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Biomedical subjects

A Montero

Publications and source records attributed to A Montero.

At least 73 records · Page 4Linked to original sources

[Empirical anti-toxoplasma therapy in cerebral AIDS and Chagas disease. Presentation of 2 cases, review of the literature and proposal of an algorithm].

Trypanosoma cruzi is the responsible agent of Chagas disease and is endemic in extended areas of South and Central America. There are many previous reports indicating that T. cruzi frequently involves the central nervous system in AIDS patients. Here, we present two cases illustrating that neurological involvement caused by T. cruzi frequently shows a clinical picture similar to that caused by Toxoplasma gondil. Since in neurological Chagas disease early treatment has been associated with a better outcome and considering that the diagnosis is easily reached by the detection of the agent in the cerebrospinal fluid, we propose a new algorithm for the management of AIDS patients presenting neurological focal lesions in endemic areas for T. cruzi.

AIDS-Related Opportunistic Infections↗

Semi-quantitative assessment of cerebral blood flow with 99mTc-HMPAO SPET in type I diabetic patients with no clinical history of cerebrovascular disease.

In 65 type I diabetic patients we prospectively evaluated brain perfusion by means of single-photon emission tomography after the injection of 740- 1110 MBq of technetium-99m hexamethylpropylene amine oxime. Thirty-five of the patients presented complications secondary to their diabetes. None showed CNS symptoms. A semiquantitative analysis was performed drawing 50 symmetrical regions of interest (ROIs) per patient. The relative contribution of each ROI to the total blood flow in each slice was compared with the relative contribution of the same ROI in a control group of ten healthy volunteers. Relative values of any ROI in the study group higher or lower than the mean +/-2 SD in respect of the same ROI in the control group were considered abnormal. The results revealed hypoperfusion in 207 ROIs in the 65 patients with diabetes mellitus: of these ROIs, 113 were frontal, 10 frontotemporal, 20 temporal, 18 parietal, 11 occipital and 35 cerebellar. A total of 137 ROIs showed hyperperfusion: 17 frontal, 3 frontotemporal, 19 temporal, 18 parietal, 19 parieto-occipital, 29 occipital and 32 cerebellar. Out of 65 type I diabetic patients, 61 showed at least one hypoperfused ROI (P = 0.0064 vs. controls) and 25 showed more than three hypoperfused ROIs. None of the control subjects showed more than three hypoperfused regions (P<0.001). The results obtained demonstrate the existence of subclinical abnormalities of brain blood perfusion in patients with type I diabetes mellitus and no history of cerebrovascular disease, thereby allowing the initiation of intensive preventive measures.

Adult↗

Contrasting effects of proinflammatory and T-helper lymphocyte subset-2 cytokines on the 5-lipoxygenase pathway in monocytes.

Human peripheral blood monocytes (HPBMs) express 5-lipoxygenase (5-LO) and 5-LO activating protein (FLAP), and hence have an ability to synthesize proinflammatory leukotrienes (LTs). Regulation of 5-LO and FLAP expression is a major determinant of cellular LT synthesis. We examined the effects of proinflammatory [interleukin (IL)-1 and interferon (IFN)-gamma] and T helper lymphocyte subset 2 (TH-2; IL-4 and IL-13) cytokines on (1) LTB4 production, and (2) 5-LO and FLAP expression in HPBMs. We show that IL-1 and IFN-gamma stimulate, whereas IL-4 and IL-13 inhibit ionophore-activated LTB4 release. The stimulatory effects of IL-1 and IFN-gamma were apparent at 16 to 36 hours of incubation. IL-1 modestly increased FLAP mRNA and significantly increased 5-LO mRNA steady state levels at 24 and 36 hours of incubation, respectively. IFN-gamma did not change the mRNA or protein expression of either 5-LO or FLAP. The inhibitory effects of IL-4 and IL-13 were associated with decreased FLAP mRNA and protein steady state levels. These results demonstrate that regulation of monocyte LTB4 biosynthesis by different cytokines proceeds via different pathways that partly involve modulation of the expression of the key proteins, 5-LO and FLAP. In addition, the contrasting effects of proinflammatory and TH-2-derived cytokines on monocyte LTB4 production demonstrate mechanisms by which cytokine subpopulations may modulate monocyte function in inflammation.

5-Lipoxygenase-Activating Proteins↗

A novel locus for non-syndromic sensorineural deafness (DFN6) maps to chromosome Xp22.

Non-syndromic X-linked deafness is highly heterogeneous. At least five different clinical forms have been described, but only two loci have been mapped. Here we report a Spanish family affected by a previously undescribed X-linked form of hearing impairment. Deafness is non-syndromic, sensorineural, and progressive. In affected males, the auditory impairment is first detected at school age, affecting mainly the high frequencies. Later it evolves to become severe to profound, involving all frequencies for adulthood. Carrier females manifest a moderate hearing impairment in the high frequencies, with the onset delayed to the fourth decade of life. Deafness was assumed to be X-linked dominant, with incomplete penetrance and variable expressivity in carrier females. The family was genotyped for a set of microsatellite markers evenly spaced at intervals of about 10 cM. We found evidence of linkage to markers in the Xp22 region (maximum lod score of 5.30 at theta = 0.000 for DXS8036 and for DXS8022). The position of the novel deafness locus (DFN6) was refined by haplotype analysis. Mapping of the breakpoints in two critical recombinants allowed us to define an interval for DFN6, delimited by DXS7108 on the distal side and by DXS7105 on the proximal side, and spanning a genetic distance of about 15 cM.

Audiometry, Pure-Tone↗

Comparative study of propofol versus midazolam in the sedation of critically ill patients: results of a prospective, randomized, multicenter trial.

OBJECTIVES: To compare the effectiveness, characteristics, duration of action, hemodynamic and biochemical effects, and side effects of propofol and midazolam used for continuous intravenous sedation of ventilated critically ill patients. DESIGN: Multicenter, prospective, randomized, nonblinded study. SETTING: Nine Spanish general intensive care units (ICUs). PATIENTS: Ninety-eight patients admitted to the ICU who were mechanically ventilated and required sedation for a minimum of 48 hrs. INTERVENTIONS: Propofol or midazolam was used for induction and maintenance of continuous intravenous sedation for a maximum of 5 days. The effectiveness of those two regimens was assessed according to their effects on ventilatory management and the presence of agitation. MEASUREMENTS AND MAIN RESULTS: In 93% of the patients studied, there was a medical cause necessitating mechanical ventilation. The mean (+/-SD) duration of sedation was 81 +/- 25 hrs and 88 +/- 27 hrs for the propofol and midazolam groups, respectively. The induction dose was 2.24 +/- 0.43 mg/kg over 318 +/- 363 secs for propofol, and 0.22 +/-0.07 mg/kg over 33 +/-29 secs for midazolam. The maintenance dose was 2.8 +/-1.1 mg/kg/hr for propofol and 0.14 +/- 0.10 mg/kg/hr for midazolam. There was no difference regarding the opiate and muscle relaxant requirements between the two groups. Sedation with propofol was more effective in achieving patient-ventilator synchrony than that with midazolam after the first hour of treatment (p < .01). Patients sedated with propofol awoke more rapidly and with less variability that those patients sedated with midazolam (23 +/- 16 mins vs. 137 +/- 185 mins, respectively, p < .05), particularly in those patients requiring deep sedation (27 +/- 16 mins vs. 237 +/- 222 mins, respectively, p < .01). No hemodynamic or biochemical changes were detected in any of the treatment groups. During induction, five patients in the propofol group and two patients in the midazolam group had hypotension. CONCLUSIONS: In this population of critically ill patients, propofol is an effective and safe alternative for sedation, with some advantages, such as short duration of action and high effectiveness over the conventional regimen with benzodiazepines and opiates.

Adolescent↗

Prognosis and clinical relevance of anisocoria-craniotomy latency for epidural hematoma in comatose patients.

OBJECTIVE: To determine whether the time between onset of anisocoria and surgery for hematoma evacuation in the head-injured patient is a useful prognostic variable for outcome in the comatose patient with an acute epidural hematoma. DESIGN: Prospective. MATERIALS AND METHODS: Twenty-one patients with an acute traumatic epidural hematoma and an admission Glasgow Coma Scale score of less than 8 were analyzed. RESULTS: Anisocoria was present in 14 (67%) patients. Mortality rate was three times higher in this group than in the patients without anisocoria; however, this difference was not statistically significant (p = 0.21, Fisher's exact test). None of the patients with an anisocoria-craniotomy latency of 70 minutes or less died and all of these patients had a good or reasonable outcome. Analysis of the anisocoria-craniotomy latency in ten patients revealed that a lapse of more than 90 minutes was associated with a greater mortality compared with patients with a latency of less than 90 minutes (p = 0.0238, Fisher's exact test). CONCLUSIONS: In patients with an acute epidural hematoma, reducing the anisocoria-surgery interval below 90 minutes is significantly associated with a better outcome (p = 0.0238, Fisher's exact test).

Adolescent↗

Role of angiotensin II in the expression and regulation of transforming growth factor-beta in obstructive nephropathy.

Unilateral ureteral obstruction (UUO) leads to fibrosis of the obstructed kidney. We tested the hypothesis that interstitial fibrosis in UUO results, at least in part, from enhanced expression of transforming growth factor-beta (TGF-beta) which in turn is regulated by local angiotensin II (Ang II) generation. (The generic name TGF-beta is used to discuss properties shared by all isoforms, but special reference to other isoforms is made when specifically needed.) Using Northern blot and immunohistochemical analysis, we examined the expression of TGF-beta in rat kidneys after 24 hours (aUUO) and one week (cUUO) of obstruction. Obstructed kidneys from both periods had increased interstitial and perivascular TGF-beta immunoreactivity compared to contralateral and sham kidneys, in which immunostaining was confined to the inner medulla. Relative abundance of all TGF-beta mRNA isoforms were higher in the obstructed than in contralateral and sham kidneys in both aUUO and cUUO. Expression of TGF-beta isoforms varied according to site (cortex vs. medulla), segment of the nephron, type of cells and duration of the obstruction. The increase in TGF-beta immunoreactivity and mRNA levels in aUUO and cUUO was almost totally abolished by pretreatment with losartan. We conclude that in UUO: (a) TGF-beta gene expression is increased and differentially regulated; (b) Ang II, at least partially, mediates the overexpression of TGF-beta gene; and (c) Ang II may play a central role in fibrogenesis in this and other models of tubulointerstitial disease.

Angiotensin II↗

Sequential changes in renal expression of renin-angiotensin system genes in acute unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) alters the expression of genes encoding for the renin-angiotensin system (RAS). We tested the hypothesis that changes in RAS genes expression occur soon after obstruction. Indeed, measurements during the first 24 hours of UUO showed up-regulation of renin mRNA in the obstructed kidney at 1 hour. UUO also led to increases in PRA and renal renin content, ACE activity and Ang II concentration in the experimental kidney. The obstructed kidney relative abundance of renin mRNA was increased compared to basal at 1, 2, 6, and 24 hours; the contralateral kidney renin mRNA expression was reduced. AT1-R mRNA expression was diminished at 6 and 24 hours in the obstructed kidney compared to contralateral and sham kidneys. ACE activity was up-regulated in the obstructed kidney and transiently down-regulated in the contralateral kidney. These findings show for the first time that activation of the RAS results from as little as 1 hour of UUO and that up-regulation of renin mRNA and ACE activity lead to increase Ang II production which down-regulates AT1-R mRNA as early as 6 hours post-UUO. These studies establish a pattern of sequential, differential regulation of the RAS genes in acute UUO that provide an explanation for the hemodynamic changes in this condition.

Acetylcholinesterase↗

The effect of LU-49938 (nexopamil) on the activation by serotonin of mesangial cells.

Intraglomerular platelet activation may release vasoactive agents such as serotonin (5-hydroxytryptamine, 5-HT) that may affect local hemodynamics and promote mesangial proliferation, eventually leading to glomerular sclerosis. The main purpose of this study is to analyze whether nexopamil, a verapamil derivative, with the property of blocking simultaneously calcium channels and 5-HT2 receptors, could modify the contractile and mitogenic effects of serotonin on cultured rat mesangial cells. Serotonin caused a concentration-dependent increase in [3H]thymidine incorporation into DNA, and mesangial cell proliferation. The effects of 5-HT on thymidine uptake and cell proliferation were blocked by the selective 5-HT2 receptor blocker ketanserin 10(-5) M. Nexopamil abolished in a concentration-dependent way the serotonin-induced [3H]thymidine incorporation into DNA, and the serotonin-induced increase in number of cells. Using 5-HT 10(-4) or 10(-5) M, nexopamil had significant effects at concentration above 10(-7) M. Serotonin induced a concentration- and time-dependent reduction of planar cell surface area. This effect was also completely blocked by ketanserin. Nexopamil partially blocked the serotonin-induced mesangial cell contraction, in a dose-dependent manner. All these data suggest that nexopamil inhibits both 5-HT-induced mesangial cell contraction and proliferation by blocking 5-HT2 receptors and the voltage-operated Ca2+ channels.

Animals↗

[Absent or reverse diastolic umbilical flow].

We show our experience in the diagnostic and management of 19 pregnancies with absent or reverse diastolic blood flow velocity (ARFV) in the umbilical artery. The presence of ARFV was a rare condition (2.2% of the high risk patients), and it was associated with a poor prognosis shown by the high percentage of fetuses SGD (small for gestational age) (63.2%), malformations and hydrops fetalis (26%) and asphyxiated fetuses, giving a final perinatal mortality rate of 36.8%. In 8 cases (42.1%) the termination or pregnancy was delayed for at least 48 hours, allowing in some cases the administration of corticosteroid. There were significant differences when comparing the groups of survivors and non survivors in relation to the gestational age at the moment of delivery (33.1 +/- 3.4 vs 28.6 +/- 3.8 weeks), malformations (8.3 vs 57.1%) and C-section (91.7 vs 42.9%). Finally, we conclude that the presence of ARFV in the umbilical artery is associated with a critical fetal condition and termination of pregnancy should be considered. In this decision the gestational age and fetal and maternal well being ought to be taken into account when choosing the best moment and route of delivery.

Adult↗

Increased glomerular nitric oxide synthesis in gentamicin-induced renal failure.

Renal glomeruli isolated from normal rats and from rats with gentamicin-induced renal failure were incubated with substances that modify nitric oxide (NO) synthesis and the resulting changes in glomerular cyclic GMP (cGMP) levels were measured by radioimmunoassay. Glomeruli from normal and gentamicin-treated rats contained 0.17 +/- 0.04 and 2.02 +/- 0.63 pmol cGMP/mg protein respectively. In normal glomeruli, acetylcholine and bradykinin significantly increased cGMP levels whereas NG-nitro-L-arginine-methyl ester, an inhibitor of NO synthesis, completely blocked this increase. In glomeruli from gentamicin-treated animals, acetylcholine and bradykinin also stimulated cGMP accumulation, while NG-nitro-L-arginine-methyl ester decreased the cGMP content to levels significantly below the basal concentrations. These data suggest an increased glomerular production of NO in rats with gentamicin-induced renal failure.

Animals↗

Platelet-activating factor mediates pancreatic function derangement in caerulein-induced pancreatitis in rats.

1. We have assessed the role of platelet-activating factor in caerulein-induced acute pancreatitis (four subcutaneous injections of caerulein at a dose of 20 micrograms/kg) by measuring platelet-activating factor levels in portal blood, pancreatic tissue and peritoneal exudate in rats with and without pancreatitis. 2. We have also observed the effect of the platelet-activating factor antagonist, BN-52021, on the hyperamylasaemia and exocrine pancreatic secretion impairment associated with pancreatitis. 3. In rats with pancreatitis the basal pancreatic flow rate was increased (1.63 +/- 0.41 versus 0.25 +/- 0.03 microliters/min). Total protein output was similar in both untreated (5.98 +/- 1.93 micrograms/min) and caerulein-injected (6.5 +/- 2.0 micrograms/min) animals. Amylase output was lower in rats with pancreatitis (19.6 +/- 4.8 mu-units/min) than in controls (39.4 +/- 16.6 mu-units/min). 4. Caerulein-treated animals had significantly higher serum amylase levels than untreated animals. BN-52021 significantly reduced the caerulein-induced hyperamylasaemia. 5. Portal blood platelet-activating factor levels increased in rats with pancreatitis and in rats infused with cholecystokinin. Rats injected with caerulein and BN-52021 had portal blood levels of platelet-activating factor that were lower than those with pancreatitis. 6. Morphological derangements associated with pancreatitis (inflammatory infiltration and cell vacuolization) were also markedly reduced in BN-52021-treated animals. 7. The results of this study suggest that platelet-activating factor is involved in the development of caerulein-induced acute pancreatitis in rats.

Acute Disease↗

[Relative risk of hepatitis C virus transmission in polytransfused patients].

Hepatitis C virus (HCV) has been shown to be responsible for a significant proportion of hepatitis cases among patients undergoing frequent blood transfusions. The prevalence in blood serum of anti-HCV antibodies was studied in 48 patients who had undergone dialysis and multiple blood transfusions. In 42 of these patients the average number of transfusions during their treatment was 11.2. The patients were stratified into four groups according to the number of transfusions received (I: < 5, II:6-9, III:10-15 and IV > 15). Odds ratios were used in order to estimate the probability of finding anti-HCV antibodies in groups II, III and IV in relation to the least exposed group I. Anti-HCV antibodies were found in 59% of patients receiving transfusions. As grouped by increasing number of transfusions, each set showed 16, 66, 62.5 and 100% presence of anti-HCV antibodies, respectively. This shows a direct correspondence between the number of transfusions and the serum-born incidence of anti-HCV antibodies. These results closely coincide with those of a similar study, done in the city of Cordoba, Argentina, in 1992. The two studies confirm the necessity to check blood units in order to discard those with anti-HCV antibodies.

Blood Transfusion↗