PubMed · 5403525
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R Pigassou, F Pinçon. 1969. [Practical notes: presentation of vision tests].. https://pubmed.ncbi.nlm.nih.gov/5403525/
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In order to examine whether a polymorphism in the promoter region of the myeloperoxidase (MPO) gene is associated with lung cancer among male smokers, we conducted a case-control study nested within a Finnish clinical trial cohort. Although we found no evidence of an overall association between lung cancer risk and MPO genotype, the variant MPO genotype was associated with an increased risk of lung cancer among a subset of older men. These findings contrast with those from previous studies that report decreased lung cancer risk among MPO variant individuals.
The present study aimed to assess the role of advanced age in the development and manifestation of thiamine deficiency using an animal model of Wernicke-Korsakoff syndrome (WKS). Interactions between pyrithiamine-induced thiamine deficiency (PTD) and age were examined relative to working memory impairment and neuropathology in Fischer 344 rats. Young (2-3 months) and aged (22-23 months) F344 rats were assigned to one of two treatment conditions: PTD or pair-fed control (PF). Rats in the former group were further divided into three groups according to duration of PTD treatment. Working memory was assessed with an operant matching-to-position (MTP) task; after testing, animals were sacrificed and both gross and immunocytochemical measures of brain pathology were obtained. Aged rats exhibited acute neurological disturbances during the PTD treatment regime earlier than did young rats, and also developed more extensive neuropathology with a shorter duration of PTD. Aged rats displayed increased brain shrinkage (smaller frontal cortical and callosal thickness) as well as enhanced astrocytic activity in the thalamus and a decrease in ChAT-positive cell numbers in the medial septum; the latter two measures of neuropathology were potentiated by PTD. In both young and aged rats, and to a greater degree in the latter group, PTD reduced thalamic volume. Behaviorally, aged rats displayed impaired choice accuracy on the delayed MTP task. Regardless of age, rats with lesions centered on the internal medullary lamina of the thalamus also displayed impaired choice accuracy. Moreover, increased PTD treatment duration led to increased response times on the delayed MTP task. These results suggest that aging does indeed potentiate the neuropathology associated with experimental thiamine deficiency, supporting an age coupling hypothesis of alcohol-related neurological disorders.
Cell death is ubiquitous in the developing brain and an important regulator of cell number. The olfactory bulb, the first central relay for information from the nose, is a particularly appropriate region for studying cell death. The bulb is constantly infused with new cells, has a strictly organized anatomy, and cell survival is known to depend on levels of afferent activation. The present study examined patterns of cell death in both the normally developing and sensory-deprived rat olfactory bulb terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL). In control pups, TUNEL-labeled profiles were high at postnatal day 5 (P5, day of birth = P0), but then decreased rapidly to constant levels. In contrast, blocking airflow through half of the nasal cavity by surgically closing an external naris on P1 resulted in a gradual increase in TUNEL-positive figures within the ipsilateral olfactory bulb by P20, with the effects being seen in the mitral and granule cell layers until at least P60. The effect was largely age dependent, because subjects occluded from P30 to P60 showed only slight increases in cell death. Furthermore, although interlaminar differences were encountered, the pattern of cell death appeared uniform over much of the bulb. Finally, reopening occluded nares decreased cell death levels to control values, suggesting an inverse relationship between the level of olfactory function and the extent of cell death. Thus, the data indicate that cell death is prevalent in the normal olfactory bulb, and that it is directly regulated by the level of olfactory function.