Photonic crystal resonators for inverse-designed multi-dimensional optical interconnects.

We experimentally demonstrate a 400 Gbit/s optical communication link utilizing wavelength-division multiplexing and mode-division multiplexing for a total of 40 channels. This link utilizes a novel, to the best of our knowledge, 400 GHz frequency comb source based on a chip-scale photonic crystal resonator. Silicon-on-insulator photonic inverse-designed 4 × 4 mode-division multiplexer structures enable a fourfold increase in data capacity. We show less than -10 dBm of optical receiver power for error-free data transmission in 34 out of a total of 40 channels using a PRBS31 pattern.

Comparison of media and culture techniques for detection of Streptococcus pneumoniae in respiratory secretions.

We compared the relative efficacy of three methods for the isolation of Streptococcus pneumoniae in lower respiratory secretions. Based on results from 294 clinical specimens, we found that S. pneumoniae was isolated at a frequency of 65% with 5% sheep blood agar or 5% sheep blood agar containing 5 micrograms of gentamicin per ml, both incubated in 5% CO2. Anaerobic incubation of 5% sheep blood agar enhanced the recovery rate of S. pneumoniae to 93%. The improved efficacy with anaerobic incubation is due to the greater ease of recognition of the larger and more mucoid colonies of S. pneumoniae, and to the suppression of the growth of other oral bacteria present in the respiratory sections.

Long-term persistence of defective HSV-1 vectors in the rat brain is demonstrated by reactivation of vector gene expression.

Wild-type HSV-1 is known to persist indefinitely in neurons in the latent state; however, defective HSV-1 vectors, or amplicons, contain only approximately 1% of the HSV-1 genome and persistence of these HSV-1 vectors has not been studied even semiquantitatively in the adult rat brain. Defective HSV-1 vectors contain both an HSV-1 origin of replication and a packaging site, and in the presence of helper virus can undergo DNA replication and packaging into HSV-1 particles. Our prototype defective HSV-1 vector, pHSVlac, uses the HSV-1 immediate-early (IE) promoter to regulate expression of the Escherichia coli lacZ gene. Using cultured neuronal cells, we have previously shown that expression from pHSVlac can be augmented by superinfection with a helper virus. In this study, pHSVlac was delivered into the adult rat striatum or hippocampus, and 2-3 months after gene transfer we utilized superinfection with several replication-incompetent HSV-1 mutants to reactivate expression from pHSVlac in approximately 30% of the number of cells observed at 4 days after gene transfer. Thus, HSV-1 plasmid vectors can persist for at least 2-3 months in at least approximately 30% of the cells which are initially infected.

Modulation of rat rotational behavior by direct gene transfer of constitutively active protein kinase C into nigrostriatal neurons.

The modulation of motor behavior by protein kinase C (PKC) signaling pathways in nigrostriatal neurons was examined by using a genetic intervention approach. Herpes simplex virus type 1 (HSV-1) vectors that encode a catalytic domain of rat PKCbetaII (PkcDelta) were developed. PkcDelta exhibited a constitutively active protein kinase activity with a substrate specificity similar to that of rat brain PKC. As demonstrated in cultured sympathetic neurons, PkcDelta caused a long-lasting, activation-dependent increase in neurotransmitter release. In the rat brain, microinjection of HSV-1 vectors that contain the tyrosine hydroxylase promoter targeted expression to dopaminergic nigrostriatal neurons. Expression of pkcDelta in a small percentage of nigrostriatal neurons (approximately 0.1-2%) was sufficient to produce a long-term (>/=1 month) change in apomorphine-induced rotational behavior. Nigrostriatal neurons were the only catecholaminergic neurons that contained PkcDelta, and the amount of rotational behavior was correlated with the number of affected nigrostriatal neurons. The change in apomorphine-induced rotational behavior was blocked by a dopamine receptor antagonist (fluphenazine). D2-like dopamine receptor density was increased in those regions of the striatum innervated by the affected nigrostriatal neurons. Therefore, this strategy enabled the demonstration that a PKC pathway or PKC pathways in nigrostriatal neurons modulate apomorphine-induced rotational behavior, and altered dopaminergic transmission from nigrostriatal neurons appears to be the affected neuronal physiology responsible for the change in rotational behavior.