Single-Cell RNA Sequencing, Cell Communication, and Network Pharmacology Reveal the Potential Mechanism of Buch.-Ham in Hepatocellular Carcinoma Inhibition.

Background: Hepatocellular carcinoma (HCC), a prevalent form of primary liver malignancy, arises from liver-specific hepatocytes. Buch.-Ham(Climbing senecio) is a bitter-tasting plant of the Compositae family with anti-tumor properties.

Pgam5-mediated PHB2 dephosphorylation contributes to endotoxemia-induced myocardial dysfunction by inhibiting mitophagy and the mitochondrial unfolded protein response.

Numerous mitochondrial abnormalities are reported to result from excessive inflammation during endotoxemia. Prohibitin 2 (PHB2) and phosphoglycerate mutase 5 (Pgam5) have been associated with altered mitochondrial homeostasis in several cardiovascular diseases; however, their role in endotoxemia-related myocardial dysfunction has not been explored. Our experiments were aimed to evaluate the potential contribution of Pgam5 and PHB2 to endotoxemia-induced mitochondrial dysfunction in cardiomyocytes, with a focus on two endogenous protective programs that sustain mitochondrial integrity, namely mitophagy and the mitochondrial unfolded protein response (UPR).

Mitochondrial quality control in diabetic cardiomyopathy: from molecular mechanisms to therapeutic strategies.

In diabetic cardiomyopathy (DCM), a major diabetic complication, the myocardium is structurally and functionally altered without evidence of coronary artery disease, hypertension or valvular disease. Although numerous anti-diabetic drugs have been applied clinically, specific medicines to prevent DCM progression are unavailable, so the prognosis of DCM remains poor. Mitochondrial ATP production maintains the energetic requirements of cardiomyocytes, whereas mitochondrial dysfunction can induce or aggravate DCM by promoting oxidative stress, dysregulated calcium homeostasis, metabolic reprogramming, abnormal intracellular signaling and mitochondrial apoptosis in cardiomyocytes.

Empagliflozin activates Wnt/β-catenin to stimulate FUNDC1-dependent mitochondrial quality surveillance against type-3 cardiorenal syndrome.

Objectives: Cardiorenal syndrome type-3 (CRS-3) is an abrupt worsening of cardiac function secondary to acute kidney injury. Mitochondrial dysfunction is a key pathological mechanism of CRS-3, and empagliflozin can improve mitochondrial biology by promoting mitophagy. Here, we assessed the effects of empagliflozin on mitochondrial quality surveillance in a mouse model of CRS-3.

Effects of Extracorporeal Membrane Oxygenation Circuits on Sequestration of Antimicrobial Agents.

Our study was designed to determine the sequestration of teicoplanin, tigecycline, micafungin, meropenem, polymyxin B, caspofungin, cefoperazone sulbactam, and voriconazole in extracorporeal membrane oxygenation (ECMO) circuits. Simulated closed-loop ECMO circuits were prepared using 2 types of blood-primed ECMO. After the circulation was stabilized, the study drugs were injected into the circuit.

Circulating Tissue Factor-Positive Procoagulant Microparticles in Patients with Type 1 Diabetes.

Aim: To investigate the count of circulating tissue factor-positive (TF) procoagulant microparticles (MPs) in patients with type 1 diabetes mellitus (T1DM).

Methods: This case-control study included patients with T1DM and age and sex-matched healthy volunteers. The counts of phosphatidylserine-positive (PS) MPs and TFPSMPs and the subgroups derived from different cell types were measured in the peripheral blood sample of the two groups using multicolor flow cytometric assay.

[Digital subtract arteriographic (DSA) characteristics of lower extremities and ankle-brachial index in patients with diabetic feet].

Objective: To evaluate the Digital Subtract Arteriography (DSA) characteristics of lower limb arterial diseases in patients with diabetic feet and to explore the correlation between DSA and Ankle-brachial index (ABI).

Methods: Fifty-two patients with diabetic feet were recruited in this study. ABI and DSA of bilateral lower extremities were examined to assess the severity of vasculopathy.

Power-law strength-degree correlation from resource-allocation dynamics on weighted networks.

Many weighted scale-free networks are known to have a power-law correlation between strength and degree of nodes, which, however, has not been well explained. We investigate the dynamic behavior of resource-traffic flow on scale-free networks. The dynamical system will evolve into a kinetic equilibrium state, where the strength, defined by the amount of resource or traffic load, is correlated with the degree in a power-law form with tunable exponent.

General dynamics of topology and traffic on weighted technological networks.

For most technical networks, the interplay of dynamics, traffic, and topology is assumed crucial to their evolution. In this Letter, we propose a traffic-driven evolution model of weighted technological networks. By introducing a general strength-coupling mechanism under which the traffic and topology mutually interact, the model gives power-law distributions of degree, weight, and strength, as confirmed in many real networks.