Evaluation of sources of irreproducibility of retention indices under programmed temperature gas chromatography conditions.

Retention index under the programmed temperature gas chromatography (PTGC) conditions (I) is widely accepted despite of its unsatisfactory reproducibility. Effects of heating rate (r), stationary liquid film thickness (d), inlet pressure (p), initial temperature (T) and polarity of stationary phase (s) on I reproducibility were studied in the present work. We found that excellent reproducibility and regularity of I values are obtainable at conditions of relatively low T and relatively high r and p, as well as use of quality thick-film column under an operation in a single-retention behavior region (i.

Phenomenon of dual- and single-retention behaviors of solutes and its validation by computational simulation in linear programmed temperature gas chromatography.

The current theory of programmed temperature gas chromatography considers that solutes are focused by the stationary phase at the column head completely and does not explicitly recognize the different effects of initial temperature (To ) and heating rate (rT ) on the retention time or temperature of a homologue series. In the present study, n-alkanes, 1-alkenes, 1-alkyl alcohols, alkyl benzenes, and fatty acid methyl esters standards were used as model chemicals and were separated on two nonpolar columns, one moderately polar column and one polar column. Effects of To and rT on the retention of nonstationary phase focusing solutes can be explicitly described with isothermal and cubic equation models, respectively.

Determination and evaluation of gas holdup time with the quadratic equation model and comparison with nonlinear models for isothermal gas chromatography.

Gas holdup time (tM) is a basic parameter in isothermal gas chromatography (GC). Determination and evaluation of tM and retention behaviors of n-alkanes under isothermal GC conditions have been extensively studied since the 1950s, but still remains unresolved. The difference equation (DE) model [J.

A new accurate quadratic equation model for isothermal gas chromatography and its comparison with the linear model.

The gas holdup time (tM) is a dominant parameter in gas chromatographic retention models. The difference equation (DE) model proposed by Wu et al. (J.

Difference equation model for isothermal gas chromatography expresses retention behavior of homologues of n-alkanes excluding the influence of holdup time.

A difference equation (DE) model is developed using the methylene retention increment (Δtz) of n-alkanes to avoid the influence of gas holdup time (tM). The effects of the equation orders (1st-5th) on the accuracy of a curve fitting show that a linear equation (LE) is less satisfactory and it is not necessary to use a complicated cubic or higher order equation. The relationship between the logarithm of Δtz and the carbon number (z) of the n-alkanes under isothermal conditions closely follows the quadratic equation for C3-C30n-alkanes at column temperatures of 24-260 °C.

Spatial distribution of organochlorine contaminants in soil, sediment, and fish in Bikini and Enewetak Atolls of the Marshall Islands, Pacific Ocean.

Several nuclear tests were performed at Enewetak and Bikini Atolls in the Marshall Islands between 1946 and 1958. The events at Bikini Atoll involved several ships that were tested for durability during nuclear explosions, and 24 vessels now rest on the bottom of the Bikini lagoon. Nine soil samples were collected from different areas on the two islands of the atoll, and eighteen sediment, nine fish, and one lobster were collected in the vicinity of the sunken ships.

Divergent effects of prostaglandin receptor signaling on neuronal survival.

Induction of cyclooxygenase-2 (COX-2) with production of prostaglandins occurs in a wide spectrum of acute and chronic neurodegenerative diseases and is associated with neuronal death. Inhibition of the COX-2 pathway and downstream production of prostaglandins protect neurons in rodent models of cerebral ischemia and neurodegeneration. Recent studies investigating the functions of selected prostaglandin receptor pathways in mediating COX-2 neurotoxicity have demonstrated both toxic and paradoxically neuroprotective effects of several receptors in models of excitotoxicity.

[Analysis of volatile constituents from leaves of plants by gas chromatography/mass spectrometry with solid-phase microextraction].

A method for analyzing volatile constituents from plant leaves with gas chromatography/mass spectrometry (GC/MS) coupled with solid-phase microextraction (SPME) was developed. The volatile compounds from the plant leaves inside a sealed flask maintained at 45 degrees C in a water bath were efficiently extracted with Polyacrylate (85 microm) SPME fibers prior to perform GC/MS analysis. The GC/MS analysis indicated that the volatile compounds from the plant leaves which is easy to be damaged by Tetraychus vienneis include relative large amounts of cis-3-hexenyl ester acetic acid, cis-3-hexenyl ester butanoic acid and alpha-famesene.

Deletion of the prostaglandin E2 EP2 receptor reduces oxidative damage and amyloid burden in a model of Alzheimer's disease.

Epidemiological studies demonstrate that chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) in normal aging populations reduces the risk of developing Alzheimer's disease (AD). NSAIDs inhibit the enzymatic activity of cyclooxygenase-1 (COX-1) and inducible COX-2, which catalyze the first committed step in the synthesis of prostaglandins. These studies implicate COX-mediated inflammation as an early and potentially reversible preclinical event; however, the mechanism by which COX activity promotes development of AD has not been determined.

Neuroprotection by the PGE2 EP2 receptor in permanent focal cerebral ischemia.

Recent studies suggest a neuroprotective function of the PGE2 EP2 receptor in excitotoxic neuronal injury. The function of the EP2 receptor was examined at time points after excitotoxicity in an organotypic hippocampal model of N-methyl-D-aspartate (NMDA) challenge and in a permanent model of focal forebrain ischemia. Activation of EP2 led to significant neuroprotection in hippocampal slices up to 3 hours after a toxic NMDA stimulus.

Prostaglandin D2 mediates neuronal protection via the DP1 receptor.

Cyclo-oxygenases (COXs) catalyze the first committed step in the synthesis of the prostaglandins PGE(2), PGD(2), PGF(2alpha), PGI(2) and thomboxane A(2). Expression and enzymatic activity of COX-2, the inducible isoform of COX, are observed in several neurological diseases and result in significant neuronal injury. The neurotoxic effect of COX-2 is believed to occur through downstream effects of its prostaglandin products.

PGE2 receptors rescue motor neurons in a model of amyotrophic lateral sclerosis.

Recent studies suggest that the inducible isoform of cyclooxygenase, COX-2, promotes motor neuron loss in rodent models of ALS. We investigated the effects of PGE2, a principal downstream prostaglandin product of COX-2 activity, on motor neuron survival in an organotypic culture model of ALS. We find that PGE2 paradoxically protects motor neurons at physiological concentrations in this model.

Neuroprotective function of the PGE2 EP2 receptor in cerebral ischemia.

The cyclooxygenases COX-1 and COX-2 catalyze the first committed step of prostaglandin synthesis from arachidonic acid. Previous studies in rodent stroke models have shown that the inducible COX-2 isoform promotes neuronal injury, and the administration of COX-2 inhibitors reduces infarct volume. We investigated the function of PGE2, a principal prostaglandin product of COX-2 enzymatic activity, in neuronal survival in cerebral ischemia.

Neuronal overexpression of cyclooxygenase-2 increases cerebral infarction.

Increases in COX-2 enzymatic activity and prostaglandin production have been associated with neuronal injury in both acute and age-related degenerative neurological diseases. In this study, we tested the effects of increased COX-2 activity in a model of transient focal ischemia using a transgenic mouse model in which human COX-2 is constitutively expressed selectively in neurons of the striatum, cerebral cortex, and hippocampus. These COX-2 transgenic mice harbor elevated levels of PGE(2) that are 10-fold higher than nontransgenic levels.