Reduced coupling between cerebrospinal fluid flow and global brain activity is linked to Alzheimer disease-related pathology.

The glymphatic system plays an important role in clearing the amyloid-ß (Aß) and tau proteins that are closely linked to Alzheimer disease (AD) pathology. Glymphatic clearance, as well as Aß accumulation, is highly dependent on sleep, but the sleep-dependent driving forces behind cerebrospinal fluid (CSF) movements essential to the glymphatic flux remain largely unclear. Recent studies have reported that widespread, high-amplitude spontaneous brain activations in the drowsy state and during sleep, which are shown as large global signal peaks in resting-state functional magnetic resonance imaging (rsfMRI), are coupled with CSF movements, suggesting their potential link to glymphatic flux and metabolite clearance. By analyzing multimodal data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) project, here we showed that the coupling between the global fMRI signal and CSF influx is correlated with AD-related pathology, including various risk factors for AD, the severity of AD-related diseases, the cortical Aß level, and cognitive decline over a 2-year follow-up. These results provide critical initial evidence for involvement of sleep-dependent global brain activity, as well as the associated physiological modulations, in the clearance of AD-related brain waste.

Social Change and Race-Specific Homicide Trajectories: An Age-Period-Cohort Analysis.

Objectives: Social change and the aging process are racially bifurcated in the United States, where Black and White populations have long lived in divergent social worlds. This study examines the cohort patterns and life-course trajectories of Black and White homicide involvement over the past four decades. Data and Methods: The study uses data from the Supplemental Homicide Reports and Age-Period-Cohort-Interaction (APC-I) models to analyze race-specific trends of (alleged) homicide offending and victimization between 1976 and 2018 in the U.S. Results: Results reveal similar patterns in the age, period, and cohort effects on Black and White homicide involvement. However, while the shapes of these trajectories are comparable, the volatility in cohort effects on homicide is much more accentuated for Black cohorts than White cohorts. We also find racial differences for cohorts born after 1990, with a downward cohort pattern among the White group but a flat cohort trend among the Black group. Conclusions: Findings suggest that Black cohorts' homicide involvement is more susceptible than White cohorts' to the influence of external social changes (e.g., economic downturn, the crack epidemic). In addition, an increasing racial gap between Black and White populations is found among the recent birth cohorts. Possible mechanisms are discussed.

Identification of kukoamine a as an anti-osteoporosis drug target using network pharmacology and experiment verification.

BACKGROUND: Osteoporosis (OP) is a major and growing public health problem characterized by decreased bone mineral density and destroyed bone microarchitecture. Previous studies found that Lycium Chinense Mill (LC) has a potent role in inhibiting bone loss. Kukoamine A (KuA), a bioactive compound extract from LC was responsible for the anti-osteoporosis effect. This study aimed to investigate the anti-osteoporosis effect of KuA isolated from LC in treating OP and its potential molecular mechanism. METHOD: In this study, network pharmacology and molecular docking were investigated firstly to find the active ingredients of LC such as KuA, and the target genes of OP by the TCMSP platform. The LC-OP-potential Target gene network was constructed by the STRING database and network maps were built by Cytoscape software. And then, the anti-osteoporotic effect of KuA in OVX-induced osteoporosis mice and MC3T3-E1 cell lines were investigated and the potential molecular mechanism including inflammation level, cell apoptosis, and oxidative stress was analyzed by dual-energy X-ray absorptiometry (DXA), micro-CT, ELISA, RT-PCR, and Western Blotting. RESULT: A total of 22 active compounds were screened, and we found KuA was identified as the highest active ingredient. Glycogen Phosphorylase (PYGM) was the target gene associated with a maximum number of active ingredients of LC and regulated KuA. In vivo, KuA treatment significantly increased the bone mineral density and improve bone microarchitecture for example increased BV/TV, Tb.N and Tb.Th but reduced Tb.Sp in tibia and lumber 4. Furthermore, KuA increased mRNA expression of osteoblastic differentiation-related genes in OVX mice and protects against OVX-induced cell apoptosis, oxidative stress level and inflammation level. In vitro, KuA significantly improves osteogenic differentiation and mineralization in cells experiment. In addition, KuA also attenuated inflammation levels, cell apoptosis, and oxidative stress level. CONCLUSION: The results suggest that KuA could protect against the development of OP in osteoblast cells and ovariectomized OP model mice and these found to provide a better understanding of the pharmacological activities of KuA again bone loss.

The mobility effects hypothesis: Methods and applications.

We discuss hypotheses researchers have put forth to explain how outcomes of socially mobile and immobile individuals might differ and/or how mobility experiences are related to outcomes of interest. Next, we examine the methodological literature on this topic, culminating in the development of the diagonal mobility model (DMM, also called the diagonal reference model in some studies), the primary tool of use since the 1980's. We then discuss some of the many applications of the DMM. Although the model was proposed to examine the effects of social mobility on outcomes of interest, the estimated relationships between mobility and outcomes that researchers have called mobility effects are more appropriately regarded as partial associations. When mobility is not associated with outcomes, as is often found in empirical work, the outcomes of movers from origin o to destination d are a weighted average of the outcomes of individuals who remained in states o and d respectively, and the weights capture the relative salience of origins and destinations in the acculturation process. In light of this attractive feature of the model, we briefly develop several generalizations of the current DMM that future researchers should also find useful. Finally, we propose new estimands of mobility effects, based on the explicit notion that a unit effect of mobility is a comparison of an individual with herself under two conditions, one in which she is mobile, the other in which she is immobile, and we discuss some of the challenges in identifying such effects.

TLR9 agonist suppresses choroidal neovascularization by restricting endothelial cell motility via ERK/c-Jun pathway.

INTRODUCTION: Choroidal neovascularization (CNV) is the feature of neovascular age-related macular degeneration (AMD). It has been demonstrated that inflammation plays a key role in the development of CNV. Here we aim to investigate how TLR9 agonist (CpG-ODN), one of the key regulators of inflammatory responses, suppresses CNV in vivo. MATERIALS AND METHODS: The cell viability was assessed by MTT and EdU test after CpG-ODN treatment. Endothelial cells gap assay, tube formation assay and transwell assay were practiced to observe how CpG-ODN affected the endothelial cells functions. The choroidal explants and laser-induced CNV model were built to investigate how CpG-ODN suppressed angiogenesis. The ERK and c-Jun expression were evaluated to assess if CpG-ODN affected cell proliferation. Flow cytometry and qPCR was practiced to observe how CpG-ODN regulated cell proliferation. RESULTS: Our data showed that CpG-ODN not only reduced CNV area in vivo, but also decreased the RPE damage. CpG-ODN inhibited endothelial cells from migration and forming tubes, while the effect was not toxic. EdU test and MTT test suggested that CpG-ODN inhibited endothelial cells proliferation. CpG-ODN significantly increased protein expression of phosphorylated c-Jun but reduced phosphorylated ERK in HUVECs, which was confirmed in ERK transfected 293T cells. JNK inhibitor abolished the suppression of endothelial cells migration and tube formation by CpG-ODN. The findings were also in agreement with the observation in CpG-ODN treated CNV eyes in vivo. The flow cytometry and qPCR data revealed that the suppression of cell motility by CpG-ODN was achieved by arresting endothelial cells cell cycle at G0/G1 phase. CONCLUSIONS: Our study demonstrated that CpG-ODN suppressed endothelial cell motility by restricting the cell cycle progression at G0/G1 phase, the effect of which was achieved by interacting with ERK/c-Jun pathways.

The Age-Period-Cohort-Interaction Model for Describing and Investigating Inter-cohort Deviations and Intra-cohort Life-course Dynamics.

Social scientists have frequently sought to understand the distinct effects of age, period, and cohort, but disaggregation of the three dimensions is difficult because cohort = period - age. We argue that this technical difficulty reflects a disconnection between how cohort effect is conceptualized and how it is modeled in the traditional age-period-cohort framework. We propose a new method, called the age-period-cohort-interaction (APC-I) model, that is qualitatively different from previous methods in that it represents Ryder's (1965) theoretical account about the conditions under which cohort differentiation may arise. This APC-I model does not require problematic statistical assumptions and the interpretation is straightforward. It quantifies inter-cohort deviations from the age and period main effects and also permits hypothesis testing about intra-cohort life-course dynamics. We demonstrate how this new model can be used to examine age, period, and cohort patterns in women's labor force participation.

Heterogeneous Effects of Intergenerational Social Mobility: An Improved Method and New Evidence.

Intergenerational social mobility has immense implications for individuals' well-being, attitudes, and behaviors. However, previous methods may be unreliable for estimating heterogeneous mobility effects, especially in the presence of moderate- or large-scale intergenerational mobility. We propose an improved method, called the "mobility contrast model" (MCM). Using simulation evidence, we demonstrated that the MCM is more flexible and reliable for estimating and testing heterogeneous mobility effects, and the results are robust to the scale of intergenerational mobility. We revisited the debate about the effect of mobility on fertility and analyzed data from the 1962 Occupational Changes in a Generation Study (OCG-1) and more recent data from the 1974 through 2018 General Social Survey (GSS) using both previous models and the MCM. The MCM suggested a small association between fertility and occupational mobility in the GSS data but substantial and heterogeneous educational mobility effects on fertility in the OCG-1 and the GSS. Such effects were difficult to pinpoint using previous methods because mobility effects of different magnitudes and opposite directions among mobility groups may cancel out. The new method can be extended to investigate the effect of intergenerational mobility across multiple generations and other research areas including immigrant assimilation and heterogamy.

Severe Pulmonary Embolism, Thrombosis of Lower Extremity, Unexpected Mild Renal Disorder in MPO-ANCA Associated Vasculitis: A Case Report.

Myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) associated vasculitis is an autoimmune disease usually with severe multiple dysfunction syndrome, especially prominent acute renal failure. A 65-year-old woman was admitted with progressive dyspnoea for six months and fever, sputum with blood, pain of the lower extremities and intermittent claudication for two days, indicating multiple organ involvement (respiratory system, blood vessels). The renal involvement was relatively mild, presenting with microscopic haematuria. The chest computed tomography demonstrated multiple pulmonary embolisms. Ultrasound and computed tomography angiography for the lower extremity vessels showed venous and arterial thrombosis. Exclusion of other diseases that can cause multiple organ damage and thrombosis, the positive perinuclear ANCA and MPO-ANCA strongly support the diagnosis of MPO-ANAC-associated vasculitis. The patient's physical condition has been greatly improved by treatment with corticosteroids and anticoagulation.

The contemporary transformation of american youth: An analysis of change in the prevalence of delinquency, 1991-2015.

Youth involvement in crime has declined substantially over the past few decades, yet the reasons for this trend remain unclear. We advance the literature by examining the role of several potentially important shifts in individual attitudes and behaviors that may help to account for the observed temporal variation in youth delinquency. Our multilevel analysis of repeated cross-sectional data from high school students in the Monitoring the Future (MTF) study indicates that changes in youth offending prevalence were not associated with changes in youth attachment and commitment to school, community involvement, or parental supervision after school. In contrast, the study provides suggestive evidence that the significant reduction in youth offending prevalence observed since the early 1990s was significantly associated with a decrease in unstructured socializing and alcohol consumption and, to a lesser extent, with a decrease in youth preferences for risky activities. Implications for existing theoretical explanations and future research on youth crime trends are discussed.

Understanding Trends in the Concentration of Infant Mortality Among Disadvantaged White and Black Mothers in the United States, 1983-2013: A Decomposition Analysis.

The United States compares unfavorably with other high-income countries in infant mortality, which recent literature has attributed to the poor birth outcomes among disadvantaged (i.e., unmarried and less-educated) mothers. Describing and decomposing the trend of the concentration of infant mortality among disadvantaged mothers thus provides important clues for improving birth outcomes. We develop the infant mortality disadvantage index (IMDI) to measure such concentration. Using the 1983-2013 Birth Cohort Linked Birth and Infant Death data, we show that although the IMDI-as a measure of mortality inequality-was persistently higher for Blacks than Whites, the trends were different between the two groups. The IMDI declined for Black women; for White women, however, it increased in the 1980s, then plateaued until the early 2000s, and declined thereafter. We then use Das Gupta's decomposition method to assess the contribution of five demographic/social factors (age, education, marriage, fertility, and infant mortality) to the IMDI trend. Nonmarital fertility among women with less than 12 years of education contributed most to Whites' changing IMDI; for Blacks, a shrinking proportion of the less-educated group and declines in infant mortality among disadvantaged mothers contributed to their declining IMDI. These findings explicate links between population-level compositional changes and infant mortality inequality.

The Intrinsic Estimator, Alternative Estimates, and Predictions of Mortality Trends: A Comment on Masters, Hummer, Powers, Beck, Lin, and Finch.

In this article, we discuss a study by Masters et al. (2014), published in Demography. Masters and associates estimated age, period, and cohort (APC) effects on U.S. mortality rates between 1959 and 2009 using the intrinsic estimator (IE). We first argue that before applying the IE, a grounded theoretical justification is needed for its fundamental constraint on minimum variance of the estimates. We next demonstrate IE's high sensitivity to the type of dummy parameterization used to obtain the estimates. Finally, we discuss challenges in the interpretation of APC models. Our comments are not restricted to the article in question but pertain generally to any research that uses the IE.

For Whom Does Education Convey Health Benefits? A Two-Generation and Life Course Approach.

Scholars of social determinants of health have long been interested in how parent's and own education influence health. However, the differing effects of parent's and own education on health-that is, for what socioeconomic group education conveys health benefits-are relatively less studied. Using multilevel marginal structural models, we estimate the heterogeneous effects of parent's and own education over the life course on two health measures. Our analysis considers both parent's and respondent's pre-education covariates, such as childhood health and socioeconomic conditions. We find that the protective effects of college completion against negative health outcomes are remarkably similar regardless of parent's (measured by father's or mother's) education. Meanwhile, parent's education has a larger effect when the average educational level is low in the population. Our results also reveal distinct life course patterns between health measures. We conclude by discussing the implications of our study for understanding the education-health relationship.

Trends in sleep duration in the U.S. from 2004 to 2018: A decomposition analysis.

Average sleep duration in the United States declined in recent years, and the decline may be linked with many biopsychosocial factors. We examine how a set of biopsychosocial factors have differentially contributed to the temporal trends in self-reported sleep duration across racial groups between 2004-2005 and 2017-2018. Using repeated nationally representative cross-sections from the National Health Interview Survey, we decompose the influence of biopsychosocial factors on sleep duration trends into two components. One component corresponds to coefficient changes (i.e., changes in the associations between behaviors or exposures and sleep duration) of key biopsychosocial factors, and the other part accounts for the compositional changes (i.e., changes in the distributions of exposures) in these biopsychosocial factors during the study period. We reveal that changes in the coefficients of some biopsychosocial factors are more important than compositional changes in explaining the decline in sleep duration within each racial/ethnic group. Our findings highlight racial differences manifest across multiple biopsychosocial domains that are shifting in terms of association and composition. Methodologically, we note that the standard regression approach for analyzing temporal trends neglects the role of coefficient changes over time and is thus insufficient for fully capturing how biopsychosocial factors may have influenced the temporal patterns in sleep duration and related health outcomes.

The gingival crevicular fluid biomarkers with micropulse vibration device: A pilot study.

Purpose: The aim of this study is to investigate the impact of vibration stimulation on gingival crevicular fluid biomarkers and orthodontic tooth movement. Methods: Forty patients were randomly assigned to receive therapy with an intraoral vibration device (n = 20, AcceleDent®) or no treatment (n = 20) at a university orthodontic clinic. The quantity of fluid in the gingival sulcus, biomarkers of each fluid in the gingival sulcus, and orthodontic tooth movement were analyzed at three-time intervals (T1, T2, T3) before and after therapy (T0). Results: The results showed that vibration treatment led to higher levels of osteoclast biomarkers (RNAKL, RANKL/OPG) and inflammatory biomarkers (TNF-, IL-11, IL-18) compared to the control group. Additionally, vibration treatment at T1, T2, and T3 significantly improved tooth mobility and GCF volume. The gingival crevicular fluid biomarker levels of the T0, T1, and T2 vibration groups, as well as IL-11, IL-18, TGF-1, and TNF-α vibration groups, were significantly higher than those of the control group at different time points. Conclusion: vibration therapy was found to be closely associated with bone-breaking cells and inflammatory factor levels.

Predicting the potential mechanism of radix chimonanthi pracecocis in treating osteoarthritis by network pharmacology analysis combined with experimental validation.

ETHNOPHARMACOLOGICAL RELEVANCE: Radix Chimonanthi Pracecocis (RCP), also known as Tiekuaizi, widely used by the Miao community in Guizhou, exhibits diverse biological activities and holds promise for the treatment of osteoarthritis (OA). However, there is a lack of contemporary pharmacological research in this area. AIMS OF THE STUDY: This study aims to explore the potential of targets and mechanisms of RCP in the treatment of OA. MATERIALS AND METHODS: The chemical components of RCP were identified using UPLC-MS/MS, and active components were determined based on the Lipinski rule. RCP and OA-related targets were retrieved from public databases such as TCMSP and GeneCards. Network pharmacology approaches were employed to identify key genes. The limma package (version 3.40.2) in R 4.3.2 was used to screen for differentially expressed genes (DEGs) between OA and healthy individuals in GSE82107. DEGs were analyzed using an independent sample t-test and receiver operating characteristic analysis in GraphPad Prism 9.5.1. Additionally, molecular docking (SYBYL2.1.1) was used to analyze the binding interactions between the active components and target proteins. Finally, we established a papain-induced osteoarthritis (OA) rat model and treated it with RCP aqueous extract by gavage. We validated relevant indicators using real-time fluorescence quantitative polymerase chain reaction, Western blot, immunohistochemistry, and enzyme-linked immunosorbent assays. RESULTS: Seven active components and 53 targets were identified. The results of GO and KEGG enrichment analyses confirmed the significant role of RCP in the regulation of pyroptosis. Hypoxia-inducible factor-1α (HIF-1α) was identified as a key gene involved in the main biological functions. Molecular docking analysis revealed that Praecoxin, Isofraxidin, Esculin, and Naringenin can bind to the nucleotide-binding domain, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) (T-Score >5). Additionally, Praecoxin can bind to HIF-1α (T-Score >5). In vivo experiments demonstrated that RCP significantly affects the NLRP3 inflammasome, which is regulated by the HIF-1α pathway. RCP inhibited pyroptosis and reduced synovial inflammation. CONCLUSIONS: This study confirmed the efficacy of RCP aqueous extract in the treatment of OA and identified seven active components (esculin, dihydrokaempferol, naringenin, praecoxin, carnosol, hydroxyvalerenic acid, isofraxidin) that may play an anti-pyroptosis role in the treatment of OA by downregulating the expression of HIF-1α and NLRP3 inflammasome.

Sympathetic innervation induces exosomal miR-125 transfer from osteoarthritic chondrocytes, disrupting subchondral bone homeostasis and aggravating cartilage damage in aging mice.

INTRODUCTION: Osteoarthritis (OA) is a progressive disease that poses a significant threat to human health, particularly in aging individuals: Although sympathetic activation has been implicated in bone metabolism, its role in the development of OA related to aging remains poorly understood. Therefore, this study aimed to investigate how sympathetic regulation impacts aging-related OA through experiments conducted both in vivo and in vitro. METHODS: To analyze the effect of sympathetic regulation on aging-related OA, we conducted experiments using various mouse models. These models included a natural aging model, a medial meniscus instability model, and a load-induced model, which were used to examine the involvement of sympathetic nerves. In order to evaluate the expression levels of ß1-adrenergic receptor (Adrß1) and sirtuin-6 (Sirt6) in chondrocytes of naturally aging OA mouse models, we performed assessments. Additionally, we investigated the influence of ß1-adrenergic receptor knockout or treatment with a ß1-adrenergic receptor blocker on the progression of OA in aging mice and detected exosome release and detected downstream signaling expression by inhibiting exosome release. Furthermore, we explored the impact of sympathetic depletion through tyrosine hydroxylase (TH) on OA progression in aging mice. Moreover, we studied the effects of norepinephrine(NE)-induced activation of the ß1-adrenergic receptor signaling pathway on the release of exosomes and miR-125 from chondrocytes, subsequently affecting osteoblast differentiation in subchondral bone. RESULTS: Our findings demonstrated a significant increase in sympathetic activity, such as NE levels, in various mouse models of OA including natural aging, medial meniscus instability, and load-induced models. Notably, we observed alterations in the expression levels of ß1-adrenergic receptor and Sirt6 in chondrocytes in OA mouse models associated with natural aging, leading to an improvement in the progression of OA. Critically, we found that the knockout of ß1-adrenergic receptor or treatment with a ß1-adrenergic receptor blocker attenuated OA progression in aging mice and the degraded cartilage explants produced more exosome than the nondegraded ones, Moreover, sympathetic depletion through TH was shown to ameliorate OA progression in aging mice. Additionally, we discovered that NE-induced activation of the ß1-adrenergic receptor signaling pathway facilitated the release of exosomes and miR-125 from chondrocytes, promoting osteoblast differentiation in subchondral bone. CONCLUSION: In conclusion, our study highlights the role of sympathetic innervation in facilitating the transfer of exosomal miR-125 from osteoarthritic chondrocytes, ultimately disrupting subchondral bone homeostasis and exacerbating cartilage damage in aging mice. These findings provide valuable insights into the potential contribution of sympathetic regulation to the pathogenesis of aging-related OA.

Trends in prevalence of multimorbidity for chronic diseases in China: serial cross-sectional surveys from 2009 to 2018.

BACKGROUND: Multimorbidity, individuals suffering from two or more chronic diseases, has become a major health challenge worldwide, especially in populous and prosperous cities, where studies of this phenomenon in China are limited. We examined the prevalence, trends, patterns, and associated factors of multimorbidity from 2009 to 2018 among community-dwelling adults in Guangzhou, China. METHODS: We conducted serial cross-sectional surveys for chronic diseases in Guangzhou, China, in 2009, 2013, and 2018. General and stratified prevalence were standardized using demographic data. Multivariable logistic regression and hierarchical cluster analysis were applied to identify associated factors and to assess the correlations and patterns of multimorbidity, respectively. RESULTS: This study included 23,284 adults aged 18 and over in 2009, 18,551 in 2013, and 15,727 in 2018. The standardized prevalence of multimorbidity increased substantially, with 12.69% (95% CI: 10.45-15.33) in 2009, 25.44% (95% CI: 23.47-27.52) in 2013, and 35.13% (95% CI:32.64-37.70) in 2018 (P for trend <0.001). The highest bi- and triple-conditions of multimorbidity were dyslipidemia (DP) and overweight or obesity (OO) (12.54%, 95% CI: 11.68-13.46), and DP, OO, and Hypertension (HT) (3.99%, 95% CI: 3.47-4.58) in 2018. From 2009 to 2018, (1) The majority of multimorbidity patterns showed a high prevalence; (2) The percentage of participants with only one chronic condition was found lower, while the percentage with multiple conditions was higher. CONCLUSIONS: The prevalence of chronic disease multimorbidity in Guangzhou China, has increased substantially among adults. Effective policies targeting multimorbidity are urgently needed, especially for the health management of primary medical institutions.

Low platelet count at diagnosis of anti-neutrophil cytoplasmic antibody-associated vasculitis is correlated with the severity of disease and renal prognosis.

Antineutrophil cytoplasmic antibody-associated vasculitis (AAV) is an autoimmune disease that involves inflammation of blood vessels. There is increasing evidence that platelets play a crucial role not only in hemostasis but also in inflammation and innate immunity. In this study, we explored the relationship between platelet count, clinical characteristics, and the prognosis of patients with AAV. We divided 187 patients into two groups based on their platelet count. Clinicopathological data and prognostic information were retrospectively gathered from medical records. Univariate and multivariate regression analyses were used to identify risk factors for prognosis, including end-stage renal disease (ESRD) and mortality. The cutoff point for platelet count was set at 264.5 × 109/L, as determined by the receiver operating characteristic (ROC) curve for predicting progression to ESRD in patients with AAV. We observed patients with low platelet count (platelets < 264.5 × 109/L) had lower leukocytes, hemoglobin, complement, acute reactants, and worse renal function (P for eGFR < 0.001). They were also more likely to progress to ESRD or death compared to the high platelet count group (platelets > 264.5 × 109/L) (P < 0.0001, P = 0.0338, respectively). Low platelet count was potentially an independent predictor of poor renal prognosis in the multivariate regression analysis [HR 1.670 (95% CI 1.019-2.515), P = 0.014]. Lower platelet count at diagnosis is associated with more severe clinical characteristics and impaired renal function. Therefore, platelet count may be an accessible prognostic indicator for renal outcomes in patients with AAV.

Isolation, identification, and induced differentiation of satellite cells from skeletal muscle of adult tree shrews.

A method for the in vitro isolation, purification, identification, and induced differentiation of satellite cells from adult tree shrew skeletal muscle was established. The mixed enzyme digestion method and differential adhesion method were used to obtain skeletal muscle satellite cells, which were identified and induced to differentiate to verify their pluripotency. The use of a mixture of collagenase II, hyaluronidase IV, and DNase I is an efficient method for isolating adult tree shrew skeletal muscle satellite cells. The P3 generation of cells had good morphology, rapid proliferation, high viability, and an "S"-shaped growth curve. Reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence staining indicated that marker genes or proteins were expressed in skeletal muscle satellite cells. After myogenic differentiation was induced, multiple-nucleated myotubes were observed, and the MyHC protein was expressed. The expression of myogenic marker genes changed with the differentiation process. After the induction of adipogenic differentiation, orange-red lipid droplets were observed, and the expression of adipogenic marker genes increased gradually with the differentiation process. In summary, satellite cells from adult tree shrew skeletal muscle were successfully isolated using a mixed enzyme digestion method, and their potential for differentiation into myogenic and adipogenic cells was confirmed, laying a foundation for further in vitro study of tree shrew muscle damage.