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131.
132.
Multiplicity activation of herpes simplex virus in mouse neuroblastoma (C1300) cells 总被引:1,自引:0,他引:1
Summary The virus yields and number of infectious centres of HSV infected mouse neuroblastoma C1300 cells (clone 41 A3) infected at different multiplicities of infection (MOI) were found to vary more than the differences of HSV concentrations of the virus suspensions used for infection of the cells. This suggested that a C1300 cell had to be infected with more than one HSV particle in order to produce progeny virus—multiplicity activation. The greater than expected enhancement of virus production of C1300 cell cultures receiving increasing MOI of HSV was probably not due to improved virus adsorption, nor influenced by non-virus factors in the virus inoculum stimulatory for HSV replication. A hypothesis, that the block in virus replication was promoted by an inhibitor of an HSV specified regulatory protein and could be overcome by the addition of HSV DNA copies in the infected cell, was supported by the results of two types of experiments. Presence of phosphonoformic acid, an inhibitor of the HSV specified DNA polymerase, in the culture medium of HSV infected permissive GMK cells resulted in non-linear relationships between virus yields and MOI. An HSV temperature sensitive mutant (ts B5), defective in a late structural protein, rescued wild type HSV in C1300 cells.With 4 Figures 相似文献
133.
134.
135.
The mutational spectrum of brachydactyly type C 总被引:3,自引:0,他引:3
Everman DB Bartels CF Yang Y Yanamandra N Goodman FR Mendoza-Londono JR Savarirayan R White SM Graham JM Gale RP Svarch E Newman WG Kleckers AR Francomano CA Govindaiah V Singh L Morrison S Thomas JT Warman ML 《American journal of medical genetics》2002,112(3):291-296
Growth/differentiation factor-5 (GDF5), also known as cartilage-derived morphogenetic protein-1 (CDMP-1), is a secreted signaling molecule that participates in skeletal morphogenesis. Heterozygous mutations in GDF5, which maps to human chromosome 20, occur in individuals with autosomal dominant brachydactyly type C (BDC). Here we show that BDC is locus homogeneous by reporting a GDF5 frameshift mutation segregating with the phenotype in a family whose trait was initially thought to map to human chromosome 12. We also describe heterozygous mutations in nine additional probands/families with BDC and show nonpenetrance in a mutation carrier. Finally, we show that mutant GDF5 polypeptides containing missense mutations in their active domains do not efficiently form disulfide-linked dimers when expressed in vitro. These data support the hypothesis that BDC results from functional haploinsufficiency for GDF5. 相似文献
136.
The manner of packing of the terminal DNA loci into nucleosomes and higher order structures may strongly influence their functional
interactions. Besides the structural flexibility of telomeric DNA sequences, conserved features of their chromatin including
short nucleosome phasing (157 bp) and nucleosome sliding have been described previously. To gain a complementary knowledge
of subtelomeres, we have analysed the chromatin structure of two subtelomeric tandem repeats from the plant Silene latifolia: X43.1 and 15Ssp. X43.1 shows two distinct nucleosome periodicities – 157 and 188 bp. Preferred positions of its two nucleosomes
have been mapped at both low and high resolution and the experimental results correspond to computer-predicted positions.
15Ssp is a newly-discovered sequence showing a telomere-associated position by PCR and a subtelomeric location by pulsed-field
gel electrophoresis and fluorescence in situ hybridisation. Its 159 bp sequence unit shows a tandem arrangement and the presence of micrococcal nuclease-hypersensitive
sites when either naked DNA or chromatin is digested. Use of a chemical nuclease results in a regular nucleosome ladder of
157 bp periodicity. Moreover, 15Ssp mononucleosomes show instability and absence of specific positioning, features typical
for telomeric chromatin.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
137.
138.
Ten members of two families with D/G translocation, three members of a family with D/D translocation, and one patient with non-familial and one with apparently non-familial D/D translocation were examined. The trdnslocation chromosomes were identified by SH-thymidine labeling and autoradio-graphy as 14q21q and 13q14q, respectively. These findings support the hypothesis of nonrandomness of D group chromosomes involved in centric-fusion translocation. The importance of the identification of Dgroup chromosomes involved in centriofusion translocation in relation to genetic counseling is discussed. 相似文献
139.
Pituitary morphologic changes in patients with Erdheim-Chester disease have not been described in detail. We report here the
histologic and immunohistochemical findings in the autopsy obtained pituitary of a 35-yr-old woman with extensively disseminated
Erdheim-Chester disease. The posterior lobe was completely replaced by xanthogranulomatous infiltrates, providing an explanation
for the patient’s diabetes insipidus. The anterior lobe was intact and immunohistochemistry demonstrated expression of GH,
TSH, FSH, LH, and alpha subunit within the normal range. A clinically observed decrease of anterior pituitary function was
interpreted as hypothalamic in origin due to massive destruction of the hypophysial stalk and compression of the hypothalamus.
Prolactin immunoreactive cells were numerous, consistent with the view that prolactin cell hyperplasia resulted from the loss
of hypothalamic dopaminergic inhibition. Massive Crooke’s hyalinization in the ACTH-producing cells was considered unrelated
to Erdheim-Chester disease and was the consequence of treatment with pharmacologic doses of glucocorticoid hormones. It can
be concluded that prolactin cell hyperplasia may be the only finding in the adenohypophysis of patients with disseminated
Erdheim-Chester disease. It appears that in our patient the clinically apparent anterior hypopituitarism was not due to the
lack of storage but rather to insufficient release of adenohypophysial hormones caused by the defect in hypothalamic regulation. 相似文献
140.
Expression of adhesion molecules in allergic lung diseases 总被引:4,自引:0,他引:4
Popper HH Pailer S Wurzinger G Feldner H Hesse C Eber E 《Virchows Archiv : an international journal of pathology》2002,440(2):172-180
Endothelial adherence and migration of leukocytes into tissue is mediated by different sets of adhesion molecules. The expression of these sets might not only preselect the types of leukocytes that enter the inflammatory sites, but also activate these leukocytes, induce adherence to epithelial cells, and cause the release of cytokines. Atopic asthma, extrinsic allergic alveolitis, and sarcoidosis as examples of immunologic lung diseases were investigated for the expression of adhesion molecules. Bronchial biopsies in chronic obstructive lung disease (COPD) and resected lung tissue of juvenile emphysema were chosen for controls. Immunohistochemistry was done on sections from bronchial and transbronchial biopsies and on smears from bronchoalveolar lavage cells. In all three types of immune disorders, lymphocytes expressed the integrins alpha4/beta1 (VLA4) and ICAM3, whereas lymphocytes in COPD bronchitis and in emphysema controls were unreactive. Eosinophils in atopic asthma bronchitis in contrast to COPD bronchitis also expressed both VLA4 and ICAM3. The expression of VCAM1 on endothelial cells was only seen in atopic asthma and was related to disease activity. The expression of other adhesion molecules was nonspecific. Expression of VCAM1 on endothelial cells and its ligand VLA4 on lymphocytes and eosinophils seems to be a specific event in atopic asthma. Expression of VLA4 and ICAM3 on lymphocytes, however, might be a specific event in all three immune reactions. 相似文献