Tabulation and summary of thermodynamic effects data for developed cavitation on ogive-nosed bodies

Thermodynamic effects data for developed cavitation on zero and quarter caliber ogives in Freon 113 and water are tabulated and summarized. These data include temperature depression (delta T), flow coefficient (C sub Q), and various geometrical characteristics of the cavity. For the delta T tests, the free-stream temperature varied from 35 C to 95 C in Freon 113 and from 60 C to 125 C in water for a velocity range of 19.5 m/sec to 36.6 m/sec. Two correlations of the delta T data by the entrainment method are presented. These correlations involve different combinations of the Nusselt, Reynolds, Froude, Weber, and Peclet numbers and dimensionless cavity length

Drug-Induced Hematologic Syndromes

Objective. Drugs can induce almost the entire spectrum of hematologic disorders, affecting white cells, red cells, platelets, and the coagulation system. This paper aims to emphasize the broad range of drug-induced hematological syndromes and to highlight some of the newer drugs and syndromes. Methods. Medline literature on drug-induced hematologic syndromes was reviewed. Most reports and reviews focus on individual drugs or cytopenias. Results. Drug-induced syndromes include hemolytic anemias, methemoglobinemia, red cell aplasia, sideroblastic anemia, megaloblastic anemia, polycythemia, aplastic anemia, leukocytosis, neutropenia, eosinophilia, immune thrombocytopenia, microangiopathic syndromes, hypercoagulability, hypoprothrombinemia, circulating anticoagulants, myelodysplasia, and acute leukemia. Some of the classic drugs known to cause hematologic abnormalities have been replaced by newer drugs, including biologics, accompanied by their own syndromes and unintended side effects. Conclusions. Drugs can induce toxicities spanning many hematologic syndromes, mediated by a variety of mechanisms. Physicians need to be alert to the potential for iatrogenic drug-induced hematologic complications

Emission of multiple dispersive waves from a single Raman-shifting soliton in an axially-varying optical fiber

International audienceWe provide the experimental demonstration of the generation of multiple dispersive waves from a single soliton propagating in the vicinity of the first zero-dispersion wavelength of an axially-varying optical fiber. The fiber is designed such that the Raman-shifting soliton successively hits three times the longitudinally evolving zero-dispersion wavelength, which results in the emission of three distinct dispersive waves at different fiber lengths. These results illustrate how suitably controlled axially-varying fibers allow to tailor the soliton dynamics in a very accurate way

Real-time measurements of dissipative solitons in a mode-locked fiber laser

Dissipative solitons are remarkable localized states of a physical system that arise from the dynamical balance between nonlinearity, dispersion and environmental energy exchange. They are the most universal form of soliton that can exist in nature, and are seen in far-from-equilibrium systems in many fields including chemistry, biology, and physics. There has been particular interest in studying their properties in mode-locked lasers producing ultrashort light pulses, but experiments have been limited by the lack of convenient measurement techniques able to track the soliton evolution in real-time. Here, we use dispersive Fourier transform and time lens measurements to simultaneously measure real-time spectral and temporal evolution of dissipative solitons in a fiber laser as the turn-on dynamics pass through a transient unstable regime with complex break-up and collision dynamics before stabilizing to a regular mode-locked pulse train. Our measurements enable reconstruction of the soliton amplitude and phase and calculation of the corresponding complex-valued eigenvalue spectrum to provide further physical insight. These findings are significant in showing how real-time measurements can provide new perspectives into the ultrafast transient dynamics of complex systems.Comment: See also M. Narhi, P. Ryczkowski, C. Billet, G. Genty, J. M. Dudley, Ultrafast Simultaneous Real Time Spectral and Temporal Measurements of Fibre Laser Modelocking Dynamics, 2017 Conference on Lasers and Electro-Optics Europe & European Quantum Electronics Conference, paper EE-3.5 (2017

Cancer epithelia-derived mitochondrial DNA is a targetable initiator of a paracrine signaling loop that confers taxane resistance.

Stromal-epithelial interactions dictate cancer progression and therapeutic response. Prostate cancer (PCa) cells were identified to secrete greater concentration of mitochondrial DNA (mtDNA) compared to noncancer epithelia. Based on the recognized coevolution of cancer-associated fibroblasts (CAF) with tumor progression, we tested the role of cancer-derived mtDNA in a mechanism of paracrine signaling. We found that prostatic CAF expressed DEC205, which was not expressed by normal tissue-associated fibroblasts. DEC205 is a transmembrane protein that bound mtDNA and contributed to pattern recognition by Toll-like receptor 9 (TLR9). Complement C3 was the dominant gene targeted by TLR9-induced NF-κB signaling in CAF. The subsequent maturation complement C3 maturation to anaphylatoxin C3a was dependent on PCa epithelial inhibition of catalase in CAF. In a syngeneic tissue recombination model of PCa and associated fibroblast, the antagonism of the C3a receptor and the fibroblastic knockout of TLR9 similarly resulted in immune suppression with a significant reduction in tumor progression, compared to saline-treated tumors associated with wild-type prostatic fibroblasts. Interestingly, docetaxel, a common therapy for advanced PCa, further promoted mtDNA secretion in cultured epithelia, mice, and PCa patients. The antiapoptotic signaling downstream of anaphylatoxin C3a signaling in tumor cells contributed to docetaxel resistance. The inhibition of C3a receptor sensitized PCa epithelia to docetaxel in a synergistic manner. Tumor models of human PCa epithelia with CAF expanded similarly in mice in the presence or absence of docetaxel. The combination therapy of docetaxel and C3 receptor antagonist disrupted the mtDNA/C3a paracrine loop and restored docetaxel sensitivity