A North American (NA) isolate of tobacco veinal necrotic strain of Potato virus Y (PVYN) (N-Jg) and a NA isolate of potato tuber necrotic strain of Potato virus Y (PVYNTN) (Tu 660) were tested for their phenotypes by inoculation to potato plants of three potato cultivars. Upon inoculation with Tu 660, tubers of the cultivars Norchip and Ranger Russet developed potato tuber necrotic ringspot disease (PTNRD) but not the tubers of Russet Burbank. N-Jg failed to induce PTNRD in the tested cultivars. The genomic RNAs of both strains were completely sequenced and analysed. High homology (98% and 99% identity on nucleotide and polyprotein, respectively) was found between Tu 660 and N-Jg. When polyproteins were compared with other isolates, high identity was observed between Tu 660 and an European (Eu) PVYN-605 (98%) and with an Eu-PVYNTN-H (96%). However, when individual mature proteins were compared, much lower identities (86.5–94%) were found between Tu 660 and PVYNTN-H compared to 98–99.5% between Tu 660 and PVYN-605 in the P3, 6K1 and CI regions. Further sequence analysis indicated that the PVYNTN-H is a hybrid molecule of the genomic RNA recombination of PVYO and Eu-PVYN as shown by Glais et al. (Arch Virol 147, 363–378), whereas NA-PVYNTN Tu 660 is free of recombination points. Phylogenetic analysis confirmed this observation, and suggested that, in light of high homology, the Tu 660 might have evolved from NA-PVYN by mutations rather than the genome recombinations. The non-recombinant nature of NA-PVYNTN Tu 660 strongly suggests that the recombinant structure of genome is not a necessary prerequisite for the PTNRD phenotype. 相似文献
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a major health problem with an estimated prevalence of 10-15% among smokers. The incidence of moderate COPD, as defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD), is largely unknown. AIM: To determine the cumulative incidence of moderate COPD (forced expiratory volume in 1 second/forced vital capacity ratio [FEV1/FVC] <0.7 and FEV1 <80% predicted) and its association with patient characteristics in a cohort of male smokers. DESIGN: Prospective cohort study. SETTING: The city of IJsselstein, a small town in the Netherlands. METHOD: Smokers aged 40-65 years who were registered with local GPs, participated in a study to identify undetected COPD. Baseline measurements were taken in 1998 of 399 smokers with normal spirometry (n = 292) or mild COPD (FEV1/FVC <0.7 and FEV1 >or=80% predicted, n = 107) and follow-up measurements were conducted in 2003. RESULTS: After a mean follow-up of 5.2 years, 33 participants developed moderate COPD (GOLD II). This showed an estimated cumulative incidence of 8.3% (95% CI = 5.8 to 11.4) and a mean annual incidence of 1.6%. No participant developed severe airflow obstruction. The risk of developing moderate COPD in smokers with baseline mild COPD (GOLD I) was five times higher than in those with baseline normal spirometry (one in five versus one in 25). CONCLUSIONS: In a cohort of middle-aged male smokers, the estimated cumulative incidence of moderate COPD (GOLD II) over 5 years was relatively high (8.3%). Age, childhood smoking, cough, and one or more GP contacts for lower respiratory tract problems were independently associated with incident moderate COPD. 相似文献
Cervical smears were reviewed from patients in whom a cytological abnormality was followed, after an interval without interference, either by regression to `negative' or else by progression to invasive carcinoma. Twenty-eight cases were from a previously analysed series with positive smears and an interval of at least two years before investigation, resulting from refusal or failure to trace. Slides were also reviewed from 25 cases in which `positive' smears had regressed to negative without escaping from surveillance, and from 10 patients subsequently developing invasive carcinoma whose previous slides, taken several years earlier, showed abnormalities on review. None of these 63 patients had any biopsy or other surgical procedure to the cervix between the initial smear and the outcome.
Slides showing `superficial cell dyskaryosis' and/or well-differentiated `parabasal cell dyskaryosis' were found only among the groups with subsequent regression. Those showing dissociated poorly differentiated dyskaryotic parabasal cells regressed to negative in two cases and progressed to invasion in nine. This suggests that many examples of spontaneous regression correspond to mild dysplasias which are not precancerous, and overdiagnosis must often have resulted in unnecessary surgical procedures in the past.
`Regressing' and `progressing' groups both included cases in which the spatula had removed coherent pieces of undifferentiated epithelium. These are difficult to interpret cytologically. In nine of them (including four which regressed) the cytological picture was that of carcinoma in situ. The remainder (14 cases) were probably examples of reserve cell hyperplasia, and it is noteworthy that, of the 21 cases subsequently progressing to invasive carcinoma, five were preceded by appearances of this type. It is concluded that cell aggregates suggesting an unusual degree of reserve cell hyperplasia are a danger signal and require careful surveillance.
Mammalian embryos cannot survive without the placenta. Development of the human placenta requires trophoblast proliferation, differentiation, and invasion as well as highly coordinated modulation of the maternal uterus. HtrA1 is a member of the recently identified mammalian HtrA (high temperature requirement factor A) serine protease family with a high level of expression in the placenta. In this study, we examined whether HtrA1 expression (mRNA and protein) is associated with placental development in the human. HtrA1 is up-regulated in both endometrial glands and decidual cells during endometrial preparation for embryo implantation and during first-trimester pregnancy at placentation. HtrA1 expression was also detected in certain trophoblast subtypes during early pregnancy. The villous syncytiotrophoblast and cytotrophoblast showed the strongest expression while the interstitial extravillous trophoblast showed the lowest or no expression of HtrA1. The distinct distribution of HtrA1 at the maternal-trophoblast interface suggests that HtrA1 may play a role in placental development. 相似文献
The muntjacs (Muntiacus, Cervidae) are famous for their rapid and radical karyotypic diversification via repeated tandem chromosome fusions, constituting
a paradigm for the studies of karyotypic evolution. Of the five muntjac species with defined karyotypes, three species (i.e.
Muntiacus reevesi, 2n = 46; M. m. vaginalis, 2n = 6/7; and M. crinifrons, 2n = 8/9) have so far been investigated by a combined approach of comparative chromosome banding, chromosome painting and
BAC mapping. The results demonstrated that extensive centromere–telomere fusions and a few centric fusions are the chromosomal
mechanisms underlying the karyotypic evolution of muntjacs. Here we have applied the same approach to two additional muntjac
species with less well-characterized karyotypes, M. feae (2n = 14♂) and M. gongshanensis (2n = 8♀). High-resolution G-banded karyotypes for M. feae and M. gongshanensis are provided. The integrated analysis of hybridization results led to the establishment of a high-resolution comparative
map between M. reevesi, M. feae, and M. gongshanensis, proving that all tandem fusions underpinning the karyotypic evolution of these two muntjac species are also centromere–telomere
fusions. Furthermore, the results have improved our understanding of the karyotypic relationships of extant muntjac species
and provided compelling cytogenetic evidence that supports the view that M. crinifrons, M. feae, and M. gongshanensis should each be treated as a distinct species. 相似文献
The Fgf/Fgfr (Fgf receptor) and Bmp signal pathways are critical for embryonic development and postnatal growth. In order
to address their roles in tongue development, preliminary study of expression patterns of some important members in the two
families, as well as of apoptosis and proliferation, were carried out in mouse developing tongue. Apoptosis in tongue is a
very late event in embryogenesis, restricted to the upper layer of the epithelium whereas proliferation is very vigorous at
the early stage of tongue development and remains active throughout embryogenesis. Bmp2, −4 and -5 were localized within the mesenchyme at the early embryonic stage of tongue development (E12 to E13), whereas Bmp3 and Bmp7 were mainly expressed in the epithelium. Most of these molecules were also seen in the tongue muscles at postnatal stages.
Among Fgfr isoforms, Fgfr1c, −2b, and -2c were detected in embryogenesis with peak expression at E11 to E13. Fgfr1c and Fgfr2c were localized within the mesenchyme, while Fgfr2b was mainly expressed in the epithelium. High expression of Fgf7 and Fgf10 was also detected in the mesenchyme at the early embryonic stage of tongue development, corresponding to the Fgfr expression, suggesting that they are among the principal ligands functioning at the early embryonic expanding stage. Fgf2 was seen in the tongue muscles at the late embryonic and postnatal stages. These results suggest that Bmp and Fgf signalling regulates tongue development at multiple stages, possibly related to proliferation and differentiation. 相似文献
Refractoriness to Gal N toxicity occurs especially in fetal rats, newborn rats, and in rats after partial hepatectomy. An injury however (laparotomy, incision on the back or ip BaSO4 suspension), prior to Gal N administration, also inhibits Gal N toxicity. In all these circumstances high levels of rat α2-macrofetoprotein (αMFP) occur. This protein is an acute phase reactant and is identical to rat α2-macroglobulin. αMFP isolated from the serum of injured rats and then administered to normal rats strongly inhibits Gal N toxicity. When time interval between the preceding injury, provoking αMFP production and Gal N administration shortens, the inhibiting effects are less and αMFP production remains low.During resistance to Gal N, the primary and secondary biochemical lesions of Gal N persist and the protecting effect of αMFP must be due to another mechanism, operating in later phases of cell injury. Very probably this is attributable to the stabilizing effect on membranes of hepatocytic organelles and the plasma membranes. As αMFP is an acute phase reactant the importance of these proteins to the course of hepatitis must be considered. 相似文献