Weight loss is often a problem in late PD.
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Biomedical subjects
Publications and source records attributed to C Jacques.
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Large amounts of type II-secreted phospholipase A2 (type II sPLA2) are secreted into inflammatory synovial fluid and they are believed to induce the synthesis of lipid mediators by articular chondrocytes. Preliminary experiments showed that insulin-like growth factor-I, which counteracts cartilage degradation in arthritis, inhibits interleukin-1beta-induced type II sPLA2 gene expression in rabbit articular chondrocytes (Berenbaum, F., G. Thomas, S. Poiraudeau, G. Bereziat, M.T. Corvol, and J. Masliah. 1994. FEBS Lett. 340: 51-55). The present study showed that IL-1beta induced the sustained synthesis of prostaglandin E2 and a parallel increase in type II sPLA2 gene expression (assessed by enzymatic activity and Northern blot analysis), but no increase in cytosolic PLA2 gene expression (assessed by Northern and Western blot analysis) or cytosolic PLA2 activity in rabbit articular chondrocytes. IGF-I inhibited both IL-1beta-stimulated PGE2 synthesis and type II sPLA2 gene expression, but had no effect on cytosolic PLA2 gene expression. Nuclear run-on experiments revealed that IL-1beta stimulated the transcription rate of type II sPLA2 gene, giving rise to long-lived mRNA in cells treated with actinomycin D. IGF-I did not affect transcription rate, suggesting that it acts as a post-transcriptional step. Sucrose density gradient analysis of the translation step showed no effect of IGF-I on the entry of type II sPLA2 mRNA into the polysomal pool or on its distribution into the various polysomal complexes, suggesting that IGF-I does not act on the translation of the mRNA. Lastly, IGF-I strongly decreased the half-life of IL-1beta-induced type II sPLA2 mRNA (from 92 to 12 h), suggesting that IGF-I destabilizes mRNA. These data demonstrate that IL-1beta stimulates the transcription rate of the type II sPLA2 gene and gives rise to a very stable mRNA. In contrast, IGF-I decreases the half-life of the type II sPLA2 message.
Advertisements were published in local newspapers asking for volunteers to participate in a study on gambling. A battery of eleven questionnaires was mailed to the subjects assessing pathological gambling behavior, sociodemographic characteristics, motivation to gamble, erroneous perceptions about gambling, superstitious beliefs, depressive symptoms, social anxiety and avoidance, alcohol and drug abuse, problem-solving skills, and marital satisfaction. Subjects received $10 when they returned the questionnaires fully completed. Response rate was over 95%. Surprisingly, 29% of the respondents met the criterion for probable pathological gambling (score of 5 or more on the SOGS) and a further 16% were identified as potential pathological gamblers (scores of 3 or 4). The potential and probable pathological gamblers showed significant differences on motivational and cognitive variables related to gambling compared to those subjects who showed no signs of pathological gambling. The probable pathological gamblers reported significantly more signs of poor psychosocial functioning than the other two groups, including depressive symptoms, poor problem orientation, drug and alcohol abuse, and interpersonal conflict. The practical and theoretical implications of these results are discussed.
This study investigates the ways in which two proinflammatory cytokines, tumor necrosis factor alpha (TNF) and interleukin-1 beta (IL1), cause increased production of prostaglandin E2 (PGE2) in rabbit articular chondrocytes (RAC). Rabbit articular chondrocytes in primary culture were incubated with IL1, TNF, or both. Arachidonic acid (AA) release, PGE2 production, and the activities of cytosolic phospholipase A2 (cPLA2), secreted phospholipase A2 (sPLA2), and cyclooxygenase (COX) were measured. The mRNA levels of cPLA2, sPLA2, and COX-2 were also measured by Northern blotting, using specific complementary DNA probes. Incubation of IL1-stimulated RAC with TNF further increased PGE2 production. This synergy did not involve PLA2 stimulation, as there were no increases in AA release, cPLA2 and sPLA2 activities, or mRNA. In contrast, TNF increased the effect of IL1 on COX-2 activity and mRNA level. These results show that TNF and IL1 act in synergy in PGE2 production in articular chondrocytes. As sPLA2 and cPLA2 do not seem to be involved, COX-2 appears to be the best target for a specific anti-inflammatory strategy against cartilage degradation.
Nitric oxide (NO) is a signalling molecule that is produced by mesangial cells and renal tubular epithelial (RTE) cells. It plays a role in the regulation of glomerular and tubular function. In renal cells, NO is synthesized by the inducible isoform of the enzyme nitric oxide synthase (NOS). Thyroid hormone modulates the activity of neuronal NOS; therefore, we examined whether triiodothyronine (T3) stimulated the activity of inducible iNOS in mesangial cells, LLC-PK1 cells (analogue of the proximal tubule) and MDCK cells (analogue of the distal tubule). T3 (concentration range: 10(-10)-10(-7) M) had no effect on NO synthesis or iNOS protein expression by the three renal cell types. In addition, T3 did not modulate NO production in RAW 264.7 cells, a murine macrophage cell line, confirming that the hormone had no effect on iNOS activity. We conclude that, unlike its effect on neuronal NOS, T3 does not regulate iNOS activity in mesangial cells, RTE cells, or macrophages, and that the effects of T3 on renal cell growth and function are not mediated by inducible increases in NO synthesis.
Secreted phospholipase A2 has been detected in numerous inflammatory and infectious diseases. Since the cloning of the type II sPLA2 in 1989 from rheumatoid arthritis synovial fluid, a direct or indirect participation of type II sPLA2 in the production of lipid mediators has been purposed. This paper reviews the different studies from the literature alleging that type II sPLA2 participates to inflammatory processes and lipid mediators synthesis.
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The DNA of mouse adenovirus strain K87 (MAd-2) was cloned and mapped with restriction endonucleases BglII, ClaI, EcoRI, HindIII and SphI. Large differences were found between the MAd-2 and MAd-1 (strain FL) DNA molecules in terms of number and location of restriction sites. The MAd-2 genome also appeared as larger in size than the MAd-1 genome (34.72 kb vs. 30.14 kb). Our results confirm the existence of two distinct adenovirus species in the mouse. Hybridization experiments, on the other hand, indicate that both MAd-1 and MAd-2 are genetically related to human adenovirus type 2 (HAd-2). Overlapping regions of DNA homology are located in genes coding for HAd-2 structural components which could explain serological relationships observed between the human and the murine adenoviruses.
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Murine adenovirus (MAd) type 1 strain FL and type 2 strain K87 genomes were cloned into plasmid pAT153 as HindIII restriction fragments. The MAd-1 and MAd-2 DNA genomes, 30.10 kb and 34.71 kb in length respectively, were mapped using BglII, ClaI, EcoRI, HindIII and SphI restriction endonuclease cleavage sites. In view of the large differences found between the MAd-1 and MAd-2 genomes in terms of the number and location of restriction sites, cross-hybridization experiments were performed. Homologous DNA sequences were located on the MAd-1 and MAd-2 physical maps. Both viruses are also genetically related to human adenovirus type 2 (HAd-2). Nucleotide sequences shared by HAd-2 and the MAds code for structural proteins, which may explain the antigenic similarities between these viruses from different origins. Our results confirm the existence of two distinct adenovirus species in the mouse.
We describe clinical and postmortem findings in a 44-year-old man with pulmonary hypertension and infection with the human immunodeficiency virus (HIV-1). Plexogenic angiopathy and veno-occlusive lesions were present, in addition to a mild, patchy pulmonary interstitial lymphoid infiltrate. The clinical data for 14 previously reported cases of HIV-associated primary pulmonary hypertension are summarized. We speculate that these vascular changes may be due to damage from a specific immune response to HIV.
Bronchial asthma is characterized by airways inflammation and airways hyperresponsiveness. It is unlikely that the pathophysiology of asthma and bronchial hyperresponsiveness can be explained on the basis of a single cell or a single class of mediators. Nevertheless, the possibility that leukotrienes may contribute to the pathogenesis of the inflammatory, vasoactive ans spasmogenic components of bronchial asthma is suggested by the properties of these lipid mediators, the preferential capacity of inflammatory cells to generate leukotrienes and the presence of leukotrienes in the airways of asthmatic subjects. The sulphidopeptide leukotrienes are potent bronchoconstrictor agonists when inhaled. The airways of asthmatic subjects are hyperresponsive to leukotrienes as to other bronchoconstrictor agonists. Nevertheless, the airways responsiveness of asthmatic subjects to these agonists demonstrate several unusual properties. While the airways of asthmatic subjects are relatively less responsive to LTC4 and LTD4, compared to agents such as histamine or methacholine, they demonstrate a marked and selective hyperresponsiveness to LTE4, suggesting a possibly unique role for this mediator in the pathogenesis of airways hyperresponsiveness. In addition an increased sensitivity of the airways to LTE4 may contribute to the mechanism of aspirin-induced asthma. The capacity of the sulphidopeptide leukotrienes to increase the airways responsiveness of normal subjects to methacholine and of asthmatic subjects to histamine is further evidence for a role for these substances in the pathogenesis of bronchial asthma.
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Bovine herpesvirus type 1 (BHV-1) DNA molecules obtained from a limited number of infected cells were cleaved with a variety of restriction endonucleases. By use of selected DNA fragments in Bgl 1, Pst 1, Pvu 1 and Pvu 11 restriction patterns, one reference, two vaccine and three wild-type strains of BHV-1 were distinguished from one another. The simplified DNA fingerprinting method described here should be most useful, not only to control the genetic stability of BHV-1 vaccines during production, but also to differentiate the vaccine strains from other isolates in clinical cases.
This study investigated the associations of Locus of Control (Children Nowicki-Strickland Internal-External Control Scale) with state and trait anxiety (State-Trait Anxiety Inventory for Children) in 302 children aged 9 to 12 yr. No significant differences were found between the groups. No significant correlations were found between the anxiety measures and externality for the 31 children from maritally disrupted families, but significant positive Pearson correlations were found for the 271 children of intact families. The results are discussed in terms of the possibility of under-reporting of marital disruption by children.
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