In vitro effects of ethanol (0.1-2.0%,v/v) on canine vasculer smooth muscle were studied. Ethanol dose-dependently produced inhibition in both the amplitude and frequency of the spontaneous rhythmic activity of the canine hepatic portal vein, and at concentration of 1.0 +/- 0.2% completely abolished the spontaneous activity. Ethanol evoked dose-dependent constriction, rather than dilatation, in all vascular smooth muscles tested, including femoral, renal, common carotid, and pulmonary arteries, and external jugular, splenic, pulmonary, femoral, renal, and hepatic portal veins. The vasoconstriction effect of ethanol was much stronger on arteries than on the corresponding veins. Based on the contractile tension developed by ethanol, the femoral artery or the external jugular vein appeared to be most sensitive to ethanol among the arteries or veins preparations tested. The present results suggested that ethanol, depending on concentration, may either enhance or decrease excitability of vascular smooth muscles. There were also regional differences of effects of ethanol on canine blood vessels.
Long stress-induced noncoding transcripts 5 (LSINCT5) has been reported to be upregulated in several human cancers and related to poor prognosis. However, its involvement in esophageal squamous cell carcinoma (ESCC) remains largely unknown. We aim to evaluate the expression and putative role of LSINCT5 on the progression of ESCC.LSINCT5 expression was first examined in the ESCC cell lines using RT-qPCR, and the next-generation RNA-Seq technology was employed to analyze and functionally annotate the differential gene expression before and after LSINCT5 knockdown in ESCC was made. Based on the functional annotation results, the effects of LSINCT5 knockdown on cell growth, migration, invasion, and epithelial-to-mesenchymal transition (EMT) were assessed in the ESCC cell lines. Finally, the expression and clinicopathological significance of LSINCT5 in ESCC and corresponding nontumor tissues were further explored using RT-qPCR.The RT-qPCR results showed that LSINCT5 expression was significantly upregulated in the ESCC cell lines. The differential gene expression analysis by next-generation RNA-Seq showed that 138 genes were up-regulated, and 227 genes were downregulated after LSINCT5 was knocked down in the ECA 109 cells. In addition, the functional annotation revealed that the differentially expressed genes were mainly functionally involved in tight junctions, ECM-receptor interactions, and MAPK signaling pathway. Further in vitro studies indicated that the knockdown of LSINCT5 significantly suppressed proliferation, migration, invasion, and EMT in ESCC cells. Finally, a comparative study of paired ESCC and corresponding nontumor tissues showed that LSINCT5 was upregulated in the ESCC tissues, and the increased LSINCT5 expression was related to late clinical stages, large tumor sizes, and lymph node metastasis.The results indicate that LSINCT5 is upregulated in ESCC and may act as an oncogene promoting the progression of ESCC.
The coexistence of neuropeptides and amine transmitters in the same neuron and the presence of postsynaptic receptors for these compounds invite speculation that the compounds may interact postsynaptically. To study this interaction, we selected the synapse between the splanchnic nerve and the chromaffin cells of adrenal medulla because the splanchnic nerve contains acetylcholine and neuropeptides (multiple molecular forms of enkephalin-like peptides), while the membranes of chromaffin cells contain receptors for acetylcholine and opiate peptides. When the opiate receptors are occupied by specific agonists, these agonists inhibit the expression of acetylcholine receptors. Both the acetylcholine binding and catecholamine release by acetylcholine were inhibited. It is suggested that peptides and acetylcholine coexisting in the splanchnic nerve might act as cotransmitters, there by modulating the sensitivity of acetylcholine receptors. Multiple molecular forms of enkephalin-like peptides are stored in chromaffin cells and are released by acetylcholine. A role for the opiate receptors in the modulation of the secretion of opiate peptides stored in chromaffin cells is not evident.
LncRNAs HULC has been reported to be important regulators in the development of various human diseases. However, the role of HULC in bone mesenchymal stem cells (BMSCs) remains unclear. The present study aimed to explore the regulatory effect of HULC on proliferation and osteogenic differentiation of BMSCs and the underlying mechanism.The expression of HULC and miR-195 in BMSCs were altered by transfection and measured by qRT-PCR. Cell viability was measured by the CCK-8 assay. Osteogenic differentiation of BMSCs was determined by evaluation of osteogenic markers (Ocn, ALP, Runx2, and Col-1) expression levels using Western blot and qRT-PCR. Furthermore, Western blot was performed to assess the expression of proliferation-related factors, Wnt/β-catenin and p38MAPK pathway-related factors.HULC overexpression significantly increased cell viability, down-regulated p21 expression but up-regulated CyclinD1 expression, and promoted the levels of osteogenic markers. However, the complete opposite effect was observed in HULC knockdown. Notably, miR-195 expression was negatively regulated by HULC and miR-195 exerted a reversed effect of HULC on BMSCs. Moreover, miR-195 mediated the regulatory effect of HULC on BMSCs proliferation and osteogenic differentiation, as miR-195 mimic abolished the effect of HULC overexpression on BMSCs. We also found that HULC overexpression enhanced the activation of Wnt/β-catenin and p38MAPK pathway through down-regulating miR-195.We revealed that HULC promoted proliferation and osteogenic differentiation of BMSCs. The potential mechanism might be involved in its negative regulation on miR-195 and enhanced activation of Wnt/β-catenin and p38MAPK pathway.
Four hundred autopsy cases of malignant tumors were analysed. Of these 321 cases (80.3%) had carcinoma and 79 (19.7%) sarcoma. In the 79 cases, 65 had malignant lymphoma, and 14 (3.5%) soft tissue and bone tumor. The tumor cells metastatic to the lung and liver were common in the autopsy cases. There were 163 cases of metastatic tumors in the lung and liver respectively (40.5%). The metastatic tumor in the liver was mainly from the breast, large intestinal, ovary, stomach and NHL, and in the lung mainly from the breast, liver, NHL, stomach and ovary. The lymph node metastasis was mainly located in the neck, mediastina, aorta. The extensive metastatic tumors were lung cancer, gastric cancer, breast cancer and NHL, However, carcinoma in uterus cervix, urinary bladder, pharynex and testis was mainly infiltrated in the original region. The tumor metastasis was related to the region, histologic type and differentiation and so on.
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