Publications by authors named "B Viuff"

Article Synopsis
  • Gremlin-1 has been linked to liver fibrosis in metabolic dysfunction-associated steatohepatitis (MASH) by inhibiting BMP signaling, making it a potential focus for therapy.* -
  • In studies using rat and human models, blocking Gremlin-1 with antibodies did not reduce liver inflammation or fibrosis, despite its increased presence in specific myofibroblast cells.* -
  • Findings indicate that Gremlin-1 does not significantly contribute to liver fibrosis development and is not a viable target for treatment due to its limited role in the disease process.*
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Obesity-related glomerulopathy and diabetic nephropathy (DN) are serious complications to metabolic syndrome and diabetes. The purpose was to study effects of a fat, fructose and cholesterol-rich (FFC) diet with and without salt in order to induce hypertension on kidney function and morphology in Göttingen Minipigs with and without diabetes. Male Göttingen Minipigs were divided into 4 groups: SD (standard diet, n = 8), FFC (FFC diet, n = 16), FFC-DIA (FFC diet + diabetes, n = 14), FFC-DIA + S (FFC diet with extra salt + diabetes, n = 14).

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Tissue fibrosis is a key driver of end-stage organ failure and cancer, overall accounting for up to 45% of deaths in developed countries. There is a large unmet medical need for antifibrotic therapies. Claudin-1 (CLDN1) is a member of the tight junction protein family.

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Background: Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are highly prevalent comorbidities in patients with Type 2 diabetes. While many of these patients eventually will need treatment with insulin, little is known about the effects of insulin treatment on histopathological parameters and hepatic gene expression in diabetic patients with co-existing NAFLD and NASH. To investigate this further, we evaluated the effects of insulin treatment in NASH diet-fed hamsters with streptozotocin (STZ) -induced hyperglycemia.

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Quantitative assessment of proliferation can be an important endpoint in toxicologic pathology. Traditionally, cell proliferation is quantified by labor-intensive manual counting of positive and negative cells after immunohistochemical staining for proliferation markers (eg, Ki67, bromo-2'-deoxyuridine, or proliferating cell nuclear antigen). Currently, there is a lot of interest in replacing manual evaluation of histology end points with image analysis tools based on artificial intelligence.

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