Eco-friendly and low-cost amidoxime-functionalized microcrystalline cellulose/mesoporous silica composite for the selective adsorption of U(VI) from aqueous solution

Journal of Radioanalytical and Nuclear Chemistry - Eco-friendly and low-cost composite, amidoxime-functionalized microcrystalline cellulose/mesoporous silica (MCC/MS-AO), were synthesized by...     

Formation of highly substituted chiral cyclohexanone derivatives using a tandem conjugate addition/cyclisation

A tandem conjugate addition/cyclisation approach, that allows the synthesis of chiral highly substituted cyclohexanones and cyclohexenones, which is applicable to natural product syntheses has been developed.     

THE PHOTOTOXICITY OF 2,5-DIPHENYLOXAZOLE (POP) AND 1,4-BIS(5-PHENYLOXAZOL-2-YL)BENZENE (POPOP)

Abstract 2,5-Diphenyloxazole (POP) is widely used for the determination of radioactivity by scintillation counting. It has been found to be phototoxic to the yeasts Saccharomyces cerevisiae and Candida utilis , to the first instar larvae of the mosquito Aedes aegypti , to the crustaceans Daphnia magna and Artemia salida , as well as to the eggs of Drosophila melanogaster . The related molecule 1,4-bis(5-phenyloxazol-2-yl)benzene (POPOP) is also phototoxic, but to a lesser degree. Both POP and POPOP can sensitize the formation of singlet oxygen.     

Synthesis of μ-hydrido-μ-phosphido heterotrimetal alkylidyne clusters: X-ray crystal structure of [Co2W(μ-H)(μ3-CMe)(μ-PPh2)(CO)6(η-C5H5]

Treatment of the μ-alkylidyne clusters [Fe₂W(μ₃-CC₆H₄Me-4)(μ-CO)- (CO)₈(η-C₅H₅)] and [Co₂W(μ₃-CMe)(CO)₈(η-C₅H₅)] with PPh₂H affords a series of new μ-phosphido-μ-hydrido alkylidyne complexes which undergo protonation with HBF₄·Et₂O to give cationic derivatives. The X-ray structure of [Co₂W(μ-H)(μ₃-CMe)(μ-PPh₂)(CO)₆(η-C₅H₅)] has been determined.     

THE EFFECTS OF THROMBOXANE INHIBITORS ON THE MICROVASCULAR AND TUMOR RESPONSE TO PHOTODYNAMIC THERAPY

Abstract— Vascular stasis and tissue ischemia are known to cause tumor cell death in several experimental models after photodynamic therapy (PDT); however, the mechanisms leading to this damage remain unclear. Because previous studies indicated that thromboxane release is implicated in vessel damage, we further examined the role of throm-boxane in PDT. Rats bearing chondrosarcoma were injected with 25 mg/kg Photofrin® (intravenously) 24 h before treatment. Light (135 J/cm ² , 630 nm) was delivered to thc tumor area after injection of one of the following inhibitors: (1) R68070: a thromboxane synthetase inhibitor; (2) SQ-29548: a thromboxane receptor antagonist; and (3) Flunarizine: an inhibitor of platelet shape change. Systemic thromboxane levels were determined. Vessel constriction and leakage were evaluated by intravital microscopy. Tumor response was assessed after treatment. Thromboxane levels were decreased more than 50% with SQ-29548 as compared to controls. Thromboxane levels in animals given R68070 and Flunarizine remained at baseline levels. SQ-29548 and R68070 reduced vessel constriction compared to controls, while Flunarizine totally prevented vessel constriction. R68070 and SQ-29548 inhibited vessel permeability compared to PDT controls; Flunarizine did not. Animals given these inhibitors showed markedly reduced tumor cure. These results indicate that the release of thromboxane is linked to the vascular response in PDT.     

High yield synthesis and reactivity of a phosphinidene bridged dimolybdenum complex

Protonation of [Mo2Cp2(mu-H)(mu-PHR*)(CO)4] (Cp = eta5-C5H5, R* = 2,4,6-C6H2tBu3) with HBF4.OEt2 gives the hydridophosphinidene complex [Mo2Cp2(mu-H)(mu-PR*)(CO)4]BF4, which is easily deprotonated with H2O to give the known phosphinidene complex [Mo2Cp2(mu-PR*)(CO)4] in 95% yield. Reaction of the latter with I2 gives the unsaturated phosphinidene complex [Mo2Cp2I2(mu-PR*)(CO)2], which exhibits an intermetallic distance of 2.960(2) A. Irradiation of solutions of [Mo2Cp2(mu-PR*)(CO)4] with UV light gives a mixture of the triply bonded [Mo2Cp2(mu-PR*)(mu-CO)2] and the hydridophosphido derivative [Mo2Cp2(mu-H){mu-P(CH2CMe2)C6H2tBu2}(CO)4] as major species. The latter complex results from an intramolecular C-H bond cleavage from a tBu group and has been characterized by spectroscopy and an X-ray study. Irradiation in the presence of HCC(p-tol) results in the insertion of the alkyne into the Mo-P bond to give [Mo2Cp2{mu-eta1:eta2,kappa-C(p-tol)CHPR*}(CO)4] structurally characterized through an X-ray study.     

PHOTODYNAMIC THERAPY INDUCED ULTRASTRUCTURAL ALTERATIONS IN MICROVASCULATURE OF THE RAT CREMASTER MUSCLE

Abstract— Photodynamic therapy disrupts blood flow to tumors and produces tumor necrosis. These effects may be due to a localized generation of singlet oxygen. The current studies used direct observations of the rat cremaster microvasculature to examine the vascular effects of PDT. The objective of the morphological examination was to delineate the structural basis for the altered blood flow in photodynamic therapy. Dihematoporphyrin ether given 30 min or 48 h prior to the experiment was activated with green light (wavelength530–560 nm, 120 J/cm²). After the in vivo activation the tissues were prepared for electron microscopy. Light alone induced little or no change in the luminal content or vessel wall. On exposure to activating light both acute (30 min) and long term (48 h) dihematoporphyrin ether pretreated samples displayed formation of luminal aggregates, granulocyte margination and migration, and endothelial cell and smooth muscle cell damage. The latter was more pronounced in the arterioles than the venules. Perivascular changes included interstitial edema and damage to striated myocytes. Some of the alterations such as interstitial edema may be transient; however, smooth and skeletal muscle cell injury are important in normal and tumor tissue necrosis after photodynamic therapy.