Phonological networks are representations of word forms and their phonological relationships with other words in a given language lexicon. A principle underlying the growth (or evolution) of those networks is preferential attachment, or the ‘rich-gets-richer’ mechanisms, according to which words with many phonological neighbors (or links) are the main beneficiaries of future growth opportunities. Due to their limited number of words, language lexica constitute node-constrained networks where growth cannot keep increasing in a linear way; hence, preferential attachment is likely mitigated by certain factors. The present study investigated aging effects (i.e., a word’s finite time span of being active in terms of growth) in an evolving phonological network of English as a second language. It was found that phonological neighborhoods are constructed by one large initial lexical spurt, followed by sublinear growth spurts that eventually lead to very limited growth in later lexical spurts during network evolution, all the while obeying the law of preferential attachment. An analysis of the strength of phonological relationships between phonological word forms revealed a tendency to attach more distant phonological neighbors in the lower proficiency levels, while phonologically more similar neighbors enter phonological neighborhoods at more advanced levels of English as a second language. Overall, the findings suggest an aging effect in growth that favors younger words. In addition, beginning learners seem to prefer the acquisition of phonological neighbors that are easier to discriminate. Implications for the second language lexicon include leveraged learning mechanisms, learning bouts focussed on a smaller range of phonological segments, and involve questions concerning lexical processing in aging networks.
Ageing is accompanied by deterioration in physical condition and a number of physiological processes and thus a higher risk of a range of diseases and disorders. In particular, we focused on the changes associated with aging, especially the role of small molecules, their role in physiological and pathophysiological processes and potential treatment options. Our previously published results and data from other authors lead to the conclusion that these unwanted changes are mainly linked to the hypothalamic-pituitary-adrenal axis can be slowed down, stopped, or in some cases even reversed by an appropriate treatment, but especially by a life-management adjustment., Martin Hill, Zdeněk Třískala, Pavla Honců, Milada Krejčí, Jiří Kajzar, Marie Bičíková, Leona Ondřejíková, Dobroslava Jandová, Ivan Sterzl., and Obsahuje bibliografii
The incidence of cerebrovascular diseases increases significantly with aging. This study aimed to test the hypothesis that aging may influence the protein kinase A (PKA)-dependent vasodilation via RyR/BKCa pathway in the middle cerebral arteries (MCA). Male Sprague-Dawley rats were randomly divided into control (4-6 month-old) and aged (24-month-old) groups. The functions of MCA and ion channel activities in smooth muscle cells were examined using myograph system and patch-clamp. Aging decreased the isoproterenol/forskolin-induced relaxation in the MCA. Large-conductance Ca2+-activated-K+ (BKCa) channel inhibitor, iberiotoxin, significantly attenuated the forskolininduced vasodilatation and hyperpolarization in the young group, but not in the aged group. The amplitude and frequency of spontaneous transient outward currents (STOCs) were significantly decreased in the aged group. Single channel recording revealed that the mean open time of BKCa channels were decreased, while an increased mean closed time of BKCa channels were found in the aged group. The Ca2+/voltage sensitivity of the channels was decreased accompanied by reduced BKCa α and β1-subunit, the expression of RyR2, PKA-Cα and PKA-Cβ subunits were also declined in the aged group. Aging induced down-regulation of PKA/BKCa pathway in cerebral artery in rats. The results provides new information on further understanding in cerebrovascular diseases resulted from agerelated cerebral vascular dysfunction.