Journal articles: 'AlSb LCQ'

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Bicchi, Ilaria, Francesco Morena, Chiara Argentati, Laura Rota Nodari, Carla Emiliani, Maurizio Gelati, Angelo L. Vescovi, and Sabata Martino. "Storage of Mutant Human SOD1 in Non-Neural Cells from the Type-1 Amyotrophic Lateral Sclerosis ratG93A Model Correlated with the Lysosomes’ Dysfunction." Biomedicines 9, no. 9 (August 24, 2021): 1080. http://dx.doi.org/10.3390/biomedicines9091080.

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Herein, we explored the impact of the lysosome dysfunction during the progression of Amyotrophic Lateral Sclerosis type-1 (ALS1). We conducted the study in non-neural cells, primary fibroblasts (rFFFs), and bone marrow-mesenchymal stem cells (rBM-MSCs), isolated from the animal model ratG93A for ALS1 at two stages of the disease: Pre-symptomatic-stage (ALS1-PreS) and Terminal-stage (ALS1-EndS). We documented the storage of human mutant Superoxide Dismutase 1, SOD1G93A (SOD1*) in the lysosomes of ALS1-rFFFs and ALS1-rBM-MSCs and demonstrated the hallmarks of the disease in non-neural cells as in ratG93A-ALS1-tissues. We showed that the SOD1* storage is associated with the altered glycohydrolases and proteases levels in tissues and both cell types from ALS1-PreS to ALS1-EndS. Only in ALS1-rFFFs, the lysosomes lost homeostasis, enlarge drastically, and contribute to the cell metabolic damage. Contrariwise, in ALS1-rBM-MSCs, we found a negligible metabolic dysfunction, which makes these cells’ status similar to WT. We addressed this phenomenon to a safety mechanism perhaps associated with an enhanced lysosomal autophagic activity in ALS1-rBM-MSCs compared to ALS1-rFFFs, in which the lysosomal level of LC3-II/LC3I was comparable to that of WT-rFFFs. We suggested that the autophagic machinery could balance the storage of SOD1* aggregates and the lysosomal enzyme dysfunction even in ALS1-EndS-stem cells.

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Weidema, Bo Pedersen. "ISO 14044 also Applies to Social LCA." International Journal of Life Cycle Assessment 10, no. 6 (November 2005): 381. http://dx.doi.org/10.1065/lca2005.11.002.

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Taran, Yu V., Jürgen Schreiber, Mark R. Daymond, and E. C. Oliver. "Fatigue Degradation and Martensitic Transformation of Austenitic Stainless Steel AlSi 321: New Results and Prospects." Materials Science Forum 524-525 (September 2006): 899–904. http://dx.doi.org/10.4028/www.scientific.net/msf.524-525.899.

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On ECRS-6 [1], we have presented first results of the researches of fatigue degradation and martensitic transformation of austenitic stainless steel AISI 321 by neutron diffraction stress analysis. A series of samples preliminary ex-situ cyclically fatigued at the frequency of 5 and 0.5 Hz was in-situ tested on the stress rig of the ENGIN instrument. In the high cycle fatigued (HCF) samples, the applied stress-elastic strain responses of austenite and martensite phases were find out to be strongly different as compared to the low cycle fatigued (LCF) samples, in which they are close. Moreover, the martensite Poisson ratio in the HCF-samples is almost twice to that of observed 0.28-0.30 in austenite and in both phases of the LCF-samples. With the purpose to search the reason of such unusual behavior of the martensite phase, one of the HCF-samples has been anew in-situ tested on the stress rig of the ENGIN-X in: 1) a LCF-mode at the frequency of 0.1 Hz to increase the fatigue level, and 2) a quasistatic mode to measure the applied stress-elastic strain responses of both phases. Also, two of the LCF-samples have been subjected to the ex-situ secondary HCF-testing at the frequency of 5 Hz and again in-situ measured on the ENGIN-X stress rig. Results of the mechanical characterization of phases in the twice fatigued austenitic stainless steel are presented and discussed.

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Holmes, Margaret A., Wendy Paulsene, Xu Jide, Colin Ratledge, and Roland K. Strong. "Siderocalin (Lcn 2) Also Binds Carboxymycobactins, Potentially Defending against Mycobacterial Infections through Iron Sequestration." Structure 13, no. 1 (January 2005): 29–41. http://dx.doi.org/10.1016/j.str.2004.10.009.

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Dreyer, Louise, and Michael Hauschild. "Scoping Must be Done in Accordance with the Goal Definition, also in Social LCA." International Journal of Life Cycle Assessment 11, no. 2 (March 2006): 87. http://dx.doi.org/10.1065/lca2006.02.004.

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Wróblewska, Barbara, Lidia Hanna Markiewicz, Anna Maria Szyc, Mariola Aleksandra Dietrich, Agata Szymkiewicz, and Joanna Fotschki. "Lactobacillus casei LcY decreases milk protein immunoreactivity of fermented buttermilk but also contains IgE-reactive proteins." Food Research International 83 (May 2016): 95–101. http://dx.doi.org/10.1016/j.foodres.2016.02.016.

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Okamura, Takayuki, Ann M. Leen, Uluhan Silli, Stephen M. Gottschalk, Stephane Vigouroux, Helen E. Heslop, Malcolm K. Brenner, and Cliona M. Rooney. "Retrovirus-Transduced T Cell Blasts Have Not Only Antigen-Presenting Capabilities but Also Suppressor Regulatory T Cell-Inducing Capability." Blood 104, no. 11 (November 16, 2004): 3855. http://dx.doi.org/10.1182/blood.v104.11.3855.3855.

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Abstract EBV-associated T/NK-lymphoproliferative diseases (LPD) are relatively rare but their prognosis is very poor. In order to understand the pathogenesis and rationalize immunotherapy, it is important to know whether EBV-infected T/NK cells have antigen-presenting capacities and how they escape the EBV-specific immunity that controls virus-infected B cells and epithelial cells. As a model for T cell antigen presenting cells (T-APC), we used activated T cells expressing pp65, the immunodominant antigen of CMV, after retroviral transduction. Two to three days after activation with CD3/28, T cells were transduced with retrovirus supernatants for 24h to 48 hr on retronectin-coated plates, and then expanded for one to two weeks with IL-2 before use as APCs or target cells. As control APCs, we used LCLs transduced with a retrovirus vector expressing pp65 (pp65-LCL). Pp65-expressing T cells functioned as target cells, since they were readily killed by pp65-specific cytotoxic T cells (CTL), reactivated using Adenovirus-pp65-pulsed dendritic cells. Furthermore, pp65T-APCs could reactivate pp65-specific CD8+ CTL from autologous PBMC. However, the pp65T-APC could not sustain prolonged pp65-specific CTL expansion. The ratio of CD4+: CD8+ T cells increased in responders after the 2nd stimulation with pp65-T-APC, and after the 3rd stimulation, the CD8+ CTL had virtually disappeared so that most of live cells were CD4+ T cells. The majority of the CD4+ T cells co-expressed CD25, the glucocoticoid-induced TNF receptor (GITR) and intracellular antigen CD152, all markers of T regulatory cells. To determine if they had regulatory function, the CD4+CD25+ population was isolated and shown to inhibit the proliferation of autologous PBMCs stimulated by pp65-LCL. In contrast, the CD4+CD25− fraction did not inhibit proliferation. Transwell experiments revealed that the inhibition required cell-to-cell contact. CFSE analysis showed that the CD4+CD25+ cells expanded while inhibiting the proliferation of stimulated PBMC. Taken together, these findings indicated that T-APC could reactivate antigen specific CD8+ CTL, but at the same time they activated regulatory CD4+ T cells, which prevented the long-term expansion of the CD8+ CTL. Similar results were found when the LMP2 antigen of EBV, which is expressed in T/NK-LPD, was used as antigen. Thus the immune escape of EBV-associated T/NK-LPD might result in part from their induction of regulatory T cells which inhibit T cell-specific CTL generation and function. T cells in general may evade immune-mediated recognition of their “novel” T cell receptors in the same way.

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Rosenfeld, Silvana A. "An Introduction to Zooarchaeology. DIANE GIFFORD-GONZALEZ. 2018. Springer International Publishing, New York. xxiii + 604 pp., 133 b/w illustrations, 4 illustrations in color. $99.00 (hardcover), ISBN 978-3-319-65680-9. Also available in paper, ISBN 978-3-030-09746-2, and ebook, ISBN 978-3-319-65682-3. DOI:10.1007/978-3-319-65682-3." Latin American Antiquity 30, no. 03 (September 2019): 661–62. http://dx.doi.org/10.1017/laq.2019.57.

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Tang, Qian, Cory M. Staub, Guofeng Gao, Qunyan Jin, Zhengke Wang, Wei Ding, Rosemarie E. Aurigemma, and Kathleen M. Mulder. "A Novel Transforming Growth Factor-β Receptor-interacting Protein That Is Also a Light Chain of the Motor Protein Dynein." Molecular Biology of the Cell 13, no. 12 (December 2002): 4484–96. http://dx.doi.org/10.1091/mbc.e02-05-0245.

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The phosphorylated, activated cytoplasmic domains of the transforming growth factor-β (TGFβ) receptors were used as probes to screen an expression library that was prepared from a highly TGFβ-responsive intestinal epithelial cell line. One of the TGFβ receptor-interacting proteins isolated was identified to be the mammalian homologue of the LC7 family (mLC7) of dynein light chains (DLCs). This 11-kDa cytoplasmic protein interacts with the TGFβ receptor complex intracellularly and is phosphorylated on serine residues after ligand-receptor engagement. Forced expression of mLC7-1 induces specific TGFβ responses, including an activation of Jun N-terminal kinase (JNK), a phosphorylation of c-Jun, and an inhibition of cell growth. Furthermore, TGFβ induces the recruitment of mLC7-1 to the intermediate chain of dynein. A kinase-deficient form of TGFβ RII prevents both mLC7-1 phosphorylation and interaction with the dynein intermediate chain (DIC). This is the first demonstration of a link between cytoplasmic dynein and a natural growth inhibitory cytokine. Furthermore, our results suggest that TGFβ pathway components may use a motor protein light chain as a receptor for the recruitment and transport of specific cargo along microtublules.

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Bar, Isabelle, Ahmad Merhi, Fadi Abdel-Sater, Abduelhakem Ben Addi, Sara Sollennita, Jean-Luc Canon, and Paul Delrée. "The MicroRNA miR-210 Is Expressed by Cancer Cells but Also by the Tumor Microenvironment in Triple-Negative Breast Cancer." Journal of Histochemistry & Cytochemistry 65, no. 6 (April 12, 2017): 335–46. http://dx.doi.org/10.1369/0022155417702849.

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The triple-negative breast cancer (TNBC) subtype occurs in about 15% of breast cancer and is an aggressive subtype of breast cancer with poor outcome. Furthermore, treatment of patients with TNBC is more challenging due to the heterogeneity of the disease and the absence of well-defined molecular targets. Microribonucleic acid (RNA) represents a new class of biomarkers that are frequently dysregulated in cancer. It has been described that the microRNA miR-210 is highly expressed in TNBC, and its overexpression had been linked to poor prognosis. TNBC are often infiltrated by immune cells that play a key role in cancer progression. The techniques traditionally used to analyze miR-210 expression such as next generation sequencing or quantitative real-time polymerase chain reaction (PCR) do not allow the precise identification of the cellular subtype expressing the microRNA. In this study, we have analyzed miR-210 expression by in situ hybridization in TNBC. The miR-210 signal was detected in tumor cells, but also in the tumor microenvironment, in a region positive for the pan-leucocyte marker CD45-LCA. Taken together, our results demonstrate that miR-210 is expressed in tumor cells but also in the tumor microenvironment. Our results also highlight the utility of using complementary approaches to take into account the cellular context of microRNA expression.

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Nodehi, Mehrab, Federico Aguayo, Nicole Madey, and Lei Zhou. "A Comparative Review of Polymer, Bacterial-based, and Alkali-Activated (also Geopolymer) Binders: Production, Mechanical, Durability, and Environmental impacts (life cycle assessment (LCA))." Construction and Building Materials 422 (April 2024): 135816. http://dx.doi.org/10.1016/j.conbuildmat.2024.135816.

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12

Duan, Yuanyuan, Guangqiang Li, Miaomiao Xu, and Zhinan Yin. "CFTR, which not only serves as a TCR signaling molecule but also function as an anion channel, dual-negatively regulates IFN-γ production and tumor immunity in γδ T cells." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 60.10. http://dx.doi.org/10.4049/jimmunol.202.supp.60.10.

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Abstract γδ T cells have been demonstrated to have the MHC independent-broad anti-tumor activities with high IFN-γ production in the infiltration of the tumor tissue, therefore, they become the strongest interest for cancer immunotherapy. Ion channels play critical roles in the cell functions, especially in the regulation of immune cells functions. Cystic fibrosis transmembrane conductance regulator (CFTR) is an important chloride channel and regulator in the apical membrane of epithelial cells. Recently, CFTR was reported to participate in the immune regulation and likely account for the risk of developing cancer. However, little is known about the effect of CFTR on γδ T cells tumor immunity. In this study, we would like to elucidate the regulatory mechanisms and indispensable functions of CFTR on γδ T cells in tumor immunity. We found that genetic deletion of CFTR displayed the increased TCR signaling and elevates IFN-γ release in peripheral γδ T cells, but not in CD4+ T cells. The absence of CFTR in γδ T cells strengthened the TCR signaling. The underlying mechanism of higher TCR signaling was likely that CFTR may participate in TCR signaling via interacting with the PLCγ-1-LCK-ZAP70 signaling complex in γδ T cells. Consistent with the data in mice, CFTR inhibition, which increased intracellular Ca2+ concentration, significantly increased the IFN-γ production in γδ T cells. Finally, CFTR−/−γδ T cells displayed higher cytolytic ability against the B16 melanoma and protected against B16 tumor growth. This study systematically defined the roles of CFTR in the activation of γδ T cells and its potential contribution to tumor immunity, which will enrich the γδ T cells biology and expand the sight for the application of CFTR in γδ T cells cancer immunotherapy.

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Subbarayalu, Panneerdoss, Daisy Medina, Pooja Yadav, Santosh Timilsina, Kunal Baxi, Ratna Vadlamudi, Yidong Chen, and Manjeet Rao. "Abstract 3528: ALKBH5 promotes cancer growth by regulating ER homeostasis via UPR, autophagy, and mitochondrial function." Cancer Research 83, no. 7_Supplement (April 4, 2023): 3528. http://dx.doi.org/10.1158/1538-7445.am2023-3528.

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Abstract Background: N6-methyladenosine (m6A) RNA methylation is a dynamic reversible epitranscriptomic modification that includes methyl transferases (writes m6A), demethylases (erases m6A) and reader proteins, which proofreads m6A marks of a specific site of transcripts. Recent studies have suggested that RNA methylation affects several fundamental cellular and molecular functions including mRNA splicing, stability, export, stem cell fate, circadian rhythms, DNA repair and cell survival. The objective of this study is to establish the mechanisms by which RNA demethylase ALKBH5 (AlkB homolog 5) facilitates tumor growth and progression. Methods: To establish the significance of RNA methylation in children’s cancers, we performed siRNA screen targeting m6A writers, erasers, and readers in osteosarcoma (OS). We used several OS cell lines including 143B, MG63, SaOS2, U2OS and multiple patient derived OS cell lines. Mechanistic studies were conducted using ALKBH5 KO and knockdown cells and by measuring the status of Autophagy and UPR associated proteins using Western blot analysis, confocal and electron microscopy. Results: Our results revealed that depletion of ALKBH5, a demethylase that erases the m6A mark from the target gene, altered the autophagy in OS cells. Interestingly, we found that level of LC3, which is the universal marker for autophagy, was significantly increased in OS cells. RNA seq analysis showed that depletion of ALKBH5 significantly altered several autophagy related genes in the OS cells. To better understand the molecular mechanism by which ALKBH5 regulates autophagy, we investigated the Endoplasmic Reticulum (ER) stress-induced Unfolded Protein Response (UPR) pathway, which is a known activator of autophagy. We discovered that ER stress induced UPR signaling pathway is highly activated in ALKBH5 depleted cancer cells. Further, mechanistic studies suggested that ALKBH5 promoted ER homeostasis by controlling the expression of ER lipid raft associated 1 (ERLIN1), which binds to the activated inositol 1, 4, 5,-triphosphate receptor and facilitates its degradation via ERAD to maintain calcium flux between ER and mitochondria. Using functional studies and electron microscopy, we show that ALKBH5-ERLIN1-IP3R-dependent calcium signaling modulates the activity of AMP kinase, and consequently mitochondrial biogenesis. These findings thus reveal that ALKBH5 serves an important role in maintaining ER homeostasis and cellular fitness. Conclusion: These findings provide novel insight into how m6A may promote cancer cell growth by regulating the crosstalk among ER signaling, UPR, autophagy, and mitochondrial function. Our study is the first to show that RNA methylation plays an important role in osteosarcoma by regulating autophagy via UPR. Citation Format: Panneerdoss Subbarayalu, Daisy Medina, Pooja Yadav, Santosh Timilsina, Kunal Baxi, Ratna Vadlamudi, Yidong Chen, Manjeet Rao. ALKBH5 promotes cancer growth by regulating ER homeostasis via UPR, autophagy, and mitochondrial function. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3528.

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Zhang, Yiguo, Lu Qiu, Shaojun Li, Yuancai Xiang, Jiayu Chen, and Yonggang Ren. "The C-Terminal Domain of Nrf1 Negatively Regulates the Full-Length CNC-bZIP Factor and Its Shorter Isoform LCR-F1/Nrf1β; Both Are Also Inhibited by the Small Dominant-Negative Nrf1γ/δ Isoforms that Down-Regulate ARE-Battery Gene Expression." PLoS ONE 9, no. 10 (October 7, 2014): e109159. http://dx.doi.org/10.1371/journal.pone.0109159.

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Tripathi, Priyanka, Haihong Guo, Alice Dreser, Alfred Yamoah, Antonio Sechi, Christopher Marvin Jesse, Istvan Katona, et al. "Pathomechanisms of ALS8: altered autophagy and defective RNA binding protein (RBP) homeostasis due to the VAPB P56S mutation." Cell Death & Disease 12, no. 5 (May 2021). http://dx.doi.org/10.1038/s41419-021-03710-y.

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AbstractMutations in RNA binding proteins (RBPs) and in genes regulating autophagy are frequent causes of familial amyotrophic lateral sclerosis (fALS). The P56S mutation in vesicle-associated membrane protein-associated protein B (VAPB) leads to fALS (ALS8) and spinal muscular atrophy (SMA). While VAPB is primarily involved in the unfolded protein response (UPR), vesicular trafficking and in initial steps of the autophagy pathway, the effect of mutant P56S-VAPB on autophagy regulation in connection with RBP homeostasis has not been explored yet. Examining the muscle biopsy of our index ALS8 patient of European origin revealed globular accumulations of VAPB aggregates co-localised with autophagy markers LC3 and p62 in partially atrophic and atrophic muscle fibres. In line with this skin fibroblasts obtained from the same patient showed accumulation of P56S-VAPB aggregates together with LC3 and p62. Detailed investigations of autophagic flux in cell culture models revealed that P56S-VAPB alters both initial and late steps of the autophagy pathway. Accordingly, electron microscopy complemented with live cell imaging highlighted the impaired fusion of accumulated autophagosomes with lysosomes in cells expressing P56S-VAPB. Consistent with these observations, neuropathological studies of brain and spinal cord of P56S-VAPB transgenic mice revealed signs of neurodegeneration associated with altered protein quality control and defective autophagy. Autophagy and RBP homeostasis are interdependent, as demonstrated by the cytoplasmic mis-localisation of several RBPs including pTDP-43, FUS, Matrin 3 which often sequestered with P56S-VAPB aggregates both in cell culture and in the muscle biopsy of the ALS8 patient. Further confirming the notion that aggregation of the RBPs proceeds through the stress granule (SG) pathway, we found persistent G3BP- and TIAR1-positive SGs in P56S-VAPB expressing cells as well as in the ALS8 patient muscle biopsy. We conclude that P56S-VAPB-ALS8 involves a cohesive pathomechanism of aberrant RBP homeostasis together with dysfunctional autophagy.

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Ledwaba, Solanka Ellen, David Thomas Bolick, Pedro Henrique Quintela Soares de Medeiros, Glynis Luanne Kolling, Afsatou Ndama Traore, Natasha Potgieter, James Paul Nataro, and Richard Littleton Guerrant. "Enteropathogenic Escherichia coli (EPEC) expressing a non-functional bundle-forming pili (BFP) also leads to increased growth failure and intestinal inflammation in C57BL/6 mice." Brazilian Journal of Microbiology, July 26, 2022. http://dx.doi.org/10.1007/s42770-022-00802-5.

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Abstract Bundle-forming pili (BFP) are implicated in the virulence of typical enteropathogenic E. coli (EPEC), resulting in enhanced colonization and mild to severe disease outcomes; hence, non-functional BFP may have a major influence on disease outcomes in vivo. Weaned antibiotic pre-treated C57BL/6 mice were orally infected with EPEC strain UMD901 (E2348/69 bfpA C129S); mice were monitored daily for body weight; stool specimens were collected daily; and intestinal tissues were collected at the termination of the experiment on day 3 post-infection. Real-time PCR was used to quantify fecal shedding and tissue burden. Intestinal inflammatory biomarkers lipocalin-2 (LCN-2) and myeloperoxidase (MPO) were also assessed. Infection caused substantial body weight loss, bloody diarrhea, and intestinal colonization with fecal and intestinal tissue inflammatory biomarkers that were comparable to those previously published with the wild-type typical EPEC strain. Here we further report on the evaluation of an EPEC infection model, showing how disruption of bfp function does not impair, and may even worsen diarrhea, colonization, and intestinal disruption and inflammation. More research is needed to understand the role of bfp in pathogenicity of EPEC infections in vivo.

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Li, Xinyue, Le Guo, Jingan Chen, Haowei Liang, Yi Liu, Wei Chen, Li Zhou, Letian Shan, and Hui Wang. "Intravenous injection of human umbilical cord-derived mesenchymal stem cells ameliorates not only blood glucose but also nephrotic complication of diabetic rats through autophagy-mediated anti-senescent mechanism." Stem Cell Research & Therapy 14, no. 1 (May 29, 2023). http://dx.doi.org/10.1186/s13287-023-03354-z.

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Abstract Background Diabetic nephropathy (DN) is one of the most severe complications of diabetes mellitus, which is characterized by early occurrence of albuminuria and end-stage glomerulosclerosis. Senescence and autophagy of podocytes play an important role in DN development. Human umbilical cord-derived mesenchymal stem cells (hucMSCs) have potential in the treatment of diabetes and its complications. However, the role of hucMSCs in the treatment of DN and the underlying mechanism remain unclear. Methods In vivo, a streptozotocin-induced diabetic male Sprague Dawley rat model was established to determine the renoprotective effect of hucMSCs on DN by biochemical analysis, histopathology, and immunohistochemical staining of renal tissues. And the distribution of hucMSCs in various organs in rats within 168 h was analyzed. In vitro, CCK8 assay, wound healing assay, and β-galactosidase staining were conducted to detect the beneficial effects of hucMSCs on high glucose-induced rat podocytes. Real-time PCR and western blot assays were applied to explore the mechanism of action of hucMSCs. Results The in vivo data revealed that hucMSCs were distributed into kidneys and significantly protected kidneys from diabetic damage. The in vitro data indicated that hucMSCs improved cell viability, wound healing, senescence of the high glucose-damaged rat podocytes through a paracrine action mode. Besides, the altered expressions of senescence-associated genes (p16, p53, and p21) and autophagy-associated genes (Beclin-1, p62, and LC3) were improved by hucMSCs. Mechanistically, hucMSCs protected high glucose-induced injury in rat podocytes by activating autophagy and attenuating senescence through the AMPK/mTOR pathway. Conclusions In conclusion, hucMSCs might be a promising therapeutic strategy for the clinical treatment of DN-induced renal damages.

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Journal articles on the topic 'AlSb LCQ'

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