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Biomedical subjects

C Peña

Publications and source records attributed to C Peña.

At least 55 records · Page 3Linked to original sources
PubMed1999

A brain Na+, K+-ATPase inhibitor (endobain E) enhances norepinephrine release in rat hypothalamus.

We have shown that synaptosomal membrane Na+, K+-ATPase activity is stimulated or inhibited by norepinephrine according to the presence or absence of a brain soluble fraction. Gel filtration of such soluble fraction has allowed the separation of two fractions, peaks I and II, able to stimulate and inhibit Na+, K+-ATPase activity, respectively. Peak II behaves much like ouabain, which has suggested the term endobain. From peak II, a subfraction termed II-E (endobain E), which highly inhibits Na+, K+-ATPase, has been separated by anionic exchange chromatography in a Synchropack AX-300 column. We determined the in vitro effect of endobain E obtained from rat cerebral cortex on neuronal norepinephrine release by incubating rat hypothalamic tissue in the presence of [3H]norepinephrine. Neuronal norepinephrine release was quantified as the factor above basal [3H]norepinephrine released to the medium at experimental and three post-experimental periods. Endobain E was found to increase norepinephrine release in a concentration-dependent fashion, reaching 200%, equivalent to the effect achieved with 400 microM ouabain. Ouabain effect persisted along three post-experimental periods whereas that of endobain E remained only during the first post-experimental period. These results led us to conclude that endobain increases norepinephrine release in hypothalamic neurons at the presynaptic nerve ending level, an effect resembling that of ouabain. It is postulated that endobain E may enhance catecholamine availability in the synaptic gap, leading to an increase in noradrenergic activity.

Animals↗
PubMed1999

Interaction of synthetic peptides from fasciculin with acetylcholinesterase.

Fasciculins (Fas) are three-looped polypeptides isolated from mamba venom which exert their toxic action by inhibiting noncompetitively acetylcholinesterase (AChE). A peptide (Fas-D) encompassing the first loop sequence was synthesized and characterized chemically, structurally, and functionally. Fas-D possesses an intramolecular disulfide bridge, present in the native toxin. Circular dichroism (CD) indicated the existence of 21.8% beta-sheet content and 24.2% beta-turn in this peptide, compatible with crystallographic data of the native toxin. The peptide showed only low partial AChE inhibition at submillimolar concentrations, much lower than that observed with Fas and a peptide (Fas-B) encompassing the second loop sequence. The simultaneous presence of Fas-D and Fas-B produced an additive inhibitory effect on AChE activity; calculated Ki and alphaKi values (7.3 +/-2.4 microM and 10.0 +/- 1.8 microM, respectively) were not significantly different, thus indicating noncompetitive inhibition. These results are consistent with site-directed mutagenesis studies and analysis of the crystal structure of the Fas-AChE complex, which indicate that residues from loops I and II contribute to Fas binding to the enzyme.

Acetylcholinesterase↗
PubMed1999

Brain soluble fractions which modulate Na+, K+-ATPase activity likewise modify muscarinic receptor.

Two brain soluble fractions, named peaks I and II, which respectively stimulate and inhibit neuronal Na+, K+-ATPase activity, have been isolated by gel filtration in Sephadex G-50. Since cholinergic transmission seems related to such enzyme activity, in this study we evaluated the effect of brain peak I, peak II, a more purified fraction II-E and commercial ouabain, on specific binding of the muscarinic antagonist [3H]quinuclidinyl benzilate to membranes from rat cerebellum, hippocampus and cerebral cortex. We found that binding was increased by peak I and decreased by peak II, II-E and ouabain, all effects proving concentration-dependent. Since the changes exerted on the muscarinic receptor followed a pattern similar to the one already described for synaptosomal membrane Na+, K+-ATPase activity, both systems seem to interact at a functional level.

Animals↗
PubMed1999

[An alternative method to determine the radiochemical purity of the 99mTC-tetrofosmine preparations].

This paper describes a new quality control method to determine the radiochemical purity (RCP) value of Technetium-99m-Tetrofosmin preparations. The results of this procedure were compared with the results obtained with the method suggested by the manufacturer of the kit (classic method), consisting in thin-layer chromatography involving the use of a single strip of ITLC/SG as the stationary phase, and a acetone:dichlorometane 35:65 (Ac:DCM) solvent mixture as the mobile phase. The method that is proposed in this paper (alternative method) uses the same stationary phase but it is developed in a single solvent, methylethylketone (MEK). This method has the following advantages: a better capacity to separate the 99mTc-Tetrofosmin complex from 99mTcO4- and 99mTcO2 impurities, a faster chromatographic developing time and the use of a single solvent in the quality control.

Acetone↗
PubMed1998

Effect of angiotensin-(1-7) on ATPase activities in several tissues.

The present investigation was undertaken to determine whether Ang-(1-7) is able to modify ATPase activities in membrane fractions prepared from several tissues. In the presence of 10(-6) M Ang-(1-7), total (Na , K+, Mg2+)-ATPase activity decreased 31% in rat atrium and 13% in sheep atrium but was unmodified in sheep liver, rat ventricle or crude brain membranes. In rat brain synaptosomal membranes, Ang-(1-7) at 10(-8) and 10(-7) M concentrations activated Na+, K+-ATPase 20 and 24%, respectively. Rat kidney Na+, K+-ATPase activity decreased roughly 40-70% with 10(-10)-10(-6) M Ang-(1-7)), but increased 22% with 10(-12) M peptide concentration, thus indicating a biphasic effect. Our findings showing that ATPase from several tissues responds differently to Ang-(1-7) are attributable to enzyme tissue specificity.

Angiotensin I↗
PubMed1998

Clinical and epidemiological findings in mechanically-ventilated patients with methicillin-resistant Staphylococcus aureus pneumonia.

Over the 5-year period from 1990 to 1994, a prospective cohort study was conducted to define the clinical and epidemiological characteristics of ventilator-associated methicillin-resistant Staphylococcus aureus (MRSA) pneumonia acquired during a large-scale outbreak of MRSA infection. Of 2411 mechanically ventilated patients, 347 (14.4%) acquired MRSA, 220 (63.4%) had MRSA positive respiratory tract samples and 41 (18.6%) developed ventilator-associated MRSA pneumonia. The overall attack rate for ventilator-associated MRSA pneumonia was 1.56 episodes/1000 ventilator days, but annual attack rates varied according to the trend of the outbreak (range 4.9-0.2). In comparison with methicillin-sensitive Staphylococcus aureus (MSSA), which was implicated in 98 episodes of ventilator-associated pneumonia, MRSA caused exclusively late-onset ventilator-associated pneumonia, while MSSA caused both early-onset [55 of 98 (56.1%) episodes] and late-onset [43 of 98 (43.8%) episodes] ventilator-associated pneumonia. Logistic regression analysis of all patients with Staphylococcus aureus pneumonia revealed intubation for more than 3 days (odds ratio (OR),1.11; confidence interval (CI):1.03-1.18) and prior bronchoscopy (OR,5.8; CI,1.85-18.19) to be independent variables associated with MRSA pneumonia. The results indicate that MRSA ventilator-associated pneumonia is a frequent complication in intensive care patients, manifesting itself as late-onset pneumonia in patients who have been intubated for prolonged periods and/or have often undergoing previous bronchoscopy.

Adult↗
PubMed1998

Na+,K+-ATPase interaction with a brain endogenous inhibitor (endobain E).

Na+,K+-ATPase activity of rat brain synaptosomal membranes was evaluated in the presence of an inhibitory fraction II-E (termed endobain E), isolated by gel filtration and anionic exchange HPLC of a rat brain soluble fraction. We studied endobain E aging, analyzed its inhibitory potency in the absence or presence of ouabain as well as its ability to block high affinity [3H]ouabain binding to cerebral cortex membranes. Similar loss of endobain E activity was observed when samples were stored either dried or in solution. Endobain E fraction inhibited synaptosomal membrane Na+,K+-ATPase activity in a concentration-dependent manner and the slope of the corresponding curve strongly resembled that of ouabain. Assays performed in the presence of endobain E and ouabain indicated that the inhibitory effect was additive or less than additive, depending on their respective concentrations during preincubation and/or incubation. High affinity [3H]ouabain binding to cerebral cortex membranes proved concentration-dependent from 0.10 to 0.50 mg protein per ml; binding inhibition by endobain E was independent of protein concentration within the above range. [3H]ouabain binding inhibition by endobain E was concentration-dependent over a 10-fold range, an effect similar to that found for Na+,K+-ATPase inhibition. The extent of endobain E effect on Na+,K+-ATPase inhibition was much higher (90-100%) than that on [3H]ouabain binding blockade (50%). Findings suggest some type of interaction between endobain E and ouabain inhibitory mechanisms and favour the view that the former behaves as an endogenous ouabain.

Animals↗
PubMed1998

Endogenous modulators of brain Na+,K(+)-ATPase at early postnatal stages of rat development.

The presence of endogenous modulators (peaks I and II) of synaptosomal Na+, K(+)-ATPase activity from adult rat cerebral cortex was previously suggested. In this study, the presence of such modulators at different postnatal stages of rat development was examined and their effect was tested on Na+, K(+)-ATPase activity. Synaptosomal membrane Na+, K(+)-ATPase activity was enhanced 20-30% by peak I and inhibited 70-75% by peak II obtained from 4-, 10-, 20- and 35-40-day-old rats. A fraction purified from peak II by anionic exchange HPLC (termed II-E) highly inhibits enzyme activity and behaves as a ouabain-like factor. Inhibitory activity of a 4-day-old II-E fraction proved higher than the corresponding fraction obtained from adult rats. Since expression of cerebral Na+, K(+)-ATPase has been shown to increase 10-fold during development whereas peak II concentration was observed to remain constant, and given the higher potency of purified neonatal II-E fraction, the effect of the latter may be greater at early postnatal stages of development than during adult life. It is suggested that the II-E fraction, which contains an ouabain-like factor, may play a role in neuronal development.

Animals↗
PubMed1998

Presence of an endogenous factor in avian CNS with agonistic action on benzodiazepine receptors.

In the present paper we describe the presence in avian CNS of an endogenous inhibitor of [3H]flunitrazepam binding. This compound was extracted from a synaptic membrane fraction isolated from chick optic lobe and brain using an exhaustive aqueous washing procedure, then purified by means of solid-phase extraction with C18 cartridges and several HPLC steps until an homogeneous peak was obtained. Its chemical structure was studied by size-exclusion chromatography of the purified material which indicated that it possesses a molecular weight below 1350. Although its inhibitory activity was lost by HCl treatment, its peptidic nature was ruled out by an amino acid and N-terminal sequence analyses. Ultraviolet absorption spectrum showed two main peaks at 230 and 280 nm. The endogenous compound was found to inhibit competitively [3H]flunitrazepam binding to its recognition site without affecting [3H]GABA binding to the same receptor complex. The behavior of the endogenous factor in an "in vitro" GABA "shift" test and GABA-dependent chloride flux experiments were similar to that of benzodiazepine receptor agonists. In conclusion, these results demonstrate the existence in avian CNS of a competitive endogenous inhibitor of benzodiazepine binding with agonistic action on benzodiazepine receptors.

Animals↗
PubMed1998

Kinetics of Na+, K+-ATPase inhibition by a rat brain endogenous factor (II-E).

Previous work from this laboratory led to the isolation by gel filtration and anionic exchange HPLC of a rat brain fraction named II-E, which highly inhibits synaptosomal membrane Na+, K+-ATPase activity. In this study we evaluated the kinetics of such inhibition and found that inhibitory potency was independent of Na+ (1.56-200 mM), K+ (1.25-40 mM), or ATP (1-8 mM) concentration. Hanes-Woolf plots indicated that II-E decreases Vmax but does not alter KM value, and suggested uncompetitive inhibition for Na+, K+ or ATP. However, II-E became a stimulator at 0.5 mM ATP concentration. It is postulated that this brain factor may modulate ionic transport at synapses, thus participating in central neurotransmission.

Adenosine Triphosphate↗
PubMed1998

Epidemiology and successful control of a large outbreak due to Klebsiella pneumoniae producing extended-spectrum beta-lactamases.

An outbreak due to extended-spectrum beta-lactamase-producing Klebsiella pneumoniae (ESBL-KP) was detected from May 1993 to June 1995. A total of 145 patients, particularly patients in intensive care units (ICUs) (107 patients [72%]), were colonized or infected. Infection developed in 92 (63%) patients, and primary bacteremia caused by ESBL-KP was the most frequent infection (40 of 92 patients [43%]). A single clone of ESBL-KP was identified by pulsed-field gel electrophoresis analysis throughout the whole period, and no molecular epidemiological relationship could be found between the epidemic strain and non-ESBL-KP isolates. To determine risk factors for ESBL-KP infection weekly rectal swabs were obtained in three serial incidence surveys (470 patients); the probabilities of carriage of ESBL-KP in the digestive tract were 33% (October and November 1993), 40% (May and June 1994), and 0% (October and November 1995) at 10 days of ICU admission. A logistic regression model identified prior carriage of ESBL-KP in the digestive tract (odds ratio, 3.4; 95% confidence interval 1.1 to 10.4) as an independent variable associated with ESBL-KP infection. A statistically significant correlation was observed between the restricted use of oxyimino-beta-lactams (189 defined daily doses [DDD]/ 1,000 patient-days to 24 DDD/1,000 patient-days) and the trends of ESBL-KP infection (r = 0.7; P = 0.03).

Anti-Bacterial Agents↗
PubMed1998

Myocardial abscess at a distant zone from the active valvular infection.

A case of an infective endocarditis with myocardial abscess due to Streptococcus anginosus at a distant location from the active valvular infection is reported. We conclude that local cardiac suppurative complications can appear in the evolution of endocarditis caused by this virulent organism.

Abscess↗