Intervertebral disc degeneration (IDD) serves as an independent risk factor for lower back pain and is closely associated with spinal musculoskeletal disorders, including lumbar disc herniation, radiculopathy, and myelopathy. , also named IL-17A, is a critical signature cytokine of T-helper 17 cells. Upon binding to
Objective To study the N6-methyladenosine (m 6 A) modification pattern of nucleus pulposus (NP) tissue during intervertebral disc degeneration (IDD). Methods A standing mouse model was generated, and staining and imaging methods were used to evaluate the IDD model. Methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-seq) was used to analyze m 6 A methylation-associated transcripts in the NP, and real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of methylation-related enzymes and conduct bio-informatics analysis. Results The standing mouse model caused IDD. Continuous axial pressure changed the expression of related methylases in degenerated NP tissue. Relative to the control group, the expression levels of KIAA1429, METTL14, METTL3, METTL4, WTAP, DGCR8, EIF3A and YTHDC1 in the experimental group were higher, while those of FTO, ELAVL1, HNRNPC1 and SRSF2 were lower. We identified 985 differentially expressed genes through MeRIP-Seq, among which 363 genes were significantly up-regulated, and 622 genes were significantly down-regulated. In addition, among the 9648 genes counted, 1319 m 6 A peaks with significant differences in methylation were identified, among which 933 were significantly up-regulated, and 386 were significantly down-regulated. Genes and pathways that were enriched in IDD have been identified. Conclusion The results of this study elucidated the m 6 A methylation pattern of NP tissue in degenerated lumbar intervertebral disc of mice and provided new perspectives and clues for research on and the treatment of lumbar disc degeneration. The Translational potential of this article As one of the important causes of low back and leg pain, intervertebral disc degeneration brings a huge economic burden to the society, family and medical system. Therefore, understanding the molecular and cellular mechanisms of intervertebral disc degeneration is of great significance for guiding clinical treatment. In this study, methylated RNA immunoprecipitation with next-generation sequencing on mice lumbar nucleus pulposus tissues found that differentially expressed genes and changes in the expression of related methylases, confirming that RNA methylation is involved in intervertebral disc degeneration. The process provides new vision and clues for future research on intervertebral disc degeneration.
Pressure overload induces cardiac hypertrophy through activation of Janus kinase 2 (Jak2), however, the underlying mechanisms remain largely unknown. In the current study, we tested whether histone deacetylase 2 (HDAC2) was involved in the process. We found that angiotensin II (Ang-II)-induced re-expression of fetal genes (Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)) in cultured cardiomyocytes was prevented by the Jak2 inhibitor AG-490 and HDAC2 inhibitor Trichostatin-A (TSA), or by Jak2/HDAC2 siRNA knockdown. On the other hand, myocardial cells with Jak2 or HDAC2 over-expression were hyper-sensitive to Ang-II. In vivo, pressure overload by transverse aorta binding (AB) induced a significant cardiac hypertrophic response as well as re-expression of ANP and BNP in mice heart, which were markedly reduced by AG-490 and TSA. Significantly, AG-490, the Jak2 inhibitor, largely suppressed pressure overload-/Ang-II-induced HDAC2 nuclear exportation in vivo and in vitro. Meanwhile, TSA or HDAC2 siRNA knockdown reduced Ang-II-induced ANP/BNP expression in Jak2 over-expressed H9c2 cardiomyocytes. Together, these results suggest that HDAC2 might be a downstream effector of Jak2 to mediate cardiac hypertrophic response by pressure overload or Ang-II.
Study Design Retrospective study. Objective To analyze the causes of and factors influencing early recurrence after TELD performed in the treatment of lumbar disc herniation. Methods We included 285 patients with single-segment lumbar disc herniation treated using transforaminal endoscopy lumbar discectomy TELD from January 2017 to December 2019 at the First Affiliated Hospital of the University of South China. Patients were classified into early recurrence and non-early recurrence groups based on clinical symptoms and MRI reexamination. Imaging data (eg, disc height index (DHI), Pfirrman grades, base width, postoperative annulus-fibrosus tear size, cross-sectional area of the foramen (CSAF), etc.)were analyzed, and multivariate, binomial logistic regression was utilized to determine which factors were associated with early recurrence after TELD. Results A total of 285 patients completed surgery and clinical follow-up, during which 19 patients relapsed within 6 months postsurgery, for an early recurrence rate of 6.7%. There were statistically significant differences between DHI, Pfirrman grades, base width, postoperative annulus-fibrosus tear size, herniation sites, CSAF and Modic changes between the early recurrence and non-early recurrence groups (P < .05). On multivariate logistic regression,the degree of disc degeneration (OR = .747, P = .037), CSAF (OR = 5.255, P = .006), degree of Modic change (OR = 1.831, P = .018) and base width of the herniation (OR = 4.942, P = .003) were significantly correlated with early recurrence after TELD. Conclusions Postoperative annulus-fibrosus tear size, DHI, and location of the disc herniation were associated with early recurrence after TELD. Increased base width of the herniation, severe disc degeneration, decreased CSAF and Modic change were risk factors for early recurrence after TELD.
3D-printed porous implants have been attracting increased attention. Although pore size is thought to be an important factor affecting the biocompatibility of implants, there is still no accurate conclusion about the optimal pore size of implants. In searching the relevant literature, it was found, that the pore size of implants is not clearly defined in many studies. Additionally, the definition methods are different in a few studies, that have clearly defined the apertures. In the current review, the definitions of pore size in different experiments are summarized and the factors affecting the definitions are analyzed, to provide an important framework for future research and design.
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