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Adv Physiol Educ. 2002 Dec;26(1-4):98-109.
Cardiovascular interactions: an interactive tutorial and mathematical model.
Rothe CF, Gersting JM.
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA. crothupui.edu
The maintenance of an adequate cardiac output and systemic arterial blood pressure is a complex process with intricacies that are often difficult to understand. Cardiovascular Interactions is an active learning tool that demonstrates the interactions between the functions of the heart and peripheral circulation. This learning package consists of a Lab Book, a Model, and an Information file. The Lab Book is an interactive tutorial for exploring the relative influences of parameter changes on the cardiovascular system under normal, stressful, or pathophysiological conditions. The learners are guided to predict the direction and relative magnitude of changes of key variables in the cardiovascular system, evaluate the accuracy of their predictions, and describe the cause-and-effect mechanisms involved. Consequences of heart failure, hemorrhage, exercise, and changes in intrathoracic pressure can be explored. The results obtained in the Lab Book are based on a five-compartment mathematical Model, which reflects our current understanding of the basic control of the cardiovascular system. The Model was designed to be complex enough to be realistic, yet not so complex as to be overwhelming. An Information File contains definitions and descriptions of classical physiology about key concepts, including figures, and a detailed description of the Model. Hypertext tags embedded in the Lab Book are used to access the Information File. The Cardiovascular Interactions learning package was designed to run from its CD and so does not need to be installed.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12031942&dopt=Abstract hemorrhage
Eur J Biochem. 2002 Dec;269(24):6052-62.
Functional analysis of DM64, an antimyotoxic protein with immunoglobulin-like structure from Didelphis marsupialis serum.
Rocha SL, Lomonte B, Neves-Ferreira AG, Trugilho MR, Junqueira-de-Azevedo Ide L, Ho PL, Domont GB, Gutierrez JM, Perales J.
Departamento de Fisiologia e Farmacodinamica, Instituto Oswaldo Cruz, Fiocruz, Rio de Janeiro, Brazil.
Bothrops snake venoms are known to induce local tissue damage such as hemorrhage and myonecrosis. The opossum Didelphis marsupialis is resistant to these snake venoms and has natural venom inhibitors in its plasma. The aim of this work was to clone and study the chemical, physicochemical and biological properties of DM64, an antimyotoxic protein from opossum serum. DM64 is an acidic protein showing 15% glycosylation and with a molecular mass of 63 659 Da when analysed by MALDI-TOF MS. It was cloned and the amino acid sequence was found to be homologous to DM43, a metalloproteinase inhibitor from D. marsupialis serum, and to human alpha1B-glycoprotein, indicating the presence of five immunoglobulin-like domains. DM64 neutralized both the in vivo myotoxicity and the in vitro cytotoxicity of myotoxins I (mt-I/Asp49) and II (mt-II/Lys49) from Bothrops asper venom. The inhibitor formed noncovalent complexes with both toxins, but did not inhibit the PLA2 activity of mt-I. Accordingly, DM64 did not neutralize the anticoagulant effect of mt-I nor its intracerebroventricular lethality, effects that depend on its enzymatic activity, and which demonstrate the dissociation between the catalytic and toxic activities of this Asp49 myotoxic PLA2. Furthermore, despite its similarity with metalloproteinase inhibitors, DM64 presented no antihemorrhagic activity against Bothrops jararaca or Bothrops asper crude venoms, and did not inhibit the fibrinogenolytic activity of jararhagin or bothrolysin. This is the first report of a myotoxin inhibitor with an immunoglobulin-like structure isolated and characterized from animal blood.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12473101&dopt=Abstract hemorrhage
J Lab Clin Med. 2002 May;139(5):303-10.
Synthetic peptides of Goodpasture's antigen in antiglomerular basement membrane nephritis in rats.
Luo AM, Fox JW, Chen L, Bolton WK.
Department of Medicine and Microbiology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
Goodpasture's syndrome (GPS) is an autoimmune disease characterized by pulmonary hemorrhage, glomerulonephritis and anti-glomerular basement membrane (GBM) antibodies. The alpha(3) noncollagenous domain (NC1) of type IV collagen [alpha(3)(IV)] is the pathogen. The disease is T-cell-dependent; thus linear peptides initiate the autoimmune process. Studies in a rat model of GPS, experimental autoimmune glomerulonephritis (EAG), have shown that the carboxy-terminal 36 amino acids (purportedly the pathogenic epitope) are not responsible for disease induction. More recent studies implicate the amino terminus of alpha(3)(IV)NC1. Finding the nephritogenic epitope(s) is crucial in the understanding of the disease and for treatment. Because alpha(3)(IV)NC1 contains the antigens that induce GN in rats and human beings, we hypothesized that regions of the alpha(3)(IV)NC1 other than the carboxy terminus were responsible for disease. We investigated overlapping peptides spanning the entire NC1 domain of the alpha(3)(IV) chain N-terminal to the 36-mer (Goodpasture epitope) using the EAG rat model. Most peptides elicited antibody responses exclusively to themselves but not to native GBM. T-cells from GBM-immunized rats proliferated in vitro after stimulation with peptides 6, 8, 14, and 15, 24-mer and 23-mer. Fifteen percent of peptide 8 and peptide 14 rats had mild glomerulonephritis. In none of the animals immunized with other peptides did glomerulonephritis develop. These data suggest that conformation-dependent sites, posttranslational modification, multiple epitopes, concomitant antibody formation, or other disturbances are important in the ability of alpha(3)(IV)NC1 to induce EAG in rats and may also be important in the induction of GPS in human beings.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12032491&dopt=Abstract hemorrhage
Can J Cardiol. 2002 May;18(5):515-22.
Effects of acute volume loading and hemorrhage on intestinal vascular capacitance: a mechanism whereby capacitance modulates cardiac output.
Scott-Douglas NW, Robinson VJ, Smiseth OA, Wright CI, Manyari DE, Smith ER, Tyberg JV.
Foothills Medical Centre, Foothills Hospital, Calgary, Alberta, Canada.
BACKGROUND: Changes in intestinal vascular capacitance during acute volume loading and hemorrhage have not been described. OBJECTIVES: To determine the effects of volume loading and hemorrhage on the intestinal vascular pressure-volume relationship and cardiac output. PATIENTS AND METHODS: In 11 alpha-chloralose-anesthetized dogs, a pneumatic portal venous constrictor and catheter were positioned to increase and measure portal venous pressure (Ppv), respectively. Relative changes in intestinal blood volume (IBV) were determined by blood-pool scintigraphy and expressed as the percentage change from control values (taken as 100%). Ppv-IBV relationships were constructed by graded portal vein constriction. RESULTS: IBV and cardiac output increased by 60 6% and 178 48%, respectively, and Ppv increased from 5.8 0.9 mmHg to 13.2 1.8 mmHg after initial volume loading (40 mL/kg of an isotonic glucose-saline solution over 7 min). IBV gradually decreased and reached near-control values after 75 min. In seven dogs, hemorrhage (sufficient to decrease mean aortic pressure by 56 4%) decreased IBV and cardiac output to 88 4% and 52 3% of control values, respectively, and Ppv decreased to 3.2 0.8 mmHg. CONCLUSIONS: A sigmoid function curve defined the relationship between cardiac output and IBV. Cardiac output remained constant over a wide range (between approximately 95% and 135% of control IBV). Outside this range, insufficient dilation or constriction resulted in a marked increase or decrease in venous pressures and cardiac output. These data indicate that vasculature capacitance modulates cardiac output during acute volume loading and hemorrhage, thereby maintaining cardiac output relatively constant over a wide range of total vascular blood volume.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12032578&dopt=Abstract hemorrhage
J Vet Diagn Invest. 2002 May;14(3):205-10.
Diagnosis of epizootic bovine abortion in Nevada and identification of the vector.
Hall MR, Hanks D, Kvasnicka W, Bosomworth A, Smith H, Stott JL, Blanchard MT, Anderson ML.
Department of Animal Biotechnology, College of Agriculture, Biotechnology and Natural Resources, University of Nevada, Reno 89557, USA.
In the 43 years since the first description in California, epizootic bovine abortion (EBA) has been considered but not definitively diagnosed as a cause of late-term abortions on Nevada ranches. Examination of aborted full-term bovine fetuses obtained from Nevada ranches revealed gross abnormalities consistent with EBA (enlarged lymph nodes, petechial hemorrhages of the oral mucosa and conjunctiva, ascites, and splenohepatomegaly), and EBA was confirmed by histologic examination of fetal tissues. The histologic thymic changes were characteristic of EBA and included severe histocytic thymusitis with depletion of thymocytes, interlobular hemorrhage, and fibrinocellular exudation. The gross enlargement of lymph nodes was the result of cortical follicular hyperplasia and histiocytic lymphadenitis. In addition, widespread, predominately nonsuppurative histologic lesions typical of EBA were observed in most organs, including the brain, lung, heart, liver, and spleen. Furthermore, the presence of Ornithodorus coriaceus, the argasid tick vector of EBA, was established by tick collection using CO2 traps. The tick was identified on ranches and in geographic areas (northern and northwestern counties of Nevada) coincident with diagnosis of multiple cases of EBA. This study establishes the presence of EBA as a cause of late-term abortion in Nevada. Additionally, identification of the EBA tick vector, O. coriaceus, in the same areas as the abortions provides strong evidence that the disease is endemic.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12033675&dopt=Abstract hemorrhage
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