HD2A-Net: A novel dual gated attention network using comprehensive hybrid dilated convolutions for medical image segmentation.

The convolutional neural networks (CNNs) have been widely proposed in the medical image analysis tasks, especially in the image segmentations. In recent years, the encoder-decoder structures, such as the U-Net, were rendered. However, the multi-scale information transmission and effective modeling for long-range feature dependencies in these structures were not sufficiently considered. To improve the performance of the existing methods, we propose a novel hybrid dual dilated attention network (HD2A-Net) to conduct the lesion region segmentations. In the proposed network, we innovatively present the comprehensive hybrid dilated convolution (CHDC) module, which facilitates the transmission of the multi-scale information. Based on the CHDC module and the attention mechanisms, we design a novel dual dilated gated attention (DDGA) block to enhance the saliency of related regions from the multi-scale aspect. Besides, a dilated dense (DD) block is designed to expand the receptive fields. The ablation studies were performed to verify our proposed blocks. Besides, the interpretability of the HD2A-Net was analyzed through the visualization of the attention weight maps from the key blocks. Compared to the state-of-the-art methods including CA-Net, DeepLabV3+, and Attention U-Net, the HD2A-Net outperforms significantly, with the metrics of Dice, Average Symmetric Surface Distance (ASSD), and mean Intersection-over-Union (mIoU) reaching 93.16%, 93.63%, and 94.72%, 0.36 pix, 0.69 pix, and 0.52 pix, and 88.03%, 88.67%, and 90.33% on three publicly available medical image datasets: MAEDE-MAFTOUNI (COVID-19 CT), ISIC-2018 (Melanoma Dermoscopy), and Kvasir-SEG (Gastrointestinal Disease Polyp), respectively.

N-Net: Lesion region segmentations using the generalized hybrid dilated convolutions for polyps in colonoscopy images.

Colorectal cancer is the cancer with the second highest and the third highest incidence rates for the female and the male, respectively. Colorectal polyps are potential prognostic indicators of colorectal cancer, and colonoscopy is the gold standard for the biopsy and the removal of colorectal polyps. In this scenario, one of the main concerns is to ensure the accuracy of lesion region identifications. However, the missing rate of polyps through manual observations in colonoscopy can reach 14%-30%. In this paper, we focus on the identifications of polyps in clinical colonoscopy images and propose a new N-shaped deep neural network (N-Net) structure to conduct the lesion region segmentations. The encoder-decoder framework is adopted in the N-Net structure and the DenseNet modules are implemented in the encoding path of the network. Moreover, we innovatively propose the strategy to design the generalized hybrid dilated convolution (GHDC), which enables flexible dilated rates and convolutional kernel sizes, to facilitate the transmission of the multi-scale information with the respective fields expanded. Based on the strategy of GHDC designing, we design four GHDC blocks to connect the encoding and the decoding paths. Through the experiments on two publicly available datasets on polyp segmentations of colonoscopy images: the Kvasir-SEG dataset and the CVC-ClinicDB dataset, the rationality and superiority of the proposed GHDC blocks and the proposed N-Net are verified. Through the comparative studies with the state-of-the-art methods, such as TransU-Net, DeepLabV3+ and CA-Net, we show that even with a small amount of network parameters, the N-Net outperforms with the Dice of 94.45%, the average symmetric surface distance (ASSD) of 0.38 pix and the mean intersection-over-union (mIoU) of 89.80% on the Kvasir-SEG dataset, and with the Dice of 97.03%, the ASSD of 0.16 pix and the mIoU of 94.35% on the CVC-ClinicDB dataset.

Polysaccharopeptide from Trametes versicolor blocks inflammatory osteoarthritis pain-morphine tolerance effects via activating cannabinoid type 2 receptor.

Analgesia with opioids such as morphine is an effective clinical strategy for the treatment of cancer pain and chronic inflammatory pain. However, long-term use of morphine can cause morphine tolerance (MT), which limits the clinical application of opioids. Polysaccharopeptide from Trametes versicolor (TPSP) is a biologically active macromolecule that exerts anti-tumor, immune-enhancing and pain-relieving effects. In order to address the clinical problem of MT, herein, we investigated the inhibitory effect and mechanism of TPSP in rats with inflammatory pain-morphine tolerance. A chronic inflammatory osteoarthritis pain-morphine tolerance model was simulated by injection of complete Freund's adjuvant (CFA) through the ankle joint cavity and continuous intrathecal administration of morphine. Different doses of TPSP (50 µg/kg, 100 µg/kg and 200 µg/kg) were intrathecally administered for consecutive 3 weeks. Our results indicate that TPSP can significantly inhibit the development of morphine dependence and acute withdrawal in rats, alleviate the decrease of paw withdrawal mechanical threshold and heat stimulation retraction latency. In addition, mechanistically at the molecular level, these effects are elicited via up-regulation of the cannabinoid type 2 receptor, up-regulating the level of ß-endorphin, and reducing the levels of IL-1, NO and PGE2. In summary, we report for the first time the application of TPSP as an adjunctive therapy strategy for the relief of MT in clinic.

Sevoflurane anesthesia alters cognitive function by activating inflammation and cell death in rats.

The present study was designed to investigate the effects of sevoflurane inhalation anesthesia on the cognitive function of rats and to investigate the molecular mechanisms mediating this effect. A total of 100 healthy male Sprague-Dawley rats were divided into four groups: i) Control (air inhalation), ii) low-dose (1.5% sevoflurane inhalation for 2 h), iii) high-dose (3% sevoflurane inhalation for 2 h), and iv) nimodipine group (3% sevoflurane inhalation for 2 h + nimodipine). Sevoflurane inhalation anesthesia resulted in cognitive dysfunction in a dose-dependent manner. Sevoflurane also upregulated the expression of tumour necrosis factor-α (TNF-α), interleukin (IL) -6, -8, and Caspase-3 in the hippocampus. The intervention with nimodipine partially recovered the cognitive function and the abnormal expression of TNF-α, IL-6, IL-8, and Caspase-3 induced by sevoflurane. The results showed that the cognitive dysfunction caused by sevoflurane inhalation in rats may be related to the activation of inflammatory and apoptotic pathways. The neuroprotective effect of nimodipine suggests that abnormal calcium transport is partially responsible for the sevoflurane toxicity.

Effects of sevoflurane pretreatment on the apoptosis of rat H9c2 cardiomyocytes and the expression of GRP78.

The protective effect of sevoflurane on apoptosis of rat H9c2 cardiomyocytes induced by H2O2 and the effect on the expression of glucose-regulated protein 78 (GRP78) were investigated. H9c2 cells were routinely cultured and divided into the control, model and sevoflurane groups. Cells in the model group were treated with 400 µM H2O2, and cells in the sevoflurane group were pretreated with sevoflurane prior to treatment with 400 µM H2O2. MTT assay was used to assess cell viability. Annexin V-propidium iodide (AV-PI) double staining flow cytometry was used to detect apoptosis. The intracellular free Ca2+ concentration was measured by the fluorescence-based assay using Fluo-3 AM as a calcium ion fluorescence probe. The mRNA expression level of GRP78 and protein expression levels of GRP78, CHOP and caspase-12 were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, respectively. The assays showed that after sevoflurane pretreatment the H9c2 cell viability was significantly increased, whereas the H2O2-induced apoptosis, intracellular Ca2+ concentration, mRNA expression of GRP78, and the protein expression of GRP78, CHOP and caspase-12 were all reduced. The results show that pretreatment with sevoflurane inhibited H2O2-induced apoptosis in H9c2 cells. The mechanism may be related to inhibition of the stress-related protein GRP78 expression in endoplasmic reticulum, resulting in decreased intracellular Ca2+ concentration and the downregulation of CHOP and caspase-12 expression levels.

The effects of dexmedetomidine on post-operative cognitive dysfunction and inflammatory factors in senile patients.

OBJECTIVE: To evaluate the effect of dexmedetomidine on post-operative cognitive dysfunction (POCD) and possible action mechanisms. METHODS: A total of 148 aged surgical patients were divided into two groups, which were treated with dexmedetomidine (Dex group) or normal saline (control group) during general anesthesia. The incidence of POCD one day after surgery was evaluated using Mini-Mental State Examination and serum levels of interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) were measured using ELISA. The correlation between the two cytokines and POCD was evaluated using quartile division assay. RESULTS: The incidence of POCD was 9.20% and 21.31% in Dex and control groups, respectively. It is significantly different between the two groups (P < 0.05). The levels of IL-6 and TNF-α were significantly increased after surgery, as compared to before surgery (P < 0.05). Compared to control group, Dexmedetomidine significantly inhibited the increase of post-operative IL-6 and TNF-α levels (P < 0.05). The incidence of POCD was significantly different between quartile divisions of IL-6 and TNF-α (P < 0.05). Pearson correlation analysis showed that IL-6 and TNF-α were positively correlated with the POCD (r = 0.689, P = 0.043 and r = 0.711, P = 0.038, respectively). CONCLUSIONS: The results demonstrate that dexmedetomidine reduces the incidence of POCD in aged patients, and inflammation suppression may underlie the action mechanism.