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J Diaz

Publications and source records attributed to J Diaz.

At least 109 records · Page 6Linked to original sources
PubMed1996

Comparison of five plating media for isolation of Salmonella species from human stools.

A comparative study was carried out to evaluate the performances of different culture media for the recovery of Salmonella spp. from 1,000 routine samples of human stools. By direct plating we tested Salmonella-Shigella agar (SS), Hektoen enteric agar (HE), bismuth sulfite agar (BS), novobiocin-brilliant green-glycerol-lactose agar (NBGL) and SM-ID medium (SM), and after selenite enrichment, we tested all of the media except HE. C8-esterase and oxidase tests were used for the screening of Salmonella spp. on SS and HE. The total number of Salmonella isolates from direct culture was 74, with respective sensitivities and positive predictive values (PPVs) of 78.4 and 61%, 64.9 and 18.7%, 36.5 and 34.2%, 55.4 and 20.7%, and 39.2 and 43.9% for NBGL, SS, HE, BS, and SMID, respectively. After enrichment, the total number of Salmonella isolates was 88. The respective sensitivities and PPVs obtained were 90.9 and 62.5%, 92 and 17%, 90.9 and 32% and 93.2 and 71.3% for NBGL, SS, BS, and SM, respectively. According to our results, NBGL in direct plating was the medium with the highest sensitivity with respect to the sensitivities of the other media, with significant statistical differences (P < 0.05). Likewise, the PPV for NBGL was also the highest (61%). After enrichment in selenite broth, the sensitivities of the four media tested were similar, with the best PPV obtained with SM (71.3%); this was followed by NBGL (62.5%). When C8-esterase was used on SS or HE, the PPVs improved from less than 40% to about 100%.

Culture Media↗
PubMed1996

Prostaglandin E2 inhibits Na-K-2Cl cotransport in medullary thick ascending limb cells.

Prostaglandin E2 (PGE2) is known to inhibit transepithelial Cl transport in medullary thick ascending limb (mTAL), but the mechanism of inhibition or the transport pathway affected has not been identified. We undertook this study to examine the effect of PGE2 on Na-K-2Cl cotransport in mouse mTAL cells in culture. In nanomolar concentrations, PGE2 inhibited the Na- and Cl-dependent, bumetanide-sensitive K influx by 45%, and this inhibition was also observed in the presence of 3 mM ouabain. Although PGE2 also inhibited ouabain-sensitive K flux, that inhibition was abolished in the presence of apical nystatin, suggesting that the pump inhibition was secondary to diminished Na entry into the cells. The effect of PGE2 was concentration dependent. Inhibition was observed at a concentration of < 1 nM, and half-maximal effect was observed at 2.5 nM. The effect of PGE2 was not mediated by an action on cytosolic Ca because cytosolic Ca was unchanged after the addition of PGE2. PGE2 reduced the maximal velocity for the cotransporter but had no effect on the affinity of the cotransporter for external Na, K, or Cl. Specific [3H]bumetanide binding was reduced in the presence of PGE2, suggesting that PGE2 affected bumetanide-sensitive K influx by downregulating the number of functioning Na-K-2Cl cotransporters. These results suggest that Na-K-2Cl cotransport in the mTAL cells may be under tonic inhibitory control of PGE2.

Animals↗
PubMed1996

Diaphragmatic fatigue following voluntary hyperpnea.

The purpose of this study was to determine whether diaphragmatic fatigue occurs after voluntary hyperpnea to task failure. Ten male subjects were asked to breathe at minute ventilation (V1) equal or slightly greater than 60% of their 12-s maximum voluntary ventilation (MVV) until task failure. Transdiaphragmatic pressure (Pdi) was measured during bilateral supramaximal stimulation of the phrenic nerves before and 10, 30, 60, and 120 min after hyperpnea. For the group, V1 averaged 107.1 +/- 7.1 L/min (SE) (range, 71-154 L/min), which represented 60 +/- 2% of the MVV. After voluntary hyperpnea, seven of the 10 subjects displayed at least a 10% reduction in twitch Pdi during transcutaneous stimulation, while all 10 subjects had a greater than 10% reduction in twitch Pdi during cervical magnetic stimulation. For the group, transcutaneous twitch Pdi was significantly decreased from 27.0 +/- 1.9 at baseline to 21.4 +/- 1.7 cm H2O (p < 0.0001) at 10 min posthyperpnea. Magnetic twitch Pdi was also significantly decreased from 36.0 +/- 2.1 at baseline to 28.7 +/- 1.9 cm H2O (p < 0.0001) at 10 min posthyperpnea. Twitch Pdi remained significantly decreased from baseline for at least 1 h after hyperpnea. After hyperpnea, the mean percentage decrease from baseline in twitch Pdi was virtually identical with the two stimulation techniques. The percentage fall in twitch Pdi after hyperpnea with the two techniques was not significantly correlated (r = 0.4). In conclusion, long-lasting contractile fatigue of the diaphragm reliably occurs after voluntary hyperpnea at levels sufficient to induce task failure. Cervical magnetic stimulation can detect diaphragmatic fatigue after a fatiguing task, but the results obtained with this technique may differ from those obtained with transcutaneous stimulation in individual subjects.

Adult↗
PubMed1995

Na+, K+, and H+/HCO3- transport in submandibular salivary ducts. Membrane localization of transporters.

The mechanisms mediating transepithelial ion transport in salivary ducts were characterized and localized by studying the regulation of [Na+]i, [K+]i, and pHi in isolated intralobular ducts and perfused main ducts of the submandibular salivary gland. A new procedure was developed for the rapid preparation of intralobular ducts. Measurements of pHi revealed the presence of Na+/H+ and Cl-/HCO3- exchange activities in intralobular duct cells. We could not obtain evidence for a coupled K+/H+ exchange activity which was postulated to exist in the luminal membrane of duct cells. Rather, a Kout+-dependent pathway which mediates the transport of H+/HCO3- and Na+ was found. This pathway was absent from acinar cells of the same gland and was active in unstimulated duct cells incubated in 5mM Kout+. Accordingly, inhibition of the Na+ pump with ouabain resulted in rapid and large Na+ influx in duct but not acinar cells. Perfusion experiments with the experimentally accessible main duct and measurements of pHi were used to provide the first direct localization of ion transporters in salivary ducts. The luminal and basolateral membranes of the duct express separate Na+/N+ and Cl-/HCO3- exchangers. Na+/H+ exchange activity in both membranes was similar, whereas the luminal Cl-/HCO3- exchange activity was higher than that in the basolateral membrane. The perfused main dust was also used to localize the newly discovered Kout(+)-dependent H+/HCO3- and Na+ transport pathway to the luminal membrane, which suggests that this pathway may play an important role in Na+ reabsorption of K+ and HCO3- secretion by the salivary ductal system.

Animals↗
PubMed1995

Regulation of [Na+]i in resting and stimulated submandibular salivary ducts.

In the preceding manuscript (Zhao, H., Xu, X., Diaz, J., and Muallem, S. (1995) J. Biol. Chem. 270, 19599-19605), we described a Kout(+)-dependent H+/HCO3- and Na+ influx pathway in the luminal membrane of salivary duct cells. In the present studies, we further characterized this pathway to show that the Kout(+)-dependent Na+ influx was not mediated by the luminal amiloride-sensitive Na+ channel, the Na+/H+ exchangers, or any electroneutral or conductive Cl(-)-dependent transport pathway. Thus, K+ efflux probably maintained electroneutrality during Na+ influx induced by removal of Kout+. Accordingly, Na+ influx was largely inhibited by 2.5mM external Ba2+. The K+ site of the Kout(+)-dependent Na+ influx showed the selectivity sequence Cs+ > K+ > NH4+ >> > Li+ which is different from that of several known K+ channels. More importantly, Na+ influx is 50% inhibited at about 20 mM Kout+, and significant Na+ influx occurred even at 80 mM Kout+. This is a critical property for the pathway to play a role in Na+ reabsorption and K+ secretion by the duct. The large Na+ influx in resting duct cells is matched by high activity of the ductal Na+ pump which is about 8-fold faster than that of acinar cells. Stimulation of submandibular ducts with various agonists increased [Na+]i in an agonist-specific manner. The parasympathetic agonist epinephrine was more effective than isoproterenol and sympathetic agonist carbachol. The use of various inhibitors of Na+ and K+ transporters suggests that different pathways mediate Na+ influx in stimulated acinar and duct cells of the gland. In duct cells, Na+ influx was inhibited only by extracellular Cs+ and Ba2+. The overall findings support a significant role for the Kout(+)-dependent pathway(s) in Na+ reabsorption and K+ and HCO3- secretion and explain several features of transepithelial electrolyte transport by salivary ducts.

Amiloride↗
PubMed1995

The value of polymorphonuclear elastase in adult respiratory distress syndrome.

The clinical usefulness of quantitative plasma polymorphonuclear elastase (PMN-elastase) determinations as prognostic markers of adult respiratory distress syndrome (ARDS) in polytraumatized patients was analyzed. PMN-elastase and C-reactive protein (CRP) levels were determined in 55 polytraumatized patients admitted into the Intensive Care Unit. Eight patients developed ARDS and 47 patients did not. These parameters were also analyzed in a control group (n = 34). PMN-elastase levels in ARDS cases reached significantly higher values than in patients who did not develop this syndrome (P < 0.01). We conclude that the increase in plasma PMN-elastase levels can be useful in predicting the development of ARDS in polytraumatized patients, in instituting prophylactic actions and monitoring the course of the disease in these high risk patients. This test is easily adaptable to the routine of any hospital laboratory.

Adolescent↗
PubMed1995

A paradoxical regulation of the dopamine D3 receptor expression suggests the involvement of an anterograde factor from dopamine neurons.

The effects of interruption of dopaminergic transmission or sustained blockade of dopamine receptors by neuroleptics on the dopamine D3 receptor in the shell of the nucleus accumbens were investigated in rats. In this brain area the D3 receptor is abundant and may mediate antipsychotic drug effects. The D3 receptor density and mRNA abundance were evaluated with 7-[3H]hydroxy-N,N-di-n-propyl-2-aminotetralin and by quantitative PCR or image analysis of in situ hybridization signals, respectively. Unilateral dopamine neuron degeneration by 6-hydroxydopamine or sections triggered, after a few days, a marked decrease (up to 50%) in D3 receptor binding and mRNA in the nucleus accumbens. In contrast, a 2-week treatment with the neuroleptic haloperidol (20 mg/kg) had no effect on D3 receptor density and mRNA but enhanced D2 receptor density and mRNA level by > 50%. In addition, tolerance to the haloperidol-induced change of neurotensin mRNA mediated by the D2 receptor developed, but there was no tolerance to the opposite change mediated by the D3 receptor. Reserpine, a monoamine-depleting drug with antipsychotic activity, did not modify D3 receptor mRNA. These observations reinforce the idea that the D3 receptor may be an important target for neuroleptics whose antipsychotic actions, but not extrapyramidal motor actions, do not display tolerance. The D3 receptor mRNA level was also decreased by a unilateral injection in dopamine cell body areas of colchicine, a drug blocking the anterograde axonal transport, or by baclofen, a type A gamma-aminobutyric acid receptor agonist reducing dopamine neuron activity, but not by sustained blockade of D1-like and D2-like, neurotensin, or cholecystokinin receptors. We therefore propose that an anterograde factor present in mesolimbic dopaminergic neurons, but distinct from dopamine and known peptide cotransmitters, plays a positive role on transcription of the D3 receptor gene.

Animals↗
PubMed1995

Synaptic transmission blockade increases plasminogen activator activity in mouse skeletal muscle poisoned with botulinum toxin type A.

Experimental denervation, either by nerve crush or axotomy, leads to a dramatic increase in muscle plasminogen activator (PA) activity, suggesting a regulation of muscle PA levels by some neural influence (Festoff et al., 1986, J. Cell Biol., 103:1415-1421; Hantaï et al., 1990, Proc. Natl. Acad. Sci. U.S.A., 87:2926-2930). The Botulinum toxin (BoTx) type A is known to selectively interrupt the release of acetylcholine without structurally altering synaptic morphology. In the present study we have used acute BoTx poisoning of hind limb muscles to further explore the neural regulation of muscle PA activities directly after poisoning and during the process of collateral reinnervation. Electromyographic recording and study of ultraterminal sprouting after zinc iodideosmium and silver-cholinesterase staining were used to monitor "denervation" and reinnervation. Muscle choline acetyltransferase activity did not decrease, as is observed after experimental denervation, but in contrast increased and, therefore, reflected the functional integrity of intramuscular nerve endings. Within 2 days of BoTx poisoning, muscle urokinase-PA, and to a lesser extent, tissue-PA activities, rose in muscle extracts as shown by an amidolytic assay and fibrin zymography. When reinnervation occurred, muscle urokinase-PA activity decreased but did not return to baseline levels within the 80 days of our study. These results suggest that cholinergic transmission-regulated events determine activity of muscle PAs and that PAs likely have a role in neuromuscular formation and plasticity.

Amino Acid Sequence↗
PubMed1995

Tumor embolism after pneumonectomy for primary pulmonary neoplasia.

We report a case of tumor embolism of the lower right extremity after right pneumonectomy. This is an infrequent complication and in most cases occurs during the intraoperative or immediate postoperative period. Our patient underwent surgery for primary pulmonary neoplasia (squamous cell carcinoma) and 4 hours later showed clinical signs of acute arterial occlusion in the lower right extremity. An emergency embolectomy was performed and a thrombus with tumor characteristics was extracted from the right common femoral artery. The pathologic features of this thrombus were identical to those of the pulmonary tumor.

Aged↗
PubMed1995

Phenotypical characterization of neurons expressing the dopamine D3 receptor in the rat brain.

We have established the cellular distribution of the dopamine D3 receptor using tritiated 7-hydroxy-N-N-di-n-propyl-2-aminotetralin and a complementary RNA probe to visualize autoradiographically the protein in binding studies and the gene transcripts by in situ hybridization, respectively. Studies with these two markers confirm the restricted expression of the D3 receptor in few brain areas, i.e. mainly the ventral striatal complex, the substantia nigra-ventral tegmental area and the cerebellum. In nucleus accumbens, the D3 receptor was mainly expressed in medium-sized neurons of the rostral pole and ventromedial shell subdivisions, but not of the core or septal pole, i.e. accumbal subdivisions expressing the D2 receptor. In the ventromedial shell, about 60% of the D3 receptor-expressing neurons were neurotensin neurons, presumably projecting to the ventral pallidum. In the islands of Calleja, both D3 receptor binding and messenger RNA were abundant in the entire population of granule cells. These cells are known to make sparse contacts with dopaminergic axons and also to express the D1 receptor. In the mesencephalon, low levels of D3 messenger RNA were detected in few dopamine neurons of substantia nigra pars lateralis and ventral tegmental area. In addition, some D3 receptor binding but not messenger RNA was detected in medial substantia nigra and lateral ventral tegmental area, where the receptor is presumably located presynaptically on afferents. In the archicerebellum, Purkinje cell perikarya in lobules 9 and 10 expressed the D3 receptor messenger RNA, whereas binding sites were found in the molecular layer, where corresponding dendrites but no known dopaminergic projection from mesencephalon are found. The occurrence of D3 receptor gene expression in some brain areas receiving low dopamine innervation supports the hypothesis that this receptor may mediate non-synaptic actions of dopamine.

Animals↗
PubMed1995

The dopamine D3 receptor and schizophrenia: pharmacological, anatomical and genetic approaches.

Antipsychotic drug therapy mainly rests on the use of antagonists of dopamine D2-like (D2, D3 and D4) receptors, for which all clinically active compounds have high affinity. The D3 receptor has a restricted expression in brain limbic areas, associated with cognitive functions and motivated behavior. D3 selective agonists and antagonists reveal an inhibitory role on motor behaviors for the D3 receptor, opposite to that of the D2 receptor. An opposing role for D2 and D3 receptors is also suggested by the contrasted effects of D2/D3 antagonists on neurotensin expression in discrete subdivisions of nucleus accumbens, where D2 and D3 receptors are selectively expressed. Tolerance to the motor but not to the therapeutic effects of neuroleptics is observed after repeated administration, which upregulates the D2, but not the D3 receptor in animals. In genetic association studies, an excess of homozygosity for both alleles of the BalI polymorphism at the D3 receptor gene was found in schizophrenic patients, suggesting that this gene may have subtle influence on the liability to develop schizophrenia. These results suggest the D3 receptor as an important target for antipsychotic drug action, and D3 receptor selective antagonists as promising therapeutic agents.

Animals↗
PubMed1995

Estrogen dependent expression of heat shock transcription factor: implications for uterine synthesis of heat shock proteins.

Transcriptional induction of heat shock protein genes is generally mediated by binding of heat shock transcription factor(s) to the heat shock element present in the promoters of heat shock genes. Although the steady-state levels of heat shock factor mRNAs vary among different tissues, at present virtually nothing is known regarding the cellular signals responsible for their synthesis and hence the observed variations. In this report we demonstrate that the heat shock transcription factor (HSTF or HSF) is under positive regulation by estrogen. The effect of estrogen was observed with both types of heat shock factors (HSF-1 and HSF-2) and occurred at both the mRNA and protein level. Immunolocalization studies emphasized the potential biological importance of these observations whereby the increase in uterine HSF-1 and HSF-2 due to estrogen was found to be associated with the endometrium, the primary tissue component which is targeted for estrogen action. This is the first demonstration of a cellular factor which can regulate HSF-1 and HSF-2 gene expression. The implications of these findings to uterine heat shock protein gene expression are discussed.

Animals↗
PubMed1995

Arteriosclerotic histologic evaluation of the internal mammary artery in patients undergoing coronary artery bypass grafting.

During 1991, 52 patients undergoing myocardial revascularization had a biopsy of the distal internal left mammary artery (IMA) taken. There were 48 male and 4 female patients with a medium age of 58 years. Arteriosclerotic involvement of the IMA was assessed according to the scale of Kay. Using this index, grade 0 corresponds to a normal artery without atherosclerosis, grade 1 represents minimal disease, grade 2 a narrowing of less than 25% of the lumen, grade 3 narrowing between 25 and 50%, and grade 4 narrowing of 50% or greater of the lumen. Of the 52 IMA examined, the arteries with degree 0, 1, 2, 3, and 4 were: 19 (36.5%), 20 (38.4%), 9 (17.6%), 4 (7.6%) and zero. Thirty-three arteries (63.4%) had some degree of atherosclerosis. Considering the arteries with some atherosclerotic narrowing, 13 (25%) of the whole group had this pathological alteration. The IMA has a low but consistent incidence of arteriosclerosis involvement. Preoperative angiographic investigation of the IMA could be routinely performed.

Adult↗
PubMed1995

Creatine kinase BB and neuron-specific enolase in cerebrospinal fluid in the diagnosis of brain insult.

Cerebrospinal fluid (CSF) markers provide useful information about the extent of brain damage. These biochemical indices may also be used when postmortem histopathological examination does not confirm antemortem brain insult. Seven biochemical parameters--creatine kinase (CK), creatine kinase BB isoenzyme (CK-BB), lactate dehydrogenase (LDH), gamma-glutamyltransferase, aldolase, leucine aminopeptidase (LAP), and neuron-specific enolase (NSE)--were analyzed in CSF from 82 cadavers. Case studies were categorized into one of four diagnostic groups. There were 15 cases of head trauma, 23 of hypoxia (hangings, carbon monoxide, and drug poisonings), 23 sudden cardiac death, and 21 miscellaneous cases. The degree of craniocerebral trauma was graded. In CSF there was a statistically significant correlation between the severity of craniocerebral trauma and levels of CK, CK-BB, aldolase, LDH, and LAP. CSF CK-BB [median U/L (range)] for the groupings of head trauma, hypoxia, sudden cardiac death, and miscellaneous were, respectively, 873 (1-12,100), 26 (2-2,780), 16 (1-42), and 18 (0-2,780). Corresponding CSF CK levels were 9,370 (28-67,842), 101 (18-36,840), 180 (10-29,622), and 264 (17-26,556). There were no statistical significant differences among the NSE concentrations in the four diagnostic groups. The testing of biochemical markers could be a reliable indicator of the degree of brain insult in support of morphological studies.

Adolescent↗
PubMed1995

Are all effects of esmolol equally rapid in onset?

The purpose of this study was to compare the time course of the bradycardic and hypotensive effects of esmolol. Ten patients undergoing craniotomy requiring hypotension were anesthetized with nitrous oxide and isoflurane. During steady state anesthesia, the response to an infusion of esmolol 500 micrograms.kg-1.min-1 for 90 s followed by 300 micrograms.kg-1.min-1 was measured over 60 min. Heart rate (HR), mean arterial pressure (MAP), and plasma renin activity (PRA) responses did not occur with equal rapidity. The half-time for the 14% decrease in HR (81 +/- 13 bpm to 70 +/- 9 bpm) was 1.2 min. MAP decreased by 26% (85 +/- 7 mm Hg to 63 +/- 6 mm Hg) with a 17.8 min half-time. This delay in MAP response may, in part, be related to the gradual 44% decline in PRA (9.5 +/- 4.5 ng.mL-1.h-1 to 5.3 +/- 2.5 ng.mL-1.h-1) occurring with a half-time of 11.9 min. The times to attainment of 90% maximum decreases were 4.8 +/- 3.0 min for HR, 42.5 +/- 8.9 min for MAP, and 32.1 +/- 15.0 min for PRA. Thus although esmolol has an ultrashort kinetic half-life, only the HR effect can be considered to have an ultrashort onset.

Adrenergic beta-Antagonists↗
PubMed1995

Aging alters the pharmacokinetics of pyridostigmine.

The duration of the antagonism to neuromuscular blockade produced by pyridostigmine is prolonged in elderly patients, and a pharmacokinetic explanation was sought. Ten elderly (71-85 yr) and 10 younger (21-51 yr) patients were anesthetized with thiopental, nitrous oxide, and isoflurane and paralyzed with a combination of d-tubocurarine and pancuronium. When twitch height returned to 5% of baseline, pyridostigmine 0.25 mg/kg was administered and blood samples were collected intermittently for 6 h. Pyridostigmine plasma concentrations were determined by radioimmunoassay and after an hour were always greater in the elderly than in the younger patients. In both groups, plasma pyridostigmine decrement curves were best described by triexponential equations. Pharmacokinetic analysis revealed that plasma clearance in the elderly group was significantly decreased compared to that in the younger group (6.7 +/- 2.2 vs 9.5 +/- 2.7 mL.kg-1.min-1, P < 0.05). Elimination half-lives and volumes of distribution were not significantly different between groups. We conclude that a possible explanation for the prolonged duration of action of pyridostigmine in the elderly is its slow plasma clearance.

Adult↗