The adsorption of environmental pollutants in gas and aqueous media utilizing nano-scale materials

In this body of work, the synthesis and characterization of several nanoporous materials have been described, as well as the application of these materials towards environmentally positive means. Largely, this work involves porous carbon materials produced from the amino acid L-histidine, a porous carbon precursor high in nitrogen and oxygen. Although pyrolysis of this precursor alone produces a non-porous foam, the introduction of any of a number of activating agents is shown here to produce a variety of amorphous and highly porous carbon materials. While applications of these materials have a very wide range, in this body of work the adsorption of pollutants is emphasized. Among the aqueous pollutants, both textile dyes and pharmaceuticals were investigated for their abilities to be taken up by these porous carbon materials. Individually, many of the porous carbons were capable of the uptake of noteworthy quantities of various pollutants. Yet, a broader finding in this work was that it appears the ‘tuning' of properties on a porous carbon is required to target each different adsorbate; no single property is universally linked to higher capacities. Apart from aqueous pollutants, the adsorption of CO2 was thoroughly investigated on many porous carbons. Given their high nitrogen content, it was expected that these materials would do well for CO2 uptake. And indeed, it was found that several histidinederived porous carbons were capable of noteworthy capacities, such as 8.30 and 5.57 mmol g-1. Through investigation of the porous carbon textural and chemical properties, these capacities are ascribed to a mixture of physisorption and chemisorption processes. Finally, the adsorption of CO2 was investigated on an amine-coated porous silica. With the purpose of making such nano-scale materials more feasible, immobilization inside a bacterial cellulose framework is investigated. Ultimately, it was found that after finetuning the loading process, a functional hybrid material can be made that successfully immobilizes the adsorbent material without sacrificing the capture abilities

Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009

Insulin resistance is a hallmark of type 2 diabetes mellitus and is associated with a metabolic and cardiovascular cluster of disorders (dyslipidaemia, hypertension, obesity [especially visceral], glucose intolerance, endothelial dysfunction), each of which is an independent risk factor for cardiovascular disease (CVD). Multiple prospective studies have documented an association between insulin resistance and accelerated CVD in patients with type 2 diabetes, as well as in non-diabetic individuals. The molecular causes of insulin resistance, i.e. impaired insulin signalling through the phosphoinositol-3 kinase pathway with intact signalling through the mitogen-activated protein kinase pathway, are responsible for the impairment in insulin-stimulated glucose metabolism and contribute to the accelerated rate of CVD in type 2 diabetes patients. The current epidemic of diabetes is being driven by the obesity epidemic, which represents a state of tissue fat overload. Accumulation of toxic lipid metabolites (fatty acyl CoA, diacylglycerol, ceramide) in muscle, liver, adipocytes, beta cells and arterial tissues contributes to insulin resistance, beta cell dysfunction and accelerated atherosclerosis, respectively, in type 2 diabetes. Treatment with thiazolidinediones mobilises fat out of tissues, leading to enhanced insulin sensitivity, improved beta cell function and decreased atherogenesis. Insulin resistance and lipotoxicity represent the missing links (beyond the classical cardiovascular risk factors) that help explain the accelerated rate of CVD in type 2 diabetic patients

HRD4/NPL4 Is Required for the Proteasomal Processing of Ubiquitinated ER Proteins

We isolated a temperature-sensitive mutant, hrd4–1, deficient in ER-associated degradation (ERAD). The HRD4 gene was identical to NPL4, a gene previously implicated in nuclear transport. Using a diverse set of substrates and direct ubiquitination assays, our analysis revealed that HRD4/NPL4 is required for a poorly characterized step in ERAD after ubiquitination of target proteins but before their recognition by the 26S proteasome. Our data indicate that this lack of proteasomal processing of ubiquitinated proteins constitutes the primary defect in hrd4/npl4 mutant cells and explains the diverse set of hrd4/npl4 phenotypes. We also found that each member of the Cdc48p-Ufd1p-Npl4p complex is individually required for ERAD