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PubMed2003

Association of porcine circovirus 2 with porcine respiratory disease complex.

A retrospective study was performed on natural cases of porcine respiratory disease complex (PRDC) to determine the association and prevalence of PRDC with porcine circovirus 2 (PCV2) and other co-existing pathogens in Korea. Histologically, alveolar septa were markedly thickened by infiltrates of mononuclear cells. Moderate to marked multifocal peribronchial and peribronchiolar fibrosis were present and often extended into the airway lamina propria. Among the 105 pigs with PRDC, 85 were positive for PCV2, 66 were positive for porcine reproductive and respiratory syndrome virus (PRRSV), 60 were positive for porcine parvovirus (PPV), and 14 were positive for swine influenza virus (SIV). There were 80 co-infections and 25 single infections. A co-infection of PCV2 with another additional bacterial pathogen is frequently diagnosed in PRDC. The combination of PCV2 and Pasteurella multocida (38 cases) was most prevalent followed by PCV2 and Mycoplasma hyopneumoniae (33 cases). The consistent presence of PCV2, but lower prevalence of other viral and bacterial pathogens in all pigs examined with PRDC, has led us to speculate that PCV2 plays an important role in PRDC.

Animals↗
PubMed2004

Establishment of genetic associations for complex diseases is independent of early study findings.

Numerous genetic association studies for complex diseases are performed. Investigators place emphasis on formal statistical significance (P-values < 0.05), but the predictive ability of early statistically significant ('positive') findings is unclear. We scrutinized 55 cumulative meta-analyses of genetic associations (579 studies), in order to assess whether having statistical significance in the earliest (first) published study or in at least half among several (> or =3) early-published studies, or high statistical significance in early studies had any predictive ability for establishing or refuting the presence of the genetic association in subsequent research. In 35 associations, a first study was 'positive' and in 15 associations more than half of the early-published reports were 'positive'. The average publication rate of subsequent studies increased 1.71-fold with a 'positive' first report. When compared against the summary results of subsequent research, sensitivity and specificity were 0.65 and 0.38 for the first reports, and 0.40 and 0.73, respectively, when at least three early studies were considered. First studies also had poor predictive ability, when we considered the estimated attributable fraction and coverage of the 95% confidence interval thereof or higher levels of statistical significance. We conclude that although 'positive' findings in the very first reports provide strong incentive for conducting more studies on a putative genetic epidemiological association, the statistical significance or even the magnitude of the effect of early studies cannot adequately predict eventual establishment of an association. Conversely, many genuine epidemiological associations would be missed, if research were abandoned after early underpowered 'negative' studies.

Causality↗
PubMedDate not supplied

[Human susceptibility to complex diseases. Genetic analysis in large populations].

Inherited susceptibility underlying the ethiopathogenity of complex diseases is based on the existence of a high number of genetic variants which are cooperating to generate different risk genetic profiles. We try to identify such profiles and construct wide data bases with this genetic information.

Bioethical Issues↗
PubMed1998

The immune system can affect learning: chronic immune complex disease in a rat model.

Evidence is presented that the immune system can affect central nervous system functioning, leading to changes in learning. Immune complex disease is induced in rats and their behavior tested using a Lashley maze. Significant differences in behavior were found between the animals with high disease activity and those with low disease activity and the non-disease controls. These changes were not due to uremia and are most likely due to the immune response. There is some evidence immune complex deposits in the choroid plexus may play some role, but not the sole or major role in the behavioral changes. This provides a model by which immunologic processes can cause neuropsychiatric manifestations in autoimmune diseases like lupus, as well as showing that immune processes can affect behavioral functioning.

Animals↗
PubMed1980

Models of immune complex disease.

An inflammatory lesion commonly develops in certain organs (e.g. skin, brain, kidneys and joints) either when antigen in the tissue spaces reacts with precipitating antibody forming microprecipitates in and around small blood vessels or when antigen in excess in the blood stream reacting with potentially precipitating antibody forms immune complexes (ICs) that lodge in the blood vessels. Other factors known to be essential for the pathogenesis of such lesions include (a) the activation of complement components, (b) chemotaxis towards ICs of PMN leucocytes and macrophages, (c) phagocytosis of ICs and (d) the formation and release by the phagocytes of prostaglandins, lysosomal enzymes, toxic metabolites of oxygen and other mediators of inflammation and tissue damage. Knowledge of these pathogenetic mechanisms opens up possibilities for chemotherapeutic attenuation or abolition of the development of antibody-dependent inflammatory lesions. The extent to which this goal has been achieved in the clinic with the aid of substances selected through the use of models of immune complex disease will be reviewed in this presentation.

Adrenocorticotropic Hormone↗
PubMed1985

[Basic studies on enzyme therapy of immune complex diseases].

Several in vitro investigations and animal experiments are described which may be used as experimental basis for the enzymatic treatment of rheumatoid arthritis and, possibly, also other immune complex diseases. Demonstration of absorption of unaltered orally-administered radiolabelled enzymes is shown in guinea pigs and rabbits. In vitro experiments with 4 types of soluble immune complexes which were incubated with gradually increasing amounts of enzymes showed dose-dependent cleavage of complexes. Antigen-induced experimental arthritis of rabbits, fed different amounts of a therapeutically used mixture of enzymes at different times, could be inhibited by this treatment, in dependence of dosage and time of feeding. With respect to the therapeutic applications of this study, the results favour the use of a high dosage repeated daily administration, since duration of effect seems limited.

Animals↗
PubMed1993

Low serum levels of oral antimycobacterial agents in patients with disseminated Mycobacterium avium complex disease.

Twenty-seven human immunodeficiency virus-infected patients with disseminated Mycobacterium avium complex disease who were treated with oral antimycobacterial agents (clofazimine, ciprofloxacin, ethambutol, and rifampin) were studied to evaluate the usefulness of monitoring serum drug concentrations and testing in vitro susceptibility of M. avium complex (MAC) isolates. Twenty patients tolerated treatment with three or four antimycobacterial agents for at least 8 weeks; mycobacteremia was eradicated in 7 (35%). The in vitro susceptibilities of MAC isolates to antimycobacterial agents were similar for these 7 and for the 13 who did not respond to antimycobacterial treatment. Serum drug levels were below the expected range in 6 of the 7 whose mycobacteremia was cleared and in 9 of the 13 nonresponders (P = .41). These low serum concentrations of antimycobacterial drugs may be due to impaired drug absorption in patients with AIDS and disseminated MAC disease.

AIDS-Related Opportunistic Infections↗
PubMed1984

Immune complex disease complicating diabetic glomerulosclerosis.

We report immunopathologic findings observed in renal biopsies of 18 patients with diabetic glomerulosclerosis and associated glomerulonephritis. 10 patients had nodular and 8 patients diffuse diabetic glomerulosclerosis. Focal proliferative glomerulonephritis (4 patients), membranous glomerulonephritis (3 patients), postinfectious glomerulonephritis, Henoch-Schönlein nephritis, IgA nephropathy of Berger (1 patient each), and mesangiopathic glomerulonephritis (8 patients) were the superimposed conditions. In patients with diabetic renal disease, a rapid loss of renal function or an atypical urinalysis could be the expression of a superimposed immune complex disease. Because of functional and biochemical alterations, the glomeruli of diabetic patients may be more susceptible to immune-mediated injury.

Adult↗
PubMed1976

Elaboration of toxic oxygen by-products by neutrophils in a model of immune complex disease.

Contact between human neutrophils and aggregated immunoglobulin G bound to micropore filters has been studied as a model of the pathogenesis of tissue damage in immune complex disease. Contact with this surface, as well as with plain filters and polystyrene petri dishes, induced neutrophils to elaborate superoxide anion and hydrogen peroxide and to generate chemiluminescence, which has been attributed to singlet oxygen. Pretreatment of the cells with cytochalasin B decreased these activities but increased release of lysosomal beta-glucuronidase, suggesting that degranulation and the burst of oxygen metabolism that characterizes phagocytes are independently regulated functions. Toxic oxygen metabolites released from neutrophils are highly reactive and could mediate tissue injury at sites of inflammation.

Anions↗
PubMed2004

Meta-analysis of linkage studies for complex diseases: an overview of methods and a simulation study.

Linkage genome scans for complex diseases have low power with the usual sample sizes, and hence meta-analysis of several scans for the same disease might be a promising approach. Appropriate data are now becoming accessible. Here we give an overview of the available statistical methods and current applications. In a simulation study, we compare the power of different methods to combine multipoint linkage scores, namely Fisher's p-value combination, the truncated product method, the Genome Search Meta-Analysis (GSMA) method and our weighting methods. In particular, we investigate the effects of heterogeneity introduced by different genetic marker sets and sample sizes between genome scans. The weighting methods explicitly take those differences into account and have more power in the simulated scenarios than the other methods.

Genetic Diseases, Inborn↗
PubMed2001

A robust identity-by-descent procedure using affected sib pairs: multipoint mapping for complex diseases.

Multipoint linkage analysis is a powerful tool to localize susceptibility genes for complex diseases. However, the conventional lod score method relies critically on the correct specification of mode of inheritance for accurate estimation of gene position. On the other hand, allele-sharing methods, as currently practiced, are designed to test the null hypothesis of no linkage rather than estimate the location of the susceptibility gene(s). In this paper, we propose an identity-by-descent (IBD)-based procedure to estimate the location of an unobserved susceptibility gene within a chromosomal region framed by multiple markers. Here we deal with the practical situation where some of the markers might not be fully informative. Rather the IBD statistic at an arbitrary within the region is imputed using the multipoint marker information. The method is robust in that no assumption about the genetic mechanism is required other than that the region contains no more than one susceptibility gene. In particular, this approach builds upon a simple representation for the expected IBD at any arbitrary locus within the region using data from affected sib pairs. With this representation, one can carry out a parametric inference procedure to locate an unobserved susceptibility gene. In addition, here we derive a sample size formula for the number of affected sib pairs needed to detect linkage with multiple markers. Throughout, the proposed method is illustrated through simulated data. We have implemented this method including exploratory and formal model-fitting procedures to locate susceptibility genes, plus sample size and power calculations in a program, GENEFINDER, which will be made available shortly.

Chromosome Mapping↗
PubMed1977

[HBs-antigen induced extrahepatic immune-complex disease (author's transl)].

A 62-year old patient was hospitalized with fever, polyarthritis and exanthema. All bacteriological, virological and biochemical findings were normal. The immunological analysis showed initially the HBs-antigen in the serum. No irregular antibody was found. Chemotherapy was failing, but application of corticosteroids was followed by a dramatic improvement. Nine weeks after the onset of the disease the patient was healthy again. Antibodies against HBs-antigen were found 3 months later. The data suggest an immune-complex disease like serum sickness based on an infection with hepatitis-B-virus without involvement of the liver.

Adrenal Cortex Hormones↗
PubMed1975

[Unusual clinical forms of pseudo-LE syndrome: an induced immune-complex disease? (author's transl)].

Two of nine patients with pseudo-LE syndrome had previously undescribed organ manifestations. In one there was the full-blown picture of cutaneous lupus erythematodes, with renal and CNS involvement, ending fatally. Immunohistologically there was severe vasculitis and nephritis, histologically generalised necrotizing angitis. It is possible that the dramatic clinical picture was due to alpha-methyldopa. In the second case lymphadenopathy with bihilar involvement and splenomegaly predominated. Histologically there was no evidence of Boeck's sarcoid. Further studies revealed systemic involvement with immune-complex nephritis, electron-dense deposits in the glomerular basal membrane, and the typical changes of lupus erythematodes in the marrow. In a third case there were similar changes in kidney and marrow. These findings support the view of an immune-complex disease which can be fatal. An unusual feature in seven of the nine patients was the proven intake of Venopyronum¿ coated tablets in temporal relationship to the manifestation of the disease. It is possible that the described cases of pseudo-LE syndrome were drug-induced. The immunological mechanism of the disease would, in that case, be analogous to penicillamine nephropathy.

Adult↗
PubMed1983

Conceptual understanding of pustulosis palmaris et plantaris as an immune complex disease due to focal tonsillar infections.

The relationship between pustulosis palmaris et plantaris (PPP) and immune complexes was studied in 17 patients who underwent tonsillectomy. By means of the Clq-binding test, immune complexes were detected in a considerable number of sera from these patients. Patients with a high serum level of immune complexes which decreased following tonsillectomy were found to benefit by a remarkable improvement in their skin lesions. There was a close association between the degree of improvement in skin lesions following tonsillectomy, and the changes in circulating immune complex levels after tonsillectomy. Immunofluorescence showed that all 6 patients with PPP tested had deposits of IgG, IgM, IgA or C3 in their skin lesions. These results suggest that PPP may be an immune complex disease, and that it may be closely associated with the tonsil as a focus for the release of antigens or immune complexes.

Adolescent↗
PubMedDate not supplied

Complex disease of the pleural space: radiographic and CT evaluation.

Pleural space disease is often complex, difficult to diagnose, and problematic to manage. At computed tomography (CT), empyema appears as an oblong fluid collection with smooth inner margins that compresses and displaces the surrounding lung and airways away from the pleural collection. CT findings in hemothorax include heterogeneous attenuation of pleural fluid, hyperattenuating areas of debris within pleural fluid, and a "fluid-hematocrit" level. Nodular pleural thickening at chest radiography or CT indicates a malignant pleural effusion; the cross-sectional capability of CT allows scrutiny of all pleural surfaces to detect enhancing tumor implants in addition to pleural effusions. Pleural plaque, rounded atelectasis, and pleural pseudotumor can mimic neoplastic disease on chest radiographs but can often be diagnosed with CT. Bronchopleural fistula may also be difficult to diagnose with radiography alone, necessitating further analysis with CT. Pleurocentesis fluid containing chyle, cerebrospinal fluid, amylase, or hyperalimentation fluid indicates pleural space disease with an unusual or iatrogenic cause. Recent advances in image-guided procedures have significantly improved treatment options for many complex pleural space processes.

Adult↗
PubMed1983

Permeability of the blood cerebrospinal fluid barrier during acute immune complex disease.

Changes in the permeability of the blood-brain barrier (BBB) and blood-cerebrospinal fluid (blood-CSF) barrier in rabbits were assessed by using a sensitive double isotope technique at different times after the induction of acute immune complex disease (AICD). Induction of AICD was done with a single large dose of bovine serum albumin, whereas controls received only saline. Animals were sacrificed 6, 9, 12, 15, and 18 days after induction. Extravasation of protein was measured by injecting rabbits i.v. with 131I-rabbit serum albumin (RSA) 24 hr before sacrifice. In order to correct for intravascular blood volume, 125I-RSA was injected 5 min before sacrifice. Extravascular blood equivalents (EVBE), a measure of barrier permeability, were elevated in the CSF of rabbits sacrificed on days 12 and 15. None of the brain regions from any of the animal groups showed any changes or significant differences from controls in EVBE values on these days. These results indicate that there was an increase in the permeability of the blood-CSF barrier to radiolabeled albumin but not in the BBB proper during the time that CSF IgG levels were elevated in AICD. The potential significance of these findings for the mechanisms mediating central nervous system involvement in systemic lupus erythematosus is discussed.

Acute Disease↗