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The results showed injury of aortic endothelium, along with reductions of the concentration of nitric oxide and generation of VEGF in diabetic rats. However, β-hydroxybutyrate treatment attenuated diabetic injury of the endothelium and up-regulated the generation of VEGF. Furthermore, β-hydroxybutyrate treatment caused marked total protein β-hydroxybutyrylation and significant elevation of H3K9bhb content in the aorta of diabetic rats. The ability of β-hydroxybutyrate to protect against diabetic injury of the aortic endothelium was greatest for its intermediate concentration. In conclusion, moderately elevated β-hydroxybutyrate could antagonize aortic endothelial injury, potentially by causing H3K9bhb to promote generation of VEGF in diabetic rats.The jugular ganglion (JG) contains sensory neurons of the vagus nerve which innervate somatic and visceral structures in cranial and cervical regions. In this study, the number of sensory neurons in the human JG was investigated. And, the morphology of sensory neurons in the human JG and nodose ganglion (NG) was compared. The estimated number of JG neurons was 2721.8-9301.1 (average number of sensory neurons ± S.D. = 7975.1 ± 3312.8). There was no significant difference in sizes of the neuronal cell body and nucleus within the JG (cell body, 1128.8 ± 99.7 μ m2; nucleus, 127.7 ± 20.8 μ m2) and NG (cell body, 963.8 ± 225.7 μ m2; nucleus, 123.2 ± 32.3 μ m2). These findings indicate that most of sensory neurons show the similar morphology in the JG and NG. Our immunohistochemical method also demonstrated the distribution of ion channels, neurotransmitter agents and calcium-binding proteins in the human JG. Numerous JG neurons were immunoreactive for transient receptor potential cation channel subfamily V member 1he external auditory canal. It is likely that sensory neurons in the human JG can transduce nociceptive and mechanoreceptive information from the external auditory canal. Theses neurons may be also associated with neurogenic inflammation in the external auditory canal and ear-cough reflex through the vagus nerve.Objective Considering the association of macrophage migration inhibitory factor with development of prostate diseases, this study aims to explore the effect and mechanism of macrophages (MAs) in inflammation and proliferation of benign prostate hyperplasia (BPH) cells. Methods Totally 85 prostate tissues (75 from BPH patients and 10 from brain death patients) were collected for determination of biomarkers of T lymphocyte (CD4 and CD8), B lymphocyte (CD20) and MAs (CD68), as well as androgen receptor (AR) and CD40/CD40L. MAs stimulated by phorbol myristate acetate (PMA) were cultured with BPH cells (BPH-1), followed by AR inhibitor or anti-CD40 L antibody treatment. Proliferation and cell apoptosis were observed by MTT assay, colony formation assay and flow cytometer. Expressions of apoptotic related proteins and MAPK signaling pathway-related proteins were determined by qRT-PCR and Western blot. Results BPH tissues had increased expressions of AR, CD40 and CD40 L, as well as elevated expressions of inflammation biomarkers (CD4, CD8, CD20 and CD68) in comparison to normal prostate tissues. MAs could increase the expressions of lymphocytes and inflammation biomarkers, in addition to promoting cell proliferation and inhibiting cell apoptosis. Cell proliferation and inflammation reaction could be attenuated by anti-CD40 L antibody and AR inhibitor in a concentration dependent manner through inhibiting the phosphorylation of JNK, ERK1/2 and p38. Conclusion MAs regulate AR and CD40/CD40L expression to promote the inflammation and proliferation as well as inhibiting apoptosis of BPH-1 cells through activation of the MAPK signaling pathway. This conclusion may provide a therapeutic strategy for BPH patients.The developmental changes of Sertoli cells were examined and described in the freshwater pearl mussel Margaritifera laevis using light and transmission electron microscopy. Sertoli cells, which are located on the basal lamina of acini in the testis, include a large number of glycogen granules, electron-dense globules, lipid droplets, and sperm morulae. Electron-dense globules are the vacuoles into which the electron-dense material is condensed. In aging Sertoli cells, the content of the globules leaks out to the extracellular area. Large lipid droplets are formed by the deposition of smaller lipid droplets into a vacuole. After the disruption of the Sertoli cell, the lipid droplets are discharged to the extracellular area and fuse with to form a larger mass. The spermatogonia which were engulfed by the Sertoli cells begin to condense their chromatin and transform themselves into sperm morulae. The constituent cells of the sperm morulae proliferate and finally differentiate into the spermatozoa. After the disruption of the Sertoli cell, the spermatozoa produced from the sperm morulae are released into the acinus lumen. Numerous matured spermatozoa in the acini gather around the large lipid droplet, to form the sperm sphere. The completed sperm spheres are subsequently released through the exhalant siphon into the stream.Oral-Facial-Digital type I (OFD1) is a rare inherited form of renal cystic disease associated with ciliary dysfunction. This disorder is due to mutations in the OFD1 gene that encodes a protein localized to centrosomes and basal bodies in different cell types. Immunofluorescence analysis demonstrated that OFD1 displays a dynamic distribution during cell cycle. Taurocholic acid High-content microscopy analysis of Ofd1-depleted fibroblasts revealed impaired cell cycle progression. Immunofluorescence analysis and cell proliferation assays also indicated the presence of a variety of defects such as centrosome accumulation, nuclear abnormalities and aneuploidy. In addition, Ofd1-depleted cells displayed an abnormal microtubule network that may underlie these defects. All together our results suggest that OFD1 contributes to the function of the microtubule organizing center (MTOC) in the cell, controlling cell cycle progression both in vitro and in vivo.Deltex-3-like (DTX3L), an E3 ligase, which is also known as B-lymphoma and BAL-associated protein (BBAP), is a member of the Deltex (DTX) family and was originally identified as a binding partner of diphtheria-toxin-like ADP-ribosyltransferase-9 (ARTD9). The present study found that DTX3L and ARTD9 were upregulated in synovial tissues obtained from rheumatoid arthritis (RA) patients compared with those from the controls. Healthy synovial tissues were obtained by arthroscopic biopsy from patients with meniscus injury (n = 10 samples) without a history of RA in the Orthopedic Department of the Affiliated Hospital of Nantong University. FLSs were isolated from RA patients who underwent total knee arthroplasty. We performed dual immunofluorescence staining on DTX3L and ARTD9, and these data strongly demonstrated that DTX3L and ARTD9 were colocalized with fibroblast-like synoviocytes (FLSs) in patients with RA. Furthermore, Western blot assays were performed to confirm that the expression levels of DTX3L and ARTD9 in the FLSs increased in a time-dependent manner and peaked at 24 h after TNF-α stimulation.
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