Journal articles: 'Aif1'

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Wissing, Silke, Paula Ludovico, Eva Herker, et al. "An AIF orthologue regulates apoptosis in yeast." Journal of Cell Biology 166, no. 7 (2004): 969–74. http://dx.doi.org/10.1083/jcb.200404138.

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Apoptosis-inducing factor (AIF), a key regulator of cell death, is essential for normal mammalian development and participates in pathological apoptosis. The proapoptotic nature of AIF and its mode of action are controversial. Here, we show that the yeast AIF homologue Ynr074cp controls yeast apoptosis. Similar to mammalian AIF, Ynr074cp is located in mitochondria and translocates to the nucleus of yeast cells in response to apoptotic stimuli. Purified Ynr074cp degrades yeast nuclei and plasmid DNA. YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis. Conversely, overexpression of Ynr074cp strongly stimulates apoptotic cell death induced by hydrogen peroxide and this effect is attenuated by disruption of cyclophilin A or the yeast caspase YCA1. We conclude that Ynr074cp is a cell death effector in yeast and rename it AIF-1 (Aif1p, gene AIF1).

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Gong, Xiaocheng, Xuepeng Li, Xin You, et al. "AIF1 was identified as an up-regulated gene contributing to CSFV Shimen infection in porcine alveolar macrophage 3D4/21 cells." PeerJ 8 (February 17, 2020): e8543. http://dx.doi.org/10.7717/peerj.8543.

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Classical swine fever (CSF) is a disease that is characterized by diffuse hemorrhaging, high fever, and high mortality rates. The pro-inflammatory characteristics of allograft inflammatory factor 1 (AIF1) have been well documented; however, insufficient attention has been given to porcine AIF1. In the present study, AIF1 was identified as a key player contributing to CSFV Shimen infection in porcine alveolar macrophage (PAM) 3D4/21 cell line. Our evaluation showed that AIF1 mRNA and protein are expressed at a time-dependent high level in CSFV Shimen-infected PAM 3D4/21 cells. The transcription and translation of IL6 were also significantly upregulated in infected PAM 3D4/21 cells. By utilizing overexpression RNAs approach, we showed that the cellular AIF1 induced an increased IL6 in PAM 3D4/21 cells. Furthermore, silencing of AIF1 suppressed CSFV Shimen-induced IL6 production in PAM 3D4/21 cells and also inhibited CSFV replication, whereas overexpression of recombinant AIF1 was beneficial for the replication of CSFV Shimen and promoting IL6 production in CSFV Shimen-infected PAM 3D4/21 cells. It is suggested CSFV Shimen induced IL6 in PAM 3D4/21 cells via AIF1 activation, which help clarify the AIF1-related inflammatory processes that occur on CSFV Shimen infected macrophages.

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Chai, Yi, Wei Liu, Junhua Wang, Libo Hu, and Yuqi Zhang. "IMMU-29. AIF1 IS A PROGNOSTIC BIOMARKER AND CORRELATED WITH IMMUNE INFILTRATES IN GLIOMAS." Neuro-Oncology 22, Supplement_3 (2020): iii365. http://dx.doi.org/10.1093/neuonc/noaa222.383.

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Abstract Gliomas remain highly variable clinical behaviors, leading to emerging studies to identify prognostic factors. AIF1 (Allograft Inflammatory Factor 1) is critical for promoting both macrophage- and dendritic cells (DCs)-mediated inflammatory response and growth of vascular smooth muscle cells and T-lymphocytes. Through comparative analyses of primary LGG patients from The Cancer Genome Atlas (TCGA) dataset and Chinese Glioma Genome Atlas(CGGA) dataset, we reported that the expression level and methylation level of AIF1 gene vary among glioma patients and AIF1 expression or gene body methylation is significantly associated with glioma patient survival. Cox regression results confirmed that AIF1 played an independent predictor of survival in lower-grade glioma(LGG), with a cox coefficient of 0.251 indicating a worse prognosis. Moreover, AIF1 expression was positively correlated with infiltrating levels of CD4+ T and B cells, macrophages, neutrophils, and DCs in LGG and glioblastoma(GBM). AIF1 expression also showed strong correlations with specific immune cell markers in LGG and GBM. In addition, AIF1 expression potentially contributed to the regulation of glioma-associated macrophages and microglia. In conclusion, our findings suggested that AIF1 was correlated with prognosis and immune infiltrating levels, and it can be used as a prognostic factor in gliomas.

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Zheng, Wei, Dejian Zhao, Hui Zhang, Prameladevi Chinnasamy, Nicholas Sibinga, and Jeffrey W. Pollard. "Induction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases." Wellcome Open Research 6 (March 8, 2021): 52. http://dx.doi.org/10.12688/wellcomeopenres.16569.1.

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Background: Metastatic breast cancer cells recruit macrophages (metastasis-associated macrophages, or MAMs) to facilitate their seeding, survival and outgrowth. However, a comprehensive understanding of the gene expression program in MAMs and how this program contributes to metastasis remain elusive. Methods: We compared the transcriptomes of MAMs recruited to lung metastases and resident alveolar macrophages (RAMs) and identified a large variety of differentially expressed genes and their associated signaling pathways. Some of the changes were validated using qRT-PCR and immunofluorescence. To probe the functional relevance to metastatic growth, a gene-targeting mouse model of female mice in the C57BL6/J background was used to study allograft inflammatory factor 1 (AIF1, also known as ionized calcium-binding adapter molecule 1 or IBA1). Results: Interferon signaling is one of the most activated pathways in MAMs, with strong upregulation of multiple components of the pathway and a significant enrichment for the gene signatures of interferon-alpha-treated human macrophages. Aif1, an interferon-responsive gene that regulates multiple macrophage activities, was robustly induced in MAMs. Aif1 deficiency in MAMs, however, did not affect development of lung metastases, suggesting that AIF1 indicates MAM activation but is dispensable for regulating metastasis. Conclusions: The drastically different gene expression profile of MAMs as compared to RAMs suggests an important role in promoting metastatic growth. Dissection of the underlying mechanisms and functional validation of potential targets in the profile may provide novel therapeutic strategies for the treatment of metastatic diseases.

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Zheng, Wei, Dejian Zhao, Hui Zhang, Prameladevi Chinnasamy, Nicholas Sibinga, and Jeffrey W. Pollard. "Induction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases." Wellcome Open Research 6 (June 23, 2021): 52. http://dx.doi.org/10.12688/wellcomeopenres.16569.2.

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Background: Metastatic breast cancer cells recruit macrophages (metastasis-associated macrophages, or MAMs) to facilitate their seeding, survival and outgrowth. However, a comprehensive understanding of the gene expression program in MAMs and how this program contributes to metastasis remain elusive. Methods: We compared the transcriptomes of MAMs recruited to lung metastases and resident alveolar macrophages (RAMs) and identified a large variety of differentially expressed genes and their associated signaling pathways. Some of the changes were validated using qRT-PCR and immunofluorescence. To probe the functional relevance to metastatic growth, a gene-targeting mouse model of female mice in the C57BL6/J background was used to study allograft inflammatory factor 1 (AIF1, also known as ionized calcium-binding adapter molecule 1 or IBA1). Results: Interferon signaling is one of the most activated pathways in MAMs, with strong upregulation of multiple components of the pathway and a significant enrichment for the gene signatures of interferon-alpha-treated human macrophages. Aif1, an interferon-responsive gene that regulates multiple macrophage activities, was robustly induced in MAMs. Aif1 deficiency in MAMs, however, did not affect development of lung metastases, suggesting that AIF1 indicates MAM activation but is dispensable for regulating metastasis. Conclusions: The drastically different gene expression profile of MAMs as compared to RAMs suggests an important role in promoting metastatic growth. Dissection of the underlying mechanisms and functional validation of potential targets in the profile may provide novel therapeutic strategies for the treatment of metastatic diseases.

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Han, Binsong, Yaqiong Jian, Xubin Xia, Wei Hu, Lina Zhang, and Peng Zhou. "Studying the effects of sea cucumber ovum powder on nonalcoholic fatty liver disease by proteomics techniques in a rat model." Food & Function 11, no. 7 (2020): 6139–47. http://dx.doi.org/10.1039/d0fo00741b.

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Schmitt, Emmanuelle, Pierre-Damien Coureux, Auriane Monestier, Etienne Dubiez, and Yves Mechulam. "Start Codon Recognition in Eukaryotic and Archaeal Translation Initiation: A Common Structural Core." International Journal of Molecular Sciences 20, no. 4 (2019): 939. http://dx.doi.org/10.3390/ijms20040939.

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Understanding molecular mechanisms of ribosomal translation sheds light on the emergence and evolution of protein synthesis in the three domains of life. Universally, ribosomal translation is described in three steps: initiation, elongation and termination. During initiation, a macromolecular complex assembled around the small ribosomal subunit selects the start codon on the mRNA and defines the open reading frame. In this review, we focus on the comparison of start codon selection mechanisms in eukaryotes and archaea. Eukaryotic translation initiation is a very complicated process, involving many initiation factors. The most widespread mechanism for the discovery of the start codon is the scanning of the mRNA by a pre-initiation complex until the first AUG codon in a correct context is found. In archaea, long-range scanning does not occur because of the presence of Shine-Dalgarno (SD) sequences or of short 5′ untranslated regions. However, archaeal and eukaryotic translation initiations have three initiation factors in common: e/aIF1, e/aIF1A and e/aIF2 are directly involved in the selection of the start codon. Therefore, the idea that these archaeal and eukaryotic factors fulfill similar functions within a common structural ribosomal core complex has emerged. A divergence between eukaryotic and archaeal factors allowed for the adaptation to the long-range scanning process versus the SD mediated prepositioning of the ribosome.

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Zhou, Jing, Jun Wu, Bo Li, et al. "PU.1 Is Essential For MLL Leukemia Via Activation Of The Meis/HOX Pathway and A Monocytic Cytokine Mediated Anti-Apoptotic Inflammatory Program." Blood 122, no. 21 (2013): 1276. http://dx.doi.org/10.1182/blood.v122.21.1276.1276.

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Abstract Aberrant transcriptional programs play a critical role in the development of acute myeloid leukemias (AMLs). Although persistent over-expression of MEIS1 and HOXA9 has been shown to be essential for the initiation and maintenance of MLL-associated leukemia, it is still poorly understood what additional transcriptional regulators, independent of the MLL fusion-driven MEIS/HOX pathway, dictate the development of MLL leukemia. Considering that AMLs with MLL translocation are typically associated with the monocytic lineage (FAB M4 and M5), we explored the potential role of the monocytic lineage-specific transcriptional program in MLL leukemia. Using 97 genome-wide expression profiles of human MLL leukemias, we constructed an MLL distinctive transcriptional regulatory network. In addition to well-known transcriptional factors in leukemia development such as MEIS1 and HOXA family genes, we identified a highly active monocyte-specific gene signature that includes transcription factor PU.1. In our effort to determine the functional role of PU.1 in MLL leukemia, we found that lower PU.1 expression significantly delayed the onset of MLL- AF9 induced leukemia in primary bone marrow transplantation assay. MLL leukemia failed to maintain in vivo upon induced deletion of the PU.1 gene. To examine the clinical relevance of the PU.1 in AML patients, we further performed multivariate Cox proportional-hazards regression analysis in four published datasets of patients with AML, for whom gene expression and time-to-event data were available. We found that a PU.1-regulated 40-gene signature showed profound concordance with prognosis in segregating high-risk and low-risk AML patients. When specific subgroups of AMLs were examined, the PU.1 expression signature could predict patient outcome for MLL patients, but not in other major AMLs, such as t(8;21), t(15;17) and inv(16). We further explored the molecular mechanisms underlying the critical role of the PU.1 program in MLL leukemia. Functional annotation of this PU.1 expression signature identified the MEIS/HOX pathway (MEIS1, FLT3, KIT), as well as key genes in the inflammatory response (AIF1, NF-KB1 and CD180). We showed that PU.1 is required to maintain high expression of Meis1 and Pbx3 and also important downstream genes in the MEIS/HOX pathway that includes known MEIS/HOX targets c-Kit and Flt3. Using ChIP-sequencing, we demonstrated that PU.1 interacts with the MEIS/HOX regulatory program through co-binding with MEIS1 at the target genomic regions in a MLL-ENL cell line. In our effort to determine the role of PU.1-controlled inflammatory response genes, we found that the growth inhibition in PU.1 knockdown MLL leukemic cells was partially rescued by addition of the monocytic inflammatory cytokine AIF1. AIF1 provides an anti-apoptotic effect through activation of the NF-ƒÛB pathway and additional known apoptosis regulators. Interestingly, AML patients with higher expression of both AIF1 and MEIS1 had a significantly shorter overall survival time than those with lower expression of both genes. Patients with high expression of either MEIS1 or AIF1 had medium survival possibilities. Notably, the prognostic value of AIF1 and MEIS1 remained in those with monocytic AMLs (P=0.00079), but not in the non- monocytic group of patients (p=0.105). Collectively, these results strongly suggest that the monocyte-specific inflammatory cytokine AIF1 is an MEIS/HOX independent essential regulator in monocytic AMLs such as MLL leukemia. Loss of function PU.1 is leukemogenic in mouse models. Suppression of PU.1 activity is also required for the development of human myelocytic M2/M3 leukemia. Here we reveal a converse role for PU.1 as an essential positive regulator in the development of MLL myeloid leukemia, mostly M4/M5 monocytic AMLs. Our study demonstrats that the monocyte-specific PU.1-driven transcriptional program independently contributes to the development of myeloid MLL leukemia, in parallel with the MLL fusion pathway. PU.1 and downstream macrophage specific inflammatory cytokine AIF1 have important prognostic value and may serve as novel therapeutic targets for MLL leukemias. Disclosures: No relevant conflicts of interest to declare.

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Cai, Linzhi, Sabrina V. Kirchleitner, Dongxu Zhao, et al. "Glioblastoma Exhibits Inter-Individual Heterogeneity of TSPO and LAT1 Expression in Neoplastic and Parenchymal Cells." International Journal of Molecular Sciences 21, no. 2 (2020): 612. http://dx.doi.org/10.3390/ijms21020612.

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Molecular imaging is essential for diagnosis and treatment planning for glioblastoma patients. Positron emission tomography (PET) with tracers for the detection of the solute carrier family 7 member 5 (SLC7A5; also known as the amino acid transporter light chain L system, LAT1) and for the mitochondrial translocator protein (TSPO) is successfully used to provide additional information on tumor volume and prognosis. The current approaches for TSPO-PET and the visualization of tracer ([18F] Fluoroethyltyrosine, FET) uptake by LAT1 (FET-PET) do not yet exploit the full diagnostic potential of these molecular imaging techniques. Therefore, we investigated the expression of TSPO and LAT1 in patient glioblastoma (GBM) samples, as well as in various GBM mouse models representing patient GBMs of different genetic subtypes. By immunohistochemistry, we found that TSPO and LAT1 are upregulated in human GBM samples compared to normal brain tissue. Next, we orthotopically implanted patient-derived GBM cells, as well as genetically engineered murine GBM cells, representing different genetic subtypes of the disease. To determine TSPO and LAT1 expression, we performed immunofluorescence staining. We found that both TSPO and LAT1 expression was increased in tumor regions of the implanted human or murine GBM cells when compared to the neighboring mouse brain tissue. While LAT1 was largely restricted to tumor cells, we found that TSPO was also expressed by microglia, tumor-associated macrophages, endothelial cells, and pericytes. The Cancer Genome Atlas (TCGA)-data analysis corroborates the upregulation of TSPO in a bigger cohort of GBM patient samples compared to tumor-free brain tissue. In addition, AIF1 (the gene encoding for the myeloid cell marker Iba1) was also upregulated in GBM compared to the control. Interestingly, TSPO, as well as AIF1, showed significantly different expression levels depending on the GBM genetic subtype, with the highest expression being exhibited in the mesenchymal subtype. High TSPO and AIF1 expression also correlated with a significant decrease in patient survival compared to low expression. In line with this finding, the expression levels for TSPO and AIF1 were also significantly higher in (isocitrate-dehydrogenase wild-type) IDHWT compared to IDH mutant (IDHMUT) GBM. LAT1 expression, on the other hand, was not different among the individual GBM subtypes. Therefore, we could conclude that FET- and TSPO-PET confer different information on pathological features based on different genetic GBM subtypes and may thus help in planning individualized strategies for brain tumor therapy in the future. A combination of TSPO-PET and FET-PET could be a promising way to visualize tumor-associated myeloid cells and select patients for treatment strategies targeting the myeloid compartment.

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Romanowski, Maciej, Karolina Kłoda, Sławomir Milczarek, et al. "Influence of AIF1 Gene Polymorphisms on Long-Term Kidney Allograft Function." Annals of Transplantation 20 (2015): 506–11. http://dx.doi.org/10.12659/aot.893885.

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Arvanitis, D. A., G. A. Flouris, and D. A. Spandidos. "Genomic rearrangements on VCAM1, SELE, APEG1 and AIF1 loci in atherosclerosis." Journal of Cellular and Molecular Medicine 9, no. 1 (2005): 153–59. http://dx.doi.org/10.1111/j.1582-4934.2005.tb00345.x.

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Muzaffar, Suhail, and Bharat B. Chattoo. "Apoptosis-inducing factor (Aif1) mediates anacardic acid-induced apoptosis in Saccharomyces cerevisiae." Apoptosis 22, no. 3 (2016): 463–74. http://dx.doi.org/10.1007/s10495-016-1330-6.

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Piotrowska, Katarzyna, Sylwia Słuczanowska-Głabowska, Mateusz Kurzawski, et al. "Over-Expression of Allograft Inflammatory Factor-1 (AIF-1) in Patients with Rheumatoid Arthritis." Biomolecules 10, no. 7 (2020): 1064. http://dx.doi.org/10.3390/biom10071064.

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Allograft inflammatory factor-1 (AIF-1) is a cytoplasmic protein that is encoded by the AIF1 gene. The main functions of AIF-1 are the activation of macrophages and enhancing the production of pro-inflammatory cytokines. To date, three different AIF-1 isoforms have been identified. In this study, we examined the expression of AIF-1 isoforms on the level of mRNA, and we compared the percentage of AIF-1-positive white blood cells (WBCs) in blood and AIF-1/CD68 cells in the synovial membranes in patients with rheumatoid arthritis (RA) and osteoarthritis (OA). We examined 15 patients with RA and 15 patients with OA who had previously undergone knee arthroplasty. Peripheral blood and synovial membranes (SMs) were collected from these patients during knee arthroplasty. We identified three AIF-1 mRNA expression variants in peripheral mononuclear cells (PBMCs) and SMs from patients in both groups. Spearman’s rank correlation coefficient tests showed strong, positive, and significant correlations between the three AIF-1 mRNA expression variants in PBMCs and/or SMs in patients with RA and OA. There were no statistically significant correlations for any of the AIF-1 mRNA expression variants between PBMCs and SMs in patients with RA and OA. We observed a statistically significant increased percentage of AIF-1-positive cells in patients with RA in comparison to patients with OA. The percentage of AIF-1-positive cells in the blood of patients with RA and OA was 1.35 ± 0.81% and 0.71 ± 0.25% (p < 0.01), respectively, whereas the percentage of AIF-1/CD68-positive WBC cells in the SMs was 24.05 ± 7.17% and 4.78 ± 1.52% (p < 0.001), respectively. In conclusion, three AIF-1 mRNA expression variants occurred in PBMCs and SM cells in patients with RA and OA. The AIF-1 mRNA expression levels of the variants correlated with each other in PBMCs and SM cells, but there were no statistically significant correlations for AIF-1 mRNA expression variants between PBMCs and SM cells in patients with RA and OA. Both in the blood and SMs, we observed an increased percentage of AIF-1-positive cells in patients with RA in comparison to patients with OA. The above results suggested that AIF-1 was the cytokine involved in the pathogenesis of RA. The precise knowledge of the role of AIF-1 in RA pathogenesis and the development of inflammatory response requires further investigations.

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Chang, Sue-Ling, André Tchernof, Francine Durocher, and Caroline Diorio. "Associations of Biomarkers of Inflammation and Breast Cancer in the Breast Adipose Tissue of Women with Combined Measures of Adiposity." Journal of Obesity 2021 (August 13, 2021): 1–10. http://dx.doi.org/10.1155/2021/3620147.

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Background. Mechanisms underlying the obesity-breast cancer link involve inflammation but need to be elucidated. Determining obesity by combining body mass index (BMI) with the waist circumference (WC) may clarify the role of inflammatory and hormonally related markers in breast cancer. We examined the effect of combining adiposity indices (BMI/WC) with the gene expression of several biomarkers involved in breast cancer. Methods. Expression of cytochrome P450 family 19 subfamily A member 1 (CYP19A1), estrogen receptor-alpha (ER-α), allograft inflammatory factor 1 (AIF1), cyclooxygenase-2 (COX2), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and leptin (LEP) in 141 adipose breast tissues was quantified using qPCR method. BMI and WC were measured by a trained nurse and categorized using the median split, BMILOWCLO, BMILOWCHI, BMIHIWCLO, and BMIHIWCHI. Results. Gene expression of IL-6 (3-fold), TNF-α (2-fold), and LEP (2-fold) was higher in the breast adipose tissue of women with high WC regardless of BMI, that is, BMILOWCHI and BMIHIWCHI women (all P < 0.01). Compared to BMILOWCLO women, gene expression of CYP19A1, COX2, and AIF1 was increased by two-fold in breast adipose tissue of BMIHIWCHI women ( P < 0.10). ER-α was not different across adiposity categories. Conclusions. The expression of some biomarkers, particularly those related to inflammation, is elevated in breast adipose tissue of women with a high WC independent of BMI. Obesity monitoring should also include women with normal or low BMI, but with central adiposity.

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Cao, C., R. Yu, Y. Xia, D. Liu, and Q. Gao. "AIF1 drives tumor progression via a cellular cross-talk with the tumor microenvironment." Gynecologic Oncology 159 (October 2020): 146. http://dx.doi.org/10.1016/j.ygyno.2020.05.200.

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Azzouz, Doua F., Nathalie Balandraud, Sami B. Kanaan, et al. "A7.2 Allograft Inflammatory Factor 1 (AIF1) Polymorphisms in French Caucasians with Rheumatoid Arthritis." Annals of the Rheumatic Diseases 72, Suppl 1 (2013): A48.2—A48. http://dx.doi.org/10.1136/annrheumdis-2013-203221.2.

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Ma, Feiyang, Yueqi Zhang, Yuzhou Wang, et al. "Role of Aif1 in regulation of cell death under environmental stress inCandida albicans." Yeast 33, no. 9 (2016): 493–506. http://dx.doi.org/10.1002/yea.3167.

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Tixhon, E., E. Robert, and B. Gilbert. "Molten KF-AIF3 System: A Study by Raman Spectroscopy." Applied Spectroscopy 48, no. 12 (1994): 1477–82. http://dx.doi.org/10.1366/0003702944027769.

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Molten AIF3-KF mixtures have been investigated in a wide composition range by Raman spectroscopy and with the use of a graphite windowless cell. The results of this study clearly show that the most intense spectrum components are made of three distinct bands whose intensities vary when the composition is changed. The most probable interpretation of our data is to consider the existence of an equilibrium between AIF63–, AIF52–, and AIF4−. This explanation is a confirmation of the conclusions of recent papers suggesting the presence of these species in similar AIF3-NaF mixtures. The presence of only one major polarized band for AIF52– is explained by considering a fast exchange between the axial and equatorial fluoride at the elevated experimental temperature (1300 K). A quantitative analysis of the distribution of the fluoroaluminate species has been performed by decomposition of the Raman-band envelope. The calculated equilibrium constants (expressed in mole fraction units) for AIF52– ⇌ AIF4− + F− and AIF63– ⇌ AIF52– + F− are KA = 0.11 ± 0.01 and KB = 5 ± 1, respectively. Compared with the NaF-AIF, system, these constants correspond to a stabilization of less coordinated fluoroaluminates when the size of the counterion increases.

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Amigoni, Loredana, Gianluca Frigerio, Enzo Martegani, and Sonia Colombo. "Involvement of Aif1 in apoptosis triggered by lack of Hxk2 in the yeastSaccharomyces cerevisiae." FEMS Yeast Research 16, no. 3 (2016): fow016. http://dx.doi.org/10.1093/femsyr/fow016.

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Xu, T., J. Xie, B. Zhu, M. Luo, X. Liu, and X. Wu. "Identification and function study of a novel AIF1 from the oyster, Crassostrea ariakensis Gould." Fish & Shellfish Immunology 34, no. 6 (2013): 1685–86. http://dx.doi.org/10.1016/j.fsi.2013.03.160.

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Biedenkapp, Joseph C., and Lisa R. Leon. "Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 9 (2013): R978—R986. http://dx.doi.org/10.1152/ajpregu.00011.2013.

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Heat stroke (HS) is characterized by a systemic inflammatory response syndrome (SIRS) consisting of profound core temperature (Tc) changes in mice. Encephalopathy is common at HS collapse, but inflammatory changes occurring in the brain during the SIRS remain unidentified. We determined the association between inflammatory gene expression changes in the brain with Tc disturbances during HS recovery in mice. Gene expression changes of heat shock protein (HSP)72, heme oxygenase (hmox1), cytokines (IL-1β, IL-6, TNF-α), cyclooxygenase enzymes (COX-1, COX-2), chemokines (MCP-1, MIP-1α, MIP-1β, CX3CR1), and glia activation markers (CD14, aif1, vimentin) were examined in the hypothalamus (HY) and hippocampus (HC) of control (Tc ∼ 36.0°C) and HS mice at Tc,Max (42.7°C), hypothermia depth (HD; 29.3 ± 0.4°C), and fever (37.8 ± 0.3°C). HSP72 (HY<HC) and IL-1β (HY only) were the only genes that showed increased expression at Tc,Max. HSP72 (HY < HC), hmox1 (HY < HC), cytokine (HY = HC), and chemokine (HY = HC) expression was highest at HD and similar to controls during fever. COX-1 expression was unaffected by HS, whereas HD was associated with approximately threefold increase in COX-2 expression (HY only). COX-2 expression was not increased during fever and indomethacin (COX inhibitor) had no effect on this Tc response indicating fever is regulated by other inflammatory pathways. CD14, aif1, and vimentin activation at HD coincided with maximal cytokine and chemokine expression suggesting glia cells are a possible source of brain cytokines and chemokines during HS recovery. The inflammatory gene expression changes during HS recovery suggest cytokines and/or chemokines may be initiating development or rewarming from hypothermia, whereas fever pathway(s) remain to be elucidated.

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Harney, S. M. J., C. Vilariño-Güell, I. E. Adamopoulos, et al. "Fine mapping of the MHC Class III region demonstrates association of AIF1 and rheumatoid arthritis." Rheumatology 47, no. 12 (2008): 1761–67. http://dx.doi.org/10.1093/rheumatology/ken376.

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Cai, Hao, Xiao-Dong Zhu, Jian-Yang Ao, et al. "Colony-stimulating factor-1-induced AIF1 expression in tumor-associated macrophages enhances the progression of hepatocellular carcinoma." OncoImmunology 6, no. 9 (2017): e1333213. http://dx.doi.org/10.1080/2162402x.2017.1333213.

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Sanfilippo, Cristina, Paola Castrogiovanni, Rosa Imbesi, and Michelino Di Rosa. "CHI3L2 Expression Levels Are Correlated with AIF1, PECAM1, and CALB1 in the Brains of Alzheimer’s Disease Patients." Journal of Molecular Neuroscience 70, no. 10 (2020): 1598–610. http://dx.doi.org/10.1007/s12031-020-01667-9.

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Raj, Abhishek, and Vasanthi Nachiappan. "Hydroquinone exposure accumulates neutral lipid by the activation of CDP-DAG pathway in Saccharomyces cerevisiae." Toxicology Research 10, no. 2 (2021): 354–67. http://dx.doi.org/10.1093/toxres/tfab005.

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Abstract Benzene metabolites (HQ and BQ) are toxic compounds and their presence in human cause alteration in cellular respiration and kidney damage. In the current study, Saccharomyces cerevisiae has been used as a model organism and acute exposure of hydroquinone (HQ) decreased cell growth and increased reactive oxygen species (ROS). The expression of apoptosis regulatory genes (YCA1, NUC1, YSP1 and AIF1) were increased with HQ exposure in the wild-type cells. HQ exposure in the wild-type cells altered both the phospholipid and neutral lipid levels. Phosphatidylcholine is a vital membrane lipid that has a vital role in membrane biogenesis and was increased significantly with HQ. The neutral lipid results were supported with lipid droplets data and mRNA expression study. The phospholipid knockouts (Kennedy pathway) accumulated neutral lipids via the CDP-DAG (cytidine-diphosphate-diacylglycerol) pathway genes both in the presence and absence of HQ.

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Pawlik, Andrzej. "AIF1 Gene RS2269475:C>T Polymorphism is Associated With Rheumatoid Arthritis Development but not With Disease Activity." Archives of Rheumatology 30, no. 2 (2015): 91–95. http://dx.doi.org/10.5606/archrheumatol.2015.5117.

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Alkassab, F., P. Gourh, F. K. Tan, et al. "An allograft inflammatory factor 1 (AIF1) single nucleotide polymorphism (SNP) is associated with anticentromere antibody positive systemic sclerosis." Rheumatology 46, no. 8 (2007): 1248–51. http://dx.doi.org/10.1093/rheumatology/kem057.

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Willats, Lisa, Soren Christensen, Henry K Ma, Geoffrey A Donnan, Alan Connelly, and Fernando Calamante. "Validating a Local Arterial Input Function Method for Improved Perfusion Quantification in Stroke." Journal of Cerebral Blood Flow & Metabolism 31, no. 11 (2011): 2189–98. http://dx.doi.org/10.1038/jcbfm.2011.78.

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In bolus-tracking perfusion magnetic resonance imaging (MRI), temporal dispersion of the contrast bolus due to stenosis or collateral supply presents a significant problem for accurate perfusion quantification in stroke. One means to reduce the associated perfusion errors is to deconvolve the bolus concentration time-course data with local Arterial Input Functions (AIFs) measured close to the capillary bed and downstream of the arterial abnormalities causing dispersion. Because the MRI voxel resolution precludes direct local AIF measurements, they must be extrapolated from the surrounding data. To date, there have been no published studies directly validating these local AIFs. We assess the effectiveness of local AIFs in reducing dispersion-induced perfusion error by measuring the residual dispersion remaining in the local AIF deconvolved perfusion maps. Two approaches to locating the local AIF voxels are assessed and compared with a global AIF deconvolution across 19 bolus-tracking data sets from patients with stroke. The local AIF methods reduced dispersion in the majority of data sets, suggesting more accurate perfusion quantification. Importantly, the validation inherently identifies potential areas for perfusion underestimation. This is valuable information for the identification of at-risk tissue and management of stroke patients.

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Iwabuchi, K., and T. Yamashita. "Platelet-derived neutrophil adherence-inhibiting factor in humans." Blood 76, no. 11 (1990): 2368–73. http://dx.doi.org/10.1182/blood.v76.11.2368.2368.

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Abstract The effect of constituents of human platelets on leukocyte adherence was examined. Adherence-inhibiting factors (AIFs), which strongly inhibited neutrophil adherence to glass, were present in both cytosol and granule fractions of human platelets. On the Superose 6 gel chromatography (Pharmacia LKB Biotechnology, Uppsala, Sweden), the granular AIF was eluted as a single active peak (2,600 Kd), whereas cytosolic AIFs were eluted at two different positions (2,600 and 480 Kd). When platelets were stimulated by thrombin, granular AIF was released extracellularly without releasing a cytosolic marker. Using DE32 anion exchange chromatography and Superose 6 gel filtration, granular AIF was completely purified. Sodium dodecyl sulfate- polyacrylamide gel electrophoresis analysis suggests that granular AIF consists of two subunits with molecular masses of approximately 340 and 190 Kd. Purified granular AIF inhibited human neutrophil adherence to glass, plastic, and type IV collagen-coated plastic, whereas it did not affect monocyte adherence. These results suggest that granular AIF inhibits neutrophil adherence not only via nonspecific adsorption sites, but also via type IV collagen receptors.

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Iwabuchi, K., and T. Yamashita. "Platelet-derived neutrophil adherence-inhibiting factor in humans." Blood 76, no. 11 (1990): 2368–73. http://dx.doi.org/10.1182/blood.v76.11.2368.bloodjournal76112368.

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The effect of constituents of human platelets on leukocyte adherence was examined. Adherence-inhibiting factors (AIFs), which strongly inhibited neutrophil adherence to glass, were present in both cytosol and granule fractions of human platelets. On the Superose 6 gel chromatography (Pharmacia LKB Biotechnology, Uppsala, Sweden), the granular AIF was eluted as a single active peak (2,600 Kd), whereas cytosolic AIFs were eluted at two different positions (2,600 and 480 Kd). When platelets were stimulated by thrombin, granular AIF was released extracellularly without releasing a cytosolic marker. Using DE32 anion exchange chromatography and Superose 6 gel filtration, granular AIF was completely purified. Sodium dodecyl sulfate- polyacrylamide gel electrophoresis analysis suggests that granular AIF consists of two subunits with molecular masses of approximately 340 and 190 Kd. Purified granular AIF inhibited human neutrophil adherence to glass, plastic, and type IV collagen-coated plastic, whereas it did not affect monocyte adherence. These results suggest that granular AIF inhibits neutrophil adherence not only via nonspecific adsorption sites, but also via type IV collagen receptors.

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Zhang, Y., J. J. Pointon, and B. P. Wordsworth. "Comment on: An allograft inflammatory factor 1 (AIF1) single nucleotide polymorphism (SNP) is associated with anticentromere antibody positive systemic sclerosis." Rheumatology 47, no. 4 (2007): 556–57. http://dx.doi.org/10.1093/rheumatology/kem333.

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Landsman-Blumberg, Pamela, Madhav Namjoshi, Erin Thomson, and William Johnson. "Real-world aromatase inhibitor use and failure in women with metastatic ER+/HER2- breast cancer." Journal of Clinical Oncology 30, no. 15_suppl (2012): 593. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.593.

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593 Background: Aromatase Inhibitors (AIs) have replaced tamoxifen as first-line therapy for postmenopausal women with metastatic, ER+ breast cancer (BC). However, little information is available on the real-world use of AIs. The objectives of this retrospective claims study were to compare demographic, clinical and treatment characteristics of postmenopausal women with metastatic ER+/HER2- BC treated with AIs and experiencing 0, 1, 2 or ≥ 3 AI failures (AIF). Methods: Women ≥ 55 years old, newly diagnosed with metastatic BC (index) were identified in the 2006-2010 Thomson Reuters MarketScan databases and followed until chemotherapy or 03/31/2011. ER+/HER2- disease was defined as any endocrine therapy (ET: tamoxifen, fulvestrant) or AI (anastrozole, letrozole, or exemestane) use and no trastuzumab or lapatinib use in the 6-month pre-or variable post-index periods. Those with any post-index AI use were retained for study. AIF post-index was defined as a switch to an alternative AI, ET or chemotherapy, or AI discontinuation with no further BC treatment. Patients were stratified by number of post-index AIF: 0, 1, 2 or ≥ 3. Results: Among 4,274 patients identified, 61% had ≥ 1 AIF (1: 80%, 2: 15%, ≥3: 5%). There was no difference in pre-index AI use across AIF cohorts: 0, 1, 2, and ≥3 (54%, 52%, 48%, 56%; p=0.073). AIFs increased with Medicare-eligibility (51%, 56%, 60%, 61%) and bone metastases at index (48%, 53%, 62%, 63%). Among those with ≥1 AIF, median follow-up (FU) increased with each failure but there was no notable pattern to reason for FU end. Median FU of the 0 AIF cohort (408 days) fell between those of the 1 and 2 AIF cohorts, 335 and 517 days. Anastrozole was the most common first line treatment for all cohorts except ≥ 3 AIFs where letrozole was most common. Pre-index and first line fulvestrant use both increased with the number of post-index AIFs: 0.3%, 1.9%, 2.0%, 5.0% and 0.7%, 2.5%, 4.0%, 14.9% respectively. There was no association between number of AIFs and chemotherapy use (36%, 29%, 38%). Conclusions: Over 60% of women with ER+/HER2- metastatic BC treated with AIs failed at least 1 and 20% of those failed ≥ 2. Surprisingly, increased rates of prior fulvestrant treatment appear associated with increasing numbers of AIF.

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Chin, Christopher, Faith Donaghey, Katherine Helming, Morgan McCarthy, Stephen Rogers, and Nicanor Austriaco. "Deletion of AIF1 but not of YCA1/MCA1 protects Saccharomyces cerevisiae and Candida albicans cells from caspofungin-induced programmed cell death." Microbial Cell 1, no. 2 (2014): 58–63. http://dx.doi.org/10.15698/mic2014.01.119.

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Rouskas, Konstantinos, Anastasia Kouvatsi, Konstantinos Paletas, et al. "Common Variants in FTO, MC4R, TMEM18, PRL, AIF1 , and PCSK1 Show Evidence of Association With Adult Obesity in the Greek Population." Obesity 20, no. 2 (2012): 389–95. http://dx.doi.org/10.1038/oby.2011.177.

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Alkassab, F., P. Gourh, F. Tan, F. Arnett, and M. Mayes. "Comment on: An allograft inflammatory factor 1 (AIF1) single nucleotide polymorphism (SNP) is associated with anticentromere antibody positive systemic sclerosis: reply." Rheumatology 47, no. 4 (2007): 557. http://dx.doi.org/10.1093/rheumatology/ken049.

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Arpudhamary, V., S. Priya, Muhammed A. P. Manzoor, D. Mubarakali, and S. Hemalatha. "Apoptotic-inducing factor 1 (AIF1) plays a critical role in cembranoid mediated apoptosis to control cancer: Molecular docking and dynamics study." Biocatalysis and Agricultural Biotechnology 22 (November 2019): 101343. http://dx.doi.org/10.1016/j.bcab.2019.101343.

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Eike, M. C., M. Olsson, D. E. Undlien, et al. "Genetic variants of the HLA-A, HLA-B and AIF1 loci show independent associations with type 1 diabetes in Norwegian families." Genes & Immunity 10, no. 2 (2008): 141–50. http://dx.doi.org/10.1038/gene.2008.88.

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Sundar, Lalith KS, Otto Muzik, Lucas Rischka, et al. "Towards quantitative [18F]FDG-PET/MRI of the brain: Automated MR-driven calculation of an image-derived input function for the non-invasive determination of cerebral glucose metabolic rates." Journal of Cerebral Blood Flow & Metabolism 39, no. 8 (2018): 1516–30. http://dx.doi.org/10.1177/0271678x18776820.

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Absolute quantification of PET brain imaging requires the measurement of an arterial input function (AIF), typically obtained invasively via an arterial cannulation. We present an approach to automatically calculate an image-derived input function (IDIF) and cerebral metabolic rates of glucose (CMRGlc) from the [18F]FDG PET data using an integrated PET/MRI system. Ten healthy controls underwent test–retest dynamic [18F]FDG-PET/MRI examinations. The imaging protocol consisted of a 60-min PET list-mode acquisition together with a time-of-flight MR angiography scan for segmenting the carotid arteries and intermittent MR navigators to monitor subject movement. AIFs were collected as the reference standard. Attenuation correction was performed using a separate low-dose CT scan. Assessment of the percentage difference between area-under-the-curve of IDIF and AIF yielded values within ±5%. Similar test–retest variability was seen between AIFs (9 ± 8) % and the IDIFs (9 ± 7) %. Absolute percentage difference between CMRGlc values obtained from AIF and IDIF across all examinations and selected brain regions was 3.2% (interquartile range: (2.4–4.3) %, maximum < 10%). High test–retest intravariability was observed between CMRGlc values obtained from AIF (14%) and IDIF (17%). The proposed approach provides an IDIF, which can be effectively used in lieu of AIF.

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Zawada, Adam M., Kyrill S. Rogacev, Björn Rotter, et al. "SuperSAGE evidence for CD14++CD16+ monocytes as a third monocyte subset." Blood 118, no. 12 (2011): e50-e61. http://dx.doi.org/10.1182/blood-2011-01-326827.

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Abstract Monocytes are a heterogeneous cell population with subset-specific functions and phenotypes. The differential expression of CD14 and CD16 distinguishes classical CD14++CD16−, intermediate CD14++CD16+, and nonclassical CD14+CD16++ monocytes. Current knowledge on human monocyte heterogeneity is still incomplete: while it is increasingly acknowledged that CD14++CD16+ monocytes are of outstanding significance in 2 global health issues, namely HIV-1 infection and atherosclerosis, CD14++CD16+ monocytes remain the most poorly characterized subset so far. We therefore developed a method to purify the 3 monocyte subsets from human blood and analyzed their transcriptomes using SuperSAGE in combination with high-throughput sequencing. Analysis of 5 487 603 tags revealed unique identifiers of CD14++CD16+ monocytes, delineating these cells from the 2 other monocyte subsets. Gene Ontology (GO) enrichment analysis suggests diverse immunologic functions, linking CD14++CD16+ monocytes to Ag processing and presentation (eg, CD74, HLA-DR, IFI30, CTSB), to inflammation and monocyte activation (eg, TGFB1, AIF1, PTPN6), and to angiogenesis (eg, TIE2, CD105). In conclusion, we provide genetic evidence for a distinct role of CD14++CD16+ monocytes in human immunity. After CD14++CD16+ monocytes have earlier been discussed as a potential therapeutic target in inflammatory diseases, we are hopeful that our data will spur further research in the field of monocyte heterogeneity.

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Gimenez da Silva-Santi, Lorena, Marina Masetto Antunes, Marco Mori, et al. "Brain Fatty Acid Composition and Inflammation in Mice Fed with High-Carbohydrate Diet or High-Fat Diet." Nutrients 10, no. 9 (2018): 1277. http://dx.doi.org/10.3390/nu10091277.

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Both high fat diet (HFD) and high carbohydrate diet (HCD) modulate brain fatty acids (FA) composition. Notwithstanding, there is a lack of information on time sequence of brain FA deposition either for HFD or HCD. The changes in brain FA composition in mice fed with HFD or HCD for 7, 14, 28, or 56 days were compared with results of 0 (before starting given the diets). mRNA expressions of allograft inflammatory factor 1 (Aif1), cyclooxygenase-2 (Cox 2), F4/80, inducible nitric oxide synthase (iNOS), integrin subunit alpha m (Itgam), interleukin IL-1β (IL-1β), IL-6, IL-10, and tumor necrosis factor alpha (TNF-α) were measured. The HFD group had higher speed of deposition of saturated FA (SFA), monounsaturated FA (MUFA), and polyunsaturated FA (PUFA) at the beginning of the experimental period. However, on day 56, the total amount of SFA, MUFA, and PUFA were similar. mRNA expressions of F4/80 and Itgam, markers of microglia infiltration, were increased (p < 0.05) in the brain of the HCD group whereas inflammatory marker index (IMI) was higher (46%) in HFD group. In conclusion, the proportion of fat and carbohydrates in the diet modulates the speed deposition of FA and expression of inflammatory gene markers.

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Bouaita, Aicha, Sébastien Augustin, Christophe Lechauve, et al. "Downregulation of apoptosis-inducing factor in Harlequin mice induces progressive and severe optic atrophy which is durably prevented by AAV2-AIF1 gene therapy." Brain 135, no. 1 (2011): 35–52. http://dx.doi.org/10.1093/brain/awr290.

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Košuth, Ján, Martina Farkašovská, Filip Mochnacký, Zuzana Daxnerová, and Juraj Ševc. "Selection of Reliable Reference Genes for Analysis of Gene Expression in Spinal Cord during Rat Postnatal Development and after Injury." Brain Sciences 10, no. 1 (2019): 6. http://dx.doi.org/10.3390/brainsci10010006.

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In order to obtain unbiased results of target gene expression, selection of the most appropriate reference gene (RG) remains a key precondition. However, an experimental study focused on the validation of stably expressed RGs in the rat spinal cord (SC) during development or after spinal cord injury (SCI) is missing. In our study, we tested the stability of the expression of nine selected RGs in rat SC tissue during normal development (postnatal days 1–43, adulthood) and after minimal (mSCI) and contusion (cSCI) spinal cord injury. The following RGs were tested: common housekeeping genes of basal cell metabolism (Gapdh, Hprt1, Mapk6) and protein translation (Rpl29, Eef1a1, Eif2b2), as well as newly designed RGs (Gpatch1, Gorasp1, Cds2) selected according to the RefGenes tool of GeneVestigator. The stability of RGs was assessed by geNorm, NormFinder, and BestKeeper. All three applets favored Gapdh and Eef1a1 as the most stable genes in SC during development. In both models of SCI, Eif2b2 displayed the highest stability of expression, followed by Gapdh and Gorasp1/Hprt1 in cSCI, and Gapdh and Eef1a1 in the mSCI experiments. To verify our results, selected RGs were employed for normalization of the expression of genes with a clear biological context in the SC—Gfap and Slc1a3/Glast during postnatal development and Aif1/Iba1 and Cd68/Ed1 after SCI.

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Soontornniyomkij, Virawudh, Rachel C. Chang, Benchawanna Soontornniyomkij, Jan M. Schilling, Hemal H. Patel, and Dilip V. Jeste. "Loss of Immunohistochemical Reactivity in Association With Handling-Induced Dark Neurons in Mouse Brains." Toxicologic Pathology 48, no. 3 (2020): 437–45. http://dx.doi.org/10.1177/0192623319896263.

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The handling-induced dark neuron is a histological artifact observed in brain samples handled before fixation with aldehydes. To explore associations between dark neurons and immunohistochemical alterations in mouse brains, we examined protein products encoded by Cav3 (neuronal perikarya/neurites), Rbbp4 (neuronal nuclei), Gfap (astroglia), and Aif1 (microglia) genes in adjacent tissue sections. Here, dark neurons were incidental findings from our prior project, studying the effects of age and high-fat diet on metabolic homeostasis in male C57BL/6N mice. Available were brains from 4 study groups: middle-aged/control diet, middle-aged/high-fat diet, old/control diet, and old/high-fat diet. Young/control diet mice were used as baseline. The hemibrains were immersion-fixed with paraformaldehyde and paraffin-embedded. In the hippocampal formation, we found negative correlations between dark neuron hyperbasophilia and immunoreactivity for CAV3, RBBP4, and glial fibrillary acidic protein (GFAP) using quantitative image analysis. There was no significant difference in dark neuron hyperbasophilia or immunoreactivity for any protein examined among all groups. In contrast, in the hippocampal fimbria, old age seemed to be associated with higher immunoreactivity for GFAP and allograft inflammatory factor-1. Our findings suggest that loss of immunohistochemical reactivity for CAV3, RBBP4, and GFAP in the hippocampal formation is an artifact associated with the occurrence of dark neurons. The unawareness of dark neurons may lead to misinterpretation of immunohistochemical reactivity alterations.

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Zhao, Zhi-jie, Dong-po Wei, Rui-zhe Zheng, Tinghua Peng, Xiang Xiao, and Fu-sheng Li. "The Gene Coexpression Analysis Identifies Functional Modules Dynamically Changed After Traumatic Brain Injury." Computational and Mathematical Methods in Medicine 2021 (April 16, 2021): 1–12. http://dx.doi.org/10.1155/2021/5511598.

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Traumatic brain injury (TBI) is a major cause of morbidity and mortality, both in adult and pediatric populations. However, the dynamic changes of gene expression profiles following TBI have not been fully understood. In this study, we identified the differentially expressed genes (DEGs) following TBI. Remarkably, Serpina3n, Asf1b, Folr1, LOC100366216, Clec12a, Olr1, Timp1, Hspb1, Lcn2, and Spp1 were identified as the top 10 with the highest statistical significance. The weighted gene coexpression analysis (WGCNA) identified 12 functional modules from the DEGs, which showed specific expression patterns over time and were characterized by enrichment analysis. Specifically, the black and turquoise modules were mainly involved in energy metabolism and protein translation. The green yellow and yellow modules including Hmox1, Mif, Anxa2, Timp1, Gfap, Cd9, Gja1, Pdpn, and Gpx1 were related to response to wounding, indicating that expression of these genes such as Hmox1, Anxa2, and Timp1 could protect the brains from brain injury. The green yellow module highlighted genes involved in microglial cell activation such as Tyrobp, Cx3cr1, Grn, Trem2, C1qa, and Aif1, suggesting that these genes were responsible for the inflammatory response caused by TBI. The upregulation of these genes has been validated in an independent dataset. These results indicated that the key genes in microglia cell activation may serve as a promising therapeutic target for TBI. In summary, the present study provided a full view of the dynamic gene expression changes following TBI.

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Hiskens, Matthew I., Anthony G. Schneiders, Rebecca K. Vella, and Andrew S. Fenning. "Repetitive mild traumatic brain injury affects inflammation and excitotoxic mRNA expression at acute and chronic time-points." PLOS ONE 16, no. 5 (2021): e0251315. http://dx.doi.org/10.1371/journal.pone.0251315.

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The cumulative effect of mild traumatic brain injuries (mTBI) can result in chronic neurological damage, however the molecular mechanisms underpinning this detriment require further investigation. A closed head weight drop model that replicates the biomechanics and head acceleration forces of human mTBI was used to provide an exploration of the acute and chronic outcomes following single and repeated impacts. Adult male C57BL/6J mice were randomly assigned into one of four impact groups (control; one, five and 15 impacts) which were delivered over 23 days. Outcomes were assessed 48 hours and 3 months following the final mTBI. Hippocampal spatial learning and memory assessment revealed impaired performance in the 15-impact group compared with control in the acute phase that persisted at chronic measurement. mRNA analyses were performed on brain tissue samples of the cortex and hippocampus using quantitative RT-PCR. Eight genes were assessed, namely MAPT, GFAP, AIF1, GRIA1, CCL11, TARDBP, TNF, and NEFL, with expression changes observed based on location and follow-up duration. The cortex and hippocampus showed vulnerability to insult, displaying upregulation of key excitotoxicity and inflammation genes. Serum samples showed no difference between groups for proteins phosphorylated tau and GFAP. These data suggest that the cumulative effect of the impacts was sufficient to induce mTBI pathophysiology and clinical features. The genes investigated in this study provide opportunity for further investigation of mTBI-related neuropathology and may provide targets in the development of therapies that help mitigate the effects of mTBI.

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Lind, Emelie, Linda Knutsson, Freddy Ståhlberg та Ronnie Wirestam. "Dynamic contrast-enhanced QSM for perfusion imaging: a systematic comparison of ΔR2*- and QSM-based contrast agent concentration time curves in blood and tissue". Magnetic Resonance Materials in Physics, Biology and Medicine 33, № 5 (2020): 663–76. http://dx.doi.org/10.1007/s10334-020-00831-x.

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Abstract Objective In dynamic susceptibility contrast MRI (DSC-MRI), an arterial input function (AIF) is required to quantify perfusion. However, estimation of the concentration of contrast agent (CA) from magnitude MRI signal data is challenging. A reasonable alternative would be to quantify CA concentration using quantitative susceptibility mapping (QSM), as the CA alters the magnetic susceptibility in proportion to its concentration. Material and methods AIFs with reasonable appearance, selected on the basis of conventional criteria related to timing, shape, and peak concentration, were registered from both ΔR2* and QSM images and mutually compared by visual inspection. Both ΔR2*- and QSM-based AIFs were used for perfusion calculations based on tissue concentration data from ΔR2*as well as QSM images. Results AIFs based on ΔR2* and QSM data showed very similar shapes and the estimated cerebral blood flow values and mean transit times were similar. Analysis of corresponding ΔR2* versus QSM-based concentration estimates yielded a transverse relaxivity estimate of 89 s−1 mM−1, for voxels identified as useful AIF candidate in ΔR2* images according to the conventional criteria. Discussion Interestingly, arterial concentration time curves based on ΔR2* versus QSM data, for a standard DSC-MRI experiment, were generally very similar in shape, and the relaxivity obtained in voxels representing blood was similar to tissue relaxivity obtained in previous studies.

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Dudgeon, Drew D., Nannan Zhang, Olufisayo O. Ositelu, Hyemin Kim, and Kyle W. Cunningham. "Nonapoptotic Death of Saccharomyces cerevisiae Cells That Is Stimulated by Hsp90 and Inhibited by Calcineurin and Cmk2 in Response to Endoplasmic Reticulum Stresses." Eukaryotic Cell 7, no. 12 (2008): 2037–51. http://dx.doi.org/10.1128/ec.00291-08.

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ABSTRACT Endoplasmic reticulum (ER) stress can trigger apoptosis and necrosis in many types of mammalian cells. Previous studies in yeast found little or no cell death in response to the ER stressor tunicamycin, but a recent study suggested widespread apoptosis-like death. Here we show that wild-type laboratory Saccharomyces cerevisiae cells responding to tunicamycin die by nonapoptotic mechanisms in low-osmolyte culture media and survive for long periods of time in standard synthetic media. Survival requires calcineurin, a Ca2+/calmodulin-dependent protein phosphatase, but none of its known targets. The Ca2+/calmodulin-dependent protein kinase Cmk2 was identified as an indirect target of calcineurin that suppresses death of calcineurin-deficient cells. Death of Cmk2- and/or calcineurin-deficient S. cerevisiae cells was preceded by accumulation of reactive oxygen species but was not associated with hallmarks of apoptosis and was not dependent on Mca1, Aif1, Nuc1, or other factors implicated in apoptosis-like death. Cmk2 and calcineurin also independently suppressed the death of S. cerevisiae cells responding to dithiothreitol or miconazole, a common azole-class antifungal drug. Though inhibitors of Hsp90 have been shown to diminish calcineurin signaling in S. cerevisiae and to synergistically inhibit growth in combination with azoles, they did not stimulate death of S. cerevisiae cells in combination with miconazole or tunicamycin, and instead they prevented the death of calcineurin- and Cmk2-deficient cells. These findings reveal a novel prodeath role for Hsp90 and antideath roles for calcineurin and Cmk2 that extend the life span of S. cerevisiae cells responding to both natural and clinical antifungal compounds.

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Hori, Yuki, Naoki Ihara, Noboru Teramoto, et al. "Noninvasive Quantification of Cerebral Metabolic Rate for Glucose in Rats Using 18F-FDG PET and Standard Input Function." Journal of Cerebral Blood Flow & Metabolism 35, no. 10 (2015): 1664–70. http://dx.doi.org/10.1038/jcbfm.2015.104.

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Measurement of arterial input function (AIF) for quantitative positron emission tomography (PET) studies is technically challenging. The present study aimed to develop a method based on a standard arterial input function (SIF) to estimate input function without blood sampling. We performed 18F-fluolodeoxyglucose studies accompanied by continuous blood sampling for measurement of AIF in 11 rats. Standard arterial input function was calculated by averaging AIFs from eight anesthetized rats, after normalization with body mass (BM) and injected dose (ID). Then, the individual input function was estimated using two types of SIF: (1) SIF calibrated by the individual's BM and ID (estimated individual input function, EIFNS) and (2) SIF calibrated by a single blood sampling as proposed previously (EIF1S). No significant differences in area under the curve (AUC) or cerebral metabolic rate for glucose (CMRGlc) were found across the AIF-, EIFNS-, and EIF1S-based methods using repeated measures analysis of variance. In the correlation analysis, AUC or CMRGlc derived from EIFNS was highly correlated with those derived from AIF and EIF1S. Preliminary comparison between AIF and EIFNS in three awake rats supported an idea that the method might be applicable to behaving animals. The present study suggests that EIFNS method might serve as a noninvasive substitute for individual AIF measurement.

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Matangkasombut, Oranart, Roongtiwa Wattanawaraporn, Keiko Tsuruda, Masaru Ohara, Motoyuki Sugai, and Skorn Mongkolsuk. "Cytolethal Distending Toxin from Aggregatibacter actinomycetemcomitans Induces DNA Damage, S/G2 Cell Cycle Arrest, and Caspase- Independent Death in a Saccharomyces cerevisiae Model." Infection and Immunity 78, no. 2 (2009): 783–92. http://dx.doi.org/10.1128/iai.00857-09.

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ABSTRACT Cytolethal distending toxin (CDT) is a bacterial toxin that induces G2/M cell cycle arrest, cell distension, and/or apoptosis in mammalian cells. It is produced by several Gram-negative species and may contribute to their pathogenicity. The catalytic subunit CdtB has homology with DNase I and may act as a genotoxin. However, the mechanism by which CdtB leads to cell death is not yet clearly understood. Here, we used Saccharomyces cerevisiae as a model to study the molecular pathways involved in the function of CdtB from Aggregatibacter actinomycetemcomitans, a cause of aggressive periodontitis. We show that A. actinomycetemcomitans CdtB (AaCdtB) expression induces S/G2 arrest and death in a DNase-catalytic residue and nuclear localization-dependent manner in haploid yeasts. Yeast strains defective in homologous recombination (HR) repair, but not other DNA repair pathways, are hypersensitive to AaCdtB, suggesting that HR is required for survival upon CdtB expression. In addition, yeast does not harbor the substrate for the other activity proposed for CdtB function, which is phosphatidylinositol-3,4,5-triphosphate phosphatase. Thus, these results suggest that direct DNA-damaging activity alone is sufficient for CdtB toxicity. To investigate how CdtB induces cell death, we examined the effect of CdtB in yeast strains with mutations in apoptotic regulators. Our results suggest that yeast death occurs independently of the yeast metacaspase gene YCA1 and the apoptosis-inducing factor AIF1 but is partially dependent on histone H2B serine 10 phosphorylation. Therefore, we report here the evidence that AaCdtB causes DNA damage that leads to nonapoptotic death in yeast and the first mutation that confers resistance to CdtB.

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Polzella, Donald J., and David C. Hubbard. "Utility and Utilization of Aircrew Training Device Advanced Instructional Features." Proceedings of the Human Factors Society Annual Meeting 30, no. 2 (1986): 139–43. http://dx.doi.org/10.1177/154193128603000208.

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The utility and utilization of the Advanced Instructional Features (AIFs) capabilities of USAF Aircrew Training Devices (ATDs) was explored by means of a survey of 534 Simulator Instructors from Air Training Command, Military Airlift Command, Strategic Air Command, and Tactical Air Command training sites. The primary purpose of the survey was to provide a database that could be used in defining the requirements for ATD procurements and in developing future ATD training programs. In general, the features that were rated highest in utility and utilization were those used for training management, variation of task difficulty/fidelity, and monitoring student performance. The level of AIF use was affected somewhat by hardware and/or software deficiencies; however, the presumed training value of an AIF was the most important determiner of its use.

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Journal articles on the topic 'Aif1'

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