胸椎黄韧带骨化症

探讨胸椎黄韧带骨化症的诊断,治疗。方法：１９９４年２月－１９９５年１２月手术治疗胸椎黄韧带骨化症６例,男４例,女２例。年龄３８－５２岁。结果：手术６例随访时间９－１８月,平均１４．５月、皆有不同程度感觉平面下降,下肢肌力恢复１－２级。５例病理反射仍存在。结论;胸椎黄韧带骨化症应及早诊断手术治疗。病程迁延脊髓残留不可逆性损害。     

胸椎黄韧带骨化所致椎管狭窄症的诊断及手术治疗

报告胸椎黄韧带骨化所致椎管狭窄症并手术２１例。临床表现多为椎管狭窄引起的胸髓压迫症，其影像学检查具特征性表现，故可对黄韧带骨化进行早期诊断。椎板切除减压术范围应充分，包括切除部分小关节以及骨化灶上下各一椎节的椎板。随访１８例，平均随访时间２３个月，优良率６６．７％，有效率７７．８％。     

胸椎黄韧带骨化症

作者报告８例由黄韧带骨化（ＯＬＦ）引起的胸椎脊髓病。ＣＴ显示，骨化块多位于椎管的后侧和后外侧，呈结节状或山丘状改变，病变平面椎管狭窄，形态不规则。本组病例均行改进的扩大椎板切除减压手术治疗。术后平均随访４６个月，８例中４例症状完全缓解，行走接近正常，恢复轻体力工作；３例症状明显缓解、可较长距离行走，但步态僵硬；１例术前截瘫，术后可扶拐行走，括约肌功能正常。作者认为ＣＴ或ＣＴＭ是诊断ＯＬＦ的最好方法，“揭盖式”椎板减压术是一种安全有效的手术。     

胸椎黄韧带骨化症的手术治疗

目的探讨胸椎黄韧带骨化症的手术治疗方法。方法回顾分析2002年1月至2008年1月我院36例胸椎黄韧带骨化症手术治疗的病例。患者均采用胸椎管后壁切除术治疗。根据日本矫形外科学会（JOA,11分）评分标准进行术前和术后的疗效评价。结果36例患者获得6～72个月随访．平均随访时间19个月。术后平均改善率66．7％,优18例,良10例,改善8例．优良率77．8％。结论胸椎黄韧带骨化症可压迫脊髓出现神经系统症状,应尽早手术治疗．根据患者病情和影像学表现．明确胸椎黄韧带骨化部位和范围,采用胸椎管后壁切除术可获得满意的疗效。     

胸椎黄韧带骨化症的诊断与治疗

目的总结胸椎黄韧带骨化症（TOLF）的临床特点，手术方法及疗效，提高治疗效果。方法回顾性分析37例经过手术治疗的胸椎黄韧带骨化症患者的临床资料，其中30例行后路半关节突全椎板切除减压术，7例行后路半关节突全椎板切除加前路经胸腔侧前方椎管减压椎间盘切除及植骨融合内固定术。结果37例患者全部获得随访，随访时间6～78个月，平均38个月，疗效参照Epstein标准，优21例、良10例、改善5例、差1例。优良率83．78％。结论胸椎黄韧带骨化症一旦确诊，尽快手术治疗是唯一选择，手术可获得满意的疗效，手术疗效与脊髓损伤程度和病程长短有关。     

24例胸椎黄韧带骨化症的手术治疗效果观察

[目的]探讨胸椎黄韧带骨化症的手术治疗效果。[方法]回顾性分析自2004年1月～2008年1月采用半关节突全椎板切除术手术方法治疗胸椎黄韧带骨化症24例,男15例,女9例;年龄42～72岁(56±13)岁。根据JOA评分标准进行术前和术后的疗效评价。[结果]24例患者获得6～56个月随访,平均随访时间28个月。术后优16例,良4例,改善4例,优良率83.3%。[结论]胸椎黄韧带骨化症可压迫脊髓出现神经系统症状,应尽早手术治疗,半关节突全椎板切除减压是胸椎黄韧带骨化症目前较好的手术方式,术中彻底减压和实时的脊髓保护是手术取得成功的关键。     

胸椎黄韧带骨化症的诊断及手术治疗

目的：回顾性研究２５ 例胸椎黄韧带骨化症的临床表现,诊断及手术治疗效果。方法：分别对胸椎黄韧带骨化症的临床表现,影像学特征和手术治疗方法进行描述。结果：全部病例经术后随访３ 个月～６ 年,手术优良率为７２ ％ 。结论：手术治疗是胸椎黄韧带骨化症的有效方法。     

全椎板截骨再植椎管扩大成形术治疗胸椎黄韧带骨化症

目的总结胸椎黄韧带骨化症导致胸椎椎管狭窄的影像学特点，探讨改良椎管减压术的临床疗效。方法胸椎黄韧带骨化症31例，男18例，女13例；年龄26—73岁，平均45．7岁。术前均行MR、CT检查以明确诊断。合并颈椎管狭窄3例、腰椎管狭窄5例，颈胸腰椎管狭窄同时存在者2例；合并胸椎后纵韧带骨化和椎间盘突出症9例。单节段3例，双节段12例，三节段11例，四节段以上5例。局限型6例，连续型17例，跳跃型8例。共94个病变节段，其中上胸段(T1～T4)23个节段、中胸段(T5～T8)19个节段、下胸段(T9-T12)52个节段。手术采用全椎板截骨原位再植椎管扩大成形术。对9例合并胸椎后纵韧带骨化和椎间盘突出者，在后方减压的同时，行切除椎管前方突出椎间盘的环脊髓减压及后路钉棒系统内固定。术后疗效评价参照Epstein标准。结果24例患者随访6—63个月，平均15个月。术后疗效优14例、良7例、可3例，优良率87．5％。1例因术后停用脱水药物过早引起下肢瘫痪症状加重；2例出现下肢静脉血栓；2例硬脊膜撕裂。结论MR结合CT检查是诊断胸椎黄韧带骨化症最有效的手段，全椎板截骨再植椎管扩大成形术安全可靠，疗效满意。     

经皮脊柱内镜微创技术治疗胸椎黄韧带骨化症

[目的]介绍经皮内镜技术对胸椎黄韧带骨化导致脊髓病变进行彻底减压治疗经验。[方法]运用经皮脊柱内镜技术通过椎板间入路对2例胸椎黄韧带骨化导致脊髓压迫的患者进行手术减压。精确定位后,建立工作通道,磨除关节突,显露骨化的黄韧带,再将骨化物磨薄,切除。[结果]患者术前神经症状在术后均明显改善,术后复查胸椎CT显示减压效果良好。[结论]经皮内镜技术治疗胸椎黄韧带骨化导致的脊髓病变可在镜下进行直接减压,同时尽量减少创伤和术后不稳,为治疗黄韧带骨化提供一种新的选择。     

胸椎黄韧带骨化症的外科治疗

目的探讨胸椎黄韧带骨化症的诊断与手术治疗方法，分析其手术时机、手术技巧、手术效果及并发症处理。方法回顾性总结56例患者的外科治疗过程，采用胸椎管后壁切除减压及侧后方入路，术中体感诱发电位监护。结果术后55例经随访1年以上，1例随访2个月。39例，良8例，可5例，差4例。结论胸椎黄韧带骨化所致的脊髓压迫症须早期手术治疗，可根据不同情况选择胸椎管后壁切除减压及侧后方入路的次环状减压的手术方式。     

Identification of the insulin-regulated interaction of phosphodiesterase 3B with 14-3-3 beta protein

Phosphodiesterase (PDE)-3B, a major PDE isoform in adipocytes, plays a pivotal role in the antilipolytic action of insulin. Insulin-induced phosphorylation and activation of PDE3B is phosphatidylinositol 3-kinase (PI3-K) and Akt dependent, but the precise mechanism of PDE3B activation is not fully understood. We have identified 14-3-3 beta, a critical scaffolding molecule in signal transduction, as a protein that interacts with PDE3B using the yeast two-hybrid system. The interaction between PDE3B and 14-3-3 beta was then confirmed in vitro. The glutathione S-transferase (GST)-tagged 14-3-3 beta interacts with endogenous PDE3B of rat adipocytes, and this interaction is enhanced when adipocytes are treated with insulin. Coimmunoprecipitation experiments reveal that endogenous PDE3B also associates with endogenous 14-3-3 beta in rat adipocytes, and this interaction is enhanced by insulin. Two different PI3-K inhibitors, wortmannin and Ly294002, block this induction, suggesting that PI3-K is required. Synthetic 15 amino acid peptides of rat PDE3B containing phosphorylated Ser-279 or -302 inhibit this interaction, indicating that the insulin-regulated phosphorylation of these serine residues is involved. Because insulin receptor substrate-1 also associates with 14-3-3, the dimeric 14-3-3 beta could function as a scaffolding protein in the activation of PDE3B by insulin.     

H3K4m3和H3K9m3修饰对胰岛组织特异性基因表达的影响

目的 通过比较不同细胞类型之间胰腺十二指肠同源盒1(Pdx-1)、配对盒基因4(Pax4)、MafA(mast cell function associated antigen)和Nkx6.1等胰岛组织特异性基因其转录起始区的H3K4m3和H3K9m3修饰的差异,探讨H3K4m3和H3K9m3修饰对胰岛组织特异性基因表达的作用.方法 采用染色质免疫共沉淀一实时定量聚合酶链反应(PCR)法检测小鼠胚胎干细胞(mES,1×10~7)、小鼠成纤维细胞株NIH3T3细胞(1×10~7)和小鼠β细胞株NIT-1细胞(1×10~7)三者中的胰岛组织特异性基因、Oct4基因和MLH1基因转录起始区H3K4m3和H3K9m3修饰的状况.同时采用实时定量逆转录(RT)-PCR检测上述3种细胞各基因mRNA表达水平.分析H3K4m3和H3K9m3修饰改变与基因表达之间的关系.结果 NIT-1细胞中Pdx-1、Pax4、MafA、Nkx6.1等胰岛组织特异性基因转录起始区的H3K4m的修饰水平分别为:(4.84±0.05)%、(9.91±1.33)%、(10.64±0.87)%、(0.23±0.03)%,与mES细胞比较明显增高(P<0.05),基因表达;NIH3T3细胞中Pdx-1、Pax4、MafA、Nkx6.1等胰岛组织特异性基因转录起始区的H3K9m3的修饰水平分别为:(0.64±0.21)%、(7.04±1.29)%、(0.39±0.10)%、(2.35±0.81)%,与mES细胞比较明显增高(P<0.05),基因不表达.结论 H3K4m3与H3K9m3修饰能相互协调,共同调控胰岛组织特异性基因的表达.     

人钠/二羧酸协同转运蛋白3基因调控肾小管上皮细胞线粒体膜电位的研究

目的 观察人钠／二羧酸协同转运蛋白3(hNaDC3，)对人肾脏近曲小管上皮细胞(HKC)线粒体膜电位的变化及其对细胞能量代谢的影响。方法 应用亚克隆技术构建正义pcDNA3-hNaDC3和反义pcDNA3-AhNaDC3两个真核表达载体，通过脂质体LipofectAMINE将pcDNA3-hNaDC3及pcDNA3-AhNaDC3转染至HKC细胞。克隆筛选后，用RT—PCR、Northern印迹及Western印迹鉴定外源基因的整合和表达。荧光探针JC-1观察各细胞系线粒体膜电位的变化。结果 外源hNaDC3基因稳定整合到HKC细胞基因组中，并获得高、低表达。转染正义hNaDC3cDNA的HKC细胞线粒体膜电位降低，JC-1在线粒体内形成单体，发出绿色荧光；而转染反义hNaDC3cDNA的HKC细胞线粒体膜电位略微升高，JC-1形成聚合体，发出红色荧光。结论 hNaDC3过表达引起线粒体膜电位降低，反义hNaDC3则使线粒体膜电位略微升高。提示NaDC3可能通过使线粒体膜电位下降，参与了细胞能量代谢。     

RNA干扰技术沉默STAT3对人前列腺癌细胞生长的抑制作用

目的: 探讨RNA干扰技术沉默STAT3基因表达对人前列腺癌细胞PC3及LNCaP的生长抑制作用。　方法: 针对STAT3mRNA序列设计合成 3对编码小干扰RNA(siRNA)的DNA模板,构建pSilencer1. 0 U6 siRNA STAT3重组质粒,转染PC3及LNCaP细胞;采用Western印迹、Northern印迹等技术观察重组质粒对STAT3基因表达的影响;用MTT法观察重组质粒对PC3及LNCaP细胞体外生长抑制作用;用流式细胞术(FCM)及吖啶橙染色检测重组质粒诱导细胞凋亡。　结果: 成功构建pSilencer1. 0 U6 siRNA STAT3重组质粒,并成功转染PC3及LNCaP细胞;Western印迹,Northern印迹结果证实重组质粒在mRNA及蛋白水平分别显著抑制STAT3基因表达,抑制率为60% ~75%;MTT及FCM结果证明上述重组质粒可显著抑制PC3及LNCaP细胞的体外生长并诱导PC3细胞凋亡。结论: pSilencer1. 0 U6 siRNA STAT3可抑制STAT3在人前列腺癌细胞中的表达,并抑制肿瘤细胞的生长,促进其凋亡。     

C3 nephritic factor associated with C3 glomerulopathy in children

Background

C3 glomerulopathy (C3G) is characterized by predominant C3 deposits in glomeruli and dysregulation of the alternative pathway of complement. Half of C3G patients have a C3 nephritic factor (C3NeF). C3G incorporated entities with a range of features on microscopy including dense deposit diseases (DDD) and C3 glomerulonephritis (C3GN). The aim of this work was to study children cases of C3G associated with C3NeF.

Methods

We reviewed 18 cases of C3G with a childhood onset associated with C3NeF without identified mutations in CFH, CFI, and MCP genes.

Results

Clinical histories started with recurrent hematuria for seven patients, nephrotic syndrome for four, acute post-infectious glomerulonephritis for three and acute renal failure for four. Twelve patients had a low C3 at first investigation. Kidney biopsy showed ten C3GN and eight DDD. Twenty-three percent of the patients tested presented elevated sC5b9. Seven patients relapsed 3 to 6 years after the onset. At the end of follow-up, two patients were under dialysis, 11 had a persistent proteinuria, five had none; four patients did not follow any treatment. Steroids were first used in 80 % of cases.

Conclusions

C3NeF associated C3G has a heterogeneous presentation and outcome. Anti-proteinuric agents may control the disease during follow-up, even after nephrotic syndrome at the onset. The efficiency of immunosuppressive therapy remains questionable.     

Quantification and visualization of the three-dimensional inconsistency of the subthalamic nucleus in the Schaltenbrand-Wahren brain atlas

The Schaltenbrand-Wahren (SW) brain atlas has many limitations: the major two are three-dimensional (3D) inconsistency and spatial sparseness. In this work, we quantify and visualize the 3D inconsistency of the subthalamic nucleus (STN). The STN 3D models, 3D-A, 3D-C and 3D-S, are reconstructed from the SW axial, coronal, and sagittal microseries, respectively, by using a shape-based (NURBS) approach. All three models are placed in the SW coordinate system and compared quantitatively in terms of location (centroids), size (volumes), shape (normalized eigenvalues), orientation (eigenvectors), and mutual spatial relationships (overlaps and inclusions). Analysis is done in 3D within each orientation and across them. A dedicated tool is developed for quantitative validation of 3D modeling. The average error achieved is 0.088 mm, which is at the resolution limit of the digital SW atlas. The reconstructed 3D STN models differ in location, size, shape, orientation, overlap size, and inclusion rate. The 3D-S volume is 1.27 times larger than that of 3D-A and 1.38 times larger than that of 3D-C. The highest overlap size is found between 3D-A and 3D-S. The highest inclusion rates of 52.5 and 66.6% are for 3D-A and 3D-S. 3D-C has the lowest overlap size and results in the lowest inclusion rates (around 20-30%), meaning that 3D-C is substantially displaced in comparison to 3D-A and 3D-S. The lateral centroid coordinate of 3D-C is 9.18 mm while that of 3D-S is 12.17 mm. Each of the 3D models has some limitation: 3D-A in orientation, 3D-C in location, and 3D-S in shape realism. The STN in comparison to the actual almond is smaller, and relatively (i.e. normalized to the same height) 2.2-2.4 times wider and 3.7-5.5 times longer. 3D-C becomes more similar to 3D-S by scaling the SW coronal microseries laterally by 1.3257. Then the lateral coordinates of their centroids coincide, the difference between them in orientation is 0.11 mm, and 3D-S is only 1.06 times larger than the scaled 3D-C. This operation substantially improves registration of the SW atlas with the probabilistic functional atlas. However, 3D visualization shows that both 3D-S and scaled 3D-C models are heavily interwoven resulting in low inclusion rates of about 60%. The STN in the SW atlas shows severe 3D inaccuracy within each orientation and across them, and it has to be employed with great care and understanding of its limitations.     

Tacrolimus pharmacogenetics: the CYP3A5*1 allele predicts low dose-normalized tacrolimus blood concentrations in whites and South Asians

Previously, we demonstrated that the dose-normalized tacrolimus blood concentration after renal transplantation was associated with a single nucleotide polymorphism (SNP) in the CYP3AP1 gene, probably through linkage with an SNP in the CYP3A5 gene. Individuals with at least one CYP3A5*1 allele synthesize CYP3A5 and CYP3A5*3/*3 homozygotes do not. We now present results with direct typing of the CYP3A5 genotype for this group of 180 kidney-only transplant recipients from a single center. South Asian and white patients with at least one CYP3A5*1 allele achieved twofold lower dose-normalized tacrolimus blood concentrations compared with CYP3A5*3/*3 homozygotes, confirming our previous findings for the CYP3AP1 SNP. There was a significant delay in achieving target blood concentrations in those with at least one CYP3A5*1 allele. Determination of the CYP3A5*1/*3 genotype could be used to predict the tacrolimus dose requirement and, given incomplete linkage, would be better than determination of the CYP3AP1 genotype.     

Effectiveness of a second course of OKT3 monoclonal anti-T cell antibody for treatment of renal allograft rejection

A second course of OKT3 monoclonal anti-T cell antibody was given to 21 recipients of kidney transplants. Rejections reversed in 43% of patients in whom 95% of rejections had reversed with their initial OKT3 course. Reversal was highly dependent upon the timing of rejection, anti-OKT3 antibody production, and T cell CD3 modulation. Rejections treated greater than 90 days after transplantation were resistant to OKT3 reversal. High-titer anti-OKT3 antibodies prevented OKT3 reversal of rejection, and effective CD3 (the cell surface target of OKT3) modulation was necessary for successful OKT3 reversal of rejection. Reexposure to OKT3 further stimulated anti-OKT3 antibody production and broadened the specificity of the antibodies produced. OKT3 can effectively and safely be used a second time for treatment of early T cell-mediated renal allograft rejections if high-titer anti-OKT3 antibodies have not been made.     

Extrarenal metabolism of 25-hydroxycholecalciferol in the rat: regulation by 1,25-dihydroxycholecalciferol

To determine the role of the kidney in regulation of 25-hydroxycholecalciferol (25OHD3, metabolism, the effects of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] on 3H-25OHD3 were compared in intact and nephrectomized vitamin D-deficient rats. Sixteen hours after the intravenous administration of 3H-25OHD3, extracts of serum and pooled small intestinal mucosa were fractionated by Sephadex LH-20 column chromatography followed by high performance liquid chromatography. In intact rats, 1,25(OH)2D3 (50 ng/day i.p. for 7 days) increased mean serum 3H-24,25-dihydroxycholecalciferol [3H-24,25(OH)2D3] from 2 +/- 2-210 +/- 80 fmol/ml (mean +/- 1 SD), increased mean serum 3H-25,26-dihydroxycholecalciferol [3H-25,26(OH)2D3] from 2 +/- 2-12 +/- 6 fmol/ml and lowered mean serum 3H-1,25(OH)2D3 from 210 +/- 40-4 +/- 4 fmol/ml. Similarly, in nephrectomized animals, 1,25(OH)2D3 increased mean serum 3H-24,25-(OH)2D3 from 6 +/- 11-115 +/- 30 fmol/ml and increased mean serum 3H-25,26(OH)2D3 from 3 +/- 3-26 +/- 10 fmol/ml. Nephrectomy increased serum 3H-25(OH)D3 in untreated (from 1450 +/- 225-2675 +/- 225 fmol/ml serum) and 1,25(OH)2D3 treated rats (from 1600 +/- 175-3075 +/- 100 fmol/ml). 3H-1,25(OH)2D3 averaged 74 +/- 16% of total radioactivity in intestinal mucosa of untreated intact rats and was not detected in either the serum or intestinal mucosa of nephrectomized animals. The results suggest that in intact animals, extrarenal synthesis can account for substantial 24,25(OH)2D3 production and for most 25,26(OH)2D3 production.(ABSTRACT TRUNCATED AT 250 WORDS)