No abstract

BackgroundLncRNA LINC00461 has been reported to play crucial regulatory roles in a variety of biological processes, including cell migration, cell invasion and cancer progression. However, its biological role in colorectal cancer (CRC) is completely unknown. The aim of our study was to explore the function of LINC00461 on CRC cells and the underlying mechanism.Materials and methodsCRC tumor tissues and cell lines derived from hospital and corporation. The expression level of LINC00461 in CRC tissues and cell lines were analyzed by quantitative real-time PCR (qRT-PCR). The effect of LINC00461 on cell proliferation, colony formation, migration and invasion were detected by CCK-8 assay, colony formation and transwell assay, respectively. In addition, cell apoptosis was analyzed by flow cytometry, and the role of LINC00461 on tumor growth was investigated by tumor xenografts in nude mice. The targets of LINC00461 were predicted by starBase v3.0 and confirmed by a dual-luciferase reporter system. The expression level of transcription factors of nuclear factor I B (NFIB), p21 and CDK2 was determined by Western blot or qRT-PCR. The NFIB expression levels in CRC tissues and mice tumors were analyzed by immunofluorescence assay (IHC).ResultsWe found that the expression of LINC00461 was significantly overexpressed in CRC tissues and different cell lines, and the high level of LINC00461 expression was associated with poor overall survival. Downregulation of LINC00461 expression significantly suppressed the proliferation, migration and invasion of CRC cells and promoted cell apoptosis. We also found that LINC00461 could directly interact with miR-323b-3p. In addition, LINC00461 significantly increased the expression NFIB and CDK2, but, p21 was inhibited. Finally, we found that the growth of tumors in nude mice was suppressed upon LINC00461 deletion.ConclusionWe demonstrated that LINC00461 may play an oncogenic role in CRC cells through NFIB signaling pathway by targeting miR-323b-3p. Our report showed that LINC00461 may be a prognostic biomarker and candidate therapeutic target for CRC.

BACKGROUND Thyroid cancer (TC) is a common malignant tumor in the endocrine system. In recent years, the incidence and recurrence rates of TC have been raising due to increasing work pressure and irregular lifestyles. Thyroid-stimulating hormone (TSH) is a specific parameter for thyroid function screening. This study aims to explore the clinical value of TSH in regulating the progression of TC, so as to find a breakthrough for the early diagnosis and treatment of TC. AIM To explore the value and safety of TSH in the clinical efficacy of patients with TC. METHODS 75 patients with TC admitted to the Department of Thyroid and Breast Surgery of our hospital from September 2019 to September 2021 were selected as the observation group, and 50 healthy subjects were selected as the control group during the same period. The control group was treated with conventional thyroid replacement therapy, and the observation group was treated with TSH suppression therapy. The soluble interleukin (IL)-2 receptor (sIL-2R), IL-17, IL-35 levels, free triiodothyronine (FT 3 ), free tetraiodothyronine (FT 4 ), CD3 + , CD4 + , CD8 + , CD44V6, and tumor supplied group of factor (TSGF) levels were observed in the two groups. The occurrence of adverse reactions was compared between the two groups. RESULTS After treatment with different therapies, the levels of FT 3 , FT 4 , CD3 + , and CD4 + in the observation group and the control group were higher than those before treatment, while the levels of CD8 + , CD44V6, and TSGF were lower than those before treatment, and the differences were statistically significant ( P < 0.05). More importantly, the levels of sIL-2R and IL-17 in the observation group were lower than those in the control group after 4 wk of treatment, while the levels of IL-35 were higher than those in the control group, and the differences were statistically significant ( P < 0.05). The levels of FT 3 , FT 4 , CD3 + , and CD4 + in the observation group were higher than those in the control group, and the levels of CD8 + , CD44V6, and TSGF were lower than those in the control group. There was no significant difference in the overall incidence rate of adverse reactions between the two groups ( P > 0.05). CONCLUSION TSH suppression therapy can improve the immune function of patients with TC, lower the CD44V6 and TSGF levels, and improve serum FT 3 and FT 4 levels. It demo...

Purpose — To explore the immune rejection of xenotransplantation of bone fracture hematoma cells in rabbits.  Way — Lan Tu was used as the donor for allogeneic transplantation of fracture hematoma cells. Twelve New Zealand white rabbits were selected to establish the fracture model. The fracture hematoma cells of Lan Tu were transplanted to the broken end of the experimental group of New Zealand white rabbits, while the rabbits in the control group were not transplanted with allogeneic fracture hematoma cells. To observe the expression level of allogeneic fracture hematoma cells in the fracture site, and to analyze the rejection caused by xenotransplantation by observing the number of macrophages in the fracture model section and lymphoid follicles in the recipient spleen. Result — On the 7th and 12th day after transplantation, the hematoma cells in the fractured end of rabbits in the experimental group showed a decreasing trend, but their survival still met the needs of treatment. The results of immunohistochemical examination on the fractured bone tissue and spleen of the two groups of rabbits showed that there was no significant difference between the macrophage content in the fractured bone tissue and the lymphocyte follicular count in the spleen tissue of the two groups of rabbits in different transplantation time (P > 0.05). Conclusion — Using allogeneic hematoma cell transplantation to treat fractures will not cause excessive rejection of receptors, which is worthy of further clinical discussion and provides a favorable scientific reference for its application in clinical treatment of fractures.

Objective:To observe the changes of cytokines in serum of rabbits with acute pulmonary embolism, and to provide scientific basis for clinical treatment of the disease.Methods: The animal models of pulmonary embolism were established in 26 healthy rabbits by autologous thrombus reinfusion and normal saline injection, and the serum levels of cytokines (TNF-α, IL-1β, HGF) in the two groups were monitored by enzyme-linked immunosorbent assay.Results: The expression levels of serum inflammatory cytokines (TNF-α, IL-1β) increased in both groups of rabbits within 1-3 hours of the acute stage of embolism, but the expression levels of serum inflammatory cytokines in experimental group of rabbits with pulmonary embolism caused by thrombosis increased more obviously；There was no significant change in serum HGF of rabbits before and after embolization in group B. The serum HGF content of experimental rabbits at 1h, 3h, 12h, 24h and 48h after embolization was significantly higher than that before embolization.And in the acute stage of embolism (1-12 hours), it showed a gradual upward trend.Conclusion: The expression level of serum growth factor is different in different acute stages of pulmonary embolism. Detecting serum cytokines in rabbits with acute pulmonary embolism is of great reference significance for improving clinical diagnosis.