PubMed · 4187005
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E Turner. 1969-11-22. Hippocampus and memory.. https://doi.org/10.1016/s0140-6736(69)90718-1
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We have considered trends in incidence and mortality in 28 European countries using incidence data from successive volumes of Cancer Incidence in Five Continents and mortality from the WHO database. Countries with the highest rates in the early 1960s included the Nordic countries, Austria, Germany and the United Kingdom, but trends in these areas have tended to decline over recent calendar periods, particularly with regard to mortality. Southern European countries showed upward trends, at least until the early 1980s for France and Italy. Likewise, in most central and eastern European countries, ovarian cancer incidence and mortality rates were originally relatively low, but tended to rise over time. Falls in mortality, but not in incidence, over recent years were observed in the Czech Republic and Hungary. In several countries, mainly in northern Europe, trends were more favorable at younger age (25-49 years) than in the subsequent age groups. Thus, recent trends in ovarian cancer have led to a leveling of rates across various areas of the continent, although a 2.5-fold variation was still observed in the late 1990s between the highest mortality rate of 9.3/100,000 in Denmark and the lowest one of 3.6 in Portugal. These patterns should be viewed in the light of an observed reduction in parity, mainly in southern and eastern Europe, and the spread of oral contraceptive use, mainly in northern Europe, since these are the best recognized protective factors with regard to ovarian carcinogenesis. The declining mortality trends can also in part be ascribed to improvements in treatment.
Nerve growth factor (NGF) and related neurotrophins are target-derived survival factors for sensory neurons. In addition, these peptides modulate neuronal differentiation, axon guidance, and synaptic plasticity. We tested axonal behavior of embryonic trigeminal neurons towards localized sources of NGF in collagen gel assays. Trigeminal axons preferentially grow towards lower doses of localized NGF and grow away from higher concentrations at earlier stages of development, but do not show this response later. Dorsal root ganglion axons also show similar responses to NGF, but NGF-dependent superior cervical ganglion axons do not. Such axonal responses to localized NGF sources were also observed in Bax-/- mice, suggesting that the axonal effects are largely independent of cell survival. Immunocytochemical studies indicated that axons, which grow towards or away from localized NGF are TrkA-positive, and TrkA-/- TG axons do not respond to any dose of NGF. We further show that axonal responses to NGF are absent in TG derived from mice that lack the p75 neurotrophin receptor (p75NTR). Collectively, our results suggest that localized sources of NGF can direct axon outgrowth from trigeminal ganglion in a dose- and age-dependent fashion, mediated by p75NTR signaling through TrkA expressing axons.
Hamsters repeatedly exposed to cocaine during adolescence display high levels of offensive aggression compared to saline-treated littermates. The escalated offensive phenotype observed in adolescent cocaine-treated animals is modulated by serotonin (5-HT) signaling and can be suppressed by inhibiting 5-HT type 3 receptors, suggesting that these receptors might play an important role in the aggression-stimulating effects of adolescent cocaine exposure. The current study examined this hypothesis and extended earlier studies investigating the relationship between 5HT(3) receptor neural signaling and the offensive response patterns of aggressive, adolescent cocaine-treated animals compared to non-aggressive, saline-treated littermates. Adolescent cocaine-treated hamsters and saline-treated littermates were tested for offensive aggression after the administration of either the 5-HT(3) antagonist 3-tropanylindole-3-carboxylate methiodide (tropisetron) or the 5-HT(3) agonist 1-(m-chlorophenyl)-biguanide hydrochloride (mCPBG). Tropisetron significantly reduced the high levels of offensive responding observed in adolescent cocaine-treated animals, whereas treatment with the 5-HT(3) receptor agonist mCPBG failed to affect the escalated offensive response. Conversely, tropisetron failed to affect very low, baseline levels of aggressive responding seen in adolescent saline-treated animals, while 5-HT(3) receptor activation via mCPBG triggered highly escalated levels of offensive aggression in these animals. Together, these data support a stimulatory role for 5-HT(3) neural signaling in offensive aggression.