Seizure prediction : ready for a new era

Acknowledgements: The authors acknowledge colleagues in the international seizure prediction group for valuable discussions. L.K. acknowledges funding support from the National Health and Medical Research Council (APP1130468) and the James S. McDonnell Foundation (220020419) and acknowledges the contribution of Dean R. Freestone at the University of Melbourne, Australia, to the creation of Fig. 3.Peer reviewedPostprin

Hepatic stellate cells:central modulators of hepatic carcinogenesis

Hepatocellular carcinoma (HCC) represents the second most common cause of cancer-related death worldwide, and is increasing in incidence. Currently, our therapeutic repertoire for the treatment of HCC is severely limited, and therefore effective new therapies are urgently required. Recently, there has been increasing interest focusing on the cellular and molecular interactions between cancer cells and their microenvironment. HCC represents a unique opportunity to study the relationship between a diseased stroma and promotion of carcinogenesis, as 90 % of HCCs arise in a cirrhotic liver. Hepatic stellate cells (HSC) are the major source of extracellular proteins during fibrogenesis, and may directly, or via secreted products, contribute to tumour initiation and progression. In this review we explore the complex cellular and molecular interplay between HSC biology and hepatocarcinogenesis. We focus on the molecular mechanisms by which HSC modulate HCC growth, immune cell evasion and angiogenesis. This is followed by a discussion of recent progress in the field in understanding the mechanistic crosstalk between HSC and HCC, and the pathways that are potentially amenable to therapeutic intervention. Furthermore, we summarise the exciting recent developments in strategies to target HSC specifically, and novel techniques to deliver pharmaceutical agents directly to HSC, potentially allowing tailored, cell-specific therapy for HCC

Structural and magnetic conformation of a cerocene [Ce(COT′′)2]− exhibiting a uniconfigurational f1 ground state and slow-magnetic relaxation

Magnet-like behaviour, in the form of slow relaxation of the magnetization, was observed for a monometallic cerium(III) sandwich complex. The use of trimethylsilyl substituted COT ligands (COT′′) led to the formation of a staggered COT′′ arrangement in the cerocene-type sandwich complex with a well-defined oxidation state of +3 for the Ce ion

Structural and magnetic conformation of a cerocene [Ce(COT′′)2]− exhibiting a uniconfigurational f1 ground state and slow-magnetic relaxation

Magnet-like behaviour, in the form of slow relaxation of the magnetization, was observed for a monometallic cerium(III) sandwich complex. The use of trimethylsilyl substituted COT ligands (COT′′) led to the formation of a staggered COT′′ arrangement in the cerocene-type sandwich complex with a well-defined oxidation state of +3 for the Ce ion

C-H Bond Addition across a Transient Uranium-Nitrido Moiety and Formation of a Parent Uranium Imido Complex

Uranium complexes in the +3 and +4 oxidation states were prepared using the anionic PN- (PN- = (N-(2-(diisopropylphosphino) -4-methylphenyl)-2,4,6-trimethylanilide) ligand framework. New complexes include the halide starting materials, (PN)(2)(UI)-I-III (1) and (PN)(2)(UCl2)-Cl-IV (2), which both yield (PN)(2)U-IV(N-3)(2) (3) by reaction with NaN3. Compound 3 was reduced with potassium graphite to produce a putative, transient uranium-nitrido moiety that underwent an intramolecular C-H activation to form a rare example of a parent imido complex, [K(THF)(3)][(PN)U-IV(= NH)[(Pr2P)-Pr-i(C6H3Me)N(C6H2Me2CH2)]] (4). Calculated reaction energy profiles strongly suggest that a C-H insertion becomes unfavorable when a reductant is present, offering a distinctively different reaction pathway than previously observed for other uranium nitride complexes. © 2018 American Chemical Societ