Fluorescent Visualization of Chemical Profiles across the Air-Water Interface.

Chemical transfer across the air-water interface is one of the most important geochemical processes of global significance. Quantifying such a process has remained extremely challenging due to the lack of suitable technologies to measure chemical diffusion across the air-water microlayer. Herein, we present a fluorescence optical system capable of visualizing the formation of the air-water microlayer with a spatial resolution of 10 µm and quantifying air-water diffusion fluxes using pyrene as a target chemical. We show for the first time that the air-water microlayer is composed of the surface microlayer in water (∼290 ± 40 µm) and a diffusion layer in air (∼350 ± 40 µm) with 1 µg L-1 of pyrene. The diffusion flux of pyrene across the air-water interface is derived from its high-resolution concentration profile without any pre-emptive assumption, which is 2 orders of magnitude lower than those from the conventional method. This system can be expanded to visualize diffusion dynamics of other fluorescent chemicals across the air-water interface and provides a powerful tool for furthering our understanding of air-water mass transfer of organic chemicals related to their global cycling.

Improving axial resolution for holographic tracking of colloids and bacteria over a wide depth of field by optimizing different factors.

Improving the axial resolution for multiparticle three-dimensional (3D) holographic tracking is crucial but challenging. Here we study the impacts of incident light power, uniformity of the illumination as well as image pixel size on the axial tracking resolution for digital holographic microscopy (DHM). We demonstrate that the resolution highly depends on the image pixel size and the uniformity of the illumination. A 3D localization algorithm based on local-intensity-maxima searching and a Gaussian fit to the integrated intensity of the reconstructed lateral images along the axial direction proves a robust strategy to enhance the axial resolution for colloids and bacteria within a wide depth of field over several tens of micrometers.

Research Progress and New Perspectives of Anticancer Effects of Emodin.

Emodin is a natural compound found in several traditional Chinese medicines, including Rheum palmatum and Polygonum cuspidatum. Recent studies have shown that emodin exhibits potent anticancer effects against a variety of cancer types, including liver, breast, lung, and colon cancer. Emodin's anticancer effects are mediated through several mechanisms, including inhibition of cell proliferation, induction of apoptosis, and suppression of tumor angiogenesis and metastasis. In this review, we provide an overview of recent research progress and new perspectives on emodin's anticancer effect. We summarize the current understanding of the molecular mechanisms underlying emodin's anticancer activity, including its effects on signaling pathways such as the PI3K/Akt, MAPK, and NF-[Formula: see text]B pathways. We also discuss the potential of emodin as a therapeutic agent for cancer treatment, including its use in combination with conventional chemotherapeutic drugs and as a sensitizer for radiotherapy. Furthermore, we highlight recent advances in the development of emodin derivatives and their potential as novel anticancer agents. Finally, we discuss the challenges and opportunities for the translation of emodin's anticancer properties into clinical applications, including the need for further preclinical and clinical studies to evaluate its safety and efficacy. In conclusion, emodin represents a promising natural compound with potent anticancer properties, and its potential as a therapeutic agent for cancer treatment warrants further investigation. This review provides a comprehensive overview of the current research progress and new perspectives on emodin's anticancer effects, which may facilitate the development of novel therapeutic strategies for cancer treatment.

Doxorubicin induced cardio toxicity through sirtuins mediated mitochondrial disruption.

The chemotherapeutic drug Doxorubicin is the most commonly prescribed in the world. However, its clinical wide application is limited due to harmful side effects like cardiotoxicity. The cardiotoxic mechanism of DOX is not fully clear, however, it is considered as a potential etiological factor to the generation of ROS and Iron complexes, impairment, Ca2⁺homeostasis, mitochondrial dysfunction, and cell membrane damage. Moreover, it is generally believed that mitochondrial dysfunction plays a central role in the cardiotoxic effect of DOX. Additionally, SIRTs are considered to play an important role, which is activated by small energy molecules to generate energy by stimulation of transcription factors and enzymatic regulation of cardiac energy metabolism. In the heart tissue, SIRT1 and SIRT3 are present in large amounts. This review paper focuses on "DOX mediated cardiomyopathy & cardiomyocytes death" and "The modulation of mitochondrial processes by SIRT1, SIRT3, and DOX". This paper expounds from the following aspects, respectively. 1. A target to mitochondria; (1) ROS overproduction under mitochondrial dysfunction; (2) Lipid peroxidation by oxidative stress after ROS overproduction; (3) Disturbance of calcium homeostasis and mitochondrial permeability transition; 2. SIRTs participate in the process of cardiotoxicity; (1) SIRT1 and toxic myocardial injury; ①Over-expression of SIRT1 in toxic myocardial injury; ②SIRT1 mediated DOX-induced cardiotoxicity; (2) SIRT3 and mitochondrial damage; ①A central role of SIRT3 in cardiac metabolism; ② Role of SIRT3 in DOX-induced cardiotoxicity; This review is based on SIRTs mediated role in the regulation of mitochondrial function, and evaluates their role on DOX induced cardiotoxicity.