[Viral hepatitis. A complication of extracorporeal circulations that does not spare the medical staff].
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Adult↗
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Increased soluble CD40 ligand levels in cystic fibrosis.
Chronic inflammation represents a key pathogeneric event in the progression of lung disease in cystic fibrosis (CF). To identify novel mechanisms of the inflammatory reaction in CF and analyze its relation with coagulative activation, we carried-out a cross-sectional study to evaluate circulating levels of the inflammatory mediators soluble (s) CD40L, C-reactive protein (CRP), interleukin (IL)-1beta, the coagulation markers activated factor VII (FVIIa) and prothrombin fragment (F) 1+2, as well as urinary 11-dehydro-thromboxane (TX)B2, an index of in vivo platelet activation, in 34 CF patients and 34 matched healthy subjects. We observed that CF patients displayed significantly increased circulating levels of sCD40L compared to controls [2.8 (0.4-15.6) vs 1.1 (0.2-2.7) ng mL(-1), P = 0.0003]. sCD40L levels inversely correlated with forced expiratory volume at 1 second (FEV1) (rho = -0.788, P = 0.0001), whereas it directly correlated with CRP and IL-1beta levels (rho = 0.621, P = 0.0004; and rho = 0.745, P = 0.0001, respectively), which were also elevated in CF patients. CF patients had also enhanced levels of FVIIa and F1+2 compared to controls [39.2 (22.6-69.8) vs 22.3 (16.2-32.4) mU mL(-1), P = 0.0001; 0.60 (0.30-1.80) vs 0.17 (0.10-0.40) nmol L(-1), P = 0.0001, respectively]. A direct correlation was observed between sCD40L and both plasma FVIIa (rho = 0.691, P = 0.0001) and F1+2 (rho = 0.545, P = 0.0017) as well as between sCD40L and urinary 11-dehydro-TXB2 (rho = 0.433, P = 0.0129). Our findings suggest that in CF patients, sCD40L could represent a biochemical link between the inflammatory state, and endothelial damage and coagulative activation, leading to progressive impairment of pulmonary function.
Adolescent↗
The fate of antibodies and their radiolabels bound to tumor cells in vitro: the effect of cross-linking at the cell surface and of anti-idiotype antibodies.
In order to obtain rapid blood clearance of circulating antibodies (Ab) at a desired time, cross-linking reagents such as second Ab are often employed. Such reagents will generally bind to Ab located at the tumor site as well as free Ab, and we therefore investigated whether the cross-linking of Ab bound to the surface of tumor cells affects the processing of those Ab. Cross-linking was induced in various ways: a polyclonal second Ab [rabbit anti-(mouse IgG)], a monoclonal rat anti-(mouse IgG constant region) Ab, and streptavidin used in conjunction with a biotinylated first Ab. Processing was followed for 3 days, to allow nearly all of the bound Ab to reach its ultimate fate. Results depended strongly on the particular first Ab used. Two basic effects were observed. First, the second Ab efficiently prevented the early dissociation of intact Ab from the cell; once the second Ab bound, there was virtually no dissociation of the primary Ab bound to the cells. For most Ab, where only a small proportion of bound Ab dissociated intact, this effect was relatively small. However, for an unusual Ab, where the majority dissociated intact (L6) the effect of a second Ab in prolonging Ab retention by the cell was dramatic. Second, cross-linking sometimes resulted in markedly accelerated internalization and degradation of the bound Ab, coupled with the release of degradation products into the medium. This process resulted in much shorter retention of the radioisotope by the cell. If a "residualizing" radiolabel was used, 125I-dilactitoltyramine, which is probably trapped within lysosomes after Ab catabolism, the effect of the second Ab in accelerating loss from the cell was largely prevented. We also tested anti-idiotype Ab as cross-linking reagents. In addition to testing anti-idiotype Ab known to react with the cell-bound primary Ab, we also tested anti-idiotype Ab not expected to bind to cell-bound Ab, initially as a negative control. Unexpectedly, all anti-idiotype Ab tested induced rapid release of the primary Ab from the cell. This effect was similar to the effect of a large excess of unlabeled Ab, and we attribute it to the blocking of the free binding site of a "wobbling" Ab, which prevents its rebinding to a second antigen molecule. We conclude that the use of selected anti-idiotype Ab to clear circulating Ab, while not reacting with cell-bound Ab, must be done cautiously.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
[Effect of extra corporeal circulation on cardiac function and myocardial ultrastructure--A comparative study in the groups with and without aortic cross-clamping and left ventricular hypertrophy].
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Animals↗
Cross-reactive antibodies induced by a monovalent influenza B virus vaccine.
Influenza viruses related to the markedly antigenically divergent strains B/Yamagata/16/88 and B/Victoria/2/87 are circulating in human populations. Adults develop cross-reacting antibodies against recent and earlier influenza B virus strains after vaccination with B/Yamagata/16/88, probably because of previous influenza B virus infections or immunizations. Vaccines containing B/Yamagata/16/88 should adequately protect adults against B/Victoria/2/87 infections.
Adult↗
Long-term body weight variability is associated with elevated C-reactive protein independent of current body mass index among Japanese men.
OBJECTIVE: To elucidate the effect of long-term weight variability on C-reactive protein (CRP) levels. DESIGN: Cross-sectional study of the circulating CRP. SUBJECTS: A total of 637 Japanese men aged 40-49 y in1997. MEASUREMENTS: Serum CRP levels, body mass index in 1997 (current BMI), the slope of weight on age (weight-slope) representing an individual's weight trend of direction and magnitude, and the root mean square error around the slope of weight on age (weight-RMSE) representing the weight fluctuation magnitude, as calculated by a simple linear regression model in which each value of the subject's five actual weights (aged 20, 25, 30 y, five years ago, and current) was a dependent variable and the subject's ages independent variables. RESULTS: After adjustment for age and confounders, including smoking and health status, the odds ratios of elevated CRP (> or =0.06 mg/dl) were 1.83 (95% CI: 1.25-2.69), 2.63 (1.69-4.11), and 10.31 (2.17-48.98) for upper normal-weight (BMI: 22-<25 kg/m(2)), overweight (25-<30), and obese (> or =30) persons, respectively, compared with lower normal-weight persons (18.5-<22). Adjusting for age, confounders, and current BMI, weight-slope was positively associated with CRP level especially among subjects with BMI> or =25 kg/m(2) (trend P<0.01), and weight-RMSE was positively associated with CRP level particularly among subjects with BMI <25 kg/m(2) (trend P<0.05). CONCLUSION: Our results suggest a state of low-grade systemic inflammation not only in overweight and obese persons, but also in normal-weight persons with large weight fluctuation, possibly explaining in part the positive association between weight fluctuation and CVD.
Adipose Tissue↗
The uptake of isoflurane by the foetal lamb in utero: effect on regional blood flow.
Because isoflurane has recently been approved for clinical use in anaesthesia, we have studied the effect of this agent in the foetus using the pregnant ewe as an animal model. Eight pregnant ewes of 120-125 days gestation were surgically prepared with indwelling catheters and tracheostomy. Prior to anaesthesia, labelled microspheres were injected into the foetal circulation to determine cardiac output and regional blood flows to all organs. The ewes were anaesthetized with a constant inspired concentration of 2.0 per cent isoflurane in oxygen. Blood samples were drawn to construct an uptake curve for both mother and foetus. At 60 and 96 minutes of anaesthesia, microspheres were injected into the foetal circulation to measure changes in organ blood flow from the control period. Isoflurane crossed the placenta and appeared in the foetal circulation within two minutes. By 96 minutes, maternal and foetal arterial levels were 116.3 +/- 9.9 and 99.3 +/- 9.1 mEq/L (0.98 vol% and 0.75 vol%). There were no significant changes in foetal blood pressure or pulse rate but foetal pH decreased significantly from 7.39 +/- 0.02 to 7.26 +/- 0.2 (mean +/- SEM) and base excess decreased from -1.1 +/- 1.5 to -6.2 +/- 0.7. Foetal cardiac index decreased from 390.8 +/- 26.9 ml X kg-1 X min-1 to 292.0 +/- 13.8 after 96 minutes of anaesthesia. There were no significant changes in any of the maternal cardiovascular or acid-base parameters.
Animals↗
Cross-clade CD8(+) T-cell responses with a preference for the predominant circulating clade.
Human immunodeficiency virus (HIV) genetic diversity is a major impediment to the design of a successful vaccine. Even if an HIV vaccine is proven effective, it remains to be seen whether this protection will extend to inter-clade, intra-clade, and recombinant strains. We used recombinant vaccinia-based interferon gamma (IFN) Elispot assays to test the inter-clade crossreactivity of clades A, B, C, and D HIV Env in two cohorts of HIV-infected Kenyans. Despite the tremendous diversity in this HIV protein, a substantial proportion of multi-clade responses were observed. Although these multi-clade responses correlated well with each other in regression analyses, clade A responses were seen at a higher frequency and at greater relative magnitudes in a proportion of these patients, when compared to the other three clades. Epitope mapping indicates CD8(+) T cell recognition of conserved regions of Env, accounting for the high degree of cross-reactivity but not the clade A preference. A better understanding of cross-clade CD8(+) T cell responses to HIV may help to predict whether a successful vaccine could be used to stop geographically and genetically distinct HIV epidemics.
CD8-Positive T-Lymphocytes↗
Procoagulant microparticles: disrupting the vascular homeostasis equation?
Apoptosis and vascular cell activation are main contributors to the release of procoagulant microparticles (MPs), deleterious partners in atherothrombosis. Elevated levels of circulating platelet, monocyte, or endothelial-derived MPs are associated with most of the cardiovascular risk factors and appear indicative of poor clinical outcome. In addition to being a valuable hallmark of vascular cell damage, MPs are at the crossroad of atherothrombosis processes by exerting direct effects on vascular or blood cells. Under pathological circumstances, circulating MPs would support cellular cross-talk leading to vascular inflammation and tissue remodeling, endothelial dysfunction, leukocyte adhesion, and stimulation. Exposed membrane phosphatidylserine and functional tissue factor (TF) are 2 procoagulant entities conveyed by circulating MPs. At sites of vascular injury, P-selectin exposure by activated endothelial cells or platelets leads to the rapid recruitment of MPs bearing the P-selectin glycoprotein ligand-1 and blood-borne TF, thereby triggering coagulation. Within the atherosclerotic plaque, sequestered MPs constitute the main reservoir of TF activity, promoting coagulation after plaque erosion or rupture. Lesion-bound MPs, eventually harboring proteolytic and angiogenic effectors are additional actors in plaque vulnerability. Pharmacological strategies aimed at modulating the release of procoagulant MPs appear a promising therapeutic approach of both thrombotic processes and bleeding disorders.
Animals↗
Monoamine innervation of the organum vasculosum laminae terminalis (OVLT): a high resolution radioautographic study in the rat.
The monoamine innervation of the organum vasculosum laminae terminalis (OVLT) was examined in the adult rat by light and electron microscope radioautography after intraventricular administration of tritiated serotonin [( 3H]5-HT) or dopamine [( 3H]DA). Radioautographic and biochemical controls after 5,7-dihydroxytryptamine or 6-hydroxydopamine lesioning established the respective serotonin (5-HT) and catecholamine (CA) identities of the axonal varicosities labeled under the conditions of the present experiments. For descriptive purposes, the OVLT was subdivided in three parts: two parenchymal zones, one juxtaventricular, the other juxtavascular, and the vascular core. Almost 10% of all axonal varicosities in the OVLT were found to be labeled with [3H]5-HT. This 5-HT innervation was most prominent in the rostrocaudal and ventrodorsal portions of the juxtaventricular zone and the dorsal aspect of the juxtavascular zone; there was none in the vascular core. [3H]DA-labeled varicosities were much less abundant and yet more numerous than earlier histofluorescent and immunohistochemical studies would have predicted. They predominated in the juxtavascular zone, where a majority presumably had a dopamine (DA) rather than a noradrenaline identity. Some were also found in the vascular core, where they most likely corresponded to peripheral autonomic noradrenaline endings. In the juxtaventricular zone of the OVLT, a significant proportion of the [3H]5-HT-labeled varicosity profiles could be observed to form axodendritic synapses, but in the juxtavascular zone no 5-HT or any [3H]DA-labeled ones were ever seen in synaptic junction. In the juxtavascular zone, the 5-HT and the presumed DA endings established close relationships with neurosecretory axons, and with astrocytic or tanycytic processes on which they occasionally formed "synaptoid contacts." A few endings of either type were also seen to about directly on the outer basement membrane of the perivascular space. It therefore appears probable that in OVLT monoamines influence neural and nonneural elements. At a proximal level of regulation (juxtaventricular zone), 5-HT could act both synaptically and nonsynaptically as an interneuronal transmitter or modulator. In contrast, distally (juxtavascular zone), both DA and 5-HT could be released as neurohormones in addition to modulating neurosecretion. 5-HT and DA varicosities in the OVLT could also behave as sensors for circulating factors that do not cross the blood-brain barrier.
Animals↗
Immunization does not interfere with uptake and transport by motor neurons of the binding fragment of tetanus toxin.
The nontoxic binding domain of tetanus toxin (fragment C or TTC) readily undergoes retrograde axonal transport from an intramuscular injection site. This property has led to investigation of TTC as a possible vector for delivering therapeutic proteins to motor neurons. However, the vast majority of individuals in the developed world have been vaccinated with tetanus toxoid and have circulating antitetanus antibodies that cross-react with TTC and may block the delivery of a TTC-linked therapeutic protein. However, it is uncertain whether the immune response is capable of completely neutralizing an intramuscular depot of protein prior to its internalization by presynaptic nerve terminals, where it is inaccessible to antibody. We have evaluated uptake of rhodamine-labeled TTC following intramuscular injection in normal animals and animals vaccinated with tetanus toxoid prior to injection of fluorescently labeled TTC. All animals demonstrated uptake of TTC, with fluorescence appropriately localized to the hypoglossal nerve and nucleus. The distribution and intensity of fluorescence within neurons and processes were indistinguishable between the two groups and were characteristic of TTC. Vaccinated animals showed levels of uptake of TTC into the brain comparable to those of immunologically naïve animals as measured by quantitative fluorimetry. All vaccinated animals had protective levels of antitetanus antibodies as measured by ELISA. Uptake of TTC by nerve terminals from an intramuscular depot is an avid and rapid process and is not blocked by vaccination associated with protection from tetanus toxin.
Animals↗
Contribution of maternal circulation to blood-borne progesterone in the fetus. I. Studies on human subjects.
Tritiated progesterone was infused intravenously at a constant rate into three pregnant volunteers in labor, for at least two hours before delivery. Blood samples from a maternal peripheral vein and from unbilical vessels were taken at birth. Comparison of the specific activities of progesterone in these samples indicated that 10 per cent or less of the hormone in fetal circulation is derived from transfer of maternally circulating progesterone. After consideration of reported values of umbilical vein blood flow at term and measured arteriovenous differences in concentrations of progesterone in umbilical vessels, the secretion rate of the placental hormone toward the fetus was estimated to be about 1/10 of the rate of secretion of progesterone toward the maternal circulation. About 1 per cent of the maternally circulating hormone was found to cross the placenta.
Female↗
Infusion of gonadotropin-releasing hormone agonist during pregnancy: maternal and fetal responses in primates.
To determine whether a gonadotropin-releasing hormone agonist could cross the placenta to the fetus, each pregnant rhesus monkey (110 to 155 days' gestation, n = 10) and her in utero fetus had indwelling cannulas placed in the femoral veins. Gonadotropin-releasing hormone agonist (1000 micrograms intravenously) was injected into the mother (n = 8) or fetus (n = 2); serial blood samples were collected from mother and fetus for luteinizing hormone and follicle-stimulating hormone determination. None of the mothers responded to the gonadotropin-releasing hormone agonist bolus. In contrast, some of the fetal monkeys receiving gonadotropin-releasing hormone agonist via placental transfer and all fetal monkeys injected directly with the agonist responded as indicated by increased luteinizing hormone (2.8- to 12.3-fold) and follicle-stimulating hormone (1.5- to 8.9-fold) concentrations. In evaluating maternal and fetal effects, we found that continuous maternal infusion with either gonadotropin-releasing hormone agonist (n = 14) or saline solution (n = 11) throughout pregnancy did not alter maternal hormonal profiles. Histologically, gonads from their infants, removed within 3 days post partum, were normal. Although neonatal ovarian weights were unaffected by the in utero treatment, the testes weighed less (p less than 0.05) in male infants born of mothers treated with gonadotropin-releasing hormone agonist compared to controls. Thus gonadotropin-releasing hormone agonist can cross from maternal to fetal circulation, and the fetus can respond (at least during the third trimester).
Animals↗
Polyclonal antibodies to the encephalitogenic neighborhoods of myelin basic protein: singular affinity populations neutralized by specific synthetic peptide probes.
Specific ligand neutralization was used to probe the extent to which singular antibody affinity populations signified specific determinants in the neighborhood myelin basic protein (MBP) encephalitogens. The probes were individual members of a panel of synthetic peptide analogs subsuming encephalitogenic regions. Comparative Scatchard analyses of neutralized and unneutralized antisera helped to identify the particular peptide determinants involved in the original polyclonal antibody responses to the multiple antigenic determinants of encephalitogenic peptides. The range of affinities for an antibody population against a singular MBP peptide determinant was found to be relatively restricted while the range of affinities overall for all populations within a given antipeptide antiserum was found to be relatively wide and invariably discontinuous. Consequently, the individual discontinuous affinity populations could readily be dissected by application of the Rosenthal method of Scatchard curve analysis. It was found that the singular high affinity antibody population (5.6 x 10(7) M-1) of a Lewis rat antiserum to rat encephalitogenic GSLPQKAQRPQDENG (S49) was against a determinant near the N-terminal non-encephalitogenic end of the peptide. Only the low affinity antibody populations were found that had reactivity for determinants within the encephalitogenic region itself. The singular high affinity antibody population (5.97 x 10(7) M-1) of a rabbit antiserum to rabbit encephalitogenic TTHYGSLPQKAQGHRPQDEG (S82) was against a determinant centered about the tyrosyl residue, within the encephalitogenic region for the rabbit, but was completely cross-reactive with a specific circulating endogenous inhibitor. The results obtained with the rat and rabbit EAE sera were consistent with a previously advanced hypothesis that antibodies to determinants within encephalitogenic neighborhoods would effectively block the onset of EAE if high enough in affinity and not neutralized by an endogenous inhibitor.
Animals↗
Role of the blood-brain barrier in the establishment of the immune response against polyoma virus-induced cerebral tumours in hamsters.
The existence of an immunological blood-brain barrier (BBB) is well established but its role in cerebral tumour immunology is less well defined. Attempting to clarify this problem we tested the graft rejection of polyoma virus-induced central nervous (CNS) tumours in hamsters after systemic or intracerebral immunization with polyoma virus. Animals were immunized by intracerebral or subcutaneous inoculations of polyoma virus before tumours were induced by intracerebral or intramuscular graft of polyoma-transformed hamster neuroglial cells. The growth of cerebral and muscular tumours was significantly inhibited in animals immunized subcutaneously. In animals immunized intracerebrally the inhibition of growth was highly significant for cerebral tumours and only very slight for intramuscular tumours. These results suggest that the blood-brain barrier allowed immunocompetent effector cells to penetrate inside the CNS but prevented the locally elicited cell-mediated immune response from diffusing outside the CNS. The ability of the brain to develop a local immune response and the partial lack of circulation of immunocompetent cells to cross the BBB could be mainly responsible for the special immune status of the CNS and may greatly interfere with the establishment of an efficient immune response toward brain tumours.
Animals↗
Reversible association of the cytokines MIP-1 alpha and MIP-1 beta with the endothelia of the blood-brain barrier.
Macrophage inflammatory proteins (MIP)-1 alpha and -1 beta have been postulated to exert their pyrogenic effects by acting directly at sites within the brain. Such activity would require circulating MIP-1s to cross the blood-brain barrier (BBB). We examined the ability of the monomer and polymer of MIP-1 alpha and the polymer of MIP-1 beta radioactively labeled with 125iodine (I-MIP-1) to cross the BBB. These I-MIP-1s behaved very similarly to each other but in a manner not previously seen for other cytokines. The I-MIP-1s immediately associated to a high degree and in a reversible manner with the vascular space of the brain. This association did not increase over time nor was it self-inhibitable. These results make it unlikely that the MIP-1s are transported into the brain by saturable transport systems in the manner found for some of the other cytokines. Other mechanisms, such as interactions with brain endothelia, leakage into brain through extracellular pathways, and binding at circumventricular organs, are more likely to provide the mechanisms through which blood-borne MIP-1s affect the central nervous system.
Animals↗
Current concepts on Escherichia coli K1 translocation of the blood-brain barrier.
The mortality and morbidity associated with neonatal gram-negative meningitis have remained significant despite advances in antimicrobial chemotherapy. Escherichia coli K1 is the most common gram-negative organism causing neonatal meningitis. Our incomplete knowledge of the pathogenesis of this disease is one of the main reasons for this high mortality and morbidity. We have previously established both in vitro and in vivo models of the blood-brain barrier (BBB) using human brain microvascular endothelial cells (HBMEC) and hematogenous meningitis in neonatal rats, respectively. With these in vitro and in vivo models, we have shown that successful crossing of the BBB by circulating E. coli requires a high-degree of bacteremia, E. coli binding to and invasion of HBMEC, and E. coli traversal of the BBB as live bacteria. Our previous studies using TnphoA, signature-tagged mutagenesis and differential fluorescence induction identified several E. coli K1 determinants such as OmpA, Ibe proteins, AslA, TraJ and CNF1 contributing to invasion of HBMEC in vitro and traversal of the blood-brain barrier in vivo. We have shown that some of these determinants interact with specific receptors on HBMEC, suggesting E. coli translocation of the BBB is the result of specific pathogen-host cell interactions. Recent studies using functional genomics techniques have identified additional E. coli K1 factors that contribute to the high degree of bacteremia and HBMEC binding/invasion/transcytosis. In this review, we summarize the current knowledge on the mechanisms underlying the successful E. coli translocation of the BBB.
Animals↗
Structural determinants of natriuretic peptide receptor specificity and degeneracy.
Cardiovascular homeostasis and blood pressure regulation are reliant, in part, on interactions between natriuretic peptide (NP) hormones and natriuretic peptide receptors (NPR). The C-type NPR (NPR-C) is responsible for clearance of NP hormones from the circulation, and displays a cross-reactivity for all NP hormones (ANP, BNP, and CNP), in contrast to other NPRs, which are more restricted in their specificity. In order to elucidate the structural determinants for the binding specificity and cross-reactivity of NPR-C with NP hormones, we have determined the crystal structures of the complexes of NPR-C with atrial natriuretic peptide (ANP), and with brain natriuretic peptide (BNP). A structural comparison of these complexes, with the previous structure of the NPR-C/CNP complex, reveals that NPR-C uses a conformationally inflexible surface to bind three different, highly flexible, NP ligands. The complex structures support a mechanism of rigid promiscuity rather than conformational plasticity by the receptor. While ANP and BNP appear to adopt similar receptor-bound conformations, the CNP structure diverges, yet shares sets of common receptor contacts with the other ligands. The degenerate versus selective hormone recognition properties of different NPRs appears to derive largely from two cavities on the receptor surfaces, pocket I and pocket II, that serve as anchoring sites for hormone side-chains and modulate receptor selectivity.
Amino Acid Sequence↗