The Extremely Brilliant Source storage ring of the European Synchrotron Radiation Facility.

The Extremely Brilliant Source (EBS) is the experimental implementation of the novel Hybrid Multi Bend Achromat (HMBA) storage ring magnetic lattice concept, which has been realised at European Synchrotron Radiation Facility. We present its successful commissioning and first operation. We highlight the strengths of the HMBA design and compare them to the previous designs, on which most operational synchrotron X-ray sources are based. We report on the EBS storage ring's significantly improved horizontal electron beam emittance and other key beam parameters. EBS extends the reach of synchrotron X-ray science confirming the HMBA concept for future facility upgrades and new constructions.

Few electron limit of n-type metal oxide semiconductor single electron transistors.

We report the electronic transport on n-type silicon single electron transistors (SETs) fabricated in complementary metal oxide semiconductor (CMOS) technology. The n-type metal oxide silicon SETs (n-MOSSETs) are built within a pre-industrial fully depleted silicon on insulator (FDSOI) technology with a silicon thickness down to 10 nm on 200 mm wafers. The nominal channel size of 20 × 20 nm(2) is obtained by employing electron beam lithography for active and gate level patterning. The Coulomb blockade stability diagram is precisely resolved at 4.2 K and it exhibits large addition energies of tens of meV. The confinement of the electrons in the quantum dot has been modeled by using a current spin density functional theory (CS-DFT) method. CMOS technology enables massive production of SETs for ultimate nanoelectronic and quantum variable based devices.

Cardiovascular and survival effects of sympatho-inhibitors in adriamycin-induced cardiomyopathy in rats.

Adriamycin (ADR) is a widely used drug for the treatments of cancers. This study evaluates the effects of moxonidine and metoprolol on cardiac hemodynamics and survival in ADR-induced left ventricular dysfunction (total dose of 20 mg/kg in a 4-week regimen). Rats were treated with the centrally acting I(1)R agonist sympatho-inhibitor, moxonidine, or with the non-selective beta-adrenergic antagonist, metoprolol, during 1 month or until death. Treatments began 1 week after the onset of the ADR administration. Low doses (0.5 and 1 mg/kg/day) of moxonidine and metoprolol (10 mg/kg/day) improved cardiovascular function. High doses of moxonidine (3 mg/kg/day) and metoprolol (150 mg/kg/day) were cardiodepressive. Moxonidine and metoprolol both failed to improve survival. These data indicate that a treatment with these sympatho-inhibitors can reduce the left ventricular dysfunction induced by ADR. Moreover, these cardioprotective effects where obtained even when ADR was used at a dose regimen usually employed for its antineoplastic effects in rodents. Nevertheless, in this particular cardiomyopathy, we did not find any association between improvements of functional parameters and survival whatever the drug and the dose used. This problem points out the difficulty to prevent, at least with sympatho-inhibitory drugs alone, the mortality linked to the chronic cardiotoxicity of ADR.

Effect of i1 imidazoline receptor agonist, moxonidine, in nitric oxide-deficient hypertension in pregnant rats.

Decreased nitric oxide production has been reported in preeclampsia, which is also frequently associated with glucose intolerance. It was thus considered of interest to investigate the effects of moxonidine, a centrally acting antihypertensive drug that reduces insulin resistance, in a rat model of preeclampsia. Hypertension was induced in Wistar rats by dietary l-NNA (N(omega)-nitro-L-arginine, 0.063%, 31 mg/kg/d, days 13-19 of gestation) and, over the same period, moxonidine or vehicle was administered orally (2 mg/kg/d by gavage). On day 20, blood pressure was measured in the pentobarbital anesthetized animals, glucose tolerance was tested (2 g/kg glucose i.p.), and morphologic studies were conducted on the litter to determine the benefits with respect to fetal outcome. Hypertension was reduced with daily moxonidine treatment (P < 0.05). Basal plasma insulin and insulin/glucose index were decreased with moxonidine treatment evidencing improved insulin sensitivity in the control and l-NNA-treated pregnant rats (P < 0.05). After glucose challenge, plasma insulin increased in all the groups as expected and plasma insulin and insulin/glucose index were significantly higher in the l-NNA group than in the control, moxonidine, or l-NNA + moxonidine groups (P < 0.05 for time 60 minutes). Thus, moxonidine improved glucose tolerance in l-NNA-treated pregnant rats. Moreover, moxonidine treatment very effectively decreased the number of necroses (1 necrosis in 71 fetuses in the l-NNA + moxonidine group versus 15 necroses in 79 fetuses in the l-NNA group, P < 0.01). In conclusion, the 7-day treatment with moxonidine suppressed hypertension and reduced glucose intolerance and fetal necrosis, thus demonstrating the effectiveness of moxonidine in the preeclamptic model.

Purification of two Bacillus subtilis proteins which cross-react with antibodies directed against eukaryotic protein kinase C, the His HPr kinase and trigger factor.

As in eukaryotes, phosphorylation of Ser residues in proteins appears to be common phenomenon in bacteria. Surprisingly, however, very few Ser/Thr protein kinases have been identified and in this study antibodies directed against mammalian protein kinase C (PKC) have been used in attempts to isolate conserved Ser/Thr protein kinases. Using the mAb M7 against rat brain PKC, a single 70 kDa band was identified in total cell extracts of Bacillus subtilis by Western blotting after SDS-PAGE, whilst using polyclonal antibody alpha-PKC1p against Saccharomyces cerevisiae PKC a single 67 kDa band was identified by the same procedure. The two proteins were purified independently on the basis of antibody recognition employing two-dimensional gel electrophoresis as a final step, which allowed subsequent microsequencing. The 70 kDa band was thus identified as the phosphoenolpyruvate-dependent His HPr kinase, Enzyme 1 of the phosphotransferase system. This identity was confirmed using a mutant deleted for ptsl, encoding Enzyme 1. The 67 kDa protein was identified as a previously unknown B. subtilis 'trigger factor', homologous to an Escherichia coli protein-folding enzyme, peptidylprolyl cis-trans-isomerase implicated in cell division.