CDC20, TOP2A and NEK2 Expression in Esophageal Squamous Cell Carcinoma and Its Clinical Significance

Objective: to study the expression and clinical significance CDC20,TOP2A, NEK2 esophageal squamous cell carcinoma. Methods: Toselect 70 patients with esophageal squamous cell carcinoma, Between August 2018 - August 2020, All intraoperative pathological specimens,A group -35 cases), Cancer tissue, B group, adjacent tissues), two groups of CDC20, TOP2A, NEK 2 expression were detected and analyzed by immunohistochemistry and semi-quantitative reverse transcription polymerase chain reaction -RT-PcR) assay.Results: the values of CDC20,TOP2A, NEK2 expression level in A group were significantly higher thanthose in B group -P<0.05). The expression level CDC20, TOP2A, NEK2esophageal squamous cell carcinoma was positively correlated with TNMstage and lymphatic metastasis, and negatively correlated with tumordifferentiation. Conclusion: CDC20, TOP2A, NEK2 high expression leveldirectly affects the metastasis, recurrence and prognosis of esophagealsquamous cell carcinoma. The combination of three indexes can accuratelyevaluate the pathological status of patients with esophageal squamous cellcarcinoma and help to judge the prognosis of patients accuratel

A Small Amount of Dietary Carbohydrate Can Promote the HFD-Induced Insulin Resistance to a Maximal Level

Both dietary fat and carbohydrates (Carbs) may play important roles in the development of insulin resistance. The main goal of this study was to further define the roles for fat and dietary carbs in insulin resistance. C57BL/6 mice were fed normal chow diet (CD) or HFD containing 0.1–25.5% carbs for 5 weeks, followed by evaluations of calorie consumption, body weight and fat gains, insulin sensitivity, intratissue insulin signaling, ectopic fat, and oxidative stress in liver and skeletal muscle. The role of hepatic gluconeogenesis in the HFD-induced insulin resistance was determined in mice. The role of fat in insulin resistance was also examined in cultured cells. HFD with little carbs (0.1%) induced severe insulin resistance. Addition of 5% carbs to HFD dramatically elevated insulin resistance and 10% carbs in HFD was sufficient to induce a maximal level of insulin resistance. HFD with little carbs induced ectopic fat accumulation and oxidative stress in liver and skeletal muscle and addition of carbs to HFD dramatically enhanced ectopic fat and oxidative stress. HFD increased hepatic expression of key gluconeogenic genes and the increase was most dramatic by HFD with little carbs, and inhibition of hepatic gluconeogenesis prevented the HFD-induced insulin resistance. In cultured cells, development of insulin resistance induced by a pathological level of insulin was prevented in the absence of fat. Together, fat is essential for development of insulin resistance and dietary carb is not necessary for HFD-induced insulin resistance due to the presence of hepatic gluconeogenesis but a very small amount of it can promote HFD-induced insulin resistance to a maximal level

Machine Learning-Based Investigation on the Impact of Chinese Venture Capital Institutions&rsquo; Performance: Evaluation Factors of Venture Enterprises to Venture Capital Institutions

Studying the influencing factors of venture capital fund investment performance is crucial for the decision making of venture capital institutions. This paper explored the influencing factors of venture capital institutions from the perspective of startups, aiming to elucidate the mechanisms of these factors on the performance of venture capital funds and to propose a novel and effective predictive model of investment performance. Linear regression and one-way ANOVA were used to analyze the influence of each variable on investment performance, and the weight proportion of each influencing factor was obtained under the linear model. Two machine learning models, including the random forest algorithm and extreme learning machine algorithm, are established, and the particle swarm algorithm and machine learning algorithm were combined to optimize the random parameters in the two models. Compare the reliability and accuracy of machine learning models and multivariate linear regression models. The analysis results indicate that the PSO-ELM hybrid model has a better predictive performance than other prediction models. A convenient machine learning algorithm provided in this paper can quickly and effectively predict the investment performance of various investment portfolios and provide investors with decision-making assistance

A small amount of dietary carbohydrate can promote the HFD-induced insulin resistance to a maximal level.

Both dietary fat and carbohydrates (Carbs) may play important roles in the development of insulin resistance. The main goal of this study was to further define the roles for fat and dietary carbs in insulin resistance. C57BL/6 mice were fed normal chow diet (CD) or HFD containing 0.1-25.5% carbs for 5 weeks, followed by evaluations of calorie consumption, body weight and fat gains, insulin sensitivity, intratissue insulin signaling, ectopic fat, and oxidative stress in liver and skeletal muscle. The role of hepatic gluconeogenesis in the HFD-induced insulin resistance was determined in mice. The role of fat in insulin resistance was also examined in cultured cells. HFD with little carbs (0.1%) induced severe insulin resistance. Addition of 5% carbs to HFD dramatically elevated insulin resistance and 10% carbs in HFD was sufficient to induce a maximal level of insulin resistance. HFD with little carbs induced ectopic fat accumulation and oxidative stress in liver and skeletal muscle and addition of carbs to HFD dramatically enhanced ectopic fat and oxidative stress. HFD increased hepatic expression of key gluconeogenic genes and the increase was most dramatic by HFD with little carbs, and inhibition of hepatic gluconeogenesis prevented the HFD-induced insulin resistance. In cultured cells, development of insulin resistance induced by a pathological level of insulin was prevented in the absence of fat. Together, fat is essential for development of insulin resistance and dietary carb is not necessary for HFD-induced insulin resistance due to the presence of hepatic gluconeogenesis but a very small amount of it can promote HFD-induced insulin resistance to a maximal level

Dietary carb is not necessary for the HFD-induced oxidative stress.

<p>Levels of GSH/GSSG ratio, MnSOD activity, malondialdehyde (MDA) in liver (<b>A, C, E</b>) and gastrocnemius (<b>B, D, F</b>) of the mice described in Fig. 1 were measured and normalized to protein levels of the same samples as detailed in “<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0100875#s2" target="_blank">Methods and Materials</a>”. Results represent results of mean ± SD of 10 animals per group. *: P<0.05 vs. CD. **: P<0.01 vs. CD. #: P<0.05 vs. HFD +0.1% carbs. ##: P<0.01 vs. HFD +0.1% carbs. $$: P<0.01 vs. HFD +5% carbs.</p

Dietary carb is not necessary for the HFD-induced insulin resistance but a small amount of it can induce a maximal level of insulin resistance in mice on HFD.

<p>(<b>A</b>) Fasting blood glucose was measured once a week after an 8-hour fast. (<b>B</b>) Plasma level of insulin was evaluated at the end of the 5-week experiment after an 8 hour fast. (<b>C–D</b>) Insulin tolerance test (ITT) was performed at the end of the 5-week experiment after an 8 hour fast and the area under curve was calculated. Results represent mean ± SD of 8 mice/group. *: P<0.05 vs. CD. **: P<0.01 vs. CD. #: P<0.05 vs. HFD +0.1% carbs. ##: P<0.01 vs. HFD +0.1% carbs. $$: P<0.01 vs. HFD +5% carbs. ++: P<0.01 vs. HFD +10% carbs.</p

Dietary carbohydrates (carbs) are not necessary for the high fat diet (HFD)-mediated body weight gain but can promote the HFD-mediated weight gain in a dose-dependent manner.

<p>C57BL/6 (B6) mice were fed the regular chow diet (CD) <i>ad libitum</i> or HFD plus 0.1%, 5%, 10% or 25.5% carbs for 5 weeks. (A–B) Food and calorie intakes were recorded weekly. The ratio of food calories over body weight daily was calculated. *: P<0.05 CD vs. either HFD +5% carbs or HFD +10% carbs. **: P<0.01 vs. CD. ##: P<0.01 vs. HFD +0.1% carbs. $$: P<0.01 HFD +5$$: P<0.01 HFD +5% carbs vs. HFD +25.5% carbs. &: P<0.05 HFD +10% carbs vs. HFD +25.5% carbs. (D) Epididymis fat pads were collected and weighed. The ratio of epididymis fat over body weight was calculated. Results represent mean ± SD of 10 mice/group. **: P<0.01 vs. CD. ##: P<0.01 vs. HFD +0.1% carbs. $$: P<0.01 vs. HFD +5% carbs. ++: P<0.01 vs. HFD +10% carbs.</p

Dietary carb is not necessary for the HFD-induced insulin resistance.

<p>At the end of the 5-week experiment, animals were fasted for 8 h. Liver (<b>A</b>) and skeletal muscle samples (<b>B</b>) were collected promptly after animals were sacrificed. Levels of total and phosphorylated IRS1, total and phosphorylated Akt, total and phosphorylated mTOR, and β-actin were detected with immunoblotting. The level of each target protein was quantified and normalized to control. The average of 3 mice was set at 1. Results were presented as mean ± SD of 6 animals/group for Akt and 3 animals for IRS1. *: P<0.05 vs. no acute insulin treatment in control. **: P<0.01 vs. no acute insulin treatment in control.</p

Inhibition of hepatic gluconeogenesis prevented the HFD-induced insulin resistance.

<p>(<b>A</b>) Levels of key hepatic gluconeogenic genes (PEPCK and glucose-6-phosphatase (G6P) were measured by using RT-PCR as detailed in “<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0100875#s2" target="_blank">Methods and Materials</a>”. Results represent mean ± SD of 4 mice per group. *: P<0.05 vs. CD. #: P<0.05 vs. HFD +0.1% carbs. (<b>B</b>) B6 mice were fed either the regular chow diet (CD) <i>ad libitum</i> or HFD plus 0.1% carbs for 5 weeks. Some mice were treated with adenoviral shRNA against p300 (10⁹ pfu/mouse) or the control shRNA at the beginning of week 5. After an 8 h fast, IIT was performed. Protein levels of p300 in liver were verified by using immunoblotting. Results represent mean ± SD of 5 mice per group. *: P<0.05 vs. CD. #: P<0.05 vs. HFD + shRNAp300 or CD.</p