Flexible, Fully Printable, and Inexpensive Paper-Based Chipless Arabic Alphabet-Based RFID Tags.

This work presents the design and analysis of newly developed reconfigurable, flexible, inexpensive, optically-controlled, and fully printable chipless Arabic alphabet-based radio frequency identification (RFID) tags. The etching of the metallic copper tag strip is performed on a flexible simple thin paper substrate (ϵr = 2.31) backed by a metallic ground plane. The analysis of investigated tags is performed in CST MWS in the frequency range of 1-12 GHz for the determination of the unique signature resonance characteristics of each tag in terms of its back-scattered horizontal and vertical mono-static radar cross section (RCS). The analysis reflects that each tag has its own unique electromagnetic signature (EMS) due to the changing current distribution of metallic resonator. This EMS of each tag could be used for the robust detection and recognition of all realized 28 Arabic alphabet tags. The study also discusses, for the first time, the effect of the change in font type and size of realized tags on their EMS. The robustness and reliability of the obtained EMS of letter tags is confirmed by comparing the RCS results for selective letter tags using FDTD and MoM numerical methods, which shows very good agreement. The proposed tags could be used for smart internet of things (IoT) and product marketing applications.

Prednisone and Its Active Metabolite Prednisolone Attenuate Lipid Accumulation in Macrophages.

BACKGROUND: Synthetic forms of glucocorticoids (GCs; eg, prednisone, prednisolone) are anti-inflammatory drugs that are widely used in clinical practice. The role of GCs in cardiovascular diseases, including atherosclerosis, is highly controversial, and their impact on macrophage foam cell formation is still unknown. We investigated the effects of prednisone and prednisolone on macrophage oxidative stress and lipid metabolism. METHODS AND RESULTS: C57BL/6 mice were intraperitoneally injected with prednisone or prednisolone (5 mg/kg) for 4 weeks, followed by lipid metabolism analyses in the aorta and peritoneal macrophages. We also analyzed the effect of serum samples obtained from 9 healthy human volunteers before and after oral administration of prednisone (20 mg for 5 days) on J774A.1 macrophage atherogenicity. Finally, J774A.1 macrophages, human monocyte-derived macrophages, and fibroblasts were incubated with increasing concentrations (0-200 ng/mL) of prednisone or prednisolone, followed by determination of cellular oxidative status, and triglyceride and cholesterol metabolism. Prednisone and prednisolone treatment resulted in a significant reduction in triglyceride and cholesterol accumulation in macrophages, as observed in vivo, ex vivo, and in vitro. These effects were associated with GCs' inhibitory effect on triglyceride- and cholesterol-biosynthesis rates, through downregulation of diacylglycerol acyltransferase 1 and HMG-CoA reductase expression. Glucocorticoid-induced reduction of cellular lipid accumulation was mediated by the GC receptors on the macrophages, because the GC-receptor antagonist (RU486) abolished these effects. In fibroblasts, unlike macrophages, GCs showed no effects. CONCLUSION: Prednisone and prednisolone exhibit antiatherogenic activity by protecting macrophages from lipid accumulation and foam cell formation.

Atherogenicity of amino acids in the lipid-laden macrophage model system in vitro and in atherosclerotic mice: a key role for triglyceride metabolism.

Atherosclerosis-related research has focused mainly on the effects of lipids on macrophage foam cell formation and atherogenesis, whereas the role of amino acids (AAs) was understudied. The current study aimed to identify anti- or pro-atherogenic AA in the macrophage model system and to elucidate the underlying metabolic and molecular mechanisms. J774A.1 cultured macrophages were treated with increasing concentrations of each 1 of the 20 AAs. Macrophage atherogenicity was assessed in terms of cellular toxicity, generation of reactive oxygen species (ROS) and cellular cholesterol or triglyceride content. At nontoxic concentrations (up to 1 mM), modest effects on ROS generation or cholesterol content were noted, but six specific AAs significantly affected macrophage triglyceride content. Glycine, cysteine, alanine and leucine significantly decreased macrophage triglyceride content (by 24%-38%), through attenuated uptake of triglyceride-rich very low-density lipoprotein (VLDL) by macrophages. In contrast, glutamate and glutamine caused a marked triglyceride accumulation in macrophages (by 107% and 129%, respectively), via a diacylglycerol acyltransferase-1 (DGAT1)-dependent increase in triglyceride biosynthesis rate with a concurrent maturation of the sterol regulatory element-binding protein-1 (SREBP1). Supplementation of apolipoprotein E-deficient (apoE-/-) mice with glycine for 40 days significantly decreased the triglyceride levels in serum and in peritoneal macrophages (MPMs) isolated from the mice (by 19%). In contrast, glutamine supplementation significantly increased MPM ROS generation and the accumulation of cholesterol and that of triglycerides (by 48%), via enhanced uptake of LDL and VLDL. Altogether, the present findings reveal some novel roles for specific AA in macrophage atherogenicity, mainly through modulation of cellular triglyceride metabolism.

The nectarine pit as a cause for small bowel obstruction and perforation: a case report.

Ingestion of a foreign body is a rare cause of small bowel obstruction. Ingested foreign bodies will usually pass without clinical sequelae, however on occasion can contribute to significant morbidity. Here we present an unusual case of small bowel obstruction and perforation as a result of accidental ingestion of a nectarine pit.

Non-healing leg ulcers in a patient with dystrophic calcification and crest syndrome: a challenging clinical case.

The management of non-healing leg ulcers in patients with CREST syndrome and subdermal calcification is rarely reported in medical literature. Only one similar case was found in the literature (1). Dealing with such patients can be a challenge for wound specialists. In this article, we discuss the clinical progress of an interesting case of extensive non-healing leg ulcers in a CREST patient with dystrophic calcification. The combination of systemic physiological deficits and immune compromise, along with the local physical abnormalities associated with the wound pose a complex multifactorial aetiological mix. There is no conclusive data on the optimal management of these wounds in CREST patients. It seems that ablation of the calcific deposits may offer some hope.