Macroscopic self ordering of solution processible poly (3,3'-dialkylquaterthiophene) by floating film transfer method

Ordering and alignment of p-conjugated polymer chains are highly desirable for high performance and long life organic electronic devices. We report here self assembly of ordered and aligned solution processible Poly(3,3‴-dialkylquaterthiophene) (PQT-12) polymer at macroscopic level using Floating Film Transfer Method (FTM). PQT-12 polymer film is formed over solution of ethylene glycol and glycerol at different temperatures viz. 22, 26, 33, and 38 C. PQT-12 films formed by FTM technique are further characterized for optical and morphological properties. UV-vis absorption (for polarize and unpolarize light) and surface topography/phase imaging are carried out by using UV-vis spectrometer and atomic force microscope (AFM), respectively. UV-vis spectra show the polymer chains alignment perpendicular to the film propagation direction and it is well supported by AFM images. The effect of temperature on ordering and alignment of PQT-12 shows 33 C as an optimum temperature for alignment of polymer chains (a little compromise in ordering). The heating of polymer films at 110 C for 2 h in ambient causes significant changes in UV-vis absorbance spectra, optical anisotropy, and AFM topography/phase imaging. Our studies provide better understanding of ordering and alignment of PQT-12 chains and also disordering on heating. This work further provides a facile and user-friendly technique for the long range ordered self assembly of PQT-12, which shows enormous potential for various electronic applications

Carbon nanotubes — chitosan nanobiocomposite for immunosensor

Carboxylic group functionalized single walled (SW) and multi walled (MW) carbon nanotubes (CNT) have been incorporated into biopolymer matrix of chitosan (CH) to fabricate nanobiocomposite film onto indium– tin–oxide (ITO) coated glass plate for co-immobilization of rabbit-immunoglobulin (r-IgGs) and bovine serum albumin (BSA) to detect ochratoxin-A (OTA). The results of electrochemical studies reveal that presence of both CNT results in increased electro-active surface area of CH leading to enhanced electron transport in these nanobiocomposites. Moreover, in CH–SWCNT and CH–MWCNT nanobiocomposites the availability of NH2/OH group in CH and surface charged CNT also increases loading of the r-IgGs resulting in enhanced electron transport responsible for improved sensing characteristics. Compared to BSA/r-IgGs/CH– MWCNT/ITO immunoelectrode, electrochemical response studies of BSA/r-IgGs/CH–SWCNT/ITO immunoelectrode carried out as a function of OTA concentration exhibits improved linearity as 0.25–6 ng/dL, detection limit as 0.25 ng/dL, response time as 25 s, and sensitivity as 21 μA ng dL−1cm−2 with the regression coefficient as 0.998

Aldose Reductase Gene Polymorphisms and Diabetic Retinopathy Susceptibility

OBJECTIVE: Aldose reductase (ALR) is involved in diabetic microvascular damage via the polyol pathway. A recent meta-analysis found genetic variation in the ALR gene (AKR1B1) to be significantly associated with diabetic retinopathy (DR). We investigated the genetic association of AKR1B1 with DR. RESEARCH DESIGN AND METHODS: The study enrolled 909 individuals with diabetes. Participants were genotyped for an AKR1B1 (CA)n microsatellite and 14 tag single nucleotide polymorphisms, and ophthalmological assessment was performed. RESULTS: A total of 514 individuals were found to have DR. rs9640883 was significantly associated with DR (P = 0.0005). However, AKR1B1 variation was not independently associated with DR development after adjusting for relevant clinical parameters. rs9640883 was associated with duration of diabetes (P = 0.002). CONCLUSION: Many previous reports have failed to account for known risk factors for DR. The commonly reported association of AKR1B1 with DR may be due to an association of the gene with younger age at onset of diabetes.Sotoodeh Abhary, Kathryn P. Burdon, Kate J. Laurie, Stacey Thorpe, John Landers, Lucy Goold, Stewart Lake, Nikolai Petrovsky, and Jamie E. Crai

Selective Inactivation of c-Jun NH2-Terminal Kinase in Adipose Tissue Protects Against Diet-Induced Obesity and Improves Insulin Sensitivity in Both Liver and Skeletal Muscle in Mice

OBJECTIVE Obesity is associated with increased activation of the c-Jun NH2-terminal kinase (JNK) in several metabolic organs, including adipose tissue, liver, and skeletal muscle. In this study, we aimed to define the role of JNK activation in adipose tissue in the development of obesity-related insulin resistance. RESEARCH DESIGN AND METHODS Transgenic mice with adipose tissue–specific overexpression of dominant-negative JNK (ap2-dn-JNK) under the transcriptional control of the aP2 gene promoter were generated and subjected to metabolic characterization together with the wild-type littermates. RESULTS On a high-fat diet (HFD), the ap2-dn-JNK mice displayed a marked suppression of both JNK1 and JNK2 activation in their adipose tissue, accompanied by a marked reduction in weight gain, fat mass, and size of the adipocytes. The transgenic mice were resistant to the deleterious impact of an HFD on systemic insulin sensitivity, glucose tolerance, and hepatic steatosis. Reduced hepatic gluconeogenesis was evident in in vivo and ex vivo studies and showed greater insulin-induced glucose uptake in skeletal muscles. These changes were accompanied by reduced macrophage infiltration in adipose tissue, decreased production of proinflammatory adipokines, and increased expression of adiponectin. Indirect calorimetry analysis showed that the transgenic mice had significant increases in oxygen consumption and reductions in respiration exchange rates compared with their wild-type littermates. CONCLUSIONS Selective suppression of JNK activation in adipose tissue alone is sufficient to counteract HFD-induced obesity and its associated metabolic dysregulations, in part through an increase in energy expenditure and a decrease in systemic inflammation

Strain-dependent host transcriptional responses to toxoplasma infection are largely conserved in mammalian and avian hosts

Toxoplasma gondii has a remarkable ability to infect an enormous variety of mammalian and avian species. Given this, it is surprising that three strains (Types I/II/III) account for the majority of isolates from Europe/North America. The selective pressures that have driven the emergence of these particular strains, however, remain enigmatic. We hypothesized that strain selection might be partially driven by adaptation of strains for mammalian versus avian hosts. To test this, we examine in vitro, strain-dependent host responses in fibroblasts of a representative avian host, the chicken (Gallus gallus). Using gene expression profiling of infected chicken embryonic fibroblasts and pathway analysis to assess host response, we show here that chicken cells respond with distinct transcriptional profiles upon infection with Type II versus III strains that are reminiscent of profiles observed in mammalian cells. To identify the parasite drivers of these differences, chicken fibroblasts were infected with individual F1 progeny of a Type II x III cross and host gene expression was assessed for each by microarray. QTL mapping of transcriptional differences suggested, and deletion strains confirmed, that, as in mammalian cells, the polymorphic rhoptry kinase ROP16 is the major driver of strain-specific responses. We originally hypothesized that comparing avian versus mammalian host response might reveal an inversion in parasite strain-dependent phenotypes; specifically, for polymorphic effectors like ROP16, we hypothesized that the allele with most activity in mammalian cells might be less active in avian cells. Instead, we found that activity of ROP16 alleles appears to be conserved across host species; moreover, additional parasite loci that were previously mapped for strain-specific effects on mammalian response showed similar strain-specific effects in chicken cells. These results indicate that if different hosts select for different parasite genotypes, the selection operates downstream of the signaling occurring during the beginning of the host's immune response. © 2011 Ong et al

A Predominant Role for Parenchymal c-Jun Amino Terminal Kinase (JNK) in the Regulation of Systemic Insulin Sensitivity

It has been established that c-Jun N-terminal kinase 1 (JNK1) is essential to the pathogenesis of insulin resistance and type 2 diabetes. Although JNK influences inflammatory signaling pathways, it remains unclear whether its activity in macrophages contributes to adipose tissue inflammation and ultimately to the regulation of systemic metabolism. To address whether the action of this critical inflammatory kinase in bone marrow-derived elements regulates inflammatory responses in obesity and is sufficient and necessary for the deterioration of insulin sensitivity, we performed bone marrow transplantation studies with wild type and JNK1-deficient mice. These studies illustrated that JNK1-deficiency in the bone marrow-derived elements (BMDE) was insufficient to impact macrophage infiltration or insulin sensitivity despite modest changes in the inflammatory profile of adipose tissue. Only when the parenchymal elements lacked JNK1 could we demonstrate a significant increase in systemic insulin sensitivity. These data indicate that while the JNK1 activity in BMDE is involved in metabolic regulation and adipose milieu, it is epistatic to JNK1 activity in the parenchymal tissue for regulation of metabolic homeostasis