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51.
目的 研究HIV-1膜蛋白(Env)特定中和表位的改造对功能性假病毒形成及中和活性的影响.方法 采用环形诱变及Dpn I筛选的方法对Env进行定点突变,将2G12和2F5两个中和表位整合入不含该表位的BC亚型的Env上,比较改造对假病毒的形成情况及对2G12和2F5单抗的中和活性的影响.结果 对5株假病毒(BC02、BE03、BC04、BC05和BC12)的Env特定中和表位进行改造,其中BC04和BCl2的2G12表位改造后,不能形成假病毒,BC02、BC03和BC05增加2G12和2F5两个表位后,仍能够形成假病毒,且假病毒滴度较改造前无明显变化,改造后的BC03假病毒较改造前对单抗2G12和2175的中和活性均有所提高,而改造后的BE02和BC05假病毒较改造前对单抗2F5的中和活性增强,而对单抗2G12的中和活性无变化.结论 2G12中和表位部分位点的改造影响假病毒的形成,中和表位的增加能够提高单抗2G12的中和活性,为免疫原的优化提供了新思路. 相似文献
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Morphological analysis of degeneration and regeneration of syncytiotrophoblast in first trimester placental villi during organ culture 总被引:3,自引:1,他引:3
We have recently shown using dansyl-L-lysine exclusion studies that the
release of human chorionic gonadotrophin (HCG) in conjunction with L-
lactate dehydrogenase (LDH) from first trimester villi during organ culture
is symptomatic of syncytiotrophoblast degeneration. The purpose of this
study was to examine chorionic villi at the ultrastructural level in order
to determine events occurring during organ culture. The tissue was sampled
after 0, 24, 48 and 120 h in culture and processed for electron microscopy.
In addition to confirming the previously recorded syncytial degeneration,
the electron micrographs showed clearly the generation of a new
syncytiotrophoblast layer. The new layer, derived from differentiating
cytotrophoblast cells, was largely formed by 48 h and was maintained for at
least 120 h in culture. This study demonstrates a model which provides an
opportunity to study the differentiation of cytotrophoblast cells whilst
they retain their anatomical relationships within the villous structure.
相似文献
55.
A second locus (GLC3B) for primary congenital glaucoma (Buphthalmos) maps to the 1p36 region 总被引:10,自引:0,他引:10
Akarsu AN; Turacli ME; Aktan SG; Barsoum-Homsy M; Chevrette L; Sayli BS; Sarfarazi M 《Human molecular genetics》1996,5(8):1199-1203
Primary congenital glaucoma (gene symbol: GLC3) is an ocular disorder that
occurs for 0.01-0.04% of blind people. In the majority of familial cases
reported so far, this condition is inherited as an autosomal recessive
trait. We have recently used a group of 17 GLC3 families with a minimum of
two affected offspring and consanguinity in most of the parental generation
and mapped the first GLC3 locus (GLC3A) to the 2p21 region. Six families
did not show any linkage to the GLC3A locus and thus provided evidence for
genetic heterogeneity of this disorder. A total of eight families unlinked
to the 2p21 region were used to search for the chromosomal location of the
second GLC3 locus. Herein, we describe mapping of a new locus (designated
GLC3B) for primary congenital glaucoma to the short arm of chromosome 1
(1p36.2-36.1) that is situated centromeric to the neuroblastoma and
Charcot-Marie-Tooth type 2A (CMT2A) loci. A total of 17 DNA markers were
genotyped from this region of chromosome 1. Four families showed no
recombination with the two markers D1S2834 and D1S402 with a maximum lod
score of 4.510 and 4.157 respectively. Pairwise and multipoint linkage
analysis and inspection of the haplotypes revealed that the remaining four
families are not linked to this part of chromosome 1, thus providing
further evidence that at least one more locus for the autosomal recessive
form of GLC3 must exist in the genome. Based on the recombination events,
the overall linkage map of this region is: tel-D1S1192-D1S1635-D1S1193 -
(D1S1597/-D1S489/D1S228)- [GLC3B/D1S2834/D1S402] - (D1S1176/D1S507/D1S407)
- D1S2728-(MFAP2/D1S170) - D1S1368 - D1S436- D1S1592-cen.
相似文献
56.
S Stoppa‐Vaucher T Ayabe J Paquette N Patey D Francoeur J‐M Vuissoz J Deladoëy ME Samuels T Ogata CL Deal 《Clinical genetics》2012,82(6):505-513
Stoppa‐Vaucher S, Ayabe T, Paquette J, Patey N, Francoeur D, Vuissoz J‐M, Deladoëy J, Samuels ME, Ogata T, Deal CL. 46, XY gonadal dysgenesis: new SRY point mutation in two siblings with paternal germ line mosaicism. Familial recurrence risks are poorly understood in cases of de novo mutations. In the event of parental germ line mosaicism, recurrence risks can be higher than generally appreciated, with implications for genetic counseling and clinical practice. In the course of treating a female with pubertal delay and hypergonadotropic hypogonadism, we identified a new missense mutation in the SRY gene, leading to somatic feminization of this karyotypically normal XY individual. We tested a younger sister despite a normal onset of puberty, who also possessed an XY karyotype and the same SRY mutation. Imaging studies in the sister revealed an ovarian tumor, which was removed. DNA from the father's blood possessed the wild type SRY sequence, and paternity testing was consistent with the given family structure. A brother was 46, XY with a wild type SRY sequence strongly suggesting paternal Y‐chromosome germline mosaicism for the mutation. In disorders of sexual development (DSDs), early diagnosis is critical for optimal psychological development of the affected patients. In this case, preventive karyotypic screening allowed early diagnosis of a gonadal tumor in the sibling prior to the age of normal puberty. Our results suggest that cytological or molecular diagnosis should be applied for siblings of an affected DSD individual. 相似文献
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