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PubMed1992

The dielectric parameters of excised EMT-6 tumours and their change during hyperthermia.

The electrical impedance from 100 Hz to 40 MHz of freshly excised EMT-6 tumours was measured periodically while the tumours were exposed to typical hyperthermia heating regimens. During hyperthermia, the EMT-6 tumour displays a characteristic response sequence which includes cellular swelling, progressive membrane damage, cellular shrinking and subsequent progressive histolysis. It was found that the changes in the tumour tissue dielectric properties reflected these hyperthermia-induced histological changes. In particular the parameters delta epsilon, sigma s and fc progressed to, reached, and retreated from extrema as the cells swelled to a maximum and then contracted. These parameters continued retreating beyond their original values as the beta-dispersion progressively collapsed during the period of progressive histolysis. The Cole-Cole parameter alpha increased during most of these histological changes, indicating a broadening of the dispersion, which suggests differential cell response during this period. Differences in the time-course between dielectric components may reflect the combined effects of cellular swelling and concurrent progressive membrane changes. Changes in rate and shape of the dielectric response with hyperthermia temperature are discussed in terms of possible cellular responses during hyperthermia.

Animals↗

PubMed1975

Emergency medical technician (EMT-A) training in a medical school environment.

A 22-week training program for EMT-A technicians, developed at the University of Connecticut Health Center, has been described. The program is coordinated by a trauma surgeon and a security officer, and teaching is carried out by faculty, residents, emergency-room nurses, experienced rescue-team members, EMT firemen, and the like. Lectures and videotaped practical problems are used. High levels of teaching and cooperation between the university health center and the community were maintained.

Allied Health Personnel↗

PubMed2006

A critical look at growth factors and epithelial-to-mesenchymal transition in the adult kidney. Interrelationships between growth factors that regulate EMT in the adult kidney.

In the adult kidney, the cellular phenotypes are maintained by a strict balance of growth factors. Epithelial-to-mesenchymal transition (EMT) is a program whereby injured epithelial cells that function as ion and fluid transporters become matrix remodelling mesenchymal cells. This process requires either transcriptional repression of genes that maintain the epithelial phenotype and transcriptional activation, or relieved repression of genes needed for functional myofibroblasts. The transcriptional regulators are controlled by several integrated signalling pathways which are triggered by growth factors. Emerging evidence indicates that the growth factors TGFbeta/CTGF and BMP-7/HGF are the main determinants that maintain the two cellular phenotypes. Both TGFbeta and BMP-7 counteract the activity of each other by cross-inducing their respective inhibitory Smads. Both growth factors may also induce the expression of other factors that can change the cellular environment and enhance their function. Chronic kidney diseases (regardless of the aetiology of the disease) are associated with increased TGFbeta and CTGF expression levels which, in turn, have an inverse effect on the activity level of BMP-7 and HGF, leading to an EMT of injured tubular epithelial cells and a progression of the disease. A detailed understanding of the complex interrelationship between these growth factors may lead to the development of novel drugs.

Animals↗

PubMed2026

Stromal ARHGEF15 Correlates With Inflammatory EMT and Stromal-Immune Crosstalk During Inflammatory Bowel Disease-To-Colorectal Cancer Progression.

Patients with inflammatory bowel disease (IBD) have an increased risk of colorectal cancer (CRC), but how chronic intestinal inflammation drives malignant transformation remains unclear. We retrospectively reanalyzed published single-cell transcriptomic datasets from intestinal biopsies of healthy individuals and patients with IBD; differential expression was assessed using independent t tests with Benjamini-Hochberg false discovery rate correction. We then integrated those single-cell findings with the Cancer Genome Atlas bulk transcriptomes and pharmacogenomic cohorts to trace stromal programs across the IBD-to-cancer continuum. ARHGEF15 emerged as a stromal gene enriched in CD74hi HLA-DRB1hi arterial pericytes within inflamed tissue. Its expression rose steadily from IBD to CRC and tracked with epithelial-mesenchymal transition (EMT) activity. In CRC, higher ARHGEF15 expression was associated with shorter overall and progression-free survival. These retrospective, in silico findings identify ARHGEF15 as an exploratory stromal biomarker associated with inflammatory EMT and stromal-immune remodeling during IBD-to-CRC progression. Prospective experimental and clinical validation is required to establish its prognostic or therapeutic relevance.

ARHGEF15↗

PubMed2025

PRMT5 regulates alternative splicing of TCF3 under hypoxia to promote EMT and invasion in breast cancer.

Tumor hypoxia induced alterations in the epigenetic landscape and alternative splicing influence cellular adaptations. PRMT5 is a type II protein arginine methyltransferase that regulates several tumorigenic events in many cancer types. However, the regulation of PRMT5 and its direct implication on aberrant alternative splicing under hypoxia remains unexplored. In this study, we observed hypoxia-induced upregulation of PRMT5 via the CTCF in human breast cancer cells. Further, PRMT5-mediated symmetric arginine dimethylation H4R3me2s and H3R8me2s directly regulated the alternative splicing of TCF3. Under hypoxia, PRMT5-mediated histone dimethylation at the intronic conserved region (ICR) present between TCF3 exon 18a and exon 18b recruits DNMT3A, resulting in DNA methylation. DNA methylation at the TCF3-ICR is recognized and bound by MeCP2 resulting in RNA-Pol II pausing, promoting the recruitment of the negative splicing factor PTBP1 to the splicing locus of TCF3 pre-mRNA. PTBP1 promotes the exclusion of exon 18a which results in the production of the pro-invasive TCF3-18B (E47) isoform which promotes EMT and invasion of breast cancer cells under hypoxia. Collectively, our results indicate PRMT5-mediated symmetric arginine dimethylation of histones regulates alternative splicing of TCF3 gene thereby enhancing EMT and invasion in breast cancer hypoxia.

Humans↗

PubMed2005

Kallikrein 4 (hK4) and prostate-specific antigen (PSA) are associated with the loss of E-cadherin and an epithelial-mesenchymal transition (EMT)-like effect in prostate cancer cells.

Prostate-specific antigen (PSA) and the related kallikrein family of serine proteases are current or emerging biomarkers for prostate cancer detection and progression. Kallikrein 4 (KLK4/hK4) is of particular interest, as KLK4 mRNA has been shown to be elevated in prostate cancer. In this study, we now show that the comparative expression of hK4 protein in prostate cancer tissues, compared with benign glands, is greater than that of PSA and kallikrein 2 (KLK2/hK2), suggesting that hK4 may play an important functional role in prostate cancer progression in addition to its biomarker potential. To examine the roles that hK4, as well as PSA and hK2, play in processes associated with progression, these kallikreins were separately transfected into the PC-3 prostate cancer cell line, and the consequence of their stable transfection was investigated. PC-3 cells expressing hK4 had a decreased growth rate, but no changes in cell proliferation were observed in the cells expressing PSA or hK2. hK4 and PSA, but not hK2, induced a 2.4-fold and 1.7-fold respective increase, in cellular migration, but not invasion, through Matrigel, a synthetic extracellular matrix. We hypothesised that this increase in motility displayed by the hK4 and PSA-expressing PC-3 cells may be related to the observed change in structure in these cells from a typical rounded epithelial-like cell to a spindle-shaped, more mesenchymal-like cell, with compromised adhesion to the culture surface. Thus, the expression of E-cadherin and vimentin, both associated with an epithelial-mesenchymal transition (EMT), was investigated. E-cadherin protein was lost and mRNA levels were significantly decreased in PC-3 cells expressing hK4 and PSA (10-fold and 7-fold respectively), suggesting transcriptional repression of E-cadherin, while the expression of vimentin was increased in these cells. The loss of E-cadherin and associated increase in vimentin are indicative of EMT and provides compelling evidence that hK4, in particular, and PSA have a functional role in the progression of prostate cancer through their promotion of tumour cell migration.

Cadherins↗

PubMed2000

Comparison of two intraosseous infusion techniques in an EMT training program

OBJECTIVE: To compare placement of IO lines using a traditional method with placement using a new device called the bone injection gun (BIG). METHODS: A prospective cross-over study was conducted to compare the time to line placement and ease of insertion for both traditional (Jamshidi) and BIG methods. EMT-P students and practicing paramedics provided information about their previous experience with IO line placement. They were assigned to establish an IO line in a pediatric leg mannequin using each technique, and rated the ease-of-use of each method. RESULTS: Thirty-eight participants (28 EMT-P students and 10 paramedics) completed both of the IO skills. Only two (5%) had ever placed an IO line in a patient previously. Time to placement of the IO device was faster in the BIG group (16.91 sec. vs. 11.93 sec., p = 0.02). There was no statistical difference in ease-of-use ratings between the methods (p = 0.816). Student times for establishing the IO line with the BIG device were faster than the times of the practicing paramedics (11. 18 sec. vs. 16.25 sec., p = 0.049). CONCLUSIONS: In the education setting, times to establishment of an IO line were similar using both the traditional method of insertion and the BIG device. Ratings of both the students and paramedics were similar with respect to each-of-use for both the methods.

Journal Article↗

PubMed1986

Comparison of antithrombotic activity of two heparin fragments PK 10169 (mol. wt. 5,000) and EMT 680 (mol. wt. 2,500) and unfractionated heparin in a rabbit experimental thrombosis model: relative importance of systemic anti-Xa and anti-IIa activities.

Two fragments obtained by chemical depolymerization of heparin from porcine mucosal origin PK 10169 (mol. wt. 5,000) and EMT 680 (mol. wt. 2,500) were compared to the original heparin in a rabbit experimental thrombosis model. Thrombosis was induced either by human serum or by bovine Xa. Various doses of heparins (6 animals per dose and per inducer) were injected in order to find the lowest systemic levels of anti-Xa and anti-IIa activities able to inhibit venous-induced thrombogenesis. The systemic activities associated with an inhibition of 50% of the generated thrombi were as follows: 0.17 +/- 0.02 anti-Xa and 0.16 +/- 0.03 anti-IIa units obtained after injection of 97 micrograms/kg (14 anti-Xa and anti-IIa units/kg) of unfractionated heparin, 0.28 +/- 0.04 anti-Xa and 0.14 +/- 0.03 anti-IIa units obtained after injection of 250 micrograms/kg (15 anti-Xa and 7.5 anti-IIa units/kg of PK 10169, and 2.6 +/- 0.2 anti-Xa and 0.06 +/- 0.01 anti-IIa units obtained after injection of 5000 micrograms/kg (260 anti-Xa and 5 anti-IIa units/kg) of EMT 680. These results suggest that the presence of an anti-IIa activity associated with the anti-Xa activity strongly increases the thrombogenesis inhibition in the serum and Xa-induced thrombosis for the heparin fragments of low and very low molecular weight used in this study.

Animals↗

PubMed1979

A transferrin-mediated uptake of gallium-67 by EMT-6 sarcoma. II. Studies in vivo (BALB/c mice): concise communication.

The EMT-6 sarcoma-like tumor of BALB/c mice can be grown as a solid subcutaneous transplantable tumor in vivo or as a monolayer culture in vitro. We have studied the uptake of gallium-67 by this tumor growing subcutaneously on the backs of 6-week-old BALB/c mice. After i.v. administration of Ga-67 citrate, tumor uptakes were as high as any others reported for mouse tumors. Also, for unknown reasons, there was appreciable reduction in tumor uptake with increasing amounts of Ga-67 citrate, even in the microcurie range. Furthermore, when mouse serum is prelabeled with Ga-67 and then injected, the EMT-6 uptake is greater than with Ga-67 administered as citrate (p less than 0.02). We believe that the finding of avid Ga-67 uptake in vivo helps to establish this unique in vivo/in vitro tumor system as a valid experimental model for studies regarding the mechanism of Ga-67 accumulation by neoplastic tissue.

Animals↗

PubMed1998

Activation of inducible nitric oxide synthase results in nitric oxide-mediated radiosensitization of hypoxic EMT-6 tumor cells.

EMT-6 cells treated for 16 h with 1-10 units/ml IFN-gamma showed a gradual activation of inducible nitric oxide synthase (iNOS) in Western and Northern blots, a simultaneous raise in NO output, and an increase in hypoxic cell radiosensitivity almost to the level of aerobic cells. Both the NO signal and radiosensitization were counteracted by the NO scavenger oxyhemoglobin, by the specific iNOS inhibitor aminoguanidine, and by the L-arginine analogue N(G)-monomethyl-L-arginine. Collectively, these data demonstrate that IFN-gamma can radiosensitize EMT-6 cells through iNOS induction and that NO is the effector molecule responsible for radiosensitization. Compared with the spontaneous NO releaser (2)-1-[N-(3-ammoniopropyl)-N-(n-propyl)amino)diazen-1-ium -1,2-diolate], the iNOS-generated NO signal appeared to be 10 times lower yet resulting in the same enhancement ratio of 2.4. Direct stimulation of NO synthesis in tumor cells through the L-arginine/iNOS pathway represents a novel approach to exploit the radiosensitizing properties of NO.

Animals↗

PubMed2024

Exploring Regulatory Roles of Transposable Elements in EMT and MET through Data-Driven Analysis: Insights from regulaTER.

Gene expression is regulated at the transcriptional and translational levels and a plethora of epigenetic mechanisms. Regulation of gene expression by transposable elements is well documented. However, a comprehensive analysis of their regulatory roles is challenging due to the lack of dedicated approaches to define their contribution. Here, we present regulaTER, a new R library dedicated to deciphering the regulatory potential of transposable elements in a given phenotype. regulaTER utilizes a variety of genomics data of any origin and combines gene expression level information to predict the regulatory roles of transposable elements. We further validated its capabilities using data generated from an epithelial-mesenchymal and mesenchymal-epithelial transition cellular model. regulaTER stands out as an essential asset for uncovering the impact of transposable elements on the regulation of gene expression, with high flexibility to perform a range of transposable element-focused analyses. Our results also provided insights on the contribution of the MIR and B element subfamilies in regulating EMT and MET through the FoxA transcription factor family. regulaTER is publicly available and can be downloaded from https://github.com/karakulahg/regulaTER.

DNA Transposable Elements↗

PubMed1980

Effect of tumor dissaggregation on results of in vitro cell survival assay after in vivo treatment of the EMT-6 tumor: x-rays, cyclophosphamide, and bleomycin.

EMT-6 tumors were treated in vivo with 300 kVp X-rays, cyclophosphamide, or bleomycin. Tumor cell suspensions were prepared by digesting tumors with trypsin or a collagenase-deoxyribonuclease-pronase cocktail, and cells were plated in vitro for determination of fractional cell survival. Cell survival after X-rays was identical for the two disaggregation methods. Trypsin-derived cells were far more sensitive to bleomycin but less sensitive to cyclophosphamide than those prepared with the mixed enzyme cocktail. Interaction of drug produced and enzyme caused damage was the probable cause for these discrepancies. The nature of the interaction may be drug specific and therefore unpredictable. The results were unlikely to be due to different nonrepresentative tumor cell samples being produced by the two digestion methods, because the X-ray cell survival curves were so similar for the two products.

Animals↗

PubMed1986

Cross-link formation and chemopotentiation of EMT-6/Ro cells exposed to MISO after CCNU treatment in vitro.

Experiments were designed to measure cross-link formation following combined treatment of EMT-6/Ro tumor cells with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) and misonidazole (MISO) in vitro. To avoid MISO-induced glutathione (GSH) depletion, which might contribute to enhanced monoadduct formation by reducing the protective GSH pools, a post-incubation (i.e. treatment with CCNU for one hour in air followed by MISO treatment in hypoxia) protocol was adopted. Utilizing this treatment scheme, it was possible to significantly enhance CCNU toxicity by post-treating with MISO immediately after exposure to CCNU. Enhanced cross-link formation detected by alkaline elution, at this time, correlated well with the magnitude of cell-kill enhancement, thereby implicating enhanced cross-link formation in the mechanism of potentiation. However, if the cells were allowed to incubate for various intervals between CCNU and MISO treatments, the magnitude of potentiation progressively diminished. Beyond approximately 8-10 hours (corresponding to the time required for maximal cross-link formation after CCNU treatment), treatment with MISO was ineffective at potentiating CCNU cytotoxicity. These experiments suggest that chemopotentiation can be produced by treating with MISO after treatment with CCNU (post-incubation) and that enhanced cross-link formation is involved in the mechanism of MISO chemopotentiation of CCNU activity. The kinetic studies, using the post-incubation protocol, further suggest that the chemopotentiating effect of MISO is exerted subsequent to monoadduct formation and probably does not involve inhibition of DNA-DNA cross-link repair.

Animals↗

PubMed1992

5-chlorodeoxycytidine, a radiosensitizer effective against RIF-1 and Lewis lung carcinoma, is also effective against a DMBA-induced mammary adenocarcinoma and the EMT-6 tumor in BALB/c mice.

5-Chlorodeoxycytidine (CldC), coadministered with modulators of pyrimidine metabolism, is an effective radiosensitizer of murine tumors. Past studies that utilized RIF-1 tumors in C3H mice and Lewis lung carcinoma (LLC) in BDF1 mice have been extended with an emphasis on using multiple cycles of drug administration followed by irradiation of LLC and the use of two additional tumor models. Four of seven cures of BDF1 mice bearing LLC were obtained with three doses of 20 Gy irradiation, in which the first and third dose were preceded by a "Standard Protocol" that includes N-(phosphonacetyl)-L-aspartic acid (PALA), 5-fluorodeoxycytidine (FdC), tetrahydrouridine, and the radiosensitizer, 5-chlorodeoxycytidine. No cures were obtained in groups of mice receiving radiation alone or drugs alone, and there were no "no takes" in untreated control groups (six mice/group). Extensive tumor inhibition, exceeding that obtained with drugs or radiation alone, was obtained with two cycles of drugs and radiation combined when a dimethybenzanthracene-induced mammary adenocarcinoma was used in BALB/c mice. With the EMT-6 tumor in BALB/c mice, doses of 10 and 20 Gy were administered 9 and 16 days after tumor implantation, each preceded with the Standard Protocol; this resulted in a tumor growth delay of 24 days. No tumor growth delay occurred with drugs or radiation alone. The omission of PALA, FdC or CldC from the Standard Protocol resulted in loss of tumor control, which was obtained with the complete protocol. The fact that 5-chlorodeoxycytidine is an effective radiosensitizer in four rodent tumor systems is compelling evidence that it has potential as a radiosensitizer of human tumors, especially in view of its tumor selectivity and its resistance to catabolism when used with modulators of its metabolism, and in view of the high levels of the key enzymes in human tumors, which can convert 5-chlorodeoxycytidine to 5-chlorodeoxyuridine triphosphate, the proximate radiosensitizer.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1986

Comparative studies of radiocitrates in oncological models--I. 99mTc citrate and 67Ga citrate uptake by EMT-6 tumors in mice.

67Ga citrate and 99mTc citrate (Solcocitran) were injected sequentially, with an interval of 48 h, into Balb/c mice bearing transplanted EMT-6 tumors. Tissue distributions of 67Ga and 99mTc were measured simultaneously at intervals of 1, 3, 5 and 8 h after injection of the 99mTc citrate (49, 51, 53 and 56 h after 67Ga citrate). Maximal tumor:blood ratios for 67Ga and 99mTc were 13.8 +/- 3.2 and 4.0 +/- 1.0 respectively, both occurring at the final period. The maximum tumor index (T.I. = T:B X % dose/g) for 67Ga was 71 +/- 23% 56 h after injection, and for 99mTc was 13 +/- 12% 1 h after injection. Liver, kidney and spleen had equal or higher concentrations of radioactivity than tumor for either radiotracer. The somewhat higher tumor:blood ratio for 67Ga citrate was offset by the time required for this optimum to be reached. Alternatively, the best 99mTc citrate tumor:blood ratios were attained within 8 h, with less liver and gut radioactivity. These data fall within the range of results from other clinical and animal model studies of 67Ga citrate and 99mTc citrate. In view of the radiation dose, the inconvenience of the 48-72 h wait, and the cost of 67Ga, and because neither radiopharmaceutical is tumor specific, 99mTc citrate may have a place in early oncological screening. The results are discussed as part of a comprehensive review of the 99mTc citrate literature.

Animals↗

PubMed1993

Characterization of sodium cations in dehydrated faujasites and zeolite EMT by 23Na DOR, 2D nutation, and MAS NMR.

Sodium cations localized at crystallographically distinct cation sites in dehydrated zeolites were characterized using 23Na double rotation, two-dimensional nutation, and magic-angle-spinning nuclear magnetic resonance spectroscopy. The new DOR NMR technique has been applied at different magnetic field strengths to determine the quadrupole parameters of the overlapping quadrupole patterns. In the NMR spectra of dehydrated NaY and NaEMT two signals of sodium cations were identified, a low-field gaussian line at -12 +/- 1 ppm and a high-field quadrupole pattern, with an isotropic chemical shift of -8 +/- 1 ppm and a quadrupole coupling constant of about 4 MHz. By comparison of the 23Na MAS NMR intensities of these signals with the population of the cation sites determined by XRD and by calculation of the electric field gradients, the former signal was attributed to sodium cations at the sites SI and the latter one to sodium cations at the sites SI' as well as SII in faujasite and zeolite EMT. This assignment has further been confirmed by 23Na MAS NMR studies of dehydrated HNaY and BaNaY zeolites.

Cations↗

PubMed1998

8-Methoxypsoralen potentiates the photocytotoxic effect of Photofrin II towards EMT-6 murine tumor cells.

Pretreatment of EMT-6 murine tumor cells for 24 h with 10(-4) M 8-methoxypsoralen (8-MOP) increased the photocytotoxicity of Photofrin II (P2) after cell exposure to low doses (1-1.5 J/cm2) of UVA by two- to three-fold. 8-MOP alone had no cytotoxic action under these experimental conditions and did not significantly change the amount of P2 recovered in cells. 8-MOP enhanced the lipid peroxidation end product formation measured as thiobarbituric acid reactive substances (TBARS) during cell photosensitization by P2. The psoralen alone also slightly increased the TBARS level after UVA exposure. These results suggest that 8-MOP, albeit non-photocytotoxic by itself under our experimental conditions, could enhance the efficiency of P2 by increasing cellular lipid peroxidation following light exposure.

Animals↗

PubMed1979

Emergency medical technician (EMT-A) instruction of medical students.

In 1977 the Department of Anesthesiology of the Medical College of Virginia coordinated a compulsory 72-hour course for first-year medical students fulfilling all requirements of the Department of Transportation and leading to eligibility for certification of the medical student as an Emergency Medical Technician (EMT-A). We describe the methodology and content of this course, as well as problems encountered and lessons learned. This sound foundation in emergency care concepts will enable the medical student to develop greater competence in critical skills during the clinical years.

Allied Health Personnel↗