Synthesis, structure and biological evaluation of bis salicylaldehyde-4(N)-ethylthiosemicarbazone ruthenium(iii) triphenylphosphine

Bis salicylaldehyde-4(N)-ethylthiosemicarbazone ruthenium(iii) triphenylphosphine [Ru(Sal-etsc)(H-Sal-etsc)(PPh(3))] was synthesized and structurally characterized by spectral and X-ray crystallographic studies and it showed 100% inhibition on the DPPH radical. It also exhibited a significant lymphocyte activity and inhibitory effect on the lung carcinoma A549 cell.     

Gene flow in genetically modified wheat

Understanding gene flow in genetically modified (GM) crops is critical to answering questions regarding risk-assessment and the coexistence of GM and non-GM crops. In two field experiments, we tested whether rates of cross-pollination differed between GM and non-GM lines of the predominantly self-pollinating wheat Triticum aestivum. In the first experiment, outcrossing was studied within the field by planting "phytometers" of one line into stands of another line. In the second experiment, outcrossing was studied over distances of 0.5-2.5 m from a central patch of pollen donors to adjacent patches of pollen recipients. Cross-pollination and outcrossing was detected when offspring of a pollen recipient without a particular transgene contained this transgene in heterozygous condition. The GM lines had been produced from the varieties Bobwhite or Frisal and contained Pm3b or chitinase/glucanase transgenes, respectively, in homozygous condition. These transgenes increase plant resistance against pathogenic fungi. Although the overall outcrossing rate in the first experiment was only 3.4%, Bobwhite GM lines containing the Pm3b transgene were six times more likely than non-GM control lines to produce outcrossed offspring. There was additional variation in outcrossing rate among the four GM-lines, presumably due to the different transgene insertion events. Among the pollen donors, the Frisal GM line expressing a chitinase transgene caused more outcrossing than the GM line expressing both a chitinase and a glucanase transgene. In the second experiment, outcrossing after cross-pollination declined from 0.7-0.03% over the test distances of 0.5-2.5 m. Our results suggest that pollen-mediated gene flow between GM and non-GM wheat might only be a concern if it occurs within fields, e.g. due to seed contamination. Methodologically our study demonstrates that outcrossing rates between transgenic and other lines within crops can be assessed using a phytometer approach and that gene-flow distances can be efficiently estimated with population-level PCR analyses.     

Predictors of health-related quality of life in obese youth

Objective: Recent literature has documented the psychosocial consequences of pediatric obesity, including poor health‐related quality of life (HRQOL). The present study examines HRQOL and its association with depressive symptoms and perceived social support in African‐American and white youth pursuing weight management treatment. Research Methods and Procedures: Study participants were 166 obese youth (mean = 12.7 years, 70% females, 57% African American, mean BMI = 37.0) referred to a pediatric weight management program. Parents of participants completed a demographics form and the parent‐proxy Pediatric Quality of Life Inventory (PedsQL). Youth completed the Children's Depression Inventory, PedsQL, and Perceived Social Support Scale for Children. Results: HRQOL scores were quite impaired relative to published norms on healthy youth (p < 0.001). Approximately 11% of the sample met criteria for clinically significant depressive symptoms. Simultaneous regression analyses revealed that depressive symptoms, perceived social support from classmates, degree of overweight, and socioeconomic status seem to be strong predictors of HRQOL. Discussion: Obesity has a clear impact on HRQOL regardless of respondent (e.g., parent, youth) or racial group. It is likely that assessing and treating depressive symptoms and fostering social support in the context of pediatric intervention have implications for both improved HRQOL and weight management outcomes.     

Reconstruction of coral reef fisheries catches in American Samoa, 1950–2002

Fisheries catches from Pacific Island coral reefs are rarely recorded in official statistics. Reconstruction of catch estimates with limited hard data requires interpolation and assumptions, justifiable only by the unsatisfactory alternative of continued substitution of zero catches, a common policy interpretation for ‘no data’. Uncertainties associated with reconstructions are high, requiring conservative estimation. American Samoan domestic fisheries consist of an artisanal, small-boat sector, whose commercial catches are reported, and a shore-based subsistence sector, with no regular reporting. Our catch reconstruction (with large pelagic species removed) suggested a 79% decrease in catches between 1950 (752 t) and 2002 (155 t). Accounting for rapid human population growth on the main island, the per capita catch rate may have declined from 36.3 kg·person⁻¹ year⁻¹ in 1950 to 1.3 kg·person⁻¹ year⁻¹ by 2002, while the catch rate for the inhabited outer islands has been independently reported as 58.6 kg·person⁻¹ year⁻¹. Catch per area of coral reef (to 50-m depth) may have declined from 5.5 to 0.7 t km⁻² year⁻¹ for the main island, and from 9.1 to 4.9 t km⁻² year⁻¹ for the outer islands, for 1950 and 2002, respectively. Summed for 1950–2002, our reconstruction suggested a 17-fold difference between reconstructed estimates and reported statistics.     

N-glycoside neoglycotrimers from 2,3,4,6-tetra-O-acetyl-beta-D-glucopyranosyl azide

2,3,4,6-Tetra-O-acetyl-beta-D-glucopyranosyl azide is available on large scale from D-glucose by means of a three-step sequence involving acetylation, activation as the glycosyl bromide, and stereospecific displacement with azide anion. The azide functionality then serves as a convenient anchor upon which to introduce new functionality, usually with retention of the beta-stereochemistry. Here we report the synthesis of an amide-linked N-glycosyl trimer, by employing a Staudinger-aza-Wittig process on the azide, as well as a hybrid N-glycosyl triazole-amide-linked trimer in which the sugars are separated by 1,2,3-triazole heterocycles. Both of these neoglycotrimers are isolated in good yield with high beta-selectivity in each case.     

Retroviral MDR1 gene transfer into marrow-engrafting human peripheral blood progenitor cells results in preferential transgene expression in the immature myeloid compartment rather than in mature myeloid progeny in vivo

BACKGROUND: The objective of multidrug resistance-1 (MDR1) gene therapy is protection of the myeloid cell lineage. It is therefore important to examine the effect of retroviral transduction on myeloid maturation. Transfer of the human MDR1 gene can confer resistance to a variety of cytostatic drugs. For a safe application in humans it is paramount to follow-up the development of transduced cells. METHODS: We transduced human mobilized peripheral blood progenitor cells (PBPC) with a viral vector containing the human MDR1 cDNA and transplanted the transduced cells into non-obese diabetic severe combined immunodeficient (NOD/SCID) mice. The progeny of the transduced cells was analyzed in detail by flow cytometry. RESULTS: A detailed analysis by four-color flow cytometry showed that MDR1 transgene-expressing CD33+ myeloid cells were preferentially negative for the maturation-associated myeloid markers CD11b and CD10, while the untransduced CD33+ myeloid cells expressed significantly higher proportions of these Ag (P<0.01 each). There was no difference in the expression of B- or T-lymphoid Ag among the MDR1-transduced and untransduced lymphoid cells. DISCUSSION: These data indicate that retroviral MDR1 gene transfer results in preferential P-glycoprotein expression in myeloid progenitor cells, which is the target cell population for myelotoxicity of cytostatic drugs.     

Failure of catecholamines to shift T-cell cytokine responses toward a Th2 profile in patients with rheumatoid arthritis

To further understand the role of neuro-immunological interactions in the pathogenesis of rheumatoid arthritis (RA), we studied the influence of sympathetic neurotransmitters on cytokine production of T cells in patients with RA. T cells were isolated from peripheral blood of RA patients or healthy donors (HDs), and stimulated via CD3 and CD28. Co-incubation was carried out with epinephrine or norepinephrine in concentrations ranging from 10(-5) M to 10(-11) M. Interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha, interleukin (IL)-4, and IL-10 were determined in the culture supernatant with enzyme-linked immunosorbent assay. In addition, IFN-gamma and IL-10 were evaluated with intracellular cytokine staining. Furthermore, basal and agonist-induced cAMP levels and catecholamine-induced apoptosis of T cells were measured. Catecholamines inhibited the synthesis of IFN-gamma, TNF-alpha, and IL-10 at a concentration of 10(-5) M. In addition, IFN-gamma release was suppressed by 10(-7) M epinephrine. Lower catecholamine concentrations exerted no significant effect. A reduced IL-4 production upon co-incubation with 10(-5) M epinephrine was observed in RA patients only. The inhibitory effect of catecholamines on IFN-gamma production was lower in RA patients as compared with HDs. In RA patients, a catecholamine-induced shift toward a Th2 (type 2) polarised cytokine profile was abrogated. Evaluation of intracellular cytokines revealed that CD8-positive T cells were accountable for the impaired catecholaminergic control of IFN-gamma production. The highly significant negative correlation between age and catecholamine effects in HDs was not found in RA patients. Basal and stimulated cAMP levels in T-cell subsets and catecholamine-induced apoptosis did not differ between RA patients and HDs. RA patients demonstrate an impaired inhibitory effect of catecholamines on IFN-gamma production together with a failure to induce a shift of T-cell cytokine responses toward a Th2-like profile. Such an unfavorable situation is a perpetuating factor for inflammation.