Effect of Inoculant Alloy Selection and Particle Size on Efficiency of Isomorphic Inoculation of Ti-Al.

The process of isomorphic inoculation relies on precise selection of inoculant alloys for a given system. Three alloys, Ti-10Al-25Nb, Ti-25Al-10Ta, and Ti-47Ta (at %) were selected as potential isomorphic inoculants for a Ti-46Al alloy. The binary Ti-Ta alloy selected was found to be ineffective as an inoculant due to its large density difference with the melt, causing the particles to settle. Both ternary alloys were successfully implemented as isomorphic inoculants that decreased the equiaxed grain size and increased the equiaxed fraction in their ingots. The degree of grain refinement obtained was found to be dependent on the number of particles introduced to the melt. Also, more new grains were formed than particles added to the melt. The grains/particle efficiency varied from greater than one to nearly twenty as the size of the particle increased. This is attributed to the breaking up of particles into smaller particles by dissolution in the melt. For a given particle size, Ti-Al-Ta and Ti-Al-Nb particles were found to have a roughly similar grain/particle efficiency.

Sinusitis: a rare cause for galactorrhoea.

A 32-year-old woman presented to the endocrinology clinic with recent onset galactorrhoea. Investigations revealed raised prolactin levels. An MRI scan demonstrated a normal pituitary gland, and an incidental finding of sphenoid sinusitis with expansion of the sphenoid sinus was thought to be due to a mucocele. It is postulated that either the direct local pressure by the mucocele or localised inflammation secondary to sinusitis might cause hyperprolactinaemia. The patient underwent endoscopic surgery to drain the mucocele, after which her galactorrhoea resolved. A review of the literature reveals only one previously documented case of sinusitis causing hyperprolactinaemia and galactorrhoea.

Use of watershed factors to predict consumer surfactant risk, water quality, and habitat quality in the upper Trinity River, Texas.

Surfactants are high production volume chemicals that are used in a wide assortment of "down-the-drain" consumer products. Wastewater treatment plants (WWTPs) generally remove 85 to more than 99% of all surfactants from influents, but residual concentrations are discharged into receiving waters via wastewater treatment plant effluents. The Trinity River that flows through the Dallas-Fort Worth metropolitan area, Texas, is an ideal study site for surfactants due to the high ratio of wastewater treatment plant effluent to river flow (>95%) during late summer months, providing an interesting scenario for surfactant loading into the environment. The objective of this project was to determine whether surfactant concentrations, expressed as toxic units, in-stream water quality, and aquatic habitat in the upper Trinity River could be predicted based on easily accessible watershed characteristics. Surface water and pore water samples were collected in late summer 2005 at 11 sites on the Trinity River in and around the Dallas-Fort Worth metropolitan area. Effluents of 4 major waste water treatment plants that discharge effluents into the Trinity River were also sampled. General chemistries and individual surfactant concentrations were determined, and total surfactant toxic units were calculated. GIS models of geospatial, anthropogenic factors (e.g., population density) and natural factors (e.g., soil organic matter) were collected and analyzed according to subwatersheds. Multiple regression analyses using the stepwise maximum R(2) improvement method were performed to develop prediction models of surfactant risk, water quality, and aquatic habitat (dependent variables) using the geospatial parameters (independent variables) that characterized the upper Trinity River watershed. We show that GIS modeling has the potential to be a reliable and inexpensive method of predicting water and habitat quality in the upper Trinity River watershed and perhaps other highly urbanized watersheds in semi-arid regions.

Malaria: a vaccine concept based on sickle haemoglobin's augmentation of an innate autoimmune process to band 3.

The protection from malaria afforded by sickle haemoglobin (and certain other haemoglobinopathies) suggests that it may be possible to utilise a common property that their erythrocytes share with both malaria-infected erythrocytes and senescent erythrocytes to develop a vaccine. All three conditions cause clustering of a specific protein molecule, band 3, on their erythrocyte's surface and this protein, when present on senescent erythrocytes at least, results in the immune recognition and removal of these by naturally occurring antibodies. It is hypothesised that if an up-regulated immune response to this protein on sickle cells is responsible for the benefit afforded to malaria patients then a vaccine using antigenic band 3 peptides may provide similar protection.

Reactive arthritis: the result of an anti-idiotypic immune response to a bacterial lipopolysaccharide antigen where the idiotype has the immunological appearance of a synovial antigen.

The term reactive arthritis (ReA) was first used in 1969 to describe sterile joint disease that follows infection elsewhere in the body. This is an attempt to explain the immunological basis of this disease, give a rationale for the presence of a single bacterial antigen in the involved joints, explain why the class I MHC molecule HLA-B27 is necessary and to suggest possible therapy. This paper proposes an anti-idiotypic (anti-id) model for this disease where a bacterial lipopolysaccharide (LPS) epitope is recognized by idiotypic (Id) T cell receptors and antibody Fab immune recognition surfaces (IRS) which have the immunologic appearance of an antigen on the synovial surface. These Id immune effectors utilize an HLA-B27 molecule to present their IRS on their surface, which results in an anti-id response that can also target the synovial antigen. The anti-id IRS have the immunologic appearance of LPS and their detection in the arthritic joint falsely suggests the presence of bacterial LPS. Evidence is presented which supports this reactive arthritis model in which there is a synovial antigen that is attacked by an anti-id response against the LPS of arthritogenic bacteria. Therapeutic vaccination is supported by this hypothesis.

The effects of the organophosphorous insecticides Dursban and Lorsban on the ciliated epithelium of the frog palate in vitro.

The ciliotoxic potential of the organophosphorous insecticides Dursban and Lorsban, their active ingredient, chlorpyrifos, and their carrier ingredients (Blanks) were assessed. Since chlorpyrifos inhibits acetylcholinesterase, the acetylcholine-innervated ciliated epithelial cultures of frog palate were used as the model. All compounds caused a decrease in frequency of ciliary beat overtime. EC50 values followed the same order as the time to inhibition. The orders were Lorsban > Dursban > chlorpyrifos, and Lorsban > Dursban approximately Lorsban Blank > Dursban Blank. Stimulation of ciliary beating occurred immediately after exposure to all compounds, followed by inhibition. Dursban, Lorsban, and both Blanks elicited stimulatory effects in the presence of atropine. Atropine only blocked the initial stimulatory response with chlorpyrifos. In addition to chlorpyrifos, some component(s) of the inert ingredients were initially stimulatory but ultimately inhibitory to ciliary beating in the frog palate model. All compounds caused mitochondrial damage, including swelling, disruption of cristae, and loss of matrix.

The effects of benomyl and its breakdown products carbendazim and butyl isocyanate on the structure and function of tracheal ciliated cells.

The effects of the fungicide benomyl and its breakdown products, carbendazim and butyl isocyanate, were examined on canine tracheal epithelial tissue in primary culture. Changes in ciliary frequencies were monitored with an optical spectrum analysis system. Serial dilutions of the test compounds were prepared in 100% corn oil and applied to the cell cultures for intervals up to 6 hours and frequencies measured at intervals of 15 minutes to 1 hour. Benomyl and butyl isocyanate caused concentration-dependent decreases in ciliary beat frequency. Benomyl at 300 micrograms/ml (3 mM) caused ciliostasis within 75 minutes of exposure. Butyl isocyanate at a molar concentration three times lower than benomyl (1 mM) caused a similar response, although within 30 minutes. The IBC50 for benomyl was 0.75 mM, while for butyl isocyanate it was 0.52 mM. Carbendazim caused a moderate decrease in frequency over a 6 hour exposure period. Benomyl caused moderate to severe swelling of the mitochondria of ciliated epithelial cells with other cell organelles appearing normal. Butyl isocyanate did not cause any noticeable effect on cell ultrastructure and the apparently low rate of penetration of carbendazim into cells made it impossible to obtain an effect which justified ultrastructural analysis. It appears, at least for benomyl and butyl isocyanate, that while the physiological effect of these two compounds (inhibition of ciliary beat) is the same, the sites of action in the cell may be different.

Reflections on an interface.

This discusses an immune recognition model of autoimmunity and tolerance which is based on an idiotypic and an anti-idiotypic immune network response at a virus receptor interface.

Intra-epithelial palatine nerve endings and their regulation of ciliary activity of frog palate epithelium.

1. Direct contact between intra-epithelial nerve endings and ciliated cells was observed in frog (Rana pipiens) palate epithelium. 2. Electrical stimulation of the palatine nerve to the explant or the explant culture induced an increase in ciliary beat frequency in explant and outgrowth cells. 3. Atropine inhibited electrically stimulated ciliary beat frequency increase in the explant and outgrowth cells. 4. Gap junctional intercellular communication appears to be involved in the propagation of stimulated ciliary beat frequency increase from innervated to non-innervated ciliated cells.

Transdifferentiation of outgrowth cells and cultured epithelial cells from swine trachea.

The morphologic and functional properties of explant out-growth cells and epithelial cells isolated from swine trachea epithelium by proteolysis were examined. A mixed population of ciliated, serous, and basal cells, obtained from out-growths, from proteolysis of trachea epithelium, and from unattached explants in organ culture, all yielded cell cultures that werecomposed almost entirely of mucus-secreting cells. When the cells were grown in primary or secondary culture on a modified collagen matrix in supplemented HAM:DMEM (1:1) medium they expressed a mucus-secreting phenotype with numerous mucus granules at various stages of maturation and incorporated [3H]GlcN and 35SO4 into secreied mucin glycoproteins. Results obtained in these studies suggest that extensive transdifferentiation of ciliated and serous cells to mucus-secreting-cells occurs after the release and during subsequent attachment and culture. Ciliated cells containing mucus granules were seen in various stages of cilia resorption. Basal cells containing mucus granules were also frequently observed. The number of mucus-secreting cells and the synthesis of mucin glycoproteins increased dramatically with time of attachment and culture, whereas cell proliferation, population doubling time of 72 h, and incorporation of [3H]-thymidine into DNA increased much more slowly. The number of mucus-secreting cells correlated closely with the level of secretion of mucin glycoproteins. Taken collectively, these studies help to elucidate the transdifferentiation process, which dramatically increases the number of mucus-secreting cells after disruption and release of epithelial cells from swine tracheobronchial epithelium. A similar mechanism involving disruption of the extracellular matrix may be involved in the stimulation of hypersecretion of mucus and mucin glycoproteins by chemical and infections irritants.

Does HIV disrupt a naturally occurring immune modulation system?

An immune modulation complex is proposed which recognizes and is driven by an MHC presented epitope of the CD4 molecule present on the surface of up regulated CD4+ lymphocytes. Immune modulation is affected by both CD4 lymphocyte destruction and impairment of their potential for immune recognition. These two processes are carefully controlled by an idiotypic, anti-idiotypic feedback mechanism. The CD4 tropic area of HIV impersonates some components of that feedback loop resulting in increased CD4 lymphocyte destruction.

Primary ciliary dyskinesia in the dog.

A disorder caused by congenital ciliary dysfunction occurs in dogs. Most of the clinical signs are directly or indirectly attributable to immotile or dyskinetic cilia and spermflagella. Due to severely impaired mucociliary clearance, a continuous mucoid nasal discharge and intermittent sneezing and coughing are typically observed during the neonatal period. Recurrent bacterial rhinosinusitis and bronchopneumonia usually start within a few weeks of birth. Hypoplastic nasal sinuses and atresia of the frontal sinuses are variable features of the disease that may be caused by neonatal colonization of these structures by specific bacteria. Bronchiectasis is an acquired lesion resulting from chronic inflammation and obstruction of airways. A secretory otitis media is caused by dysfunction of the cilia in the middle ear, and is manifested in some dogs by sclerotic tympanic bullae. Male infertility is caused by live, but immotile to hypomotile spermatozoa; however, unexplained oligospermia and azoospermia have been reported. Hydrocephalus and situs inversus are common but variable features of the disease; the genesis of these lesions has not yet been determined. The probable mode of inheritance is autosomal recessive, but dominant mutations cannot be excluded. The diagnosis can be confirmed by demonstrating the absence or near absence of nasal or tracheal mucociliary clearance and the presence of a specific ultrastructural lesion in a large percentage of cilia from multiple sites (airways, middle ear, or oviduct). The ultrastructure of sperm flagella should mirror that of the cilia. Not all dogs have ultrastructural ciliary lesions, and in these cases, results of in vitro analysis of ciliary activity may be highly suggestive, if not diagnostic. In dogs without mucociliary clearance in which structural and functional analysis of cilia are not diagnostic, confirmation of congenital ciliary dysfunction can be established only by ruling out other diseases with similar signs (e.g., congenital immunodeficiency syndromes). The clinical course in an longevity of affected dogs are highly variable. Appropriate antibiotic treatment and pulmonary physical therapy may result in prolonged survival, although cor pulmonale and reactive systemic amyloidosis are potential sequelae of chronic hypoxia and chronic bacterial infection of the airways, respectively.

AIDS--an autoimmune model.

In AIDS a complementary interface between the HIV virus and the CD4 molecule of the T4 lymphocyte suggest a possible cause of immune self-recognition. Because of this complementarity, an anti-idiotypic immune response to the CD4 attachment area of HIV should result in an autoimmune reaction to CD4 positive lymphocytes. Experimental demonstration of such an immune recognition model by autoreactive lymphocytes is presented and a hypothetical immune response unit is suggested.

The immediate effects of silicon carbide whiskers upon ciliated tracheal epithelium.

Considering the relationship between toxicity of dust and particle geometry, as exhibited by asbestos, we have examined short-term biological effects of SiC whiskers (SiCW) in vitro and in vivo. Cultured explants of tracheal epithelium were exposed to a range of SiCW concentrations. There were no dramatic effects on ciliary function as measured by an optical spectrum analysis system that provided discrete ciliary frequencies. Particles were swept by ciliary activity into nonciliated regions where foci of extensive cell damage and death were observed with whiskers penetrating epithelial layers into the underlying tissues. Similar necrotic foci were observed in tracheae from rats exposed by intratracheal instillation to SiC whiskers in vivo.

An immune model defined by AIDS.

An immune control system is proposed which is made up of a pair of idiotypic T4 and T8 cells which recognize self-antigen, and a pair of anti-idiotypic T4 and T8 cells which recognize those idiotypic receptors. The protective and destructive elements of the control cells and their induced immunoglobulins are in equilibrium, allowing self-recognition and tolerance. One of the self-antigens monitored by the system is CD4, the T4 surface marker and also the HIV attachment site. In AIDS the HIV attachment antigen is immunologically identical to one of the CD4 control cell receptors. This disrupts the equilibrium of the system causing chronic T4 cell destruction.