Deep learning methods for diagnosis of graves' ophthalmopathy using magnetic resonance imaging.

Background: The effect of diagnosing Graves' ophthalmopathy (GO) through traditional measurement and observation in medical imaging is not ideal. This study aimed to develop and validate deep learning (DL) models that could be applied to the diagnosis of GO based on magnetic resonance imaging (MRI) and compare them to traditional measurement and judgment of radiologists. Methods: A total of 199 clinically verified consecutive GO patients and 145 normal controls undergoing MRI were retrospectively recruited, of whom 240 were randomly assigned to the training group and 104 to the validation group. Areas of superior, inferior, medial, and lateral rectus muscles and all rectus muscles on coronal planes were calculated respectively. Logistic regression models based on areas of extraocular muscles were built to diagnose GO. The DL models named ResNet101 and Swin Transformer with T1-weighted MRI without contrast as input were used to diagnose GO and the results were compared to the radiologist's diagnosis only relying on MRI T1-weighted scans. Results: Areas on the coronal plane of each muscle in the GO group were significantly greater than those in the normal group. In the validation group, the areas under the curve (AUCs) of logistic regression models by superior, inferior, medial, and lateral rectus muscles and all muscles were 0.897 [95% confidence interval (CI): 0.833-0.949], 0.705 (95% CI: 0.598-0.804), 0.799 (95% CI: 0.712-0.876), 0.681 (95% CI: 0.567-0.776), and 0.905 (95% CI: 0.843-0.955). ResNet101 and Swin Transformer achieved AUCs of 0.986 (95% CI: 0.977-0.994) and 0.936 (95% CI: 0.912-0.957), respectively. The accuracy, sensitivity, and specificity of ResNet101 were 0.933, 0.979, and 0.869, respectively. The accuracy, sensitivity, and specificity of Swin Transformer were 0.851, 0.817, and 0.898, respectively. The ResNet101 model yielded higher AUC than models of all muscles and radiologists (0.986 vs. 0.905, 0.818; P<0.001). Conclusions: The DL models based on MRI T1-weighted scans could accurately diagnose GO, and the application of DL systems in MRI may improve radiologists' performance in diagnosing GO and early detection.

Piezoelectric Micromachined Ultrasonic Transducers with a Cost-Effective Bottom-Up Fabrication Scheme for Millimeter-Scale Range Finding.

This study proposes a novel piezoelectric micromachined ultrasonic transducer (PMUT), fabricated on a metal foil. Using a bottom-up, cost-effective micromachining technique, the PMUTs made of electrodes, a piezoelectric film, or electrode-sandwiched structures with versatile patterns were implemented on a large-area foil thinner rather than regular paper. The proposed microfabrication facilitated the PMUT to be able to generate ultrasonic waves with fundamental and harmonic resonances. The fourth-order resonances of the fabricated PMUT functionally operated at an ultrasonic spectrum of approximately 30 kHz as an ultrasonic emitter. The developed PMUT was paired with a microelectromechanical system (MEMS) microphone module for range-finding applications in the range of several tens of millimeters. A signal-processing scheme was developed to extract the representative pattern from the acquired signals that were emitted and received. The pattern enabled finding the distance between the PMUT and the microphone using time-of-flight and strength-variation technology. The developed PMUT-microphone pair demonstrated its range-finding performance, displaying an error of less than 0.7% using the time-of-flight method.

Sonic hedgehog signaling regulates hypoxia/reoxygenation-induced H9C2 myocardial cell apoptosis.

The sonic hedgehog (Shh) signaling pathway has been reported to protect cells against hypoxia/reoxygenation (H/R) injury; however, the role of Shh and relevant molecular mechanisms remain unclear. In the present study, the rat cardiomyoblast cell line H9C2 was subjected to hypoxia and serum-starvation for 4 h. Cells were subsequently reoxygenated using 95% O2 and 5% CO2. Reverse transcription-quantitative polymerase chain reaction was performed to quantify the expression of Shh mRNA, while cell apoptosis was assessed using flow cytometry. Caspase-3 activity and p53 expression were measured by western blotting and an MTT assay was subsequently used to assess cell viability. In addition, reactive oxygen species levels were measured using dichlorofluorescein and H/R-induced changes in the activation of superoxide dismutase, catalase, phosphorylated-endothelial nitric oxide synthase, phosphorylated-protein kinase B (Akt) and mammalian target of rapamycin activation were assessed using western blotting. H/R treatment decreased the cell viability of H9C2 cells, but activated endogenous Shh signaling. The activation of Shh signaling protected H9C2 myocardial cells from H/R-induced apoptosis and restored cell viability. In the present study, Shh signaling was demonstrated to serve a protective role against H/R by activating the phosphoinositol 3-kinase (PI3K)/Akt pathway and promoting the expression of anti-oxidant enzymes to ameliorate oxidative stress. In summary, Shh signaling attenuated H/R-induced apoptosis through via the PI3K/Akt pathway.

Diosgenin Protects Rats from Myocardial Inflammatory Injury Induced by Ischemia-Reperfusion.

BACKGROUND Diosgenin, a phytosteroid sapogenin, has anti-inflammatory properties shown to reduce myocardial ischemia-reperfusion injury (MIRI). However, the specific mechanism by which this is achieved is not clear. This study investigated the protective effects of diosgenin on myocardial ischemia/reperfusion (I/R) and the potential anti-inflammatory mechanisms. MATERIAL AND METHODS Healthy adult male SD rats, body weight (b.w.) 250-280 g, were used to model ischemia-reperfusion injury (IRI) and were administered diosgenin (50 mg/kg and 100 mg/kg b.w.) intragastrically for 4 consecutive weeks before surgery. The left anterior descending artery (LAD) was ligated to induce myocardial ischemia for 30 min and reperfusion for 30 min, 60 min, and 120 min while relevant indicators were detected. RESULTS Both 50 mg and 100 mg diosgenin oral administration increased left ventricular developed pressure (LVDP) and maximum changing rate of ventricular pressure (±dp/dtmax), decreased left ventricular end-diastolic pressure (LVEDP), and myocardial enzyme markers. TTC staining suggested that diosgenin reduced myocardial infarct size in the rat model. Pathological results showed that myocardial ischemia and inflammation were alleviated by diosgenin. In addition, the increased expression of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß) in serum, and myeloperoxidase (MPO) in myocardium were significantly suppressed by diosgenin administration. Diosgenin further inhibited the phosphorylation of transcription factor NF-κB and modulated the expression of downstream inflammatory cytokines by regulating the activation of p38-MAPK and JNK pathways. CONCLUSIONS Results demonstrate diosgenin plays an anti-inflammatory role in the protection of MIRI through regulation of p38-MAPK and JNK pathways and phosphorylation of NF-κB.

The effects of subclinical hypothyroidism on serum lipid level and TLR4 expression of monocyte in peripheral blood of rats.

OBJECTIVE: To observe effect of subclinical hypothyroidism (SCH) on serum lipid level and expression of toll-like receptor 4 (TLR4) in rats' peripheral blood mononuclear cells (PBMC). METHODS: Fifty Wistar female rats were divided into three groups: normal control (NC group; n=10), sham group (n=10), and L-T-4 (L-thyroxine) group (n=30, with thyroidectomy, fed with rich-calcium water after operation. 5 weeks later, abdominal subcutaneous injection of L-T-4: 0.95 µg/100g/d). 8 weeks later, the rats were killed then the peripheral blood was collected to determine the levels of serum thyroid-stimulating hormone (TSH), total thyroid hormone (TT4), total cholesterol (TC) and low density lipoprotein cholesterin (LDL-C). Rats in L-T-4 group were divided into normal lipid (NL) group) and high lipid (HL) group) according to lipid value of NC group. Monocytes were separated from blood to determine TLR4 expression by flow cytometry. RESULTS: In NL and HL groups TSH were higher than in NC and Sham groups (p<0.05). TT4 have no significant differences (p>0.05). TLR4, TLR4 mRNA, NF-κB (p65) were increased (p<0.05). TNF-α, IL-6 and IL-1ß were higher than in NC and sham groups (p<0.01). There were no significant differences of TLR4, TLR4 mRNA, NF-κB (p65), TNF-α, IL-6 and IL-1ß expression between NL and HL groups (p>0.05). CONCLUSION: TLR4, TLR4 mRNA, NF-κB (p65) of PBMC and TNF-α, IL-6, IL-1ß expression in serum were all increased in SCH rats, which was not related to serum dyslipidemia.

Ginkgo biloba extract reducing myocardium cells apoptosis by regulating apoptotic related proteins expression in myocardium tissues.

The Bax, cyt-c and caspase-3 proteins play an important role in regulating the myocardial apoptosis. Although very little is known about the specific signal pathways modulated by Ginkgo biloba extract (GBE), it seems advisable to suppose that GBE-induced antiapoptotic effect might be attributed to the regulation of the expression of these proteins. Our aim was to investigate whether GBE could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. In the myocardium ischemia reperfusion (IR) rat model, treatment of GBE (400 mg/kg) significantly decreased the cardiomyocyte cell apoptosis and myocardium infarction. Immunohistochemical analysis showed that GBE significantly inhibited I/R-induced increase of myocardial Bax, caspase-3, and cyt-c proteins expression. Western blot analysis confirmed results of immunohistochemical analysis. It is most likely that multiple pathways are involved in IR-induced apoptosis in rat myocardium cells. Therefore, these results demonstrate that GBE exhibits significant protective effect against myocardial I/R injury in rat heart, which is related to down-regulate Bax, cyt-c and caspase-3. Bcl-2 overexpression might prevent IR-induced apoptosis by inhibiting cytochrome c release from the mitochondria and block activation of caspase-3.