Childhood Lead Exposure Linked to Apple Cinnamon Fruit Puree Pouches - North Carolina, June 2023-January 2024.

Lead exposure is toxic even at low levels, resulting in impairments that can affect a child's lifelong success. In North Carolina, testing for lead is encouraged for all children at ages 1 and 2 years and required for children covered by Medicaid; investigations are performed to identify potential exposure sources for children with blood lead levels (BLLs) ≥5 μg/dL. During June-August 2023, routine lead testing identified four asymptomatic North Carolina children with BLLs ≥5 μg/dL.

The Small-Molecule Enhancers of Autophagy AUTEN-67 and -99 Delay Ageing in Striated Muscle Cells.

Autophagy (cellular self-degradation) plays a major role in maintaining the functional integrity (homeostasis) of essentially all eukaryotic cells. During the process, superfluous and damaged cellular constituents are delivered into the lysosomal compartment for enzymatic degradation. In humans, age-related defects in autophagy have been linked to the incidence of various age-associated degenerative pathologies (e.

Neural stem cells deriving from chick embryonic hindbrain recapitulate hindbrain development in culture.

Neural stem cells (NSCs) are self-renewing multipotent cells that line the neural-tube and generate all the nervous system. Understanding NSC biology is fundamental for neurodevelopmental research and therapy. Many studies emphasized the need to culture NSCs, which are typically purified from mammalian embryonic/adult brains.

The small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptoms.

Autophagy functions as a main route for the degradation of superfluous and damaged constituents of the cytoplasm. Defects in autophagy are implicated in the development of various age-dependent degenerative disorders such as cancer, neurodegeneration and tissue atrophy, and in accelerated aging. To promote basal levels of the process in pathological settings, we previously screened a small molecule library for novel autophagy-enhancing factors that inhibit the myotubularin-related phosphatase MTMR14/Jumpy, a negative regulator of autophagic membrane formation.

AUTEN-67 (Autophagy Enhancer-67) Hampers the Progression of Neurodegenerative Symptoms in a Drosophila model of Huntington's Disease.

Background: Autophagy, a lysosome-mediated self-degradation process of eukaryotic cells, serves as a main route for the elimination of cellular damage [1-3]. Such damages include aggregated, oxidized or misfolded proteins whose accumulation can cause various neurodegenerative pathologies, including Huntington's disease (HD).

Objective: Here we examined whether enhanced autophagic activity can alleviate neurophatological features in a Drosophila model of HD (the transgenic animals express a human mutant Huntingtin protein with a long polyglutamine repeat, 128Q).