Cold thermopeaking-induced drift of nase Chondrostoma nasus larvae.

Research on how intermittent water releases from hydropower plants affect the early life stages of fish has advanced in the last years, focusing not only on the direct impacts of rapid flow changes (hydropeaking), but also on the short-term fluctuations in water temperature (thermopeaking). Flow and thermal fluctuations caused by hydropeaking may affect fish movement patterns and migration at critical stages of a species' life cycle, e.g., by inducing passive downstream drift. Using two experimental outdoor channels, we investigated how nase (Chondrostoma nasus, Cypriniformes) larvae respond to a rapid drop in water temperature during hydropeaking (simulating a cold thermopeaking event), reaching on average 5.5 °C under peak flow (maximum discharge) conditions, in comparison with a hydropeaking treatment with a constant water temperature regime. Responses of fish larvae were analyzed during acclimation, up-ramping (increase in discharge), peak flow and down-ramping (decrease in discharge) phases. Fish drift increased during peak flow in the cold thermopeaking treatment compared to hydropeaking. Higher drift rates were also negatively associated with pronounced water temperature drops during peak flow conditions. In addition, the starting temperature of the experiment influenced drift during up-ramping. Overall, the results suggest that cold thermopeaking may increase drift in the early life stages of cypriniform fish compared with hydropeaking with stable water temperature. Hence, monitoring and active water temperature adjustments following hydropower releases should be adopted as strategies to mitigate power plant-related impacts on aquatic organisms. Supplementary Information: The online version contains supplementary material available at 10.1007/s00027-023-00955-x.

Clean carbon nanotubes coupled to superconducting impedance-matching circuits.

Coupling carbon nanotube devices to microwave circuits offers a significant increase in bandwidth (BW) and signal-to-noise ratio. These facilitate fast non-invasive readouts important for quantum information processing, shot noise and correlation measurements. However, creation of a device that unites a low-disorder nanotube with a low-loss microwave resonator has so far remained a challenge, due to fabrication incompatibility of one with the other. Employing a mechanical transfer method, we successfully couple a nanotube to a gigahertz superconducting matching circuit and thereby retain pristine transport characteristics such as the control over formation of, and coupling strengths between, the quantum dots. Resonance response to changes in conductance and susceptance further enables quantitative parameter extraction. The achieved near matching is a step forward promising high-BW noise correlation measurements on high impedance devices such as quantum dot circuits.

Safety and immunogenicity of a V3 loop synthetic peptide conjugated to purified protein derivative in HIV-seronegative volunteers.

OBJECTIVES: To develop a peptide-based model for a preventive vaccine for HIV-1 infection. DESIGN: Phase I trial in HIV-1-seronegative volunteers. PARTICIPANTS: Adult healthy subjects HIV-1-antibody-seronegative in an enzyme-linked immunosorbent assay, screened for tuberculin [purified protein derivative (PPD)] reactivity with 2 tuberculin units PPD-administered intradermally. INTERVENTIONS: Submicrogram doses of a PPD conjugate with a peptide of the primary neutralizing domain (PND) of HIV-1MN (PPD-MN-PND) were administered intradermally to tuberculin skin-test-positive and -negative volunteers. RESULTS: Antibodies to the MN-PND were measured after two immunizations in 10 out of 11 PPD skin-test-positive volunteers. After the fourth immunization high-affinity antibodies were detected, which persisted for over 1 year. High titers of MN-PND-specific immunoglobulin (Ig) G and IgA were detected in the serum and saliva of all volunteers tested. Serum antibodies were cross-reactive with PND peptide from some other HIV-1 strains but neutralized only the HIV-1MN prototype. Human leukocyte antigen (HLA)-B7-restricted MN-PND-specific cytotoxic T lymphocytes (CTL) were also detected. CONCLUSIONS: The PPD-MN-PND vaccine at submicrogram doses is safe and immunogenic in PPD skin-test-positive healthy adult volunteers. Long lasting humoral immune responses in the serum and saliva were possibly accompanied by HLA-B7-restricted CTL responses. This is a vaccine prototype that can be rapidly and inexpensively modified to include other peptide epitopes. It is especially suitable for use in a worldwide multibillion Bacillus Calmette-Guérin (BCG)-primed or tuberculosis-exposed population at risk for HIV-1 infection.

Plasmodium falciparum-infected erythrocyte receptor(s) for CD36 and thrombospondin are restricted to knobs on the erythrocyte surface.

Adherence of Plasmodium falciparum-infected RBCs (PRBC) to endothelial cells causes PRBC sequestration in cerebral microvessels and is considered to be a major contributor to the pathogenesis of cerebral malaria. Both CD36 and thrombospondin (TSP) are glycoproteins that mediate PRBC adherence to endothelial cells in vitro. Because they are both expressed on the surface of endothelial cells, they probably contribute to PRBC sequestration and vascular occlusion in vivo. By applying affinity labeling of receptor binding sites with purified ligands, we showed for the first time that both CD36 and TSP can bind independently to the PRBC surface and that the PRBC receptor(s) for CD36 and TSP are localized specifically to the electron-dense knob protrusions of the PRBC surface. These findings may help in efforts to develop a malaria vaccine to prevent cerebral malaria.

A primate model for human cerebral malaria: Plasmodium coatneyi-infected rhesus monkeys.

A major factor in the pathogenesis of human cerebral malaria is blockage of cerebral microvessels by the sequestration of parasitized human red blood cells (PRBC). In vitro studies indicate that sequestration of PRBC in the microvessels is mediated by the attachment of knobs on PRBC to receptors on the endothelial cell surface such as CD36, thrombospondin (TSP), and intercellular adhesion molecule-1 (ICAM-1). However, it is difficult to test this theory in vivo because fresh human brain tissues from cerebral malarial autopsy cases are not easy to obtain. Although several animal models for human cerebral malaria have been proposed, none have shown pathologic findings that are similar to those seen in humans. In order to develop an animal model for human cerebral malaria, we studied brains of rhesus monkeys infected with the primate malaria parasite, Plasmodium coatneyi. Our study demonstrated PRBC sequestration and cytoadherence of knobs on PRBC to endothelial cells in the cerebral microvessels of these monkeys. Cerebral microvessels with sequestered PRBC were shown by immunohistochemical analysis to possess CD36, TSP, and ICAM-1. These proteins were not evident in the cerebral microvessels of uninfected control monkeys. Thus, our study indicates, for the first time, that rhesus monkeys infected with P. coatneyi can be used as a primate model to study human cerebral malaria. By using this animal model, we may be able to evaluate strategies for the development of vaccines to prevent human cerebral malaria.

Surface molecules on Plasmodium falciparum-infected erythrocytes involved in adherence.

The identity of cell surface receptor molecules on Plasmodium falciparum-infected erythrocytes is of great interest since the functional sites involved in attachment to endothelial cells may be structurally conserved in wild isolates. Such conserved sites may represent suitable antigenic targets for a vaccine-induced immune response that would block or reverse infected cell sequestration in vivo. Identification of the infected cell receptor sites may also lead to novel methods for treatment of acute cerebral malaria. We review the likely roles, either direct or indirect, for the participation of knob protrusions, malarial proteins expressed at the cell surface, and modified host membrane proteins in the specific receptor properties acquired by infected erythrocytes.

An improved microassay for Plasmodium falciparum cytoadherence using stable transformants of Chinese hamster ovary cells expressing CD36 or intercellular adhesion molecule-1.

Stable transformants of Chinese hamster ovary (CHO) cell lines expressing high levels of human CD36 or intercellular adhesion molecule-1 (ICAM-1) have been produced as target cells for cytoadherence of Plasmodium falciparum-infected erythrocytes. An improved adherence microassay has been designed using small sample volumes and allowing convenient and reliable measurements on a large number of samples. The assay can be used both with purified proteins spotted on plastic and with the stably transformed CHO cell lines. The same assay plate can be evaluated either microscopically or by scintillation counting after use of 3H-hypoxanthine-labeled parasites. Using the microassay, functional expression of the transfected receptor molecules on CHO-CD36 and CHO-ICAM was confirmed using parasites with different cytoadherence phenotypes and cytoadherence inhibition experiments with a panel of anti-CD36 antibodies. The use of isolates from The Gambia confirmed the applicability of these assays for laboratory studies of these isolates.

Safety and immunogenicity of a Haemophilus influenzae type B polysaccharide-tetanus toxoid conjugate vaccine combined with diphtheria, tetanus and pertussis vaccines in Thai infants.

A randomized, open, multicenter trial was conducted to determine the safety and immunogenicity of a Haemophilus influenzae type b polysaccharide-tetanus toxoid (PRP-T) conjugate vaccine combined with tetanus, diphtheria and pertussis (DTP) vaccine in 271 Thai infants born to mothers immunized against tetanus during pregnancy. Infants were immunized at approximately 2, 4 and 6 months of age with these vaccines. To determine if elevated levels of anti-tetanus toxin antibodies suppressed the anti-PRP antibody response, a second group of infants were immunized with PRP complexed with outer membrane proteins of Neisseria meningitidis (Pedvax HIB) in one limb at 2 and 4 months of age and DTP vaccine in the other limb at 2, 4 and 6 months of age. A third group of infants received only DTP vaccine at 2, 4 and 6 months of age. The occurrence of both local and systemic adverse reactions were comparable in all 3 groups. The geometric mean anti-tetanus antibody titer was > 1 IU/ml at baseline. Approximately 1 month after the administration of the third dose of vaccine, 98.5%, 99.3% and 9.7% of the children immunized with DTP+Pedvax HIB, DTP-PRP-T or DTP possessed > or = 0.15 microgram of anti-PRP antibody per ml. No child in the DTP group achieved > or = 1 microgram/ml while 74.2% and 89.3% did so after immunization with DTP+Pedvax HIB, or DTP-PRP-T, respectively (p < 0.05). Immune responses to diphtheria, tetanus and pertussis antigens were similar in all vaccine groups. These results demonstrate that elevated tetanus antibody titers do not diminish the anti-PRP antibody response following immunization with a PRP-T conjugate combined with DTP vaccine.

Purification and characterization of 6-pyruvoyl tetrahydropterin synthase from salmon liver.

Salmon liver was chosen for the isolation of 6-pyruvoyl tetrahydropterin synthase, one of the enzymes involved in tetrahydrobiopterin biosynthesis. A 9500-fold purification was obtained and the purified enzyme showed two single bands of 16 and 17 kDa on SDS/PAGE. The native enzyme (68 kDa) consists of four subunits and needs free thiol groups for enzymatic activity as was shown by reacting the enzyme with the fluorescent thiol reagent N-(7-dimethylamino-4-methylcoumarinyl)-maleimide. The enzyme is heat-stable up to 80 degrees C, has an isoelectric point of 6.0-6.3, and a pH optimum at 7.5. The enzyme is Mg2+ -dependent and has a Michaelis constant for its substrate dihydroneopterin triphosphate of 2.2 microM. The turnover number of the purified salmon liver enzyme is about 50 times as high as that of the enzyme purified from human liver. It does not bind to the lectin concanavalin A, indicating that it is free of mannose and glucose residues. Polyclonal antibodies raised against the purified enzyme in Balb/c mice were able to immunoprecipitate enzyme activity. The same polyclonal serum was not able to immunoprecipitate enzyme activity of human liver 6-pyruvoyl tetrahydropterin synthase, nor was any cross-reaction in ELISA tests seen.

[Gardner's syndrome (author's transl)]. / Das Gardner-Syndrom. Definition, Ausdrucksformen, Frühdiagnostik und Therapie.

An exact history was taken and clinical, endoscopic and histologic studies were performed in 14 family members of a case of Gardner's syndrome with triple symptomatology documented with biopsy and autopsy findings. Among the symptom-free probands five cases of colonic polyposis and three cases with gastric polyps were found. All polyps were histologically adenomatous. Dysplasias grade I and II were found repeatedly, in one 16-year-old adolescent there was already severe dysplasia within the gastric mucosal polyps. A warning is given against sub-classification of familial colonic polyposis and other syndromes within the definition of Gardner's syndrome. In future during diagnostic investigations for cases of Gardner's syndrome isolated gastric polyposis should be sought for as well as monosymptomatic colonic polyposis. Diagnostic procedures and treatment should depend on endoscopic and histological findings. Regular follow-up with endoscopic biopsies are to be encouraged not only in the diseased cases but also in all family members available.

Peptide immunization in humans: a combined CD8+/CD4+ T cell-targeted vaccine restimulates the memory CD4 T cell response but fails to induce cytotoxic T lymphocytes (CTL).

Immunization with short antigenic peptides represents a potential strategy to induce peptide-specific CTL in vivo. In this study, a synthetic vaccine consisting of an HIV-derived, HLA-A2.1-binding CTL epitope and a tetanus toxin-derived T helper epitope was evaluated for its capacity to induce peptide-specific CTL in humans. Thirteen volunteers were immunized and boosted twice with 100 micrograms of the CTL epitope plus 300 micrograms of the T helper peptide (p30). Peripheral blood mononuclear cells (PBMC) were regularly analysed for cytotoxic and proliferative responses before, between and after the immunizations, and the serum was tested for anti-peptide antibodies. No unequivocal induction of HIV peptide-specific CTL in any of the volunteers was observed. However, a wide pattern of mild and transient side reactions was observed, ranging from local redness at the injection site to generalized exanthema, myalgias, arthralgias and fever. The side-effects were related to the T helper epitope, as they were similar to the side-effects experienced after tetanus immunization, correlated to the magnitude of the p30-specific in vitro proliferative response, and occurred only if p30 was co-injected. No antibodies against the HIV-derived peptides nor against p30 were detectable in the serum after repeated immunizations. The data suggest that the CTL peptide, at the concentration used in this study, failed to induce a cytotoxic immune response in vivo, although the T helper peptide seems to be capable of restimulating the specific memory T cells.

Plasmodium falciparum-infected erythrocytes do not adhere well to C32 melanoma cells or CD36 unless rosettes with uninfected erythrocytes are first disrupted.

Plasmodium falciparum malaria parasites modify the human erythrocytes in which they grow so that some parasitized erythrocytes (PE) can cytoadhere (C+) to host vascular endothelial cells or adhere in rosettes (R+) to uninfected erythrocytes. These C+ and R+ adherence properties of PE appear to mediate much of the pathogenesis of severe malaria infections, in part by blocking blood flow in microvessels. From one parasite strain, PE were selected in vitro for C+ R+ or C+ R- adherence properties and examined in model adherence assays. The C+ R+ PE cytoadhered poorly to C32 melanoma cells or to immobilized CD36 in a settled-cell assay when uninfected human erythrocytes were present and formed rosettes with PE. C+ R- PE adhered well in the same assays. However, C+ R+ PE adhered very well, even better than C+ R- PE, when the rosettes were disrupted and the C+ R+ PE were purified. Adding back rabbit erythrocytes, which do not form rosettes with C+ R+ PE, had simply a dilutional effect. The ability of rosettes to interfere with the detection of adherence must be dealt with in all future assays of malarial PE adherence. Individual PE were observed attached simultaneously to C32 cells and to a few erythrocytes, suggesting that C+ and R+ adherence properties are coexpressed on the same PE. Coexpression of these adherence properties on the same PE may have pathological importance in vivo, where passage of rosettes through capillaries may shear uninfected erythrocytes from rosetted PE and allow direct PE attachment to postcapillary venule walls before rosettes reform.

The cytochrome c peroxidase-cytochrome c electron transfer complex. The role of histidine residues.

The histidine-selective reagent diethyl pyrocarbonate and dye-sensitized photooxidation have been used to study the functional role of histidines in cytochrome c peroxidase. Of the 6 histidines in cytochrome c peroxidase, 5 are modified by diethyl pyrocarbonate at alkaline pH and 4 by photooxidation. The sixth histidine serves as the proximal heme ligand and is unavailable for reaction. Both modification reactions result in the loss of enzymic activity. However, photooxidized peroxidase retains its ability to react with H2O2 and to form a 1:1 cytochrome c peroxidase-cytochrome c complex. It is, therefore, concluded that the extra histidine modified by diethyl pyrocarbonate is the catalytic site distal histidine, His 52. In the presence of cytochrome c, no enzymic activity is lost by photooxidation and a single histidine, His 181, is protected from oxidative destruction. This finding provides strong support for the hypothetical model of the cytochrome c peroxidase-cytochrome c complex in which His 181 lies near the center of the intermolecular interface where it seems to provide an important link in the electron transfer process.

cDNA cloning, structural features, and eucaryotic expression of human TAG-1/axonin-1.

Axonal surface glycoproteins, composed of repeated immunoglobulin-like and fibronectin-type-III(FNIII)-like domains, mediate adhesion between axons or between axons and non-neuronal cells or extracellular matrix proteins. Several representatives of this group promote neurite outgrowth, when presented as substratum to neurons in culture, and have been implicated in axonal guidance mechanisms. TAG-1 and axonin-1 are presumptive species homologues of the rat and the chick, respectively; together with F11/F3, they form a subgroup of Ig/FNIII-like molecules containing a glycosyl-PtdIns membrane anchor. Recent reports on tumor suppressor genes encoding Ig-like and FNIII-like sequences prompted us to isolate the human homologue to TAG-1 and axonin-1. Polymerase chain reaction (PCR) primers were designed to regions conserved in both TAG-1 and axonin-1 using deoxyinosine at ambiguous positions. An expected 1000-bp fragment was obtained from cDNA derived from adult human cerebellum. Using this PCR fragment as a probe, several clones were isolated from a human fetal brain cDNA library. Nucleotide sequence analysis of a full-length clone, as expected, revealed a high degree of similarity to rat TAG-1 (91% identity) and chicken axonin-1 (75% identity) at the amino acid level. The encoded protein was then transiently expressed in monkey COS1 cells, and a stable mouse myeloma cell line was established expressing human TAG-1/axonin-1. The transfected COS1 and myeloma cells showed immunoreactivity on the cell surface with polyclonal anti-(chicken axonin-1) serum. On Western blots, the same antibodies recognized the recombinant protein migrating slightly slower on SDS/PAGE than chicken axonin-1. A comparison of chicken and human brain-tissue proteins by Western-blot analysis revealed a similar apparent molecular mass difference between the two species, which might be due to three additional N-glycosylation sites present on human TAG-1/axonin-1. Immunostaining of cryostat sections of embryonic retinas with polyclonal anti-(axonin-1) serum showed similar expression patterns in chicken and human samples at corresponding developmental stages. An additional shared feature of human TAG-1/axonin-1, rat TAG-1 and chick axonin-1 is their attachment to the cell membrane with a glycosyl-PtdIns anchor.

A comparison of the anthropometric, strength, endurance and flexibility characteristics of female elite and recreational climbers and non-climbers.

There is limited information on the anthropometry, strength, endurance and flexibility of female rock climbers. The aim of this study was to compare these characteristics in three groups of females: Group 1 comprised 10 elite climbers aged 31.3 +/- 5.0 years (mean +/- s) who had led to a standard of 'hard very severe'; Group 2 consisted of 10 recreational climbers aged 24.1 +/- 4.0 years who had led to a standard of 'severe'; and Group 3 comprised 10 physically active individuals aged 28.5 +/- 5.0 years who had not previously rock-climbed. The tests included finger strength (grip strength, finger strength measured on climbing-specific apparatus), flexibility, bent arm hang and pull-ups. Regression procedures (analysis of covariance) were used to examine the influence of body mass, leg length, height and age. For finger strength, the elite climbers recorded significantly higher values (P < 0.05) than the recreational climbers and non-climbers (four fingers, right hand: elite 321 +/- 18 N, recreational 251 +/- 14 N, non-climbers 256 +/- 15 N; four fingers, left hand: elite 307 +/- 14 N, recreational 248 +/- 12 N, non-climbers 243 +/- 11 N). For grip strength of the right hand, the elite climbers recorded significantly higher values than the recreational climbers only (elite 338 +/- 12 N, recreational 289 +/- 10 N, non-climbers 307 +/- 11 N). The results suggest that elite climbers have greater finger strength than recreational climbers and non-climbers.

Structural, functional, and antigenic differences between bovine heart endothelial CD36 and human platelet CD36.

Endothelial cell CD36 (glycoprotein IV) has been purified from bovine heart tissue by detergent partitioning and immunoaffinity chromatography. Bovine CD36 differs from human CD36 in its apparent mass (85 versus 88 kDa), primary structure, and immunological cross-reactivity. Of the 18 N-terminal residues identified, 17 conformed to the human CD36 sequence. Mouse monoclonal antibodies E-1 and 8A6 defined bovine- and human-specific epitopes, respectively. Because human CD36 has been identified as a receptor for erythrocytes infected with the malaria parasite Plasmodium falciparum, we examined the ability of bovine CD36 to bind infected erythrocytes. Bovine CD36, unlike human CD36, did not bind infected erythrocytes, suggesting that human CD36-specific structural features are responsible for recognition of the infected erythrocyte ligand.

Prenatal diagnosis of "dihydrobiopterin synthetase" deficiency, a variant form of phenylketonuria.

Amniocentesis was performed at 19 weeks gestation in a mother who had previously delivered a boy with "dihydrobiopterin synthetase" (DHBS) deficiency. The amniotic fluid contained neopterin in high (136 nmol/l) and biopterin in very low concentrations (1.8 nmol/l). The activity of the phosphate-eliminating enzyme (PEE, also called 6-pyruvoyl tetrahydropterin synthase, substrate: 7,8-dihydroneopterin triphosphate) which is present in liver and erythrocytes and defective in DHBS deficiency, was measured in the erythrocytes of the family members. The fetal sample showed only 2% of the activity of healthy adult controls and was comparable with that of the affected sibling. Obligate heterozygotes had activities around 20% of the controls. Two fetal control samples showed even higher activities than adult erythrocytes, Sepiapterin reductase activities wer normal in all cases. At autopsy, PEE deficiency was confirmed in the liver of the fetus. We concluded that DHBS deficiency (and most probably also GTP cyclohydrolase I deficiency) can be diagnosed by metabolite measurements in amniotic fluid. PEE activity is measurable in erythrocytes, although the assay needs to be improved. Since maternal tetrahydrobiopterin does not cross the placenta, treatment of a tetrahydrobiopterin-deficient fetus with tetrahydrobiopterin in utero is not possible.

Epithelial membrane glycoprotein PAS-IV is related to platelet glycoprotein IIIb binding to thrombospondin but not to malaria-infected erythrocytes.

Glycoprotein (GP) IIIb (also termed GPIV or CD36) is an integral platelet membrane protein, and has been identified as a binding site for thrombospondin, collagen, and malaria-infected erythrocytes. PAS-IV is an integral membrane protein found in lactating mammary epithelial cells and capillary endothelial cells. The N-terminal sequence of PAS-IV is nearly identical to that of GPIIIb and monospecific anti-PAS-IV antibody reacts with GPIIIb, indicating that PAS-IV is structurally related to GPIIIb. In this study, human platelet GPIIIb and bovine epithelial PAS-IV were compared in terms of structural, immunologic, and functional characteristics. The two-dimensional tryptic peptide map of both intact and deglycosylated PAS-IV was highly similar but not identical to that of GPIIIb. PAS-IV and GPIIIb reacted to an equal extent with monoclonal antibodies OKM5 and OKM8 by enzyme-linked immunosorbent assay. GPIIIb bound to surface immobilized thrombospondin (TSP) in a concentration-dependent and saturable manner, with approximately 60% reduction in binding in the presence of EDTA. PAS-IV bound to TSP with similar characteristics except that maximum binding was consistently approximately 50% of that of GPIIIb and binding was not inhibited by EDTA. GPIIIb supported adhesion of Plasmodium falciparum-infected erythrocytes (PRBC) in a dose-dependent manner while no significant adhesion of PRBC to PAS-IV was observed. Our data demonstrate that while epithelial PAS-IV and platelet GPIIIb are structurally and immunologically related, there are significant differences in their functional properties. Whether this result is due to different posttranslational glycosylation modifications or that PAS-IV and GPIIIb represent a family of related cell adhesive protein receptors remains to be determined.

Involvement of CD36 on erythrocytes as a rosetting receptor for Plasmodium falciparum-infected erythrocytes.

Plasmodium falciparum-infected erythrocytes (parasitized red blood cells [PRBCs]) can adhere to uninfected erythrocytes (RBCs) to form rosettes, and adhere to the endothelial cell (EC) surface antigen CD36. These adherence phenomena have previously been considered quite different. We show that anti-CD36 monoclonal antibodies (MoAbs) reverse rosetting of PRBCs from both a culture-adapted line (Malayan Camp [MC] strain) and a natural isolate, GAM425. Three MoAbs that block adherence of PRBCs to ECs or C32 melanoma cells also reversed rosetting by greater than 50% at levels of less than 1 microgram/mL (OKM5, OKM8, and 8A6). Two other MoAbs that react with purified CD36 (1D3 and 1B1), but do not react with the surface of C32 cells, failed to reverse rosetting. When rosettes were disrupted and the RBCs and PRBCs were pretreated separately with antibodies before mixing to allow rosette reformation, only pretreatment of RBCs had an effect. MoAb 8A6 pretreatment of RBCs blocked rosette reformation, while MoAb 1B1 pretreatment did not. Rosetting was also reversed by purified human platelet CD36. In conjunction with evidence that CD36 is expressed on normal human erythrocytes (van Schravendijk et al, Blood 80:2105, 1992), we conclude that this CD36 is able to act as a host receptor for rosetting in the MC strain and some natural isolates of P falciparum.