Self-Organized Similarity based Kernel Fuzzy Clustering Model and Its Applications

The purpose of this paper is to improve the performance of the kernel fuzzy clustering model by introducing a self-organized algorithm. A conventional kernel fuzzy clustering model is defined as a model which is an improved additive fuzzy clustering. The purpose of this conventional model is to obtain a clearer result by consideration of the interaction of clusters. This paper proposes a fuzzy clustering model based on the idea of self-organized dissimilarity between two objects

Successful reprogramming of epiblast stem cells by blocking nuclear localization of β-catenin.

Epiblast stem cells (EpiSCs) in mice and rats are primed pluripotent stem cells (PSCs). They barely contribute to chimeric embryos when injected into blastocysts. Reprogramming of EpiSCs to embryonic stem cell (ESC)-like cells (rESCs) may occur in response to LIF-STAT3 signaling; however, low reprogramming efficiency hampers potential use of rESCs in generating chimeras. Here, we describe dramatic improvement of conversion efficiency from primed to naive-like PSCs through upregulation of E-cadherin in the presence of the cytokine LIF. Analysis revealed that blocking nuclear localization of β-CATENIN with small-molecule inhibitors significantly enhances reprogramming efficiency of mouse EpiSCs. Although activation of Wnt/β-catenin signals has been thought desirable for maintenance of naive PSCs, this study provides the evidence that inhibition of nuclear translocation of β-CATENIN enhances conversion of mouse EpiSCs to naive-like PSCs (rESCs). This affords better understanding of gene regulatory circuits underlying pluripotency and reprogramming of PSCs

A New Cell Death Inhibitor, Bax-inhibiting-peptide (BIP) Derived from Ku70(Animal Biology, Animal Reproduction)

Programmed cell death (apoptosis) plays a pivotal role in the homeostasis of multicellular organisms. Bax is a key mediator of apoptosis. Apoptotic stress induces the translocation of Bax from the cytosol to mitochondria, and then Bax induces mitochondria-dependent cell death. Recently, we have found that Ku70 inhibits the translocation of Bax from the cytosol to mitochondria, suggesting that Ku70 inhibits mitochondria-dependent cell death (Sawada et al., 2003b). Moreover, we have designed a new type of cell death inhibitor, Bax-inhibiting-peptide (BIP) derived from Ku70 (Sawada et al., 2003b; Yoshida et al., 2004). We have demonstrated that BIPs inhibit the cell death induced by anti-cancer drugs, UVC irradiation, and tropic factor deprivation (Sawada et al., 2003b; Yoshida et al., 2004). BIP directly binds Bax and inhibits the cytotoxic activity of Bax. BIP may become a new tool to control degenerative diseases.ApoptosisKu70BaxBax-inhibiting-peptide (BIP)cell death inhibito

Can Reinforcement Learning Be Applied to Surgery?

Background: Remarkable progress has recently been made in the field of artificial intelligence (AI).Objective: We sought to investigate whether reinforcement learning could be used in surgery in the future.Methods: We created simple 2D tasks (Tasks 1–3) that mimicked surgery. We used a neural network library, Keras, for reinforcement learning. In Task 1, a Mac OS X with an 8 GB memory (MacBook Pro, Apple, USA) was used. In Tasks 2 and 3, a Ubuntu 14. 04LTS with a 26 GB memory (Google Compute Engine, Google, USA) was used.Results: In the task with a relatively small task area (Task 1), the simulated knife finally passed through all the target areas, and thus, the expected task was learned by AI. In contrast, in the task with a large task area (Task 2), a drastically increased amount of time was required, suggesting that learning was not achieved. Some improvement was observed when the CPU memory was expanded and inhibitory task areas were added (Task 3).Conclusions: We propose the combination of reinforcement learning and surgery. Application of reinforcement learning to surgery may become possible by setting rules, such as appropriate rewards and playable (operable) areas, in simulated tasks

Morbillivirus Receptors and Tropism: Multiple Pathways for Infection

Morbilliviruses, which include measles virus (MeV), canine distemper virus, and rinderpest virus, are among the most important pathogens in their respective hosts and cause severe syndromes. Morbilliviruses are enveloped viruses with two envelope proteins, one of which is hemagglutinin (H) protein, which plays a role in binding to cellular receptors. During morbillivirus infection, the virus initially targets lymphoid cells and replicates efficiently in the lymph nodes. The principal cellular receptor for morbillivirus is signaling lymphocyte activation molecule (SLAM, also called CD150), which is exclusively expressed on immune cells. This feature reflects the strong lymphoid cell tropism and viral spread in the infected body. Morbillivirus infection, however, affects various tissues in the body, including the lung, kidney, gastrointestinal tract, vascular endothelium, and brain. Thus, other receptors for morbilliviruses in addition to SLAM might exist. Recently, nectin-4 has been identified as a novel epithelial cell receptor for MeV. The expression of nectin-4 is localized to polarized epithelial cells, and this localization supports the notion of cell tropism since MeV also grows well in the epithelial cells of the respiratory tract. Although two major receptors for lymphoid and epithelial cells in natural infection have been identified, morbillivirus can still infect many other types of cells with low infectivity, suggesting the existence of inefficient but ubiquitously expressed receptors. We have identified other molecules that are implicated in morbillivirus infection of SLAM-negative cells by alternative mechanisms. These findings indicate that morbillivirus utilizes multiple pathways for establishment of infection. These studies will advance our understanding of morbillivirus tropism and pathogenesis

Complex coevolutionary history of symbiotic Bacteroidales bacteria of various protists in the gut of termites

<p>Abstract</p> <p>Background</p> <p>The microbial community in the gut of termites is responsible for the efficient decomposition of recalcitrant lignocellulose. Prominent features of this community are its complexity and the associations of prokaryotes with the cells of cellulolytic flagellated protists. Bacteria in the order Bacteroidales are involved in associations with a wide variety of gut protist species as either intracellular endosymbionts or surface-attached ectosymbionts. In particular, ectosymbionts exhibit distinct morphological patterns of the associations. Therefore, these Bacteroidales symbionts provide an opportunity to investigate not only the coevolutionary relationships with the host protists and their morphological evolution but also how symbiotic associations between prokaryotes and eukaryotes occur and evolve within a complex symbiotic community.</p> <p>Results</p> <p>Molecular phylogeny of 31 taxa of Bacteroidales symbionts from 17 protist genera in 10 families was examined based on 16S rRNA gene sequences. Their localization, morphology, and specificity were also examined by fluorescent in situ hybridizations. Although a monophyletic grouping of the ectosymbionts occurred in three related protist families, the symbionts of different protist genera were usually dispersed among several phylogenetic clusters unique to termite-gut bacteria. Similar morphologies of the associations occurred in multiple lineages of the symbionts. Nevertheless, the symbionts of congeneric protist species were closely related to one another, and in most cases, each host species harbored a unique Bacteroidales species. The endosymbionts were distantly related to the ectosymbionts examined so far.</p> <p>Conclusion</p> <p>The coevolutionary history of gut protists and their associated Bacteroidales symbionts is complex. We suggest multiple independent acquisitions of the Bacteroidales symbionts by different protist genera from a pool of diverse bacteria in the gut community. In this sense, the gut could serve as a reservoir of diverse bacteria for associations with the protist cells. The similar morphologies are considered a result of evolutionary convergence. Despite the complicated evolutionary history, the host-symbiont relationships are mutually specific, suggesting their cospeciations at the protist genus level with only occasional replacements.</p