Congestive heart failure in a marsupial (Monodelphis domestica).
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Animals↗
Biomedical subjects
M Rodriguez
Publications and source records attributed to M Rodriguez.
[Cerebral abscesses. The clinical and evolutionary aspects of 17 cases treated surgically].
Seventeen cases of cerebral abscesses undergoing surgery were reviewed, underlying the characteristics of predisposing factors, infectious sources, microbiological and radiological studies, as well as clinical and evolutive aspects. The average age of the patients was 34 years, with a higher incidence in the second (35%) and sixth (22%) decades. The young patients (< 40 years) showed a greater frequency of adjacent infectious sources (83%) and the older patients (> 40 years), distant infectious sources (75%). The average time gap between the onset of symptoms and the diagnosis was 7 +/- 13 days. CAT showed in all the patients typical hypodense images with a peripheral ring; three patients had multiple abscesses and the remainder, single abscesses. In 12 patients (70.5%), microbiological cultures were positive, 3 (25%) for aerobe germs, 7 (50.3%) for anaerobe germs, 1 (8.33%) for multiple germs and 1 (8.33%) for fungi. Eleven patients underwent surgical drainage, four of which required latter exeresis. Six other patients underwent exeresis as the only surgical treatment. One patient died and the remainder showed a positive evolution. The hospital length of stay was 42.3 +/- 52.3 days. The most frequent sequela was the epilepsia present in 23.5% of the patients. Our findings are similar to the results of recent works, although in our series, there is a higher frequency of anaerobe germs. No differences were observed between the surgical techniques used nor between the past and current antibiotherapy patterns.
Adolescent↗
Monoclonal autoantibodies promote central nervous system repair in an animal model of multiple sclerosis.
Susceptible strains of mice infected intracerebrally with Theiler's murine encephalomyelitis virus develop a chronic, progressive, immune-mediated CNS demyelinating disease similar both pathologically and clinically to multiple sclerosis. Previous reports indicated that polyclonal immunoglobulins from mice injected with homogenized spinal cord promote CNS remyelination when given to SJL/J mice chronically infected with Theiler's virus. To explore further both the mechanism(s) and potential therapeutic usefulness of antibodies in the treatment of CNS demyelinating diseases, we made a panel of monoclonal antibodies derived from splenocytes of SJL/J mice injected with homogenized spinal cord, and screened them for their autoantigen-binding capability. Monoclonal IgM autoantibodies from two clones, designated SCH94.03 and SCH94.32, promoted fourfold more CNS remyelination than controls when given to chronically infected SJL/J mice. CNS remyelination, assessed morphologically by the presence of abnormally thin myelin sheaths relative to axonal diameter, correlated with the absence of clinical disease progression. In titration experiments, treatment with SCH94.03 and remyelination had a positive dose-response relationship, and as little as 10 micrograms of antibody promoted remyelination. Both SCH94.03 and SCH94.32 showed multiorgan autoreactivity, and recognized both surface and cytoplasmic determinants on glial cells. We propose that this model provides a unique system to elucidate the mechanism(s) and test the reparative potential of autoantibodies in the treatment of CNS injury.
Animals↗
Application of the ATP-cell viability assay for assessment of in vitro radiation treatment response in gynecologic cancer cell lines.
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Adenosine Triphosphate↗
[Home care services. Landmarks and perspectives].
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France↗
Frequency of sister chromatid exchanges in humans at 14-16 week foetal stage and at birth.
In order to identify transplacental induced mutagenicity in humans the baseline frequency of sister chromatid exchanges (SCEs) in amniotic fluid cells (8.56 +/- 0.28 per cell) from 14 to 16-week-old foetuses as well as in peripheral blood lymphocytes (7.96 +/- 0.26 per cell) from newborns was determined. A group of twelve patients who were analysed both at 14-16 weeks gestation and at birth showed no SCE variations. These results suggest that foetal amniocytes and T lymphocytes from newborns present a similar sensitivity to the mutagenic activity of the thymidine analogue 5-bromodeoxyuridine employed in the sister chromatid differentiation.
Adult↗
Treatment of early stages of Hodgkin's disease with novantrone, vincristine, vinblastine, prednisone, and radiotherapy.
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Antineoplastic Combined Chemotherapy Protocols↗
Spontaneous firing of nigrostriatal dopaminergic neurons in split-brain rats.
The regulatory action of the contralateral brain side on nigrostriatal dopaminergic (NSDA) neurons was examined in anesthetized rats using extracellular single-unit recording techniques. The spontaneous activity of NSDA cells was recorded from split-brain, sham-lesioned or intact-brain rats. The three groups of cells did not differ in antidromic latency and firing rate. However, cells from split-brain rats exhibited a more regular pattern of discharge than those recorded in the two control groups as shown by autocorrelograms and the standard deviation and variation coefficient of the interspike intervals. In addition, burst firing was found to be markedly reduced in the split-brain group. It is concluded that decussating pathways are involved in the regulation of the discharge pattern of NSDA neurons.
Action Potentials↗
Synthesis and biological evaluation of cholecystokinin analogs in which the Asp-Phe-NH2 moiety has been replaced by a 3-amino-7-phenylheptanoic acid or a 3-amino-6-(phenyloxy)hexanoic acid.
Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-2-phenylethyl ester (JMV180), an analog of the C-terminal octapeptide of cholecystokinin (CCK-8), shows interesting biological activities behaving as an agonist at the high-affinity CCK binding sites and as an antagonist at the low-affinity CCK binding sites in rat pancreatic acini. Although we did not observe any major hydrolysis of the ester bond of Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-2-phenylethyl ester in our in vitro studies, we were aware of a possible and rapid cleavage of this ester bond during in vivo studies. To improve the stability of Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-2-phenylethyl ester, we decided to synthesize analogs in which the ester bond would be replaced by a carba (CH2-CH2) linkage. We synthesized the 3-amino-7-phenylheptanoic acid (beta-homo-Aph) with the R configuration in order to mimic the Asp-2-phenylethyl ester moiety and the 3-amino-6-(phenyloxy)hexanoic acid (H-beta-homo-App-OH), an analog of H-beta-homo-Aph-OH in which a methylene group has been replaced by an oxygen. (R)-beta-Homo-Aph and (R)-H-beta-homo-App-OH were introduced in the CCK-8 sequence to produce Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-(R)-beta-homo-Aph-OH and Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-(R)-beta-homo-App-OH. Both compounds were able to recognize the CCK receptor on rat pancreatic acini (IC50 = 12 +/- 8 nM and 13 +/- 5 nM, respectively), on brain membranes (IC50 = 32 +/- 2 nM and 57 +/- 5 nM, respectively), and on Jurkat T cells (IC50 = 75 +/- 15 nM and 65 +/- 21 nM, respectively). Like Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-2-phenylethyl ester, both compounds produced maximal stimulation of amylase secretion (EC50 = 6 +/- 2 nM and 4 +/- 2 nM, respectively) with no decrease of the secretion at high concentration indicating that these compounds probably act as agonists at the high-affinity peripheral CCK-receptor and as antagonists at the low-affinity CCK-receptor. Replacing the tryptophan by a D-tryptophan in such analogs produced full CCK-receptor antagonists. All these analogs might be more suitable for in vivo studies than Boc-Tyr(SO3H)-Nle-Gly-Trp-Nle-Asp-2-phenylethyl ester.
Amino Acid Sequence↗
Differential expression of H-2K and H-2D in the central nervous system of mice infected with Theiler's virus.
A model of demyelination induced by Theiler's murine encephalomyelitis virus (TMEV) was used to study differential regulation of class I MHC gene products in the brain and spinal cord of resistant (B10) and susceptible (B10.Q and B10.RBQ) mice. Allelic polymorphisms in the H-2D region, but not the H-2K region, play a primary role in determining susceptibility to late demyelinating disease. However, even though significant structural diversity distinguishes class I alleles, there are no discernible K or D-specific patterns of structural diversity within the peptide binding domains of these glycoproteins. Our hypothesis was that D region association of susceptibility to demyelination was related to differences in the expression of the K and D Ag in the central nervous system (CNS) after TMEV infection. Using allele-specific mAb and an immunoperoxidase technique, we demonstrated transient but equivalent increases in K and D Ag expression in the brain and spinal cord of resistant mice beginning 7 days after TMEV infection, which returned to baseline by 90 days. However, when genetically susceptible animals were examined, a significantly greater increase in D expression relative to K expression was seen in the brain and spinal cord at all post-infection observation periods. Immunosuppression of genetically resistant animals before TMEV infection, which results in viral persistence, was accompanied by equivalent increases in both the K and D Ag. Depletion of CD8+ T cells, but not CD4+ T cells, in susceptible mice ablated class I expression in the CNS in response to TMEV infection, implying that CD8+ cells contribute to the differential regulation of K and D Ag in the CNS. These findings are consistent with the hypothesis that differences in gene regulation may account for different roles of the K and D loci play in determining resistance and susceptibility to TMEV-induced demyelinating disease.
Animals↗
Abrogation of resistance to Theiler's virus-induced demyelination in H-2b mice deficient in beta 2-microglobulin.
Intracerebral infection of susceptible strains of mice with Theiler's virus, a picornavirus, results in central nervous system demyelination, which is similar to multiple sclerosis. Immunogenetic experiments indicate that the MHC (H-2) and, in particular, the D region that controls class I-restricted immune responses, is an important determinant to development of demyelination. We tested whether disruption of beta 2-microglobulin (beta 2-m) would abrogate resistance to demyelinating disease normally observed in H-2b mice. All (C57BI/6 x 129)F3 mice transgenic for homozygous beta 2-m gene disruption (-/-) developed chronic demyelination after Theiler's murine encephalomyelitis virus infection, whereas none of the infected littermates with normal expression of class I MHC (beta 2-m, +/+) developed demyelination. Demyelinated lesions showed class II MHC expression, macrophages, and TNF but no class I MHC expression or CD8+ T cells. No correlation was observed between development of demyelination and delayed-type hypersensitivity responses to virus Ag. Despite the presence of demyelinating lesions, none of the infected beta 2-m (-/-) mice developed neurologic deficits. Infectious virus and virus Ag persisted in the central nervous systems of infected beta 2-m (-/-) mice but not in beta 2-m (+/+) mice. These experiments support the hypothesis that a class I immune response mediated by CD8+ T cells is important in resistance to Theiler's murine encephalomyelitis virus-induced demyelination. Development of chronic neurologic deficits as observed in immunocompetent susceptible strains of mice may be dependent on the presence of class I MHC and CD8+ T cells.
Animals↗
Molecular cloning of a human beta 3-adrenergic receptor cDNA.
We report the molecular cloning of a beta 3-adrenergic receptor [beta 3-AR] cDNA from human brown adipose tissue. The cDNA-encoded protein is identical to the previously cloned beta 3-AR but with 6 additional amino acids at the C-terminus. The C-terminus is shared by the beta 3 receptors expressed in human neuroblastoma cells [SK-N-MC] [Mol. Pharmacol. 42 (1992) 964-970]. Furthermore, using a polymerase chain reaction strategy we have cloned and sequenced the beta 3-AR introns. Sequence analysis demonstrates that the human beta 3-AR gene comprises at least 3 exons and 2 introns and that the most abundant beta 3-AR transcripts encode a protein with an exon 3-derived C-terminus. Interestingly, although a similar organization has been found in rodent genes, the rat beta 3-AR transcripts encode a receptor with an exon 2-derived C-terminus.
Adipose Tissue, Brown↗
Synthesis and analgesic effects of N-[3-[(hydroxyamino) carbonyl]-1-oxo-2(R)-benzylpropyl]-L-isoleucyl-L-leucine, a new potent inhibitor of multiple neurotensin/neuromedin N degrading enzymes.
The synthesis of N-[3-[(hydroxyamino) carbonyl]-1-oxo-2(R)-benzylpropyl]-L-isoleucyl-L-leucine (JMV-390-1, 6a), a multipeptidase inhibitor based on the C-terminal sequence common to neurotensin (NT) and neuromedin N (NN), is described. This compound behaves as a full inhibitor of the major NT/NN degrading enzymes in vitro, e.g. endopeptidase 24.16, endopeptidase 24.15, endopeptidase 24.11, and leucine aminopeptidase (type IV-S), in the nanomolar range (IC50's from 30 to 60 nM). Compound 6a was found to increase endogenous recovery of NT and NN from slices of mice hypothalamus depolarized with potassium. In various assays commonly used to select analgesics, e.g. hot-plate test, tail-flick test, acetic acid-induced writhing test, in mice, compound 6a proved to be potent when intracerebroventricularly (icv) injected. The analgesic effects observed were totally (hot-plate test) or largely (tail-flick test) reversed by the opioid antagonist naltrexone. Furthermore, icv injection of compound 6a (10 micrograms/mouse) was found to significantly potentiate the hypothermic effects of NT or NN.
Analgesics↗
The rat beta 3-adrenergic receptor gene contains an intron.
We report that the rat beta 3-adrenergic receptor (beta 3-AR) gene has an intron. The intron starts with an in-frame stop codon with the result that unspliced transcripts will encode a C-terminal truncated protein. The reported protein sequences of mouse and human beta 3-AR were both deduced from genomic DNA sequences. Given the heterogeneity at the C-termini of the otherwise highly similar rat, mouse and human sequences, we discuss the intriguing possibility that the beta 3-AR gene of the latter two species also contain an intron near the extremity of the open reading frame. A beta-adrenergic receptor (beta-AR) cDNA we have cloned from rat colonic tissue which has a sequence essentially identical to that previously reported for the rat adipose beta 3-AR cDNA [(1991) J. Chem. 266, 24053], encodes the spliced version of the beta 3-AR.
Amino Acid Sequence↗
Human class I major histocompatibility complex transgene prevents virus-induced demyelination in susceptible mutant B10.D2dml mice.
Theiler's murine encephalomyelitis virus (TMEV) induces immune-mediated demyelination in susceptible strains of mice, providing an excellent model for multiple sclerosis. Class I genes within the major histocompatibility complex locus (H-2D region) play a major role in determining whether strains of mice develop chronic demyelination and TMEV persistence. B10.D2dml mice with deletion in the 3' end of Dd and the 5' end of Ld genes develop the most prominent demyelination in comparison with resistant B10.D2 mice with normal complementation of H-2D region genes. We tested whether expression of a class I human transgene (HLA-B27) would modulate virus-induced demyelination in mutant B10.D2dml mice. Transgenic B10.D2dml (HLA-B27+) mice infected with virus showed dramatic decrease in the extent of demyelination (p < 0.0001) and virus antigen expression in spinal cord compared with littermate controls without the human class I transgene. These experiments demonstrate that transgenic expression of a human class I major histocompatibility complex locus molecule can prevent demyelination induced by a virus in mutant mice.
Animals↗
Platelet adhesion/aggregation in an in vitro model of coronary artery stenosis.
Platelet adhesion/aggregation (PAA) at a site of coronary artery stenosis is believed to be a process strongly modulated by local shear rates and the functional state of neighboring endothelium. One purpose of the present work, therefore, is to describe an in vitro model for the direct imaging of such PAA. Another is to apply the model to the question as to whether the use of nonionic vs. ionic contrast media (CM) in the presence of vascular endothelium contributes to PAA at the stenosis site. Toward these ends, we utilized a special flow chamber which incorporates a monolayer of endothelial cells (ECs), a step 66% flowpath constriction at a site preadsorbed with microfibrillar collagen, and arterial shear rates. By epifluorescence microscopy and digital image analysis of video recordings, PAA was found to be greater with dysfunctional ECs (pretreated with lysine acetylsalicyclate) than with normal ECs, thereby confirming a modulatory role in PAA of functionally intact ECs. When nonionic (iohexol) or ionic (ioxaglate, diatrizoate) CM was added to the flowing blood at a concentration of 20% by non-red cell volume, PAA was inhibited in the order diatrizoate > ioxaglate > iohexol > saline control. No inhibition by any CM was seen, however, when chamber prefill culture medium containing 20% by volume CM was displaced by CM-free blood, in simulation of bolus administration of CM. In terms of inhibition of PAA during percutaneous transluminal coronary angioplasty (PTCA), therefore, our model provides a conceptual basis by which one may anticipate in flowing blood no clear benefit of ionic over nonionic CM.(ABSTRACT TRUNCATED AT 250 WORDS)
Aspirin↗
Detection of human papillomavirus L1 protein in condylomata acuminata from adults with defects in cell-mediated immunity.
Immunohistochemical assays for human papillomavirus (HPV) L1 protein, using antiserum directed against the L1 major capsid protein of bovine papillomavirus (anti-BPV serum), were performed on 101 condylomata acuminata biopsy samples from 47 men (40 of whom had intact cell mediated immunity [CMI], and 7 with conditions known to cause CMI defects), and 54 women (48 with normal CMI, and 6 with CMI defects). L1 protein was detected in 28% of all biopsies, including 20.5% of samples from patients with normal CMI and 76.9% of patients with CMI defects (P = .00002). For both males and females, L1 protein was detected significantly more often in samples from patients with CMI defects than those with normal CMI. Immunohistochemical assays of HPV 11-infected human foreskin implants grown in athymic mice were performed to optimize the conditions of the assay. Three dilutions of anti-BPV serum or preimmune rabbit serum were used. A 1:500 dilution provided readily interpretable results, while preimmune serum at this dilution did not stain to any significant degree. However, at 1:10 and 1:100 dilution, both the anti-BPV serum and preimmune serum caused an unacceptable amount of nuclear staining, making results uninterpretable. Defects in CMI may allow active viral particle assembly at an increased rate, as judged by detection of L1 protein in condylomata acuminata from these patients.
Capsid↗