Graph Signal Restoration Using Nested Deep Algorithm Unrolling

Graph signal processing is a ubiquitous task in many applications such as sensor, social, transportation and brain networks, point cloud processing, and graph neural networks. Graph signals are often corrupted through sensing processes, and need to be restored for the above applications. In this paper, we propose two graph signal restoration methods based on deep algorithm unrolling (DAU). First, we present a graph signal denoiser by unrolling iterations of the alternating direction method of multiplier (ADMM). We then propose a general restoration method for linear degradation by unrolling iterations of Plug-and-Play ADMM (PnP-ADMM). In the second method, the unrolled ADMM-based denoiser is incorporated as a submodule. Therefore, our restoration method has a nested DAU structure. Thanks to DAU, parameters in the proposed denoising/restoration methods are trainable in an end-to-end manner. Since the proposed restoration methods are based on iterations of a (convex) optimization algorithm, the method is interpretable and keeps the number of parameters small because we only need to tune graph-independent regularization parameters. We solve two main problems in existing graph signal restoration methods: 1) limited performance of convex optimization algorithms due to fixed parameters which are often determined manually. 2) large number of parameters of graph neural networks that result in difficulty of training. Several experiments for graph signal denoising and interpolation are performed on synthetic and real-world data. The proposed methods show performance improvements to several existing methods in terms of root mean squared error in both tasks

Atherosclerotic plaque behind the stent changes after bare-metal and drug-eluting stent implantation in humans: Implications for late stent failure?

Background and aims The natural history and the role of atherosclerotic plaque located behind the stent (PBS) are still poorly understood. We evaluated the serial changes in PBS following bare-metal (BMS) compared to first-generation drug-eluting stent (DES) implantation and the impact of these changes on in-stent neointimal hyperplasia (NIH). Methods Three-dimensional coronary reconstruction by angiography and intravascular ultrasound was performed after intervention and at 6–10-month follow-up in 157 patients with 188 lesions treated with BMS (n = 89) and DES (n = 99). Results There was a significant decrease in PBS area (−7.2%; p  <  0.001) and vessel area (−1.7%; p  <  0.001) after BMS and a respective increase in both areas after DES implantation (6.1%; p  <  0.001 and 4.1%; p  <  0.001, respectively). The decrease in PBS area significantly predicted neointimal area at follow-up after BMS (β: 0.15; 95% confidence interval [CI]: 0.10–0.20, p  <  0.001) and DES (β: 0.09; 95% CI: 0.07–0.11; p  <  0.001) implantation. The decrease in PBS area was the most powerful predictor of significant NIH after BMS implantation (odds ratio: 1.13; 95% CI: 1.02–1.26; p = 0.02). Conclusions The decrease in PBS area after stent implantation is significantly associated with the magnitude of NIH development at follow-up. This finding raises the possibility of a communication between the lesion within the stent and the underlying native atherosclerotic plaque, and may have important implications regarding the pathobiology of in-stent restenosis and late/very late stent thrombosis

Arterial Remodeling and Endothelial Shear Stress Exhibit Significant Longitudinal Heterogeneity Along the Length of Coronary Plaques

Atherosclerosis is determined by both systemic risk factors and local vascular mechanisms. The arterial remodeling in response to plaque development plays a key role in atherosclerosis. Compensatory expansive remodeling is an adaptive mechanism that maintains lumen patency as a plaque develops. In contrast, excessive expansive remodeling, signifying an enlargement in vascular and lumen volume as a result of local plaque buildup, is a consistent attribute of high-risk plaques. Local hemodynamic factors, in particular low endothelial shear stress (ESS), is an intensely proinflammatory and proatherogenic stimulus and largely accounts for the spatially diverse distribution of atherosclerotic plaques. However, plaque, remodeling and ESS have hitherto been investigated only in the cross-sectional arterial axis and their distribution in the longitudinal axis of individual plaques has not been characterized

Tilt Angle and Theoretical Target Strength of the Japanese Sandeel, Ammodytes personatus Captured on the Northern Coast of Hokkaido, Japan.

The tilt angle, i.e., the angle from horizontal made by the fish body as its head dives down or up, affects the readings on fish echo soundings. We measured the tilt angle of Japanese sandeels (Ammodytes personatus Girard) in a water tank, and calculated the acoustic target strength (TS) using a theoretical scattering model. This study examined the TS of sandeels from the northern coast of Hokkaido, which have a larger body size than those in other regions in Japan. TS values for sandeels, a swimbladderless fish, were estimated using a distorted-wave Born approximation (DWBA) model at two frequencies: 38 and 120 kHz. The mean tilt angle was 20.4?? (S.D. = 18.5??), which differed slightly from that of the lesser sandeel, Ammodytes marinus. The regression equations of the average TS values were TS38kHz = 8.2 log10SL ??? 74.2 and TS120kHz = 20.9 log10SL ??? 92.6, respectively. At 120 kHz, the slope was close to 20, suggesting that the acoustic backscattering strength was proportional to the square of the body length. This value was smaller at 38 kHz, suggesting that the acoustic backscattering strength was stable to differences in body length. We obtained a small discrepancy for both frequencies (??TS = TS120kHz???TS38kHz) were TS120kHz < TS38kHz. Discrepancies of ???1.3 dB for the maximum TS, and ???1.8 dB for averaged TS were found in 72 fish samples, which would be useful for identifying sandeel schools in practical analysis using TS differences

Targeting Ovarian Cancer Cells Overexpressing CD44 with Immunoliposomes Encapsulating Glycosylated Paclitaxel

Paclitaxel (PTX) is one of the front-line drugs approved for the treatment of ovarian cancer. However, the application of PTX is limited due to the significant hydrophobicity and poor pharmacokinetics. We previously reported target-directed liposomes carrying tumor-selective conjugated antibody and encapsulated glycosylated PTX (gPTX-L) which successfully overcome the PTX limitation. The tubulin stabilizing activity of gPTX was equivalent to that of PTX while the cytotoxic activity of gPTX was reduced. In human ovarian cancer cell lines, SK-OV-3 and OVK18, the concentration at which cell growth was inhibited by 50% (IC50) for gPTX range from 15⁻20 nM, which was sensitive enough to address gPTX-L with tumor-selective antibody coupling for ovarian cancer therapy. The cell membrane receptor CD44 is associated with cancer progression and has been recognized as a cancer stem cell marker including ovarian cancer, becoming a suitable candidate to be targeted by gPTX-L therapy. In this study, gPTX-loading liposomes conjugated with anti-CD44 antibody (gPTX-IL) were assessed for the efficacy of targeting CD44-positive ovarian cancer cells. We successfully encapsulated gPTX into liposomes with the loading efficiency (LE) more than 80% in both of gPTX-L and gPTX-IL with a diameter of approximately 100 nm with efficacy of enhanced cytotoxicity in vitro and of convenient treatment in vivo. As the result, gPTX-IL efficiently suppressed tumor growth in vivo. Therefore gPTX-IL could be a promising formulation for effective ovarian cancer therapies

Chronic Hepatitis B Virus Infection and Rubella Susceptibility Among Obstetric Population in Metropolis Antenatal Centre Kano, Nigeria

It is well known that hepatitis B virus (HBV) infection is endemic in Nigeria. However, increased rubella susceptibility has been shown in patients from the Asian pacific region where chronic HBV infection is endemic. This study was carried out to assess the relationship between chronic HBV infection and rubella susceptibility in obstetric population aged 15–47 years attending Antenatal Clinic at Muhammad Abdullahi Wase Specialist Hospital Kano, Nigeria. From a total of 288 patients screened, 31 (10.76%) were reactive for HBsAg, meanwhile 50 (17.36%) were reactive to rubella IgM. Among the 31 infected patients 15 (48.39%) were from 20 – 24 years age bracket representing the most  susceptible age group while the infection rate was lowest (0.35%) in 45 – 49  age group (P = 0.00). The results of serological markers shows that HBsAg (+) was found in all 31 subjects (100%), anti HBs (+) 0 (0.00%), HBeAg (+) 3 (9.68%); anti HBe (+) and anti HBc (+) 24 (77.42%) respectively (P = 0.09). The study of liver enzymes activity among the HBV positive patients shows abnormal Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) among HBsAg (+) and HBeAg (+) group. However, abnormal Alkaline phospatase (ALP) was found to be non-significantly different between HBsAg (+) and HBeAg (+) vsHBsAg (+) and HBeAg (-) groups (P=0.00). Moreover, obstetric histories such as abortion still birth and neonatal deaths among various age groups with respect to rubella was also studied, it implies that  out of the 50 reactive patients, 35(12.15%) had a previous abnormal obstetric history (P=0.02). In a comparative study conducted, it was observed that HBV carriers were (25.81%) susceptible to rubella as against (12.91%) observed in HBV free subjects (positive correlation). The study demonstrates strong associations between chronic HBV infection and rubella susceptibility among the studied population

Chloroquine potentiates the anti-cancer effect of 5-fluorouracil on colon cancer cells

<p>Abstract</p> <p>Background</p> <p>Chloroquine (CQ), the worldwide used anti-malarial drug, has recently being focused as a potential anti-cancer agent as well as a chemosensitizer when used in combination with anti-cancer drugs. It has been shown to inhibit cell growth and/or to induce cell death in various types of cancer. 5-Fluorouracil (5-FU) is the chemotherapeutic agent of first choice in colorectal cancer, but in most cases, resistance to 5-FU develops through various mechanisms. Here, we focused on the combination of CQ as a mechanism to potentiate the inhibitory effect of 5-FU on human colon cancer cells.</p> <p>Methods</p> <p>HT-29 cells were treated with CQ and/or 5-FU, and their proliferative ability, apoptosis and autophagy induction effects, and the affection of the cell cycle were evaluated. The proliferative ability of HT-29 was analyzed by the MTS assay. Apoptosis was quantified by flow-cytometry after double-staining of the cells with AnnexinV/PI. The cell cycle was evaluated by flow-cytometry after staining of cells with PI. Autophagy was quantified by flow-cytometry and Western blot analysis. Finally, to evaluate the fate of the cells treated with CQ and/or 5-FU, the colony formation assay was performed.</p> <p>Results</p> <p>5-FU inhibited the proliferative activity of HT-29 cells, which was mostly dependent on the arrest of the cells to the G0/G1-phase but also partially on apoptosis induction, and the effect was potentiated by CQ pre-treatment. The potentiation of the inhibitory effect of 5-FU by CQ was dependent on the increase of p21^Cip1and p27^Kip1and the decrease of CDK2. Since CQ is reported to inhibit autophagy, the catabolic process necessary for cell survival under conditions of cell starvation or stress, which is induced by cancer cells as a protective mechanism against chemotherapeutic agents, we also analyzed the induction of autophagy in HT-29. HT-29 induced autophagy in response to 5-FU, and CQ inhibited this induction, a possible mechanism of the potentiation of the anti-cancer effect of 5-FU.</p> <p>Conclusion</p> <p>Our findings suggest that the combination therapy with CQ should be a novel therapeutic modality to improve efficacy of 5-FU-based chemotherapy, possibly by inhibiting autophagy-dependent resistance to chemotherapy.</p

Potential use of COX-2–aromatase inhibitor combinations in breast cancer

Cyclooxygenase-2 (COX-2) is overexpressed in several epithelial tumours, including breast cancer. Cyclooxygenase-2-positive tumours tend to be larger, higher grade, node-positive and HER-2/neu-positive. High COX-2 expression is associated with poor prognosis. Cyclooxygenase-2 inhibition reduces the incidence of tumours in animal models, inhibits the development of invasive cancer in colorectal cancer and reduces the frequency of polyps in familial adenomatous polyposis (FAP). These effects may be as a result of increased apoptosis, reduced angiogenesis and/or proliferation. Studies of COX-2 inhibitors in breast cancer are underway both alone and in combination with other agents. There is evidence to suggest that combining COX-2 inhibitors with aromatase inhibitors, growth factor receptor blockers, or chemo- or radiotherapy may be particularly effective. Preliminary results from combination therapy with celecoxib and exemestane in postmenopausal women with advanced breast cancer showed that the combination increased the time to recurrence. Up to 80% of ductal carcinomas in situ (DCISs) express COX-2, therefore COX-2 inhibition may be of particular use in this situation. Cyclooxygenase-2 expression correlates strongly with expression of HER-2/neu. As aromatase inhibitors appear particularly effective in patients with HER-2/neu-positive tumours, the combination of aromatase inhibitors and COX-2 inhibitors may be particularly useful in both DCIS and invasive cancer

Effects of Low Endothelial Shear Stress After Stent Implantation on Subsequent Neointimal Hyperplasia and Clinical Outcomes in Humans

Background: In‐stent hyperplasia (ISH) may develop in regions of low endothelial shear stress (ESS), but the relationship between the magnitude of low ESS, the extent of ISH, and subsequent clinical events has not been investigated. Methods and Results: We assessed the association of poststent ESS with neointimal ISH and clinical outcomes in patients treated with percutaneous coronary interventions (PCI). Three‐dimensional coronary reconstruction was performed in 374 post‐PCI patients at baseline and 6 to 10 months follow‐up as part of the PREDICTION Study. Each vessel was divided into 1.5‐mm‐long segments, and we calculated the local ESS within each stented segment at baseline. At follow‐up, we assessed ISH and the occurrence of a clinically indicated repeat PCI for in‐stent restenosis. In 246 total stents (54 overlapping), 100 (40.7%) were bare‐metal stents (BMS), 104 (42.3%) sirolimus‐eluting stents, and 42 (17.1%) paclitaxel‐eluting stents. In BMS, low ESS post‐PCI at baseline was independently associated with ISH (β=1.47 mm2 per 1‐Pa decrease; 95% CI, 0.38–2.56; P<0.01). ISH was minimal in drug‐eluting stents. During follow‐up, repeat PCI in BMS was performed in 21 stents (8.5%). There was no significant association between post‐PCI ESS and in‐stent restenosis requiring PCI. Conclusions: Low ESS after BMS implantation is associated with subsequent ISH. ISH is strongly inhibited by drug‐eluting stents. Post‐PCI ESS is not associated with in‐stent restenosis requiring repeat PCI. ESS is an important determinant of ISH in BMS, but ISH of large magnitude to require PCI for in‐stent restenosis is likely attributed to factors other than ESS within the stent