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Biomedical subjects

M Rodriguez

Publications and source records attributed to M Rodriguez.

At least 595 records · Page 33Linked to original sources
PubMed1988

[1.5 T MRI, arthrography and arthroscopy in the evaluation of knee lesions].

It has been previously demonstrated that MRI can show the knee joint non-invasively and without radiation. Forty-two patients with lesions of the knee were examined using 1.5 Tesla and flexible surface coils. The findings were compared with those of arthroscopy, arthrography and, where possible, with those at surgery. For the evaluation of cruciate ligament injuries, MRI proved to have a sensitivity of 100% and a specificity of 82% with an overall accuracy of 92%. Thirty-nine cruciate ligaments were correctly evaluated. Three times a false positive diagnosis was made. Examination of the menisci was less reliable. Sensitivity was 88% and specificity was 83% with an overall accuracy of 94%. Fifteen meniscus lesions were correctly diagnosed. Three times a false positive and twice a false negative diagnosis was made. Four of the five incorrect diagnoses concerned the posterior horn of the meniscus and three were situated laterally.

Adolescent↗
PubMed1988

Isolation and characterization of two plaque size variants of Theiler's murine encephalomyelitis virus (DA strain).

We have isolated two plaque size variants of Theiler's murine encephalomyelitis virus (TMEV) strain DA. One variant, TMEV-CL (CL), produced large plaques, while the other, TMEV-DS (DS), produced small plaques in L-2 cells. The DS variant yielded a lower titre in BHK cells and had a significantly slower growth rate when compared to CL and DA. In contrast, DS replicated to a higher titre in the central nervous system (CNS) of infected mice than the large plaque counterpart and DA. Furthermore, the DS (but not CL) variant was temperature-sensitive, replicating 130- to 500-fold more at 37 degrees C than at 39 degrees C. Although DS, CL and DA were able to establish persistent CNS infections in mice, only the DS variant and DA induced demyelinating disease in SJL/J mice. Therefore persistence of TMEV in the CNS is not sufficient to produce demyelinating disease. These two variants of the DA strain of TMEV will be useful for study of the viral genetic elements important in the mechanism of virus-induced demyelination.

Animals↗
PubMed1988

2-Phenylethyl ester and 2-phenylethyl amide derivative analogues of the C-terminal hepta- and octapeptide of cholecystokinin.

Syntheses of analogues of the C-terminal octa- and heptapeptide of cholecystokinin are described. These analogues were obtained by replacing the C-terminal phenylalanine residue by 2-phenylethyl alcohol or by 2-phenylethylamine derivatives and by replacing the tryptophan residue by a D-tryptophan. The CCK-derivatives were tested for their ability to inhibit binding of labeled CCK-8 to rat pancreatic acini and to guinea pig brain membranes, and for their action on stimulation of amylase release from rat pancreatic acini. Some of these derivatives appeared to exhibit only part of the CCK-activity on amylase release, the D-Trp analogues behaving as CCK-antagonists.

Amino Acid Sequence↗
PubMed1988

Mechanisms of virus-induced demyelination and remyelination.

Viral models of demyelination and remyelination provide important clues to the pathogenesis of multiple sclerosis. Determining the precise viral polypeptides recognized by T cells during the demyelinating process will be important in understanding the mechanisms of viral-induced myelin destruction. Isolation, purification, and characterization of factors that promote remyelination and proliferation of oligodendrocytes may provide hope in the treatment of patients with chronic demyelinating disorders.

Animals↗
PubMed1988

Structure-activity relationship studies on cholecystokinin: analogues with partial agonist activity.

In the present study, hepta- and octapeptide analogues of the C-terminal part of cholecystokinin, modified on the C-terminal phenylalanine residue, were synthesized. CCK analogues were prepared in which the peptide bond between aspartic acid and phenylalanine had or had not been modified and were lacking the C-terminal primary amide function. These CCK derivatives were able to cause full stimulation of amylase release from rat pancreatic acini but without a decrease in amylase release at supramaximal concentrations. There was a close relationship between the abilities of these derivatives to stimulate amylase release and their abilities to inhibit binding of 125I-BH-CCK-9 to CCK receptors on rat and guinea pig pancreatic acini. These CCK analogues were also able to recognize the guinea pig brain CCK receptors, some of them being particularly potent. The findings indicate that the aromatic ring of phenylalanine is important for the binding to brain and pancreatic CCK receptors, whereas the C-terminal primary amide function is not essential for the binding to pancreatic CCK receptors but is crucial for biological activity of rat pancreatic acini.

Amylases↗
PubMed1988

Autoimmune paraneoplastic cerebellar degeneration: ultrastructural localization of antibody-binding sites in Purkinje cells.

Sera from three of four patients with paraneoplastic cerebellar degeneration (PCD) associated with gynecologic cancer had antibodies that stained the cytoplasm of Purkinje cells in a characteristic discrete and coarsely granular pattern. No such antibodies were found in PCD patients with small cell cancer of the lung, in patients with cerebellar degeneration without cancer, in nonneurologic patients with small cell carcinoma or gynecologic cancer, or in normal subjects. Immunoelectron microscopy revealed that the antibodies of PCD bound to clusters of ribosomes, granular endoplasmic reticulum, and the trans-face of the vesicles of the Golgi complex in Purkinje cells. Immunostaining was localized in orderly arrays of stacked parallel cisternae of the endoplasmic reticulum in the perikaryon and dendritic processes. This pattern suggested that at least one autoantigen of PCD may be a glycoprotein specific cerebellar tissue that is associated with the endoplasmic reticulum. Some patches of Purkinje plasma membrane also were immunostained.

Aged↗
PubMed1988

Acquired C1-inhibitor deficiency associated with a lupus-like anticoagulant activity.

A patient with two attacks of glottis angioedema in a 15-day period without any apparent stimulus was studied. The complement profile of the patient revealed depletion of C4, C2, C1 inhibitor (C1INH) and C1q, with normal values of C3. Patient's offspring had a normal complement profile. Cytofluorographic analysis of the peripheral blood cells showed a marked increase of B cells. In the clotting study, a circulating lupus-like anticoagulant activity (LLA) was detected with a noticeable decrease of prothrombin time. Hepatosplenomegaly was confirmed by abdominal echography and CAT. From the liver biopsy it was concluded to be a lymphoproliferative process compatible with germinal center lymphoma. It is suggested that the neoplasm is probably the origin of the LLA and the cause of C1 activation, producing the biochemical defect of C1INH and the clinical symptoms of angioedema.

Aged↗
PubMed1987

Conditioned response to apomorphine in nigro-striatal system-lesioned rats: the origin of undrugged rotational response.

Development and time-course characteristics of Early rotational response (ER) to apomorphine in 6-hydroxydopamine-lesioned rats is explored. We show here how this ER can be considered a conditioned response that arises when the drug is repeatedly administered, according to a classical conditioning paradigm. In this way, the ER to apomorphine can be considered a non-pharmacological, conditioned, placebo response, the drug action being the unconditioned stimulus (UCS). In our model, the undrugged rotational response elicited by saline injections two weeks after drug treatment can be considered as the conditioned response (CR) to the conditioned stimulus, the CS being the environment associated with the drug treatment. This CR had not previously been identified during the drug treatment. Thus, we studied the acquisition of the ER, nonexistent after the first injection of apomorphine. Furthermore, we distinguish between this ER and the later, strictly pharmacological rotational response (LR) to apomorphine. Finally, we related this ER to the undrugged, paradoxical response to saline. In conclusion, we demonstrate the paradigm of pharmacological conditioning using this animal model of Parkinson's disease, supported by our own results and those of Silverman and Ho (1981).

Animals↗
PubMed1987

A synthetic peptide derivative that is a cholecystokinin receptor antagonist.

So far, there are no known peptidic effective receptor antagonists of both peripheral and central effects of cholecystokinin (CCK). Here, we describe a synthetic peptide derivative of CCK, t-butyloxycarbonyl-Tyr(SO3-)-Met-Gly-D-Trp-Nle-Asp 2-phenylethyl ester 1 (where Nle is norleucine), which is a potent CCK receptor antagonist. In rat and guinea pig dispersed pancreatic acini, this peptide derivative did not alter amylase secretion, but was able to antagonize the stimulation caused by cholecystokinin-related agonists. It caused a parallel rightward shift in the dose-response curve for the stimulation of amylase secretion with half-maximal inhibition of CCK-8-stimulated amylase release at a concentration of about 0.1 microM. Compound 1 was able to inhibit the binding of labeled CCK-9 (the C-terminal nonapeptide of CCK) to rat and guinea pig pancreatic acini (IC50 = 5 X 10(-8) M) as well as to guinea pig cerebral cortical membranes (IC50 = 5 X 10(-7) M). These results indicate that Compound 1 is a potent competitive CCK receptor antagonist.

Amylases↗
PubMed1987

Immune response gene products (Ia antigens) on glial and endothelial cells in virus-induced demyelination.

Theiler's murine encephalomyelitis virus induced central nervous system demyelination in susceptible strains of mice with s, q, v, p, and f H-2D alleles. We used immunoelectron microscopy to look for differential production of class II immune response gene products (Ia) within astrocytes, oligodendrocytes, microglia, and endothelial cells. Spinal cord sections from susceptible mice (B10.S and B10.ASR2) showed increased content of Ia in glial and endothelial cells. In contrast, resistant mice [B10.S(9R)] showed minimal Ia production within the CNS. The findings indicate an important role of class II immune response products on glial cells during demyelination after virus infection.

Animals↗
PubMed1987

Characterization of immunologic and neuropathologic abnormalities in wasted mice.

Mice bearing the autosomal recessive gene "wasted" (wst/wst) have been reported to develop low or absent secretory immune responses, abnormal DNA repair mechanisms, and uncoordinated body movements. We have performed a detailed immunologic and neuropathologic investigation of the disease. Con A and LPS mitogenic responses of splenic lymphocytes as well as total serum Ig levels were equivalent in wst/wst and undiseased control littermates (wst/+ and +/+). Amounts of serum IgM, IgG2a, IgG2b, IgG3, and IgA, however, were reduced in wst/wst animals. FACS analyses of Ig+ and isotype-specific B cell populations revealed similar percentages of Ig+, mu +, gamma +, and alpha + cells in wst/wst and control mice. However, the percentage of "very bright" Ig+ cells as well as "very bright" heavy and light chain-specific B cell subpopulations was increased at least 10-fold in wst/wst B cells as compared with littermate controls. In addition, studies of Ig-specific mRNA accumulation in these animals revealed significant decreases in all isotypes except gamma 3 in spleens of wst/wst mice as compared with littermate controls. Neuropathologic studies in wst/wst mice showed prominent vacuolar degeneration of neurons within anterior horns of the spinal cord and the motor nuclei of the brain stem. No abnormalities were noted in Purkinje cells of the cerebellum nor within myelin sheaths. The abnormalities in the nervous system resembled human motor neuron disease rather than ataxia-telangiectasia as had been reported previously. The immunologic studies suggest that splenic B cells from wst/wst mice have a defect in the ability to "switch" from membrane to secreted Ig. In addition, this mutation provides a mechanism to study regulatory interactions between the immune and nervous systems.

Animals↗
PubMed1987

Pulmonary acinus: geometry and morphometry of the peripheral airway system in rat and rabbit.

The geometry and morphometry of intraacinar airways in rat and rabbit lungs were studied from silicone rubber casts. Acini, defined as the complex of alveolated airways distal to the "terminal" bronchiole, were trimmed off the bronchial tree. In both species, the acinar volume followed a log-normal distribution over a range in size of one order of magnitude. At an inflation level of 60% total lung capacity, their mean volume was 1.86 mm3 in the rat and 3.46 mm3 in the rabbit. On a representative sample of acini of different volumes, the branching pattern was characterized as irregular dichotomy, and the segment length and inner and outer diameters were measured. The average acinus had a mean of six generations in the rat and seven in the rabbit. Both showed a decrease in segment length and inner diameter with each generation. The mean longitudinal pathway length--that is, the distance from the initial acinar segment to the terminal sacs--was found to depend on the cube root of the acinar volume in both species. It was calculated at 1.46 and 1.95 mm for rat and rabbit, respectively.

Animals↗
PubMed1987

Direct evidence that insulin does not down-regulate its own receptors in circulating monocytes of human newborns.

To determine the effect of insulin on its own receptor concentrations in circulating monocytes of normal human adults and full-term newborns, these cells were chronically exposed (2-18 h) to 10(-9) to 10(-7) mol/l insulin at 37 degrees C in vitro. The reduced 125I-insulin binding observed in monocytes from adult individuals was dependent on the concentration of unlabelled insulin and on the duration of exposure, while in the monocytes obtained from umbilical cord blood, insulin did not induce any reduction of insulin binding. The modifications observed in insulin binding were accounted for by changes in receptor concentrations rather than by any change in receptor affinity for the hormone. These findings show that insulin does not down-regulate its own receptors in monocytes of human newborns.

Humans↗
PubMed1987

Osteomyelitis deriving from BCG-vaccination.

Secondary complications after BCG-vaccination are unusual. There is an almost invariably lethal generalized infection affecting the immunodepressed. Late dissemination of BCG to bone is characterized by lytic lesions, it is not normally associated with immunologic changes and has a good prognosis. The histology of BCG-osteomyelitis resembles that produced by Koch bacillus. We present a rare case of a lytic lesion in the femur improving after specific treatment.

BCG Vaccine↗