Blind Detection of Broadband Signal Based on Weighted Bi-Directional Feature Pyramid Network.

With the development of wireless technology, signals propagating in space are easy to mix, so blind detection of communication signals has become a very practical and challenging problem. In this paper, we propose a blind detection method for broadband signals based on a weighted bi-directional feature pyramid network (BiFPN). The method can quickly perform detection and automatic modulation identification (AMC) on time-domain aliased signals in broadband data. Firstly, the method performs a time-frequency analysis on the received signals and extracts the normalized time-frequency images and the corresponding labels by short-time Fourier transform (STFT). Secondly, we build a target detection model based on YOLOv5 for time-domain mixed signals in broadband data and learn the features of the time-frequency distribution image dataset of broadband signals, which achieves the purpose of training the model. The main improvements of the algorithm are as follows: (1) a weighted bi-directional feature pyramid network is used to achieve a simple and fast multi-scale feature fusion approach to improve the detection probability; (2) the Efficient-Intersection over Union (EIOU) loss function is introduced to achieve high accuracy signal detection in a low Signal-Noise Ratio (SNR) environment. Finally, the time-frequency images are detected by an improved deep network model to complete the blind detection of time-domain mixed signals. The simulation results show that the method can effectively detect the continuous and burst signals in the broadband communication signal data and identify their modulation types.

Enhanced Cerebral Microbleeds by Long-Term Air Pollution Exposure in Spontaneously Hypertensive Rats.

BACKGROUND: Cerebral microbleeds (CMBs) are associated with a high risk for stroke . The present study determined whether long-term exposure to PM2.5 results in progressive worsening of CMBs and induction of systemic inflammation and microvascular oxidative stress. METHODS: Sixteen male Spontaneously hypertensive rats (SHR) and eight Wistar-Kyoto (WKY) rats were exposed to either filtered air or PM2.5 for 12 months. To detect CMBs, rats were imaged using a 7-T MRI. To determine systemic inflammation and oxidative stress, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), as well as reactive oxygen species (ROS), NADPH activity and its subunits p22/47/67phox & gp91phox were measured. RESULTS: During the exposure period, the mean daily concentration of PM2.5 was 59.2 ± 1.0 µg/m3. PM2.5 exposure significantly increased the incidence of CMBs compared to the PM2.5 (-) group (37.5% vs 12.5% incidence rate, p < 0.001). Animals exposed to PM2.5 also had significantly increased systolic blood pressures (SBPs) at 3 months (173 ± 5 vs 157 ± 5 mmHg, p < 0.05), 6 months (218 ± 6 vs 193 ± 7 mmHg, p < 0.01), 9 months (222 ± 6 vs 203 ± 8 mmHg, p < 0.05), and 12 months (231 ± 4 vs 207 ± 5 mmHg, p = 0.01). Additionally, there were significant elevations in IL-6, MCP-1, and TNF-α in the exposed group. Furthermore, PM2.5 significantly increased NOX activity and protein levels of gp91phox and p22/47/67phox. CONCLUSION: In the SHR model, long-term exposure to PM2.5 worsened CMBs, increased SBPs, induced systemic inflammation and oxidative stress. Therefore, PM2.5 is potentially a controllable risk factor that promotes CMBs in certain patients, such as those with hypertension.

Breast Carcinoma with a Special Histological Pattern of Sebaceous Differentiation and High-Frequency Microsatellite Instability: A Case Report and Review of the Literature.

The World Health Organization in its 2019 Classification of Breast Tumors termed breast sebaceous carcinoma as invasive breast carcinoma of no special type (IBC-NST), with a sebaceous pattern. Approximately 30 cases of IBC-NST with a sebaceous pattern have been reported in the literature, and in all cases the expression of mismatch repair proteins in tumors was normal. Here, we report a case of IBC-NST with a sebaceous pattern and high-frequency microsatellite instability (MSI-H). This case was a sporadic sebaceous pattern of IBC-NST with MSI-H and was unrelated to Muir-Torre syndrome. Its histopathological characteristics were similar to those of MSI-H-associated triple-negative breast carcinoma (TNBC) with a high histological grade but were without tumor-infiltrating lymphocytes (TILs). The tumor did not recur after 20 months of follow-up.

Omega-3 fatty acid supplement prevents development of intracranial atherosclerosis.

OBJECTIVES: Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of stroke worldwide and, in particular, has been implicated as a leading cause of recurrent ischemic stroke. We adapted a rat model of atherosclerosis to study brain intracranial atherosclerosis, and further investigated the effect of omega-3 fatty acids (O3FA) in attenuating development of ICAS. MATERIALS AND METHODS: Adult male Sprague-Dawley rats were divided into control normal-cholesterol or high-cholesterol diet groups with or without O3FA for up to 6weeks. During the first 2weeks, NG-nitro-l-arginine methyl ester (l-NAME, 3mg/mL) was added to the drinking water of the high-cholesterol groups. The rats received supplementation with O3FA (5mg/kg/day) by gavages. Blood lipids including low density lipoprotein (LDL), cholesterol (CHO), triglycerides (TG) and high density lipoprotein (HDL) were measured at 3 and 6weeks. The lumen of middle cerebral artery (MCA) and the thickness of the vessel wall were assessed. Inflammatory molecular markers were assessed by Western blot. RESULTS: A high-cholesterol diet exhibited a significant increase in the classic blood markers (LDL, CHO, and TG) for atherosclerosis, as well as a decrease in HDL. These markers were found to be progressively more severe with time. Lumen stenosis and intimal thickening were increased in MCA. O3FA showed attenuation of blood lipids with an absence of morphological changes. O3FA significantly reduced the inflammatory marker CD68 in MCA and prevented monocyte chemotactic protein (MCP-1) and interferon-γ (IFN-γ) expression in the brain. O3FA similarly decreased inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6), markers affiliated with monocyte activity in atherosclerosis. Furthermore, O3FA significantly inhibited the expression of vascular cell adhesion molecule-1 (VCAM-1), a marker for endothelial activation. Lastly, O3FA increased ATP-binding cassette transporter A1 (ABCA1) protein expression via silent information regulator 1 (SIRT1) activation, thus increasing cholesterol efflux from macrophages to HDL. CONCLUSIONS: Long-term O3FA dietary supplementation prevents the development of intracranial atherosclerosis. This O3FA effect appears to be mediated by its prevention of macrophage infiltration into the vessel wall, therefore reducing inflammation and intimal thickening. While similar effects in humans need to be determined, O3FA dietary supplement shows promising results in the prevention of ICAS.

A new clinically relevant model for intracranial atherosclerosis in rats.

INTRODUCTION: Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of stroke worldwide and, in particular, has been implicated as a leading cause of recurrent ischemic stroke. We developed a new rat model to study intracranial atherosclerosis. METHODS: Twelve-week-old male Sprague-Dawley rats were divided into a control (on a maintain diet) and a high-cholesterol group (on a daily 1% cholesterol diet) for up to 6 weeks. During the first two weeks, NG-nitro-L-arginine methylester (L-NAME, 3 mg/mL) was added to the drinking water in the high-cholesterol group to induce intimal changes making the rats susceptible to atherosclerosis. Blood lipids, including low-density lipoprotein (LDL), cholesterol (CHO), triglycerides (TG), and high-density lipoprotein (HDL), were measured after 3 and 6 weeks. Histological sections of the brains, including internal carotid artery (ICA), middle cerebral artery (MCA), and basilar artery (BA), were prepared to study intracranial artery morphometry and intimal thickening. The levels of CD68, an inflammatory marker, within the vessel walls as determined by immunohistochemistry were also measured. RESULTS: The high-cholesterol diet increased the levels of classic blood markers of atherosclerosis, LDL, CHO, and TG as well as decreased HDL, which became progressively more intensive with time. Rats showed increased intimal thickening in the ICA, MCA, and BA. This protocol also increased the levels of CD68 immunoreactivity within the vessel walls. CONCLUSIONS: A rat model of intracranial atherosclerosis was effectively developed by high-cholesterol diet and L-NAME administration. This clinically relevant model would be beneficial for studying ICAS.