升高

The test shows that the bed temperature is gradually reduced along the height of furnace in case of lower volatile matter content in the coal sort,but the temperature of returned material is obviously en- hanced;the bed temperature is entirely increased in the event of increasing the load,but the temperature difference be...

试验表明，煤挥发分含量较低时，床温沿炉膛高度逐渐降低，但返料温度明显升高；负荷提高，床温整体升高，但炉膛底部与中部的温差减小；一次风量增加，会导致烟气从密相区带走的热量大于燃烧放热而使床温降低。

Octadecanoic acid、tetradecanoic acid、hexadecanoic acid、eicosanoic acid、9-octadecenoic acid、9,12,15-Octadecatrienoic acid、5,8,11,14-Eicosatetraenoic acid and 9,12-Octadecadienoic acid were increased dramatically in NASH group (P.05). Moreover,ω-6/ω-3 polyunsaturated fatty acids ratio is raised.

1脂肪酸分析结果提示NASH肝组织中正十二烷酸含量显著降低(P.05)，硬脂酸、十四烷酸、十六烷酸、二十烷酸、油酸、α-亚麻酸、花生四烯酸和亚油酸含量显著升高(P.05)，ω-6：ω-3多不饱和脂肪酸的比值升高。

Results: Compared with sham operation group, the ability of vascular dementia model mouse for learning and memory reduced, which showed extending the time for swimming the whole process, and increasing times of mistakes, and the activity of SOD in hippocamp was decreased and the content of MDA was increased(P.01). Compared with model group, Danggui Shaoyao-San could make the time for swimming the whole process shorten and times of mistakes decreased, and increase the activity of SOD and decrease the content of MDA in hippocamp, which were excellent than that of contrast medicine.

结果：与假手术组比较，模型小鼠学习与记忆能力下降，表现为游全程时间延长，错误次数增加(P.01)，脑海马SOD活性明显降低，MDA含量明显升高(P.01)；与模型组比较，当归芍药散组可使游全程时间缩短，错误次数减少，脑海马SOD活性明显升高，MDA含量明显降低(P.01)，并优于对照药物(P.05)。

The results show that the hyperthyroidism group has elevated levels of choline, glucose and declined levels of VLDL, LDL, cholesterol, lactate, glycoprotein and alanine in serum samples relative to the healthy group. In urine samples, the hyperthyroidism group show increased levels of glucose, citrate, taurine and creatinine as well as decreased levels of hippurate, trimethylamine-N-oxide, formate and succinate.

结果表明，甲亢组血清中的胆碱、葡萄糖和三甲胺等物质的含量升高，而VLDL，LDL和胆固醇等脂质以及乳酸、糖蛋白和丙氨酸等代谢物的含量下降；甲亢组尿液中的葡萄糖、柠檬酸、牛磺酸以及肌氨酸等代谢物的含量升高，而马尿酸、TMAO、甲酸和琥珀酸等代谢物的含量下降。

Results At 2 h after damage in cerebral cortex 5-hydroxyindolecetic acid (5-HIAA) elevated remarkably; At 8 h after da-mage 5-hydroxytryptamine (5-HT), homovanillic acid elevated; but there was no obvious change on norepinephrine and 3,4-dihydroxyphenyl acetic acid.

结果 大脑皮质运动区在损伤后2小时5-羟吲哚乙酸（5-HIAA〕明显升高；8小时后5-羟色胺(5-HT)、高香草酸升高；去甲肾上腺素及3、4-双羟苯乙酸变化不明显。

Results Compared with low-salt diet control group, the renal changes in CsA-L group were not obvious at the 2nd weeks, the urine volume and the level of BUN were remarkably increased in CsA-H group. At the 4th weeks, the urine volume was decreased; the levels of Crea and BUN were significantly increased and showed a significant positive correlation with the blood CsA concentration. Morphologic changes consisted of vacuolization of renal tubular cells, hyalinization of small arterioles and the light renal interstitial fibrosis.

结果 与低盐对照组相比，药后第2周CsA-L组各指标无明显变化，CsA-H组尿量增多，尿蛋白降低，尿素氮升高；药后第4周时，尿量呈减少趋势，肌酐和BUN明显升高，且与CsA血药浓度呈显著正相关，病理表现为肾小管细胞空泡变性及小动脉和肾间质病变，CsA-H组各种变化较CsA-L组更为明显。

All of the antinociceptive effects of CPF in three hyperalgesic models could be reversed by α-FMH (50 mg·kg-1, ip).

使用福尔马林后，小鼠脑和脊髓中NO和PGE2水平升高，而CPF能明显抑制这种升高作用，该抑制作用不被α-FMH所拮抗。

And more, ERK contents between group A and B, group C and D were not dramatically different. The pathological lesions indicated that intestinal tissue necrosis was severe in group C and D, which were graded 3 points, but obviously lessened in group A and B, which was graded 1 point, with ITF interfering. Conclusion: Intestinal inflammation was ameliorated after ITF was injected hypodermically or intraperitoneally.

结果：A、B组组织匀浆中ERK的面密度值各为87.68±19.24、82.65±21.35，较C、D组(30.23±7.79、30.74±8.19)明显升高(P＜0.01)，C、D组与E组(5.41±1.46)比较也有升高(P＜0.05)；并且随著ERK的激活伴随著明显的核转位。A、B组间及C、D组间ERK含量无显著差异(P＞0.05)；病理切片显示C、D组HE染色切片见肠壁损伤轻重不一，可见全肠粘膜绒毛坏死，病理评分的中位积分为3分；A、B组肠上皮细胞少量脱落，顶端绒毛坏死，病理评分的中位积分为1分。

Activation of NF-κB(p65) with evident nuclear translocation was found in neonatal rat NEC model. The pathological lesions indicated that intestinal tissue necrosis in varying degrees in group C and D, which were 2-4 points, but obviously lessened in group E, which were 0-2 points. Conclusions Intestinal inflammation is ameliorated after the ITF is injected hypodermically.

结果 C、D组组织中NF-κB(p65)阳性表达较A、B及E组显著升高P(下标 a.01，E组与A、B组比较也有升高P(下标 a.01，且随NF-κB(p65)的激活有明显的核转移；病理切片示C、D组HE染色见肠壁损伤轻重不一，可见全肠黏膜绒毛坏死，病理评分2~4分；E组轻度肠上皮细胞脱落，顶端绒毛坏死，肠组织病理评分0~2分。

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。