71 research outputs found
Feature Article: Altered morpho-functional features of bones in autoimmune disease-prone BXSB/MpJ-Yaa mice
No full textBones play crucial roles in motility, electrolyte metabolism, and immunity. Clinical cases have suggested bone dysfunction in several systemic autoimmune diseases. This study exhibited altered bone morpho-functions in BXSB/MpJ-Yaa as a murine autoimmune disease model. During clinical examinations, the serum Ca level was significantly higher in BXSB/MpJ-Yaa than the healthy control BXSB/MpJ at the early stage (two to four months), but that in BXSB/MpJ-Yaa decreased with advancing age. Further, the increase of urinary Ca with nephritis and white blood cells with mild anemia proceeded in BXSB/MpJ-Yaa with advancing age. The thyroid and parathyroid gland morphologies and serum parathormone level did not differ among strains, but the tibia was smaller in BXSB/MpJ-Yaa than in BXSB/MpJ especially during the late stage (six months). Histologically, osteoclasts and osteoblasts showed increased and decreased tendencies, respectively, in BXSB/MpJ-Yaa during the early stage, and osteoclasts and bone area significantly increased and decreased, respectively, compared with BXSB/MpJ at later stages. The bone morphological indices were affected by the expression of BXSB/MpJ-Yaa mutation genes and inflammatory genes in BXSB/MpJ-Yaa. In conclusion, systemic autoimmune diseases in BXSB/MpJ-Yaa are associated with the morpho-functional abnormalities of bones, calcium dynamics, and hematopoiesis, and each factor contributes to forming the phenotypes in this disease. Impact statement Bone disease, such as osteoporosis and rheumatoid arthritis, increases because of the progression of an aging society. Autoimmune disease are important and predisposing factors for the pathogenesis of the bone disease; however, the pathological mechanism is unclear. We have demonstrated that systemic autoimmune disease in BXSB/MpJ-Yaa is closely associated with the morpho-functional abnormalities of bones including bone marrow and has complicated pathology. The abnormalities are characterized by altered regulations of serum calcium, anemia tendency, and hematopoiesis with increased WBCs and decreased PLs, short length and low mass of long bones, imbalance in the populations of osteoclasts and osteoblasts, and increased expression of candidate genes for causing and/or exacerbating their phenotypes. Therefore, BXSB/MpJ-Yaa serves as a model to elucidate bone phenotypes in systemic autoimmune disease that would be affected by the factors in the bone as well as the other immune and/or mineral metabolism organs both in human and experimental medicine
BXSB/MpJ-Yaa mouse model of systemic autoimmune disease shows increased apoptotic germ cells in stage XII of the seminiferous epithelial cycle
No full textIn mammals, the reproductive system and autoimmunity regulate mutual functions. Importantly, systemic autoimmune diseases are thought to cause male infertility but the underlying pathological mechanism remains unclear. In this study, the morpho-function of the testes in BXSB/MpJ-Yaa mice was analyzed as a representative mouse model for systemic autoimmune diseases to investigate the effect of excessive autoimmunity on spermatogenesis. At 12 and 24 weeks of age, BXSB/MpJ-Yaa mice showed splenomegaly and increased levels of serum autoantibodies, whereas no controls showed a similar autoimmune condition. In histological analysis, the enlarged lumen of the seminiferous tubules accompanied with scarce spermatozoa in the epididymal ducts were observed in some of the BXSB/MpJ-Yaa and BXSB/MpJ mice but not in C57BL/6N mice. Histoplanimetrical analysis revealed significantly increased residual bodies and apoptotic germ cells in the seminiferous tubules in BXSB/MpJ-Yaa testes without apparent inflammation. Notably, in stage XII of the seminiferous epithelial cycles, the apoptotic germ cell number was remarkably increased, showing a significant correlation with the indices of systemic autoimmune disease in BXSB/MpJ-Yaa mice. Furthermore, the Sertoli cell number was reduced at the early disease stage, which likely caused subsequent morphological changes in BXSB/MpJ-Yaa testes. Thus, our histological study revealed the altered morphologies of BXSB/MpJ-Yaa testes, which were not observed in controls and statistical analysis suggested the effects of an autoimmune condition on this phenotype, particularly the apoptosis of meiotic germ cells. BXSB/MpJ-Yaa mice were shown to be an efficient model to study the relationship between systemic autoimmune disease and the local reproductive system
ESCRAVIDÃO E DIÁSPORA: UMA ANÁLISE DE O CAMINHO DE CASA, DE YAA GYASI
No full textThis article aims to analyze the novel Homegoing (2016), by the Ghanaian author Yaa Gyasi, which focuses on the African diaspora, in order to demonstrate how the author critically revisits the past and promotes a representation of the impact of captivty on the descendants of slaves. We will also approach the representation of the cultural identity of the diasporic individual. For this, we will use the theories of African Diaspora by Kevin Kenny (2013) and Paul Gilroy (2001), and also the concept of diasporic identity by Stuart Hall (2008).Este artigo visa à analise do romance O Caminho de Casa (2016), da autora ganesa Yaa Gyasi, que focaliza a diáspora africana, de modo a demonstrar como a autora revisita criticamente o passado e promove uma representação do impacto do cativeiro nos descendentes de escravos. Abordaremos igualmente a representação da identidade cultural do sujeito diaspórico. Para isso, utilizaremos as teorias de diáspora africana de Kevin Kenny (2013) e Paul Gilroy (2001), bem como o conceito de identidade diaspórica de Stuart Hall (2008).Este artículo tiene como objetivo analizar la novela Volver a Casa (2016), de la escritora de origen ghanés Yaa Gyasi, con enfoque en la diáspora africana, para demostrar cómo el autor revisita críticamente el pasado y promueve una representación del impacto del cautiverio en los descendientes de esclavos. También abordaremos la representación de la identidad cultural del sujeto diaspórico. Para esto, use las teorías de la diáspora africana de Kevin Kenny (2013) y Paul Gilroy (2001), así como el concepto de identidad diaspórica de Stuart Hall (2008)
Castrated autoimmune glomerulonephritis mouse model shows attenuated glomerular sclerosis with altered parietal epithelial cell phenotype
No full textSex hormones help in maintaining proper immunity as well as renal homeostasis in mammals, and these multi-functional properties characterize the onset of sex-dependent diseases. To clarify the contribution of sex hormones to autoimmune disease-related renal pathogenesis, BXSB/MpJ-Yaa was investigated as a murine autoimmune glomerulonephritis model. BXSB/MpJ-Yaa and its wild-type, BXSB/MpJ-Yaa(+) were castrated or sham-operated at three weeks and examined until six months of age. Both castrated strains showed significantly lower serum testosterone levels and body weights than sham-operated mice. Castration did not change the disease phenotypes in BXSB/MpJ-Yaa(+). At three months, both sham-operated and castrated BXSB/MpJ-Yaa manifested splenomegaly, autoantibody production, and glomerulonephritis, and castrated BXSB/MpJ-Yaa tended to show heavier spleen weights than the sham-operated group. At six months, both the treated BXSB/MpJ-Yaa showed equivalent autoimmune disease conditions; however, castrated mice clearly showed milder glomerular sclerotic lesions than the sham-operated groups. Urinary albumin excretion in castrated BXSB/MpJ-Yaa was significantly milder than in sham-operated mice at four months, but those of both the treated BXSB/MpJ-Yaa were comparable at six months. The examined renal histopathological indices in parietal epithelial cells were remarkably altered by castration. Briefly, castration decreased the height of parietal epithelial cells and total parietal epithelial cell number in BXSB/MpJ-Yaa at six months. For immunostaining, parietal epithelial cells facing the injured glomeruli of BXSB/MpJ-Yaa expressed CD44, an activated parietal epithelial cell marker, and CD44-positive parietal epithelial cells showed nuclear localization of the androgen receptor and proliferation marker Ki67. CD44- or Ki67-positive parietal epithelial cells were significantly fewer in castrated group than in sham-operated BXSB/MpJ-Yaa at six months. Further, quantitative indices for CD44-positive parietal epithelial cell number and frequency in renal corpuscles positively correlated with glomerular sclerotic severity in BXSB/MpJ-Yaa. In conclusion, androgen seemed to have an effect on both systemic immunity and renal morpho-function; however, the effect on the latter could be more clearly observed in BXSB/MpJ-Yaa, as parietal epithelial cell activation resulted in glomerular sclerosis
Ventos que cruzam o atlântico: intersecções, violência e subalternidade feminina na poética de Yaa Gyasi
No full textThe objective of this research is to analyze female characters, highlighting the aspects of violence and subalternity, as an analytical category. The work examines the poetic performance of the African author, of Ghanaian origin, Yaa Gyasi. The aforementioned author uses the space of fiction and uses it as a tool to denounce the sociocultural imbalances caused by segregationist behaviors that aim at social fragmentation in order to preserve the status of supremacy. The intersection of indicators of subalternization, such as race, social class, gender, nationality and ethnic origin, are mechanisms used for the effective exercise of hegemonic institutions, legitimized by the patriarchal regime that gives the male entity decision-making power, leadership and moral authority over marginalized social layers. To consolidate the theoretical-argumentative measurements, we use the novel Homegoing (2017), as a corpus of analysis. The development of this thesis is relevant to the promotion of further studies in the field of literary theory, as well as expanding the critical-expository contributions related to post-colonial and gender reflexive interventions. In this way, we contribute to promoting the critical fortune inherent to the novelist Yaa Gyasi and provide, in the space of academic discussion, the products of her creative disposition. That said, in order to legitimize the argumentative assumptions and systematize the discussion, we resorted to the theoretical conjectures of AIDOO (1983, 2009), ACHOLONU (1995), AMADIUME (1987), ARNDT (2002), COLLINS (2019), DAVIS (2016), HUDSON-WEEMS (2020), BONNICI (2000), BHABHA (2014), BAMISILE (2021), ACHEBE (2012), ALENCASTRO (1998), MBEMBE (2014), APPIAH (2012), FANON (1968, 1983), among other epistemological frameworks necessary for the evolution of the thesis.A concretização desta pesquisa tem o objetivo de analisar as personagens femininas, realçando os aspectos da violência e subalternidade, enquanto categoria analítica. O trabalho ausculta o desempenho poético da autora africana, de origem ganense, Yaa Gyasi. A autoria citada recorre ao espaço da ficção e o utiliza como ferramenta à denúncia dos desequilíbrios socioculturais suscitados por condutas segregacionistas que tencionam a fragmentação social a fim de preservarem o status de supremacia. A intersecção dos indicadores de subalternização, a exemplo de raça, classe social, gênero, nacionalidade e origem étnica, são mecanismos utilizados ao efetivo exercício das instituições hegemônicas, legitimadas pelo regime patriarcal que confere à entidade masculina poder de decisão, liderança e autoridade moral sobre as camadas sociais marginalizadas. Para a consolidação das aferições teórico-argumentativas nos valemos da obra O caminho de Casa (2017), enquanto corpus de análise. O desenvolvimento desta tese é relevante à fomentação de estudos posteriores, no campo da teoria literária, assim como amplia os aportes crítico-expositivos relacionados às intervenções reflexivas pós-coloniais e de gênero. Deste modo, contribuímos para promoção da fortuna crítica inerente à romancista Yaa Gyasi e dispomos, ao espaço da discussão acadêmica, os produtos de sua disposição criativa. Isto posto, com a finalidade de legitimar os pressupostos argumentativos e sistematizar a discussão recorremos às conjecturas teóricas de AIDOO (1983, 2009), ACHOLONU (1995), AMADIUME (1987), ARNDT (2002), COLLINS (2019), DAVIS (2016), HUDSON-WEEMS (2020), BONNICI (2000), BHABHA (2014), BAMISILE (2021), ACHEBE (2012), ALENCASTRO (1998), MBEMBE (2014), APPIAH (2012), FANON (1968, 1983), entre outros arcabouços epistemológicos necessários à evolução da tese
Histopathological changes in tear-secreting tissues and cornea in a mouse model of autoimmune disease
No full textThe tear film covers the cornea, and its abnormalities (including immunological) induce dry eye. Using autoimmune disease model mice, BXSB/MpJ-Yaa (BXSB-Yaa), histopathological changes in the eye and tear-secreting tissues were examined using histopathology, immunohistochemistry, and electron microscopy at 8, 20, and 28 weeks for early, middle, and late disease stages. Early and middle stage BXSB-Yaa showed increased serum autoantibody and spleen weight-to-body weight (S/B) ratio, respectively, and higher tear volume than controls, BXSB/MpJ (BXSB), at early stages, which decreased with ageing and negatively correlated with autoimmune disease indices. Smaller Meibomian gland acini, intraorbital lacrimal glands, and Harderian gland acinar cells were seen in late stage BXSB-Yaa than in BXSB; the latter two indices decreased with ageing and negatively correlated with the S/B ratio. Cell infiltration occurred in the middle stage BXSB-Yaa extraorbital lacrimal gland, and acinar cells were smaller than BXSB. The conjunctival goblet cells decreased from early to middle stages in both strains, but in BXSB-Yaa, they increased at late stages with a partial lack of microvilli on the cornea and were inversely altered with anterior epithelium thickness through ageing, suggesting that they compensated for anterior epithelium damage. In conclusion, the tear film was unstable due to an autoimmune disease condition in BXSB-Yaa. Impact statement Cornea, an outermost layer of mammalian eye, is protected by tear film and abnormalities of tear film causes dry eye. Dry eye injures the cornea which results lower vision in patients. Several factors cause dry eye, including altered systemic conditions, environment, and immunological abnormality of the patient in autoimmune disease like Sjogren's syndrome (SS). However, the detailed pathology of autoimmune abnormality-mediated dry eye is unclear. Here we demonstrated that systemic autoimmune abnormality in BXSB-Yaa mice was associated with histological changes in the exocrine glands and cornea of the eyes. We also showed that BXSB-Yaa mice developed mild or early stage dry eye-like disease and explain the existence of a compensatory mechanism associated with the dysfunction of these tissues. Thus, BXSB-Yaa could be a model for SS-like disease-associated dry eye and these data would contribute to the understanding of the pathogenesis of autoimmune-related dry eye disease
Altered Renal Pathology in an Autoimmune Disease Mouse Model After Induction of Diabetes Mellitus
No full textDiabetes mellitus (DM) is a predisposing factor for renal disorder progression and is referred to as diabetic kidney disease (DKD). However, there are no reports of DKD with an underlying autoimmune disorder. In this study, we compared the pathophysiological changes caused by DM induction after streptozotocin (STZ) injection in comparison with that in a control group receiving citrate buffer (CB) in the autoimmune disease model mice "BXSB/MpJ-Yaa" (Yaa) and the wild-type strain BXSB/MpJ. Both strains showed hyperglycemia after 12 weeks of STZ injection. Interestingly, the Yaa group developed membranous and proliferative glomerulonephritis, which tended to be milder glomerular lesions in the STZ group than in the CB group, as indicated by a decreased mesangial area and ameliorated albuminuria. Statistically, the indices for hyperglycemia and autoimmune abnormalities were negatively and positively correlated with the histopathological parameters for mesangial matrix production and glomerular proliferative lesions, respectively. STZ treatment induced renal tubular anisonucleosis and dilations in both strains, and they were more severe in Yaa. Significantly decreased cellular infiltration was observed in the Yaa group compared to the CB group. Thus, in DKD related to autoimmune nephritis, hyperglycemia modifies its pathology by decreasing the mesangial area and interstitial inflammation and aggravating renal tubular injury
Journeys: Camosun Stories of Indigenization (2018)
No full text"Journeys: Camosun Stories of Indigenization" features stories of Indigenization from the diverse and multiple perspectives
of Camosun staff.Contributors include: John Borass, Vice President, Education; Sybil Harrison, Director, Learning Services; Suzanne Thiessen, School of Business; Shane Johnson, Facilities; Chivonne Graff, Child Care Services and Early Learning & Care; Andrew Brice, Digital Communication; Kelly Pitman, English Department; Nicole Kilburn, Anthropology Department; Brenda Petays, Visual Arts Department; Steve Walker-Duncan, Culinary Arts Department; Joan Humphries, Nursing Department; Anita Ferriss, Human Resources; Daryl Thomson, Human Resources; Merry Watts, Human Resources; Dianne Biin, Centre for Indigenous Education & Community Connections. Messages from Camosun President, Sherri Bell and Dawn Smith, Education Developer, Indigenization & Sustainability are also featured.
Art work of, and information about, Nuu-chah-nulth artist Art Thompson (Tsa Qwa Supp) is included. Additional information about Art Thompson's work in the Camosun Art Collection can be found at: https://cc.arcabc.ca/islandora/object/cc%3Apubar
Induced expression of Toll-like receptor 9 in peritubular capillary endothelium correlates with the progression of tubulointerstitial lesions in autoimmune disease-prone mice
No full textBackground Toll-like receptor (Tlr) 9 is capable of recognizing exogenous and/or endogenous nucleic acids and plays a crucial role in innate and adaptive immunity. Recently, we showed that Tlr9 is overexpressed in podocytes, a component of the blood-urine barrier (BUB), in glomeruli of autoimmune glomerulonephritis (AGN) model mice. This study investigated the activation of peritubular capillary (PTC) endothelial cells (ECs), a component of the BUB in the tubulointerstitium, through overexpressing Tlr9, and the subsequent development of tubulointerstitial lesions (TILs) in AGN model mice. Methods Lupus-prone BXSB/MpJ-Yaa (Yaa) and BXSB/MpJ (BXSB) mice were used as an AGN model and control, respectively. In addition to histopathological and ultrastructural techniques, protein and mRNA levels were also evaluated. The relationship between Tlr9 and TIL indices was analyzed by statistical correlation analysis. Results Yaa mice developed TILs and showed strong Tlr9 mRNA expression in PTC ECs at 24 weeks (wks) of age. However, BXSB mice showed no TIL but faint expression of Tlr9 mRNA at 8 and 24wks of age. Tlr9 protein localization on PTC was almost absent in BXSB mice at both ages but intense expression was found in Yaa mice only at 24wks of age. Relative mRNA expression of Tlr9 and its putative downstream cytokines, including interleukin 1 beta (Il1b), Il6, interferon gamma (Ifng), and tumor necrosis factor alpha (Tnf) was markedly increased in isolated tubulointerstitium from Yaa mice at 24wks of age. Furthermore, electron microscopy examination revealed PTC injury and TIL in Yaa mice at 24wks. The expression level of Tlr9 in the tubulointerstitium was correlated with inflammatory cells in TILs, injured PTC, Ilb and Tnf expression, and damaged tubules (P<0.05 and 0.01). Conclusion Induced expression of Tlr9 in ECs correlates with PTC injury and the development of TILs in lupus-prone AGN model mice
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