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21.
Abstract It has been suggested that cardioplegic arrest during cardiopulmonary bypass (CPB) produces global myocardial ischemia with a risk of myocardial stunning. It has also been postulated that anesthetic technique may affect the course of post-CPB myocardial stunning via exaggerated myocardial depression. However, we have previously found that global ventricular and regional myocardial responses to halothane do not differ in post-CPB and pre-CPB dogs. Our examination of the effects of CPB on the beta-adrenergic function revealed that beta-adrenergic receptor function is only slightly decreased immediately following (i.e., 1 min) and 30 minutes post-CPB. A dose-response relationship was established for dobutamine, with decreased responsiveness noted at both times. Since other data show normal inotropic stimulation of stunned myocardium, decreases in dobutamine responsiveness cannot be explained by beta-receptor desensitization. Overall, these data indicate that CPB does not result in myocardial stunning. The differences between these data and others showing myocardial stunning following CPB may be due to several factors, such as anesthetic regimen, lack of coronary blood flow abnormalities, and a reduction in sarcoplasmic reticular damage due to the hypothermic conditions used. 相似文献
22.
Optic nerve pseudomeningioma secondary to localized amyloidosis 总被引:1,自引:0,他引:1
A 55-year-old woman presented with a mass of the optic nerve sheath suggestive of a meningioma. On excision, this proved to be amyloid. No systemic involvement could be found. Although amyloid may arise as a solitary lesion of the orbit or extraocular muscle, this "pseudomeningiomatous" pattern has not been previously noted. A magnetic resonance scan was helpful because the amyloid imaged at a density similar to vitreous and cerebral white matter, unlike meningiomas, which appear more like bone. The diagnosis of localized amyloidosis, however, still remains dependent on histopathology and cannot be made on a clinical basis. 相似文献
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25.
Lucia MB Rutella S Leone G Larocca LM Vella S Cauda R 《Journal of acquired immune deficiency syndromes (1999)》2002,30(4):369-378
P-glycoprotein (P-gp) transports a wide range of structurally unrelated drugs, such as HIV protease inhibitors (PIs) and cytotoxic compounds such as anthracyclines. Because modification of P-gp phenotype and function is an important underlying mechanism of drug interactions, the current study was conducted in order to evaluate whether highly active antiretroviral therapy (HAART), HIV plasma viral load (VL), or cancer chemotherapy may induce in vivo changes of P-gp phenotype in peripheral blood mononuclear cells (PBMCs) from HIV-infected treatment-naive and -experienced subjects at different stages of HIV infection and/or disease, including patients with HIV-associated Kaposi sarcoma (KS). Our results show that neither HAART nor HIV VL, nor the stage of HIV infection and/or disease, significantly alter P-gp expression on PBMCs. In particular, surface P-gp expression is expressed at low levels by T-cell subsets, B cells, and NK cells, whereas almost all monocytes are double positive and these results are not modified by HIV PI-containing regimens. By contrast, a significant phenotype modification is detected in PBMCs from AIDS/KS patients after challenge with the liposomal formulation of the anthracycline doxorubicin (L-DOX) with the higher expression reached 24 hours after the end of the drug infusion. In addition, accumulation of L-DOX is unaffected by P-gp-mediated drug efflux as documented by in vitro experiments, in sharp contrast to the kinetic of free DOX, based on HIV PI blockade experiments. Finally, P-gp expression was found in KS spindle cells from HIV-infected treatment-naive AIDS/KS patients. We conclude that P-gp phenotype in PBMCs and specific subsets is not altered by HAART and/or HIV, whereas a significant increase is induced by specific anticancer drugs such as L-DOX. Moreover, HIV PIs possess an inhibitory effect on P-gp function that may improve DOX sensitivity in KS spindle cells. 相似文献
26.
Rafaella Barbieri Anna Paola Rimondi Daniele Buzzoni Leone Luppi Claudio Nastruzzi Patrizia Orlando Dr Roberto Gambari 《Clinical & experimental metastasis》1989,7(4):417-426
The methylation pattern of the human HLA-DR gene was analyzed in normal breast tissues, breast primary tumors and lymphonodal metastases isolated from patients carrying breast carcinomas. In breast adenomas and also in normal tissues (including breast, muscle, brain, sperm and T- and B-lymphocytes), the HLA-DR gene is hypermethylated at the CCGG and GCGC sites. In all tissues studied, the only constantly unmethylated region is located in the 5 portion of the gene, near the promoter sequence. Further, the results indicate that the HLA-DR gene is hypomethylated in carcinomas and in the relative metastatic lymph nodes. It is suggested that hypomethylation of the human HLA-DR gene could be proposed as a molecular marker of malignant breast tumors. 相似文献
27.
Hart TC; Bowden DW; Bolyard J; Kula K; Hall K; Wright JT 《Human molecular genetics》1997,6(13):2279-2284
Tricho-dento-osseous syndrome (TDO), MIM# 190320, is transmitted as a
highly penetrant autosomal dominant trait that is characterized by variable
clinical expression. The principal clinical features include kinky/curly
hair in infancy, enamel hypoplasia, taurodontism, as well as increased
thickness and density of cranial bones. Possible genetic linkage has been
reported for TDO with the ABO blood group locus, but the gene defect
remains unknown. We have identified four multiplex families (n = 63, 39
affected, 24 unaffected) from North Carolina segregating TDO. We previously
have excluded a major locus for TDO in the ABO region for these families.
Utilizing a genome-wide search strategy, we obtained conclusive evidence
for linkage of the TDO syndrome locus to markers on chromosome 17q21
(D17S791, Z max = 10.54, Theta = 0.00) with no indication of genetic
heterogeneity. Multipoint analysis suggests the TDO locus is located in a 7
cM chromosomal segment flanked by D17S932 and D17S941. This finding
represents the first step towards isolation and cloning of the TDO gene.
Identification of this gene has important implications for understanding
normal and abnormal craniofacial development of hair, teeth and bone.
相似文献
28.
Paradiso A Ranieri G Silvestris N Naccarato G Bevilacqua G Mangia A Leone B Vallejo C Simone G Schittulli F De Lena M 《Clinical and experimental medicine》2001,1(3):127-132
In the present study, the primary tumor angiogenesis characteristics of 81 stage IV previously untreated breast cancers with
synchronous metastasis to different distant sites (10 patients with soft tissue metastases, 31 with bone metastases, and 40
with visceral metastases) were analyzed. The primary intratumor microvessel density was assessed by immunohistochemical assay
on paraffin-embedded primary tumor samples, using a monoclonal anti-CD34 antibody. The mean primary intratumor microvessel
density (at 400× fields) was 78±39 (SD) microvessels per field. The microvessel density was not significantly related to the
main clinical/pathological features of the tumor (age, cytohistological grade, DNA ploidy, diameter, and receptor status).
The percentage of tumor cases with high primary intratumor microvessel density (cut-off median value of the series 73±39 microvessels/field)
did not significantly differ in patients with bone, soft tissue, or visceral metastatic disease. Aanalysis of clinical outcome
showed a significantly shorter time to progression and overall survival for patients with visceral metastases (P<0.001 and P<0.0002 by log-rank, respectively). Presence of visceral metastases was confirmed to be the only independent prognostic factor
related to a worse TTP (hazard risk 2.15, 95% confidence interval 1.14–4.03, P<0.02) and overall survival (hazard risk 1.81, 95% confidence interval 0.98–3.35, P<0.06) by multivariate analysis. In conclusion, the assessment of neoangiogenesis of primary breast cancer by CD34 expression
does not provide information predictive of different distant sites of metastasis.
Received: 15 June 2001 / Accepted: 12 September 2001 相似文献
29.
Missense mutation in a von Willebrand factor type A domain of the alpha 3(VI) collagen gene (COL6A3) in a family with Bethlem myopathy 总被引:2,自引:0,他引:2
Pan TC; Zhang RZ; Pericak-Vance MA; Tandan R; Fries T; Stajich JM; Viles K; Vance JM; Chu ML; Speer MC 《Human molecular genetics》1998,7(5):807-812
The Bethlem myopathy is a rare autosomal dominant proximal myopathy
characterized by early childhood onset and joint contractures. Evidence for
linkage and genetic heterogeneity has been established, with the majority
of families linked to 21q22.3 and one large family linked to 2q37,
implicating the three type VI collagen subunit genes, COL6A1 (chromosome
21), COL6A2 (chromosome 21) and COL6A3 (chromosome 2) as candidate genes.
Mutations of the invariant glycine residues in the triple-helical
domain-coding region of COL6A1 and COL6A2 have been reported previously in
the chromosome 21-linked families. We report here the identification of a
G-->A mutation in the N-terminal globular domain-coding region of COL6A3
in a large American pedigree (19 affected, 12 unaffected), leading to the
substitution of glycine by glutamic acid in the N2 motif, which is
homologous to the type A domains of the von Willebrand factor. This
mutation segregated to all affected family members, to no unaffected family
members, and was not identified in 338 unrelated Caucasian control
chromosomes. Thus mutations in either the triple-helical domain or the
globular domain of type VI collagen appear to cause Bethlem myopathy.
相似文献
30.