The quantitative and demographic features of infant-corpse-carrying behavior in Japanese macaques (Macaca fuscata) at Takasakiyama, southern Japan, have been studied over 24 years. More than 91% of the dead infants that were carried by their mothers were abandoned within a week. Mothers of all age classes exhibited this behavior and neither the carrying rate (number of carriers/number of deaths) nor the duration were significantly different between young and older mothers. The sex of the infant was not a decisive factor. Nearly 80% of all cases observed involved infants that had died within 30 days of birth. The oldest infant whose corpse was observed being carried had died at 253 days. The overall carrying rate was 15% when death had occurred within 253 days and 28.7% for infants that died within 30 days of birth. Most mothers whose infants had lived for more than a month abandoned the corpse soon after death. Some females persist in exhibiting behaviors performed towards live infants but the exact reasons for this are unclear at present.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective and progressive loss of motor neurons. The purpose of this study was to clarify effects of brazilian green propolis and the active ingredient against ALS-associated mutant copper-zinc superoxide dismutase (SOD1)-mediated toxicity. Ethanol extract of brazilian green propolis (EBGP) protected N2a cells against mutant SOD1-induced neurotoxicity and reduced aggregated mutant SOD1 by induction of autophagy. Kaempferide and kaempferol, the active ingredients of EBGP, also inhibited mutant SOD1-induced cell death and reduced the intracellular mutant SOD1 aggregates. Both kaempferide and kaempferol significantly suppressed mutant SOD1-induced superoxide in mitochondria. Western blot analysis showed that kaempferol potentially induced autophagy via the AMP-activated protein kinase (AMPK) - the mammalian target of rapamycin (mTOR) pathway. These results suggest that EBGP containing the active ingredient against mutant SOD1-mediated toxicity is a promising medicine or health food for prevention and treatment of ALS.

Epidemiological and laboratory studies suggested that exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects glucose homeostasis and increases the incidence of type 2 diabetes mellitus. To evaluate the effects of TCDD on insulin secretion from islets of Langerhans (islets), we designed in vivo, ex vivo and in vitro experiments. For the in vivo experiment, male C57BL/6J and aryl hydrocarbon receptor (AhR)-null mice were injected intraperitoneally with TCDD (10 microg kg(-1) b.w.), fasted for 12 h and administered glucose 24 h post-administration. TCDD exposure significantly decreased the plasma insulin concentration at 60 and 120 min after a glucose challenge in C57BL/6J mice but not in AhR-null mice. In contrast, the plasma glucose concentration was not changed by TCDD exposure in both C57BL/6J and AhR-null mice. For the ex vivo experiment, we isolated islets 24 h after TCDD administration and determined the glucose-stimulated insulin secretion from the islets. The insulin secretion level was found to be significantly decreased by TCDD exposure at 60 min after glucose treatment. For the in vitro experiment, islets harvested from untreated C57BL/6J mice were exposed to 0.1, 1, 10 or 100 nM TCDD for 24 h and analyzed for glucose-stimulated insulin secretion. Insulin secretion from the islets remained unchanged regardless of TCDD dose. In conclusion, TCDD exposure impaired the second phase of glucose-stimulated secretion of insulin from the islets via the AhR signaling pathway.

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Congenital heart disease (CHD) is the most common congenital abnormality and one of the leading causes of newborn death throughout the world. Despite much emerging scientific information, the precise etiology of this disease remains elusive. Here, we show that the aryl hydrocarbon receptor (AHR) regulates the expression of crucial cardiogenesis genes and that interference with endogenous AHR functions, either by gene ablation or by agonist exposure during early development, causes overlapping structural and functional cardiac abnormalities that lead to altered fetal heart physiology, including higher heart rates, right and left ventricle dilation, higher stroke volume, and reduced ejection fraction. With striking similarity between AHR knockout (Ahr(-/-)) and agonist-exposed wild type (Ahr(+/+)) embryos, in utero disruption of endogenous AHR functions converge into dysregulation of molecular mechanisms needed for attainment and maintenance of cardiac differentiation, including the pivotal signals regulated by the cardiogenic transcription factor NKH2.5, energy balance via oxidative phosphorylation and TCA cycle and global mitochondrial function and homeostasis. Our findings suggest that AHR signaling in the developing mammalian heart is central to the regulation of pathways crucial for cellular metabolism, cardiogenesis, and cardiac function, which are potential targets of environmental factors associated with CHD.