Progress on the study of nucleosome reorganization during cellular reprogramming.

Cellular reprogramming is the process during which epigenetic markers of nuclear genome are deleted and remodeled during sperm-egg binding or nuclear transplantation, thereby rendering differentiated cells totipotent. The main cellular reprogramming methods are cell fusion, somatic cell nuclear transplantation, and induced pluripotent stem cells. Nucleosomes are the basic structural and functional units of chromatin, and nucleosome localization has an important role in regulating gene expression and the state of the cell. The occupancy and location of nucleosomes also change dramatically during cellular reprogramming, while the occupancy of nucleosomes around the transcriptional start site also decreases to promote the expression of pluripotency genes. In this review, we summarize the role of nucleosome localization in gene activation and repression, chromatin remodeling, and transcription factor recognition, with the aim of providing an important basis for an in-depth analysis of cellular reprogramming mechanisms.

Activation of AMPK participates hydrogen sulfide-induced cyto-protective effect against dexamethasone in osteoblastic MC3T3-E1 cells.

Long-time glucocorticoids (GCs) usage causes osteoporosis. In the present study, we explored the potential role of hydrogen sulfide (H2S) against dexamethasone (Dex)-induced osteoblast cell damage, and focused on the underlying mechanisms. We showed that two H2S-producing enzymes, cystathionine ß-synthase (CBS) and cystathionine γ-lyase (CSE), were significantly downregulated in human osteonecrosis tissues as well as in Dex-treated osteoblastic MC3T3-E1 cells. H2S donor NaHS as well as the CBS activator S-adenosyl-l-methionine (SAM) inhibited Dex-induced viability reduction, death and apoptosis in MC3T3-E1 cells. NaHS activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling, which participated its cyto-protective activity. AMPK inhibition by its inhibitor (compound C) or reduction by targeted-shRNA suppressed its pro-survival activity against Dex in MC3T3-E1 cells. Further, we found that NaHS inhibited Dex-mediated reactive oxygen species (ROS) production and ATP depletion. Such effects by NaHS were again inhibited by compound C and AMPKα1-shRNA. In summary, we show that H2S inhibits Dex-induced osteoblast damage through activation of AMPK signaling. H2S signaling might be further investigated as a novel target for anti-osteoporosis treatment.

[Arthroscopic assistance of latissimus dorsi tendon transposition for the treatment of unrepairable rotator cuff tear].

OBJECTIVE: To explore clinical effect of arthroscopy-assisted rotator cuff tendon transfer in treating irreparable rotator cuff tears (IRCT). METHODS: From May 2015 to May 2018, 23 patients with unrepairable rotator cuff tears were treated with arthroscopy-assisted rotator cuff tendon transfer, and 21 patients were followed up finally, including 8 males and 13 females, aged from 48 to 82 years old with an average of(64.3±9.1) years old;the courses of disease ranged from 6 to 36 months with an average of (14.0±6.4) months. American Rotator and Elbow Surgeons Score(ASES) and Constant-Murley score were used to evaluate clinical efficacy before surgery and at the latest follow-up. RESULTS: All 21 patients were followed up for 36 to 54 months with an average of (39.4±4.4) months. Axillary incision of 1 patient was redness, swelling and exudation after surgery, which healed after 3 weeks of dressing change, and exudate culture was negative. At the latest follow-up, MRI showed partial tearing of the metastatic tendon in 2 patients, but pain and movement of the affected shoulder were still better than before surgery. ASES increased from preoperative (41.0±9.6) scores to the latest follow-up (75.6±14.0) scores, and had statistical difference (t=10.50, P<0.01). Constant-Murley score increased from (49.8±7.1) scores before operation to (67.5±11.6) scores at the latest follow-up (t=11.27, P<0.01). CONCLUSION: Arthroscopic assisted latissimus dorsalis tendon transposition restores physiological and anatomical structure of glenohumeral joint by reconstructing balance of horizontal and vertical couples of shoulder joint, thus achieving the stability of the shoulder joint, relieving shoulder pain and improving shoulder joint function.

Expression changes of transforming growth factor-beta1 and thrombospondin-1 in cavernous tissues of diabetic rats.

OBJECTIVE: To assess transforming growth factor-beta1 (TGF-beta1) and thrombospondin-1 (TSP-1) expression in the cavernous tissue of rats with streptozotocin (STZ)-induced diabetes. MATERIALS AND METHODS: Twenty male Sprague-Dawley rats were randomly divided into 2 groups: diabetics and controls. We injected STZ intraperitoneally to induce diabetes, and studied the alterations in TGF-beta1 and TSP-1 expression in the cavernous tissue of the 2 groups by immunohistochemistry and real-time quantitative reverse transcription polymerase chain reaction. HE staining was also applied to determine morphological changes. Weight, blood sugar and urine sugar were measured before and after model induction in both groups. RESULTS: Expression of TGF-beta1 and TSP-1 increased significantly in the cavernous tissue of the diabetic rats compared to the control group. CONCLUSIONS: TGF-beta1 and TSP-1 expression changes in cavernous tissues may play an important role in diabetic erectile dysfunction.

[Anterior instrumentation for the treatment of tuberculotic spinal deformity].

OBJECTIVES: To summarize the clinical results in the treatment of spinal tuberculosis with debridement, bone grafting and anterior fixation and to evaluate the safety and the value of this procedure. METHODS: From June 1997 to May 2001, 18 patients with spinal tuberculosis were treated using anterior debridement, autograft of bone and primary internal instrumentation. They were 8 men and 10 women, aged from 25 to 59 years (mean 41 years). The degree of kyphosis before surgery was 27.0 degrees to 75.5 degrees (mean 47.5 degrees +/- 11.4 degrees ). The involved spines included cervical spine (1 patient), thoracic spine (10), thoracic-lumbar spine (2), and lumbar spine (5). Average 2.8 intervertebral bodies in each patient were afflicted with tuberculosis disease. Spinal fusions were done with iliac bone grafts. RESULTS: All patients were followed up for an average of 25 months. No deep wound infection and sinus were observed after surgery. The grafted bones were fused in all patients with an average time of 3.6 months. The degree of spine kyphosis correction was 32.7 degrees +/- 8.3 degrees, and 3.2 degrees +/- 2.8 degrees was lost on average in the late stage. CONCLUSION: Anterior instrumentation for spinal tuberculosis could stabilize the spine, correct kyphosis and fuse the grafted bone.

Effect of siRNA-mediated downregulation of VEGF in Tca8113 cells on the activity of monocyte-derived dendritic cells.

Vascular endothelial growth factor (VEGF) is a tumor angiogenesis factor that is important in immune regulation. In our previous study, we found that VEGF expression in the peripheral blood and neoplasm nest from patients with oral squamous cell carcinoma (OSCC) was positively correlated with the course of disease, while an inverse correlation between VEGF expression and dendritic cells (DCs) was identified in the peripheral blood. Therefore, in the present study, we investigated whether inhibition of human VEGF in the human tongue carcinoma cell line Tca8113 had effects on the activity of monocyte-derived DCs. We knocked down the expression of human VEGF in Tca8113 cells using the small interfering RNA (siRNA) technique. Tca8113 cells pre-transfected with siRNA targeting VEGF were co-cultured with monocyte­derived immature and mature DCs. Cell proliferation was evaluated by a WST-8 assay. Cell apoptosis, cell cycle and cell phenotypes were determined by flow cytometry. The data revealed that downregulation of the human VEGF significantly inhibited the proliferation of Tca8113 cells and increased apoptosis. Inhibition of human VEGF arrested the cell cycle of Tca8113 cells at the G0/G1 phase. Our results showed that the co-culture of DCs with Tca8113 cells markedly inhibited the expression of the mature markers of DCs including HLA-DR, CD80, CD86, CD40 and CD1a, as well as the immature marker CD83, while inhibition of human VEGF in Tca8113 cells significantly reversed these effects. Therefore, human VEGF in Tca8113 cells may not only regulate the cell proliferation and apoptosis of oral squamous cell carcinoma cells, but may also inhibit DC maturation.

[Research on the correlation of vascular endothelial growth factor and dendritic cell in patients with oral squamous cell carcinoma].

OBJECTIVE: To investigate the effect of vascular endothelial growth factor (VEGF) on the differentiation, formation and function of the dendritic cell (DC) in peripheral blood of patients with oral squamous cell carcinoma (OSCC). METHODS: Flow cytometry was used to detect the number of DC in peripheral blood of 81 patients with OSCC, and ELISA applied to test serum VEGF concentration the OSCC patients, and immunohistochemistry used to observe the expression of VEGF in primary foci of 57 patients with OSCC. DC from CD-14 peripheral blood mononuclear cells were cultured with VEGF(165) in vitro to investigate the cytokine's effect on DC. RESULTS: In comparison with controls [(325.70 +/- 117.54) ng/L], the level of serum VEGF [(764.33 +/- 263.64) ng/L] was significantly increased (P < 0.01) and the DC numbers was significantly decreased (P < 0.01) in patients with OSCC. There was a negative correlation between serum VEGF concentration and the level of DC (P < 0.01). The expression of VEGF in primary focus was positively correlated with serum VEGF concentration, but was negatively correlated with the level of peripheral blood DC (P < 0.01). DC cultured in vitro with VEGF(165) decreased the expression of CD-1a, CD-40, CD-80, CD-86, CD-83, HLA-DR, and revealed a lower ability of stimulating T lymphocyte proliferation but a higher ability of uptake, compared to controls. CONCLUSIONS: The overexpressed VEGF in patients with OSCC might be one of the important reasons for blocking the differentiation and maturation of DC.