The data suggest that feedback interactions between dysbiosis in F prausnitzii and dysregulation of gut epithelial inflammation might underlie the chronic progression of AD by resulting in impairment of the gut epithelial barrier, which ultimately leads to aberrant TH2-type immune responses to allergens in the skin.

The equine-associated obligate pathogen Burkholderia mallei was developed by reductive evolution involving a substantial portion of the genome from Burkholderia pseudomallei, a free-living opportunistic pathogen. With its short history of divergence (∼3.5 myr), B. mallei provides an excellent resource to study the early steps in bacterial genome reductive evolution in the host. By examining 20 genomes of B. mallei and B. pseudomallei, we found that stepwise massive expansion of IS (insertion sequence) elements ISBma1, ISBma2, and IS407A occurred during the evolution of B. mallei. Each element proliferated through the sites where its target selection preference was met. Then, ISBma1 and ISBma2 contributed to the further spread of IS407A by providing secondary insertion sites. This spread increased genomic deletions and rearrangements, which were predominantly mediated by IS407A. There were also nucleotide-level disruptions in a large number of genes. However, no significant signs of erosion were yet noted in these genes. Intriguingly, all these genomic modifications did not seriously alter the gene expression patterns inherited from B. pseudomallei. This efficient and elaborate genomic transition was enabled largely through the formation of the highly flexible IS-blended genome and the guidance by selective forces in the host. The detailed IS intervention, unveiled for the first time in this study, may represent the key component of a general mechanism for early bacterial evolution in the host.

BACKGROUND Telomerase activation is thought to be essential for the stabilization of telomere length, through which immortalization and oncogenesis are achieved, but little is known about the regulation of telomerase in human gastric carcinoma cells. METHODS A total of 27 primary gastric tumors, 29 cases of intestinal metaplasia, and 30 cases of normal mucosa, as well as 8 gastric carcinoma cell lines, were examined for the relation between telomerase activation and gastric carcinogenesis. Telomerase activity was detected by telomeric repeat amplification protocol, and the expression of each telomerase subunit was evaluated by Northern blot analysis or reverse transcriptase–‐polymerase chain reaction. RESULTS Telomerase activity was found in all 8 gastric carcinoma cell lines and in 25 of 27 gastric carcinoma tissue samples (93%), and weakly observed in 11 of 29 gastric intestinal metaplasia samples (38%). None of 30 normal gastric tissue samples displayed telomerase activity. The mRNA expression of human telomerase catalytic subunit (hTERT) was up‐regulated in 26 of 26 tumor tissue samples (100%) and in 19 of 24 intestinal metaplasia (79%) in which telomerase activity was weak or negative. Normal gastric mucosa expressed the telomerase gene, albeit at low levels. In contrast to hTERT, human telomerase RNA component and human telomerase‐associated protein expression did not parallel telomerase activity, which was independent of tumor stage and histology. CONCLUSIONS hTERT expression is up‐regulated during an early stage in the carcinogenic process, and telomerase activation may be a critical step in gastric carcinogenesis. Cancer 1999;86:559–65. © 1999 American Cancer Society.

Ginkgo trees of four different ages were selected as experimental material. Telomeric restriction fragment (TRF) lengths, as an indicator of telomere length, were determined for different tissues by Southern hybridization analysis. Statistical analysis was performed to compare two aspects of TRF length. By determining TRF lengths for different tissues for each age, a latent tendency was found. TRF length varied from short to long in these tissues in the order microspore < embryonal callus < leaf < branchlet. TRF lengths for leaf tissue and branchlet tissue were dissimilar for female and male mature trees, although this difference between TRF lengths for the two sexes was not statistically significant. Evaluation of TRF lengths for each tissue for trees of all four ages revealed TRF lengths increased with age to some extent. Different rates of change were found for leaf tissue and for branchlet tissue, although tendencies to increase were not linear for either. Finally, a simple mathematical model was formulated to describe the relationship between telomere length and age for Ginkgo biloba L.

Telomeres have lately received considerable attention in the development of broad-leaved tree species. In order to determine tissue-, sex-, season- and age-specific changes in telomerase activity in ginkgo trees, analyses of the telomerase repeat amplification protocol were carried out. In all of the tissues detected (embryonal callus, microspore tissues and leaves) telomerase activity was found, with differences between these activities statistically significant (P < 0.05). The highest telomerase activity was found in embryonal callus, suggesting that ginkgo trees have tissue-specific telomerase activity. Tissues containing high levels of dividing cells also have high levels of telomerase activity. No significant difference of telomerase activity was found between male and female trees (P > 0.05). In the annual development cycle, the highest telomerase activity was found in April and a decreasing trend over time in the four age groups studied: 10, 20, 70 and 700 year. The most obvious decline appeared in trees of the 700 year old group, suggesting that ginkgo trees have season-specific telomerase activities and trees of various ages react differently to seasonal changes. The mean annual telomerase activity showed a regular decreasing trend in all leaf samples analyzed from 10 to 700 year old ginkgo trees. We conclude that maintenance of telomere length depends on season- and age- associated telomerase activity. An optimal telomere length is regulated and maintained by telomerase in Ginkgo biloba L.