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91.
92.
Bisphosphonate associated osteonecrosis of the jaws (ONJ) usually commences at the alveolus. Comparison is made between the structure and function of long bones and alveolar bone and the differing susceptibilities of the bisphosphonates at these different sites are explored. Current concepts of the causation of ONJ are discussed. The clinical implications of these findings to dentists managing periodontal conditions are presented. 相似文献
93.
94.
Donor and recipient-transforming growth factor-beta 1 polymorphism and cardiac transplant-related coronary artery disease 总被引:1,自引:0,他引:1
BACKGROUND: Transforming growth factor-beta1 (TGF-beta1) has been implicated in the pathogenesis of coronary vasculopathy following cardiac transplantation. The TGFB1 gene contains polymorphisms at positions +915* (Arg25Pro) and +869* (Leu10Pro) which may influence TGF-beta1 expression. We investigated the relationship between the development of coronary vasculopathy and the prevalence of these alleles in a cardiac transplant population. METHODS: Vasculopathy was diagnosed at routine surveillance post-transplant coronary angiography. Using sequence-specific polymerase chain reaction we identified the TGFB1 +915* and +869* genotypes in 147 cardiac transplant recipients and 134 cardiac donors. RESULTS: TGFB1 +915*C allele carriers (low producers) made up 10.5% of the recipient population but were significantly less likely to develop coronary vasculopathy (P=0.03). Median time to diagnosis was 6.0 years (3.9-8.72) in +915*C allele carriers compared to 2.75 years (2.10-4.22) in *G/G homozygotes (p=0.002). Pre- and 1 year post-transplant clinical variables were equivalent between the two groups. Multivariate analysis identified the recipient +915*G/G genotype (hazard ratio 2.96 (95% CI, 1.09-9.98); p=0.039), donor age (hazard ratio 1.05 (95% CI, 1.02-1.09); p=0.008) and number of acute rejection episodes of ISHLT grade 3 or greater in the first year (hazard ratio 1.12 (95% CI, 1.01-1.23); p=0.03) as significant predictors of vasculopathy. The recipient TGFB1 +869*, and both alleles in the donor, had no influence on vasculopathy development. CONCLUSIONS: Recipient TGFB1 +915* genotype influences the development of cardiac transplant-related coronary vasculopathy. This gives an important insight to the pathophysiology of the disease. On the contrary, donor TGFB1 +915* and TGFB1 +869* polymorphisms do not appear to be important and cannot be used as genetic risk factors. 相似文献
95.
96.
Rat ferritin-H: cDNA cloning, differential expression and localization during hepatocarcinogenesis 总被引:2,自引:0,他引:2
Wu CG; Groenink M; Bosma A; Reitsma PH; van Deventer SJ; Chamuleau RA 《Carcinogenesis》1997,18(1):47-52
Elevated serum ferritin levels, especially of the H subunit, accompany many
clinical malignancies. By using the subtraction-enhanced display technique,
we have recently isolated several cDNA clones which are over- expressed in
rat hepatocellular carcinoma induced by diethylnitrosamine. One
830-base-pair clone was 88% similar to human ferritin-H cDNA and encoded a
182 amino acid protein which is 97% homologous to human ferritin-H chain.
Hepatic mRNA levels of ferritin-H were increased markedly at the early
stage of diethylnitrosamine- induced hepatocarcinogenesis in the rat (6
weeks) and appeared more than 10-fold overexpressed as the tumour
progressed. In contrast, hepatic ferritin-H mRNA remained constant during
liver regeneration after a 70% partial hepatectomy. In situ hybridization
showed that over- expression of ferritin-H was exclusively localized to
preneoplastic foci, to tumour nodules and to tumour cells invading blood
vessels. These findings suggest that ferritin-H is a highly conserved
protein, its over-expression during tumour development is phenotypically
correlated with tumour initiation and/or progression, and it is useful as
an early marker for hepatocellular carcinoma.
相似文献
97.
Genomic screening for beta-sarcoglycan gene mutations: missense mutations may cause severe limb-girdle muscular dystrophy type 2E (LGMD 2E) 总被引:7,自引:3,他引:7
Bonnemann CG; Passos-Bueno MR; McNally EM; Vainzof M; de Sa Moreira E; Marie SK; Pavanello RC; Noguchi S; Ozawa E; Zatz M; Kunkel LM 《Human molecular genetics》1996,5(12):1953-1961
Autosomal recessive limb-girdle muscular dystrophies (LGMDs) are
genetically heterogeneous. A subgroup of these disorders is caused by
mutations in the dystrophin-associated sarcoglycan complex. Truncating
mutations in the 43 kDa beta-sarcoglycan gene (LGMD 2E) were originally
identified in a sporadic case of Duchenne-like muscular dystrophy, and a
common missense mutation (T151R) was identified independently in Indiana
Amish pedigrees with a milder form of LGMD. To facilitate mutational
analysis of larger numbers of patients directly from genomic DNA, as
opposed to reverse transcribed RNA from muscle biopsies, we have determined
the genomic structure of the beta-sarcoglycan gene. The open reading frame
of the beta-sarcoglycan coding region extends over six exons. Primers were
designed for PCR amplification of single exons from genomic DNA and
subsequent single strand conformation polymorphism (SSCP) analysis. We
screened 15 patients from the Brazilian LGMD patient population, 13 of whom
followed a severe course. Most of the patients had been assessed previously
for deficiency of alpha- sarcoglycan immunofluorescence on muscle biopsy
sections as a marker for disease of the sarcoglycan complex. Novel
mutations in two familial and two sporadic cases of severe childhood-onset
LGMD were identified. Only one of these patients carried a truncating
mutation (homozygous 2 bp deletion, FS164TER), while the other three
carried missense mutations (homozygous R91P, homozygous M100K, heterozygous
recessive L108R; only one allele could be identified in this family). All
three missense mutations occurred in exon 3, coding for the immediate
extracellular domain. Complete absence for all three of the known
sarcoglycans was noted by immunohistochemistry on muscle biopsy sections of
the patients.
相似文献
98.
99.
Summary of mutations underlying autosomal recessive congenital ichthyoses (ARCI) in Arabs with four novel mutations in ARCI‐related genes from the United Arab Emirates
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100.
目的:观察承载丸含药血清对甲基强的松龙预处理的MC3T3-E1成骨细胞L-钙通道电流的影响。方法:实验于2006-04/06在中国中医科学院望京医院药理实验室及吉林大学基础医学院生理教研室完成。①实验材料:MC3T3-E1(购于北京协和细胞中心);8个月龄SD大鼠10只,雌雄各半;中药制剂承载丸(由鹿角霜、肉苁蓉、续断、黄芪、当归、炙水蛭、杜仲、蛋衣、皂角刺、香附、乌药等21味中药组成);甲基强的松龙(批号H20040338,Pharmacia NV/SA生产)。②实验干预:成骨细胞(MC3T3-E1)传代培养。承载丸药粉60g,加水至200mL搅匀,取大鼠6只(雌雄各半),每只灌服2.5mL/d,灌服4d后动脉取血,制备含药血清。另取大鼠4只,同法灌服生理盐水,制成不含药血清。甲基强的松龙的浓度为1×10-5mol/L。③实验分组:将培养后的成骨细胞株分为4组:正常组(加入正常大鼠不含药血清)、模型组(加入正常大鼠不含药血清及甲基强的松龙)、承载丸低剂量组(加入甲基强的松龙及0.5mL承载丸含药血清)和承载丸高剂量组(加入甲基强的松龙及0.1mL承载丸含药血清)。④实验评估:24h后,用全细胞膜片钳技术记录每组10个细胞的L-钙通道电流,并测定其峰值电流。结果:①各组电流峰值测定结果:模型组峰值电流比正常组下降19.5%[(0.1839±0.0179),(0.2284±0.0209)nA,P<0.01];承载丸低剂量组和高剂量组比模型组分别升高37.4%和45.2%[(0.2526±0.0093),(0.2671±0.0120),(0.1839±0.0179)nA,P<0.01];承载丸高低剂量组相比差异有显著性意义(P<0.05)。②MG3T3E1细胞钙电流的特性分析:正常组,钙通道大约在-20mV时开放,最大峰值电流在 20~ 30mV,反转电位在 60~ 70mV。当在浴液中加入Co2 ,可阻断此电流的大部分电流成份,其峰值电流为(0.1050±0.0097)nA,而钙离子激活剂Bayk8644增加了此电流(0.3335±0.0323)nA。结论:①甲基强的松龙抑制成骨细胞L-钙通道电流。②承载丸含药血清可升高甲基强的松龙预处理的成骨细胞L-钙通道电流。 相似文献