. However, the biological functions and regulatory mechanisms of circular RNAs (circRNAs) remain unclear in HF. The present study aimed to elucidate the novel role of circMcph1 in HF. MAIN METHODS: HF mouse model was established by injecting CCl4 intraperitoneally and validated using hematoxylin and eosin staining, immunohistochemistry, and serological tests in vivo. RAW264.7 cells were treated with lipopolysaccharide (LPS) and interferon-γ (IFN-γ) in vitro inflammatory damage model. Gel electrophoresis, DNA sequencing, RNase R and actinomycin D treatment, random 6 primers and oligo dT primers assay, nuclear and cytoplasmic fractionation assay, and fluorescence in situ hybridization were performed to identify the characteristics of circMcph1. Functional assays such as ELISA, flow cytometry, and adeno-associated virus administration in vivo and liposome delivery gene therapy in vitro were used to determine the functional effects of circMcph1/miR-370-3p/interleukin-1 receptor-associated kinase 2 (Irak2) axis. Mechanistic assays such as luciferase reporter analysis, and chromatin immunoprecipitation revealed the molecular mechanism of the Myc/circMcph1/miR-370-3p/Irak2 axis in HF. KEY FINDINGS: CircMcph1 expression was upregulated in liver tissues and primary Kupffer cells of CCl4-induced HF mice, as well as in LPS and IFN-γ-treated RAW264.7 cells. Knockdown of circMcph1 ameliorated liver fibrogenesis and inflammatory damage in HF mice and reduced the inflammatory response in LPS and IFN-γ-treated RAW264.7 cells. Mechanically, circMcph1 mediated by Myc regulated the expression of Irak2 by sponging miR-370-3p in HF. SIGNIFICANCE: The study findings suggested that the Myc/circMcph1/miR-370-3p/Irak2 axis might be a novel identifier and therapeutic target for HF.

Nanozyme-assisted ratiometric photoelectrochemical aptasensor over Cu2O nanocubes mediated photocurrent-polarity-switching based on S-scheme FeCdS@FeIn2S4 heterostructure.

The controllable modulation of the response mode is highly attractive for the construction of photoelectrochemical (PEC) sensors with improved sensitivity and anti-interference ability in complex real samples matrix. Here, we present a charming proof-of-concept ratiometric PEC aptasensor of enrofloxacin (ENR) analysis via the controllable signal transduction. Different with the traditional sensing mechanism, this ratiometric PEC aptasensor integrates the anodic PEC signal induced by PtCuCo nanozyme-catalyzed precipitation reaction and the polarity-switching cathodic PEC response mediated by Cu2O nanocubes on S-scheme FeCdS@FeIn2S4 heterostructure. Taking advantages of the photocurrent-polarity-switching signal response model and the superior performance of the photoactive substrate material, the proposed ratiometric PEC aptasensor displays a good detection linear range for ENR analysis from 0.01 pg mL-1 to 10 ng mL-1, with a detection limit of 3.3 fg mL-1. This study provides a general platform for detecting interested trace analytes in real samples and expands the diversity of sensing strategy design.

N6-methyladenosine-modified circIRF2, identified by YTHDF2, suppresses liver fibrosis via facilitating FOXO3 nuclear translocation.

Circular RNA (circRNA) has been implicated in liver fibrosis and modulated by multiple elusive molecular mechanisms, while the effects of N6-methyladenosine (m6A) modification on circRNA are still elusive. Herein, we identify circIRF2 from our circRNA sequencing data, which decreased in liver fibrogenesis stage and restored in resolution stage, indicating that dysregulated circIRF2 may be closely associated with liver fibrosis. Gain/loss-of-function analysis was performed to evaluate the effects of circIRF2 on liver fibrosis at both the fibrogenesis and resolution in vivo. Ectopic expression of circIRF2 attenuated liver fibrogenesis and HSCs activation at the fibrogenesis stage, whereas downregulation of circIRF2 impaired mouse liver injury repair and inflammation resolution. Mechanistically, YTHDF2 recognized m6A-modified circIRF2 and diminished circIRF2 stability, partly accounting for the decreased circIRF2 in liver fibrosis. Microarray was applied to investigate miRNAs regulated by circIRF2, our data elucidate cytoplasmic circIRF2 may directly harbor miR-29b-1-5p and competitively relieve its inhibitory effect on FOXO3, inducing FOXO3 nuclear translocation and accumulation. Clinically, circIRF2 downregulation was prevalent in liver fibrosis patients compared with healthy individuals. In summary, our findings offer a novel insight into m6A modification-mediated regulation of circRNA and suggest that circIRF2 may be an exploitable prognostic marker and/or therapeutic target for liver fibrosis.

Bioactive isoquinoline alkaloids from Corydalis saxicola.

Twelve isoquinoline alkaloids including two new nitro-containing tetrahydroprotoberberines, (-)-2,9-dihydroxyl-3,11-dimethoxy-1,10-dinitrotetrahydroprotoberberine (1) and (+)-4-nitroisoapocavidine (2), were isolated from the whole plant of Corydalis saxicola Bunting. The structures of the new compounds were established by spectroscopic analysis and chemical evidence. The inhibitory activity of these isolates against cholinesterase and canine parvovirus were evaluated. Compounds 1 and 1A, (+)-1-nitroapocavidine (5), berberine (8), palmatine (9), dehydrocavidine (10), and sanguinarine (11) showed potent inhibitory activity against acetylcholinesterase with IC(50) values of less than 10 µM, while only compound 1 possessed weak activity against canine parvovirus. Structure-activity studies demonstrated that the nitro substituents at ring A in the tetrahydroprotoberberines led to an increase in the anti-acetylcholinesterase activity.

Ultrasensitive electrochemiluminescence sensor based on perovskite quantum dots coated with molecularly imprinted polymer for prometryn determination.

A highly effective molecularly imprinted electrochemiluminescence sensor was constructed for prometryn determination in environmental and biological samples by using perovskite quantum dots coated with a molecularly imprinted silica layer (MIP/CsPbBr3-QDs) as the recognition and response element. MIP/CsPbBr3-QDs were immobilized on a glassy carbon electrode (GCE) through electropolymerization, and the electrochemiluminescence (ECL) response of MIP/CsPbBr3-QDs could be motivated under the condition of H2O2 as co-reactant. ECL signal was selectively quenched with prometryn by hindering electron transfer and directly proportional to the logarithm of prometryn concentration (0.10-500.0 µg/L) with a correlation coefficient of 0.9960. Limits of detection in fish and seawater samples were 0.010 µg/kg and 0.050 µg/L, respectively. Excellent recoveries of 88.0%-106.0% were acquired for fish and seawater samples with a relative standard deviation below 4.2%. The constructed MIECL sensor based on MIP/CsPbBr3-QDs showed good stability, accuracy, and precision for sensitive detection of prometryn in aquaculture products and environmental samples.

Ginsenoside Rb1 preconditioning enhances eNOS expression and attenuates myocardial ischemia/reperfusion injury in diabetic rats.

Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (P < 0.05). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (P < 0.05). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.

Protective effect of ginsenoside Rb1 against myocardial ischemia/reperfusion injury in streptozotocin-induced diabetic rats.

The objective of the current study is to investigate whether ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with ginsenoside Rb1 in the diabetic myocardium.

Cytotoxic amide alkaloids from Piper boehmeriaefolium.

Eight new amide alkaloids (1-8) and 19 known ones were isolated from the whole plant of Piper boehmeriaefolium. Their structures were determined through spectroscopic data analyses. Cytotoxic activity of these amides against human cervical carcinoma HeLa cells was evaluated, and 1-[(9E)-10-(3,4-methylenedioxyphenyl)-9-decenoyl]pyrrolidine (9) exhibited significant inhibitory activity with an IC(50) value of 2.7 µg/mL.

Development and application of fluorescence sensor and test strip based on molecularly imprinted quantum dots for the selective and sensitive detection of propanil in fish and seawater samples.

Molecularly imprinted quantum dots (MIP-QDs) were successfully synthesized via reversed-phase microemulsion and used as the specific recognition element and signal probe of a fluorescence sensor or test strip to achieve the highly sensitive detection of propanil. The physical-chemical characteristics and excellent selectivity of MIP-QDs were elucidated. Under optimized parameters, the MIP-QDs had good linearity at the propanil concentration range of 1.0 µg/L to 20.0 × 103 µg/L by fluorescence quenching. The developed MIP-QD-based fluorescence sensor showed good recoveries ranging from 87.2 % to 112.2 %, and the relative standard deviation was below 6.0 % for the fish and seawater samples. In addition, the limits of detection (LODs) for fish and seawater were 0.42 µg/kg and 0.38 µg/L, respectively. The fluorescence test strip developed on the basis of the MIP-QDs also displayed satisfactory recoveries of 90.1 %-111.1 %, and the LOD for propanil in the seawater sample was 0.6 µg/L. The proposed fluorescence sensor and test strip were successfully used in propanil determination in environment and aquatic products.

Hyperbaric oxygen treatment for Parkinson's disease with severe depression and anxiety: A case report.

RATIONALE: Patients with Parkinson's disease (PD) frequently suffer from psychiatric disorders, and treating these symptom whereas managing the motor symptoms associated with PD can be a therapeutic challenge. PATIENT CONCERNS: We report a case of PD patient with severe depression and anxiety that refused to be treated with dopaminagonists or SSRIs, the most common treatments for PD patients suffering from psychiatric symptoms. DIAGNOSES: Parkinson's disease with severe depression and anxiety. INTERVENTIONS: This man was treated with hyperbaric oxygen treatment for 30 days. OUTCOMES: Clinical assessment scores for depression and anxiety, including Unified Parkinson's Disease Rating ScaleI (UPDRS I), UPDRS II, Hanmilton Depression Rating Scale, and Hamiliton Anxiety Rating Scale, were improved following the hyperbaric oxygen treatment. LESSONS: Hyperbaric oxygen treatment may be a potential therapeutic method for PD patient suffering from depression and anxiety. Further research is needed to validate this finding and explore a potential mechanism.

Microscopic study on the concretion of ceramics in the "Nanhai I" shipwreck of China, Southern Song Dynasty (1,127-1,279 A.D.).

"Nanhai I" shipwreck of China Southern Song Dynasty is the oldest and the most integrally preserved shipwreck in the world. The related conservation and archeological research have caught great attention of different experts all over the world. In this study, different types of concretion covered on the surface of the ceramics in "Nanhai I" shipwreck were analyzed by X-ray diffractometer, micro-Raman spectrometer, and scanning electron microscope equipped with energy dispersive spectroscopy. Based on the analyses, we found that the grey concretion was mainly composed of quartz, aragonite, and calcite while the reddish concretion was mainly composed of pyrite and quartz. Our study indicated that the formation process of the grey concretion probably included the crystallization and transformation of aragonite, while the corrosion of iron implements and crystallization of pyrite were highly involved in the formation of reddish concretion.