Clinical and serologic features of herpes simplex virus infection in patients with AIDS.

We studied the natural history of herpes simplex virus (HSV) infection and its association with specific serum antibody in a sample of 68 HIV-infected patients with a first episode of Pneumocystis carinii pneumonia at San Francisco General Hospital in 1986. Seroprevalence was 66 and 77% for HSV-1 and HSV-2 antibody, respectively, by immunoblot assay. Twenty-seven patients had 45 HSV outbreaks diagnosed during 739 patient-months of follow-up. Median frequency of recurrence resulting in a medical visit was once every 6.5 months, and median duration of treated outbreak was 10 days. Fourteen of 48 evaluable patients seropositive for HSV-2 had no outbreak of HSV during a median follow-up of 7.5 months. Our data suggests that neither frequency nor severity of HSV were substantially increased in this group of patients, despite severe immunosuppression caused by HIV. However, validation of these results by a prospective study is required.     

Effects of chronic monocular enucleation on calcium binding proteins calbindin-D28k and parvalbumin in the lateral geniculate nucleus of adult rhesus monkeys

The calcium binding proteins parvalbumin and calbindin-D_28k were localized immunocytochemically within the lateral geniculate nucleus of adult monkeys at 1–7 months after monocular enucleation. Within the deafferented magno- and parvocellular layers, parvalbumin and calbindin-D_28k immunoreactive fibers were depleted at all post-enucleation times. The neuronal staining for parvalbumin was similar in numerical density and intensity between the deafferented and intact layers. In hemispheres examined at 5 and 7 months post-enucleation, parvalbumin-immunoreactive fibers were also lost within the deprived ocular dominance bands in layers IVA, IVC and VI of the visual cortex, suggesting that cellular expression or axonal transport of parvalbumin may be decreased in the deafferented geniculate laminae. While the intact magno- and parvocellular layers contained very few neurons that were immunoreactive for calbindin-D_28k, the density of calbindin-D_28k-positive neurons increased in these layers after deafferentation. The counts of calbindin-D_28k and parvalbumin immunostained neurons were not statistically different at 4–7 months post-enucleation. Because virtually all magno- and parvocellular projection neurons express parvalbumin, many parvalbumin neurons that normally do not contain calbindin-D_28k may co-express this in response to injury. The findings suggest that long-term deafferentation imposes additional calcium buffering requirements on lateral geniculate neurons.     

Accreditation of occupational therapy educational programmes in Australia: Time to do it our way?

Australia currently uses the World Federation of Occupational Therapists' guidelines and standards for the professional accreditation of occupational therapy educational programmes. The case for developing Australian accreditation standards and guidelines is presented.     

Trauma in pregnancy

The care of the pregnant trauma patient provides unique challenges and holds profound implications for both fetal and maternal outcomes. The management of these patients is influenced by unique anatomic and physiologic changes, increased concern for deleterious radiation and medication exposures, and the need for multidisciplinary care. This article reviews the critical features necessary in the assessment, diagnosis, treatment, and disposition of pregnant trauma patients with a focus on recent developments reported in the literature as pertinent to emergency management.     

A latex-safe environment is in everyone's best interest

Given the increasing number of both health care workers and patients who are allergic to latex, it has become critical for hospitals to create latex-safe environments. Though not an easy task, it is possible when departments work together especially with materials management. But due to financial implications, administration should be involved at the inception of an interdisciplinary committee charged with effecting change. One of the many issues to be addressed is constructing a comprehensive latex policy.     

An empirical evaluation of the performance of antibody identification tasks

Four empirical studies were conducted for better understanding of the nature of problem-solving activities by medical technologists and medical technology students when performing antibody identification tasks. The results indicated the importance of strategies that ensure the collection of converging evidence, as these strategies protect against the fallibility of commonly used heuristics and against errors due to simple slips. The results also indicate that not only do students make significant numbers of errors, but so do practicing technologists. In one of the studies covering a 1-year period, for instance, a group of 16 technologists made a total of 41 errors in 1057 cases. On the basis of these findings, several alternatives are proposed to reduce errors.     

Analysis of p53 mutations in a large series of lymphoid hematologic malignancies of childhood

p53 mutations are found in a wide variety of cancers, including hematologic malignancies. These alterations apparently contribute to development of the malignant phenotype. We analyzed a large series of lymphoid (330 cases) and a smaller series of myeloid (29 cases) malignancies of childhood for p53 mutations by single-strand conformational polymorphism (SSCP) following polymerase chain reaction. Samples with abnormal SSCP were reamplified and analyzed by direct sequencing method. p53 mutations were detected within the known mutational hotspots (exons 5 to 8) in 8 of 330 lymphoid malignancies, and in none of 29 myeloid malignancies, showing that the frequency of p53 mutations in childhood lymphoid malignancies was very low (8 of 330 cases [2%]). Four of these patients had very aggressive, fatal acute lymphocytic leukemia (ALL). None of 13 infants and none of 48 patients with T-lineage leukemia had detectable p53 mutations in their ALL cells. Exceptionally, p53 mutations were comparatively frequent in a small sample of B-cell non-Hodgkin's lymphomas (2 of 8 cases). Mutations were detected in samples from two patients with ALL at relapse; these were not detected in samples at initial diagnosis from the same patients, suggesting that p53 mutations may be associated with progression to a more malignant phenotype. Seven of eight alterations of p53 were missense mutations, and seven of eight samples may be heterozygous for the mutant p53, indicating that p53 protein may act in a dominant negative fashion.     

Detection of minimal residual disease in acute lymphoblastic leukemia by in vitro amplification of rearranged T-cell receptor delta chain sequences

Human T-cell receptor (TCR) delta-chain diversity mainly originates from high junctional variability, since only a limited number of germline elements is available. This extraordinary diversity at the V.J junction, due to the use of two D delta elements and extensive incorporation of N nucleotides, constitutes a specific clonal marker for cell populations exhibiting rearranged TCR delta genes. To this end we amplified in vitro by polymerase chain reaction (PCR) the TCR delta junctional region of five acute lymphoblastic leukemias (ALL), isolated respective DNA fragments, and used them directly as clonospecific probes. The combination of PCR technology and hybridization to clonospecific probes permitted the detection of leukemia DNA at dilution of 1:100,000 in all five cases. Moreover, we were able to investigate one of the ALL patients 11 months after achieving continuous complete remission. Conventional Southern blot analysis failed to detect rearranged TCR genes at this stage. However, residual leukemic cells could readily be detected by PCR technique. We conclude that the strategy proposed here is a very sensitive tool to detect minimal residual disease in a significant proportion of human lymphoid neoplasias.     

A point mutation in the integrin beta 3 cytoplasmic domain (S752-->P) impairs bidirectional signaling through alpha IIb beta 3 (platelet glycoprotein IIb-IIIa)

Agonist-induced inside-out signaling results in an increased affinity of integrin alpha IIb beta 3 (platelet glycoprotein IIb-IIIa) for soluble ligands (fibrinogen [Fg] and PAC1). Ligand binding to integrins initiates outside-in signaling that leads to cellular responses such as cell spreading and focal adhesion formation. A point mutation in the beta 3 cytoplasmic domain (S752-->P) is associated with blocked inside- out alpha IIb beta 3 signaling in a variant Glanzmann's thrombasthenia. This mutation was introduced into beta 3 and cotransfected into Chinese hamster ovary cells with a chimeric alpha subunit consisting of the alpha IIb extracellular and transmembrane domains and the alpha 6B cytoplasmic domain. The substitution of the alpha IIb cytoplasmic domain with that of alpha 6 led to activation of alpha IIb beta 3 to bind PAC1, mimicking inside-out signaling. This effect was reversed by the S752-->P mutation, indicating a disruption of inside-out signaling by the mutation. In addition, transfectants expressing this beta 3 variant showed reduced alpha IIb beta 3-mediated cell spreading on immobilized Fg, focal adhesion, and fibrin clot retraction, suggesting an impairment in outside-in alpha IIb beta 3 signaling. Therefore, a single point mutation in the beta 3 cytoplasmic domain impaired bidirectional signaling through alpha IIb beta 3.