Congenital Abdominal Aortic Aneurysm: A Case Report and Literature Review.

Congenital abdominal aortic aneurysm is a rare disease with unknown etiology, and the common symptoms are abdominal pulsatile mass and pain caused by aneurysm rupture. The disease has a high mortality rate and fewer reports of surgical treatment. Here, we present a case of an idiopathic congenital abdominal aortic aneurysm. A 4-year-old boy had an abdominal pulsatile mass, and computed tomography angiography revealed an isolated infrarenal abdominal aortic aneurysm. To prevent rupture of the aneurysm, we repaired the aneurysm with artificial graft transplantation. No genetic mutation of the known congenital aneurysmal diseases was found in the whole-exome sequencing of the patient and his parents. There was no graft obstruction, and the patient grew well 40 months after surgery. Open surgery is the best treatment for idiopathic congenital abdominal aortic aneurysms. Surgical details such as timing and graft selection need to be further explored.

LncRNA ZEB1-AS1 facilitates ox-LDL-induced damage of HCtAEC cells and the oxidative stress and inflammatory events of THP-1 cells via miR-942/HMGB1 signaling.

AIMS: The role of long noncoding RNA ZEB1 antisense 1 (lncRNA ZEB1-AS1) in carotid artery atherosclerosis remains barely explored. MATERIALS AND METHODS: The viability and apoptosis of HCtAEC cells were measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Caspase-3 activity detection assay and flow cytometry. The oxidative stress status and inflammation of THP-1 cells were detected by oxidative stress indicator detection kit and Enzyme-linked immunosorbent assay (ELISA). The abundance of ZEB1-AS1, miR-942 and high-mobility group box 1 (HMGB1) was measured by quantitative real time polymerase chain reaction (qRT-PCR). The targets of ZEB1-AS1 and miR-942 in HCtAEC and THP-1 cells were predicted by DIANA tool, and the combination was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA-pull down assay. Western blot was conducted to examine the protein expression of HMGB1. KEY FINDINGS: ZEB1-AS1 promoted ox-LDL-mediated injury in HCtAEC and THP-1 cells. MiR-942 was a direct target of ZEB1-AS1, and it was negatively modulated by ZEB1-AS1 in HCtAEC and THP-1 cells. HMGB1 could bind to miR-942, and it was regulated by ZEB1-AS1/miR-942 axis in HCtAEC and THP-1 cells. HMGB1 overexpression or miR-942 depletion reversed the inhibitory effects of ZEB1-AS1 intervention on the injury and apoptosis of HCtAEC cells and the oxidative stress and inflammation of THP-1 cells. SIGNIFICANCE: LncRNA ZEB1-AS1 contributed to ox-LDL-mediated injury and apoptosis of HCtAEC cells and the oxidative stress and inflammation of THP-1 cells through up-regulating HMGB1 via sponging miR-942. ZEB1-AS1/miR-942/HMGB1 axis might provide a new direction to treatment carotid artery atherosclerosis.

Upregulation of circulating miR130a is correlated with development of Barrett's esophagus and esophageal adenocarcinoma.

BACKGROUND: Barrett's esophagus (BE) is one of the major known risk factors for esophageal adenocarcinoma (EAC). Circulating miRNAs are emerging as predictive biomarkers for early detection of malignancy. However, the potential for circulating miRNAs to be used as biomarkers for BE neoplastic progression to EAC has not been well characterized. METHOD: We performed a systematic screening approach to identify spectrum miRNAs in the serum of both BE and EAC patients. RESULTS: miRNA-array web-based software identified 116 sequences differentially expressed between BE patients and healthy controls. Subsequent study revealed that miR130a was significantly upregulated in serum samples of BE and EAC patients compared to healthy controls. We found an increase in serum miR130a in low-grade and high-grade dysplasia BE patients compared to individuals with metaplasia. We also observed that miR130a expression levels increased gradually from early-stage (I, II) to advanced-stage (III, IV) EAC patients. CONCLUSION: Our preliminary results provide evidence that circulating miR130a is correlated with the development of BE and EAC.

The Role of Gastroesophageal Reflux in Provoking High Blood Pressure Episodes in Patients With Hypertension.

GOALS: We assessed the relationship between gastroesophageal reflux disease (GERD) and hypertension and whether antiacid therapy could be used to control blood pressure (BP) on hypertension in patients with GERD. BACKGROUND: Gastroesophageal reflux disease (GERD) may provoke cardiovascular disease. Many factors are involved in the development of essential hypertension, but whether GERD has a role needs further study. STUDY: Patients with essential hypertension (n=86) were studied by 24-hour continuous BP monitoring and esophageal impedance and pH monitoring. Patients fulfilling the GERD criteria received 14-day therapy with omeprazole (20 mg twice a day), and the effect on BP was studied. RESULTS: Of the 86 essential hypertension patients, 38 (44.2%) had GERD. Among these 38 patients, 494 episodes of pathologic reflux (PR), and 684 episodes of high BP were recorded. PR was significantly more common at nighttime especially when supine. Of the 684 episodes of hypertension, 102 (14.9%) were synchronous with PR. GERD patients had significantly higher nocturnal BP than non-GERD patients. Antiacid therapy brought about significant reduction in all esophageal monitoring parameters as well as in BP parameters in GERD patients. CONCLUSIONS: This study demonstrated that there is significant correlation between hypertension and GERD. Antiacid therapy can restore normal esophageal pH and help maintain normal BP.

Angiotensin II type 1 receptor-associated protein regulates carotid intimal hyperplasia through controlling apoptosis of vascular smooth muscle cells.

Intimal hyperplasia is the main cause of restenosis after carotid artery injury, and the underlying mechanism involves the proliferation and migration of vascular smooth muscle cells (VSMCs). Angiotensin II Type 1 Receptor-Associated Protein (ATRAP) has been reported to withstand intimal hyperplasia by inhibiting VSMCs proliferation and migration; however, whether the beneficial effect of ATRAP associates with VSMCs apoptosis remains unclarified. We demonstrated that the adenoviral-mediated overexpression of ATRAP induced VSMC apoptosis, alleviating the balloon injury-induced neointima formation in rats. Under the condition of Angiotensin-II stimulation, ATRAP overexpression induced the apoptosis of rat VSMCs by depressing the PI3K-Akt signaling; whereas up-regulation of Akt by PTEN inhibitor abolished the apoptotic death. Thus, ATRAP regulates carotid intimal hyperplasia through controlling the PI3K-Akt signal-mediated VSMCs apoptosis.

Contribution of hiatal hernia to asthma in patients with gastroesophageal reflux disease.

BACKGROUND: To determine the correlation between asthma and hiatal hernia (HH) in patients with gastroesophageal reflux disease (GERD)-related asthma requiring laparoscopic anti-reflux surgery. METHODS: One hundred and thirty-six GERD patients with medically refractory asthma with (80 patients) or without HH (56 patients) were enrolled. Gastroesophageal reflux disease was assessed by endoscopy, esophageal manometry, reflux monitoring and symptom questionnaires, and treated with laparoscopic Nissen fundoplication (LNF) or LNF with concomitant hiatal hernia repair (LNF-HHR). The outcome measures included patients' satisfaction and drug independence. RESULTS: The patients with HH had lower esophageal sphincters (P = .005) and higher DeMeester scores (P = .014) than those without HH. After an average follow-up of 24 months, symptom scores were significantly decreased from the preoperative values (P < .05). Compared to LNF, LNF-HHR showed a better improvement in both esophageal and asthmatic symptoms (P < .0001 and P = .016, respectively). CONCLUSIONS: The patients with GERD with asthma have a high prevalence of HH. The presence of HH maybe correlated with asthma and severe GERD. Actively treating HH not only improved reflux, but also controlled asthma symptoms.