Focusing and Compression of Ultrashort Pulses through Scattering Media

Light scattering in inhomogeneous media induces wavefront distortions which pose an inherent limitation in many optical applications. Examples range from microscopy and nanosurgery to astronomy. In recent years, ongoing efforts have made the correction of spatial distortions possible by wavefront shaping techniques. However, when ultrashort pulses are employed scattering induces temporal distortions which hinder their use in nonlinear processes such as in multiphoton microscopy and quantum control experiments. Here we show that correction of both spatial and temporal distortions can be attained by manipulating only the spatial degrees of freedom of the incident wavefront. Moreover, by optimizing a nonlinear signal the refocused pulse can be shorter than the input pulse. We demonstrate focusing of 100fs pulses through a 1mm thick brain tissue, and 1000-fold enhancement of a localized two-photon fluorescence signal. Our results open up new possibilities for optical manipulation and nonlinear imaging in scattering media

Spatial and Spectral Coherent Control with Frequency Combs

Quantum coherent control (1-3) is a powerful tool for steering the outcome of quantum processes towards a desired final state, by accurate manipulation of quantum interference between multiple pathways. Although coherent control techniques have found applications in many fields of science (4-9), the possibilities for spatial and high-resolution frequency control have remained limited. Here, we show that the use of counter-propagating broadband pulses enables the generation of fully controlled spatial excitation patterns. This spatial control approach also provides decoherence reduction, which allows the use of the high frequency resolution of an optical frequency comb (10,11). We exploit the counter-propagating geometry to perform spatially selective excitation of individual species in a multi-component gas mixture, as well as frequency determination of hyperfine constants of atomic rubidium with unprecedented accuracy. The combination of spectral and spatial coherent control adds a new dimension to coherent control with applications in e.g nonlinear spectroscopy, microscopy and high-precision frequency metrology.Comment: 12 page

Shaping speckles: spatio-temporal focussing of an ultrafast pulse through a multiply scattering medium

The multiple scattering of coherent light is a problem of both fundamental and applied importance. In optics, phase conjugation allows spatial focussing and imaging through a multiply scattering medium; however, temporal control is nonetheless elusive, and multiple scattering remains a challenge for femtosecond science. Here, we report on the spatially and temporally resolved measurement of a speckle field produced by the propagation of an ultrafast optical pulse through a thick strongly scattering medium. Using spectral pulse shaping, we demonstrate the spatially localized temporal recompression of the output speckle to the Fourier-limit duration, offering an optical analogue to time-reversal experiments in the acoustic regime. This approach shows that a multiply scattering medium can be put to profit for light manipulation at the femtosecond scale, and has a diverse range of potential applications that includes quantum control, biological imaging and photonics.Comment: 7 pages, 3 figures, published in Nature Communication

Caspase Inhibitors of the P35 Family Are More Active When Purified from Yeast than Bacteria

Many insect viruses express caspase inhibitors of the P35 superfamily, which prevent defensive host apoptosis to enable viral propagation. The prototypical P35 family member, AcP35 from Autographa californica M nucleopolyhedrovirus, has been extensively studied. Bacterially purified AcP35 has been previously shown to inhibit caspases from insect, mammalian and nematode species. This inhibition occurs via a pseudosubstrate mechanism involving caspase-mediated cleavage of a “reactive site loop” within the P35 protein, which ultimately leaves cleaved P35 covalently bound to the caspase's active site. We observed that AcP35 purifed from Saccharomyces cerevisae inhibited caspase activity more efficiently than AcP35 purified from Escherichia coli. This differential potency was more dramatic for another P35 family member, MaviP35, which inhibited human caspase 3 almost 300-fold more potently when purified from yeast than bacteria. Biophysical assays revealed that MaviP35 proteins produced in bacteria and yeast had similar primary and secondary structures. However, bacterially produced MaviP35 possessed greater thermal stability and propensity to form higher order oligomers than its counterpart purified from yeast. Caspase 3 could process yeast-purified MaviP35, but failed to detectably cleave bacterially purified MaviP35. These data suggest that bacterially produced P35 proteins adopt subtly different conformations from their yeast-expressed counterparts, which hinder caspase access to the reactive site loop to reduce the potency of caspase inhibition, and promote aggregation. These data highlight the differential caspase inhibition by recombinant P35 proteins purified from different sources, and caution that analyses of bacterially produced P35 family members (and perhaps other types of proteins) may underestimate their activity

Dopamine in the dorsal hippocampus impairs the late-consolidation of cocaine-associated memory

Cocaine is thought to be addictive because it elevates dopamine levels in the striatum, reinforcing drug-seeking habits. Cocaine also elevates dopamine levels in the hippocampus, a structure involved in contextual conditioning as well as in reward function. Hippocampal dopamine promotes the late phase of consolidation of an aversive step-down avoidance memory. Here, we examined the role of hippocampal dopamine function in the persistence of the conditioned increase in preference for a cocaine-associated compartment. Blocking dorsal hippocampal D1-type receptors (D1Rs) but not D2-type receptors (D2Rs) 12 h after a single training trial extended persistence of the normally short-lived memory; conversely, a general and a specific phospholipase C-coupled D1R agonist (but not a D2R or adenylyl cyclase-coupled D1R agonist) decreased the persistence of the normally long-lived memory established by three-trial training. These effects of D1 agents were opposite to those previously established in a step-down avoidance task, and were here also found to be opposite to those in a lithium chloride-conditioned avoidance task. After returning to normal following cocaine injection, dopamine levels in the dorsal hippocampus were found elevated again at the time when dopamine antagonists and agonists were effective: between 13 and 17 h after cocaine injection. These findings confirm that, long after the making of a cocaine-place association, hippocampal activity modulates memory consolidation for that association via a dopamine-dependent mechanism. They suggest a dynamic role for dorsal hippocampal dopamine in this late-phase memory consolidation and, unexpectedly, differential roles for late consolidation of memories for places that induce approach or withdrawal because of a drug association.Fil: Kramar, Cecilia Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaFil: Chefer, Vladimir I.. National Institutes of Health; Estados UnidosFil: Wise, Roy A.. National Institutes of Health; Estados UnidosFil: Medina, Jorge Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; ArgentinaFil: Barbano, María Flavia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentin

A database of chlorophyll a in Australian waters

© The Author(s) 2018. Chlorophyll a is the most commonly used indicator of phytoplankton biomass in the marine environment. It is relatively simple and cost effective to measure when compared to phytoplankton abundance and is thus routinely included in many surveys. Here we collate 173, 333 records of chlorophyll a collected since 1965 from Australian waters gathered from researchers on regular coastal monitoring surveys and ocean voyages into a single repository. This dataset includes the chlorophyll a values as measured from samples analysed using spectrophotometry, fluorometry and high performance liquid chromatography (HPLC). The Australian Chlorophyll a database is freely available through the Australian Ocean Data Network portal (https://portal.aodn.org.au/). These data can be used in isolation as an index of phytoplankton biomass or in combination with other data to provide insight into water quality, ecosystem state, and relationships with other trophic levels such as zooplankton or fish

A database of marine phytoplankton abundance, biomass and species composition in Australian waters

There have been many individual phytoplankton datasets collected across Australia since the mid 1900s, but most are unavailable to the research community. We have searched archives, contacted researchers, and scanned the primary and grey literature to collate 3,621,847 records of marine phytoplankton species from Australian waters from 1844 to the present. Many of these are small datasets collected for local questions, but combined they provide over 170 years of data on phytoplankton communities in Australian waters. Units and taxonomy have been standardised, obviously erroneous data removed, and all metadata included. We have lodged this dataset with the Australian Ocean Data Network (http://portal.aodn.org.au/) allowing public access. The Australian Phytoplankton Database will be invaluable for global change studies, as it allows analysis of ecological indicators of climate change and eutrophication (e.g., changes in distribution; diatom:dinoflagellate ratios). In addition, the standardised conversion of abundance records to biomass provides modellers with quantifiable data to initialise and validate ecosystem models of lower marine trophic levels

Corrigendum: A database of marine phytoplankton abundance, biomass and species composition in Australian waters (Scientific Data (2016) 3 (160043) DOI: 10.1038/sdata201643))

© The Author(s) 2016. A series of errors in our database were brought to our attention by readers, and have been corrected in an updated version of this database, which is accessible via the AODN at the following link: https://portal.aodn.org.au/search?uuid =75f4f1fc-bee3-4498-ab71-aa1ab29ab2c0 The custodian details of several datasets were incorrect. These fields in the metadata table have been updated to correctly assign P744, P746, P748, and P778 to the Australian Antarctic Division, and P752 to the Royal Belgian Institute of Natural Sciences. Species names and functional group assignments have been changed for a small number of records to fix identified errors. Tripos brevis and Tripos arietinus were spelt incorrectly, and have been duly corrected. Pedinellaceae was wrongly assigned to dinoflagellate as a functional group, and has now been re-assigned to flagellate. The 'Naked flagellate' group has been renamed 'Flagellate' as there is some inconsistency in the use of the term 'Naked flagellate' and what precisely would be included. The functional group 'Other', has also been excluded as this contained data that was not necessarily phytoplankton but had been found in phytoplankton counts. The macroalgae Murrayella australica, Cladophora spp., Chlorohormidium sp., Eudorina spp., Tribonema spp., Chlorohormidium spp. were also removed. In addition to these corrections, three datasets have been extended to include more recently acquired data: P 597 IMOS Australian Continuous Plankton Recorder survey (ongoing dataset, 59089 new records as of 2016-08-31); P599 IMOS National Reference Stations (ongoing dataset, 14669 new records as of 2016-08-31); and P1068 Great Barrier Reef Expedition 1928-29 (new dataset, 1340 new records). Table 1 provides a summary of the overall change in database contents. (Table Presented). This dataset will continue to grow and will be regularly updated with new data and any further corrections to the data. Users can email imos-planktonatcsiro.au with any comments, which will be reviewed and included in future updates if applicable. The AODN portal will always direct the user to the most recent version, the original version will remain available at http://dx.doi.org/10.4225/69/ 56454b2ba2f79, and interim versions will be available on request

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.