Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depression of reticuloendothelial (RE) phagocytic function has been clearly documented following trauma and operation. This phagocytic failure is mediated in part by depletion of an opsonic glycoprotein. Depletion of this opsonic protein may result in prolonged blood retention of potentially harmful particulates that may interfere with the microcirculation and may possibly result in altered organ function. Isolation and identification of this opsonic protein has led to the finding of the identity between opsonic glycoprotein and cold insoluble globulin (CIg) or so-called plasma fibronectin. Since CIg is concentrated in cryoprecipitate, this blood component was used as a readily available source of opsonic protein for replacement studies. Nine patients were studied following a 1-hour infusion of cryoprecipitate obtained from 10 units of plasma and suspended in a volume of 250 ml. Both the pulmonary shunt fraction and the fraction of dead space ventilation decreased significantly (P = 0.02) after cryoprecipitate administration. Limb blood flow (P = 0.001), limb oxygen consumption (P = 0.001), and reactive hyperemia of the limb (P = 0.05) increased significantly following cryoprecipitate infusion. Cardiac output, total oxygen consumption did not change consistently. The data demonstrate that the infusion of cryoprecipitate resulted in improved pulmonary and microcirculatory function--possibly due to opsonic glycoprotein replacement.
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PMID:Cardiovascular hemodynamics after opsonic alpha-2-surface binding glycoprotein therapy in injured patients. 8 71

Plasma fibronectin (cold-insoluble globulin) is known to be cross-linked to fibrin during the final stage of blood coagulation and is probably the major nonspecific opsonin of blood. We measured the concentration of plasma fibronectin in 36 hospitalized patients (11 with malignancy, 12 with infection, 13 with other underlying diseases) with evidence of fibrin depostion and lysis. Plasma fibronectin concentration was greater than 2 S.D. below the mean of normals in 17 of the patients (p less than 0.001). Depression of fibronectin was not related to severity of disseminated intravascular coagulation, as assessed by fibrinogen concentration and the quantity of FDP in serum. Depressed plasma fibronectin concentration and the quantity of FDP in serum. Depressed plasma fibronectin concentration was an unfavorable prognostic finding, inasmuch as 12 of the 17 patients with depressed fibronectin concentrations died during hospitalization as compared to five of the 19 patients with normal fibronectin concentrations (p less than 0.02). We speculate that specific depletion of plasma fibronectin, because of codeposition with fibrin or due to increased utilization as a nonspecific opsonin, may contribute to the organ failure seen in severely ill patients.
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PMID:Fibronectin concentration is decreased in plasma of severely ill patients with disseminated intravascular coagulation. 64 97

Liver and spleen phagocytic clearance of blood-borne microparticulate tissue debris and products of intravascular coagulation after trauma and surgical injury is an important mechanism to limit the deposition of debris in the pulmonary vascular bed. Plasma fibronectin (pFn) modulates this clearance process. We evaluated the effect of a localized peripheral ischemia and reperfusion injury on liver and spleen phagocytic function. Male rats (250 to 350 g) underwent 4 hours of tourniquet-induced bilateral hindlimb ischemia, followed by 18 hours of reperfusion after release of the tourniquet. Rats subjected to ether anesthesia alone or anesthesia followed by groin incision without ischemia were the control and sham groups, respectively. Reticuloendothelial (RE) phagocytic function was assessed at 15 minutes and 18 hours after the start of reperfusion by the in vivo liver and spleen removal of blood-borne iodine 125 (125I)-test microparticles, which were coated with gelatin (denatured collagen) to enhance their interaction with pFn. Liver and spleen particle uptake in control and sham rats was similar. In contrast, after 4 hours of ischemic injury with 15 minutes of reperfusion, we observed a 30% to 40% decrease (p less than 0.05) in liver and spleen particle uptake as compared with sham controls with partial restoration of this removal mechanism by 18 hours. This depression in liver and spleen phagocytic function was associated with a significant (p less than 0.05) increase in the deposition of the 125I-test particles in the lung. RE depression was not due to a deficiency of pFn; indeed, a marked elevation (588 +/- 12 micrograms/mL versus 1,083 +/- 40 micrograms/mL) of pFn was observed by immunoassay over the 18-hour reperfusion interval. Comparative bioassay of humoral (opsonic) versus cellular (Kupffer's cell) activity revealed that Kupffer's cells in livers from controls or ischemia-reperfusion rats exhibited normal phagocytic function when incubated in plasma harvested from either control or 4-hour ischemic rats. The opsonic activity of plasma harvested after ischemia and reperfusion was also more than adequate, consistent with the immunoassay analysis. Thus, the impaired liver and spleen clearance mechanism after peripheral ischemia and reperfusion injury did not appear to be due to either a macrophage cellular deficit or a lack of pFn. This clearance depression may be mediated by splanchnic malperfusion, which is known to develop after peripheral ischemia and reperfusion and associated soft tissue injury.
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PMID:Liver and spleen phagocytic depression after peripheral ischemia and reperfusion. 141 24

Adherence to extracellular matrix proteins modulates the functional and secretory activities of mononuclear phagocytes, although the mechanisms regulating these adherence-dependent changes are poorly understood. In this study, the ability of rat inflammatory peritoneal macrophages (PM) to adhere to an endothelial cell-derived extracellular matrix or a denatured collagen/fibronectin-coated surface and perform antibody dependent cell cytotoxicity (ADCC) and secrete reactive oxygen intermediates was compared with PM adherent to tissue culture plastic. Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2), two major cyclooxygenase products released by inflammatory macrophages, were also measured by PM adherent to the protein coated surfaces. Rat exudate PM were equally adherent to tissue culture plastic or wells coated with either endothelial cell derived matrix or denatured collagen (gelatin)/fibronectin. PM adherent to a denatured collagen/fibronectin-coated wells demonstrated significantly less cytolytic activity (15 +/- 2% lysis) when compared with either tissue culture plastic adherent PM (43 +/- 7% lysis) or PM adherent to extracellular matrix (59 +/- 11% lysis). PM adherent to extracellular matrix released twofold more TxB2 than plastic adherent PM, while PM adherent to denatured collagen/fibronectin released 40% more PGE2 than cells adherent to tissue culture plastic or 80% more PGE2 than PM adherent to the extracellular matrix. PM adherent to denatured collagen/fibronectin release less superoxide anion (27 +/- .9 nmoles/10(6) PM) than PM adherent to either tissue culture plastic (43 +/- 1 nmoles/10(6) PM) or the extracellular matrix (60 +/- 0.5 nmoles/10(6) PM). Furthermore, incubation of plastic adherent PM with exogenous PGE2 reduced superoxide production in a dose-dependent manner. These results demonstrate that the inhibition of ADCC and secretion of reactive oxygen intermediates by PM adherent to a denatured collagen/fibronectin surface correlated with an increased release of the immunosuppressive prostanoid PGE2. Furthermore, the addition of exogenous PGE2 to plastic adherent PM reproduced the depression in ADCC and superoxide anion production observed by PM adherent to a denatured collagen/fibronectin surface. These studies suggest that the increased production and release of PGE2 by inflammatory macrophages adherent to a denatured collagen surface may act to suppress cytotoxic mechanisms and thereby constitutes part of an autocrine feedback mechanism regulating macrophage function during wound injury.
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PMID:Surface contact modulation of inflammatory macrophage antibody dependent cytotoxicity and prostanoid release. 166 Aug 99

Sequence-specific resonance assignments for the isolated second or b domain of the bovine seminal fluid protein PDC-109 have been obtained from analysis of two-dimensional 1H NMR experiments recorded at 500 MHz. These assignments include the identification of all aromatic and most aliphatic amino acid resonances. Stereospecific assignment of resonances stemming from the Val2 CH3 gamma,gamma' groups and from seven CH beta,beta' geminal pairs has been accomplished by analysis of 3J alpha beta coupling constants in conjunction with patterns of cross-peak intensities observed in two-dimensional nuclear Overhauser effect (NOESY) spectra. Analysis of NOESY and 3J alpha NH data reveals a small antiparallel beta-sheet involving stretches containing residues 25-28 and 39-42, a cis-proline residue (Pro4), antiparallel strands consisting of residues 1-3, 5-7, and 10-13, and an aromatic cluster composed of Tyr7, Trp26, and Tyr33. The results of distance geometry and restrained molecular dynamics calculations indicate that the global fold of the PDC-109 b domain, a type II module related to those found in fibronectin, is somewhat different from that predicted by modeling the structure on the basis of homology between type II and kringle units. A shallow depression in the molecular surface which presents a solvent-exposed hydrophobic area--a potential ligand-binding site-is identified in the NMR-based models.
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PMID:Sequence-specific 1H NMR assignments and structural characterization of bovine seminal fluid protein PDC-109 domain b. 199 83

Fibronectin is a large-molecular-weight glycoprotein present on most cell surfaces, in extracellular fluids, and in plasma. Both cell-associated and soluble fibronectin are thought to have important roles in the inflammatory response and host defense and may contribute to the maintenance of microvascular integrity during septic episodes. Newborn infants have levels of fibronectin in plasma that are one-third to one-half those found in the healthy adult. In addition, neonates with respiratory distress syndrome, perinatal asphyxia, bacterial sepsis, intrauterine growth retardation, or postnatal malnutrition have a further depression in their plasma levels of fibronectin. The low plasma concentration of fibronectin in newborn infants may contribute to the hypofunction of the neonatal reticuloendothelial system and predispose to the development of sepsis. Rates of synthesis of plasma fibronectin are diminished in the neonate, and an inverse correlation between fibronectin half-life and gestational age exists. The role of fibronectin in treatment or prophylaxis of neonatal sepsis remains to be determined.
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PMID:Role of fibronectin in diseases of newborn infants and children. 219 69

There is evidence that undernutrition may contribute to the reduction in plasma fibronectin concentration and the depression of the reticuloendothelial (RE) system associated with severe sepsis. We have investigated the effects of fasting, surgical trauma and sepsis on plasma fibronectin concentrations and RE function. In experiment 1, plasma fibronectin was measured in rabbits (n = 14) before and 48 h after fasting. In experiment 2, sepsis was induced by devascularization of the appendix in animals on a normal diet (sepsis group, n = 7). A third group of animals underwent only a laparotomy (laparotomy only group, n = 7). Plasma fibronectin concentrations and the blood clearance and organ distribution of 99mtechnetium tin colloid (TTC) were measured 24 h after operation. Compared with pooled reference plasma, fasting in experiment 1 resulted in a reduction in mean(s.e.m.) plasma fibronectin concentration from 98(1.5) per cent to 86(3.7) per cent (T = 2, P less than 0.005). Mean(s.e.m.) plasma fibronectin concentration was raised in the sepsis group to 117(4.6) per cent, compared with 97(2.5) per cent in the laparotomy only group (U = 5, P less than 0.02), but there was no such increase in the fasting and sepsis group. There was a delay in the blood clearance and reduced hepatic uptake of TTC in both sepsis groups. The dissociation between fibronectin concentrations and RE function in animal models of sepsis casts doubt on the importance of fibronectin in RE function.
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PMID:Effect of acute starvation on plasma fibronectin response to sepsis. 231 81

Reconstituted, 100-microns-thick collagen sheets were crosslinked with either UV light, chromium, or cysteine for use as a burn covering. The sheets were also exposed to a "surface agent" (hydroxyproline, fibronectin, or soluble basement membrane matrix containing Type IV collagen) as a preliminary step in planned adherence studies. Since some chemicals render the collagen toxic, the modified sheets were tested for cytotoxicity using human keratinocytes and fibroblasts. Autoradiography and 3H-thymidine incorporation were used to quantitate the proliferative rate of these cells in vitro. There was a universal depression of keratinocyte incorporation of 3H-thymidine following a 1-day exposure to any collagen sheet when compared to cells not exposed to any collagen. This effect had lessened by 5 days' exposure to the collagen. Conversely, the fibroblasts the collagen. Conversely, the fibroblasts showed an enhancement in rate of incorporation after 1-day exposure, especially for cells exposed to collagen sheets cross-linked by UV light. This effect had also lessened by 5 days' exposure. Autoradiography showed few significant variations for any of the cells exposed for either time period. Chromium leaching was determined, with no values greater than 30% of the allowable maximum set by both the British and American Pharmacopeia.
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PMID:In vitro properties of crosslinked, reconstituted collagen sheets. 239 65

In the present study plasma fibronectin levels were determined in patients with hematopoietic malignancy, particularly leukemias, in an effort to clarify their clinical implications. Among leukemia patients, those with AML, ALL, ATL or CLL had various plasma fibronectin levels that were higher in some cases, while lower in others, as compared to normal control values. An elevation of the fibronectin level was noted often in APL, while lower fibronectin values were observed in many instances of CML. In these types of leukemia, acute exacerbation as well as supervention of infection tended to be associated with lower than normal levels of fibronectin. An especially marked depression of fibronectin occurred, when leukemia was complicated by sepsis or DIC, in which a good parallel was noted between the progress of disease and the fibronectin level. In lymphoproliferative diseases, the fibronectin value varied widely, but low fibronectin levels were frequently associated with intercurrent infection or an extreme deterioration of the general physical conditions.
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PMID:Variation of plasma fibronectin levels in leukemia patients. 248 45

Severe sepsis leads to depression of the reticuloendothelial (RE) system with delayed bloodstream clearance of particulate matter and bacteria. Fibronectin may be an important opsonin of the RE system and low fibronectin levels often accompany severe sepsis in man. We have investigated the effect of prolonged intra-abdominal sepsis on plasma fibronectin concentrations and RE function. Serial plasma fibronectin concentrations were determined in rabbits for 2 weeks after either the induction of sepsis (appendix abscess) (n = 6) or laparotomy only (n = 6). RE function was measured at 2 weeks by determining the clearance kinetics and organ distribution of low dose technetium tin colloid (TTC). There was an early transient depression in plasma fibronectin values followed by elevated concentrations at 48-72 h which were more marked in the sepsis group. There was a delay in the blood clearance with reduced hepatic and increased bone uptake of TTC. We conclude that depletion of opsonic fibronectin is unlikely to be an important factor contributing to the impairment of RE function associated with intra-abdominal sepsis and that RE depression in septic animals is due to intrinsic Kupffer cell dysfunction.
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PMID:Reticuloendothelial failure in chronic intra-abdominal sepsis: the role of opsonic fibronectin. 270 51


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