Complex [ t BuOCO]W^C( t Bu)(THF) 2 (1) {where t BuOCO ¼ [2,6-( t BuC 6 H 3 O) 2 C 6 H 3 ] 3À , THF ¼ tetrahydrofuran} polymerizes acetylenes (R-phenylacetylene (R ¼ H, p-OMe, p-F, 3,5-diCF 3 ), 1-decyne, 3,3-dimethyl-1-butyne, and trimethylsilylacetylene) to form p-conjugating polymers. Upon treating 1 with 2 equiv. of phenylacetylene in toluene-d 8 at À35 C, two isolable products form. These two products are 4À } and derived from an apparent reductive alkylidyne migratory insertion into a metal-arene bond. Complexes 2-t Bu and 2-Ph polymerize acetylene and a wide variety of monosubstituted acetylenes including phenylacetylene derivatives, 1-decyne, 3,3-dimethyl-1-butyne and trimethylsilylacetylene. With a substrate to catalyst loading ratio of 25 000 : 1, complex 2-t Bu polymerizes phenylacetylene with a turnover number (TON) of 17 233. Additionally, 2-t Bu polymerizes phenylacetylene and 1-decyne with catalytic activities up to 5.64 Â 10 6 g PPA mol À1 h À1 and 7.98 Â 10 6 g PA mol À1 h À1 , respectively. 2-t Bu also polymerizes the disubstituted acetylene, 1-phenyl-1-propyne. NMR spectroscopic and single crystal X-ray structural studies provide compelling evidence for polymer chain growth via an insertion ring-expansion mechanism.

Synthesis, characterization, and catalytic alkyne polymerization results for the first trianionic pincer alkylidyne complex, [(t)BuOCO]W≡CC(CH(3))(3)(THF)(2) (6), are described. Complex 6 is a highly active catalyst for the polymerization of acetylenes and exhibits a high turnover number (4371), activity (1.05 × 10(6) g(PPA) mol(cat)(-1) h(-1)),and yield (87%) for the polymerization of 1-ethynyl-4-fluorobenzene.

This report details the synthesis of new NCN trianionic pincer ligand precursors and metalation reactions to form group (IV) complexes. N,N'-[1,3-phenylenebis(methylene)]bis-2,6-diisopropylaniline [2,6-(i)PrNCN]H(3) (8) was converted to the N,N'-substituted Si(IV), Sn(IV), Mg(II), and Zn(II) derivatives. [2,6-(i)PrNCHN](SiMe(3))(2) (9-Si) and [2,6-(i)PrNCHN](SnMe(3))(2) (9-Sn) form by first treating 8 with MeLi followed by Me(3)MCl, where M = Si or Sn. Single crystal X-ray experiments indicate 8, 9-Si, and 9-Sn have similar structural features in the solid state. [2,6-(i)PrNCHN](mu-MgCl.THF)(2) (12) forms by treating 8 with MeMgCl, and its solid state structure revealed a bis-mu-MgCl bridging unit. The (1)H NMR spectrum of 12 reveals a dynamic process occurs in solution. A variable temperature (1)H NMR experiment failed to quench the dynamic process. {[2,6-(i)PrNCHN]Zn}(2) (13) forms upon treating {[2,6-(i)PrNCHN]Li(2)}(2) (10) with anhydrous ZnCl(2) and is a dimer in the solid state. Again, dynamic (1)H NMR behavior is observed, and a mechanism is provided to explain the apparent low symmetry of 13 in solution. Extension of the aliphatic arm of the NCN ligand provides the new N(C)C(C)N pincer ligand precursors N,N'-(2,2'-(1,3-phenylene)bis(ethane-2,1-diyl))bis(3,5-bis(trifluoromethyl)aniline) [3,5-CF(3)N(C)C(C)N]H(3) (16) and [3,5-CF(3)N(C)CH(C)N](SiMe(3))(2) (17). A more rigid ligand architecture was accessed by synthesis of the anthracene derived pincer ligand anthracene-1,8-diylbis(N-3,5-bistrifluormethylaniline) [3,5-CF(3)N(C)C(anth)(C)N]H(3) (18). Treating {Zr(NMe(2))(4)}(2) with 2 equiv of 16 provides the dimer {(mu-3,5-CF(3)N(C)CH(C)N)Zr(NMe(2))(3)NHMe(2)}(2) (19). Treating Hf(NMe(2))(4) with 18 provides the bimetallic complex (mu-3,5-CF(3)N(C)CH(anth)(C)N){Hf(NMe(2))(3)NHMe(2)}(2) (20) in which one ligand bridges two Hf(IV) ions. Salt metathesis between 10 and ZrCl(2)(NMe(2))(2)(THF)(2) provides the mononuclear complex [2,6-(i)PrNCHN]Zr(NMe(2))(2) (21) in which the NCN ligand is bound as a chelating diamide. Thermoysis of 21 does not lead to formation of a trianionic pincer complex. Instead, treating HfCl(4) with {[2,6-(i)PrNCN]Li(3)}(2) (11) followed by MeLi provides the trianionic pincerate complex [2,6-(i)PrNCNHfMe(2)][Li(DME)(2)] (23). In the solid state the Hf ion has distorted trigonal bipyramidal geometry.

The synthesis and characterization of a series of four Cr complexes in the +2, +3, +4, and +5 oxidation states supported by an NCN trianionic pincer ligand are reported. Treating CrMeCl2(THF)3 with the dilithio salt pincer ligand precursor {[2,6- i PrNCHN]Li2}2 provides the CrIII complex [2,6- i PrNCN]CrIII(THF)3 (1), CrIV complex [2,6- i PrNCN]CrIVMe(THF) (2), and CrII complex [2,6- i PrNHCN]CrII(THF)2 (3). Complexes 2 and 3 are the result of disproportionation. Treating 1 with 1 equiv of styrene oxide in THF converts the CrIII complex to the CrV(O) species [2,6- i PrNCN]CrV(O)(THF) (4). Complex 2, characterized by single-crystal X-ray diffraction, is a rare CrIV methyl complex that is kinetically stable at 25 °C; at 85 °C, Cr–Me bond homolysis occurs. The homolytic cleavage results in CH4 formation and biphenyl via a radical mechanism. The metal-containing product from thermolysis is the same CrII species formed during metalation, except one of the protons is substituted for a deuterium from C6D6 (3- d ). Complex 2 is a precatalyst for the selective isomerization of 1-hexene and 1-octene to the corresponding 2-alkenes. An induction period occurs during the catalytic isomerization, and the active catalyst was determined to be the CrII complex 3, not 2.

We show that mesenchymal insulin-like growth factor-1 (IGF-1) promotes intestinal crypt repair following stem cell loss from whole-body irradiation. IGF-1 signals through mTORC1 to activate facultative stem cells to repopulate the damaged intestinal epithelium. BACKGROUND & AIMS: Intestinal crypts have a remarkable capacity to regenerate after injury from loss of crypt base columnar (CBC) stem cells. After injury, facultative stem cells (FSCs) are activated to replenish the epithelium and replace lost CBCs. Our aim was to assess the role of insulin-like growth factor-1 (IGF-1) to activate FSCs for crypt repair. METHODS: The intestinal regenerative response was measured after whole body 12-Gy g-irradiation of adult mice. IGF-1 signaling or its downstream effector mammalian target of rapamycin complex 1 (mTORC1) was inhibited by administering BMS-754807 or rapamycin, respectively. Mice with inducible Rptor gene deletion were studied to test the role of mTORC1 signaling in the intestinal epithelium. FSC activation post-irradiation was measured by lineage tracing. RESULTS: We observed a coordinate increase in growth factor expression, including IGF-1, at 2 days postirradiation, followed by a surge in mTORC1 activity during the regenerative phase of crypt repair at day 4. IGF-1 was localized to pericryptal mesenchymal cells, and IGF-1 receptor was broadly expressed in crypt progenitor cells. Inhibition of IGF-1 signaling via BMS-754807 treatment impaired crypt regeneration after 12-Gy irradiation, with no effect on homeostasis. Similarly, rapamycin inhibition of mTORC1 during the growth factor surge blunted the regenerative response. Analysis of Villin-CreER T2 ;Rptor fl/fl mice showed that epithelial mTORC1 signaling was essential for crypt regeneration. Lineage tracing from Bmi1marked cells showed that rapamycin blocked FSC activation post-irradiation. CONCLUSIONS: Our study shows that IGF-1 signaling through mTORC1 drives crypt regeneration. We propose that IGF-1 release from pericryptal cells stimulates mTORC1 in FSCs to regenerate lost CBCs.