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1.  Antifouling phenyl ethers and other compounds from the invertebrates and their symbiotic fungi collected from the South China Sea 
AMB Express  2016;6:102.
Marine organism-derived secondary metabolites are promising potential sources for discovering environmentally safe antifouling agents. In present study, 55 marine secondary metabolites and their synthesized derivatives were tested and evaluated for their antifouling activities and security. These compounds include 44 natural products isolated from marine invertebrates and their symbiotic microorganisms collected from the South China Sea and 11 structural modified products derived from the isolated compounds. The natural secondary metabolites, covering phenyl ether derivatives, terpenoids, 9, 11-secosteroids, anthraquinones, alkaloids, nucleoside derivatives and peptides, were isolated from two corals, one sponge and five symbiotic fungi. All of the isolated and synthesized compounds were tested for their antifouling activities against the cyprids of barnacle Balanus (Amphibalanus) amphitrite Darwin. Noticeably, five phenyl ether derivatives (9, 11, 13–15) exhibited potent anti-larval settlement activity with the EC50 values lower than 3.05 μM and the LC50/EC50 ratios higher than 15. The study of structure–activity relationship (SAR) revealed that the introduction of acetoxy groups and bromine atoms to phenyl ether derivatives could significantly improve their antifouling activities. This is the first report on the SAR of phenyl ether derivatives on antifouling activity against barnacle B. amphitrite. The polybrominated diphenyl ether derivative, 2, 4, 6, 2′, 4′, 6′-hexabromo-diorcinol (13), which displayed excellent antifouling activity, was considered as a promising candidate of environmentally friendly antifouling agents.
Electronic supplementary material
The online version of this article (doi:10.1186/s13568-016-0272-2) contains supplementary material, which is available to authorized users.
PMCID: PMC5081312  PMID: 27785778
Antifouling; Anti-larval settlement; Balanus amphitrite; Marine natural product; Phenyl ether derivative
2.  Activin A Stimulates Aromatase via the ALK4-Smad Pathway in Endometriosis 
BioMed Research International  2016;2016:5791510.
Endometriosis is an estrogen-dependent disease. We previously found that the expression of Activin A was upregulated in the peritoneal fluid of patients with endometriosis. The results of the present study indicated that Activin A induced estradiol secretion and P450arom expression in endometrial stromal cells (ESCs) derived from endometriosis patients. The mechanism of estrogenic synthesis was regulated by the Activin-Smad pathway in endometrial lesions. The data showed that the effect of Activin A on ESCs was partially abrogated by pretreatment with an inhibitor of ALK4 (the type I receptor, ActRIB) and Smad4-siRNA. Cumulatively, these data suggest that Activin A promotes the secretion of estradiol from ESCs by increasing the expression of P450arom via the ALK4-Smad pathway. These findings indicate the ALK4-Smad pathway may promote ectopic lesion survival and development.
PMCID: PMC5090068  PMID: 27833918
3.  Nitric oxide and hyperoxic acute lung injury 
Medical Gas Research  2016;6(2):85-95.
Hyperoxic acute lung injury (HALI) refers to the damage to the lungs secondary to exposure to elevated oxygen partial pressure. HALI has been a concern in clinical practice with the development of deep diving and the use of normobaric as well as hyperbaric oxygen in clinical practice. Although the pathogenesis of HALI has been extensively studied, the findings are still controversial. Nitric oxide (NO) is an intercellular messenger and has been considered as a signaling molecule involved in many physiological and pathological processes. Although the role of NO in the occurrence and development of pulmonary diseases including HALI has been extensively studied, the findings on the role of NO in HALI are conflicting. Moreover, inhalation of NO has been approved as a therapeutic strategy for several diseases. In this paper, we briefly summarize the role of NO in the pathogenesis of HALI and the therapeutic potential of inhaled NO in HALI.
PMCID: PMC5110127  PMID: 27867474
hyperoxic acute lung injury; hyperoxia; nitric oxide; nitric oxide synthase; reactive oxygen species; reactive nitrogen species; inhaled nitric oxide; nitro-L-arginine methyl ester
4.  Glucose and Palmitate Differentially Regulate PFKFB3/iPFK2 and Inflammatory Responses in Mouse Intestinal Epithelial Cells 
Scientific Reports  2016;6:28963.
The gene PFKFB3 encodes for inducible 6-phosphofructo-2-kinase, a glycolysis-regulatory enzyme that protects against diet-induced intestine inflammation. However, it is unclear how nutrient overload regulates PFKFB3 expression and inflammatory responses in intestinal epithelial cells (IECs). In the present study, primary IECs were isolated from small intestine of C57BL/6J mice fed a low-fat diet (LFD) or high-fat diet (HFD) for 12 weeks. Additionally, CMT-93 cells, a cell line for IECs, were cultured in low glucose (LG, 5.5 mmol/L) or high glucose (HG, 27.5 mmol/L) medium and treated with palmitate (50 μmol/L) or bovine serum albumin (BSA) for 24 hr. These cells were analyzed for PFKFB3 and inflammatory markers. Compared with LFD, HFD feeding decreased IEC PFKFB3 expression and increased IEC proinflammatory responses. In CMT-93 cells, HG significantly increased PFKFB3 expression and proinflammatory responses compared with LG. Interestingly, palmitate decreased PFKFB3 expression and increased proinflammatory responses compared with BSA, regardless of glucose concentrations. Furthermore, HG significantly increased PFKFB3 promoter transcription activity compared with LG. Upon PFKFB3 overexpression, proinflammatory responses in CMT-93 cells were decreased. Taken together, these results indicate that in IECs glucose stimulates PFKFB3 expression and palmitate contributes to increased proinflammatory responses. Therefore, PFKFB3 regulates IEC inflammatory status in response to macronutrients.
PMCID: PMC4937440  PMID: 27387960
5.  Berberine Ameliorates Hepatic Steatosis and Suppresses Liver and Adipose Tissue Inflammation in Mice with Diet-induced Obesity 
Scientific Reports  2016;6:22612.
Increasing evidence demonstrates that berberine (BBR) is beneficial for obesity-associated non-alcoholic fatty liver disease (NAFLD). However, it remains to be elucidated how BBR improves aspects of NAFLD. Here we revealed an AMP-activated protein kinase (AMPK)-independent mechanism for BBR to suppress obesity-associated inflammation and improve hepatic steatosis. In C57BL/6J mice fed a high-fat diet (HFD), treatment with BBR decreased inflammation in both the liver and adipose tissue as indicated by reduction of the phosphorylation state of JNK1 and the mRNA levels of proinflammatory cytokines. BBR treatment also decreased hepatic steatosis, as well as the expression of acetyl-CoA carboxylase and fatty acid synthase. Interestingly, treatment with BBR did not significantly alter the phosphorylation state of AMPK in both the liver and adipose tissue of HFD-fed mice. Consistently, BBR treatment significantly decreased the phosphorylation state of JNK1 in both hepatoma H4IIE cells and mouse primary hepatocytes in both dose-dependent and time-dependent manners, which was independent of AMPK phosphorylation. BBR treatment also caused a decrease in palmitate-induced fat deposition in primary mouse hepatocytes. Taken together, these results suggest that BBR actions on improving aspects of NAFLD are largely attributable to BBR suppression of inflammation, which is independent of AMPK.
PMCID: PMC4776174  PMID: 26936230
6.  Blocking Nuclear Factor-Kappa B Protects against Diet-Induced Hepatic Steatosis and Insulin Resistance in Mice 
PLoS ONE  2016;11(3):e0149677.
Inflammation critically contributes to the development of various metabolic diseases. However, the effects of inhibiting inflammatory signaling on hepatic steatosis and insulin resistance, as well as the underlying mechanisms remain obscure. In the current study, male C57BL/6J mice were fed a chow diet or high-fat diet (HFD) for 8 weeks. HFD-fed mice were respectively treated with p65 siRNA, non-silence control siRNA or vehicle every 4th day for the last 4 weeks. Vehicle-treated (HF) and non-silence siRNA-treated (HFNS) mice displayed overt inflammation, hepatic steatosis and insulin resistance compared with chow-diet-fed (NC) mice. Upon treatment with NF-κB p65 siRNA, HFD-fed (HFPS) mice were protected from hepatic steatosis and insulin resistance. Furthermore, Atg7 and Beclin1 expressions and p-AMPK were increased while p-mTOR was decreased in livers of HFPS mice in relative to HF and HFNS mice. These results suggest a crosslink between NF-κB signaling pathway and liver AMPK/mTOR/autophagy axis in the context of hepatic steatosis and insulin resistance.
PMCID: PMC4773172  PMID: 26930600
7.  Liraglutide prevents fast weight gain and β-cell dysfunction in male catch-up growth rats 
Experimental Biology and Medicine  2015;240(9):1165-1176.
We reported recently that after a nutritional growth retardation, rats showed significant weight gain, central fat accumulation, dyslipidemia, and β-cell dysfunction during a catch-up growth (CUG) phase. Here, we investigated whether glucagon-like peptide-1 (GLP-1) ameliorated the rapid weight gain, central fat deposition, and β-cell dysfunction during the CUG in rats. Sixty-four male Sprague Dawley rats were stratified into four groups including normal control group, CUG group, catch-up growth with liraglutide treatment group, and catch-up growth with liraglutide and exendin 9–39 treatment group. Energy intake, body weight, and body length were monitored. Fat mass percentage was analyzed by dual energy X-ray absorptiometry scan. Plasma triglyceride and non-esterified fatty acid were measured. The β-cell mass was analyzed by morphometric analysis and signaling molecules were examined by Western blot and real-time PCR. Insulin secretion capability was evaluated by hyperglycemic clamp test. Liraglutide prevented weight gain and improved lipid and glucose metabolism in rats under CUG conditions, which were associated with reduced fasting insulin levels and improved glucose-stimulated insulin secretion. Improved β-cell function is found to be associated with increased β-cell replication as determined by β-cell density and insulin-Ki67 dual staining. Furthermore, liraglutide increased islet pancreatic duodenal homeobox-1 (Pdx-1) and B-cell lymphoma-2 transcript and protein expression, and reduced Procaspase-3 transcript and Caspase-3 p11 subunit protein expression, suggesting that expression of Pdx-1 and reduction of apoptosis may be the mechanisms involved. The therapeutic effects were attenuated in rats co-administered with exendin 9–39, suggesting a GLP-1 receptor-dependent mechanism. These studies revealed that incretin therapy effectively prevented fast weight gain and β-cell dysfunction in rats under conditions of nutrition restriction followed by nutrition excess, which is in part due to enhanced functional β-cell mass and insulin secretory capacity.
PMCID: PMC4935360  PMID: 25710926
Catch-up growth; liraglutide; β-cell dysfunction; GLP-1
8.  Metformin and metabolic diseases: a focus on hepatic aspects 
Frontiers of medicine  2015;9(2):173-186.
Metformin has been widely used as a first-line anti-diabetic medicine for the treatment of type 2 diabetes (T2D). As a drug that primarily targets the liver, metformin suppresses hepatic glucose production (HGP), serving as the main mechanism by which metformin improves hyperglycemia of T2D. Biochemically, metformin suppresses gluconeogenesis and stimulates glycolysis. Metformin also inhibits glycogenolysis, which is a pathway that critically contributes to elevated HGP. While generating beneficial effects on hyperglycemia, metformin also improves insulin resistance and corrects dyslipidemia in patients with T2D. These beneficial effects of metformin implicate a role for metformin in managing non-alcoholic fatty liver disease. As supported by the results from both human and animal studies, metformin improves hepatic steatosis and suppresses liver inflammation. Mechanistically, the beneficial effects of metformin on hepatic aspects are mediated through both adenosine monophosphate-activated protein kinase (AMPK)-dependent and AMPK-independent pathways. In addition, metformin is generally safe and may also benefit patients with other chronic liver diseases.
PMCID: PMC4567274  PMID: 25676019
metformin; diabetes; hepatic steatosis; inflammatory response; insulin resistance
9.  Resveratrol supplementation restores high-fat diet-induced insulin secretion dysfunction by increasing mitochondrial function in islet 
Experimental Biology and Medicine  2015;240(2):220-229.
Resveratrol (RSV), a natural compound, is known for its effects on energy homeostasis. Here we investigated the effects of RSV and possible mechanism in insulin secretion of high-fat diet rats. Rats were randomly divided into three groups as follows: NC group (animals were fed ad libitum with normal chow for 8 weeks), HF group (animals were fed ad libitum with high-fat diet for 8 weeks), and HFR group (animals were treated with high-fat diet and administered with RSV for 8 weeks). Insulin secretion ability of rats was assessed by hyperglycemic clamp. Mitochondrial biogenesis genes, mitochondrial respiratory chain activities, reactive oxidative species (ROS), and several mitochondrial antioxidant enzyme activities were evaluated in islet. We found that HF group rats clearly showed low insulin secretion and mitochondrial complex dysfunction. Expression of silent mating type information regulation 2 homolog- 1 (SIRT1) and related mitochondrial biogenesis were significantly decreased. However, RSV administration group (HFR) showed a marked potentiation of glucose-stimulated insulin secretion. This effect was associated with elevated SIRT1 protein expression and antioxidant enzyme activities, resulting in increased mitochondrial respiratory chain activities and decreased ROS level. This study suggests that RSV may increase islet mitochondrial complex activities and antioxidant function to restore insulin secretion dysfunction induced by high-fat diet.
PMCID: PMC4935315  PMID: 25228148
Resveratrol; insulin secretion; mitochondrial
10.  Bioactive 7-Oxabicyclic[6.3.0]lactam and 12-Membered Macrolides from a Gorgonian-Derived Cladosporium sp. Fungus 
Marine Drugs  2015;13(7):4171-4178.
One new bicyclic lactam, cladosporilactam A (1), and six known 12-membered macrolides (2–7) were isolated from a gorgonian-derived Cladosporium sp. fungus collected from the South China Sea. Their complete structural assignments were elucidated by comprehensive spectroscopic investigation. Quantum chemistry calculations were used in support of the structural determination of 1. The absolute configuration of 1 was determined by calculation of its optical rotation. Cladosporilactam A (1) was the first example of 7-oxabicyclic[6.3.0]lactam obtained from a natural source. Compound 1 exhibited promising cytotoxic activity against cervical cancer HeLa cell line with an IC50 value of 0.76 μM.
PMCID: PMC4515610  PMID: 26198234
gorgonian-derived fungus; Cladosporium sp.; bicyclic lactam; 12-membered macrolides; cytotoxic activity
11.  Combating non-Hodgkin lymphoma by targeting both CD20 and HLA-DR through CD20–243 CrossMab 
mAbs  2014;6(3):739-747.
Although rituximab has revolutionized the treatment of hematological malignancies, the acquired resistance is one of the prime obstacles for cancer treatment, and development of novel CD20-targeting antibodies with potent anti-tumor activities and specificities is urgently needed. Emerging evidence has indicated that lysosomes can be considered as an “Achilles heel” for cancer cells, and might serve as an effective way to kill resistant cancer cells. HLA-DR antibody L243 has been recently reported to elicit potent lysosome-mediated cell death in lymphoma and leukemia cells, suggesting that HLA-DR could be used as a potential target against lymphoma. In this study, we generated a bispecific immunoglobulin G-like antibody targeting both CD20 and HLA-DR (CD20–243 CrossMab) through CrossMab technology. We found that the CrossMab could induce remarkably high levels of complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity and anti-proliferative activity. Notably, although HLA-DR is expressed on normal and malignant cells, the CrossMab exhibited highly anti-tumor specificity, showing efficient eradication of hematological malignancies both in vitro and in vivo. Our data indicated that combined targeting of CD20 and HLA-DR could be an effective approach against malignancies, suggesting that CD20–243 CrossMab would be a promising therapeutic agent against lymphoma.
PMCID: PMC4011918  PMID: 24670986
CD20 antibody; rituximab; HLA-DR; lysosome-mediated cell death; CrossMab; resistant cancer cell
12.  Pre- and Posttreatment With Edaravone Protects CA1 Hippocampus and Enhances Neurogenesis in the Subgranular Zone of Dentate Gyrus After Transient Global Cerebral Ischemia in Rats 
ASN NEURO  2014;6(6):1759091414558417.
Edaravone is clinically used for treatment of patients with acute cerebral infarction. However, the effect of double application of edaravone on neurogenesis in the hippocampus following ischemia remains unknown. In the present study, we explored whether pre- and posttreatment of edaravone had any effect on neural stem/progenitor cells (NSPCs) in the subgranular zone of hippocampus in a rat model of transient global cerebral ischemia and elucidated the potential mechanism of its effects. Male Sprague-Dawley rats were divided into three groups: sham-operated (n = 15), control (n = 15), and edaravone-treated (n = 15) groups. Newly generated cells were labeled by 5-bromo-2-deoxyuridine. Immunohistochemistry was used to detect neurogenesis. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling was used to detect cell apoptosis. Reactive oxygen species (ROS) were detected by 2,7-dichlorofluorescien diacetate assay in NSPCs in vitro. Hypoxia-inducible factor-1α (HIF-1α) and cleaved caspase-3 proteins were quantified by western blot analysis. Treatment with edaravone significantly increased the number of NSPCs and newly generated neurons in the subgranular zone (p < .05). Treatment with edaravone also decreased apoptosis of NSPCs (p < .01). Furthermore, treatment with edaravone significantly decreased ROS generation and inhibited HIF-1α and cleaved caspase-3 protein expressions. These findings indicate that pre- and posttreatment with edaravone enhances neurogenesis by protecting NSPCs from apoptosis in the hippocampus, which is probably mediated by decreasing ROS generation and inhibiting protein expressions of HIF-1α and cleaved caspase-3 after cerebral ischemia.
PMCID: PMC4357607  PMID: 25388889
neurogenesis; cerebral ischemia; neural stem/progenitor cells; neuroprotection; edaravone; reactive oxygen species
13.  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
14.  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
15.  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
16.  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
17.  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
18.  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
19.  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
20.  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
21.  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
22.  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
23.  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 1-23 (23)