Hidradenitis suppurativa: A neglected disease in Indigenous Australians

We report the first case series of hidradenitis suppurativa in patients of Indigenous Australian heritage. The incidence and ethnicity of populations affected by this condition are not known. The high comorbid disease burden and socioeconomic disadvantage that is well recognised in the Indigenous Australian population poses significant challenges to therapeutic outcomes.     

Lung function and immunological changes in poultry breeders

Summary The results of the study of 61 persons occupationally exposed to the inhalation of dust from waste materials in chicken breeding are presented. The subjects were divided into three groups: 1. females in permanent exposure, 2. males in permanent exposure, 3. males in intermittent exposure. The following examinations were performed: case histories with special reference to symptoms of allergic alveolitis and/or chronic nonspecific lung disease, testing of skin hypersensitivity to allergens prepared from material collected in working places, blood analysis for the precipitins against chicken dropping and cock serum, testing of ventilatory lung function including measurements of residual volume, and testing of lung diffusion capacity. A very high prevalence of positive early and late skin reaction was found with no large differences between different groups of subjects. The highest percentage of precipitins was found in permanently exposed women. FVC, FEV₁ and MEF 25% values were significantly lower than predicted normal values. A statistically significant increase of the residual volume was recorded in all subjects in permanent exposure. Lung diffusion capacity in all the subjects was normal. The prevalence of acute respiratory symptoms indicative of allergic alveolitis was significantly higher in subjects in permanent than in those in intermittent exposure.     

The role of core antigen detection in management of hepatitis C: a critical review.

Several assays in research format and two commercial assays for the detection of hepatitis C virus (HCV) core protein or HCV core antigen have been developed in recent years. In order to elucidate the role and significance of HCV core antigen detection in the diagnosis and management of hepatitis C, we reviewed 56 studies published in peer-reviewed journals until September 2004. Evaluations in transfusion settings showed that the HCV core antigen assay detects HCV infection, similarly as nucleic acid techniques (NAT), between 40 and 50 days earlier than the current third generation HCV antibody screening assays. HCV core antigen levels closely track HCV RNA dynamics, and allow clinical monitoring of a patient's therapy, independently of HCV genotype, however, mainly in the samples with HCV RNA levels above 20,000 IU/ml. Considering the lower sensitivity of HCV core antigen detection in comparison to NAT, the HCV core antigen assay is not practical for the determination of the end of treatment response and sustained viral response, but could be useful for the determination of early viral response in the pegylated interferon-alpha and ribavirin treated patients infected with HCV genotype 1. The HCV core antigen detection is a viable tool for study of hepatitis C pathogenesis. The HCV core antigen can be used as a marker of HCV replication in anti-HCV positive individuals in the areas of the world that cannot afford NAT and/or in the settings that are not equipped or competent to perform HCV RNA testing. Because the manufacturer of HCV core antigen assays recently stopped an active marketing of these assays in several countries, it will, unfortunately and probably, never be possible to determine the actual potential and usefulness of HCV core antigen testing in the management of hepatitis C.     

Development of laboratory information system--quality standards

The aim of the study was to determine structural modules of laboratory information system (LIS) for the application of new biomedical and information technologies by utilizing current organizational trends. The method used included definition of structural modules according to significant LIS properties, e.g., a large number of data, automation of analyses and rapid exchange of information, and according to the process of information establishment the collection, organization, selection, synthesis and distribution. Thus, outdated distributed software at the Clinical Institute of Laboratory Diagnosis has now been replaced by modular organization. Modules have been developed for the following: data input, online operation of laboratory instruments, preparation of results, compilation of medical documentation on quality assurance based on the application of quality standards, management of finances, and for point of care testing. The method of re-engineering as well as adherence to EN and ISO quality standards were utilized in planning the development of LIS based on the application of new information technologies and in shaping business processes. The application of re-engineering in LIS development results in quality improvement, reduces the cost and time necessary for performance of procedures, and improves relations in organizational structure.     

T cells specific for the myelin oligodendrocyte glycoprotein mediate an unusual autoimmune inflammatory response in the central nervous system

Myelin oligodendrocyte glycoprotein (MOG)-specific T cells mediate an autoimmune inflammatory response in the central nervous system (CNS) that differs radically from conventional models of T cell-mediated experimental allergic encephalomyelitis (EAE). Using synthetic peptides an encephalitogenic T cell epitope of MOG for the Lewis rat was identified within the extracellular IgG V-like domain of the protein, amino acids 44-53 (FSRVVHLYRN).The adoptive transfer of CD4⁺ T cells specific for this epitope induce an intense, dose-dependent inflammatory response in the CNS of naive syngeneic recipients. However, unlike the inflammatory response induced by myelin basic protein (MBP)-specific T cell lines, inflammation mediated by the MOG peptide-specific T cells failed to induce a gross neurological deficit. This unexpected observation was not due to a reduction in the overall inflammatory response in the CNS, but was specifically associated with a decrease in the extent of parenchymal (as opposed to perivascular) inflammation, a selective decrease in the number of ED1⁺ macrophages infiltrating the CNS, and a total lack of peripheral nerve inflammation. The decreased recruitment of macrophages into the CNS could not be ascribed to deficiences in the synthesis of interferon-γ, tumor necrosis factor-a, interleukin (IL)-6 or IL-2 by the T cell line. Moreover, this sub-clinical inflammatory response induced severe blood-brain barrier dysfunction as demonstrated by the induction of severe clinical disease following intravenous injection of a demyelinating MOG-specific monoclonal antibody. The neurological deficit in EAE thus exhibits an unexpected dependence on the identity of the target autoantigen, which determines the extent and nature of the local inflammatory response and ultimately the extent of the neurological deficit.     

Post-injury immunosuppression and secondary infections are caused by an AIM2 inflammasome-driven signaling cascade

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Efficient induction of cytotoxic CD8+ T cells against exogenous proteins: establishment and characterization of a T cell line specific for the membrane protein ActA of Listeria monocytogenes

The property of listeriolysin (LLO) to introduce soluble passenger proteins into the cytosol of antigen-presenting cells allows the induction of CD8⁺ cytotoxic T cells against such antigens. To overcome the potential problem of presentation of the immunodominant epitope LLO91-99 by H-2K^d, a variant LLO92A was established in which Tyr 92 was replaced by Ala. Immunization of BALB/c mice with purified LLO92A failed to stimulate cytotoxic T cells specific for either the epitope LLO91-99 or for any other LLO-derived peptide. Injection of mixtures of purified LLO92A and soluble nucleoprotein (NP) of influenza virus into mice resulted in a strong cytotoxic T cell response exclusively directed against NP. The LLO92A variant was successfully used to generate, propagate and characterize a CD8⁺ T cell line specific for the membrane-bound virulence factor ActA of Listeria monocytogenes. Interestingly, wild-type ActA bound to the surface of live L. monocytogenes was not presented by MHC class I molecules to the CD8⁺ T cell line.