Ordered growth of vanadyl phthalocyanine (VOPc) on an iron phthalocyanine (FePc) monolayer

The growth and characterisation of a non-planar phthalocyanine (Vanadyl Phthalocyanine, VOPc) on a complete monolayer (ML) of a planar phthalocyanine (Iron (II) Phthalocyanine, FePc) on an Au (111) surface, has been investigated using ultra-high vacuum (UHV) scanning tunnelling microscopy (STM) and low energy electron diffraction (LEED). The surface mesh of the initial FePc monolayer has been determined and shown to correspond to an incommensurate overlayer, not commensurate as previously reported. Ordered islands of VOPc, with (1x1) epitaxy, grow on the FePc layer at submonolayer coverages. The individual VOPc molecules occupy sites directly atop the underlying FePc molecules, indicating that significant intermolecular bonding must occur. It is proposed that this interaction implies that the V=O points down into the surface, allowing a Fe-O bond to form. The detailed appearance of the STM images of the VOPc molecules is consistent with previous studies in other VOPc growth studies in which this molecular orientation has been proposed

Structural templating in a nonplanar phthalocyanine using single crystal copper iodide

Solution-grown copper iodide crystals are used as substrates for the templated growth of the nonplanar vanadyl phthalocyanine using organic molecular beam deposition. Structural characterization reveals a single molecular orientation produced by the (111) Miller plane of the copper iodide crystals. These fundamental measurements show the importance of morphology and structure in templating interactions for organic electronics applications

Monitoring erosive toothwear: BEWE, a simple tool to protect patients and the profession.

Erosive tooth wear is the third most commonly observed oral condition after caries and periodontal disease, with a prevalence similar to that of dentine hypersensitivity. However, it is not a condition that is routinely screened, or monitored, as part of the standard dental examination. Following a meeting held in 2018, this paper considers the outlook for erosive tooth wear and the need for dental professionals to monitor for signs of the condition as part of an oral health assessment, to provide protection for patients and the profession. The use of the basic erosive wear examination (BEWE) is proposed as a simple screening tool designed to detect erosive tooth wear in clinical practice

The Human Lipodystrophy Gene BSCL2/Seipin May Be Essential for Normal Adipocyte Differentiation

OBJECTIVE—Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2) is a recessive disorder featuring near complete absence of adipose tissue. Remarkably, although the causative gene, BSCL2, has been known for several years, its molecular function and its role in adipose tissue development have not been elucidated. Therefore, we examined whether BSCL2 is involved in the regulation of adipocyte differentiation and the mechanism whereby pathogenic mutations in BSCL2 cause lipodystrophy

Alterations on peripheral B cell subsets following an acute uncomplicated clinical malaria infection in children

<p>Abstract</p> <p>Background</p> <p>The effects of <it>Plasmodium falciparum </it>on B-cell homeostasis have not been well characterized. This study investigated whether an episode of acute malaria in young children results in changes in the peripheral B cell phenotype.</p> <p>Methods</p> <p>Using flow-cytofluorimetric analysis, the B cell phenotypes found in the peripheral blood of children aged 2–5 years were characterized during an episode of acute uncomplicated clinical malaria and four weeks post-recovery and in healthy age-matched controls.</p> <p>Results</p> <p>There was a significant decrease in CD19⁺B lymphocytes during acute malaria. Characterization of the CD19⁺B cell subsets in the peripheral blood based on expression of IgD and CD38 revealed a significant decrease in the numbers of naive 1 CD38^-IgD⁺B cells while there was an increase in CD38⁺IgD^-memory 3 B cells during acute malaria. Further analysis of the peripheral B cell phenotype also identified an expansion of transitional CD10⁺CD19⁺B cells in children following an episode of acute malaria with up to 25% of total CD19⁺B cell pool residing in this subset.</p> <p>Conclusion</p> <p>Children experiencing an episode of acute uncomplicated clinical malaria experienced profound disturbances in B cell homeostasis.</p

Identification and Characterisation of a Novel Pathogenic Mutation in the Human Lipodystrophy Gene AGPAT2 : C48R: A Novel Mutation in AGPAT2.

Loss-of-function mutations in AGPAT2, encoding 1-acylglycerol-3-phosphate-O-acyltransferase 2 (AGPAT2), produce congenital generalised lipodystrophy (CGL). We screened the AGPAT2 gene in two siblings who presented with pseudoacromegaly, diabetes and severe dyslipidaemia and identified a novel mutation in AGPAT2 causing a single amino acid substitution, p.Cys48Arg. We subsequently investigated the molecular pathogenic mechanism linking both this mutation and the previously reported p.Leu228Pro mutation to clinical disease. Wild-type and mutant AGPAT2 were expressed in control and AGPAT2-deficient preadipocyte cell lines. mRNA and protein expression was determined, and the ability of each AGPAT2 species to rescue adipocyte differentiation in AGPAT2-deficient cells was assessed. Protein levels of both p.Cys48Arg and p.Leu228Pro AGPAT2 were significantly reduced compared with that of wild-type AGPAT2 despite equivalent mRNA levels. Stable expression of wild-type AGPAT2 partially rescued adipogenesis in AGPAT2 deficient preadipocytes, whereas stable expression of p.Cys48Arg or p.Leu228Pro AGPAT2 did not. In conclusion, unusually severe dyslipidaemia and pseudoacromegaloid overgrowth in patients with diabetes should alert physicians to the possibility of lipodystrophy. Both the previously unreported pathogenic p.Cys48Arg mutation in AGPAT2, and the known p.Leu228Pro mutation result in decreased AGPAT2 protein expression in developing adipocytes. It is most likely that the CGL seen in homozygous carriers of these mutations is largely accounted for by loss of protein expression