ABSTRACT
Although a relationship between epigenetics and aging phenotypic changes has been established, a theoretical explanation of the intrinsic connection between the epigenetics and aging is lacking. In this essay, we propose that epigenetic recording of varied cell environment and complex history could be an origin of cellular aging. Through epigenetic modifications, the environment and historical events can induce the chromatin template into an activated or repressive accessible structure, thereby shaping the DNA template into a spectrum of chromatin states. The inner nature of diversity and conflicts born by the cell environment and its historical events are hence recorded into the chromatin template. This could result in a dissipated spectrum of the chromatin state and chaos in overall gene expression. An unavoidable degradation of epigenome entropy, similar to Shannon entropy, would be consequently induced. The resultant disorder in epigenome, characterized by corrosion of epigenome entropy as reflected in chromatin template, can be stably memorized and propagated through cell division. Furthermore, the hysteretic nature of epigenetics responding to the emerging environment could exacerbate the degradation of epigenome entropy. As well as stochastic errors, we propose that outside entropy (or chaos) derived from the varied environment and complex cell history, gradually input and imprinted into the chromatin via epigenetic modifications, would lead inevitably to cellular aging, the extent of which could be aggravated by hysteresis of epigenetics without error erasing and correction.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the image characteristics of bone metastasis of primary lung carcinoma.</p><p><b>METHODS</b>Whole-body bone imaging ((99)Tc(m)-MDP) was performed in 258 patients with pathologically proven lung carcinoma. The rate of bone metastasis, distribution of the metastatic lesions and their characteristics were analyzed.</p><p><b>RESULTS</b>Among the 258 cases, 142 patients developed bone metastasis. The overall rate of bone metastasis was 55.0%. The metastases located in axial skeleton were 49.6%, appendicular skeleton 36.0%, trunk bones of the axial skeleton 48.4%, and appendicular girdle skeleton 31.4%. Ribs, thoracic vertebrae, ilium and lumbar vertebrae had a higher rate of bone metastasis, higher than 20%, respectively. 1252 lesions were detected including 406 at the left side of the body, 387 in the axial skeleton and 459 at the right side of the body. There was no significant difference in terms of number of lesions between left side and right side (chi(2) = 3.3, P = 0.072). 1224 bone metastatic foci (97.8%) were presented as strong radioactive, 26 (2.1%) mixed lesion, and 2 (0.2%) low radioactive. According to the shape of the lesions, there were 810 punctate lesions (71.5%), 159 (14.0%) lump form, 108 (9.5%) strip form and 56 (4.9%) lamellar form. The accumulative bone metastasis rate was 28.7% for the patients with one to three lesions. The metastasis rate decreased gradually with the increasing number of metastatic lesions.</p><p><b>CONCLUSION</b>Bone metastasis is very common in patients with lung cancer. Most bone metastases are characterized by strong radioactive and earlier punctate form, often occurs in the trunk bones of axial skeleton or appendicular girdles. The distribution of earlier metastases has not obvious regularity, and advanced bone metastases are often concurrent, multiple and multiform, widely and randomly distributed in the body.</p>