Finally, the high-throughput sequencing of gut microbiota (16S) showed that the MSC+EPC treatment can inhibit the Enterococcus population ( less then 0.5%) and stabilize the Akkermansia population (~15%), with the Akkermansia population showing significant positive correlations with p38 MAPK/phos-p38, HSP27/phos-HSP27, IL-17A, and occludin. Taken together, our results show that MSC+EPC combined therapy is beneficial for the repair of injured intestine and drives gut microbial community stability by regulating the intestinal microenvironment. Adaptive or memory natural killer (NK) cells with epigenetic imprints similar to memory T cells have been shown to develop in response to cytomegalovirus (CMV) infection with upregulation of activating receptor NKG2C. These cells have been shown to possess strong anti-tumour efficacy both in-vitro as well as in-vivo. To determine if reconstitution of adaptive NK cells (CD56 NKG2C NKG2A ) in patients with advanced leukemia undergoing haploidentical HCT had any impact on disease progression (DP). The study cohort comprised of 60 patients with advanced acute leukemia, aged 2-65 years, receiving myeloablative PTCy based haploidentical transplantation from CMV seropositive donors, followed by CTLA4Ig-primed donor lymphocyte infusions (DLI). They were evaluated for the kinetics of reconstitution of adaptive NK cells, both phenotypic and functional, at days +30,+60, +90 and at regular intervals, to 3 years of follow-up, in relation to DP. Reconstitution of adaptive NK cells was compared with a retrospectiveitution of adaptive NK cells in those receiving CTLA4Ig-DLI (p < 0.0001). Our study suggests that myeloablative transplantation from CMV seropositive haploidentical donors augmented with CTLA4Ig-primed DLI might favor early and sustained expansion of functionally competent adaptive NK cells irrespective of CMV reactivation, with a favorable outcome.Our study suggests that myeloablative transplantation from CMV seropositive haploidentical donors augmented with CTLA4Ig-primed DLI might favor early and sustained expansion of functionally competent adaptive NK cells irrespective of CMV reactivation, with a favorable outcome.The impact of the coronavirus disease 2019 (COVID-19) pandemic on hematopoietic cell transplant (HCT) donor registries and transplant center (TC) practices is underreported. This article reports on the National Marrow Donor Program (NMDP) Be The Match Registry and its coordinating the provision of unrelated donor (URD) products to domestic and international TCs during the initial 3 months of the COVID-19 pandemic (March through May 2020). Specifically, NMDP data are presented for disease indications for transplant, URD search volumes and availability, graft requests and processing, courier utilization and performance, and conversion rates from formal donor search and workup to graft collection and shipment. selleck products Data following the onset of COVID-19 are compared to the immediate 3 months prior to the COVID-19 pandemic (December 2019 through February 2020) and the same quarter 1 year prior to COVID-19 (March through May 2019). During the initial onset of COVID-19 and compared to 1 year prior, TCs requested and the NHCT recipients. A growing number of older patients with cancer require well-founded clinical decision-making. Frailty screening is suggested as a service to improve outcomes in vulnerable older patients with cancer. This prospective study examined the value of frailty screening to predict rapid functional decline, rapid progressive disease (PD) and shorter overall survival (OS) in older patients with gastrointestinal cancer receiving palliative chemotherapy. Patients aged ≥70years were screened for frailty in an oncologic department after clinical decision but before starting palliative chemotherapy. Screening was repeated at first response evaluation after approximately two months of chemotherapy. Frailty screening tools included performance status (PS), Charlson Comorbidity Index, G-8 using two different cut-offs (G8 ,G8 ), VES-13, Timed-Up-and-Go, Handgrip strength and falls. A total of 170 patients were included, median age was 75.5 (70-88) years and 65.9% were male. The frequency of frailty varied from 14% to 74% according to the chosen frailty tool. In multivariate analysis G8 predicted OS (HR 1.5; 95%CI 1.0-2.4), whereas G8 predicted PD (OR 2.4; 1.1-5.6) and OS (HR 2.1; 1.4-2.9). VES-13 predicted functional decline (OR 3.5; 1.0-11.6), PD (OR 3.5; 1.5-8.4) and OS (HR 1.7; 1.2-2.4). Timed-Up-and-Go predicted OS (HR 1.8; 1.1-2.7). Handgrip strength and falls predicted functional decline (OR 4.5; 1.1-19 and OR 6.1; 1.4-25.8, respectively). PS predicted PD (OR 6.2; 2.6-14.7) and OS (HR 2.2; 1.5-3.2). VES-13 was useful for predicting all three endpoints of interest. Frailty tools covering domains of functioning and nutrition are suggested for older patients with advanced gastrointestinal cancer.VES-13 was useful for predicting all three endpoints of interest. Frailty tools covering domains of functioning and nutrition are suggested for older patients with advanced gastrointestinal cancer.Innate immune cellular effectors are actively consumed during systemic inflammation, but the systemic traffic and the mechanisms that support their replenishment remain unknown. Here, we demonstrate that acute systemic inflammation induces the emergent activation of a previously unrecognized system of rapid migration of granulocyte-macrophage progenitors and committed macrophage-dendritic progenitors, but not other progenitors or stem cells, from bone marrow (BM) to regional lymphatic capillaries. The progenitor traffic to the systemic lymphatic circulation is mediated by Ccl19/Ccr7 and is NF-κB independent, Traf6/IκB-kinase/SNAP23 activation dependent, and is responsible for the secretion of pre-stored Ccl19 by a subpopulation of CD205+/CD172a+ conventional dendritic cells type 2 and upregulation of BM myeloid progenitor Ccr7 signaling. Mature myeloid Traf6 signaling is anti-inflammatory and necessary for lymph node myeloid cell development. This report unveils the existence and the mechanistic basis of a very early direct traffic of myeloid progenitors from BM to lymphatics during inflammation.