المؤلفون: Sritha, P.¹ (AUTHOR) srithaeee@gmail.com, Valarmathi, R.S.² (AUTHOR), Poongodi, C.³ (AUTHOR)

المصدر: Journal of Intelligent & Fuzzy Systems. 2023, Vol. 45 Issue 6, p10193-10211. 19p.

مصطلحات موضوعية: *ADVANCED Encryption Standard, SPACE-time block codes, HEART beat, INFANT health, MACINTOSH (Computer), HEART rate monitors

مستخلص: One of the best methods for assessing a baby's health is foetal electrocardiography (FECG). Previously restricted to more widespread global disorders such as common ischemia, it is new way to investigating foetal heart rate irregularities. Current prenatal monitoring practices ignore critical FECG waveform elements that are the foundation of both pediatric, adult cardiac assessment, and instead of focusing solely on the foetal heart rate. In this paper we proposed Double Multiply-and-Accumulate (MAC) approach used for package operators into a single DSP block of commercial FPGAs, theoretically doubling the calculation speed for FECG monitoring. For a variety of technical reasons, they were using the Space-Time Block Code (STBC) monitoring mode of operation. To strengthen the security of FECG monitoring, the Advanced Encryption Standard (AES) method may be used with the double MAC operators using STBC based FECG monitoring that has been developed. The solution was then assessed using state-of-the-art the Space-Time Block Code (STBC) based FECG techniques, and its validity was confirmed using Verilog simulation and FPGA synthesis. The calculation throughput of an STBC-based FECG monitoring system was found to be doubled using the Double MAC approach. Our implementation result demonstrates that keys are necessary for 128-bit AES encoding and decoding operations via VHDL-coded transformations. It is now more vital than ever to do a feasibility analysis of any hardware design due to the increase in the number of ways presented for minimizing noise. The efficiency increased (92%), and the delay was decreased to 19.35 ns by employing this double MAC architecture. The simulation results demonstrate that transformations for coding on an FPGA are implemented using the Xilinx VIVADO tool. [ABSTRACT FROM AUTHOR]

: Copyright of Journal of Intelligent & Fuzzy Systems is the property of IOS Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Held, Martina¹ (AUTHOR) martina.held@mef.hr, Kozmar, Ana² (AUTHOR) ana.kozmar@kbc-zagreb.hr, Sestan, Mario¹ (AUTHOR) mario.sestan@gmail.com, Turudic, Daniel¹ (AUTHOR) danielturudic@gmail.com, Kifer, Nastasia¹ (AUTHOR) nastasia.ce@gmail.com, Srsen, Sasa³ (AUTHOR) ssrsen@kbsplit.hr, Gagro, Alenka⁴ (AUTHOR) alenka.gagro@gmail.com, Frkovic, Marijan¹ (AUTHOR) mfrkovic1@gmail.com, Jelusic, Marija¹ (AUTHOR) marija.jelusic@mef.hr

المصدر: International Journal of Molecular Sciences. Apr2024, Vol. 25 Issue 8, p4383. 16p.

مصطلحات موضوعية: *RECEPTOR for advanced glycation end products (RAGE), *ADVANCED glycation end-products, *ERYTHROCYTES, *IMMUNOGLOBULIN A, *ENZYME-linked immunosorbent assay, *VASCULITIS

مستخلص: The pathogenesis of IgAV, the most common systemic vasculitis in childhood, appears to be complex and requires further elucidation. We aimed to investigate the potential role of galactose-deficient immunoglobulin A1 (Gd-IgA1), high-mobility group box 1 (HMGB1), receptor for advanced glycation end products (RAGE) and protocadherin 1 (PCDH1) in the pathogenesis of IgAV. Our prospective study enrolled 86 patients with IgAV and 70 controls. HMGB1, RAGE, Gd-IgA1 and PCDH1 in serum and urine were determined by the enzyme-linked immunosorbent assay (ELISA) method at the onset of the disease and after a six-month interval in patients and once in the control group. Serum concentrations of HMGB1, RAGE and PCDH1 and urinary concentrations of HMGB1, RAGE, Gd-IgA1 and PCDH1 were significantly higher in patients with IgAV than in the control group (p < 0.001). Concentrations of HMGB1 (5573 pg/mL vs. 3477 pg/mL vs. 1088 pg/mL, p < 0.001) and RAGE (309 pg/mL vs. 302.4 pg/mL vs. 201.3 pg/mL, p = 0.012) in the serum of patients remained significantly elevated when the disease onset was compared with the six-month follow-up interval, and thus could be a potential marker of disease activity. Urinary concentration of HMGB1 measured in the follow-up period was higher in patients with nephritis compared to IgAV without nephritis (270.9 (146.7–542.7) ng/mmol vs. 133.2 (85.9–318.6) ng/mmol, p = 0.049) and significantly positively correlated with the urine albumine to creatinine ratio (τ = 0.184, p < 0.05), the number of erythrocytes in urine samples (τ = 0.193, p < 0.05) and with the outcome of nephritis (τ = 0.287, p < 0.05); therefore, HMGB1 could be a potential tool for monitoring patients with IgAV who develop nephritis. Taken together, our results imply a possible interplay of Gd-IgA1, HMGB1, RAGE and PCDH1 in the development of IgAV. The identification of sensitive biomarkers in IgAV may provide disease prevention and future therapeutics. [ABSTRACT FROM AUTHOR]

المؤلفون: You, Xujun¹ (AUTHOR), Qiu, Junfeng² (AUTHOR), Li, Qixin¹ (AUTHOR), Zhang, Qing¹ (AUTHOR), Sheng, Wen^3,4 (AUTHOR), Cao, Yiguo⁵ (AUTHOR) caoyiguo82@gzucm.edu.cn, Fu, Wei¹ (AUTHOR) fuwei84@gzucm.edu.cn

المصدر: BMC Cancer. 4/15/2024, Vol. 24 Issue 1, p1-12. 12p.

مصطلحات موضوعية: *PROSTATE cancer, *RECEPTOR for advanced glycation end products (RAGE), *GUT microbiome, *TUMOR growth, *PROSTATE tumors, *ADVANCED glycation end-products, *FECAL microbiota transplantation

مستخلص: Background: Prostate cancer (PCa) is becoming the most common malignancy in men worldwide. We investigated the effect of astragaloside IV combined with PESV on the gut microbiota and metabolite of PCa mice and the process of treating PCa. Methods: Nude mice were genetically modified to develop tumors characteristic of PCa. The treatment of PCa mice involved the administration of a combination of astragaloside IV and peptides derived from scorpion venom (PESV). Feces were collected for both 16 S rDNA and metabolic analysis. Fecal supernatant was extracted and used for fecal transplantation in PCa mice. Tumor development was observed in both PCa mice and nude mice. Tumor histopathology was examined, and the expression of inflammatory factors and the AGE-RAGE axis in PCa tissues were analyzed. Results: PCa mice treated with Astragaloside IV in combination with PESV showed a significant reduction in tumor volume and weight, and stabilization of gut microbiota and metabolites. At the Genus level, significant differences were observed in Porphyromonas, Corynebacterium, Arthromitus and Blautia, and the differential metabolites were PA16_016_0, Astragaloside+, Vitamin A acid, Nardosinone, a-Nortestoster, D-Pantethine, Hypoxanthine, Pregnenolone, cinnamic acid, Pyridoxa, Cirtruline and Xanthurenate. There was a correlation between gut microbiota and metabolites. After the fecal transplantation, tumor growth was effectively suppressed in the PCa mice. Notably, both the mRNA and protein levels of the receptor for advanced glycation end products (RAGE) were significantly decreased. Furthermore, the expression of inflammatory factors, namely NF-κB, TNF-α, and IL-6, in the tumor tissues was significantly attenuated. Conversely, upregulation of RAGE led to increased inflammation and reversed tumor growth in the mice. Conclusion: Astragaloside IV combined with PESV could treat PCa by intervening in gut microbiota composition and metabolite by targeting RAGE. [ABSTRACT FROM AUTHOR]

المؤلفون: Dascalu, Anca‐Elena^1,2,3 (AUTHOR), Furman, Christophe^2,4 (AUTHOR), Landrieu, Isabelle^2,5 (AUTHOR), Cantrelle, François‐Xavier^2,5 (AUTHOR), Mortelecque, Justine^2,5 (AUTHOR), Grolaux, Gaëlle² (AUTHOR), Gillery, Philippe⁶ (AUTHOR), Tessier, Frédéric^2,4 (AUTHOR), Lipka, Emmanuelle^2,4 (AUTHOR), Billamboz, Muriel^1,2 (AUTHOR), Boulanger, Eric² (AUTHOR), Ghinet, Alina^1,2,3 (AUTHOR) alina.ghinet@junia.com

المصدر: Chemistry - A European Journal. 4/5/2024, Vol. 30 Issue 20, p1-10. 10p.

مصطلحات موضوعية: *RECEPTOR for advanced glycation end products (RAGE), *ADVANCED glycation end-products, *COMBINATORIAL chemistry, *LIGANDS (Chemistry), *IMMUNOGLOBULIN receptors, *DRUG target

مستخلص: RAGE is a transmembrane receptor of immunoglobulin family that can bind various endogenous and exogenous ligands, initiating the inflammatory downstream signaling pathways, including inflammaging. Therefore, RAGE represents an attractive drug target for age‐related diseases. For the development of small‐molecule RAGE antagonists, we employed protein‐templated dynamic combinatorial chemistry (ptDCC) using RAGE′s VC1 domain as a template, the first application of this approach in the context of RAGE. The affinities of DCC hits were validated using microscale thermophoresis. Subsequent screening against AGE2 (glyceraldehyde‐modified AGE)‐sRAGE (solubleRAGE) (AGE2‐BSA/sRAGE) interaction using ELISA tests led to the identification of antagonists with micromolar potency. Our findings not only demonstrate the successful application of ptDCC on RAGE but also highlight its potential to address the pressing need for alternative strategies for the development of small‐molecule RAGE antagonists, an area of research that has experienced a slowdown in recent years. [ABSTRACT FROM AUTHOR]

المؤلفون: Zglejc-Waszak, Kamila¹ (AUTHOR) kamila.zglejc@uwm.edu.pl, Korytko, Agnieszka¹ (AUTHOR), Pomianowski, Andrzej² (AUTHOR), Wojtkiewicz, Joanna¹ (AUTHOR), Wąsowicz, Krzysztof³ (AUTHOR), Juranek, Judyta K.¹ (AUTHOR) judyta.juranek@uwm.edu.pl

المصدر: Animal Science Papers & Reports. 2024, Vol. 42 Issue 2, p203-216. 14p.

مصطلحات موضوعية: *RECEPTOR for advanced glycation end products (RAGE), *NERVE conduction studies, *ADVANCED glycation end-products, *TYPE 1 diabetes, *LABORATORY mice, *ESTRUS

مستخلص: A growing body of literature has shown that type 1 diabetes (T1D) and high-fat diet (HFD) affect female reproductive function and may be involved in a chronic inflammatory state. Our previous studies indicated that T1D as well as HFD may evoke perturbations in the receptor for advanced glycation end products (RAGE) signaling pathway. The aim of the study was to determine the amount of RAGE protein and its proinflammatory ligands in uterine tissues harvested from T1D and HFD/pre-diabetic mice (n = 5 per group). We sought the impact of T1D and HFD on the activity of the RAGE signaling pathway in uterine tissues during the estrous cycle. The abundance of RAGE and its ligands were estimated using immunohistochemical staining. However, we also performed nerve conduction velocity studies to confirm diabetic neuropathy. The highest amount of RAGE and its ligands were observed in uterine tissues of T1D mice. Moreover, myometrial activity of the RAGE signaling pathway was increased in HFD in comparison to the control group (P≤0.05). We observed a strong relationship between RAGE, Nε-(carboxymethyl)lysine (CML) and tumor necrosis factor alpha (TNFα) proteins in mice myometrium. These data suggest that T1D and HFD could modulate the activity of RAGE and thus RAGE signaling pathway in uterine tissues during estrous cycle. Long-term diabetes and HFD may induce malfunctions in the uterine milieu. In the future RAGE protein may serve as a molecular marker in the diagnosis of malfunctions in pre- and diabetic uterus milieu. [ABSTRACT FROM AUTHOR]

المؤلفون: Rojas, Armando¹ (AUTHOR) arojasr@ucm.cl, Lindner, Cristian² (AUTHOR) clindner@udec.cl, Schneider, Ivan³ (AUTHOR) ivan.schneider96@gmail.com, Gonzalez, Ileana¹ (AUTHOR) ileanag@ucm.cl, Uribarri, Jaime⁴ (AUTHOR) jaime.uribarri@mountsinai.org

المصدر: Biomolecules (2218-273X). Apr2024, Vol. 14 Issue 4, p412. 24p.

مصطلحات موضوعية: *PATTERN perception receptors, *ADVANCED glycation end-products, *CELL receptors, *RECEPTOR for advanced glycation end products (RAGE), *HYPERGLYCEMIA, *PRORENIN receptor, *DIABETES complications, *CARDIOVASCULAR development

مستخلص: In 1992, a transcendental report suggested that the receptor of advanced glycation end-products (RAGE) functions as a cell surface receptor for a wide and diverse group of compounds, commonly referred to as advanced glycation end-products (AGEs), resulting from the non-enzymatic glycation of lipids and proteins in response to hyperglycemia. The interaction of these compounds with RAGE represents an essential element in triggering the cellular response to proteins or lipids that become glycated. Although initially demonstrated for diabetes complications, a growing body of evidence clearly supports RAGE's role in human diseases. Moreover, the recognizing capacities of this receptor have been extended to a plethora of structurally diverse ligands. As a result, it has been acknowledged as a pattern recognition receptor (PRR) and functionally categorized as the RAGE axis. The ligation to RAGE leads the initiation of a complex signaling cascade and thus triggering crucial cellular events in the pathophysiology of many human diseases. In the present review, we intend to summarize basic features of the RAGE axis biology as well as its contribution to some relevant human diseases such as metabolic diseases, neurodegenerative, cardiovascular, autoimmune, and chronic airways diseases, and cancer as a result of exposure to AGEs, as well as many other ligands. [ABSTRACT FROM AUTHOR]

المؤلفون: Parwani, Kirti¹ (AUTHOR), Patel, Farhin¹ (AUTHOR), Bhagwat, Pranav² (AUTHOR), Dilip, Haritha² (AUTHOR), Patel, Dhara¹ (AUTHOR), Thiruvenkatam, Vijay³ (AUTHOR), Mandal, Palash¹ (AUTHOR) palashmandal.bio@charusat.ac.in

المصدر: Archives of Physiology & Biochemistry. Apr2024, Vol. 130 Issue 2, p136-154. 19p.

مصطلحات موضوعية: *RECEPTOR for advanced glycation end products (RAGE), *ADVANCED glycation end-products, *RENAL fibrosis, *DIABETIC nephropathies, *KIDNEY diseases, *HIGH-fat diet

مستخلص: The molecular mechanism by which Swertiamarin (SM) prevents advanced glycation end products (AGEs) induced diabetic nephropathy (DN) has never been explored. To evaluate the effect of SM in preventing the progression of DN in high fat diet-streptozotocin-induced diabetic rats. After 1 week of acclimatisation, the rats were divided randomly into five groups as follows: (1) Control group, which received normal chow diet; (2) High-fat diet (HFD) group which was fed diet comprising of 58.7% fat, 27.5% carbohydrate and 14.4% protein); (3) Aminoguanidine (AG) group which received HFD + 100 mg/k.b.w.AG (intraperitoneal); (4) Metformin (Met) group which received HFD + 70 mg/k.b.w. the oral dose of Met and (5) SM group which was supplemented orally with 50 mg/k.b.w.SM along with HFD. After 12 weeks all HFD fed animals were given a single 35 mg/k.b.w. dose of streptozotocin with continuous HFD feeding for additional 18 weeks. Later, various biochemical assays, urine analyses, histopathological analysis of kidneys, levels of AGEs, expression of various makers, and in-silico analysis were performed. The diabetic group demonstrated oxidative stress, increased levels of AGEs, decreased renal function, fibrosis in the renal tissue, higher expression of the receptor for advanced glycation end products (RAGE), which were ameliorated in the SM treated group. In-silico analysis suggests that SM can prevent the binding of AGEs with RAGE. SM ameliorated DN by inhibiting the oxidative stress induced by AGEs. SM reduces the levels of hyperglycaemia-induced advanced glycation end products in serum and renal tissue. SM prevents renal fibrosis by inhibiting the EMT in the kidney tissue. The in-silico analysis proves that SM can inhibit the binding of various AGEs with RAGE, thereby inhibiting the AGE-RAGE axis. [ABSTRACT FROM AUTHOR]

المؤلفون: Olson, Lucas C.^1,2 (AUTHOR), Nguyen, Tri¹ (AUTHOR), Sabalewski, Eleanor L.¹ (AUTHOR), Puetzer, Jennifer L.^1,3 (AUTHOR), Schwartz, Zvi^1,4 (AUTHOR), McClure, Michael J.^1,3 (AUTHOR) mccluremj2@vcu.edu

المصدر: American Journal of Physiology: Cell Physiology. Apr2024, Vol. 326 Issue 4, pC1080-C1093. 14p.

مصطلحات موضوعية: *RECEPTOR for advanced glycation end products (RAGE), *ADVANCED glycation end-products, *MYOBLASTS, *MUSCLE aging, *COLLAGEN, *SKELETAL muscle

مستخلص: Advanced glycation end-products (AGEs) stochastically accrue in skeletal muscle and on collagen over an individual's lifespan, stiffening the muscle and modifying the stem cell (MuSC) microenvironment while promoting proinflammatory, antiregenerative signaling via the receptor for advanced glycation end-products (RAGEs). In the present study, a novel in vitro model was developed of this phenomenon by cross linking a 3-D collagen scaffold with AGEs and investigating how myoblasts responded to such an environment. Briefly, collagen scaffolds were incubated with d -ribose (0, 25, 40, 100, or 250 mM) for 5 days at 37°C. C2C12 immortalized mouse myoblasts were grown on the scaffolds for 6 days in growth conditions for proliferation, and 12 days for differentiation and fusion. Human primary myoblasts were also used to confirm the C2C12 data. AGEs aberrantly extended the DNA production stage of C2C12s (but not in human primary myoblasts) which is known to delay differentiation in myogenesis, and this effect was prevented by RAGE inhibition. Furthermore, the differentiation and fusion of myoblasts were disrupted by AGEs, which were associated with reductions in integrins and suppression of RAGE. The addition of S100b (RAGE agonist) recovered the differentiation and fusion of myoblasts, and the addition of RAGE inhibitors (FPS-ZM1 and Azeliragon) inhibited the differentiation and fusion of myoblasts. Our results provide novel insights into the role of the AGE-RAGE axis in skeletal muscle aging, and future work is warranted on the potential application of S100b as a proregenerative factor in aged skeletal muscle. NEW & NOTEWORTHY: Collagen cross-linked by advanced glycation end-products (AGEs) induced myoblast proliferation but prevented differentiation, myotube formation, and RAGE upregulation. RAGE inhibition occluded AGE-induced myoblast proliferation, while the delivery of S100b, a RAGE ligand, recovered fusion deficits. [ABSTRACT FROM AUTHOR]

المؤلفون: Chen, Xi¹ (AUTHOR) chenxi_1009@126.com, Wang, Ruichun² (AUTHOR), Yu, Haixia¹ (AUTHOR), Huang, Yingying¹ (AUTHOR), Zhang, Simin² (AUTHOR) zhangsm0701@163.com

المصدر: Journal of Aquatic Food Product Technology. 2024, Vol. 33 Issue 3, p275-290. 16p.

مصطلحات موضوعية: *AROMATIC amines, *RECEPTOR for advanced glycation end products (RAGE), *ADVANCED glycation end-products, *HAZARDOUS substances, *LIPIDS

مستخلص: The formation of hazardous substances, heterocyclic aromatic amines (HAAs) and two representative advanced glycation end products (AGEs), Nε-carboxymethyl-lysine (CML) and Nε-carboxyethyl-lysine (CEL) in five kinds of fish with different fat contents during thermal processing was investigated. The results indicated that HAAs, AGEs produced is related to the lipids in varying degrees. The variation of key precursors were examined to explain the relationship between fat oxidation and molecular pathway of HAAs and AGEs formation. The current research may help us better understand the overall generation of hazardous substances in food systems, and provide new ideas for formulating prevention in future production. [ABSTRACT FROM AUTHOR]

المؤلفون: Lee, Jeonghoon¹ (AUTHOR), Huh, Seonghoo² (AUTHOR), Park, Kyungtaek³ (AUTHOR), Kang, Nuree¹ (AUTHOR), Yu, Hyun Sook² (AUTHOR), Park, Hong Geun² (AUTHOR), Kim, Yong Sik⁴ (AUTHOR), Kang, Ung Gu^1,5 (AUTHOR), Won, Sungho^3,6,7,8 (AUTHOR), Kim, Se Hyun¹ (AUTHOR) sh3491@snu.ac.kr

المصدر: Psychopharmacology. Apr2024, Vol. 241 Issue 4, p817-832. 16p.

مصطلحات موضوعية: *RECEPTOR for advanced glycation end products (RAGE), *NF-kappa B, *ADVANCED glycation end-products, *TUMOR necrosis factors, *NEURAL inhibition, *ELECTROCONVULSIVE therapy

مستخلص: Rationale: Electroconvulsive therapy (ECT) is an effective treatment modality for schizophrenia. However, its antipsychotic-like mechanism remains unclear. Objectives: To gain insight into the antipsychotic-like actions of ECT, this study investigated how repeated treatments of electroconvulsive seizure (ECS), an animal model for ECT, affect the behavioral and transcriptomic profile of a neurodevelopmental animal model of schizophrenia. Methods: Two injections of MK-801 or saline were administered to rats on postnatal day 7 (PN7), and either repeated ECS treatments (E10X) or sham shock was conducted daily from PN50 to PN59. Ultimately, the rats were divided into vehicle/sham (V/S), MK-801/sham (M/S), vehicle/ECS (V/E), and MK-801/ECS (M/E) groups. On PN59, prepulse inhibition and locomotor activity were tested. Prefrontal cortex transcriptomes were analyzed with mRNA sequencing and network and pathway analyses, and quantitative real-time polymerase chain reaction (qPCR) analyses were subsequently conducted. Results: Prepulse inhibition deficit was induced by MK-801 and normalized by E10X. In M/S vs. M/E model, Egr1, Mmp9, and S100a6 were identified as center genes, and interleukin-17 (IL-17), nuclear factor kappa B (NF-κB), and tumor necrosis factor (TNF) signaling pathways were identified as the three most relevant pathways. In the V/E vs. V/S model, mitophagy, NF-κB, and receptor for advanced glycation end products (RAGE) pathways were identified. qPCR analyses demonstrated that Igfbp6, Btf3, Cox6a2, and H2az1 were downregulated in M/S and upregulated in M/E. Conclusions: E10X reverses the behavioral changes induced by MK-801 and produces transcriptional changes in inflammatory, insulin, and mitophagy pathways, which provide mechanistic insight into the antipsychotic-like mechanism of ECT. [ABSTRACT FROM AUTHOR]