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by hyperglycemia
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  高血糖
     Expression of Pax3 and Cx43 in NTD embryos induced by hyperglycemia
     高血糖致畸小鼠胚胎Pax3与Cx43基因的表达及定量研究
短句来源
     Type 2 diabetes mellitus (T2DM) is a common disease characterized by hyperglycemia, insulin resistance, and impaired insulin secretion.
     2型糖尿病(T2DM)是胰岛素抵抗和β细胞分泌缺陷导致高血糖的一种复杂多基因疾病。
短句来源
     Results The rat models were characterized by hyperglycemia,hyperlipemia and hyperinsulinemia which resembled the clinical phenotype of type 2 diabetes.
     结果生化指标结果显示糖尿病大鼠存在高血糖、高血脂和高胰岛素血症,符合2型糖尿病的特征,证明本研究制作的2型糖尿病模型成功。
短句来源
     Uca/Ucr in the diabetic group was significantly higher than that in the control (0.23±0. 21 vs 0. 14±0. 08, P<0. 05), and positively correlated with the concentrations of blood glucose and FRM (r=0. 32 and 0. 41, P<0.05), indicating that bone loss in diabetics relate to hypercalcinuria. Osmotic diuresis caused by hyperglycemia may be one of the major factors for hypercalcinuria.
     NIDDM组的Uca/Ucr明显升高(0.23±0.21比0.14±0.08,P<0.05),并且与血糖和血清果糖胺浓度呈正相关(r=0.32和0.41,P<0.05),提示NIDDM出现骨量降低与高尿钙有关,而且高血糖引起高尿糖状态所致渗透性利尿很可能是高尿钙的主要原因之一。
短句来源
     Objective To explore the relationship between expression of p38MAPK and cerebral ischemia exacerbated by hyperglycemia.
     目的探讨p38MAPK与脑缺血及高血糖脑缺血损害的关系。
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  高血糖引起
     Conclusion: Streptozocin induced hyperglycemia can significantly retard the development of amygdala and PTZ kindling in rats, which mechanism could be related to the functional defects of insulin/insulin receptors in the brain induced by hyperglycemia.
     结论:链脲霉素引起的高血糖延缓大鼠杏仁核和PTZ点燃进程,其机制可能与高血糖引起的脑内胰岛素/胰岛素受体功能缺陷有关。
短句来源
     Uca/Ucr in the diabetic group was significantly higher than that in the control (0.23±0. 21 vs 0. 14±0. 08, P<0. 05), and positively correlated with the concentrations of blood glucose and FRM (r=0. 32 and 0. 41, P<0.05), indicating that bone loss in diabetics relate to hypercalcinuria. Osmotic diuresis caused by hyperglycemia may be one of the major factors for hypercalcinuria.
     NIDDM组的Uca/Ucr明显升高(0.23±0.21比0.14±0.08,P<0.05),并且与血糖和血清果糖胺浓度呈正相关(r=0.32和0.41,P<0.05),提示NIDDM出现骨量降低与高尿钙有关,而且高血糖引起高尿糖状态所致渗透性利尿很可能是高尿钙的主要原因之一。
短句来源
     Conclusion: The increased expression of NF-κB, VEGF and bFGF induced by hyperglycemia is of great significance in early diabetic macrovasculopathy.
     结论:高血糖引起的NF-κB、VEGF及bFGF表达增加在糖尿病早期大血管病变的发生发展中可能有重要意义。
短句来源
     Conclusion The formation and accumulation of AGE in glomeruli is directly related to abnormal alterations in structure and function of glomeruli and is an important link in development of nephropathy by hyperglycemia.
     结论 AGE在肾小球内的大量形成和堆积与肾小球结构和功能的异常改变直接有关 ,是高血糖引起肾脏病变的一个重要环节。
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  “by hyperglycemia”译为未确定词的双语例句
     Fatty liver disease (FLD) includes alcoholic liver disease (ALD) by alcohol and non-alcoholic fatty liver disease (NAFLD) by hyperglycemia and obesity.
     脂肪性肝病(Fatty liver disease, FLD)包括由酒精所致的酒精性肝病(Alcoholic liver disease , ALD)和高脂、肥胖等因素所致的非酒精性脂肪性肝病(non- Alcoholic fatty liver disease,NAFLD)。
短句来源
     Analysis of 113 Cases of Burn Complicated by Hyperglycemia
     烧伤并发高血糖症113例分析
短句来源
     Objective This study is to investigate whether phospholipase A 2(PLA 2) activity may affect the proliferation of their vascular smooth muscle cell (VSMC) in cultured rats induced by hyperglycemia and/or hyperinsulinemia.
     目的 观察磷脂酶 A2 (phospholipase A2 ,PL A2 )活性变化对高糖或 (和 )高胰岛素 (Ins)环境下培养大鼠血管平滑肌细胞 (vascular smooth muscle cell,VSMC)增殖的影响。
短句来源
     Conclusion The level of plasma ET 1 and P selec elevated by hyperglycemia and hyperlipoidemia in the rabbit models( P <0.01),but which it was prominence elevated in level of ET 1 and P selec after 2h after infarction( P <0.05~0.01). The biomolecule changes was remarkable in PSS group which compared with the Urokinase,Nimodiping and the coutrast group( P <0.05~0.01).
     结论 高脂、高糖血症兔模型的血浆 ET- 1和 P- selec水平升高 (P<0 .0 1) ,脑梗死后 2 h ET- 1和 P- selec水平明显升高 (P<0 .0 5~ 0 .0 1) ,尿激酶、PSS和尼莫地平与对照组比较 ,PSS组对血浆生物分子改变最为显著 (P<0 .0 5~ 0 .0 1)。
短句来源
     Effects of Catalase on Decrease of Pax6 Expression Induced by Hyperglycemia
     过氧化氢酶对高糖诱导NIT-1胰岛β细胞Pax6基因表达下降的影响
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  by hyperglycemia
We postulate that the concomitant mobilization of p53 protein to the mitochondria and the subsequent changes on the Δ >amp;lt; eqid2 >amp;gt; m, lead to an important pancreatic β-cell apoptosis mechanism induced by oxidative stress caused by hyperglycemia.
      
Rats were injected with single dose of streptozotocin (45 mg/kg, i.v.), and after 1 week the disease was manifested by hyperglycemia and cardiac dysfunction.
      
Diabetic rats were characterized by hyperglycemia (4-fold increase), hypoinsulinemia (81% decrease) and a significant (P>amp;lt;0.01) increase in hepatic insulin receptor numbers.
      
Our findings alsodemonstrate that anal sphincter motor function is notappreciably modified by hyperglycemia.
      
To facilitate our understanding of the PKC- and FAK-modulating mechanism, we developed an in vitro model of mouse mesangial cell hypocontractility induced by hyperglycemia or mannitol.
      
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This Paper reports an Observation of three hundred and twenty one cases of acute cerebral hemor- rhage. The result showed that the level of blood glucose was positively correlated with disturbance in consciousness. the increase of intracranial pressure and pathological changes in median line structures but bore on obvious relation with the number of cells in the cerebrospinal fluid. The death rate of hy- perglycemic patients was very high. Most of them died from intracranial diseases,such as cerebral her- nia....

This Paper reports an Observation of three hundred and twenty one cases of acute cerebral hemor- rhage. The result showed that the level of blood glucose was positively correlated with disturbance in consciousness. the increase of intracranial pressure and pathological changes in median line structures but bore on obvious relation with the number of cells in the cerebrospinal fluid. The death rate of hy- perglycemic patients was very high. Most of them died from intracranial diseases,such as cerebral her- nia. But the death rate of patients with normal blood glucoser was lower and mostly died from extra cranial diseases, such as lung infection. Glucose treatment should be avoided in severe cerebral hemor- rhage accompanied by hyperglycemia. Dynamic observation on blood glucose was of important value in the prognosis of cerebral hemorrhag.

本文报告321例脑出血急性期血糖测定结果;血糖水平与意识障碍、颅压增高及中线结构病损呈正相关;与脑脊液细胞数无明显关系;高血糖者死亡率很高,且多死于脑疝等颅内原因;血糖正常者死亡率较低,且多死于肺部感染等颅外原因。认为重症脑出血合并高糖血症者应避免使用葡萄糖治疗;血糖动态观察对脑出血患者的预后判断有重要价值。

Effects of different blood sucar levels on the mitochondria responding to succnic dehydrogenase (SDH),of forebrain in rats undergoing bilateral occlusion of common carotid arteries for 30 minutes were studied bv using electron microscope en-zymlogy combined with texture analysis technique (TAS).The ultrastructure of the mitochondria was also observed in each group.The results showed that the mean number of the mitochondria in hyperglycemic group was significantly lower than in normo-and hypoplycemic groups.The...

Effects of different blood sucar levels on the mitochondria responding to succnic dehydrogenase (SDH),of forebrain in rats undergoing bilateral occlusion of common carotid arteries for 30 minutes were studied bv using electron microscope en-zymlogy combined with texture analysis technique (TAS).The ultrastructure of the mitochondria was also observed in each group.The results showed that the mean number of the mitochondria in hyperglycemic group was significantly lower than in normo-and hypoplycemic groups.The mean mitochondrial area in hypoglycemie group was significantly lower than in hyper and normo-glycemic groups.The asfrocvte and glial membrane of BBB were obviously swelling in hyper-glycemic group.It was revealed that brain ischemia can be aggravated by hyperglycemia and rnild hypo-glycemia may have a protective effect on it.

本文采用电镜酶细胞化学方法及图像分析技术(TAS),对不同血糖水平条件下,大鼠双侧颈总动脉闭塞30分钟后,前脑皮质神经元内有琥珀酸脱氢酶(SDH)反应产物的线粒体进行了精确的形态学计量,并对相应的超微结构进行了观察。结果表明高血糖能加剧缺血时线粒体的肿胀和破坏;高血糖组胶质细胞水肿,血脑屏障的胶质膜高度水肿,而正常血糖组及低血糖脑缺血组改变不明显。

GFR was studied in 24 normal subjects as control and 39 patients with early stage N1D- DM turned from impaired glucose tolerance within 2 years.The results showed that GFR in early stage NIDDM patients without hypertension was elevated and in those with hypertension was low- ered significantly than that in normal subjects.There was a negative correlation between diastolic blood pressure and GFR in NIDDM patients.GFR was enhanced by hyperglycemia,and was re- duced by hypertension.

观察39例在2a 内由糖耐量低减转为糖尿病的早期非胰岛素依赖型(NIDDM)糖尿病患者及24例正常人的肾小球滤过率(GFR),结果表明,早期 NIDDM 病例中血压正常者 GFR 较正常人高,伴有高血压者 GFR 较正常人低;舒张压与 GFR 呈显著负相关关系,高血糖使 GFR 升高,高血压使 GFR 降低,高血压对 GFR 的影响较其它因素更突出。

 
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