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This article presents the findings of a study on paroxysmal nocturnal haemoglobinuria (PNH), a rare blood disorder. The study used single-cell sequencing to analyze bone marrow cells from PNH patients and healthy controls. The researchers discovered alterations in the differentiation of bone marrow haematopoietic cells in PNH patients, which may contribute to the development of the disorder. The article includes clinical data on four PNH patients and discusses the mechanisms involved in PNH. The study highlights the differences in bone marrow cells between PNH patients and healthy individuals, providing insights into the impact of PNH on the distribution and function of hematopoietic cells in the bone marrow. [Extracted from the article]

Municipal solid waste incineration (MSWI) fly ash is classified as hazardous waste due to high leachable heavy metals, and incineration leachate belongs to organic wastewater with high biodegradability. Electrodialysis (ED) has shown potential for the removal of heavy metals from fly ash, and bioelectrochemical system (BES) employs biological and electrochemical reactions to generate electricity and remove contaminants from a wide range of substrates. In this study, the ED-BES coupled system was constructed for the co-treatment of fly ash and incineration leachate, where the ED was driven by BES. The treatment effect of fly ash by varying additional voltage, initial pH and liquid-to-solid (L/S) ratio was evaluated. Results showed that the highest removal rates of Pb, Mn, Cu and Cd were 25.43%, 20.13%, 32.14% and 18.87% after 14 days treatment of the coupled system, respectively. These values were obtained under 300 mV of additional voltage, L/S 20 and initial pH3. After the treatment of the coupled system, the fly ash leaching toxicity was lower than the threshold of GB5085.3-2007. The highest energy saving for removed Pb, Mn, Cu and Cd were 6.72, 15.61, 8.99 and 17.46 kWh/kg, respectively. The ED-BES can be considered a cleanliness approach to treating fly ash and incineration leachate simultaneously. [ABSTRACT FROM AUTHOR]

Despite new efficacy drugs and cell therapy have been used for multiple myeloma (MM) patients, some patients will relapse over time. We wonder the immune system play a vital role as well as MM cell during the development of disease. It is clear that the characteristic of myeloma cell is associated with the survival of MM patients. However, the link between the immune profiling and the prognosis of the disease is still not entirely clear. As more study focus on the role of immunity on multiple myeloma pathogenesis. There are plenty of study about the predictive role of immunity on the survival of multiple myeloma patients. Up to mow, the majority reviews published have focused on the immunotherapy and immune pathogenesis. It is indispensable to overlook the predictive role of immunity on multiple myeloma patients. Here, we give a review of vital previous works and recent progress related to the predictive role of immune profiling on multiple myeloma, such as absolute lymphocyte count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, lymphocytes and cytokines.

The mechanism underlying autophagy in paroxysmal nocturnal hemoglobinuria (PNH) remains largely unknown. We previously sequenced the entire genome exon of the CD59– cells from 13 patients with PNH and found genes such as CUX1 encoding Cut-like homeobox 1. Peripheral blood samples from 9 patients with PNH and 7 healthy control subjects were obtained to measure CUX1 expression. The correlation between CUX1 messenger RNA expression and PNH clinical indicators was analyzed. To simulate CUX1 expression in patients with PNH, we generated a panel of PNH cell lines by knocking out PIGA in K562 cell lines and transfected lentivirus with CUX1. CCK-8 and EDU assay assessed cell proliferation. Western blotting was used to detect Beclin-1, LC3A, LC3B, ULK1, PI3K, AKT, p-AKT, mTOR, and p-mTOR protein levels. Autophagosomes were observed with transmission electron microscopy. Chloroquine was used to observe CUX1 expression in PNH after autophagy inhibition. Leukocytes from patients with PNH had lower levels of CUX1 messenger RNA expression and protein content than healthy control subjects. The lactose dehydrogenase level and the percentage of PNH clones were negatively correlated with CUX1 relative expression. We reduced CUX1 expression in a PIGA knockout K562 cell line, leading to increased cell proliferation. Levels of autophagy markers Beclin-1, LC3B, LC3A, and ULK1 increased, and autophagosomes increased. Furthermore, PI3K/AKT/mTOR protein phosphorylation levels were lower. CUX1 expression did not change and cell proliferation decreased in CUX1 knocked down PNH cells after inhibition of autophagy by chloroquine. In brief, CUX1 loss-of-function mutation resulted in stronger autophagy in PNH. [ABSTRACT FROM AUTHOR]