Search PubMedSearch

Biomedical subjects

M Rodriguez

Publications and source records attributed to M Rodriguez.

At least 145 records · Page 8Linked to original sources

Direct inhibitory effect of calcitriol on parathyroid function (sigmoidal curve) in dialysis.

The effect of intravenous calcitriol on parathyroid function was evaluated in nine chronic hemodialysis patients with secondary hyperparathyroidism. Two micrograms of calcitriol were administered intravenously after dialysis thrice weekly for ten weeks. Parathyroid function was assessed by inducing hypo- and hypercalcemia with low calcium (1.0 mEq/liter) and high calcium (4.0 mEq/liter) dialyses before and after ten weeks of intravenous calcitriol therapy. To avoid hypercalcemia during calcitriol administration, the dialysate calcium was reduced to 2.5 mEq/liter. Parathyroid hormone (PTH) values (pg/ml) from dialysis-induced hypo- and hypercalcemia were plotted against serum ionized calcium, and the sigmoidal relationship between PTH and calcium was evaluated. Basal PTH levels fell from 902 +/- 126 pg/ml to 466 +/- 152 pg/ml (P less than 0.01) after therapy without a significant change in the serum total calcium concentration. The ionized calcium-PTH sigmoidal curve shifted to the left and downward after calcitriol therapy. The maximal PTH response during hypocalcemia decreased after calcitriol from 1661 +/- 485 pg/ml before calcitriol to 1031 +/- 280 pg/ml afterward (P less than 0.05). The PTH level at maximal inhibition due to hypercalcemia decreased from 281 +/- 76 pg/ml before calcitriol to 192 +/- 48 pg/ml afterward (P less than 0.05). The slope of the sigmoidal curve changed from -2125 +/- 487 to -1563 +/- 385 (P less than 0.05). The set point of ionized calcium (4.60 +/- .11 mg/dl before vs. 4.44 +/- .07 mg/dl after) did not change significantly with calcitriol therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitriol

Silent genes in the mouse major urinary protein gene family.

To date, two classes of mouse major urinary protein (MUP)-encoding genes have been described, the expressed genes and the intervening-sequence-containing pseudogenes. The data presented in this paper define a third class, the silent Mup genes, which are potentially functional but appear not to be expressed under normal circumstances. We describe a MUP subfamily (Mup-1.5) containing two genes, Mup-1.5a and Mup-1.5b, that are nearly identical, differing at only three positions (greater than 99.9% identity) over the entire 4-kilobase (kb) transcription unit and approximately 1 kb of flanking DNA. The similarity between these two genes extends over greater than 35 kb. Using specific oligonucleotides, we have shown that the 5a gene is expressed in BALB/cByJ mice, primarily in the submaxillary gland, whereas the 5b gene is not expressed. However, we found that when a 9.4-kb DNA fragment containing the Mup-1.5b gene was introduced into the mouse germ line, mice in two of the four transgenic lines expressed this gene at a high level and with the tissue-specificity characteristic of the Mup-1.5a gene. These results suggest that the inactivity of the endogenous Mup-1.5b gene is due not to a lack of functional positive regulatory elements, but to long-range, inhibitory position effects.

Animals

Ultrastructural, morphometric, and immunocytochemical study of anterior horn cells in mice with "wasted" mutation.

Mice with the autosomal recessive gene "wasted" (wst/wst) manifest hindlimb paralysis and tremulousness, develop reduced secretory immune responses, and have abnormal DNA repair mechanisms. There is prominent vacuolar degeneration of neurons within anterior horns of the spinal cord and motor nuclei of the brainstem. A morphometric analysis of motor neurons in the spinal cord was performed on 2-hydroxyethyl methacrylate-embedded tissue from ten wst/wst mice, ten littermates (wst/+, +/+) without clinical deficits, and ten parental (+/+) control mice. Vacuolated neurons were present only in wst/wst mice (p = 0.0008). Fibrillary neurons were more numerous in the wst/wst mice than in littermates (p = 0.01) or controls (p = 0.007). The number of total or normal neurons did not differ significantly among the three groups. Volume measurements for normal, fibrillary, vacuolated, and total neurons were greater in wst/wst mice (p less than 0.008). Electron microscopic studies revealed vacuolar degeneration exclusively within neurons of wst/wst mice with the prominent accumulation of neurofilaments. Immunocytochemical staining of Araldite-embedded sections with monoclonal antibodies (MAb) to 68 kDa, 160 kDa, and 200 kDa neurofilament proteins showed prominent staining of vacuolated and fibrillary neurons in wst/wst mice exclusively with the MAb to 200 kDa neurofilaments. Dephosphorylation of tissue reduced the staining of 200 kDa neurofilaments in wst/wst mice. These studies suggest that phosphorylated neurofilaments may be important in events producing neuronal dysfunction. Therefore the "wasted" mutation may be an excellent model for the study of motor neuron disease.

Animals

Clinical pharmacokinetics of intravenous flecainide in critically ill patients.

Plasma flecainide (FLC) levels versus time were measured in a group of 10 acute myocardial infarction (AMI) patients at our Intensive Care Unit. These patients were treated with single doses of 150 mg FLC as a 30-min intravenous infusion. Mean FLC plasma concentration values at 0, 1, 2, 4, and 8 h following administration were 562 +/- 271, 342 +/- 129, 270 +/- 90m, 240 +/- 80 and 210 +/- 60 ng/ml, respectively. Flecainide pharmacokinetics fitted an open two-compartment model, with a rapid distribution phase and a slow elimination phase. Mean values for the terminal plasma half-life (t1/2 beta) was 22.0 +/- 9.7 h and the volume of distribution (V beta) was 7.99 +/- 3.02 1/kg. FLC is different to other i.v. antiarrhythmics in having a prolonged plasma half-life which is a decided advantage. In contrast to lidocaine, FLC has a pharmacokinetic profile that enables it to be used for treating ventricular arrhythmia without constant-rate i.v. infusion and without the need for complicated loading dosages in order to avoid a 'pharmacokinetic dip' over the first hour of treatment.

Acute Disease

Synthesis and biological activities of some cholecystokinin analogues substituted in position 29 by a beta-alanine.

Syntheses of analogues of the C-terminal heptapeptide of cholecystokinin are described. These analogues were obtained by replacing glycine 29 by a beta-alanine. The C-terminal phenylalanine amide was in some cases substituted by 2-phenylethyl alcohol and/or residues of the C-terminal tetrapeptide by their D-enantiomers. These compounds were tested for their action on stimulation of amylase release from rat pancreatic acini and for their ability to inhibit binding of labeled CCK to rat pancreatic acini and guinea pig brain membranes. Some of these derivatives behaved as CCK receptor antagonists.

Alanine

Treatment of encephalomyocarditis virus-induced central nervous system demyelination with monoclonal anti-T-cell antibodies.

Infection of BALB/c mice with the M variant of encephalomyocarditis virus resulted in the development of a paralytic syndrome in 7 to 10 days. The paralysis was maximal during the period of viral clearance; most of the animals recovered from the initial deficit and showed no delayed recurrences. Pathologically, the white matter of brain and spinal cord showed well-demarcated areas of perivascular cuffing, demyelination, and, during recovery, remyelination by oligodendrocytes--all suggestive of postinfectious encephalomyelitis. Depletion of either the CD4 or CD8 subset of T cells in vivo with the appropriate monoclonal antibody, GK1.5 or 2.43, respectively, administered one day (24 h) prior to infection was sufficient to limit the development of the paralytic syndrome by 79% (GK1.5) and 82% (2.43).

Animals

The prevalence of the Wernicke-Korsakoff syndrome in Sydney, Australia: a prospective necropsy study.

In a prospective necropsy study, the prevalence of the Wernicke-Korsakoff syndrome (WKS) in Sydney, Australia was 2.1% of adults over the age of 15 years. The population studied encompassed a wide spectrum of socio-economic and cultural backgrounds. Abuse of alcohol appeared to be the major predisposing factor to the development of the WKS in cases which were adequately documented. This high prevalence rate is in line with other clinical and pathological Australian studies and provides additional support for the idea of prevention of the WKS by the use of thiamin supplements in the Australian diet in flour, bread and perhaps alcoholic beverages.

Adolescent

Catheter-induced aortic thrombus masquerading as coarctation of the aorta.

The placement of an umbilical artery catheter is firmly established as an essential technique in the care of ill neonates. This simple procedure involves well recognized risks. Thrombotic complications are frequently seen with umbilical artery catheter (UAC) placement. The occurrence, however, of an aortic thrombus presenting as classical aortic coarctation has not been reported previously. This report describes two infants with classical symptomatology of coarctation of the aorta who were found instead to have aortic thrombus formation in association with umbilical artery catheter placement.

Aortic Coarctation

The coexistence of Taenia solium cysticerci and the pig: role of the antigen B.

A review of data on the antigen B of Taenia solium (AgB) is presented. The biochemical, immunological and physiological properties of AgB are discussed in the context of the host-parasite relationship. It is proposed that AgB facilitates survival of cysticerci by impairing augmentation of the host inflammatory response through the inhibition of the classical pathway of the complement cascade. In this way, AgB not only allows evasion of the host immune attack but also decreases the host-parasite confrontation, facilitating their coexistence.

Animals

Detection of bovine herpesvirus type 1 via an immunoperoxidase method, using monoclonal antibodies.

The sensitivity and specificity of the immunoperoxidase technique, using monoclonal antibodies, for the detection of bovine herpesvirus type 1 (BHV-1) was assessed and compared with viral isolation methods. In this study, BHV-1 antigens were detected in impression smears of brain obtained from calves in which BHV-1 was isolated. False-positive results were not observed after double-blind examination. Preliminary identification of isolates as antigenic variants was possible by use of 3 monoclonal antibodies reactive with neurotropic and/or pneumotropic strains of BHV-1. Results were consistent with previous work in which characterization was performed by use of immunofluorescense and ELISA. The immunoperoxidase technique, using monoclonal antibodies, was determined to be specific and sensitive, compared with viral isolation, for the diagnosis of BHV-1 encephalitis. In addition, it has operative advantages in that the assay does not require tissue culture facilities, and results can be obtained within hours after specimens are obtained.

Animals

[Comparative study of Uromiron and 38% Lipiodol in sialography].

A comparative study was undertaken to assess the properties of uromiron and lipiodol 38%, which are used as radiopaque materials in sialographic techniques, on 25 young adult outpatients of both sexes that were seen at the Dental School, University of Chile, Santiago. It was found that, although the radiopaque properties of uromiron were less than lipiodol 38%, the can be improved by increasing the amount of material injected into the duct system of the salivary glands. Likewise, uromiron exhibited a proper biological tolerance and a rapid emptying time, therefore the use of uromiron in sialographic techniques seems to be a proper alternative to lipiodol 38%.

Adult

Intrathecal somatostatin in cat and mouse studies on pain, motor behavior, and histopathology.

Effects of intrathecal (i.t.) somatostatin (SST) on nociception, motor function, and spinal cord pathology were evaluated in cats and mice. Cats chronically implanted with i.t. lumbar catheters received either a single injection of 2 mg SST i.t. (group I, N = 4), four repetitive injections on consecutive days of 2 mg SST i.t. (group II, N = 4) or saline i.t. (group III, N = 2). No analgesic effects were observed following single or repeated SST injections as evaluated by the skin twitch response. However, significant impairment of hind leg motor function ranging from unbalanced gait to paralysis was observed following the first SST i.t. injection. Histological examination of spinal cords six days after the first SST injection in group II showed multiple pyknotic neurons in all cats. Some cats showed focal demyelination in the posterior column of the spinal cord white matter. Mice received a single percutaneous injection of 50 micrograms SST i.t. (group I, N = 7), 5 micrograms SST i.t. (group II, N = 3), or saline i.t., (group III, N = 5). No analgesic effects were observed in groups II and III as evaluated by the hot plate (HP) and tail flick (TF) tests. Injection of 50 micrograms SST i.t. (group I) caused reversible flaccid hind leg paralysis in all mice and concomitant increases in HP and TF latencies. Histologic examination revealed focal demyelination in the spinal cord in three out of seven mice in this group. Present data substantiate neurotoxic effects of i.t. SST and lack of behaviorally defined antinociception at innocuous dosages.

Animals

Refractory potassium repletion due to cisplatin-induced magnesium depletion.

Cisplatin is a common cause of hypomagnesemia and hypokalemia due to renal magnesium (Mg) and potassium (K) losses. Magnesium plays an important role in the maintenance of intracellular K. An unrecognized and untreated Mg depletion can lead to a refractory K repletion. We describe two patients with hypomagnesemia-associated refractory hypokalemia following cisplatin following cisplatin therapy. Potassium supplementation failed to replace the K deficit. Profound hypokalemia persisted until hypomagnesemia was recognized and corrected. In neither patient was the concurrent hypomagnesemia recognized until the 11th and 9th hospital days. These two cases demonstrated the association of a refractory K repletion and an Mg deficiency. Thus, both serum K ion and Mg levels should routinely be assessed in patients who require cisplatin therapy.

Adult

Successful therapy of Theiler's virus-induced demyelination (DA strain) with monoclonal anti-Lyt-2 antibody.

The effects of therapy with mAb to T cell subsets were studied in mice with Theiler's murine encephalomyelitis virus-induced demyelination. mAb GK1.5 (directed at class II-restricted T cells) and mAb 2.43 (directed at class I-restricted T cells) depleted the appropriate subset of T cells in lymph nodes, spleens, and peripheral blood for 6 to 8 wk after a single i.p. injection of 1 mg of purified mAb. Early treatment with mAb GK1.5 (days -1, 0, and +1 relative to virus injection) resulted in death, encephalitis, and increased demyelination in the majority of animals tested. Treatment with mAb 2.43 resulted in less meningeal inflammation and fewer demyelinating lesions in the spinal cord, irrespective of whether the mAb was given early or after demyelinating disease was established (days 15, 16, and 17). Beneficial response to mAb therapy did not correlate with titers of virus isolated from the central nervous system or serum. These results indicate an important role of class II-restricted T cells during early disease in preventing overwhelming encephalitis; class I-restricted T cells may be critical during demyelination.

Animals

Structural mutation affecting intracellular transport and cell surface expression of murine class II molecules.

We have selected Ia variants from the Ia+ (H-2d) M12.4.1 B cell lymphoma that are negative on the cell surface for one or both Ia isotypes. The molecular analysis of two such independently selected cell lines, M12.A2 and M12.C3, is reported here. This analysis revealed that the genes encoding Ad beta (M12.A2) and Ed beta (M12.C3) contained identical single-nucleotide transitions that resulted in the substitution of Ser (mutant) for Asn (wild-type) at residue 82/83 of the extracellular NH2-terminal (membrane distal) beta 1 domain. This conservative substitution caused a cytoplasmic accumulation of I-A or I-E molecules in the respective cell line although predicted secondary-structure analysis suggests a minimal effect on protein conformation. Thus, the mutation appears to have either created a negative signal that stops transport or eliminated a positive signal that is required for transport and targeting to the cell surface.

Amino Acid Sequence

Immunoglobulins and complement in demyelination induced in mice by Theiler's virus.

Intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV) produces chronic demyelination and persistent infection in the central nervous system (CNS) of susceptible SJL mice. This series of experiments examined the contribution of humoral immunity and C to myelin destruction. As in multiple sclerosis, mice persistently infected with TMEV had elevated levels of IgG and oligoclonal bands in the cerebrospinal fluid (CSF). Immunoblot studies revealed that even in animals exhibiting profound demyelination, IgG in the serum and CSF was directed primarily at virus antigen rather than at normal myelin components. Inflammatory cells positive for Ig were distributed mainly around blood vessels, but occasionally they infiltrated the spinal cord parenchyma. Rare examples of myelin sheaths positive for IgG were found by immunoelectron microscopy in spinal cord sections from infected mice; the third component of complement (C3) was commonly found in the walls of CNS blood vessels but not on myelin. Neither serum nor CSF IgG from infected mice bound to myelin sheaths or other CNS components in sections of normal syngeneic spinal cord. There were significantly more demyelinating lesions in infected mice depleted of C components with cobra venom factor. These data do not support a humoral autoimmune basis for the CNS demyelination that occurs in association with persistent TMEV infection. However, the humoral immune response directed at TMEV antigens may either limit virus spread or promote virus persistence.

Animals

The tubulin genes of Trypanosoma cruzi.

The organization of the alpha- and beta-tubulin genes in the genome of Trypanosoma cruzi have been analysed by Southern blotting using tubulin probes derived from Trypanosoma brucei. The tubulin array appears to be more complex in this organism than in other members of the same family. Some tubulin genes are tightly clustered in an alternating (alpha-beta)n array with a basic repeat unit length of 4.3 kb. However, other pairs of alternating alpha- and beta-tubulin sequences appear to be physically separated from the basic group. This finding indicates that the tubulin gene cluster present in T. cruzi is less perfectly conserved than in T. brucei. T. (Herpetosoma) rangeli is similar to T. (Schizotrypanum) cruzi in its tubulin gene organization whereas most of these genes are tandemly clustered in the genome of T. (Trypanozoon) evansi, with a basic repeat unit length of 3.6 kb as previously described for T. (Trypanozoon) brucei. Two overlapping recombinant clones containing T. cruzi tubulin sequences have been isolated from a genomic cosmid library of T. cruzi epimastigotes using the T. brucei tubulin probes. Partial sequencing of the T. cruzi beta-tubulin gene has confirmed its identity and shows more than 70% homology with the sea urchin, chicken and T. b. rhodesiense beta-tubulin reported gene sequences. Analysis of tubulin gene organization through the parasite life cycle does not show evidence of major rearrangements within the repeat unit. Several T. cruzi strains and cloned lines whilst sharing the 4.3-kb tubulin repeat unit, exhibited very variable tubulin gene organization with tubulin probes. These striking differences in the organization of this structural gene among T. cruzi strains and cloned lines suggest that the heterogeneity previously reported in parasite populations may be related to a very dynamic, diploid genome.

Animals