In recent years, the interest in the comprehension of the fasciae has significantly grown, together with the necessity of finding a consensus for a terminology of the fasciae in the research and clinical fields. Furthermore, it is becoming necessary to categorize the various types of fascia (superficial, deep, visceral, neural) since they possess different anatomical characteristics, and are implicated in different pathophysiological pathways. While in the past we have described the deep/muscular fascia, the aim of this work is to summarize and catalog the information relating to the human superficial fascia (thickness, cellular end extracellular matrix component, innervation, vascularization).

Macrophages play a crucial role in the progression of atherosclerotic lesions. In the current study, we analyzed the expression and function of sestrin1 (SESN1) in the aorta macrophages in a murine atherosclerosis model. We identified high SESN1 expression in the aorta macrophages in atherosclerotic mice. Using lentivirus‐mediated SESN1 overexpression in macrophages, we found that SESN1 inhibited oxidized low‐density lipoprotein–induced NLRP3 inflammasome activation in lipopolysaccharide (LPS)‐primed macrophages, as evidenced by less ASC‐NLRP3 complex formation, lower caspase‐1 activation, and lower generation of mature IL‐1β. Besides, SESN1 impeded oxidized low‐density lipoprotein–induced activation of NK‐κB signaling in macrophages. Furthermore, SESN1 suppressed cholesterol crystal‐induced NLRP3 inflammasome activation and foam cell formation. Adoptive transfer of SESN1 overexpressing macrophages reduced the expression of pro‐inflammatory cytokines in infiltrating macrophages and the whole aorta tissue. Adoptive transfer of SESN1 knockdown macrophages enhanced the expression of pro‐inflammatory cytokines in infiltrating macrophages and the whole aorta tissue. Overall, our study sheds light on the significance of SESN1 for macrophage‐mediated aorta inflammation.

Muscle spindles have unique anatomical characteristics that can be directly affected by the surrounding tissues under physiological and pathological conditions. Understanding their spatial distribution and density in different muscles is imperative to unravel the complexity of motor function. In the present study, the distribution and number/density of muscle spindles in human and animal muscles were reviewed. We identified 56 articles focusing on muscle spindle distribution; 13 articles focused on human muscles and 43 focused on animal muscles. The results demonstrate that spindles are located at the nerve entry points and along distributed vessels and they relate to the intramuscular connective tissue. Muscles’ deep layers and middle segments are the main topographic distribution areas. Eleven articles on humans and thirty-three articles on animals (totaling forty-four articles) focusing on muscle spindle quantity and density were identified. Hand and head muscles, such as the pronator teres/medial pterygoid muscle/masseter/flexor digitorum, were most commonly studied in the human studies. For animals, whole-body musculature was studied. The present study summarized the spindle quantity in 77 human and 189 animal muscles. We identified well-studied muscles and any as-yet unfound data. The current data fail to clarify the relationship between quantity/density and muscle characteristics. The intricate distribution of the muscle spindles and their density and quantity throughout the body present some unique patterns or correlations, according to the current data. However, it remains unclear whether muscles with fine motor control have more muscle spindles since the study standards are inconsistent and data on numerous muscles are missing. This study provides a comprehensive and exhaustive approach for clinicians and researchers to determine muscle spindle status.

To explore the correlation between UGT1A1 variant and neonatal hyperbilirubinemia in Chinese Uighur and Han populations. We conducted this study in Urumqi, China. Umbilical cord blood specimens and clinical information of term infants born in the studied center were collected. Variation status of UGT1A1 was determined by direct sequencing or capillary electrophoresis analysis. 102 Uighur and 99 Han normal term neonates, together with 19 hospitalized term newborns (10 Uighur and 9 Han) due to significant hyperbilirubinemia were enrolled into the final analysis. The incidence of neonates with high-risk transcutaneous bilirubin level (TCB) were much higher in Han newborns than in Uighur newborns(P = 0.01). Also, there was statistically significant difference in (TA) 7 promoter mutation of UGT1A1 between Han and Uighur group(χ2 = 4.675, P = 0.03). Furthermore, exon mutation (c.211 and /or c.1091) in UGT1A1 gene was significantly associated with increased TCB level (OR_adj = 1.41, 95%CI: 0.25–2.51, P = 0.002) and higher risk of hyperbilirubinemia in both Han and Uighur infants after adjusted for covariates (OR_adj = 2.21, 95%CI: 1.09–4.49, P = 0.03). In conclusion, UGT1A1 promoter polymorphism seem to be an important genetic modulator of plasma bilirubin level and neonatal hyperbilirubinemia risk within ethnic groups. Genetic assessment of UGT1A1 coding variants may be useful for clinical diagnosis of neonatal jaundice.