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Physical activity in infancy is associated with body composition at age three

The prevalence of obesity in the pediatric population is increasing, driven by a multifactorial etiology that includes genetic predisposition as well as both prenatal and postnatal influences. We aimed to explore associations between child physical activity (PA) at ages one and three years and body composition at age three. Furthermore, we investigated associations between maternal PA during pregnancy and child body composition at age three.

Mother-child pairs (n = 68) from a pregnancy PA intervention study were included. Children’s PA was assessed at one-and three-year follow-ups using 7-day accelerometry and categorized into 24-hour PA and daytime PA (6 a.m. – 8 p.m.). Child body composition was measured by Dual-energy X-ray absorptiometry and expressed as fat-free mass (FFM) and body fat percentage (BF%). Maternal moderate-to-vigorous intensity PA (MVPA) was measured using a commercial activity tracker. Associations between maternal and child PA and child body composition were examined using linear regression. Variables used for model adjustment included maternal pre-pregnancy body mass index, gestational weight gain, maternal educational level at baseline, parity, maternal age at baseline, child walking status at age one, child sex, and child age at the three-year follow-up.

We found a positive association between daytime PA at age one and child FFM at age three. Daytime PA at age three was positively associated with FFM, and 24-hour PA at age three was negatively associated with BF% and positively associated with FFM. A 10% increase in 24-hour PA was associated with approximately 400 g higher FFM. Maternal MVPA during pregnancy showed no association with child body composition at age three.

A nucleolar view of neuromuscular disease

The nucleolus is a master regulator of ribosome biogenesis and cellular homeostasis, as well as an increasingly key determinant of neuromuscular diseases. Across these conditions, diverse genetic and molecular lesions converge on alterations in nucleolar organization and function. These changes impact ribosomal RNA synthesis and reshape translational output, linking nuclear events to cytoplasmic protein homeostasis in disease-relevant contexts. In this review, we propose a comprehensive framework in which the nucleolus integrates RNA dysfunction, genome organization, and translational control across neuromuscular disorders. This perspective provides a conceptual basis for interpreting disease heterogeneity and highlights nucleolar pathways as potential, underexploited targets for therapeutic intervention.

Two hours of sleep restored: Researchers make Alzheimer’s breakthrough

There’s a small fire isolated in your kitchen. If you had the right tool, you might be able to put it out. But before you can, the sprinklers turn on and flood your entire house. An automatic response to an issue has now damaged everything you own.

That’s akin to what happens in the brains of people with Alzheimer’s: Amyloid plaques, sticky protein clumps that build up in the brain, are the fire in the kitchen. Microglia, the brain’s resident immune cells, are the sprinklers. A mechanism designed to protect the body ends up hurting it.

Researchers at the University of Kentucky have discovered this harmful process for the first time—and figured out how to turn it off.

Activation mechanism and structural assembly of the Mycobacterium tuberculosis ClpP1P2 protease and its associated ATPases

Weinhäupl et al. determine the cryo-EM structure of the ClpC1P1P2 complex from Mycobacterium tuberculosis, revealing an asymmetric architecture and selective activator binding. They show that molecular crowding promotes assembly and activation of Clp complexes, suggesting a mechanism for ClpP1P2 activation under physiological conditions.

Early warning signs of potential drug resistance in schistosomiasis parasite revealed

Scientists have identified genetic changes in wild populations of the parasitic worm that causes schistosomiasis that may reduce its response to praziquantel, the only available treatment. The study provides an early warning for disease control and elimination programs.

Researchers from the Wellcome Sanger Institute, the Royal Veterinary College (RVC) and Medical College of Wisconsin (MCW) led a large-scale international collaboration analyzing hundreds of Schistosoma mansoni genomes collected from people in several African and Caribbean countries. The study is the largest genomic analysis of the parasite from human infections to date.

Published in Science Advances, the findings highlight the need for ongoing genomic surveillance to help protect the long-term effectiveness of praziquantel.

Postnatal Development of Pyramidal Neurons Excitability and Synaptic Inputs in Mouse Gustatory Cortical Circuits

During postnatal development, mammals shift from relying on their mother’s milk to foraging for food. Early experience with feeding independence influences the development of taste preferences (Schiff et al., 2023). While the postnatal development of gustatory cortical circuits is not well studied, there is some experimental evidence for protracted maturation of neuronal morphology and early-life experience-dependent effects on neurons in other regions of the taste system. In mice, taste receptor cells begin to reliably fire action potentials during the third postnatal week (Bigiani et al., 2002) and the refinement of their excitability extends into adulthood (Bigiani et al., 2002; Ohtubo et al., 2012). Postnatal anatomical rewiring was observed in the first central relay in the gustatory system, the nucleus of the solitary tract (NTS) after postnatal day 21 (P21), with the inputs to the NTS reaching adult connectivity by P35 and undergoing additional refinement into adulthood (Hill et al., 1983; Sollars et al., 2006; May et al., 2008; Sun et al., 2017). In the gustatory portion of the parabrachial nucleus, dendritic arborization of multipolar and fusiform cells reach adult morphology by P35 (Lasiter and Kachele, 1988). Together, these studies identify the postnatal window between P15–P21, P21–P35, and P50–P65 as periods of maturation for different circuits in the gustatory system.

In primary visual, auditory, and somatosensory cortices, developmental time windows of heightened sensitivity to changes in sensory inputs extending between the third and fifth postnatal week have been identified (Micheva and Beaulieu, 1995; Antonini et al., 1999; Maffei et al., 2006, 2010; Maffei and Turrigiano, 2008b; Wang et al., 2011; Takesian et al., 2012, 2018; Gainey and Feldman, 2017; Gainey et al., 2018). During these periods, known as critical periods, cortical circuits undergo a maturation process that is shaped by experience and reach their adult properties.

GABAergic inhibitory synapses in particular play a crucial role in postnatal cortical circuit maturation and refinement. Inhibitory cortical circuits themselves undergo extended postnatal maturation (Hensch, 2004; Tatti et al., 2017; Takesian et al., 2018), with increases in GABAergic inhibition opening the critical period for circuit refinement. For instance, in a knock-out mouse in which GABA is severely diminished (GAD-KO), the critical period may never open unless GABA receptors are activated pharmacologically (Fagiolini and Hensch, 2000). Changes in inhibitory circuits during critical periods are primarily ascribed to parvalbumin-expressing interneurons (PV+ INs). Reports show an increase in the number of PV+ INs (Gonchar et al., 2007; Tatti et al., 2017) along with increased perisomatic innervation of pyramidal neurons (Chattopadhyaya et al., 2004). This process is associated with increases in the expression of PV in PV+ INs (Murase et al.

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