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The gyrotron installation on the DIII-D tokamak has been in operation at the second harmonic of the electron cyclotron resonance since the mid-1990s. Prior to that a large installation of ten 60 GHz tubes was operated at the fundamental resonance. The system has been upgraded regularly and is an everyday tool for experiments on DIII-D.

The National Spherical Torus Experiment Upgrade (NSTX-U) will operate at axial toroidal fields of ≤ 1 T and plasma currents, Ip ≤ 2 MA. The development of non-inductive (NI) plasmas is a major long-term research goal for NSTX-U. Time dependent numerical simulations of 28 GHz electron cyclotron (EC) heating of low density NI start-up plasmas generated by Coaxial Helicity Injection (CHI) in NSTX-U predict a significant and rapid increase of the central electron temperature (Te(0)) before the plasma becomes overdense. The increased Te(0) will significantly reduce the Ip decay rate of CHI plasmas, allowing the coupling of fast wave heating and neutral beam injection. A megawatt-level, 28 GHz electron heating system is planned for heating NI start-up plasmas in NSTX-U. In addition to EC heating of CHI start-up discharges, this system will be used for electron Bernstein wave (EBW) plasma start-up, and eventually for EBW heating and current drive during the Ip flattop.

The DIII-D ECH complex is being upgraded with three new depressed collector gyrotrons. The performance of the existing system has been very good. As more gyrotrons having higher power are added to the system, diagnostics of gyrotron operation, optimization of the performance and qualification of components for higher power become more important. A new FPGA-based gyrotron control system is being installed, additional capabilities for rapid real time variation of the rf injection angles by the DIII-D Plasma Control System are being tested and infrastructure enhancements are being completed. Longer term plans continue to include ECH as a major component in the DIII-D heating and current drive capabilities.

The National Spherical Torus Experiment Upgrade (NSTX-U) will operate at an axial toroidal field of up to 1 T, about twice the field available on NSTX. A 28 GHz electron cylotron resonance heating (ECRH) system is currently being planned for NSTX-U. A 1 MW 28 GHz gyrotron will be employed. Intially the system will use short, 10-50 ms, 1 MW pulses for ECRH-assisted discharge start-up. Later the pulse length will be extended to 1-5 s to study electron Bernstein wave heating (EBWH) during the plasma current flat top. A mirror launcher will be used to couple microwave power to the plasma via O-mode to the slow X-mode to EBW (O-X-B) double mode conversion. This paper presents a pre-conceptual design for the ECRH/EBWH system proposed for NSTX-U and includes ray tracing and Fokker-Planck modeling results for 28 GHz ECRH during plasma start-up and EBW heating and current drive during the plasma current flattop of a NSTX-U advanced H-mode plasma scenario.

Summary: Background: For patients with early American Joint Committee on Cancer (AJCC)‐stage melanoma the combined loss of the autophagy regulatory protein AMBRA1 and the terminal differentiation marker loricrin in the peritumoral epidermis is associated with a significantly increased risk of metastasis. Objectives: The aim of the present study was to evaluate the potential contribution of melanoma paracrine transforming growth factor (TGF)‐β signalling to the loss of AMBRA1 in the epidermis overlying the primary tumour and disruption of epidermal integrity. Methods: Immunohistochemistry was used to analyse AMBRA1 and TGF‐β2 in a cohort of 109 AJCC all‐stage melanomas, and TGF‐β2 and claudin‐1 in a cohort of 30 or 42 AJCC stage I melanomas, respectively, with known AMBRA1 and loricrin (AMLo) expression. Evidence of pre‐ulceration was analysed in a cohort of 42 melanomas, with TGF‐β2 signalling evaluated in primary keratinocytes. Results: Increased tumoral TGF‐β2 was significantly associated with loss of peritumoral AMBRA1 (P < 0·05), ulceration (P < 0·001), AMLo high‐risk status (P < 0·05) and metastasis (P < 0·01). TGF‐β2 treatment of keratinocytes resulted in downregulation of AMBRA1, loricrin and claudin‐1, while knockdown of AMBRA1 was associated with decreased expression of claudin‐1 and increased proliferation of keratinocytes (P < 0·05). Importantly, we show loss of AMBRA1 in the peritumoral epidermis was associated with decreased claudin‐1 expression (P < 0·05), parakeratosis (P < 0·01) and cleft formation in the dermoepidermal junction (P < 0·05). Conclusions: Collectively, these data suggest a paracrine mechanism whereby TGF‐β2 causes loss of AMBRA1 overlying high‐risk AJCC early‐stage melanomas and reduced epidermal integrity, thereby facilitating erosion of the epidermis and tumour ulceration. [ABSTRACT FROM AUTHOR]