Hypoadiponectinemia predicts impaired endothelium-independent vasodilation in newly diagnosed type 2 diabetic patients: an 8-year prospective study.

Background: Adiponectin is an adipokine with insulin-sensitising and anti-atherogenic properties. The aim of this study was to investigate whether low adiponectin levels predict the impairment of endothelial function in newly diagnosed type 2 diabetic patients in an 8-year prospective study.

Methods: In the prospective study, we enrolled 133 newly diagnosed type 2 diabetic patients without subclinical atherosclerosis and gave them intensive therapy; the mean treatment period was 8 years.

A continued saga of Boc5, the first non-peptidic glucagon-like peptide-1 receptor agonist with in vivo activities.

Glucagon-like peptide-1 (GLP-1)-based therapy presents a promising option for treating type 2 diabetes. However, there are several limitations relative to the peptidic GLP-1 mimetics currently on the market or under development. This concern has led to a continued interest in the search for non-peptidic agonists for GLP-1 receptor (GLP-1R).

(Z)-Ethyl 2-(2,4-dimethyl-benzyl-idene)-7-methyl-3-oxo-5-phenyl-3,5-dihydro-2H-thia-zolo[3,2-a]pyrimidine-6-carboxyl-ate.

In the title compound, C(25)H(24)N(2)O(3)S, the dihedral angles between the thia-zole ring and the phenyl and substituted benzene rings are 84.91 (11) and 11.58 (10)°, respectively.

Dual effects of phloretin on aflatoxin B1 metabolism: activation and detoxification of aflatoxin B1.

Typically, chemopreventive agents involve either induction of phase II detoxifying enzymes and/or inhibition of cytochrome P450 enzymes (CYPs) that are required for the activation of procarcinogens. In this study, we investigated the protective effects of phloretin against aflatoxin B1 (AFB1) activation to the ultimate carcinogenic intermediate, AFB(1)-8, 9-epoxide (AFBO), and its subsequent detoxification. Phloretin markedly inhibited formation of the epoxide with human liver microsomes in a dose-dependent manner.

4-[Tris(1H-pyrazol-1-yl)meth-yl]phenol.

The title compound, C(16)H(14)N(6)O, was prepared by the condensation of 4-(trifluoro-meth-yl)phenol and sodium pyrazol-1-ide in a yield of 58%. The dihedral angles formed by the planes of the pyrazole rings are 50.7 (2), 71.

1,1',1''-{[4-(3,4-Ethyl-ene-dioxy-thio-phen-2-yl)phen-yl]methane-tri-yl}tris-(1H-pyra-zole).

In the title complex, C(22)H(18)N(6)O(2)S, two of the pyrazole rings are disordered over two sets of sites with ratios of refined occupancies of 0.58 (2):0.42 (2) and 0.

CRABP-II methylation: a critical determinant of retinoic acid resistance of medulloblastoma cells.

Medulloblastoma cells exhibit varied responses to therapy by all-trans retinoic acid (RA). The underlying mechanism for such diverse effects however remains largely unclear. In this study, we attempted to elucidate the molecular basis of RA resistance through the study of RA signaling components in both RA-sensitive (Med-3) and RA-resistant (UW228-2 and UW228-3) medulloblastoma cells.

Temperature-directed structural recurrence in low-symmetric Co(II) complexes and nanocrystals.

Low-symmetric complexes {[Co(μ(2)-L)(H(2)O)(2)]·H(2)O}(n) (1) and {[Co(μ(3)-L)(H(2)O)]·0.5H(2)O}(n) (2) and corresponding nanocrystals were obtained, which exhibit structural recurrence behaviour at various temperatures as well as changes of chiral, nonlinear optical and ferroelectric properties.

Metabolic patterns and biotransformation activities of resveratrol in human glioblastoma cells: relevance with therapeutic efficacies.

Background: Trans-resveratrol rather than its biotransformed monosulfate metabolite exerts anti-medulloblastoma effects by suppressing STAT3 activation. Nevertheless, its effects on human glioblastoma cells are variable due to certain unknown reason(s).

Methodology/principal Findings: Citing resveratrol-sensitive UW228-3 medulloblastoma cell line and primarily cultured rat brain cells/PBCs as controls, the effect of resveratrol on LN-18 human glioblastoma cells and its relevance with metabolic pattern(s), brain-associated sulfotransferase/SULT expression and the statuses of STAT3 signaling and protein inhibitor of activated STAT3 (PIAS3) were elucidated by multiple experimental approaches.

CRABP-II- and FABP5-independent all-trans retinoic acid resistance in COLO 16 human cutaneous squamous cancer cells.

The effect of all-trans retinoic acid (ATRA) on cutaneous squamous cell carcinomas (c-SCC) has been poorly described. Because the imbalance of CRABP-II-mediated anticancer signalling and FABP5-mediated growth-promoting signalling was supposed to be related with ATRA sensitivities of cancer cells, COLO16 human c-SCC cell line was selected to check underlying mechanism leading to ATRA resistance by multiple experimental approaches. The results revealed that COLO 16 cells were resistant to 15 μm ATRA treatment.

Pharmacokinetics of tacrolimus converted from twice-daily formulation to once-daily formulation in Chinese stable liver transplant recipients.

Aim: To evaluate the pharmacokinetics of tacrolimus in Chinese stable liver transplant recipients converted from immediate release (IR) tacrolimus-based immunosuppression to modified release (MR) tacrolimus-based immunosuppression.

Methods: Open-label, multi-center study with a one-way conversion design was conducted. Eighty-three stable liver recipients (6-24 months post-transplant) with normal renal and stable hepatic function were converted from IR tacrolimus twice-daily treatment to MR tacrolimus once-daily treatment on a 1:1 (mg: mg) total daily dose basis.

Anti-apoptotic effect of phloretin on cisplatin-induced apoptosis in HEI-OC1 auditory cells.

Cisplatin is a highly effective chemotherapeutic agent, but it has significant ototoxic side effects. Apoptosis is an important mechanism of cochlear hair cell loss following exposure to cisplatin. The present study examined the effects of phloretin, a natural polyphenolic compound found in apples and pears, on cisplatin-induced apoptosis.

(1E,4E)-1,5-Bis(2,6-difluoro-phen-yl)penta-1,4-dien-3-one.

The mol-ecule of the title compound, C(17)H(10)F(4)O, is roughly planar, with a dihedral angle of 5.59 (14)° between the two phenyl rings. The mol-ecule has an E conformation with respect to the olefinic bonds.

Differential Notch1 and Notch2 expression and frequent activation of Notch signaling in gastric cancers.

Context: The biologic effects of Notch1 and Notch2 vary with cancer types and their potential role(s) in gastric cancers (GCs) remains largely unknown.

Objectives: This study aimed to address the previously mentioned issue by checking the expression of Notch1, Notch2, and Notch target gene Hes1 in GCs, premalignant gastric lesions, and noncancerous endoscopic gastric mucosa and by inhibiting Notch signal transduction in GC cells.

Design: The status of Notch1, Notch2, and Hes1 expression in 74 GC surgical specimens, 10 endoscopic samples, and 4 human GC cell lines was evaluated by tissue microarray-based immunohistochemical staining, Western blotting, and reverse transcription-polymerase chain reaction, and the importance of Notch signaling was elucidated by treating 2 GC cell lines with 2 γ-secretase inhibitors.

[Metabolites of injected chlorogenic acid in rats].

Chlorogenic acid (5-CQA) is one of the major components in some Chinese herbal injections. However, the metabolism of 5-CQA in rats after intravenous injection has not been determined. An ultra-high performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF MS) method was applied to identify the metabolites in bile, urine, feces and plasma after a single intravenous administration of 10 mg x kg(-1) 5-CQA to rats.

[Comparison and significance of DCDF probe and ES probe in the detection of BCR/ABL fusion gene].

Objective: To investigate the signal patterns of dual color dual fusion (DCDF) probe and extra signal (ES) probe in the detection of BCR/ABL fusion gene, and illustrate the relation between the fluorescence in situ hybridization (FISH) pattern and the karyotype.

Methods: Sixty-five cases of chronic myelocytic leukemia (CML) and 50 cases of acute lymphoblastic leukemia (ALL) were detected by FISH with DCDF probe, the BCR/ABL positive samples were detected by FISH with ES probe. Among these cases, 47 cases of CML and 40 cases of ALL perform conventional cytogenetics simultaneously.

[Effects of human Livin gene down-regulation by RNA interference on xenograft of transplantation tumor induced by SPC-A1 in nude mice].

Objective: To explore the in vivo inhibitory effect of Livin gene silencing by RNA interference on xenograft of lung adenocarcinoma SPC-A-1 cells in BALB/C nude mice.

Methods: Three different BALB/C nude mice models were established by subcutaneously inoculating differently treated SPC-A-1 cells into 3 nude mice groups: the blank control group was inoculated with blank SPC-A-1 cells, while the negative group was inoculated with cells transfected with lentivirus-delivered negative shRNA, the experimental group was inoculated with cells with lentivirus-delivered Livin shRNA. Then the growth of tumors was observed, and the volume and weight of the tumors were measured at different time points.

Inhibition of NF-κB signaling commits resveratrol-treated medulloblastoma cells to apoptosis without neuronal differentiation.

Resveratrol promotes differentiation and apoptosis of medulloblastoma cells by suppressing STAT3 signaling and a range of cancer-associated gene expression. However, Bcl-2, a common target of STAT3 and NF-κB signaling, is distinctly up-regulated in resveratrol-treated medulloblastoma cells, indicating potential effects of NF-κB in Bcl-2 expression and anti-medulloblastoma efficiency of resveratrol. To clarify this point, the status of NF-κB signaling and the consequence of NF-κB inhibition in UW228-2 and UW228-3 medulloblastoma cells without and with resveratrol treatment were evaluated by several experimental approaches.

Changes of inflammation and apoptosis in adrenal gland after experimental injury in rats with acute necrotizing pancreatitis.

We hypothesize that adrenal insufficiency in acute necrotizing pancreatitis (ANP) is attributable to hemorrhagic inflammation, necrosis, and apoptosis of the adrenal cortex. Arguments to support this view are presented in the study that investigated morphological and functional changes of adrenal and the distinct roles of inflammatory mediator secretory phospholipase A(2) (sPLA(2)) and apoptosis-related genes Bax and Bcl-2 played in acute adrenal injury in ANP. After ANP model was induced, pancreatic histology, serum amylase, sPLA(2), and corticosterone were analyzed.

[Pathogenetic mechanism of beta-arrestin1 in experimental colitis of rats and intervention effects of oxymatrine].

Objective: To investigate the pathogenetic mechanism of beta-arrestin1 in the rat's experimental colitis, whether the delta opioid receptor-beta-arrestin1 -Bcl-2 signal transduction pathway involves the pathological process of experimental colitis in rats, and whether oxymatrine could attenuate colitis through this pathway.

Methods: Twenty-six SD rats were randomly divided into four groups, the normal control group, the model group, the mesalazine treated group and the oxymatrine treated group (8 rats in the last group and 6 each in the others). The colitis model was established with trinitrobenzene sulfonic acid (TNBS), and rats in the latter two groups were treated by oxymatrine (intramuscular injection) and mesalazine (3 mL solution gavaged) for 15 days, respectively, while rats in the former two groups were fed with equal volume of distilled water.

Global histone modification patterns as prognostic markers to classify glioma patients.

Background: An altered pattern of epigenetic modifications is central to the development and progression of various tumors. We studied epigenetic changes involving multiple modifications of histones to better predict prognosis of glioma patients.

Methods: Immunohistochemistry was done to investigate global histone modification expression of histone 3 lysine 4 dimethylation (H3K4diMe), histone 4 arginine 3 monomethylation (H4R3monoMe), histone 4 lysine 20 trimethylation (H4K20triMe), and acetylation of histone 3 lysine 9 (H3K9Ac), histone 3 lysine 18 (H3K18Ac), histone 4 lysine 12 (H4K12Ac), and histone 4 lysine 16 (H4K16Ac) in resected tumor samples of 230 glioma patients.

Grifolin, a potent antitumour natural product upregulates death-associated protein kinase 1 DAPK1 via p53 in nasopharyngeal carcinoma cells.

Grifolin, a secondary metabolite isolated from the fresh fruiting bodies of the mushroom Albatrellus confluens, has been shown to inhibit the growth of some cancer cell lines in vitro by induction of apoptosis in previous studies of our group. However, the mechanisms of action are not completely understood. An apoptosis-related gene expression profiling analysis provided a clue that death-associated protein kinase 1 (dapk1) gene was upregulated at least twofold in response to grifolin treatment in nasopharyngeal carcinoma cell CNE1.

Flower-like hierarchically nanostructured hydroxyapatite hollow spheres: facile preparation and application in anticancer drug cellular delivery.

Flower-like nanostructured hydroxyapatite hollow spheres (NHHS) assembled with nanosheets with a hierarchical morphology are fabricated by a rapid microwave-assisted hydrothermal route. The presence and concentration of block copolymer poly(lactide)-block-poly(ethylene glycol) (PLA-PEG) are important parameters for the formation of the hollow structure. The possible formation mechanism of NHHS is proposed.

Sulforaphane induces glutathione S-transferase isozymes which detoxify aflatoxin B(1)-8,9-epoxide in AML 12 cells.

The aflatoxin B(1)-8,9-epoxide (AFBO) is hepatocarcinogenic intermediate of aflatoxin B(1) (AFB(1)) and is detoxified by glutathione S-transferases (GSTs). In this study, we investigated whether sulforaphane (SFN) could increase the rate of conjugation between AFBO and glutathione (GSH) as well as which of the GST isozymes were involved in the conjugation reaction. The conjugation potential was inhibited dose dependently with curcumin, an inhibitor of GSTs.

Chronic morphine treatment impaired hippocampal long-term potentiation and spatial memory via accumulation of extracellular adenosine acting on adenosine A1 receptors.

Chronic exposure to opiates impairs hippocampal long-term potentiation (LTP) and spatial memory, but the underlying mechanisms remain to be elucidated. Given the well known effects of adenosine, an important neuromodulator, on hippocampal neuronal excitability and synaptic plasticity, we investigated the potential effect of changes in adenosine concentrations on chronic morphine treatment-induced impairment of hippocampal CA1 LTP and spatial memory. We found that chronic treatment in mice with either increasing doses (20-100 mg/kg) of morphine for 7 d or equal daily dose (20 mg/kg) of morphine for 12 d led to a significant increase of hippocampal extracellular adenosine concentrations.