Seasonal food changes and feeding behaviour adaptations of savanna chimpanzees at Nguye in Ugalla, Tanzania.

We studied the feeding strategies of savanna chimpanzees (Pan troglodytes) at Nguye in Ugalla, Western Tanzania (05°13'S, 30°28'E). Among the driest most open chimpanzee habitats, Ugalla is covered mainly by woodlands. We analysed undigested contents in chimpanzee faeces, and conducted a vegetation survey and a 1-year phenology survey every 2 weeks. The fruits of some trees with the highest biomass had high appearance rates in faeces (e.g. Parinari curatellifolia and Diplorhynchus condylocarpon). Herbaceous Aframomum mala fruits grew in large patches in savanna woodland near forest edges along rivers and had the highest appearance frequency over the longest seasonal period in faeces. Other species with higher appearance rates in faeces for long seasonal periods included Grewia mollis at the forest edge and Thespesia garckeana growing on termite mounds at the forest edge. These two tree species had low biomass. Thus, savanna chimpanzees fed on some tree foods with higher biomass, herbaceous fruits instead of scarcer tree fruits, and fruits at forest edges and in forests which occupy a small portion of the study area, in addition to woodlands which occupy a large proportion. The forest edge and interior run continuously for long distances along rivers. Forest occupies 2% of this area, but chimpanzees can continuously obtain food by moving along riverine forest. To compensate for fruit scarcity in the non-fruiting (early rainy) season, chimpanzees ate fibrous, low-quality plant parts. Chimpanzees formed smaller parties when ripe fruits and unripe legumes were scarcer. Using these feeding strategies, chimpanzees adapted to savanna woodlands.

Increased production of inflammatory cytokines and activation of microglia in the fetal brain of preeclamptic mice induced by angiotensin II.

Preeclampsia (PE) is a hypertensive obstetric disorder with poor prognosis for both the mother and offspring. Infants born to mothers with PE are known to be at increased risk of developing higher brain dysfunction, such as autism. However, how maternal PE can affect the environment in the fetal brain has not been fully elucidated. Here, we examined the impact of PE on the fetal brain in a mouse model of PE induced by angiotensin II (Ang II), focusing on changes in the inflammatory condition. We confirmed that pregnant mice which were continuously administered Ang II exhibited PE phenotypes, including high blood pressure, proteinuria, and fetal growth restriction. Quantitative RT-PCR analysis demonstrated that the brain of fetuses on embryonic day 17.5 (E17.5) in the Ang II-administered pregnant mice showed increased expression of cytokines, interleukin (IL)- 6, IL-17a, tumor necrosis factor-α, interferon-γ, IL-12, IL-4, and IL-10. Immunohistochemical analysis over a wide area, from the tip of the frontal lobe to the posterior cerebral end, on E17.5 revealed that the microglia in the fetal brain of the Ang II-administered group displayed higher solidity and circularity than those of the control group, indicating that the microglia had transformed to an amoeboid morphology and were activated. Our findings suggest that maternal PE may cause altered inflammatory conditions in the fetal brain, which might be associated with the pathological mechanism connecting maternal PE and brain dysfunction in the offspring.

A Case of Preeclampsia with Uterine Necrosis after Uterine Artery Embolization for Postpartum Hemorrhage.

Uterine necrosis is a rare complication in uterine artery embolization (UAE) for postpartum hemorrhage (PPH). Preeclampsia (PE) is a condition characterized with systemic endothelial damage and intravascular volume depletion. Whether a patient with PE is at high risk for uterine necrosis after UAE for PPH has been unknown. A 30-year-old primipara woman was diagnosed with PE based on hypertension and proteinuria during delivery. UAE was performed for PPH after forceps delivery. After UAE, the patient presented with pleural effusion and massive ascites as well as persistent fever unresponsive to antibiotics. Ultrasonography and contrast-enhanced magnetic resonance imaging (MRI) led to the diagnosis of uterine necrosis, for which we performed total laparoscopic hysterectomy. It should be kept in mind that patients with PE associated with massive ascites may be at high risk for uterine necrosis after UAE due to decreased uterine perfusion. Therefore, it is important to pay attention to persistent symptoms such as fever and abdominal pain after UAE to diagnose uterine necrosis.

Chimpanzees (Pan troglodytes) in savanna landscapes.

Chimpanzees (Pan troglodytes) are the only great apes that inhabit hot, dry, and open savannas. We review the environmental pressures of savannas on chimpanzees, such as food and water scarcity, and the evidence for chimpanzees' behavioral responses to these landscapes. In our analysis, savannas were generally associated with low chimpanzee population densities and large home ranges. In addition, thermoregulatory behaviors that likely reduce hyperthermia risk, such as cave use, were frequently observed in the hottest and driest savanna landscapes. We hypothesize that such responses are evidence of a "savanna landscape effect" in chimpanzees and offer pathways for future research to understand its evolutionary processes and mechanisms. We conclude by discussing the significance of research on savanna chimpanzees to modeling the evolution of early hominin traits and informing conservation programs for these endangered apes.

Elevated placental histone H3K4 methylation via upregulated histone methyltransferases SETD1A and SMYD3 in preeclampsia and its possible involvement in hypoxia-induced pathophysiological process.

INTRODUCTION: Disturbance in placental epigenetic regulation contributes to the pathogenesis of preeclampsia (PE). Although aberrant placental DNA methylation status in PE has been thoroughly studied, the role of histone modifications, including histone methylation, in PE remains unclear. Moreover, no study has ever reported the association between PE and placental histone methylation status by focusing on histone methyltransferases. The present study aimed to investigate the possible involvement of placental epigenetic regulation by histone methylation via histone methyltransferases in the pathophysiology of PE. METHODS: Placental mRNA expression of histone methyltransferases was examined using quantitative RT-PCR. Protein expression of histone methyltransferases and histone methylation status in placentas and trophoblast cell lines were assessed by immunoblotting and immunohistochemistry. RESULTS: Expression profile of histone methyltransferases in the placentas using quantitative RT-PCR revealed that the mRNA expression levels of histone 3 lysine 4 (H3K4) methyltransferases, SETD1A and SMYD3, were significantly increased in placentas from PE patients. Immunoblotting and immunohistochemistry revealed that not only protein expression levels of SETD1A and SMYD3, but also H3K4 methylation status was increased in the trophoblasts from PE placentas. In vitro studies using HTR-8/SV-neo and BeWo cells showed that hypoxia induced the expression levels of SETD1A and SMYD3, and subsequently enhanced H3K4 methylation. Furthermore, the overexpression of SETD1A and SMYD3 in HTR-8/SV-neo cells enhanced H3K4 methylation in response to hypoxia. DISCUSSION: Our study results suggest that placental epigenetic alteration by enhanced histone H3K4 methylation through upregulated SETD1A and SMYD3 might play a role in the pathophysiological process of PE associated with hypoxia.

Risk-taking behavior of bull-headed shrikes that recently colonized islands.

Individuals which have invaded urbanized environments are reported to engage in riskier behaviors, possibly influenced by the scarcity of predators in urbanized areas. Here, we studied the risk-taking behavior of birds which had invaded a new natural environment, rather than an artificial urban environment, using recently established populations of the bull-headed shrike Lanius bucephalus, which naturally colonized three subtropical islands in Japan. We compared flight initiation distance (FID), the distance at which an individual approached by a human initiates flight, between the islands and the temperate mainland. FID was longer for the insular shrikes compared with the mainland shrikes after controlling for other factors, indicating that the individuals which had invaded a new natural environment had a lower propensity for risk-taking. A possible explanation for these results is that low risk-taking behavior might be adaptive on the islands due to predation by the black rat Rattus rattus, an unfamiliar predator not found in shrike habitats on the temperate mainland. Further studies are needed to examine the nest predation rate, predator species, and nest site selection of these insular shrike populations.

ASK1 promotes uterine inflammation leading to pathological preterm birth.

It is widely accepted that enhanced uterine inflammation associated with microbial infection is a main causative factor for preterm birth. However, little is known about the molecular basis by which inflammation is associated with preterm birth. Here, we demonstrate that apoptosis signal-regulating kinase 1 (ASK1), a member of the mitogen-activated protein 3-kinase family, facilitates inflammation-induced preterm birth and that inhibition of ASK1 activity is sufficient to suppress preterm birth. ASK1-deficient pregnant mice exhibited reduced incidence of lipopolysaccharide (LPS)-induced preterm birth. ASK1 was required for the induction of LPS-induced inflammatory responses related to preterm birth, including pro-inflammatory cytokine production in the uterus and peritoneal cavities. In addition, selective suppression of uterine ASK1 activity through a chemical genetic approach reduced the incidence of LPS-induced preterm birth. Moreover, translational studies with human choriodecidua demonstrated that ASK1 was required for LPS-induced activation of JNK and p38 and pro-inflammatory cytokine production. Our findings suggest that ASK1 activation is responsible for the induction of inflammation that leads to preterm birth and that the blockade of ASK1 signaling might be a promising therapeutic target for preventing preterm birth.

Increased LIGHT leading to sFlt-1 elevation underlies the pathogenic link between hydatidiform mole and preeclampsia.

Hydatidiform moles are known to pose an extremely high risk of severe early-onset preeclampsia if left untreated. TNF superfamily cytokine, LIGHT has recently been reported to contribute to pathophysiology of preeclampsia. The present study aimed to investigate the involvement of LIGHT in hydatidiform moles. We measured the serum levels of LIGHT and sFlt-1 by ELISA in 17 women with complete hydatidiform mole (HM) and 20 gestational-age-matched normal pregnant women (control). As a result, the serum LIGHT levels were significantly higher in HM as compared with those in control (69.9 ± 9.6 pg/ml vs 25.4 ± 5.3 pg/ml, p = 0.0001) and the serum levels of LIGHT were significantly positively correlated with those of sFlt-1 in HM (r = 0.68, p = 0.0029). Immunohistochemical analysis revealed that the expression levels of LIGHT were increased in HM placentas as compared with controls, and LIGHT and sFlt-1 were co-localized in the trophoblast cells of HM. In vitro studies using primary syncytiotrophoblast cells demonstrated that LIGHT directly induced sFlt-1 expression in trophoblast cells. Our results indicated that elevated LIGHT in the trophoblast cells of hydatidiform mole induces sFlt-1, which might underlie the pathogenic mechanism of early-onset preeclampsia developing secondary to molar pregnancies.

Sleeping site selection by savanna chimpanzees in Ugalla, Tanzania.

We examined sleeping site selection by chimpanzees (Pan troglodytes) in the Ugalla savanna woodland area, western Tanzania, from 1994 to 2012. We established 488 km of line transects and recorded 379 chimpanzee beds within 30 m perpendicular to the transects. Comparisons between 60 × 60 m(2) quadrats containing new and recent beds and the remaining quadrats without beds along the transects indicated that evergreen forests accounted for disproportionately more area in quadrats with beds than in those without beds during both the dry and rainy seasons. In Ugalla, chimpanzees coexist with lions (Panthera leo) and leopards (Panthera pardus). They may sleep in forests to reduce predation risk by these carnivores, as trees are dense and the canopy is high and closed. The angle of slope was steeper in quadrats containing beds than in those without beds during the dry season, whereas the angle was less steep in quadrats with beds than in those without beds during the rainy season. Additionally, fewer beds were found further from forests. The distance between beds and forests during the dry season was shorter than that during the rainy season. Chimpanzees may sleep in or near forests and on slopes because of water pools in the valley forests along the slopes during the dry season. Quadrats with beds were at slightly higher altitude than those without beds during the rainy season; however, the difference was not significant during the dry season. The number of beds found in or close to feeding trees was not related to the fruiting period. Sleeping site selection by chimpanzees may be affected by predation pressure and water availability in the savanna woodland area.