ABSTRACT
Reaction of 2,2'-bipyridine (bpy) with dinuclear complexes [RuCl(dfppe)(µ-Cl)3Ru(dmso-S)3] (dfppe = 1,2-bis(dipentafluorophenyl phosphino)ethane (C6F5)2PCH2CH2P(C6F5)2; dmso = dimethyl sulfoxide) (1) or [RuCl(dfppe)(µ-Cl)3RuCl(dfppe)] (2) affords the mononuclear species trans-[RuCl2(bpy)(dfppe)] (3). Using this precursor complex (3), a series of new cationic Ru(II) electrophilic complexes [RuCl(L)(bpy)(dfppe)][Z] (L = P(OMe)3 (5), PMe3 (6), CH3CN (7), CO (8), H2O (9); Z = OTf (5, 6, 7, 8), BAr(F)4 (9) have been synthesized via abstraction of chloride by AgOTf or NaBAr(F)4 in the presence of L. Complexes 5 and 6 were converted into the corresponding isomeric hydride derivatives [RuH(PMe3)(bpy)(dfppe)][OTf] (10a, 10b) and [RuH(P(OMe)3)(bpy)(dfppe)][OTf] (11a, 11b) respectively, when treated with NaBH4. Protonation of the cationic monohydride complex (11a) with HOTf at low temperatures resulted in H2 evolution accompanied by the formation of either solvent or triflate bound six coordinated species [Ru(S)(P(OMe)3)(bpy)(dfppe)][OTf]n [(S = solvent (n = 2), triflate (n = 1)] (13a/13b); these species have not been isolated and could not be established with certainty. They (13a/13b) were not isolated, instead the six-coordinated isomeric aqua complexes cis-[Ru(bpy)(dfppe)(OH2)(P(OMe)3)][OTf]2 (14a/14b) were isolated. Reaction of the aqua complexes (14a/14b) with 1 atm of H2 at room temperature in acetone-d6 solvent resulted in heterolytic cleavage of the H-H bond. Results of the studies on H2 lability and heterolytic activation using these complexes are discussed. The complexes 3, 5, 11a, and 14a have been structurally characterized.
Subject(s)
Deuterium/chemistry , Deuterium/metabolism , Ruthenium/chemistry , Ruthenium/metabolism , Crystallography, X-RayABSTRACT
Cortical sinovenous thrombosis in a child with nephrotic syndrome and iron deficiency anaemia is described. The most probable mechanism for the hypercoagulable state was thrombocytosis associated with iron deficiency anaemia. The other possible contributing factor might have been the diuretic therapy during the phase of relapse.
Subject(s)
Anemia, Iron-Deficiency/complications , Intracranial Thrombosis/etiology , Nephrotic Syndrome/complications , Venous Thrombosis/etiology , Child, Preschool , Cranial Sinuses , Humans , Intracranial Thrombosis/diagnostic imaging , Male , Tomography, X-Ray Computed , Venous Thrombosis/diagnostic imagingSubject(s)
Athetosis/etiology , Brain Diseases/etiology , Calcinosis/etiology , Chorea/etiology , Hypoparathyroidism/complications , Kinesthesis , Adult , Athetosis/diagnosis , Athetosis/physiopathology , Brain Diseases/diagnosis , Brain Diseases/physiopathology , Calcinosis/diagnosis , Calcinosis/physiopathology , Chorea/diagnosis , Chorea/physiopathology , Diagnosis, Differential , Female , Humans , Hypoparathyroidism/diagnosis , Hypoparathyroidism/physiopathology , Kinesthesis/physiologyABSTRACT
A case of cerebral infarction after viper bite is described; the patient also had features of diffuse encephalopathy. Findings on MRI were suggestive of subacute hemorrhagic infarcts. Possible mechanisms for cerebral infarction in these circumstances were discussed. The mechanism of cerebral infarction in this case seemed to be vasospasm due to the action of the toxin, hemorrhagin, present in the venom.
