Über Bildung und Reaktionen der CH2Li‐Derivate von tBu2P–P=P(CH3)tBu2 und (Me3Si)tBuP–P=P(CH3)tBu2

Formation and Reactions of the CH₂Li‐Derivatives of ^tBu₂P–P=P(CH₃)^tBu₂ and (Me₃Si)^tBuP–P=P(CH₃)^tBu₂ With ⁿBuLi, (Me₃Si)^tBuP–P=P(CH₃)^tBu₂ ( 1 ) and ^tBu₂P–P=P(CH₃)^tBu₂ ( 2 ) yield (Me₃Si)^tBuP–P=P(CH₂Li)^tBu₂ ( 3 ) and ^tBu₂P–P=P(CH₂Li)^tBu₂ ( 4 ), wich react with Me₃SiCl to give (Me₃Si)^tBuP–P=P(CH₂–SiMe₃)^tBu₂ ( 5 ) and ^tBu₂P–P=P(CH₂–SiMe₃)^tBu₂ ( 6 ), respectively. With ^tBu₂P–P(SiMe₃)–P^tBuCl ( 7 ), compound 3 forms 5 as well as the cyclic products [H₂C–P(^tBu)₂=P–P(^tBu)–P^tBu] ( 8 ) and [H₂C–P(^tBu)₂=P–P(P^tBu₂)–P(^tBu)] ( 9 ). Also 3 forms 8 with ^tBuPCl₂. The cleavage of the Me₃Si–P‐bond in 1 by means of C₂Cl₆ or N‐bromo‐succinimide yields (Cl)^tBuP–P=P(CH₃)^tBu₂ ( 10 ) or (Br)^tBuP–P=P(CH₃)^tBu₂ ( 11 ), resp. With LiP(SiMe₃)₂, 10 forms (Me₃Si)₂P–P(^tBu)–P=P(CH₃)^tBu₂ ( 12 ), and Et₂P–P(^tBu)–P=P(CH₃)^tBu₂ ( 13 ) with LiPEt₂. All compounds are characterized by ³¹P NMR Data and mass spectra; the ylide 5 and the THF adduct of 4 additionally by X‐ray structure analyses.     

Serial MR imaging of intracranial metastases after radiosurgery

Purpose: To evaluate the spatiotemporal evolution of radiosurgical induced changes both in metastases and in normal brain tissue adjacent to the lesions by serial magnetic resonance (MR) imaging. Methods and Materials: Thirty-five intracranial metastases of different primaries were treated in 25 patients by single high-dose radiosurgery. MR images acquired before radiosurgery were available in all patients. Sixty-three follow-up MR studies were performed in these patients including T₂- and contrast-enhanced T₁-weighted MR images. The average follow-up time was 9 ± 5 months (mean ± standard deviation [SD]). Based on contrast-enhanced T₁-weighted MR images, tumor response was radiologically classified in the following four groups: stable disease was assumed if the average tumor diameter after treatment did not show a tumor shrinkage of more than 50% and an increase of more than 25%, partial remission as a shrinkage of tumor size of more than 50%, a disappearance of contrast-enhancing tumor as a complete remission, and an increase of tumor diameter of more than 25% as tumor progress. Moreover, we analysed signal changes on T₂-weighted images in brain parenchyma adjacent to the enhancing metastases. Results: The overall mean survival time was 10.5 ± 7 months, with a 1-year actuarial survival rate of 40%. Stable disease, partial or complete remission of the metastatic tumor was observed in 22 patients (88%). Central or homogeneous loss of contrast enhancement appeared to be a good prognostic sign for stable disease or partial remission. This association was statistically significant (p < 0.05). Three patients (12%) suffered from tumor progression. In eight patients (32%) with stable disease or partial remission, signal changes on T₂-weighted images were observed in tissue adjacent to the contrast enhancing lesions. A progression of the high signal on T₂-weighted images was seen in seven of the eight patients between 3 and 6 months after therapy, followed by a signal regression 6–18 months after irradiation. Conclusion: MR imaging is a sensitive imaging tool to evaluate tumor response as well as the presence or absence of adjacent parenchymal changes following radiosurgery. Loss of homogeneous or central contrast enhancement on Gd-enhanced MR images appeared to be a good prognostic sign for tumor response. Tumor shrinkage seems not to be dependent on time. In addition, most cases of radiation induced changes in normal brain parenchyma observed on T₂-weighted images seem to be self limited.     

Zum Einfluß der PR3‐Liganden auf Bildung und Eigenschaften der Phosphinophosphiniden‐Komplexe [{η2‐tBu2P–P}Pt(PR3)2] und [{η2‐tBu2P1–P2}Pt(P3R3)(P4R′3)]

Coordination Chemistry of P‐rich Phosphanes and Silylphosphanes XXI The Influence of the PR₃ Ligands on Formation and Properties of the Phosphinophosphinidene Complexes [{η²‐^tBu₂P–P}Pt(PR₃)₂] and [{η²‐^tBu₂P¹–P²}Pt(P³R₃)(P⁴R′₃)] (R₃P)₂PtCl₂ and C₂H₄ yield the compounds [{η²‐C₂H₄}Pt(PR₃)₂] (PR₃ = PMe₃, PEt₃, PPhEt₂, PPh₂Et, PPh₂Me, PPh₂ⁱPr, PPh₂^tBu and P(p‐Tol)₃); which react with ^tBu₂P–P=PMe^tBu₂ to give the phosphinophosphinidene complexes [{η²‐^tBu₂P–P}Pt(PMe₃)₂], [{η²‐^tBu₂P–P}Pt(PEt₃)₂], [{η²‐^tBu₂P–P}Pt(PPhEt₂)₂], [{η²‐^tBu₂P–P}Pt(PPh₂Et)₂], [{η²‐^tBu₂P–P}Pt(PPh₂Me)₂], [{η²‐^tBu₂P–P}Pt(PPh₂ⁱPr], [{η²‐^tBu₂P–P}Pt(PPh₂^tBu)₂] and [{η²‐^tBu₂P–P}Pt(P(p‐Tol)₃)₂]. [{η²‐^tBu₂P–P}Pt(PPh₃)₂] reacts with PMe₃ and PEt₃ as well as with ^tBu₂PMe, PⁱPr₃ and P(c‐Hex)₃ by substituting one PPh₃ ligand to give [{η²‐^tBu₂P¹–P²}Pt(P³Me₃)(P⁴Ph₃)], [{η²‐^tBu₂P¹–P²}Pt(P³Ph₃)(P⁴Me₃)], [{η²‐^tBu₂P¹–P²}Pt(P³Et₃)(P⁴Ph₃)], [{η²‐^tBu₂P¹–P²}Pt(P³Me^tBu₂)(P⁴Ph₃)], [{η²‐^tBu₂P¹–P²}Pt(P³ⁱPr₃)(P⁴Ph₃)] and [{η²‐^tBu₂P¹–P²}Pt(P³(c‐Hex)₃)(P⁴Ph₃)]. With ^tBu₂PMe, [{η²‐^tBu₂P–P}Pt(P(p‐Tol)₃)₂] forms [{η²‐^tBu₂P¹–P²}Pt(P³Me^tBu₂)(P⁴(p‐Tol)₃)]. The NMR data of the compounds are given and discussed with respect to the influence of the PR₃ ligands.