本文選題：高分辨率CT + 核磁共振��； 參考：《山東大學(xué)》2014年博士論文

【摘要】：第一部分：POU3F4基因突變所致X連鎖的遺傳性非綜合征型耳聾患者內(nèi)耳畸形影像學(xué)分析 1.研究目的： 用MPR后處理技術(shù)在最佳層面顯示內(nèi)耳結(jié)構(gòu)和聽(tīng)神經(jīng),CT仿真內(nèi)鏡技術(shù)顯示蝸神經(jīng)孔,VRT技術(shù)顯示內(nèi)耳立體形態(tài),與正常組對(duì)照,回顧性分析POU3F4基因突變所致的X連鎖的非綜合征型遺傳性耳聾患者內(nèi)耳發(fā)育畸形影像學(xué)表現(xiàn)及特征。 2.材料與方法： 收集自2004年-2014年收集6例經(jīng)基因診斷確診的POU3F4基因突變所致的X連鎖的非綜合征型遺傳性耳聾患者HRCT和MRI影像學(xué)資料,男性,年齡2-19歲,其中2例來(lái)自同一家庭,另4例分別來(lái)自不同家庭。電測(cè)聽(tīng)結(jié)果：3例重度感音神經(jīng)性耳聾,3例混合性耳聾。同時(shí)收集3例致病基因攜帶者影像資料,分別來(lái)自病例組三個(gè)不同家庭,均為女性,年齡28歲-52歲,2例聽(tīng)力正常,1例輕度混合性聽(tīng)力減低。另收集30例因眩暈、外傷就診患者HRCT、MRI掃描數(shù)據(jù)作為對(duì)照組,男18例,女12例,年齡2歲-46歲所有患者聽(tīng)力正常,均否認(rèn)中內(nèi)耳疾病史。用MPR技術(shù)重組耳蝸、內(nèi)聽(tīng)道、半規(guī)管等相關(guān)結(jié)構(gòu),用CTVE技術(shù)顯示蝸神經(jīng)孔,VRT技術(shù)顯示內(nèi)耳立體形態(tài),與正常組比較,分析病例組和致病基因攜帶組患者內(nèi)耳形態(tài)學(xué)變化。 3.結(jié)果： 3.1病例組內(nèi)耳結(jié)構(gòu)形態(tài)學(xué)異常主要有： 病例組6例病人所見(jiàn)內(nèi)耳畸形在同一病例均為雙側(cè)對(duì)稱性。 (1)6例(12耳)均存在耳蝸發(fā)育異常,耳蝸畸形形態(tài)學(xué)表現(xiàn)相似,HRCT和MRI表現(xiàn)為耳蝸外殼相對(duì)正常,略呈葫蘆形,耳蝸各轉(zhuǎn)均已發(fā)育,底轉(zhuǎn)/中轉(zhuǎn)和中轉(zhuǎn)/頂轉(zhuǎn)之間骨性分隔存在；耳蝸蝸軸及蝸螺旋板缺如,被液體密度/信號(hào)影取代,蝸管內(nèi)腔開(kāi)放,與耳蝸內(nèi)腔相通；蝸神經(jīng)管增寬；耳蝸與內(nèi)聽(tīng)道直接相通,無(wú)骨性或軟組織分隔。 (2)6例(12耳)雙側(cè)內(nèi)聽(tīng)道外側(cè)端對(duì)稱性擴(kuò)張,中段及內(nèi)側(cè)端無(wú)擴(kuò)張。 (3)6例(12耳)面神經(jīng)管迷路段和水平段擴(kuò)張,前庭上神經(jīng)管擴(kuò)張,兩者之間Bill’s嵴肥大、部分氣化；單孔神經(jīng)管均開(kāi)口于內(nèi)聽(tīng)道近端,其中1例(2耳)單孔神經(jīng)管擴(kuò)張；前庭下神經(jīng)管未見(jiàn)擴(kuò)張。 (4)6例(12耳)上、水平及后半規(guī)管外形正常,其中3例(6耳)水平半規(guī)管和后半規(guī)管擴(kuò)張,水平半規(guī)管內(nèi)骨島變��；1例(2耳)后半規(guī)管下壁骨質(zhì)不連續(xù)。 (5)2例病例(4耳)前庭導(dǎo)水管起始段擴(kuò)張,內(nèi)淋巴囊無(wú)擴(kuò)張；余4例患者前庭導(dǎo)水管形態(tài)正常。 (6)2例病例(4耳)前庭內(nèi)上緣見(jiàn)小囊狀突起,并向上突入上半規(guī)管兩腳之間。 (7)6例(12耳)蝸神經(jīng)孔CTVE成像可見(jiàn)螺旋形耳蝸內(nèi)腔,而非正常組螺旋形蝸神經(jīng)孔列。Bill's嵴肥大,上前庭神經(jīng)孔與面神經(jīng)孔距離增大。 (8)6例(12耳)蝸神經(jīng)均存在,由內(nèi)聽(tīng)道直接進(jìn)入耳蝸內(nèi)腔。 3.2致病基因攜帶者內(nèi)耳結(jié)構(gòu)形態(tài)學(xué)異常 3例(6耳)致病基因攜帶者僅見(jiàn)內(nèi)聽(tīng)道外側(cè)端擴(kuò)張,其中1例(2耳)伴有內(nèi)聽(tīng)道底面神經(jīng)管和前庭上神經(jīng)管擴(kuò)張(圖21)；耳蝸、前庭、半規(guī)管、前庭導(dǎo)水管均未見(jiàn)異常形態(tài)學(xué)改變。 4.結(jié)論 (1)6例不同POU3F4基因突變位點(diǎn)耳聾患者具有共同的影像學(xué)表現(xiàn),包括雙側(cè)對(duì)稱性耳蝸發(fā)育畸形(蝸軸缺如,外形大致正常,與內(nèi)聽(tīng)道直接交通)、內(nèi)聽(tīng)道外側(cè)端擴(kuò)張、面神經(jīng)迷路段和前庭上神經(jīng)管擴(kuò)張,為本組POU3F4基因突變所致X連鎖的非綜合征型耳聾患者典型的影像學(xué)特征； (2)本組部分患者可合并有前庭畸形,前庭導(dǎo)水管起始部擴(kuò)大,單孔神經(jīng)管擴(kuò)大及水平、后半規(guī)管擴(kuò)大； (3)致病基因攜帶者表現(xiàn)為內(nèi)聽(tīng)道外側(cè)端擴(kuò)張,部分病例可合并面神經(jīng)管和前庭上神經(jīng)管的擴(kuò)張。 第二部分：POU3F4基因異常所致X連鎖的遺傳性非綜合征型耳聾患者鐙骨HRCT評(píng)價(jià) 1.研究目的： 采用多層螺旋CT MPR技術(shù)重組鐙骨結(jié)構(gòu)同層顯示圖像,與正常組對(duì)照,對(duì)POU3F4基因異常所致X連鎖的遺傳性非綜合征型耳聾患者及致病基因攜帶者鐙骨底板、鐙骨形態(tài)及鐙骨前間隙進(jìn)行評(píng)價(jià)。 2.材料與方法： 收集自2004年-2014年收集6例POU3F4基因異常所致的X連鎖的非綜合征型遺傳性耳聾患者HRCT影像學(xué)資料,男性,年齡2-19歲,其中2例來(lái)自同一家庭,另4例分別來(lái)自不同家庭。電測(cè)聽(tīng)結(jié)果：3例重度感音神經(jīng)性耳聾,3例混合性耳聾。3例致病基因攜帶者影像資料也被收集,分別來(lái)自病例組三個(gè)不同家庭,均為女性,年齡28歲-52歲,2例聽(tīng)力正常,1例輕度混合性聽(tīng)力減低。另收集30例因眩暈、外傷就診患者HRCT掃描數(shù)據(jù)作為對(duì)照組,男18例,女12例,年齡2歲-46歲所有患者聽(tīng)力正常,均否認(rèn)中內(nèi)耳疾病史。用MPR技術(shù)重組鐙骨結(jié)構(gòu)同層顯示圖像,與正常組比較,分析各組鐙骨形態(tài)學(xué)改變,同時(shí)分析各組鐙骨底板厚度及鐙骨前間隙顯示率有無(wú)差異。所有統(tǒng)計(jì)學(xué)處理均在SPSS17.0軟件中完成。 3.結(jié)果： (1)病例組與正常組鐙骨底板厚度和鐙骨前間隙顯示率存在差異； (2)致病基因攜帶組與正常組鐙骨底板厚度和鐙骨前間隙顯示率無(wú)明顯差異； (3)病例組鐙骨形態(tài)學(xué)改變主要有5例(9耳)鐙骨底板增厚和鐙骨前間隙消失,其中1例(1耳)鐙骨前弓發(fā)育不全,1例(1耳)鐙骨后弓發(fā)育不全,1例(1耳)鐙骨前弓發(fā)育不良,2例(耳)柱狀鐙骨；1例(2耳)雙側(cè)鐙骨底板瘺。致病基因攜帶組3例(6耳)鐙骨形態(tài)學(xué)無(wú)明顯異常。 4.結(jié)論 (1) POU3F4基因突變所致X連鎖的非綜合征型耳聾患者鐙骨底板厚于正常人； (2) POU3F4基因突變所致X連鎖的非綜合征型耳聾患者鐙骨前間隙顯示率明顯低于正常人； (3) POU3F4基因突變所致X連鎖的非綜合征型耳聾患者鐙骨底板具有典型影像學(xué)特征,包括鐙骨底板增厚和鐙骨前間隙消失,部分病例可合并鐙骨前后弓發(fā)育不良、柱狀鐙骨及鐙骨底板瘺；本組致病基因攜帶者鐙骨形態(tài)無(wú)異常發(fā)現(xiàn)。
[Abstract]:Part one: imaging analysis of inner ear malformation of X linked hereditary nonsyndromic hearing loss caused by POU3F4 gene mutation
1. the purpose of the study:
MPR post-processing technique was used to display the inner ear structure and auditory nerve at the best level. The CT simulation endoscopy showed the cochlear nerve hole, and the VRT technique showed the three-dimensional shape of the inner ear. Compared with the normal group, the imaging findings and characteristics of the malformation of the inner ear development of the non syndromic hereditary deafness induced by the X linked POU3F4 gene mutation were analyzed retrospectively.
2. materials and methods:
The HRCT and MRI imaging data of 6 non syndromic hereditary deafness patients were collected from 6 cases of POU3F4 gene mutation diagnosed by gene diagnosis in 2004. Male, age 2-19 years old, 2 of them from the same family and 4 from different families. Electrical audiometry results were found in 3 cases of severe sensorineural deafness and 3 mixed cases. At the same time, 3 patients were collected from three different families, all of which were female, 28 years old -52 years old, 2 cases with normal hearing and 1 mild mixed hearing loss, and 30 cases of vertigo and trauma patients were collected as the control group, 18 men, 12 women, and all -46 years old at the age of 2, all -46 years old. MPR technique was used to reconstruct the cochlea, the inner auditory canal, the semicircular canal and other related structures, and the CTVE technique was used to display the cochlear nerve foramen. The VRT technique was used to display the three-dimensional shape of the inner ear, and the morphological changes of the inner ear of the patients and the patients with the disease gene were compared with the normal group.
3. results:
3.1 the morphological abnormality of inner ear structure in case group was mainly:
The inner ear malformations seen in 6 patients in the case group were bilateral symmetry in the same case.
(1) 6 cases (12 ears) had cochlear dysplasia, and cochlear malformation was similar in morphology. HRCT and MRI showed that the cochlear shell was relatively normal, slightly gourd, the cochlea was developed, the bottom / transfer and the transfer / top rotation existed between the cochlea, the cochlear and cochlear spiral plates were absent, and the liquid density / signal shadow was replaced and the inner cavity of the cochlear tube opened. It is connected with the inner cavity of the cochlea; the cochlear canal is widened; the cochlea is directly interconnected with the internal auditory canal without any bony or soft tissue separation.
(2) 6 cases (12 ears) had symmetrical expansion on the lateral side of the inner auditory canal and no expansion in the middle and medial side.
(3) the dilation of the labyrinth and horizontal segments of the facial nerve canal in 6 cases (12 ears), the dilatation of the superior vestibular nerve canal, the Bill 's ridge hypertrophy and partial gasification, and the opening of the single hole nerve tube to the proximal end of the inner auditory canal, of which 1 cases (2 ears) were dilated by the single hole nerve canal, and no dilation was found in the vestibular canal.
(4) in 6 cases (12 ears), the horizontal and posterior semicircular canals were normal, of which 3 cases (6 ears) were dilated in the horizontal semicircular canal and posterior semicircular canal, and the inner bone island in the horizontal semicircular canal became smaller, and the inferior wall of the posterior semicircular canal was discontinuous in the posterior wall of the 1 cases (2 ears).
(5) in 2 cases (4 ears), the vestibular aqueduct began to expand, and the endolymphatic sac did not expand. In 4 cases, the vestibular aqueduct was normal.
(6) in 2 cases (4 ears), small vesicular protuberances were seen in the upper part of the vestibule, and upward to the upper semicircular canal between the feet.
(7) 6 cases (12 ears) of the cochlear cochlear cavity were seen in the CTVE of the cochlear cochlea, but not in the normal group of spiral cochlear.Bill's, and the distance between the upper vestibular and facial nerve holes increased.
(8) in 6 cases (12 ears), the cochlear nerve was present and entered the cochlea cavity directly from the internal auditory canal.
3.2 the inner ear structure is abnormal in the carriers of disease causing genes.
In 3 cases (6 ears), only 1 cases (2 ears) were accompanied by the dilatation of the inner auditory canal and the superior vestibular canal (Figure 21). There were no abnormal morphological changes in the cochlea, the vestibule, the semicircular canal and the vestibular aqueduct.
4. conclusion
(1) 6 cases of deafness with different POU3F4 gene mutation sites have common imaging features, including bilateral symmetric cochlear development (abnormal cochlear axis, normal shape, direct traffic with the inner auditory), external lateral dilatation of the inner auditory canal, facial nerve labyrinth and vestibular canal dilation, which are the non synthesis of X linked POU3F4 gene mutations in this group. Typical imaging features of patients with syndromic deafness.
(2) some patients may have vestibular deformities, enlargement of the vestibular aqueduct, enlargement of the single canal, and expansion of the posterior semicircular canal.
(3) the carriers of the pathogenic gene showed expansion of the lateral side of the inner auditory canal, and some cases could be expanded with facial nerve canal and vestibular nerve canal.
The second part: stapes HRCT evaluation of X linked hereditary nonsyndromic hearing loss caused by POU3F4 gene abnormality.
1. the purpose of the study:
Multislice spiral CT MPR technique was used to reconstruct the stapes structure in the same layer. Compared with the normal group, the stapes floor, the stapes shape and the stapes gap of the X linked genetic nonsyndromic deafness patients and the carriers of the POU3F4 gene were evaluated.
2. materials and methods:
The HRCT imaging data of X linked non syndromic deafness patients were collected from 6 cases of POU3F4 gene abnormalities in -2014 2004. Men were 2-19 years old, 2 of them were from the same family and 4 from different families. 3 cases of severe sensorineural deafness and 3.3 cases of mixed deafness were carried out. The band image data were also collected from three different families of the case group, all of which were female, age 28 -52 years, 2 cases of normal hearing and 1 mild mixed hearing loss, and 30 cases of vertigo, HRCT scan data were collected as the control group, 18 men, 12 women, and 2 years old -46 years old, all denied middle hearing. MPR technique was used to reconstruct the stapes structure and the image of the same layer. Compared with the normal group, the morphological changes of stapes were analyzed. At the same time, there was no difference in the thickness of the stapes floor and the display rate of the stapes gap in each group. All the statistical treatments were completed in the SPSS17.0 software.
3. results:
(1) there were differences in the thickness of stapes floor and the stapes anterior space between case group and normal group.
(2) there was no significant difference in the thickness of the stapes floor and the stapes space between the pathogenic gene carrier group and the normal group.
(3) the morphological changes of stapes in the case group were mainly 5 cases (9 ears) thickening of the stapes floor and disappearance of the anterior stapes space, of which 1 cases (1 ears) had dysplasia of the stapes anterior arch, 1 (1 ears) stapapapapstal arch dysplasia, 1 (1 ears) dysplasia of the stapes anterior arch, 2 cases (ears) columnar stapes, 1 (2) bilateral stapes floor fistula. Pathogenic gene carrying group 3 cases (6 ears) stapes There was no obvious abnormality in morphology.
4. conclusion
(1) the stapes floor of X linked non syndromic hearing loss caused by POU3F4 mutation is thicker than that of normal persons.
(2) the rate of stapes anterior space in X linked non syndromic hearing loss caused by POU3F4 mutation was significantly lower than that in normal subjects.
(3) the stapes floor of the X linked non syndromic deafness patients with POU3F4 gene mutation has typical imaging features, including the thickening of the stapes floor and the disappearance of the anterior stapes space. Some cases may be associated with the dysplasia of the stapes, the stapes and the stapes floor fistula, and the stapes form in this group has no abnormal discovery of the stapes.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2014
【分類號(hào)】：R764.43;R816.96

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 朱學(xué)駿,陳喜雪,李冠群,楊勇,馬玲蕾,董慧婷,吳安,謝艷秋;角蛋白相關(guān)遺傳性皮膚病基因突變的研究進(jìn)展[J];中華皮膚科雜志;2001年05期

2 耿稚江;;構(gòu)成長(zhǎng)壽的基因突變被成功鑒定[J];國(guó)外醫(yī)學(xué)情報(bào);2004年09期

3 李勝光;黃烽;劉湘源;鄧心新;徐明;丁玉珍;叢賢滋;;熒光雜交探針實(shí)時(shí)聚合酶鏈?zhǔn)椒磻?yīng)快速檢測(cè)甘露聚糖結(jié)合凝集素啟動(dòng)子區(qū)基因變異方法的建立[J];中華臨床醫(yī)師雜志(電子版);2008年06期

4 朱佳杰;;肺癌發(fā)生相關(guān)基因的研究進(jìn)展[J];醫(yī)藥論壇雜志;2011年07期

5 高福平;魏謹(jǐn);;P53與肺癌關(guān)系的研究進(jìn)展[J];臨床肺科雜志;2012年01期

6 路俊生;何勝虎;;家族性擴(kuò)張型心肌病的基因突變[J];國(guó)際心血管病雜志;2012年03期

7 張廣宇，孫以瑜，王孟山，朱春賢;肺癌K－ras基因突變的檢測(cè)及臨床應(yīng)用[J];中華結(jié)核和呼吸雜志;1995年05期

8 但凌;一種基因、四種綜合征[J];國(guó)外醫(yī)學(xué).遺傳學(xué)分冊(cè);1995年03期

9 張磊;吸煙致癌與P53基因[J];解放軍健康;1998年03期

10 吳小軍,李清泉,陳雪芹,胡克,丁續(xù)紅,楊炯;肺癌患者組織和痰液中p53基因、K-ras基因突變[J];腫瘤防治研究;2000年01期

相關(guān)會(huì)議論文 前10條

1 吳雪瓊;張俊仙;李洪敏;梁建琴;鐘敏;王巍;;結(jié)核分支桿菌耐藥基因的研究[A];中國(guó)防癆協(xié)會(huì)全國(guó)學(xué)術(shù)會(huì)議大會(huì)學(xué)術(shù)報(bào)告[C];2001年

2 楊芳;金佩佩;王學(xué)鋒;丁秋蘭;王鴻利;李薇;王冠軍;;2例新的基因突變導(dǎo)致遺傳性蛋白S缺陷癥[A];第11次中國(guó)實(shí)驗(yàn)血液學(xué)會(huì)議論文匯編[C];2007年

3 馮義國(guó);白轉(zhuǎn)麗;肖生祥;譚升順;吳佳紋;;先天性厚甲癥Ⅰ型的基因突變研究[A];中華醫(yī)學(xué)會(huì)第14次全國(guó)皮膚性病學(xué)術(shù)年會(huì)論文匯編[C];2008年

4 劉第墉;;HOX基因熱潮:又一次爆發(fā)性抄炒[A];中國(guó)古生物學(xué)會(huì)第21屆學(xué)術(shù)年會(huì)論文摘要集[C];2001年

5 殷鑫湞;張寶榮;;脊髓小腦共濟(jì)失調(diào)7型的臨床特征及基因突變研究[A];第九次全國(guó)神經(jīng)病學(xué)學(xué)術(shù)大會(huì)論文匯編[C];2006年

6 陸舜;李子明;;驅(qū)動(dòng)基因和轉(zhuǎn)化型研究的治療策略[A];第13屆全國(guó)肺癌學(xué)術(shù)大會(huì)論文匯編[C];2013年

7 呂鶴;呼群;袁云;;中國(guó)CADASIL的臨床和基因改變規(guī)律[A];第九次全國(guó)神經(jīng)病學(xué)學(xué)術(shù)大會(huì)論文匯編[C];2006年

8 沈楊;朱勇梅;樊星;施靜藝;王琴榮;顏曉菁;顧朝暉;王彥艷;陳冰;姜春雷;嚴(yán)晗;陳菲菲;陳海敏;陳竺;金潔;陳賽娟;;1185例急性髓細(xì)胞白血病基因突變和預(yù)后影響研究[A];第13屆全國(guó)實(shí)驗(yàn)血液學(xué)會(huì)議論文摘要[C];2011年

9 楊芳;周榮富;付啟華;王學(xué)鋒;丁秋蘭;王鴻利;楊芳;李薇;王冠軍;;5例新的基因突變導(dǎo)致遺傳性抗凝血酶缺陷癥[A];中華醫(yī)學(xué)會(huì)第七次全國(guó)檢驗(yàn)醫(yī)學(xué)學(xué)術(shù)會(huì)議資料匯編[C];2008年

10 周向平;張成;粱秀齡;;Charcot-Marie-Tooth病Cx32基因突變研究[A];第四次全國(guó)中西醫(yī)結(jié)合神經(jīng)系統(tǒng)疾病學(xué)術(shù)研討會(huì)論文集[C];2002年

相關(guān)重要報(bào)紙文章 前10條

1 本報(bào)記者 李禾;吸煙導(dǎo)致的基因突變可代代相傳？[N];科技日?qǐng)?bào);2010年

2 實(shí)習(xí)生 劉冰玉;檢測(cè)癌癥基因能否一紙完成？[N];科技日?qǐng)?bào);2012年

3 記者 耿建擴(kuò) 通訊員 李晉陶 程益聰;人類8種新發(fā)基因突變被發(fā)現(xiàn)[N];光明日?qǐng)?bào);2013年

4 查莉 武佼芳;市中心醫(yī)院發(fā)現(xiàn)人類8種新發(fā)基因突變[N];邯鄲日?qǐng)?bào);2013年

5 吳汐;英科學(xué)家發(fā)現(xiàn)語(yǔ)言基因[N];遼寧日?qǐng)?bào);2001年

6 奇云;基因檢測(cè)預(yù)知疾病幾多風(fēng)險(xiǎn)[N];大眾科技報(bào);2007年

7 張?zhí)锟?基因的對(duì)壘與相互依存[N];大眾科技報(bào);2000年

8 馬曉燕;查一下基因，，能預(yù)知你容易得啥病[N];新華每日電訊;2005年

9 本報(bào)記者 夏雄偉;我們走在國(guó)內(nèi)基因產(chǎn)業(yè)的最前列[N];證券時(shí)報(bào);2000年

10 吉吉邋編譯;科學(xué)家已發(fā)現(xiàn)吸煙基因[N];第一財(cái)經(jīng)日?qǐng)?bào);2008年

相關(guān)博士學(xué)位論文 前10條

1 楊昭慶;云南省兩種遺傳性血液疾病的基因突變研究[D];中國(guó)協(xié)和醫(yī)科大學(xué);2001年

2 茅江峰;不同基因突變對(duì)特發(fā)性低促性腺激素性性腺功能減退癥患者的臨床特點(diǎn)、隱睪和生精療效的影響[D];北京協(xié)和醫(yī)學(xué)院;2013年

3 張軍航;肺癌組織中p16基因mRNA和蛋白表達(dá)及基因異常甲基化的研究[D];中國(guó)醫(yī)科大學(xué);2002年

4 李冰;第一部分 原發(fā)性骨髓纖維化患者基因突變的研究 第二部分 原發(fā)性骨髓纖維化患者的細(xì)胞遺傳學(xué)研究 第三部分 血清鐵蛋白是中國(guó)骨髓增生異常綜合征中危-1組患者的獨(dú)立預(yù)后因素[D];北京協(xié)和醫(yī)學(xué)院;2014年

5 段妍;單純型和顯性營(yíng)養(yǎng)不良型大皰性表皮松解癥基因突變研究[D];南方醫(yī)科大學(xué);2014年

6 李紅梅;聯(lián)合檢測(cè)p53基因和端粒酶對(duì)肺癌的診斷意義[D];天津醫(yī)科大學(xué);2010年

7 李劍;Ndr2基因在人類淋巴造血系統(tǒng)中的功能研究[D];第四軍醫(yī)大學(xué);2002年

8 潘洪明;漢族人群RAGE基因和APE1基因多態(tài)性與肺癌易感性的關(guān)聯(lián)研究[D];大連理工大學(xué);2013年

9 陳棟;BRAF基因突變與惡性腫瘤的系統(tǒng)評(píng)價(jià)及其痕量檢測(cè)方法的構(gòu)建[D];第三軍醫(yī)大學(xué);2014年

10 尹光浩;非小細(xì)胞肺癌的磷酸化EGFR與EGFR基因突變的比較分析[D];吉林大學(xué);2009年

相關(guān)碩士學(xué)位論文 前10條

1 李君;潰瘍性結(jié)腸炎和潰瘍性結(jié)腸炎相關(guān)癌的有關(guān)基因改變[D];浙江大學(xué);2001年

2 孫文夏;脂代謝相關(guān)三基因突變小鼠模型的建立與動(dòng)脈粥樣硬化機(jī)理研究[D];浙江大學(xué);2004年

3 焦衛(wèi)云;一種新的凝血因子X(jué)III基因突變導(dǎo)致的遺傳性FXIII缺陷癥[D];安徽醫(yī)科大學(xué);2007年

4 李長(zhǎng)毅;nm23-H_1基因雜合性缺失與肺癌生物學(xué)特性[D];重慶醫(yī)科大學(xué);2004年

5 彭亞婷;RAD51基因G135C單核苷酸多態(tài)性在肺癌中的意義[D];南昌大學(xué);2011年

6 謝艷秋;表皮松解性角化過(guò)度家系基因突變研究[D];天津醫(yī)科大學(xué);2002年

7 石文;中國(guó)南方漢族和西藏藏族RHCE基因多態(tài)性研究[D];廣州中醫(yī)藥大學(xué);2012年

8 呂衛(wèi)剛;家族性腺瘤性息肉病基因診斷流程的建立及三個(gè)家系的突變分析[D];中南大學(xué);2010年

9 劉曉蕾;肺癌EGFR基因突變檢測(cè)方法的建立及臨床應(yīng)用[D];遼寧醫(yī)學(xué)院;2012年

10 臧文巧;豫醫(yī)無(wú)毛小鼠無(wú)毛基因突變部位的定位和分析[D];鄭州大學(xué);2004年

本文編號(hào)：1898540