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1 f oral premalignancies (dysplasias) are also mortal.
2 e strand breaks induces cell cycle arrest in mortal and immortal human cells.
3  for the first time that there are divergent mortal and immortal pathways for oral SCC development vi
4 rmatic techniques showed that development of mortal and immortal SCCs involves distinct transcription
5                                          The mortal and immortal tumors are generated in vivo as judg
6 activator of endogenous target genes both in mortal and immortalized cells.
7 flow cytometric analysis, we found that both mortal and immortalized HMEC, which contain wild-type p5
8 l lung cancer (NSCLC) is a highly morbid and mortal cancer type that is difficult to eradicate using
9 cells, but is low or absent in most diploid, mortal cells such as those of somatic tissues.
10 irus abolished telomerase activity, creating mortal cells with varying telomere lengths.
11 mere shortening at a rate similar to that of mortal cells.
12 5-fold higher in immortal cell lines than in mortal cells.
13 ngthen its telomeres and then was fused with mortal cells.
14           Stroke is a morbid and potentially mortal complication among patients hospitalized with acu
15 cytic lymphohistiocytosis (sHLH) is a highly mortal complication associated with sepsis.
16 cterial infection is a frequent, morbid, and mortal complication of liver transplantation.
17  dysfunctions are intimately involved in the mortal complications of hematopoietic stem cell transpla
18 ork training, scientific computing and even 'mortal computing'(25,29,30).
19 was not linked to variation in resistance to mortal disease and that Bd infection altered bacterial c
20 ess, public knowledge of PAD as a morbid and mortal disease has not been previously assessed.
21 de polymorphisms (SNPs) increase the risk of mortal disease.
22 the expression of hTERT in two other typical mortal dyplasia cultures (that retain RAR-beta and p16IN
23               Phages are often thought of as mortal enemies of bacteria.
24  underlying pathology and mechanisms driving mortal events.
25 is progress has been a decline in morbid and mortal events.
26 e human endogenous plastic somatic cells are mortal, express low telomerase activity, expand for an e
27                                   In normal, mortal fibroblasts this block to proliferation is perman
28    We show here that following DNA damage in mortal fibroblasts, the induction of p21 and p53 is to a
29  receptor fusion protein, MYC-ERTM, in human mortal fibroblasts, WI38, on cell-cycle entry, apoptosis
30 isolated Caenorhabditis elegans mutants with mortal germ lines--worms that can reproduce for several
31 ensitive embryonic lethality, sterility, and mortal germ lines.
32                                          The mortal germline (Mrt) mutants in Caenorhabditis elegans
33                                 One of these mortal germline (mrt) mutants, mrt-2, exhibits progressi
34 bp-2 mutants display shorter telomeres and a Mortal Germline.
35 reast cancer cell lines relative to "normal" mortal human mammary epithelial cells and benign, immort
36 t length but did not affect the frequency of mortal hybrids following MMCT of chromosome 4.
37 t approximately 40% of primary oral SCCs are mortal in culture, and these have a better prognosis.
38 s a pandemic disease that is more severe and mortal in people with immunodeficiency, such as those wi
39 an hosts, but the dosage required to achieve mortal infection varies greatly.
40 the susceptibilities of these two species to mortal infection, there was no significant difference in
41 mmatory response syndrome (SIRS) is a highly mortal inflammatory disease, associated with systemic in
42 ing to prevent the occurrence of a morbid or mortal ischemic event.
43 ce an activin A-dependent stress response in mortal nontumorigenic human mammary epithelial cells tha
44 tifying biomarker combinations predictive of mortal outcomes in older adults, as well as the multipli
45  so does the occurrence of highly morbid and mortal outcomes, including heart failure and thromboembo
46  was still present in hybrids displaying the mortal phenotype.
47  3' G-rich tails at human chromosome ends in mortal primary fibroblasts, umbilical vein endothelial c
48 ven prevent it and thus avoid the morbid and mortal scourge of human heart failure.
49               In contrast to normal lung and mortal short-term bronchial epithelial cultures, WNT7a w
50  words, we must guard against committing the mortal sin of genomics by confusing throughput with outp
51 entially immortal germ line separated from a mortal soma, and evolutionary biologists regard senescen
52                   Volvox has two cell types: mortal somatic cells and immortal germ cells.
53 olvox carteri possesses only two cell types: mortal somatic cells and potentially immortal asexual re
54 ith external regulators, which suggests that mortal somatic lineages with cells that reproducibly int
55 ng the effects of telomerase activity in two mortal SVLT-Rasval12-transformed human pancreatic cell l
56 causes superficial infection and can lead to mortal systemic infections, especially in immunocompromi
57 o-resident aggression can be both morbid and mortal; therefore, intervention research is needed to pr
58 r, we demonstrate that aging lineages become mortal when damage accumulation rates surpass a threshol