Ruegeria sp. Strains Isolated from the Reef-Building Coral Galaxea fascicularis Inhibit Growth of the Temperature-Dependent Pathogen Vibrio coralliilyticus

2018 ◽  
Vol 21 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Natsuko Miura ◽  
Keisuke Motone ◽  
Toshiyuki Takagi ◽  
Shunsuke Aburaya ◽  
Sho Watanabe ◽  
...  
Keyword(s):  
Temperature Dependent ◽  
Galaxea Fascicularis ◽  
Vibrio Coralliilyticus

scholarly journals Vibrio coralliilyticus sp. nov., a temperature-dependent pathogen of the coral Pocillopora damicornis

2003 ◽  
Vol 53 (1) ◽  
pp. 309-315 ◽  
Author(s):  
Y. Ben-Haim ◽  
F. L. Thompson ◽  
C. C. Thompson ◽  
M. C. Cnockaert ◽  
B. Hoste ◽  
...  
Keyword(s):  
Pocillopora Damicornis ◽  
Temperature Dependent ◽  
Vibrio Coralliilyticus

scholarly journals Vibrio coralliilyticus Strain OCN008 Is an Etiological Agent of Acute Montipora White Syndrome

2014 ◽  
Vol 80 (7) ◽  
pp. 2102-2109 ◽  
Author(s):  
Blake Ushijima ◽  
Patrick Videau ◽  
Andrew H. Burger ◽  
Amanda Shore-Maggio ◽  
Christina M. Runyon ◽  
...  
Keyword(s):  
Type Strain ◽  
Disease Onset ◽  
Tissue Loss ◽  
Temperature Dependent ◽  
Content Type ◽  
Infectious Dose ◽  
White Syndrome ◽  
Porites Compressa ◽  
Sensing Systems ◽  
Vibrio Coralliilyticus

ABSTRACTIdentification of a pathogen is a critical first step in the epidemiology and subsequent management of a disease. A limited number of pathogens have been identified for diseases contributing to the global decline of coral populations. Here we describeVibrio coralliilyticusstrain OCN008, which induces acuteMontiporawhite syndrome (aMWS), a tissue loss disease responsible for substantial mortality of the coralMontipora capitatain Kāne‘ohe Bay, Hawai‘i. OCN008 was grown in pure culture, recreated signs of disease in experimentally infected corals, and could be recovered after infection. In addition, strains similar to OCN008 were isolated from diseased coral from the field but not from healthyM. capitata. OCN008 repeatedly induced the loss of healthyM. capitatatissue from fragments under laboratory conditions with a minimum infectious dose of between 107and 108CFU/ml of water. In contrast,Porites compressawas not infected by OCN008, indicating the host specificity of the pathogen. A decrease in water temperature from 27 to 23°C affected the time to disease onset, but the risk of infection was not significantly reduced. Temperature-dependent bleaching, which has been observed with theV. coralliilyticustype strain BAA-450, was not observed during infection with OCN008. A comparison of the OCN008 genome to the genomes of pathogenicV. coralliilyticusstrains BAA-450 and P1 revealed similar virulence-associated genes and quorum-sensing systems. Despite this genetic similarity, infections ofM. capitataby OCN008 do not follow the paradigm forV. coralliilyticusinfections established by the type strain.

(111) Monocrystalline Nickel Films

1972 ◽  
Vol 30 ◽  
pp. 512-513
Author(s):  
T.E. Pratt ◽  
R.W. Vook
Keyword(s):  
Film Thickness ◽  
Deposition Rate ◽  
Room Temperature ◽  
Narrow Range ◽  
High Vacuum ◽  
Residual Pressure ◽  
Temperature Dependent ◽  
Deposition Parameters ◽  
Transmission Electron ◽  
Substrate Temperatures

(111) oriented thin monocrystalline Ni films have been prepared by vacuum evaporation and examined by transmission electron microscopy and electron diffraction. In high vacuum, at room temperature, a layer of NaCl was first evaporated onto a freshly air-cleaved muscovite substrate clamped to a copper block with attached heater and thermocouple. Then, at various substrate temperatures, with other parameters held within a narrow range, Ni was evaporated from a tungsten filament. It had been shown previously that similar procedures would yield monocrystalline films of CU, Ag, and Au.For the films examined with respect to temperature dependent effects, typical deposition parameters were: Ni film thickness, 500-800 A; Ni deposition rate, 10 A/sec.; residual pressure, 10-6 torr; NaCl film thickness, 250 A; and NaCl deposition rate, 10 A/sec. Some additional evaporations involved higher deposition rates and lower film thicknesses.Monocrystalline films were obtained with substrate temperatures above 500° C. Below 450° C, the films were polycrystalline with a strong (111) preferred orientation.

In Vitro Effects of Urokinase — Prevention by Different Inhibitors

1990 ◽  
Vol 64 (03) ◽  
pp. 402-406 ◽  
Author(s):  
M D Oethinger ◽  
E Seifried
Keyword(s):  
In Vitro Study ◽  
Thrombin Time ◽  
Plasma Samples ◽  
Temperature Dependent ◽  
Chloromethyl Ketone ◽  
Control Value ◽  
Dose Time ◽  
In Vitro Effects ◽  
Full Protection

SummaryThe present in vitro study investigated dose-, time- and temperature-dependent effects of two-chain urokinase plasminogen activato(u-PA, urokinase) on normal citrated plasma. When 10 μg/ml u-PA wereadded to pooled normal plasma and incubated for 30 min at an ambient temperature (25° C), α2-antiplas-min decreased to 8% of the control value. Incubation on ice yielded a decrease to 45% of control,whereas α2-antiplasmin was fully consumed at 37° C. Fibrinogen and plasminogen fell to 46% and 39%, respectively, after a 30 min incubation at 25° C. Thrombin time prolonged to 190% of control.Various inhibitors were studied with respect to their suitability and efficacy to prevent these in vitro effects. Aprotinin exhibited a good protective effect on fibrinogen at concentrations exceeding 500 KlU/ml plasma. Its use, however, was limited due to interferences with some haemostatic assays. We could demonstrate that L-Glutamyl-L-Glycyl-L-Arginyl chloromethyl ketone (GGACK) and a specific polyclonal anti-u-PA-antibody (anti-u-PA-IgG) effectively inhibited urokinase-induced plasmin generation without interfering with haemostatic assays. The anti-u-PA-antibody afforded full protection ofα2-antiplasmin at therapeutic levels of u-PA.It is concluded that u-PA in plasma samples from patients during thrombolytic therapy may induce in vitro effects which should be prevented by the use of a suitable inhibitor such as GGACK or specific anti-u-PA-antibody.

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