Bergmann's rule states that, within species of mammals, individuals tend to be larger in cooler environments. However, the validity of the rule has been debated. We examined the relationship between size and latitude as well as size and temperature within various species of mammals. We also tested the idea that smaller mammals follow Bergmann's rule more strongly than larger mammals, as expected if heat conservation is the cause of the rule. When all studies were included, the percentage of species showing a positive correlation between size and latitude was significantly >50% (78 of 110 species). Similarly, the percentage of species showing a negative correlation between size and temperature was significantly >50% (48 of 64). Analyses using only significant studies or only studies that sampled extensively also support Bergmann's rule. The size-latitude and size-temperature trends were consistent within all orders and most families for which data are available. We did not find support for the hypothesis that smaller mammals conform more strongly to Bergmann's rule than larger mammals. Thus, we found broad support for Bergmann's rule as a general trend for mammals; however, our analyses do not support heat conservation as the explanation.
AbstractBackgroundBacterial meningitis (BM) causes apoptotic damage to the hippocampus and homocysteine (Hcy) accumulation to neurotoxic levels in the cerebrospinal fluid of children. The Hcy pathway controls bioavailability of methyl and its homeostasis can be modulated by vitamin B12, cofactor of the methionine synthase enzyme. Herein, the neuroprotective potential and the underlying mode of action of vitamin B12 adjuvant therapy were assessed in an infant rat model of BM.MethodsEleven-day old rats were intracysternally infected with Streptococcus pneumoniae serotype 3, or saline, treated with B12 or placebo, and, 24h after infection, their hippocampi were analyzed for apoptosis in the dentate gyrus, sulfur amino acids content, global DNA methylation, transcription and proximal promoter methylation of candidate genes. Differences between groups were compared using 2-way ANOVA 2-way followed by Bonferroni post-hoc test. Correlations were tested with Spearman’s test.ResultsB12 attenuated BM-induced hippocampal apoptosis in a Hcy dependent manner (r = 0.80, P < 0.05). BM caused global DNA hypomethylation, however B12 restored this parameter. Accordingly, B12 increased the methylation capacity of hippocampal cells from infected animals, as inferred from the ratio S-adenosyl methionine (SAM):S-adenosyl homocysteine (SAH) in infected animals. BM upregulated selected pro-inflammatory genes, and this effect was counteracted by B12, which also increased methylation of CpGs at the promoter of Ccl3 of infected animals.ConclusionHcy is likely to play a central role in hippocampal damage in the infant rat model of BM, and B12 shows an anti-inflammatory and neuroprotective action through methyl-dependent epigenetic mechanisms.
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