1. Rapid resolution of retinoschisis with acetazolamide.

    Documenta Ophthalmologica 131(1):63 (2015) PMID 25796216 PMCID PMC4504776

    To report the results of an acetazolamide (Diamox(®)) treatment regimen in a genetically confirmed case of X-linked juvenile retinoschisis (XLRS). A patient with XLRS was prescribed acetazolamide (Diamox(®)) at a dose of 500 mg/day, then discontinued the treatment due to non-compliance for 4 day...
  2. Erratum. PD-L1-Driven Tolerance Protects Neurogenin3-Induced Islet Neogenesis to Reverse Established Type 1 Diabetes in NOD Mice. Diabetes 2015;64:529-540.

    Diabetes 64(7):2685 (2015) PMID 26106199

  3. Genome-Wide Analysis of ChREBP Binding Sites on Male Mouse Liver and White Adipose Chromatin.

    Endocrinology 156(6):1982 (2015) PMID 25751637 PMCID PMC4430618

    Glucose is an essential nutrient that directly regulates the expression of numerous genes in liver and adipose tissue. The carbohydrate response element-binding protein (ChREBP) links glucose as a signaling molecule to multiple glucose-dependent transcriptional regulatory pathways, particularly ...
  4. Bone marrow-derived TNF-α causes diabetic neuropathy in mice.

    Diabetologia 58(2):402 (2015) PMID 25399355 PMCID PMC4289451

    Dysregulation of biochemical pathways in response to hyperglycaemia in cells intrinsic to the nervous system (Schwann cells, neurons, vasa nervorum) are thought to underlie diabetic peripheral neuropathy (DPN). TNF-α is a known aetiological factor; Tnf-knockout mice are protected against DPN. We...
  5. Bone marrow-derived TNF-α causes diabetic neuropathy in mice.

    Diabetologia 58(2):402 (2015) PMID 25399355 PMCID PMC4289451

    Dysregulation of biochemical pathways in response to hyperglycaemia in cells intrinsic to the nervous system (Schwann cells, neurons, vasa nervorum) are thought to underlie diabetic peripheral neuropathy (DPN). TNF-α is a known aetiological factor; Tnf-knockout mice are protected against DPN. We...
  6. PD-L1-driven tolerance protects neurogenin3-induced islet neogenesis to reverse established type 1 diabetes in NOD mice.

    Diabetes 64(2):529 (2015) PMID 25332429 PMCID PMC4303975

    A breakdown in self-tolerance underlies autoimmune destruction of β-cells and type 1 diabetes. A cure by restoring β-cell mass is limited by the availability of transplantable β-cells and the need for chronic immunosuppression. Evidence indicates that inhibiting costimulation through the PD-1/PD...
  7. Bone marrow-derived TNF-α causes diabetic neuropathy in mice.

    Diabetologia 58(2):402 (2015) PMID 25399355

    Dysregulation of biochemical pathways in response to hyperglycaemia in cells intrinsic to the nervous system (Schwann cells, neurons, vasa nervorum) are thought to underlie diabetic peripheral neuropathy (DPN). TNF-α is a known aetiological factor; Tnf-knockout mice are protected against DPN. We...
  8. PD-L1-Driven Tolerance Protects Neurogenin3-Induced Islet Neogenesis to Reverse Established Type 1 Diabetes in NOD Mice.

    Diabetes 64(2):529 (2015) PMID 25332429 PMCID PMC4303975

    A breakdown in self-tolerance underlies autoimmune destruction of β-cells and type 1 diabetes. A cure by restoring β-cell mass is limited by the availability of transplantable β-cells and the need for chronic immunosuppression. Evidence indicates that inhibiting costimulation through the PD-1/PD...
  9. Bone marrow-derived TNF-α causes diabetic neuropathy in mice.

    Diabetologia 58(2):402 (2015) PMID 25399355

    Dysregulation of biochemical pathways in response to hyperglycaemia in cells intrinsic to the nervous system (Schwann cells, neurons, vasa nervorum) are thought to underlie diabetic peripheral neuropathy (DPN). TNF-α is a known aetiological factor; Tnf-knockout mice are protected against DPN. We...
  10. Bone marrow-derived TNF-α causes diabetic neuropathy in mice.

    Diabetologia 58(2):402 (2015) PMID 25399355

    Dysregulation of biochemical pathways in response to hyperglycaemia in cells intrinsic to the nervous system (Schwann cells, neurons, vasa nervorum) are thought to underlie diabetic peripheral neuropathy (DPN). TNF-α is a known aetiological factor; Tnf-knockout mice are protected against DPN. We...
  11. Bone marrow-derived TNF-α causes diabetic neuropathy in mice.

    Diabetologia 58(2):402 (2015) PMID 25399355 PMCID PMC4289451

    Dysregulation of biochemical pathways in response to hyperglycaemia in cells intrinsic to the nervous system (Schwann cells, neurons, vasa nervorum) are thought to underlie diabetic peripheral neuropathy (DPN). TNF-α is a known aetiological factor; Tnf-knockout mice are protected against DPN. We...
  12. Development and rescue of human familial hypercholesterolaemia in a xenograft mouse model.

    Nature Communications 6:7339 (2015) PMID 26081744

    Diseases of lipid metabolism are a major cause of human morbidity, but no animal model entirely recapitulates human lipoprotein metabolism. Here we develop a xenograft mouse model using hepatocytes from a patient with familial hypercholesterolaemia caused by loss-of-function mutations in the low...
  13. Effects of High Fat Feeding and Diabetes on Regression of Atherosclerosis Induced by Low-Density Lipoprotein Receptor Gene Therapy in LDL Receptor-Deficient Mice.

    PLoS ONE 10(6):e0128996 (2015) PMID 26046657 PMCID PMC4457481

    We tested whether a high fat diet (HFD) containing the inflammatory dietary fatty acid palmitate or insulin deficient diabetes altered the remodeling of atherosclerotic plaques in LDL receptor knockout (Ldlr-/-) mice. Cholesterol reduction was achieved by using a helper-dependent adenovirus (HDA...
  14. MondoA deficiency enhances sprint performance in mice.

    Biochemical Journal 464(1):35 (2014) PMID 25145386

    MondoA is a basic helix-loop-helix (bHLH)/leucine zipper (ZIP) transcription factor that is expressed predominantly in skeletal muscle. Studies in vitro suggest that the Max-like protein X (MondoA:Mlx) heterodimer senses the intracellular energy status and directly targets the promoter region of...
  15. MondoA deficiency enhances sprint performance in mice.

    Biochemical Journal 464(1):35 (2014) PMID 25145386

    MondoA is a basic helix-loop-helix (bHLH)/leucine zipper (ZIP) transcription factor that is expressed predominantly in skeletal muscle. Studies in vitro suggest that the Max-like protein X (MondoA:Mlx) heterodimer senses the intracellular energy status and directly targets the promoter region of...
  16. MondoA deficiency enhances sprint performance in mice.

    Biochemical Journal 464(1):35 (2014) PMID 25145386

    MondoA is a basic helix-loop-helix (bHLH)/leucine zipper (ZIP) transcription factor that is expressed predominantly in skeletal muscle. Studies in vitro suggest that the Max-like protein X (MondoA:Mlx) heterodimer senses the intracellular energy status and directly targets the promoter region of...
  17. MondoA deficiency enhances sprint performance in mice.

    Biochemical Journal 464(1):35 (2014) PMID 25145386 PMCID PMC4410994

    MondoA is a basic helix-loop-helix (bHLH)/leucine zipper (ZIP) transcription factor that is expressed predominantly in skeletal muscle. Studies in vitro suggest that the Max-like protein X (MondoA:Mlx) heterodimer senses the intracellular energy status and directly targets the promoter region of...
  18. Molecular mechanisms underlying fasting modulated liver insulin sensitivity and metabolism in male lipodystrophic bscl2/seipin-deficient mice.

    Endocrinology 155(11):4215 (2014) PMID 25093462 PMCID PMC4197977

    Bscl2(-/-) mice recapitulate many of the major metabolic manifestations in Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2) individuals, including lipodystrophy, hepatomegly, hepatic steatosis, and insulin resistance. The mechanisms that underlie hepatic steatosis and insulin resistance...
  19. Molecular mechanisms underlying fasting modulated liver insulin sensitivity and metabolism in male lipodystrophic Bscl2/Seipin-deficient mice.

    Endocrinology 155(11):4215 (2014) PMID 25093462 PMCID PMC4197977

    Bscl2(-/-) mice recapitulate many of the major metabolic manifestations in Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2) individuals, including lipodystrophy, hepatomegly, hepatic steatosis, and insulin resistance. The mechanisms that underlie hepatic steatosis and insulin resistance...
  20. Molecular mechanisms underlying fasting modulated liver insulin sensitivity and metabolism in male lipodystrophic bscl2/seipin-deficient mice.

    Endocrinology 155(11):4215 (2014) PMID 25093462 PMCID PMC4197977

    Bscl2(-/-) mice recapitulate many of the major metabolic manifestations in Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2) individuals, including lipodystrophy, hepatomegly, hepatic steatosis, and insulin resistance. The mechanisms that underlie hepatic steatosis and insulin resistance...