Shape transformations of lipid vesicles by insertion of bulky-head lipids

Lipid vesicles, in particular Giant Unilamellar Vesicles (GUVs), have been increasingly important as compartments of artificial cells to reconstruct living cell-like systems in a bottom-up fashion. Here, we report shape transformations of lipid vesicles induced by polyethylene glycol-lipid conjugate (PEG lipids). Statistical analysis of deformed vesicle shapes revealed that shapes vesicles tend to deform into depended on the concentration of the PEG lipids. When compared with theoretically simulated vesicle shapes, those shapes were found to be more energetically favorable, with lower membrane bending energies than other shapes. This result suggests that the vesicle shape transformations can be controlled by externally added membrane molecules, which can serve as a potential method to control the replications of artificial cells

Regulatory Mechanism of Skeletal Muscle Glucose Transport by Phenolic Acids

Type 2 diabetes mellitus (T2DM) is one of the most severe public health problems in the world. In recent years, evidences show a commonness of utilization of alternative medicines such as phytomedicine for the treatment of T2DM. Phenolic acids are the most common compounds in non-flavonoid group of phenolic compounds and have been suggested to have a potential to lower the risk of T2DM. Skeletal muscle is the major organ that contributes to the pathophysiology of T2DM. Studies have shown that several phenolic acids (caffeic acid, chlorogenic acid, gallic acid, salicylic acid, p-coumaric acid, ferulic acid, sinapic acid) have antidiabetic effects, and these compounds have been implicated in the regulation of skeletal muscle glucose metabolism, especially glucose transport. Glucose transport is a major regulatory step for whole-body glucose disposal, and the glucose transport processes are regulated mainly through two different systems: insulin-dependent and insulin-independent mechanism. In this chapter, we reviewed recent experimental evidences linking phenolic acids to glucose metabolism focusing on insulin-dependent and insulin-independent glucose transport systems and the upstream signaling events in skeletal muscle

Caffeine modulates phosphorylation of insulin receptor substrate-1 and impairs insulin signal transduction in rat skeletal muscle

Caffeine decreases insulin sensitivity and insulin-stimulated glucose transport in skeletal muscle; however, the precise mechanism responsible for this deleterious effect is not understood fully. We investigated the effects of incubation with caffeine on insulin signaling in rat epitrochlearis muscle. Caffeine (≥1 mM, ≥15 min) suppressed insulin-stimulated insulin receptor substrate (IRS)-1 Tyr[612] phosphorylation in a dose- and time-dependent manner. These responses were associated with inhibition of the insulin-stimulated phosphorylation of phosphatidylinositol 3-kinase (PI3K) Tyr[458], Akt Ser[473], and glycogen synthase kinase-3β Ser9 and with inhibition of insulin-stimulated 3-O-methyl-D-glucose (3MG) transport but not with inhibition of the phosphorylation of insulin receptor-β Tyr[1158/62/63]. Furthermore, caffeine enhanced phosphorylation of IRS-1 Ser[307] and an IRS-1 Ser307 kinase, inhibitor-κB kinase (IKK)-α/β Ser[176/180]. Blockade of IKK/IRS-1 Ser[307] by caffeic acid ameliorated the caffeine-induced downregulation of IRS-1 Tyr[612]phosphorylation and 3MG transport. Caffeine also increased the phosphorylation of IRS-1 Ser789 and an IRS-1 Ser[789] kinase, 5′-AMP-activated protein kinase (AMPK). However, inhibition of IRS-1 Ser[789] and AMPK phosphorylation by dantrolene did not rescue the caffeine-induced downregulation of IRS-1 Tyr612 phosphorylation or 3MG transport. In addition, caffeine suppressed the phosphorylation of insulin-stimulated IRS-1 Ser[636/639] and upstream kinases, including the mammalian target of rapamycin and p70S6 kinase. Intravenous injection of caffeine at a physiological dose (5 mg/kg) in rats inhibited the phosphorylation of insulin-stimulated IRS-1 Tyr[612] and Akt Ser[473] in epitrochlearis muscle. Our results indicate that caffeine inhibits insulin signaling partly through the IKK/IRS-1 Ser[307] pathway, via a Ca[2+]- and AMPK-independent mechanism in skeletal muscle

Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells

Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs

Penyahwarnaan efluen kilang minyak kelapa sawit (POME) melalui proses pengoksidaan Fenton secara berterusan menggunakan limonit sebagai pemangkin

Industri minyak sawit mempunyai impak yang besar ke atas alam sekitar terutama di Malaysia. Efluen kilang minyak sawit (POME) merupakan air buangan yang mengandungi sebatian organik yang berasal daripada bahan boleh urai dan sedia direput oleh mikroorganisma. Teknologi rawatan POME masa kini banyak bertumpu kepada kaedah biologi untuk mengurangkan permintaan oksigen kimia (COD), permintaan oksigen bio-kimia (BOD) dan jumlah karbon organik (TOC). Walau bagaimanapun, kebanyakan proses biologi tidak dapat menguraikan warna yang terdapat dalam POME. Kajian ini mengkaji potensi teknologi pengoksidaan Fenton menggunakan biji limonit sebagai pemangkin kepada hidrogen peroksida untuk merawat POME selepas proses rawatan biologi yang diperoleh daripada kilang minyak kelapa sawit. Keputusan menunjukkan dengan hanya 50 mM H2O2 boleh menyahwarnakan POME sebanyak 800-1000 PtCo secara berterusan dengan pengekalan masa 1 jam pada pH 3

Development of Skin Flaps for Reconstructive Surgery : Random Pattern Flap to Perforator Flap

Flap transplantation has been an important procedure in plastic and reconstructive surgery to cover and fill various defects. Flap necrosis due to blood circulation failure leads to severe complications, especially in a patient undergoing reconstruction concerning the body cavity after tumor ablation. Surgical procedures for flap transplantation have been further improved and developed. We have reviewed from the random pattern flap to the newest procedure, the perforator flap. Perforator vessels were investigated in the process of development of the fasciocutaneous flap and have become important for blood supply of the skin flap. Blood circulation of the flap has become more stable and reliable than ever with the development and findings of the perforator vessels. Further development of a skin flap will be based on the perforasome concept, which involves the study of the territory and linking of perforator vessels

A type of familial cleft of the soft palate maps to 2p24.2–p24.1 or 2p21–p12

Cleft of the soft palate (CSP) and the hard palate are subtypes of cleft palate. Patients with either condition often have difficulty with speech and swallowing. Nonsyndromic, cleft palate isolated has been reported to be associated with several genes, but to our knowledge, there have been no detailed genetic investigations of CSP. We performed a genome-wide linkage analysis using a single-nucleotide polymorphism-based microarray platform and successively using microsatellite markers in a family in which six members, across three successive generations, had CSP. A maximum LOD score of 2.408 was obtained at 2p24.2-24.1 and 2p21-p12, assuming autosomal dominant inheritance. Our results suggest that either of these regions is responsible for this type of CSP