Design of the first fusion experiment to achieve target energy gain G>1.

In this work we present the design of the first controlled fusion laboratory experiment to reach target gain G>1 N221204 (5 December 2022) [Phys. Rev. Lett. 132, 065102 (2024)10.1103/PhysRevLett.132.065102], performed at the National Ignition Facility, where the fusion energy produced (3.15 MJ) exceeded the amount of laser energy required to drive the target (2.05 MJ). Following the demonstration of ignition according to the Lawson criterion N210808, experiments were impacted by nonideal experimental fielding conditions, such as increased (known) target defects that seeded hydrodynamic instabilities or unintentional low-mode asymmetries from nonuniformities in the target or laser delivery, which led to reduced fusion yields less than 1 MJ. This Letter details design changes, including using an extended higher-energy laser pulse to drive a thicker high-density carbon (also known as diamond) capsule, that led to increased fusion energy output compared to N210808 as well as improved robustness for achieving high fusion energies (greater than 1 MJ) in the presence of significant low-mode asymmetries. For this design, the burnup fraction of the deuterium and tritium (DT) fuel was increased (approximately 4% fuel burnup and a target gain of approximately 1.5 compared to approximately 2% fuel burnup and target gain approximately 0.7 for N210808) as a result of increased total (DT plus capsule) areal density at maximum compression compared to N210808. Radiation-hydrodynamic simulations of this design predicted achieving target gain greater than 1 and also the magnitude of increase in fusion energy produced compared to N210808. The plasma conditions and hotspot power balance (fusion power produced vs input power and power losses) using these simulations are presented. Since the drafting of this manuscript, the results of this paper have been replicated and exceeded (N230729) in this design, together with a higher-quality diamond capsule, setting a new record of approximately 3.88MJ of fusion energy and fusion energy target gain of approximately 1.9.

Reduced mixing in inertial confinement fusion with early-time interface acceleration.

In inertial confinement fusion (ICF) implosions, the interface between the cryogenic DT fuel and the ablator is unstable to shock acceleration (the Richtmyer-Meshkov instability, RM) and constant acceleration (Rayleigh-Taylor instability, RT). Instability growth at this interface can reduce the final compression, limiting fusion burnup. If the constant acceleration is in the direction of the lighter material (negative Atwood number), the RT instability produces oscillatory motion that can stabilize against RM growth. Theory and simulations suggest this scenario occurred at early times in some ICF experiments on the National Ignition Facility, possibly explaining their favorable performance compared to one-dimensional simulations. This characteristic is being included in newer, lower adiabat designs, seeking to improve compression while minimizing ablator mixing into the fuel.

Design of an inertial fusion experiment exceeding the Lawson criterion for ignition.

We present the design of the first igniting fusion plasma in the laboratory by Lawson's criterion that produced 1.37 MJ of fusion energy, Hybrid-E experiment N210808 (August 8, 2021) [Phys. Rev. Lett. 129, 075001 (2022)10.1103/PhysRevLett.129.075001]. This design uses the indirect drive inertial confinement fusion approach to heat and compress a central "hot spot" of deuterium-tritium (DT) fuel using a surrounding dense DT fuel piston. Ignition occurs when the heating from absorption of α particles created in the fusion process overcomes the loss mechanisms in the system for a duration of time. This letter describes key design changes which enabled a ∼3-6× increase in an ignition figure of merit (generalized Lawson criterion) [Phys. Plasmas 28, 022704 (2021)1070-664X10.1063/5.0035583, Phys. Plasmas 25, 122704 (2018)1070-664X10.1063/1.5049595]) and an eightfold increase in fusion energy output compared to predecessor experiments. We present simulations of the hot-spot conditions for experiment N210808 that show fundamentally different behavior compared to predecessor experiments and simulated metrics that are consistent with N210808 reaching for the first time in the laboratory "ignition."

Impact of Localized Radiative Loss on Inertial Confinement Fusion Implosions.

The impact to fusion energy production due to the radiative loss from a localized mix in inertial confinement implosions using high density carbon capsule targets has been quantified. The radiative loss from the localized mix and local cooling of the reacting plasma conditions was quantified using neutron and x-ray images to reconstruct the hot spot conditions during thermonuclear burn. Such localized features arise from ablator material that is injected into the hot spot from the Rayleigh-Taylor growth of capsule surface perturbations, particularly the tube used to fill the capsule with deuterium and tritium fuel. Observations, consistent with analytic estimates, show the degradation to fusion energy production to be linearly proportional to the fraction of the total emission that is associated with injected ablator material and that this radiative loss has been the primary source of variations, of up to 1.6 times, in observed fusion energy production. Reducing the fill tube diameter has increased the ignition metric χ_{no α} from 0.49 to 0.72, 92% of that required to achieve a burning hot spot.

The JAK inhibitor ruxolitinib reduces inflammation in an ILC3-independent model of innate immune colitis.

Innate immunity contributes to the pathogenesis of inflammatory bowel disease (IBD). However, the mechanisms of IBD mediated by innate immunity are incompletely understood and there are limited models of spontaneous innate immune colitis to address this question. Here we describe a new robust model of colitis occurring in the absence of adaptive immunity. RAG1-deficient mice expressing TNFAIP3 in intestinal epithelial cells (TRAG mice) spontaneously developed 100% penetrant, early-onset colitis that was limited to the colon and dependent on intestinal microbes but was not transmissible to co-housed littermates. TRAG colitis was associated with increased mucosal numbers of innate lymphoid cells (ILCs) and depletion of ILC prevented colitis in TRAG mice. ILC depletion also therapeutically reversed established colitis in TRAG mice. The colitis in TRAG mice was not prevented by interbreeding to mice lacking group 3 ILC nor by depletion of TNF. Treatment with the JAK inhibitor ruxolitinib ameliorated colitis in TRAG mice. This new model of colitis, with its predictable onset and colon-specific inflammation, will have direct utility in developing a more complete understanding of innate immune mechanisms that can contribute to colitis and in pre-clinical studies for effects of therapeutic agents on innate immune-mediated IBD.

Publisher's Note: X-ray shadow imprint of hydrodynamic instabilities on the surface of inertial confinement fusion capsules by the fuel fill tube [Phys. Rev. E 95, 031204(R) (2017)].

This corrects the article DOI: 10.1103/PhysRevE.95.031204.

X-ray shadow imprint of hydrodynamic instabilities on the surface of inertial confinement fusion capsules by the fuel fill tube.

Measurements of hydrodynamic instability growth for a high-density carbon ablator for indirectly driven inertial confinement fusion implosions on the National Ignition Facility are reported. We observe significant unexpected features on the capsule surface created by shadows of the capsule fill tube, as illuminated by laser-irradiated x-ray spots on the hohlraum wall. These shadows increase the spatial size and shape of the fill tube perturbation in a way that can significantly degrade performance in layered implosions compared to previous expectations. The measurements were performed at a convergence ratio of ∼2 using in-flight x-ray radiography. The initial seed due to shadow imprint is estimated to be equivalent to ∼50-100 nm of solid ablator material. This discovery has prompted the need for a mitigation strategy for future inertial confinement fusion designs as proposed here.

Development of a krypton-doped gas symmetry capsule platform for x-ray spectroscopy of implosion cores on the NIF.

The electron temperature at stagnation of an ICF implosion can be measured from the emission spectrum of high-energy x-rays that pass through the cold material surrounding the hot stagnating core. Here we describe a platform developed on the National Ignition Facility where trace levels of a mid-Z dopant (krypton) are added to the fuel gas of a symcap (symmetry surrogate) implosion to allow for the use of x-ray spectroscopy of the krypton line emission.

Erratum: First Measurements of Fuel-Ablator Interface Instability Growth in Inertial Confinement Fusion Implosions on the National Ignition Facility [Phys. Rev. Lett. 117, 075002 (2016)].

This corrects the article DOI: 10.1103/PhysRevLett.117.075002.

First Measurements of Fuel-Ablator Interface Instability Growth in Inertial Confinement Fusion Implosions on the National Ignition Facility.

Direct measurements of hydrodynamic instability growth at the fuel-ablator interface in inertial confinement fusion (ICF) implosions are reported for the first time. These experiments investigate one of the degradation mechanisms behind the lower-than-expected performance of early ICF implosions on the National Ignition Facility. Face-on x-ray radiography is used to measure instability growth occurring between the deuterium-tritium fuel and the plastic ablator from well-characterized perturbations. This growth starts in two ways through separate experiments-either from a preimposed interface modulation or from ablation front feedthrough. These experiments are consistent with analytic modeling and radiation-hydrodynamic simulations, which say that a moderately unstable Atwood number and convergence effects are causing in-flight perturbation growth at the interface. The analysis suggests that feedthrough from outersurface perturbations dominates the interface perturbation growth at mode 60.

Improved Performance of High Areal Density Indirect Drive Implosions at the National Ignition Facility using a Four-Shock Adiabat Shaped Drive.

Hydrodynamic instabilities can cause capsule defects and other perturbations to grow and degrade implosion performance in ignition experiments at the National Ignition Facility (NIF). Here, we show the first experimental demonstration that a strong unsupported first shock in indirect drive implosions at the NIF reduces ablation front instability growth leading to a 3 to 10 times higher yield with fuel ρR>1 g/cm(2). This work shows the importance of ablation front instability growth during the National Ignition Campaign and may provide a path to improved performance at the high compression necessary for ignition.

Inhibition of turbulence in inertial-confinement-fusion hot spots by viscous dissipation.

Achieving ignition in inertial confinement fusion (ICF) requires the formation of a high-temperature (>10 keV) central hot spot. Turbulence has been suggested as a mechanism for degrading the hot-spot conditions by altering transport properties, introducing colder, mixed material, or reducing the conversion of radially directed kinetic energy to hot-spot heating. We show, however, that the hot spot is very viscous, and the assumption of turbulent conditions in the hot spot is incorrect. This work presents the first high-resolution, three-dimensional simulations of National Ignition Facility (NIF) implosion experiments using detailed knowledge of implosion dynamics and instability seeds and including an accurate model of physical viscosity. We find that when viscous effects are neglected, the hot spot can exhibit a turbulent kinetic energy cascade. Viscous effects, however, are significant and strongly damp small-scale velocity structures, with a hot-spot Reynolds number in the range of only 10-100.

Targeted deletion of MyD88 in intestinal epithelial cells results in compromised antibacterial immunity associated with downregulation of polymeric immunoglobulin receptor, mucin-2, and antibacterial peptides.

Intestinal epithelial cells (IECs) form a physical and immunological barrier that separates the vast gut microbiota from host tissues. MyD88-dependent Toll-like receptor signaling is a key mediator of microbial-host cross-talk. We examined the role of epithelial MyD88 expression by generating mice with an IEC-targeted deletion of the Myd88 gene (MyD88(ΔIEC)). Loss of epithelial MyD88 signaling resulted in increased numbers of mucus-associated bacteria; translocation of bacteria, including the opportunistic pathogen Klebsiella pneumoniae, to mesenteric lymph nodes; reduced transmucosal electrical resistance; impaired mucus-associated antimicrobial activity; and downregulated expression of polymeric immunoglobulin receptor (the epithelial IgA transporter), mucin-2 (the major protein of intestinal mucus), and the antimicrobial peptides RegIIIγ and Defa-rs1. We further observed significant differences in the composition of the gut microbiota between MyD88(ΔIEC) mice and wild-type littermates. These physical, immunological, and microbial defects resulted in increased susceptibility of MyD88(ΔIEC) mice to experimental colitis. We conclude that MyD88 signaling in IECs is crucial for maintenance of gut homeostasis.

Allosteric regulation of Na/Ca exchange current by cytosolic Ca in intact cardiac myocytes.

The cardiac sarcolemmal Na-Ca exchanger (NCX) is allosterically regulated by [Ca](i) such that when [Ca](i) is low, NCX current (I(NCX)) deactivates. In this study, we used membrane potential (E(m)) and I(NCX) to control Ca entry into and Ca efflux from intact cardiac myocytes to investigate whether this allosteric regulation (Ca activation) occurs with [Ca](i) in the physiological range. In the absence of Ca activation, the electrochemical effect of increasing [Ca](i) would be to increase inward I(NCX) (Ca efflux) and to decrease outward I(NCX). On the other hand, Ca activation would increase I(NCX) in both directions. Thus, we attributed [Ca](i)-dependent increases in outward I(NCX) to allosteric regulation. Ca activation of I(NCX) was observed in ferret myocytes but not in wild-type mouse myocytes, suggesting that Ca regulation of NCX may be species dependent. We also studied transgenic mouse myocytes overexpressing either normal canine NCX or this same canine NCX lacking Ca regulation (Delta680-685). Animals with the normal canine NCX transgene showed Ca activation, whereas animals with the mutant transgene did not, confirming the role of this region in the process. In native ferret cells and in mice with expressed canine NCX, allosteric regulation by Ca occurs under physiological conditions (K(mCaAct) = 125 +/- 16 nM SEM approximately resting [Ca](i)). This, along with the observation that no delay was observed between measured [Ca](i) and activation of I(NCX) under our conditions, suggests that beat to beat changes in NCX function can occur in vivo. These changes in the I(NCX) activation state may influence SR Ca load and resting [Ca](i), helping to fine tune Ca influx and efflux from cells under both normal and pathophysiological conditions. Our failure to observe Ca activation in mouse myocytes may be due to either the extent of Ca regulation or to a difference in K(mCaAct) from other species. Model predictions for Ca activation, on which our estimates of K(mCaAct) are based, confirm that Ca activation strongly influences outward I(NCX), explaining why it increases rather than declines with increasing [Ca](i).

Intraoperative nasal transillumination for maxillary sinus augmentation procedures: a technical note.

This article presents a simple, inexpensive method for precisely locating the floor of the maxillary sinus, as well as the presence of any septa, at the time of sinus augmentation surgery. Using an anesthesia light wand placed transnasally to illuminate the sinus, the surgeon can reliably elevate the lateral maxillary wall overlying the sinus with relative ease without fear of placing the osteotomy cuts too far from the sinus floor. The same procedure can be used postoperatively to evaluate the density of the bone graft placed into the sinus prior to closure.

Control of maximum sarcoplasmic reticulum Ca load in intact ferret ventricular myocytes. Effects Of thapsigargin and isoproterenol.

In steady state, the Ca content of the sarcoplasmic reticulum (SR) of cardiac myocytes is determined by a balance among influx and efflux pathways. The SR Ca content may be limited mainly by the ATP-supplied chemical potential that is inherent in the gradient between SR and cytosol. That is, forward Ca pumping from cytosol to SR may be opposed by energetically conservative reverse pumping dependent on intra-SR free [Ca]. On the other hand, SR Ca loading may be limited by dissipative pathways (pump slippage and/or pump-independent leak). To assess how SR Ca content is limited, we loaded voltage-clamped ferret ventricular myocytes cumulatively with known amounts of Ca via L-type Ca channels (ICa), using Na-free solutions to prevent Na/Ca exchange. We then measured the maximal resulting caffeine-released SR Ca content under control conditions, as well as when SR Ca pumping was accelerated by isoproterenol (1 micro M) or slowed by thapsigargin (0.2-0.4 micro M). Under control conditions, SR Ca content reached a limit of 137 micro mol.liter cytosol-1 (nonmitochondrial volume) when measured by integrating caffeine-induced Na/Ca exchange currents lintegraINaCaXdt) and of 119 micro mol.liter cytosol-1 when measured using fluorescence signals dependent on changes in cytosolic free Ca ([Ca]i). When Ca-ATPase pumping rate was slowed 39% by thapsigargin, the maximal SR Ca content decreased by 5 (integralINaCaXdt method) or 23% (fluorescence method); when pumping rate was increased 74% by isoproterenol, SR Ca content increased by 10% (fluorescence method) or 20% (integralINaCaXdt method). The relative stability of the SR Ca load suggests that dissipative losses have only a minor influence in setting the SR Ca content. Indeed, it appears that the SR Ca pump in intact cells can generate a [Ca] gradient approaching the thermodynamic limit.

Evaluation of dexamethasone for reducing postoperative edema and inflammatory response after orthognathic surgery.

A randomized, prospective, double-blind study was conducted to determine the efficacy of intravenous dexamethasone in reducing postoperative edema after bilateral sagittal split osteotomies of the mandible. Twenty-three patients were enrolled in the study and randomly assigned to one of the three groups. Each patient received one preoperative infusion and three postoperative infusions every 6 hours. Seven patients served as controls and received placebos for all infusions. Eight patients received dexamethasone, 16 mg preoperatively and three placebo postoperative doses. Eight patients received dexamethasone, 16 mg preoperatively and three 8-mg postoperative doses. Facial edema was quantified by computer scanning of standardized photographs. The underlying inflammatory process also was measured using C-reactive protein, erythrocyte sedimentation rate, and complete blood counts. Five sets of photographic and laboratory data were obtained for each patient: preoperative, day of surgery, and postoperative days 1, 2, and 3. Patients receiving dexamethasone demonstrated significantly less postoperative edema only on postoperative day 1 (P < .05) when measured photographically. C-reactive protein was significantly reduced on postoperative days 1, 2, and 3 (P < .05) in both dexamethasone groups. No significant difference was found between the two dexamethasone groups. Measurement of C-reactive protein seems to be the most sensitive method for comparing the effect of dexamethasone on postoperative inflammation. Preoperative intravenous dexamethasone significantly reduced postoperative inflammation and its associated edema after orthognathic surgery.

Undiagnosed shrapnel of the tongue.

A case of a large metal fragment in the tongue is reported in a soldier injured in Operation Desert Storm. The fragment was not diagnosed for 57 days as the patient was evacuated through multiple U.S. Army medical facilities for other injuries. Diagnosis and treatment of the case are discussed.