Quality of Type 2 Diabetes Management in the States of The Co-Operation Council for the Arab States of the Gulf: A Systematic Review

Type 2 diabetes mellitus is a growing, worldwide public health concern. Recent growth has been particularly dramatic in the states of The Co-operation Council for the Arab States of the Gulf (GCC), and these and other developing economies are at particular risk. We aimed to systematically review the quality of control of type 2 diabetes in the GCC, and the nature and efficacy of interventions. We identified 27 published studies for review. Studies were identified by systematic database searches. Medline and Embase were searched separately (via Dialog and Ovid, respectively; 1950 to July 2010 (Medline), and 1947 to July 2010 (Embase)) on 15/07/2009. The search was updated on 08/07/2010. Terms such as diabetes mellitus, non-insulin-dependent, hyperglycemia, hypertension, hyperlipidemia and Gulf States were used. Our search also included scanning reference lists, contacting experts and hand-searching key journals. Studies were judged against pre-determined inclusion/exclusion criteria, and where suitable for inclusion, data extraction/quality assessment was achieved using a specifically-designed tool. All studies wherein glycaemic-, blood pressure- and/or lipid- control were investigated (clinical and/or process outcomes) were eligible for inclusion. No limitations on publication type, publication status, study design or language of publication were imposed. We found the extent of control to be sub-optimal and relatively poor. Assessment of the efficacy of interventions was difficult due to lack of data, but suggestive that more widespread and controlled trial of secondary prevention strategies may have beneficial outcomes. We found no record of audited implementation of primary preventative strategies and anticipate that controlled trial of such strategies would also be useful

Flavonoids and Triterpenoid Saponins from <i>Pimenta dioica</i> (Merr.) L

The defatted and desalted 80% methanolic extract of the leaves of Pimenta dioica (Mirr.) L. resulted in the isolation of three triterpenoid saponins, 23-hydroxy-3α-[( O-α-L-rhamnopyranosyl-(1→2)- O-α-L-arabinopyranosyl) oxy] olean-12-en-28-oic acid O-α-L-rhamnopyranosyl-(1→4)- O-β-D-galactopyranosyl-(1→6)- O-β-D-galactopyranosyl ester (1), 2α,3α,23-trihydroxyolean-12-en-28-oic acid O-β-D-glucopyranosyl ester (2), and 2α,3α,23-trihydroxyolean-13(18)-en-28-oic acid O-β-D-glucopyranosyl ester (3), along with a novel dihydrokaempferol glucoside, namely, 3-carboxy-6,8-di- C-methyl-dihydrokaempferol 3- O-β-D-glucopyranoside (4), together with three known flavonoids, quercetin 3- O-β-D-glucuronopyranoside (5), quercitrin (6) and mernesitin (7), all for the first time from the genus Pimenta. The structures were identified on the basis of chemical and physicochemical analysis (UV, HRESI-MS, 1 and 2D NMR). </jats:p

SRC-like adaptor protein 2 (SLAP2) is a negative regulator of KIT-D816V-mediated oncogenic transformation

KIT is a receptor tyrosine kinase (RTK) involved in several cellular processes such as regulation of proliferation, survival and differentiation of early hematopoietic cells, germ cells and melanocytes. Activation of KIT results in phosphorylation of tyrosine residues in the receptor, and recruitment of proteins that mediate downstream signaling and also modulate receptor signaling. Here we show that the SRC-like adaptor protein 2 (SLAP2) binds to wild-type KIT in a ligand-dependent manner and is furthermore found constitutively associated with the oncogenic mutant KIT-D816V. Peptide fishing analysis mapped pY568 and pY570 as potential SLAP2 association sites in KIT, which overlaps with the SRC binding sites in KIT. Expression of SLAP2 in cells expressing the transforming mutant KIT-D816V led to reduced cell viability and reduced colony formation. SLAP2 also partially blocked phosphorylation of several signal transduction molecules downstream of KIT such as AKT, ERK, p38 and STAT3. Finally, SLAP2 expression enhanced ubiquitination of KIT and its subsequent degradation. Taken together, our data demonstrate that SLAP2 negatively modulates KIT-D816V-mediated transformation by enhancing degradation of the receptor