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The COVID-19 pandemic has disrupted our collective normal patterns of behavior in almost all aspects of our personal and professional lives. While many K-12 and post-secondary subject area curricula lend themselves more easily to a migration to online and remote learning, technology education faces unique challenges. This research paper sought to understand the challenges, benefits, and lessons learned through an analysis of the process of re-organizing a pre-service technology education diploma for remote, blended, and face-to-face learning during the early stages of the COVID-19 pandemic. The investigation followed a collaborative autoethnographic methodology as the authors constructed two narratives based on their roles of administering and instructing in a pre-service technology education diploma program. An interpretive descriptive analysis suggests a number of challenges associated with the organizational changes, but also a number of positive outcomes related to the instructional shifts. Challenges included maintaining equitable access to physical materials and technologies for all students, scheduling issues related to changing pandemic rules and regulations, and a loss of social presence with students. Benefits included more student autonomy, less dependence on group work for technical skill development, and the development of alternative delivery models for pre-service technology education that could be used to expand program offerings to non-traditional students.

This paper presents a new optical imaging survey of four deep drilling fields (DDFs), two Galactic and two extragalactic, with the Dark Energy Camera (DECam) on the 4-m Blanco telescope at the Cerro Tololo Inter-American Observatory (CTIO). During the first year of observations in 2021, >4000 images covering 21 deg2 (seven DECam pointings), with ∼40 epochs (nights) per field and 5 to 6 images per night per filter in g, r, i, and/or z have become publicly available (the proprietary period for this program is waived). We describe the real-Time difference-image pipeline and how alerts are distributed to brokers via the same distribution system as the Zwicky Transient Facility (ZTF). In this paper, we focus on the two extragalactic deep fields (COSMOS and ELAIS-S1) characterizing the detected sources, and demonstrating that the survey design is effective for probing the discovery space of faint and fast variable and transient sources. We describe and make publicly available 4413 calibrated light curves based on difference-image detection photometry of transients and variables in the extragalactic fields. We also present preliminary scientific analysis regarding the Solar system small bodies, stellar flares and variables, Galactic anomaly detection, fast-rising transients and variables, supernovae, and active Galactic nuclei.

How are we preparing teachers to design and foster learning through making where disciplinary knowledge and skills are applied and developed? One approach that addresses this question can be found from the International Maker Educational Network (IMEN); an online professional learning community built upon shared interests in educational making. Members meet regularly to share their maker context and experiences and what can be gleaned to help support developing capacity to design and facilitate learning through making. In further studying their professional practice using a self-study methodology, four IMEN members shared their respective maker contexts, illustrating examples of making in formal and informal learning environments and what is being learned from their experiences. These cases provide examples of strategies and approaches that are being used to support learning through making and provide insight into developing and utilizing knowledge and skills in fostering learning through making in P-16 educational contexts. The article concludes with three recommendations for practice to support educators and teacher educators in fostering learning through making.

Many information technology services firms now offer services and consider software availability to be a critical component of achieving excellence and competing in the industry. The most crucial factor for customers is the quality of service, consumer needs, the state of the organization/company, and the present market should all be considered when improving their service. In this study, an ITSM analysis will be carried out at an oil palm plantation company based in West Kalimantan Province using ITIL framework V3 by focusing on continual service improvement, which largely relies on service measurement because a process must be measurable to be regulated and improved. To achieve continuous service improvement (CSI) throughout the service life cycle, we use the 7-step process to improve is used to establish and take care of the stages involved in identifying, defining, collecting, processing, analyzing, presenting, and implementing changes. The result of this analysis is CSF and KPI analysis that produce metrics, such as the average resolution time, the percentage of events allocated more than once, and the initial response time, then create a measurement system that is in accordance with the needs and can be used as a reference for the company's system assessment.

Purpose: To report bilateral retinal vascular occlusive disease in limb-girdle muscular dystrophy (LGMD). Methods: Case report. Results: A 34-year-old Asian woman was referred for evaluation and management of central retinal vein occlusion. Ultra-wide-field fluorescein angiography showed resolving initial peripheral retinal vein occlusion in one eye and peripheral venular segmental staining in the fellow asymmetric eye. Genetic testing established the diagnosis of LGMD. Conclusion: Similar to other forms of muscular dystrophy, LGMD is caused by genetic abnormalities in sarcolemma proteins, a key structural component that connects the intracellular cytoskeleton of a myofiber to the extracellular matrix. Like other muscular dystrophies, LGMD may be associated with retinal vascular abnormalities noted. In this case, retinal vascular smooth muscle dysfunction was seen in LGMD, analogous to reported vascular abnormalities in other muscular dystrophies such as facioscapulohumeral dystrophy and Duchenne muscular dystrophy. [ABSTRACT FROM AUTHOR]

The analysis of costs of National Institutes of Health (NIH) bio-medical research demonstrates that the increased expenditures for research project grants are due to such factors as real growth in the program, artifacts of the calculation method, and the extent to which project periods of awards have lengthened. (Author/DB)

While heparin has been used almost exclusively as a blood anticoagulant, important literature demonstrates that it also has broad anti-inflammatory activity. Herein, using low anti-coagulant 2-O,3-O-desulfated heparin (ODSH), we demonstrate that most of the anti-inflammatory pharmacology of heparin is unrelated to anticoagulant activity. ODSH has low affinity for anti-thrombin III, low anti-Xa, and anti-IIa anticoagulant activities and does not activate Hageman factor (factor XII). Unlike heparin, ODSH does not interact with heparin-platelet factor-4 antibodies present in patients with heparin-induced thrombocytopenia and even suppresses platelet activation in the presence of activating concentrations of heparin. Like heparin, ODSH inhibits complement activation, binding to the leukocyte adhesion molecule P-selectin, and the leukocyte cationic granular proteins azurocidin, human leukocyte elastase, and cathepsin G. In addition, ODSH and heparin disrupt Mac-1 (CD11h/CD18)-mediated leukocyte adhesion to the receptor for advanced glycation end products (RAGE) and inhibit ligation of RAGE by its many proinflammatory ligands, including the advanced glycation end-product carboxymethyl lysine-bovine serum albumin, the nuclear protein high mobility group box protein-1 (HMGB-1), and S100 calgranulins. In mice, ODSH is more effective than heparin in reducing selectin-mediated lung metastasis from melanoma and inhibits RAGE-mediated airway inflammation from intratracheal HMGB-1. In humans, 50% inhibitory concentrations of ODSH for these anti-inflammatory activities can be achieved in the blood without anticoagulation. These results demonstrate that the anticoagulant activity of heparin is distinct from its anti-inflammatory actions and indicate that 2-O and 3-O sulfate groups can be removed to reduce anticoagulant activity of heparin without impairing its anti-inflammatory pharmacology. receptor for advanced glycation end products; P-selectin; high mobility group box protein-l; S100 calgranulins; human research; translational research doi: 10.1152/ajpcell.00009.2010.

Am J Physiol Heart Circ Physiol 298: H102-H111, 2010. First published October 23, 2009; doi: 10.1152/ajpheart.00316.2009.--Heparin desulfated at the 2-0 and 3-0 positions (ODSH) decreases canine myocardial reperfusion injury. We hypothesized that this occurs from effects on ion channels rather than solely from anti-inflammatory activities, as previously proposed. We studied closed-chest pigs with balloon left anterior descending coronary artery occlusion (75-min) and reperfusion (3-h). ODSH effects on [[[Na.sup.+]].sub.i] (Na Green) and [[[Ca.sup.2+]].sub.i] (Fluo-3) were measured by flow cytometry in rabbit ventricular myocytes after 45-min of simulated ischemia [metabolic inhibition with 2 mM cyanide, 0 glucose, 37[degrees]C, pacing at 0.5 Hz; i.e., pacing-metabolic inhibition (PMI)]. [Na.sup.+]/[Ca.sup.2+] exchange (NCX) activity and [Na.sup.+] channel function were assessed by voltage clamping. ODSH (15 mg/kg) 5 min before reperfusion significantly decreased myocardial necrosis, but neutrophil influx into reperfused myocardium was not consistently reduced. ODSH (100 [micro]g/ml) reduced [[[Na.sup.+]].sub.i] and [[[Ca.sup.2+]].sub.i] during PMI. The NCX inhibitor KB-R7943 (10 [micro]M) or the late [Na.sup.+] current ([1.sub.Na-L]) inhibitor ranolazine (10 [micro]M) reduced [[[Ca.sup.2+]].sub.i] during PMI and prevented effects of ODSH on [Ca.sup.2+] loading. ODSH also reduced the increase in [Na.sup.+] loading in paced myocytes caused by l0 nM sea anemone toxin II, a selective activator of [I.sub.Na-L]. ODSH directly stimulated NCX and reduced [I.sub.Na-L]. These results suggest that in the intact heart ODSH reduces [Na.sup.+] influx during early reperfusion, when [I.sub.Na-L] is activated by a burst of reactive oxygen production. This reduces [Na.sup.+] overload and thus [Ca.sup.2+] influx via NCX. Stimulation of [Ca.sup.2+] extrusion via NCX later after reperfusion may also reduce myocyte [Ca.sup.2+] loading and decrease infarct size. metabolic inhibition; sodium-calcium exchange; late sodium current; ranolazine; myocardial reperfusion injury; nonanticoagulant heparin

NAD(P)H oxidase is one of the critical enzymes mediating cellular production of reactive oxygen species and has a central role in airway smooth muscle (ASM) cell proliferation. Since reactive oxygen species also affect ASM contractile response, we hypothesized a regulatory role of NAD(P)H oxidase in ASM contractility. We therefore studied ASM function in wild-type mice (C57BL/6J) and mice deficient in a component ([p47.sup.phox]) of NAD(P)H oxidase. In histological sections of the trachea, we found that the area occupied by ASM was 17% more in [p47.sup.phox-/-] than in wild-type mice. After correcting for the difference in ASM content, we found that force generation did not vary between the two genotypes. Similarly, their ASM shortening velocity, maximal power, and sensitivity to acetylcholine, as well as airway responsiveness to methacholine in vivo, were not significantly different. The main finding of this study was a significantly reduced ASM relaxation in [p47.sup.phox-/-] compared with wild-type mice both during the stimulus and after the end of stimulation. The tension relaxation attained at the 20th second of electric field stimulation was, respectively, 17.6 [+ or -] 2.4 and 9.2 [+ or -] 2.3% in null and wild-type mice (P < 0.01 by t-test). Similar significant differences were found in the rate of tension relaxation and the time required to reduce tension by one-half. Our data suggest that NAD(P)H oxidase may have a role in the structural arrangement and mechanical properties of the airway tissue. Most importantly, we report the first evidence that the [p47.sup.phox] subunit of NAD(P)H oxidase plays a role in ASM relaxation. airways; airway responsiveness; contractility; reactive oxygen species

Transforming growth factor-[beta]1 (TGF-[beta]1) plays a pivotal role in increasing airway smooth muscle mass in severe asthma by inducing proliferation and hypertrophy of human airway smooth muscle. The mechanism(s) for these effects of TGF-[beta]1 have not been fully elucidated. In this study, we demonstrate that TGF-[beta]1 is a potent inducer of expression of the nonphagocyte NAD(P)H oxidase catalytic homolog Nox4, diphenylene iodonium-inhibitable reactive oxygen species production, proliferation, and hypertrophy in cultured human airway smooth muscle cells. By confocal microscopy, TGF-[beta]1-induced Nox4 was localized with the endoplasmic reticulum and the nucleus, implying a role for Nox4 in regulation of both the cell cycle and protein synthesis. Consistent with this hypothesis, TGF-[beta]1 increased retinoblastoma protein phosphorylation at both Ser807/811 and Ser780. Silencing Nox4 prevented TGF-[beta]1-mediated retinoblastoma protein phosphorylation, proliferation, and cell hypertrophy. TGF-[beta]1 also increased phosphorylation of eukaryotic translation initiation factor 4E binding protein-1 at Thr37/46, and this was likewise blocked by silencing Nox4. This is the first report to suggest a functional role for Nox4 in cell cycle transition and to demonstrate that Nox4 influences the pathobiochemistry of asthma by generating reactive oxygen species that promote TGF-[beta]1-induced proliferation and hypertrophy of human airway smooth muscle. Myc; cdc2; eukaryotic translation initiation factor 4E binding protein- 1; nicotinamide adenine dinucleotide phosphate oxidase; reactive oxygen species; translation doi: 10.1152/ajplung.00430.2006

Transforming growth factor-[beta]1 (TGF-[beta]1) is abundantly expressed in pulmonary hypertension, but its effect on the pulmonary circulation remains unsettled. We studied the consequences of TGF-[beta]1 stimulation on freshly isolated human pulmonary artery smooth muscle cells (HPASMC). TGF-[beta]1 initially promoted differentiation, with upregulated expression of smooth muscle contractile proteins. TGF-[beta]1 also induced expression of Nox4, the only NAD(P)H oxidase membrane homolog found in HPASMC, through a signaling pathway involving Smad 2/3 but not mitogen-activated protein (MAP) kinases. TGF-[beta]1 likewise increased production of reactive oxygen species (ROS), an effect significantly reduced by the NAD(P)H oxidase flavoprotein inhibitor diphenylene iodonium (DPI) and by Nox4 siRNAs. In the absence of TGF-[beta]1, Nox4 was present in freshly cultured cells but progressively lost with each passage in culture, paralleling a decrease in ROS production by HPASMC over time. At a later time point (72 h), TGF-[beta]1 promoted HPASMC proliferation in a manner partially inhibited by Nox4 small interfering RNA and dominant negative Smad 2/3, indicating that TGF-[beta]1 stimulates HPASMC growth in part by a redox-dependent mechanism mediated through induction of Nox4. HPASMC activation of the MAP kinases ERK1/2 was reduced by the NAD(P)H oxidase inhibitors DPI and 4-(2-aminoethyl)benzenesulfonyl fluoride, suggesting that TGF-[beta]1 may facilitate proliferation by upregulating Nox4 and ROS production, with transient oxidative inactivation of phosphatases and augmentation of growth signaling cascades. These findings suggest that Nox4 is the relevant Nox homolog in HPASMC. This is the first observation that TGF-[beta]1 regulates Nox4, with important implications for mechanisms of pulmonary vascular remodeling. Smad 2/3; pulmonary arterial hypertension; hypertrophy; superoxide anion; rac 1; ERK 1/2; phosphatases

The efficacy of sodium bicarbonate compared with sodium chloride for preventive hydration before and after radiographic contrast is examined. The results indicate that hydration with sodium bicarbonate before contrast exposure is more effective than hydration with sodium chloride for prophylaxis of contrast-induced renal failure.

Reactive oxygen species (ROS) appear to play an important role in regulating growth and survival of prostate cancer. However, the sources for ROS production in prostate cancer cells have not been determined. We report that ROS are generated by intact American Type Culture Collection DU 145 cells and by their membranes through a mechanism blocked by NAD(P)H oxidase inhibitors. ROS are critical for growth in these cells, because NAD(P)H oxidase inhibitors and antioxidants blocked proliferation. Components of the human phagocyte NAD(P)H oxidase, [p22.sup.phox] and [gp91.sup.phox] as well as the [Ca.sup.2+] concentration-responsive [gp.syup.91phox] homolog NOX5 were demonstrated in DU 145 cells by RT-PCR and sequencing. Although the protein product for [p22.sup.phox] was not detectable, both [gp91.sup.phox] and NOX5 were identified throughout the cell by immunostaining and confocal microscopy and NOX5 immunostaining was enhanced in a perinuclear location, corresponding to enhanced ROS production adjacent to the nuclear membrane imaged by 2',7'-dichlorofluorescin diacetate oxidation. The calcium ionophore ionomycin dramatically stimulated ferricytochrome c reduction in cell media, further supporting the importance of NOX5 for ROS production. Antisense oligonucleotides for NOX5 inhibited ROS production and cell proliferation in DU 145 cells. In contrast, antisense oligonucleotides to [p22.sup.phox] or [gp91.sup.phox] did not impair cell growth. Inhibition of ROS generation with antioxidants or NAD(P)H oxidase inhibitors increased apoptosis in cells. These results indicate that ROS generated by the newly described NOX5 oxidase are essential for prostate cancer growth, possibly by providing trophic intracellular oxidant tone that retards programmed cell death. superoxide anion; diphenylene iodonium; [p22.sup.phox]; [gp91.sup.phox]; adenosine 3',5'-cyclic monophosphate response element; caspases

The iron chelator deferoxamine has been reported to inhibit both xanthine oxidase (XO) and xanthine dehydrogenase activity, but the relationship of this effect to the availability of iron in the cellular and tissue environment remains unexplored. XO and total xanthine oxidoreductase activity in cultured V79 cells was increased with exposure to ferric ammonium sulfate and inhibited by deferoxamine. Lung XO and total xanthine oxidoreductase activities were reduced in rats fed an iron-depleted diet and increased in rats supplemented with iron, without change in the ratio of XO to total oxidoreductase. Intratracheal injection of an iron salt or silica-iron, but not aluminum salts or silica-zinc, significantly increased rat lung XO and total xanthine oxidoreductase activities, immunoreactive xanthine oxidoreductase, and the concentration of urate in bronchoalveolar fluid. These results suggest the possibility that the production of uric acid, a major chelator of iron in extracellular fluid, is directly influenced by iron-mediated regulation of the expression and/or activity of its enzymatic source, xanthine oxidase. xanthine dehydrogenase; deferoxamine; silica; uric acid

Evidence is rapidly accumulating that low-activity-reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases homologous to that in phagocytic cells generate reactive oxygen species as signaling intermediates in both endothelium and vascular smooth muscle. We therefore explored the possibility of such an oxidase regulating growth of airway smooth muscle (AWSM). Proliferation of human AWSM cells in culture was inhibited by the antioxidants catalase and N-acetylcysteine, and by the flavoprotein inhibitor diphenylene iodonium (DPI). Membranes prepared from human AWSM cells generated superoxide anion ([O.sup.-.sub.2]) measured by superoxide dismutase-inhibitable lucigenin chemiluminescence, with a distinct preference for NADPH instead of reduced nicotinamide adenine dinucleotide as substrate. Chemiluminescence was also inhibited by DPI, suggesting the presence of a flavoprotein containing oxidase generating ([O.sup.-.sub.2]) as a signaling molecule for cell growth. Examination of human AWSM cells by reverse transcriptase-polymerase chain reaction consistently demonstrated transcripts with sequences identical to those reported for [p22.sup.phox]. Transfection with p22phox antisense oligonucleotides reduced human AWSM proliferation. Inhibition of NADPH oxidase activity with DPI prevented serum-induced activation of nuclear factor-[kappa]B (NF-[kappa]B), and overexpression of a superrepressor form of the NF-[kappa]B inhibitor I[kappa]B[alpha] significantly reduced human AWSM growth. These findings suggest that an NADPH oxidase containing [p22.sup.phox] regulates growth-factor responsive human AWSM proliferation, and that the oxidase signals in part through activation of the prototypical redox-regulated transcription factor NF-[kappa]B. superoxide anion; diphenylene iodonium; [p22.sup.phox]