Bilateral sino-orbital pseudotumour

The authors present a case of histopathologically proved bilateral idiopathic inflammatory pseudotumour of the orbits with involvement of the paranasal sinuses in a child. Clinically, the bilateral proptosis was manifest at the age of 5 years. While extraorbital manifestations are rare, orbital pseudotumour should be considered in such cases.     

Recovery after chronic stress fails to reverse amygdaloid neuronal hypertrophy and enhanced anxiety-like behavior

The hippocampus and amygdala are important components of the neural circuitry mediating stress responses. While structural plasticity in the hippocampus may mediate cognitive aspects of behavioral impairments caused by severe stress, changes in the amygdala are more likely to contribute to the affective aspects of stress disorders. Recent reports have identified cellular and molecular correlates of stress-induced amygdaloid plasticity that may underlie anxiety. Hence, we examined the impact of chronic stress, in terms of its duration, at the cellular and behavioral levels in rats. We found that, even after 21 days of stress-free recovery, animals exposed to chronic immobilization stress (CIS) continue to exhibit enhanced anxiety, as manifested by a significant reduction in open-arm exploration and risk-assessment behavior in the elevated plus-maze. At the cellular level, we tested if CIS-induced dendritic remodeling in the amygdala is also as long-lasting as enhanced anxiety after 21 days of recovery. Indeed, long-lasting facilitation of CIS-induced anxiety is accompanied by a persistent increase in dendritic arborization of basolateral amygdala (BLA) spiny neurons. Moreover, CIS-induced BLA hypertrophy is distinct from hippocampal CA3 atrophy, which is reversible within the same period of stress-free recovery. These findings on persistent dendritic remodeling in the amygdala, in addition to highlighting important differences with hippocampal structural plasticity, may provide a cellular basis for examining anxiety and mood disorders triggered by chronic stress.     

Comparison of four erythrocyte fragility tests as indicators of vitamin E status in adult dogs.

Plasma alpha-tocopherol (alpha-T) concentrations, erythrocyte osmotic fragility and detergent sensitivity were measured at 8 week intervals in two 1-year-old male beagle dogs fed a vitamin E-deficient diet (< 0.08 mg per kg alpha-T) and in two control beagles fed the same diet supplemented with vitamin E (> 90 mg per kg alpha-T). Beginning at 24 weeks, dialuric acid haemolysis and spontaneous haemolysis were evaluated also. In the vitamin E-deficient dogs, plasma alpha-T concentrations declined progressively from baseline values of 20.5 and 31.3 micrograms per ml to 0.11 and 0.07 micrograms per ml, respectively, by 90 weeks. The supplemented dogs maintained alpha-T concentrations between 18.3 and 38.4 micrograms per ml. Both dialuric acid haemolysis (R = -0.89) and spontaneous haemolysis (R = -0.91) increased with declining plasma alpha-T concentration. In the dialuric acid haemolysis assay, 50 per cent haemolysis occurred when plasma alpha-T declined to 1.7 micrograms per ml, compared with spontaneous haemolysis in which 50 per cent haemolysis occurred when plasma alpha-T declined to 0.5 micrograms per ml. Osmotic fragility and detergent sensitivity remained unchanged in the vitamin E-deficient dogs throughout the study. Of the four tests, dialuric acid haemolysis was the most sensitive in-vitro assay for vitamin E deficiency in adult dogs.     

Hyperpolarization of myenteric neurons by opioids does not involve cyclic adenosine-3',5'-monophosphate.

To investigate the role of cyclic adenosine-3'5'-monophosphate on the inhibitory actions of opioids in guinea-pig ileum, we made intracellular recordings from the two electrophysiologically defined classes of neurons (S and AH) in the myenteric plexus. The selective opioid mu agonist (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin caused a membrane hyperpolarization in 34 out of 67 S neurons but did not affect the membrane potential of AH neurons. The mean amplitude (+/- S.E.M.) of the hyperpolarization was 8.2 +/- 0.8 mV. Forskolin, which activates adenylate cyclase and increases intracellular cyclic adenosine-3',5'-monophosphate levels, caused a membrane depolarization in AH neurons (9.4 +/- 1.9 mV) but did not alter the resting membrane potential of S neurons. Similarly, neither the phosphodiesterase inhibitor, isobutylmethylxanthine, nor the membrane permeable analogue of cyclic adenosine-3',5'-monophosphate, dibutyryl cyclic adenosine-3'-5'-monophosphate, altered the resting membrane properties of S neurons. Furthermore, none of these agents affected significantly the amplitude of the hyperpolarization of S neurons by (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin. The experiments indicate that changes in intracellular cyclic adenosine-3',5'-monophosphate are not important in the processes that link occupation of mu receptors to the opening of potassium channels on myenteric neurons.     

The BPV-1 E5 oncoprotein expressed in Schizosaccharomyces pombe exhibits normal biochemical properties and binds to the endogenous 16-kDa component of the vacuolar proton-ATPase

The 44-amino-acid E5 oncoprotein of bovine papillomavirus type 1 transforms immortalized murine fibroblast cell lines. This highly hydrophobic protein forms homodimers, localizes to intracellular membrane compartments (including the Golgi apparatus), and forms a complex with the 16-kDa membrane-embedded constituent (16k) of the vacuolar proton-ATPase. To develop a system for the genetic and biochemical analysis of the E5/16k interaction, the E5 gene was cloned into a new vector which was designed for expression in the fission yeast Schizosaccharomyces pombe. The E5 protein synthesized in this system dimerized normally and bound to endogenous and overexpressed S. pombe 16k protein. Comparison of the S. pombe and mammalian 16k proteins showed strong conservation in carboxyl-terminal amino acids but greater variation in the amino-terminal sequences, suggesting that E5 was interacting with the 16k carboxyl domains. Finally, a new protein epitope tag is described which permitted for the first time the coprecipitation of E5 with antibodies directed against the 16k protein.     

Distinct pattern of antibody reactivity with oligomeric or polymeric forms of the capsular polysaccharide of Haemophilus influenzae type b.

The chain length of oligosaccharides required for antibody binding has been studied by using the capsular polysaccharide from Haemophilus influenzae type b or oligosaccharides derived from it. The concentration of competing antigens required to achieve a 50% inhibition of antibody binding by human polyclonal antisera in an in vitro competition enzyme-linked immunosorbent assay decreased progressively from greater than 10(-3) to 5 x 10(-7) M as the inhibiting saccharide chain length increased from 1 to 262 repeat units. Even small oligosaccharides (one or two repeat units) are potentially capable of competing to a significant level if a high enough concentration of saccharides is used. A similar pattern of reactivity was seen with a monoclonal anti-polyribosyl ribitol phosphate antibody, suggesting that the differences in the avidity of the antibody subpopulations in the polyclonal antisera do not contribute to the binding patterns observed. The binding reaction was specific as evaluated with pneumococcal saccharides. Furthermore, an oligosaccharide-protein conjugate binds antibody better than the free oligosaccharides do. Such a difference in binding was not observed between the polysaccharide and a polysaccharide-protein conjugate. Overall, the data suggest that identical epitopes are expressed by oligomeric and polymeric forms of the antigen and that a particularly more stable conformation in polysaccharides is preferred by antibodies. Covalent coupling of oligomers to protein increases the expression of stable conformation of epitopes. The data further suggest that this kind of antigenic analysis may be important for the design and synthesis of glycoconjugate vaccines.     

Immediate breast reconstruction-impact on radiation management

Breast reconstruction is an option for women undergoing modified radical mastectomy due to a diagnosis of breast cancer. In certain patients, breast reconstruction is performed by insertion of a temporary tissue expander prior to the placement of permanent breast implants. Some of these patients, following mastectomy, may require chest wall irradiation to prevent loco regional relapse. The compatibility of radiation and tissue expanders placed in the chest wall is of major concern to the radiation oncologist. Clinically undetectable changes can occur in the tissue expander during the course of radiation therapy. This can lead to radiation treatment set-up changes, variation in tissue expansion resulting in unwanted cosmesis, and deviation from the prescribed radiation dose leading to over and/or under dosing of tumor burden. At Howard University hospital, a CT scan was utilized to evaluate the status of the temporary tissue expander during radiation treatment to enable us to prevent radiation treatment related complications resulting from dosimetric discrepancies. CT images of the tissue expander were obtained through the course of treatment. To avoid a 'geographic miss' the amount of fluid injected into the tissue expander was kept constant following patient's satisfaction with the size of the breast mound. The CT scans allowed better visualization of the prosthesis and its relation to the surrounding tumor bed. This technique ensured that anatomical changes occurring during radiation treatment, if any, were minimized. Repeated dosimetry evaluations showed no changes to the prescribed dose distribution. A CT of the reconstructed breast provides an important quality control. Further studies with greater number of patients are required for confirming this impact on radiation treatment.