Complex Blood Research Articles

High serum C1q-adiponectin/total adiponectin ratio correlates with coronary artery disease in Japanese type 2 diabetics

ObjectiveAdiponectin, an adipocyte-derived protein, has potential antiatherogenic properties. Low levels of serum total-adiponectin (Total-APN) correlate with diabetes and coronary artery disease (CAD). Adiponectin and C1q form a protein complex in blood, and serum C1q-binding adiponectin (C1q-APN) can be measured. We investigated the correlation between C1q-APN and CAD in patients with type 2 diabetes mellitus (T2DM). MethodsThe study subjects were 107 outpatients with T2DM who underwent evaluation for CAD. Blood C1q, Total-APN, high-molecular weight-adiponectin (HMW-APN) and C1q-APN were measured by enzyme-linked immunosorbent assays. ResultsSerum levels of C1q-APN/Total-APN ratio were higher in patients diagnosed with CAD (10.47±0.59, mean±SEM, n=54) than those without CAD (8.88±0.60, n=53, p=0.0482). Age- and sex-adjusted logistic regression analysis identified serum C1q-APN/Total-APN ratio and hypertension as significant and independent determinants of CAD. A high serum C1q-APN/Total-APN ratio was associated with 3.965-fold increase in CAD prevalence. ConclusionsHigh serum C1q-APN/Total-APN ratio correlates with CAD in T2DM.

Goodpasture Antigen-binding Protein/Ceramide Transporter Binds to Human Serum Amyloid P-Component and Is Present in Brain Amyloid Plaques

Serum amyloid P component (SAP) is a non-fibrillar glycoprotein belonging to the pentraxin family of the innate immune system. SAP is present in plasma, basement membranes, and amyloid deposits. This study demonstrates, for the first time, that the Goodpasture antigen-binding protein (GPBP) binds to human SAP. GPBP is a nonconventional Ser/Thr kinase for basement membrane type IV collagen. Also GPBP is found in plasma and in the extracellular matrix. In the present study, we demonstrate that GPBP specifically binds SAP in its physiological conformations, pentamers and decamers. The START domain in GPBP is important for this interaction. SAP and GPBP form complexes in blood and partly colocalize in amyloid plaques from Alzheimer disease patients. These data suggest the existence of complexes of SAP and GPBP under physiological and pathological conditions. These complexes are important for understanding basement membrane, blood physiology, and plaque formation in Alzheimer disease.

99mTc(CO)3-tosufloxacin dithiocarbamate complexation and radiobiological evaluation in male Wister rat model

In the current investigation tosufloxacin (TSN) was derivatized to its dithiocarbamate (TSND) derivative and its radiolabeling with technetium-99m using [99mTc(CO)3(H2O)3]+ precursor. The labeled TSND (99mTc(CO)3-TSND) was radiochemically characterized in saline and serum and biologically its in vitro binding with Proteus mirabilis (P. mirabilis) and biodistribution in male Wister rats (MWR) artificially infected with live and heat killed P. mirabilis. Radiochemically a stable radio-tricarbonyl TSND complex was observed with a maximum stability of 98.15 ± 0.32% and it remained more than 90% up to 4 h after reconstitution. The stability decreased to 91.00 ± 0.30% from 98.15 ± 0.32% within 4 h. In serum at 37 °C the growth of some unwanted side product decreased the stability by 15.65% within 16 h. The complex showed saturated in vitro binding with P. mirabilis up to 78.50% (90 min). In MWR infected with live P. mirabilis the percent (%) uptake of the complex in blood, liver, spleen, stomach, intestines and kidneys were almost similar to the MWR infected with heat killed. However, the % accumulation of the complex in the infected muscle was six times higher than in the inflamed and normal muscle in MWR infected with live P. mirabilis. On the basis of immovability of the 99mTc(CO)3-TSND complex in normal saline, in vitro permanence in serum, saturated in vitro binding with P. mirabilis and six fold uptake in the infected muscle of the MWR infected with live P. mirabilis as compared to the normal muscle, the suitability of the 99mTc(CO)3-TSND complex is established as a promising infection radiotracer.

Multifocal choroidopathy syndrome: A case report

Multifocal choroidopathy syndromes are a group of rare disorders, which involve a primary pathologic process occurring at or near the level of the retinal pigment epithelium, with or without choriocapillaris involvement. The aetiology of multifocal choroidopathy syndrome is still unknown. We present a case of multifocal choroidopathy syndrome. A 54-year-old woman was referred to our department with blurred vision on both eyes, mild ocular pain, accompanied by metamorphopsia, floaters, scotomas and photopsia. The anterior segment examination showed small to medium size keratic precipitates, posterior synechiae, and iris atrophy. Mild to moderate aqueous inflammation with cells and flair was present in the anterior chamber. The fundus examination showed multiple small yellow--white spots, round-shaped changes located at the level of the retinal pigment epithelium and choriocapillaris. According to the fluorescein angiography the active lesions exhibited blockage of the early choroidal fluorescence followed by late staining The old inactive lesions corresponded to the retinal pigment epithelium windows defects. The laboratory examination showed high level of blood glucose, C reactive protein, cholesterol HDL, LDL, triglycerides. According to the immunological examination the C3 component of complement was lower (0.630), as well as the C4 component of complement (0.158), and the immunological complex in blood was elevated (171). ELIZA test on viral infection showed Citomegalo viruses IgG positive, Herpes Simpler Virus lgG positive, Varichela Zoster Virus lgG positive. The results of human leucocyte antigen typization were humuan leucocyte antigen A1:A2, human leucocyte antigen A2:A24(9), human leucocyte antigen B1:B44(12), human leucocyte antigen B2:B60(40), human leucocte antigen C1:Cw3, human leucocyte antigen C2:Cw5. The radiological examination of lungs, the Mantoux test, Treponemnal serology, Toxocara and Toxoplasma serology, magnetic resonance of endocranium and orbit were also performed. The multiple viral infection, which was detected in our patient with immunological abnormalities pointed to an underlying autoimmune mechanisnm, possibly triggered by an infectious agent, a virus.

Reconstitution of Recombinant Factor VIII In fVIII-/- mice Restores Von Willebrand Factor Homeostasis

AbstractAbstract 2213Coagulation factor VIII (FVIII) binds von Willebrand factor (VWF) at the D′D3 domain with high affinity. FVIII almost always circulates as a FVIII-VWF complex in blood. Our recent study has demonstrated that FVIII accelerates proteolytic cleavage of VWF by ADAMTS13 under mechanically induced fluid shear stress (Cao et al, PNAS, 2008). In this study, we sought to determine: 1) the domain of FVIII required for the enhancing effect on VWF proteolysis by ADAMTS13 under these conditions; 2) the physiological relevance of this enhancing effect on plasma VWF homeostasis in a murine model. First, we employed the novel vortex-based shear assay developed in the laboratory to assess the rate enhancing effect of various recombinant FVIII variants on VWF proteolysis by ADAMTS13. In these experiments, purified plasma VWF (150 nM) was incubated for 10 min with recombinant ADAMTS13 (50 nM) in the presence of various concentrations of recombinant FVIII variants (0-20 nM) in a total volume of 20 μl under constant fluid shear generated with a bench top mini-vortexer. This maneuver appears to produce ∼75 dyn/cm2 of fluid shear stress. Proteolytic cleavage product (∼350 kDa, the dimer of two C-terminal fragments linked by a disulfide bond) was then determined by 5% SDS-polyacrylamide gel electrophoresis and Western blotting. We showed that addition of a recombinant light chain of FVIII (FVIII-LC) increased the formation of proteolytic cleavage product as a function of increasing FVIII-LC concentrations. This rate enhancing effect was similar to that of full-length recombinant FVIII and B-domainless FVIII (FVIII-SQ). However, addition of a heavy chain of FVIII (FVIII-HC) or a light chain variant lacking the acidic (a3) region (FVIII-Δa3LC) did not increase the formation of cleavage product under the same conditions. These results suggest that FVIII-light chain is sufficient for accelerating VWF proteolysis by ADAMTS13 under physiological conditions. The rate enhancing effect of FVIII-LC depends on its high affinity interaction with VWF. Second, we determined plasma VWF antigen and multimer distribution in fVIII-/- and fVIII+/+ (WT) mice with same genetic background (C57BL/6) prior to and after reconstitution with recombinant FVIII-SQ and variants via a hydrodynamic approach. Plasma VWF antigen was determined by a sandwich ELISA assay and plasma VWF multimers were determined by 1% agarose gel electrophoresis and Western blotting. We showed that plasma VWF antigen levels in the fVIII-/- mice (n=18) were increased by ∼2.0 fold as compared with those in the WT mice (n=14). No difference in the ratio of ultra large (UL)-VWF to dimer was observed between the fVIII-/- mice and the WT mice (p>0.05). These data suggest that lack of FVIII may impair plasma VWF homeostasis. To assess whether plasma FVIII affects VWF proteolysis in vivo, plasma VWF multimer distribution was determined by agarose (1%) gel electrophoresis and Western blotting in the fVIII-/- mice 48 hours after injection of a series of endotoxin-free expression plasmids encoding various FVIII variants/fragments (i.e. plasmids diluted in 2 ml normal saline and injected into tail vein within 5 seconds). We showed that the ratio of the UL-VWF multimers to the dimer in plasma of fVIII-/- mice receiving normal saline alone was 1.70 ± 0.59 (means ± SD) (n=10). However, the ratios in plasma of fVIII-/- mice receiving plasmids encoding canine FVIII-SQ, human FVIII-SQ, human FVIII-HC+LC, and FVIII-LC were 0.44 ± 0.37 (n=20), 0.88 ± 0.18 (n=9), 0.40 ± 0.20 (n=5), and 0.97 ± 0.29 (n=9), respectively. These ratios were dramatically reduced compared with that in fVIII-/- mice receiving normal saline alone (p values<0.05∼0.001). Our hydrodynamic injection approach resulted in plasma levels of FVIII-SQ, FVIII-LC+HC and FVIII-LC between 150% and 200% of the WT. In contrast, a hydrodynamic injection of plasmid encoding human FVIII-HC or FVIII-Δa3LC did not prevent the accumulation of plasma UL-VWF multimers in fVIII-/- mice. We therefore conclude that FVIII, through the high affinity binding interaction between its light chain and D′D3 domain of VWF, may play a critical role in maintaining VWF homeostasis under (patho) physiological conditions. Disclosures:No relevant conflicts of interest to declare.

ProMMP-2: TIMP-1 Complexes Identified in Plasma of Healthy Individuals

Activation of MMPs in tissues is an important component of tissue injury. Based on earlier reports that (latent) proMMP-2 is incapable of forming a complex with TIMP-1, we reasoned that the identification of MMP-2:TIMP-1 complexes in blood might serve as a surrogate marker (“smoking gun”) of MMP-2 activation in tissues. Using specific antibodies, we developed a sensitive and specific assay to detect MMP-2:TIMP-1 complexes. We were perplexed to find that approximate 40% of plasma specimens from healthy individuals had detectable levels of the MMP-2:TIMP-1 complexes. Employing recombinant TIMP-1 bound Sepharose beads and Western blots, we demonstrated binding between recombinant proMMP-2 and TIMP-1 proteins. Recombinant MMP-2 lacking the catalytic domain also bound to TIMP-1 coated beads. These data are consistent with TIMP-1 binding to the hemopexin or hinge domain of proMMP-2. The explanation for the presence of plasma proMMP-2:TIMP-1 complexes in selected healthy individuals remains to be determined. In contrast to our immunoassay and bead-binding experiments, proMMP-2 failed to bind to immobilized TIMP-1 employing surface plasmon resonance technology. Additional studies are needed to clarify these contrasting results.

Cationic lipid/DNA complexes induce TNF-α secretion in splenic macrophages

Cationic lipids are widely used as vectors to deliver DNA into mammalian cells in vitro and in vivo. However, cationic lipid/DNA lipoplexes induce an inflammatory response, characterized by pro-inflammatory cytokine secretion, which severely limits their use. The main goal of this work is to identify the organs and the cell type involved in TNF-α secretion after lipoplex injection. We determined the kinetics of distribution of the cationic lipid/DNA complex in blood, lung, liver and spleen and quantified the TNF-α amount in organ homogenates and in the serum at different points of times. Increase in TNF-α production was only observed in the spleen and no significant increase of TNF-α production could be observed in the other organs. Fractionation of spleen cells revealed that macrophages were mainly responsible for TNF-α secretion. This observation was verified in vivo by using macrophage-removing agents. In conclusion, we show here that the TNF-α secreted in the serum after intravenous injection of lipoplexes comes mainly from the splenic macrophages.

Inhaled Nitric Oxide Attenuates Reperfusion Inflammatory Responses in Humans

Reduced bioavailability of endothelium-derived nitric oxide associated with reperfusion could potentially exacerbate the inflammatory response during reperfusion. Evidence suggests the pharmacologic effects of inhaled nitric oxide may extend beyond the pulmonary vasculature, and this is attributed to nitric oxide-derived complexes in blood that ultimately orchestrate antiinflammatory effects. In this study, the authors evaluated the potential for inhaled nitric oxide (80 ppm) to attenuate inflammation instigated by ischemia-reperfusion in a human model using patients undergoing knee surgery where a tourniquet was used to produce a bloodless surgical field. Inhaled nitric oxide (80 ppm) was administered before tourniquet application and continued throughout reperfusion until the completion of surgery. Venous blood samples were collected before and after reperfusion, for the measurements of nitrate and nitrite, CD11b/CD18, soluble P-selectin, and lipid hydroperoxide. Muscle biopsies were obtained from the quadriceps muscle before skin closure and analyzed for myeloperoxide, conjugated dienes, and nuclear factor-kappaB translocation. Administration of inhaled nitric oxide (80 ppm) significantly attenuated the inflammatory response characterized by reduced expression of CD11b/CD18, P-selectin, and nuclear factor kappaB compared with the control group. This was accompanied by increased plasma levels of nitrate and nitrite and reduced oxidative stress. Administration of inhaled nitric oxide at 80 ppm significantly reduces inflammation in lower extremity ischemia-reperfusion in humans. This observation supports the concept that during diseases characterized by dysfunction in nitric oxide metabolism, inhaled nitric oxide may be an effective therapy to replenish systemic nitric oxide, thus retarding inflammatory-mediated injury.

Effect of Drotrecogin alfa (activated) on platelet receptor expression in vitro

Thrombocytopenia is a common problem in critically ill patients, which is associated with increased mortality. Recently, Drotrecogin alfa (activated) (recombinant human activated protein C (APC)) was shown to reduce mortality in patients with severe sepsis. Only minimal effect of APC on coagulation markers was demonstrated. Nevertheless, low platelet count was identified as a risk factor for bleeding with use of this drug. We conducted this study to evaluate possible influence of APC on in vitro expression of platelet receptors at therapeutic and supra-therapeutic concentrations. Blood samples of volunteers and patients with severe sepsis were adjusted with APC to final concentrations of 0.045 µg mL−1 APC (APC-45, therapeutic dose) and 0.225 µg mL−1 APC (APC-225, five-fold therapeutic dose), respectively. The activation of platelets was mediated by two different agonists. APC had no significant influence on platelet activation, with or without stimulation at both concentrations. In group APC-225, CD62P showed a non-significant decrease. This in vitro study demonstrates that therapeutic plasma concentrations of Drotrecogin alfa (activated) have neither influence on expression of platelet activation markers nor on platelet-granulocyte complexes in blood of volunteers and patients with severe sepsis. Thus, a direct drug-platelet interaction seems unlikely.

Association between nitric oxide synthesis and vaccination-acquired resistance to murine hepatitis virus by spf mice

Murine hepatitis virus strain 3 (MHV-3) produces a strain-dependent pattern of disease, with A/J and BALB/c mice being considered models of resistance and susceptibility, respectively. A role for nitric oxide in controlling infection remains debatable; thus, we monitored nitric oxide levels in blood and liver of immunized and nonimmunized spf mice during infection by electron paramagnetic resonance. In parallel, liver histology, virus titers, and plasma alanine aminotransferase (ALT) activity were monitored. Nitric oxide synthesis was barely detectable in BALB/c mice, which showed a progressive increase in virus titers and ALT activity. These animals died with a shorter survival time than A/J mice. The latter displayed a less severe infection and presented detectable levels of nitric oxide as nitrosyl complexes in blood and liver at 72 hpi. Immunized mice from both strains became resistant to MHV-3 and showed comparable levels of nitrosyl complexes in blood and liver at an early time (24 hpi). Thereafter, nitric oxide levels decreased but remained detectable in blood up to 96 hpi. Immunized mice were capable of clearing the virus and clearance was inhibited by administration of a nitric oxide synthase inhibitor. Overall, the results support a role for nitric oxide in controlling MHV-3 infection.

Phenotypic characteristics of immunocompetent cells in blood of patients with pneumonia and new effective method of immunotherapy

Rationale Prevention of secondary immunodeficiency in pneumonia is a topical problem in modern medicine. Methods We studied bactericidal phagocyte activity, functional lymphocyte activity in blast-transformation reaction with PHA; CD3, CD4, CD8, CD16, CD20, IgA, IgM, IgG, circulating immune complexes in blood of patients with mild, moderate and severe pneumonia. Results Phenotypic characteristics of peripheral blood immunocompetent cells is given. Complex evaluation of background disturbances of the immune system in patients with pneumonia depending on the severity of the pathologic process was carried out. An decrease in the number of CD3 +, CD4 +, CD16 +, IgA level, functional lymphocyte activity, and an increase in the level of circulating immune complexes and CD20 + (p<0.05) were revealed. Direct correlation between the level of immune disturbances and clinical indices characterizing the severity of the disease was also revealed. The method of paravasal lymphotropic immunotherapy along with several immunomodulators possessing differently targeted action was elaborated and applied to treat pneumonia. Conclusion The application of lymphotropic immunotherapy promotes restoration of quantitative subsets and functional activity of immune regulatory cells, it decreases the period of arresting of X-ray symptoms, increases the efficacy of the treatment, and prevents the development of complications.

Artificial Blood: An Update on Current Red Cell and Platelet Substitutes

To begin, it should be clarified that the term “artificial blood” is really a misnomer. The complexity of blood is far too great to allow for absolute duplication in a laboratory. Instead, researchers have focused their efforts on creating artificial substitutes for 2 important functions of blood: oxygen transport by red blood cells and hemostasis by platelets. A number of driving forces have led to the development of artificial blood substitutes (1). One major force is the military, which requires a large volume of blood products that can be easily stored and readily shipped to the site of casualties. Another force is HIV; with the advent of this virus, the medical community and the public suddenly became aware of the significance of transfusion-transmitted diseases and became concerned about the safety of the national blood supply. A third force is the growing shortage of blood donors. Approximately 60% of the population is eligible to donate blood, but fewer than 5% are regular blood donors (2). A unit of blood is transfused every 3 seconds in the USA, and the number of units transfused each year has been increasing at twice the rate of donor collection. Artificial blood products offer many important benefits (3). First, they are readily available and have a long shelf life, allowing them to be stocked in emergency rooms and ambulances and easily shipped to areas of need. Second, they can undergo filtration and pasteurization processes to virtually eliminate microbial contamination. No product can claim to be 100% risk-free for infectious agents, but these substitutes have a greatly increased level of safety. Third, they do not require blood typing, so they can be infused immediately and for all patient blood types. Fourth, they do not appear to cause immunosuppression in the recipient. In the sections that follow, the different types of red cell and platelet substitutes currently under development will be briefly reviewed.

Circulating immune complexes in blood of patients with positive family history of schizophrenia.

Circulating immune complexes in blood of patients with positive family history of schizophrenia.

Low Density Lipoprotein as a Carrier of Cytostatics in Cancer Chemotherapy: Study of Stability of Drug-carrier Complexes in Blood

Several solid tumour and leukemia cell types have a higher low density lipoprotein (LDL) uptake than the corresponding normal cells. We are investigating the possibilities to use LDL as a drug carrier to increase the selectivity of antineoplastic drugs in cancer chemotherapy. We have developed a method to incorporate lipophilic cytotoxic agents without interfering with the in vitro and in vivo properties of LDL. In this study, we examined the stability of some drug-LDL complexes in blood and plasma as this is an important prerequisite to achieve a selective therapy.The in vitro dialysis of N-trifluoroacetyl-adriamycin-14-valerat-LDL (AD-32-LDL) against plasma revealed a slow dissociation of the complex. The same method showed a fast and total leakage of paclitaxel from paclitaxel—LDL into the plasma chamber. The dissociation of paclitaxel was confirmed by an autoradiographic study of the distribution of paclitaxel—LDL in tumour-bearing mice. In patients with leukemia the rapid plasma dissociation of AD-32 from LDL illustrated a much higher in vivo instability of this complex. With this method, cholesteryl-linoleate only could be incorporated into LDL in a stable manner as shown by dialysis and autoradiography results. The incorporation of cytotoxic drug derivatives, containing lipophilic anchors, is now under study in order to obtain LDL complexes with better plasma stability.

Determination of the Complex between Urokinase and Its Type-1 Inhibitor in Plasma from Healthy Donors and Breast Cancer Patients

The complex between urokinase (uPA) and its type-1 inhibitor (PAI-1) is formed exclusively from the active forms of these components; thus, the complex concentration in a biological sample may reflect the ongoing degree of plasminogen activation. Our aim was to establish an ELISA for specific quantification of the uPA:PAI-1 complex in plasma of healthy donors and breast cancer patients. A kinetic sandwich format immunoassay was developed, validated, and applied to plasma from 19 advanced-stage breast cancer patients, 39 age-matched healthy women, and 31 men. The assay detection limit was <2 ng/L, and the detection of complex in plasma was validated using immunoabsorption, competition, and recovery tests. Eighteen cancer patients had a measurable complex concentration (median, 68 ng/L; range, <16 to 8700 ng/L), whereas for healthy females and males the median signal values were below the detection limit (median, <16 ng/L; range, <16 to 200 ng/L; P <0.0001). For patient plasma, a comparison with total uPA and PAI-1 showed that the complex represented a variable, minor fraction of the uPA and PAI-1 concentrations of each sample. The reported ELISA enables detection of the uPA:PAI-1 complex in blood and, therefore, the evaluation of the complex as a prognostic marker in cancer.

Cell-generated nitric oxide inactivates rat hepatocyte mitochondria in vitro but reacts with hemoglobin in vivo

BACKGROUND & AIMS: Nitric oxide forms inactive iron-nitrosyl complexes within hepatic mitochondria in vitro. However, when formed in vivo, NO might react instead with hemoglobin. The aim of this study was to compare the effects of cell-derived NO on rat hepatocyte mitochondria in vitro and in vivo. METHODS: First, hepatocytes were cultured in vitro for 24 hours under a porous membrane supporting macrophages that were stimulated by endotoxin. Second, hepatic macrophage hyperplasia was induced in vivo by preadministration of killed Corynebacterium parvum; 7 days later, rats received endotoxin and were killed after 6 hours. Third, mitochondria were exposed to sodium nitroprusside in vitro, washed, mixed with blood, and recovered. RESULTS: Iron-nitrosyl complexes and hepatocyte mitochondrial dysfunction were observed in the in vitro model and prevented by an NO synthase inhibitor. In the in vivo model, however, despite a 130-fold increase in plasma nitrate levels and formation of hemoglobin-NO complexes in blood, no iron- nitrosyl complex was detected in hepatic mitochondria, and hepatic mitochondrial function was not impaired. In the third model, mitochondria lost preformed iron-nitrosyl complexes when exposed to blood. CONCLUSIONS: Although NO reacts with hepatocyte mitochondria in vitro, in vivo it reacts with sinusoidal hemoglobin without detectable impairment of hepatic mitochondrial function. (Gastroenterology 1996 Jan;110(1):210-20)

Immunoglobulin and complement complexes in blood following infection with human immunodeficiency virus type 1.

Freely soluble and complexed plasma immunoglobulin A (IgA), IgG, IgM, C1q, C3, and factor B in 36 human immunodeficiency virus type I (HIV-1)-seronegative controls, 69 asymptomatic HIV+ subjects, and 117 individuals with symptomatic HIV-associated disease were characterized. Levels of free and complexed IgG and IgA, and to a lesser extent free C1q and complexed IgM, increased with HIV-1 infection. In stark contrast, both HIV+ groups showed three- to sixfold declines in complexed C3, C1q, and factor B levels. The asymptomatic HIV+ population showed declines in levels of C3-bound IgA, IgG2, and IgG4 complexes. The asymptomatic group showed reductions in C3-complexed IgM, IgA, IgG2, and IgG4 levels. HIV infection is associated with complement-deficient immune complexes.

Stability of cisplatin and its monohydrated complex in blood, plasma and ultrafiltrate — implications for quantitative analysis

The stability of cisplatin and its monohydrated complex has been studied in blood, plasma and plasma ultrafiltrate at 37°C (pH 7.4). Intact cisplatin and the monohydrated complex were determined by liquid chromatography with post-column derivatization. The half lives for cisplatin and the monohydrated complex were 1.43 ± 0.03 h (SEM) and 0.36 ± 0.03 h (SEM), respectively, in blood and 0.88 ± 0.05 h (SEM) and 0.26 ± 0.02 h (SEM), respectively, in plasma. The compounds were unstable at −25°C ( t 1 2 for cisplatin was 52 ± 5 h (SEM) and for the monohydrated compound 26 ± 2 h (SEM)), but at −70°C both compounds were stable for at least 3 weeks. The monohydrated complex was found to be formed to a small extent when cisplatin was added to plasma (37°C, pH 7.4). A sampling procedure using centripetal ultrafiltration of whole blood was evaluated and found applicable if the samples were stored at 0°C and ultracentrifuged within 1 h.

IgM antibodies directed to HIV: the neglected issue?

AIDS Research and Human RetrovirusesVol. 10, No. 5 IgM Antibodies Directed to HIV: The Neglected Issue?PHILIPPE VAN de PERRE, CLAUDE DESGRANGES, and ARSÈNE BURNYPHILIPPE VAN de PERRESearch for more papers by this author, CLAUDE DESGRANGESSearch for more papers by this author, and ARSÈNE BURNYSearch for more papers by this authorPublished Online:16 Mar 2009https://doi.org/10.1089/aid.1994.10.517AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited ByIncreased Serpin A5 levels in the cervicovaginal fluid of HIV-1 exposed seronegatives suggest that a subtle balance between serine proteases and their inhibitors may determine susceptibility to HIV-1 infectionVirology, Vol. 458-459Dissecting the antibody constant region protective immune parameters in HIV infectionFuture Virology, Vol. 9, No. 4Characterization of a Novel Human Anti-HIV-1 gp41 IgM Monoclonal Antibody Designated Clone 37 Chuanhai Cao, Yun Bai, Mary Jolene Holloway, Rebecca L. Edgeworth, Eugene A. Jackson, Joseph Cotropia, and Kenneth E. Ugen10 December 2004 | DNA and Cell Biology, Vol. 23, No. 12Intracellular Neutralization of HIV Transcytosis across Tight Epithelial Barriers by Anti-HIV Envelope Protein dIgA or IgMImmunity, Vol. 9, No. 2Humoral immune response to the capsid components of recombinant adenoviruses: Routes of immunization modulate virus-induced Ig subclass shiftsEuropean Journal of Immunology, Vol. 27, No. 3Immunoglobulin and complement complexes in blood following infection with human immunodeficiency virus type 1Clinical Diagnostic Laboratory Immunology, Vol. 3, No. 1 Volume 10Issue 5May 1994 To cite this article:PHILIPPE VAN de PERRE, CLAUDE DESGRANGES, and ARSÈNE BURNY.IgM Antibodies Directed to HIV: The Neglected Issue?.AIDS Research and Human Retroviruses.May 1994.517-520.http://doi.org/10.1089/aid.1994.10.517Published in Volume: 10 Issue 5: March 16, 2009PDF download

Diphasic Increase in Thrombin-Antithrombin III Complex in Blood from the Internal Jugular Vein Following Severe Head Injury

Diphasic Increase in Thrombin-Antithrombin III Complex in Blood from the Internal Jugular Vein Following Severe Head Injury