How tyramine β-hydroxylase controls the production of octopamine, modulating the mobility of beetles

Biogenic amines perform many kinds of important physiological functions in the central nervous system (CNS) of insects, acting as neuromodulators, neurotransmitters, and neurohormones. The five most abundant types of biogenic amines in invertebrates are dopamine, histamine, serotonin, tyramine, and octopamine (OA). However, in beetles, an important group of model and pest insects, the role of tyramine beta-hydroxylase (T beta H) in the OA biosynthesis pathway and the regulation of behavior remains unknown so far. We therefore investigated the molecular characterization and spatiotemporal expression profiles of T beta H in red flour beetles (Triboliun castaneum). Most importantly, we detected the production of OA and measured the crawling speed of beetles after dsTcT beta H injection. We concluded that TcT beta H controls the biosynthesis amount of OA in the CNS, and this in turn modulates the mobility of the beetles. Our new results provided basic information about the key genes in the OA biosynthesis pathway of the beetles, and expanded our knowledge on the physiological functions of OA in insects

Correlation of survivin, p53 and Ki-67 in laryngeal cancer Hep-2 cell proliferation and invasion

AbstractObjectiveTo investigate the mechanism of survivin, p53 and Ki-67 on Hep-2 human laryngeal cancer endothelial cell proliferation and invasion.MethodsLaryngeal squamous cell carcinoma and paracancerous normal tissues were collected, total RNA was extracted from tissues, survivin, p53 and Ki-67 gene mRNA expression levels in laryngeal cancer and the adjacent tissues were detected by Real-time PCR. Human laryngeal cancer Hep-2 epithelial cells were selected, survivin gene was overexpressed, and cell proliferation was detected by MTT. p53 and Ki-67 gene expression changes in overexpressed survivin gene were detected by Western blot. Changes in Hep-2 cell invasive ability were studied when survivin was overexpressed as detected by Transwell invasion assay.ResultsIn the adjacent tissues, survivin, p53 and Ki-67 gene relative expression levels were 1.72 ± 0.9, 13.7 ± 5.7 and 5.7 ± 1.3, respectively; while in cancer tissues, gene relative expression levels were 53.7 ± 8.3, 66.7 ± 5.2 and 61.0 ± 3.1, respectively, which was significantly increased. As detected by MTT, relative cell survival rate within 12 h of survivin overexpression were: load control group (88.5 ± 1.6)%; overexpressed group (90.3 ± 1.9)%. Transwell invasion assay results indicated that overexpressed survivin could significantly increase the relative survival rate of cells.ConclusionsExpressions of p53, Ki67 and survivin are increased in cancer; and there is a positive correlation between survivin, p53 and Ki67 expressions in laryngeal carcinoma

The Impacts of Swimming Exercise on Hippocampal Expression of Neurotrophic Factors in Rats Exposed to Chronic Unpredictable Mild Stress

Depression is associated with stress-induced neural atrophy in limbic brain regions, whereas exercise has antidepressant effects as well as increasing hippocampal synaptic plasticity by strengthening neurogenesis, metabolism, and vascular function. A key mechanism mediating these broad benefits of exercise on the brain is induction of neurotrophic factors, which instruct downstream structural and functional changes. To systematically evaluate the potential neurotrophic factors that were involved in the antidepressive effects of exercise, in this study, we assessed the effects of swimming exercise on hippocampal mRNA expression of several classes of the growth factors (BDNF, GDNF, NGF, NT-3, FGF2, VEGF, and IGF-1) and peptides (VGF and NPY) in rats exposed to chronic unpredictable mild stress (CUMS). Our study demonstrated that the swimming training paradigm significantly induced the expression of BDNF and BDNF-regulated peptides (VGF and NPY) and restored their stress-induced downregulation. Additionally, the exercise protocol also increased the antiapoptotic Bcl-xl expression and normalized the CUMS mediated induction of proapoptotic Bax mRNA level. Overall, our data suggest that swimming exercise has antidepressant effects, increasing the resistance to the neural damage caused by CUMS, and both BDNF and its downstream neurotrophic peptides may exert a major function in the exercise related adaptive processes to CUMS

Glycine ethyl ester hydro­chloride

In the crystal structure of the title compound, C4H10NO2 +·Cl− (systematic name: 3-eth­oxy-3-oxopropan-1-aminium chlor­ide), there are strong inter­molecular N—H⋯Cl, C—H⋯Cl and C—H⋯O hydrogen-bonding inter­actions between the free chloride anion and the organic cation, resulting in a two-dimensional supra­molecular network in the ab plane

Discovering multiple transcripts of human hepatocytes using massively parallel signature sequencing (MPSS)

<p>Abstract</p> <p>Background</p> <p>The liver is the largest human internal organ – it is composed of multiple cell types and plays a vital role in fulfilling the body's metabolic needs and maintaining homeostasis. Of these cell types the hepatocytes, which account for three-quarters of the liver's volume, perform its main functions. To discover the molecular basis of hepatocyte function, we employed Massively Parallel Signature Sequencing (MPSS) to determine the transcriptomic profile of adult human hepatocytes obtained by laser capture microdissection (LCM).</p> <p>Results</p> <p>10,279 UniGene clusters, representing 7,475 known genes, were detected in human hepatocytes. In addition, 1,819 unique MPSS signatures matching the antisense strand of 1,605 non-redundant UniGene clusters (such as <it>APOC1</it>, <it>APOC2</it>, <it>APOB </it>and <it>APOH</it>) were highly expressed in hepatocytes.</p> <p>Conclusion</p> <p>Apart from a large number of protein-coding genes, some of the antisense transcripts expressed in hepatocytes could play important roles in transcriptional interference via a <it>cis</it>-/<it>trans</it>-regulation mechanism. Our result provided a comprehensively transcriptomic atlas of human hepatocytes using MPSS technique, which could be served as an available resource for an in-depth understanding of human liver biology and diseases.</p

Trimebutine Promotes Glioma Cell Apoptosis as a Potential Anti-tumor Agent

Gliomas are the most common primary brain tumors with a usually fatal malignancy. They are associated with a poor prognosis although multiple therapeutic options have been available. Trimebutine is one of the prokinetic agents and it has been mainly used for treatment of disorders of the gastrointestinal (GI) tract such as irritable bowel syndrome. However, its effects on glioma cells remain unknown. Here, we used various concentrations of trimebutine to treat SHG44, U251, and U-87 MG human glioma/glioblastoma cells. And combined experiments of MTT, colony formation assay, and wound healing assay, as well as western blot and immunofluorescence staining were used to evaluate the effects of trimebutine on glioma cells. The results demonstrated that trimebutine significantly inhibited cell viability and colony formation. A significant inhibition of glioma cell migration was also indicated by wound healing assay. In addition, trimebutine promoted cell apoptosis and induced Bcl-2 downregulation, accompanied with Bax upregulation. Both immunofluorescence staining and western blot results showed that trimebutine increased the level of active Caspase-3. Moreover, trimebutine reduced the activation of both AKT and ERK signaling pathways. In subcutaneous U-87 MG cell xenograft tumors in nude mice, trimebutine significantly inhibited tumor growth. More TUNEL-positive apoptotic cells in tumor sections were observed in trimebutine-treated mice when compared to the vehicle control. Reduced Bcl-2 and upregulated Bax, as well as perturbed p-AKT and p-ERK signaling pathways were also observed in trimebutine-treated xenograft tissues. Our combined data indicated that trimebutine may be potentially applied for the clinical management of glioma/glioblastoma

Exploring cellular memory molecules marking competent and active transcriptions

<p>Abstract</p> <p>Background</p> <p>Development in higher eukaryotes involves programmed gene expression. Cell type-specific gene expression is established during this process and is inherited in succeeding cell cycles. Higher eukaryotes have evolved elegant mechanisms by which committed gene-expression states are transmitted through numerous cell divisions. Previous studies have shown that both DNase I-sensitive sites and the basal transcription factor TFIID remain on silenced mitotic chromosomes, suggesting that certain trans-factors might act as bookmarks, maintaining the information and transmitting it to the next generation.</p> <p>Results</p> <p>We used the mouse globin gene clusters as a model system to examine the retention of active information on M-phase chromosomes and its contribution to the persistence of transcriptional competence of these gene clusters in murine erythroleukemia cells. In cells arrested in mitosis, the erythroid-specific activator NF-E2p45 remained associated with its binding sites on the globin gene loci, while the other major erythroid factor, GATA-1, was removed from chromosome. Moreover, despite mitotic chromatin condensation, the distant regulatory regions and promoters of transcriptionally competent globin gene loci are marked by a preserved histone code consisting in active histone modifications such as H3 acetylation, H3-K4 dimethylation and K79 dimethylation. Further analysis showed that other active genes are also locally marked by the preserved active histone code throughout mitotic inactivation of transcription.</p> <p>Conclusion</p> <p>Our results imply that certain kinds of specific protein factors and active histone modifications function as cellular memory markers for both competent and active genes during mitosis, and serve as a reactivated core for the resumption of transcription when the cells exit mitosis.</p

Effects of Dioscorea polystachya \u27yam gruel\u27 on the cognitive function of diabetic rats with focal cerebral ischemia-reperfusion injury via the gut-brain axis

© 2020 Pang et al. Published by IMR press. Focal cerebral ischemia-reperfusion injury is closely related to hyperglycemia and gut microbiota imbalance, while gut microbiota contributes to the regulation of brain function through the gut-brain axis. Previous studies in patients with diabetes have found that \u27yam gruel\u27 is a classic medicated diet made from Dioscorea polystachya, increases the content of Bifidobacterium, regulates oxidative stress, and reduces fasting blood glucose levels. The research reported here investigated the effects of \u27yam gruel\u27 on the cognitive function of streptozotocin-induced diabetic rats with focal cerebral ischemia-reperfusion injury and explored the mechanism underlying the role of the gut-brain axis in this process. \u27Yam gruel\u27 was shown to improve cognitive function as indicated by increased relative content of probiotic bacteria, and short-chain fatty acids in the intestinal tract and cerebral cortex reduced oxidative stress and inflammatory response and promotion of the expression of neurotransmitters and brain-derived neurotrophic factor. Thus, it is concluded that \u27yam gruel\u27 has a protective effect on cognitive function via a mechanism related to the gut-brain axis

Proteomic analysis of sex conversion induced by CPPU in male grapevine of Vitis amurensis

If N-(2-chloro-4-pyridyl)-N′-phenylurea (CPPU) could induce sex conversion in male plants of Vitis amurensis Rupr., this would reduce blindness of selection for male parents according to the fruit characters in cold-tolerant and disease-tolerant grape crossbreeding. Flower bud samples of male plants were treated with 100 mg∙L-1 CPPU at 15 days before anthesis. Two-dimensional gel electrophoresis (2-DE) was used to analyze the proteins related to sex conversion at different development time points. More than 600 protein spots were detected. Among them, 31 differentially expressed proteins were identified by MALDI-TOF/TOF, and 24 protein spots could be assigned to a probable function. Seventeen proteins participated in the sex conversion and with complex interaction. Sex conversion might receive the ROS signal in the beginning, and then pollen tube proteins were proposed to down-regulate to repress the stamen development, while the up-regulated cell elongation protein might promote the development of pistil. Adenine phosphoribosyl transferase 3 was proposed as the key protein in the sex organ conversion that was up-regulated by CPPU in the male V. amurensis achieving the ability to fruit in the end.

Continuous and low-energy 125I seed irradiation changes DNA methyltransferases expression patterns and inhibits pancreatic cancer tumor growth

<p>Abstract</p> <p>Background</p> <p>Iodine 125 (¹²⁵I) seed irradiation is an effective treatment for unresectable pancreatic cancers. However, the radiobiological mechanisms underlying brachytherapy remain unclear. Therefore, we investigated the influence of continuous and low-energy ¹²⁵I irradiation on apoptosis, expression of DNA methyltransferases (DNMTs) and cell growth in pancreatic cancers.</p> <p>Materials and methods</p> <p>For <it>in vitro </it>¹²⁵I seed irradiation, SW-1990 cells were divided into three groups: control (0 Gy), 2 Gy, and 4 Gy. To create an animal model of pancreatic cancer, the SW 1990 cells were surgically implanted into the mouse pancreas. At 10 d post-implantation, the 30 mice with pancreatic cancer underwent ¹²⁵I seed implantation and were separated into three groups: 0 Gy, 2 Gy, and 4 Gy group. At 48 or 72 h after irradiation, apoptosis was detected by flow cytometry; changes in DNMTs mRNA and protein expression were assessed by real-time PCR and western blotting analysis, respectively. At 28 d after ¹²⁵I seed implantation, <it>in vivo </it>apoptosis was evaluated with TUNEL staining, while DNMTs protein expression was detected with immunohistochemical staining. The tumor volume was measured 0 and 28 d after ¹²⁵I seed implantation.</p> <p>Results</p> <p>¹²⁵I seed irradiation induced significant apoptosis, especially at 4 Gy. DNMT1 and DNMT3b mRNA and protein expression were substantially higher in the 2 Gy group than in the control group. Conversely, the 4 Gy cell group exhibited significantly decreased DNMT3b mRNA and protein expression relative to the control group. There were substantially more TUNEL positive in the ¹²⁵I seed implantation treatment group than in the control group, especially at 4 Gy. The 4 Gy seed implantation group showed weaker staining for DNMT1 and DNMT3b protein relative to the control group. Consequently, ¹²⁵I seed implantation inhibited cancer growth and reduced cancer volume.</p> <p>Conclusion</p> <p>¹²⁵I seed implantation kills pancreatic cancer cells, especially at 4 Gy. ¹²⁵I-induced apoptosis and changes in DNMT1 and DNMT3b expression suggest potential mechanisms underlying effective brachytherapy.</p