Annals of medicine
-
Background: Bladder cancer (BC) is one of the most common human malignancies worldwide. Previous researches have shown that the unfolded protein response (UPR) pathway could contribute to the tumorigenesis of BC. However, the role of UPR in the immune infiltration, progression, and prognosis of BC is unclear. ⋯ The UPR score was positively correlated with the infiltration abundance of many tumor immune cells in TCBC. Besides, we constructed predictive models based on the UPR score, and good performance was observed, with c-indexes ranging from 0.74 to 0.87. Conclusions: Our study proved that the UPR pathway may have an important impact on the progression, prognosis, and tumor immune infiltration in TCBC, and the models we built may provide effective and reliable guides for prognosis assessment and treatment decision-making for TCBC patients.
-
Low triiodothyronine syndrome (LT3S) is a common endocrine disease in preterm neonates. Various serious acute or chronic diseases result in LT3S. Few studies have investigated the causal relationship between perinatal factors and LT3S in preterm neonates with a gestational age (GA) of 28-35 weeks. The present study comprehensively analyzed the perinatal factors of LT3S in preterm neonates. ⋯ LT3S in preterm neonates was associated with multiple perinatal factors, including smaller gestational age, lower birth weight, RDS, sepsis, and dopamine use. Preterm neonates with a GA of 28-35 weeks who are exposed to a series of high-risk perinatal factors must be closely observed, diagnosed early and treated for primary diseases promptly to reduce the occurrence of LT3S and improve the outcomes.Key Message:Few studies have investigated the relationship between perinatal factors and Low triiodothyronine syndrome (LT3S) in preterm neonates with a gestational age (GA) of 28-35 weeks.LT3S was associated with multiple perinatal factors, including smaller gestational age, lower birth weight, respiratory distress syndrome (RDS), sepsis, and dopamine use.
-
Background: Recent evidence indicates that host-gut microbiota crosstalk has nonnegligible effects on host skeletal muscle, yet gut microbiota-regulating mechanisms remain obscure. Methods: C57BL/6 mice were treated with a cocktail of antibiotics (Abx) to depress gut microbiota for 4 weeks. The profiles of gut microbiota and microbial bile acids were measured by 16S rRNA sequencing and ultra-performance liquid chromatography (UPLC), respectively. ⋯ Mechanistically, circulating FGF15 was decreased, which downregulated skeletal muscle protein synthesis through the extracellular-signal-regulated protein kinase 1/2 (ERK1/2) signaling pathway. Treating Abx mice with FGF19 (human FGF15 ortholog) partly reversed skeletal muscle loss. Conclusions: These findings indicate that the BA-FXR-FGF15/19 axis acts as a regulator of gut microbiota to mediate host skeletal muscle.
-
Objectives: Early fetal demise (absence of cardiac activity in a visible fetus) is a very common event, but there are no reliable biomarkers to predict it. The purpose of the study was to assess the association of platelet parameters with early fetal demise. Methods: In this case-control study, we included women with normal deliveries or those ultrasound diagnosed as early fetal demise. ⋯ In addition, platelet reactivity is higher in the normal delivery group than those in early fetal demise group (p < .05). High levels of platelet counts resulted in an adjusted odds ratio (OR) of 2.075 (95% confidence interval [95% CI], 1.215-3.544; p = .008) for early fetal demise. Conclusions: Increased platelet counts in the first trimester may be a predictor for the risk of early fetal demise.
-
Background: Exosomes-encapsulated microRNAs (miRNAs) have been established to be implicated in the pathogenesis of different diseases. Nevertheless, circulating exosomal miRNAs of thromboangiitis obliterans (TAO) remains poorly understood. This study aimed to explore the effects of exosomal miRNAs associated with TAO on human vascular smooth muscle cells (HVSMCs). ⋯ Additionally, the expressions of VCAM1 and IGF1R were down-regulated by exosomes and miR-223-5p mimics, and were abrogated by miR-223-5p inhibitor. Dual-luciferase report showed that VCAM1 was the target of miR-223-5p. Conclusions: Our findings imply that circulating exosomal miR-223-5p may play an essential role in the pathogenesis of TAO, and provide a basis for miR-6515-5p/VCAM1 as novel therapeutic targets and pathways for TAO treatment.