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Therma Bright Inc V.THRM

Alternate Symbol(s):  TBRIF

Healthcare Medical Devices
Therma Bright Inc. is a Canada-based company, which is a developer and partner in a range of diagnostic and medical device technologies. It focuses on providing consumers and medical professionals with solutions that address medical and healthcare challenges. It is involved in developing, acquiring, manufacturing, and marketing proprietary healthcare and medical devices for the consumer and institutional marketplace. Its product offerings include Covid-19 diagnostic test product line, such as AcuVid COVID-19 Rapid Antigen Saliva Test and AcuVid COVID-19 Rapid Antibody Test; Sores & Bite Inflammation Therapy product line, such as InterceptCS Cold Sore Prevention System and TherOZap, and Muscle Pain & Blood Circulation Health Therapy product line, such as Venowave, which is a circulation booster designed to improve circulation in the lower extremities. Its products include Benepod, Inretio, AI4LYF, Invixa and Instatin, and others.


TSXV:THRM - Post by User

Therma Bright Inc
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Post by mariaroseon Aug 18, 2020 12:31am
3112 Views
Post# 31421232

Orpheus Medica CEO Babaei's research

Orpheus Medica CEO Babaei's research

Saeid Babaei's research while affiliated with University of Toronto and other places

Publications (8)

Defective Lung Vascular Development and Fatal Respiratory Distress in Endothelial NO Synthase-Deficient Mice A Model of Alveolar Capillary Dysplasia?
Article
  • May 2004
Endothelium-derived NO plays a critical role in the regulation of cardiovascular function and structure, as well as acting as a downstream mediator of the angiogenic response to numerous vascular growth factors. Although endothelial NO synthase (eNOS)-deficient mice are viable, minor congenital cardiac abnormalities have been reported and homozygou...
Defective lung vascular development and fatal respiratory distress in endothelial NO synthase-deficient mice: a model of alveolar capillary dysplasia? Circ
Article
  • Apr 2004
Endothelium-derived NO plays a critical role in the regulation of cardiovascular function and structure, as well as acting as a downstream mediator of the angiogenic response to numerous vascular growth factors. Although endothelial NO synthase (eNOS)-deficient mice are viable, minor congenital cardiac abnormalities have been reported and homozygou...
Phospholipids and Oxophospholipids in Atherosclerotic Plaques at Different Stages of Plaque Development
Article
  • Mar 2004
We identified and quantified the hydroperoxides, hydroxides, epoxides, isoprostanes, and core aldehydes of the major phospholipids as the main components of the oxophospholipids (a total of 5-25 pmol/micromol phosphatidylcholine) in a comparative study of human atheroma from selected stages of lesion development. The developmental stages examined i...
Decorin Inhibition of PDGF-Stimulated Vascular Smooth Muscle Cell Function
Article
  • Sep 2003
Angiogenic Actions of Angiopoietin-1 Require Endothelium-Derived Nitric Oxide
Article
  • Jul 2003
Angiopoietin1 (Ang1) is a novel angiogenic factor with important actions on endothelial cell (EC) differentiation and vascular maturation. Ang1 has been shown to prevent EC apoptosis through activation of PI3-kinase/Akt, a pathway that is also known to activate endothelium nitric oxide synthase (eNOS). Therefore, we hypothesized that the angiogenic...
Paraoxonase-1 reduces monocyte chemotaxis and adhesion to endothelial cells due to oxidation of palmitoyl, linoleoyl glycerophosphorylcholine
Article
  • Jan 2003
High-density lipoprotein (HDL) is postulated to protect against the development of atherosclerosis, in part, by inhibiting the oxidation of low density lipoprotein (LDL) in the sub-endothelial space and thus inhibiting activation of the endothelium. The HDL-associated enzyme, paraoxonase-1, is proposed to be a major protective factor. However, HDL...
Overexpression of endothelial NO synthase induces angiogenesis in a co-culture model
Article
  • Jul 2002
Angiogenesis is a complex multistep process that involves endothelial cell (EC) migration, proliferation and differentiation into vascular tubes. NO has been reported to be a downstream mediator in the angiogenic response to a variety of growth factors, but the mechanisms by which NO promotes neovessel formation is not clear. We hypothesized that N...
Effects of VasoCare (TM) therapy on the initiation and progression of atherosclerosis
Article
  • May 2002
VasoCare therapy, which involves the administration of autologous blood following the ex vivo exposure to physico-chemical stressors, has been shown to modulate immune responses. Since immune mechanisms have been recognized to be pivotal in the pathogenesis of atherosclerosis, we hypothesized that VasoCare treatment would inhibit atherosclerosis in...

Citations

... Accumulating evidence has shown that decorin binding multiple growth factors such as transforming growth factor (TGF-β) [49], TNFα [50], fibroblast growth factor (FGF) [51], and platelet-derived growth factor (PDGF) [52]. Decorin also antagonizes several receptor tyrosine kinases (RTKs), including toll-like receptors (TLRs) [53], insulin-like growth factor receptor (IGFR) [54], ErbB family [55], epidermal growth factor receptor (EGFR) [56], and vascular endothelial growth receptor factor (VEGFR) [57]. ...
Reference: Decorin knockdown affects the gene expression profile of adhesion, growth and extracellular matrix metabolism in C-28/I2 chondrocytes
 
Decorin Inhibition of PDGF-Stimulated Vascular Smooth Muscle Cell Function
Citing article
  • Sep 2003
... On the other hand, phosphatidylcholine (PC), the most abundant surfactant lipid component was reduced in broncho-alveolar lavage fluid from lungs of eNOS knock-out neonatal mice at birth in comparison with WT. The major and most surface-active phospholipid species, dipalmitoyl PC, was also significantly reduced in BAL fluid (Han et al. 2004). In SP-D and iNOS double knockout mice model the loss of alveoli and alterations of elastic properties of lung parenchyma with no changes in surfactant system where reported suggesting that surfactant homeostasis is mediated by different mechanisms (Knudsen et al. 2014). ...
Reference: Physiology of Nitric Oxide in the Respiratory System
 
Defective lung vascular development and fatal respiratory distress in endothelial NO synthase-deficient mice: a model of alveolar capillary dysplasia? Circ
Citing article
  • Apr 2004
... PON1 also has phospholipase-like activity that allows it to hydrolyze phosphatidylcholine core aldehydes and to produce lysophosphatidylcholine (LysoPC) and free oxidized fatty acids (Ahmed et al. 2002;Loued et al. 2012). It has been suggested that the hydrolysis of these oxidized phospholipids may explain the anti-inflammatory activity of PON1 (Ahmed et al. 2003). Intriguingly, the hydrolysis of oxidized phospholipids in oxidized LDL (oxLDL) contributes to the formation of LysoPC and oxidized free fatty acids, both of which are pro-inflammatory (Ahmed et al. 2002;Rozenberg et al. 2003;Schilling and Eder 2009). ...
Reference: The role of paraoxonase 1 in regulating HDL functionality during aging
 
Paraoxonase-1 reduces monocyte chemotaxis and adhesion to endothelial cells due to oxidation of palmitoyl, linoleoyl glycerophosphorylcholine
Citing article
  • Jan 2003
  • PubMed
... Lung ECs adapt to these dynamic environmental changes and regulate post-natal pulmonary circulation by secreting various vasoactive molecules including NO (Gao and Raj, 2010;Gao et al., 2016). Endothelial NO synthase (eNOS)-deficient mice exhibit paucity of alveolar capillary ECs and arrested alveolarization (Han et al., 2004), suggesting that EC-derived NO not only regulates pulmonary vascular tone, but also contributes to alveolarization at this stage. ...
Reference: Vascular Niche in Lung Alveolar Development, Homeostasis, and Regeneration
 
Defective Lung Vascular Development and Fatal Respiratory Distress in Endothelial NO Synthase-Deficient Mice A Model of Alveolar Capillary Dysplasia?
Citing article
  • May 2004
  • PubMed
... The main lipid peroxidation products contained in oxidized low-density lipoprotein (LDL) are cholesterol ester hydroperoxide (CEOOH) and phosphatidylcholine hydroperoxide (PCOOH), which are the primary products generated by the oxidation of cholesterol ester (CE) and phosphatidylcholine (PC), respectively [1][2][3][4][5]. Increased contents of CEOOH and PCOOH have been detected in the actual blood and organs of patients with diseases such as arteriosclerosis, hyperlipidemia, and diabetes [6][7][8][9][10]. Therefore, CEOOH and PCOOH in oxidized LDL are considered to be closely related to the onset and development of such diseases. ...
Reference: Direct Separation of the Diastereomers of Cholesterol Ester Hydroperoxide Using LC-MS/MS to Evaluate Enzymatic Lipid Oxidation
 
Phospholipids and Oxophospholipids in Atherosclerotic Plaques at Different Stages of Plaque Development
Citing article
  • Mar 2004
  • PubMed
... The hypothesis of this trial was that an anti-inflammatory stimuli could produce an endogenous anti-inflammatory state in the recipient HF patient, which would suppress ongoing low-grade pathological chronic inflammation-a concept supported by animal data. 49 Although nonspecific in nature, ACCLAIM utilized a technology called Immune Modulation therapy (celecade), where the patients' own blood would be stressed to induced cell death, and then the mixture of apoptotic cells was injected intramuscularly into the same patient (average follow-up of 10.2 months). Although there was no difference in the primary end point (all-cause mortality or cardiovascular admission) in the entire cohort, there was improvement in patients with NICM and with more mild (New York Heart Association-II) symptoms. ...
Reference: Chronic Heart Failure and Inflammation: What Do We Really Know?
 
Effects of VasoCare (TM) therapy on the initiation and progression of atherosclerosis
Citing article
  • May 2002
  • PubMed
... These angiogenic pathways are coordinated by ANGII during kidney development under normal physiological conditions and are activated by eNOSinduced Akt/PI3K signaling (35) and endothelial NO production. Phosphorylation of eNOS by Akt resulted in activation, and increased production of NO. (36). In vitro and in vivo studies have shown that increased eNOS activity resulted in endothelial cell proliferation and migration, and increased angiogenesis (37,38). ...
Reference: Effect of Calcitriol on the Renal Microvasculature Differentiation Disturbances Induced by AT1 Blockade During Nephrogenesis in Rats
 
Overexpression of endothelial NO synthase induces angiogenesis in a co-culture model
Citing article
  • Jul 2002
  • PubMed
... MSCs secrete Ang-1, especially during wound healing, which recruits macrophages and endothelial lineage cells [75][76][77]. Ang-1 phosphorylates the Tie-2 receptor and this Ang-1/Tie-2 interaction regulates maturation of newly formed vasculature, which ultimately results in complex functional vascular network formation [78,79]. Our previous research indicated that hMSCs cultured on the ECM in hypoxic environments promoted expression of Ang-1 [39]. ...
Reference: Engineering stem cell cardiac patch with microvascular features representative of native myocardium
 
Angiogenic Actions of Angiopoietin-1 Require Endothelium-Derived Nitric Oxide
Citing article
  • Jul 2003
  • PubMed

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