Objective To explore the application value of triggered angiography non-contrast enhanced (TRANCE) technology in diagnosing lower limb arterial occlusive disease.Methods Totally 22 lower limb arterial occlusive disease patients were randomly selected,and then underwent TRANCE and DSA examinations.The arteries from the abdomen to the lower limb were divided into abdominal aorta,common iliac artery,external iliac artery,internal iliac artery,superficial femoral artery,deep femoral artery,popliteal artery,anterior tibial artery,posterior tibial artery and peroneal artery.Totally 337 sections displayed clearly were chosen to go through examinations by TRANCE and DSA.Results Of the 337 sections there were 312 ones with the same stenoses found by TRANCE and DSA,TRANCE found 16 sections with worse stenoses and 9 milder ones than by DSA.There were 153 sections with the same moderate stenoses (≥50％) displayed by TRANCE and DSA;Of the 153 sections,there were 15 ones with worse stenoses and 6 ones with milder stenoses found by TRANCE than by DSA.Kappa value of the two methods was 0.905.Conclusion TRANCE technology is a non-invasive,safe and nonradiative diagnosing method for the lower limb arterial occlusive disease.

As the place for gas exchange, the lungs are metabolically active, and their energy consumption are essential for regulating common cell functions and maintaining the unique function of lung tissues to synthesize pulmonary surfactants. The metabolic pathways of pulmonary cells mainly include glycolysis, pentose phosphate pathway, and tricarboxylic acid cycle. Recent studies have found that changes in pulmonary cells metabolism are closely related to a variety of lung diseases. Herein, we review the main pathways of pulmonary cells metabolism and the relationship between changes in cell metabolism and the four lung diseases of chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), and pulmonary hypertension (PH), to find new ways to treat lung diseases.

Ahmed glaucoma drainage valve (AGV) implantation is one of the main methods for the treatment of refractory glaucoma with a higher success rate than conventional filtration surgery.However, as a foreign body, the AGV often causes hyperplasia of scar tissue in the filtration area, wrapping around the drainage plate, thereby inhibiting aqueous fluid outflow and causing the intraocular pressure to rise again, leading to surgical failure.Although multiple injections of anti-metabolic drugs during and after AGV implantation can inhibit postoperative scarring, multiple postoperative subconjunctival injections will not only cause discomfort to patients, but also lead to complications.Therefore, it is necessary to improve the AGV to avoid repeated injection of the drug, achieve slow local release of the drug, and reduce the foreign body reaction of AGV at the same time.Recently, the development of new materials, such as Ologen collagen, poly (2-hydroxyethyl methacrylate), poly lactic-co-glycolic acid and opal shale and new techniques provides new methods to inhibit the scarring of filtration area after AGV implantation.This article reviews the methods and progress of inhibition of scar formation in filtration area from the aspects of development of AGV drainage plate materials, construction of drug delivery system of AGV combined with new materials, and improvement of AGV drainage plate structure.

The human brain undergoes rapid development during childhood, with significant improvement in a wide spectrum of cognitive and affective functions. Mapping domain- and age-specific brain activity patterns has important implications for characterizing the development of children’s cognitive and affective functions. The current mainstay of brain templates is primarily derived from structural magnetic resonance imaging (MRI), and thus is not ideal for mapping children’s cognitive and affective brain development. By integrating task-dependent functional MRI data from a large sample of 250 children (aged 7 to 12) across multiple domains and the latest easy-to-use and transparent preprocessing workflow, we here created a set of age-specific brain functional activity maps across four domains: attention, executive function, emotion, and risky decision-making. Moreover, we developed a toolbox named Developmental Brain Functional Activity maps across multiple domains that enables researchers to visualize and download domain- and age-specific brain activity maps for various needs. This toolbox and maps have been released on the Neuroimaging Informatics Tools and Resources Clearinghouse website (http://www.nitrc.org/projects/dbfa). Our study provides domain- and age-specific brain activity maps for future developmental neuroimaging studies in both healthy and clinical populations.

Drug-associated reward memories are conducive to intense craving and often trigger relapse. Simvastatin has been shown to regulate lipids that are involved in memory formation but its influence on other cognitive processes is elusive. Here, we used a mass spectrometry-based lipidomic method to evaluate the impact of simvastatin on the mouse brain in a cocaine-induced reinstatement paradigm. We found that simvastatin blocked the reinstatement of cocaine-induced conditioned place preference (CPP) without affecting CPP acquisition. Specifically, only simvastatin administered during extinction prevented cocaine-primed reinstatement. Global lipidome analysis showed that the nucleus accumbens was the region with the greatest degree of change caused by simvastatin. The metabolism of fatty-acids, phospholipids, and triacylglycerol was profoundly affected. Simvastatin reversed most of the effects on phospholipids induced by cocaine. The correlation matrix showed that cocaine and simvastatin significantly reshaped the lipid metabolic pathways in specific brain regions. Furthermore, simvastatin almost reversed all changes in the fatty acyl profile and unsaturation caused by cocaine. In summary, pre-extinction treatment with simvastatin facilitates cocaine extinction and prevents cocaine relapse with brain lipidome remodeling.
Animals ; Brain ; Cocaine ; Conditioning, Operant ; Extinction, Psychological ; Lipidomics ; Male ; Mice ; Simvastatin/therapeutic use*

Drug-associated reward memories are conducive to intense craving and often trigger relapse. Simvastatin has been shown to regulate lipids that are involved in memory formation but its influence on other cognitive processes is elusive. Here, we used a mass spectrometry-based lipidomic method to evaluate the impact of simvastatin on the mouse brain in a cocaine-induced reinstatement paradigm. We found that simvastatin blocked the reinstatement of cocaine-induced conditioned place preference (CPP) without affecting CPP acquisition. Specifically, only simvastatin administered during extinction prevented cocaine-primed reinstatement. Global lipidome analysis showed that the nucleus accumbens was the region with the greatest degree of change caused by simvastatin. The metabolism of fatty-acids, phospholipids, and triacylglycerol was profoundly affected. Simvastatin reversed most of the effects on phospholipids induced by cocaine. The correlation matrix showed that cocaine and simvastatin significantly reshaped the lipid metabolic pathways in specific brain regions. Furthermore, simvastatin almost reversed all changes in the fatty acyl profile and unsaturation caused by cocaine. In summary, pre-extinction treatment with simvastatin facilitates cocaine extinction and prevents cocaine relapse with brain lipidome remodeling.