A series of porous poly(styrene-divinylbenzene) monoliths (polyHIPE) was synthesized by high internal phase emulsions (HIPE). The effects of the ethanol contents on the microstructure of the polyHIPE were characterized by scanning electron microscopy and mercury intrusion porosimeter. The adsorption and release behaviors of the polyHIPE for a monomer mixture consisting of dicyclopentadiene (DCPD) /styrene (St) (DS, mass ratio of 9/1) were investigated. The polymerization of the mixture DS within pores of the polyHIPE was studied. The results showed that the microstructure of the polyHIPE was significantly influenced by the ethanol content. The increase of ethanol in the HIPE increased the internal pore diameter and decreased the pore volume of the polyHIPE, thus decreased the DS absorption and increased the release rate. The DS monomer can enter the pores(cavities, windows) and fill the original holes after the polymerization. Compared with conventional polymerization of DCPD/St, the poly(DCPD/St) (pDS) obtained from confined spaces possess higher molecular weight, broader molecular weight distribution, and higher Tg. As the pore diameter increased, the effect of space confinement reduced, and the performances of pDS were closed to that prepared by conventional polymerization.
Carlos R. Plata‐Saláman, Joseph R. Vasselli, Gayatri Sonti
AbstractPathophysiological and pharmacological concentrations of tumor necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β) in the cerebrospinal fluid (CSF) induce anorexia in normal rats. Obesity in humans and rodents is associated with increased TNF‐α messenger RNA and protein levels in various cell types. This suggests that obese individuals may have differential regulation of cytokine production and dissimilar responsiveness to cytokines. In the present study, we investigated the effects of the intracerebroventricular (ICV) microinfusion of TNF‐α (50, 100, and 500 ng/rat), IL‐1β (1.0, 4.0, and 8.0 ng), and TNF‐α (100 ng) plus IL‐1β (1.0 ng) on obese (fa/fa) and lean (Fa/Fa) Zucker rats. The results show that: TNF‐α and IL‐1β, and the concomitant administration of TNF‐a and IL‐ip decreased the short‐term (4 hours), nighttime (12 hours), and total daily food intakes in obese and lean rats; IL‐1β was more potent relative to TNF‐α; obese rats showed greater responsiveness to IL‐1β: 8.0 ng IL‐1β, for example, decreased the 12‐hour food intake by 52% in obese and 22% in lean rats. On the other hand, obese and lean rats did not exhibit a significantly different responsiveness to the anorexia induced by 50,100, or 500 ng TNF‐α at the 4‐hour period; and the concomitant ICV administration of TNF‐α and IL‐1β induced anorexia with additive (4‐hour period) or synergistic (12‐hour and 24‐hour periods) effects in obese rats. The effect of TNF‐α plus IL‐1β in lean rats was greater than additive for the 12‐hour and 24‐hour periods. The difference in suppression of total daily food intake by TNF‐α plus IL‐1β in obese (‐43%) versus lean (‐23%) rats was significantly different (p<0.01). The results show that obese (fa/fa) and lean (Fa/Fa) Zucker rats have differential responsiveness to the ICV microinfusion of two different classes of cytokines.
Laszlo Koranyi, Yukio Tanizawa, Luc Penicaud
et al.
Obese individuals are hyperinsulinemic and insulin resistant. Because amylin is cosecreted with insulin and may contribute to the insulin resistance of obesity, this study tested the hypothesis that insulin and amylin genes are coordinately regulated by obesity and carbohydrate feeding. Insulin and amylin gene expression were measured during the suckling/weaning transition in lean (Fa/Fa) and obese (fa/fa) Zucker rats, a period associated with marked changes in tissue insulin sensitivity. There was a decline in insulin mRNA (−90 ± 15%, P < 0.01) and amylin mRNA (−72 ± 21%, P < 0.01) content in pancreases of lean rats maintained on a high-fat diet from days 15 to 30, probably reflecting the relative increase in exocrine/endocrine development during this neonatal period and the effects of fat feeding. Weaning on high-carbohydrate versus high-fat diets resulted in enhanced expression of both insulin (P < 0.05) and amylin (P < 0.05) mRNAs. In contrast to the decline in pancreatic insulin and amylin mRNA content observed in lean rats, there was an increase in insulin mRNA (421.3 ± 57.5%, P < 0.05) and no change in amylin mRNA in obese rats maintained on a high-fat diet from days 15 to 30. There was no enhancement of insulin or amylin gene expression in obese rats with high carbohydrate relative to high-fat feeding, perhaps reflecting maximum rates of transcription in these obese insulin-resistant rats. Direct comparisons of insulin and amylin mRNA content between lean and obese rats revealed no differences at days 15–22 but enhanced expression of both mRNA types in obese rats by day 30, whether weaned on high-fat (P < 0.01) or high-carbohydrate (P < 0.05) diets. There was a significant correlation between pancreatic content of insulin and amylin mRNA (r = 0.749, P = <0.001) for all of the rats and nutritional conditions studied. These studies show enhanced expression of insulin and amylin genes with carbohydrate feeding and obesity and suggest coordinate expression of the genes that encode these two copackaged and secreted peptides.