Adaptive cascaded transformer U-Net for MRI brain tumor segmentation.

Objective.Brain tumor segmentation on magnetic resonance imaging (MRI) plays an important role in assisting the diagnosis and treatment of cancer patients. Recently, cascaded U-Net models have achieved excellent performance via conducting coarse-to-fine segmentation of MRI brain tumors. However, they are still restricted by obvious global and local differences among various brain tumors, which are difficult to solve with conventional convolutions.Approach.To address the issue, this study proposes a novel Adaptive Cascaded Transformer U-Net (ACTransU-Net) for MRI brain tumor segmentation, which simultaneously integrates Transformer and dynamic convolution into a single cascaded U-Net architecture to adaptively capture global information and local details of brain tumors. ACTransU-Net first cascades two 3D U-Nets into a two-stage network to segment brain tumors from coarse to fine. Subsequently, it integrates omni-dimensional dynamic convolution modules into the second-stage shallow encoder and decoder, thereby enhancing the local detail representation of various brain tumors through dynamically adjusting convolution kernel parameters. Moreover, 3D Swin-Transformer modules are introduced into the second-stage deep encoder and decoder to capture image long-range dependencies, which helps adapt the global representation of brain tumors.Main results.Extensive experiment results evaluated on the public BraTS 2020 and BraTS 2021 brain tumor data sets demonstrate the effectiveness of ACTransU-Net, with average DSC of 84.96% and 91.37%, and HD95 of 10.81 and 7.31 mm, proving competitiveness with the state-of-the-art methods.Significance.The proposed method focuses on adaptively capturing both global information and local details of brain tumors, aiding physicians in their accurate diagnosis. In addition, it has the potential to extend ACTransU-Net for segmenting other types of lesions. The source code is available at:https://github.com/chenbn266/ACTransUnet.

Vibrational and electrochemical studies of pectin-a candidate towards environmental friendly lithium-ion battery development.

Pectin polymers are considered for lithium-ion battery electrodes. To understand the performance of pectin as an applied buffer layer, the electrical, magnetic, and optical properties of pectin films are investigated. This work describes a methodology for creating pectin films, including both pristine pectin and Fe-doped pectin, which are optically translucent, and explores their potential for lithium-ion battery application. The transmission response is found extended in optimally Fe-doped pectin, and prominent modes for cation bonding are identified. Fe doping enhances the conductivity observed in electrochemical impedance spectroscopy, and from the magnetic response of pectin evidence for Fe3+ is identified. The Li-ion half-cell prepared with pectin as binder for anode materials such as graphite shows stable charge capacity over long cycle life, and with slightly higher specific capacity compare with the cell prepared using polyvinylidene fluoride (PVDF) as binder. A novel enhanced charging specific capacity at a high C-rate is observed in cells with pectin binder, suggesting that within a certain rate (∼5 C), pectin has higher capacity at faster charge rates. The pectin system is found as a viable base material for organic-inorganic synthesis studies.

Correlation between connexin and traumatic brain injury in patients.

BACKGROUND: Identification of molecular alterations of damaged tissue in patients with neurological disorders can provide novel insight and potential therapeutic target for treatment of the diseases. It has been suggested by animal studies that connexins (CXs), a family of gap junction proteins, could contribute to neuronal cell death and associate with neurological deficits during trauma-induced damage. Nevertheless, whether specific CXs are involved in traumatic brain injury (TBI) has remained unexplored in human patients. METHODS: In a clinical setting, we performed a correlation study of 131 TBI patients who received brain surgery. CXs (including CX40, CX43, and CX45) were examined in the harvested brain tissues for studying the relationships with the Glasgow Coma Scale scores of the patients. RESULTS: Specifically, the protein levels of CX43 (negatively) and CX40 (positively) are associated with the extent of disease severity. Meanwhile, the phosphorylation status of CX43 was strongly associated with the severe TBI patients who contain relatively high kinase activities of PKC (protein kinase C) and MAPK (mitogen-activated protein kinase), two possible activators for CX43 phosphorylation. CONCLUSION: These data highlight that a cluster of connexin family gap junction proteins not previously studied in humans is significantly correlated with the disease progression of TBI.

Resveratrol inhibits lung cancer growth by suppressing M2-like polarization of tumor associated macrophages.

In cancer, tumor associated macrophages (TAMs) play an important role in the cancer progression, evasion of immunity and dissemination of cancer cells. Inhibition of the activation or the M2 polarization of TAMs is an effective therapy for cancer. In the present study, we investigated the ability of resveratrol (RES) to inhibit lung cancer growth using in vitro and in vivo studies, and examined the underlying mechanisms. We demonstrated that M2 polarization of human monocyte derived macrophage (HMDMs) induced by the lung cancer cells conditioned medium was inhibited by RES. Additionally, RES exhibited inhibitory function in lung cancer cells co-cultured with human macrophages. The activity of signal transducer and activator of transcription 3 (STAT3) was significantly decreased by RES. Moreover, in a mouse lung cancer xenograft model, RES significantly inhibited the tumor growth, which was associated with inhibition of cell proliferation and decreased expression of p-STAT3 in tumor tissues. Further, RES inhibits F4/80 positive expressing cells and M2 polarization in the tumors. These results suggest that RES can effectively inhibit lung cancer progression by suppressing the protumor activation of TAMs.