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Gracefield, New Zealand

Beal J.H.L.,Victoria University of Wellington | Beal J.H.L.,MacDiarmid Institute for Advanced Materials and Nanotechnology | Beal J.H.L.,Trinity Bioactives Ltd. | Etchegoin P.G.,Victoria University of Wellington | And 3 more authors.
Journal of Physical Chemistry C

The metal polysulfide complexes [M(N-MeIm)6]S8 (M ) Fe, Ni) and ZnS6(N-MeIm)2 (N-MeIm ) N-methylimidazole) were synthesized and used as single-source precursors for the synthesis of metal sulfide nanocrystals. Rapid injection of [Ni(N-MeIm)6]S8 into oleylamine at 300 °C, followed by immediate cooling, led to the formation of spherical, monodisperse 6 nm NiS2 nanocrystals. Whereas reaction of [Ni(N-MeIm)6]S8 by gradual heating in oleylamine to 300 °C led to the formation of irregularly shaped 45 nm R-Ni1-xS nanocrystals. Rapid injection of [Fe(N-MeIm)6]S8 into oleylamine at 300 °C, followed by immediate cooling, led to the formation of 16 nm Fe3S4 nanocrystals. Whereas reaction of [Fe(N-MeIm)6]S8 in oleylamine at 300 °C for 4 h led to the formation of faceted, submicrometer Fe1-xS crystallites. Reaction of ZnS6(N-MeIm)2 in oleylamine at 300 °C for 30 min led to the formation of monodisperse 11 × 5 nm ZnS nanorods. Metal polysulfide complexes were shown to be viable single-source precursors for a range of transition metal sulfide nanocrystals, with all samples demonstrating a high degree of crystallinity and excellent phase-purity. © 2010 American Chemical Society. Source

Chan Y.K.,University of Auckland | Davis P.F.,University of Otago | Davis P.F.,Trinity Bioactives Ltd. | Poppitt S.D.,University of Auckland | And 7 more authors.
Laboratory Animals

Blood is collected during animal experimentation to measure haematological and metabolic parameters. It cannot be assumed that circulating blood has the same composition irrespective of its location, and indeed, differences in the composition of blood sampled from the arterial and venous compartments have been reported. Here we investigated whether blood collected by cardiac puncture (CP) versus that collected following removal of the distal 1 mm of the tail tip (TT) differs with respect to glucose and lipid profiles in male C57BL/6J mice at 4, 7, 20 and 28 weeks of age. Blood was first collected from the TT of unanaesthetized mice, which were then immediately anaesthetized using ketamine/xylazine, and a second blood sample was collected by CP. The CP glucose concentration was significantly higher than TT glucose by a positive bias averaging +80% (P < 0.01), irrespective of the age of the mice. Conversely, the concentrations of the CP lipids, including total cholesterol, high-density lipoprotein cholesterol and triglyceride were lower than TT lipids by a negative bias averaging -25% (P < 0.05). These observations highlight the difficulty in measuring and comparing metabolic parameters such as glucose and lipid between one blood compartment and another. They illustrate the need to standardize sampling sites, especially when repeated blood sampling is required. Source

Irvine S.M.,Mesynthes | Irvine S.M.,University of Otago | Cayzer J.,Estendart Ltd | Todd E.M.,Mesynthes | And 14 more authors.

Ovine forestomach matrix (OFM) biomaterial acts as a biomimetic of native extracellular matrix (ECM) by providing structural and functional cues to orchestrate cell activity during tissue regeneration. The ordered collagen matrix of the biomaterial is supplemented with secondary ECM-associated macromolecules that function in cell adhesion, migration and communication. As angiogenesis and vasculogenesis are critical processes during tissue regeneration we sought to quantify the angiogenic properties of the OFM biomaterial. In vitro studies demonstrated that soluble OFM components stimulated human umbilical vein endothelial cell (HUVEC) migration and increased vascular sprouting from an aorta. Blood vessel density and branch points increased in response to OFM in an ex ovo chicken chorioallantoic membrane (CAM) assay. The OFM biomaterial was shown to undergo remodeling in a porcine full-thickness excisional model and gave rise to significantly more blood vessels than wounds treated with small intestinal submucosa decellularized ECM or untreated wounds. © 2011 Elsevier Ltd. Source

Hunt S.,Promisia Integrative Ltd | Yoshida M.,Trinity Bioactives Ltd. | Davis C.E.,Trinity Bioactives Ltd. | Greenhill N.S.,Trinity Bioactives Ltd. | Davis P.F.,Trinity Bioactives Ltd.
Journal of Inflammation Research

Purpose: To investigate the ability of a commercial extract from the medicinal plant Artemisia annua to modulate production of the cytokine, tumor necrosis factor-alpha (TNF-α), and the cyclooxygenase (COX) inflammatory marker, prostaglandin E2 (PGE2) in activated neutrophils. Methods: Neutrophils were harvested from rat whole blood and cultured in the presence of plant extract or control samples. Neutrophils, except unactivated control cells, were activated with 10 μg/mL lipopolysaccharide (LPS). The cells were cultured with a range of different concentrations of the A. annua extracts (400–1 μg/mL) and artemisinin (200 and 100 μg/mL) and the supernatants were then tested by enzyme-linked immunosorbent assay (ELISA) for the concentrations of TNF-α and PGE2. Each sample was assayed in triplicate. Positive controls with an inhibitor were assayed in triplicate: chloroquine 2.58 and 5.16 μg/mL for TNF-α, and ibuprofen 400 μg/mL for PGE2. An unsupplemented group was also assessed in triplicate as a baseline control. Results: Neutrophils were stimulated to an inflammatory state by the addition of LPS. A. annua extract significantly inhibited TNF-α production by activated neutrophils in a dose-dependent manner. There was complete inhibition by the A. annua extract at 200, 100, and 50 μg/mL (all P≤0.0003). At A. annua extract concentrations of 25, 10, and 5 μg/mL, TNF-α production was inhibited by 89% (P<0.0001), 54% (P=0.0002), and 38% (P=0.0014), respectively. A. annua 1 μg/mL did not significantly inhibit TNF-α production (8.8%; P>0.05). Concentrations of 400, 200, and 100 μg/mL A. annua extract significantly inhibited PGE2 production by 87% (P=0.0128), 91% (P=0.0017), and 93% (P=0.0114), respectively. Conclusion: An extract of A. annua was shown to be a potent inhibitor of TNF-α and a strong inhibitor of PGE2 production in activated neutrophils at the concentrations tested. Further studies are warranted with this promising plant extract. © 2015 Hunt et al. Source

Nielsen S.,Aarhus University Hospital | Nielsen K.,Aarhus University Hospital | Ivarsen A.,Aarhus University Hospital | Greenhill N.S.,University of Otago | And 4 more authors.

Purpose: The purpose of this study was to investigate the pathophysiologic heterogeneity of Fuchs endothelial corneal dystrophy (FECD). Methods: We conducted a systematic immunofluorescence study on 39 Descemet membrane samples from FECD patients and compared these with 10 Descemet membrane samples from patients with pseudophakic bullous keratopathy (PBK) and 7 normal corneas. Samples were analyzed with immunofluorescence using antibodies to the a1-chain [collagen VIII a1-chain (COL8A1)] and a2-chain (COL8A2). Intensity of staining was assessed using a subjective grading scale from 0 to 3. The presence of specific staining patterns was noted. Results: The overall distribution of COL8A1 staining intensity between groups was significantly different (P = 0.002). There was marked/intense staining in 85% (33/39) of the FECD samples, 40% (4/10) of the PBK samples (P = 0.034), and 29% (2/7) of normal samples (P = 0.004). The overall distribution of COL8A2 staining intensity was not significantly different between groups (P = 0.39). There was marked/intense staining in 33% (13/39) of the FECD samples, 10% (1/10) of PBK samples, and 14% (1/7) of the normal samples. There was substantial variation in staining intensity in the FECD group, a phenomenon that was especially pronounced for the COL8A2 antibody. Conclusions: We found increased staining for COL8A1, but not COL8A2 in FECD samples. Further, there was striking variation of staining intensity in FECD patients, indicating pathophysiological heterogeneity. © 2016 Wolters Kluwer Health, Inc. All rights reserved. Source

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