Nima Purvis
I am an outgoing and enthusiastic researcher that has experience working in Biomedical Science and Physiology research fields. I completed a PhD from the University of Otago where I demonstrated the pathophysiological role of microRNAs in diabetic cardiac stem cells. Prior to this, I completed an Honours degree (first class) in Biomedical Sciences (Functional human biology) where I characterised the functional properties of the mucosal folds at the pancreaticobiliary junction. I am experienced in performing a variety of molecular techniques associated with stem cell research, and possess data analysis and interpretation skills at a high level.
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Objective: To investigate if deregulated miRs are the underlying molecular mechanism responsible for functional deterioration of diabetic CSCs.
Methods and Results: CSCs were isolated from type-2 diabetic and age-matched non-diabetic mice hearts (n=9 each) using collagenase digestion, followed by purification of the cells using stem cell specific antigen-1 (Sca-1) magnetic labelling. Following one week of culture, total RNA was extracted and miR expression profiles were analysed using an nCounter miR expression assay (Nanostring Technologies). Among 601 miRs evaluated, 14 miRs were significantly altered (12 up-regulated and 2 down-regulated, based on minimum of ±2 fold change and P<0.01) in diabetic CSCs. The online tool, ‘MiRPath’ narrowed this to 4 miRs (upregulation of miR-376c, miR-329 and miR-495 and downregulation of miR-30c) that are involved in regulation of stem cell proliferation and differentiation. Mass spectrometry analysis confirmed the downregulation of CDK6 and upregulation of VDAC1, target proteins for miR-376c and miR-30c respectively (P<0.05). Finally in vitro functional analysis using loss- or gain-of function in diabetic CSCs demonstrated marked improvement in the survival, proliferation and differentiation in diabetic CSCs only following the restoration of miR-30c and miR-376c (P<0.05 for all the parameters).
Conclusion: Therapeutic restoration of miR-30c and miR-376c improves the in vitro functional ability of diabetic CSCs.
AIMS: The principal aim of this study was to investigate the distribution and length of the mucosal folds within the terminal bile and pancreatic ducts. A secondary aim was to identify features within the folds that are consistent with an active function, including smooth muscle, innervation and hormonal receptors.
METHODS: PBJ specimens from 10 human cadavers (five male, 66-90 years old) were embedded in paraffin and sectioned transversely (3-4 μm thickness) at 200 μm intervals, beginning at the major duodenal papilla. These sections were stained with hematoxylin and eosin, and immunohistochemically with anti-actin, anti-S100, and anti-cholecystokinin A for detection of smooth muscle actin, innervation, and cholecystokinin A receptors, respectively. Three surgical specimens (2 male, 63-72 years old) were also evaluated. ImageJ software was used to measure mean fold length and distribution, as well as the relative distribution of S100 and the density of smooth muscle actin staining within the folds of the terminal bile and pancreatic ducts. The morphology of the folds was also examined in one additional specimen under scanning electron microscopy.
Objective: To investigate if deregulated miRs are the underlying molecular mechanism responsible for functional deterioration of diabetic CSCs.
Methods and Results: CSCs were isolated from type-2 diabetic and age-matched non-diabetic mice hearts (n=9 each) using collagenase digestion, followed by purification of the cells using stem cell specific antigen-1 (Sca-1) magnetic labelling. Following one week of culture, total RNA was extracted and miR expression profiles were analysed using an nCounter miR expression assay (Nanostring Technologies). Among 601 miRs evaluated, 14 miRs were significantly altered (12 up-regulated and 2 down-regulated, based on minimum of ±2 fold change and P<0.01) in diabetic CSCs. The online tool, ‘MiRPath’ narrowed this to 4 miRs (upregulation of miR-376c, miR-329 and miR-495 and downregulation of miR-30c) that are involved in regulation of stem cell proliferation and differentiation. Mass spectrometry analysis confirmed the downregulation of CDK6 and upregulation of VDAC1, target proteins for miR-376c and miR-30c respectively (P<0.05). Finally in vitro functional analysis using loss- or gain-of function in diabetic CSCs demonstrated marked improvement in the survival, proliferation and differentiation in diabetic CSCs only following the restoration of miR-30c and miR-376c (P<0.05 for all the parameters).
Conclusion: Therapeutic restoration of miR-30c and miR-376c improves the in vitro functional ability of diabetic CSCs.
AIMS: The principal aim of this study was to investigate the distribution and length of the mucosal folds within the terminal bile and pancreatic ducts. A secondary aim was to identify features within the folds that are consistent with an active function, including smooth muscle, innervation and hormonal receptors.
METHODS: PBJ specimens from 10 human cadavers (five male, 66-90 years old) were embedded in paraffin and sectioned transversely (3-4 μm thickness) at 200 μm intervals, beginning at the major duodenal papilla. These sections were stained with hematoxylin and eosin, and immunohistochemically with anti-actin, anti-S100, and anti-cholecystokinin A for detection of smooth muscle actin, innervation, and cholecystokinin A receptors, respectively. Three surgical specimens (2 male, 63-72 years old) were also evaluated. ImageJ software was used to measure mean fold length and distribution, as well as the relative distribution of S100 and the density of smooth muscle actin staining within the folds of the terminal bile and pancreatic ducts. The morphology of the folds was also examined in one additional specimen under scanning electron microscopy.