The Fastest Capillary Flow in Root-like Networks under Gravity.

Capillary flow has garnered significant attention due to its unique dynamic characteristics that require no external force. Creating a quantitative analytical model to evaluate capillary flow behaviors in root-like networks is essential for enhancing fluid control properties in functional textiles. In this study, we explore the capillary dynamics within root-like networks under the influence of gravity and derive the most rapid capillary flow via structural optimization. The flow time in a capillary is dominated by the capillary pressure, viscous pressure loss, and gravity, each of which exhibits diverse sensitivities to the structures of root-like networks. We scrutinize various structural parameters to understand their impact on capillary flow in root-like networks. Subsequently, optimal structural parameters (namely, the mother tube diameter and diameter ratio) are identified to minimize capillary flow time. Moreover, we discovered that the correlation between flow time and distance for capillary flow in root-like networks does not obey the classical Lucas-Washburn equation. These results affirm that root-like networks can enhance capillary flow, providing critical insights for numerous capillary-flow-dependent engineering applications.

Two distinct and competitive pathways confer the cellcidal actions of artemisinins.

The biological actions of artemisinin (ART), an antimalarial drug derived from Artemisia annua, remain poorly understood and controversial. Besides potent antimalarial activity, some of artemisinin derivatives (together with artemisinin, hereafter referred to as ARTs), in particular dihydroartemisinin (DHA), are also associated with anticancer and other antiparasitic activities. In this study, we used baker's yeast Saccharomyces cerevisiae as cellular and genetic model to investigate the molecular and cellular properties of ARTs. Two clearly separable pathways exist. While all ARTs exhibit potent anti-mitochondrial actions as shown before, DHA exerts an additional strong heme-dependent, likely mitochondria-independent inhibitory action. More importantly, heme antagonizes the mitochondria-dependent cellcidal action. Indeed, when heme synthesis was inhibited, the mitochondria-dependent cellcidal action of ARTs could be dramatically strengthened, and significant yeast growth inhibition at as low as 100 nM ART, an increase of about 25 folds in sensitivity, was observed. We conclude that ARTs are endowed with two major and distinct types of properties: a potent and specific mitochondria-dependent reaction and a more general and less specific heme-mediated reaction. The competitive nature of these two actions could be explained by their shared source of the consumable ARTs, so that inhibition of the heme-mediated degradation pathway would enable more ARTs to be available for the mitochondrial action. These properties of ARTs can be used to interpret the divergent antimalarial and anticancer actions of ARTs.

[Effects of various compounds on efficacy of artemisinin in a yeast model].

Artemisinin is a key anti-malarial drug and few clinically meaningful resistant cases about its application have so far been reported. The World Health Organization (WHO) officially recommended the use of ACT (Artemisinin-based Combination Therapy) as the first line antimalarial application to increase its inhibitory efficacy and prevent the likely resistance development. Based on our current understanding of artemisinin, a set of compounds were selected to study their interaction with artemisinin by using the yeast (S. cerevisiae) model, in the hope that knowledge gained might provide some references for clinical investigations. In this research, yeast strain (BY4742) was cultured in the nonfermentable YPGE solid medium with 4 µmol · L(-1) artemisinin and one of the selected compounds for 48 hours, and the combined drug efficiency was evaluated by the inhibition of yeast growth. The compounds belong to the categories of oxygenants, antioxidants, metal ions, ion chelators and uncouplers. Among them, 0.2 mmol L(-1) FeCl3, 60 µmol · L(-1) BPS, 1 mmol · L(-1) CuCl2, 0.75 mmol · L(-1) VE and 1 mmol · L(-1) VC antagonized the action of artemisinin, while 40 µmol · L(-1) DNP, 0.1 µmol · L(-1) CCCP and 0.25 mmol · L(-1) H2O2 had synergistic effects. These results suggested that redox-active and mitochondria-dysfunctional compounds could affect artemisinin's potency, supporting our prior proposed mitochondrial model for artemisinin's action. This research in addition provided a convenient method to screen likely artemisinin-interacting compounds.