Background: Angiotensin-converting enzyme 2 (ACE2), a primary component of the vasoprotective axis in the renin-angiotensin system (RAS), has recently been found to have regulatory actions in hypoxic pulmonary hypertension and monocrotaline-induced pulmonary hypertension. We explored the hypothesis that the level of ACE2 protein contents may be decreased in patients with pulmonary arterial hypertension (PAH) due to congenital heart disease (CHD). Objective: We observed the serum ACE2 protein contents in patients with PAH due to CHD (CHD-PAH), and investigated their correlation with mean pulmonary arterial pressure (mPAP). Methods: One hundred and four patients with CHD and 33 normal control patients (group A) were involved in the research. The patients with CHD were divided into 55 cases of nonpulmonary hypertension (group B), 25 cases of mild to moderate pulmonary hypertension (group C) and 24 cases of severe pulmonary hypertension (group D). The serum level of ACE2 protein contents were detected by enzyme-linked immunosorbent assay (ELISA), and the relationship between these contents and mPAP were analyzed. Results: ACE2 protein contents significantly declined as mPAP increased. The mPAP was negatively correlated with the level of ACE2 protein contents. Conclusions: These results demonstrated that ACE2 may play an important regulatory role in CHD-PAH.
Objective To investigate the effect of antisense senquences of epidermal growth factor receptor(EGFR) on proliferation of vascular smooth muscle cells(VSMCs) activated by angiotensinⅡ(AngⅡ).Methods Sprague-Rat VSMCs were transfected with antisense senquences of EGFR.EGFR mRNA and protein in VSMCs were detected by reverse transcription polymerase chain reaction(RT-PCR) and Western-Bloting.The three groups were stimulated by AngⅡ;Proliferation of VSMCs was detected by()~3H-Tdr incorperation.Result The expression of EGFR mRNA and protein in VSMCs transfected with antisense senquences of EGFR were significantly lower than that transfected with sense senquences of EGFR and control(P0.05).The()~3H-Tdr incorperation of VSMCs transfected with antisense senquences of EGFR was markedly lower than that transfected with sense senquences of EGFR and control(P0.05).Conclusion Antisense senquences of EGFR attenuated the proliferation of VSMCs activated by AngⅡ,These indicate that EGFR play an important role in the proliferation of VSMCs activated by AngⅡ.
Visuospatial dysfunction is one predominant symptom in many atypical Alzheimer's disease (AD) patients, however, until now its neural correlates still remain unclear. For the accumulation of intracellular hyperphosphorylated tau proteins is a major pathogenic factor in neurodegeneration of AD, the distributional pattern of tau could highlight the affected brain regions associated with specific cognitive deficits.We investigated the brain regions particularly affected by tau accumulation in patients with visuospatial dysfunction to explore its neural correlates.Using 18F-AV-1451 tau positron emission tomography (PET), voxel-wise two-sample t-tests were performed between AD patients with obvious visuospatial dysfunction (VS-AD) and cognitively normal subjects, AD patients with little-to-no visuospatial dysfunction (non VS-AD) and cognitively normal subjects, respectively.Results showed increased tau accumulations mainly located in occipitoparietal cortex, posterior cingulate cortex, precuneus, inferior and medial temporal cortex in VS-AD patients, while increased tau accumulations mainly occurred in the inferior and medial temporal cortex in non VS-AD patients.These findings suggested that occipitoparietal cortex, posterior cingulate cortex and precuneus, which were particularly affected by increased tau accumulation in VS-AD patients, may associate with visuospatial dysfunction of AD.
To probe the safety and clinical results of percutaneous transcatheter intervention therapy in patients with combined congenital heart deformities in the same session.
Methods
Thirty patients (14 males and 16 females) with combined congenital heart deformities underwent simultaneous transcatheter intervention therapy, including 7 patients with atrial septal defect (ASD) and patent ductus arteriosus (PDA), 10 patients with ASD and ventricular septal defect (VSD), six patients with ASD and pulmonary stenosis (PS), 5 patients with ASD and PDA, 1 patient with PDA and PS, 1 patient with VSD, PDA and ASD. Their mean age was (17.9±13.5) years. Their mean weight was (38.8±22.0) kg. They underwent transcatheter therapy simultaneously with the sequential algorithm as balloon pulmonary valvuloplasty at first, followed by the occlusion of VSD, then the occlusion of PDA, then ASD, which can be adjusted depending on the circumstances. Follow-up with electrocardiogram (ECG) and transthoracie echocardiography (TTE) was undertaken 2 d, l m, 3 m, 6 m and 12 m after the procedures.
Results
30 patients were treated successfully. In the 7 patients complicated with PS, the systolic pressure gradient across the pulmonary valve decreased from (46.1±15.1) mm Hg(1 mm Hg=0.133 kPa) to (17.6±3.8) mm Hg and the difference was significant(p<0.01). 1 patient showed incomplete right bundle branch block, one patient showed complete right bundle branch block and 1 patient showed incomplete left bundle branch block after intervention therapy, and ECG showed normal after treatment with dexamethasone. one patient with VSD and ASD, preoperative and 10 days after the procedure whose ECG showed Bifascicular block. The patient was given a permanent implanted cardiac pacemaker. Among two patients with VSD, a slight crevice shunt was detected after the procedure by TTE, they were detected disappearance of the crevice shunt by TTE at 6 months after the procedure. No patient encountered complications during follow-up.
Conclusions
Simultaneous transcatheter therapy of combined congenital heart deformities can obtain satisfactory effect by strict indication control and procedure manipulations.
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