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.     

Experimental axonopathy induced by immunization with campylobacter jejuni lipopolysaccharide from a patient with guillain‐barré syndrome

Campylobacter jejuni (C. jejunj) infection is the most common antecedent in the axonal variant of Guillain‐Barré syndrome (GBS). Antibodies against nerve gangliosides found in GBS patients recognize cross‐reactive epitopes in the lipopolysaccharide (LPS) of C. jejuni. This led to the molecular mimicry hypothesis of GBS. We immunized eleven rabbits with a LPS extracted from HS:19 C. jejuni strain isolated from a patient with GBS and complete Freund's adjuvant (CFA)(group I). In a second experiment we immunized seven rabbits with LPS, CFA and keyhole limpet hemocyanin (KLH)(group II). All group I rabbits developed high titers of anti‐LPS, anti‐GM1, anti‐GD1b antibodies and lower titers of anti‐GD1a. One rabbit, 50 days after initial inoculation, showed tremor and weakness. All rabbits of group II developed high titres of antiganglioside antibodies and six animals showed weakness 59–113 days after initial inoculation. Two rabbits died. Pathology showed mild to moderate, tendentially grouped, axonal degeneration in sciatic nerves of four out of five animals. Control rabbits of group I (immunized with CFA only) did not develop antibodies, controls of group II (immunized with CFA + KLH) developed low titers of IgG anti‐GM1. None developed neurological signs or showed axonal degeneration. C. jejuni LPS is a potent B‐cell stimulator capable to induce a strong antiganglioside response in rabbits. However, to induce the neuropathy is crucial to employ KLH, a glycoprotein known to stimulate both humoral and cellular responses. This animal model reproduces the pathogenetic process hypothesized in axonal GBS with antiganglioside antibodies post C. jejuni infection.     

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.     

Disorders of perfusion of the anterior segment of the eye

Background: We have investigated the vascular perfusion of a wide variety of conditions of the anterior segment using fluorescein angiography.
Methods: The conditions were classified and findings reported according to the system set out below. Patients underwent full ocular examination. Fluorescein angiography of the anterior segment was carried out when indicated to investigate iris atrophy and neovascularisation. Specular microscopy of the corneal endothelium was used to detect changes in this tissue.
Results: The hypoperfusion was variable in degree and accompanied by varying degrees of iris hypoplasia and atrophy with neovascularisation. The degree of neovascularisation depended upon its rapidity of development, the pre-existing state of vascular perfusion and the underlying pathological condition.
Conclusions: Hypoperfusion with resultant ischaemia and neovascularisation is common in conditions of the anterior segment. An understanding of the changes is valuable in treating many conditions affecting the anterior segment. The changes observed may also occur elsewhere in the physical system and may be a significant part of the ageing process, either as scattered, disparate processes or as part of a general disease process.     

Postoperative radiation therapy in the management of lung cancer

Postoperative radiation therapy for lung cancer is still controversial. In a 9-year period, 69 patients with non-oat-cell carcinoma of the lung (16% stage I, 26% stage II, and 58% stage III) received such therapy. The radiation dose was less than 5,000 cGy in 42 patients, 5,000-5,900 cGy in 16, and 6,000 cGy or more in 11; follow-up ranged from 24 to 64 months. Actuarial survival at 2 and 4 years was 50% and 16%, respectively, for squamous cell carcinoma, and 40% and 26% for adenocarcinoma. The 5-year survival for stages I, II, and III cancer was 29%, 17%, and 19%, respectively. Histologic findings and type of surgery did not affect survival, but the radiation dose apparently did. The 3-year survival for patients who received less than 6,000 cGy was 35%, compared with 73% for patients who received higher doses. In eight patients, treatment failed within the irradiated volume: all had received doses of less than 6,000 cGy, and the volume in three was judged to be inadequate.     

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.