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Biomedical subjects

J F Wright

Publications and source records attributed to J F Wright.

At least 19 recordsLinked to original sources
PubMed2005

ISBT Code 128 implementation at a regional blood center.

BACKGROUND: Application specifications for ISBT 128 bar code symbology and the International Council for Commonality in Blood Bank Automation (ICCBBA) were created in 1994. By June 2000, the FDA considered ISBT 128 a standard for uniform labeling of blood and blood components. Our blood center initiated a change process for ISBT 128 implementation and "went live" in 2003. STUDY DESIGN AND METHODS: The intention to adopt ISBT 128 symbology with hospitals was actively communicated in October 2001. A Codabar-ISBT label cross-reference book was developed, FDA approval for the fullface label format in April 2002 was requested, and FDA approval was received in March 2003. In December 2002, donor identification labels and number sets were ordered, and an integration test plan was subsequently developed with departmental process flowcharts for each of the nine affected departments. Each step was tested, the labeling changes were approved in May 2003, training was completed in June 2003, and ISBT bar code symbology was implemented on July 1, 2003. A written survey was sent to hospital transfusion services in April 2004. RESULTS: Implementation went smoothly except for an unanticipated high rate of "no-reads" on some analyzers in the testing lab. The hospitals spent an average of 18 hours preparing for changes, 14 hours on validation, 4 hours on documentation and procedure development, and 8 hours on training. CONCLUSION: ISBT bar code symbology was successfully implemented. Hospital transfusion services made some adjustments and, overall, readily accepted the new bar code symbology.

Blood Banks↗
PubMed2002

A comparison of the macrophyte cover and macroinvertebrate fauna at three sites on the River Kennet in the mid 1970s and late 1990s.

In 1974-1976, baseline studies were carried out on the flora and macroinvertebrate fauna of the R. Kennet at two sites downstream of Marlborough (Savernake Upper and Lower) and at one site upstream of Hungerford (Littlecote). Simplified maps of each site, showing the cover of macrophytes, were obtained monthly between April 1974 and April/June 1976, and replicated quantitative samples of the macroinvertebrates were collected on the dominant macrophyte and on gravel in June 1974, and also in June and December 1975. As a consequence of two major droughts and increasing concern over water quality in the Upper Kennet in the 1990s, the studies recommenced in the summer of 1997 using the same sites and methodologies. Maps and macroinvertebrate samples were obtained in early July and December 1997 and in June of both 1998 and 1999. At the Savernake sites, mapping in summer 1997 confirmed what had been apparent for some years. That is, macrophyte cover (both Ranunculus and Schoenoplectus) was much lower than in the 1970s. In contrast, the site downstream at Littlecote retained a relatively high cover of Ranunculus, despite the drought. In late autumn 1997, phosphate stripping commenced at Marlborough Sewage Treatment Works, the drought ended and in addition, the spring of 1998 was unusually wet. Ranunculus recolonised both Savernake sites with remarkable speed by summer 1998 and retained this dominant position in 1999. Quantitative samples of macroinvertebrates collected on gravel and the dominant macrophyte at each of the three study sites indicated that there was no evidence of major loss of family richness between the 1970s and 1990s as a result of the low flows or enrichment. However, at Savernake (but not Littlecote) in summer 1997, the macroinvertebrate assemblage was affected by low flows and/or enrichment. This took the form of changes in the abundance of some families, with lentic forms being favoured in relation to some lotic families. Following the end of the drought, many macroinvertebrate families at Savernake showed a rapid response to the new conditions and the assemblages reverted to those expected in a fast-flowing cretaceous chalk stream. Continued monitoring through the next drought is advisable to provide a greater understanding of the interplay between water quality, the discharge regime, habitat quality (including macrophyte growth) and the response of the macroinvertebrate fauna.

Animals↗
PubMed2001

Teratoma in desert grassland whiptail lizards (Cnemidophorus uniparens).

The clinical, gross necropsy, and histopathology findings in two unrelated desert grassland whiptail lizards (Cnemidophorus uniparens) with teratoma are described. The desert grassland whiptail is a parthenogenic lizard species with a polyploid chromosomal complement. The chromosome composition of the teratomas from these lizards was not determined.

Animals↗
PubMed2000

Cholesterol granulomas in three meerkats (Suricata suricatta).

Cholesterol granulomas are uncommon pathologic lesions in animals, although they are important intracranial tumors in humans. This report describes cholesterol granulomas associated with multiple organ systems of three captive meerkats. In the most severe case, meerkat No. 1, the pathologic behavior of the cholesterol granuloma was unique in that it appeared to locally invade the cerebrum and calvarium, possibly contributing to neurological deficits observed antemortem. A review of other meerkat necropsies revealed incidental, asymptomatic cholesterol granulomas in organs of two other individuals, meerkat Nos. 2 and 3. Histologically, all lesions were composed of cholesterol clefts admixed with large, foamy macrophages containing hemosiderin, multinucleated giant cells, lymphocytes, plasma cells, and foci of mineralization. Hypercholesterolemia was documented in two of the three meerkats.

Animals↗
PubMed1999

Annexin II enhances cytomegalovirus binding and fusion to phospholipid membranes.

A number of studies have suggested that the anionic phospholipid (anPL)-binding protein annexin II may play a role in cytomegalovirus (CMV) infection. Since annexin II has been shown to mediate aggregation and fusion of certain membranes, we investigated whether these properties could be exploited by CMV directly. The experiments showed that purified annexin II, but not the homologous protein annexin V (AnV), can mediate the binding of 35S-CMV (strain AD169) to anPL-coated microtiter wells. This association required Ca2+, could be titrated by varying either annexin II (apparent Kd = 4 x 10(-)8 M) or 35S-CMV, was inhibited by unlabeled CMV, and was observed for the heterotetrameric or monomeric form of annexin II. In experiments utilizing the fluorescence dequenching of octadecyl rhodamine incorporated into the CMV envelope, annexin II was furthermore found to enhance the rate of virus-anPL vesicle fusion. The observed fusion was dependent on the concentration of annexin II, Ca2+, and anPL and was mediated principally by the heterotetramer. Interestingly, AnV was observed to inhibit the effects of annexin II on CMV fusion but not binding to anPL, which indicates that annexin II enhances these processes by distinct mechanisms. The results presented here provide the first direct evidence that annexin II has the capacity to bridge CMV to a phospholipid membrane and to enhance virus-membrane fusion. These observations furthermore suggest that AnV may regulate the fusogenic function of annexin II.

Anions↗
PubMed1999

Characterization of platelet glycoproteins and platelet/endothelial cell antibodies in patients with thrombotic thrombocytopenic purpura.

Platelets and sera from 12 patients with thrombotic thrombocytopenic purpura (TTP) and 12 healthy normal control subjects were examined. As determined by quantitative flow cytometry, prior to plasma exchange therapy platelet surface glycoprotein (GP) Ib levels were similar in TTP patients and normal controls (mean 20 188 and 20 226 molecules/platelet, respectively). Platelets from patients with TTP did, however, have significantly reduced levels of GPIIb/IIIa prior to plasmapheresis (mean 36 348 v 52 505 molecules/platelet in controls; P = 0.0004) and of GPIV (mean 13 321 v 26 212 molecules/platelet in controls; P = 0.0002). An increase in activated platelets, as determined by CD62 expression, was observed in 82% of patients. Increased platelet-associated immunoglobulins and/or complement was also seen in approximately 60% of the patients. In general, with return of platelet counts to normal levels following seven plasmaphereses, the above abnormalities were reversed, although often not to normal levels. Western blot analysis indicated the presence of antibodies reactive to platelet GPIV (88 kD) in 70% of pretreatment sera from patients with TTP; a similar band was observed in 80% of patient sera against microvascular endothelial cells. Immunofluorescence microscopic examination indicated the presence of antibody in pretreatment sera from patients with TTP to microvascular (73%) and large vessel (36%) endothelial cells. As measured by an indirect flow cytometric assay, pretreatment sera from 55% of patients with TTP were reactive with large vessel endothelial cells and 100% reacted with microvascular endothelial cells; reactivity was significantly greater against the microvascular endothelial cells (P = 0.0048) and was reduced following plasma exchange therapy. These results indicate abnormalities in platelet glycoprotein expression in TTP and suggest that anti-platelet and anti-endothelial cell antibodies play a role in the thrombocytopenia and vasculitis characteristic of this disorder.

Adult↗
PubMed1999

Bioassays and biological stability.

The development of the concept of < >, made possible through the power and detail afforded by modern biochemical and biophysical techniques, has resulted in questions being raised about the value of the more variable bioassay. However bioassays, particularly in a routine stability monitoring situation, continue to be useful and often provide unique information not obtained by other techniques. They have advantages in that they are relatively easy to perform and generally have better sensitivity than most structural techniques. They can be used to monitor for previously undetected changes - particularly those associated with conformational alterations, and can be used to monitor the effective combination of all individual changes.

Biological Assay↗
PubMed1998

Virus-associated idiopathic thrombocytopenic purpura.

Two-thirds of children with acute idiopathic thrombocytopenic purpura (ITP) have a history of an infectious illness a few days to a few weeks before the onset of thrombocytopenia. In a subset of affected children, identification of a specific virus can be made, such as varicella zoster virus, rubella, Epstein-Barr virus, influenza, or human immunodeficiency type 1 virus, indicating an etiological role for preceding viral infection in these children with ITP. While inhibition of thrombopoiesis has been established to play a role in thrombocytopenia associated with infection with some viruses, it does not appear to play a major role in the etiology of most typical ITP cases. Rather, enhanced clearance of platelets by the reticuloendothelial system is considered to be, at least in part, responsible for the thrombocytopenia which occurs during the viremic phase of acute virus infection or which develops days to weeks following the virus illness. Molecular mimicry between viral antigens and host proteins has been implicated in a number of autoimmune phenomena, and may be involved in the enhanced platelet clearance in virus-associated ITP.

Acute Disease↗
PubMed1998

Characterization of HIV-1-specific antibodies and HIV-1-crossreactive antibodies to platelets in HIV-1-infected haemophiliac patients.

Sera from HIV-1-infected haemophiliacs were examined for human immunodeficiency virus (HIV) specific antibodies and for platelet crossreactive antibodies. Using HIV sepharose 4B affinity columns for serum absorption, antibodies against various HIV antigens, including HIV lysate. HIV-p24 and HIV-gp120, were eluted either by low or by high pH buffer. The eluates were examined by ELISA for HIV specificity and by flow cytometry for platelet crossreactivity. Two types of HIV antibodies could be eluted, i.e. acid-sensitive and alkaline-sensitive antibodies. HIV antibodies were obtained in 26/29 acid eluates and in 25/29 of the alkaline eluates from HIV-lysate columns; 96% (25/26) of the acid-eluted antibodies were HIV-specific but 48% (12/ 25) of the alkaline-eluted antibodies also showed crossreactivity to platelets. Of the 20 alkaline-eluted HIV-p24 antibodies, 40% (8/20) reacted specifically with HIV-p24 and 60% (12/20) were platelet crossreactive. In contrast, of the alkaline-eluted HIV-gp120 antibodies (n=17), 88% (15/17) were HIV gp120-specific and only 12% (2/17) were platelet crossreactive. Western blot analysis of platelets demonstrated that the anti-p24 antibodies recognized three bands with approximate molecular weights of 72000 to 95000. 69% of the serum antiplatelet antibodies showed platelet glycoprotein IIbIIIa specificity. Anti-HIV antibodies could be eluted from platelets. Hence, platelet crossreactive antibodies in HIV infection are primarily alkaline-sensitive and are associated predominantly with HIV p24 antibody; these antibodies may play a role in the immune thrombocytopenia of HIV-infected haemophiliacs.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Coagulation initiated on herpesviruses.

Herpesviruses have been previously correlated to vascular disease and shown to cause thrombogenic and atherogenic changes to host cells. Herein we show that even in the absence of cells, purified cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) can initiate thrombin production. Functional assays demonstrated that purified HSV-1 and HSV-2 provide the necessary phospholipid (proPL) for assembling the coagulation factors Xa and Va into prothrombinase, which is responsible for generating thrombin. These observations are consistent with our earlier studies involving CMV. The presence of proPL on all three herpesviruses was confirmed directly by flow cytometry and electron microscopy by using annexin V and factor Va, respectively, as proPL-specific probes. Of equal importance, we found that CMV, HSV-1, and HSV-2 were also able to facilitate factor Xa generation from the inactive precursor factor X, but only when factor VII/VIIa and Ca2+ were present. Monoclonal antibodies specific for tissue factor (TF), the coagulation initiator, inhibited this factor X activation and, furthermore, enabled identification of TF antigen on each virus type by flow cytometry and electron microscopy. Collectively, these data show that CMV, HSV-1, and HSV-2 can initiate the generation of thrombin by having essential proPL and TF activities on their surface. Unlike the normal cellular source, the viral activity is constitutive and, therefore, not restricted to sites of vascular injury. Thus cell-independent thrombin production may be the earliest event in vascular pathology mediated by herpesviruses.

Blood Coagulation↗
PubMed1997

The connectionist simulation of aphasic naming.

The simulation of language disorders using interactive activation (IA) networks and connectionist systems is discussed. An existing IA account of aphasic naming is described, in which two network parameters (decay rate and connection strength) are varied to fit the error production of an aphasic patient. Fairly similar results can be obtained through modification of additional parameters, including the so-called "shared weight increase factor" linking lexical and semantic units. This leads us to consider simulation of aphasic naming using connectionist networks which do not require explicit variation of network parameters. A modular connectionist architecture is presented, in which semantic-lexical and phonological knowledge are instantiated using self-organizing Kohonen maps, while connections between them are implemented using Hebbian networks; a linear connectionist network (Madaline) is used to simulate nonword repetition. The Hebbian connections are lesioned in order to reproduce the patient's naming errors.

Aphasia↗
PubMed1997

Flow cytometric analysis of platelets from children with the Wiskott-Aldrich syndrome reveals defects in platelet development, activation and structure.

The pathophysiology of platelet dysfunction in the Wiskott-Aldrich immune deficiency syndrome (WAS) remains unclear. Using flow cytometry, we have characterized the functional properties of platelets from 10 children with WAS. Patients with WAS had thrombocytopenia, small platelets, increased platelet-associated IgG and reduced platelet-dense granule content. Levels of reticulated 'young' platelets were normal in the WAS patients. Although the mean numbers of platelet glycoprotein (GP) Ib, GPIIbIIIa and GPIV molecules per platelet appeared lower in WAS patients than in healthy controls, analysis of similar-sized platelets revealed the mean number of GPIb molecules per platelet to be comparable in patients and normal controls. Surface GPIIbIIIa and GPIV expression was, however, significantly lower on the WAS platelets than on normal platelets. Compared with normal platelets, WAS platelets showed a reduced ability to modulate GPIIbIIIa expression following thrombin stimulation. In addition, thrombin- and ADP-induced expression of CD62P and CD63 was defective in WAS platelets. Phallacidin staining of the WAS platelets revealed less F-actin content than in normal platelets. Together, these data suggest that the reduced platelet number and function in WAS reflects, at least in part, a defect in bone marrow production as well as an intrinsic platelet abnormality.

Actins↗
PubMed1996

Characterization of platelet-reactive antibodies in children with varicella-associated acute immune thrombocytopenic purpura (ITP).

Biochemical analyses were performed on blood samples obtained from two children (P1, P2) who presented with acute immune thrombocytopenic purpura (ITP) following a recent varicella zoster virus (VZV) infection. Patient sera had antibodies that were reactive with normal blood-group O platelets as measured by flow-cytometric assay. Western blot analysis of electrophoretically separated normal blood-group O platelets under reducing and non-reducing conditions demonstrated that these sera were reactive with platelet antigens of approximately 50 and approximately 110 kD, respectively. These 50/110 kD antigens were not reactive with seven sera from acute ITP patients whose illness was not preceded by VZV infection, with serum from a patient with a prior history of VZV and no thrombocytopenia, nor with normal healthy control sera. VZV antibodies (IgG and IgM), isolated from patient sera by affinity chromatography using immobilized purified VZV glycoproteins, were found to bind to gel-filtered autologous platelets and with normal blood-group O platelets, as analysed by flow cytometry. No binding was observed using antibodies similarly prepared from healthy volunteer sera. To investigate their ability to sensitize platelets to complement activation, affinity-purified VZV antibodies were incubated with platelets and then with purified complement components C1 and 125 I-labelled C4. Platelets reacted with VZV-specific antibodies from the two patients and showed increases of 2.3-2.4-fold of platelet-surface deposition of 125 I-C4b, compared to controls. These data provide evidence that virus-specific antibodies occurring in children with varicella-associated acute ITP cross-react with normal platelet antigens, and may contribute to platelet clearance.

Antibodies, Viral↗
PubMed1995

Applications of flow cytometry in the analysis of blood leukocytes.

Flow cytometric analysis of blood leukocytes is currently used for both routine clinical measurements as well as for cutting edge research applications. This technology has enabled rapid and accurate determination of leukocyte antigens and quantitative analysis of leukocyte subsets, tests of leukocyte function, determination of the presence of antineutrophil and antilymphocyte antibodies in plasma and on cells, measurement of CD34+ hematpoietic stem cells in peripheral blood and bone marrow samples, measurement of apoptosis, and detection of virus-infected leukocytes. This review will focus on the use of the flow cytometer for investigations of blood leukocytes in transfusion medicine.

Flow Cytometry↗
PubMed1995

Analysis of platelets by flow cytometry.

Transfusion medicine has become a multi-disciplinary field with many recent technical developments and the flow cytometer has had a significant impact in transfusion medicine, especially at the level of platelet immunobiology. Many routine tests in platelet immunology are now performed by flow cytometry laboratories, including assessment of platelet-associated allo- and auto-antibodies and complement components. Platelet analysis by flow cytometry has been applied to detection of platelet antigens, platelet surface-bound proteins, platelet activation, measurement of reticulated platelets, intracellular calcium studies, and the measurement of platelet microparticles in vivo and in vitro. This review will focus on the use of the flow cytometer in these applications in investigations of platelet immunology.

Antigens, Human Platelet↗
PubMed1995

An investigation into the use of hypertext as a user interface to taxonomic keys.

In an attempt to overcome some of the drawbacks of existing taxonomic keys, we have experimented with a computerized version of a key, changing the interface to the key, but leaving the information contained in the key essentially unchanged. This is in contrast to most previous work on the use of computers in taxonomy, where work has concentrated on alternative identification techniques and techniques for manipulating taxonomic data. Hopkin's (1991) Key to the Woodlice of Britain and Ireland was converted (including the diagrams and colour photographs), into a hypertext document using the Unix Guide hypertext system. An experiment was conducted where test subjects with a wide range of experience of taxonomic keys and computing skills were asked to identify woodlouse specimens using the paper and hypertext forms of the keys. The results showed that test subjects were more likely to obtain an identification with the hypertext version of the key, they found it easier to use and preferred using it to the paper version of the key. However, there were indications that test subjects were more likely to obtain a misidentification using the hypertext key than the paper version of the key. Further work is needed to discover the possible causes of the increased frequency of misidentifications, and ways in which the usability of hypertext keys can be further enhanced.

Classification↗
PubMed1995

Host cellular annexin II is associated with cytomegalovirus particles isolated from cultured human fibroblasts.

A significant amount of host cellular annexin II was found to be associated with human cytomegalovirus isolated from cultured human fibroblasts (approximately 1,160 molecules per virion). This composition was established by four different analytical approaches that included (i) Western blot (immunoblot) analysis of gradient-purified virions with a monoclonal antibody specific for annexin II, (ii) peptide mapping and sequence analysis of virus-associated proteins and proteins dissociated from virus following EDTA treatment, (iii) electron microscopic immunocytochemistry of gradient-purified virions, and (iv) labeling of virus-associated proteins by lactoperoxidase-catalyzed radioiodination. These results indicated that annexin II was primarily localized to the viral surface, where it bound in a divalent cation-dependent manner. In functional experiments, a rabbit antiserum raised against annexin II inhibited cytomegalovirus plaque formation in human foreskin fibroblast monolayers in a concentration-dependent manner. Cumulatively, these studies demonstrate an association of host annexin II with cytomegalovirus particles and provide evidence for the involvement of this cellular protein in virus infectivity.

Animals↗