Capture of Electroweak Multiplet Dark Matter in Neutron Stars

If dark matter has a sizable scattering cross section with nucleons, it can efficiently be captured by a neutron star. Its energy is then transferred to the neutron star as heat through the scattering and annihilation inside the star. This heating effect may be detectable via dedicated temperature observations of nearby old pulsars, providing an alternative method for dark matter searches. In this paper, we show that for electroweak multiplet dark matter this search strategy can probe the parameter region which is out of reach of future dark matter direct detection experiments. To see this systematically, we classify such dark matter candidates in terms of their electroweak charges and investigate the effect of ultraviolet physics by means of higher-dimensional effective operators. We then show that if the effect of ultraviolet physics is sizable, the dark matter-nucleon elastic scattering cross section becomes sufficiently large, whilst if it is suppressed, then the mass splittings among the components of the DM multiplet get small enough so that the inelastic scattering processes are operative. In any case, the electroweak multiplet dark matter particles are efficiently captured in neutron stars, making the search strategy with the temperature observation of old neutron stars promising.Comment: 33 pages, 7 figures, 1 tabl

New chemically induced skin tumour susceptibility loci identified in a mouse backcross between FVB and dominant resistant PWK

<p>Abstract</p> <p>Background</p> <p>A variety of skin cancer susceptibility among mouse strains has allowed identification of genes responsible for skin cancer development. Fifteen <it>Skts </it>loci for skin tumour susceptibility have been mapped so far by using the two-stage skin carcinogenesis model [induced by 7.12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)]. A few responsible genes have been identified using wild-derived dominant resistant <it>Mus spretus </it>mice, and one has been confirmed as a low penetrance cancer susceptibility gene in a variety of human cancers.</p> <p>Results</p> <p>In the present study, we found that wild-derived PWK mice developed no tumour by treatment with the two-stage skin carcinogenesis protocol. This phenotype is dominant resistant when crossed with the highly susceptible strain FVB. By analyzing the F1 backcross generation between PWK and FVB, we found empirical evidence of significant linkage at the new loci <it>Skts-fp1 </it>on chromosome 4 and suggestive linkage on chromosomes 1, 3, 11, 12 and 14 for skin tumour susceptibility. <it>Skts-fp1 </it>includes the <it>Skts7 </it>interval, which was previously mapped by a <it>Mus spretus </it>and NIH backcross. We also observed suggestive linkage on chromosomes 1 and 2 in the female population only, while suggestive linkage on chromosomes 14 and 15 only was observed in the male population. A significant genetic interaction was seen between markers of <it>D11Mit339</it> and <it>D16Mit14</it>.</p> <p>Conclusion</p> <p>Analysis of this new cross may facilitate the identification of genes responsible for mouse skin cancer susceptibility and may reveal their biological interactions.</p

Vortex Creep Heating vs. Dark Matter Heating in Neutron Stars

Dark matter particles captured in neutron stars deposit their energy as heat. This DM heating effect can be observed only if it dominates over other internal heating effects in NSs. In this work, as an example of such an internal heating source, we consider the frictional heating caused by the creep motion of neutron superfluid vortex lines in the NS crust. The luminosity of this heating effect is controlled by the strength of the interaction between the vortex lines and nuclei in the crust, which can be estimated from the many-body calculation of a high-density nuclear system as well as through the temperature observation of old NSs. We show that both the temperature observation and theoretical calculation suggest that the vortex creep heating dominates over the DM heating. The vortex-nuclei interaction must be smaller than the estimated values by several orders of magnitude to overturn this.Comment: 8 pages, 2 figure

Involvement of Fusobacterium Species in Oral Cancer Progression : A Literature Review Including Other Types of Cancer

Chronic inflammation caused by infections has been suggested to be one of the most important cause of cancers. It has recently been shown that there is correlation between intestinal bacteria and cancer development including metastasis. As over 700 bacterial species exist in an oral cavity, it has been concerning that bacterial infection may cause oral cancer. However, the role of bacteria regarding tumorigenesis of oral cancer remains unclear. Several papers have shown that Fusobacterium species deriving the oral cavities, especially, play a crucial role for the development of colorectal and esophageal cancer. F. nucleatum is a well-known oral bacterium involved in formation of typical dental plaque on human teeth and causing periodontal diseases. The greatest characteristic of F. nucleatum is its ability to adhere to various bacteria and host cells. Interestingly, F. nucleatum is frequently detected in oral cancer tissues. Moreover, detection of F. nucleatum is correlated with the clinical stage of oral cancer. Although the detailed mechanism is still unclear, Fusobacterium species have been suggested to be associated with cell adhesion, tumorigenesis, epithelial-to-mesenchymal transition, inflammasomes, cell cycle, etc. in oral cancer. In this review, we introduce the reports focused on the association of Fusobacterium species with cancer development and progression including oral, esophageal, and colon cancers

Oral environment and cancer

Cancer is now the leading cause of death in Japan. A rapid increase in cancer mortality is expected as Japan is facing a super-aged society. Many causes of cancer are known to be closely linked to life style factors, such as smoking, drinking, and diet. The oral environment is known to be involved in the pathogenesis and development of various diseases such as bronchitis, pneumonia, diabetes, heart disease, and dementia. Because the oral cavity acts as the bodily entrance for air and food, it is constantly exposed to foreign substances, including bacteria and viruses. A large number of bacteria are endemic to the oral cavity, and indigenous oral flora act to prevent the settlement of foreign bacteria. The oral environment is influenced by local factors, including dental plaque, tartar, teeth alignment, occlusion, an incompatible prosthesis, and bad lifestyle habits, and systemic factors, including smoking, consumption of alcohol, irregular lifestyle and eating habits, obesity, stress, hormones, and heredity. It has recently been revealed that the oral environment is associated with cancer. In particular, commensal bacteria in the oral cavity are involved in the development of cancer. Moreover, Candida, human papilloma virus and Epstein-Barr virus as well as commensal bacteria have been reported to be associated with the pathogenesis of cancer. In this review, we introduce recent findings of the correlation between the oral environment and cancer

ヘルシンキ メトロポリア オウヨウ カガク ダイガク エノ タンキ リュウガク ニオケル カツドウ ホウコク

We visited Helsinki Metropolia University of Applied Sciences from August 14th to 22nd as a short-term study abroad supported by Japan Student Services Organization (JASSO). We participated in the basic and clinical training of the oral hygiene course. Furthermore, we also visited the institution for elderly in Espoo and the orthopedic hospital in Helsinki. We reported the outline of the study abroad here

Perfluorooctanoic acid-induced cell death via the dual roles of ROS-MAPK/ERK signaling in ameloblast-lineage cells

Perfluorooctanoic acid (PFOA) is an artificial fluorinated organic compound that has generated increased public attention due to its potential health hazards. Unsafe levels of PFOA exposure can affect reproduction, growth and development. During tooth enamel development (amelogenesis), environmental factors including fluoride can cause enamel hypoplasia. However, the effects of PFOA on ameloblasts and tooth enamel formation remain largely unknown. In the present study we demonstrate several PFOA-mediated cell death pathways (necrosis/necroptosis, and apoptosis) and assess the roles of ROS-MAPK/ERK signaling in PFOA-mediated cell death in mouse ameloblast-lineage cells (ALC). ALC cells were treated with PFOA. Cell proliferation and viability were analyzed by MTT assays and colony formation assays, respectively. PFOA suppressed cell proliferation and viability in a dose dependent manner. PFOA induced both necrosis (PI-positive cells) and apoptosis (cleaved-caspase-3, γH2AX and TUNEL-positive cells). PFOA significantly increased ROS production and up-regulated phosphor-(p)-ERK. Addition of ROS inhibitor N-acetyl cysteine (NAC) suppressed p-ERK and decreased necrosis, and increased cell viability compared to PFOA alone, whereas NAC did not change apoptosis. This suggests that PFOA-mediated necrosis was induced by ROS-MAPK/ERK signaling, but apoptosis was not associated with ROS. Addition of MAPK/ERK inhibitor PD98059 suppressed necrosis and increased cell viability compared to PFOA alone. Intriguingly, PD98059 augmented PFOA-mediated apoptosis. This suggests that p-ERK promoted necrosis but suppressed apoptosis. Addition of the necroptosis inhibitor Necrostatin-1 restored cell viability compared to PFOA alone, while pan-caspase inhibitor Z-VAD did not mitigate PFOA-mediated cell death. These results suggest that 1) PFOA-mediated cell death was mainly caused by necrosis/necroptosis by ROS-MAPK/ERK signaling rather than apoptosis, 2) MAPK/ERK signaling plays the dual roles (promoting necrosis and suppressing apoptosis) under PFOA treatment. This is the initial report to indicate that PFOA could be considered as a possible causative factor for cryptogenic enamel malformation. Further studies are required to elucidate the mechanisms of PFOA-mediated adverse effects on amelogenesis

A Study on High School and Undergraduate Students’ Learning Motivation : A Case of Joint Management of the Educational Relationship between K Agricultural High School and A University for the “K Agricultural High School & A University Program"

This paper introduces the joint management of an educational relationship between K Agricultural High School and A University, and reports the program's effects to increase students' motivation for learning at both schools. In the program, first, the high school students presented the results of their project based learning, and the university students and university instructor gave comments. Next, the high school students received a lecture from the university instructor and a research report from the university student. Finally, the high school students, university students, and instructors attended a social gathering. An analysis of responses to the study questionnaire suggests that students’ motivation for learning increased at both schools, except the university students who have high motivation originally

Porphyromonas gingivalis attenuates the insulin-induced phosphorylation and translocation of forkhead box protein O1 in human hepatocytes

Objective: Porphyromonas gingivalis (P. gingivalis) is a pathogen involved in periodontal disease. Recently, periodontal disease has been demonstrated to increase the risk of developing diabetes mellitus, although the molecular mechanism is not fully understood. Forkhead box protein O1 (FoxO1) is a transcriptional factor that regulates gluconeogenesis in the liver. Gluconeogenesis is a key process in the induction of diabetes mellitus; however, little is known regarding the relationship between periodontal disease and gluconeogenesis. In this study, to investigate whether periodontal disease influences hepatic gluconeogenesis, we examined the effects of P. gingivalis on the phosphorylation and translocation of FoxO1 in insulin-induced human hepatocytes. Design: The human hepatocyte HepG2 was treated with insulin and Akt and FoxO1 phosphorylation was detected by western blot analysis. The localization of phosphorylated FoxO1 was detected by immunocytochemistry and western blot analysis. HepG2 cells were treated with SNAP26b-tagged P. gingivalis (SNAP-P. g.) before insulin stimulation, and then the changes in Akt and FoxO1 were determined by western blot analysis and immunocytochemistry. Results: Insulin (100 nM) induced FoxO1 phosphorylation 60 min after treatment in HepG2 cells. Phosphorylated FoxO1 translocated to the cytoplasm. SNAP-P.g. internalized into HepG2 cells and decreased Akt and FoxO1 phosphorylation induced by insulin. The effect of insulin on FoxO1 translocation was also attenuated by SNAP-P.g. Conclusions: Our study shows that P. gingivalis decreases the phosphorylation and translocation of FoxO induced by insulin in HepG2 cells. Our results suggest that periodontal disease may increase hepatic gluconeogenesis by reducing the effects of insulin on FoxO1