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Biomedical subjects

I Valdés

Publications and source records attributed to I Valdés.

11 recordsLinked to original sources
PubMed2001

Succinylation of cyclodextrin glycosyltransferase from Thermoanaerobacter sp. 501 enhances its transferase activity using starch as donor.

A simple modification procedure, the succinylation of amino groups, was suitable to increase the transferase (disproportionation) activity of cyclodextrin glycosyltransferase (CGTase) from Thermoanaerobacter sp. 501 using different linear oligosaccharides as acceptors. On the contrary, the synthesis of cyclodextrins (CDs), the coupling of CDs with oligosaccharides, and the hydrolysis of starch decreased after chemical modification. The degree of succinylation of amino groups (45%) was accurately determined by MALDI-TOF mass spectrometry. The formation of CDs under industrial conditions was analyzed for native and succinylated CGTases, showing similar selectivity to alpha-, beta-, gamma-CD. The acceptor reaction with D-glucose using soluble starch as glucosyl donor was studied at 60 degrees C and pH 5.5. Malto-oligosaccharides (MOS) production was notably higher using the semisynthetic enzyme at different ratios (w/w) starch:D-glucose. Thus, more than 90% of the initial starch was converted into MOS (G2-G7) in 48 h employing a ratio donor:acceptor 1:2 (w/w).

Acylation↗
PubMed1998

An innovative sandwich ELISA system based on an antibody cocktail for gluten analysis.

A cocktail sandwich ELISA based on the employ of two monoclonal antibodies (MAbs) as coating antibodies and a third MAb conjugated to horseradish peroxidase has been developed for the analysis of gluten in foods. Given that each MAb displays a wide specificity spectrum for wheat, barley, rye and oats prolamins, their combination for ELISA ensures a high crossreactivity with most of the potentially toxic gliadin, hordein, secalin and avenin protein family. One of the unprecedented features of the cocktail sandwich ELISA is that it permits for the first time analysis of barley hordeins in foods, which is unattainable using conventional or commercial ELISA kits. Besides, gliadins, hordeins and secalins are recognised to the same extent. The system provides a high detection sensitivity for gliadins, hordeins, secalins and avenins (1.5, 0.05, 0.15 and 12 ng/ml, respectively). The working linear range comprises 3-100 ng/ml with a gliadin detection limit of 1.5 ppm. This limit of detection is even better than that demanded in the latest Codex recommendation, 10 ppm. Cocktail ELISA data were contrasted with those of commercial ELISA kits and confirmed by mass spectrometry, a non-immunological technique which provides evidence for the occurrence of false positive results with the commercial kits.

Antibodies, Monoclonal↗
PubMed1997

Acute respiratory illnesses in the first 18 months of life.

To help assess the causes and frequency of acute respiratory illnesses (ARI) during the first 18 months of life in Chile, a cohort of 437 children born in good health between May 1991 and April 1992 was followed at an urban health clinic in northern Santiago. Information was obtained from medical checkups performed at the clinic, from emergency health care services, from private physicians, and from interviews with each child's mother when the child was enrolled in the study and when it was 6, 12, and 18 months old. Followup was completed for 379 (87%) of the children. ARI accounted for 67% of all 3762 episodes of illness recorded for these children in the 18-month study period, 1384 (55%) of the ARI episodes affecting the upper respiratory tract and the remaining 1144 (45%) affecting the lower. The overall rate of ARI observed was 33 episodes per 100 child-months of observation. The incidences of upper, lower, and total ARI episodes decreased significantly in the third six months of life. A statistically significant association was found between upper ARI (> or = 2 episodes) and maternal smoking (> or = 5 cigarettes per day), but no significant associations were found with any of the other risk factors studied. However, lower ARI (> or 2 episodes) was significantly associated with maternal schooling (< 8 years), a family history of atopic allergy, and substandard housing conditions; and lower ARI (> or = 4 episodes) was significantly associated with these factors and also with the existence of one or more siblings, birth in a cold season, limited breast-feeding (< 4 months), and low socioeconomic status. Significant associations were found between obstructive bronchitis episodes and most of the risk factors studied (gender, siblings, season of birth, duration of breast-feeding, maternal schooling, smoking, use of polluting fuels in the home, and a family history of atopic allergy); similarly, significant associations were found between the occurrence of pneumonia and many risk factors (including siblings, season of birth, duration of breast-feeding, maternal schooling, smoking, and socioeconomic level). Overall, 42 of the study children were hospitalized during the study period for lower tract ARI, and two children died of pneumonia at home during their first 6 months of life. The rate of hospitalization fell significantly with increasing age.

Acute Disease↗
PubMed1996

[Infant pneumonia at periodic check-ups. Characteristics and associated factors].

BACKGROUND: Each year, pneumonia is the cause of death of forty thousand children under four years of age in America. AIM: To follow children from birth until two years of age and record episodes of pneumonia, their features and associated factors. PATIENTS AND METHODS: Four hundred thirty seven healthy newborns were followed in a public out patient clinic of Northern Santiago until two years of age. Pneumonia was diagnosed using clinical or radiological criteria. The mothers of each child were interviewed in each follow up visit. RESULTS: Two hundred ten episodes of pneumonia were detected during the study, 0.6 episodes per child and 1.8 episodes per affected child. Sixty six percent of episodes occurred during the first year of age. Total prevalence was 22.4 and 14.3% during the first and second year of age respectively. Semi annual incidence was 13.8 and 5.5% during the first and fourth semester respectively. Children that had pneumonia, were male in a higher proportion, had a lower birth weight, had higher number of brothers, mothers with less that 8 years of school courses and a lower socioeconomic level. During the first year of life, breast feeding during less than four months and a birth date during spring and summer were associated with a higher incidence of pneumonia. Seventy seven episodes, that occurred in 48 children, required hospitalization. The hospitalization rate for the whole cohort was 13.4% percent and 41.2% for affected children. Mean hospital stay was 5.8 days. Risk factors for hospitalization were male sex, less than four months of breast feeding, low birth weight, to have brothers, a lower mother education and lower socioeconomic level. Two children died. CONCLUSIONS: One out of three healthy newborns had pneumonia during the first year of life and a low socioeconomic level was an important risk factor.

Episode of Care↗
PubMed1991

Comparative effect of transient global ischemia on extracellular levels of glutamate, glycine, and gamma-aminobutyric acid in vulnerable and nonvulnerable brain regions in the rat.

We evaluated whether regional differences in the magnitude of glutamate, gamma-aminobutyric acid (GABA), and glycine release could explain why some regions are vulnerable to ischemia whereas others are spared. By means of the microdialysis technique, the temporal profile of ischemia-induced changes in extracellular levels of glutamate, GABA, and glycine was compared in regions that demonstrate differing susceptibilities to a 10- and 20-min ischemic insult (dorsal hippocampus, anterior thalamus, somatosensory cortex, and dorsolateral striatum). The degree of ischemia (as established by local cerebral blood flow reduction) and the magnitude of histopathological neuronal damage were also evaluated in these regions. The blood flow reduction was severe and uniform in all regions; however, the histopathological outcome illustrated a different pattern. Whereas the CA1 sector of the hippocampus was severely damaged, the thalamus and cortex were relatively spared from both 10 and 20 min of ischemia. Striatal neurons were resistant to a 10-min insult but severely damaged after 20 min of ischemia. Ischemia-induced increase in glutamate and GABA content were of a similar magnitude and temporal profile in all four brain regions. A uniform increase in extracellular glycine levels was also observed in all four brain structures. The postischemic response, however, was different. Glycine levels remained twofold higher than baseline in the hippocampus but fell to baseline in the cortex and thalamus after both 10- and 20-min insults. In the striatum, glycine levels returned to baseline after 10 min of ischemia but remained relatively high after a 20-min insult.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Ischemia induces release of glutamate in regions spared from histopathologic damage in the rat.

Excessive release of glutamate is thought to play a major role in the susceptibility of neurons to ischemia. In the present study, we evaluated whether differences in the magnitude of glutamate release resulted in some regions being vulnerable to ischemia, but others being spared from irreversible histopathologic damage. Specifically, we compared the temporal profile of ischemia-induced changes in extracellular levels of glutamate in a region selectively vulnerable to 10 minutes of transient ischemia (CA1 sector of the hippocampus) to the changes occurring in regions that, although rendered ischemic, are usually unaffected by a 10-minute insult (i.e., thalamus, cortex, and dorsolateral striatum). In an attempt to correlate the regional changes in glutamate release to the magnitude of the ischemic insult, the degree of ischemia (e.g., ATP depletion, lactate accumulation, and local cerebral blood flow reduction) and the final histopathologic outcome were also evaluated in these regions. Blood flow reduction and energy depletion were severe and uniform in all regions. However, the histopathologic outcome illustrated a different pattern. Although the CA1 sector of the hippocampus was severely damaged, all other brain regions were unaffected by the 10-minute insult. Extracellular glutamate levels, measured by microdialysis, were significantly elevated during ischemia in all four regions. These levels continued to increase during the early recirculation period and gradually returned to baseline by 30 minutes of reperfusion, with a similar temporal changes in all four brain structures. These results, taken with our previous findings, demonstrate that elevated intraischemic glutamate levels are insufficient to independently engender ischemic damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1989

Direct evidence for acute and massive norepinephrine release in the hippocampus during transient ischemia.

Recent studies suggest the norepinephrine (NE) may play a regulatory role in neuronal cell death in the hippocampus after transient ischemia. However, ischemia-induced changes in extracellular NE release have not been demonstrated. In the present study, we utilized the microdialysis technique to measure extracellular NE levels in the hippocampus before, during, and after 20 min of global ischemia induced by two-vessel occlusion combined with systemic hypotension in the rat. Stable basal concentrations of extracellular NE were detected in three consecutive samples collected prior to ischemia (1.86 +/- 1.21 pmol/ml of perfusate mean +/- SEM). During ischemia, NE levels increased to 30.1 +/- 5.5 pmol/ml, representing an 18-fold increase. The levels gradually returned to baseline by 40 min of reperfusion. These results are the first to demonstrate that acute and massive extracellular release of NE occurs in the hippocampus during ischemia and early recirculation. These results support the hypothesis that the activation of the noradrenergic system may play a significant role in modulating the development of ischemic neuronal damage.

Animals↗
PubMed1989

Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain.

We have demonstrated previously that mild intraischemic hypothermia confers a marked protective effect on the final histopathological outcome. The present study was carried out to evaluate whether this protective effect involves changes in the degree of local cerebral blood flow reductions, tissue accumulation of free fatty acids, or alterations in the extracellular release of glutamate and dopamine. Rats whose intraischemic brain temperature was maintained at 36 degrees C, 33 degrees C, or 30 degrees C were subjected to 20 minutes of ischemia by four-vessel occlusion combined with systemic hypotension. Levels of local cerebral blood flow, as measured autoradiographically, were reduced uniformly in all experimental animals at the end of ischemia by gas chromatography after tissue extraction and separation by thin layer chromatography. A massive ischemia-induced accumulation of individual free fatty acids was observed in animal groups whose intraischemic brain temperature was maintained at either 36 degrees C or 30 degrees C. Extracellular neurotransmitter levels were measured by microdialysis; the perfusate was collected before, during, and after ischemia. In rats whose intraischemic brain temperature was maintained at 36 degrees C, dopamine and glutamate increased significantly during ischemia and the early period of recirculation (by 500-fold and sevenfold, respectively). In animals whose brain temperature was maintained at 33 degrees C and 30 degrees C, the release of glutamate was completely inhibited, and the release of dopamine was significantly attenuated (by 60%). These results suggest that mild intraischemic hypothermia does not affect the ischemia-induced local cerebral blood flow reduction or free fatty acid accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Small differences in intraischemic brain temperature critically determine the extent of ischemic neuronal injury.

We have tested whether small intraischemic variations in brain temperature influence the outcome of transient ischemia. To measure brain temperature, a thermocouple probe was placed stereotaxically into the left dorsolateral striatum of rats prior to 20 min of four-vessel occlusion. Rectal temperature was maintained at 36-37 degrees C by a heating lamp, and striatal temperature prior to ischemia was 36 degrees C in all animals. Six animal subgroups were investigated, including rats whose intraischemic striatal brain temperature was not regulated, or was maintained at 33, 34, 36, or 39 degrees C. Postischemic brain temperature was regulated at 36 degrees C, except for one group in which brain temperature was lowered from 36 degrees C to 33 degrees C during the first hour of recirculation. Energy metabolites were measured at the end of the ischemic insult, and histopathological evaluation was carried out at 3 days after ischemia. Intraischemic variations in brain temperature had no significant influence on energy metabolite levels measured at the conclusion of ischemia: Severe depletion of brain ATP, phosphocreatine, glucose, and glycogen and elevation of lactate were observed to a similar degree in all experimental groups. The histopathological consequences of ischemia, however, were markedly influenced by variations in intraischemic brain temperature. In the hippocampus, CA1 neurons were consistently damaged at 36 degrees C, but not at 34 degrees C. Within the dorsolateral striatum, ischemic cell change was present in 100% of the hemispheres at 36 degrees C, but in only 50% at 34 degrees C. Ischemic neurons within the central zone of striatum were not observed in any rats at 34 degrees C, but in all rats at 36 degrees C. In rats whose striatal temperature was not controlled, brain temperature fell from 36 to 30-31 degrees C during the ischemic insult. In this group, no ischemic cell change was seen within striatal areas and was only inconsistently documented within the CA1 hippocampal region. These results demonstrate that (a) rectal temperature unreliably reflects brain temperature during ischemia; (b) despite severe depletion of brain energy metabolites during ischemia at all temperatures, small increments of intraischemic brain temperature markedly accentuate histopathological changes following 3-day survival; and (c) brain temperature must be controlled above 33 degrees C in order to ensure a consistent histopathological outcome. Lowering of the brain temperature by only a few degrees during ischemia confers a marked protective effect.

Adenosine Triphosphate↗