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PubMed2001

The extinction program for Homo sapiens and cloning humans: trinucleotide expansion as a one-way track to extinction.

It has been uncovered that expansion of trinucleotide repeats in the human genome are causing a variety of genetic diseases. They are also identified in other loci that are not clearly related to particular diseases, which indicates such repeat expansion is one of the general forms of evolution occurring throughout the human genome. Trinucleotide repeat expansion has been shown to occur during meiosis, and is generally irreversible. In consequence, every human chromosome suffers from the burden of accumulating trinucleotide repeats along with the passage of generation, which eventually ends up in a deficiency of replication. Thus, all the human chromosomes are predicted to be 'mortal', so far as they replicate through meiosis. Naturally, the mortality of human chromosomes leads to the mortality of Homo sapiens as a species on earth. Although it is quite controversial, a radical breakthrough for humans to survive might be found through cloning reproduction without meiosis.

Animals↗
PubMed2000

Resurgence: the role of extinction.

Three hens were trained to door push and three were trained to head bob using food as the reinforcer (Behaviour 1 training). A period of extinction followed. Each hen was then trained to perform the other behaviour (Behaviour 2) and this was followed by seven sessions of extinction. This whole sequence was repeated six times, with two sessions of extinction following Behaviour 1 training. Over the repeated extinction conditions there were decreases in responding early in extinction, for both Behaviours 1 and 2, compared with the first condition. Behaviour in the later extinction sessions could be studied for Behaviour 2 only, and it was found to increase relative to the first condition, over repeated extinction conditions. The occurrence of Behaviour 1 during the extinction following the training of Behaviour 2, that is the resurgence of Behaviour 1, both over the whole of and in the first session of each extinction phase, was variable and tended to increase over these six conditions. Thus it is possible to study resurgence using a within-subject design but the effect of repeated extinction conditions needs to be considered. The period of extinction immediately following Behaviour 1 training was then increased to nine sessions for two replications of the whole sequence. This was followed by two repeats of the sequence with no sessions of this extinction and then by another repeat, with nine sessions of this extinction phase. Over these five conditions the total resurgence of Behaviour 1 was generally greater when there were no sessions of extinction immediately following Behaviour 1 training, than when there were nine sessions. This result was more marked for the resurgence of Behaviour 1 in the first session of the extinction of Behaviour 2. Thus, these data support the hypothesis that the resurgence of Behaviour 1 is the result of the prevention of the extinction of Behaviour 1 by training Behaviour 2. At a similar point in extinction, the number of occurrences of Behaviour 1 in its own extinction was not significantly different from the number of occurrences of Behaviour 1 during the extinction of Behaviour 2. This fails to support the hypothesis that resurgence is induced by the extinction of Behaviour 2.

Journal Article↗
PubMed2006

Neural correlates of modality-specific spatial extinction.

Sites of lesions responsible for visual, tactile, and/or motor extinction have not been clearly identified. We sought to determine the frequency of extinction in various modalities immediately after acute ischemic stroke, the rate of co-occurrence of extinction across modalities, and areas of infarct and/or hypoperfusion associated with each modality of extinction. A total of 148 patients with right supratentorial stroke were studied. In Study 1, 88 patients without hemiplegia, hemianesthesia, or visual field cuts were tested within 24 hours of onset for visual, tactile, and motor extinction, and underwent magnetic resonance diffusion and perfusion imaging. Associations between modality of extinction and areas of neural dysfunction (hypoperfusion/infarct) were identified. Of the 88 patients, 19 had only tactile extinction, 8 had only visual extinction, 12 had only motor extinction, 14 had extinction in two or more modalities, and 35 had no extinction. Tactile extinction was associated with neural dysfunction in the inferior parietal lobule; visual extinction was associated with dysfunction in the visual association cortex; and motor extinction was associated with neural dysfunction in the superior temporal gyrus. In Study 2, data from 60 patients who were excluded from Study 1 because of motor deficits were analyzed in the same way to determine whether frontal lesions contributed to visual or tactile extinction. Results again demonstrated that tactile extinction is associated with inferior parietal dysfunction, and visual extinction is associated with dysfunction of the visual association cortex. Potential accounts of the results, based on the "hemisphere rivalry" model of extinction and the limited attentional capacity model, are considered.

Aged↗