Competitive Swarm Optimized SVD Clutter Filtering for Ultrafast Power Doppler Imaging.

Ultrafast power Doppler imaging (uPDI) can significantly increase the sensitivity of resolving small vascular paths in ultrasound. While clutter filtering is a fundamental and essential method to realize uPDI, it commonly uses singular value decomposition (SVD) to suppress clutter signals and noise. However, current SVD-based clutter filters using two cutoffs cannot ensure sufficient separation of tissue, blood, and noise in uPDI. This article proposes a new competitive swarm-optimized SVD clutter filter to improve the quality of uPDI. Specifically, without using two cutoffs, such a new filter introduces competitive swarm optimization (CSO) to search for the counterparts of blood signals in each singular value. We validate the CSO-SVD clutter filter on public in vivo datasets. The experimental results demonstrate that our method can achieve higher contrast-to-noise ratio (CNR), signal-to-noise ratio (SNR), and blood-to-clutter ratio (BCR) than the state-of-the-art SVD-based clutter filters, showing a better balance between suppressing clutter signals and preserving blood signals. Particularly, our CSO-SVD clutter filter improves CNR by 0.99 ± 0.08 dB, SNR by 0.79 ± 0.08 dB, and BCR by 1.95 ± 0.03 dB when comparing a spatial-similarity-based SVD clutter filter in the in vivo dataset of rat brain bolus.

Fasudil hydrochloride hydrate, a Rho-kinase inhibitor, ameliorates hepatic fibrosis in rats with type 2 diabetes.

BACKGROUND: Hyperglycemia may accelerate liver fibrosis. Currently, there is no effective treatment for liver fibrosis induced by type 2 diabetes. The study aim was to investigate whether RhoA/Rho kinase (ROCK) pathway is involved in liver fibrosis in the rats with type 2 diabetes and define the protective effects of fasudil on livers. METHODS: A rat model of type 2 diabetes was established by high fat diet combined with streptozotocin (30 mg/kg, intraperitoneal injection). Animals were randomly assigned to 3 groups: control rats, untreated diabetic rats that received vehicle and fasudil-treated diabetic rats that received ROCK inhibitor fasudil hydrochloride hydrate (10 mg/kg per day, intraperitoneal injection, for 14 weeks). The morphological features of liver were observed by HE staining. Accumulation of collagen in livers was determined by Masson staining and the measurement of hydroxyproline. The mRNA expression of transforming growth factor-ß1 (TGFß1), connective tissue growth factor (CTGF), type-I, and type-III procollagen was assessed with real-time polymerase chain reaction. The phosphorylation of myosin phosphatase target subunit-1 (MYPT1) and the protein levels of TGFß1 and α-smooth muscle actin (a-SMA) were evaluated by Western blotting. RESULTS: Compared with control rats, untreated diabetic rats showed higher values of collagen and hydroxyproline in livers (P < 0.01), the phosphorylation of MYPT1 and the protein levels of TGFß1 and α-SMA were increased (P < 0.01), and the mRNA expression of TGFß1, CTGF, type-I, and type-III procollagen was upregulated (P < 0.01); compared with untreated diabetic rats, treatment with fasudil signifcantly reduced values of collagen and hydroxyproline (P < 0.01), and decreased the phosphorylation of MYPT1 and the levels of TGFß1 and α-SMA (P < 0.01), concomitant with the downregulation of TGFß1/CTGF, type-I, and type-III procollagen mRNA expression (P < 0.01). CONCLUSIONS: Fasudil ameliorates liver fibrosis in rats with type 2 diabetes at least partly by inhibiting TGFß1/CTGF pathway and α-SMA expression. Inhibition of RhoA/ROCK may be a novel therapeutic target for liver fibrosis in diabetic non-alcoholic steatohepatitis.

Involvement of RhoA/ROCK in myocardial fibrosis in a rat model of type 2 diabetes.

AIM: To investigate whether activation of RhoA/Rho kinase (ROCK) is involved in myocardial fibrosis in diabetic hearts. METHODS: A rat model of type 2 diabetes was established using high fat diet combined with streptozotocin (30 mg/kg, ip). Animals were randomly divided into 3 groups: control rats, untreated diabetic rats that received vehicle and treated diabetic rats that received Rho-kinase inhibitor fasudil hydrochloride hydrate (10 mg·kg(-1)·d(-1), ip, for 14 weeks). Cardiac contractile function was evaluated in vivo. The morphological features of cardiac fibrosis were observed using immunohistochemistry and TEM. The mRNA expression of JNK, TGFß1, type-I, and type-III procollagen was assessed with RT-PCR. The phosphorylation of MYPT1, JNK and Smad2/3, as well as the protein levels of TGFß1 and c-Jun, were evaluated using Western blotting. RESULTS: In untreated diabetic rats, myocardial fibrosis was developed and the heart contractility was significantly reduced as compared to the control rats. In the hearts of untreated diabetic rats, the mRNA expression level and activity of JNK were upregulated; the expression of TGFß1 and phosphorylation of Smad2/3 were increased. In the hearts of treated diabetic rat, activation of JNK and TGFß/Smad was significantly decreased, myocardial fibrosis was reduced, and cardiac contractile function improved. CONCLUSION: The data suggest that fasudil hydrochloride hydrate ameliorates myocardial fibrosis in rats with type 2 diabetes at least in part through inhibiting the JNK and TGFß/Smad pathways. Inhibition of RhoA/ROCK may be a novel therapeutic target for prevention of diabetic cardiomyopathy.