276 research outputs found
Synthetic and Mechanistic Studies of the Ring Opening and Denitrogenation of Pyridine and Picolines by Ti−C Multiple Bonds
No full textThe neopentylidene-neopentyl complex (PNP)Ti=CH(t)Bu(CH(2)(t)Bu) (1; PNP(-) = N[2-P(CHMe(2))2-4-methylphenyl]2) extrudes neopentane in neat pyridine or picoline (3- or 4-picoline) under mild conditions (25 degrees C), to generate the transient titanium alkylidyne intermediate (PNP)Ti C(1)Bu (A), which subsequently ring-opens the pyridine by ring-opening metathesis of the aromatic N=C bond across the Ti C linkage, generating the metallaazabicycles (PNP)Ti(C((t)Bu)C(5)H(3)RNH) (R = H (2), 3-Me (3), 4-Me (4)). Kinetic studies suggest that the C N activation process obeys a pseudo-first-order process in titanium, with a-hydrogen abstraction being the rate-determining step (the KIE for 1/1-d(3) conversion to 2 was 3.8(3) at 25 degrees C). The activation parameters are Delta H* = 23(3) kcal/mol and Delta S* = -4(3) cal/(mol K). The intermolecular k(H)/k(D) ratio is close to unity, 1.07(3) at 25 C, for the conversion of 1 to 2 in pyridine versus pyridine-d(5). Detailed theoretical studies suggest the 1 -> 2 transformation proceeds in the following order: (i) formation of A in an overall endergonic step by a-hydrogen abstraction, (ii) an exergonic binding of pyridine, and (iii) concerted, exergonic 1,2 + 21 cycloaddition followed by (iv) exergonic ring-opening metathesis and finally (v) a concerted hydrogen atom migration. Complexes 2-4 can denitrogenate, that is, completely remove N of the heterocycle at 65 C over 7211, when treated with silyl chlorides such as ClSi R(3) (R = Me, (i)Pr, Ph) to cleanly afford the titanium silylimides (PNP)Ti=NSiR(3)(Cl) (R = Me (8), (i)Pr (9), Ph (10)) and the corresponding (1)Bu-arene organic byproduct. [Et(3)Si][B(C(6)F(5))(4)] also promotes denitrogenation of 2 to yield (t)Bu-benzene, but the metal complex could not be characterized from such a reaction. The conversion 2 -> 8 was found to have activation parameters Delta H* = 30(6) kcal/mol and Delta S* = 10(2) cal/(mol K), therefore yielding activation parameters Delta H* = 30(6) kcal/mol and Delta S* = 10(2) cal/(mol K), therefore yielding Delta G*approximate to kcal/mol at 298.15 K. A KIE of 1.6(2) at 85 degrees C was observed when 2/2-d(5) were denitrogenated to 8 in the presence of ClSiMe(3), with the rate of the reaction being insensitive to both the steric nature and concentration of the trialkylsilyl chloride. Denitrogenation leading to 8-10 is proposed to occur via a series of steps including a 1,3-hydrogen migration, an electrocyclic rearrangement, a retrocycloaddition, and a Si-Cl addition. The transformations 1 -> 2/3/4 and 2/3/4 -> 8 can be made cyclic by a series of steps such as deimination of the imide moiety in 8 with 2 equiv of MoCl(5), followed by reduction and transmetalation with LiCH(2)(t)Bu and then oxidatively induced a-hydrogen abstraction. The reactivity of 1 with other heterocycles such as THF, thiophene, and piperidine is also discussed
Processing multi-join query in parallel systems
No full textApplied Computing: Technological Challenges of the 1990's283-29
The Effect of Social Support on the Effectiveness of College Counseling for International Students
No full textBuffer and load balancing in locally distributed database systems
No full textProceedings - Sixth International Conference on Data Engineering545-55
Lipid Droplet–Mitochondria Contacts in Health and Disease
No full textThe orchestration of cellular metabolism and redox balance is a complex, multifaceted process crucial for maintaining cellular homeostasis. Lipid droplets (LDs), once considered inert storage depots for neutral lipids, are now recognized as dynamic organelles critical in lipid metabolism and energy regulation. Mitochondria, the powerhouses of the cell, play a central role in energy production, metabolic pathways, and redox signaling. The physical and functional contacts between LDs and mitochondria facilitate a direct transfer of lipids, primarily fatty acids, which are crucial for mitochondrial β-oxidation, thus influencing energy homeostasis and cellular health. This review highlights recent advances in understanding the mechanisms governing LD–mitochondria interactions and their regulation, drawing attention to proteins and pathways that mediate these contacts. We discuss the physiological relevance of these interactions, emphasizing their role in maintaining energy and redox balance within cells, and how these processes are critical in response to metabolic demands and stress conditions. Furthermore, we explore the pathological implications of dysregulated LD–mitochondria interactions, particularly in the context of metabolic diseases such as obesity, diabetes, and non-alcoholic fatty liver disease, and their potential links to cardiovascular and neurodegenerative diseases. Conclusively, this review provides a comprehensive overview of the current understanding of LD–mitochondria interactions, underscoring their significance in cellular metabolism and suggesting future research directions that could unveil novel therapeutic targets for metabolic and degenerative diseases
The Effect of Social Support on the Effectiveness of College Counseling for International Students
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