Direct fluorescence-based lipase activity assay.
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Bacillus↗
Biomedical subjects
P Diaz
Publications and source records attributed to P Diaz.
Effect of clonidine on heart rate variability in congestive heart failure.
In patients with congestive heart failure, abnormal heart rate variability is a predictor of total mortality and sudden cardiac death. Drugs that improve heart rate variability may have a potential role for improving the survival among these patients. The effects of clonidine were studied in 24 patients with congestive heart failure, sinus rhythm, a left ventricular ejection fraction <0.40, and systolic blood pressure > 115 mm Hg. A 6-minute corridor walk test and 24-hour Holter monitoring were performed before and 42+/-24 days after initiation of clonidine therapy (Catapres-TTS patch, mean dose: 0.33+/-0.21 mg). Changes in other medications used at baseline were not allowed. One patient died suddenly. Two patients did not complete the protocol due to worsening congestive heart failure, which required changes in medications, 1 patient discontinued due to hypotension, and 2 for personal reasons. Among the 18 patients who completed the protocol, the mean RR interval of sinus beats increased from 760+/-106 to 822+/-125 ms (p=0.001) and the distance covered during the 6-minute walk test increased from 1,148+/-277 to 1,255+/-359 feet (p=0.042). Systolic blood pressure decreased from 139+/-15 to 119+/-10 mm Hg (p <0.0001). The following increases were noted in the heart rate variability measurements: high-frequency power in 0.15 to 0.40 Hz: 4.58+/-1.07 to 4.94+/-1.17 In (ms), p=0.002; SD: 47.0+/-16.9 to 52.5+/-18.4 ms, p=0.034; SD of the mean of all RR intervals in 24 hours: 116+/-94 to 130+/-19 ms, p=0.033; SD of all 5-minute mean RR intervals: 106+/-44 to 124+/-66 ms, p=0.042; root-mean square of difference of successive RR intervals: 28.8+/-10.7 to 34.1+/-14.2 ms, p=0.017. Clonidine improves heart rate variability in the patients with congestive heart failure by increasing the parasympathetic tone. It is well tolerated by most patients with heart failure and may have a beneficial effect on exercise capacity.
Adrenergic alpha-Agonists↗
The production of free oxygen radicals and nitric oxide in the rat cochlea.
Rat cochleas were analysed for free oxygen radicals (FOR) and nitric oxide (NO) production by the chemiluminescent oxidation of luminol. 4Beta-phorbol-12beta-myristate-13alpha-acetate (PMA), a well-known agonist of protein kinase C, induced the release of FOR after a time lag close to 30 s and reverted to basal values in approximately 10 min. Sphingosine inhibited by nearly 50% the response to PMA, whereas staurosporine caused an inhibition of 100%. The incubation of rat cochleas with 0.5 mM arginine potentiated the chemiluminescent reaction induced by PMA causing an additional oxidation of luminol that was inhibited by the NO synthase inhibitor N-methyl-arginine (NMA). Our results show for the first time the presence in the cochlea of cell populations producing FOR and NO and the real time production following cell activation. This procedure may help to explain the mechanisms involved in ototoxicity, as in the case of streptomycin and gentamicin that enhanced PMA-dependent production of FOR and NO.
Animals↗
Serum vitamin E decreases in HIV-seropositive subjects over time.
Vitamin E is an important lipid soluble antioxidant that has a number of crucial functions including protecting lipids from oxidative damage. It also may play an important role in enhancing the immune response in subjects with Human Immunodeficiency Virus (HIV) infection. The current study measured the serum level of vitamin E in 121 HIV seropositive subjects with no prior pulmonary complications. Although the mean level was normal at 9.0 +/- 0.5 microg/ml, 22.3% of the subjects had a deficient level of less than 5 microg/ml. In addition, 42 subjects were studied longitudinally and serum vitamin E levels were determined at baseline and 12 months later. The mean serum vitamin E level in this group significantly decreased after 12 months compared with baseline levels (5.9 +/- 0.5 microg/ml compared with 9.6 +/- 0.9 microg/ml, p = 0.001). The CD4 counts also were significantly decreased after 12 months (460.6 +/- 36.0 cells/mm3 versus 390.5 +/- 37.7 cells/mm3, p = 0.032). No significant correlations were observed between the decrease in serum vitamin E and the change in CD4 count, body mass index (BMI), or serum albumin levels over the 12-month period. In conclusion, a significant portion of HIV-seropositive subjects have a deficiency in serum vitamin E early in the course of their disease. Furthermore, there is a significant decrease in serum vitamin E levels in these subjects over 12 months.
Adult↗
Alveolar fluid glutathione is not reduced in asymptomatic HIV-seropositive subjects.
Glutathione is an important antioxidant tripeptide that is found in high concentrations in the epithelial lining fluid (ELF) of the lung. Previous investigators demonstrated a deficiency of glutathione (GSH) in the epithelial lining fluid of human immunodeficiency virus (HIV)-seropositive patients. The current investigation performed bronchoalveolar lavage (BAL) on 59 asymptomatic HIV-seropositive subjects (mean CD4: 365.9 +/- 31.2 cells/mm3) and 12 normal control subjects. The volume of ELF and the concentration of glutathione and oxidized glutathione were determined. The concentration of total GSH in ELF was not significantly different in HIV-seropositive individuals compared with normal subjects (628.1 +/- 63.9 microM versus 499.9 +/- 86.0 microM, p = 0.38). However, there was a significantly higher concentration of ELF GSH in HIV-seropositive cigarette smokers (n = 30) compared with nonsmokers (n = 29) (800.3 +/- 107.7 microM versus 443.6 +/- 45.3 microM, p = 0.004). The percentage of total GSH in the oxidized form (GSSG) was similar in both the HIV-seropositive and the normal subject groups (3.4 +/- 0.3% versus 3.0 +/- 0.4%, p = 0.559). There were no significant correlations between ELF GSH or GSSG concentrations and age, CD4 count, or pulmonary function. There was, however, a significant negative correlation between BAL lymphocyte percentage and GSH. The current study suggests that for those patients whose HIV infection is at a relatively early phase, the levels of GSH in the lung ELF are normal.
Adult↗
Alveolar fluid glutathione decreases in asymptomatic HIV-seropositive subjects over time.
BACKGROUND: Initial investigations demonstrated a deficiency of glutathione (GSH) in the epithelial lining fluid (ELF) of HIV-seropositive patients. In a recent study, our laboratory was unable to document such a deficiency. The current study was performed in an attempt to reconcile those disparate findings. STUDY OBJECTIVES: To determine if ELF GSH decreases over time in asymptomatic HIV-seropositive subjects. DESIGN: Prospective, longitudinal study. SETTING: Major university medical center. PATIENTS OR PARTICIPANTS: Thirty-three asymptomatic HIV-seropositive volunteers. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: BAL was performed on 33 asymptomatic HIV-seropositive subjects at baseline, 6 months later, and 12 months later. The volume of ELF and the concentration of GSH and oxidized GSH were determined. The concentration of total GSH in ELF was 689.0+/-100.4 microM. This significantly decreased when measured 6 and 12 months later (355.9+/-41.7 microM, and 397.9+/-52.7 microM, respectively, p=0.01, compared with baseline, both comparisons). Significant decreases were also noted in the HIV-seropositive subjects who smoked cigarettes (baseline--762.6+/-142.4 microM; 6 months--373.7+/-45.9 microM; 12 months--459.3+/-73.8 microM, p<0.03, for baseline vs 6 months, and baseline vs 12 months). In nonsmoking HIV-seropositive subjects, there was a decrease in ELF GSH over time, but it did not reach statistical significance (baseline--589.1+/-138.2 microM; 6 months--335.3+/-74.1 microM; 12 months--345.8+/-74.0 microM, p>0.1, all comparisons). The percentage of total GSH in the oxidized form was similar at all three time points (baseline--3.8+/-0.5%; 6 months--3.1+/-0.5%; 12 months--3.9+/-0.9%, p>0.1, all comparisons). CONCLUSIONS: The current study demonstrates that the GSH level in ELF is significantly decreased in HIV-seropositive subjects 6 and 12 months after the initial determination.
Adult↗
Erythromycin interaction with risperidone or clomipramine in an adolescent.
An adverse event is described which appeared when the macrolide antibiotic erythromycin was added to a regimen of risperidone 0.5 mg bid and clomipramine 50 mg tid in a 15-year-old male being treated for Tourette's, obsessive-compulsive, and attention-deficit hyperactivity disorders. An acute onset of behavioral symptoms, including agitation, labile mood, incessant talking, and argumentativeness, began within 24 h of starting the erythromycin and persisted for 9 days after its discontinuation. It was followed by a return to stable functioning on the prior risperidone-clomipramine regimen. Erythromycin, risperidone, and clomipramine are all metabolized by the hepatic cytochrome P450 system. It is postulated that the addition of erythromycin, a known inhibitor of CYP3A and CYP1A2, resulted in alterations in the metabolism of clomipramine and risperidone. Clomipramine metabolism is dependent upon the isoenzymes CYP2D6 and CYP1A2, and risperidone is a substrate for CYP2D6. Erythromycin would inhibit demethylation of clomipramine at the 1A2 isoenzyme and lead to a dual interaction between risperidone and clomipramine at the CYP2D6 isoenzyme. The subsequent increases in plasma levels of clomipramine, risperidone, their metabolites, or a combination of these agents could explain the adverse effects noted in this patient. In the absence of risperidone, clomipramine could have been metabolically cleared by CYP2D6. In the absence of clomipramine, risperidone clearance would not be affected by erythromycin. So the proposed mechanism requires an interaction involving all three agents: erythromycin, clomipramine, and risperidone. Alterations in plasma protein binding may also have played a role, because all three agents are extensively protein bound. Caution is urged when prescribing erythromycin with psychotropic drugs that are highly protein bound and/or are metabolized by the same P450 isoenzymes.
Acne Vulgaris↗
Administration of oral acyclovir suppressive therapy after neonatal herpes simplex virus disease limited to the skin, eyes and mouth: results of a phase I/II trial.
BACKGROUND: Neonatal herpes simplex virus (HSV) infections limited to the skin, eyes and mouth (SEM) can result in neurologic impairment. A direct correlation exists between the development of neurologic deficits and the frequency of cutaneous HSV recurrences. Thus, the National Institutes of Allergy and Infectious Diseases Collaborative Antiviral Study Group conducted a Phase I/II trial of oral acyclovir therapy for the suppression of cutaneous recurrences after SEM disease in 26 neonates. METHODS: Infants < or = 1 month of age with virologically confirmed HSV-2 SEM disease were eligible for enrollment. Suppressive oral acyclovir therapy (300 mg/m2/dose given either twice daily or three times per day) was administered for 6 months. RESULTS: Twelve (46%) of the 26 infants developed neutropenia (< 1000 cells/mm3) while receiving acyclovir. Thirteen (81%) of the 16 infants who received drug 3 times per day experienced no recurrences of skin lesions while receiving therapy. In comparison, a previous Collaborative Antiviral Study Group study found that only 54% of infants have no cutaneous recurrences in the 6 months after resolution of neonatal HSV disease if oral acyclovir suppressive therapy is not initiated. In one infant, HSV DNA was detected in the cerebrospinal fluid during a cutaneous recurrence, and an acyclovir-resistant HSV mutant was isolated from another patient during the course of the study. CONCLUSIONS: Administration of oral acyclovir can prevent cutaneous recurrences of HSV after neonatal SEM disease. The effect of such therapy on neurologic outcome must be assessed in a larger, Phase III study. As such, additional investigation is necessary before routine use of suppressive therapy in this population can be recommended.
Acyclovir↗
Occurrence of the Cys311 DRD2 variant in a pedigree multiply affected with panic disorder.
Following the detection of the rare DRD2 codon 311 variant (Ser-->Cys) in an affected member from a large, multiply affected panic disorder family, we investigated the occurrence of this variant in other family members. The variant occurred in both affected and unaffected individuals. Further screening in panic disorder sib pairs unrelated to this family failed to detect the Cys311 variant. Our data suggests that this variant has no pathogenic role in panic disorder.
Base Sequence↗
Evidence that the APOE locus influences rate of disease progression in late onset familial Alzheimer's Disease but is not causative.
An association has been observed in several independent data sets between late onset Alzheimer's Disease (AD) and the APOE locus on chromosome 19. We have examined the genotype in family history positive (FHP) and family history negative (FHN) cases and find a distortion of the APOE allele frequencies in accord with previous studies. However, when we examined the allele distribution of the at-risk siblings of the FHP group we found an excess of the epsilon 4 allele which also differs significantly from historic controls but not from the affected siblings. The age distribution of the affected and unaffected siblings was similar, suggesting that the allelic frequency distortion in the unaffected siblings was not due to their being below the mean age of onset. Lod score linkage analysis, with age dependent onset and non-stringent specification of the genetic parameters, did not suggest linkage to the APOE locus. Furthermore, an analysis of variance of the age of disease free survival suggested that APOE genotype contributes a small fraction of the total variance indicating that the APOE locus is a poor predictor of disease free survival age within late onset families. One explanation for the age dependent association reported by other groups, and our results, is that the APOE locus enhances the rate of progression of the disease process in otherwise predisposed individuals and that variation at this locus is not able in and of itself to cause the disease. We suggest this hypothesis is compatible with the current literature regarding APOE and AD.
Age Factors↗
Asymptomatic neurocysticercosis in a patient with AIDS and cryptococcal meningitis.
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AIDS-Related Opportunistic Infections↗
Environmental regulation of alpha-haemolysin expression in Escherichia coli.
The effect of osmolarity, temperature and anaerobiosis on the expression of Escherichia coli alpha-haemolysin was investigated. Low osmolarity of the culture medium, growth at high temperature (37 degrees C) and anaerobiosis increase haemolysin production in E. coli cells harbouring the haemolytic plasmid pHly152 as well as in haemolytic strains isolated from urinary-tract infections.
Anaerobiosis↗
Quantitation of soluble HLA class I heterodimers and beta 2-microglobulin in patients with active pulmonary tuberculosis.
Beta 2m serum levels have been shown to be increased in patients with tuberculosis and HIV infection. We determined the stability of beta 2m and of sHLA-I dimers in serum, and then determined the levels of both molecules in 60 non-HIV-infected patients with active pulmonary tuberculosis and in 55 adult controls. The levels of sHLA-I in samples kept at room temperature declined by 8% at 30 minutes, 16% at 60 minutes, and 36% at 120 minutes. Beta 2m levels remained stable at all times tested. Mean sHLA-I levels were 0.99 +/- 0.16 micrograms/ml in controls and 1.34 +/- 0.11 micrograms/ml in patients with tuberculosis (P < 0.0001). Beta 2m levels were 1.23 +/- 0.26 micrograms/ml in controls and 2.26 +/- 0.64 micrograms/ml in patients with tuberculosis (P < 0.0001). All patients with tuberculosis had elevation of sHLA-I and/or beta 2m above 1 standard deviation of normal values. However, there was no correlation between sHLA-I and beta 2m levels in individual samples. Evaluation of sHLA-I holds the promise of further understanding of the biology and genetic regulation of the immune response to mycobacterial infection.
Adolescent↗
A locus control region in the T cell receptor alpha/delta locus.
A locus control region (LCR) is a set of cis-acting elements that regulate chromatin accessibility of a gene locus. In the T cell receptor (TCR) alpha/delta locus, an LCR might regulate the differential tissue and developmental expression and the rearrangement of TCR alpha and delta genes. We have localized a region 3' of the TCR alpha/delta locus containing eight T cell-specific nuclease hypersensitive domains (HS-1 to HS-8), which fit the characteristics of an LCR. In transgenic mice, a TCR alpha gene linked to this region is expressed at a high level, independent of the site of integration and correlates with gene copy number. The transgene is expressed in the alpha beta but not the gamma delta T cell subset and is activated at the right time during development. Proper LCR function requires the region containing HS-2 to HS-6. We propose a model of LCR competition to explain the differential regulation of TCR alpha versus delta genes during development.
Animals↗
Neurocysticercosis in Houston, Texas. A report of 112 cases.
Neurocysticercosis (NCC) is a common disease among Hispanic immigrants to the American Southwest. The experience in this series suggests a higher incidence of disease than has been reported by public health personnel. Symptoms at presentation correlate with the anatomic site of disease. Parenchymal disease and inactive calcifications present primarily with seizures; ventricular disease with headaches and symptoms of acute hydrocephalus; and cisternal disease with basilar meningitis, hydrocephalus, or seizures from coexisting parenchymal disease. Current treatment regimens are suboptimal, although symptoms may resolve in the absence of therapy. Patients may not respond to a single course of praziquantel therapy. Procedures to divert cerebrospinal fluid are often needed and frequently require revision. We found an association between corticosteroid treatment and the need for repeat therapy with praziquantel, but controlled studies are needed to clarify the role of antiparasitic agents in all forms of neurocysticercosis.
Adolescent↗
[Cardiovascular surgery in the elderly. Preoperative and postoperative care].
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Aged↗
Loss of activity in the secreted form of Escherichia coli haemolysin caused by an rfaP lesion in core lipopolysaccharide assembly.
A transposon mutant of Escherichia coli 5K was isolated which reduced 10- to 50-fold the secreted extracellular haemolytic activity of cells carrying the complete hlyCABD operon while leaving unaffected the intracellular haemolytic activity and the levels of intracellular and extracellular haemolysin protein, HlyA. The transposon insertion was identified within the rfaP gene (required for attachment of phosphate-containing substituents to the lipopolysaccharide inner core), and extracellular haemolytic activity was restored in trans by the intact rfaP gene. The loss in cytolytic activity of the secreted HlyA protein was not related to the HlyC-directed acylation of the protoxin. Activity of the secreted toxin was restored by chaotropic agents and during rate-zonal centrifugation the mutant-secreted HlyA migrated as a larger species than the wild type. The results indicate that the rfaP mutation affects the aggregation behaviour of the active toxin during or following the signal peptide-independent secretion process.
Bacterial Proteins↗
A locus for familial early-onset Alzheimer's disease on the long arm of chromosome 14, proximal to the alpha 1-antichymotrypsin gene.
Although mutations in the beta-amyloid precursor protein gene (APP) on chromosome 21 cause some cases of early-onset Alzheimer's disease (AD), most cases evidently do not have mutations in APP. We analysed ten early-onset families for linkage to APP and markers elsewhere in the genome. One family (F172) was consistent with linkage to chromosome 21 and was subsequently found to have an APP Val to Ile mutation. Of the others, all but one were consistent with linkage to markers in the middle long arm of chromosome 14. However, no family showed independent evidence of linkage with two point analysis and only one showed independent evidence of linkage on multipoint analysis. Therefore, we cannot rule out heterogeneity at these loci although tests for heterogeneity were not significant.
Adult↗