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Purpose@#Although the popularity of Descemet membrane endothelial keratoplasty (DMEK) is increased, there is still few clinical studies in Korea. In this study, we aimed to report the initial clinical outcomes of DMEK in patients followed up for more than 6 months. @*Methods@#A total of 96 eyes that underwent DMEK by a single surgeon for Fuchs endothelial corneal dystrophy, pseudophakic bullous keratopathy, or other indications were evaluated for best-corrected visual acuity (BCVA), endothelial cell density (ECD), central corneal thickness (CCT), postoperative complications, and graft survival. @*Results@#The postoperative BCVA significantly increased compared to the preoperative BCVA by 59.4% (1.00 ± 0.77 logarithm of the minimum angle of resolution vs. 0.67 ± 0.76 logarithm of the minimum angle of resolution, p < 0.001). The average preoperative ECD was 754 ± 382 cells/mm2, increasing to 1,333 ± 562 cells/mm2 at 3 months (76.8%, p < 0.001), 1,334 ± 632 cells/mm2 at 6 months (76.9%, p < 0.001), 1,121 ± 474 cells/mm2 at 12 months (48.7%, p = 0.024), and 972 ± 458 cells/mm2 at 24 months postoperatively (28.9%, p = 0.445). Compared to 3 months, the ECD declined by 15.9% at 12 months (p = 0.009) and 27.1% at 24 months postoperatively (p = 0.158). The average CCT was 675 ± 113 μm preoperatively, decreasing to 581 ± 102, 574 ± 101, and 594 ± 94 μm at 6, 12, and 24 months after DMEK, respectively (p < 0.001 between all follow-up time points). Allograft rejection was detected in three (3.1%) and 14 eyes (14.6%) underwent retransplantation at an average of 10.1 ± 8.4 months after DMEK. @*Conclusions@#DMEK is promising for maintaining corneal clarity, low postoperative complication rates, and stable graft longevity.
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Purpose@#Although there is still no consensus on the best animal model for dry eye disease research, a model based on lacrimal gland extraction (LGE) model is widely used. In this study, we aimed to investigate the histopathological changes taking place on the contralateral eye after unilateral LGE to determine whether it is useful as a control. @*Methods@#Seven-week-old male C57BL/6 mice were divided into naive control, environmental chamber model, and LGE groups. Corneal fluorescein staining was scored to quantify the severity of damage. Morphological changes in the cornea, conjunctiva, and lacrimal gland (LG) were determined by hematoxylin and eosin staining and compared to those on naive control animals. @*Results@#Compared to naive subjects, the unilateral LGE model showed enhanced corneal erosion scores and loss of conjunctival goblet cells, not only on the ipsilateral but also on the contralateral side. These changes in the ocular surface became more pronounced in a time-dependent manner. Furthermore, loss of LG acinar cells and leukocyte infiltration were detected in the contralateral LGs of the LGE model. @*Conclusions@#Considering the changes observed in the ocular surface and LGs, the contralateral side of the LGE model may not offer proper control conditions for the experimental comparison of the effects of dry eye disease in vivo. There may be regulatory feedback or crosstalk system between both eyes activated in response to LGE.
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Stroke causes systemic immunosuppression. T lymphocytes are involved in infarct size in the early stages of stroke. However, the phenotypes of T lymphocytes and their functions in peripheral immune organs and the brain have not been well analyzed in the acute and chronic phases of stroke. Here, we investigated pathological phenotypic alterations in the systemic immune response, especially changes in T lymphocytes, from one day to six months after ischemic stroke in mice. Impairment in thymocyte numbers, development, proliferation, and apoptosis were observed for up to two weeks. The number of mature T cells in the spleen and blood decreased and showed reduced interferon-γ production. Increased numbers of CD4-CD8-CD3+ double-negative T cells were observed in the mouse brain during the early stages of stroke, whereas interleukin (IL)-10+Foxp3+ regulatory T lymphocytes increased from two weeks during the chronic phase. These phenotypes correlated with body weight and neurological severity scores. The recovery of T lymphocyte numbers and increases in IL-10+Foxp3+ regulatory T lymphocytes may be important for long-term neurological outcomes. Dynamic changes in T lymphocytes between the acute and chronic phases may play different roles in pathogenesis and recovery. This study provides fundamental information regarding the T lymphocyte alterations from the brain to the peripheral immune organs following stroke.
RESUMO
Stroke causes systemic immunosuppression. T lymphocytes are involved in infarct size in the early stages of stroke. However, the phenotypes of T lymphocytes and their functions in peripheral immune organs and the brain have not been well analyzed in the acute and chronic phases of stroke. Here, we investigated pathological phenotypic alterations in the systemic immune response, especially changes in T lymphocytes, from one day to six months after ischemic stroke in mice. Impairment in thymocyte numbers, development, proliferation, and apoptosis were observed for up to two weeks. The number of mature T cells in the spleen and blood decreased and showed reduced interferon-γ production. Increased numbers of CD4-CD8-CD3+ double-negative T cells were observed in the mouse brain during the early stages of stroke, whereas interleukin (IL)-10+Foxp3+ regulatory T lymphocytes increased from two weeks during the chronic phase. These phenotypes correlated with body weight and neurological severity scores. The recovery of T lymphocyte numbers and increases in IL-10+Foxp3+ regulatory T lymphocytes may be important for long-term neurological outcomes. Dynamic changes in T lymphocytes between the acute and chronic phases may play different roles in pathogenesis and recovery. This study provides fundamental information regarding the T lymphocyte alterations from the brain to the peripheral immune organs following stroke.