Keratitis due to Chaetomium sp.

Aim. To describe keratitis due to Chaetomium sp. occurring in a 65-year-old woman who presented with a corneal ulcer with hypopyon of the right eye with a history of trauma by vegetable matter. Method. Multiple scrapings were obtained from the ulcer. A lactophenol cotton blue wet mount and a Gram-stained smear of the scrapings were made. Scrapings were also inoculated onto various culture media. Results. Direct microscopy of corneal scrapings revealed moderate numbers of septate fungal hyphae. Greenish-yellow-coloured fungal colonies with aerial mycelium were observed in culture of the corneal scrapes. On the basis of colony characteristics and conidial structure, the fungal isolate was identified as Chaetomium sp. The patient was treated with topical natamycin (5%) hourly and cyclopentolate 1% drops 3 times a day. After 4 weeks of therapy, the hypopyon had disappeared, the epithelial defect had healed, and the stromal infiltration had almost completely resolved; the visual acuity of the eye improved from hand movements to (1/2)/60. Conclusion. Fungi of the genus Chaetomium, which are rare causes of human disease (systemic mycosis, endocarditis, subcutaneous lesions), may also cause ocular lesions

Behaviour of Innovative Concrete Sandwich Panels with Pervious Concrete Core under Flexural Bending

Research studies investigating the possibility of using new core material (other than polystyrene) in concrete sandwich panels are being reported in the literature. In this paper, lightweight pervious concrete core is proposed as a new alternative. In this paper, the flexural behaviour of concrete sandwich panels with pervious concrete core is investigated under three-point and four-point bending conditions. The geometrical variables considered are core thickness and number of shear connector lines. Test results showed that, sandwich panels without shear connector trusses failed due to separation of wythes, and the panels with shear connector trusses achieved composite action. The variables considered were found to influence the initial stiffness, cracking moment, ultimate moment, load-deflection behaviour and load-strain behaviour of the panels. Analytical study indicated that the equation given in ACI 318 underestimated the strength of the tested panels. The equation have to be modified by explicitly including the shear connector details in the equation for predicting the flexural strength with reasonable accuracy. Further experimental and analytical studies on prototype concrete sandwich panels with pervious concrete core produced using lightweight aggregates are required in view of developing design guidelines for practical applications

Interferon γ (IFN-γ) Is Necessary for the Genesis of Acetylcholine Receptor–induced Clinical Experimental Autoimmune Myasthenia gravis in Mice

Experimental autoimmune myasthenia gravis (EAMG) is an animal model of human myasthenia gravis (MG). In mice, EAMG is induced by immunization with Torpedo californica acetylcholine receptor (AChR) in complete Freund's adjuvant (CFA). However, the role of cytokines in the pathogenesis of EAMG is not clear. Because EAMG is an antibody-mediated disease, it is of the prevailing notion that Th2 but not Th1 cytokines play a role in the pathogenesis of this disease. To test the hypothesis that the Th1 cytokine, interferon (IFN)-γ, plays a role in the development of EAMG, we immunized IFN-γ knockout (IFN-gko) (−/−) mice and wild-type (WT) (+/+) mice of H-2b haplotype with AChR in CFA. We observed that AChR-primed lymph node cells from IFN-gko mice proliferated normally to AChR and to its dominant pathogenic α146–162 sequence when compared with these cells from the WT mice. However, the IFN-gko mice had no signs of muscle weakness and remained resistant to clinical EAMG at a time when the WT mice exhibited severe muscle weakness and some died. The resistance of IFN-gko mice was associated with greatly reduced levels of circulating anti-AChR antibody levels compared with those in the WT mice. Comparatively, immune sera from IFN-gko mice showed a dramatic reduction in mouse AChR-specific IgG1 and IgG2a antibodies. However, keyhole limpet hemocyanin (KLH)–priming of IFN-gko mice readily elicited both T cell and antibody responses, suggesting that IFN-γ regulates the humoral immune response distinctly to self (AChR) versus foreign (KLH) antigens. We conclude that IFN-γ is required for the generation of a pathogenic anti-AChR humoral immune response and for conferring susceptibility of mice to clinical EAMG

Autoantibodies to Agrin in Myasthenia Gravis Patients

To determine if patients with myasthenia gravis (MG) have antibodies to agrin, a proteoglycan released by motor neurons and is critical for neuromuscular junction (NMJ) formation, we collected serum samples from 93 patients with MG with known status of antibodies to acetylcholine receptor (AChR), muscle specific kinase (MuSK) and lipoprotein-related 4 (LRP4) and samples from control subjects (healthy individuals and individuals with other diseases). Sera were assayed for antibodies to agrin. We found antibodies to agrin in 7 serum samples of MG patients. None of the 25 healthy controls and none of the 55 control neurological patients had agrin antibodies. Two of the four triple negative MG patients (i.e., no detectable AChR, MuSK or LRP4 antibodies, AChR-/MuSK-/LRP4-) had antibodies against agrin. In addition, agrin antibodies were detected in 5 out of 83 AChR+/MuSK-/LRP4- patients but were not found in the 6 patients with MuSK antibodies (AChR-/MuSK+/LRP4-). Sera from MG patients with agrin antibodies were able to recognize recombinant agrin in conditioned media and in transfected HEK293 cells. These sera also inhibited the agrin-induced MuSK phosphorylation and AChR clustering in muscle cells. Together, these observations indicate that agrin is another autoantigen in patients with MG and agrin autoantibodies may be pathogenic through inhibition of agrin/LRP4/MuSK signaling at the NMJ