Work Relation and the Second Law of Thermodynamics in Nonequilibrium Steady States

We extend Jarzynski's work relation and the second law of thermodynamics to a heat conducting system which is operated by an external agent. These extensions contain a new non equilibrium contribution expressed as the violation of the (linear) response relation caused by the operation. We find that a natural extension of the minimum work principle involves information about the time-reversed operation, and is far from straightforward. Our work relation may be tested experimentally especially when the temperature gradient is small.Comment: 5 pages, 2 figure

Hidden heat transfer in equilibrium states implies directed motion in nonequilibrium states

We study a class of heat engines including Feynman's ratchet, which exhibits a directed motion of a particle in nonequilibrium steady states maintained by two heat baths. We measure heat transfer from each heat bath separately, and average them using a careful procedure that reveals the nature of the heat transfer associated with directed steps of the particle. Remarkably we find that steps are associated with nonvanishing heat transfer even in equilibrium, and there is a quantitative relation between this ``hidden heat transfer'' and the directed motion of the particle. This relation is clearly understood in terms of the ``principle of heat transfer enhancement'', which is expected to apply to a large class of highly nonequilibrium systems.Comment: 4 pages, 4 figures; revise

An expression for stationary distribution in nonequilibrium steady state

We study the nonequilibrium steady state realized in a general stochastic system attached to multiple heat baths and/or driven by an external force. Starting from the detailed fluctuation theorem we derive concise and suggestive expressions for the corresponding stationary distribution which are correct up to the second order in thermodynamic forces. The probability of a microstate $\eta$ is proportional to $\exp[{\Phi}(\eta)]$ where ${\Phi}(\eta)=-\sum_k\beta_k\mathcal{E}_k(\eta)$ is the excess entropy change. Here $\mathcal{E}_k(\eta)$ is the difference between two kinds of conditioned path ensemble averages of excess heat transfer from the $k$-th heat bath whose inverse temperature is $\beta_k$. Our expression may be verified experimentally in nonequilibrium states realized, for example, in mesoscopic systems.Comment: 4 pages, 2 figure

A heat pump at a molecular scale controlled by a mechanical force

We show that a mesoscopic system such as Feynman's ratchet may operate as a heat pump, and clarify a underlying physical picture. We consider a system of a particle moving along an asymmetric periodic structure . When put into a contact with two distinct heat baths of equal temperature, the system transfers heat between two baths as the particle is dragged. We examine Onsager relation for the heat flow and the particle flow, and show that the reciprocity coefficient is a product of the characteristic heat and the diffusion constant of the particle. The characteristic heat is the heat transfer between the baths associated with a barrier-overcoming process. Because of the correlation between the heat flow and the particle flow, the system can work as a heat pump when the particle is dragged. This pump is particularly effective at molecular scales where the energy barrier is of the order of the thermal energy.Comment: 7 pages, 5 figures; revise

Regenerative Rehabilitation for Stroke Recovery by Inducing Synergistic Effects of Cell Therapy and Neurorehabilitation on Motor Function: A Narrative Review of Pre-Clinical Studies

Neurological diseases severely affect the quality of life of patients. Although existing treatments including rehabilitative therapy aim to facilitate the recovery of motor function, achieving complete recovery remains a challenge. In recent years, regenerative therapy has been considered as a potential candidate that could yield complete functional recovery. However, to achieve desirable results, integration of transplanted cells into neural networks and generation of appropriate microenvironments are essential. Furthermore, considering the nascent state of research in this area, we must understand certain aspects about regenerative therapy, including specific effects, nature of interaction when administered in combination with rehabilitative therapy (regenerative rehabilitation), and optimal conditions. Herein, we review the current status of research in the field of regenerative therapy, discuss the findings that could hold the key to resolving the challenges associated with regenerative rehabilitation, and outline the challenges to be addressed with future studies. The current state of research emphasizes the importance of determining the independent effect of regenerative and rehabilitative therapies before exploring their combined effects. Furthermore, the current review highlights the progression in the treatment perspective from a state of compensation of lost function to that of a possibility of complete functional recovery

Molecular Mechanism Underlying Derepressed Male Production in Hexaploid Persimmon

Sex expression in plants is often flexible and contributes to the maintenance of genetic diversity within a species. In diploid persimmons (the genus Diospyros), the sexuality is controlled by the Y chromosome-encoded small-RNA gene, OGI, and its autosomal counterpart, MeGI. Hexaploid Oriental persimmon (Diospyros kaki) evolved more flexible sex expression, where genetically male individuals carrying OGI can produce both male and female flowers (monoecy). This is due to (semi-)inactivation of OGI by the Kali-SINE retrotransposon insertion on the promoter region and the resultant DNA methylations. Instead, flower sex determination in Oriental persimmon is also dependent on DNA methylation states of MeGI. Here, we focused on a cultivar, Kumemaru, which shows stable male flower production. Our results demonstrated that cv. Kumemaru carries OGI with Kali-SINE, which was highly methylated as well as in other monoecious cultivars; nevertheless, OGI gene could have a basal expression level. Transcriptomic analysis between cv. Kumemaru and 14 cultivars that predominantly produce female flowers showed differentially expressed genes (DEGs) specific to cv. Kumemaru, which is mainly involved in stress responses. Co-expression gene networks focusing on the DEGs also suggested the involvement of stress signals, mainly via gibberellin (GA), salicylic acid (SA), and especially jasmonic acid (JA) signal pathways. We also identified potential regulators of this co-expression module, represented by the TCP4 transcription factor. Furthermore, we attempted to identify cv. Kumemaru-specific transcript polymorphisms potentially contributing to derepressed OGI expression by cataloging subsequences (k-mers) in the transcriptomic reads from cv. Kumemaru and the other 14 female cultivars. Overall, although the direct genetic factor to activate OGI remains to be solved, our results implied the involvement of stress signals in the release of silenced OGI and the resultant continuous male production

Chemopreventive effects and anti-tumorigenic mechanisms of Actinidia arguta, known as sarunashi in Japan toward 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)- induced lung tumorigenesis in a/J mouse

Background Previously, we reported the inhibitory effect of Actinidia arguta juice, known as sarunashi juice (sar-j) in Japan, on mutagenesis, inflammation, and mouse skin tumorigenesis. The components of A. arguta responsible for the anti-mutagenic effects were identified to be water-soluble, heat-labile phenolic compounds. We proposed isoquercetin (isoQ) as a candidate anticarcinogenic component. In this study, we sought to investigate the chemopreventive effects of A. arguta juice and isoQ on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice, and identify the possible mechanisms underlying the anti-tumorigenic effects of A. arguta. Results The number of tumor nodules per mouse lung in the group injected with NNK and administered A. arguta juice orally was significantly lower than that in the group injected with NNK only. Oral administration of isoQ also reduced the number of nodules in the mouse lungs. As expected, the mutagenicity of NNK and 1-methyl-3-nitro-1-nitrosoguanidine (MNNG) detected using S. typhimurium TA1535 decreased in the presence of sar-j. However, NNK and MNNG mutagenicity detected using S. typhimurium YG7108, a strain lacking the O6-methylguanine DNA methyltransferases (ogtST and adaST) did not decrease in the presence of sar-j suggesting that sar-j may mediate its antimutagenic effect by enhancing the DNA damage repair by ogtST and adaST. Phosphorylation of Akt, with or without epidermal growth factor stimulation, in A549 cells was significantly decreased following sar-j and isoQ treatment, indicating that components in sar-j including isoQ suppressed the PI3K/AKT signaling pathways. Conclusions Sar-j and isoQ reduced NNK-induced lung tumorigenesis. Sar-j targets both the initiation and growth/progression steps during carcinogenesis, specifically via anti-mutagenesis, stimulation of alkyl DNA adduct repair, and suppression of Akt-mediated growth signaling. IsoQ might contribute in part to the biological effects of sar-j via suppression of Akt phosphorylation, but it may not be the main active ingredient

Reduction of total E2F/DP activity induces senescence-like cell cycle arrest in cancer cells lacking functional pRB and p53

E2F/DP complexes were originally identified as potent transcriptional activators required for cell proliferation. However, recent studies revised this notion by showing that inactivation of total E2F/DP activity by dominant-negative forms of E2F or DP does not prevent cellular proliferation, but rather abolishes tumor suppression pathways, such as cellular senescence. These observations suggest that blockage of total E2F/DP activity may increase the risk of cancer. Here, we provide evidence that depletion of DP by RNA interference, but not overexpression of dominant-negative form of E2F, efficiently reduces endogenous E2F/DP activity in human primary cells. Reduction of total E2F/DP activity results in a dramatic decrease in expression of many E2F target genes and causes a senescence-like cell cycle arrest. Importantly, similar results were observed in human cancer cells lacking functional p53 and pRB family proteins. These findings reveal that E2F/DP activity is indeed essential for cell proliferation and its reduction immediately provokes a senescence-like cell cycle arrest