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A platinum cobalt wire and silver sheathed Bi-2223 tape were used to investigate bubble formation and critical heat flux to boiling state for cyclic heat inputs.

Magnetic bearings using a high-Tc superconductor have been studied. Generally the bearing makes use of the pinning effects to get the levitation force. The stiffness of the bearing, however, is extremely low as compared with industrial-scale conventional one. To improve the bearing stiffness we propose a disc-type repulsive superconducting thrust bearing with a slit for the restraint of the flux. Both theoretical and experimental evaluation on the load performance was carried out, and it is clarified that the proposed superconducting bearing has higher stiffness.

In this paper, the influence of a macro-flow, which is some kind of natural convection caused by heat-in leak in rotational cryostats, has been investigated. A macro cooling channel unit which generates a main flow counter to the buoyancy direction has been made to simulate the macro-flow influence. A high-speed camera has been used to observe the transient local convection. Also a thin film thermometer has been used to detect the transient temperature variation. As the result, some fluctuation caused by the macro-flow has been observed in the transient convection. The degradations of the transient temperature variation and the maximum heat flux have been measured.

Stabilities of magnets in a high gravitational field up to 2000 G are discussed, based upon the experimental results of forced quench tests in a set of rotating magnets, in order to establish the stability design criterion of field windings of superconducting generators. Relations of propagation velocities, recovery currents, minimum quench energy and heat transfer characteristics are studied, a good agreement between the experimental results and a theory confirmed the improvement of magnet stability in a high gravitational field because of the enhanced heat transfer characteristics.

Electrical breakdown behavior of liquid helium was investigated under high speed rotating field. In the development of superconducting turbine generator it is essential to get the knowledge of electrical insulation characteristics of liquid helium under high speed rotating field. When the current of the field magnet of a superconducting generator is changed, changing magnetic field generates heat in the conductor and it causes bubbles in the liquid helium around the conductor. The behavior of the bubbles is affected largely by the buoyancy which is generated by the centrifugal force. Electrical breakdown behavior of the liquid helium is strongly dependent on the gas bubbles in the liquid. Electrical breakdown voltage between electrodes was measured in a rotating cryostat with and without heater input for bubble formation. Decrease of the breakdown voltage by the heater power was smaller in the rotating field than that in the non rotating field.

This paper proposes a goods transportation system with a pinning-type superconducting magnetic levitation guide setting in a vacuum passage and describes the system outline. Load characteristics of the superconducting levitation guide used this system are analyzed by a newly developed electromagnetic field analysis program; then, it is evaluated for whether it has sufficient load characteristics as a non-contact guide for this system. Calculation results show that the superconducting levitation guide has sufficient levitation force in the large gap, which become an effective space for thermal insulation between the magnetic rail at room temperature and superconductors cooled to cryogenic temperatures. Comparison between calculated and measured values was done to examine program validity in a small model; it showed good agreement both quantitatively and qualitatively. [Copyright &y& Elsevier]

Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a progressive increase in pulmonary artery pressure caused by pathological pulmonary artery remodeling. Here, we demonstrate that endothelial cell (EC) senescence plays a negative role in pulmonary hypertension via juxtacrine interaction with smooth muscle cells (SMCs). By using EC-specific progeroid mice, we discovered that EC progeria deteriorated vascular remodeling in the lungs, and exacerbated pulmonary hypertension in mice. Mechanistically, senescent ECs overexpressed Notch ligands, which resulted in increased Notch signaling and activated proliferation and migration capacities in neighboring SMCs. Pharmacological inhibition of Notch signaling reduced the effects of senescent ECs on SMCs functions in vitro , and improved the worsened pulmonary hypertension in EC-specific progeroid mice in vivo . Our findings show that EC senescence is a critical disease-modifying factor in PAH and that EC-mediated Notch signaling is a pharmacotherapeutic target for the treatment of PAH, particularly in the elderly., Competing Interests: The authors declare no competing interests., (© 2023 The Authors.)

Acute respiratory distress syndrome (ARDS) with COVID-19 is aggravated by hyperinflammatory responses even after the peak of the viral load has passed; however, its underlying mechanisms remain unclear. In the present study, analysis of the alveolar tissue injury markers and epithelial cell death markers in patients with COVID-19 revealed that COVID-19-induced ARDS was characterized by alveolar epithelial necrosis at an early disease stage. Serum levels of HMGB-1, one of the DAMPs released from necrotic cells, were also significantly elevated in these patients. Further analysis using a mouse model mimicking COVID-19-induced ARDS showed that the alveolar epithelial cell necrosis involved two forms of programmed necrosis, namely necroptosis, and pyroptosis. Finally, the neutralization of HMGB-1 attenuated alveolar tissue injury in the mouse model. Collectively, necrosis, including necroptosis and pyroptosis, is the predominant form of alveolar epithelial cell death at an early disease stage and subsequent release of DAMPs is a potential driver of COVID-19-induced ARDS., Competing Interests: The authors declare no competing interests., (© 2022 The Author(s).)

Alveolar epithelial cell (AEC) death, which is classified as apoptosis or necrosis, plays a critical role in the pathogenesis of acute respiratory distress syndrome (ARDS). In addition to apoptosis, some types of necrosis are known to be molecularly regulated, and both apoptosis and necrosis can be therapeutic targets for diseases. However, the relative contribution of apoptosis and necrosis to AEC death during ARDS has not been elucidated. Here, we evaluated which type of AEC death is dominant and whether regulated necrosis is involved in lipopolysaccharide (LPS)-induced lung injury, an experimental ARDS model. In the bronchoalveolar lavage fluid from the LPS-induced lung injury mice, both the levels of cytokeratin 18-M65 antigen (a marker of total epithelial cell death) and cytokeratin 18-M30 antigen (an epithelial apoptosis marker) were increased. The M30/M65 ratio, which is an indicator of the proportion of apoptosis to total epithelial cell death, was significantly lower than that in healthy controls. In addition, the number of propidium iodide-positive, membrane-disrupted cells was significantly higher than the number of TUNEL-positive apoptotic cells in the lung sections of lung injury mice. Activated neutrophils seemed to mediate AEC death. Finally, we demonstrated that necroptosis, a regulated necrosis pathway, is involved in AEC death during LPS-induced lung injury. These results indicate that necrosis including necroptosis, rather than apoptosis, is the dominant type of AEC death in LPS-induced lung injury. Although further studies investigating human ARDS subjects are necessary, targeting necrosis including its regulated forms might represent a more efficient approach to protecting the alveolar epithelial barrier during ARDS.

Pulmonary hypertension is a progressive lung disease with poor prognosis due to the consequent right heart ventricular failure. Pulmonary artery remodeling and dysfunction are culprits for pathologically increased pulmonary arterial pressure, but their underlying molecular mechanisms remain to be elucidated. Previous genome-wide association studies revealed a significant correlation between the genetic locus of family with sequence similarity 13, member A (FAM13A) and various lung diseases such as chronic obstructive pulmonary disease and pulmonary fibrosis; however whether FAM13A is also involved in the pathogenesis of pulmonary hypertension remained unknown. Here, we identified a significant role of FAM13A in the development of pulmonary hypertension. FAM13A expression was reduced in the lungs of mice with hypoxia-induced pulmonary hypertension. We identified that FAM13A was expressed in lung vasculatures, especially in endothelial cells. Genetic loss of FAM13A exacerbated pulmonary hypertension in mice exposed to chronic hypoxia in association with deteriorated pulmonary artery remodeling. Mechanistically, FAM13A decelerated endothelial-to-mesenchymal transition potentially by inhibiting β-catenin signaling in pulmonary artery endothelial cells. Our data revealed a protective role of FAM13A in the development of pulmonary hypertension, and therefore increasing and/or preserving FAM13A expression in pulmonary artery endothelial cells is an attractive therapeutic strategy for the treatment of pulmonary hypertension., Competing Interests: The authors have declared that no competing interests exist.

Background: While hemodynamics and exercise capacity in patients with chronic thromboembolic pulmonary hypertension (CTEPH) can be improved by invasive therapy such as pulmonary endarterectomy (PEA) and balloon pulmonary angioplasty (BPA), there has been little data on the health-related quality of life (HRQOL) in such patients. Methods and Results: This single-center and observational study compared the impact of invasive therapy on HRQOL. We utilized the Medical Outcome Study 36-Item Short Health Survey (SF-36) to measure HRQOL and compared HRQOL changes after PEA and BPA. A total of 48 patients were diagnosed with CTEPH. Of these, 39 patients completed questionnaires before and after invasive therapy. The PEA group (n=15) and the BPA group (n=24) had similar improvements in clinical parameters. With regard to HRQOL score, both groups had fairly low scores in physical functioning (PF), role physical (RP), general health (GH), social functioning (SF), role emotional (RE), and physical component summary (PCS) at baseline. PF, GH, vitality (VT), mental health (MH), and PCS had significant improvements in the PEA group while PCS and all subscales except for bodily pain (BP) had significant improvements in the BPA group. Furthermore, changes between baseline and follow-up were not significantly different between the 2 groups. Conclusions: BPA for patients who are ineligible for PEA can recover HRQOL to a similar level to that achieved by PEA., Competing Interests: Sources of Funding: There is no grant support for this manuscript. Conflict of Interest Statement: K.N. has received research grants from Actelion Pharmaceuticals Japan, Bayer Holding, and GlaxoSmithKline. K.H. received research grants from Actelion Pharmaceuticals Japan, and Bayer Holding. The other authors declare no conflicts of interest., (Copyright © 2019, THE JAPANESE CIRCULATION SOCIETY.)

Rheumatoid vasculitis is a rare etiology for pulmonary hypertension (PH) in patients with connective tissue disease. We encountered a case of acute PH crisis in a case with rheumatoid vasculitis eight months after undergoing adalimumab reduction. Since no repetition of arthralgia occurred after the adalimumab reduction, we decided to not increase the dose of adalimumab. However, hemodynamic collapse thereafter developed and even though steroid pulse therapy was administered, the patient nevertheless died. The autopsy showed clusters of acute and chronic inflammation around the remodeled pulmonary arteries along with micro-thrombi in the vessel lumen. We should consider the possibility of critical worsening of PH as a phenotype of vasculitis related to immunosuppressive therapy reduction.

Antiphospholipid syndrome (APS) is a cause of chronic thromboembolic pulmonary hypertension (CTEPH) and it is associated with an increased risk of postoperative neurological complications. We experienced a case of reversible parkinsonism after pulmonary endarterectomy (PEA) and subsequent multiple cerebral infarctions under standard anticoagulation therapy in a patient with CTEPH associated with APS. Strict management using a combination of antiplatelet and anticoagulation therapy should be considered in patients with a high titer of triple antiphospholipid antibodies in the perioperative period. We should be aware of the high risk of postoperative neurologic manifestations in patients with APS.

Background: Residual symptoms after pulmonary endarterectomy (PEA) remain as the clinical issues to be solved. Additional balloon pulmonary angioplasty (BPA) after PEA showed its efficacy with symptoms in a case series, although long-term spontaneous recovery of exercise ability after PEA was also reported. However, no studies have validated the clinical efficacy of additional BPA by directly comparing PEA with and without BPA. The aim of this study was to retrospectively evaluate the efficacy of additional BPA as a sequential hybrid therapy for chronic thromboembolic pulmonary hypertension after PEA., Methods and Results: Among 44 patients with chronic thromboembolic pulmonary hypertension, 20 patients had residual symptoms after PEA. Of those, 10 patients underwent additional BPA (hybrid group) and were compared with the other 10 patients, who were followed up without BPA (PEA group). The period from PEA to additional BPA was 7.3±2.3 months. In hybrid group, mean pulmonary arterial pressure was significantly improved by PEA (40.6±1.8 to 26.9±3.1 mm Hg, P =0.001) and improved further (to 16.7±1.8 mm Hg, P =0.002) with additional BPA, which resulted in remarkable improvement in World Health Organization (WHO) functional class (pre- to post-BPA: class I/II/III/IV, 0/5/4/1 to 7/3/0/0; P <0.001). Compared with the PEA group at follow-up, the hybrid group achieved better mean pulmonary arterial pressure (18.7±1.7 versus 30.2±3.2 mm Hg, P =0.008), WHO functional class (class I/II/III/IV, 7/3/0/0 versus 0/8/2/0; P =0.001), and 6-minute walking distance (429±38 versus 319±22 m, P =0.028)., Conclusions: A sequential hybrid strategy improved residual symptoms and exercise capacity compared with single-PEA therapy., (© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)