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  • 1
    Electronic Resource
    Electronic Resource
    Relationship between mesangial deposition of IgA1 and IgA2 subclasses and complement activation in IgA glomerulonephritis (2002)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 7 (2002), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.7.s.30.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Mesangial deposition of IgA2 subclass and lectin pathway-mediated complement activation in IgA glomerulonephritis (2001)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 6 (2001), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Three pathways are recognized in the complement activation cascade. The aim of our study was to elucidate immunohistologically which complement pathway is associated with the activation in IgA glomerulonephritis (GN) and the relation of IgA subclass to the complement activation. Immunohistological staining was performed on biopsied renal specimens from 36 patients with IgA GN, 10 with systemic lupus erythematosus (SLE) and 16 with other glomerulonephritides using polyclonal antibodies of IgG, IgA, IgM, C3c, C4, C1q and monoclonal antibodies of IgA1, IgA2, mannose-binding lectin (MBL) and MBL-associated serine protease-1 (MASP-1). Mesangial deposits of IgA1, IgA2, C3c, C4, MBL and MASP-1 were detected in 19 of the 36 patients with IgA GN, and IgA2 and MBL/MASP-1 were colocalized in the mesangium in these 19 patients. The remaining 17 patients showed mesangial deposition of IgA1 alone. Twelve of these 17 patients presented mesangial deposition of C3c without deposition of C4, MBL and MASP-1. No deposition of C1q was evident in IgA GN patients. Three of the 10 SLE patients showed glomerular deposition of MBL and MASP-1 without deposition of IgA2. No patient with other glomerulonephritides showed glomerular deposition of IgA1, IgA2, MBL and MASP-1. There was no correlation in clinical and pathological indicators between IgA2-positive and IgA2-negative patients with IgA GN. In conclusion, alternative pathway-mediated complement activation is associated in patients with mesangial deposition of IgA1 alone in IgA GN. In those with the deposition of both IgA1 and IgA2, both alternative and lectin pathways are activated, and mesangial deposition of IgA2 is associated with the lectin pathway-mediated complement activation in IgA GN.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2001.00006.x
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  • 3
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    Kalinga ornata Alder & Hancock, 1864 (Nudibranchia: Polyceridae): a unique case of a sea slug feeding on echinoderms (2011)
    Oxford University Press
    Details
    Publication Date: 2011-11-24
    Print ISSN: 0260-1230
    Electronic ISSN: 1464-3766
    Topics: Biology
    Published by Oxford University Press
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  • 4
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    Recognition of viruses in the cytoplasm by RLRs and other helicases--how conformational changes, mitochondrial dynamics and ubiquitination control innate immune responses (2012)
    Oxford University Press
    Details
    Publication Date: 2012-11-28
    Description: Mammalian cells possess multiple sensors for recognition of invasion by a broad range of microbes. This recognition occurs through specific molecular signatures found across various pathogens. Toll-like receptors (TLRs), retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and C-type lectin receptors (CLRs) are the major cellular pathogen-recognition receptors (PRRs) responsible for this recognition. TLRs are transmembrane sensors, whereas other PRRs mainly localize in the cytoplasm for the activation of type I interferons and pro-inflammatory cytokines. Among these PRRs, RLRs are well known for their indispensable role in sensing the invasion of RNA viruses. This review summarizes recent advances in knowledge about viral recognition by RLRs and their signalling pathways, and introduces newly emerging RNA helicases involved in innate immune responses.
    Print ISSN: 0953-8178
    Electronic ISSN: 1460-2377
    Topics: Medicine
    Published by Oxford University Press
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  • 5
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    Importance of endothelial NF-{kappa}B signalling in vascular remodelling and aortic aneurysm formation (2012)
    Oxford University Press
    Details
    Publication Date: 2012-12-22
    Description: Aims Vascular remodelling and aortic aneurysm formation are induced mainly by inflammatory responses in the adventitia and media. However, relatively little is known about the mechanistic significance of endothelium in the pathogenesis of these vascular disorders. The transcription factor nuclear factor-kappa B (NF-B) regulates the expressions of numerous genes, including those related to pro-inflammatory responses. Therefore, to investigate the roles of endothelial pro-inflammatory responses, we examined the impact of blocking endothelial NF-B signalling on intimal hyperplasia and aneurysm formation. Methods and results To block endothelial NF-B signalling, we used transgenic mice expressing dominant-negative IBα selectively in endothelial cells (E-DNIB mice). E-DNIB mice were protected from the development of cuff injury-induced neointimal formation, in association with suppressed arterial expressions of cellular adhesion molecules, a macrophage marker, and inflammatory factors. In addition, the blockade of endothelial NF-B signalling prevented abdominal aortic aneurysm formation in an experimental model, hypercholesterolaemic apolipoprotein E-deficient mice with angiotensin II infusion. In this aneurysm model as well, aortic expressions of an adhesion molecule, a macrophage marker, and inflammatory factors were suppressed with the inhibited expression and activity of matrix metalloproteinases in the aorta. Conclusion Endothelial NF-B activation up-regulates adhesion molecule expression, which may trigger macrophage infiltration and inflammation in the adventitia and media. Thus, the endothelium plays important roles in vascular remodelling and aneurysm formation through its intracellular NF-B signalling.
    Print ISSN: 0008-6363
    Electronic ISSN: 1755-3245
    Topics: Medicine
    Published by Oxford University Press
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  • 6
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    Extracellular vesicles derived from human vestibular schwannomas associated with poor hearing damage cochlear cells (2016)
    Oxford University Press
    Details
    Publication Date: 2016-10-14
    Description: Background Vestibular schwannoma (VS) is a tumor of the vestibular nerve that transmits balance information from the inner ear to the brain. Sensorineural hearing loss occurs in 95% of patients with these tumors, but the cause of this loss is not well understood. We posit a role of VS-secreted extracellular vesicles (EVs) as a major contributing factor in cochlear nerve damage. Methods Using differential centrifugation, we isolated EVs from VS cell line HEI-193 and primary cultured human VS cells from patients with good hearing or poor hearing. The EVs were characterized using a Nanosight device and transmission electron microscopy and by extracting their RNA content. The EVs' effects on cultured murine spiral ganglion cells and organotypic cochlear cultures were studied using a transwell dual-culture system and by direct labeling of EVs with PKH-67 dye. EV-induced changes in cochlear cells were quantified using confocal immunohistochemistry. Transfection of VS cells with a green fluorescent protein–containing plasmid was confirmed with reverse transcription PCR. Results Human VS cells, from patients with poor hearing, produced EVs that could damage both cultured murine cochlear sensory cells and neurons. In contrast, EVs derived from VS cells from patients with good hearing did not damage the cultured cochlear cells. Conclusions This is the first report on EVs derived from VSs and on the capacity of EVs from VSs from patients with hearing loss to selectively damage cochlear cells, thereby identifying a potential novel mechanism of VS-associated sensorineural hearing loss.
    Print ISSN: 1522-8517
    Electronic ISSN: 1523-5866
    Topics: Medicine
    Published by Oxford University Press on behalf of The Society for Neuro-Oncology (SNO).
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  • 7
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    The Role of Aldosterone in Obesity-Related Hypertension (2016)
    Oxford University Press
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    Publication Date: 2016-03-11
    Description: Obese subjects often have hypertension and related cardiovascular and renal diseases, and this has become a serious worldwide health problem. In obese subjects, impaired renal-pressure natriuresis causes sodium retention, leading to the development of salt-sensitive hypertension. Physical compression of the kidneys by visceral fat and activation of the sympathetic nervous system, renin–angiotensin systems (RAS), and aldosterone/mineralocorticoid receptor (MR) system are involved in this mechanism. Obese subjects often exhibit hyperaldosteronism, with increased salt sensitivity of blood pressure (BP). Adipose tissue excretes aldosterone-releasing factors, thereby stimulating aldosterone secretion independently of the systemic RAS, and aldosterone/MR activation plays a key role in the development of hypertension and organ damage in obesity. In obese subjects, both salt sensitivity of BP, enhanced by obesity-related metabolic disorders including aldosterone excess, and increased dietary sodium intake are closely related to the incidence of hypertension. Some salt sensitivity-related gene variants affect the risk of obesity, and together with salt intake, its combination is possibly associated with the development of hypertension in obese subjects. With high salt levels common in modern diets, salt restriction and weight control are undoubtedly important. However, not only MR blockade but also new diagnostic modalities and therapies targeting and modifying genes that are related to salt sensitivity, obesity, or RAS regulation are expected to prevent obesity and obesity-related hypertension.
    Print ISSN: 0895-7061
    Electronic ISSN: 1879-1905
    Topics: Medicine
    Published by Oxford University Press
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  • 8
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    Decreased serum osmolality promotes ductus arteriosus constriction (2014)
    Oxford University Press
    Details
    Publication Date: 2014-11-01
    Description: Aims At birth, dynamic changes occur in serum components and haemodynamics, such as closure of the ductus arteriosus (DA). A previous study demonstrated that, in full-term human neonates, serum osmolality decreased transiently after birth, but recovered over the next few days. However, the significance of this transient decrease in osmolality has never been addressed. The objective of the present study was to examine the role of changes in serum osmolality after birth in DA closure. Methods and results We found that rats exhibited a similar transient hypoosmolality after birth. Hypotonic stimulation induced constriction of DA rings and increased Ca 2+ transient in DA smooth muscle cells, but not in the aorta. The hypoosmotic sensor transient receptor potential melastatin 3 (TRPM3) was highly expressed in the rat DA, and TRPM3 silencing abolished the Ca 2+ response to hypoosmolality. Pregnenolone sulfate stimulation of TRPM3 induced rat DA constriction ex vivo and in vivo. Furthermore, hyper tonic fluid injection impaired rat DA closure. In humans, neonatal serum hypoosmolality was observed in relatively mature preterm infants (≥28 weeks). In extremely preterm infants (〈28 weeks), however, this hypoosmolality was absent. Instead, a rapid increase in osmolality occurred thereafter. Such an increase was greater, in particular, among patent DA (PDA) patients. Conclusions A transient decrease in serum osmolality may promote DA closure during the first few days of life. Adjusting serum osmolality to proper levels might help to prevent the onset of PDA, improving the therapeutic outcome in extremely preterm infants.
    Print ISSN: 0008-6363
    Electronic ISSN: 1755-3245
    Topics: Medicine
    Published by Oxford University Press
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  • 9
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    Prognostic value of tumor-infiltrating lymphocytes differs depending on histological type and smoking habit in completely resected non-small-cell lung cancer (2016)
    Oxford University Press
    Details
    Publication Date: 2016-10-29
    Description: Background T-cell infiltration in tumors has been used as a prognostic tool in non-small-cell lung cancer (NSCLC). However, the influence of smoking habit and histological type on tumor-infiltrating lymphocytes (TILs) in NSCLC remains unclear. Patients and methods We evaluated the prognostic significance of TILs (CD4 + , CD8 + , CD20 + , and FOXP3 + ) according to histological type and smoking habit using automatic immunohistochemical staining and cell counting in 218 patients with NSCLC. Results In multivariate survival analyses of clinical, pathological, and immunological factors, a high ratio of FOXP3 + to CD4 + T cells (FOXP3/CD4) [hazard ratio (HR): 4.46, P 〈 0.01 for overall survival (OS); HR: 1.96, P 〈 0.05 for recurrence-free survival (RFS)] and a low accumulation of CD20 + B cells (HR: 2.45, P = 0.09 for OS; HR: 2.86, P 〈 0.01 for RFS) were identified as worse prognostic factors in patients with adenocarcinoma (AD). In non-AD, a low number of CD8 + T cells were correlated with an unfavorable outcome (HR: 7.69, P 〈 0.01 for OS; HR: 3.57, P 〈 0.02 for RFS). Regarding smoking habit in AD, a high FOXP3/CD4 ratio was poorly prognostic with a smoking history (HR: 5.21, P 〈 0.01 for OS; HR: 2.38, P 〈 0.03 for RFS), whereas a low accumulation of CD20 + B cells (HR: 4.54, P = 0.03 for OS; HR: 2.94, P 〈 0.01 for RFS) was confirmed as an unfavorable factor in non-smokers with AD. Conclusions A low number of CD8 + T cells in non-AD, a high FOXP3/CD4 ratio in smokers with AD, and a low number of CD20 + B cells in non-smokers with AD were identified as independent unfavorable prognostic factors in resected NSCLC. Evaluating the influence of histological type and smoking habit on the immunological environment may lead to the establishment of immunological diagnosis and appropriate individualized immunotherapy for NSCLC.
    Print ISSN: 0923-7534
    Electronic ISSN: 1569-8041
    Topics: Medicine
    Published by Oxford University Press
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