Fiber Bragg grating sensor array for detecting heat flux in vacuum.

In TAE Technologies' current experimental device, C-2W (also called "Norman"), record-breaking, advanced beam-driven field-reversed configuration plasmas are produced and sustained in steady state utilizing variable energy neutral beams, advanced divertors, edge-biasing electrodes, and an active plasma control system [Gota et al., Nucl. Fusion 61, 106039 (2021)]. A novel diagnostic has been developed by TAE Technologies to leverage an industrial fiber Bragg grating (FBG) sensor array to detect heat flux along the wall of the vacuum vessel from a plasma discharge. The system consists of an optical fiber with FBG sensors distributed along its length, housed in a pressurized steel sheath. Each FBG sensor is constructed to reflect a different wavelength, the exact value of which is sensitive to the strain and temperature at the location of the grating in the fiber. The fiber is illuminated with broadband light, and the data acquisition system analyzes the spectrum of reflected light to determine the temperature at the location of each FBG. We have installed four of these vacuum-rated FBG sensor arrays on the C-2W experiment, each with 30 individual FBG sensors spaced at 0.15 m intervals along the 5 m fiber, with a 100 Hz acquisition rate. The measurement of temperature change due to a plasma discharge provides a single data point at each sensor location, creating a 120-point heat map of the vacuum vessel.

T-bet controls intestinal mucosa immune responses via repression of type 2 innate lymphoid cell function.

Innate lymphoid cells (ILCs) play an important role in regulating immune responses at mucosal surfaces. The transcription factor T-bet is crucial for the function of ILC1s and NCR+ ILC3s and constitutive deletion of T-bet prevents the development of these subsets. Lack of T-bet in the absence of an adaptive immune system causes microbiota-dependent colitis to occur due to aberrant ILC3 responses. Thus, T-bet expression in the innate immune system has been considered to dampen pathogenic immune responses. Here, we show that T-bet plays an unexpected role in negatively regulating innate type 2 responses, in the context of an otherwise intact immune system. Selective loss of T-bet in ILCs leads to the expansion and increased activity of ILC2s, which has a functionally important impact on mucosal immunity, including enhanced protection from Trichinella spiralis infection and inflammatory colitis. Mechanistically, we show that T-bet controls the intestinal ILC pool through regulation of IL-7 receptor signalling. These data demonstrate that T-bet expression in ILCs acts as the key transcriptional checkpoint in regulating pathogenic vs. protective mucosal immune responses, which has significant implications for the understanding of the pathogenesis of inflammatory bowel diseases and intestinal infections.

Field reversed configuration confinement enhancement through edge biasing and neutral beam injection.

Field reversed configurations (FRCs) with high confinement are obtained in the C-2 device by combining plasma gun edge biasing and neutral beam injection. The plasma gun creates an inward radial electric field that counters the usual FRC spin-up. The n = 2 rotational instability is stabilized without applying quadrupole magnetic fields. The FRCs are nearly axisymmetric, which enables fast ion confinement. The plasma gun also produces E × B shear in the FRC edge layer, which may explain the observed improved particle transport. The FRC confinement times are improved by factors 2 to 4, and the plasma lifetimes are extended from 1 to up to 4 ms.

Gene expression in endoprosthesis loosening: chitinase activity for early diagnosis?

The aim of the study was to identify markers for the early diagnosis of endoprosthesis loosening, for the differentiation between wear particle-induced and septic loosening and to gather new insights into the pathogenesis of endoprosthesis loosening. Gene expression profiles were generated from five periprosthetic membranes of wear particle-induced and five of infectious (septic) type using Affymetrix HG U133A oligonucleotide microarrays. The results of selected differentially expressed genes were validated by RT-PCR (n = 30). The enzyme activity and the genotype of chitinase-1 were assessed in serum samples from 313 consecutive patients hospitalized for endoprosthesis loosening (n = 54) or for other reasons, serving as control subjects (n = 259). Eight hundred twenty-four genes were differentially expressed with a fold change greater than 2 (data sets on http://www.ncbi.nlm.nih.gov/geo/ GSE 7103). Among these were chitinase 1, CD52, calpain 3, apolipoprotein, CD18, lysyl oxidase, cathepsin D, E-cadherin, VE-cadherin, nidogen, angiopoietin 1, and thrombospondin 2. Their differential expression levels were validated by RT-PCR. The chitinase activity was significantly higher in the blood from patients with wear particle-induced prosthesis loosening (p = 0.001). However, chitinase activity as a marker for early diagnosis has a specificity of 83% and a sensitivity of 52%, due to a high variability both in the disease and in the control group.

Spontaneously and pharmacologically provoked coronary arterial spasm in Prinzmetal variant angina.

Eleven of 21 consecutive patients with Prinzmetal angina (PMA) exhibited no significant fixed stenoses of the coronary arteries. Spontaneous coronary arterial spasm was demonstrated in 3 patients. Ergonovine maleate produced near-total occlusion of a major vessel in 3 of 4 other patients with PMA, but did not provoke spasm in 10 without PMA. The current study documents spasm as the mechanism of myocardial ischemia in some patients with normal coronary arteries and provides initial and favorable diagnostic results with provocative pharmacoangiography in this entity.