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Ever since Endel Tulving first distinguished between episodic and semantic memory, the remember/know paradigm has become a standard means of probing the phenomenology of participants' memorial experiences by memory researchers, neuropsychologists, neuroscientists, and others. However, this paradigm has not been without its problems and has been used to capture many different phenomenological experiences, including retrieval from episodic versus semantic memory, recollection versus familiarity, strength of memory traces, and so on. We first conducted a systematic review of its uses across the literature and then examined how memory experts, other cognitive psychology experts, experts in other areas of psychology, and lay participants (Amazon Mechanical Turk workers) define what it means when one says "I remember" and "I know." From coding their open-ended responses using a number of theory-bound dimensions, it seems that lay participants do not see eye to eye with memory experts in terms of associating "I remember" responses with recollection and "I know" responses with familiarity. However, there is general consensus with Tulving's original distinction, linking remembering with memory for events and knowing with semantic memory. Recommendations and implications across fields are discussed.Objective To evaluate memory in patients with drug-resistant epilepsy. Methods Following an examination, 50 patients were diagnosed in accordance with the 2005 proposal of the International League Against Epilepsy and the definition of drug-resistant epilepsy from 2010. The neuropsychological examination used the Wechsler Memory Scale. It assessed seven structural types of memory general knowledge, orientation, mental control, logical memory, number memory, associative memory, and visual reproduction. The values were compared with 50 subjects without epilepsy. Results Patients with epilepsy had statistically significantly lower values in five of seven structural units of memory. The average value of overall memory efficacy in subjects with epilepsy was 96.5 ± 19.6, while in subjects without epilepsy it was 118 ± 15.6 (p = 0.0002). Memory impairments are greater in those taking polytherapy (p = 0.0429). The overall memory efficiency correlated significantly negatively with seizure frequency (p = 0.0015) and insignificantly negative with the duration of epilepsy (p = 0.1935). Conclusion Patients with drug-resistant epilepsy have lower memory efficiency. Memory impairments are greater in those taking polytherapy, as with those with more frequent seizures. The duration of epilepsy has no significant effect on overall memory performance.The cause of chronic inflammatory periodontitis, which leads to the destruction of periodontal ligament and alveolar bone, is multifactorial. An increasing number of studies have shown the clinical significance of NLRP3-mediated low-grade inflammation in degenerative disorders, but its causal linkage to age-related periodontitis has not yet been elucidated. In this study, we investigated the involvement of the NLRP3 inflammasome and the therapeutic potential of NLRP3 inhibition in age-related alveolar bone loss by using in vivo and in vitro models. The poor quality of alveolar bones in aged mice was correlated with caspase-1 activation by macrophages and elevated levels of IL-1β, which are mainly regulated by the NLRP3 inflammasome, in periodontal ligament and serum, respectively. Aged mice lacking Nlrp3 showed better bone mass than age-matched wild-type mice via a way that affects bone resorption rather than bone formation. In line with this finding, treatment with MCC950, a potent inhibitor of the NLRP3 inflammasome, significantly suppressed alveolar bone loss with reduced caspase-1 activation in aged mice but not in young mice. In addition, our in vitro studies showed that the addition of IL-1β encourages RANKL-induced osteoclastogenesis from bone marrow-derived macrophages and that treatment with MCC950 significantly suppresses osteoclastic differentiation directly, irrelevant to the inhibition of IL-1β production. Our results suggest that the NLRP3 inflammasome is a critical mediator in age-related alveolar bone loss and that targeting the NLRP3 inflammasome could be a novel option for controlling periodontal degenerative changes with age.Guided bone regeneration (GBR) is a process that involves the regeneration of bone defects through the application of occlusive membranes that mechanically exclude the population of non-osteogenic cells from the surrounding soft tissue. Interestingly, platelet-rich fibrin (PRF) has previously been proposed as an autologous GBR membrane despite its short-term resorption period of 2-3 weeks. Recent clinical observations have demonstrated that, by heating a liquid platelet-poor plasma (PPP) layer and mixing the cell-rich buffy coat zone, the resorption properties of heated albumin gel with liquid-PRF (Alb-PRF) can be significantly improved. The aim of this study was to evaluate the inflammatory reaction, biocompatibility, and extended degradation properties of a new autologous Alb-PRF membrane in comparison to commonly utilized standard PRF after nude mice implantation, according to ISO 10993-6/2016. Two standard preparations of PRF (L-PRF and H-PRF) were compared to novel Alb-PRF following subcutaneous implantation at 7, 14, and 21 days. All groups demonstrated excellent biocompatibility owing to their autologous sources. However, it is worth noting that, while both L-PRF and H-PRF membranes demonstrated significant or complete resorption by 21 days, the Alb-PRF membrane remained volume-stable throughout the duration of the study. Selleck GSK2110183 This study demonstrates-for the first time, to the best of our knowledge-a marked improvement in the membrane stability of Alb-PRF. This indicates its future potential for use as a biological barrier membrane for GBR procedures with a long-lasting half-life, or as a biological filler material in esthetic medicine applications. Thus, further studies are warranted to explore future clinical applications in various fields of medicine.The 140,000 or so fungal species reported so far are heterogeneously defined based on varying criteria such as morphological, physiological, mating, and/or molecular features. Incongruences are common among traits used to separating closely related species and it is often difficult to compare fungal taxonomic groups defined based on different species recognition criteria. Though DNA sequence-based classification and identification have been made, a consensus has not been reached, primarily due to intrinsic limitations in the proposed one or a few genes. Here, I argue that the fundamental reason for the observed inconsistencies is that speciation is a stochastic process with the emergence and fixation of different traits influenced differently by many non-deterministic factors such as population size, random mutation, mode(s) of reproduction, selection imposed by interacting biotic and abiotic factors, and chance events. Each species concept attempts to capture one or a few traits emerged in the continuous process of speciation.
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