scholarly journals The effects of feed naturally contaminated with Fusarium mycotoxins on the thymus in suckling piglets

2020 ◽  
Vol 68 (2) ◽  
pp. 186-192
Author(s):  
Igor Ujčič-Vrhovnik ◽  
Tanja Švara ◽  
Tadej Malovrh ◽  
Breda Jakovac-Strajn
Keyword(s):  
Cellular Proliferation ◽  
Fusaric Acid ◽  
Perinatal Period ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Fusarium Mycotoxins ◽  
Tunel Method ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Suckling Piglets ◽  
Experimental Group

AbstractIn this study, feed naturally containing Fusarium mycotoxins was fed to gilts during the perinatal period, and the effects on the thymus were investigated in one-week-old piglets. Twenty gilts were divided into equal control (0.26 mg deoxynivalenol, DON) and experimental (5.08 mg DON, 0.09 mg zearalenone and 21.61 mg fusaric acid per kg of feed) groups. One suckling piglet from each litter (n = 20) was sacrificed at one week of age to obtain thymus samples for further analysis. The cortex to medulla ratio of the thymus was morphometrically analysed using NIS Elements BR (Nikon) software. Paraffin-embedded thymus sections were stained to quantify apoptosis (with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling – TUNEL method), cellular proliferation (Ki-67) and macrophages (MAC 387). The results showed that the thymus cortex (P = 0.023) to medulla (P = 0.023) ratio was significantly lower in the experimental group. The number of apoptotic cells (cortex, P = 0.010, medulla, P = 0.001) and the number of proliferating cells in the thymus cortex (P = 0.001) and medulla (P < 0.001) were significantly higher in the experimental group. Our results indicate that feeding Fusarium mycotoxins to a parent animal during the perinatal period induces significant alterations in the thymus of one-week-old piglets, which indicates an immunosuppressive effect in piglets.

scholarly journals The Influence of Fusarium Mycotoxins on the Liver of Gilts and Their Suckling Piglets

Animals ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 2534
Author(s):  
Tamara Dolenšek ◽  
Tanja Švara ◽  
Tanja Knific ◽  
Mitja Gombač ◽  
Boštjan Luzar ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Animal Species ◽  
Animal Feed ◽  
Fusaric Acid ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Fusarium Mycotoxins ◽  
Experimental Diet ◽  
Proliferation Activity ◽  
Suckling Piglets ◽  
Inflammatory Infiltrates

Mycotoxins are common fungal secondary metabolites in both animal feed and human food, representing widespread toxic contaminants that cause various adverse effects. Co-contamination with different mycotoxins is frequent; therefore, this study focused on feed contaminated with Fusarium mycotoxins, namely, deoxynivalenol (5.08 mg/kg), zearalenone (0.09 mg/kg), and fusaric acid (21.6 mg/kg). Their effects on the liver of gilts and their piglets were chosen as the research subject as pigs are one of the most sensitive animal species that are also physiologically very similar to humans. The gilts were fed the experimental diet for 54 ± 1 day, starting late in their pregnancy and continuing until roughly a week after weaning of their piglets. Livers of gilts and their piglets were assessed for different histopathological changes, apoptosis, and proliferation activity of hepatocytes. On histopathology, gilts fed the experimental diet had a statistically significant increase in hepatocellular necrosis and apoptosis (p = 0.0318) as well as sinusoidal leukocytosis with inflammatory infiltrates of hepatic lobules (p = 0.0004). The amount of interlobular connective tissue in the liver of experimental gilts was also significantly decreased (p = 0.0232), implying a disruption in the formation of fibrous connective tissue. Apoptosis of hepatocytes and of cells in hepatic sinusoids, further assessed by the terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assay, showed a statistically significant increase (p = 0.0224 and p = 0.0007, respectively). No differences were observed in piglet livers. These results indicated that Fusarium mycotoxins elicited increased apoptosis, necrosis, and inflammation in the liver of gilts, but caused no effects on the liver of piglets at these concentrations.

scholarly journals Using Ki-67 Mitotic Activity Markers as a Predictor of the Progression of Adhesions in the Abdominal Cavity

2020 ◽  
Vol 10 (4) ◽  
pp. 412-415
Author(s):  
Irina Shurygina ◽  
Michael Shurygin ◽  
Elena Chepurnykh ◽  
Nataliya Ayushinova
Keyword(s):  
Mitotic Activity ◽  
Proliferative Activity ◽  
Abdominal Cavity ◽  
Control Group ◽  
Proliferative Potential ◽  
Proliferating Cells ◽  
Maximum Increase ◽  
Ki 67 ◽  
Male Wistar Rats ◽  
Experimental Group

Background: Ki-67 is a nuclear protein expressed in all proliferating cells of vertebrates during mitotic cycle phases S, G1, G2, and M, except for G0. Studying this marker is widely used to diagnose the proliferative activity of tumors. However, studying Ki-67 in non-neoplastic diseases attracts much less attention among the researchers. The aim of this study was to assess the possibility of using staining for Ki-67 to identify the proliferative potential of fibroblasts during the formation of adhesions in the abdominal cavity (AC). Methods and Results: Experiments were carried out on male Wistar rats. The adhesion process in AC was simulated in the control group (n=25), and in the experimental group (n=25) with the administration of Seroguard®. Animals were sacrificed on Days 1–30, and the severity of the adhesive process in AC was assessed. Histological sections were prepared and stained for Ki-67. It was found that the animals of the control group had increased severity of the adhesive process in AC during the observation. Maximum increase in severity was registered on Day 30 – 12[9-13] points in the control group and 4[4-4] points in the experimental group (P=0.0079). High proliferative activity of fibroblasts in the control group was detected on Days 3, 7, 14 and 30, which may indicate an active division of fibroblasts and the formation of adhesions in the damaged area. In the experimental group, single Ki-67 positive cells were noted during the entire observation period, which may point to a reduced potential for the formation of adhesions. Conclusion: Our study showed the prospects of using Ki-67 staining to determine the severity of the developing adhesive process in AC, and also revealed one of the possible mechanisms that inhibit the formation of the adhesive process when using Seroguard® – a decrease in the mitotic activity of fibroblasts in the area of peritoneal injury.

scholarly journals Optimization of the method for isolation of epithelial cells from the non-glandular part of the rat stomach for flow cytometry

2020 ◽  
Vol 90 (5) ◽  
pp. 517-525
Author(s):  
Gordana Joksić ◽  
◽  
Jelena Filipović Tričković ◽  
Mileva Mićić ◽  
Ivana Joksić ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Epithelial Cells ◽  
Propidium Iodide ◽  
Cellular Proliferation ◽  
Immunohistochemical Detection ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Tert Butyl ◽  
Flow Cytometric ◽  
Propidium Iodide Staining

Traditional methods in cell proliferation studies are based on immunohistochemical detection of proliferating cells in the target tissue. Since they are time consuming, optimization of novel, more efficient methods is important for large scale proliferation studies. In this study, we aimed to optimize the isolation of single epithelial rat forestomach cells for flow cytometry. As a marker of cellular proliferation we used the Ki-67 antibody to detect this nuclear protein expressed in proliferating cells. We also performed immunohistochemical detection of Ki-67 positive cells and propidium iodide staining to validate the results. 3-tert- butyl -4-hydroxyanisole was used as the positive control to ensure cellular proliferation. The results showed that isolation of epithelial cells with collagenase, trypsin and cell strainer ensures great cell viability (>95%) and the purity of the samples. Flow cytometry and immunostaining with the Ki-67 antibody indicated that 3-tert- butyl-4-hydroxyanisole treatment leads to a significant increase in proliferation. A significant positive correlation was observed between the results obtained by immunohistochemistry and flow cytometry, but the flow cytometric data had a smaller measurement error, suggesting the equal sensitivity and greater accuracy of this method. Propidium iodide staining showed that the percentage of cells in the G2+S phase of the cell cycle correlated positively with the percentage of Ki-67 positive cells assessed by flow cytometry, indicating that Ki-67 positive cells reflect an active dividing cell pool. We conclude that the isolation of forestomach epithelial cells described is a simple and reliable method for obtaining viable cells for use in flow cytometry. Compared to immunohistochemistry, flow cytometric detection of the Ki-67 antigen is equally sensitive, but much faster and provides more accurate results.

Tissue Ki67 proliferative index expression and pathological changes in hemodialysis arteriovenous fistulae: Preliminary single-center results

2021 ◽  
pp. 112972982110154
Author(s):  
Raffaella Mauro ◽  
Cristina Rocchi ◽  
Francesco Vasuri ◽  
Alessia Pini ◽  
Anna Laura Croci Chiocchini ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Hot Spot ◽  
Wall Thickening ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Group A ◽  
The Mean ◽  
Set Up ◽  
Group B

Background: Arteriovenous fistula (AVF) for hemodialysis integrates outward remodeling with vessel wall thickening in response to drastic hemodynamic changes. Aim of this study is to determine the role of Ki67, a well-established proliferative marker, related to AVF, and its relationship with time-dependent histological morphologic changes. Materials and methods: All patients were enrolled in 1 year and stratified in two groups: (A) pre-dialysis patients submitted to first AVF and (B) patients submitted to revision of AVF. Morphological changes: neo-angiogenesis (NAG), myointimal thickening (MIT), inflammatory infiltrate (IT), and aneurysmatic fistula degeneration (AD). The time of AVF creation was recorded. A biopsy of native vein in Group A and of arterialized vein in Group B was submitted to histological and immunohistochemical (IHC) analysis. IHC for Ki67 was automatically performed in all specimens. Ki67 immunoreactivity was assessed as the mean number of positive cells on several high-power fields, counted in the hot spots. Results: A total of 138 patients were enrolled, 69 (50.0%) Group A and 69 (50.0%) Group B. No NAG or MIT were found in Group A. Seven (10.1%) Group A veins showed a mild MIT. Analyzing the Group B, a moderate-to-severe MIT was present in 35 (50.7%), IT in 19 (27.5%), NAG in 37 (53.6%); AD was present in 10 (14.5%). All AVF of Group B with the exception of one (1.4%) showed a positivity for Ki67, with a mean of 12.31 ± 13.79 positive cells/hot spot (range 0–65). Ki67-immunoreactive cells had a subendothelial localization in 23 (33.3%) cases, a myointimal localization in SMC in 35 (50.7%) cases. The number of positive cells was significantly correlated with subendothelial localization of Ki67 ( p = 0.001) and with NA ( p = 0.001). Conclusions: Native veins do not contain cycling cells. In contrast, vascular cell proliferation starts immediately after AVF creation and persists independently of the time the fistula is set up. The amount of proliferating cells is significantly associated with MIT and subendothelial localization of Ki67-immunoreactive cells, thus suggesting a role of Ki-67 index in predicting AVF failure.

scholarly journals Characterization of Cytokines and Proliferation Marker Ki67 in Chronic Rhinosinusitis with Nasal Polyps: A Pilot Study

Medicina ◽  
2021 ◽  
Vol 57 (6) ◽  
pp. 607
Author(s):  
Rudolfs Janis Viksne ◽  
Gunta Sumeraga ◽  
Mara Pilmane
Keyword(s):  
Connective Tissue ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Cellular Proliferation ◽  
Rank Correlation ◽  
Control Group ◽  
Relative Distribution ◽  
Proliferation Marker ◽  
Ki 67 ◽  
Stimulation Of

Background and Objectives: Chronic rhinosinusitis (CRS) is a condition that affects as much as 10.9% of the population and, along with presence of nasal polyps, is associated with significant morbidity and decreased quality of life. Studies on molecular pathways that have been activated in nasal polyp tissue are mainly based on cytokine concentration detection. Therefore, our aim is to investigate the complex appearance, relative distribution and interlinks of IL-1, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12 and Ki 67 in chronic rhinosinusitis with nasal polyps (CRSwNP) affected human nasal mucosa. Materials and Methods: Samples of nasal polyps were obtained from 12 patients with previously diagnosed CRSwNP and no prior surgery. Control group consisted of samples from 17 otherwise healthy individuals with isolated nasal septum deviation. Tissues were stained for IL-1, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12 and Ki67 immunohistochemically. Non-parametric statistic, Mann–Whitney U test and Spearman’s rank correlation coefficient were used. Results: All factors, except connective tissue cytokine IL-10 and proliferation marker Ki-67, had increased presence in connective tissue and decreased presence in epithelium of nasal polyps when compared to controls. Very strong and strong positive correlations between factors were observed. Conclusions: Decreased appearance of IL-1α, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12 positive structures in the nasal epithelium with selective increase of IL-1α and IL-12 in nasal subepithelial connective tissue characterize the cytokine endotype with dysfunctional epithelial barrier and local stimulation of immune response in the connective tissue in case of chronic rhinosinusitis with polyps. Decrease of IL-6 in both—epithelium and connective tissue with strong correlation between it and IL-7 and IL-10 in connective tissue suggests significant stimulation of this regulatory cytokine and, possibly, the important role in pathogenesis of the development in nasal polyps. Correlations between Ki67 and cytokines indicate possible involvement of IL-4, IL-7 and IL-12 in regulation of cellular proliferation.

scholarly journals Mice lacking β-carotene-15,15’-dioxygenase exhibit reduced serum testosterone, prostatic androgen receptor signaling, and prostatic cellular proliferation

2016 ◽  
Vol 311 (6) ◽  
pp. R1135-R1148 ◽  
Author(s):  
Joshua W. Smith ◽  
Nikki A. Ford ◽  
Jennifer M. Thomas-Ahner ◽  
Nancy E. Moran ◽  
Eric C. Bolton ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Cellular Proliferation ◽  
Serum Testosterone ◽  
Cell Number ◽  
Immunofluorescent Staining ◽  
Receptor Signaling ◽  
Ki 67 ◽  
Androgen Receptor Signaling ◽  
Testosterone Levels ◽  
Β Carotene

β-Carotene-15,15’-dioxygenase (BCO1) cleaves dietary carotenoids at the central 15,15’ double bond, most notably acting on β-carotene to yield retinal. However, Bco1 disruption also impacts diverse physiological end points independent of dietary carotenoid feeding, including expression of genes controlling androgen metabolism. Using the Bco1−/− mouse model, we sought to probe the effects of Bco1 disruption on testicular steroidogenesis, prostatic androgen signaling, and prostatic proliferation. Male wild-type (WT) and Bco1−/− mice were raised on carotenoid-free AIN-93G diets before euthanasia between 10 and 14 wk of age. Weights of the prostate and seminal vesicles were significantly lower in Bco1−/− than in WT mice (−18% and −29%, respectively). Serum testosterone levels in Bco1−/− mice were significantly reduced by 73%. Bco1 disruption significantly reduced Leydig cell number and decreased testicular mRNA expression of Hsd17b3, suggesting inhibition of testicular testosterone synthesis. Immunofluorescent staining of the androgen receptor (AR) in the dorsolateral prostate lobes of Bco1−/− mice revealed a decrease in AR nuclear localization. Analysis of prostatic morphology suggested decreases in gland size and secretion. These findings were supported by reduced expression of the proliferation marker Ki-67 in Bco1−/− prostates. Expression analysis of 200 prostate cancer- and androgen-related genes suggested that Bco1 loss significantly disrupted prostatic androgen receptor signaling, cell cycle progression, and proliferation. This is the first demonstration that Bco1 disruption lowers murine circulating testosterone levels and thereby reduces prostatic androgen receptor signaling and prostatic cellular proliferation, further supporting the role of this protein in processes more diverse than carotenoid cleavage.

Immunohistochemical study of p53 expression in endometrial carcinomas: correlation with markers of proliferating cells and clinicopathologic features

1993 ◽  
Vol 3 (6) ◽  
pp. 363-368 ◽  
Author(s):  
T. Hachisuga ◽  
K. Fukuda ◽  
M. Uchiyama ◽  
N. Matsuo ◽  
T. Iwasaka ◽  
...  
Keyword(s):  
Dna Polymerase ◽  
Proliferative Activity ◽  
P53 Protein ◽  
Myometrial Invasion ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Normal Endometrium ◽  
P53 Expression ◽  
Dna Polymerase Α ◽  
Endometrial Carcinomas

Using anti-p53 (PAb1801 and PAb240), anti-DNA polymerase α and Ki-67 monoclonal antibodies, the expression of p53 was studied in 11 normal endometria, 14 endometrial hyperplasias and 27 endometrial carcinomas and its relationship to the proliferative activity of the tumors was examined. Normal endometria and simple hyperplasias were completely negative for p53. The PAb1801 indices of complex hyperplasias and complex atypical hyperplasias were 2.5±1.8% and 5.0±3.2%, respectively. The PAb1801 indices of grade 1, grade 2 and grade 3 endometrial carcinomas were 10.2±14.2%, 44.4±29/0% and 45.0±32.5%, respectively. These results indicate a progressively enhanced p53 expression in the sequence from normal endometrium, through hyperplasia to carcinoma. A significant correlation between p53 expression and labeling indices of Ki-67 and DNA polymerase α was observed in endometrial carcinomas. The endo-metrial carcinomas with p53 overexpression developed mainly in post-menopausal patients and were frequently high-grade tumors with deep myometrial invasion. These findings may indicate that overexpression of p53 protein contributes to the proliferative activity of the tumor cells.

The murine Ki-67 cell proliferation antigen accumulates in the nucleolar and heterochromatic regions of interphase cells and at the periphery of the mitotic chromosomes in a process essential for cell cycle progression

1996 ◽  
Vol 109 (1) ◽  
pp. 143-153 ◽  
Author(s):  
M. Starborg ◽  
K. Gell ◽  
E. Brundell ◽  
C. Hoog
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Tandem Repeats ◽  
Sequence Motifs ◽  
Mitotic Chromosomes ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Cycle Progression ◽  
Conserved Sequence ◽  
Interphase Cells

We have isolated the murine homologue of the human Ki-67 antigen. The Ki-67 antigen is used as a marker to assess the proliferative capacity of tumour cells; however, its cellular function is not known. The murine Ki-67 cDNA sequence (TSG126) was found to contain 13 tandem repeats, making up more than half of the total protein size. A comparison of this repetitive sequence block to its human counterpart, which contains 16 consecutive repeat units, revealed several conserved sequence motifs, including one motif frequently observed in proteins interacting with DNA. An antiserum developed against the product of the TSG126 cDNA clone identified a protein with an apparent molecular mass of 360 kDa, mainly expressed in proliferating cells. The TSG126 protein begins to accumulate during the late G1 stage of the cell cycle and is first seen as numerous small granules evenly distributed throughout the nucleus. During the S and the G2 phases, larger foci that overlap with the nucleoli and the heterochromatic regions are formed. At the onset of mitosis the TSG126 protein undergoes a dramatic redistribution process and becomes associated with the surface of the condensed chromosomes. The relative absence of the TSG126 protein from G1 interphase cells strongly argues against a model where the association of the TSG126 protein with mitotic chromosomes merely reflects a mechanism for the symmetrical distribution of nucleolar proteins between daughter cells. Instead, the intracellular distribution of the TSG126 protein during the cell cycle suggests that it could have a chromatin-associated function in both interphase and mitotic cells. Microinjection of anti-TSG126 antibodies into proliferating Swiss-3T3 fibroblasts was found to delay cell cycle progression, indicating that the TSG126 protein has an essential nuclear function.

Ki-67/MIB-1 and Recurrence in Pituitary Adenoma

2021 ◽  
Author(s):  
Kent Tadokoro ◽  
Colten Wolf ◽  
Joseph Toth ◽  
Cara Joyce ◽  
Meharvan Singh ◽  
...  
Keyword(s):  
Systematic Review ◽  
Pituitary Adenoma ◽  
Recurrence Rate ◽  
Pituitary Adenomas ◽  
Cellular Proliferation ◽  
Published Data ◽  
Ki 67 ◽  
Institutional Data ◽  
Mib 1

Abstract Objectives Ki-67/MIB-1 is a marker of cellular proliferation used as a pathological parameter in the clinical assessment of pituitary adenomas, where its expression has shown utility in predicting the invasiveness of these tumors. However, studies have shown variable results when using Ki-67/MIB-1 association with recurrence. The purpose of this study is to determine if a high Ki-67/MIB-1 labeling index (LI) is predictive of recurrence in pituitary adenomas. Methods A retrospective chart review was performed for patients undergoing pituitary adenoma resection with at least 1 year of follow-up. Additionally, systematic data searches were performed and included studies that correlated recurrence rate to Ki-67/MIB-1 LI. Our institutional data were included in a synthesis with previously published data. Results Our institutional review included 79 patients with a recurrence rate of 26.6%. We found that 8.8% of our patients had a high Ki-67/MIB-1 LI (>3%); however, high Ki-67/MIB-1 was not associated with recurrence. The systematic review identified 244 articles and 49 full-text articles that were assessed for eligibility. Quantitative analysis was performed on 30 articles including our institutional data and 18 studies reported recurrence by level of Ki-67/MIB-1 LI. Among studies that compared Ki-67/MIB-1 ≥3 vs. <3%, 10 studies reported odds ratios (OR) greater than 1 of which 6 were statistically significant. A high Ki-67/MIB-1 had higher odds of recurrence via the pooled odds ratio (OR = 4.15, 95% confidence interval [CI]: 2.31–7.42). Conclusion This systematic review suggests that a high Ki-67/MIB-1 should prompt an increased duration of follow-up due to the higher odds of recurrence of pituitary adenoma.

Abstract 1414: Pim-1 Stimulates Cardiac Progenitor Cell Proliferation And Asymmetric Division

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Christopher T Cottage ◽  
Savilla Tuck ◽  
Kimberlee Fischer ◽  
Natalie Gude ◽  
John Muraski ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cell Fate ◽  
Cellular Proliferation ◽  
Gene Promoter ◽  
Asymmetric Division ◽  
Postnatal Growth ◽  
Chain Gene ◽  
Ki 67 ◽  
Population Number ◽  
Mechanistic Basis

Cardiac progenitor cells (CPCs) blunt cardiomyopathic damage and increase survival following adoptive transfer into hearts subjected to myocardial infarction (MI), but the initial survival, persistence, and long term engraftment of the donated cell population remains problematic. Previous studies from our group have demonstrated that transgenes driven by the α -myosin heavy chain gene promoter are expressed in the CPC population allowing for enhanced proliferation and survival. This study details a genetic engineering strategy to augment the salutary effects of CPCs through the use of a serine/threonine kinase named Pim-1 that promotes cellular proliferation and survival. Transgenic mice created with cardiac-specific Pim-1 overexpression (Pim-wt) exhibit enhanced Pim-1 activity in both cardiomyocytes and CPCs, both of which show increased proliferative activity assessed using BrdU or Ki-67 markers relative to non-transgenic (NTG) controls. However, CPC population number was not increased in the Pim-wt hearts during normal postnatal growth or after infarction challenge, suggesting that Pim-1 expression promotes asymmetric division resulting in maintenance of the CPC pool as well as expansion of the cardiomyocyte population. Localization and quantitation of cell fate determinants Numb and α -adaptin by confocal microscopy were employed to assess levels of asymmetric division in the CPC population. Polarization of Numb in mitotic phospho-histone positive cells demonstrates asymmetric division in 65% of the CPC population in hearts of Pim-wt mice versus 26% in NTG hearts after infarction challenge. Similarly, Pim-wt hearts had fewer cells with uniform α -adaptin staining indicative of symmetrically dividing CPCs, with in 36% of the CPCs versus vs. 73% in NTG sections. These findings define a mechanistic basis for enhanced myocardial regeneration in transgenic mice overexpressing Pim-1 kinase in the myocardial lineage cells.

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