Effect of osmotic pressure and simultaneous heat-moisture phosphorylation treatments on the physicochemical properties of mung bean, water caltrop, and corn starches.

This study aimed to investigate the physicochemical properties of modified starch prepared through the simultaneous heat-moisture and phosphorylation treatment (HMPT) and osmotic pressure treatment (OPT) for water caltrop starch (WCS), mung bean starch (MBS), and amylose-rich corn starch (CS) for different time periods. Furthermore, variations in starch content [amylose and resistant starch (RS)], swelling powder (SP), water solubility index (WSI), crystallinity, thermal properties, gelatinization enthalpy (ΔH), and glycemic index (GI) were examined. This study demonstrates that neither HMPT nor OPT resulted in a significant increase in the resistant starch (RS) content, whereas all samples succeeded in heat-treating at 105 °C for another 10 min exhibited a significant increase in RS content compared to their native counterparts. Moreover, the gelatinization temperatures of the three starches increased (To, Tp, and Tc), whereas their gelatinization enthalpy (ΔH) and pasting viscosity decreased. In particular, the GI of all three modified starches subjected to HMPT or OPT showed a decreasing trend with modification time, with OPT exhibiting the best effect. Therefore, appropriate modification through HMPT or OPT is a viable approach to develop MBS, WCS, and CS as processed foods with low GI requirements, which exceptionally may be suitable for canned foods, noodles, and bakery products.

What subjective experiences determine the perception of falling asleep during sleep onset period?

Sleep onset is associated with marked changes in behavioral, physiological, and subjective phenomena. In daily life though subjective experience is the main criterion in terms of which we identify it. But very few studies have focused on these experiences. This study seeks to identify the subjective variables that reflect sleep onset. Twenty young subjects took an afternoon nap in the laboratory while polysomnographic recordings were made. They were awakened four times in order to assess subjective experiences that correlate with the (1) appearance of slow eye movement, (2) initiation of stage 1 sleep, (3) initiation of stage 2 sleep, and (4) 5 min after the start of stage 2 sleep. A logistic regression identified control over and logic of thought as the two variables that predict the perception of having fallen asleep. For sleep perception, these two variables accurately classified 91.7% of the cases; for the waking state, 84.1%.

Flexible Epoxy Resins Formed by Blending with the Diblock Copolymer PEO-b-PCL and Using a Hydrogen-Bonding Benzoxazine as the Curing Agent.

In this study, we enhanced the toughness of epoxy resin by blending it with the diblock copolymer poly(ethylene oxide⁻b⁻ε-caprolactone) (PEO-b-PCL) with a benzoxazine monomer (PA-OH) as the thermal curing agent. After thermal curing, Fourier transform infrared spectroscopy revealed that intermolecular hydrogen bonding existed between the OH units of the epoxy⁻benzoxazine copolymer and the C⁻O⁻C (C=O) units of the PEO (PCL) segment. Differential scanning calorimetry and dynamic mechanical analysis revealed that the glass transition temperature and storage modulus of the epoxy⁻benzoxazine matrix decreased significantly upon increasing the concentration of PEO-b-PCL. The Kwei equation predicted a positive value of q, consistent with intermolecular hydrogen bonding in this epoxy⁻benzoxazine/PEO-b-PCL blend system. Scanning electron microscopy revealed a wormlike structure with a high aspect ratio for PEO-b-PCL as the dispersed phase in the epoxy⁻benzoxazine matrix; this structure was responsible for the improved toughness.

The involvement of hypoxia-inducible transcription factor-1-dependent pathway in nickel carcinogenesis.

Nickel is a potent environmental pollutant in industrial countries. Because nickel compounds are carcinogenic, exposure to nickel represents a serious hazard to human health. The understanding of how nickel exerts its toxic and carcinogenic effects at a molecular level may be important in risk assessment, as well as in the treatment and prevention of occupational diseases. Previously, using human and rodent cells in vitro, we showed that hypoxia-inducible signaling pathway was activated by carcinogenic nickel compounds. Acute exposure to nickel resulted in the accumulation of hypoxia-inducible transcription factor (HIF)-1, which strongly activated hypoxia-inducible genes, including the recently discovered tumor marker NDRG1 (Cap43). To further identify HIF-1-dependent nickel-inducible genes and to understand the role of the HIF-dependent signaling pathway in nickel-induced transformation, we used the Affymetrix GeneChip to compare the gene expression profiles in wild-type cells or in cells from HIF-1 alpha knockout mouse embryos exposed to nickel chloride. As expected, when we examined 12,000 genes for expression changes, we found that genes coding for glycolytic enzymes and glucose transporters, known to be regulated by HIF-1 transcription factor, were induced by nickel only in HIF-1 alpha-proficient cells. In addition, we found a number of other hypoxia-inducible genes up-regulated by nickel in a HIF-dependent manner including BCL-2-binding protein Nip3, EGLN1, hypoxia-inducible gene 1 (HIG1), and prolyl 4-hydroxylase. Additionally, we found a number of genes induced by nickel in a HIF-independent manner, suggesting that Ni activated other signaling pathways besides HIF-1. Finally, we found that in HIF-1 alpha knockout cells, nickel strongly induced the expression of the whole group of genes that were not expressed in the presence of HIF-1. Because the majority of modulated genes were induced or suppressed by nickel in a HIF-1-dependent manner, we elucidated the role of HIF-1 transcription factor in cell transformation. In HIF-1 alpha-proficient cells, nickel exposure increased soft agar growth, whereas it decreased soft agar growth in HIF-1 alpha-deficient cells. We hypothesize that the induction of HIF-1 transcription factor by nickel may be important during the nickel-induced carcinogenic process.