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Purpose. Retinal ischemia–reperfusion injury (RIRI) is the basis of the pathology that leads to many retinal diseases and induces necroptosis and apoptosis. Tumor necrosis factor-α (TNF-α) is critically involved in necroptosis and apoptosis. Delta-opioid receptor (DOR) activation inhibits TNF-α release in our previous studies, it might prevent necroptosis and apoptosis by inhibiting the release of TNF-α. However, the role of TNF-α and DOR in necroptosis and apoptosis of retinal pigment epithelial (RPE) cells remains largely unknown. Here, we explored the mechanisms of TNF-α and DOR in necroptosis and apoptosis using an oxygen-glucose deprivation/reoxygenation (OGD/R) model of adult retinal pigment epithelial cell line-19 (ARPE19) cells. Materials and Methods. ARPE19 cells were exposed to OGD/R conditions to mimic RIRI in vitro. Cell viability was quantified using the Cell Counting Kit-8 (CCK-8) assay. Morphological changes were observed by inverted microscopy. TNF-α protein levels in cell lysates were measured by enzyme-linked immunosorbent assay (ELISA). The DOR agonist TAN-67 and antagonist naltrindole (NTI) were used to pretreat cells for 1 or 2 hours before OGD24/R36 administration. Calcein acetoxymethylester/propidium iodide (Calcein-AM/PI) and Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining were used to detect necroptotic and apoptotic ARPE19 cells, respectively. The protein expression of DOR, p-RIP1 (RIP1), p-RIP3 (RIP3), p-MLKL (MLKL), and cleaved Caspase3 (Caspase3) was measured by western blotting. Results. OGD severely damaged ARPE19 cells. Prolonged reoxygenation significantly increased TNF-α level and decreased DOR expression in ARPE19 cells. Pretreatment with the DOR agonist TAN-67 (10 µM) significantly improved ARPE19 cell viability after OGD24/R36 by reducing the number of necroptotic and apoptotic cells. Furthermore, DOR activation significantly inhibited TNF-α release and suppressed the expression of proteins related to necroptosis and apoptosis, including p-RIP1, p-RIP3, p-MLKL, and cleaved Caspase3, after OGD24/R36. This effect was reversed by the DOR antagonist NTI. Conclusion. These results strongly suggest that DOR activation inhibits necroptosis and apoptosis by decreasing TNF-α release, leading to the prevention of OGD/R-induced injury in ARPE19 cells. This study provides an innovative idea for clinical treatment strategies for retinal damage and vision loss due to RIRI.

T cell lymphoblastic lymphoma (T-LBL) is regarded as the leukemic phase of T cell acute lymphoblastic leukemia (T-ALL). The early T cell precursors ALL/LBL (ETP-LBL/ALL) are derived from thymic cells at the ETP differentiation stage and recognized as a high-risk subgroup of T-ALL/LBL. Most of these cases presented with ALL at the disease onset, but the ETP-LBL phase is uncommon. Here, we report a patient who presented with ETP-LBL at the disease onset. In this case, ALL developed even despite receiving chemotherapy, but the patient achieved a complete remission with intensive chemotherapy.

Malaria, which is responsible for a substantial amount of deaths in endemic countries, has been shown to have both direct and indirect effects on the hematological parameters. Notwithstanding, some hematological parameters among populations living in malaria endemic regions have not been described consistently, as a standard for measuring malaria burden. Based on the above fact, this study was designed to assess some hematological changes and their diagnostic values in malaria infected patients. A total of 160 malaria positive adult patients, together with 81 healthy control adults were recruited for the study. For the malaria positive group, the female to male ratio was 1.38 : 1. Specifically, 74.38%, 10.00%, and 15.62% of those in the malaria positive group had mild, moderate, and severe parasitaemia, respectively. Leukemia, anemia, and thrombocytopenia were found to be significantly associated with malaria and were all estimated to be specific for the diagnosis of malaria. Anemia was, however, estimated to be both sensitive and specific for malaria diagnosis. Therefore, anemia offers the most diagnostic value in the malaria infected patients of this study.

Objective. To investigate the quantity of CD4+T, CD4+T, CD8+T, and γδT cells in peripheral blood of HIV-infected/AIDS patients as well as to explore the possible role of CD4/CD8 ratio and γδT cells in the progression of HIV/AIDS, aimed at providing evidence for the diagnosis and treatment of AIDS. Methods. The quantity levels of CD3+T cells, CD4+T cells, CD8+T cells, and γδT cells in peripheral blood of 46 HIV-infected/AIDS patients and 30 healthy controls were detected by using flow cytometry. Results. The count of CD3+T, CD4+T, CD8+T, and γδT cells (x ¯ ± s , A/μl) in the peripheral blood was 1183.64 ± 132.58 , 278.39 ± 122.38 , 863.13 ± 82.38 , and 22.53 ± 1.74 in the experimental group as well as 1456.46 ± 124.37 , 788.74 ± 189.67 , 569.61 ± 46.49 , and 10.96 ± 0.28 in the control group, respectively. The p values of the two groups were <0.005 after the t -test, revealing a statistically significant difference. The proportion of CD3+T, CD4+T, CD8+T, and γδT cells in total lymphocytes in the two groups (x ¯ ± s , %) was 71.83 ± 5.37 , 13.39 ± 2.23 , 62.93 ± 5.81 , and 3.67 ± 0.87 in the experimental group, respectively. In the control group, the values were expressed as 66.72 ± 5.48 , 42.77 ± 3.38 , 31.41 ± 3.62 , and 1.73 ± 0.36 , respectively. After performing the t -test, p values in the two groups were <0.005 except CD3+T, with statistically significant differences. Besides, CD4/CD8 was 0.33 ± 0.11 in the experimental group and 1.48 ± 0.29 in the control group, t = 26.528 , p < 0.001 , exhibiting a significant statistical difference. Conclusion. HIV infection induces the activation and proliferation of CD8+T and γδT cells, contributing to the decrease of CD4+T cells, while CD8+T and γδT cells are involved in the immune response and tissue damage after HIV infection. [ABSTRACT FROM AUTHOR]