Role for BLT1 in regulating inflammation within adipose tissue immune cells of aged mice.

Background: Aging is a complex biological process characterized by obesity and immunosenescence throughout the organism. Immunosenescence involves a decline in immune function and the increase in chronic-low grade inflammation, called inflammaging. Adipose tissue expansion, particularly that of visceral adipose tissue (VAT), is associated with an increase in pro-inflammatory macrophages that play an important role in modulating immune responses and producing inflammatory cytokines.

Age-associated accumulation of B cells promotes macrophage inflammation and inhibits lipolysis in adipose tissue during sepsis.

Non-canonical lipolysis induced by inflammatory cytokines or Toll-like receptor ligands is required for the regulation of inflammation during endotoxemia and sepsis. Canonical lipolysis induced by catecholamines declines during aging due to factors including an expansion of lymphocytes, pro-inflammatory macrophage polarization, and an increase in chronic low-grade inflammation; however, the extent to which the non-canonical pathway of lipolysis is active and impacted by immune cells during aging remains unclear. Therefore, we aimed to define the extent to which immune cells from old mice influence non-canonical lipolysis during sepsis.

Lambda transition and Bose-Einstein condensation in liquid ^{4}He.

We present the theory describing Bose-Einstein condensation (BEC) and superfluidity in a liquid ^{4}He based on the concept that for some temperature interval, there exist metastable diatomic clusters or diatomic quasiparticles which are the bound states of two atoms of ^{4}He. It is shown that in liquid ^{4}He for the temperature region 1K≤T≤T_{λ} diatomic quasiparticles macroscopically populate the ground state which leads to BEC in liquid ^{4}He. The approach yields the lambda temperature as T_{λ}=2.

Inflammaging and fatty acid oxidation in monocytes and macrophages.

Fatty acid oxidation (FAO), primarily known as β-oxidation, plays a crucial role in breaking down fatty acids within mitochondria and peroxisomes to produce cellular energy and preventing metabolic dysfunction. Myeloid cells, including macrophages, microglia, and monocytes, rely on FAO to perform essential cellular functions and uphold tissue homeostasis. As individuals age, these cells show signs of inflammaging, a condition that includes a chronic onset of low-grade inflammation and a decline in metabolic function.