Multi-dimensional Circular Supply Chain Management: A Comparative Review of the State-of-the-art Practices and Research

The circular economy (CE) concept has gained wide attention in practice as well as in academia in recent years. This paper reviews the state-of-the-art practices and research in “circular supply chain management” (CSCM), i.e., the integration of CE thinking into supply chain management (SCM) with the goal of achieving “zero wastes”. The review covers 68 real-life CE implementation cases collected by the Ellen MacArthur Foundation and 124 publications in well-established, high-ranking academic journals in operations and supply chain management. The comparative review shows that CSCM encompasses multiple dimensions, including closed-loop SCM, reverse SCM, remanufacturing SCM, recycling SCM, and industrial symbiosis. A multi-dimensional CSCM (MD-CSCM) framework is developed to synthesize their interrelationships and to categorize academic publications into multiple research themes. Based on the identified research-practice gaps and pressing research needs, this study discusses important directions for future studies to advance supply chain circularity

Gastrojejunocolic fistula after gastrojejunostomy: a case series

<p>Abstract</p> <p>Introduction</p> <p>Gastrojejunocolic (GJC) fistulae represent a significant post-surgical cause of morbidity and mortality. GJC fistulae represent rare post-surgical complications, and most are associated with gastric surgery. In the past, this complication has been under-recognized because a fistula may form years after surgery.</p> <p>Case presentation</p> <p>We describe two cases of gastrojejunocolic fistula in men aged 67 and 60 who both initially presented with watery diarrhea and weight loss. Upper GI studies with small bowel follow-through or barium contrast enema studies allowed a conclusive diagnosis to be made. Both patients underwent one-stage en bloc resection, and their postoperative course was uneventful.</p> <p>Conclusion</p> <p>With surgery, this condition is entirely correctable. Pre-operative nutritional status should be evaluated in patients undergoing corrective surgery, and total parenteral nutrition plays a major role in the provision of bowel rest to allow recovery in malnourished patients.</p

A3^{3}COSMOS: Dissecting the gas content of star-forming galaxies across the main sequence at 1.2 ≤z\leq z < 1.6

We aim to understand the physical mechanisms that drive star formation in a sample of mass-complete (>10$^{9.5}M_{\odot}$) star-forming galaxies (SFGs) at 1.2 $\leq z$ < 1.6. We selected SFGs from the COSMOS2020 catalog and applied a $uv$-domain stacking analysis to their archival Atacama Large Millimeter/submillimeter Array (ALMA) data. Our stacking analysis provides precise measurements of the mean molecular gas mass and size of SFGs. We also applied an image-domain stacking analysis on their \textit{HST} $i$-band and UltraVISTA $J$- and $K_{\rm s}$-band images. Correcting these rest-frame optical sizes using the $R_{\rm half-stellar-light}$-to-$R_{\rm half-stellar-mass}$ conversion at rest 5,000 angstrom, we obtain the stellar mass size of MS galaxies. Across the MS (-0.2 < $\Delta$MS < 0.2), the mean molecular gas fraction of SFGs increases by a factor of $\sim$1.4, while their mean molecular gas depletion time decreases by a factor of $\sim$1.8. The scatter of the MS could thus be caused by variations in both the star formation efficiency and molecular gas fraction of SFGs. The majority of the SFGs lying on the MS have $R_{\rm FIR}$ $\approx$ $R_{\rm stellar}$. Their central regions are subject to large dust attenuation. Starbursts (SBs, $\Delta$MS>0.7) have a mean molecular gas fraction $\sim$2.1 times larger and mean molecular gas depletion time $\sim$3.3 times shorter than MS galaxies. Additionally, they have more compact star-forming regions ($\sim$2.5~kpc for MS galaxies vs. $\sim$1.4~kpc for SBs) and systematically disturbed rest-frame optical morphologies, which is consistent with their association with major-mergers. SBs and MS galaxies follow the same relation between their molecular gas mass and star formation rate surface densities with a slope of $\sim1.1-1.2$, that is, the so-called KS relation.Comment: 20 pages, 17 figure

Optimal Design and Operation for a No-Moving-Parts-Valve (NMPV) Micro-Pump with a Diffuser Width of 500 μm

A no-moving-parts-valve (NMPV) with a diffuser width of D = 500 microns was investigated in this study by numerical simulations at Reynolds numbers, ReD, ranging from 20 to 75, and expansion valve angles ranging from 30° < θ1 < 57° and 110° < θ2 < 120°. The Dp,i value, 1.02 < Dp,i < 1.14, is larger within the proposed range of the expansion valve angles. A flow channel structure with a depth of 500 micron is manufactured using yellow light lithography in this study. From prior analyses and experiments, it is found that piezoelectric films work better at a buzz driving frequency of f < 30Hz and the best operating frequency is at a driving frequency of f = 10Hz because it produces the largest net flow. In addition, the expansion angles θ1 = 30° and θ2 = 120° are the best expansion angles because they produce the largest net flow. These related results are very helpful for the actual design of no-moving-parts-valve micro-pump

Deactivation of TBP contributes to SCA17 pathogenesis

Spinocerebellar ataxia type 17 (SCA17) is an autosomal dominant cerebellar ataxia caused by the expansion of polyglutamine (polyQ) within the TATA box-binding protein (TBP). Previous studies have shown that polyQexpanded TBP forms neurotoxic aggregates and alters downstream genes. However, how expanded polyQ tracts affect the function of TBP and the link between dysfunctional TBP and SCA17 is not clearly understood. In this study, we generated novel Drosophila models for SCA17 that recapitulate pathological features such as aggregate formation, mobility defects and premature death. In addition to forming neurotoxic aggregates, we determined that polyQ-expanded TBP reduces its own intrinsic DNA-binding and transcription abilities. Dysfunctional TBP also disrupts normal TBP function. Furthermore, heterozygous dTbp amorph mutant flies exhibited SCA17-like phenotypes and flies expressing polyQ-expanded TBP exhibited enhanced retinal degeneration, suggesting that loss of TBP function may contribute to SCA17 pathogenesis. We further determined that the downregulation of TBP activity enhances retinal degeneration in SCA3 and Huntington&apos;s disease fly models, indicating that the deactivation of TBP is likely to play a common role in polyQ-induced neurodegeneration

Nationwide Surveillance of Influenza during the Pandemic (2009–10) and Post-Pandemic (2010–11) Periods in Taiwan

INTRODUCTION: Although WHO declared the world moving into the post-pandemic period on August 10, 2010, influenza A(H1N1) 2009 virus continued to circulate globally. Its impact was expected to continue during the 2010-11 influenza season. This study describes the nationwide surveillance findings of the pandemic and post-pandemic influenza periods in Taiwan and assesses the impact of influenza A(H1N1) 2009 during the post-pandemic period. METHODS: The Influenza Laboratory Surveillance Network consisted of 12 contract laboratories for collecting and testing samples with acute respiratory tract infections. Surveillance of emergency room visits and outpatient department visits for influenza-like illness (ILI) were conducted using the Real-Time Outbreak and Disease Surveillance system and the National Health Insurance program data, respectively. Hospitalized cases with severe complications and deaths were reported to the National Notifiable Disease Surveillance System. RESULTS: During the 2009-10 influenza season, pandemic A(H1N1) 2009 was the predominant circulating strain and caused 44 deaths. However, the 2010-11 influenza season began with A(H3N2) being the predominant circulating strain, changing to A(H1N1) 2009 in December 2010. Emergency room and outpatient department ILI surveillance displayed similar trends. By March 31, 2011, there were 1,751 cases of influenza with severe complications; 50.1% reported underlying diseases. Of the reported cases, 128 deaths were associated with influenza. Among these, 93 (72.6%) were influenza A(H1N1) 2009 and 30 (23.4%) A(H3N2). Compared to the pandemic period, during the immediate post-pandemic period, increased number of hospitalizations and deaths were observed, and the patients were consistently older. CONCLUSIONS: Reemergence of influenza A(H1N1) 2009 during the 2010-11 influenza season had an intense activity with age distribution shift. To further mitigate the impact of future influenza epidemics, Taiwan must continue its multifaceted influenza surveillance systems, remain flexible with antiviral use policies, and revise the vaccine policies to include the population most at risk

Role of the CCAAT-Binding Protein NFY in SCA17 Pathogenesis

Spinocerebellar ataxia 17 (SCA17) is caused by expansion of the polyglutamine (polyQ) tract in human TATA-box binding protein (TBP) that is ubiquitously expressed in both central nervous system and peripheral tissues. The spectrum of SCA17 clinical presentation is broad. The precise pathogenic mechanism in SCA17 remains unclear. Previously proteomics study using a cellular model of SCA17 has revealed reduced expression of heat shock 70 kDa protein 5 (HSPA5) and heat shock 70 kDa protein 8 (HSPA8), suggesting that impaired protein folding may contribute to the cell dysfunction of SCA17 (Lee et al., 2009). In lymphoblastoid cells, HSPA5 and HSPA8 expression levels in cells with mutant TBP were also significantly lower than that of the control cells (Chen et al., 2010). As nuclear transcription factor Y (NFY) has been reported to regulate HSPA5 transcription, we focused on if NFY activity and HSPA5 expression in SCA17 cells are altered. Here, we show that TBP interacts with NFY subunit A (NFYA) in HEK-293 cells and NFYA incorporated into mutant TBP aggregates. In both HEK-293 and SH-SY5Y cells expressing TBP/Q61∼79, the level of soluble NFYA was significantly reduced. In vitro binding assay revealed that the interaction between TBP and NFYA is direct. HSPA5 luciferase reporter assay and endogenous HSPA5 expression analysis in NFYA cDNA and siRNA transfection cells further clarified the important role of NFYA in regulating HSPA5 transcription. In SCA17 cells, HSPA5 promoter activity was activated as a compensatory response before aggregate formation. NFYA dysfunction was indicated in SCA17 cells as HSPA5 promoter activity reduced along with TBP aggregate formation. Because essential roles of HSPA5 in protection from neuronal apoptosis have been shown in a mouse model, NFYA could be a target of mutant TBP in SCA17