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Biomedical subjects

M Rodriguez

Publications and source records attributed to M Rodriguez.

At least 487 records · Page 27Linked to original sources
PubMed1991

Human T-cell lymphotropic virus type I sequences detected by nested polymerase chain reactions are not associated with multiple sclerosis.

The hypothesis that human T-cell lymphotropic virus type I (HTLV-I) infection is associated with multiple sclerosis (MS) was tested by using primers specific to gag and pol regions of HTLV-I in an analysis that used polymerase chain reactions. No amplification of DNA from patients with MS was detected with primers for either region. After application of a more sensitive scheme with use of nested primers, however, half the samples, including patients with MS and normal control subjects, were found to contain pol DNA sequences. No sequences related to the HTLV-I gag region were detected among patients with MS by using nested primers. Sequences of the amplified HTLV-I pol genomes were determined. Regardless of their origin (MS or normal control), the pol region sequences were similar to HTLV-I sequences reported by other investigators. We conclude that HTLV-I does not have a distinct association with MS, but HTLV-I-related sequences, although in extremely low copy number, may be present in human genomes.

Adult↗
PubMed1991

Calcitonin, an important factor in the calcemic response to parathyroid hormone in the rat.

The role of calcitonin on the calcemic response to parathyroid hormone (PTH) in renal failure has not been evaluated previously. Often animal studies evaluating the calcemic response to PTH in renal failure are performed in thyroparathyroidectomized (TPTX) animals, and thus eliminate any potential physiologic effect of calcitonin. In addition, parathyroidectomy (PTX), presumably by reduction of high PTH levels, has corrected the calcemic response to PTH in animals with renal failure. The present study was designed to evaluate the effect of endogenous calcitonin production on the calcemic response to PTH in rats with renal failure and secondary hyperparathyroidism, and in rats with normal renal function with diet induced hyperparathyroidism. Four groups of rats were evaluated: 1) chronic renal failure plus TPTX with autotransplant of the parathyroid gland, (CT-) CRF; 2) chronic renal failure plus selective PTX with autotransplant of the parathyroid gland, (CT+) CRF; 3) normal renal function plus TPTX with autotransplant of the parathyroid gland, (CT-) NRF; and 4) normal renal function plus selective PTX with autotransplant of the parathyroid gland, (CT+) NRF. Renal failure was surgically induced by a two-stage 5/6 nephrectomy, and exogenous thyroxine was administered to the two thyroidectomized (CT-) groups. Hyperparathyroidism was induced with a high phosphate diet (1.2%), and thus at the time of PTH infusion, PTH levels were (CT-) CRF 84 +/- 16, (CT+) CRF 89 +/- 21, (CT-) NRF 37 +/- 7, and (CT+) NRF 31 +/- 4 pg/ml, respectively (normal 21 +/- 3 pg/ml). Rat 1-34 PTH (2.6 U/hr) was infused for 48 hours via a subcutaneously implanted Alzet pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Sigmoidal relationship between calcitonin and calcium: studies in normal, parathyroidectomized, and azotemic rats.

Calcitonin secretion is stimulated by acute hypercalcemia. Furthermore, in the rat, the calcemic response to parathyroid hormone (PTH) is decreased by calcitonin stimulation. However, in renal failure, it is not known if an increase in the serum calcium concentration within the physiologic range of serum calcium stimulates calcitonin and whether the increased calcitonin decreases the calcemic response to PTH. In the present study, four groups of pair-fed rats were evaluated: normals (N); parathyroidectomy (PTX); and two groups with renal failure (RF)--basal serum calcium less than 8.5 mg/dl (RFa) and basal serum calcium greater than 8.5 mg/dl (RFb). Hypocalcemia was induced by parathyroidectomy or in the RFa group, by a high phosphate diet. Increases in the serum calcium were produced by a 48 hour infusion of rat 1-34 PTH. In the RFa and PTX groups, stimulation of calcitonin was observed as the serum calcium increased from hypocalcemia to normal levels of calcium (P less than 0.01). In all four groups, increasing the serum calcium from normal levels to hypercalcemia increased the serum calcitonin level (P less than 0.05). The relationship between serum calcitonin and calcium was best expressed as a sigmoidal curve. In the two groups with basal hypocalcemia, PTX and RFa, the calcitonin-calcium curve was shifted to the left of the N and RFb groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Calcemic response to parathyroid hormone in renal failure: role of phosphorus and its effect on calcitriol.

The calcemic response to parathyroid hormone (PTH) is decreased in renal failure. The reduction of hyperphosphatemia improves the calcemic response to PTH in animals with advanced renal failure. However, since low calcitriol levels in renal failure may also contribute to the decreased calcemic response to PTH, the improved calcemic response observed during the reduction of serum phosphorus may be partially mediated by an increase in serum calcitriol levels. The present study evaluated the calcemic response to PTH in rats with moderate and advanced renal failure and how this response was modified by a high and a low phosphorus diet. In addition, the effect of a change in dietary phosphorus on calcitriol levels was also evaluated. A 48-hour continuous infusion of 1-34 rat PTH increased the serum calcium level to 18.2 +/- 0.4 mg/dl in normal rats, versus 13.7 +/- 0.9 and 12.1 +/- 0.2 mg/dl in rats with moderate and advanced renal failure, respectively. During the PTH infusion, a high phosphorus diet increased the serum phosphorus and resulted in a reduced calcemic response to PTH at each level of renal function; respective serum calcium levels were 13.8 +/- 0.6 mg/dl in normals, 11.2 +/- 0.2 mg/dl in moderate renal failure and 9.6 +/- 0.5 mg/dl in advanced renal failure. In normal rats and in rats with moderate renal failure, dietary phosphorus restriction during the PTH infusion increased serum calcitriol levels. In rats with advanced renal failure, serum calcitriol levels were lower than in the other two groups and were not affected by changes in dietary phosphorus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Calcemic response to parathyroid hormone in renal failure: role of calcitriol and the effect of parathyroidectomy.

Hyperparathyroidism due to renal failure begins in the early stages of renal insufficiency and is in part secondary to skeletal resistance to the calcemic action of parathyroid hormone (PTH). Factors which have been reported to reduce the calcemic response to PTH include: decreased calcitriol levels, hyperphosphatemia and down regulation of PTH receptors in bone. While hyperphosphatemia may directly decrease the calcemic response to PTH, it may also act indirectly by a suppression of calcitriol synthesis. In this study, the effect of calcitriol on the calcemic response to PTH was evaluated in normal rats and in rats with moderate and advanced renal failure. To determine the combined effect of calcitriol and phosphorus on the calcemic response to PTH, rats receiving calcitriol were fed either a high (1.0%) or low (0.2%) phosphorus diet during a 48-hour PTH infusion. In advanced renal failure, calcitriol administration increased the calcemic response to PTH independent of the dietary phosphorus intake. During ingestion of a low phosphorus diet, a 48 hour PTH infusion resulted in a serum calcium level of 13.7 +/- 0.5 and 12.1 +/- 0.2 mg/dl (P less than 0.02) with and without calcitriol administration, respectively. In normal rats and in rats with moderate renal failure, calcitriol administration improved the calcemic response only during a high phosphorus intake. After a 48-hour PTH infusion in normal rats, the serum calcium levels with and without calcitriol were 16.1 +/- 0.9 and 14.8 +/- 0.6 mg/dl, P less than 0.01 respectively; in rats with moderate renal failure, calcitriol administration increased serum calcium, 13.2 +/- 0.5 versus 11.2 +/- 0.4 mg/dl, P less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of aluminium on osteocalcin production in the rat.

In renal failure, aluminium is an important factor in the development of osteomalacia. The mechanism by which aluminium produces osteomalacia is not clear; it may be toxic to the osteoblast, and as a result of its effect on osteoblasts, impair mineralisation. Another possibility is that aluminium may directly impair mineralisation independent of osteoblast function. Osteocalcin is considered to be a specific marker of osteoblast activity and its production is stimulated by calcitriol. In the present study, calcitriol-stimulated production of osteocalcin was studied as a marker of osteoblast activity in aluminium toxicity. Four groups of rats were evaluated: (1) normals; (2) normal renal function plus aluminium; (3) renal failure; and (4) renal failure plus aluminium. Osteocalcin production was determined by measuring serum osteocalcin at baseline and after stimulation with calcitriol. In rats receiving aluminium, the baseline serum osteocalcin levels were not different from their respective controls. After stimulation with calcitriol, the increase in serum osteocalcin was less in the renal failure group receiving aluminium. However, when corrected for the number of osteoblasts, the increase in serum osteocalcin was not decreased. In summary, although aluminium administration decreased the number of osteoblasts in rats with renal failure, osteocalcin production by the remaining osteoblasts was not decreased.

Aluminum↗
PubMed1991

A comparison of parathyroid-gland function in haemodialysis patients with different forms of renal osteodystrophy.

Parathyroid function was studied in three different histological forms of renal osteodystrophy: osteitis fibrosa (OF), low-turnover aluminium-associated bone disease (LTAABD), and aplastic bone disease without aluminium (ABD). Parathyroid function was determined by the evaluation of the sigmoidal parathyroid hormone-(PTH)-calcium curve, which was obtained by the performance of a reduced calcium and an increased calcium haemodialysis. Parameters of the sigmoidal PTH-calcium curve evaluated included maximally stimulated (PTHMax) and inhibited (PTHMin) PTH, the set point of calcium for PTH (ICA50), defined as the ionised calcium concentration at which PTHMax was reduced by 50%, the ratio of basal PTH to maximally stimulated PTH (PTHBase:PTHMax), the ionised calcium concentration at which basal (ICABase), maximally stimulated (ICAMax), and maximally inhibited (ICAMin) PTH values were observed, and the slope of the PTH-calcium curve. Both PTHMax and PTHMin were greater in OF than the other two groups (P less than 0.02). The ratio of basal to maximally stimulated PTH was greater (P less than 0.02) in OF (61 +/- 7%) than LTAABD (33 +/- 5%) and ABD (36 +/- 7%). The ICA50 and the ICAMax were greater (P less than 0.03) in OF than the other two groups; however, no differences were observed in the ICABase and ICAMin. The slope of the PTH-calcium curve (% maximal PTH), which should indicate the sensitivity of parathyroid cells, was greater in OF than LTAABD (P less than 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1991

Apomorphine lowers dopamine synthesis for up to 48 h: implications for drug sensitization.

Previous reports have shown that tolerance or sensitization to apomorphine depends on the dosage interval. The effect of apomorphine on behaviour increases when there is a drug-free period between successive injections. Here we studied the biochemical action of apomorphine during a drug-free period. The experiments showed that dopamine level and dopamine turn-over are persistently inhibited for at least 48 h after apomorphine administration. At 24 h after drug injection, there was a decrease of both DOPAC level and tyrosine hydroxylase activity. The results suggest that apomorphine induces long-lasting dopaminergic inhibition action that increases drug-induced behavioural response, perhaps after development of postsynaptic hypersensitivity.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Persistence of Theiler's virus infection following promotion of central nervous system remyelination.

Chronic infection of SJL/J mice with the Daniel's strain of Theiler's virus develop primary demyelination, viral persistence but minimal central nervous system (CNS)-type remyelination. In contrast, treatment of virus-infected mice with sera or immunoglobulin G (IgG) from mice immunized with homogenized spinal cord (SCH) emulsified in incomplete Freund's adjuvant promotes CNS remyelination. We measured levels of infectious virus, virus antigen and virus-specific antibody to determine if treatments which promote CNS remyelination are able to modulate infection. Levels of virus-specific antibody were higher in mice treated with SCH/IgG than control treatment groups and correlated positively with extent of remyelination. Although number of virus antigen-positive cells in spinal cord was less in mice treated with SCH/IgG than mice treated with phosphate buffered saline (PBS)/IgG, there was only a slight negative correlation with extent of remyelination by regression analysis. Titers of infectious virus isolated three to six months following infection were not different among treatment groups. Even though treatment of mice with SCH/IgG reduced number of virus antigen-positive cells and enhanced levels of virus-specific antibody, CNS remyelination can occur despite presence of infectious virus.

Animals↗
PubMed1991

Synthetic CCK8 analogs with antagonist activity on pancreatic receptors: in vivo study in the rat, compared to non-peptidic antagonists.

The cholecystokinin octapeptide (CCK8)-derived synthetic peptides Boc-Tyr(SO3H)-Nle-Gly-DTrp-Nle-Asp-O-CH2-CH2-C6H5 (JMV179) and Boc-Tyr(SO3H)-Nle-Gly-DTrp-Nle-Asp-NH-CH2-CH2-C6H5 (JMV167) are antagonists of peripheral cholecystokinin (CCK) receptors in vitro. In the present study, antagonist activity of these peptides was studied on rat pancreatic secretion in vivo, and compared to those of other peptidic molecules and to the non-peptidic antagonists L364718, D-, L-, DL-lorglumide, and proglumide. The decreasing order of antagonist potencies on amylase release in vitro was L364718 greater than JMV179 greater than lorglumide greater than JMV167 greater than proglumide; JMV179 was 25 times less potent than L364718 and 300 times more potent than JMV167. The decreasing order of antagonist potencies on protein output in pancreatic juice in vivo was L364718 greater than JMV167 greater than JMV179 greater than lorglumide greater than proglumide; JMV167 was two times more potent than JMV179 and only 8 times less potent than L364718. Increased potency of JMV167, relative to JMV179 under in vivo conditions, is probably due to the slower rate of catabolism of the phenylethylamide group, relative to the phenylethylester group, since the metabolite issued from hydrolysis of the ester bond was totally inactive. This study shows that it is possible to obtain peptidic CCK antagonists, which are active and potent in vivo, and provides a quantitative measurement of potency changes occurring in vivo for several peptidic and non-peptidic antagonists.

Amino Acid Sequence↗
PubMed1991

Synthesis and biological activity of 2-phenylethyl ester analogues of C-terminal heptapeptide of cholecystokinin modified in Trp 30 region.

We have tried to evaluate the significance of the tryptophan side chain residue and of the surrounding peptide bonds in the antagonist activity of cholecystokinin analogues lacking the C-terminal amide function and having a D-tryptophan. In order to perform this study, analogues of the C-terminal heptapeptide of cholecystokinin were synthesized by replacing the C-terminal phenylalanine residue with 2-phenylethyl alcohol and by either replacing the tryptophan residue with an alanine, a norleucine and a phenylalanine residue, or introducing a "reduced peptide bond" in the tryptophan 30 region. Most of these compounds were able to reproduce only part of the response of cholecystokinin in stimulating amylase release from rat pancreatic acini, as was already observed for 2-phenylethyl ester analogues of CCK. These results point out the key role of tryptophan 30 in the biological response of cholecystokinin.

Amino Acid Sequence↗
PubMed1991

Gel electrophoretic analysis of Zymomonas mobilis glycolytic and fermentative enzymes: identification of alcohol dehydrogenase II as a stress protein.

The 13 major enzymes which compose the glycolytic and fermentative pathways in Zymomonas mobilis are particularly abundant and represent one-half of the soluble protein in exponential-phase cells. One- and two-dimensional polyacrylamide gel electrophoresis maps were developed for 12 of these enzymes. Assignments were made by comigration with purified proteins, comparison with overexpressed genes in recombinant strains, and Western blots (immunoblots). Although most glycolytic enzymes appeared resistant to turnover and accumulated in stationary-phase cells, the protein levels of pyruvate kinase, alcohol dehydrogenase I, and glucokinase declined. Alcohol dehydrogenase II was identified as a major stress protein and was induced both by exposure to ethanol and by elevated temperature (45 degrees C). This enzyme, encoded by the adhB gene, is expressed from tandem promoters which share partial sequence identity with the Escherichia coli consensus sequence for heat shock proteins.

Alcohol Dehydrogenase↗
PubMed1991

Cytotoxic T cells isolated from the central nervous systems of mice infected with Theiler's virus.

Intracerebral inoculation of resistant mice (C57BL/10SNJ) with Theiler's murine encephalomyelitis virus (TMEV) results in acute encephalitis followed by subsequent clearance of virus from the central nervous system (CNS). In contrast, infection of susceptible mice (SJL/J) results in virus persistence and chronic immune-mediated demyelination. Both resistance and susceptibility to TMEV-induced disease appear to be immune mediated, since immunosuppression results in enhanced encephalitis in resistant mice but diminished demyelination in susceptible mice. The purpose of these experiments was to determine whether anti-TMEV cytotoxic T lymphocytes (CTLs) are generated during acute and chronic TMEV infection. Nonspecific lectin-dependent cellular cytotoxicity was used initially to detect the cytolytic potential of lymphocytes infiltrating the CNS irrespective of antigen specificity. Using TMEV-infected targets, H-2-restricted TMEV-specific CTLs of the CD8+ phenotype were demonstrated in lymphocytes from the CNS of susceptible and resistant mice, arguing against the hypothesis that the ability to generate CD8+ CTLs mediates resistance. In chronically infected SJL/J mice, TMEV-specific CTL activity was detected in the CNS as late as 226 days postinfection. These experiments demonstrate that virus-specific CTLs are present in the CNS during both acute and chronic TMEV infection. Anti-TMEV CTLs in the CNS of chronically infected SJL/J mice may play a role in demyelination through their ability to lyse TMEV-infected glial cells.

Animals↗
PubMed1991

Identification of an enhancer required for the expression of a mouse major urinary protein gene in the submaxillary gland.

The MUP1.5b gene was previously found to be expressed specifically in the submaxillary gland and at high levels when introduced into mice as a transgene including 4.7 kb of 5'-flanking DNA and 0.3 kb of 3'-flanking DNA. To localize regulatory elements responsible for this tissue-specific pattern of expression, we tested the expression of three additional MUP1.5b transgenes including various amounts of 5'-flanking DNA. These experiments indicated that sequences between -1.85 and -3.46 kb from the transcription initiation site were required for high-level expression in the submaxillary gland. The presence of regulatory elements in this region was also suggested by the detection of a DNase I-hypersensitive site, seen only in submaxillary gland nuclei, at position -2.5 kb upstream from the MUP1.5a gene, a member of the same MUP gene subfamily and virtually identical to the MUP1.5b gene. Further evidence for enhancer activity was provided by the ability of the 1.6-kb DNA fragment including sequences between -1.85 and -3.46 kb to stimulate the expression of an otherwise inactive MUP1.5b-chloramphenicol acetyltransferase fusion gene specifically in the submaxillary gland. The nucleotide sequence of this 1.6-kb DNA fragment was found to be identical for the MUP1.5a and MUP1.5b genes. Together, these results provide the first localization of a cis-acting regulatory sequence involved in the differential tissue-specific expression of the MUP gene family.

Animals↗
PubMed1991

Multiple sclerosis: histopathologic and MR and/or CT correlation in 37 cases at biopsy and three cases at autopsy.

The authors retrospectively reviewed the cases of 40 patients with biopsy- or autopsy-proved inflammatory demyelination consistent with multiple sclerosis (MS); each patient underwent magnetic resonance (MR) and/or computed tomographic (CT) imaging. In review of the 32 MR and 30 CT examinations, three predominant radiologic patterns were apparent: (a) relatively small homogeneous lesions with no or minimal diffuse enhancement; (b) hypoattenuating lesions on CT scans and hypointense lesions on short-TR MR images, with a contrast material-enhanced, isoattenuating or isointense ring; and (c) lesions that were more infiltrative and ill defined, with mixed attenuation and signal intensity and scattered enhancement. A common radiologic feature was lack of mass effect or edema in white matter surrounding even large lesions. In all but four patients the lesions were classified as active by using both histologic and clinical criteria. Histologically active lesions had various radiologic appearances; however, in all contrast-enhanced studies they demonstrated some form of enhancement. Inactive lesions were homogeneously hypoattenuating on CT scans, hypointense on short-TR MR images, and hyperintense on unenhanced, long-TR MR images.

Adolescent↗