Correction to: ‘Violence in the prehistoric period of Japan: the spatio-temporal pattern of skeletal evidence for violence in the Jomon period’

Whether man is predisposed to lethal violence, ranging from homicide to warfare, and how that may have impacted human evolution, are among the most controversial topics of debate on human evolution. Although recent studies on the evolution of warfare have been based on various archaeological and ethnographic data, they have reported mixed results: it is unclear whether or notwarfare among prehistoric hunter–gathererswas common enough to be a component of human nature and a selective pressure for the evolution of human behaviour. This paper reports the mortality attributable to violence, and the spatio-temporal pattern of violence thus shown among ancient hunter–gatherers using skeletal evidence in prehistoric Japan (the Jomon period: 13 000 cal BC–800 cal BC). Our results suggest that the mortality due to violence was low and spatio-temporally highly restricted in the Jomon period, which implies that violence including warfare in prehistoric Japan was not common

Violence and warfare in prehistoric Japan

The origins and consequences of warfare or largescale intergroup violence have been subject of long debate. Based on exhaustive surveys of skeletal remains for prehistoric hunter-gatherers and agriculturists in Japan, the present study examines levels of inferred violence and their implications for two different evolutionary models, i.e., parochial altruism model and subsistence model. The former assumes that frequent warfare played an important role in the evolution of altruism and the latter sees warfare as promoted by social changes induced by agriculture. Our results are inconsistent with the parochial altruism model but consistent with the subsistence model, although the mortality values attributable to violence between hunter-gatherers and agriculturists were comparable

Relationship between Protection against Cold and the Physiological Index during a Cold Environment

A snow cave is a bivouac shelter used in mountain climbing that is widely used as a shelter against the cold during winter. In the outdoors, wind velocity and air temperature have an influence on temperature change. It could stabilize body temperature if it can control the convection of ambient air. This paper could develop a theory focusing on the relation between physiological indexes and the protection against the cold while staying in a snow cave. For example, protection against the cold could be thermal insulation underwear, thermal insulation gloves, thermal insulation socks, a steam warmed temperature sheet and a rescue sheet. Measurement items were heart rate, blood pressure, rectal temperature, score of a subjective thermal sensation and the activity of the parasympathetic nervous system. It was clarified that the protection against the cold could be effective for the decrease of the physiological index. These field studies suggest that they would enable the adaptation in the adjustment range of the autonomic nervous system given these protections against the cold

Magnetic Resonance Imaging Diagnosis of Dandy-Walker-Like Syndrome in a Wire-Haired Miniature Dachshund

A 12-week-old female Wire-haired miniature dachshund presented with non-progressive ataxia and hypermetria. Due to the animal’s clinical history and symptoms, cerebellar malformations were suspected. Computed tomography (CT) and magnetic resonance imaging (MRI) detected bilateral ventriculomegaly, dorsal displacement of the cerebellar tentorium, a defect in the cerebellar tentorium and a large fluid-filled cystic structure that occupied the regions where the cerebellar vermis and occipital lobes are normally located. The abovementioned cystic structure and the defect in the cerebellar tentorium were comparable to those seen in humans with Dandy-Walker syndrome. However, the presence of the cystic structure in the occipital lobe region was unique to the present case. During necropsy, the MRI findings were confirmed, but the etiology of the condition was not determined

Effectiveness of a digital device providing real-time visualized tooth brushing instructions: A randomized controlled trial

Introduction: The aim of this trial was to investigate whether a digital device that provides real-time visualized brushing instructions would contribute to the removal of dental plaque over usual brushing instructions. Methods: We conducted a single-center, parallel-group, stratified permuted block randomized control trial with 1:1 allocation ratio. Eligibility criteria included people aged ≥ 18 years, and exclude people who met the following criteria: severely crowded teeth; using interdental cleaning implement; having external injury in the oral cavity, or stomatitis; having less than 20 teeth; using orthodontic apparatus; visited to a dental clinic; having the possibility of consulting a dental clinic; having a dental license; not owning a smartphone or tablet device; smoker; taken antibiotics; pregnant; an allergy to the staining fluid; and employee of Sunstar Inc. All participants received tooth brushing instructions using video materials and were randomly assigned to one of two groups for four weeks: (1) an intervention group who used the digital device, providing real-time visualized instructions by connection with a mobile application; and (2) a control group that used a digital device which only collected their brushing logs. The primary outcome was the change in 6-point method plaque control record (PCR) score of all teeth between baseline and week 4. The t-test was used to compare the two groups in accordance with intention-to-treat principles. Results: Among 118 enrolled individuals, 112 participants were eligible for our analyses. The mean of PCR score at week 4 was 45.05% in the intervention group and 49.65% in the control group, and the change of PCR score from baseline was −20.46% in the intervention group and −15.77% in the control group (p = 0.088, 95% confidence interval −0.70–10.07). Conclusions: A digital device providing real-time visualized brushing instructions may be effective for the removal of dental plaque

The DNA Repair Enzyme Apurinic/Apyrimidinic Endonuclease (Apex Nuclease) 2 Has the Potential to Protect against Down-Regulation of Chondrocyte Activity in Osteoarthritis

Apurinic/apyrimidinic endonuclease 2 (Apex 2) plays a critical role in DNA repair caused by oxidative damage in a variety of human somatic cells. We speculated that chondrocyte Apex 2 may protect against the catabolic process of articular cartilage in osteoarthritis (OA). Higher levels of Apex 2 expression were histologically observed in severely compared with mildly degenerated OA cartilage from STR/OrtCrlj mice, an experimental model which spontaneously develops OA. The immunopositivity of Apex 2 was significantly correlated with the degree of cartilage degeneration. Moreover, the OA-related catabolic factor interleukin-1β induced the expression of Apex 2 in chondrocytes, while Apex 2 silencing using small interfering RNA reduced chondrocyte activity in vitro. The expression of Apex 2 in chondrocytes therefore appears to be associated with the degeneration of articular cartilage and could be induced by an OA-related catabolic factor to protect against the catabolic process of articular cartilage. Our findings suggest that Apex 2 may have the potential to prevent the catabolic stress-mediated down-regulation of chondrocyte activity in OA

The NAD-Dependent Deacetylase Sirtuin-1 Regulates the Expression of Osteogenic Transcriptional Activator Runt-Related Transcription Factor 2 (Runx2) and Production of Matrix Metalloproteinase (MMP)-13 in Chondrocytes in Osteoarthritis

Aging is one of the major pathologic factors associated with osteoarthritis (OA). Recently, numerous reports have demonstrated the impact of sirtuin-1 (Sirt1), which is the NAD-dependent deacetylase, on human aging. It has been demonstrated that Sirt1 induces osteogenic and chondrogenic differentiation of mesenchymal stem cells. However, the role of Sirt1 in the OA chondrocytes still remains unknown. We postulated that Sirt1 regulates a hypertrophic chondrocyte lineage and degeneration of articular cartilage through the activation of osteogenic transcriptional activator Runx2 and matrix metalloproteinase (MMP)-13 in OA chondrocytes. To verify whether sirtuin-1 (Sirt1) regulates chondrocyte activity in OA, we studied expressions of Sirt1, Runx2 and production of MMP-13, and their associations in human OA chondrocytes. The expression of Sirt1 was ubiquitously observed in osteoarthritic chondrocytes; in contrast, Runx2 expressed in the osteophyte region in patients with OA and OA model mice. OA relating catabolic factor IL-1βincreased the expression of Runx2 in OA chondrocytes. OA chondrocytes, which were pretreated with Sirt1 inhibitor, inhibited the IL-1β-induced expression of Runx2 compared to the control. Since the Runx2 is a promotor of MMP-13 expression, Sirt1 inactivation may inhibit the Runx2 expression and the resultant down-regulation of MMP-13 production in chondrocytes. Our findings suggest thatSirt1 may regulate the expression of Runx2, which is the osteogenic transcription factor, and the production of MMP-13 from chondrocytes in OA. Since Sirt1 activity is known to be affected by several stresses, including inflammation and oxidative stress, as well as aging, SIRT may be involved in the development of OA

DPP-4 inhibition protects human umbilical vein endothelial cells from hypoxia-induced vascular barrier impairment

Dipeptidyl peptidase-4 (DPP-4) inhibitors are relatively new class of anti-diabetic drugs. Some protective effects of DPP-4 on cardiovascular disease have been described independently from glucose-lowering effect. However, the detailed mechanisms by which DPP-4 inhibitors exert on endothelial cells remain elusive. The purpose of this research was to determine the effects of DPP-4 inhibitor on endothelial barrier function. Human umbilical vein endothelial cells (HUVECs) were cultured and exposed to hypoxia in the presence or absence of Diprotin A, a DPP-4 inhibitor. Immunocytochemistry of vascular endothelial (VE-) cadherin showed that jagged VE-cadherin staining pattern induced by hypoxia was restored by treatment with Diprotin A. The increased level of cleaved β-catenin in response to hypoxia was significantly attenuated by Diprotin A, suggesting that DPP-4 inhibition protects endothelial adherens junctions from hypoxia. Subsequently, we found that Diprotin A inhibited hypoxia-induced translocation of NF-κB from cytoplasm to nucleus through decreasing TNF-α expression level. Furthermore, the tube formation assay showed that Diprotin A significantly restored hypoxia-induced decrease in number of tubes by HUVECs. These results suggest that DPP-4 inhibitior protects HUVECs from hypoxia-induced barrier impairment