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BioWorld - Tuesday, April 28, 2026
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Liver disease
Gastrointestinal

Researchers develop novel murine model of MAFLD progressing to HCC

March 2, 2023
Metabolic-associated fatty liver disease (MAFLD) has emerged as a leading cause of progressive liver disease, even leading to a risk of hepatocellular carcinoma (HCC). Animal models that mimic the key etiological and histological features of the liver in the context of metabolic dysfunction represent the basis of preclinical research in MAFLD. The aim of work from researchers at Guangdong Pharmaceutical University was to develop a diet-induced murine model of MAFLD progressing to fibrosis and HCC.
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Biocom space-panel
Drug Design, Drug Delivery & Technologies

Biocom 2023: There’s science going on 250 miles above your head

March 2, 2023
By Brian Orelli
Performing experiments and potentially manufacturing products in space offers some unique advantages in a near-zero gravity environment. Space changes buoyancy, hydrostatic pressure and convective heat flow. Researchers are studying how those changes affect cells, but also looking to take advantage of the changes to create products in manufacturing processes that wouldn’t be possible on earth.
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Gastrointestinal

Eosinophilic gastroenteritis murine model shows dependence on ILC2/IL-25 axis

March 2, 2023
The pathogenesis of eosinophilic gastroenteritis (EGE), a chronic inflammatory disease characterized by eosinophil infiltration in the gastrointestinal tract, is still not well understood.
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Biomarkers

RELMβ as novel biomarker and pathogenic player in children with food allergy

March 2, 2023
Resistin-like molecule beta (RELMβ) is a gut-derived cytokine involved in both allergic responses and protection from pathogens, and it has been previously found to be dysregulated in mouse models of food allergy (FA). Researchers from Boston Children’s Hospital aimed assess the potential of RELMβ as a novel biomarker in children with FA.
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Genetic/Congenital

Researchers report development of DNL-126, a novel brain-penetrant therapy for MPS IIIA

March 2, 2023
Mucopolysaccharidosis type IIIA (MPS IIIA) is a genetic disorder where mutations in SGSH lead to the accumulation of heparan sulfate (HS) and lysosomal dysfunction that translate into developmental delay and cognition decline in humans. To date, there is no cure for MPS IIIA and that is why finding new strategies is an urgent need.
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Mast cell releasing histamine during allergic response
Immune

MOD-000001, a novel orally available KIT inhibitor with efficacy in models of allergic disease

March 1, 2023
It has been demonstrated that stem cell factor (SCF) and its receptor KIT play key roles in the differentiation, proliferation, survival, migration and activation of mast cells, which in turn play a central role in the development of IgE-mediated allergic diseases, including allergic urticaria and food allergy.
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Neurology/Psychiatric

Astroglial TNFR2 as therapeutic target for counteracting cognitive dysfunction in MS

March 1, 2023
Previous studies indicated a protective function of TNFR2 signaling in multiple sclerosis (MS) as well as experimental autoimmune encephalomyelitis.
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Biomarkers

Study reveals novel upregulated markers in atopic dermatitis skin lesions

March 1, 2023
Atopic dermatitis (AD) is an inflammatory skin disease with complex pathogenesis. Researchers from the Swiss Institute of Allergy and Asthma Research and their collaborators have investigated biomarkers tied to AD and its severity.
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Immune

BTK inhibition ameliorates clinical reactivity to peanuts in allergic patients

Feb. 28, 2023
It is known that Bruton tyrosine kinase (BTK) is an essential enzyme for the FcεRI signaling pathway and is thought to be a target to prevent IgE-mediated allergic reactions. Researchers have hypothesized that the BTK inhibitor acalabrutinib may prevent reactivity to peanuts in patients with peanut allergy.
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Hands holding brain
Neurology/Psychiatric

Targeting paranodal potassium channels for neuroprotection in multiple sclerosis

Feb. 28, 2023
Previous research has suggested that neurons in multiple sclerosis (MS) exhibit metabolic exhaustion, believed to be caused by chronic hyperexcitability, which can lead to neurodegeneration. Researchers from Heidelberg University and affiliated organizations aimed to investigate the role of nodal Kv7 (outward rectifying) and perinodal oligodendroglial Kir4.1 (inward rectifying) channels as potential therapeutic targets for neuroprotection through balancing of neuronal excitability caused by inflammatory demyelination.
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