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Deep learning based multi-atlas segmentation (DL-MA) has achieved the state-of-the-art performance in many medical image segmentation tasks, e.g., brain parcellation. In DL-MA methods, atlas-target correspondence is the key for accurate segmentation. In most existing DL-MA methods, such correspondence is usually established using traditional or deep learning based registration methods at image level with no further feature level adaption. This could cause possible atlas-target feature inconsistency. As a result, the information from atlases often has limited positive and even counteractive impact on the final segmentation results. To tackle this issue, in this paper, we propose a new DL-MA framework, where a novel differentiable atlas feature warping module with a new smooth regularization term is presented to establish feature level atlas-target correspondence. Comparing with the existing DL-MA methods, in our framework, atlas features containing anatomical prior knowledge are more relevant to the target image feature, leading the final segmentation results to a high accuracy level. We evaluate our framework in the context of brain parcellation using two public MR brain image datasets: LPBA40 and NIREP-NA0. The experimental results demonstrate that our framework outperforms both traditional multi-atlas segmentation (MAS) and state-of-the-art DL-MA methods with statistical significance. Further ablation studies confirm the effectiveness of the proposed differentiable atlas feature warping module.

The purpose of the present study was to analyze the clinical phenotypes of a girl with oculo-facio-cardio-dental (OFCD) syndrome and to identify the potential pathogenic mutation responsible for her disease. The patient underwent detailed clinical examinations and phenotype data were collected over a follow-up period of 9 years. Mutation analysis of the candidate gene BCORwas performed with polymerase chain reaction and Sanger sequencing. BCORof 60 unrelated normal individuals were also sequenced as a control group. Clinical phenotyping and follow-up study results indicate that this patient had multiple system anomalies including ocular, facial, cardiac, dental, and limb malformations. In addition, papilloma of the choroid plexus was identified, which represents the first report of this phenotype in an OFCD patient. A novel deletion mutation, c.1296delT in exon 4 of the BCORgene, was identified in this patient and was not found in her parents or in 60 normal unrelated individuals. This deletion was a frameshift mutation and is proposed to encode a premature stop codon, thus producing a truncated protein. Our patient fitted the diagnostic criteria for OFCD syndrome and we report the first papilloma of the choroid plexus in an OFCD patient, expanding the recognized phenotypic spectrum of this disease. Meanwhile, we identified a novel deletion mutation that may cause OFCD syndrome.

In the present study, we aimed to establish a rabbit atherosclerosis model and examine atherosclerotic plaques by using optical coherence tomography (OCT) and intravascular ultrasonography (IVUS) to evaluate the clinical usefulness of these diagnostic tools in the detection of atherosclerotic plaques. Twenty healthy New Zealand rabbits were fed on a high-fat diet for 4 weeks and then subjected to abdominal aortic intimal injury. The OCT and IVUS were performed after 8 weeks. The distal and proximal plaque images were marked to observe the plaque thickness and features of the lesions at the tunica intima and tunica media. Moreover, a pathological examination was performed to evaluate the efficacies of OCT and IVUS. The mean (SD) plaque thickness on OCT and IVUS images was 386.5 (125.3) μm and 412.7 (165.8) μm, respectively. Pathological examinations indicated a mean (SD) plaque thickness of 360.2 (98.l) μm (P> 0.05). No significant differences were noted between the 2 methods. The intimal and medial thickness measured with OCT showed greater correlation with pathologically measured thickness (r = 0.95, P< 0.001 for OCT; r = 0.88, P< 0.001 for IVUS); in particular, the intimal thickness measurements on OCT showed a higher correlation (r = 0.98, P< 0.001). However, the measurements obtained using IVUS were not accurate. Thus, compared with IVUS, OCT was more accurate in determining the nature and thickness of vascular plaques.

Abstract: Nitrous oxide (N2O) and methane (CH4) emissions were measured using a static chamber method in two adjacent plots of freshwater marsh predominated by Calamagrostis angustifolia, one is seasonal waterlogged (SW) and the other without surface water accumulation (NW), in Sanjiang Plain wetland (47°35’N, 133°31’E), northeast China, during 2002–2004. The diurnal and seasonal flux variations of both gases were significantly correlated with 5-cm-soil temperature. The NW marsh is a source of N2O and sink of CH4, while the SW marsh is sink of N2O and source of CH4. Remarkably, we observed a N2O emission peak under Eh of −300 to −100 mV, and CH4 emission peak under Eh of +300 to +400 mV, which indicate additional sources of N2O and CH4 for the freeze-thaw induced emission peaks of N2O and CH4 observed between late July and early August. Further study shows that the additional N2O and CH4 were emitted under the frozen soil after thawing.

Electroacupuncture (EA) therapy has widely been accepted as a useful therapeutic technique with low risk in the clinical setting for prevention from cardiac disease. However, the physiological mechanism under which this protective effect works remains unclear. The present study investigated the effects of EA pretreatment on myocardial ischaemia/reperfusion (MI/R) injury in mice and its possible signalling pathway. Mice were randomly divided into Sham, MI/R, EA + MI/R, EA(−) + MI/R, and AM630 + EA + MI/R groups. We reported that EA pretreatment significantly ameliorated MI/R injury, evidenced by increased cardiac function, reduced infarct size, and decreased apoptosis. This was associated with a reduction of oxidative stress in the infarcted myocardium, which was through CB2. The CB2 expression was up-regulated in the heart after EA pretreatment, as well as heart tissue content of N-arach-idonoylethanolamine-anandamide and 2-arachidonylglycerol. Furthermore, the expression of adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) in the left ventricular myocardial tissue was decreased in the MI/R group, whereas increased in the EA pretreatment group. Administration of AM630 before EA pretreatment did not improve cardiac function and inhibit oxidative stress. Preinjection of AM630 or AMPK inhibitor compound C could partially decrease the expression of EA pretreatment-mediated AMPK or PGC-1α. Pretreatment with EA increased the production of endocannabinoid, which elicited protective effects against MI/R injury through CB2 activation. The mechanism of this effect was related to the activation of AMPK/PGC-1α pathway, followed by an inhibition of oxidative stress.