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1.
Inorg Chem ; 59(23): 17415-17420, 2020 Dec 07.
Article in English | MEDLINE | ID: mdl-33211488

ABSTRACT

The reaction of 3,6-ditert-butyl-1,8-bis(diphenylphosphino)-9-methyl-9H-carbazole (L) with CuBr resulted in the isolation of tetranuclear copper(I) complex Cu4Br4L2 as two colorless crystal morphs, i.e., green-emitting 1G and yellow-emitting 1Y. As demonstrated by X-ray crystallography, the Cu4Br4 moiety in both 1G and 1Y adopts the same chair conformations. When L is bonded perpendicularly to the Cu4 plane, 1G with green emission is obtained, while it gives a yellow emission of 1Y once the L is parallelly bonded to Cu4 plane. Theoretical computational studies suggest that the variation in ligand orientation results in a different degree of structural distortion in triplet state and thus different luminescent energy. Particularly, 1Y undergoes dramatic structural distortion from the ground (S0) to triplet excied state (T1). Interestingly, 1G can be converted into 1Y upon exposed to saturated hexane vapor, which would return to 1G upon exposure to acetonitrile vapor. As demonstrated experimentally and theoretically, the reversible luminescence transformation between 1G and 1Y is ascribed to the variation of ligand L orientations.

2.
Proc Natl Acad Sci U S A ; 114(23): E4631-E4640, 2017 06 06.
Article in English | MEDLINE | ID: mdl-28533408

ABSTRACT

Like many complex human diseases, esophageal squamous cell carcinoma (ESCC) is known to cluster in families. Familial ESCC cases often show early onset and worse prognosis than the sporadic cases. However, the molecular genetic basis underlying the development of familial ESCC is mostly unknown. We reported that SLC22A3 is significantly down-regulated in nontumor esophageal tissues from patients with familial ESCC compared with tissues from patients with sporadic ESCCs. A-to-I RNA editing of the SLC22A3 gene results in its reduced expression in the nontumor esophageal tissues of familial ESCCs and is significantly correlated with lymph node metastasis. The RNA-editing enzyme ADAR2, a familial ESCC susceptibility gene identified by our post hoc genome-wide association study, is positively correlated with the editing level of SLC22A3 Moreover, functional studies showed that SLC22A3 is a metastasis suppressor in ESCC, and deregulation of SLC22A3 facilitates cell invasion and filopodia formation by reducing its direct association with α-actinin-4 (ACTN4), leading to the increased actin-binding activity of ACTN4 in normal esophageal cells. Collectively, we now show that A-to-I RNA editing of SLC22A3 contributes to the early development and progression of familial esophageal cancer in high-risk individuals.


Subject(s)
Carcinoma, Squamous Cell/genetics , Esophageal Neoplasms/genetics , Organic Cation Transport Proteins/genetics , RNA Editing , Actinin/metabolism , Adenosine Deaminase/genetics , Adenosine Deaminase/metabolism , Adult , Aged , Animals , Carcinoma, Squamous Cell/pathology , Carcinoma, Squamous Cell/secondary , Cell Line , Cell Line, Tumor , Cell Movement , Disease Progression , Down-Regulation , Esophageal Neoplasms/pathology , Esophageal Neoplasms/secondary , Esophageal Squamous Cell Carcinoma , Esophagus/cytology , Esophagus/metabolism , Gene Knockdown Techniques , Genome-Wide Association Study , Humans , Lymphatic Metastasis/genetics , Male , Mice , Mice, SCID , Middle Aged , Neoplasm Invasiveness/genetics , Organic Cation Transport Proteins/deficiency , Organic Cation Transport Proteins/metabolism , RNA-Binding Proteins/genetics , RNA-Binding Proteins/metabolism , Risk Factors
3.
Carcinogenesis ; 38(1): 94-104, 2017 01.
Article in English | MEDLINE | ID: mdl-27879277

ABSTRACT

Reprogramming of intracellular metabolism is common in liver cancer cells. Understanding the mechanisms of cell metabolic reprogramming may present a new basis for liver cancer treatment. In our previous study, we reported that a novel oncogene eukaryotic translation initiation factor 5A2 (EIF5A2) promotes tumorigenesis under hypoxic condition. Here, we aim to investigate the role of EIF5A2 in cell metabolic reprogramming during hepatocellular carcinoma (HCC) development. In this study, we reported that the messenger RNA (mRNA) level of EIF5A2 was upregulated in 59 of 105 (56.2%) HCC clinical samples (P = 0.015), and EIF5A2 overexpression was significantly associated with shorter survival time of patients with HCC (P = 0.021). Ectopic expression of EIF5A2 in HCC cell lines significantly promoted cell growth and accelerated glucose utilization and lipogenesis rates. The high rates of glucose uptake and lactate secretion conferred by EIF5A2 revealed an abnormal activity of aerobic glycolysis in HCC cells. Several key enzymes involved in glycolysis including glucose transporter type 1 and 2, hexokinase 2, phosphofructokinase liver type, glyceraldehyde 3-phosphate dehydrogenase, pyruvate kinase M2 isoform, phosphoglycerate mutase 1 and lactate dehydrogenase A were upregulated by overexpression of EIF5A2. Moreover, EIF5A2 showed positive correlations with FASN and ACSS2, two key enzymes involved in the fatty acid de novo biosynthetic pathway, at both protein and mRNA levels in HCC. These results indicated that EIF5A2 may regulate fatty acid de novo biosynthesis by increasing the uptake of acetate. In conclusion, our findings demonstrate that EIF5A2 has a critical role in HCC cell metabolic reprogramming and may serve as a prominent novel therapeutic target for liver cancer treatment.


Subject(s)
Biomarkers, Tumor/metabolism , Carcinoma, Hepatocellular/metabolism , Glucose/metabolism , Lipogenesis , Liver Neoplasms/metabolism , Metabolic Networks and Pathways , Peptide Initiation Factors/metabolism , RNA-Binding Proteins/metabolism , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/pathology , Case-Control Studies , Cell Proliferation , Cells, Cultured , Cellular Reprogramming , Female , Follow-Up Studies , Gene Expression Regulation, Neoplastic , Glycolysis , Humans , Liver/metabolism , Liver/pathology , Liver Neoplasms/genetics , Liver Neoplasms/pathology , Male , Middle Aged , Neoplasm Invasiveness , Neoplasm Staging , Peptide Initiation Factors/genetics , Prognosis , RNA-Binding Proteins/genetics , Survival Rate , Eukaryotic Translation Initiation Factor 5A
4.
Inorg Chem ; 56(19): 11917-11928, 2017 Oct 02.
Article in English | MEDLINE | ID: mdl-28933540

ABSTRACT

A hexadentate macrocyclic N-heterocyclic carbene (NHC) ligand precursor (H4L)(PF6)4 containing four benzimidazolium and two secondary amine groups, has been synthesized and characterized. Coordination chemistry of this new macrocyclic diamine-tetracarbene ligand has been studied by the synthesis of its Ag(I), Au(I), Ni(II), and Pd(II) complexes. Reactions of (H4L)(PF6)4 with different equiv of Ag2O result in Ag(I) complexes [Ag(H2L)](PF6)3 (1) and [Ag2(H2L)](PF6)4 (2). A mononuclear Au(I) complex [Au(H2L)](PF6)3 (3) and a trinuclear Au(I) complex [Au3(H2L)(Cl)2](PF6) (4) are obtained by transmetalation of 1 and 2 with AuCl(SMe2), respectively. Reactions of (H4L)(PF6)4 with Ni(OAc)2 and Pd(OAc)2 in the presence of NaOAc yield [Ni(L)](PF6)2 (5) and [Pd(L)](PF6)2 (6), respectively, containing one Ni(II) and Pd(II) ion with distorted square-planar geometry. Using more NaOAc results in the formation of unusual dinuclear complexes [Ni2(L-2H)](PF6)2 (7) and [Pd2(L-2H)](PF6)2 (8) (L-2H = deprotonated ligand after removing two H+ ions from two secondary amine groups in L), respectively, featuring a rare M2N2 core formed by two bridging amides. 7 is also formed by the reaction of 5 with 1.0 equiv of Ni(OAc)2·4H2O in the presence of NaOAc. Transmetalation of 2 with 2.0 equiv of Ni(PPh3)2Cl2 gives [Ni2(L)(µ-O)](PF6)2 (9), the first example of a dinuclear Ni(II) complex with a singly bridging oxo group. 9 is converted to 7 in good yield through the treatment with NaOAc.

5.
Carcinogenesis ; 37(3): 320-332, 2016 Mar.
Article in English | MEDLINE | ID: mdl-26785734

ABSTRACT

Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy; its mechanisms of development and progression are poorly understood. By high-throughput transcriptome sequencing (RNA-Seq) profiling of three pairs of primary ESCCs and their corresponding non-tumorous tissues, we identified that prostate stem cell antigen (PSCA), a gene that encodes a glycosylphosphatidylinositol-anchored protein, is significantly downregulated in ESCC. Here, we reported decreased expression of PSCA in 188/218 (86.2%) of primary ESCC cases and was negatively regulated by its transcription factor sex-determining region Y-box5 that was significantly associated with the poor differentiation (P = 0.003), increased lymph node metastasis (P < 0.0001), advanced stage (P = 0.007), and disease-specific survival (P < 0.0001), but not associated with the recently reported transcrible rs2294008 (C > T) polymorphism in ESCC. Functional studies showed that PSCA could arrest cell cycle progression and promote cell differentiation independent of the start codon polymorphism. Further mechanistic studies revealed that retinoblastoma 1-inducible coiled-coil 1 (RB1CC1), a key signaling node to regulate cellular proliferation and differentiation, interacted specifically with PSCA in ESCC cells. Binding of PSCA and RB1CC1 in cytoplasm resulted in stabilization and translocation of RB1CC1 into nucleus, thereby activating key factors involved in cell cycle arrest and differentiation. Collectively, our data provide a novel molecular mechanism for the tumor suppressor role of PSCA and may help design effective therapy targeting PSCA-RB1CC1 pathway to control esophageal cancer growth and differentiation.


Subject(s)
Antigens, Neoplasm/metabolism , Carcinoma, Squamous Cell/pathology , Esophageal Neoplasms/pathology , Neoplasm Proteins/metabolism , Protein Transport/physiology , Protein-Tyrosine Kinases/metabolism , Tumor Suppressor Proteins/metabolism , Animals , Autophagy-Related Proteins , Chromatin Immunoprecipitation , Electrophoretic Mobility Shift Assay , Esophageal Squamous Cell Carcinoma , GPI-Linked Proteins/metabolism , Heterografts , High-Throughput Nucleotide Sequencing , Humans , Immunohistochemistry , Mice , Mice, Nude , Tissue Array Analysis
6.
Compr Psychiatry ; 69: 216-24, 2016 Aug.
Article in English | MEDLINE | ID: mdl-27423364

ABSTRACT

This study investigated the correlation between the level of microRNA expression in peripheral blood mononuclear cells (PBMCs) and symptomatology in patients with generalized anxiety disorder (GAD). MicroRNA array was performed in peripheral blood mononuclear cells (PBMCs) obtained from GAD patients with gender, age, ethnicity-matched healthy controls. Then real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to verify the top 7 miRNAs with the highest fold-change values in 76 GAD patients and 39 healthy controls. It demonstrated that 5 miRNAs showed significantly differences in expression levels (P<0.01). These 5 GAD-associated miRNAs were finally selected into our study to analyze the association between the plasma level of miRNAs expression and symptomatology scores in Hamilton Anxiety Scale (HAMA). Results showed that the level of miR-4505 and miR-663 was negatively correlated with the total HAMA scores in GAD patients (r=0.2228, r=0.264 P<0.05). MiR-663 was selected into the regression equation of HAMA total scores and psychic anxiety symptomatology scores, and it could explain 5.3% of the HAMA total scores and 15.3% of the anxiety symptomatology scores. This study analyzed preliminarily possible circulating miRNAs expression changes in GAD patients, and the expression level of miR-663 highly correlated with psychic anxiety symptoms, further molecular mechanism of which needs to be explored.


Subject(s)
Anxiety Disorders/diagnosis , Anxiety Disorders/genetics , MicroRNAs/blood , MicroRNAs/genetics , Adult , Anxiety Disorders/psychology , Female , Humans , Leukocytes, Mononuclear/metabolism , Male , Middle Aged , Real-Time Polymerase Chain Reaction , Reference Values , Statistics as Topic
7.
Psychol Health Med ; 21(4): 460-468, 2016 Jun.
Article in English | MEDLINE | ID: mdl-26498318

ABSTRACT

This study aimed to investigate the maladjustment of Asian (Bangladeshi, Pakistani) and African (Nigerian, Namibian, Ghanaian) peacekeepers and its major influence factors. By random cluster sampling, 300 Asian peacekeepers and 271 African peacekeepers were administered the military psychological maladjustment scale (MPMS) and risk factors questionnaire. Investigation at Day 7 and Day 120 into the peacekeeping deployment period indicated that MPMS total score and factor scores of the Asian peacekeepers were significantly lower than those of the African peacekeepers (p < .01). The total score and each factor score of MPMS of the Asian peacekeepers significantly decreased (p < .01); for the African peacekeepers, only the factor score of emotional disorder of MPMS significantly decreased (p < .05). Stepwise regression analysis showed that the education duration was the influence factor for the emotional disorder factor score in the Asian peacekeepers, and the two factors were positively correlated. Age, military service duration, education duration and marital status were the major influence factors for the MPMS factors of the African peacekeepers, among which age was negatively correlated with the total score and each factor score, and military service duration, education duration and marital status were positively related. We conclude that the Asian peacekeepers are more adaptable and resilient than the African peacekeepers. Education duration was the major influence factor for Emotional Disorder in the Asian peacekeepers. The major influence factors for maladjustment in the African peacekeepers were age, military service duration, education duration and marital status.

8.
Am J Med Genet B Neuropsychiatr Genet ; 168B(3): 170-8, 2015 Apr.
Article in English | MEDLINE | ID: mdl-25656957

ABSTRACT

MicroRNAs (miRNA, miR) have been implicated as promising blood-based biomarkers for schizophrenia patients. This study aimed to clinically validate miRNA as potential schizophrenia biomarkers. Plasma levels of 10 miRNAs were analyzed using qPCR in a cohort of 61 schizophrenia patients and 62 normal controls, as well as 25 patients particularly selected for a six-week antipsychotic treatment course. Positive And Negative Syndrome Scale (PANSS), Global Assessment Scale (GAS) and Clinical Global Impression (CGI) were administered to assess the clinical symptoms. The results demonstrated that a panel of miRNAs consisting of miR-30e, miR-181b, miR-34a, miR-346 and miR-7 had significantly increased expression levels with significant combined diagnostic value (AUC:0.713; sensitivity:35.5%; specificity:90.2%). In response to pharmacological treatment, expression levels of miR-132, miR-181b, miR-432 and miR-30e were significantly decreased. In addition, the improvement of clinical symptomatology was significantly correlated with the changes of miR-132, miR-181b, miR-212 and miR-30e expression levels. Furthermore, the decreases of plasma levels of miR-132 and miR-432 were significantly greater in high-effect subgroup than those in low-effect subgroup after six-week treatment course. We conclude that miR-30e, miR-181b, miR-34a, miR-346 and miR-7 combined as a panel are potentially useful non-invasive biomarkers for schizophrenia diagnosis. Markers miR-132, miR-181b, miR-30e and miR-432 are potential indicators for symptomatology improvements, treatment responses and prognosis for schizophrenia patients.


Subject(s)
Antipsychotic Agents/therapeutic use , Biomarkers, Tumor/genetics , Gene Expression Regulation, Neoplastic/drug effects , MicroRNAs/genetics , Schizophrenia/genetics , Adolescent , Adult , Biomarkers, Tumor/blood , Case-Control Studies , Female , Follow-Up Studies , Gene Expression Profiling , Humans , Male , MicroRNAs/blood , Middle Aged , Prognosis , Real-Time Polymerase Chain Reaction , Schizophrenia/blood , Schizophrenia/drug therapy , Young Adult
9.
Carcinogenesis ; 35(5): 1154-61, 2014 May.
Article in English | MEDLINE | ID: mdl-24510112

ABSTRACT

Here, we report the characterization of a candidate tumor suppressor gene leucine-rich glioma inactivated 1 (LGI1) in human esophageal squamous cell carcinoma (ESCC). Downregulation of LGI1 has been detected in approximately 50% of primary ESCCs, which was significantly associated with advanced clinical stage (P < 0.001), lymph node metastasis (P < 0.001), tumor invasion (P = 0.009) and poor disease-specific survival (P < 0.001). Functional studies found that LGI1 could inhibit cell growth, clonogenicity, cell motility and tumor formation in nude mice. Mechanistic investigations suggested that LGI1 acted through extracellular signal-regulated kinase (ERK1/2) signaling to downregulate matrix metalloproteinase (MMP)-3 expression and subsequently suppressed tumor metastasis. Taken together, our study revealed that LGI1 plays an important tumor suppressive role in the development and progression of ESCC, with possible application in clinics as a biomarker and a potential new therapeutic target.


Subject(s)
Carcinoma, Squamous Cell/genetics , Carcinoma, Squamous Cell/pathology , Esophageal Neoplasms/genetics , Esophageal Neoplasms/pathology , Gene Expression Regulation, Neoplastic , Proteins/genetics , Adult , Aged , Carcinoma, Squamous Cell/metabolism , Carcinoma, Squamous Cell/mortality , Cell Line, Tumor , Cell Movement/genetics , Down-Regulation , Esophageal Neoplasms/metabolism , Esophageal Neoplasms/mortality , Esophageal Squamous Cell Carcinoma , Female , Gene Silencing , Humans , Intracellular Signaling Peptides and Proteins , MAP Kinase Signaling System , Male , Matrix Metalloproteinase 3/metabolism , Middle Aged , Neoplasm Grading , Neoplasm Metastasis , Neoplasm Staging , Prognosis , RNA Interference , Tumor Suppressor Proteins/genetics
10.
Int J Behav Med ; 21(4): 730-5, 2014 Aug.
Article in English | MEDLINE | ID: mdl-24337952

ABSTRACT

BACKGROUND: A devastating earthquake registering 8.0 on the Richter Scale struck Wenchuan County in Northwest Sichuan Province in China on May 12, 2008, claiming over 69,200 lives, seriously wounding more than 374,600 people, and rendering more than 18,400 people missing. The epicenter was close to Yingxiu Township in Wenchuan County. PURPOSE: This study aimed to investigate the psychosomatic conditions of the children and adolescents exposed to the devastating earthquake and explore the risk factors for psychosomatic symptoms. METHOD: A total of 1,828 participants aged 6 to 16 years, of whom 842 from the affected area and 986 from non-affected area, were administered a Psychosomatic Conditions Scale. RESULTS: Each factor score, total somatic score, total psychological score, and total psychosomatic score of the experimental group were significantly higher than those of the control group (P < 0.001). Positive correlation was found between the psychological state and somatic symptoms in the experimental group(r = 0.157 ~ 0.489, P < 0.01). Respiratory system, cardiovascular system, nervous system, digestive system, urogenital system, emotion, behavior, and language, combined as a panel, were significantly differentiated between the two groups, accounting for 73.4% of the total difference. In the experimental group, the factor scores of anxiety, behavior, total psychological score, and total psychosomatic score of the girls were obviously higher than those of the boys (P < 0.01 ~ 0.05); most somatic factors and psychological factors, total somatic score, total psychological score, and total psychosomatic score of the elder adolescents were significantly higher than those of the younger children (P < 0.01 ~ 0.05). CONCLUSION: The children and adolescents exposed to 5.12 earthquake greatly suffered from terrible psychosomatic conditions, among whom the elder girls had more severe symptoms, particularly in terms of anxiety and behavior.


Subject(s)
Anxiety/epidemiology , Earthquakes , Psychophysiologic Disorders/epidemiology , Adolescent , Age Factors , Anxiety/etiology , Child , China/epidemiology , Female , Humans , Male , Psychophysiologic Disorders/etiology , Risk Factors , Sex Factors
11.
Carcinogenesis ; 34(2): 454-63, 2013 Feb.
Article in English | MEDLINE | ID: mdl-23125220

ABSTRACT

Nasopharyngeal carcinoma (NPC) is a type of head and neck cancer with significantly high prevalence in Southern China. Unlike other head and neck cancers, mutations or deletions of tumor suppressor genes in NPC are not common. Recently, downregulation of tumor suppressor genes expression by microRNA (miRNA) is increasingly recognized as an important mechanism of nasopharyngeal tumorigenesis. In this study, we reported that microRNA-144 (miR-144) was frequently upregulated in NPC specimens and cell lines. Repression of miR-144 significantly decreased cell proliferation, clonogenicity, migration, invasion and tumor formation in nude mice, while restoring miR-144 in miR-144-attenuated NPC cells exhibited a strong tumorigenic role. Further, we found that miR-144 was inversely correlated with the tumor suppressor gene phosphatase and tensin homolog (PTEN) in NPC specimens and cell lines, and then we identified PTEN as a direct target of miR-144 in NPC cell lines. PTEN downregulation in miR-144-attenuated cells could increase cell growth, migration and invasion. Mechanistic investigations revealed that miR-144 suppressed the expression of PTEN to increase the expression of pAkt and cyclin D1 to promote G(1)-phase transition and decrease E-cadherin to promote migration and invasion. Taken together, we provide compelling evidence that miR-144 functions as an onco-miRNA in NPC, and its oncoeffects are mediated chiefly by repressing PTEN expression to activate the PI3K/Akt pathway.


Subject(s)
Cell Movement , Cell Proliferation , Gene Expression Regulation, Neoplastic , MicroRNAs/genetics , Nasopharyngeal Neoplasms/pathology , Nasopharynx/metabolism , PTEN Phosphohydrolase/antagonists & inhibitors , Adult , Aged , Animals , Apoptosis , Blotting, Western , Carcinoma , Case-Control Studies , Cell Adhesion , Cell Cycle , Female , Humans , Immunoenzyme Techniques , Male , Mice , Mice, Inbred BALB C , Mice, Nude , Middle Aged , Nasopharyngeal Carcinoma , Nasopharyngeal Neoplasms/genetics , Neoplasm Invasiveness , PTEN Phosphohydrolase/genetics , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , RNA, Messenger/genetics , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain Reaction , Tumor Cells, Cultured
12.
Mol Cell Biochem ; 375(1-2): 105-13, 2013 Mar.
Article in English | MEDLINE | ID: mdl-23291919

ABSTRACT

Paroxetine is a widely used antidepressant in clinic. Besides its role in inhibition of serotonin reuptake, resent studies indicate that the increase of hippocampal neurogenesis is also involved in its pharmacology. However, only limited data are available in this regard and its effect on the hippocampus-derived neural stem cell (NSCs) has not been well elucidated. In present study, we utilized hippocampus-derived NSCs from fetal rats to investigate the direct effect of paroxetine on the neurogenesis of NSCs and explore the possible cellular and molecular mechanisms. The results showed that paroxetine not only promoted the proliferation of NSCs, but also promoted NSCs to differentiate into neurons other than glial cells. In addition, the elevated protein levels of phosphorylated ERK1/2, Bcl-2, and brain-derived neurotrophic factor were also observed after paroxetine was administered. Furthermore, the proliferative effect and promotion of NSCs differentiating predominantly into neurons of paroxetine was inhibited by U0126, an ERK1/2 phosphorylation inhibitor. In conclusion, these data indicate that paroxetine can promote neurogenesis of neural stem cells, and this effect might be mediated by ERK1/2 signal pathways.


Subject(s)
Antidepressive Agents, Second-Generation/pharmacology , Hippocampus/cytology , Neural Stem Cells/physiology , Neurogenesis/drug effects , Paroxetine/pharmacology , Animals , Brain-Derived Neurotrophic Factor/metabolism , Butadienes/pharmacology , Cell Proliferation , Cells, Cultured , Extracellular Signal-Regulated MAP Kinases/metabolism , Fetus/cytology , Glial Fibrillary Acidic Protein/metabolism , MAP Kinase Signaling System , Neural Stem Cells/drug effects , Nitriles/pharmacology , Proto-Oncogene Proteins c-bcl-2/metabolism , Rats , Rats, Sprague-Dawley , Spheroids, Cellular/drug effects , Spheroids, Cellular/physiology , Tubulin/metabolism , Up-Regulation
13.
Genome ; 56(6): 351-8, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23957675

ABSTRACT

The aim of this study was to measure genetic diversity and population structure among 92 Canadian barley cultivars using two types of molecular markers (SSRs and DArTs) and pedigree data. A total of 368 alleles were identified at 50 SSR loci. The number of alleles per locus ranged between 2 and 13 ([Formula: see text] = 7.36) and PIC values ranged from 0.34 to 0.86 ([Formula: see text] = 0.69). For the biallelic DArT markers, the genetic distance matrix was based on 971 markers whose PIC values ranged between 0.06 and 0.50 ([Formula: see text] = 0.39). A third distance matrix was computed based on the kinship coefficient. Clustering of genotypes was performed based on the genetic distance matrix and the three dendrograms obtained showed the genetic relationships among barley cultivars. The topological similarity of the three dendrograms was estimated using a congruence index and showed the three dendrograms to be in very good agreement. Statistical analysis also showed a highly significant correlation between the SSR and DArT matrices (r = 0.80, p < 0.002) compared with lower yet significant correlations of the pedigree data with both marker types (r = 0.46, p < 0.002; r = 0.52, p < 0.002). Finally, we assessed linkage disequilibrium in this germplasm and found it to be quite extensive, as the mean distance between marker pairs with significant (P < 0.001) r(2) values >0.5 was 3.8 cM. Information obtained from comparing results of different genetic diversity estimation methods should be useful for the improvement and conservation of barley genetic resources.


Subject(s)
Genetic Variation , Hordeum/genetics , Alleles , Canada , Cluster Analysis , Genetic Markers , Linkage Disequilibrium , Microsatellite Repeats
14.
Inorg Chem ; 52(9): 5167-75, 2013 May 06.
Article in English | MEDLINE | ID: mdl-23581521

ABSTRACT

A series of highly phosphorescent PtAg2 heterotrinuclear alkynyl complexes with bis(diphenylphosphinomethyl)phenylphosphine (dpmp) were prepared and characterized structurally. The solution phosphorescence with various emitting colors is systematically modulated by modifying substituents as well as π-conjugated systems in aromatic acetylides. The crystals, powders, or films exhibit reversible stimuli-responsive phosphorescence changes upon exposure to vapor of MeCN, pyridine, DMF, etc., resulting from perturbation of d(8)-d(10) metallophilic interaction in the excited states as a consequence of the formation/disruption of Ag-solvent bonds. Both experimental and time-dependent density functional theory (TD-DFT) studies demonstrate that d(8)-d(10) metallophilic interaction exerts a crucial role on phosphorescent characteristics due to the PtAg2 cluster-based (3)[d → p] state. This study affords a paradigm for phosphorescence modulation in d(8)-d(10) heteronuclear complexes.


Subject(s)
Alkynes/chemistry , Luminescent Agents/chemistry , Phosphines/chemistry , Platinum Compounds/chemistry , Silver/chemistry , Alkynes/chemical synthesis , Luminescent Agents/chemical synthesis , Luminescent Measurements , Models, Molecular , Phosphines/chemical synthesis , Platinum Compounds/chemical synthesis , Spectrophotometry, Ultraviolet
15.
Zhongguo Shi Yan Xue Ye Xue Za Zhi ; 31(4): 1171-1178, 2023.
Article in Zh | MEDLINE | ID: mdl-37551494

ABSTRACT

OBJECTIVE: To explore molecular mechanisms by which umbilical cord-derived mesenchymal stem cells suppress the development of GVHD after bone marrow hematopoietic stem cell transplantation. METHODS: A mouse model of aGVHD was constructed after bone marrow hematopoietic stem cell transplantation, and the umbilical cord-derived mesenchymal stem cells were cultured, and then injected into the aGVHD mouse model, so as to investigate its prophylactic efficacy. Prophylactic effect of the exosomes isolated from umbilical cord-derived mesenchymal stem cells on aGVHD mice was assessed. Sequencing analysis of miRNA from exosomes was performed. RESULTS: aGVHD model was successfully constructed after hematopoietic stem cell transplantation. By injecting umbilical cord-derived mesenchymal stem cells into the GVHD mouse model, it was found that the treatment significantly prolonged survival time of mice compared to the untreated group. Injection exosomes derived from umbilical cord-derived mesenchymal stem cells into the GVHD mouse model significantly prolonged the survival time of mice compared to the untreated group. High-throughput sequencing data showed that microRNA such as miR-21 in exosomes isolated from umbilical cord-derived mesenchymal stem cells, which mainly affected the signaling pathways such as cell adhesion, RNA degradation. CONCLUSION: The umbilical cord-derived mesenchymal stem cells can prevent the occurrence of aGVHD after HSCT, which is mediate by MicroRNA in the exosomes derived from umbilical cord-derived mesenchymal stem cells.

17.
Inorg Chem ; 51(17): 9508-16, 2012 Sep 03.
Article in English | MEDLINE | ID: mdl-22880548

ABSTRACT

A Zn(2+)-responsive bimodal magnetic resonance imaging (MRI) and luminescence imaging probe GdL was synthesized. The relaxivity and luminescence properties were examined. In the presence of 0.5 equiv of Zn(2+), the longitudinal relaxivity is increased from 3.8 mM(-1) s(-1) to 5.9 mM(-1) s(-1) at 23 MHz and 25 °C with 55% enhancement, whereas the fluorescence exhibits a 7-fold increase. The Zn(2+) responsive imaging probe shows favorable selectivity and tolerance over a variety of biologically relevant anions and metal ions in physiological pH range for both relaxivity and luminescence. In vitro phantom images and confocal fluorescence images in living cells show that the bimodal Zn(2+) probe can effectively enhance T(1)-weighted imaging contrast and luminescence imaging effect through Zn(2+) coordination with excellent cellmembrane permeability and biocompatibility. Spectral and electrospray ionization mass spectrometry (ESI-MS) studies indicate that two different Zn(2+)-bound species, (GdL)(2)Zn and GdLZn, are formed when 0.5 and 1 equiv of Zn(2+) are bound to GdL complex, respectively. Crystal structural determination and dysprosium-induced (17)O NMR shift (DIS) experiment demonstrate that the increased molecular weight and the improved molecular rigidity upon complexation of Zn(2+) with GdL is the primary factor for relaxivity enhancement. Significant enhancement of the luminescence is due to a heavy atom effect and much increased molecular rigidity upon Zn(2+) binding to 8-sulfonamidoquinoline chromophore.


Subject(s)
Gadolinium/chemistry , Magnetic Resonance Imaging/methods , Molecular Imaging/methods , Organometallic Compounds/chemistry , Zinc/metabolism , Cell Line, Tumor , Cell Membrane Permeability , Cell Survival , Humans , Materials Testing , Molecular Probes/chemistry , Molecular Probes/metabolism , Molecular Probes/toxicity , Organometallic Compounds/metabolism , Organometallic Compounds/toxicity , Spectrometry, Fluorescence
18.
Inorg Chem ; 51(10): 5569-79, 2012 May 21.
Article in English | MEDLINE | ID: mdl-22551081

ABSTRACT

Planar platinum(II) complex Pt(Me(3)SiC≡CbpyC≡CSiMe(3))(C≡CC(6)H(4)CF(3)-4)(2) (6) with 5,5'-bis(trimethylsilylethynyl)-2,2'-bipyridine and 4-trifluoromethylphenylacetylide exhibits remarkable luminescence vapochromic and mechanochromic properties and a thermo-triggered luminescence change. Solid-state 6 is selectively sensitive to vapors of oxygen-containing volatile compounds such as tetrahydrofuran (THF), dioxane, and tetrahydropyrane (THP) with phosphorescence vapochromic response red shifts from 561 and 608 nm to 698 nm (THF), 689 nm (dioxane), and 715 nm (THP), respectively. Upon being mechanically ground, desolvated 6, 6·CH(2)Cl(2), and 6·(1)/(2)CH(2)ClCH(2)Cl exhibit significant mechanoluminescence red shifts from 561 and 608 nm to 730 nm, while vapochromic crystalline species 6·THF, 6·dioxane, or 6·THP affords a mechanoluminescence blue shift from 698 nm (THF), 689 nm (dioxane), or 715 nm (THP) to 645 nm, respectively. When the compounds are heated, a thermo-triggered luminescence change occurs, in which bright yellow luminescence at 561 and 608 nm turns to red luminescence at 667 nm with a drastic red shift. The multi-stimulus-responsive luminescence switches have been monitored by the changes in emission spectra and X-ray diffraction patterns. Both X-ray crystallographic and density functional theory studies suggest that the variation in the intermolecular Pt-Pt interaction is the key factor in inducing an intriguing luminescence switch.

19.
Chin J Cancer ; 31(5): 215-22, 2012 May.
Article in English | MEDLINE | ID: mdl-22360856

ABSTRACT

Nasopharyngeal carcinoma (NPC) is among the most common malignancies in southern China. Deletion of genomic DNA, which occurs during the complex pathogenesis process for NPC, represents a pivotal mechanism in the inactivation of tumor suppressor genes (TSGs). In many circumstances, loss of TSGs can be detected as diagnostic and prognostic markers in cancer. The short arm of chromosome 3 (3p) is a frequently deleted chromosomal region in NPC, with 3p21.1-21.2 and 3p25.2-26.1 being the most frequently deleted minimal regions. In recent years, our research group and others have focused on the identification and characterization of novel target TSGs at 3p, such as RASSF1A, BLU, RBMS3, and CHL1, in the development and progression of NPC. In this review, we summarize recent findings of TSGs at 3p and discuss some of these genes in detail. A better understanding of TSGs at 3p will significantly improve our understanding of NPC pathogenesis, diagnosis, and treatment.


Subject(s)
Chromosome Deletion , Chromosomes, Human, Pair 3/genetics , Genes, Tumor Suppressor , Nasopharyngeal Neoplasms/genetics , Tumor Suppressor Proteins/genetics , Cell Adhesion Molecules/genetics , Cytoskeletal Proteins , Epigenesis, Genetic , Gene Expression Regulation, Neoplastic , Heterotrimeric GTP-Binding Proteins/genetics , Humans , RNA-Binding Proteins/genetics , Trans-Activators/genetics , Transducin
20.
Gut ; 60(12): 1635-43, 2011 Dec.
Article in English | MEDLINE | ID: mdl-21672941

ABSTRACT

OBJECTIVES: Interaction between neoplastic and stromal cells plays an important role in tumour progression. It was recently found that WNT2 was frequently overexpressed in fibroblasts isolated from tumour tissue tumour fibroblasts (TF) compared with fibroblasts from non-tumour tissue normal fibroblasts in oesophageal squamous cell carcinoma (OSCC). This study aimed to investigate the effect of TF-secreted Wnt2 in OSCC development via the tumour-stroma interaction. METHODS: Quantitative PCR, western blotting, immunohistochemistry and immunofluorescence were used to study the expression pattern of Wnt2 and its effect on the Wnt/ß-catenin pathway. A Wnt2-secreting system was established in Chinese hamster ovary cells and its conditioned medium was used to study the role of Wnt2 in cell proliferation and invasion. RESULTS: Expression of Wnt2 could only be detected in TF but not in OSCC cancer cell lines. In OSCC tissues, Wnt2(+) cells were mainly detected in the boundary between stroma and tumour tissue or scattered within tumour tissue. In this study, Wnt2-positive OSCC was defined when five or more Wnt2(+) cells were observed in 200× microscopy field. Interestingly, Wnt2-positive OSCC (22/51 cases) was significantly associated with lymph node metastases (p=0.001), advanced TNM stage (p=0.001) and disease-specific survival (p<0.0001). Functional study demonstrated that secreted Wnt2 could promote oesophageal cancer cell growth by activating the Wnt/ß-catenin signalling pathway and subsequently upregulated cyclin D1 and c-myc expression. Further study found that Wnt2 could enhance cell motility and invasiveness by inducing epithelial-mesenchymal transition. CONCLUSIONS: TF-secreted Wnt2 acts as a growth and invasion-promoting factor through activating the canonical Wnt/ß-catenin signalling pathway in oesophageal cancer cells.


Subject(s)
Esophageal Neoplasms/metabolism , Wnt Signaling Pathway/physiology , Wnt2 Protein/metabolism , Animals , Blotting, Western , CHO Cells , Cell Line, Tumor , Cell Movement/physiology , Cell Proliferation , Cricetinae , Esophageal Neoplasms/physiopathology , Fibroblasts/metabolism , Fibroblasts/physiology , Neoplasm Invasiveness/physiopathology , Reverse Transcriptase Polymerase Chain Reaction , Wnt2 Protein/physiology
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