AutoShrink: A Topology-aware NAS for Discovering Efficient Neural Architecture

Resource is an important constraint when deploying Deep Neural Networks (DNNs) on mobile and edge devices. Existing works commonly adopt the cell-based search approach, which limits the flexibility of network patterns in learned cell structures. Moreover, due to the topology-agnostic nature of existing works, including both cell-based and node-based approaches, the search process is time consuming and the performance of found architecture may be sub-optimal. To address these problems, we propose AutoShrink, a topology-aware Neural Architecture Search(NAS) for searching efficient building blocks of neural architectures. Our method is node-based and thus can learn flexible network patterns in cell structures within a topological search space. Directed Acyclic Graphs (DAGs) are used to abstract DNN architectures and progressively optimize the cell structure through edge shrinking. As the search space intrinsically reduces as the edges are progressively shrunk, AutoShrink explores more flexible search space with even less search time. We evaluate AutoShrink on image classification and language tasks by crafting ShrinkCNN and ShrinkRNN models. ShrinkCNN is able to achieve up to 48% parameter reduction and save 34% Multiply-Accumulates (MACs) on ImageNet-1K with comparable accuracy of state-of-the-art (SOTA) models. Specifically, both ShrinkCNN and ShrinkRNN are crafted within 1.5 GPU hours, which is 7.2x and 6.7x faster than the crafting time of SOTA CNN and RNN models, respectively

Insulin autoimmune syndrome caused by esomeprazole in a Chinese patient

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Autotaxin expression and its connection with the TNF-alpha-NF-κB axis in human hepatocellular carcinoma

<p>Abstract</p> <p>Background</p> <p>Autotaxin (ATX) is an extracellular lysophospholipase D that generates lysophosphatidic acid (LPA) from lysophosphatidylcholine (LPC). Both ATX and LPA have been shown to be involved in many cancers. However, the functional role of ATX and the regulation of ATX expression in human hepatocellular carcinoma (HCC) remain elusive.</p> <p>Results</p> <p>In this study, ATX expression was evaluated in tissues from 38 human HCC and 10 normal control subjects. ATX was detected mainly in tumor cells within tissue sections and its over-expression in HCC was specifically correlated with inflammation and liver cirrhosis. In addition, ATX expression was examined in normal human hepatocytes and liver cancer cell lines. Hepatoma Hep3B and Huh7 cells displayed stronger ATX expression than hepatoblastoma HepG2 cells and normal hepatocytes did. Proinflammtory cytokine tumor necrosis factor alpha (TNF-α) promoted ATX expression and secretion selectively in Hep3B and Huh7 cells, which led to a corresponding increase in lysophospholipase-D activity. Moreover, we explored the mechanism governing the expression of ATX in hepatoma cells and established a critical role of nuclear factor-kappa B (NF-κB) in basal and TNF-α induced ATX expression. Further study showed that secreted enzymatically active ATX stimulated Hep3B cell invasion.</p> <p>Conclusions</p> <p>This report highlights for the first time the clinical and biological evidence for the involvement of ATX in human HCC. Our observation that links the TNF-α/NF-κB axis and the ATX-LPA signaling pathway suggests that ATX is likely playing an important role in inflammation related liver tumorigenesis.</p

Acute Iloprost Inhalation Improves Right Ventricle Function in Pulmonary Artery Hypertension: A Cardiac Magnetic Resonance Study

Background: Right ventricle (RV) function is among the most important prognostic factors for pulmonary arterial hypertension (PAH) patients. Inhaled iloprost, an inhaled member of the prostacyclin family, is effective for the treatment of severe PAH and acute RV failure. However, the acute effects of iloprost on RV physiology have not been thoroughly explored in the past.Materials and Methods: This prospective study involved 69 incident PAH patients, including 23 idiopathic PAH (IPAH) patients, 26 patients with PAH associated with connective tissue disease (CTD-PAH) and 20 with PAH associated with congenital heart disease (CHD-PAH). All patients underwent both right heart catheterization and cardiac magnetic resonance imaging at baseline and 20 min after 5 μg iloprost inhalation.Results: Acute iloprost inhalation reduced PVR from 13 ± 7 to 10 ± 6 Wood U (P &lt; 0.001), increased RV ejection fraction (RVEF) from 31 ± 11 to 35 ± 12 % (P &lt; 0.001), increased RV stroke volume from 53 ± 21 to 57 ± 22 ml (P &lt; 0.001) and decreased RV end-diastolic volume from 179 ± 67 to 172 ± 69 ml (P &lt; 0.001). Acute iloprost inhalation-induced RVEF improvement was correlated with the degree of PVR reduction (P &lt; 0.001) in IPAH patients, but not in CTD-PAH or CHD-PAH patients.Conclusion: Acute iloprost inhalation improved RVEF, RV stroke volume and decreased RV volume in IPAH and CTD-PAH patients. Iloprost-induced RVEF increase was proportional to PVR reduction in IPAH patients, but not in CTD-PAH or CHD-PAH patients

Expression of the Splicing Factor Gene SFRS10 Is Reduced in Human Obesity and Contributes to Enhanced Lipogenesis

SummaryAlternative mRNA splicing provides transcript diversity and may contribute to human disease. We demonstrate that expression of several genes regulating RNA processing is decreased in both liver and skeletal muscle of obese humans. We evaluated a representative splicing factor, SFRS10, downregulated in both obese human liver and muscle and in high-fat-fed mice, and determined metabolic impact of reduced expression. SFRS10-specific siRNA induces lipogenesis and lipid accumulation in hepatocytes. Moreover, Sfrs10 heterozygous mice have increased hepatic lipogenic gene expression, VLDL secretion, and plasma triglycerides. We demonstrate that LPIN1, a key regulator of lipid metabolism, is a splicing target of SFRS10; reduced SFRS10 favors the lipogenic β isoform of LPIN1. Importantly, LPIN1β-specific siRNA abolished lipogenic effects of decreased SFRS10 expression. Together, our results indicate that reduced expression of SFRS10, as observed in tissues from obese humans, alters LPIN1 splicing, induces lipogenesis, and therefore contributes to metabolic phenotypes associated with obesity

Prevalence and Characterization of Staphylococcus aureus Isolated From Women and Children in Guangzhou, China

The prevalent Staphylococcus aureus clones and antibiotic susceptibility profiles are known to change dynamically and geographically; however, recent S. aureus strains causing infections in women and children in China have not been characterized. In this study, we analyzed the molecular epidemiology and antimicrobial resistance of S. aureus isolated from patients in four centers for women and children in Guangzhou, China. In total, 131 S. aureus isolates (100 from children and 31 from women) were analyzed by spa typing, multi-locus sequence typing, virulence gene and antimicrobial resistance profiling, staphylococcal chromosomal cassette mec typing, and mutation analyses of rpoB. A total of 58 spa types, 27 sequence types (STs), and 10 clonal complexes (CCs) were identified. While CC59 (ST59-IV, 48.8%; ST338-III, 35.7%) and CC45 (ST45-IV, 100%) were the major clones (84.4%) among MRSA isolates, CC5 (ST188, 24.3%; ST1, 21.6%) and CC398 (ST398, 70%) were the major ones (70.1%) among MSSA isolates. ST338-MRSA-III mostly found in pus but hardly in respiratory tract samples while ST45-MRSA-IV was on the opposite, even though they both found in blood and cerebrospinal fluid sample frequently. Staphylococcal enterotoxin genes seb-seq-sek were strongly associated with ST59 and ST338, while sec was associated with ST45, ST121, ST22, and ST30. All ST338, ST1232, and SCCmec III isolates carried lukF/S-PV genes. A total of 80% of ST338 isolates were resistant to erythromycin, clindamycin, and tetracycline. All ST45 isolates exhibited intermediate or complete resistance to rifampicin. In total, 481 HIS/ASN mutations in rpoB were found in rifampicin-resistant or intermediate-resistant isolates. ST338-III and ST45-IV emerged as two of three major clones in MRSA isolates from women and children in Guangzhou, China, though ST59-MRSA-IV remained the most prevalent MRSA clone. Clonal distribution of S. aureus varied, depending on the specimen source. Virulence genes and antibiograms were closely associated with the clonal lineage. These results clarified the molecular epidemiology of S. aureus from women and children in Guangzhou, China, and provide critical information for the control and treatment of S. aureus infections

Abnormalities in Osteoclastogenesis and Decreased Tumorigenesis in Mice Deficient for Ovarian Cancer G Protein-Coupled Receptor 1

Ovarian cancer G protein-coupled receptor 1 (OGR1) has been shown to be a proton sensing receptor in vitro. We have shown that OGR1 functions as a tumor metastasis suppressor gene when it is over-expressed in human prostate cancer cells in vivo. To examine the physiological functions of OGR1, we generated conditional OGR1 deficient mice by homologous recombination. OGR1 deficient mice were viable and upon gross-inspection appeared normal. Consistent with in vitro studies showing that OGR1 is involved in osteoclastogenesis, reduced osteoclasts were detected in OGR1 deficient mice. A pH-dependent osteoclasts survival effect was also observed. However, overall abnormality in the bones of these animals was not observed. In addition, melanoma cell tumorigenesis was significantly inhibited in OGR1 deficient mice. OGR1 deficient mice in the mixed background produced significantly less peritoneal macrophages when stimulated with thioglycolate. These macrophages also showed altered extracellular signal-regulated kinases (ERK) activation and nitric oxide (NO) production in response to lipopolysaccharide. OGR1-dependent pH responses assessed by cAMP production and cell survival in macrophages or brown fat cells were not observed, presumably due to the presence of other proton sensing receptors in these cells. Our results indicate that OGR1's role in osteoclastogenesis is not strong enough to affect overall bone development and its role in tumorigenesis warrants further investigation. The mice generated can be potentially used for several disease models, including cancers or osteoclast-related diseases