Diacetonitrile[N,N′-bis(2,6-diisopropyl-phenyl)ethane-1,2-diimine] dichloridochromium(II) acetonitrile solvate

The title compound, [CrCl2(CH3CN)2(C 26H36N2)]·CH3CN, was synthesized by the reaction of CrCl2(THF)2 with N,N′-bis-(2,6- diisopropyl-phen-yl)ethane-1,2-diimine in dichloro-methane/acetonitrile. The chromium center is coordinated by two N atoms of the chelating diimine ligand, two chloride ions in a trans configuration with respect to each other, and by two N atoms of two acetonitrile mol-ecules in a distorted octa-hedral geometry

Trans-Di-μ-acetato-[μ-N,N-bis-(diphenyl-phosphino)aniline] bis-[chlorido-molybdenum(II)](Mo - Mo)-dichloro-methane-tetra-hydro-furan (1/0.3/1.7)

The mol-ecular structure of the title compound, [Mo2(CH 3COO)2Cl2(C30H25NP 2)]·0.3CH2Cl2·1.7C 4H8O, features an Mo - Mo dumbbell bridged by two acetate groups which are trans to each other. Perpendicular to the plane spanned by the acetate groups, the Ph2PN(Ph)PPh2 ligand bridges both Mo atoms, having a P - N - P angle of 114.09 (19)°. In a trans position to the PNP ligand are two Cl atoms, one on each molybdenum centre. The Mo - Mo bond distance is 2.1161 (9) Å, within the range known for Mo - Mo quadruple bonds. The Mo complex is located on a crystallographic twofold rotation axis which runs through the N - C bond of the ligand. The site occupation factors of the disordered solvent molecules were fixed to 0.15 for dichloromethane and 0.85 for tetrahydrofuran. © 2009

[2,2-Bis(diphenylphosphanyl)propane κ2P,P0] tetracarbonylchromium(0)dichloromethane monosolvate

The title compound, [Cr(C27H26P2)(CO) 4]·CH2Cl2, was obtained by the reaction of Ph2PCMe2PPh2 with Cr(CO)6 in refluxing toluene by substitution of two carbonyl ligands. The CrC 4P2 coordination geometry at the Cr atom is distorted octa-hedral, with a P - Cr - P bite angle of 70.27 (2)°

[N,N-Bis(diphenyl­phosphino)isopropyl­amine]dibromidonickel(II)

The title compound, [NiBr2(C27H27NP2)], was synthesized by the reaction of NiBr2(dme) (dme is 1,2-dimethoxy-ethane) with N,N-bis-(diphenyl-phosphino)isopropyl-amine in methanol/tetra-hydro-furan. The nickel(II) center is coordinated by two P atoms of the chelating PNP ligand, PH2PN(iPr)PPH2, and two bromide ions in a distorted square-planar geometry

Ectopic Expression of Neurogenin 2 Alone is Sufficient to Induce Differentiation of Embryonic Stem Cells into Mature Neurons

Recent studies show that combinations of defined key developmental transcription factors (TFs) can reprogram somatic cells to pluripotency or induce cell conversion of one somatic cell type to another. However, it is not clear if single genes can define a cell̀s identity and if the cell fate defining potential of TFs is also operative in pluripotent stem cells in vitro. Here, we show that ectopic expression of the neural TF Neurogenin2 (Ngn2) is sufficient to induce rapid and efficient differentiation of embryonic stem cells (ESCs) into mature glutamatergic neurons. Ngn2-induced neuronal differentiation did not require any additional external or internal factors and occurred even under pluripotency-promoting conditions. Differentiated cells displayed neuron-specific morphology, protein expression, and functional features, most importantly the generation of action potentials and contacts with hippocampal neurons. Gene expression analyses revealed that Ngn2-induced in vitro differentiation partially resembled neurogenesis in vivo, as it included specific activation of Ngn2 target genes and interaction partners. These findings demonstrate that a single gene is sufficient to determine cell fate decisions of uncommitted stem cells thus giving insights into the role of key developmental genes during lineage commitment. Furthermore, we present a promising tool to improve directed differentiation strategies for applications in both stem cell research and regenerative medicine

A Systematic Proteomic Study of Irradiated DNA Repair Deficient Nbn-Mice

BACKGROUND: The NBN gene codes for the protein nibrin, which is involved in the detection and repair of DNA double strand breaks (DSBs). The NBN gene is essential in mammals. METHODOLOGY/PRINCIPAL FINDINGS: We have used a conditional null mutant mouse model in a proteomics approach to identify proteins with modified expression levels after 4 Gy ionizing irradiation in the absence of nibrin in vivo. Altogether, amongst approximately 8,000 resolved proteins, 209 were differentially expressed in homozygous null mutant mice in comparison to control animals. One group of proteins significantly altered in null mutant mice were those involved in oxidative stress and cellular redox homeostasis (p<0.0001). In substantiation of this finding, analysis of Nbn null mutant fibroblasts indicated an increased production of reactive oxygen species following induction of DSBs. CONCLUSIONS/SIGNIFICANCE: In humans, biallelic hypomorphic mutations in NBN lead to Nijmegen breakage syndrome (NBS), an autosomal recessive genetic disease characterised by extreme radiosensitivity coupled with growth retardation, immunoinsufficiency and a very high risk of malignancy. This particularly high cancer risk in NBS may be attributable to the compound effect of a DSB repair defect and oxidative stress

Short-term triple therapy with azithromycin for Helicobacter pylori eradication: Low cost, high compliance, but low efficacy

<p>Abstract</p> <p>Background</p> <p>The Brazilian consensus recommends a short-term treatment course with clarithromycin, amoxicillin and proton-pump inhibitor for the eradication of <it>Helicobacter pylori </it>(<it>H. pylori)</it>. This treatment course has good efficacy, but cannot be afforded by a large part of the population. Azithromycin, amoxicillin and omeprazole are subsidized, for several aims, by the Brazilian federal government. Therefore, a short-term treatment course that uses these drugs is a low-cost one, but its efficacy regarding the bacterium eradication is yet to be demonstrated. The study's purpose was to verify the efficacy of <it>H. pylori </it>eradication in infected patients who presented peptic ulcer disease, using the association of azithromycin, amoxicillin and omeprazole.</p> <p>Methods</p> <p>Sixty patients with peptic ulcer diagnosed by upper digestive endoscopy and <it>H. pylori </it>infection documented by rapid urease test, histological analysis and urea breath test were treated for six days with a combination of azithromycin 500 mg and omeprazole 20 mg, in a single daily dose, associated with amoxicillin 500 mg 3 times a day. The eradication control was carried out 12 weeks after the treatment by means of the same diagnostic tests. The eradication rates were calculated with 95% confidence interval.</p> <p>Results</p> <p>The eradication rate was 38% per intention to treat and 41% per protocol. Few adverse effects were observed and treatment compliance was high.</p> <p>Conclusion</p> <p>Despite its low cost and high compliance, the low eradication rate does not allow the recommendation of the triple therapy with azithromycin as an adequate treatment for <it>H. pylori </it>infection.</p

Boosting scientific publications in Africa: which IPRs protection channels matter?

This paper examines how Africa’s share in the contribution to global scientific knowledge can be boosted with existing Intellectual Property Rights (IPRs) mechanisms. The findings which broadly indicate that tight IPRs are correlated with knowledge contribution can be summarized in two main points. First, the enshrinement of IPRs laws in a country’s Constitution is a good condition for knowledge economy. Secondly, while Main IP laws, WIPO treaties and Bilateral treaties are positively correlated with scientific publications, the IPRs law channel have a negative correlation. Whereas the study remains expositional, it does however offer interesting insights into the need for IPRs in the promotion of knowledge contribution within sampled countries of the continent. Other policy implications are discussed