Successful treatment of concomitant pulmonary Nocardiosis and aspergillosis in an immunocompromised renal patient

A case is reported of rapid onset concomitant pulmonary infection withNocardia andAspergillus fumigatus in a patient six weeks after the institution of immunosuppressive therapy for renal vasculitis. Pulmonary lesions completely resolved on treatment with a combination of imipenem, cotrimoxazole and a prolonged course of itraconazole.     

Initial studies on the behavior of salivary proteins at liquid/air interfaces.

The mode of adsorption of salivary proteins at air/liquid interfaces was studied by using the drop volume technique to measure the kinetics of surface tension decay of aqueous salivary solutions. Adsorption of salivary proteins from whole saliva was fast, with a plateau value of the surface tension of 43 (+/- 2) mNm-1. As the concentration of saliva was reduced, the plateau value of surface tension increased and was achieved more slowly. The reduction in surface tension of aqueous solutions was larger for salivary proteins than for many other proteins reported.     

Cellular degeneration and synaptogenesis in the developing retina of the rat

We have investigated the time course and magnitude of cellular degeneration in the ganglion cell layer and the presumptive amacrine and bipolar regions of the inner nuclear layer during the development of the retina in the rat. Pyknotic profiles are present in the ganglion cell layer during the first 2 postnatal weeks, reaching peak numbers during the first 4 postnatal days (corresponding to the time of greatest loss of ganglion cells and their axons: Potts et al., '82; Lam et al., '82; Perry et al., '83). Two observations suggest that the majority of pyknotic profiles present in the ganglion cell layer during the second postnatal week are not ganglion cells. First, following injection of kainic acid into one superior colliculus, degenerating ganglion cells in the contralateral retina are cleared within 24-48 hours. Therefore, since most ganglion cell and axon loss occurs within the first postnatal week, few of the pyknotic profiles present in the second week are likely to be ganglion cells. Second, the time course of cellular degeneration in the ganglion cell layer during the second postnatal week follows a very similar pattern to that seen in the presumptive amacrine sublayer of the inner nuclear layer. Such a correspondence suggests that two phases of cell death occur in the ganglion cell layer: during the first postnatal week the majority of dying cells are ganglion cells, and in the second, most cell death is due to a loss of displaced amacrine cells. In the inner nuclear layer pyknotic profiles are most numerous in the presumptive amacrine region on postnatal days 6 and 7, and in the presumptive bipolar region on day 10. Synaptogenesis in the inner plexiform layer occurs later but reflects the order of cell death. Thus, conventional (presumed amacrine) synapses were first observed on day 11 and synaptic ribbons (indicative of bipolar synapses) on day 13. These observations suggest that amacrine and bipolar cells initiate synapses only after their numbers have stabilized.     

Frequent ongoing T-cell receptor rearrangements in childhood B- precursor acute lymphoblastic leukemia: implications for monitoring minimal residual disease

Crosslineage T-cell receptor delta (TCR delta) rearrangements are widely used as tumor markers for the follow up of minimal residual disease in childhood B-precursor acute lymphoblastic leukemia (ALL) by polymerase chain reaction (PCR). The major drawback of this approach is the risk of false-negative results due to clonal evolution. We investigated the stability of V delta 2D delta 3 rearrangements in a group of 56 childhood B-precursor ALL patients by PCR and Southern blot analysis. At the PCR level, V delta 2D delta 3-to-J alpha rearranged subclones (one pathway for secondary TCR delta recombination) were demonstrated in 85.2% of V delta 2D delta 3-positive patients tested, which showed that small subclones are present in the large majority of patients despite apparently monoclonal TCR delta Southern blot patterns. Sequence analysis of V delta 2D delta 3J alpha rearrangements showed a biased J alpha gene usage, with HAPO5 and J alpha F in 26 of 32 and 6 of 32 clones, respectively. Comparison of V delta 2D delta 3 rearrangement status between diagnosis and first relapse showed differences in seven of eight patients studied. In contrast, from first relapse onward, no clonal changes were observed in six patients studied. To investigate the occurrence of crosslineage TCR delta rearrangements in normal B and T cells, fluorescence-activated cell sorter-sorted peripheral blood CD19+/CD3- and CD19-/CD3+ cell populations from three healthy donors were analyzed. V delta 2D delta 3 rearrangements were detected at low frequencies in both B and T cells, which suggests that V delta 2-to-D delta 3 joining also occurs during normal B-cell differentiation. A model for crosslineage TCR delta rearrangements in B-precursor ALL is deduced that explains the observed clonal changes between diagnosis and relapse and is compatible with multistep leukemogenesis of B-precursor ALL.     

Reaction of poly(acrylamide-co-vinylamine) with tresyl-PEG in the presence of PC12 cells

Tresylation of an amine containing polymer film in the presence of PC12 cells did not result in a significant loss of cell viability, at least as assessed by trypan blue exclusion or MTT assay. PC12 cells were cultured atop reactive poly(acrylamide-co-vinyl amine) films or tissue culture polystyrene and exposed for 2 h to tresylated polyethylene glycol (TPEG) or unreactive hydrolyzed TPEG in 0.1M TES (N-tris hydroxymethyl-2-aminoethane sulfonic acid). The loss in trypan blue viability was limited ( approximately 80% retained), provided the TPEG concentration was 10 micromol/g or less. Similarly when microencapsulated PC12 cells (in a non-reactive polyacrylate hydrogel) were exposed to TPEG (10 micromol/g in 0.1M TES) the loss of MTT activity was small. The loss of vaibility was attributed to the toxicity of the tresyl leaving group and not the reaction itself. Thus, it may be possible to surface modify cell containing microcapsules, at least under limited conditions, in order to improve their biocompatibility without compromising the viability of the enclosed cells. This should lead to the development of new (reactive) polymers for microencapsulation since biocompatibility need not be a design consideration in the first instance.     

Heparinized styrene-butadiene-styrene elastomers.

A heparinized high-strength elastomer has been developed which is potentially useful as a nonthrombogenic vascular prosthesis. A surface hydroxylated styrene-butadiene-styrene (SBS) block copolymer with at least 40% extent of reaction after glow-discharge cleaning was coated with a 20% acetylated polyvinyl alcohol/heparin mixture containing glutaraldehyde and magnesium chloride. After curing at 80 degrees C for 100 min, the polyvinyl alcohol, heparin, and hydroxylated SBS were covalently bound to each other by acetal bridges. The effects of the various substrate and coating parameters were optimized to achieve very strong adhesion between the coating layer and the surface hydroxylated SBS. Heparin was not leached from the surface of the new material using 3M saline at pH 7.4 despite a detection limit of 10(-5) micrograms heparin/cm2 min. Prolonged partial thromboplastin times of greater than 1200 sec were observed (control: PTT = 120 sec). Preliminary ex vivo testing using a simple arteriovenous shunt in the leg of a rabbit showed good thromboresistance. The heparinized SBS shunt chamber remained patent for more than two hours without desorption of heparin. It was concluded that surface hydroxylated SBS heparinized by acetal coupling owed its thromboresistance to the heparin covalently bound to the surface and not to a microenvironment of heparin in solution at the blood/material interface.