Upregulating vascular endothelial K2.3 channels alleviates pulmonary hypertension in mice.

Endothelial dysfunction of pulmonary arteries is important in the initiation of pulmonary hypertension (PH). Pulmonary vascular tone is regulated by endothelium-dependent hyperpolarization (EDH) that induces vasodilation. Although K2.

Glutaminolysis and α-ketoglutarate-stimulated K3.1 expression contribute to β-adrenoceptor activation-induced myocardial fibrosis in mice.

Heart failure is associated with myocardial fibrosis, a pivotal histopathological feature arising from β-adrenergic receptor (β-AR) stimulation through sympathetic nervous system activation. Augmented glutaminolysis with increased bioavailability of α-ketoglutarate (α-KG) is suggested to contribute to fibrogenesis and changes in cellular gene expression. K3.

Hippo pathway activation mediates cardiomyocyte ferroptosis to promote dilated cardiomyopathy through downregulating NFS1.

Cardiomyocyte loss by regulated death modes, like apoptosis and ferroptosis, has been implicated in the development of dilated cardiomyopathy (DCM). It remains unclear whether cardiomyocyte ferroptosis occurs as a consequence of Hippo pathway activation. Using a mouse model of DCM by overexpression of Mst1 transgene (Mst1-TG) leading to Hippo pathway activation, we showed that cardiomyocyte ferroptosis was evident by transcriptomic profiles, elevated mitochondrial Fe content, increased levels of lipid peroxidation and obvious mitochondrial damage.

Green one-step synthesis of N-doped carbon quantum dots for fluorescent detection of lemon yellow in soft drinks.

A new fluorescent sensor for the determination of lemon yellow was developed based on nitrogen-doped carbon quantum dots (N-CQDs), which were prepared via a hydrothermal method with dried pomelo peel and L-tyrosine. The N-CQDs exhibited the blue fluorescence with a quantum yield of 28 %. The sensing principle of N-CQDs was quenched by lemon yellow via static quenching.

[L-arginine decreases P-selectin expression in traumatic shock].

Objective: To investigate the changes of P-selectin distribution in the vital organs and plasma during traumatic shock and explore the significance of these changes.

Methods: Twenty-four normal SD rats were randomly assigned into 3 groups (n=8), namely traumatic shock group, L-arginine (L-Arg) treatment and control group. The rats in the former 2 groups were subjected to traumatic shock with L-Arg treatment group given 100 mg/kg L-Arg during resuscitation while the other receiving no medication.

[Therapeutic effect of L-arginine on traumatic shock in rats].

Objective: To evaluate the therapeutic effect of L-arginine (L-Arg) on traumatic shock in rats and explore the possible mechanisms.

Methods: Rat models of traumatic shock were established in Sprague-Daulay rats, which were randomly divided into two groups either to receive L-Arg treatment or not. The plasma concentration of endothelin (ET) and oxygen partial pressure in the tissues from the skeletal muscles, liver and small intestine were measured before and after the shock and 1, 3, and 5 h after resuscitation.

Dynamic changes in serum level of nitric oxide and its mechanisms in rats with traumatic shock.

Objective: To investigate the dynamic changes of serum nitric oxide (NO) level and its mechanisms in rats in traumatic shock.

Methods: Rat models of traumatic shock were established by fracturing the posterior limb of the rats. Serum levels of nitrate/nitrite were measured with the method described by Griess.