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Trisomy 21, characterized by the presence of an additional chromosome 21, leads to a set of clinical features commonly referred to as Down syndrome (DS). The pathological phenotypes observed in DS are caused by a combination of factors, such as mitochondrial dysfunction, neuroinflammation, oxidative stress, disrupted metabolic patterns, and changes in protein homeostasis and signal transduction, and these factors collectively induce neurological alterations. In DS, the triplication of chromosome 21 and the micronuclei arising from the missegregation of chromosomes are closely associated with inflammation and the development of redox imbalance. Autophagy, an essential biological process that affects cellular homeostasis, is a powerful tool to facilitate the degradation of redundant or dysfunctional cytoplasmic components, thereby enabling the recycling of their constituents. Targeting the autophagy process has been suggested as a promising method to balance intracellular inflammation and oxidative stress and improve mitochondrial dysfunction. In this review, we summarize the role of autophagy in regulating inflammation and redox homeostasis in DS and discuss their crosslinks. A comprehensive elucidation of the roles of autophagy in DS offers novel insights for the development of therapeutic strategies aimed at aneuploidy-associated diseases. [ABSTRACT FROM AUTHOR]

Spermatogenesis in mammalian testes is essential for male fertility, ensuring a continuous supply of mature sperm. The testicular microenvironment finely tunes this process, with retinoic acid, an active metabolite of vitamin A, serving a pivotal role. Retinoic acid is critical for various stages, including the differentiation of spermatogonia, meiosis in spermatogenic cells, and the production of mature spermatozoa. Vitamin A deficiency halts spermatogenesis, leading to the degeneration of numerous germ cells, a condition reversible with retinoic acid supplementation. Although retinoic acid can restore fertility in some males with reproductive disorders, it does not work universally. Furthermore, high doses may adversely affect reproduction. The inconsistent outcomes of retinoid treatments in addressing infertility are linked to the incomplete understanding of the molecular mechanisms through which retinoid signaling governs spermatogenesis. In addition to the treatment of male reproductive disorders, the role of retinoic acid in spermatogenesis also provides new ideas for the development of male non-hormone contraceptives. This paper will explore three facets: the synthesis and breakdown of retinoic acid in the testes, its role in spermatogenesis, and its application in male reproduction. Our discussion aims to provide a comprehensive reference for studying the regulatory effects of retinoic acid signaling on spermatogenesis and offer insights into its use in treating male reproductive issues. [ABSTRACT FROM AUTHOR]

Context: Degenerative spondylolisthesis (DS) is a prevalent degenerative condition affecting the lumbar spine. Local spinal parameters play a pivotal role in surgical complications and in the QoL that adults with spinal deformities experience. Treatment can effectively alleviate radicular symptoms, but it doesn't significantly mitigate postoperative axial symptoms (AS)., Objective: The study intended to investigate the correlation between postoperative axial symptoms (AS) and spinal-pelvic parameters for patients with DS of the lumbar spine., Design: The research team conducted a prospective cohort study., Setting: The study took place at the Huai'an Hospital of Huai'an City in the Huai'an District of Huai'an City in JiangSu Province, China., Participants: Participants were 120 patients with DS who had been admitted to the department of orthopedics at the hospital between January 2016 and December 2022 and 120 healthy volunteers during the same period., Intervention: The research team created two groups, each with 120 participants: (1) the intervention group with DS who received posterior laminar decompression + pedicle-screw internal fixation + intervertebral-space bone grafting and fusion, and (2) the control group, the healthy volunteers., Outcome Measures: The research team: (1) measured both group's spinal-pelvic parameters at baseline and at 6 months postintervention, (2) evaluated both group's motor functions at baseline and at 6 months postintervention, using the Japanese Orthopedic Association (OAS) scale and the Oswestry Disability Index (ODI), (3) examined the intervention group's postoperative AS, and (4) analyzed the correlation between the intervention group's spinal-pelvic parameters and its postoperative AS and motor function., Results: At 6 months postintervention, the intervention group's spinal-pelvic parameters-lumbar lordosis (LL) and sacral slope (SS) were significantly lower-and-pelvic incidence (PI), pelvic tilt (PT), thoracic kyphosis (TK), segmental lumbar lordosis (SLL), and sagittal vertical axis (SVA) were significantly higher than those of the control group (all P = .000). The intervention group's JOA and ODI scores were significantly lower than those of the control group postintervention (both P = .000). Postintervention compared to the non-AS group, the AS group's LL (P = .000), PI (P = .000), and SS (P = .020) were significantly lower and PT (P = .002), TK (P = .000), SLL (P = .002), and SVA (P = .000) were significantly higher. Postoperative AS was negatively correlated with LL, PI, SS, and positively correlated with PT, TK, SLL, and SVA (all P = .000). The JOA and ODI scores were positively correlated with LL, PI, and SS, and negatively correlated with PT, TK, SLL, and SVA (all P = .000)., Conclusions: Postoperative AS in patients with DS is significantly correlated with spinal-pelvic parameters, providing convincing evidence for the evaluation of postoperative dysfunction. However, generalizing to other patients is limited due to the small sample size, which might have resulted in bias in spinal-pelvic parameters. Hence, ongoing trials with large samples are warranted.