Cooling mechanical resonators to quantum ground state from room temperature

Ground-state cooling of mesoscopic mechanical resonators is a fundamental requirement for test of quantum theory and for implementation of quantum information. We analyze the cavity optomechanical cooling limits in the intermediate coupling regime, where the light-enhanced optomechanical coupling strength is comparable with the cavity decay rate. It is found that in this regime the cooling breaks through the limits in both the strong and weak coupling regimes. The lowest cooling limit is derived analytically at the optimal conditions of cavity decay rate and coupling strength. In essence, cooling to the quantum ground state requires $Q_{\mathrm{m}}>2.4n_{\mathrm{th}}$, with $Q_{\mathrm{m}}$ being the mechanical quality factor and $n_{\mathrm{th}}$ being the thermal phonon number. Remarkably, ground-state cooling is achievable starting from room temperature, when mechanical $Q$-frequency product $Q_{\mathrm{m}}{\nu>1.5}\times10^{13}$, and both of the cavity decay rate and the coupling strength exceed the thermal decoherence rate. Our study provides a general framework for optimizing the backaction cooling of mesoscopic mechanical resonators

Parameter-tuning Networks: Experiments and Active Walk Model

The tuning process of a large apparatus of many components could be represented and quantified by constructing parameter-tuning networks. The experimental tuning of the ion source of the neutral beam injector of HT-7 Tokamak is presented as an example. Stretched-exponential cumulative degree distributions are found in the parameter-tuning networks. An active walk model with eight walkers is constructed. Each active walker is a particle moving with friction in an energy landscape; the landscape is modified by the collective action of all the walkers. Numerical simulations show that the parameter-tuning networks generated by the model also give stretched exponential functions, in good agreement with experiments. Our methods provide a new way and a new insight to understand the action of humans in the parameter-tuning of experimental processes, is helpful for experimental research and other optimization problems.Comment: 4 pages, 5 figure

The Arabidopsis EAR-motif-containing protein RAP2.1 functions as an active transcriptional repressor to keep stress responses under tight control

<p>Abstract</p> <p>Background</p> <p>Plants respond to abiotic stress through complex regulation of transcription, including both transcriptional activation and repression. Dehydration-responsive-element binding protein (DREB)-type transcription factors are well known to play important roles in adaptation to abiotic stress. The mechanisms by which DREB-type transcription factors activate stress-induced gene expression have been relatively well studied. However, little is known about how DREB-type transcriptional repressors modulate plant stress responses. In this study, we report the functional analysis of RAP2.1, a DREB-type transcriptional repressor.</p> <p>Results</p> <p>RAP2.1 possesses an APETALA2 (AP2) domain that binds to dehydration-responsive elements (DREs) and an ERF-associated amphiphilic repression (EAR) motif, as the repression domain located at the C-terminus of the protein. Expression of <it>RAP2.1 </it>is strongly induced by drought and cold stress via an ABA-independent pathway. Arabidopsis plants overexpressing <it>RAP2.1 </it>show enhanced sensitivity to cold and drought stresses, while <it>rap2.1-1 </it>and <it>rap2.1-2 </it>T-DNA insertion alleles result in reduced sensitivity to these stresses. The reduced stress sensitivity of the plant containing the <it>rap2.1 </it>allele can be genetically complemented by the expression of <it>RAP2.1</it>, but not by the expression of EAR-motif-mutated <it>RAP2.1</it>. Furthermore, chromatin immunoprecipitation (ChIP) analysis has identified <it>Responsive to desiccation/Cold-regulated </it>(<it>RD/COR</it>) genes as downstream targets of RAP2.1 <it>in vivo</it>. Stress-induced expression of the <it>RD/COR </it>genes is repressed by overexpression of <it>RAP2.1 </it>and is increased in plants expressing the <it>rap2.1 </it>allele. In addition, RAP2.1 can negatively regulate its own expression by binding to DREs present in its own promoter. Our data suggest that RAP2.1 acts as a negative transcriptional regulator in defence responses to cold and drought stress in Arabidopsis.</p> <p>Conclusions</p> <p>A hypothetical model for the role of RAP2.1 in modulating plant responses to cold and drought is proposed in this study. It appears that RAP2.1 acts as a negative "subregulon" of DREB-type activators and is involved in the precise regulation of expression of stress-related genes, acting to keep stress responses under tight control.</p

Roles of TGFβ and FGF signals during growth and differentiation of mouse lens epithelial cell in vitro.

Transforming growth factor β (TGFβ) and fibroblast growth factor (FGF) signaling pathways play important roles in the proliferation and differentiation of lens epithelial cells (LECs) during development. Low dosage bFGF promotes cell proliferation while high dosage induces differentiation. TGFβ signaling regulates LEC proliferation and differentiation as well, but also promotes epithelial-mesenchymal transitions that lead to cataracts. Thus far, it has been difficult to recapitulate the features of germinative LECs in vitro. Here, we have established a LEC culture protocol that uses SB431542 (SB) compound to inhibit TGFβ/Smad activation, and found that SB treatment promoted mouse LEC proliferation, maintained LECs' morphology and distinct markers including N-cadherin, c-Maf, Prox1, and αA-, αB-, and β-crystallins. In contrast, low-dosage bFGF was unable to sustain those markers and, combined with SB, altered LECs' morphology and β-crystallin expression. We further found that Matrigel substrate coatings greatly increased cell proliferation and uniquely affected β-crystallin expression. Cultured LECs retained the ability to differentiate into γ-crystallin-positive lentoids by high-dosage bFGF treatment. Thus, a suppression of TGFβ/Smad signaling in vitro is critical to maintaining characteristic features of mouse LECs, especially expression of the key transcription factors c-Maf and Prox1