Dichloridobis(di-tert-butylmethylphosphine oxide-[kappa]O)diphenyltin(IV)

The complete molecule of the title compound, [Sn(C6H5)2Cl2(C9H21OP)2], is generated by crystallographic inversion symmetry, the Sn atom is located on a special position of site symmetry \overline{1}. The Sn atom adopts an all-trans SnC2O2Cl2 octahedral geometry. As a consequence of the bulky substituents at the O atom, the P-O-Sn bond angle is 163.9 (3)°. Key indicators: single-crystal X-ray study; T = 173 K; mean σ(C–C) = 0.012 Å; R factor = 0.058; wR factor = 0.099; data-to-parameter ratio = 18.6

[my]-Hydroxido-bis[(2,20-bipyridine)-tricarbonylrhenium(I)] perrhenate

The title compound, [Re2(OH)(C10H8N2)2(CO)6][ReO4], is a mixed-valence rhenium compound containing discrete anions and cations. The ReI atoms are in a slightly distorted octahedral environment, whereas the ReVII atoms show the typical tetrahedral coordination mode. The dihedral angle between the two bipyridine groups is 34.3 (7)°. Key indicators: single-crystal X-ray study; T = 173 K; mean σ(C–C) = 0.044 Å; R factor = 0.093; wR factor = 0.262; data-to-parameter ratio = 13.9

Metallicity evolution of AGNs from UV emission-lines based on a new index

We analyzed the evolution of the metallicity of the gas with the redshift for a sample of AGNs in a very wide redshift range (0<z<4) using ultraviolet emission-lines from the narrow-line regions (NLRs) and photoionization models. The new index C43=log(CIV+CIII])/HeII is suggested as a metallicity indicator for AGNs. Based on this indicator, we confirmed the no metallicity evolution of NLRs with the redshift pointed out by previous works. We found that metallicity of AGNs shows similar evolution than the one predicted by cosmic semi-analytic models of galaxy formation set within the Cold Dark Matter merging hierarchy (for z < 3). Our results predict a mean metallicity for local objects in agreement with the solar value (12+log(O/H)=8.69). This value is about the same that the maximum oxygen abundance value derived for the central parts of local spiral galaxies. Very low metallicity log(Z/Z_{\odot})~ -0.8 for some objects in the range 1.5 < z <3 is derived.Comment: 25 pages, 10 figures, accepted MNRA

ELUSIDASI SENYAWA ANTIDIABETES DARI KULIT AKAR TUMBUHAN KULU (ARTOCARPUS CAMANSI)

ABSTRACTAntidiabetic testing of the crude extract of n-hexane, the fraction groups A, B, C, D and C43 isolates from kulu root bark (Artocarpus camansi) have been performed. The greatest result of the power of reducing blood glucose was group of fraction A, at minute 60, followed by crude extract of n-hexane, group of fraction B, group of fraction C, group of fraction D and isolate C43. While group of isolate C43, the greatest ability to lower blood glucose in the 30th minute, but in the 90th minute raised blood glucose mice. Group A fraction at minute 120, had higher mean glucose level and significantly different than positive control with 95% confidence level (

Tetra­butyl­ammonium tris­(methyl­sulfanylmeth­yl)phenyl­borate

In the title molecular salt, C16H36N+·C12H20BS3-, three of the four n-butyl chains show a trans conformation, whereas the fourth has the C—C—C—C torsion angle in a gauche conformation [-77.8 (5)°]. In the crystal, mol­ecules are packed in layers parallel to the (101) plane

The Formyl Peptide Receptor 2 Regulates Microglial Phenotype Through Immunometabolism: Implications for Alzheimer’s Disease

Microglia are key players in the pathology of Alzheimer’s disease (AD), driving chronic inflammation, oxidative stress, and the altered metabolism seen in the brains of patients. With clinical trials continuing to fail, new approaches towards drug development are critical. Strategies to reduce microglial activation may therefore be a viable therapeutic approach to tackling AD. Formyl peptide receptor 2 (Fpr2), which drives peripheral inflammatory resolution, is expressed in microglia. However, its functional role in neuroinflammation is unclear. This thesis provides evidence to support the peripheral findings of Fpr2 stimulation, wherein it may also hold promise for exploitation as a therapeutic for neurodegenerative disorders, including AD. We also highlight novel findings surrounding the modulation of both oxidative stress and microglial metabolism associated with Fpr2 activation. Under inflammatory conditions, we report that selective agonists for Fpr2 modulate the microglial inflammatory response, actively shifting from a pro-inflammatory to a pro-resolving phenotype, emphasised by the reduction of pro-inflammatory cytokines and concomitant increases in both pro-resolving cytokines and phagocytosis. Metabolic shifting away from glycolysis was also observed for pro-resolving microglia. Moreover, we describe for the first time that Fpr2 completely reverses reactive oxygen species (ROS) production from the mitochondria and NADPH oxidase enzymes following an inflammatory stimulus. We also highlight that the toxic oligomeric amyloid (oAβ) facilitates microglial ROS production and subsequent metabolic changes without triggering an inflammatory response. oAβ facilitated NADPH oxidase activation, which in turn resulted in the activation of glucose 6-phosphate dehydrogenase (G6PD), the rate limiting step for the pentose phosphate pathway. This metabolic pathway is responsible for producing NADPH, which in turn NADPH oxidases exploit for further ROS production. These changes resulted in noticeable reductions in both microglial glycolysis and oxidative phosphorylation. We present data underlining that Fpr2/3 stimulation reverses oAβ-induced ROS production, with a resultant reduction in G6PD activity and the return of homeostatic glycolysis. These oAβ-induced microglial changes triggered the apoptosis of SH-SY5Y cells in co-culture with BV-2 microglia. However, supporting our interest in Fpr2/3 for therapeutic approaches to neurodegenerative diseases, post-treatment with a select agonist for the receptor successfully prevented apoptosis of these neuronal like SH-SY5Y cells. This original data unveils novel functions of Fpr2/3 in the central nervous system (CNS), supplementing the well-established pro-resolving functions the receptor facilitates within the periphery. The combination of pro-resolving, anti-oxidative, immunometabolic and anti-apoptotic functions of Fpr2/3 support the exploitation of this receptor for therapeutic research into multiple different CNS disorders, including AD

[my]-Bis(diphenylphosphanyl)borato-[kappa]2P:P'-bis[dicarbonyl([eta]5-cyclopentadienyl)iron(II)] tetrachloridoferrate(III) chloroform solvate

The title compound, [Fe2(C5H5)2(C24H22BP2)(CO)4][FeCl4]·CHCl3, is an oxidation product of CpFe(CO)2PPh2BH3. One pair of phenyl rings attached to the two different P atoms are almost parallel, as are the other pair [dihedral angles = 8.7 (5) and 8.9 (5)°]. The planes of the two cyclopentadienyl rings are inclined by 26.8 (7)° with respect to each other. The carbonyl groups at each Fe atom are almost perpendicular [C-Fe-C = 92.6 (6) and 94.3 (5)°]. Key indicators: single-crystal X-ray study; T = 173 K; mean &#963;(C–C) = 0.019 Å; R factor = 0.112; wR factor = 0.177; data-to-parameter ratio = 16.8