PRK,LASIK技术在中国的应用

准分子激光屈光性角膜切削术（ＰＲＫ）和准分子激光原位角膜磨镶术（ＬＡＳＩＫ）是一种治疗眼球屈光不正的新技术,美国、德国、日本和中国（台湾）等国发展了多种准分子激光屈光治疗机以及相应的手术器械及软件,我国从１９９３年引进第一台ＰＲＫ机以来,已引进近百台机器,治疗屈光不正病例已超过十万。作者通过问卷调查和专家访问,对ＰＲＫ、ＬＡＳＩＫ技术在中国的应用状况进行了调查,在调查的基础上进行了分析,并对ＰＲＫ     

准分子激光原位角膜磨镶术的护理体会

准分子激光原位角膜磨镶术（LASIK）是目前安全性、准确性、稳定性以及疗效的预测性都较好的一种屈光不正矫治术．是目前治疗近视及近视散光首选的屈光手术之一。其原理是用显微板层成形系统掀开一个角膜瓣．在瓣下角膜基质层上用准分子激光根据近视、远视和散光度数进行精确切削。我院于2008年2月从德国引进世界上先进的第八代爱丽丝智能高速扫描准分子激光治疗系统。自4月份开展该术以来。共有212例（408只眼）患者要求手术,通过术前资料评估及术前检查．筛查确定出198例进行LASIK术。通过术前的心理护理、术中密切配合以及术后的详细指导及定期复查随访．疗效满意．现将护理体会总结如下。     

近视的药物治疗及手术治疗研究进展

近视是最常见的眼病之一,近年来,由于近视的发病率逐年上升,已成为世界性医学问题,近视眼的治疗也成为研究重点。药物研究和手术治疗是近视的治疗目前的研究热点,并已经取得一定得成果。药物方面,阿托品,托品酰胺,哌仑西平,消旋山莨菪碱对近视的控制作用都有被证实,但由于应用上还有一定的副作用,远期效果也不明确,需要进一步研究。手术方面,近视眼手术主要分为角膜屈光手术和眼内屈光手术。LASIK手术是目前应用最广泛的角膜屈光手术方法,SBK手术,飞秒激光手术等技术也日趋成熟。但是,角膜手术存在着一定的风险,应用范围也较为局限,需要进一步研究。眼内屈光手术主要为有晶体眼的人工晶体植入术(PIOL)和屈光性晶状体置换术,矫正的范围更加大,但是眼内手术并发症较多,也需要进一步研究和改进。     

准分子激光表层无痕术治疗近视患者的临床疗效分析

目的:研究准分子激光表层无痕术治疗近视患者的临床疗效。方法:选择2014年6月~2015年11月在我院进行准分子激光表层无痕术治疗的近视患者110例(198眼),根据眼屈光度数分为低(-1.00~-3.00 D)、中(-3~-6 D)、高(≥-6 D)度近视组。应用准分子激光对上皮层、前弹力层和前部基质层采取屈光性的切削,使眼球的表面稍微变平,角膜曲率进而改变。于术后复查眼部症状、上皮愈合情况、裸眼视力、矫正视力和屈光度。结果:仅少数患者于术后有不同程度的异物感,182眼(91.92%)角膜上皮在3天内愈合;术后所有患者的眼部均出现了不同程度的疼痛,但随着时间的增长逐渐好转,术后6 d疼痛感消失;与术前裸眼视力相比,三组在术后1天、1周、2周、1月和3月视力均明显升高,差异有统计学意义(P0.05);高度近视组在术后各时期的视力均明显低于低度近视组(P0.05);随着术后时间的延长,三组术后不同时间残余屈光度≤±1.00 D的百分比均有不同程度的升高,差异无统计学意义(P0.05);高度近视组在术后不同时间残余屈光度≤±1.00 D的百分比均明显低于低度近视组(P0.05);所有患者均无严重并发症发生,在随访期间无一例发生高眼压。结论:准分子激光表层无痕术能做到角膜无创口,有较高的预测性、安全性及有效性,且术后并发症少,有较好的应用前景。     

准分子激光原位角膜磨镶术前术后客观验光和主观验光的比较

目的比较准分子激光原位角膜磨镶术前后客观验光和主观验光的准确性和相关性。方法对在我中心接受LASIK手术69例123眼,在术前和术后一个月进行客观验光(NIDEKARK-700)和主观验光(RODENSTOCK综合验光头),对获得的数据进行相关分析。结果LASIK术后,客观验光的准确性较术前下降,客观验光和主观验光测量结果的差值明显增加;术前近视度越高,术后客观验光和主观验光测量结果的差别越大。在测量散光中,术后1月,客观验光和主观验光测量散光的差值明显增加,客观验光不能准确测量散光的量和轴向。结论LASIK术前用自动验光仪进行的客观验光可靠性较高,与主观验光法测量屈光不正的结果接近;术后,客观验光的准确性较术前下降,不能有效评判屈光不正的性质和量。     

准分子激光治疗近视眼

本文对准分子激光PRK治疗近视眼息者503例的早期临床结果进行分析,近视范围为－2．0至－15．0D,根据术前屈光度不同分为三组,术后随访三个月．结果证实准分子激光是一种安全、有效、预测性较好的治疗近视眼方法．全部病人提高了裸眼视力,绝大部分保持了最佳矫正视力,且没有产生危及视力的并发症．     

高度近视准分子激光原位角膜磨镶术后屈光回退的相关分析

目的:探讨高度近视准发子激光原位角膜镶术(laser insitu keratomileusis,LASIK)手术后屈光回退与术前各项检查结果间的相关性。方法:将135例(241只眼)近视患者按屈光度数分为A组126只眼(-6.00 D~-9.00 D)和B组115只眼(≥-9.00 D)。记录术前的屈光度数、眼压和角膜厚度,依据预期校正屈光度数计算理论残余角膜厚度,行LASIK手术后记录术后视力、屈光度数,进行统计学分析。术后平均随访时间19.14个月。结果:A组中正常术眼108只眼(85.7%),回退术眼18只眼(14.3%);B组中正常术眼74只眼(64.3%),回退术眼41只眼(35.7%);两组比较差异有非常显著意义(P<0.01)。术后平均视力A组为1.17±0.20,B组为0.99±0.28,两组比较差异有非常显著意义(P<0.01)。两组术后的平均屈光度数比较,差异有非常显著意义(P<0.01)。平均理论残余角膜厚度A组为(452.53±28.47)μm,B组为(439.61±30.11)μm,两者比较,差异有非常显著意义(P<0.01)。屈光回退度数与术前近视屈光度数显著正相关(r=0.35,P<0.001),与理论残余角膜厚度显著负相关(r=0.13,P=0.04),与术前眼压及术前角膜厚度无相关性(r=-0.48,P=0.46;r=-0.39,P=0.55)。结论:LASIK手术术前屈光度数越大,术前计算的理论残余角膜厚度越小,术后越易出现回退。对于-6.0 D~-9.00 D的高度近视患者,LASIK手术的预测性和术后稳定性相对较好;对于≥-9.00 D的超高度近视患者,应结合手术技术和术前计算的理论残余角膜厚度慎重选择进行手术。     

近视眼激光角膜切除术原理及控制方法

本文从理论上研究了激光人眼角膜切除术的原理和控制方法。详细分析了角膜前表面的曲率半径对近发消融深度和治疗结果的影响。     

角膜屈光手术后屈光回退的手术治疗进展*

屈光回退是角膜屈光手术后的并发症之一,其治疗方法主要为药物治疗和手术治疗。对于需要再次手术的患者,应根据初次手术方式、距离初次手术时间、回退度数,在充分评价角膜情况后合理选择增效术,确保手术的安全性和有效性。目前,准分子激光原位角膜磨镶术和飞秒激光小切口角膜基质透镜取出术是治疗近视和近视散光的主要手术方式。本文就两者术后屈光回退手术治疗的适应症、不同增效术的优缺点及注意事项作一综述。     

LASIK治疗高度近视的护理配合

目的:对高度近视患者行准分子激光原位角膜磨镶手术进行术前、术中和术后护理,观察高度近视患者LASIK手术矫治前后视功能的变化,评价LASIK矫治高度近视的疗效.方法:对90例(162眼)屈光度在-6.00 D以上的高度近视患者进行散瞳眼底检查,并就患者高度近视程度、眼底病变程度与患者手术后视力进行比较分析.结果:所有患者(162只眼)都接受了LASIK手术治疗.①手术后超高度近视组的矫正视力低于普通高度近视组,差异具有显著性意义(P<0.05).②手术前及手术后较严重眼底病变组的矫正视力均低于普通眼底病变组,差异具有显著性意义(P<0.05).结论:LASIK手术矫治高度近视眼是安全有效的,但其高度近视程度和眼底病变程度会影响手术疗效.     

Long-term evaluation of corneal sub-basal nerve recovery after photorefractive keratectomy and influence of pars plana vitrectomy

The corneal sub-basal nerve (SBN) plexus is destroyed during photorefractive keratectomy (PRK) and its recovery is still a matter of debate. In vivo confocal microscopy (IVCM) was used to evaluate SBN plexus in 23 patients at a distance of 10–25 years (mean 15.6 years) from myopic PRK. Because 8 out of the 23 PRK patients underwent pars plana vitrectomy (PPV) for rhegmatogenous retinal detachment, IVCM was also performed on those patients 6 months after PPV. Thirteen patients matched for age and myopia served as controls (non-PRK). SBN plexus was markedly reduced after PRK compared with non-PRK eyes and showed a slow, continuous but incomplete recovery up to the end of our follow-up (range 10–25 years). PRK and non-PRK eyes showed a marked reduction in SBN density 6 months after PPV, thus demonstrating a detrimental effect exerted by PPV on SBN plexus.     

Biomechanical modeling of refractive corneal surgery

The aim of refractive corneal surgery is to modify the curvature of the cornea to improve its dioptric properties. With that goal, the surgeon has to define the appropriate values of the surgical parameters in order to get the best clinical results, i.e., laser and geometric parameters such as depth and location of the incision, for each specific patient. A biomechanical study before surgery is therefore very convenient to assess quantitatively the effect of each parameter on the optical outcome. A mechanical model of the human cornea is here proposed and implemented under a finite element context to simulate the effects of some usual surgical procedures, such as photorefractive keratectomy (PRK), and limbal relaxing incisions (LRI). This model considers a nonlinear anisotropic hyperelastic behavior of the cornea that strongly depends on the physiological collagen fibril distribution. We evaluate the effect of the incision variables on the change of curvature of the cornea to correct myopia and astigmatism. The obtained results provided reasonable and useful information in the procedures analyzed. We can conclude from those results that this model reasonably approximates the corneal response to increasing pressure. We also show that tonometry measures of the IOP underpredicts its actual value after PRK or LASIK surgery.     

MEK kinase 2 binds and activates protein kinase C-related kinase 2. Bifurcation of kinase regulatory pathways at the level of an MAPK kinase kinase

MEK kinase 2 (MEKK2) is a 70-kDa protein serine/threonine kinase that has been shown to function as a mitogen-activated protein kinase (MAPK) kinase kinase. MEKK2 has its kinase domain in the COOH-terminal moiety of the protein. The NH(2)-terminal moiety of MEKK2 has no signature motif that would suggest a defined regulatory function. Yeast two-hybrid screening was performed to identify proteins that bind MEKK2. Protein kinase C-related kinase 2 (PRK2) was found to bind MEKK2; PRK2 has been previously shown to bind RhoA and the Src homology 3 domain of Nck. PRK2 did not bind MEKK3, which is closely related to MEKK2. The MEKK2 binding site maps to amino acids 637-660 in PRK2, which is distinct from the binding sites for RhoA and Nck. This sequence is divergent in the closely related kinase PRK1, which did not bind MEKK2. In cells, MEKK2 and PRK2 are co-immunoprecipitated and PRK2 is activated by MEKK2. Similarly, purified recombinant MEKK2 activated PRK2 in vitro. MEKK2 activation of PRK2 is independent of MEKK2 regulation of the c-Jun NH(2)-terminal kinase pathway. MEKK2 activation of PRK2 results in a bifurcation of signaling for the dual control of MAPK pathways and PRK2 regulated responses.     

cAMP Level Modulates Scleral Collagen Remodeling,a Critical Step in the Development of Myopia

The development of myopia is associated with decreased ocular scleral collagen synthesis in humans and animal models. Collagen synthesis is, in part, under the influence of cyclic adenosine monophosphate (cAMP). We investigated the associations between cAMP, myopia development in guinea pigs, and collagen synthesis by human scleral fibroblasts (HSFs). Form-deprived myopia (FDM) was induced by unilateral masking of guinea pig eyes. Scleral cAMP levels increased selectively in the FDM eyes and returned to normal levels after unmasking and recovery. Unilateral subconjunctival treatment with the adenylyl cyclase (AC) activator forskolin resulted in a myopic shift accompanied by reduced collagen mRNA levels, but it did not affect retinal electroretinograms. The AC inhibitor SQ22536 attenuated the progression of FDM. Moreover, forskolin inhibited collagen mRNA levels and collagen secretion by HSFs. The inhibition was reversed by SQ22536. These results demonstrate a critical role of cAMP in control of myopia development. Selective regulation of cAMP to control scleral collagen synthesis may be a novel therapeutic strategy for preventing and treating myopia.     

Characterization of the novel cardiolipin binding regions identified on the protease and lipid activated PKC‐related kinase 1

Protein kinase C‐related kinase 1 (PRK1) or PKN is a protease and lipid activated protein kinase that acted downstream of the RhoA or Rac1 pathway. PRK1 comprises a unique regulatory domain and a PKC homologous kinase domain. The regulatory domain of PRK1 consists of homologous region ?1 (HR1) and ?2 (HR2). PRK1‐(HR1) features a pseudosubstrate motif that overlapped with the putative cardiolipin and known RhoA binding sites. In fact, cardiolipin is the most potent lipid activator for PRK1 in respect of its either auto‐ or substrate phosphorylation activity. This study was thus aimed to characterize the binding region(s) of cardiolipin that was previously suggested for the regulatory domain of PRK1. The principal findings of this work established (i) PRK1‐(HR1) folded into an active conformation where high affinity binding sites (mainly located in HR1a subdomain) were accessible for cardiolipin binding to protect against limited Lys‐C digestion, (ii) the binding nature between acidic phospholipids and PRK1 (HR1) involved both polar and nonpolar components consistent with the amphipathic nature of the known cardiolipin‐binding motifs, (iii) identification of the molecule masses of the Lys‐C fragments of PRK1‐(HR1) complexed with cardiolipin molecule, and (iv) appreciable reductions in the secondary structural contents at 222 nm measured by circular dichroism analyses demonstrated the binding of cardiolipin elicited the disruptive effect that was most evident among all phospholipids tested, suggestive of a functional correlation between the extents of helical disruption and PRK1 activation.     

Isolation and compositional analysis of a CP12-associated complex of calvin cycle enzymes from Nicotiana tabacum

Two Calvin Cycle enzymes, NAD(P)-dependent glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and phosphoribulokinase (PRK) form a multiprotein complex with CP12, a small intrinsically-unstructured protein. Under oxidizing conditions, association with CP12 confers redox-sensitivity to the otherwise redox-insensitive A isoform of GAPDH (GapA) and provides an additional level of down-regulation to the redox-regulated PRK. To determine if CP12-mediated regulation is specific for GAPDH and PRK in vivo, a high molecular weight complex containing CP12 was isolated from tobacco chloroplasts and leaves and its protein composition was characterized. Gel electrophoresis and immunoblot analyses after separation of stromal proteins by size fractionation verified that the GAPDH (both isoforms) and PRK co-migrated with CP12 in dark- but not light-adapted chloroplasts. Nano-liquid-chromatography-mass-spectrometry of the isolated complex identified only CP12, GAPDH and PRK. Since nearly all of the CP12 from darkened chloroplasts migrates with GADPH and PRK as a high molecular mass species, these data indicate that the tight association of tobacco CP12 with GAPDH and PRK is specific and involves no other Calvin Cycle enzymes.