Compact ring resonators of silicon nanorods for strong optomechanical interaction.

Optomechanical interaction in microstructures plays a more and more important role in the fields of quantum technology, information processing, and sensing, among others. It is still a challenge to obtain a strong optomechanical interaction in a compact device. Here, we propose and demonstrate that compact ring resonators consisting of silicon nanorods can realize strong optomechanical interaction even surpassing that of most optical microcavities.

Fibroblast growth factor 10 ameliorates renal ischaemia-reperfusion injury by attenuating mitochondrial damage.

Ischaemia-reperfusion (I/R) injury is one of the leading causes of acute kidney injury (AKI). Its pathologic mechanism is quite complex, involving oxidative stress, inflammatory response, autophagy, and apoptosis. Fibroblast growth factor 10 (FGF10) and 5-hydroxydecanoate (5-HD) play essential roles in kidney injury.

Strong optomechanical coupling in chain-like waveguides of silicon nanoparticles with quasi-bound states in the continuum.

We propose and demonstrate that strong optomechanical coupling can be achieved in a chain-like waveguide consisting of silicon nanorods. By employing quasi-bound states in the continuum and mechanical resonances at a frequency around 10 GHz, the optomechanical coupling rate can be above 2 MHz and surpass most microcavities. We have also studied cases with different optical wave numbers and size parameters of silicon, and a robust coupling rate has been verified, benefiting the experimental measurements and practical applications.

Protective effect of apigenin magnesium complex on HO-induced oxidative stress and inflammatory responses in rat hepatic stellate cells.

Apigenin displays antioxidant and anti-inflammatory effects. However, effects of apigenin magnesium (AM) complex on these aspects remain unknown. This study investigated the effects of AM complex on oxidative stress and inflammatory responses in hydrogen peroxide (HO)-induced rat hepatic stellate cells (HSCs).

-diacetylcystine ameliorates inflammation in experimental non-alcoholic steatohepatitis by regulating nuclear transcription factor kappa B activation.

Non-alcoholic fatty liver disease (NAFLD) is one of the most common diseases worldwide that has been continuously increasing recently. NAFLD embraces a spectrum of liver histological alterations, ranging from simple steatosis (NAFL) to severe non-alcoholic steatohepatitis (NASH), that is characterized by fat accumulation, lobular inflammation, and ballooning degeneration in the hepatocytes in the absence of alcohol abuse. The innate immune system has an important role in NASH pathogenesis.

N-acetylcysteine protects against liver injure induced by carbon tetrachloride via activation of the Nrf2/HO-1 pathway.

Chronic liver injury is an important clinical problem which eventually leads to cirrhosis, hepatocellular carcinoma and end-stage liver failure. It is well known that cell damage induced by reactive oxygen species (ROS) is an important mechanism of hepatocyte injure. N-acetylcysteine (NAC), a precursor of glutathione (GSH), is well-known role as the antidote to acetaminophen toxicity in clinic.

[Effect of apigenin on protein expressions of PPARs in liver tissues of rats with nonalcoholic steatohepatitis].

Objective: To investigate the effect of apigenin on the protein expression levels of peroxisome proliferator-activated receptors (PPARs) in liver tissues of rats with nonalcoholic steatohepatitis (NASH).

Methods: The NASH rat model was established by feeding of a high-fat diet. Unmodeled rats served as the normal controls.

Protective effects of -acetylcysteine on cisplatin-induced oxidative stress and DNA damage in HepG2 cells.

Hepatocyte injury is a common pathological effect of cisplatin (CDDP) in various solid tumor therapies. Thus, strategies for minimizing CDDP toxicity are of great clinical interest. -acetylcysteine (NAC), a known antioxidant, is often used as an antidote for acetaminophen overdose in the clinic due to its ability to increase the levels of glutathione (GSH).

[The protective effect of N-acetylcysteine magnesium against liver cirrhosis with portal hypertension in rat].

Objective: To study the effects of acetylcysteine magnesium on the vasoactive substances and hepatic fibrosis indexes in liver cirrhosis and portal hypertension of rats.

Methods: The rat liver cirrhosis model was made with 12 microg/kg dimethylnitrosamines. Then acetylcysteine magnesium was injected respectively with 25, 50, and 100 mg x kg(-1) dose daily into abdominal cavity.