Conductive poly(α,ω-bis(3-pyrrolyl)alkanes)-coated wool fabrics

Cross-linked poly(α,ω-bis(3-pyrrolyl)alkanes) were directly applied to woven wool substrates by either chemical, vapour or mist polymerization methods. Choice of dopant could greatly improve the surface resistance. The optimum coating on textiles with the lowest surface resistance, highest colour-fastness and stability was achieved using a mist polymerization method with 1,8-bis(pyrrolyl)octane, iron(III) chloride (FeCl₃) as the oxidant and p-toluene sulfonic acid sodium salt (pTSA) as the dopant.

(1,3-benzo[d]dioxol-5-yl)(2-pyridyl)methyl cyanide

In the title compound, C₁₄H₁₀N₂O₂, the dihedral angle formed between the substituted pyridine ring and 1,3-benzodioxole group is 67.73 (6)°. The crystal features chains of molecules held together by alternating [π]...[π] and C-H...[π] interactions.

Synthesis and structure of tris(triphenyltin)benzene-1,3,5-tricarboxylate and its tri-DMSO adduct

The molecular structure of (Ph₃SnO₂C)₃C₆H₃ reveals distorted tetrahedral C₃O geometries for each tin atom. No intermolecular Sn...O associations occur between the molecules so that the trinuclear molecule may be considered monomeric. An increase in coordination number at tin is indicated by ¹¹⁹Sn NMR measurements conducted in d₆-DMSO solution and this has been confirmed by a structure analysis of (DMSO·Ph₃SnO₂C)₃C₆H₃·2 DMSO. In this structure, the tin atom geometries are distorted trigonal bipyramidal, existing within trans-C₃O₂ donor sets. Thus, while is it possible for the tin atoms to increase their coordination numbers in (Ph₃SnO₂C)₃C₆H₃, molecular aggregation to form polymeric arrays is precluded, most likely due to steric constraints.

Synthesis and structure of 1,3,5-tris(diorganohydroxysilyl)benzenes. Novel building blocks in supramolecular silanol chemistry

The 1,3,5-tris(diorganohydroxysilyl)benzenes 1,3,5-(HOR₂Si)₃C₆H₃ (TMSB, R = Me; TPSB, R = Ph) have been prepared and fully characterized by X-ray crystallography. The crystal structure of TMSB features pairwise connected layers, in which the molecules are involved in interlayer hydrogen bonding. The supramolecular hydrogen bond motif may be described as a 12-membered ring that adopts a chair conformation. TPSB forms an equimolar inclusion complex with water, which is associated via hydrogen bonding and apparently fills a void in the crystal packing. In this case, the supramolecular hydrogen bond motif may be described as an eight-membered ring. Two of the water molecules are also associated, giving rise to a water dimer entrapped in the silanol matrix. Besides the hydrogen bonds, the crystal structure of the TPSB·H₂O complex reveals intra- and intermolecular C-H··· π stacking of most of the phenyl groups. Electrospray mass spectrometry shows that TPSB undergoes supramolecular complex formation with a variety of N-donors such as 4-(dimethylamino)pyridine, N,N,N',N'-tetramethylethylenediamine, imidazole, 2-(dimethylamino)pyridine, and 2,2'-dipyridylamine.

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Oligomethylene-bridged dinuclear triorganotin triflates and diphenylphosphinates. Ion pairing in the solid state and electrolytic dissociation in solution of [Ph2Sn(CH2)nSnPh2X](O3SCF3) (X = OH, O2PPh2; n = 1-3)

The condensation of [Ph₂(OH)Sn(CH₂)_nSn(OH)Ph₂] (1-3; n = 1-3) with HO₃SCF₃ and HO₂PPh₂ provided [Ph₂Sn(CH₂)_nSnPh₂(OH)](O₃SCF₃) (4-6; n = 1-3) and [Ph₂(O₂PPh₂)Sn(CH₂)_nSn(O₂PPh₂)Ph₂] (10-12; n = 1-3), respectively. The reaction of [Ph₂Sn(CH₂)_nSnPh₂(OH)](O₃SCF₃) (4-6; n = 1-3) with HO₂PPh₂ and NaO₂PPh₂ gave rise to the formation of [Ph₂Sn(CH₂)_nSnPh₂(O₂PPh₂)](O₃SCF₃) (7-9; n = 1-3) and [Ph₂(OH)Sn(CH₂)_nSn(O₂PPh₂)Ph₂] (13-15; _n = 1-3), respectively. In the solid state, compounds 4-9 comprise ion pairs of cationic cyclo-[Ph₂SnCH₂SnPh₂(OH)]₂²⁺, cyclo-[Ph₂Sn(CH₂)_nSnPh₂(OH)]⁺ (n = 2, 3), and cyclo-[Ph₂Sn(CH₂)_nSnPh₂(O₂PPh₂)]⁺ (n = 1-3) and triflate anions. In MeCN, the eight-membered-ring system cyclo-[Ph₂SnCH₂SnPh₂(OH)]₂²⁺ appears to be in equilibrium with the four-membered-ring system cyclo-[Ph₂SnCH₂SnPh₂(OH)]⁺. In contrast, compounds 10-15 show no ionic character. Compounds 1-15 were characterized by multinuclear NMR spectroscopy in solution and in the solid state, IR spectroscopy, conductivity measurements, electrospray mass spectrometry, osmometric molecular weight determinations, and X-ray crystallography (4, 5, 7, and 12).

Plasma phospholipid and dietary fatty acids as predictors of type 2 diabetes: interpreting the role of linoleic acid 1-3

Background: Dietary fatty acids may be associated with diabetes but are difficult to measure accurately.

Objective: We aimed to investigate the associations of fatty acids in plasma and diet with diabetes incidence.

Design: This was a prospective case-cohort study of 3737 adults aged 36-72 y. Fatty acid intake (/kJ) and plasma phospholipid fatty acids (%) were measured at baseline, and diabetes incidence was assessed by self-report 4 y later. Logistic regression excluding (model 1) and including (model 2) body mass index and waist-hip ratio was used to calculate odds ratios (ORs) for plasma phospholipid and dietary fatty acids.

Results: In plasma phospholipid, positive associations with diabetes were seen for stearic acid [OR model 1, highest versus lowest quintile: 4.14 (95% CI: 2.65, 6.49), P for trend < 0.0001] and total saturated fatty acids [OR model 1: 3.76 (2.43, 5.81), P for trend < 0.0001], whereas an inverse association was seen for linoleic acid [OR model 1: 0.22 (0.14, 0.36), P for trend < 0.0001]. Dietary linoleic [OR model 1: 1.77 (1.19, 2.64), P for trend = 0.002], palmitic [OR model 1: 1.65 (1.12, 2.43), P for trend = 0.012], and stearic [OR model 1: 1.46 (1.00, 2.14), P for trend = 0.030] acids were positively associated with diabetes incidence before adjustment for body size. Within each quintile of linoleic acid intake, cases had lower baseline plasma phospholipid linoleic acid proportions than did controls.

Conclusions: Dietary saturated fat intake is inversely associated with diabetes risk. More research is required to determine whether linoleic acid is an appropriate dietary substitute.

Microwave-accelerated 1,3-dipolar cycloaddition for the formation of fused [n]polynorbornanes

Microwave irradiation induces the 1,3-dipolar cycloaddition of cyclobutane epoxides with norbornenes to afford [n]polynorbornane scaffolds. Greatly enhanced reaction rates and significantly reduced levels of decomposition were observed.

Scores on the dietary guideline index for children and adolescents are associated with nutrient intake and socio-economic position but not adiposity 1-3

Diet quality indices reflect overall dietary patterns better than single nutrients or food groups. The study aims were to develop a measure of adherence with dietary guidelines applicable to child and adolescent populations in Australia and determine the association between index scores and food and nutrient intake, socio-demographic characteristics, and measures of adiposity. Data were analyzed from 4- to 16-y-old participants of the 2007 Australian Children’s Nutrition and Physical Activity Survey (n = 3416). The Dietary Guideline Index for Children and Adolescents (DGI-CA) comprises 11 components: 5 core food groups, wholegrain bread, reduced-fat dairy foods, extra foods (nutrient poor and high in fat, salt, and added sugar), healthy fats/oils, water, and diet variety (possible score of 100). The index criteria were age specific. The mean DGI-CA score was low (53.6 ± 0.4), similar between boys and girls, and differed by age; the youngest children scored higher than the oldest children (P < 0.0001). Higher DGI-CA scores were associated with lower energy intake, energy density, total and saturated fat, and sugar intake; higher protein, carbohydrate, fiber, calcium, iron, vitamin C, vitamin A, folate, phosphorous, magnesium, zinc, and iodine intakes; and a higher polyunsaturated:saturated fat ratio (P < 0.0001). DGI-CA scores were associated with socio-economic characteristics and measures of family circumstance. Weak positive associations were observed between DGI-CA score and BMI or waist circumference Z-scores in the 4- to 10-y and 12- to 16-y age groups only. This index is the first validated index in Australia and one of the few international indices to describe the diet quality of children and adolescents.

Dietary salt loading impairs arterial vascular reactivity 1-3

BACKGROUND: Studies of sodium have shown improvements in vascular function and blood pressure (BP). The effect of chronic sodium loading from a low-sodium diet to a Western diet on vascular function and BP has been less well studied.

OBJECTIVE: The objective was to examine the effects of dietary salt intake on vascular function and BP.

DESIGN: Thirty-five hypertensive volunteers met the inclusion criteria. After a 2-wk run-in with a low-sodium diet (60 mmol/d), the participants maintained their diets and were randomly assigned to receive sequentially 1 of 3 interventions for 4 wk, with a 2-wk washout between interventions: sodium-free tomato juice (A), tomato juice containing 90 mmol Na (B), and tomato juice containing 140 mmol Na (C). The outcomes were changes in pulse wave velocity (PWV), systolic BP (SBP), and diastolic BP (DBP).

RESULTS: The difference in PWV between interventions B and A was 0.39 m/s (95% CI: 0.18, 0.60 m/s; P = 0.001) and between C and A was 0.35 m/s (95% CI: 0.13, 0.57 m/s; P = 0.01). Differences in SBP and DBP between interventions B and A were 4.4 mm Hg (95% CI: 1.2, 7.8 mm Hg; P = 0.01) and 2.4 mm Hg (95% CI: 0.8, 4.1 mm Hg; P = 0.001), respectively, and between interventions C and A were 5.6 mm Hg (95% CI: 2.7, 8.4 mm Hg; P = 0.01) and 3.3 mm Hg (95% CI: 1.5, 5.0 mm Hg; P = 0.001), respectively. Changes in PWV correlated with changes in SBP (r = 0.52) and DBP (r = 0.58).

CONCLUSIONS: Dietary salt loading produced significant increases in PWV and BP in hypertensive volunteers. Correlations between BP and PWV suggest that salt loading may have a BP-independent effect on vascular wall function. This further supports the importance of dietary sodium restriction in the management of hypertension. This trial was registered with the Australian and New Zealand Clinical Trials Registry as ACTRN12609000161224.