钳夹法制备猫急性眼外肌损伤模型的研究
摘要
急性眼外肌损伤是临床上常见的眼病,常由于外伤、代谢性疾病等引起,造成神经、肌肉、血管等的损伤导致一条或多条眼外肌运动受限,往往形成麻痹性斜视,出现复视和代偿头位。眼外肌损伤所引起的这些症状和体征不仅影响患者的形象外观,同时由于复视等亦影响其正常工作和生活。急性眼外肌损伤的治疗主要是药物治疗和必要时进行手术矫正斜视和复视,但尚无系统和规范的治疗方式。由于目前对急性眼外肌损伤的研究缺乏合适的动物模型,制约了对其发生发展、疾病转归、药物及手术治疗等的研究。
在我们前期的兔眼眼外肌损伤模型的研究中,尝试使用钳夹法制备急性眼外肌损伤的兔模型,在一定程度上可供急性眼外肌损伤的基础和临床研究(2010 WOC, Berlin)。但兔眼模型尚存在不足,如使用钳夹时间来控制损伤程度类似于缺血再灌注损伤而不完全符合外伤性急性损伤、无法进行眼位的观察等,不能满足急性眼外肌损伤的发病机制、功能改变和药物防治的深入研究。猫是额面化的动物,双眼的联合视野与人类接近,能够进行眼位的观察。因此,本研究拟在原有眼外肌损伤模型研究的基础上,应用钳夹法进行猫急性眼外肌损伤模型的制备,以期能够更好地反映和评价眼外肌损伤,为研究眼外肌损伤的发病机制和药物防治提供合适的动物模型。
目的:利用钳夹法制备猫急性眼外肌损伤模型,为急性眼外肌损伤病理机制及治疗方法的研究提供模型。方法:家猫72只,随机分为A、B、C、D、E、F六组,每组12只,
以30 mg/kg体重腹腔注射1%戊巴比妥钠溶液麻醉动物后,通过实施手术的方法分离出左眼外直肌,然后用12.5 cm直型细针(小血管)持针器直视下分别以2 kg(A、D组)、4 kg(B、E组)、6 kg(C、F组)大小的钳夹力钳夹猫左眼外直肌造成损伤,右眼不做处理作为对照。每组的6只猫分别于术后第4 d(A、B、C组)及第7 d(D、E、F组)利用眼底血管造影仪拍摄猫双眼眼底像,通过投射法测量猫眼眼位斜视度的方法以观测眼位;测量眼位之后,分别于第4 d(A、B、C组)、第7 d(D、E、F组)将猫处死,取双眼外直肌标本进行HE染色、电镜切片以观察肌肉损伤后的病理变化,并进行增殖细胞核抗原(PCNA)和肌球蛋白重链(MHC)免疫组织化学染色;每组的其余6只猫分别于第4 d(A、B、C组)、第7 d(D、E、F组)在活体上分离出外直肌,连接于生物机能实验系统,设定起始刺激强度为0 V,频率100 Hz,刺激次数100次,增量为0.05 V及0.5 V,双眼分别测定,比较眼外肌损伤后肌力的改变。结果:在光学显微镜下观察各实验组猫外直肌损伤的HE染色病理切片,可观察到较正常对照组出现不同程度的肌纤维断裂、坏死和肌浆溶解,损伤后4 d主要表现为炎性浸润、出血水肿及变性坏死等;损伤后7 d主要表现为水肿减轻,纤维组织增生;钳夹力为2 kg、4 kg、6 kg所造成的肌肉损伤分别符合肌肉损伤Ⅱ度中轻度、中度、重度损伤标准。电镜观察下,主要表现为肌浆网扩张,肌小节模糊、连接断裂,Z线、H带及明暗带结构破裂、杂乱,肌丝排列紊乱,线粒体增生、空泡样改变等。PCNA及MHC免疫组化染色可证实损伤区的肌纤维增殖,在高倍镜下进行PCNA阳性细胞核计数,损伤各组的阳性细胞核比例均较正常对照组升高,其平均阳性率约为17.83%;损伤后各组猫的外直肌表现出对电刺激阈值的升高,同时较对侧外直肌肌力明显下降;第4 d,A组(557.333±206.507 mg)与B组(283.167±91.777 mg)、C组(169.167±60.261 mg)的肌力之间有差别(F=12.559,P<0.05);而第7 d,D组(360.833±113.118 mg)、E组(392.667±154.859 mg)、F组(536±311.995 mg)三组间的肌力差别无统计学意义(F=1.169,P>0.05);钳夹伤后第4、7 d各实验组猫的眼位观测均提示眼位较术前均有不同程度的向内偏斜,分别为A组(13.3°±5.785°)、B组(23.3°±4.476°)、C组(16.7°±9.973°)、D组(11.3°±4.885°)、E组(15.0°±5.745°)、F组(15.2°±4.535°),但除A组与B、C组之间有差别(F=3.015,P<0.05)外,其余各组间两两比较无统计学意义(F=1.006,P>0.05)。
结论:钳夹法可制备出猫急性眼外肌损伤模型,并可以按照需要制作不同的病理损伤分级,为进一步研究眼外肌损伤的病理变化、疾病转归、药物治疗等提供了稳定的模型。
创新点
1、首次采用钳夹法制作出猫急性眼外肌损伤模型,并进行了眼外肌损伤的病理分级,为进一步研究其机制和药物治疗等研究提供了稳定和可重复的实验模型。
2、采用了改良的猫活体眼位观察方法,应用于猫急性眼外肌损伤模型,能够为更好地评价急性眼外肌损伤眼位的变化提供依据。
Acute extraocular muscle injury is one of the most frequent clinical ocular disease, which constantly caused by trauma or metabolic diseases. Injury of nerves, myofibers and blood vessels often lead to restricted motions of one or more extraocular muscles, which result in paralytic strabismus with diplopia and compensative head position. Such symptoms and physical signs of extraocular muscles may disturb normal work and daily life. The treatment for acute extraocular muscle injury include medication and surgery with which dealing with strabismus and diplopia, and there is no systematic and normative treatment. At present, due to lack of proper animal model, the study of development, consequences, medication and surgery treatment of acute extraocular muscle injury has been limited.
In our previous study, we have established a rabbit model of acute extraocular injury by clamping, which can be used to the basic and clinical research (2010 WOC, Berlin). However, the previous model has shortcomings, prolonged clamping in the rabbit model may lead to a damage similar to ischemia/reperfusion injury rather than traumatic injury. Moreover, rabbit is incapable for eye position observation. Cat is similar to human beings in orbital structure and combine visual fields, which is suitable for observation of eye position. Therefore, the aim of present study was to establish a cat model of acute extraocular injury by clamping in order to get the better evaluation to the extraocular muscle injury and apply to the investigation of medications in the extroocular muscle injury, which is being developed in our laboratory. Objective To establish a model of acute extraocular muscle injury by clamping in cat, which is suitable for the experimental research of its pathological mechanism and medication.
Methods Seventy-two cat were randomly divided into A、B、C、D、E、F groups (12 cats in each group). After 1% Phenobarbital sodium (30 mg/kg) was injected into abdominal cavity of the cat, the left lateral rectus were set apart, and then clamped it with a 12.5cm needle holder for 15s. The intensity of clamping were set as 2 kg (group A、D)、4 kg (group B、E) and 6 kg (group C、F) respectively. There were no any treatment in the right eyes as a control group. On the 4th day (group A、B、C) and the 7th day (group D、E、F), fundus photographs of 6 cats in each group were screened by fundus angiography instrument with modification in order to measure the ocular alignment via projection. After that, they were sacrificed at the 4th day (group A、B、C) and the 7th day (group D、E、F) respectively, and the pathological changes of bilateral muscles by light and electron microscopy were investigated accordingly. Then proliferating cell nuclear antigen (PCNA) and myosin heavy chain (MHC) were performed by using imunohistochemistry staining methods. On the 4th day (group A、B、C) and the 7th day (group D、E、F), the other 6 cats in each group were anaesthetized, and the bilateral lateral rectus were set apart in vivo and connected to the organism function experimental system. The primary stimulus intensity at 0 V, stimulus frequency at 100 Hz, stimulus times at 100, increment at 0.05 V and 0.5 V were set up to measure the muscle forces in vivo. Muscle forces of both lateral rectus were measured by the same methods.
Results The morphological changes in all the groups can be classified in grades as mild, moderate, severe by HE dyeing and electron microscopy. PCNA and MHC immunohistochenical staining displayed proliferation of the muscle fibers in the damage area. The numbers of PCNA positive cell nuclei were counted at high magnification. And the percentage of them in all the injury muscles, with a average positive rate of 17.83%, were higher than that of the normal controls. On the 4th day and the 7th day after clamping, threshold to the electric stimulation of the injuried lateral muscle appeared elevated. The muscle forces of the group A (557.333±206.507 mg)、group B (283.167±91.777 mg) and group C (169.167±60.261 mg) were statistically significant (F=12.559, P<0.05), but there were no significant differences among the group D (360.833±113.118 mg)、group E (392.667±154.859 mg) and group F (536±311.995 mg) (F=1.169, P>0.05). All groups had different degrees with medial deviation in ocular alignment after 4 days or 7 days from operation, group A (13.3°±5.785°)、group B (23.3°±4.476°)、group C (16.7°±9.973°)、group D (11.3°±4.885°)、group E (5.0°±5.745°)、group F(15.2°±4.535°), respectively. But there were no statistically significant differences among the groups (F=1.006, P>0.05) except when it came to group B and group C compared with group A (F=3.015, P<0.05).
Conclusions A model of acute extraocular muscle injury can be successfully established by clamping rectus in cat in vivo.
在我们前期的兔眼眼外肌损伤模型的研究中,尝试使用钳夹法制备急性眼外肌损伤的兔模型,在一定程度上可供急性眼外肌损伤的基础和临床研究(2010 WOC, Berlin)。但兔眼模型尚存在不足,如使用钳夹时间来控制损伤程度类似于缺血再灌注损伤而不完全符合外伤性急性损伤、无法进行眼位的观察等,不能满足急性眼外肌损伤的发病机制、功能改变和药物防治的深入研究。猫是额面化的动物,双眼的联合视野与人类接近,能够进行眼位的观察。因此,本研究拟在原有眼外肌损伤模型研究的基础上,应用钳夹法进行猫急性眼外肌损伤模型的制备,以期能够更好地反映和评价眼外肌损伤,为研究眼外肌损伤的发病机制和药物防治提供合适的动物模型。
目的:利用钳夹法制备猫急性眼外肌损伤模型,为急性眼外肌损伤病理机制及治疗方法的研究提供模型。方法:家猫72只,随机分为A、B、C、D、E、F六组,每组12只,
以30 mg/kg体重腹腔注射1%戊巴比妥钠溶液麻醉动物后,通过实施手术的方法分离出左眼外直肌,然后用12.5 cm直型细针(小血管)持针器直视下分别以2 kg(A、D组)、4 kg(B、E组)、6 kg(C、F组)大小的钳夹力钳夹猫左眼外直肌造成损伤,右眼不做处理作为对照。每组的6只猫分别于术后第4 d(A、B、C组)及第7 d(D、E、F组)利用眼底血管造影仪拍摄猫双眼眼底像,通过投射法测量猫眼眼位斜视度的方法以观测眼位;测量眼位之后,分别于第4 d(A、B、C组)、第7 d(D、E、F组)将猫处死,取双眼外直肌标本进行HE染色、电镜切片以观察肌肉损伤后的病理变化,并进行增殖细胞核抗原(PCNA)和肌球蛋白重链(MHC)免疫组织化学染色;每组的其余6只猫分别于第4 d(A、B、C组)、第7 d(D、E、F组)在活体上分离出外直肌,连接于生物机能实验系统,设定起始刺激强度为0 V,频率100 Hz,刺激次数100次,增量为0.05 V及0.5 V,双眼分别测定,比较眼外肌损伤后肌力的改变。结果:在光学显微镜下观察各实验组猫外直肌损伤的HE染色病理切片,可观察到较正常对照组出现不同程度的肌纤维断裂、坏死和肌浆溶解,损伤后4 d主要表现为炎性浸润、出血水肿及变性坏死等;损伤后7 d主要表现为水肿减轻,纤维组织增生;钳夹力为2 kg、4 kg、6 kg所造成的肌肉损伤分别符合肌肉损伤Ⅱ度中轻度、中度、重度损伤标准。电镜观察下,主要表现为肌浆网扩张,肌小节模糊、连接断裂,Z线、H带及明暗带结构破裂、杂乱,肌丝排列紊乱,线粒体增生、空泡样改变等。PCNA及MHC免疫组化染色可证实损伤区的肌纤维增殖,在高倍镜下进行PCNA阳性细胞核计数,损伤各组的阳性细胞核比例均较正常对照组升高,其平均阳性率约为17.83%;损伤后各组猫的外直肌表现出对电刺激阈值的升高,同时较对侧外直肌肌力明显下降;第4 d,A组(557.333±206.507 mg)与B组(283.167±91.777 mg)、C组(169.167±60.261 mg)的肌力之间有差别(F=12.559,P<0.05);而第7 d,D组(360.833±113.118 mg)、E组(392.667±154.859 mg)、F组(536±311.995 mg)三组间的肌力差别无统计学意义(F=1.169,P>0.05);钳夹伤后第4、7 d各实验组猫的眼位观测均提示眼位较术前均有不同程度的向内偏斜,分别为A组(13.3°±5.785°)、B组(23.3°±4.476°)、C组(16.7°±9.973°)、D组(11.3°±4.885°)、E组(15.0°±5.745°)、F组(15.2°±4.535°),但除A组与B、C组之间有差别(F=3.015,P<0.05)外,其余各组间两两比较无统计学意义(F=1.006,P>0.05)。
结论:钳夹法可制备出猫急性眼外肌损伤模型,并可以按照需要制作不同的病理损伤分级,为进一步研究眼外肌损伤的病理变化、疾病转归、药物治疗等提供了稳定的模型。
创新点
1、首次采用钳夹法制作出猫急性眼外肌损伤模型,并进行了眼外肌损伤的病理分级,为进一步研究其机制和药物治疗等研究提供了稳定和可重复的实验模型。
2、采用了改良的猫活体眼位观察方法,应用于猫急性眼外肌损伤模型,能够为更好地评价急性眼外肌损伤眼位的变化提供依据。
Acute extraocular muscle injury is one of the most frequent clinical ocular disease, which constantly caused by trauma or metabolic diseases. Injury of nerves, myofibers and blood vessels often lead to restricted motions of one or more extraocular muscles, which result in paralytic strabismus with diplopia and compensative head position. Such symptoms and physical signs of extraocular muscles may disturb normal work and daily life. The treatment for acute extraocular muscle injury include medication and surgery with which dealing with strabismus and diplopia, and there is no systematic and normative treatment. At present, due to lack of proper animal model, the study of development, consequences, medication and surgery treatment of acute extraocular muscle injury has been limited.
In our previous study, we have established a rabbit model of acute extraocular injury by clamping, which can be used to the basic and clinical research (2010 WOC, Berlin). However, the previous model has shortcomings, prolonged clamping in the rabbit model may lead to a damage similar to ischemia/reperfusion injury rather than traumatic injury. Moreover, rabbit is incapable for eye position observation. Cat is similar to human beings in orbital structure and combine visual fields, which is suitable for observation of eye position. Therefore, the aim of present study was to establish a cat model of acute extraocular injury by clamping in order to get the better evaluation to the extraocular muscle injury and apply to the investigation of medications in the extroocular muscle injury, which is being developed in our laboratory. Objective To establish a model of acute extraocular muscle injury by clamping in cat, which is suitable for the experimental research of its pathological mechanism and medication.
Methods Seventy-two cat were randomly divided into A、B、C、D、E、F groups (12 cats in each group). After 1% Phenobarbital sodium (30 mg/kg) was injected into abdominal cavity of the cat, the left lateral rectus were set apart, and then clamped it with a 12.5cm needle holder for 15s. The intensity of clamping were set as 2 kg (group A、D)、4 kg (group B、E) and 6 kg (group C、F) respectively. There were no any treatment in the right eyes as a control group. On the 4th day (group A、B、C) and the 7th day (group D、E、F), fundus photographs of 6 cats in each group were screened by fundus angiography instrument with modification in order to measure the ocular alignment via projection. After that, they were sacrificed at the 4th day (group A、B、C) and the 7th day (group D、E、F) respectively, and the pathological changes of bilateral muscles by light and electron microscopy were investigated accordingly. Then proliferating cell nuclear antigen (PCNA) and myosin heavy chain (MHC) were performed by using imunohistochemistry staining methods. On the 4th day (group A、B、C) and the 7th day (group D、E、F), the other 6 cats in each group were anaesthetized, and the bilateral lateral rectus were set apart in vivo and connected to the organism function experimental system. The primary stimulus intensity at 0 V, stimulus frequency at 100 Hz, stimulus times at 100, increment at 0.05 V and 0.5 V were set up to measure the muscle forces in vivo. Muscle forces of both lateral rectus were measured by the same methods.
Results The morphological changes in all the groups can be classified in grades as mild, moderate, severe by HE dyeing and electron microscopy. PCNA and MHC immunohistochenical staining displayed proliferation of the muscle fibers in the damage area. The numbers of PCNA positive cell nuclei were counted at high magnification. And the percentage of them in all the injury muscles, with a average positive rate of 17.83%, were higher than that of the normal controls. On the 4th day and the 7th day after clamping, threshold to the electric stimulation of the injuried lateral muscle appeared elevated. The muscle forces of the group A (557.333±206.507 mg)、group B (283.167±91.777 mg) and group C (169.167±60.261 mg) were statistically significant (F=12.559, P<0.05), but there were no significant differences among the group D (360.833±113.118 mg)、group E (392.667±154.859 mg) and group F (536±311.995 mg) (F=1.169, P>0.05). All groups had different degrees with medial deviation in ocular alignment after 4 days or 7 days from operation, group A (13.3°±5.785°)、group B (23.3°±4.476°)、group C (16.7°±9.973°)、group D (11.3°±4.885°)、group E (5.0°±5.745°)、group F(15.2°±4.535°), respectively. But there were no statistically significant differences among the groups (F=1.006, P>0.05) except when it came to group B and group C compared with group A (F=3.015, P<0.05).
Conclusions A model of acute extraocular muscle injury can be successfully established by clamping rectus in cat in vivo.
引文
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22. Stewart CE, Rotwein P. Insulin-like growth factor-2 is an autocrinesurvival factor for differentiating myoblasts. J Biol Chem. 1996. 271:11330-11338
23. Gagnon J, Ho-Kim MA, Chagnon YC, et al. Absence of linkage between VO2max and its response to training with markers spanning chromosome
22. Med Sci Sports Exerc. 1997, 29(11):1448-1453
24. Bozyczko D, Decker C, Muschler J, et al. Integrin on developing and adult skeletal muscle. Exp Cell Res. 1989, 183(1):72-91
25. Taftachi R, Ayhan A, Ekici S, et al. Proliferating cell nuclear antigen(PCNA) as an independent prognostic marker in patients after prostatectomy: a comparisom of PCNA and Ki67. BJU Int. 2005, 95(4):650-654
26. Takata T, Lu Y, Ogawa I, et al. Proliferative activity of calcifying odontogenic cysts as evaluated by proliferating cell nuclear antigen labeling index. Pathol Int. 1998, 48(11):877-881.
27. Morris GF, Mathews MB. Regulation of proliferation cell nuclear antigen during the cell cycle. J Biol chem. 1989, 264:13856-13864
28. Mocquet V, LainéJP, Riedl T, et al. Sequential recruitment of the repair factors during NER: the role of XPG in initiating the resynthesis step. EMBO J. 2008, 27(1):155-167
29. Brun J, Chiu RK, Wouters BG, et al. Regulation of PCNA polyubiquitination in human cells. BMC Res Notes. 2010, 3:85
30. Kannabiran C, Morris GF, Mathews MB. Dual action of the adenovirus E1A 243R oncoprotein on the human proliferating cell nuclear antigen promoter: repression of transcriptional activation by P53. Oncogene. 1999, 18(54):7825-7833
31. Spangenburg EE, Chakravarthy NV, Booth FW. P27 kipl: a key regulatorof skeletal muscle satellite cell. Clin Orthop. 2002, 403:221-227
32. Koyuncuo?lu M, Kargi A, Cing?z S, et al. Investigation of P53, c-erbB-2, PCNA irnmunoreactivity, DNA content, AgNOR and apoptosis in bladder carcinoma as prognostic parameters. Cancer Lett. 1998, 126(2): 143-148
33. Huang JZ, Xia SS, Ye QF, et al. Effects of p16 gene on biological behaciors in hepatocellular carcinoma cell. World J Gastroenterol. 2003, 9(1): 84-88
34. B?r A, Pette D. Three fast myosin heavy chain in adult rat skeletal muscle. FEBS Left. 1998, 235 (1-2):153-155
35. Baldwin KM, Haddad F. Effects of different activity and inactivity paradigms on myosin heavy chain gene expression in striated muscle. J Appl Physiol. 2001, 90(1):345-357
36. Staron RS, Pette D. The multiplicity of combinations of myosin light chains and heavy chains in histochemically typed single fibres. Rabbit tibialis anterior muscle. Biochem J. 1987, 243(3):695-699
37. Fitts RH, Bodine SC, Romatowski JG, et al. Velocity, force, power, and Ca2+ sensitivity of fast and slow monkey skeletal muscle fibers. J Appl Physiol. 1998, 84(5):1776-1787
38. Talmadge RJ. Myosin heavy chain isoform expression following reduced neuromuscular activity: potential regulatory mechanisms. Muscle Nerve. 2000, 23(5):661-679
39. Majerczak J, Szkutnik Z, Karasinski J, et al. High content of MYHC II in vastus lateralis is accompanied by higher VO2/power output ratio during moderate intensity cycling performed both at low and at high pedalling rates. J Physiol Pharmacol. 2006, 57(2):199-215
40. Briggs MM, Schachat F. Early specialization of the superfast myosin inextraocular and laryngeal muscles. J Exp Biol. 2000, 203(16):2485-2494
41. Rubinstein NA, Hoh JF. The distribution of myosin heavy chain isoforms among rat extraocular muscle ?ber types. Invest Ophthalmol Vis Sci. 2000, 41(11):3391-3398
42. Spencer RF, Porter JD. Structural organization of the extraocular muscles. Rev Oculomotor Res. 1988, 2:33-79
43. Porter JD, Baker RS, Ragusa RJ, et al. Extraocular muscles: Basic and clinical aspects of structure and function. Surv Ophthalmol. 1995, 39:451-448
44. Lucas CA, Hoh JF. Extraocular fast myosin heavy chain expression in the levator palpebrae and retractor bulbi muscles. Invest Ophthalmol Vis Sci. 1997, 38(13):2817-2825
45. Jacoby J, Ko K, Weiss C, et al. Systematic variation in myosin expression along extraocular muscle ?bres of the adult rat. J Muscle Res Cell Motil. 1990, 11(1):25-40
46. Bicer S, Reiser PJ. Myosin Isoform Expression in Dog Rectus Muscles:Patterns in Global and Orbital Layers and among Single Fibers. Invest Ophthalmol Vis Sci. 2009, 50(1):157-167
47. Porter JD, Baker RS, Ragusa RJ, et al. Extraocular muscles: basic and clinical aspects of structure and function. Surv Ophthalmol. 1995, 39(6):451-484
48. Kranjc BS, Sketelj J, Albis AD, et al. Fibre types and myosin heavy chain expression in the ocular medial rectus muscle of the adult rat. J Muscle Res Cell Motil. 2000, 21(8):753-761
49. Kranjc BS, Sketelj J, D'Albis A, et al. Long-term changes in myosin heavy chain composition after botulinum toxin a injection into rat medial rectusmuscle. Invest Ophthalmol Vis Sci. 2001, 42(13):3158-3164
50. Talmadge RJ, Roy RR, Edgerton VR. Myosin heavy chain profile of cat soleus following chronic reduced activity or inactivity. Muscle Nerve. 1996, 19(8):980-988
51. Roy RR, Talmadge RJ, Hodgson JA, et al. Differential response of fast hindlimb extensor and flexor muscles to exercise in adult spinalized cats. Muscle Nerve. 1999, 22(2):230-241
52. Willoughby DS, Nelson MJ. Myosin heavy-chain mRNA expression after a single session of heavy-resistance exercise. Med Sci Sports Exerc. 2002, 34 (8):1262-1269
53. Jaschinski F, Schuler M, Peuker H, et al. Changes in myosin heavy chain mRNA and protein isoforms of rat muscle during forced contractile activity. Am J Physiol. 1998, 274(1):365-370
54. Cerny LC, Bandman E. Expression of myosin heavy chain isoforms in generating myotubes of innervated and denervated chicken pectoral muscle. Dev Biol. 1987, 119:350-362
55. d'Albis A, Couteaux R, Janmot C, et al. Regeneration after cardiotoxin injury of innervated and denervated slow and fast muscles of mammals. Myosin isoform analysis. Eur J Biochem. 1988, 174(1):103-110
56.孙春华,赵堪兴.不同种属眼外肌Pulley结构形态学的研究进展.国际眼科纵览. 2006, 30(2):133-136
57. Schoppmann A, Hoffmann KP. The Development of Eye Alignment in Normal and Naturally Microstrabismic Kittens. Invest Ophthalmol Vis Sci. 1985, 26(3):350-358
58. Sherman SM. Development of interocular alignment in cats. Brain Res. 1972, 37(2):187-203
59. Cynader M. Role of visual cortex in interocular alignment. Invest Ophthalmol Vis Sci. 1979, 18(7):742-751
60. Duke-Elder S, Wybar K. Ocular motility and strabismus. In System of Ophthalmology. St. Louis: The C. V. Mosby Co., 1973
61. Olson CR, Freeman RD. Development of eye alignment in cats. Nature. 1978, 271:446-467
62. Cynader M. Interocular alignment following visual deprivation in the cat. Invest Ophthalmol Vis Sci. 1979, 18(7):726-741
63. Bishop PO, Kozak W, Vakkur GJ. Some quantitative aspects of the cat's eye: axes and plane of reference, visual field coordinates and optics. J Physiol. 1963, 163:466-502
64. Olson CR, Freeman RD. Eye alignment in kittens. J Neurophysiol. 1978, 41 (4):848-859
65. Berman N, Blakemore C, Cynader M. Binocular interaction in the cat's superior colliculus. J Physiol. 1975, 246(3):595-615
66. Joshua DE, Bishop PO. Binocular single vision and depth discrinuna-tion. Receptive field disparities for central and peripheral vision and binocular interaction on peripheral single units in cat striate cortex. Expl Brain Res. 1970, 10:389-416
67. Cynader M, Berman N. Receptive-field organization of monkey superior colliculus. J. Neurophysiol. 1972, 35:187-201
68. Berman N, Cynader M. Comparison of receptive-field organization of the superior colliculus in Siamese and normal cats. J Physiol. 1972, 224(2):363-389
69. Dürsteler MR, von der Heydt R. Plasticity in the binocular correspondence of striate cortical receptive fields in kittens. J Physiol. 1983, 345:87-105
70. H?nny P, von der Heydt R. The effect of horizontal-plane environment on the development of binocular receptive fields of cells in cat visual cortex. J Physiol. 1982, 329:75-92
71. Baek SH, Lee EY. Clinical analysis of internal orbital fractures in children. Korean J Ophthalmol. 2003, 17(1):44-49
72. Sherman SM. Development of interocular alignment in cats. Brain Res. 1972, 37(2):187-203
73.张海平,宋吉锐.急性骨骼肌损伤动物实验模型构建及应用.中国组织工程研究与临床康复. 2007, 11(49):9984-9988
74. Sun LH, Yan H. Establishment of an animal model for acute extraocular muscle infury with clamping. Int J Ophthalmol. 2009, 9(6):1069-1071
75.孙礼华. IGF-I促进急性眼外肌损伤修复的研究.第四军医大学硕士学位论文. 2009
76. Wang NC, Ma L, Wu SY, et al. Orbital blow-out fractures in children: characterization and surgical outcome. Chang Gung Med J. 2010, 33(3):313-320
77. Kwon JH, Moon JH, Kwon MS, et al. The differences of blowout fracture of the inferior orbital wall between children and adults. Arch Otolaryngol Head Neck Surg. 2005, 131(8):723-727
78. Boutin RD, Fritz RC, Steinbach LS. Imaging of sports-related muscle injuries. Radiol Clin North Am. 2002, 40(2):333-362
79.洪汛宁,王德杭,王小宁,等.肌肉损伤磁共振成像的病理基础研究.南京医科大学学报. 2000, 20(10):362-364
80. Fielding RA, Manfredi TJ, Ding W, et al. Acute phase response in exercise. III. Neutrophil and IL-1 beta accumulation in skeletal muscle. Am J Physiol. 1993, 265(2):166–172
81. Rhoads RP, Fernyhough ME, Liu X, et al. Extrinsic regulation of domestic animal-derived myogenic satellite cellsⅡ. Domest Anim Endocrinol. 2009, 36:111-126
82. ChargéSB, Rudnicki MA. Cellular and molecular regulation of muscle regeneration. Physiol Rev. 2004, 84:209–238
83. Hail PA, Levision DA. Review: assessment of cell proliferation in histological material. Chins Pathol. 1990, 43:184-187
84. Rubinstein NA, Hoh JF. The distribution of myosin heavy chain isoforms among rat extraocular muscle fiber types. Invest Ophthalmol Vis Sci. 2000, 41(11):3391-3398
85. Anderson BC, Christiansen SP, McLoon LK, et al. Myogenic Growth Factors Can Decrease Extraocular Muscle Force Generation: A Potential Biological Approach to the Treatment of Strabismus. Invest Ophthalmol Vis Sci. 2008, 49(1):221-229
86. English AW, Wolf SL, Segal RL. Compartmentalization of muscles and their motor nuclei: the partitioning hypothesis. Phys Ther. 1993, 73(12):857-867
87. Dimitrova DM, Shall MS, Goldberg SJ. Stimulation-evoked eye movements with and without the lateral rectus muscle pulley. J Neurophysiol. 2003, 90:3809-3815
88. Huang CB, Zhou J, Zhou Y, et al. Contrast and phase combination in binocular vision. PLoS One. 2010, 5(12):15075
89. Dimitrova DM, Shall MS, Goldberg SJ. Stimulation-evoked eye movements with and without the lateral rectus muscle pulley. J Neurophysiol. 2003, 90:3809-3815
90. Miller JM. Understanding and misunderstanding extraocular musclepulleys. J Vis. 2007, 7(11): 1–15
2. Li YJ, Yan H, Wang WN, et al. Analysis of causes and management on acute extraocular muscles paralysis primarily tolerated diplopia. Int J Ophthalmal, 2004, 4(6):1140-1142
3.蔡晓红.外伤性眼肌麻痹临床分析.浙江创伤外科. 2006, 11(6): 517-518
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7.周全,陈金城,刘斯润,等.眼外肌病变的MRI表现.临床放射学杂志. 2007, 26(5):456-460
8. Chen W, Ruell PA, Ghoddusi M, et al. Ultrastructural changes and sarcoplasmic reticulum Ca2+ regulation in red vastus muscle following eccentric exercise in the rat. Exp Physiol. 2007, 92(2):437-447
9. Lauritzen F, Paulsen G, Raastad T, et al. Gross ultrastructural changes and necrotic fiber segments in elbow flexor muscles after maximal voluntary eccentric action in humans. J Appl Physiol. 2009, 107(6):1923-1934
10. Husmann I, Soulet L, Gautron J, et al. Growth factors in skeletal muscle regeneration. Cytokine Growth Factor Rev. 1996, 7(3):249-258
11. JancsóG. Pathobiological reactions of C-fibre primary sensory neurones to peripheral nerve injury. Exp Physiol. 1992, 77(3):405-431
12. Holland GR. Experimental trigeminal nerve injury. Crit Rev Oral Biol Med. 1996, 7(3):237-258
13. Demonbreun AR, Lapidos KA, Heretis K, et al. Myoferlin regulation by NFAT in muscle injury, regeneration and repair. J Cell Sci. 2010, 123(14):2413-2422
14. Gibson MC, Schultz E. The distribution of satellite cells and their relationship to specific fiber types in soleus and extensor digetorum longus muscles. Anat Rec. 1982, 202:329-337
15. Garry DJ, Meeson A, Elterman J, et al. Myogenic stem cell function is impaired in mice lacking the forkhead/winged helix protein MNF. Proc Natl Acad Sci. 2000, 97:5416-5421
16. Cooper RN, Tajbakhsh S, Mouly V, et al. In vivo satellite cell activation via Myf5 and MyoD in regenerating mouse skeletal muscle. J Cell Sci. 1999, 122(17):2895-2901
17. Dorfman J, Duong M, Zibatis A, et al. Myocardial tissue engineering with autologous myoblast implantation. Cardiovasc Surg. 1998, 116(5):744-751
18. Irintcher A, Langer M, Zweyer M, et al. Functional improvement of damaged adult mouse by implantation of primary myoblasts. J Physiol(Lond). 1997, 500(3):775-785
19. Evans CH, Robbins PD. Genetically augmented tissue engineering of the musculoskeletal system. Clin Orthop Relat Res. 1999, 367:410-418
20.郑江,邓忠良,李开南.肌肉损伤修复治疗的研究进展.广东医学. 2009, 30(5): 818-820
21. Hill M, Wernig A, Goldspink G. Muscle satellite(stem) cell activation during local tissue injury and repair. J Aanat. 2003, 203(1):89-99
22. Stewart CE, Rotwein P. Insulin-like growth factor-2 is an autocrinesurvival factor for differentiating myoblasts. J Biol Chem. 1996. 271:11330-11338
23. Gagnon J, Ho-Kim MA, Chagnon YC, et al. Absence of linkage between VO2max and its response to training with markers spanning chromosome
22. Med Sci Sports Exerc. 1997, 29(11):1448-1453
24. Bozyczko D, Decker C, Muschler J, et al. Integrin on developing and adult skeletal muscle. Exp Cell Res. 1989, 183(1):72-91
25. Taftachi R, Ayhan A, Ekici S, et al. Proliferating cell nuclear antigen(PCNA) as an independent prognostic marker in patients after prostatectomy: a comparisom of PCNA and Ki67. BJU Int. 2005, 95(4):650-654
26. Takata T, Lu Y, Ogawa I, et al. Proliferative activity of calcifying odontogenic cysts as evaluated by proliferating cell nuclear antigen labeling index. Pathol Int. 1998, 48(11):877-881.
27. Morris GF, Mathews MB. Regulation of proliferation cell nuclear antigen during the cell cycle. J Biol chem. 1989, 264:13856-13864
28. Mocquet V, LainéJP, Riedl T, et al. Sequential recruitment of the repair factors during NER: the role of XPG in initiating the resynthesis step. EMBO J. 2008, 27(1):155-167
29. Brun J, Chiu RK, Wouters BG, et al. Regulation of PCNA polyubiquitination in human cells. BMC Res Notes. 2010, 3:85
30. Kannabiran C, Morris GF, Mathews MB. Dual action of the adenovirus E1A 243R oncoprotein on the human proliferating cell nuclear antigen promoter: repression of transcriptional activation by P53. Oncogene. 1999, 18(54):7825-7833
31. Spangenburg EE, Chakravarthy NV, Booth FW. P27 kipl: a key regulatorof skeletal muscle satellite cell. Clin Orthop. 2002, 403:221-227
32. Koyuncuo?lu M, Kargi A, Cing?z S, et al. Investigation of P53, c-erbB-2, PCNA irnmunoreactivity, DNA content, AgNOR and apoptosis in bladder carcinoma as prognostic parameters. Cancer Lett. 1998, 126(2): 143-148
33. Huang JZ, Xia SS, Ye QF, et al. Effects of p16 gene on biological behaciors in hepatocellular carcinoma cell. World J Gastroenterol. 2003, 9(1): 84-88
34. B?r A, Pette D. Three fast myosin heavy chain in adult rat skeletal muscle. FEBS Left. 1998, 235 (1-2):153-155
35. Baldwin KM, Haddad F. Effects of different activity and inactivity paradigms on myosin heavy chain gene expression in striated muscle. J Appl Physiol. 2001, 90(1):345-357
36. Staron RS, Pette D. The multiplicity of combinations of myosin light chains and heavy chains in histochemically typed single fibres. Rabbit tibialis anterior muscle. Biochem J. 1987, 243(3):695-699
37. Fitts RH, Bodine SC, Romatowski JG, et al. Velocity, force, power, and Ca2+ sensitivity of fast and slow monkey skeletal muscle fibers. J Appl Physiol. 1998, 84(5):1776-1787
38. Talmadge RJ. Myosin heavy chain isoform expression following reduced neuromuscular activity: potential regulatory mechanisms. Muscle Nerve. 2000, 23(5):661-679
39. Majerczak J, Szkutnik Z, Karasinski J, et al. High content of MYHC II in vastus lateralis is accompanied by higher VO2/power output ratio during moderate intensity cycling performed both at low and at high pedalling rates. J Physiol Pharmacol. 2006, 57(2):199-215
40. Briggs MM, Schachat F. Early specialization of the superfast myosin inextraocular and laryngeal muscles. J Exp Biol. 2000, 203(16):2485-2494
41. Rubinstein NA, Hoh JF. The distribution of myosin heavy chain isoforms among rat extraocular muscle ?ber types. Invest Ophthalmol Vis Sci. 2000, 41(11):3391-3398
42. Spencer RF, Porter JD. Structural organization of the extraocular muscles. Rev Oculomotor Res. 1988, 2:33-79
43. Porter JD, Baker RS, Ragusa RJ, et al. Extraocular muscles: Basic and clinical aspects of structure and function. Surv Ophthalmol. 1995, 39:451-448
44. Lucas CA, Hoh JF. Extraocular fast myosin heavy chain expression in the levator palpebrae and retractor bulbi muscles. Invest Ophthalmol Vis Sci. 1997, 38(13):2817-2825
45. Jacoby J, Ko K, Weiss C, et al. Systematic variation in myosin expression along extraocular muscle ?bres of the adult rat. J Muscle Res Cell Motil. 1990, 11(1):25-40
46. Bicer S, Reiser PJ. Myosin Isoform Expression in Dog Rectus Muscles:Patterns in Global and Orbital Layers and among Single Fibers. Invest Ophthalmol Vis Sci. 2009, 50(1):157-167
47. Porter JD, Baker RS, Ragusa RJ, et al. Extraocular muscles: basic and clinical aspects of structure and function. Surv Ophthalmol. 1995, 39(6):451-484
48. Kranjc BS, Sketelj J, Albis AD, et al. Fibre types and myosin heavy chain expression in the ocular medial rectus muscle of the adult rat. J Muscle Res Cell Motil. 2000, 21(8):753-761
49. Kranjc BS, Sketelj J, D'Albis A, et al. Long-term changes in myosin heavy chain composition after botulinum toxin a injection into rat medial rectusmuscle. Invest Ophthalmol Vis Sci. 2001, 42(13):3158-3164
50. Talmadge RJ, Roy RR, Edgerton VR. Myosin heavy chain profile of cat soleus following chronic reduced activity or inactivity. Muscle Nerve. 1996, 19(8):980-988
51. Roy RR, Talmadge RJ, Hodgson JA, et al. Differential response of fast hindlimb extensor and flexor muscles to exercise in adult spinalized cats. Muscle Nerve. 1999, 22(2):230-241
52. Willoughby DS, Nelson MJ. Myosin heavy-chain mRNA expression after a single session of heavy-resistance exercise. Med Sci Sports Exerc. 2002, 34 (8):1262-1269
53. Jaschinski F, Schuler M, Peuker H, et al. Changes in myosin heavy chain mRNA and protein isoforms of rat muscle during forced contractile activity. Am J Physiol. 1998, 274(1):365-370
54. Cerny LC, Bandman E. Expression of myosin heavy chain isoforms in generating myotubes of innervated and denervated chicken pectoral muscle. Dev Biol. 1987, 119:350-362
55. d'Albis A, Couteaux R, Janmot C, et al. Regeneration after cardiotoxin injury of innervated and denervated slow and fast muscles of mammals. Myosin isoform analysis. Eur J Biochem. 1988, 174(1):103-110
56.孙春华,赵堪兴.不同种属眼外肌Pulley结构形态学的研究进展.国际眼科纵览. 2006, 30(2):133-136
57. Schoppmann A, Hoffmann KP. The Development of Eye Alignment in Normal and Naturally Microstrabismic Kittens. Invest Ophthalmol Vis Sci. 1985, 26(3):350-358
58. Sherman SM. Development of interocular alignment in cats. Brain Res. 1972, 37(2):187-203
59. Cynader M. Role of visual cortex in interocular alignment. Invest Ophthalmol Vis Sci. 1979, 18(7):742-751
60. Duke-Elder S, Wybar K. Ocular motility and strabismus. In System of Ophthalmology. St. Louis: The C. V. Mosby Co., 1973
61. Olson CR, Freeman RD. Development of eye alignment in cats. Nature. 1978, 271:446-467
62. Cynader M. Interocular alignment following visual deprivation in the cat. Invest Ophthalmol Vis Sci. 1979, 18(7):726-741
63. Bishop PO, Kozak W, Vakkur GJ. Some quantitative aspects of the cat's eye: axes and plane of reference, visual field coordinates and optics. J Physiol. 1963, 163:466-502
64. Olson CR, Freeman RD. Eye alignment in kittens. J Neurophysiol. 1978, 41 (4):848-859
65. Berman N, Blakemore C, Cynader M. Binocular interaction in the cat's superior colliculus. J Physiol. 1975, 246(3):595-615
66. Joshua DE, Bishop PO. Binocular single vision and depth discrinuna-tion. Receptive field disparities for central and peripheral vision and binocular interaction on peripheral single units in cat striate cortex. Expl Brain Res. 1970, 10:389-416
67. Cynader M, Berman N. Receptive-field organization of monkey superior colliculus. J. Neurophysiol. 1972, 35:187-201
68. Berman N, Cynader M. Comparison of receptive-field organization of the superior colliculus in Siamese and normal cats. J Physiol. 1972, 224(2):363-389
69. Dürsteler MR, von der Heydt R. Plasticity in the binocular correspondence of striate cortical receptive fields in kittens. J Physiol. 1983, 345:87-105
70. H?nny P, von der Heydt R. The effect of horizontal-plane environment on the development of binocular receptive fields of cells in cat visual cortex. J Physiol. 1982, 329:75-92
71. Baek SH, Lee EY. Clinical analysis of internal orbital fractures in children. Korean J Ophthalmol. 2003, 17(1):44-49
72. Sherman SM. Development of interocular alignment in cats. Brain Res. 1972, 37(2):187-203
73.张海平,宋吉锐.急性骨骼肌损伤动物实验模型构建及应用.中国组织工程研究与临床康复. 2007, 11(49):9984-9988
74. Sun LH, Yan H. Establishment of an animal model for acute extraocular muscle infury with clamping. Int J Ophthalmol. 2009, 9(6):1069-1071
75.孙礼华. IGF-I促进急性眼外肌损伤修复的研究.第四军医大学硕士学位论文. 2009
76. Wang NC, Ma L, Wu SY, et al. Orbital blow-out fractures in children: characterization and surgical outcome. Chang Gung Med J. 2010, 33(3):313-320
77. Kwon JH, Moon JH, Kwon MS, et al. The differences of blowout fracture of the inferior orbital wall between children and adults. Arch Otolaryngol Head Neck Surg. 2005, 131(8):723-727
78. Boutin RD, Fritz RC, Steinbach LS. Imaging of sports-related muscle injuries. Radiol Clin North Am. 2002, 40(2):333-362
79.洪汛宁,王德杭,王小宁,等.肌肉损伤磁共振成像的病理基础研究.南京医科大学学报. 2000, 20(10):362-364
80. Fielding RA, Manfredi TJ, Ding W, et al. Acute phase response in exercise. III. Neutrophil and IL-1 beta accumulation in skeletal muscle. Am J Physiol. 1993, 265(2):166–172
81. Rhoads RP, Fernyhough ME, Liu X, et al. Extrinsic regulation of domestic animal-derived myogenic satellite cellsⅡ. Domest Anim Endocrinol. 2009, 36:111-126
82. ChargéSB, Rudnicki MA. Cellular and molecular regulation of muscle regeneration. Physiol Rev. 2004, 84:209–238
83. Hail PA, Levision DA. Review: assessment of cell proliferation in histological material. Chins Pathol. 1990, 43:184-187
84. Rubinstein NA, Hoh JF. The distribution of myosin heavy chain isoforms among rat extraocular muscle fiber types. Invest Ophthalmol Vis Sci. 2000, 41(11):3391-3398
85. Anderson BC, Christiansen SP, McLoon LK, et al. Myogenic Growth Factors Can Decrease Extraocular Muscle Force Generation: A Potential Biological Approach to the Treatment of Strabismus. Invest Ophthalmol Vis Sci. 2008, 49(1):221-229
86. English AW, Wolf SL, Segal RL. Compartmentalization of muscles and their motor nuclei: the partitioning hypothesis. Phys Ther. 1993, 73(12):857-867
87. Dimitrova DM, Shall MS, Goldberg SJ. Stimulation-evoked eye movements with and without the lateral rectus muscle pulley. J Neurophysiol. 2003, 90:3809-3815
88. Huang CB, Zhou J, Zhou Y, et al. Contrast and phase combination in binocular vision. PLoS One. 2010, 5(12):15075
89. Dimitrova DM, Shall MS, Goldberg SJ. Stimulation-evoked eye movements with and without the lateral rectus muscle pulley. J Neurophysiol. 2003, 90:3809-3815
90. Miller JM. Understanding and misunderstanding extraocular musclepulleys. J Vis. 2007, 7(11): 1–15
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