I. DETERMINING MASTER CURVES FOR THE INERTIAL AND VISCOUS REGIMEFig. S 1: Time history of drop shapes as a function of film viscosity (µo), indicated to the left. At the point of detachment from the needle the drop shape is independent of the film viscosity.An inertial (τ ρ ) and a viscous (τ µ ) time scale are found to describe the drop deformation after contact with the oil film ( Fig. 5), where Fig. S1 shows the time history of the drop shapes. A similar scaling law is also expected for the apparent radius (r). By scaling r with the initial drop size (R) and time (t) with τ ρ or τ µ two distinct spreading regimes appear (Fig. S2). The inertial scaling ( Fig. S2a) shows that the data for Oh < 0.2 follows nearly the same curve, where as Oh > 0.2 the data remains scattered. If r is instead scaled with τ µ the data for Oh < 0.2 is reduced to nearly a single curve (Fig. S2b). The data in the transitional regime (0.2 < Oh < 2) follows neither of the two scaling laws.A log-log plot of the non-dimensional apparent radius (r/R) in Figs. S2a,b shows that it follows a power-law like behavior (Figs. S3, S4). We fit a master curve through each data set to determine the range of the exponents and the pre-factors for the two regimes. Since the experimental data show that these two regimes are bounded within a certain time span we only use the data in these regions for the fitting, which is illustrated by dashed square in Figs. S3a, S4a. Each data set inside the dashed area is fitted onto a curve of the form r/R = a(t/τ ρ ) b or r/R = a(t/τ µ ) b , where a and b are constants determined by the best fit. For clarity, the data in the transitional regime (0.2 < Oh < 2) has been omitted below.The inertial regime is defined before drop detachment from the needle (t/τ ρ < 2). Each data set is fitted by a single curve (Fig. S3), which is represented by the dashed line. We find the the inertial regime to be represented by a curve r/R ≈ 1.1( t τρ ) 0.45 , where the pre-factor varies between 1.09 -1.13 and the exponent is ≈ 0.45.
Bone marrow (BM)-resident hematopoietic stem and progenitor cells (HSPCs) are often activated by bacterial insults to replenish the host hemato-immune system, but how they integrate the associated tissue damage signals to initiate distal tissue repair is largely unknown. Here, we showed that acute gut inflammation expands HSPCs in the BM through GM-CSFR activation, and directs them to inflamed mesenteric lymph nodes for further differentiation into myeloid cells specialized in gut tissue repair. We also identified that this process is exclusively mediated by Bacteroides, a commensal gram-negative bacteria, that activates innate immune signaling. In contrast, chronic gut inflammation reduces HSC potential for hematopoietic reconstitution and immune response against infection. Similarly, microbial signals contribute to aging-associated HSPC expansion. These findings establish a cross-organ communication that promotes tissue regeneration, but if sustained, impairs tissue homeostasis that may be relevant to aging and chronic disorders.
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