A one-stone-two-birds strategy for cellulose dissolution, regeneration, and functionalization as a photocatalytic composite membrane for wastewater purification.

Photocatalytic membranes integrate membrane separation and photocatalysis to deliver an efficient solution for water purification, while the top priority is to exploit simple, efficient, renewable, and low-cost photocatalytic membrane materials. We herein propose a facile one-stone-two-birds strategy to construct a multifunctional regenerated cellulose composite membrane decorated by Prussian blue analogue (ZnPBA) microspheres for wastewater purification. The hypotheses are that: 1) ZnCl2 not only serves as a cellulose solvent for tuning cellulose dissolution and regeneration, but also functions as a precursor for in-situ growth of spherical-like ZnPBA; 2) More homogeneous reactions including coordination and hydrogen bonding among Zn2+, [Fe(CN)6]3- and cellulose chains contribute to a rapid and uniform anchoring of ZnPBA microspheres on the regenerated cellulose fibrils (RCFs). Consequently, the resultant ZnPBA/RCM features a high loading of ZnPBA (65.3 wt%) and exhibits excellent treatment efficiency and reusability in terms of photocatalytic degradation of tetracycline (TC) (90.3 % removal efficiency and 54.3 % of mineralization), oil-water separation efficiency (>97.8 % for varying oils) and antibacterial performance (99.4 % for E. coli and 99.2 % for S. aureus). This work paves a simple and useful way for exploiting cellulose-based functional materials for efficient wastewater purification.

Chronic circadian rhythm disorder induces heart failure with preserved ejection fraction-like phenotype through the Clock-sGC-cGMP-PKG1 signaling pathway.

Emerging evidence has documented that circadian rhythm disorders could be related to cardiovascular diseases. However, there is limited knowledge on the direct adverse effects of circadian misalignment on the heart. This study aimed to investigate the effect of chronic circadian rhythm disorder on heart homeostasis in a mouse model of consistent jetlag. The jetlag model was induced in mice by a serial 8-h phase advance of the light cycle using a light-controlled isolation box every 4 days for up to 3 months. Herein, we demonstrated for the first time that chronic circadian rhythm disorder established in the mouse jetlag model could lead to HFpEF-like phenotype such as cardiac hypertrophy, cardiac fibrosis, and cardiac diastolic dysfunction, following the attenuation of the Clock-sGC-cGMP-PKG1 signaling. In addition, clock gene knock down in cardiomyocytes induced hypertrophy via decreased sGC-cGMP-PKG signaling pathway. Furthermore, treatment with an sGC-activator riociguat directly attenuated the adverse effects of jetlag model-induced cardiac hypertrophy, cardiac fibrosis, and cardiac diastolic dysfunction. Our data suggest that circadian rhythm disruption could induce HFpEF-like phenotype through downregulation of the clock-sGC-cGMP-PKG1 signaling pathway. sGC could be one of the molecular targets against circadian rhythm disorder-related heart disease.

Cardiac Lymphatic Insufficiency Leads to Diastolic Dysfunction Via Myocardial Morphologic Change.

Although cardiac lymphatic vessels have received increasing attention in recent years, there is still a knowledge gap between cardiac lymphatics and heart homeostasis in a normal heart. In the present study, we established a mouse model of cardiac lymphatic insufficiency ablating cardiac lymphatic collector vessels to reveal the crucial role of cardiac lymphatic vessels in maintaining cardiac homeostasis and the impact on cardiac function both in physiological and pathologic settings. Furthermore, therapeutic lymphangiogenesis improved the adverse effect on cardiac morphologic changes and functions. These findings suggest that the cardiac lymphatic system would be a novel therapeutic target for heart disease.

Therapeutic Lymphangiogenesis Is a Promising Strategy for Secondary Lymphedema.

Secondary lymphedema is caused by lymphatic insufficiency (lymphatic drainage failure) following lymph node dissection during the surgical treatment or radiation therapy of breast or pelvic cancer. The clinical problems associated with lymphedema are reduced quality of life in terms of appearance and function, as well as the development of skin ulcers, recurrent pain, and infection. Currently, countermeasures against lymphedema are mainly physical therapy such as lymphatic massage, elastic stockings, and skin care, and there is no effective and fundamental treatment with a highly recommended grade. Therefore, there is a need for the development of a fundamental novel treatment for intractable lymphedema. Therapeutic lymphangiogenesis, which has been attracting attention in recent years, is a treatment concept that reconstructs the fragmented lymphatic network to recover lymphatic vessel function and is revolutionary to be a fundamental cure. This review focuses on the translational research of therapeutic lymphangiogenesis for lymphedema and outlines the current status and prospects in the development of therapeutic applications.

Hydrogen Sulfide Attenuates Lymphedema Via the Induction of Lymphangiogenesis Through a PI3K/Akt-Dependent Mechanism.

Background Accumulating evidence suggests that hydrogen sulfide ( H2S ), an endogenously produced gaseous molecule, plays a critical role in the regulation of cardiovascular homeostasis. However, little is known about its role in lymphangiogenesis. Thus, the current study aimed to investigate the involvement of H2S in lymphatic vessel growth and lymphedema resolution using a murine model and assess the underlying mechanisms. Methods and Results A murine model of tail lymphedema was created both in wild-type mice and cystathionine γ-lyase-knockout mice, to evaluate lymphedema up to 28 days after lymphatic ablation. Cystathionine γ-lyase-knockout mice had greater tail diameters than wild-type mice, and this phenomenon was associated with the inhibition of reparative lymphangiogenesis at the site of lymphatic ablation. In contrast, the administration of an H2S donor, diallyl trisulfide, ameliorated lymphedema by inducing the formation of a considerable number of lymphatic vessels at the injured sites in the tails. In vitro experiments using human lymphatic endothelial cells revealed that diallyl trisulfide promoted their proliferation and differentiation into tube-like structures by enhancing Akt (protein kinase B) phosphorylation in a concentration-dependent manner. The blockade of Akt activation negated the diallyl trisulfide-induced prolymphangiogenic responses in lymphatic endothelial cells. Furthermore, the effects of diallyl trisulfide treatment on lymphangiogenesis in the tail lymphedema model were also negated by the inhibition of phosphoinositide 3'-kinase (P13K)/Akt signaling. Conclusions H2S promotes reparative lymphatic vessel growth and ameliorates secondary lymphedema, at least in part, through the activation of the Akt pathway in lymphatic endothelial cells. As such, H2S donors could be used as therapeutics against refractory secondary lymphedema.