A Self-Supervised Deep Learning Method for Seismic Data Deblending Using a Blind-Trace Network.

The simultaneous-source technology for high-density seismic acquisition is a key solution to efficient seismic surveying. It is a cost-effective method when blended subsurface responses are recorded within a short time interval using multiple seismic sources. A following deblending process, however, is needed to separate signals contributed by individual sources. Recent advances in deep learning and its data-driven approach toward feature engineering have led to many new applications for a variety of seismic processing problems. It is still a challenge, though, to collect enough labeled data and avoid model overfitting and poor generalization performance over different datasets with a low resemblance from each other. In this article, we propose a novel self-supervised learning method to solve the deblending problem without labeled training datasets. Using a blind-trace deep neural network and a carefully crafted blending loss function, we demonstrate that the individual source-response pairs can be accurately separated under three different blended-acquisition designs.

Altered Jagged1-Notch1 Signaling in Enhanced Dysfunctional Neovascularization and Delayed Angiogenesis After Ischemic Stroke in HFD/STZ Induced Type 2 Diabetes Rats.

Diabetes exacerbates brain damage in cerebral ischemic stroke. Our previous study has demonstrated that after cerebral ischemia, type 2 diabetes rats displayed worse neurological outcomes, larger cerebral infarction and severer blood-brain barrier disruption. However, our knowledge of the mechanisms of how diabetes impacts the cerebrovascular repair process is limited. This study was aimed to characterize structural alterations and potential mechanisms in brain microvessels before and after ischemic stroke in type 2 diabetic rats treated with high-fat diet and streptozotocin (HFD/STZ). Furtherly, we tested our hypothesis that dysregulated intercellular Jagged1-Notch1 signaling was involved in the dysfunctional cerebral neovascularization both before and after ischemic stroke in HFD/STZ rats. In our study, we found increased yet dysfunctional neovascularization with activated Jagged1-Notch1 signaling in the cerebrovasculature before cerebral ischemia in HFD/STZ rats compared with non-diabetic rats. Furthermore, we observed delayed angiogenesis as well as suppressed Jagged1-Notch1 signaling after ischemic stroke. Our results elucidate the potential mechanisms underlying diabetes-related cerebral microvasculature dysfunction after ischemic stroke.

Clarifying the effects of diabetes on the cerebral circulation: Implications for stroke recovery and beyond.

Given the sheer increased number of victims per year and the availability of only one effective treatment, acute ischemic stroke (AIS) remains to be one of the most under-treated serious diseases. Diabetes not only increases the incidence of ischemic stroke, but amplifies the ischemic damage, upon which if patients with diabetes suffer from stroke, he/she will confront increased risks of long-term functional deficits. The grim reality makes it a pressing need to intensify efforts at the basic science level to understand how diabetes impairs stroke recovery. This review retrospects the clinical and experimental studies in order to elucidate the detrimental effect of diabetes on cerebrovascular circulation including the major arteries/arterioles, collateral circulation, and neovascularization to shed light on further exploration of novel strategies for cerebral circulation protection before and after AIS in patients with diabetes.

Mild hypothermia alleviates diabetes aggravated cerebral ischemic injury via activating autophagy and inhibiting pyroptosis.

Diabetic patients manifest with more severe neurological deficits than non-diabetes after ischemic stroke. It has been shown that hypothermia has neuroprotective effects on cerebral ischemia, but whether it is effective for cerebral ischemia in diabetic patients remains unknown. The aim of this study was to investigate whether hypothermia can alleviate cerebral ischemic injury in diabetic rats and the regulation of autophagy and pyroptosis of the treatment. We introduced permanent middle cerebral artery occlusion (pMCAO) in a model of type 2 diabetic rats prepared by high-fat diet combined with intraperitoneal injection of STZ in vivo and mimicked cerebral ischemia with diabetes by employing high glucose stimulation and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro. Moreover, 3-methyladenine and bafilomycin A1 were used to evaluate the association between autophagy and pyroptosis in vitro. Our results showed that diabetes aggravated neurological deficits, increased the volume of cerebral infarction and brain edema as well as the blood brain barrier permeability after cerebral ischemia, which were alleviated by mild hypothermia. Compared with the pMCAO model in non-diabetic rats and OGD/R model without high glucose stimulation in vitro, the expression of P62, NOD-like receptor protein 3 (NLRP3), cleaved caspase-1 and Gasdermin-N increased and the ratio of microtubule-associated protein 1 light chain 3B (LC3B) Ⅱ/Ⅰ decreased in the pMCAO model in diabetic rats and OGD/R model with high glucose stimulation, which could be reversed by mild hypothermia. In conclusion, mild hypothermia alleviated diabetes aggravated cerebral ischemic injury via activating autophagy and inhibiting pyroptosis.

Decreased vesicular acetylcholine transporter related to memory deficits in epilepsy: A [18 F] VAT positron emission tomography brain imaging study.

OBJECTIVE: Vesicular acetylcholine transporter (VAChT) is a rate-limiting factor for synaptic acetylcholine transport. Our study focused on whether [18 F] VAT, a novel positron emission tomography (PET) tracer, could be used in detecting cognitive deficits in epilepsy. METHODS: Morris water maze test was used to evaluate learning and memory deficits in pilocarpine-induced chronic epilepsy rats 12 weeks after status epilepticus. Interictal [18 F] VAT PET was performed 13 weeks after status epilepticus to evaluate the level of VAChT in cholinergic pathways compared with [18 F] fluorodeoxyglucose PET. The association between VAChT levels and memory measures was analyzed. Neuropathological tests were performed. RESULTS: Epileptic rats exhibited significant memory deficits in Morris water maze test. [18 F] VAT uptake decreased in septum, hippocampus, thalamus, and basal forebrain, and correlated to memory function. Of note, the level of VAChT in basal forebrain significantly decreased, yet no glucose hypometabolism was detected. Immunofluorescence and Western blot demonstrated decreased expression of VAChT in hippocampus and basal forebrain in the epilepsy group, but no change of expression of acetyltransferase or activity of acetylcholinesterase was detected. SIGNIFICANCE: [18 F] VAT PET is a promising method to test the level of VAChT as a valuable biomarker for memory deficits in pilocarpine-induced chronic epileptic rats.

Therapeutic time window and regulation of autophagy by mild hypothermia after intracerebral hemorrhage in rats.

Although recent studies have shown that mild hypothermia has neuroprotective effects on intracerebral hemorrhage (ICH), the therapeutic time window of the therapy and the role of autophagy as a potential neuroprotective mechanism remain unclear. This study was aimed to investigate the appropriate time window of mild hypothermia and the regulation of autophagy during the treatment in a rat model of autologous blood-injected ICH injury. The rats were divided into Sham, normothermic (NT) and hypothermic (HT) groups. HT groups received mild hypothermia (33 °C-35 °C) for 48 h starting from 3 h (HT3), 6 h (HT6), and 12 h (HT12) respectively after ICH. The neurological function, brain edema, blood brain barrier (BBB) permeability and volume of tissue loss were tested. The expression of metrix metalloproteinase 9 (MMP-9) and tight junction (TJ) protein including Occludin and Claudin-5 around the hematoma were detected by Western blot. Moreover, autophagy after ICH was detected by the ratio of LC3B-II/I, and the expression of Beclin-1 and p62, while apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dURP nick end labelling (TUNEL) staining and expression of Bcl-2, Bim, cleaved Caspase-3. Compared with NT group, neurological deficit, brain edema and BBB permeability were attenuated in HT6 and HT12 groups, but not in HT3 group, while volume of tissue loss was reduced only in HT12 group. The expression of MMP-9 and the degradation of Occludin and Claudin-5 were suppressed only in HT6 and HT12 groups, especially in the latter one. Moreover, neuronal autophagy and apoptosis induced by ICH were downregulated in HT12 group. The results suggested that mild hypothermia initiated at 6 h or 12 h post-injury was neuroprotective in ICH model of rats, especially at 12 h post-injury, via suppression of autophagy upregulated by ICH.

Vascular Remodeling, Oxidative Stress, and Disrupted PPARγ Expression in Rats of Long-Term Hyperhomocysteinemia with Metabolic Disturbance.

Hyperhomocysteinemia, a risk factor for vascular disease, is associated with metabolic syndrome. Our study was aimed at exploring the effect of long-term hyperhomocysteinemia with metabolic disturbances on vascular remodeling. We also studied oxidative stress and expression of PPARγ in the coronary arteriole as a possible mechanism underlying vascular remodeling. Rats were treated with standard rodent chow (Control) or diet enriched in methionine (Met) for 48 weeks. Plasma homocysteine, blood glucose, serum lipids, malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels were measured. Coronary arteriolar and carotid arterial remodeling was assessed by histomorphometric techniques and the expression of PPARγ in vessel wall was investigated. In Met group, an increase in the level of fasting blood glucose, serum triglyceride, total cholesterol, MDA, and NO, a decline in the serum SOD level, and increased collagen deposition in coronary and carotid arteries were found. Moreover, we detected decreased expression of PPARγ in the coronary arterioles in Met group. In summary, our study revealed metabolic disturbances in this model of long-term hyperhomocysteinemia together with vascular remodeling and suggested that impaired oxidative stress, endothelium dysfunction, and decreased PPARγ expression in the vessel wall could be underlying mechanisms.

Mild hypothermia protects rat neuronal injury after intracerebral hemorrhage via attenuating endoplasmic reticulum response induced neuron apoptosis.

BACKGROUND AND PURPOSE: Mild hypothermia has been proved to reduce global and focal cerebral ischemic injury in rodents by preventing cellular apoptosis through several pathways. However, whether hypothermia will be beneficial for intracerebral hemorrhage (ICH) and its underlying mechanisms haven't reached a consensus. It has been implicated that endoplasmic reticulum (ER) stress plays a role in the secondary injury after ICH in rats. In this study, we aimed to investigate whether mild hypothermia would attenuate ICH induced neuronal injury via regulating ER stress. METHODS: The model of ICH was induced by injecting autologous blood (120µl) into the rat striatum. Rats were divided into sham, normothermic (NT) and hypothermic (HT) groups. HT group were subjected to mild hypothermia (33°C-35°C) for 2days starting from 6h after ICH. Neurological deficits were evaluated. The ER stress related proteins (GRP78, CHOP and p-eIF2α) and the apoptosis associated indicators (cleaved caspase3, Bcl-2 and Bim) around hematoma were assessed by western blot, qRT-PCR (quantificational real-time polymerase chain reaction), immunofluorescence and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling) assay. RESULTS: Neurological deficits following ICH were reduced in HT group compared to NT group. Protein levels of GRP78, CHOP and p-eIF2α significantly increased after ICH in both NT and HT group compared to sham group, which was consistent with the trend of cleaved-caspase3 at protein level, and Bim, Bcl-2 at gene level. In comparison to NT group, GRP78, CHOP, p-eIF2α, cleaved caspase-3 and Bim all decreased, while Bcl-2 increased in HT group. Additionally, apoptotic cells detected by TUNEL staining significantly decreased in the HT group. CONCLUSION: Mild hypothermia could attenuate ICH caused neuron injury by decreasing ER response-induced neuron apoptosis.

Acute phase homocysteine related to severity and outcome of atherothrombotic stroke.

BACKGROUND: Homocysteine (HCY) is associated with risk of stroke, but whether HCY affects stroke severity and prognosis remains controversial. We hypothesized HCY has an impact on atherothrombosis and this prospective study was aimed to explore the association between acute phase HCY with stroke severity and outcome in patients with atherothrombosis. METHODS: Patients <72 h after symptom onset were categorized by the modified Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification and those typed as atherothrombosis were included. Neurologic function was assessed with National Institute of Health Stroke Score (NIHSS) <72 h after symptom onset and Modified Rankin Scale (mRS) and Barthel Index (BI) 6-month, 12-month and 18-month poststroke respectively. HCY was recorded <72 h after symptom onset. Participants were divided into hHCY (HCY>15 µmol/l) and nhHCY (HCY≤15 µmol/l). The correlation between HCY and mRS was analyzed. RESULTS: 125 of 130 participants without HCY interventional therapy completed the 18-month follow-up. There was no difference in demographics, histories of hypertension, diabetes mellitus, coronary heart disease, previous cerebral vascular event, and plasma low-density lipoprotein between hHCY and nhHCY. NIHSS, mRS were significantly higher and BI was significantly lower in hHCY than in nhHCY. The 18-month recurrence rate in hHCY (21.0%) was significantly higher than that in nhHCY (6.8%). Spearman correlation analysis revealed correlation between HCY and mRS (p=0.000). By ordinal logistic regression, HCY was an independent predictor of 18-month mRS (odds ratio 1.08, 95% confidence interval 1.04-1.13, p=0.000). CONCLUSIONS: Acute phase elevated HCY correlated with severity and prognosis in patients with atherothrombotic stroke.

Embedding topic discovery in conditional random fields model for segmenting nuclei using multispectral data.

Segmentation of cells/nuclei is a challenging problem in 2-D histological and cytological images. Although a large number of algorithms have been proposed, newer efforts continue to be devoted to investigate robust models that could have high level of adaptability with regard to considerable amount of image variability. In this paper, we propose a multiclassification conditional random fields (CRFs) model using a combination of low-level cues (bottom-up) and high-level contextual information (top-down) for separating nuclei from the background. In our approach, the contextual information is extracted by an unsupervised topic discovery process, which efficiently helps to suppress segmentation errors caused by intensity inhomogeneity and variable chromatin texture. In addition, we propose a multilayer CRF, an extension of the traditional single-layer CRF, to handle high-dimensional dataset obtained through spectral microscopy, which provides combined benefits of spectroscopy and imaging microscopy, resulting in the ability to acquire spectral images of microscopic specimen. The approach is evaluated with color images, as well as spectral images. The overall accuracy of the proposed segmentation algorithm reaches 95% when applying multilayer CRF model to the spectral microscopy dataset. Experiments also show that our method outperforms seeded watershed, a widely used algorithm for cell segmentation.

Multispectral microscopy and cell segmentation for analysis of thyroid fine needle aspiration cytology smears.

This paper discusses the needs for automated tools to aid in the diagnosis of thyroid nodules based on analysis of fine needle aspiration cytology smears. While conventional practices rely on the analysis of grey scale or RGB color images, we present a multispectral microscopy system that uses thirty-one spectral bands for analysis. Discussed are methods and results for system calibration and cell delineation.