Programmable system on chip for controlling an atomic physics experiment.

Most atomic physics experiments are controlled by a digital pattern generator used to synchronize all equipment by providing triggers and clocks. Recently, the availability of well-documented open-source development tools has lifted the barriers to using programmable systems on chip (PSoCs), making them a convenient and versatile tool for synthesizing digital patterns. Here, we take advantage of these advancements in the design of a versatile clock and pattern generator using a PSoC. We present our design with the intent of highlighting the new possibilities that PSoCs have to offer in terms of flexibility. We provide a robust hardware carrier and basic firmware implementation that can be expanded and modified for other uses.

Confinement of an alkaline-earth element in a grating magneto-optical trap.

We demonstrate a compact magneto-optical trap (MOT) of alkaline-earth atoms using a nanofabricated diffraction grating chip. A single input laser beam, resonant with the broad 1S0 → 1P1 transition of strontium, forms the MOT in combination with three diffracted beams from the grating chip and a magnetic field produced by permanent magnets. A differential pumping tube limits the effect of the heated, effusive source on the background pressure in the trapping region. The system has a total volume of around 2.4 l. With our setup, we have trapped up to 5 × 106 88Sr atoms at a temperature of ∼6 mK, and with a trap lifetime of ∼1 s. Our results will aid the effort to miniaturize quantum technologies based on alkaline-earth atoms.

Drug survival is not significantly different between biologics in patients with psoriasis vulgaris: a single-centre database analysis.

BACKGROUND: Drug survival depends on several factors such as dosing, effectiveness, quality-of-life improvement and safety, and could be seen as an overall marker for treatment success. Such data for biologics in psoriasis treatment are sparse. OBJECTIVES: To determine differences in drug survival between different biologics for psoriasis. METHODS: Drug survival, dosing, Psoriasis Area and Severity Index (PASI) and Skindex-29 at weeks 12 and 52, and adverse events of patients with psoriasis treated with a biologic registered in the local database of the Academic Medical Center, Amsterdam, were analysed. Patients were divided into those naive or non-naive for treatment episodes with biologics. RESULTS: Drug survival did not differ significantly for naive treatment episodes between the biologics (etanercept 85% to 64%, adalimumab 77% to 77%, infliximab 75% to 75% for year 1-4), or for non-naive treatment episodes (etanercept 86% to 42%, adalimumab 84% to 56%, infliximab 68% to 43% for year 1-4; ustekinumab 84% to 57% for year 1-3). The naive group showed better drug survival and PASI 75 response at week 12, although the difference was not significant. A similar improvement of mean ∆PASI and mean ∆Skindex-29 was observed at weeks 12 and 52 for all biologics for both groups, although no significant difference was seen between groups. Treatment termination was due mainly to nonresponse for all biologics. CONCLUSIONS: There was no significant difference in drug survival, mean ∆PASI or Skindex-29 response at weeks 12 or 52 between the biologics or between the naive and non-naive groups. Treatment termination was due mostly to nonresponse. Sequential treatment with the available biologics can be effective.

Functional nucleotide excision repair is required for the preferential removal of N-ethylpurines from the transcribed strand of the dihydrofolate reductase gene of Chinese hamster ovary cells.

Transcription-coupled repair of DNA adducts is an essential factor that must be considered when one is elucidating biological endpoints resulting from exposure to genotoxic agents. Alkylating agents comprise one group of chemical compounds which modify DNA by reacting with oxygen and nitrogen atoms in the bases of the double helix. To discern the role of transcription-coupled DNA repair of N-ethylpurines present in discrete genetic domains, Chinese hamster ovary cells were exposed to N-ethyl-N-nitrosourea, and the clearance of the damage from the dihydrofolate reductase gene was investigated. The results indicate that N-ethylpurines were removed from the dihydrofolate reductase gene of nucleotide excision repair-proficient Chinese hamster ovary cells; furthermore, when repair rates in the individual strands were determined, a statistically significant bias in the removal of ethyl-induced, alkali-labile sites was observed, with clearance occurring 30% faster from the transcribed strand than from its nontranscribed counterpart at early times after exposure. In contrast, removal of N-ethylpurines was observed in the dihydrofolate reductase locus in cells that lacked nucleotide excision repair, but both strands were repaired at the same rate, indicating that transcription-coupled clearance of these lesions requires the presence of active nucleotide excision repair.

3-Methyladenine and 7-methylguanine exhibit no preferential removal from the transcribed strand of the dihydrofolate reductase gene in Chinese hamster ovary B11 cells.

The removal of cylclobutane pyrimidine dimers from cellular DNA occurs preferentially in actively transcribed genes of cells subjected to ultraviolet radiation. In contrast, reports concerning the transcription-dependent repair of N-methylpurines formed in cellular DNA following exposure to methylating agents are quite conflicting, with some studies suggesting that no biased clearance of these lesions occurs and others indicating that preferential removal of these adducts transpires in active genetic loci. Even in the cases where no preferential clearance was demonstrated, a slight but statistically insignificant biased removal of N-methylpurines from the transcribed strand of active genes was often evident. We proposed that these results might be due to the preferential clearance of only one of the two principal N-methylpurines formed, 3-methyladenine, or to the source of the methylating species to which the cells were exposed. Therefore, we investigated the clearance of 3-methyladenine and 7-methylguanine as individual lesions from the amplified dihydrofolate reductase gene of Chinese hamster ovary cells, and we examined the gene-specific removal of N-methylpurines formed by several different methylating agents as well. We observed no biased clearance of 3-methyladenine toward the transcribed strand of the locus being examined. This result indicates that any minor gene-specific preferential repair that has been observed previously for N-methylpurines in toto--which actually reflects the removal of the predominant methylated purine 7-methylguanine--is not due to biased clearance of the transcription-inhibiting 3-methyladenine lesion.(ABSTRACT TRUNCATED AT 250 WORDS)