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Background • Chemotherapy-induced peripheral neuropathy (CIPN) is a common troublesome side effect and affects long-term activities of daily living. This neuropathic disorder is still difficult to treat with current clinical treatments. The aim of this study was to investigate and offer an updated perspective of complementary therapies for CIPN. Methods • This review included current databases, including PubMed, Embase, the Cochrane Database, Google Scholar, and Ovid Medline, published up to May 2019 in the English language, to summarize the role of nutrient supplements in CIPN, based on evidence from both animal and clinical studies. Results • A total of 58 studies were included in this review. There were 19 preclinical studies that reported mechanisms of effects and 31 clinical studies corroborated preclinical findings, including 22 randomized controlled trials and 3085 patients with CIPN. Interventions included vitamin E, vitamin B complex, glutamine, acetyl-L-carnitine, alpha lipoic acid, glutathione, omega-3 fatty acids, and calcium/magnesium (Ca2+/Mg2+). The administration of various nutrients remains inconsistent, and limited evidence of effective ones for treating CIPN is available. However, glutamine and omega-3 fatty acids present potential as treatment options for CIPN. The evidence on vitamin E and vitamin B complex is inconclusive, and some forms of vitamin B, such as B6 or B12, await confirmation of their potential to offer protection from CIPN. Less robust evidence was found for nutrients such as acetyl-L-carnitine, α-Lipoic acid, glutathione, and Ca2+/Mg2+ for CIPN. Conclusion • Nutritional therapists seem to recommend nutrient supplements as potential anti-inflammatory and neuroprotective agents for both the prevention and management of CIPN. An understanding of this evolving literature is useful in exploring these therapies with patients who are considering using them. However, their effects against CIPN are still controversial due to the undetermined neuropathic mechanisms of different antineoplastic agents and complex drug interactions. Further research on these agents is warranted. [ABSTRACT FROM AUTHOR]

Background: Although the prognosis of gastric cancer patients have a favorable progression, there are some patients with unusual patterns of locoregional and systemic recurrence. Therefore, a better understanding of early molecular events of the disease is needed. Current evidences demonstrate that long noncoding RNAs (lncRNAs) may be an important class of functional regulators involved in human gastric cancers development. Our previous studies suggest that HOTAIR contributes to gastric cancer development, and the overexpression of HOTAIR predicts a poor prognosis. In this study, we investigated the characteristic of the LncRNA FEZF1-AS1 in gastric cancer. Methods: QRT-PCR was used to detect the expression of FEZF1-AS1 in gastric cancer tissues and cells. MTT assays, clonogenic survival assays and nude mouse xenograft model were used to examine the tumorigenesis function of FEZF1-AS1 in vitro and in vivo. Bioinformatics analysis were used to select downstream target genes of FEZF1-AS1. Cell cycle analysis, ChIP, RIP,RNA Pulldown assays were examined to dissect molecular mechanisms. Results: In this study, we reported that FEZF1-AS1, a 2564 bp RNA, was overexpressed in gastric cancer, and upregulated FEZF1-AS1 expression indicated larger tumor size and higher clinical stage; additional higher expression of FEZF1-AS1 predicted poor prognosis. Further experiments revealed that knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis, whereas endogenous expression FEZF1-AS1 promoted cell growth. Additionally, RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase. ChIP assays demonstrated that LSD1 could directly bind to the promoter of P21, inducing H3K4me2 demethylation. Conclusion: In summary, these data demonstrated that FEZF1-AS1 could act as an "oncogene" for gastric cancer partly through suppressing P21 expression; FEZF1-AS1 may be served as a candidate prognostic biomarker and target for new therapies of gastric cancer patients. [ABSTRACT FROM AUTHOR]

The effect of a copper-embedded barrel on the performance of a helix slow-wave structure (SWS) has been studied theoretically and experimentally. The heat dissipation capability and cold-test characteristics of the SWSs with a monel barrel, a normal copper barrel, and a copper-embedded monel barrel have been analyzed and compared. With its combination of high mechanical strength and good thermal conductivity, the copper-embedded monel barrel enables better heat dissipation capability than the other barrel types and has low RF losses. [ABSTRACT FROM AUTHOR]

The effect of the plated metal film on the heat dissipation capability and cold-test characteristics of the helix slow-wave structure (SWS) have been studied in several experimental tests and computer simulations. The thermal conduction and the power losses of the helix SWS were improved by using a plated helix. A brazed SWS with end-plated rods exhibits excellent heat dissipation capability. The side-plated rods affect the cold-test characteristics of the SWS. [ABSTRACT FROM AUTHOR]

A novel and effective analytical method using ANSYS has been developed for studying the heat-dissipation capability of a helix traveling-wave-tube slow-wave structure (SWS). This method, which is based on calibrating theoretical calculations with experimental data, is able to precisely predict the SWS heat dissipation, thereby reducing material costs and saving time. The consistency and feasibility of this method have been verified by experimental tests on SWSs using copper-plated helices and both BeO and BN support rods. [ABSTRACT FROM AUTHOR]

A new experimental evaluation method is presented for evaluating and comparing the heat dissipation capability of the slow-wave structures (SWSs) of helix traveling-wave tube (TWT). The practicality and simplicity of the evaluation method have been validated through experimental tests in some components with different assembling and processing methods, such as the cold stuffing, the heat shrink, the hot insertion, the molybdenum wrapping methods, and so on. Experimental results demonstrate that our evaluation method can be used effectively and conveniently to estimate and compare the thermal dissipation capability of the SWSs of the helix TWT. [ABSTRACT FROM AUTHOR]

Background: Long noncoding RNAs (lncRNAs) are emerging as key regulators governing fundamental biological processes, and their disorder expression involves in tumorigenesis. SPRY4-IT1 (SPRY4 intronic transcript 1), a lncRNA derived from an intron within SPRY4 gene, involves in multiple cancers development. However, the expression pattern and biological function of SPRY4-IT1 in gastric cancer is still not well documented. Hence, we carried out the present study to investigate the potential role of SPRY4-IT1 in gastric carcinogenesis. Methods: QRT-PCR was performed to detect the expression of SPRY4-IT1 in 61 pairs of gastric cancer samples. Over-expression and RNA interference (RNAi) approaches were used to investigate the biological functions of SPRY4- IT1. The effect of SPRY4-IT1 on proliferation was evaluated by MTT and colony formation assays. Gastric cancer cells transfected with pCDNA-SPRY4-IT1 were injected into nude mice to study the effect of SPRY4-IT1 on tumorigenesis and metastasis in vivo. Protein levels of SPRY4-IT1 targets were determined by western blot or fluorescence immunohistochemistry. ChIP assays were performed to investigate the effect of DNMT1 on SPRY4-IT1 expression. Differences between groups were tested for significance using Student's t test (two-tailed). Results: SPRY4-IT1 expression is decreased in gastric cancer tissues and associated with larger tumor size, advanced pathological stage, deeper depth of invasion and lymphatic metastasis. Patients with lower SPRY4-IT1 expression had a relatively poor prognosis. DNA methylation may be a key factor in controlling the SPRY4-IT1 expression. Furthermore, SPRY4-IT1 contributed to gastric cancer cells metastasis might partly via regulating epithelial-mesenchymal transition (EMT) process. Conclusion: Low expression of SPRY4-IT1 is involved in progression and metastasis of gastric cancer and may represent a novel biomarker of poor prognosis in patients with gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Gastric cancer is the second leading cause of cancer death and remains a major clinical challenge due to poor prognosis and limited treatment options. Long noncoding RNAs (lncRNAs) have emerged recently as major players in tumor biology and may be used for cancer diagnosis, prognosis, and potential therapeutic targets. Although downregulation of lncRNA GAS5 (Growth Arrest-Specific Transcript) in several cancers has been studied, its role in gastric cancer remains unknown. Our studies were designed to investigate the expression, biological role and clinical significance of GAS5 in gastric cancer. Methods: Expression of GAS5 was analyzed in 89 gastric cancer tissues and five gastric cancer cell lines by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Over-expression and RNA interference (RNAi) approaches were used to investigate the biological functions of GAS5. The effect of GAS5 on proliferation was evaluated by MTT and colony formation assays, and cell apoptosis was evaluated by hochest stainning. Gastric cancer cells transfected with pCDNA3.1-GAS5 were injected into nude mice to study the effect of GAS5 on tumorigenesis in vivo. Protein levels of GAS5 targets were determined by western blot analysis. Differences between groups were tested for significance using Student's t-test (two-tailed). Results: We found that GAS5 expression was markedly downregulated in gastric cancer tissues, and associated with larger tumor size and advanced pathologic stage. Patients with low GAS5 expression level had poorer disease-free survival (DFS; P = 0.001) and overall survival (OS; P < 0.001) than those with high GAS5 expression. Further multivariable Cox regression analysis suggested that decreased GAS5 was an independent prognostic indicator for this disease (P = 0.006, HR = 0.412; 95%CI = 2.218-0.766). Moreover, ectopic expression of GAS5 was demonstrated to decrease gastric cancer cell proliferation and induce apoptosis in vitro and in vivo, while downregulation of endogenous GAS5 could promote cell proliferation. Finally, we found that GAS5 could influence gastric cancer cells proliferation, partly via regulating E2F1 and P21 expression. Conclusion: Our study presents that GAS5 is significantly downregulated in gastric cancer tissues and may represent a new marker of poor prognosis and a potential therapeutic target for gastric cancer intervention. [ABSTRACT FROM AUTHOR]

Background Gastric cancer is the second leading cause of cancer death and remains a major clinical challenge due to poor prognosis and limited treatment options. Long noncoding RNAs (IncRNAs) have emerged recently as major players in tumor biology and may be used for cancer diagnosis, prognosis, and potential therapeutic targets. Although downregulation of IncRNA GAS5 (Growth Arrest-Specific Transcript) in several cancers has been studied, its role in gastric cancer remains unknown. Our studies were designed to investigate the expression, biological role and clinical significance of GAS5 in gastric cancer. Methods Expression of GAS5 was analyzed in 89 gastric cancer tissues and five gastric cancer cell lines by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Overexpression and RNA interference (RNAi) approaches were used to investigate the biological functions of GAS5. The effect of GAS5 on proliferation was evaluated by MTT and colony formation assays, and cell apoptosis was evaluated by hochest stainning. Gastric cancer cells transfected with pCDNA3.1 -GAS5 were injected into nude mice to study the effect of GAS5 on tumorigenesis in vivo. Protein levels of GAS5 targets were determined by western blot analysis. Differences between groups were tested for significance using Student's t-test (two-tailed). Results We found that GAS5 expression was markedly downregulated in gastric cancer tissues, and associated with larger tumor size and advanced pathologic stage. Patients with low GAS5 expression level had poorer disease-free survival (DFS; P = 0.001) and overall survival (OS; P < 0.001) than those with high GAS5 expression. Further multivariable Cox regression analysis suggested that decreased GAS5 was an independent prognostic indicator for this disease (P = 0.006, HR = 0.412; 95% CI = 2.218-0.766). Moreover, ectopic expression of GAS5 was demonstrated to decrease gastric cancer cell proliferation and induce apoptosis in vitro and in vivo, while downregulation of endogenous GAS5 could promote cell proliferation. Finally, we found that GAS5 could influence gastric cancer cells proliferation, partly via regulating E2F1 and P21 expression. Conclusion Our study presents that GAS5 is significantly downregulated in gastric cancer tissues and may represent a new marker of poor prognosis and a potential therapeutic target for gastric cancer intervention. [ABSTRACT FROM AUTHOR]

Flavonoids exist extensively in plants, and several biological effects of them have been demonstrated. Wogonin is an important flavonoid compound. In this study, wogonin showed obvious growth inhibition on Bel-7402 cells. The major mechanisms of inhibition included cell apoptosis and cytotoxic effects. Wogonin-induced cell death showed characteristics of apoptosis including DNA fragmentation, chromatin condensation, appearance of apoptotic bodies, and an increase in hypodiploid cells. However, the percentage of necrosis cells also increased with the increase of wogonin concentration. Furthermore, treatment with wogonin caused changes of reactive oxygen species (ROS) and mitochondrial membrane potentials (ΔΨm, MMP), the decrease of the ratio of reduced and oxidized glutathione (GSH/GSSG), cytochrome c release and activation of caspase-9. [ABSTRACT FROM AUTHOR]