We have realized ambipolar ionic liquid gated field-effect transistors based on WS2 mono- and bilayers, and investigated their opto-electronic response. A thorough characterization of the transport properties demonstrates the high quality of these devices for both electron and hole accumulation, which enables the quantitative determination of the band gap (Δ1L = 2.14 eV for monolayers and Δ2L = 1.82 eV for bilayers). It also enables the operation of the transistors in the ambipolar injection regime with electrons and holes injected simultaneously at the two opposite contacts of the devices in which we observe light emission from the FET channel. A quantitative analysis of the spectral properties of the emitted light, together with a comparison with the band gap values obtained from transport, show the internal consistency of our results and allow a quantitative estimate of the excitonic binding energies to be made. Our results demonstrate the power of ionic liquid gating in combination with nanoelectronic systems, as well as the compatibility of this technique with optical measurements on semiconducting transition metal dichalcogenides. These findings further open the way to the investigation of the optical properties of these systems in a carrier density range much broader than that explored until now.

When thinned down to the atomic scale, many layered van der Waals materials exhibit an interesting evolution of their electronic properties, whose main aspects can be accounted for by changes in the single-particle band structure. Phenomena driven by interactions are also observed, but identifying experimentally systematic trends in their thickness dependence is challenging. Here, we explore the evolution of gate-induced The ability to produce few-atom-thick two-dimensional (2D) materials of excellent quality 1 2 -such as graphene 3 4 5 , semiconducting transition metal dichalcogenides (TMDs) 6 7 , and phosporene 8 -is an impressive breakthrough in condensed matter physics and nanoelectronics. Upon adding an individual monolayer, the electronic properties of these 2D materials change drastically, so that multilayers of different thickness truly represent distinct

Cyclic guanosine monophosphate (cGMP) is a second messenger molecule that transduces nitric oxide (NO) and natriuretic peptide (NP) coupled signaling, stimulating phosphorylation changes by protein kinase G (PKG). Enhancing cGMP synthesis or blocking its degradation by phosphodiesterase type 5A (PDE5A) protects against cardiovascular disease1,2. However, cGMP stimulation alone is limited by counter-adaptions including PDE upregulation3. Furthermore, though PDE5A regulates NO-generated cGMP4,5, NO-signaling is often depressed by heart disease6. PDEs controlling NP-coupled cGMP remain uncertain. Here we show that cGMP-selective PDE9A7,8 is expressed in mammalian heart including humans, and is upregulated by hypertrophy and cardiac failure. PDE9A regulates NP rather than NO-stimulated cGMP in heart myocytes and muscle, and its genetic or selective pharmacological inhibition protects against pathological responses to neuro-hormones, and sustained pressure-overload stress. PDE9A inhibition reverses pre-established heart disease independent of NO-synthase (NOS) activity, whereas PDE5A inhibition requires active NOS. Transcription factor activation and phospho-proteome analyses of myocytes with each PDE selectively inhibited reveals substantial differential targeting, with phosphorylation changes from PDE5A inhibition being more sensitive to NOS activation. Thus, unlike PDE5A, PDE9A can regulate cGMP signaling independent of the NO-pathway, and its role in stress-induced heart disease suggests potential as a therapeutic target.

Significance Cardiac hypertrophy and dysfunction in response to sustained hormonal and mechanical stress are sentinel features of most forms of heart disease. Activation of non–voltage-gated transient receptor potential canonical channels TRPC3 and TRPC6 may contribute to this pathophysiology and provide a therapeutic target. Effects from combined selective inhibition have not been tested previously. Here we report the capability of highly selective TRPC3/6 inhibitors to block pathological hypertrophic signaling in several cell types, including adult cardiac myocytes. We show in vivo redundancy of each channel; individual gene deletion was not protective against sustained pressure overload, whereas combined deletion ameliorated the response. These data strongly support a role for both channels in cardiac disease and the utility of selective combined inhibition.