Group method approach to the estimation of response factors of unavailable substances in quantitative gas chromatography.

The method's accuracy of a compound quantitation by chromatography depends on the calibration procedure with a pure standard of the target analyte, if the latter is unavailable uncertainty is unavoidable. The group method is a different approach in GC quantitative analysis that shows a practicable way for avoiding this uncertainty and accurately quantify a mixture containing one or more unavailable components. This paper is concerned with the definition of the group method quantitative parameters, the application procedures for their calculation, the determination of the quantitative proportion of a group of unavailable components of a mixture and the partial or total quantitation of the latter. The paper also describes the steps for carrying out the so-called group-correlation method in the determination of the response factors of unavailable compounds, which belong to a homologous series. The GC experimental corroboration of the group method approach employing model mixtures of compounds is also presented.

Alcohol concentration determines the type of atrial arrhythmia induced in a porcine model of acute alcoholic intoxication.

Alcohol abuse has long been suspected clinically to cause paroxysmal atrial tachyarrhythmias. However, such a relationship has never been conclusively proven, partly due to the lack of experimental evidence. Although atrial fibrillation (AF) is the most common atrial arrhythmia attributed to acute alcoholic ingestion, atrial flutter has occasionally been noted. We analyzed the possible role of alcohol in initiation and/or maintenance of a variety of atrial tachyarrhythmias in a closed-chest porcine model. Nine pigs underwent nine endocardial right atrial stimulation protocols (RASP) at baseline and 17 RASPs after increasing doses of ethanol (first infusion 1,230 mg/kg, second infusion 870 mg/kg) by means of one multipolar catheter advanced under heavy sedation from the femoral vein. Each RASP included 1, 2, and 3 extrastimuli, and rapid pacing at 5 times diastolic threshold. Venous ethanol concentrations were measured (HPGC method) every 10 minutes and at the time of arrhythmia induction. Atrial tachyarrhythmias were induced in 4 of 9 baseline RASPs, and lasted for a mean of 21 seconds, and in 16 of 17 RASPs after alcohol lasting for a mean of 357 seconds. Only fibrillation was observed at the baseline RASP. The atrial tachyarrhythmias induced after alcohol were AF in 11 RASPs and atrial flutter in 5 RASPs (in 5 animals). The mean venous ethanol concentration at the time of the longest arrhythmia induced for each RASP were 200 +/- 89 mg/dL for RASP inducing fibrillation and 292 +/- 40 mg/dL for RASP inducing flutter (P < 0.05). Flutter tended to be sustained (> 1 minute in duration) more often than fibrillation (4 of 5 flutter vs 2 of 11 fibrillation P < 0.05). In three experiments, atrial flutter persisted for > 10 minutes and was terminated by overdrive atrial pacing. We concluded: (1) in this closed-chest porcine model, an ethanol infusion facilitates a variety of atrial arrhythmias related to the ethanol concentration; (2) flutter tended to be sustained, and its termination by overdrive pacing suggests the possibility of an alcohol induced reentrant mechanism; and (3) the higher concentration required for atrial flutter, exceeding that usually seen in humans, may help to explain the rarity of atrial flutter in clinical alcohol intoxication.

S100 beta stimulates inducible nitric oxide synthase activity and mRNA levels in rat cortical astrocytes.

The glia-derived, neurotrophic protein S100 beta has been implicated in development and maintenance of the nervous system. However, S100 beta has also been postulated to play a role in mechanisms of neuropathology, because of its specific localization and selective overexpression in Alzheimer's disease. To begin to address the question of whether S100 beta can induce potentially toxic signaling pathways, we examined the effects of the protein on nitric oxide synthase (NOS) activity in cultures of rat cortical astrocytes. S100 beta treatment of astrocytes induced a time- and dose-dependent increase in accumulation of the NO metabolite, nitrite, in the conditioned medium. The S100 beta- stimulated nitrite production was blocked by cycloheximide and by the NOS inhibitor N-nitro-L-arginine methylester, but not by the inactive D-isomer of the inhibitor. Direct measurement of NOS enzymatic activity in cell extracts and analysis of NOS mRNA levels showed that the NOS activated by S100 beta addition is the calcium-independent, inducible isoform. Furthermore, the specificity of the effects of S100 beta on activation of NOS was demonstrated by the inability of S100 alpha and calmodulin to induce an increase in nitrite levels. Our data indicate that S100 beta can induce a potent activation of inducible NOS in astrocytes, an observation that might have relevance to the role of S100 beta in neuropathology.

Genesis of olfactory receptor neurons in vitro: regulation of progenitor cell divisions by fibroblast growth factors.

Olfactory receptor neurons are produced continuously in mammalian olfactory epithelium in vivo, but in explant cultures neurogenesis ceases abruptly. We show that in vitro neurogenesis is prolonged by fibroblast growth factors (FGFs), which act in two ways. FGFs increase the likelihood that immediate neuronal precursors (INPs) divide twice, rather than once, before generating neurons; this action requires exposure of INPs to FGFs by early G1. FGFs also cause a distinct subpopulation of explants to generate large numbers of neurons continually for at least several days. The data suggest that FGFs delay differentiation of a committed neuronal transit amplifying cell (the INP) and support proliferation or survival of a rare cell, possibly a stem cell, that acts as a progenitor to INPs.

Yeast bZip proteins mediate pleiotropic drug and metal resistance.

Saccharomyces cerevisiae contains a group of transcription factors related to mammalian c-Jun. This yeast Jun-family of proteins consists of GCN4, a regulator of genes involved in amino acid biosynthesis, and yAP-1, a factor conferring pleiotropic drug resistance when overexpressed. In the work described here, we show that a third member of the yeast Jun-family exists. This protein has been designated CAD1 and provides resistance to cadmium when present on a high-copy plasmid. CAD1 and yAP-1 are related in their amino-terminal DNA binding domains and can recognize the same DNA target site in vitro. Overproduction of CAD1 leads to transcriptional activation of an artificial reporter gene in delta yap1 cells. High level production of either CAD1 or yAP-1 causes cells to acquire a pleiotropic drug-resistant phenotype and to be able to tolerate normally toxic levels of iron chelators and zinc. Surprisingly, disruption of the CAD1 gene has no effect on the normal cellular resistance to cadmium but delta yap1 mutants are hypersensitive to this cytotoxic metal. The cadmium hypersensitivity of the delta yap1 mutant described here indicates that one major role of YAP1 in the yeast cell is to mediate resistance to this metal.

[Helicoid ventricular tachycardia, torsade de pointes, in acute myocardial infarction]. / Taquicardia ventricular helicoidal, "torsade de pointes", en el infarto agudo del miocardio.

Helicoidal ventricular tachycardia (Torsades de Pointe), (HVT) is an arrhythmia with peculiar characteristics and therefore should be individualized. The occurrence of HVT during acute myocardial evolution has been denied by many authors. In this paper, the possibility that this association may be not only coincidental is analyzed. A group of 1,307 patients with acute myocardial infarction was studied, in 29 of them this arrhythmia was detected in the first 72 hours and these patients didn't have an associated disease and/or treatment related to HVT. This represents an incidence of 2.22% in this group. The helicoidal ventricular tachycardia had a peculiar behavior, different to the one found in HVT of other etiologies. It was triggered by early premature ventricular beats, it was found even in cases with supraventricular tachycardia and acute atrio--ventricular heart block, very seldom is autolimited and usually degenerates into ventricular fibrillation, the most important factor in association with this arrhythmia is QT prolongation. Intracavitary pacing is the treatment of choice.

Taquicardia ventricular helicoidal, "torsades de pointe", en el infarto agudo del miocardio. / Helicoidal ventricular tachycardia \"torsades de pointe\" in acute myocardial infarction

La taquicardia ventricular helicoidal o "torsades de pointe" es un trastorno del ritmo que debe ser individualizado por sus caracteristicas peculiares. Se ha negado reiteradamente que la taquicardia ventricular helicoidal sea una arritmia habitual en la evolucion de un infarto agudo del miocardio. Este trabajo estudia la posibilidad que esta asociacion no sea solo coincidental. Se estudiaron 1,307 pacientes con infarto agudo del miocardio, de los cuales se obtuvieron 29 en los que se detecto esta arritmia en las primeras 72 horas de evolucion y que no tenian asociado un padecimiento o tratamiento de los que frecuentemente se asocian a taquicardia ventricular helicoidal. Este trastorno del ritmo tuvo una incidencia de 2.22% en este lote, con un comportamiento particular, diferente a la taquicardia ventricular helicoidal producida por otras etiologias. Es desencadenada frecuentemente por extrasistoles ventriculares precoces, aparece aun en presencia de taquicardias supraventriculares y bloqueio auriculoventricular agudo, dificilmente se autolimita y generalmente degenera en fibrilacion ventricular. El factor mas importante asociado a esta arritmia es la prolongacion de QT y la terapeutica mas eficiente fue mediante electro-estimulacion intracavitaria