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0% (129/358), respectively. Also, 134 (37.3%) patients received nutritional support; the ratio of parenteral nutrition (PN) to enteral nutrition (EN) was 1.351. Further, 106 (58.9%) patients with nutritional risk received nutritional support. The number of chronic diseases and age were protective factors, and activities of daily living (ADL) were risk factors.

The overall frequencies of nutritional risk and malnutrition of oldest-old hospitalized patients were high, and the rates of EN and PN were low. Nutritional risk was associated with the number of chronic diseases, age, and ADL.

The overall frequencies of nutritional risk and malnutrition of oldest-old hospitalized patients were high, and the rates of EN and PN were low. Nutritional risk was associated with the number of chronic diseases, age, and ADL.Triple-negative breast cancer (TNBC) is an aggressive cancer, and rapidly progresses following relapse in advanced stage. This cancer is usually associated with worse overall survival, so the carcinogenesis of TNBC needs to be further explored to find more effective therapies. In this study, we intended to identify the roles of YY1-mediated long non-coding RNA Kcnq1ot1 in TNBC. First, the paired samples of tumor tissues and adjacent tissues were collected to determine YY1, lncRNA Kcnq1ot1, and PTEN expression using RT-qPCR and Western blot analysis followed by analysis of the relationship between them and patient survival. The results revealed that YY1 and lncRNA Kcnq1ot1 were upregulated in TNBC tissues, and high expression of YY1 and lncRNA Kcnq1ot1 was associated with poor patient survival. LOXO-195 Then, ChIP and MSP assays were employed to explore interactions between YY1, lncRNA Kcnq1ot1, and PTEN gene. We obtained that YY1 upregulated lncRNA Kcnq1ot1, which mediated PTEN methylation via DNMT1, thus decreasing PTEN expression. Afterward, TNBC cells were examined for their viability using functional assays with the results displaying that overexpression of YY1 facilitated TNBC cell proliferation, invasion, and migration. Mechanistically, upregulated YY1 repressed tumor growth by inhibiting PTEN via upregulation of lncRNA Kcnq1ot1. Mouse models were also constructed, and the above effects of YY1, lncRNA Kcnq1ot1, and PTEN on TNBC were also established in vivo. Taken together, this study demonstrates that the silencing of YY1 exerted tumor-suppressive effects on TNBC by modulating lncRNA Kcnq1ot1/DNMT1/PTEN pathway, in support of further investigation into anti-tumor therapy for TNBC.Understanding how species have responded to past climate change may help refine projections of how species and biotic communities will respond to future change. Here, we integrate estimates of genome-wide genetic variation with demographic and niche modeling to investigate the historical biogeography of an important ecological engineer the dusky-footed woodrat, Neotoma fuscipes. We use RADseq to generate a genome-wide dataset for 71 individuals from across the geographic distribution of the species in California. We estimate population structure using several model-based methods and infer the demographic history of regional populations using a site frequency spectrum-based approach. Additionally, we use ecological niche modeling to infer current and past (Last Glacial Maximum) environmental suitability across the species' distribution. Finally, we estimate the directionality and possible spatial origins of regional population expansions. Our analyses indicate this species is subdivided into three regionally distinct populations, with the deepest divergence occurring ~1.7 million years ago across the modern-day San Francisco-Bay Delta region; a common biogeographic barrier for the flora and fauna of California. Our models of environmental suitability through time coincide with our estimates of population expansion, with relative long-term stability in the southern portion of the range, and more recent expansion into the northern end of the range. Our study illustrates how the integration of genome-wide data with spatial and demographic modeling can reveal the timing and spatial extent of historic events that determine patterns of biotic diversity and may help predict biotic response to future change.Haematopoietic stem cell transplantation (HSCT) is a curative option for severe aplastic anemia (SAA). Finding a suitable matched donor in a timely manner is a challenge. The availability of haploidentical donors and their successful use in transplantation have expanded valid choices for SAA. In recent decades, haploidentical HSCT (haplo-HSCT) for the treatment of SAA has been continuously attempted, and great strides have been made. Nowadays, haplo-HSCT using different regimens has overcome the difficulty of graft failure and severe graft-versus-host disease (GvHD), and achieved inspiring survival outcomes in SAA. The regimens consist mainly of granulocyte colony-stimulating factor (G-CSF) plus antithymocyte globulin (ATG), posttransplantation cyclophosphamide (PT-Cy), and ex vivo graft T-cell depletion (TCD). In particular, the G-CSF and ATG-based regimen includes the largest sample size and the successful wide use of the G-CSF and ATG-based regimen has promoted haplo-HSCT a higher priority in SAA patients without matched related or unrelated donors in China. Recent studies have also indicated that haplo-HSCT using PT-Cy or TCD regimen is a practicable alternative, but the sample size is relatively small. Here, we offer an overview of clinical results obtained through the use of haploidentical transplantation in SAA, mainly focusing on current advances and future challenges.We retrospectively compared outcomes of a large series of adult patients with APL in CR2 receiving alloHSCT (n = 228) or autoHSCT (n = 341) reported to the European Society for Blood and Marrow Transplantation from January 2004 to December 2018. The 2-year cumulative incidence of non-relapse mortality was significantly higher for alloHSCT 17.3% (95% CI 12.5-22.8) compared with autoHSCT 2.7% (95% CI 1.2-5) (p = 0.001), while differences in relapse rate were not significant (28% versus 22.9%; p = 0.28). Leukemia-free survival (LFS) and overall survival (OS) favored autoHSCT with 74.5% (95% CI 69-79.2) and 82.4% (95% CI 77.3-86.5) compared with alloHSCT with 54.7% (95% CI 47.5-61.3) (p = 0.001) and 64.3% (95% CI 57.2-70.6), respectively (p = 0.001 and p = 0.001). Multivariable analysis showed significantly worse LFS after alloHSCT (HR 0.49; 95% CI 0.37-0.67; p  less then  0.0001), older age (p = 0.001), and shorter time from diagnosis to transplant (p = 0.00015). Similar results were obtained for OS. The study shows that autoHSCT resulted in better survival outcomes (LFS and OS) for APL in CR2.