| 查看: 308 | 回复: 4 | ||
| 当前主题已经存档。 | ||
| 【悬赏金币】回答本帖问题，作者zy830226将赠送您 3 个金币 | ||
[求助]
谁能帮我检验下这段英语的语法错误，谢谢！
|
||
|
Neuropathic pain can result from a peripheral or central nervous system lesion and is refractory to analgesic therapy [1-2]. Clinical symptoms commonly include stimulus- independent pain (spontaneous pain) and stimulus-evoked pain (hyperalgesia or allydynia) [2]. Of all symptoms in patients with painful neuropathy, spontaneous pain is the most burdensome [2]. Unfortunately, the behavior of spontaneous pain is more difficult occurred than stimulus-evoked pain. So there are few studies on spontaneous pain. The behavior of spontaneous pain was expressed strongly in mSNA rats [3, 25]. Lee DH [3] suggested that spontaneous pain is induced by inflammation, which was evoked by L5 SNL plus the L4 chromic gut loop in mSNA rats. Nerve injury is followed by Wallerian degeneration. A large number of proinflammatory mediators including cytokines, growth factors and proteases, are released from schwann cells, microglia cells and neuron cells [4-5,9]. And the inflammation response is the basis of neuropathic pain. TNFαis the first cytokines that plays a critical role in setting the cytokine network, contributing to macrophage recruitment to inflammatory site[6]. So TNFαappears to play a key role for the induction of neuropathic pain following never injury[7-9]. However, the results are based on studying in stimulus-evoked pain, do not show the effect of TNFαin spontaneous pain. The cellular immediate early gene c-fos is transiently induced in numerous cell types by many kinds of stimuli and conditions [10]. While the expression of c-fos is suppressed by various means, the pain behavior could be alleviated in the neuropathic pain rats [11-13]. And the result is also in the inflammatory pain rats [14]. So some people suggest using c-fos as a neural marker of pain [15]. However, as previously described in many other studies, c-fos is not a neural marker of the spontaneous pain [16-17]. Thus the relationship between c-fos and pain is not clear until now. Minocycline is a second generation semi-synthetic tetracycline that penetrates well into the central nervous system via blood-brain barrier. And it is a strong anti-inflammatory drug, which is used extensively in the studies of stimulus-evoked pain. And all studies indicated that the inflammatory response was suppressed with minocycline pre-surgery, then the symptoms of stimulus-evoked pain alleviated too [18-21]. Minocycline was able to suppress c-fos expressing in spinal dorsal horn as Cho IK reported [14]. What is minocycline effect on the expression of c-fos and TNFα? We verified the effect of TNFαand c-fos in the spontaneous pain with mSNA rats. We also verified that effect of minocycline in the spontaneous pain in our study. [ Last edited by 风风1号 on 2008-5-8 at 07:47 ] |
回复此楼» 猜你喜欢
导师各种操作恶心咋办
已经有13人回复
-
本人最近太闲了，谁有问题可以提，每天会统一回复
已经有12人回复
-
重磅！青年科学基金项目（C类）资助增幅预计超过50%
已经有4人回复
-
青C资助名额大幅增加！
已经有10人回复
-
护理论文 晋升
已经有5人回复
-
求助大佬sci投稿哪个好中
已经有4人回复
-
评审感受-评审感受-评审感受
已经有14人回复
-
这年头没有找到涵评专家，还有中面上的可能吗
已经有6人回复
-
2026博士申请求助
已经有10人回复
-
西南大学考核制博士
已经有6人回复
★
zy830226(金币+1,VIP+0):谢谢
zy830226(金币+1,VIP+0):谢谢
|
the behavior of spontaneous pain is more difficult occurred than stimulus-evoked pain. So there are few studies on spontaneous pain. 这里个人感觉occurred用错了，可以改成to be occurred或者occurring The behavior of spontaneous pain was expressed strongly in mSNA rats [3, 25]. Lee DH [3] suggested that spontaneous pain is induced by inflammation 这里was要去掉 However, the results are based on studying in stimulus-evoked pain, do not show the effect of TNFαin spontaneous pain. do not 前加一个连词吧 the pain behavior could be alleviated in the neuropathic pain rats 改成the pain behavior of the neuropathic pain rats could be alleviated And the result is also in the inflammatory pain rats 这句话最好改成And the result is the same in the inflammatory pain rats So some people suggest using c-fos as a neural marker of pain 这个，用people不是很好吧，用expert什么的好点吧 呃，请各位高手指正，呵呵，语法并非偶的强项～ |
2楼2008-05-07 21:15:53
3楼2008-05-07 21:23:11
4楼2008-05-07 21:38:09
★ ★
zy830226(金币+2,VIP+0):谢谢，请继续
zy830226(金币+2,VIP+0):谢谢，请继续
|
有异议的地方已经用引号表起来了，可以在和其他人商量一下。写得不错！ Neuropathic pain can result from a peripheral or central nervous system lesion and is refractory to analgesic therapy [1-2]. Clinical symptoms commonly include stimulus- independent pain (spontaneous pain) and stimulus-evoked pain (hyperalgesia or allydynia) [2]. Of all symptoms in patients with painful neuropathy, spontaneous pain is the most burdensome [2]. Unfortunately,“ the behaviors of spontaneous pain occur more difficultly than stimulus-evoked pain.” So there are few studies on spontaneous pain. The behavior of spontaneous pain was expressed strongly in mSNA rats [3, 25]. Lee DH [3] suggested that spontaneous pain “was” induced by inflammation, which was evoked by L5 SNL plus the L4 chromic gut loop in mSNA rats. Nerve injury is followed by Wallerian degeneration. A large number of proinflammatory mediators including cytokines, growth factors and proteases,“which”are released from schwann cells, microglia cells and neuron cells [4-5,9]. And the inflammation response is the basis of neuropathic pain. TNFα is the first cytokines that “play” a critical role in setting the cytokine network, contributing to macrophage recruitment to inflammatory site[6]. So TNFα appears to play a key role for the induction of neuropathic pain following never injury[7-9]. However, the results “ base” on studying in stimulus-evoked pain, do not show the effect of TNFα in spontaneous pain. The cellular immediate early gene c-fos is transiently induced in numerous cell types by many kinds of “stimulis” and conditions [10]. While the expression of c-fos is suppressed by various means, the pain behavior could be alleviated in the neuropathic pain rats [11-13]. And the result is also in the inflammatory pain rats [14]. So some people suggest using c-fos as a neural marker of pain [15]. However, as previously described in many other studies, c-fos is not a neural marker of the spontaneous pain [16-17]. Thus the relationship between c-fos and pain is not clear until now. Minocycline is a second generation semi-synthetic tetracycline that penetrates well into the central nervous system via blood-brain barrier. And it is a strong anti-inflammatory drug, which is used extensively in the studies of stimulus-evoked pain. And all studies indicated that the inflammatory response was suppressed with minocycline pre-surgery, then the symptoms of stimulus-evoked pain alleviated too [18-21]. Minocycline was able to suppress c-fos expressing in spinal dorsal horn as Cho IK reported [14]. What is “the effect of minocycline” on the expression of c-fos and TNFα? We verified the effect of TNFα and c-fos in the spontaneous pain with mSNA rats. We also verified that“ the” effect of minocycline in the spontaneous pain in our study. |
5楼2008-05-07 21:39:44