Preparation and Properties of Attapulgite/Brucite Fiber-Based Highly Absorbent Polymer Composite.

The ATP-BF-P(HEC-AA-AMPS) composite highly absorbent polymer was copolymerized with acrylic acid (AA) and 2-acrylamido-2-methylpropane sulfonic acid (AMPS) using an aqueous solution method with attapulgite (ATP) and attapulgite (ATP) as a matrix. The prepared ATP-BF-P(HEC-AA-AMPS) was characterized in terms of microstructure and tested for its water absorption capacity, water retention properties, and pH dynamic sensing ability. The results showed that the synthesized ATP-BF-P(HEC-AA-AMPS) had a rough and porous surface and a high water absorption capacity and rate, almost reaching the maximum water absorption around 20 min, and demonstrated excellent water retention performance at low and medium temperatures. ATP-BF-P(HEC-AA-AMPS) has a sensitive dynamic sensing ability in different pH solutions, with a high swelling capacity between pH 6.0 and 10.0. When the pH value exceeded 10.0, the swelling rate decreased rapidly. Additionally, the thermal stability and mechanical strength of the highly absorbent polymers were significantly improved after blending with ATP and BF.

Risk factors for postoperative sepsis-induced cardiomyopathy in patients undergoing general thoracic surgery: a single center experience.

BACKGROUND: The current study aimed to investigate the incidence of sepsis-induced cardiomyopathy (SICM) in patients who received general thoracic surgery, along with the risk factors and management strategies for this complication. METHODS: The clinical records of 163 patients with postoperative sepsis were retrospectively reviewed. After propensity score matching, 144 patients were divided into 2 groups by stroke volume: the SICM group (n=72) and the non-SICM group (n=72). RESULTS: The overall incidence of postoperative SICM was 53.99%. Multiple logistic regression analysis showed that stroke volume and C-reactive protein were independent predictors of mortality in patients with postoperative sepsis. Statistical analysis by t-test and χ2 test indicated that mortality (P=0.000), B-type natriuretic peptide (P=0.001), left ventricular ejection fraction (P=0.000), the mitral peak velocity of early filling/early diastolic mitral annular velocity (E/e') (P=0.049), C-reactive protein (P=0.016), procalcitonin (P=0.013), serum creatinine (P=0.016), platelets (P=0.028), and lactic acid (P=0.002) were significantly associated with the occurrence of postoperative SICM. Among these parameters, B-type natriuretic peptide was identified as the best biomarker for predicting SICM by receiver operating characteristic (ROC) curve analysis. CONCLUSIONS: It is vital to improve the diagnosis and standard management of SICM. A combined strategy comprising early detection of suspected infection, adequate use of antibiotics, close monitoring, effective drainage, and supportive care may improve the outcomes of patients with postoperative SICM.

Gax regulates human vascular smooth muscle cell phenotypic modulation and vascular remodeling.

Abnormal phenotypic modulation of vascular smooth muscle cells (VSMCs) is a hallmark of cardiovascular diseases such as atherosclerosis, hypertension and restenosis after angioplasty. Transcription factors have emerged as critical regulators for VSMCs function, and recently we verified inhibiting transcription factor Gax was important for controlling VSMCs proliferation and migration. This study aimed to determine its role in phenotypic modulation of VSMCs. Western blot revealed that overexpression of Gax increased expression of VSMCs differentiation marker genes such as calponin and SM-MHC 11. Then, Gax overexpression potently suppressed proliferation and migration of VSMCs with or without platelet-derived growth factor-induced-BB (PDGF-BB) stimuli whereas Gax silencing inhibited these processes. Furthermore, cDNA array analysis indicated that Rap1A gene was the downstream target of Gax in human VSMCs. And overexpression of Gax significantly inhibited expression of Rap1A in VSMCs with or without PDGF-BB stimuli. Moreover, overexpression of Rap1A decreased expression of VSMCs differentiation marker genes and increased proliferation and migration of VSMCs with or without PDGF-BB stimuli. Finally, Gax overexpression significantly inhibited the neointimal formation in carotid artery injury of mouse models, specifically through maintaining VSMCs contractile phenotype by decreasing Rap1A expression. In conclusion, these results indicated that Gax was a regulator of human VSMCs phenotypic modulation by targeting Rap1A gene, which suggested that targeting Gax or its downstream targets in human VSMCs may provide an attractive approach for the prevention and treatment of cardiovascular diseases.

Thoracic Endovascular Aortic Repair for Traumatic Thoracic Aortic Injury: A Single-Center Initial Experience.

BACKGROUND: Several publications have documented the technical feasibility and efficacy of stent grafting for aortic injuries. We report short- and mid-term results of thoracic endovascular repair with covered stent grafts for type B blunt thoracic aortic injury. METHODS: We performed a retrospective review of patients who had sustained blunt thoracic aortic injuries. From January 2010 to March 2014, 13 patients (12 men and 1 woman) were admitted and treated in our department for type B thoracic aortic injury. The patients' ages ranged from 19 to 62 years. Traffic accidents were responsible for 10 of the 13 blunt thoracic aortic injuries, and the remainder was caused by blunt trauma from falls. Medical records were examined to identify the clinical outcomes of the procedures, and follow-up computed tomography scans were reviewed to document the efficacy of thoracic endovascular aortic repair. RESULTS: Endovascular stent grafting was technically successful in all cases, and no paraplegia or stroke-like events were reported. No major cardiac, neurologic, or peripheral vascular complications were observed during early or late follow-up. None of the patients died from procedure-related complications. CONCLUSIONS: Our single-center experience demonstrates the feasibility of performing endovascular repair for type B blunt aortic injury. As experience with endovascular surgery accumulates, this method of treatment promises to become the first-choice option for repairing this type of aortic injury, with less associated morbidity and mortality relative to conventional surgical repair.

Midterm results of "treat and repair" for adults with non-restrictive ventricular septal defect and severe pulmonary hypertension.

BACKGROUND: A non-restrictive ventricular septal defect (VSD) can cause intracardiac left to right shunt, which leads to increased pulmonary vascular resistance (PVR) and pulmonary hypertension causes bi-directional or even right-left shunt, namely the Eisenmenger's syndrome. For patients with non-restrictive VSD with severe pulmonary hypertension at stage of near or to be Eisenmenger's syndrome, traditional VSD repair carries high mortality and poor prognosis. Recently, targeted drug therapy was used to decrease pulmonary circulation resistance in these patients before they receive defect repair surgery, namely "treat and repair" strategy, however, there is few reports about the midterm result of this strategy in adults with non-restrictive VSD with severe pulmonary hypertension at stage of near or to be Eisenmenger's syndrome. METHODS: In this study, we used this strategy to treat 41 adult VSD patients who received bosentan as the targeted therapy to decrease their PVR before and after repair surgery. RESULTS: A total of 39 patients were followed up for an average of 37 months. None of the patients died during follow-up. Among them, 36 cases continued targeted drug therapy, whose mean pulmonary artery pressure (mPAP) was significantly reduced, including 31 cases with mPAP <50 mmHg, and the valve of tap hole was closed. Besides, the SpO2 was significantly elevated. CONCLUSIONS: These results demonstrated that "treat-and-repair" strategy may be a viable approach for the adults with non-restrictive VSD with severe pulmonary hypertension at stage of near or to be Eisenmenger's syndrome.

Identification and characterization of CD4(+)AT2(+) T lymphocyte population in human thoracic aortic aneurysm.

Thoracic aortic aneurysm (TAA) is progressive fatal aortic pathological dilation. However, the underlying molecular mechanisms are still largely unknown. Evidences suggest that endothelial cells and renin-angiotensin system may participate in the pathogenesis of TAA. This study aimed to investigate whether angiotensin II type 2 receptor (AT2) positive cells are involved in TAA formation. The mRNA level of AT2 is dramatically elevated in TAA compared with in controls. CD4(+)AT2(+) cells increased in both aortic wall and circulation of TAA patients. The levels of IL-1ß and IL-17B in CD4(+)AT2(+) cells were lower than those in CD4(+)AT2(-) cells. When compared with endothelial cells (ECs) cultured alone, CD4(+)AT2(+) cells showed an inhibitory effect on proliferation and MMP2 expression in ECs, but CD4(+)AT2(-) cells promoted proliferation and MMP2 expression in ECs. Both CD4(+)AT2(+) and CD4(+)AT2(-) cells suppressed apoptosis of ECs. In conclusion, we have identified a novel population of CD4(+)AT2(+) T lymphocytes that show protective effect in TAA through inhibition of growth, apoptosis, and MMP2 expression in ECs.