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1.  Insulin-Like Growth Factor-1 as a Prognostic Marker in Patients with Acute Ischemic Stroke 
PLoS ONE  2014;9(6):e99186.
Insulin-like growth factor-1 (IGF-1) has been associated with cardiovascular risk factors and atherosclerosis. The aim of the present study was to evaluate the prognostic value of IGF-1 levels in patients with acute ischemic stroke (AIS).
All patients with first-ever AIS from August 1, 2012 to August 31, 2013 were recruited to participate in the study. Clinical data were collected. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to serum IGF-1 levels. For the assessment of functional outcome at 90 days Modified Rankin Scale (mRS) was used. On admission, serum IGF-1 levels were determined by chemiluminescence immunoassay. The influence of IGF-1 levels on functional outcome and death was assessed by multivariate logistic regression analysis.
Patients with an unfavorable outcomes and non-survivors had significantly decreased serum IGF-1 levels on admission (P<0.0001 for both). IGF-1 was an independent prognostic marker of functional outcome and death [odds ratio 0.89 (0.84–0.93) and 0.90 (0.84–0.95), respectively, P<0.0001 for both, adjusted for age, NIHSS score and other predictors] in patients with ischemic stroke. Serum IGF-1 levels ≤130 ng/mL was as an value indicator for unfavorable functional outcome (OR 3.31, 95% CI:1.87–5.62; P<0.0001), after adjusting for other significant confounders.
We reported a significant association between low serum IGF-1 levels and unfavorable functional outcome and death.
PMCID: PMC4050057  PMID: 24911265
2.  Metformin Ameliorates Hepatic Steatosis and Inflammation without Altering Adipose Phenotype in Diet-Induced Obesity 
PLoS ONE  2014;9(3):e91111.
Non-alcoholic fatty liver disease (NAFLD) is closely associated with obesity and insulin resistance. To better understand the pathophysiology of obesity-associated NAFLD, the present study examined the involvement of liver and adipose tissues in metformin actions on reducing hepatic steatosis and inflammation during obesity. C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity-associated NAFLD and treated with metformin (150 mg/kg/d) orally for the last four weeks of HFD feeding. Compared with HFD-fed control mice, metformin-treated mice showed improvement in both glucose tolerance and insulin sensitivity. Also, metformin treatment caused a significant decrease in liver weight, but not adiposity. As indicated by histological changes, metformin treatment decreased hepatic steatosis, but not the size of adipocytes. In addition, metformin treatment caused an increase in the phosphorylation of liver AMP-activated protein kinase (AMPK), which was accompanied by an increase in the phosphorylation of liver acetyl-CoA carboxylase and decreases in the phosphorylation of liver c-Jun N-terminal kinase 1 (JNK1) and in the mRNA levels of lipogenic enzymes and proinflammatory cytokines. However, metformin treatment did not significantly alter adipose tissue AMPK phosphorylation and inflammatory responses. In cultured hepatocytes, metformin treatment increased AMPK phosphorylation and decreased fat deposition and inflammatory responses. Additionally, in bone marrow-derived macrophages, metformin treatment partially blunted the effects of lipopolysaccharide on inducing the phosphorylation of JNK1 and nuclear factor kappa B (NF-κB) p65 and on increasing the mRNA levels of proinflammatory cytokines. Taken together, these results suggest that metformin protects against obesity-associated NAFLD largely through direct effects on decreasing hepatocyte fat deposition and on inhibiting inflammatory responses in both hepatocytes and macrophages.
PMCID: PMC3956460  PMID: 24638078
3.  Ochracenoids A and B, Guaiazulene-Based Analogues from Gorgonian Anthogorgia ochracea Collected from the South China Sea 
Marine Drugs  2014;12(3):1569-1579.
Two new guaiazulene-based analogues, ochracenoids A (1) and B (2), along with four known analogues (3–6), were isolated from the gorgonian Anthogorgia ochracea collected from the South China Sea. The planar structures of the new compounds were elucidated by comprehensive spectroscopic data. The absolute configuration of 1 was determined as 3R by the comparison of TDDFT calculated electronic circular dichroism with its experimental spectrum. Compound 1 is a rare guaiazulene-based analogue possessing a unique C16 skeleton. The possible generation process of 1 through an intermolecular one-carbon-transfer reaction was also discussed. Compound 2 was previously described as a presumed intermediate involved in the biogenesis of anthogorgienes A and I. Compound 3 exhibited antiproliferative effects on the embryo development of zebrafish Danio rerio.
PMCID: PMC3967227  PMID: 24637960
gorgonian; Anthogorgia ochracea; guaiazulene-based analogue; antiproliferative effect; zebrafish embryo
4.  Hyperbaric Oxygen Preconditioning Induces Tolerance against Oxidative Injury and Oxygen-Glucose Deprivation by Up-Regulating Heat Shock Protein 32 in Rat Spinal Neurons 
PLoS ONE  2014;9(1):e85967.
Hyperbaric oxygen (HBO) preconditioning (HBO-PC) has been testified to have protective effects on spinal cord injury (SCI). However, the mechanisms remain enigmatic. The present study aimed to explore the effects of HBO-PC on primary rat spinal neurons against oxidative injury and oxygen-glucose deprivation (OGD) and the relationship with heat shock proteins (HSPs).
Primary rat spinal neurons after 7 days of culture were used in this study. HSPs were detected in rat spinal neurons following a single exposure to HBO at different time points by Western blot. Using lactate dehydrogenase release assay and cell counting kit-8 assay, the injuries induced by hydrogen peroxide (H2O2) insult or OGD were determined and compared among neurons treated with HBO-PC with or without HSP inhibitors.
The results of Western blot showed that HSP27, HSP70 and HSP90 have a slight but not significant increase in primary neurons following HBO exposure. However, HSP32 expression significantly increased and reached highest at 12 h following HBO exposure. HBO-PC significantly increased the cell viability and decreased the medium lactate dehydrogenase content in cultures treated with H2O2 or OGD. Pretreatment with zinc protoporphyrin IX, a specific inhibitor of HSP32, significantly blocked the protective effects of HBO-PC.
These results suggest that HBO-PC could protect rat spinal neurons in vitro against oxidative injury and OGD mostly by up-regulating of HSP32 expression.
PMCID: PMC3895009  PMID: 24465817
5.  5-Phenyl-1,3,4-oxadiazol-2-amine 
In the title complex, C8H7N3O, the C—O [1.369 (2) and 1.364 (3) Å] and C=N [1.285 (3) and 1.289 (3) Å] bond lengths in the oxadiazole ring are each almost identical within systematic errors, although different substituents are attached to the ring. The phenyl ring is inclined to the planar oxadiazole ring [r.m.s. deviation 0.002 Å] by 13.42 (18)°. In the crystal, molecules are linked via N—H⋯N hydrogen bonds, forming double-stranded chains propagating along [010].
PMCID: PMC3470405  PMID: 23125818
6.  5-(4-Methyl­phen­yl)-1,3,4-oxadiazol-2-amine 
In the crystal structure of the title compound, C9H9N3O, adjacent mol­ecules are linked through N—H⋯N hydrogen bonds into a three-dimensional network.
PMCID: PMC3379265  PMID: 22719463
7.  Ba5Cl4(H2O)8(VPO5)8: a novel three-dimensional framework solid 
The structure of Ba5Cl4(H2O)8(PVO5)8 consists of alternating anionic oxovanadium phosphate (VPO5) and cationic barium chloride hydrate, Ba5Cl4(H2O)8, layers. These layers are linked through Ba—O bonds, generating a three-dimensional framework.
The novel hydro­thermally synthesized title compound, penta­barium tetra­chloride octa­hydrate octa­kis(oxovanadium phosphate), Ba5Cl4(H2O)8(VPO5)8, crystallizes in the ortho­­rhom­bic space group Cmca with a unit cell containing four formula units. Two Ba2+ cations, two Cl− anions and the O atoms of four water mol­ecules are situated on the (100) mirror plane, while the third independent Ba2+ cation is on the inter­section of the (100) plane and the twofold axis parallel to a. Two phosphate P atoms are on twofold axes, while the remaining independent P atom and both V atoms are in general positions. The structure is characterized by two kinds of layers, namely anionic oxovanadium phosphate (VPO5), composed of corner-sharing VO5 square pyramids and PO4 tetra­hedra, and cationic barium chloride hydrate clusters, Ba5Cl4(H2O)8, composed of three Ba2+ cations linked by bridging chloride anions. The layers are connected by Ba—O bonds to generate a three-dimensional structure.
PMCID: PMC2855588  PMID: 20203389
8.  Effect of catch-up growth after food restriction on the entero-insular axis in rats 
Catch-up growth after food restriction (CUGFR) is characterized by a significant change in food intake which could theoretically lead to the change in glucagon-like peptide-1 (GLP-1) secretion that consequently results in altered functions of pancreatic islets.
Experimental rats were divided into two groups. Rats in CUGFR group were put on food-restriction for 4 weeks, and then allowed full access to food for 0, 2, 4 weeks respectively while rats in the control group were offered ad libitum access to food. Plasma glucose, insulin and GLP-1 level during OGTT were measured in all the rats. Moreover, morphology of intestinal mucosa, number of L cells, beta cell mass, incretin effect and the expression of GLP-1 receptor (GLP-1R) gene in the islets were also determined.
The size of pancreatic islets, insulin concentration, plasma GLP-1 concentration, incretin effect, villus height-to-crypt depth ratio and L cells were all significantly decreased in CUGFR group at the end of a 4-week food-restriction period as compared with the controls. Insulin concentration and the villus height-to-crypt depth ratio were increased and finally exceeded the level of the control group over a 4-week catch-up period. Nevertheless, at the conclusion of the study, islet size, L cells number, plasma GLP-1 concentration and incretin effect increased but failed to reach the levels of the controls.
CUGFR decreases incretin effect and disturbs the entero-insular axis partially by decreasing GLP-1 concentration, which might be responsible for the increased risk of metabolic disorder during CUGFR.
PMCID: PMC2890696  PMID: 20504302
9.  Lithium diaqua­nickel(II) catena-borodiphosphate(V) monohydrate 
The title borophosphate LiNi(H2O)2[BP2O8]·H2O was synthesized under hydro­thermal conditions. The crystal structure is isotypic with the Mg analogue and features helical [BP2O8]3− borophosphate ribbons, constructed by BO4 (2 symmetry) and PO4 tetra­hedra. The borate groups share all their oxygen apices with adjacent phosphate tetra­hedra. The ribbons are connected via Ni2+ cations that are located on twofold rotation axes. The cations have a slightly distorted octa­hedral oxygen coordination by four O atoms from the anion and by two water mol­ecules. The voids within the helices are occupied by Li+ cations, likewise located on twofold rotation axes, in an irregular environment of five O atoms. The structure is stabilized by O—H⋯O hydrogen bonds between coordinated or uncoordinated water mol­ecules and O atoms that are part of the helices.
PMCID: PMC2969569  PMID: 21582977
10.  An open-framework borophosphate, LiCu2BP2O8(OH)2  
The open-framework alkaline-earth metal borophosphate, lithium dicopper(II) borophosphate dihydroxide, LiCu2BP2O8(OH)2, was synthesized hydro­thermally. Its structure may be regarded as a layer formed via BO4 and PO4 tetra­hedra bonding together with distorted CuO6 and LiO6 octa­hedral units. Each P atom is connected to B, Li and Cu atoms through a bridging O atom. The B atom lies on a crystallographic twofold axis and the Li atom lies on a center of symmetry. The two metal centers are connected to each other by Cu—O—Li bonds.
PMCID: PMC2977544  PMID: 21583730
11.  A new aqua­manganese(II) oxalate phosphate, Mn(C2O4)Mn3(PO4)2(H2O)2  
The title salt, diaquatetra­manganese(II) oxalate bis[ortho­phos­phate(V)], Mn4(C2O4)(PO4)2(H2O)2, was synthesized hydro­thermally and displays a three-dimensional framework structure. The asymmetric unit consists of two different MnII centers, half of an oxalate anion, a phosphate group and a coordinated water mol­ecule. A crystallographic inversion center is located at the mid-point of the oxalate C—C bond. The distorted octa­hedral MnO6 and the tetra­gonal pyramidal MnO5 centers are linked through bridging oxalate and phosphate groups. The water mol­ecule also has a weaker bonding contact to the five-coordinate Mn atom, which consequently exhibits a distorted octa­hedral geometry and also bridges the independent Mn atoms. The water mol­ecule is a donor for intra- and inter­molecular O—H⋯O hydrogen bonds.
PMCID: PMC2977538  PMID: 21583724

Results 1-11 (11)