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The lung is the most common extra-abdominal metastasis site of colorectal cancer (CRC). This study aimed to investigate the genetic variation of pulmonary metastases (PM) and primary tumors in resectable CRC. The clinical data of 410 patients with PM after CRC surgery and 33 paraffin-embedded tissue samples from January 2012 to July 2019 in our hospital were collected retrospectively. Next, 450-panel gene detection technologies based on next-generation sequencing (NGS) were used to analyze the changes in the gene map and the overall variation in cancer-related genes in PM and primary tumors. After quality control, 19 samples were included in the final gene analysis. The results showed that APC (89.5%), TP53 (89.5%), and KRAS (53%) were the most common mutations in PM and primary tumors, but the gene amplification variation was enriched in primary tumors (4.6% vs. 11.4%). KRAS G12D was the most common site variation of the KRAS gene in both PM and primary tumors of CRC. There was no hotspot mutation in the TP53 locus in CRC, and the TP53 mutation in the PM was consistent with that in the primary lesion. The microsatellite instability (MSI) levels of 10 patients were MSS. The mean tumor mutation burden (TMB) of the primary tumor (5.3 muts·Mb−1) was slightly higher than that of metastasis (5.0 muts·Mb−1). In our institution, the genetic characteristics of resectable PM from CRC may be highly consistent with those of the primary tumor.

Herein, we systematically studied the electronic and conducting properties of 9,10-anthraquinone (

Background Acute myeloid leukemia (AML) is a heterogeneous hematological disease. Our purpose of the research was to investigate the regulatory influence of long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1)/microRNA-338-3p (miR-338-3p)/CREB3 regulatory factor (CREBRF) in AML progression. Methods The associated RNA and protein levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. Cell growth was assessed through colony formation assay and 3-(4,5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Flow cytometry was exploited to determine the apoptosis rate. Cell migration and invasion were detected by transwell assay. The combination of miR-338-3p and NEAT1 or CREBRF was analyzed via the dual-luciferase reporter assay. Results NEAT1 and CREBRF were down-regulated in AML tissues and cells. NEAT1 up-regulation suppressed cell growth, migration and invasion but enhanced apoptosis of AML cells. Inhibition of CREBRF reverted the NEAT1-induced effects on AML cells. Moreover, NEAT1 directly targeted miR-338-3p and miR-338-3p targeted CREBRF. NEAT1/miR-338-3p could affect cellular behaviors of AML cells via the modulation of CREBRF. Conclusion NEAT1/miR-338-3p axis repressed the AML progression through regulating CREBRF, which might afford a favorable perspective for the AML treatment molecularly.

Our study mainly reports the specific mechanisms of microRNA (miR)-874-3p on drug resistance in gastric cancer (GC). Clinical specimen was collected. The upstream long non-coding RNA (lncRNA) and the downstream gene of miR-874-3p were predicted using bioinformatic analysis with the results being ascertained with dual-luciferase reporter assay. The viability, apoptosis, migration and invasion of transfected GC cells with or without cisplatin (DDP) treatment were evaluated by Cell Counting Kit-8 (CCK-8), flow cytometric, Scratch, and Transwell assays. An animal xenograft model was constructed. Expressions of long intergenic non-coding RNA 00922 (LINC00922), miR-874-3p and potential target genes were quantified by quantitative real-time polymerase-chain reaction (qRT-PCR) and Western blot. MiR-874-3p, which was lower-expressed in drug-resistant GC tissues and cells, was upregulated to repress the viability, migration and invasion but enhance the apoptosis and sensitivity in GC cells with or without DDP resistance. Downregulation of miR-874-3p eliminated the effects of silenced LINC00922, a upstream lncRNA of miR-874-3p, on cell viability, apoptosis, migration and invasion, as well as the expressions of Glycerophosphodiester Phosphodiesterase Domain Containing 5 (GDPD5) and the downstream gene of miR-874-3p in DDP-resistant GC cells. GDPD5 silencing diminished the effects of miR-874-3p downregulation on GDPD5 expression, viability, migration and invasion of DDP-resistant GC cells. Additionally, LINC00922 silencing enhanced the inhibitory effect of DDP on tumor growth, whereas reversing the effects of DDP on LINC00922, miR-874-3p and GDPD5 expressions in tumors. MiR-874-3p, an miRNA, which is sponged by LINC00922 and targets GDPD5, inhibits the GC progression yet enhances the DDP sensitivity in GC.

Resistance to chemotherapeutic drugs limits the control of gastric cancer (GC) development. The study intended to probe into the mechanism of aquaporin 3 (AQP3) on the chemoresistance of GC. Cisplatin (CDDP)-resistant cells were constructed. Parental AGS and HGC-27 cells and their respective CDDP-resistant cells were transfected with AQP3 overexpression plasmid, AQP3 short hairpin RNA (sh-AQP3) and sh-Kruppel-like factor 5 (shKLF5). The expressions of AQP3 and factors related to autophagy (LC3 I, LC3 II, Atg5, Beclin-1, p62)/epithelial-mesenchymal transition (EMT; E-cadherin and snail) were assessed by Western blot and qRT-PCR. Cell counting kit-8 assay was adopted to test cell viability and half maximal inhibitory concentration (IC 50) was determined. Transwell assay was used for the examination of cell migration and invasion. The regulatory relationship of AQP3 and KLF5 was tested by chromatin immunoprecipitation (ChIP) and dual luciferase reporter assays. AQP3 was highly-expressed in GC cells and its level was even higher in CDDP-resistant GC cells. AQP3 silencing inhibited viability, autophagy and EMT in CDDP-resistant GC cells, while AQP3 overexpression had the opposite effect. KLF5 positively modulated AQP3 in GC cells resistant to CDDP. KLF5 knockdown reversed AQP3-induced autophagy, viability, migration, invasion and EMT in CDDP-resistant GC cells. KLF5-modulated AQP3 activated autophagy to facilitate the resistance of GC to CDDP.

Novel neoadjuvant therapy regimens are needed to improve the outcomes of patients with locally advanced resectable oral squamous cell carcinoma (OSCC). We conducted a prospective, open-label, single-arm trial (n = 21, NCT04393506) to determine the safety and feasibility of neoadjuvant camrelizumab (an anti-PD-1 antibody) plus apatinib (a VEGFR inhibitor) for locally advanced resectable OSCC. The primary endpoints were safety and major pathological response (MPR). Neoadjuvant camrelizumab plus apatinib was well-tolerated and the MPR rate was 40% (8/20), meeting the primary endpoint. All five patients with CPS ˃ 10 had MPR. Additionally, patients achieving MPR showed more CD4+ T cell infiltration and a higher CD8+/FoxP3+ ratio than those without MPR (p < 0.05), and decreased CD31 and ɑ-SMA expression were observed after neoadjuvant therapy. Our findings demonstrate that neoadjuvant therapy with a chemo-free combination of camrelizumab and apatinib is safe and yields a promising MPR rate, supporting further trials.

Background: Congenital cytomegalovirus (cCMV) infection is the most common cause of childhood hearing loss (HL), although the strength of this association remains limited and inconclusive. Thus, the purpose of this study was to summarize evidence regarding the strength of the relationship between cCMV and childhood HL and to determine whether this relationship differs according to patient characteristics. Methods: The PubMed, EmBase, and Cochrane Library databases were searched for studies evaluating the relationship between cCMV and HL from inception to September 2019. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were used to calculate the investigated outcomes in a random-effects model. Sensitivity, subgroup, and publication bias analyses were also performed. Results: A total of 15 studies involving 235,026 children met the inclusion criteria and were included in the final analysis. The summary results indicated that cCMV infection was associated with an increased risk of HL (odds ratio [OR]: 8.45; 95% confidence interval [CI]: 3.95–18.10; P

The shapes of the HOMOs/LUMOs and the relative positions of adjacent molecules decide the size of the intermolecular electronic couplings., This work presents a systematic study of the conducting and optical properties of a family of aromatic di­imides reported recently and discusses the influences of side-chain substitution on the reorganization energies, crystal packing, electronic couplings and charge injection barrier of 4,5,9,10-pyrenedi­imide (PyDI). Quantum-chemical calculations combined with the Marcus–Hush electron transfer theory revealed that the introduction of a side chain into 4,5,9,10-pyrenedi­imide increases intermolecular steric interactions and hinders close intermolecular π–π stacking, which results in weak electronic couplings and finally causes lower intrinsic hole and electron mobility in t-C5-PyDI (μh = 0.004 cm2 V−1 s−1 and μe = 0.00003 cm2 V−1 s−1) than in the C5-PyDI crystal (μh = 0.16 cm2 V−1 s−1 and μe = 0.08 cm2 V−1 s−1). Furthermore, electronic spectra of C5-PyDI were simulated and time-dependent density functional theory calculation results showed that the predicted fluorescence maximum of t-C5-PyDI, corresponding to an S 1→S 0 transition process, is located at 485 nm, which is close to the experimental value (480 nm).

A new type of 3D NiS/MoS2@N-doped reduced graphene oxide (NiS/MoS2@N-rGO) hybrid composite is presented and its super-capacitive performance is studied. NiS/MoS2@N-rGO hybrid is synthesized via an easy and cost-effective hydrothermal route. By combining nickel sulfide and molybdenum disulfide with N-reduced graphene oxide, the as-prepared sample demonstrates a mesoporous nanostructure that increases the accessible area of the electrolyte ions. Due to the synergistic effect in the 3D network, such NiS/MoS2@N-rGO hybrid is used as electrode and it demonstrates a highly specific capacity of 2225 F/g at a current density of 1 A/g, and a good rate of 1347.3 F/g at 10 A/g. Furthermore, we also test a full symmetric supercapacitor based on NiS/MoS2@N-rGO, which displays excellent capacitive property up to 1028 F/g at 1 A/g, with high energy and good power density up to 35.69 W h/kg and 601.8 W/kg, and good cycle stability up to 94.5% initial capacitive retention after 50,000 loops. Moreover, the symmetric supercapacitor demonstrates excellent flexibility under different bending conditions.

OBJECTIVE: To study the change and significance of serum pentraxin-3 (PTX-3) and syndecan-4 in children with chronic heart failure (CHF). METHODS: A total of 40 children with CHF who were admitted to the Department of Pediatrics of the First Affiliated Hospital of Zhengzhou University were enrolled as the heart failure group, and 30 children who underwent physical examination in the outpatient service during the same period of time were enrolled as the control group. The serum levels of PTX-3, syndecan-4, and N-terminal pro-brain natriuretic peptide (NT-proBNP) were compared between the two groups. RESULTS: The children with CHF had significant reductions in the serum levels of PTX-3, syndecan-4, and NT-proBNP after treatment. The levels of these markers in children with CHF were significantly higher than the control group before and after treatment (P < 0.05). The CHF children with grade Ⅱ/Ⅲ/Ⅳ cardiac function had significantly higher serum levels of PTX-3 and syndecan-4 than the control group (P < 0.05). The levels of PTX-3 and syndecan-4 were related to the severity of cardiac function. Compared with the grade Ⅱ cardiac function group, the grade Ⅳ cardiac function group had significant increases in the serum levels of PTX-3 and syndecan-4 (P < 0.05). The serum level of PTX-3 was positively correlated with that of syndecan-4 in children with CHF (r(s)=0.999, P < 0.05); the serum level of PTX-3 was positively correlated with NT-proBNP, left ventricular mass index (LVMI), and cardiac function grade (r(s)=0.726, 0.736, and 0.934 respectively, P < 0.05) and was negatively correlated with left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) (r(s)=-0.852 and -0.767 respectively, P < 0.05); the serum level of syndecan-4 was positively correlated with NT-proBNP, LVMI, and cardiac function grade (r(s)=0.733, 0.743, and 0.934 respectively, P < 0.05) and was negatively correlated with LVEF and LVFS (r(s)=-0.856 and -0.771 respectively, P < 0.05). CONCLUSIONS: Serum PTX-3 and syndecan-4 may be involved in the development and progression of ventricular remodeling in children with CHF and may be used as markers for the diagnosis, cardiac function grading, and treatment outcome evaluation of children with heart failure.

Background Colorectal cancer (CRC) has a high incidence and mortality. In CRC, the lung is the most common extra-abdominal site of metastasis. Understanding the genetic characteristics and clonal evolution of primary tumor and lung metastases (LM) will help oncologists better outline treatments. To date, few studies for CRC with LM exist. As such, revealing the genetic characteristics and clonal evolution of resectable CRC with LM was the goal of this study. Methods From January 2012 to July 2019, clinical data and formalin-fixed, paraffin-embedded samples were collected from 33 Chinese CRC patients. Nineteen (19) primary tumors and 10 matched LM samples were examined using a 450 cancer gene next-generation sequencing assay. Genomic alterations, including single base substitutions, indels, copy number variations (CNVs), and gene fusion and rearrangement, were assessed. A phylogenetic reconstruction of sequencing data using LICHeE was also performed for each patient. Results Median patient age was 60 years old (48-67 years), with most having right lung metastasis. A significant difference existed between single (21/33, 63.6%) and multiple LM (12/33, 36.4%) (P < 0.01). Median disease-free survival was 20 months (95% CI, 0-84), from primary CRC to LM. The most frequently mutated genes were TP53 (90%), APC (90%), KRAS (53%), MUC16 (26%), ARID1A (21%). A comparison of mutational profiles for primary and matched LM samples revealed that 65.70% of alterations were consistent and that the most frequently mutated genes, including APC, TP53, and KRAS, of the primary tumor were completely consistent with LM. However, some differences between metastatic and primary samples were determined. More CNVs were found in primary samples (11.4% vs. 4.6%), indicating that CNVs are early molecular events for tumorigenesis and disease progression. SMAD4 was only present in two primary samples, while LRP1B was only present in two LM samples. Clonal evolution for eight patients indicated that phylogenetic structure was similar across patients. All patients had at least seven mutations on trunks. In trunks, TP53 (87.5%), APC (87.5%), KRAS (50%), and LRP2 (37.5%) were frequently identified. A new actionable gene (BRCA2) emerged in LM sample was identified in one patient. The mean value of TMB for the primary was almost the same as that for the LM site (5.3 vs. 5 muts/Mb, P > 0.05). Conclusions Our data indicated that the genetic characteristics and clonal evolution of LM are highly consistent with those of the primary tumor, suggesting that suitable treatments can be selected based on the genetic characteristics of primary tumor in CRC patients with LM that cannot be surgically treated. Citation Format: Yong Cheng, Ming-Jian Ge, Peng Dong, Yan-Yu Qiu, Xin-Peng Shu, Jin-Dou Li, Jun-Wei Wang, Xiao-Fang Qi. Genetic characteristics & clonal evolution of Chinese resectable colorectal cancer patients with lung metastases [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5133.

This article summarizes and analyzes the clinical features and gene mutation characteristics of children with noncompaction of the ventricular myocardium (NVM). For the 6 children with NVM (4 boys and 2 girls), the age of onset ranged from 3 months to 12 years. Of the 6 children, 5 had arrhythmia, 3 had cardiac insufficiency, 1 had poor mental state, and 1 had chest distress and sighing. NVM-related gene mutations were detected in 4 children, among whom 2 had MYH7 gene mutation, 1 had PRDM16 gene mutation, and 1 had mutations in the ACTN2 and TNNT2 genes. Four children had improvement in cardiac function. The two children with no significant improvement in cardiac function had a younger age of onset, a greater reduction in systolic function on echocardiography, and greater increases in myocardial enzyme and N-terminal pro-brain natriuretic peptide. It is concluded that for children with the initial symptoms of chest distress, sighing, arrhythmia, enlarged heart shadow, and increased myocardial enzyme, echocardiography and cardiac magnetic resonance are recommended for the diagnosis of NVM. NVM can have various genetic mutations.

Long noncoding RNAs (lncRNAs) have drawn growing attention owing to their important effects in various tumors, including hepatocellular carcinoma (HCC). Recently, a newly identified lncRNA, ZFPM2 antisense RNA 1 (ZFPM2-AS1), was reported to serve as an oncogene in gastric cancer. However, its function in tumors remains largely unknown. In this study, we identified ZFPM2-AS1 as a novel HCC-related lncRNA, which was observed to be distinctly upregulated in HCC tissues and associated with shorter overall survival. Luciferase reporter and chromatin immunoprecipitation assays suggested that overexpression of ZFPM2-AS1 was induced by STAT1. Functional investigations suggested that the inhibition of ZFPM2-AS1 suppressed cell proliferation, metastasis, cell cycle progression while accelerated cell apoptosis. Mechanistic studies showed that there were two binding sites of miR-653 within the sequence of ZFPM2-AS1 and the levels of ZFPM2-AS1 were negatively correlated with miR-653. In addition, ZFPM2-AS1 could reverse the suppressor effects of miR-653 on the proliferation and metastasis of HCC cells by the modulation of GOLM1, a target gene of miR-653. To conclude, we provided a better understanding of the interaction mechanism between ZFPM2-AS-miR-653-GOLM1 axis, which may help develop prognostic biomarkers and therapeutic target for HCC.

Background: Previous studies had investigated the association between polymorphism of IVS5N+5 G>A in SCN1A and the risk of febrile seizure and epilepsy. However, the results were inconsistent. We aimed to conduct a systematic review and meta-analysis to evaluate the association between SCN1A IVS5N+5 G>A polymorphism and risk of febrile seizures and epilepsy.Methods: We searched Embase, Medline, Scopus, and CNKI for studies on the association between SCN1A IVS5N+5 G>A polymorphism and risk of febrile seizures and epilepsy up to 19 February 2020. We pooled odds ratios (ORs) and 95% confidence intervals (CIs) by different genetic models. To explore the source of heterogeneity, we performed the subgroup analysis by ethnicity and source of control.Results: We included a total of 12 studies in the meta-analysis. We found a significant negative association between G allele SCN1A IVS5N+5 G>A polymorphism, febrile seizures [G vs. A: OR (95% CI): 0.690 (0.530–0.897); GG vs. AA: 0.503 (0.279–0.908); AG vs. AA: 0.581 (0.460–0.733); GG + AG vs. AA: 0.543 (0.436–0.677); AA + GG vs. AG: 1.309 (1.061–1.615)], and epilepsy [G vs. A: 0.822 (0.750–0.902); GG vs. AA: 0.655 (0.515–0.832); AG vs. AA: 0.780 (0.705–0.862); GG vs. AG + AA: 0.769 (0.625–0.947); GG + AG vs. AA: 0.743 (0.663–0.833); AA + GG vs. AG: 1.093 (1.001–1.193)]. The subgroup analysis shows the association varied by type of disease, ethnicity, and source of control.Conclusion: The present meta-analysis suggests that G allele in SCN1A IVS5N+5 G>A polymorphism is a protective factor of febrile seizures and epilepsy. It is possible to determine the vulnerability of each individual to develop febrile seizures or epilepsy genotype by these genetic variants. Future studies with better study designs are needed to confirm the results.Study Registration: This study was registered in the International Prospective register of systematic reviews (PROSPERO, CRD42020163318).

WUSCHEL (WUS) protein regulates stem cell function in shoot apical meristem of Arabidopsis. The expression of WUS gene is strictly regulated by developmental cues and environmental factors. As DnaJ domain-containing proteins, SDJ1 and SDJ3 have been proven to play an important role in transcriptional activation of promoter methylated genes. Here, we showed that three DnaJ domain-containing proteins including SDJ1 and SDJ3 can bind WUS protein as a complex, which further maintain the expression of WUS gene by binding to WUS promoter. We propose a model how DnaJ domain-containing proteins are involved in the self-regulation of WUS gene in stem cells maintenance of Arabidopsis.

Background: Breast cancer is a kind of malignant tumor that severely threatens women’s health and life worldwide. Macrophages have been reported to mediate tumor progression, while the potential mechanism still needs further identification.Methods: Human monocytic cell line THP-1 was used to induce M2-macrophage. Real-time PCR and western blot were performed to determine gene expression in mRNA and protein level, respectively. Cell proliferation was determined using MTT assays, while cell migration was detected based on the scratch wound healing assays.Results: The supernatant medium of M2-macrophages incubated breast cancer cells showed increased cell proliferation and reduced expression of IRF-7. Overexpression of IRF-7 reversed the increased level of M2-macrophage induced cell proliferation and migration. The supernatant medium of M2-macrophages incubation promoted miR-1587 expression in breast cancer cells. miR-1587 overexpression promoted cell proliferation and migration of breast cancer. In addition, miR-1587 knockdown suppressed cell proliferation and migration that induced by M2-macrophages. miR-1587 targets IRF-7 to regulate its expression. Knockdown of IRF-7 reversed the effects of miR-1587 knockdown on cell proliferation and migration.Conclusion: Collectively, this study revealed that miR-1587/IRF-7 mediated the mechanism of M2-macrophages-induced breast cancer progression, and this would shed light on the further clinical therapy of breast cancer.

MiR-301a is as an oncogene involved in the regulation of gastric cancer (GC) progression, but the underlying mechanism is unclear. This study was to explore the lncRNA PCAT18/miR-301a/TP53INP1 axis in regulating the GC cell proliferation and metastasis. In the present study, GC tissues and cell lines were collected for the detection of PCAT18 expression. Herein, we found that PCAT18 is significantly decreases in human GC tissues and five GC cell lines. Overexpression of PCAT18 inhibits cell viability, invasion and migration of GC cells and tumour growth of GC xenograft tumours. PCAT18 negatively regulates the expression level of miR-301a. The interaction between PCAT18 and miR-301a is confirmed by RIP and RNA pull down. MiR-301a mimic increases cell viability and promotes cell migration and invasion and reverses the inhibitory action of PCAT18. TP53INP1 expression is negatively regulated by miR-301a and TP53INP1/miR-301a is involved in GC viability, migration and invasion. The promoting of PCAT18 on TP53INP1 expression is abolished by miR-301a overexpression. In conclusion, lncRNA PCAT18 acts as a tumour suppressor for GC and lncRNA PCAT18, miR-301a and TP53INP1 comprise a signal axis in regulating GC cell proliferation, migration and invasion.

The conducting and optical properties of a series of indeno[1,2-b]fluorene-6,12-dione (IFD)-based molecules have been systematically studied and the influences of butyl, butylthio and dibutylamino substituents on the reorganization energies, intermolecular electronic couplings and charge-injection barriers of IFD have been discussed. The quantum-chemical calculations combined with electron-transfer theory reveal that the incorporation of sulfur-linked side chains decreases reorganization energy associated with hole transfer and optimizes intermolecular π–π stacking, which results in excellent ambipolar charge-transport properties (μh = 1.15 cm2 V−1 s−1 and μe = 0.08 cm2 V−1 s−1); in comparison, addition of dibutylamino side chains increases intermolecular steric interactions and hinders perfect intermolecular π–π stacking, which results in the weak electronic couplings and finally causes the low intrinsic hole mobility (μh = 0.01 cm2 V−1 s−1). Furthermore, electronic spectra of butyl-IFD, butylthio-IFD and dibutylamino-IFD were simulated and compared with the reported experimental data. Calculations demonstrate that IFD-based molecules possess potential for developing novel infrared and near-infrared probe materials via suitable chemical modifications.

BACKGROUND Congenital cytomegalovirus (cCMV) infection is the most common cause of childhood hearing loss (HL), although the strength of this association remains limited and inconclusive. Thus, the purpose of this study was to summarize evidence regarding the strength of the relationship between cCMV and childhood HL and to determine whether this relationship differs according to patient characteristics. METHODS The PubMed, EmBase, and Cochrane Library databases were searched for studies evaluating the relationship between cCMV and HL from inception to September 2019. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were used to calculate the investigated outcomes in a random-effects model. Sensitivity, subgroup, and publication bias analyses were also performed. RESULTS A total of 15 studies involving 235,026 children met the inclusion criteria and were included in the final analysis. The summary results indicated that cCMV infection was associated with an increased risk of HL (odds ratio [OR]: 8.45; 95% confidence interval [CI]: 3.95-18.10; P

Taking 4-(1,2,2-triphenylvinyl)­aniline salicylaldehyde hydrazone (A) as an example, the relationship between molecular packing and charge-transport parameters has been computed and analysed. The conducting properties of A are also predicted within the framework of hopping models., Based on first-principles calculations, the relationship between molecular packing and charge-transport parameters has been investigated and analysed in detail. It is found that the crystal packing forces in the flexible organic molecule 4-(1,2,2-triphenylvinyl)­aniline salicylaldehyde hydrazone (A) can apparently overcome the dynamic intramolecular rotations and the intramolecular steric repulsion, effectively enhancing the molecular rigidity and decreasing the internal reorganization energy. The conducting properties of A have also been simulated within the framework of hopping models, and the calculation results show that the intrinsic electron mobility in A is much higher than the corresponding intrinsic hole mobility. These theoretical investigations provide guidance for the efficient and targeted control of the molecular packing and charge-transport properties of organic small-molecule semiconductors and conjugated polymeric materials.

The prevalence rate of nonalcoholic fatty liver disease (NAFLD) has been increasing year by year. However, since the complex pathogenesis of NAFLD has not been fully clarified, there still lacks a gold standard for the diagnosis and treatment of NAFLD. 5-Hydroxytryptamine (5-HT) can affect the development and progression of NAFLD via several links and thus change the course of NAFLD. This article introduces the association between 5-HT and NAFLD, the role of 5-HT in the pathogenesis of NAFLD, and its future application in treatment.

In this work, excited-state intramolecular single and double proton transfer mechanisms for 2,5-bis(benzoxazol-2-yl)thiophene-3,4-diol were investigated using time-dependent density functional theory (TDDFT) method for the first time. Our calculations showed that the intramolecular hydrogen bond N⋯H O is strengthened in the excited state, which provides a driving force to effectively facilitate the proton transfer process. The constructed potential energy surface of the excited state demonstrated that the double proton transfer reaction occurs more readily in both dynamics and thermodynamics aspects, and it is implemented by simultaneous double proton transfer, or successive single transfers. Furthermore, the assignments of multiple fluorescence bands in experiment were confirmed by fluorescence spectral simulation. The calculated emission spectra indicated that the experimental fluorescence maxima at 475 nm should be attributed to normal Stokes shifted emission; the large Stokes shifted fluorescence with peaks at 550 nm originates from the double proton transfer phototautomer emission, and the experimentally observed shoulder peak at ∼493 nm results from the excited state single proton transfer tautomer.

Background Aquaporin 3(AQP3) has been implicated in gastric intestinal metaplasia and gastric cancer, and considered as a biomarker to improve treatment strategy. Accumulating evidence suggests that AQP3 is involved in the gastric carcinogenesis and the disease progression. However, whether AQP3 is involved in the transformation from gastritis to gastric cancer remain elusive. In this study, we intended to realized the expression pattern and its significance of AQP3 in different gastric diseases. Methods A total of 101 patients diagnosed with gastric diseases were included in the study. A gastric tissue biopsy was taken from the gastric antrum during endoscopic examination. Expression of AQP3 protein is determined by immunohistochemistry using polyclonal rabbit anti-AQP3 antibody. Percentage of positive cells and staining intensity were counted and measured. Results The frequency of AQP3 positivity was similar between the disease types of chronic gastritis, gastric ulcer, gastric erosion, and atrophic gastritis, whereas the frequency of AQP3 positivity was significantly higher in patients with gastric intestinal metaplasia、gastric dysplasia 、gastric polyps and intestinal-type gastric adenocarcinoma than that in patients with gastritis, gastric ulcer, gastric erosion, or atrophic gastritis(p

Metabolomics is the study of the investigation of small molecules derived from cellular and organism metabolism, which reflects the outcomes of the complex network of biochemical reactions in living systems. As the most recent member of the omics family, there has been notable progress in metabolomics in the last decade, mainly driven by the improvement in mass spectrometry (MS). MS-based metabolomic strategies in modern health and medical science studies provide innovative tools for novel diagnostic and prognostic approaches, as well as an augmented role in drug development, nutrition science, toxicology, and forensic science. In the present review, we not only introduce the application of MS-based metabolomics in the above fields, but also discuss the MS analysis technologies commonly used in metabolomics and the application of metabolomics in precision medicine, and further explore the challenges and perspectives of metabolomics in the field of health and medical science, which are expected to make a little contribution to the better development of metabolomics.

A new type of 3D NiS/MoS

The optical absorption properties and fluorescence properties of 3-hydroxy-2-(thiophen-2-yl)chromen-4-one (3-HTC) were simulated by the time-dependent density functional theory (TDDFT) method. The experimental absorption spectrum and fluorescence spectrum were reproduced well by the calculated vertical excitation energies of 3-HTC-a, which corresponds to the intramolecular hydrogen bond O2⋯H1–O1. The excited state intramolecular proton transfer (ESIPT) mechanism of 3-HTC has been systematically investigated. The constructed potential energy curves (PECs) of 3-HTC-a in the S0 and S1 states indicate that, after photo-excitation, the intramolecular proton transfer reaction with the H1 atom moving from O1 to O2 occurs more readily in both the dynamics and thermodynamics aspects. In sharp contrast, the weak S⋯H1–O1 bond in 3-HTC-b was weakened in the S1 state compared with that in the S0 state, suggesting that the ESIPT process is forbidden. For the first time, it is found that the strong hydrogen bond is further strengthened and the weak hydrogen bond is further weakened in the excited state of 3-HTC. Moreover, the vibrational frequencies of the CO and O–H groups involved in the hydrogen bonds were also studied, and a more clear-cut signature of the hydrogen-bonding dynamics of 3-HTC is provided in this work.

We systematically studied the electronic structures and conducting properties of rubrene and its derivatives reported recently, and disscussed the influences of electron-withdrawing groups and chemical oxidation on the reorganization energies, crystal packing, electronic couplings, and charge injection barrier of rubrene. Hirshfeld surface analysis and quantum-chemical calculations revealed that the introduction of CF3 groups into rubrene decreases the H···H repulsive interaction and increases intermolecular F···H/H···F attractive interactions, which resulted in the tight packing arrangement and the increase of the electronic couplings, and finally cause the higer intrinsic hole-mobility in bis(trifluoromethyl)-dimethyl-rubrene crystal (μh = 19.2 cm2 V−1 s−1) than in rubrene crystal (μh = 15.8 cm2 V−1 s−1). In comparison, chemical oxidation reduces charge-carrier mobility of rubrene crystal by 2~4 orders of magnitude and increased the hole and electron injection barrier, which partly explains the rubrene-based field-effect transistor performance degrades upon exposure to air. Furthermore, we also discussed the influence of structural parameters of carbon nanotube (CNT) electrode on charge injection process, which suggests that the regulation of CNT diameters and increasing in thickness is an effective strategy to optimize CNT work functions and improve n-type OFET performances based on these organic materials.

OBJECTIVE: To examine the changes in serum chromogranin A (CgA) and urotensin Ⅱ (U Ⅱ) levels in children with chronic heart failure (CHF) and their clinical significance. METHODS: A total of 58 children with CHF, among whom 17 had endocardial fibroelastosis (EFE) and 41 had dilated cardiomyopathy (DCM), were selected as CHF group, and 20 healthy children were selected as control group. Serum levels of CgA and U Ⅱ were measured using enzyme-linked immunosorbent assay, and the level of N-terminal pro-brain natriuretic peptide (NT-proBNP) was determined by bi-directional lateral flow immunoassay. Ventricular remodeling indices were measured using echocardiography. The correlation between serum CgA and U Ⅱ levels and ventricular remodeling was evaluated by Pearson correlation or Spearman's rank correlation analysis. RESULTS: There were no significant differences in serum CgA and NT-proBNP levels between children with grade Ⅱ heart function and the control group (P > 0.05). However, the serum CgA and NT-proBNP levels gradually increased as the heart function grade increased, and were significantly higher in grade Ⅲ and IV children compared to those in the control group (P < 0.05). U Ⅱ levels were lower in children with grade Ⅱ, Ⅲ, or IV heart function than those in the control group (P < 0.05), and significantly decreased with the aggravation of CHF (P < 0.05). There were no significant differences in CgA and U Ⅱ levels between patients with EFE and DCM (P > 0.05). Serum CgA concentration was positively correlated with left ventricular mass index (LVMI), NT-proBNP, and cardiac function classification (r=0.279, 0.649, and 0.778 respectively; P < 0.05), but was negatively correlated with left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and U Ⅱ (r=-0.369, -0.322, and-0.718 respectively; P < 0.05). Serum U Ⅱ concentration was negatively correlated with NT-proBNP and cardiac function classification (r=-0.472 and-0.591 respectively; P < 0.05), but was not correlated with LVMI, LVEF, and LVFS (P > 0.05). CONCLUSIONS: CgA may play a role in ventricular remodeling in children with CHF. Serum CgA and U Ⅱ may serve as a reference for the diagnosis and functional classification of heart failure.