Fast bilateral weighted least square for the detail enhancement of COVID-19 chest X-rays.

Background: X-ray is an effective measure in the diagnosis of coronavirus disease 2019. However, it suffers from low visibility and poor details. A plausible solution is to decompose the captured images and enhance the details. The bilateral weighted least square model can be an effective tool for this task. However, it is highly computationally expensive. Method: In this article, we propose an efficient algorithm for the bilateral weighted least square model. We approximate the bilateral weight with the bilateral grid and then incorporate it into the optimization model. This significantly reduces the number of variables in the linear system. Therefore, the model can be efficiently solved. We employ the proposed algorithm to decompose the input X-rays into base and detail layers. The detail layers are then boosted and added back to the input to derive the detail-enhanced results. Results: The subjective results indicate that our method achieves higher contrast than the best-performing method (442.30>410.09, 426.40>403.34, 564.51>531.38). Furthermore, our method is highly efficient. It takes 0.92 s to process a 720P color image on an Intel i7-6700 CPU. The objective results derive from the chi-square test indicate that subjects hold more positive attitudes toward our detail-enhanced images than the original X-ray images (3.53>2.72, 3.42>2.61, 3.5>2.56). Conclusion: We have conducted extensive experiments to evaluate the proposed image detail enhancement method. It can be concluded that (1) our method could significantly improve the visibility of the X-ray images. (2) our method is fast and effective, thus facilitating real applications.

Lin28b delays vasculature aging by reducing platelet-derived growth factor-beta resistance in senescent vascular smooth muscle cells.

BACKGROUND AND AIMS: Platelet-derived growth factor-ß (PDGFB) is an important mediator of vascular smooth muscle cell (VSMC) proliferation, and PDGFB resistance is observed in senescent VSMCs. Lin28b is a stemness regulator in the embryo; however, its role in vasculature aging and VSMC senescence is unknown. We aimed to investigate whether Lin28b could restore the VSMC response to PDGFB and delay vasculature aging. METHODS: ApoE-/- mice were fed a high-fat diet for different weeks to establish an aging model. PDGFB resistance was observed using EdU staining in vessel culture in vitro. Quantitative polymerase chain reaction and in situ hybridization were used to detect let-7 expression. Senescence was identified by Western blotting, senescence-associated beta-galactosidase activity or Sudan Black B staining, and VSMC function was determined using CCK-8, migration, and enzyme-linked immunosorbent assays. RESULTS: Vessels from aged mice showed poor responses to PDGFB stimulation compared with those from young mice; similar results were found in senescent VSMCs. The expression levels of Lin28b and PDGF receptor-ß were downregulated in aging vasculature and senescent VSMCs, whereas let-7 family levels increased with aging and VSMC passage growth. Transfection of VSMCs with let-7c induced PDGFB resistance and accelerated VSMC senescence, whereas blocking let-7c restored PDGFB reactions in VSMCs. Overexpression of Lin28b protein by lentivirus resulted in the restoration of PDGFB reactions and delayed VSMC senescence, which was blocked by a let-7c mimic. CONCLUSIONS: This study reveals the role of Lin28b in delaying vasculature aging by decreasing senescent VSMC PDGFB resistance mediated by let-7.

Higenamine exerts an antispasmodic effect on cold-induced vasoconstriction by regulating the PI3K/Akt, ROS/α2C-AR and PTK9 pathways independently of the AMPK/eNOS/NO axis.

The present study aimed to investigate the antispasmodic effect of higenamine on cold-induced cutaneous vasoconstriction and the underlying molecular mechanisms. A cold-induced cutaneous vasoconstriction rat model was established and different doses of higenamine were delivered by intravenous injection. The changes of cutaneous regional blood flow (RBF) between groups were analyzed. In vitro, the proliferation of human dermal microvascular endothelial cells was measured by MTT. The NO concentration was detected by a nitrate reductase assay. Flow cytometry was applied to measure reactive oxygen species (ROS) levels. The protein expression levels were detected by western blotting. The results demonstrated that in the model group, RBF declined compared with the normal control group, but was reversed by treatment with higenamine. The expression of endothelial nitric oxide synthase (eNOS), phosphorylated (p)-eNOS, protein kinase B (Akt1), p-Akt1, AMP-activated protein kinase (AMPK) α1 and p-AMPKα1 was upregulated by hypothermic treatment but was reversed by higenamine treatment. Treatment with higenamine significantly reduced the level of intracellular α2C-adrenoreceptor (AR) compared with the hypothermia group (P<0.05). Furthermore, the expression of twinfilin-1 (PTK9) was downregulated in the higenamine and positive control groups compared with the hypothermia group (P<0.05). Compared with the hypothermia group, the levels of ROS and α2C-AR (intracellular & membrane) were decreased in higenamine and the positive control group (P<0.05 and P<0.01, respectively). This study, to the best of our knowledge, is the first to assess the effects of higenamine on cold-induced vasoconstriction in vivo and its molecular mechanisms on the PI3K/Akt, AMPK/eNOS/nitric oxide, ROS/α2C-AR and PTK9 signaling pathways under hypothermia conditions. Higenamine may be a good therapeutic option for Raynaud's phenomenon (RP) and cold-induced vasoconstriction.

[Clinical studies on level of N-terminal portion of brain natriuretic in the treatment and prognosis of Chinese patients with chronic left heart failure].

OBJECTIVE: To study the relationship of the level of N-terminal portion of brain natriuretic (NT-ProBNP) with the treatment and prognosis of patients with acute attack of chronic left heart failure. METHODS: Patients (age range 18-80 years) with decompensated heart failure treated in the emergency department in Fuwai Hospital were included in this study. Dynamic changes of plasma levels of NT-ProBNP, angiotensin (AO), renin activity (PRA), angiotensin II (AT II) and aldosterone (ALD) were detected by enzyme linked immunoadsorbent assay (ELISA) before anti-cardiac failure treatment and 3-5, 5-7 days after the treatment. All enrolled patients were followed up for 2 years after leaving hospital, and cardiovascular events such as death, myocardial infarction, worsening of heart failure, severe arrhythmia or delayed discharge from hospital were recorded. RESULTS: Compared with baseline level at admission, plasma NT-ProBNP levels were lowered on 3rd -5th day and 5th-7th day after admission and treatment (both P<0.05) in 44 patients with chronic left heart failure, but there was no difference in NT-ProBNP levels between the 3rd-5th and 5th -7th day after treatment. The levels of plasma NT-ProBNP increased much higher at all observation times in patients with cardiovascular events than without the events (all P<0.05), but the changes in AO, PRA, ATII and ALD showed no significant difference between two groups (all P>0.05). CONCLUSION: During acute onset, plasma NT-ProBNP levels in patients with chronic left heart failure can be lowered at 3-7 days after admission and treatment. Higher baseline levels of plasma NT-ProBNP may have certain predictive values for long term prognosis in patients with chronic left heart failure.

[Prognostic value of N-terminal-pro-brain natriuretic peptide on admission in patients with chronic heart failure].

OBJECTIVE: Heart failure is responsible for a huge burden in hospital care. Our goal was to evaluate the value of N-terminal-pro-brain natriuretic peptide (Nt-proBNP) on predicting death or hospital readmission after hospital discharge in patients with chronic heart failure (CHF). METHODS: From March 2003 to April 2005, 135 consecutive patients (97 male and 38 female, mean age 60.7 years +/- 13.1 years) with chronic heart failure [dilated cardiomyopathy (44%) and coronary heart disease (35%)] were included in this study. Plasma concentrations of the Nt-proBNP were measured by ELISA on admission. All patients received conventional therapy and were followed up for 24 months. The primary end point was death or readmission. RESULTS: (1) During the follow up period (640 days +/- 100 days), 11 patients died and 39 patients rehospitalized, the median Nt-proBNP level on admission was significantly higher in patients died during the follow up period (5908 ng/L) than that of rehospitalized patients (2768 ng/L, P = 0.038). Plasma Nt-proBNP level on admission were significantly higher in primary end point group (n = 50, 2947 ng/L) than that in non-primary end point group (n = 85, 917 ng/L, P < 0.01). (2) Variables associated with an increased hazard of death and/or rehospitalization were Nt-proBNP and NYHA degree when analyzed by logistic regression models. Increased Log Nt-proBNP was the strongest independent predictor of an adverse outcome of CHF (odds ratio 13.8, 95% confidence interval 2.29 to 2.78, P < 0.01). (3) Area under the curve for Nt-proBNP in evaluating prognosis of CHF patients was 0.885 (positive predictive value 88.5%, negative predictive value 11.5%). CONCLUSION: Nt-proBNP level on admission is a strong predictor of rehospitalization and death within 24 months after hospital discharge in patients with chronic heart failure.