Ono Pharmaceutical Co. Ltd. has entered an option and research collaboration agreement with Monash University to discover and develop antibodies targeting G protein-coupled receptors (GPCRs) with the aim of creating novel therapeutics for the treatment of autoimmune and inflammatory diseases.

An Icelandic genome-wide association study that linked variants in a gene which regulates retinoic acid synthesis to severe osteoarthritis (OA) of the hands, has led on to the discovery of an anti-inflammatory role for the vitamin A metabolite and pointed to a new class of potentially disease-modifying drugs. A proof-of-concept clinical trial of talarozole, a retinoic acid metabolism blocking agent, is now taking place to assess if increasing retinoic acid production suppresses inflammation in the joint tissues of patients with OA.

Blood vessels supplying adipose tissue in females and males differed in their biological characteristics and gene expression programs, researchers at York University in Toronto, Canada, have demonstrated. The findings, which will appear in the Jan. 20, 2023, print issue of Iscience after earlier publication online, give new insights into sex differences in metabolic health.

Fat tissue can be detrimental to health, but the relationship between fat, BMI and health is increasingly acknowledged as being highly complex. One factor that affects the relationship between fat and health is how well adipose tissue is vascularized. Any new tissue that forms in the body needs to be vascularized to ensure its blood supply, and fat is no exception.

Unlike amphibians, mammals do not regenerate appendages. Except when they do. “If you amputate one of the branches off of the antler [of a reindeer], it will also regenerate,” Jeff Biernaskie told BioWorld. Even without amputation, the antlers of both male and female reindeer regenerate annually, including their skin. That regeneration is “the only large mammal model of true skin regeneration,” he said.

The most common cause of anemia in chronically ill hospitalized patients is due to inflammatory anemia (IA) that is caused indirectly by diseases such as autoimmune, cancer, chronic kidney disease, congestive heart failure, or pulmonary disease. The precise and common etiology of these diseases involves hypercytokinemia that leads to excessive increases in hepcidin, a master regulator of iron homeostasis that blocks intestinal iron absorption when levels are too persistently high.

Lung cancer associated transcript 1 (LUCAT1) is a long noncoding RNA and has been identified as a negative feedback regulator of interferon I and inflammatory cytokine expression in myeloid cells; the anti-inflammatory protein nuclear receptor 4A2 (NR4A2) was identified as a LUCAT1-binding protein involved in regulating splicing and processing of mRNAs. NR4A2 inhibits the inflammatory process driven by NF-κB. It was observed that cells lacking LUCAT1 expression had their splicing of immune genes altered, with reduced expression of NR4A2 (altered splicing on exon 7) in those cells lacking LUCAT1, as shown by ChIRP-MS assay in THP-1 cells.

Obesity and chronic inflammation in the liver trigger the most severe form of nonalcoholic fatty liver disease (NAFLD), steatohepatitis. Scientists at the University of Texas (UT) have shown how damaged hepatocytes accumulated in the liver after a vicious cycle of cytokine expression induced shedding of a critical liver receptor.