Tanreqing Injection Regulates Cell Function of Hypoxia-Induced Human Pulmonary Artery Smooth Muscle Cells (HPASMCs) through TRPC1/CX3CL1 Signaling Pathway.

Hypoxia-induced pulmonary arterial hypertension (HPAH) is due to hypoxia caused by vascular endothelial cell remolding and damage. Previous studies have suggested that CX3CL1 plays an important role in HPAH which is affected by oxidative stress. Ca channel activation correlated with increasing NF-B levels induced by ROS.

Non-Tuberculous Mycobacteria Pulmonary Infection Could Be Easily Misdiagnosed Leading to Serious Consequences.

Background: Non-tuberculous mycobacteria (NTM) infection is on the rise worldwide. Chronic pulmonary infection can be difficult to diagnose, and thus easily misdiagnosed and mistreated in clinical practice, leading to serious complications. Case presentation, methods and results: A patient with NTM pulmonary infection, who had undergone a lengthy treatment course in two different hospitals, resulting in drug related multi-organ damage, was presented.

[Effects of different patterns of hypoxia on renin angiotension system in serum and tissues of rats].

Objective: To Investigate the influences of chronic intermittent hypoxia (CIH) and continuous hypoxia (CH) on renin angiotensin system (RAS) in serum and tissues of rats, and therefore to investigate the mechanism of CIH-induced hypertension and hypoxia induced pulmonary hypertension.

Methods: Eighteen male Sprague-Dawley (SD) rats were divided into 3 groups: CIH group, CH group and control group (UC). CIH rats were subjected to alternating cycles of hypoxia (6% ∼ 8% O(2) in N(2) for 20 ∼ 25 s) and normoxia (21% O(2) in N(2) for 2 min) every 180 s for 7 h/d.

[Mechanisms of sympathetic activity in rats exposed to different patterns of hypoxia and the correlation with blood pressure].

Objective: To observe the effects of two different hypoxia patterns on blood pressure and the underlying mechanisms.

Methods: Eighteen male SD rats were randomly divided into three groups: the intermittent hypoxia group (IH group), the continuous hypoxia group (CH group) and the normal control group (NC group). The rats of the IH and CH group were subjected to intermittent hypoxia (7 h/d) and continuous hypoxia (7 h/d) for 42 days respectively.

[A study of the related pathways of oxidative stress in chronic intermittent hypoxia rats and the effect of N-acetylcysteine].

Objective: To study the relation of oxidative stress with systolic blood pressure (SBP) and renin-agiotensin system (RAS) in a rat model of chronic intermittent hypoxia (CIH), and to investigate the preventive effect and mechanism of N-acetylcysteine (NAC) in CIH-induced hypertension.

Methods: Twenty-four male Sprague-Dawley (SD) rats were divided into 4 groups: CIH+NAC group (CIH1), CIH+normal saline (NS) group (CIH2), CIH control group (CIH3) and blank control group (UC). CIH rats were subjected to alternating cycles of hypoxia (6%-8% O2 in N2 for 20-25 s) and normoxia (21% O2 in N2 for 2 min) every 180 s for 7 h per day.