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1
Santana, Lorenna Gabriella Novaes, Jose Alexandre dos Santos, Marta Pagán Martinez, and Rosamaria Cox Moura-Leite. "Práticas do disclosure voluntário socioambiental em cooperativas agropecuárias brasileiras." Revista de Administração da UFSM 11 (December 3, 2018): 812. http://dx.doi.org/10.5902/1983465932504.
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O objetivo deste artigo é descrever o disclosure voluntário socioambiental em cooperativas agropecuárias brasileiras. A fim de atingir o objetivo traçado, foram analisados os relatórios anuais presentes nos websites de uma amostra não-probabilística das maiores cooperativas agropecuárias brasileiras, referentes ao período de 2015. Para a análise dos dados, foram utilizadas as médias por subcategoria e três índices de avalição de disclosure: Índice de Disclosure (ID), Índice de Disclosure das Empresas (IDE) e Índice Geral de Disclosure das Empresas (IGDE), Índice Geral de Disclosure social (IGDs). Além disso, foi desenvolvido um quinto índice de avaliação do disclosure: o Índice Geral de Disclosure ambiental (IGDa). Os resultados obtidos permitem afirmar que há mais divulgações de informações sociais do que ambientais, com destaque para, relação com empregados, preocupação com a comunidade e com educação, e que ainda falta muito para alcançar uma boa aderência de disclosure voluntário socioambiental pelas cooperativas agropecuárias analisadas.
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Schor, S. L., I. Ellis, J. Banyard, and A. M. Schor. "Motogenic activity of IGD-containing synthetic peptides." Journal of Cell Science 112, no. 22 (1999): 3879–88. http://dx.doi.org/10.1242/jcs.112.22.3879.
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Although the IGD amino acid motif (iso-gly-asp) is a highly conserved feature of the fibronectin type I module, no biological activity has as yet been ascribed to it. We have previously reported that the gelatin-binding domain of fibronectin stimulates the migration of human skin fibroblasts into native, but not denatured, type I collagen substrata. Two IGD-containing type I modules are present within the gelatin-binding domain. The object of this study was to ascertain whether soluble synthetic peptides containing the IGD motif stimulate fibroblast migration. We found that IGD peptides stimulated fibroblast migration in the following order of activity: IGDS (as present in the ninth type I module) > IGDQ (as present in the seventh type I module) > IGD. The scrambled SDGI peptide and the well-characterised RGDS peptide were devoid of motogenic activity. The migratory response of fibroblasts to IGD-containing peptides consisted of two distinct phases: an initial period of peptide-mediated cell activation and a subsequent period of enhanced migration manifest in the absence of further IGD peptide. Cell activation was substratum-independent (occurring equally well on both native and denatured type I collagen substrata), whilst the manifestation of enhanced migration was persistent and substratum-dependent (being evident only by cells adherent to a native collagen substratum). Our data further indicated that cell activation (1) is elicited by a signal transduction cascade occurring within minutes of cell exposure to IGD-containing peptides, (2) is dependent upon integrin alphavbeta3 functionality, (3) involves the tyrosine phosphorylation of focal adhesion kinase (ppFAK125) and (4) is inhibited by signalling mediated through integrin alpha5beta1. The expression of migration stimulating activity by soluble IGD-containing peptides clearly distinguishes them from their RGD counterparts. This is the first identified biological activity of the highly conserved IGD motif and provides a rational platform for the development of a novel family of therapeutic compounds designed to stimulate cell migration in relevant clinical situations, such as impaired wound healing.
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Chen, Juliet Honglei, Meng Xuan Zhang, Chih-Hung Ko, et al. "The Development of a Screening Tool for Chinese Disordered Gamers: The Chinese Internet Gaming Disorder Checklist (C-IGDC)." International Journal of Environmental Research and Public Health 17, no. 10 (2020): 3412. http://dx.doi.org/10.3390/ijerph17103412.
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Despite the increasing research attention being paid to gaming disorder globally, a screening tool developed specifically for the Chinese population is still lacking. This study aims to address this gap by constructing a screening tool to assess Internet gaming disorder (IGD) symptomology, defined by the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), among Chinese gamers. Based on expert interviews and consultations, a focus group of gamers, a background literature review, and the IGD criteria proposed by the DSM-5, we developed the Chinese Internet Gaming Disorder Checklist (C-IGDC). This study evaluated its dimensional structure, reliability, validity, and screening efficacy with 464 Chinese past-year gamers (53% female; mean age = 19.84). The two-level structure of the 27-item C-IGDC showed a satisfactory model fit, acceptable reliability, as well as good validity via expected associations with Internet addiction, gameplay frequency, and depressive symptoms. The optimal screening cutoff score (≥20) was proposed to detect probable IGD cases. The C-IGDC is the first DSM-5-based, multidimensional IGD screening tool designed specifically for Chinese gamers. Further evaluation of the C-IGDC in epidemiological studies and clinical settings is recommended.
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Khairwa, Anju. "Indian scenario of IgA nephropathy: a systematic review and meta-analysis." African Health Sciences 21, no. 1 (2021): 159–65. http://dx.doi.org/10.4314/ahs.v21i1.21.
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Background: IgA nephropathy (IgAN) is most common primary glomerulopathy. There are variations in prevalence of IgAN and its clinical features in different studies from India.
 Aim: To summarize overall scenario of IgAN in India.
 Methods: In this systematic review, studies related to IgAN and related renal disease were included. Data searched were PubMed, EMBASE, Google scholar, and Cochrane Database from inception to 31st January 2019.
 Results: Total 49 studies (N=2480) were included: 21studies (N=2309) of primary IgAN; 19 studies (N=21) of Secondary IgAN; four studies (N=133) of IgA vasculitis nephropathy (IgAVN); and five studies (N=17) of IgA dominant nephropathy (IgADN). Prevalence of IgAN was 16.5% in India. Age of affected persons was ranging from 27.2±16.7 to 48.6±21.3 years . Male female ratio was 1.8:1. Clinical features of Primary IgAN, IgAVN, IgADN & Secondary IgAN were microscopic hematuria (49.6%, 44.4%, 15.6% & 59.5%), macroscopic hematuria (5.1%, 0.4%,40.9%,& 35.7%), Subnephrotic proteinuria (42.1%, 29.4%, 23.2%, & 52.3%), nephrotic proteinuria (16.0%, 4.4%, 76.8%,& 47.6%), and hypertension (25.8%,18.3%, 35.5%,& 47.6%).. The 24 hours proteinuria was ranging from 2.6±1.5 to 4.7±2.3 gm/day and serum creatinine (mg/dl) was ranging from 0.9±0 to 3.5±3.9 mg/dl. Histolomorphologically, all type of IgAN showed mesangial hypercellularity and Immunofluorescence revealed IgA deposition.
 Conclusion: The overall prevalence of primary IgAN in India was 16.5%. The subnephrotic proteinuria and microscopic hematuria were common clinical features.
 Keywords: IgA Nephropathy; histomorphology; prevalence; India.
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Paddock, Cathy, Dongwen Zhou, Panida Lertkiatmongkol, Peter J. Newman, and Jieqing Zhu. "Structural Basis for PECAM-1 Homophilic Binding." Blood 126, no. 23 (2015): 1041. http://dx.doi.org/10.1182/blood.v126.23.1041.1041.
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Abstract PECAM-1 is a 130 kDa member of the immunoglobulin gene (Ig) superfamily that is present on the surface of circulating platelets and leukocytes, and highly expressed at the junctions of confluent endothelial cell monolayers. PECAM-1-mediated homophilic interactions, known to be mediated by its two amino-terminal Ig homology domains, are essential for concentrating PECAM-1 at endothelial cell intercellular junctions, where it functions to sense flow, regulate leukocyte transendothelial migration, maintain vascular integrity, and transmit survival signals into the cell. Mutagenesis studies have implicated amino acids on either side of the face of IgD1 in homophilic binding, however the spatial orientation of this domain, the role that IgD2 plays in positioning IgD1 to participate in PECAM-1 homophilic interactions, and the contribution of its sialylated glycans to homophilic PECAM-1/PECAM-1 interactions remain to be critically explored. Complicating things further, PECAM-1 forms dimers and oligomers within the plane of the plasma membrane. The structural features of PECAM-1 responsible for maintaining the PECAM-1/PECAM-1 homophilic contacts necessary for carrying out these activities, however, have heretofore remained unresolved. Given the importance of PECAM-1-mediated homophilic interactions in mediating each of these cell physiological events, and to reveal the nature and orientation of the PECAM-1-PECAM-1 homophilic binding interface, we undertook studies aimed at determining the crystal structure of the PECAM-1 homophilic binding domain. The structure of IgD1-D2 was determined by multi-crystal anomalous diffraction and refined at 2.8 Å resolution. Interestingly, PECAM-1 crystallized as a strand-swapped dimer, a feature that has been seen in the crystal structures of many other members of the Ig superfamily, including cadherins, NCAM2, CTLA-4, and CD47. The homophilic interface between adjacent IgD1 domains was large, with a total buried interface of 1608 Å2. In addition to the large IgD1/IgD1 interface, interdomain contacts were found between IgD1/IgD2, and IgD2/IgD2 that likely reinforce the PECAM-1/PECAM-1 homophilic interactions that form as a consequence of the large number of PECAM-1 molecules that become concentrated at endothelial cell-cell borders as a result of diffusion trapping. Taken together, these results provide atomic-level detail to the unique architecture of the interface that forms the most abundant component of the endothelial cell intercellular junction. Disclosures No relevant conflicts of interest to declare.
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Concerto, Carmen, Alessandro Rodolico, Chiara Avanzato, et al. "Autistic Traits and Attention-Deficit Hyperactivity Disorder Symptoms Predict the Severity of Internet Gaming Disorder in an Italian Adult Population." Brain Sciences 11, no. 6 (2021): 774. http://dx.doi.org/10.3390/brainsci11060774.
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Over the last decade, internet gaming has been a fast-growing recreational activity. Gamers risk their leisure activity becoming an addiction. In the present study, we aimed to measure the prevalence of Internet Gaming Disorder (IGD) in an adult population of video game players and to investigate the association between demographic variables, Autism Spectrum Disorder (ASD) traits, Attention-Deficit Hyperactivity Disorder (ADHD) severity, and IGD in adults. Through an online survey, we recruited 4260 individuals aged between 18 and 55 years old, who were members of online communities of video gamers. We collected demographic data and administered three questionnaires: the Internet Gaming Disorder Scale-Short Form (IGD9-SF), the Autism Spectrum Quotient (AQ), and the Adult ADHD Self-Report Scale (ASRS). Of the overall sample, 29.67% scored above the cut-off of 21 points for the IGD9-SF. Multiple linear regression models showed that daily spare time, autistic traits, and ADHD symptoms were positively associated with the severity of IGD in adults, after controlling for demographic variables. Future studies are required in order to explore factors linked to IGD in adults.
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Sheptulin, A. A. I., S. S. Kardasheva, and A. Beer. "Idiopathic gastro-duodenal ulcers." Clinical Medicine (Russian Journal) 96, no. 8 (2018): 702–6. http://dx.doi.org/10.18821/0023-2149-2018-96-8-702-706.
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Idiopathic gastroduodenal ulcers (IGD) are stomach and duodenal ulcers not associated with Helicobacter pylori infection or with the administration of non-steroidal anti-inflammatory drugs. Their relative frequency ranges from 1.6 to 35%, and is likely to be overestimated due to frequent false negative test results. The etiology and pathogenesis of IGDH remain poorly understood. Factors contributing to their development can serve as old age, hereditary predisposition, disorders of gastric mucus, mesenteric ischemia. Compared to the positive peptic ulcer disease, PYLORI is characterized by less favorable course, higher frequency of gastrointestinal bleeding (including repeated), slow healing, more frequent recurrence. Treatment of IGD involves long-term use of proton pump inhibitors (PPI).
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De Pasquale, Concetta, Federica Sciacca, Valentina Martinelli, Matteo Chiappedi, Carmela Dinaro, and Zira Hichy. "Relationship of Internet Gaming Disorder with Psychopathology and Social Adaptation in Italian Young Adults." International Journal of Environmental Research and Public Health 17, no. 21 (2020): 8201. http://dx.doi.org/10.3390/ijerph17218201.
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Internet addiction is currently considered a worldwide problem, with a possible impact on mental health. This study aimed to investigate the prevalence of internet gaming disorder (IGD) among Italian young adults and to explore its association with psychopathological symptoms. Our sample included 566 young adults (324 males/242 females; age: 22.74 ± 4.83 years). Participants were asked to state their favorite games and complete the following questionnaires: the Internet Gaming Disorder Scale Short Form (IGD9-SF); the APA symptom checklist, based on DSM-5 diagnostic criteria for IGD; the Symptom Checklist-90 Revised (SCL-90 R); and the Social Adaptation Self Evaluation Scale (SASS). Use of video games was common among study participants (95% of the sample). Thirty subjects (5.3% of the sample) matched criteria for a clinical diagnosis of IGD. Data showed a positive correlation between higher use of online games and higher levels of depression (r = 0.501), anxiety (r = 0.361) and psychoticism (r = 0.431), and lower family and extra-family relationships (r = −0.383). At linear regression analysis, somatization (p = 0.002), depression (p = 0.001) and sleep disturbances (p = 0.003) were predictors of IGD diagnosis. IGD was significantly associated to mental health distress. Healthcare professionals should be aware of the problematic consequences of online gaming.
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Mei, Heng, Cathy Paddock, Jay Campbell, Ralph Albrecht, and Peter J. Newman. "Enhancement Of Endothelial Cell Barrier Function By Antibody-Driven Affinity Modulation Of PECAM-1." Blood 122, no. 21 (2013): 193. http://dx.doi.org/10.1182/blood.v122.21.193.193.
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Abstract Endothelial integrity is a critical parameter of hemostasis, and loss of barrier function contributes to the etiology and pathogenesis of both autoimmune and infectious disease. PECAM-1 is a cellular adhesion and signaling receptor comprised of six extracellular immunoglobulin (Ig) – like homology domains, a short transmembrane domain, and a 118 amino acid cytoplasmic domain that becomes serine and tyrosine phosphorylated upon activation. PECAM-1 is a major constituent of the endothelial cell intercellular junction, where up to 2 x 106 molecules concentrate upon cell-cell contact. Previous studies have shown that PECAM-1–PECAM-1 homophilic interactions mediated by N-terminal Ig domain 1 (IgD1) are required for border localization, and contribute importantly to steady-state endothelial cell barrier stability as well as the ability of the vascular endothelium to recover, both in vitro and in vivo, following inflammatory or hemostatic challenge. To examine whether the homophilic adhesive properties of PECAM-1 might be subject to regulation, we prepared phospholipid bilayer nanodiscs containing purified, full-length PECAM-1 and examined their ability to bind intact PECAM-1-expressing cells. Preliminary transmission electron microscopy studies indicated that PECAM-1-containing nanodiscs harbored a single, high-density refraction shadow, suggesting the presence of a single inserted PECAM-1 protein per nanodisc. Binding of these nanodiscs to either human umbilical vein endothelial cells or to PECAM-1-transfected HEK 293 cells required IgD1, as Fab fragments of the IgD1-specific monoclonal antibody (mAb), PECAM-1.3, completely blocked their binding. Interestingly, Fab fragments of mAbs PECAM-1.2 or 4G6, which bind closely-spaced epitopes within membrane-proximal IgD6, were found to enhance PECAM-1 nanodisc binding by 200-300%, suggesting that they induced a conformational change leading to a high-affinity form of PECAM-1. In support of this notion, rotary-shadowed electron micrographs of the purified PECAM-1 ectodomain revealed an ensemble of straight and bent molecular isoforms, reminiscent of conformational isomorphs that exist among members of the integrin family of adhesion receptors. Finally, to determine whether regulatable affinity modulation of this Ig superfamily member might be exploited to enhance or reinforce endothelial cell-cell borders, endothelial cell monolayer resistance was quantitatively measured using Electric Cell-substrate Impedance Sensing (ECIS), a real-time reporter of barrier function. As predicted, IgD1-specific mAb PECAM-1.3 delayed barrier recovery following thrombin-induced disruption of the endothelial cell monolayer, while IgD6-specific mAb PECAM-1.2 markedly enhanced the rate of barrier restoration. Both antibodies were without effect on endothelial cell monolayers in which PECAM-1 had been knocked down using a lentivirally-introduced PECAM-1 siRNA. Taken together, these data demonstrate that the homophilic binding affinity of PECAM-1 can be enhanced by IgD6-specific antibodies, and suggest a novel therapeutic modality for treating vascular endothelial injury-related disorders. Disclosures: No relevant conflicts of interest to declare.
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Reyes, Marris R. "RISK FACTORS OF INTERNET GAMING AMONG FILIPINO STUDENTS." Humanities & Social Sciences Reviews 8, no. 4 (2020): 230–37. http://dx.doi.org/10.18510/hssr.2020.8424.
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Purpose of the study: The main objective of this study is to examine the risk factors for internet gaming disorder (IGD). Specifically, it aims to: measure the severity of internet gaming among Filipino students; describe their internet gaming characteristic; and, identify which among the risk factors predict IGD.
 Methodology: Students who displayed five or more symptoms in the Internet Gaming Disorder Scale – Short Form (IGD9-SF) were identified. The internet gaming characteristics, Brief Self Control Scale (BSCS) to identify self-control levels, and Mini-IPIP for the personality of the participants were also collected. Data were analyzed using descriptive statistics and linear regression analysis to identify the significant risk factors for IGD using SPSS 17.0.
 Main Findings: Internet gaming characteristics such as time spent, money spent, and devices used were significant risk factors to IGD. Psychological factors such as self-control and personality traits (agreeableness and openness) were established and were also significant risk factors. The lower the self-control the higher the risk of developing IGD, as well as the more agreeable and open the gamers are the higher the risk to IGD.
 Applications of this study: Researchers and therapists should focus on developing intervention methods focusing on minimizing the device's exposure to lessen time and money spent in gaming as well as strengthening the self-control of the gamers. 
 Novelty/Originality of this study: This psychological inquiry contributed to the emerging psychological disorder IGD shedding light on its current debates and controversies. This established risk factors to IGD among Filipino students who are time spent, money spent, devices used, self-control, and personality factors such as agreeableness and openness.
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Lihme, Benny. "HASH IGEN-IGEN." Rus & samfunn, no. 04 (October 8, 2014): 19. http://dx.doi.org/10.18261/issn1501-5580-2014-04-08.
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Han, Le, Xian-zheng Zhang, Chen Wang та ін. "IgD-Fc-Ig fusion protein, a new biological agent, inhibits T cell function in CIA rats by inhibiting IgD-IgDR-Lck-NF-κB signaling pathways". Acta Pharmacologica Sinica 41, № 6 (2020): 800–812. http://dx.doi.org/10.1038/s41401-019-0337-2.
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Al-Harbi, F., D. Kaisarly, A. Michna, A. ArRejaie, D. Bader, and M. El Gezawi. "Cervical Interfacial Bonding Effectiveness of Class II Bulk Versus Incremental Fill Resin Composite Restorations." Operative Dentistry 40, no. 6 (2015): 622–35. http://dx.doi.org/10.2341/14-152-l.
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SUMMARY Cervical interfacial bonding quality has been a matter of deep concern. The purpose of this study was to analyze microtensile bond strength (MTBS) and cervical interfacial gap distance (IGD) of bulk-fill vs incremental-fill Class II composite restorations. Box-only Class II cavities were prepared in 91 maxillary premolars (n = 7) with gingival margin placement 1 mm above the cementoenamel junction at one side and 1 mm below it on the other side. Eighty-four maxillary premolars were divided into self-etch and total-etch groups and further subdivided into six restorative material subgroups used incrementally and with an open-sandwich technique: group 1, Tetric Ceram HB (TC) as a control; group 2, Tetric EvoFlow (EF); group 3, SDR Smart Dentin Replacement (SDR); group 4, SonicFill (SF); group 5, Tetric N-Ceram Bulk Fill (TN); and group 6, Tetric EvoCeram Bulk Fill (TE). Groups 2-6 were bulk-fill restoratives. Tetric N-Bond Self-Etch (se) and Tetric N-Bond total-etch (te) adhesive were used in subgroups 1–5, whereas AdheSE (se) and ExciTE F (te) were used in subgroup 6. In an additional group, Filtek P90 Low Shrink Restorative (P90) was used only with its corresponding self-etch bond. The materials were manipulated, light-cured (1600 mW/cm2), artificially aged (thermal and occlusal load-cycling), and sectioned. Two microrods/restoration (n = 14/group) were tested for MTBS at a crosshead-speed of 0.5 mm/min (Instron testing machine). Fracture loads were recorded (Newtons), and MTSBs were calculated (Megapascals). Means were statistically analyzed by the Kruskal-Wallis test, Conover-Inman post hoc analysis for MTBS (multiple comparisons), and Mann-Whitney U test for IGD. The ends of the fractures were examined for failure mode. One microrod/restoration (n = 7/group) was investigated by scanning electron microscopy (×1200) for IGD. MTBS values for SF/te, P90 in enamel, and TC+SDR/te in enamel and cementum were significantly higher compared with those for the control TC/te and TC/se in cementum. Most of the failures were mixed. IGDs were generally smaller at enamel margins, and the smallest IGDs were found in P90 at both enamel and cementum margins. Bulk-fill and silorane-based composites might provide better cervical interfacial quality than incremental-fill restorations.
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Schanz, Hans-Jørgen. "Wittgenstein igen." Slagmark - Tidsskrift for idéhistorie, no. 9 (February 9, 2018): 141–48. http://dx.doi.org/10.7146/sl.v0i9.103483.
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Iversen, Stefan. "Om igen." K&K - Kultur og Klasse 36, no. 105 (2008): 234–37. http://dx.doi.org/10.7146/kok.v36i105.22049.
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Larsen, Jesper Eckhardt. "Dannelse igen!" Nytt Norsk Tidsskrift 21, no. 02 (2004): 166–72. http://dx.doi.org/10.18261/issn1504-3053-2004-02-06.
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Hacken, Elisa ten, Cristina Scielzo, William G. Wierda, et al. "Ibrutinib Differentially Interferes With Surface IgM and IgD BCR Signaling Kinetics In Chronic Lymphocytic Leukemia." Blood 122, no. 21 (2013): 4143. http://dx.doi.org/10.1182/blood.v122.21.4143.4143.
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Abstract B cell receptor (BCR) signaling is a driving event in Chronic Lymphocytic Leukemia (CLL) progression. Most CLL cells express both surface IgM (sIgM) and sIgD molecules, and previous reports showed heterogeneous responses to anti-IgM stimulation: CLL cells carrying IGHV unmutated-BCRs are highly responsive in terms of intracellular signaling activation, while cells with IGHV-mutated receptors are usually anergic to BCR cross-linking. In contrast, it has been described that almost all CLL cells retain responsiveness to sIgD, suggesting that sIgD signaling may not be the most relevant event in disease progression and heterogeneity. As the clinical significance of these mechanisms still needs to be unraveled, in the present study we analyzed the kinetics of BCR signaling activation following either sIgM or sIgD stimulation in CLL cells. The activation of HS1 protein, along with BCR proximal kinases (i.e. SRC/LYN and BTK) and the downstream effector ERK, was tested by Western Blot and flow-cytometry analysis up to 60 minutes following receptor engagement. HS1 protein was chosen as an early marker of BCR signaling and cytoskeletal activation (ten Hacken E et al., Blood 2013), also in the light of its prognostic relevance, as HS1 hyperphosphorylation correlates with a dismal clinical outcome of patients. Purified B cells from 16 primary CLL samples were stimulated with either soluble anti-IgM or anti-IgD and the level of HS1 activating tyrosine (Y)397 phosphorylation was analyzed at different time points (2, 5, 15, 30, 60 minutes) by densitometric analysis of Western Blot results or Mean Fluorescent Intensity analysis of flow cytometry data. HS1 activation peaked after 2-5 minutes following stimulation, and then returned to baseline at later time points with different patterns. In 13/16 samples, we observed a protracted HS1 phosphorylation after anti-IgM stimulation. In contrast, 6/16 samples showed protracted HS1 phosphorylation after anti-IgD stimulation, while 10/16 samples showed a very transient HS1 activation that rapidly returned to baseline. The activation kinetics of the other signaling molecules (i.e. SRC/LYN, BTK and ERK) was in line with that of HS1. As protracted BCR signaling activation is linked to cell cycle entry and proliferation, the protracted IgD signaling observed in some patients suggests that not only IgMs, but also IgDs may have pathogenetic relevance in CLL progression and heterogeneity. We then analyzed how the BTK inhibitor ibrutinib affects BCR signaling activation kinetics and analyzed phosphoprotein activation patterns in 10 CLL samples after 1 hour pretreatment with ibrutinib and up to 60 minutes following anti-IgM and anti-IgD stimulation. Both IgM and IgD-induced phosphorylation of HS1, SRC/LYN, BTK and ERK was reduced by ibrutinib treatment, demonstrating that ibrutinib is effective in blocking signaling pathways downstream not only of IgM receptors, as previously demonstrated, but also downstream of IgDs. Interestingly, in 7/10 samples, HS1 partially retained the ability to be phosphorylated after BCR triggering following 1-hour ibrutinib treatment and 5-minute anti-IgM or anti-IgD stimulation, suggesting that HS1 activation can bypass BTK kinase inhibition at least at early time points following receptor stimulation. A broad analysis on a large cohort of patients will further allow the correlation between BCR signaling molecule activation and cell viability with molecular/cytogenetic prognostic factors. Overall, these results show that sIgM stimulation of CLL cells promotes protracted activation of BCR signaling, which can only be observed in a restricted set of patients after sIgD stimulation. These observations support the notion that sIgM signaling may be more relevant for CLL progression, but also suggest that sIgD signaling may contribute to CLL pathogenesis in selected patients. Both signaling pathways can be inhibited by ibrutinib, further supporting the effectiveness of ibrutinib in inhibiting BCR signaling in CLL. Disclosures: O'Brien: Pharmacyclics: Research Funding. Burger:Pharmacyclics: Membership on an entity’s Board of Directors or advisory committees, Research Funding.
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Murakami, Yoshiko, Mitsuhiro Kato, Hirotomo Saitsu, et al. "Inherited GPI-Anchor Deficiencies Caused By The Hypomorphic Mutations In PIG A gene: Comparison To Paroxysmal Nocturnal Hemogrobinuria." Blood 122, no. 21 (2013): 3701. http://dx.doi.org/10.1182/blood.v122.21.3701.3701.
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Abstract Glycosylphosphatidylinositol (GPI) is a glycolipid that anchors 150 or more kinds of proteins to the cell surface. There are at least 26 genes involved in the biosynthesis and transport of GPI anchored proteins (GPI-APs). In paroxysmal nocturnal hemogrobinuria (PNH), an acquired GPI deficiency, somatic mutation in X-linked PIGA accounts for most of the patients. A case with PNH due to a combination of inherited mutation in one allele and a somatic mutation in the other allele of autosomal gene PIGT was reported recently (Blood 2013 doi:10.1182/blood-2013-01-481499). On the other hand, many inherited GPI deficiencies (IGDs) were found recently using whole exome sequencing (Nat Genet 2010 vol.42 p827, Am J Hum Genet 2012 vol. 90 p295, p146, Am J Hum Genet 2012 vol. 91 p146, Am J Hum Genet 2013 vol. 92 p584). As the complete GPI deficiency causes embryonic death, these patients with IGD are partial deficiency. The major symptoms of IGDs include mental retardation, epilepsy, coarse facial features and multiple organ anomalies that vary in severity depending upon the degree of defect and/or position in the pathway of affected gene. We clarified a mechanism of hyperphosphatasia, an elevated release of tissue nonspecific alkaline phosphatase (TNAP, GPI-AP), seen in some of the patients with IGDs such as hyperphosphatasia mental retardation syndrome or Mabry syndrome caused by mutation in genes in the later stage of GPI biosynthesis (J Biol Chem. 2012 vol. 287 p6318) Here, we report four male patients with intellectual disabilities accompanied by seizures caused by the mutations in PIGA gene. These mutations were found by whole-exome sequencing using the Illumina HiSeq system. PIGA is X-linked gene which is involved in the first step of GPI biosynthesis pathway. These patients have germline hypomorphic mutations in PIGAgene and have completely different symptoms from patients with PNH, which is characterized by complement-mediated intravascular hemolysis. Patient 1 had a hemizygous nonsense mutation, and was diagnosed with Ohtahara syndrome (early infantile epileptic encephalopathy with suppression burst) with multiple congenital anomalies. The nonsense mutation is leaky and caused a partial deficiency. Patient 2 had a maternally inherited hemizygous missense mutation and was diagnosed with early-onset West syndrome (a severe epilepsy syndrome characterized by infantile spasm with hypsarrhythmia). Patients 3 and 4 are brothers, had maternally inherited hemizygous missense mutation and were suffering from severe intellectual disabilities with seizures but not with any anomalies. Analysis by flow cytometry of patients’ blood cells revealed that all four patients showed decreased expression of GPI-APs on the granulocytes but not in erythrocytes or lymphocytes, suggesting that FACS analysis of granulocytes is useful to screen patients with IGD. Interestingly, the FACS analysis of the granulocytes from the mother of patients 3 and 4 showed mosaic pattern in CD16 expression. The mother seemed to have no neurological symptom, raising the possibility that contribution of GPI-AP-deficient cells to neuronal system does not occur or is only limited. Although PNH and IGDs are different diseases, both are partial GPI deficiencies, the former affecting only hematopoietic cells, the latter having the hypomorphic mutations, which rescue the patients from lethality but cause the severe hematopoietic and developmental abnormalities, respectively. Disclosures: No relevant conflicts of interest to declare.
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Wong, Hiu Yan, Hoi Yi Mo, Marc N. Potenza, et al. "Relationships between Severity of Internet Gaming Disorder, Severity of Problematic Social Media Use, Sleep Quality and Psychological Distress." International Journal of Environmental Research and Public Health 17, no. 6 (2020): 1879. http://dx.doi.org/10.3390/ijerph17061879.
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Internet gaming and social media use are prevalent and integral to many people’s lives. However, excessive engagement in either could lead to negative health impacts. This study aimed to investigate relationships between severities of internet gaming disorder (IGD) and problematic social media use (operationalized as social media addiction; SMA) with sleep quality and psychological distress among young adults. A cross-sectional study with snowball sampling was conducted among Hong Kong university students in 2019. All participants (n = 300; mean (SD) age = 20.89 (1.48); 122 males (40.67%)) responded to an online survey that included Chinese versions of the Internet Gaming Disorder Scale-Short Form (IGDS9-SF), Bergen Social Media Addiction Scale (BSMAS), Pittsburgh Sleep Quality Index (PSQI), and Depression Anxiety Stress Scales (DASS-21). Multiple linear regressions demonstrated that IGDS-SF9 scores demonstrated associations with psychological distress measures (standardized coefficient (β) = 0.295 for depression, 0.325 for anxiety, 0.339 for stress, all p < 0.001). BSMAS scores showed similar albeit numerically less robust associations (β = 0.235 for depression, p < 0.001; 0.219 for anxiety, p = 0.001; 0.262 for stress, p < 0.001). BSMAS scores demonstrated associations with poorer sleep quality (β = 0.292; p < 0.001) and IGDS9-SF scores (β = 0.157; p = 0.024) showed a significantly less robust association (p = 0.01 for comparing the two βs). These findings suggest that both severities of IGD and SMA associate with more psychological distress and poorer sleep quality, although the strengths of associations may differ.
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Cho, Won-Hee, Seon-Hwa Park, Seul-Ki Choi, et al. "Characterization of IgA Deposition in the Kidney of Patients with IgA Nephropathy and Minimal Change Disease." Journal of Clinical Medicine 9, no. 8 (2020): 2619. http://dx.doi.org/10.3390/jcm9082619.
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Approximately 5% of patients with IgA nephropathy (IgAN) exhibit mild mesangial lesions with acute onset nephrotic syndrome and diffuse foot process effacement representative of minimal change disease (MCD). It is not clear whether these unusual cases of IgAN with MCD (IgAN-MCD) are variant types of IgAN or coincidental deposition of IgA in patients with MCD. In a retrospective multicenter cohort study of 18 hospitals in Korea, we analyzed 46 patients with IgAN-MCD. Patients with endocapillary proliferation, segmental sclerosis, and crescent were excluded, and the clinical features and prognosis of IgAN-MCD were compared with those of pure MCD. In addition, we performed galactose-deficient IgA1 (KM55) staining to characterize IgAN-MCD. Among the 21,697 patients with glomerulonephritis enrolled in the database, 46 patients (0.21%) were diagnosed with IgAN-MCD, and 1610 patients (7.4%) with pure MCD. The 46 patients with IgAN-MCD accounted for 0.6% of primary IgAN patients (n = 7584). There was no difference in prognosis between patients with IgAN-MCD and those with only MCD. IgA and KM55 showed double positivity in all patients with IgAN-MCD (n = 4) or primary IgAN (n = 5) under double immunofluorescent staining. However, in four patients with lupus nephritis, mesangial IgA was deposited, but galactose-deficient-IgA1 (Gd-IgA1) was not. These findings suggest that IgAN-MCD is a dual glomerulopathy in which MCD was superimposed on possibly indolent IgAN. We confirmed by KM55 staining that IgAN-MCD is true IgAN, enabling better characterizations of the disease. Furthermore, IgAN-MCD shows a good prognosis when treated according to the usual MCD treatment modality.
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Allison, Susan J. "Crescents in IgAN." Nature Reviews Nephrology 12, no. 11 (2016): 650. http://dx.doi.org/10.1038/nrneph.2016.141.
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Barratt, Jonathan, Alice C. Smith, Karen Molyneux, and John Feehally. "Immunopathogenesis of IgAN." Seminars in Immunopathology 29, no. 4 (2007): 427–43. http://dx.doi.org/10.1007/s00281-007-0089-9.
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Wang, Yamei, and Yuhong Tao. "Tuberculosis-associated IgA nephropathy." Journal of International Medical Research 46, no. 7 (2018): 2549–57. http://dx.doi.org/10.1177/0300060518774127.
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Immunoglobulin A nephropathy (IgAN) is the most frequent pathological diagnosis of tuberculosis (TB)-associated glomerulonephritis. Diagnosing TB-associated IgAN (TB-IgAN) is difficult because of its non-specific and insidious symptoms. An inaccurate diagnosis of TB-IgAN could result in the spread of TB and reduced renal function. Haematuria and proteinuria in conjunction with TB should be assessed because of the potential for diagnosis of IgAN. Renal biopsy is important in securing an accurate diagnosis prior to initiating treatment. Detection of Mycobacterium tuberculosis DNA and assessment of early secreted antigenic target of 6 kDa in renal biopsy tissues may have great potential diagnostic value in patients with TB-IgAN. Anti-TB therapy can effectively alleviate TB and TB-IgAN.
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Park, J. S., J. H. Song, W. S. Yang, S. B. Kim, Y. K. Kim, and C. D. Hong. "Cytomegalovirus is not specifically associated with immunoglobulin A nephropathy." Journal of the American Society of Nephrology 4, no. 8 (1994): 1623–26. http://dx.doi.org/10.1681/asn.v481623.
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Cytomegalovirus (CMV) has been suspected to be involved in the pathogenesis of IgA nephropathy (IgAN). Whether CMV is present in renal tissue of IgAN, however, remains controversial. To determine the presence of CMV in IgAN, compared with other glomerulonephritis (GN) as disease control, polymerase chain reaction amplifying a 159-base-pair fragment of the immediate early gene of CMV and indirect immunofluorescence staining with anti-CMV monoclonal antibody were performed on 10 IgAN and 14 non-IgAN GN renal tissues. CMV DNA was detected in 6 of 10 IgAN tissues and 10 of 14 other GN by polymerase chain reaction, whereas no CMV antigen was detected in all renal tissues by immunofluorescence. This frequent observation of CMV DNA in various types of GN as well as in IgAN would suggest that CMV is not specifically associated with the pathogenesis of IgAN seen in endemic areas of CMV infection.
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Suzuki, Hitoshi, Landino Allegri, Yusuke Suzuki, et al. "Galactose-Deficient IgA1 as a Candidate Urinary Polypeptide Marker of IgA Nephropathy?" Disease Markers 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/7806438.
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In patients with IgA nephropathy (IgAN), circulatory IgA1 and IgA1 in mesangial deposits contain elevated amounts of galactose-deficient IgA1 (Gd-IgA1). We hypothesized that a fraction of Gd-IgA1 from the glomerular deposits and/or circulation may be excreted into the urine and thus represent a disease-specific biomarker. Levels of urinary IgA and Gd-IgA1 were determined in 207 patients with IgAN, 205 patients with other renal diseases, and 57 healthy controls, recruited in USA, Japan, and Italy. Urinary IgA was similarly elevated in patients with IgAN and renal-disease controls compared with healthy controls. However, urinary Gd-IgA1 levels were higher in patients with IgAN (IgAN,28.0±17.9; disease controls,20.6±17.4units/mg urinary creatinine;P<0.0001). Lectin western blotting data confirmed these results. In IgAN patients, levels of urinary Gd-IgA1 correlated with proteinuria (P<0.001). When we purified IgA from serum and urine of an IgAN patient, the relative proportion of Gd-IgA1 to total IgA1 was higher in the urine compared with serum, suggesting selective excretion of Gd-IgA1 in IgAN. In summary, urinary excretion of Gd-IgA1 was elevated in patients with IgAN and the urinary Gd-IgA1 levels correlated with proteinuria. Urinary Gd-IgA1 may thus represent a disease-specific biomarker of IgAN.
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Chae, Yura, Hye Eun Yoon, Yoon Kyung Chang, et al. "Renal Outcome of IgM Nephropathy: A Comparative Prospective Cohort Study." Journal of Clinical Medicine 10, no. 18 (2021): 4191. http://dx.doi.org/10.3390/jcm10184191.
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Immunoglobulin M nephropathy (IgMN) is an idiopathic glomerulonephritis characterized by diffuse deposits of IgM in the glomerular mesangium. However, its renal prognosis remains unknown. We compared renal outcomes of IgMN patients with those of patients with minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), or mesangial proliferative glomerulonephritis (MsPGN) from a prospective observational cohort, with 1791 patients undergoing native kidney biopsy in eight hospitals affiliated with The Catholic University of Korea between December 2014 and October 2020. IgMN had more mesangial proliferation and matrix expansion than MsPGN and more tubular atrophy and interstitial fibrosis than MCD. IgMN patients had decreased eGFR than MCD patients in the earlier follow-up. However, there was no significant difference in urine protein or eGFR among all patients at the last follow-up. When IgMN was divided into three subtypes, patients with FSGS-like IgMN tended to have lower eGFR than those with MCD-like or MsPGN-like IgMN but higher proteinuria than MsPGN-like IgMN without showing a significant difference. The presence of hypertension at the time of kidney biopsy predicted ≥20% decline of eGFR over two years in IgMN patients. Our data indicate that IgMN would have a clinical course and renal prognosis similar to MCD, FSGS, and MsPGN.
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Zhu, Li, and Hong Zhang. "The Genetics of IgA Nephropathy: An Overview from China." Kidney Diseases 1, no. 1 (2015): 27–32. http://dx.doi.org/10.1159/000381740.
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Background: IgA nephropathy (IgAN) is the most common type of primary glomerulonephritis worldwide. Highly variable data for disease prevalence and reports of familial clustering suggest the involvement of genetic factors in IgAN. As China is an area with a high prevalence of IgAN, Chinese scholars have made a considerable effort to reveal the underlying genetic architecture of IgAN. Summary: In this review, we summarize recent achievements in the genetic studies of IgAN, focusing mainly on studies undertaken in China. Early association studies followed a population-based design and focused on a single variant or single gene. Subsequently, family-based designs and genetic interactions applied by Chinese scholars revealed an association of variants in MEGSIN and glycosyltransferase genes with IgAN. Recently, genome-wide association studies (GWAS) have been used to identify multiple susceptibility loci for IgAN, and they have, for the most part, been validated in Chinese populations. Key Messages: More efforts should be made to explore the underlying genetic mechanisms of GWAS-identified variants. In future studies in IgAN, the application of a systems genetics approach would be helpful and productive. Facts from East and West: The reported prevalence of IgAN is higher in Asia than in Europe and North America. However, differences in use of biopsy for the diagnosis of IgAN should be taken into account in analyzing data from both East and West. In Europe, IgAN affects men more frequently than women; this is not the case in Asia. Familial IgAN has been more frequently reported in Europe than in Asia. Within Europe, familial IgAN is more evident in southern than in northern populations. Changes in the pattern of serum IgA1 O-glycosylation is a common finding in IgAN patients in the East and West. SNPs within the gene coding for the enzyme C1GALT1 have been reported in Chinese and European patients. However, there is no evidence for a role of gene polymorphism of the C1GALT1 chaperone cosmc in Europeans. Genetic variants in the HLA gene family have been observed in populations from the East and West. Associations between IgAN and variants of the TAP1/PSMB and DEFA genes were observed in Asian but not in Western patients. Association with the angiotensin-converting enzyme gene was seen only in Asian patients.
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Liu, Di, Yexin Liu, Guochun Chen, et al. "Rapamycin Enhances Repressed Autophagy and Attenuates Aggressive Progression in a Rat Model of IgA Nephropathy." American Journal of Nephrology 45, no. 4 (2017): 293–300. http://dx.doi.org/10.1159/000456039.
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Background: IgA nephropathy (IgAN) has been considered to be the most frequent form of primary glomerulonephritis that occurs worldwide with a variety of factors involved in its occurrence and development. The impact of autophagy in IgAN, however, remains partially unclear. This study was designed to investigate the effects of rapamycin in an IgAN model. Method: After establishing an IgAN rat model, SD rats were divided into 4 groups: control, control + rapamycin, IgAN, IgAN + rapamycin. Proteinuria and the pathological changes and the level of autophagy of kidney were texted. Identify the expression of phosphorylation and total mammalian target of rapamycin (mTOR) and s6k1 as well as cyclin D1 in the kidney of rats through Western blot and immunohistochemistry. Results: With rapamycin treatment, we observed a significant reduction in the progression of proteinuria as well as alleviation of pathological lesions in IgAN rats. Besides, autophagy was inhibited, while the mTOR/S6k1 pathway was activated and expression of cyclin D1 was increased in IgAN. Rapamycin treatment increased autophagy and decreased the expression of cyclin D1. Conclusion: These results may suggest that mTOR-mediated autophagy inhibition may result in mesangial cell proliferation in IgAN.
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James, Christopher W., Kelly C. McNelis, David M. Cohen, Susan Szabo, and Arlene K. Bincsik. "Recurrent Ingrown Toenails Secondary to Indinavir/Ritonavir Combination Therapy." Annals of Pharmacotherapy 35, no. 7-8 (2001): 881–84. http://dx.doi.org/10.1345/aph.10386.
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OBJECTIVE: To report five cases of ingrown toenails (IGTN) associated with indinavir/ritonavir (IDV/RTV) combination therapy. CASE SUMMARY: The median onset of IGTN from initiation of IDV/RTV therapy was 18.4 weeks. Four patients previously received IDV, with one of these experiencing prior IGTN. All patients required surgical management of IGTN. All patients received virologic benefit from ongoing antiretroviral therapy, and the majority of patients elected to maintain IDV/RTV combination therapy. Two patients experienced recurrent IGTN while receiving ongoing IDV/RTV combination therapy. DISCUSSION: IGTN and paronychia have previously been reported with IDV and lamivudine. IGTN in patients with HIV infection is more likely to present acutely, involve more digits, and require surgical management. IDV increases retinoic acid signaling and, based on elevated IDV concentrations from concomitant RTV therapy, the risk of IGTN may be increased in patients receiving IDV/RTV combination therapy. CONCLUSIONS: With the increasing popularity of IDV/RTV combination therapy, clinicians should be aware of the potential increase in frequency of dose-related toxicities including IGTN. Evaluation of hands and feet on physical examination should be recommended for all patients being treated with lamivudine and IDV, especially when used in combination with RTV.
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Kim, Jin Sug, Hyeon Seok Hwang, Sang Ho Lee, et al. "Clinical Relevance of Serum Galactose Deficient IgA1 in Patients with IgA Nephropathy." Journal of Clinical Medicine 9, no. 11 (2020): 3549. http://dx.doi.org/10.3390/jcm9113549.
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New biomarkers of IgA nephropathy (IgAN) are needed for non-invasive diagnosis and appropriate treatment. There is emerging evidence that galactose deficient IgA1 (Gd-IgA1) is a pivotal molecule in the pathogenesis of IgAN. However, few studies have investigated the role of Gd-IgA1 as a biomarker in IgAN. In this study, we investigated the clinical relevance of serum Gd-IgA1 levels in patients with IgAN. Two hundred and thirty biopsy-proven IgAN patients, 74 disease controls (patients with non-IgAN nephropathy), and 15 healthy controls were enrolled in this study. Levels of serum Gd-IgA1 were measured using an ELISA kit in serum samples obtained the day of renal biopsy. We compared levels of serum Gd-IgA1 according to the type of glomerular disease and analyzed the association between Gd-IgA1 levels and clinical and pathological parameters in patients with IgAN. We then divided IgAN patients into two groups according to Gd-IgA1 level and investigated the predictive value of Gd-IgA1 for progression of chronic kidney disease (CKD). Serum Gd-IgA1 levels were significantly higher in IgAN patients than disease controls and healthy controls. In patients with IgAN, serum Gd-IA1 levels were significantly correlated with estimated glomerular filtration rate, serum IgA level, and tubular atrophy/interstitial fibrosis. CKD progression was more frequent in IgAN patients with higher serum Gd-IgA1 levels than in those with lower serum Gd-IgA1 levels. Cox proportional hazard models showed that high GdIgA1 level was an independent risk factor for CKD progression after adjusting for several confounders. Our results suggest that serum Gd-IgA1 level is a useful diagnostic and prognostic marker in IgAN patients. Further studies with a larger sample size and longer follow-up duration are needed.
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Irabu, Hitoshi, Masaki Shimizu, Shuya Kaneko, et al. "Clinical Significance of Serum Galactose-Deficient IgA1 Level in Children with IgA Nephropathy." Journal of Immunology Research 2020 (May 21, 2020): 1–10. http://dx.doi.org/10.1155/2020/4284379.
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This study was aimed at investigating the clinical significance of serum galactose-deficient IgA1 (Gd-IgA1) levels measured by a novel lectin-independent enzyme-linked immunosorbent assay (ELISA) using an anti-Gd-IgA1 monoclonal antibody (KM55) as a disease-specific biomarker for IgA nephropathy (IgAN) in children. Thirty-three children with IgAN, 40 with non-IgA glomerular diseases, and 38 age-matched healthy controls (HCs) were enrolled. Serum Gd-IgA1 levels were quantified by ELISA using KM55. Results were statistically compared with clinical features and pathological findings of IgAN. Serum Gd-IgA1 levels were significantly elevated in children with IgAN compared with children with non-IgA glomerular diseases and HCs. Serum Gd-IgA1 levels in children with IgAN were positively correlated with serum total IgA levels. However, the serum Gd-IgA1/total IgA ratio (Gd-IgA1/IgA) was also significantly elevated in children with IgAN. Serum Gd-IgA1 levels in children with IgAN increased in an age-dependent manner. The cutoff value of serum Gd-IgA1 levels for differentiating IgAN from non-IgA glomerular diseases was 3236 in children<12 years and 5284 in children≥12 years, respectively. In contrast, serum Gd-IgA1/IgA was age-independent. The cutoff value of serum Gd-IgA1/IgA for differentiating IgAN from non-IgA glomerular diseases was 0.2401. Serum Gd-IgA1 levels were negatively correlated with eGFR and positively correlated with mesangial IgA deposition. In contrast, serum Gd-IgA1/IgA levels were not correlated with any clinical parameters of IgAN. In conclusion, serum Gd-IgA1 levels were significantly elevated in children with IgAN. However, those levels were age-dependent; therefore, serum Gd-IgA1 levels classified by age and/or serum Gd-IgA1/IgA might have diagnostic values in children with IgAN.
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Li, Guanhong, Xiaoyan Wang, Zhe Yang, et al. "Serum Levels of Joining Chain-Containing IgA1 Are Not Elevated in Patients with IgA Nephropathy." Disease Markers 2019 (July 2, 2019): 1–11. http://dx.doi.org/10.1155/2019/9802839.
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Background. It has been suggested that mesangial IgA deposits are dimeric or polymeric in IgA nephropathy (IgAN). However, evidence concerning the molecular form of serum IgA in IgAN is controversial. And there is no direct evidence that the serum levels of joining chain- (J chain-) containing IgA (J-IgA) are elevated in IgAN. In this study, we aimed to measure serum J-IgA and glomerular J chain deposition with anti-J chain monoclonal antibody in IgAN. Methods. BALB/c mice were immunized with human J chain-GST recombinant peptide to obtain anti-J chain monoclonal antibody. The levels of serum total IgA and J-IgA were measured by sandwich enzyme-linked immunosorbent assay in 115 patients with IgAN and 117 healthy volunteers. J chain deposition in kidney specimens was analyzed by immunohistochemistry staining. Results. Serum levels of total IgA1 were elevated in IgAN patients compared to healthy subjects. However, serum levels of IgA, J-IgA, and J chain-containing IgA1 (J-IgA1), the J-IgA to total IgA ratio, and the J-IgA1 to total IgA1 ratio were not significantly different between IgAN patients and healthy subjects. Western blot analysis and gel filtration analysis using purified IgA1 also showed that the proportion of J chain-containing polymeric IgA1 was lower in IgAN patients compared to healthy subjects. No correlation was found between serum J-IgA or J-IgA1 and clinical features in IgAN. Immunohistochemistry analysis showed that glomerular J chain was positive in 12 IgAN patients (57.1%). The values of the J-IgA to IgA ratio and J-IgA1 to IgA ratio were significantly higher in IgAN patients with glomerular J chain deposition than those without. However, the serum levels of J-IgA and J-IgA1 and the J-IgA1 to IgA1 ratio were not significantly higher in two subgroups. Conclusions. Although serum levels of total IgA1 were elevated in IgAN, the serum levels of J-IgA1 were not elevated. And serum J-IgA, serum J-IgA1, and J chain deposition were not correlated with disease severity in IgAN.
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Qi, Yuan-yuan, Xu-jie Zhou, Fa-juan Cheng та Hong Zhang. "Elevated Plasmaα-Defensins (HNP1–3) Levels Correlated with IgA1 Glycosylation and Susceptibility to IgA Nephropathy". Disease Markers 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/8123138.
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Aim. IgA nephropathy (IgAN) is the most common form of glomerulonephritis. Recent genome-wide association study (GWAS) suggested that DEFA locus (which encodesα-defensins) may play a key role in IgAN.Methods. The levels ofα-defensins in 169 IgAN patients and 83 healthy controls were tested by ELISA.Results. We observed thatα-defensins human neutrophil peptides 1–3 (HNP1–3) in IgAN patients were elevated compared with healthy controls. The mean levels ofα-defensins of 83 healthy controls and 169 IgAN patients were 50 ng/mL and 78.42 ng/mL. When the results were adjusted to the mean levels ofα-defensins of IgAN patients, the percentage of individuals with high levels ofα-defensins increased in IgAN patients (22.5%) compared to healthy controls (9.6%) (p=0.013). The elevation ofα-defensins in IgAN patients was independent of renal function or neutrophil count, which were major sources ofα-defensins in circulation. More importantly, negative correlation was observed between galactose-deficient IgA1andα-defensins.Conclusion. Asα-defensin is a lectin-like peptide, we speculated that it might be involved in IgA galactose deficiency. The data implied that patients with IgAN had higher plasmaα-defensins levels and highα-defensins correlated with IgA galactose deficiency, further suggesting a pathogenic role ofα-defensins in IgAN.
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Lundgreen-Nielsen, Flemming. "Verdenskrøniken 1812 læst igen -." Grundtvig-Studier 64, no. 1 (2015): 92–94. http://dx.doi.org/10.7146/grs.v64i1.20910.
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Verdenskrøniken 1812 som verdenslitteraturhistorie[The World Chronicle 1812 as a history of world literature]By Flemming Lundgreen-NielsenHidden in Grundtvig’s World Chronicle, 1812, is a history of world literature, infact the first published attempt of its kind written in Danish by a single scholar.This easily escapes attention as Grundtvig’s numerous paragraphs on poetry andliterary history are not marked typographically. This paper examines and discusses his most important statements chronologically. Even if Grundtvig’s brief portrayals of poets often describe a short bloom followed by rapid decay and an inevitablefall, he ends in foreseeing a renewal of Nordic literature led by Steffens, Oehlenschläger and himself. Thus Grundtvig, as early as 1812, introduces the Danish romantic breakthrough (1802 onwards) as a poetological paradigm which otherwise is first acknowledged by literary historians writing in the 1870s, ‘80s and ‘90s. Grundtvig’s survey of world literature has been overshadowed by more conspicuous and provocative qualities of his text but deserves a sober-minded consideration.
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Sestoft, Carsten. "Kultur og klasse - igen?" K&K - Kultur og Klasse 21, no. 75 (1993): 117–36. http://dx.doi.org/10.7146/kok.v21i75.24780.
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Gömöri, George, and István Vas. "Igen is, nem is." World Literature Today 61, no. 4 (1987): 661. http://dx.doi.org/10.2307/40143938.
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Mattsson, Margareta, and Kerstin Ekman. "Gör mig levande igen." World Literature Today 71, no. 2 (1997): 405. http://dx.doi.org/10.2307/40153168.
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Sweet, Charlie, Hal Blythe, and Rusty Carpenter. "Creating an iGen Pedagogy." National Teaching & Learning Forum 28, no. 6 (2019): 1–4. http://dx.doi.org/10.1002/ntlf.30212.
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Niiler, Eric. "Igen accused of nepotism." Nature Biotechnology 19, no. 4 (2001): 297. http://dx.doi.org/10.1038/86637.
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Johansson, S. G. O. "The story of IgND." Journal of Allergy and Clinical Immunology 115, no. 3 (2005): 644–48. http://dx.doi.org/10.1016/j.jaci.2004.11.027.
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Sanders, John T., M. Colleen Hastings, Zina Moldoveanu, et al. "Serial Galactose-Deficient IgA1 Levels in Children with IgA Nephropathy and Healthy Controls." International Journal of Nephrology 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/8210641.
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Galactose-deficient IgA1 (Gd-IgA1) is a key pathogenic factor for IgA nephropathy (IgAN) and a potential biomarker for the disease. This study examined serial serum Gd-IgA1 levels over 1 year in 13 children with IgAN and 40 healthy children, to determine whether or not serum Gd-IgA1 levels changed over time. Subjects were younger than 18 years of age. Follow-up measurements were scheduled 6 and/or 12 months later. Analysis of variance and regression models for repeated measures were used to estimate group and time effects. Serum Gd-IgA1 level was higher in initial samples for IgAN patients compared to those of healthy children (P<0.0001). Serum Gd-IgA1 levels did not change over time for healthy controls but increased for IgAN patients (P=0.001). Serum Gd-IgA1 level was elevated for 9 children with IgAN at study entry and remained elevated. Two of the 4 IgAN patients with initially normal Gd-IgA1 levels had a subsequent elevated level. The persistent elevation of the serum Gd-IgA1 level in children with IgAN enhances its utility as a potential diagnostic test for IgAN.
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Wehbi, Batoul, Virginie Pascal, Lina Zawil, Michel Cogné, and Jean-Claude Aldigier. "History of IgA Nephropathy Mouse Models." Journal of Clinical Medicine 10, no. 14 (2021): 3142. http://dx.doi.org/10.3390/jcm10143142.
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IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. It was first described in 1968 by Jean Berger and Nicole Hinglais as the presence of intercapillary deposits of IgA. Despite this simple description, patients with IgAN may present very broad clinical features ranging from the isolated presence of IgA in the mesangium without clinical or biological manifestations to rapidly progressive kidney failure. These features are associated with a variety of histological lesions, from the discrete thickening of the mesangial matrix to diffuse cell proliferation. Immunofluorescence on IgAN kidney specimens shows the isolated presence of IgA or its inconsistent association with IgG and complement components. This clinical heterogeneity of IgAN clearly echoes its complex and multifactorial pathophysiology in humans, inviting further analyses of its various aspects through the use of experimental models. Small-animal models of IgAN provide the most pertinent strategies for studying the multifactorial aspects of IgAN pathogenesis and progression. Although only primates have the IgA1 subclass, several murine models have been developed in which various aspects of immune responses are deregulated and which are useful in the understanding of IgAN physiopathology as well as in the assessment of IgAN therapeutic approaches. In this manuscript, we review all murine IgAN models developed since 1968 and discuss their remarkable contribution to understanding the disease.
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Rizk, Dana V., Manish K. Saha, Stacy Hall, et al. "Glomerular Immunodeposits of Patients with IgA Nephropathy Are Enriched for IgG Autoantibodies Specific for Galactose-Deficient IgA1." Journal of the American Society of Nephrology 30, no. 10 (2019): 2017–26. http://dx.doi.org/10.1681/asn.2018111156.
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BackgroundIgA nephropathy (IgAN) is the leading primary GN worldwide. The disease is thought to result from glomerular deposition of circulating immune complexes of IgG bound to galactose-deficient IgA1 (Gd-IgA1). However, routine immunofluorescence microscopy fails to detect IgG in many kidney biopsies from patients with IgAN and the specificity of IgG in immunodeposits has not been tested.MethodsWe used remnant frozen kidney-biopsy specimens from 34 patients with IgAN; 14 were IgG-positive and 20 were IgG-negative by routine immunofluorescence microscopy. Six patients with primary membranous nephropathy (MN) and eight with lupus nephritis (LN) served as controls. IgG in the kidney tissue was extracted and its amount determined by ELISA. IgG molecular integrity was assessed by SDS-PAGE immunoblotting. Antigenic specificity of extracted IgG was determined by ELISA using phospholipase A2 receptor (PLA2R) or Gd-IgA1 as antigen. In addition, ten other IgAN cases, six IgG-positive and four IgG-negative by routine immunofluorescence, were used for colocalization studies by confocal microscopy.ResultsIgG extracted from MN but not IgAN immunodeposits reacted with PLA2R. Conversely, IgG extracted from IgAN but not MN or LN immunodeposits reacted with Gd-IgA1. Even IgAN kidney-biopsy specimens without IgG by routine immunofluorescence microscopy had IgG specific for Gd-IgA1. Confocal microscopy confirmed the presence of IgG in the IgAN biopsies with colocalization of glomerular IgA and IgG.ConclusionsThese results reveal for the first time that IgAN kidney biopsies, with or without IgG by routine immunofluorescence, contain Gd-IgA1–specific IgG autoantibodies. These findings support the importance of these autoantibodies in the pathogenesis of IgAN.
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Cassol, Clarissa A., Cherri Bott, Gyongyi M. Nadasdy, et al. "Immunostaining for galactose-deficient immunoglobulin A is not specific for primary immunoglobulin A nephropathy." Nephrology Dialysis Transplantation 35, no. 12 (2019): 2123–29. http://dx.doi.org/10.1093/ndt/gfz152.
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Abstract Background Primary immunoglobulin A nephropathy (IgAN) is characterized by IgA1-dominant or codominant glomerular deposits, postulated to be galactose deficient (Gd). However, glomerular IgA deposition can also occur in nonrenal diseases such as liver cirrhosis, psoriasis and inflammatory bowel disease (‘secondary IgAN’) or be an incidental finding in biopsies with other pathologies. A glomerulonephritis resembling IgAN can develop in patients with bacterial, mainly staphylococcal infections [staphylococcal infection-associated glomerulonephritis (SAGN)]. There are no specific histological features to distinguish between these, but differentiation is critical for appropriate management. The aim of this study was to investigate whether a recently described antibody to Gd-IgA1 (KM-55) could aid in differentiating primary IgAN from other conditions with glomerular IgA deposition, especially SAGN. Methods We performed a retrospective cohort study of patients who underwent kidney biopsy for clinical indications and were found to have glomerular IgA deposits. Results We evaluated 100 biopsies, including primary IgAN (n = 44), secondary IgAN (n = 27), SAGN (n = 13), incidental IgA deposition (n = 8) and lupus nephritis (n = 8). There was no difference in Gd-IgA staining intensity or the proportion of positive cases between primary and secondary IgAN. SAGN and cases with incidental IgA deposits had significantly lower Gd-IgA staining intensity than primary IgAN, but up to 69% of SAGN cases were positive (albeit weaker). Conclusions Gd-IgA staining is present not only in primary IgAN, but also in biopsies with secondary IgAN, SAGN and incidental IgA. Weak or negative staining may favor SAGN, especially in the setting of infection, or incidental IgA in the absence of nephritic symptoms or in the presence of other unrelated glomerular pathologies. However, positive staining for Gd-IgA alone is not specific enough for a diagnosis of primary IgAN.
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Feng, Shaozhen, Zhong Zhong, Jinjin Fan, Xiaoyan Li, Dianchun Shi, and Lanping Jiang. "Upregulated Expression of Intestinal Antimicrobial Peptide HD5 Associated with Renal Function in IgA Nephropathy." Disease Markers 2020 (February 5, 2020): 1–10. http://dx.doi.org/10.1155/2020/2078279.
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Purpose. It was reported that gut-kidney axis may play an important role in IgA nephropathy (IgAN). Previous five GWASs of different populations for IgAN have discovered several genes related to intestinal immunity, including DEFA gene. However, the roles of the encoded proteins of DEFA5/6 which were called intestinal antimicrobial peptides HD5 and HD6 were not clear in kidney disease, such as IgAN. The purpose of this study was to clarify the association of HD5 and HD6 with IgAN. Methods. We measured HD5 and HD6 in serum, urine, and kidney of IgAN patients and normal controls by ELISA, Western blot, and immunofluorescence. The association of HD5 or HD6 levels with clinical and pathologic phenotypes was analyzed. Results. Serum levels of HD5 and HD6 were significantly higher in IgAN patients than those in normal controls. Baseline serum HD5 levels were significantly associated with eGFR (P=0.002) and tubular atrophy/interstitial fibrosis (P=0.004) by stepwise multivariate regression analysis. Compared to the patients with serum HD5 below the median level, patients with elevated serum HD5 above the median level had a significantly worse renal outcome (log-rank test, P=0.009) by Kaplan-Meier analysis. A Cox regression model showed that serum HD5 was an independent prognostic factor (HR=1.239, P=0.029) after adjusting for the well-known predictors of outcome in IgAN patients. In renal biopsies of IgAN patients, HD5 was significantly expressed in the damaged proximal tubules, while no immunoreactive HD6 was found. Interestingly, the serum HD6 level of IgAN patients was significantly associated with gender. Conclusions. In IgAN patients, an elevated serum HD5 level at the time of renal biopsy was associated with poor renal outcomes. HD5 rather than HD6 was probably associated with renal function of IgAN patients.
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Schena, Francesco Paolo, Giuseppina Cerullo, Michele Rossini, Salvatore Giovanni Lanzilotta, Christian D’Altri, and Carlo Manno. "Increased Risk of End-Stage Renal Disease in Familial IgA Nephropathy." Journal of the American Society of Nephrology 13, no. 2 (2002): 453–60. http://dx.doi.org/10.1681/asn.v132453.
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ABSTRACT. Primary IgA nephropathy (IgAN) is characterized by recurrent episodes of macroscopic hematuria accompanied by upper respiratory tract infections or persistent asymptomatic microscopic hematuria with or without proteinuria. IgAN may involve one or more members of a family. Three generations of a cohort of 110 patients with biopsy-proven IgAN, living in Southern Italy, were checked for urinalysis, and the relative risk (RR) of developing the disease was evaluated. A total of 19 unrelated familial, 37 suspected, and 54 sporadic cases of IgAN were identified. Renal survival was estimated by the Kaplan-Meier method for censored data and compared by use of the log-rank test. More than 50% of the patients with IgAN clustered in kindred with more than two probably affected relatives. In 19 unrelated IgAN families, 8 had single-generation (SG) and 11 multigenerational (MG) involvement showing a prevalent vertical transmission of the trait. The RR was 16 times higher in first-degree relatives (odds ratio [OR], 16.4; 95% confidence interval [CI], 5.7 to 47.8; P < 0.0001) and >2 times higher, even if NS, in second-degree relatives (OR, 2.4; 95 % CI, 0.7 to 7.9; P = 0.145). The clinical and histologic picture of familial and sporadic IgAN appeared to be similar. The 20-yr renal survival rate from the apparent onset of the disease was significantly poorer in patients with familial (41%) than in patients with sporadic (94%) IgAN (P = 0.003). Furthermore, 15-yr renal survival from the time of renal biopsy was significantly worse in familial IgAN (P = 0.02); end-stage renal disease was present in 64% of familial and only in 8% of patients with sporadic IgAN. Finally, renal survival was significantly worse in patients belonging to families with SG rather than with MG involvement (P = 0.03). These data show, for the first time, that familial IgAN may be considered a nonbenign disease that occurs frequently in first-degree relatives. Familial IgAN has a poorer outcome than sporadic IgAN. Therefore, an accurate family history and urinalysis in all family members is urgently recommended in clinical practice. This procedure might avoid late referral of subjects with persistent and underestimated urinary abnormalities and late diagnosis of the disease.
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Feehally, John, and Jonathan Barratt. "The Genetics of IgA Nephropathy: An Overview from Western Countries." Kidney Diseases 1, no. 1 (2015): 33–41. http://dx.doi.org/10.1159/000381738.
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Background: IgA nephropathy (IgAN) is the commonest primary glomerulonephritis worldwide and a significant cause of chronic kidney disease and end-stage renal disease. It is widely accepted that genetic factors play a role in the pathogenesis of IgAN. However, the identity of these genetic factors remains uncertain. Summary: Critical to all genetic studies is a precise phenotypic definition of the disease. It is well recognised that IgAN displays striking phenotypic variation, raising the possibility that it may not be a single disease and it may not be the same disease in different parts of the world. In this review, we discuss the challenges that this phenotypic variation poses to interpreting genetic data and the current evidence for specific gene involvement in IgAN, focusing particularly on data from European IgAN cohorts. Key Messages: With advances in genetic techniques, in particular next-generation sequencing, and an increased understanding of the importance of copy number variations, epigenetics and transcriptomics, it is likely that we will gain a greater understanding of the genetic basis for IgAN. However, due to the lack of consistency in epidemiological clinicopathological studies both within and between continents, this will only be achieved if we are able to more precisely phenotype IgAN populations. Facts from East and West: The reported prevalence of IgAN is higher in Asia than in Europe and North America. However, differences in use of biopsy for the diagnosis of IgAN should be taken into account in analysing data from both East and West. In Europe, IgAN affects men more frequently than women; this is not the case in Asia. Familial IgAN has been more frequently reported in Europe than in Asia. Within Europe, familial IgAN is more evident in southern than in northern populations. Changes in the pattern of serum IgA1 O-glycosylation is a common finding in IgAN patients in the East and West. SNPs within the gene coding for the enzyme C1GALT1 have been reported in Chinese and European patients. However, there is no evidence for a role of gene polymorphism of the C1GALT1 chaperone cosmc in Europeans. Genetic variants in the HLA gene family have been observed in populations from the East and West. Associations between IgAN and variants of the TAP1/PSMB and DEFA genes were observed in Asian but not in Western patients. Association with the angiotensin-converting enzyme gene was seen only in Asian patients.
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Park, Sehoon, Seung Hee Yang, Chang Wook Jeong, et al. "RNA-Seq profiling of microdissected glomeruli identifies potential biomarkers for human IgA nephropathy." American Journal of Physiology-Renal Physiology 319, no. 5 (2020): F809—F821. http://dx.doi.org/10.1152/ajprenal.00037.2020.
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Few studies have examined gene expression changes occurring in the glomeruli of IgA nephropathy (IgAN) using a sensitive transcriptomic profiling method such as RNA sequencing (RNA-Seq). We collected glomeruli from biopsy specimens from patients with IgAN with relatively preserved kidney function (estimated glomerular filtration rate ≥ 60 mL·min−1·1.73 m−2 and urine protein-to-creatinine ratio < 3 g/g) and from normal kidney cortexes by hand microdissection and performed RNA-Seq. Differentially expressed genes were identified, and gene ontology term annotation and pathway analysis were performed. Immunohistochemical labeling and primary mesangial cell cultures were performed to confirm the findings of RNA-Seq analysis. Fourteen patients with IgAN and ten controls were included in this study. Glomerulus-specific genes were highly abundant. Principal component analysis showed clear separation between the IgAN and control groups. There were 2,497 differentially expressed genes, of which 1,380 were upregulated and 1,117 were downregulated (false discovery rate < 0.01). The enriched gene ontology terms included motility/migration, protein/vesicle transport, and immune system, and kinase binding was the molecular function overrepresented in IgAN. B cell signaling, chemokine signal transduction, and Fcγ receptor-mediated phagocytosis were the canonical pathways overrepresented. In vitro experiments confirmed that spleen tyrosine kinase (SYK), reported as upregulated in the IgAN transcriptome, was also upregulated in glomeruli from an independent set of patients with IgAN and that treatment with patient-derived IgA1 increased the expression of SYK in mesangial cells. In conclusion, transcriptomic profiling of the IgAN glomerulus provides insights in the intraglomerular pathophysiology of IgAN before it reaches profound kidney dysfunction. SYK may have a pathogenetic role in IgAN.
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Gassmann, W., T. Haferlach, K. H. Engelhardt, et al. "IgD-Plasmozytom." DMW - Deutsche Medizinische Wochenschrift 109, no. 46 (2008): 1775–79. http://dx.doi.org/10.1055/s-2008-1069453.
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Suschke, J., and J. U. Walther. "Das Hyper-IgD-Syndrom (The hyper-IgD-syndrome)." Zeitschrift f�r Rheumatologie 56, no. 1 (1997): 40–42. http://dx.doi.org/10.1007/s003930050019.
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