Multi-Task Weakly-Supervised Attention Network for Dementia Status Estimation With Structural MRI.

Accurate prediction of clinical scores (of neuropsychological tests) based on noninvasive structural magnetic resonance imaging (MRI) helps understand the pathological stage of dementia (e.g., Alzheimer's disease (AD)) and forecast its progression. Existing machine/deep learning approaches typically preselect dementia-sensitive brain locations for MRI feature extraction and model construction, potentially leading to undesired heterogeneity between different stages and degraded prediction performance. Besides, these methods usually rely on prior anatomical knowledge (e.g., brain atlas) and time-consuming nonlinear registration for the preselection of brain locations, thereby ignoring individual-specific structural changes during dementia progression because all subjects share the same preselected brain regions. In this article, we propose a multi-task weakly-supervised attention network (MWAN) for the joint regression of multiple clinical scores from baseline MRI scans. Three sequential components are included in MWAN: 1) a backbone fully convolutional network for extracting MRI features; 2) a weakly supervised dementia attention block for automatically identifying subject-specific discriminative brain locations; and 3) an attention-aware multitask regression block for jointly predicting multiple clinical scores. The proposed MWAN is an end-to-end and fully trainable deep learning model in which dementia-aware holistic feature learning and multitask regression model construction are integrated into a unified framework. Our MWAN method was evaluated on two public AD data sets for estimating clinical scores of mini-mental state examination (MMSE), clinical dementia rating sum of boxes (CDRSB), and AD assessment scale cognitive subscale (ADAS-Cog). Quantitative experimental results demonstrate that our method produces superior regression performance compared with state-of-the-art methods. Importantly, qualitative results indicate that the dementia-sensitive brain locations automatically identified by our MWAN method well retain individual specificities and are biologically meaningful.

Effect of Electromyographic Biofeedback Therapy on Muscle Strength Recovery in Children with Guillain-Barré Syndrome.

GBS, as an immune-mediated acute inflammatory peripheral neuropathy (Tan and Halpin et al.), with the characteristics of acute onset and rapid progression, is mainly manifested with damages in nerve root and peripheral nerve. The purpose of the study was to investigate the effect of electromyographic biofeedback therapy on muscle strength recovery in children with Guillain-Barré syndrome (GBS). A total of 62 GBS children patients admitted to our hospital from June 2014 to December 2018 were selected and divided into control group (n = 30) and experimental group (n = 32) according to the order of admission. The children patients in the control group received physical therapy combined with occupational therapy (PT + OT), while based on the treatment in the control group, the experimental group children patients were treated with electromyographic biofeedback therapy. After that, the recovery of nerve and muscle at different time points, muscle strength score, gross motor function measure (GMFM) score, and Barthel index (BI) score of the children patients before and after treatment were compared between the two groups. There were no significant differences in the recovery of nerve and muscle of the children patients between the two groups at T 0 and T 1 (P > 0.05), and the recovery of nerve and muscle of the children patients in the experimental group was significantly better than that in the control group at T 2, T 3, and T 4 (P < 0.001); the muscle strength score, GMFM score, and BI score of the children patients in the experimental group were significantly better than those in the control group after treatment (P < 0.001). The application of electromyographic biofeedback therapy for the treatment of GBS can effectively relieve clinical symptoms, promote rapid recovery, and improve treatment efficacy in children patients, which is worthy of application and promotion.

Macrophage 12/15 lipoxygenase expression increases plasma and hepatic lipid levels and exacerbates atherosclerosis.

12/15 lipoxygenase (12/15LO) oxidizes polyunsaturated fatty acids (PUFAs) to form bioactive lipid mediators. The role of 12/15LO in atherosclerosis development remains controversial. We evaluated atherosclerosis development and lipid metabolism in 12/15LO-LDL receptor (LDLr) double knockout (DK) vs. LDLr knockout (SK) mice fed a PUFA-enriched diet to enhance production of 12/15LO products. Compared with SK controls, DK mice fed a PUFA-enriched diet had decreased plasma and liver lipid levels, hepatic lipogenic gene expression, VLDL secretion, and aortic atherosclerosis and increased VLDL turnover. Bone marrow transplantation and Kupffer cell ablation studies suggested both circulating leukocytes and Kupffer cells contributed to the lipid phenotype in 12/15LO-deficient mice. Conditioned medium from in vitro incubation of DK vs. SK macrophages reduced triglyceride secretion in McArdle 7777 hepatoma cells. Our results suggest that, in the context of dietary PUFA enrichment, macrophage 12/15LO expression adversely affects plasma and hepatic lipid metabolism, resulting in exacerbated atherosclerosis.

[The effect of tetrandrine on the expression of the P170, LRP and TOPO II in S180's tumor cell induced by chemotherapy in the mice with acquired multi-drug resistance].

OBJECTIVE: To observe the effect of tetrandrine on the P170 production expressed by multi-drug resistance gene, lung resistant protein (LRP), and topoisomeras II and elucidate the underlying molecular mechanism. METHOD: Cellular model of multi-drug resistance was established in S180 tumor cell by means of the scheme of PFC chemotherapy at the dosage lower than that with curative effect. P170, LRP and TOPO II were measured by flow cytometry after the mouse model was treated with tetrandrine for 4 weeks. RESULT: tetrandrine obviously reduced the enhancement of express of P170, LRP and the activity of TOPO II in the tumor cells with multi-drug resistance induced by chemotherapy. CONCLUSION: Tetrandrine significantly inhibits the multi-drug resistance of tumor cells induced by chemotherapy via diminishing both the expression of multi-drug resistance gene and the activity of topoisomeras II.