Neurofibromin 2 (NF2), a potent tumor suppressor, is reported to inhibit proliferation in several cell types. The role of NF2 in neointima hyperplasia after vascular injury is unknown. We explored the role of NF2 in proliferation, migration of vascular smooth muscle cell (VSMC) and neointima hyperplasia after vascular injury. NF2 phosphorylation was elevated in VSMC subjected to platelet-derived growth factor (PDGF)-BB and in artery subjected to vascular injury. Mice deficient for Nf2 in VSMC showed enhanced neointima hyperplasia after injury, increased proliferation and migration of VSMC after PDGF-BB treatment. Mechanistically, we observed increased nuclear p-NF2, declined p-Yes-Associated Protein (YAP), nuclear translocation of YAP after PDGF-BB treatment or injury. NF2 knockdown or YAP overexpression showed similar phenotype in VSMC proliferation, migration and neointima hyperplasia. YAP inhibition abolished the above effects mediated by NF2 knockdown. Finally, NF2 knockdown further promoted
TY - JOUR. T1 - Acidophilic nuclear inclusions are specific for florid ductal hyperplasia among proliferative breast lesions. AU - Lauer, Scott. AU - Oprea-Ilies, Gabriela. AU - Cohen, Cynthia. AU - Adsay, Volkan. AU - Adams, Amy L.. PY - 2011/6/1. Y1 - 2011/6/1. N2 - Context.-Recently we have observed distinctive acidophilic intranuclear inclusions in cases of usual intraductal hyperplasia of the breast. Similar inclusions were described almost 20 years ago in cases of mammary hyperplasia. These correlated ultrastructurally with so-called helioid inclusions. However, there since has been little discussion of these inclusions in the literature. Objective.-To examine the incidence and specificity of these inclusions in proliferative lesions of the breast. Design.-Forty cases of usual intraductal hyperplasia, 15 cases of atypical ductal hyperplasia, and 34 cases of lowgrade ductal carcinoma in situ were examined for the presence of acidophilic intranuclear inclusions. Results.-Acidophilic ...
Hyperplasia may be due to any number of causes, including proliferation of basal layer of epidermis to compensate skin loss, chronic inflammatory response, hormonal dysfunctions, or compensation for damage or disease elsewhere.[11] Hyperplasia may be harmless and occur on a particular tissue. An example of a normal hyperplastic response would be the growth and multiplication of milk-secreting glandular cells in the breast as a response to pregnancy, thus preparing for future breast feeding.[12] Perhaps the most interesting and potent effect IGF has on the human body is its ability to cause hyperplasia, which is an actual splitting of cells.[13] By contrast, hypertrophy is what occurs, for example, to skeletal muscle cells during weight training and steroid use and is simply an increase in the size of the cells.[14] With IGF use, one is able to cause hyperplasia which actually increases the number of muscle cells present in the tissue.[15] Weight training with or without anabolic steroid use ...
TY - JOUR. T1 - Risk factors for atherosclerosis and the development of preatherosclerotic intimal hyperplasia. AU - Cizek, Stephanie M.. AU - Bedri, Shahinaz. AU - Talusan, Paul. AU - Silva, Nilsa. AU - Lee, Hang. AU - Stone, James R.. PY - 2007/11. Y1 - 2007/11. N2 - Background: Intimal hyperplasia or thickening is considered to be the precursor lesion for atherosclerosis in humans; however, the factors governing its formation are unclear. To gain insight into the etiology of preatherosclerotic intimal hyperplasia, we correlated traditional risk factors for atherosclerosis with the intimal hyperplasia in an atherosclerosis-resistant vessel, the internal thoracic artery. Methods: Paired internal thoracic arteries were obtained from 89 autopsies. Multivariate logistic regression and multiple regression models were used to examine the association of preatherosclerotic intimal hyperplasia with traditional risk factors for atherosclerosis: age, gender, hypertension, smoking, body mass index, ...
Neointimal hyperplasia refers to proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, resulting in the thickening of arterial walls and decreased arterial lumen space. Neointimal hyperplasia is the major cause of restenosis after percutaneous coronary interventions such as stenting or angioplasty. The term neointima is used because the cells in the hyperplastic regions of the vascular wall have histological characteristics of both intima and normal artery cells. Neointimal hyperplasia first develops with damage to the arterial wall, followed by platelet aggregation at site of injury, recruitment of inflammatory cells, proliferation and migration of vascular smooth muscle cells, and collagen deposition. Mechanical injury of arterials due to stretching of arterial walls with a balloon catheter results in the recruitment of cells such as monocytes, macrophages, and neutrophils to the site of injury. Macrophages in particular express many growth factors, ...
The p53-ull mammary epithelial model differs from the traditional mouse models of mammary tumorigenesis in several fundamental biological properties (5 , 6) . The traditional mouse models of mammary tumorigenesis, which are induced by mouse mammary tumor virus standard, arise from alveolar hyperplasias. These alveolar hyperplasias are negative for ER at the onset and generate ER-negative, hormone-independent tumors. In chemical carcinogen-treated mice, tumors arise from both alveolar hyperplasias and ductal hyperplasias. However, tumors are primarily hormone independent. Because the p53-null normal mammary epithelium and the serially transplanted, immortalized ductal outgrowths were ER positive, it was of interest to determine the hormonal dependency of preneoplastic progression in these cells.. The hormonal dependency of the p53-null normal mammary epithelium is indistinguishable from that of the p53 wild-type epithelium. Previous results demonstrated that growth and morphogenesis in ...
Roberts, Jenna, "Characterization of a cellular hyperplasia in a mutant transgenic mouse." (1989). Summer and Academic Year Student Reports. 885 ...
AIMS--To determine if allelic loss on chromosomes 16q and 17p, commonly encountered in in situ and invasive ductal carcinomas, is present in atypical ductal hyperplasia (ADH); to determine whether ADH is a neoplastic (clonal) or hyperplastic (polyclonal) proliferation. METHODS--Fourteen cases of ADH were examined for allele loss at loci on chromosome 16q and 17p using a microdissection technique, polymorphic DNA markers and the polymerase chain reaction (PCR). RESULTS--Loss of heterozygosity (LOH) was detected in five of nine informative cases on chromosome 16q at the microsatellite D16S413 and two of eight informative cases on chromosome 17p at D17S796. CONCLUSIONS--The incidence of LOH at these loci is similar to that previously observed in ductal carcinoma in situ and in invasive ductal carcinoma. Because of the nature of the technique used, our findings also demonstrate that ADH is a monoclonal, and hence, neoplastic proliferation rather than a hyperplastic (polyclonal) condition as its name ...
Atypical ductal hyperplasia is a condition that can occur in the lining of the milk ducts in the breast. ADH is not a form of breast cancer.
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Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue. Hyperplasia may result in the gross enlargement of an organ, the formation of a benign tumor. Hyperplasia is considered to be a physiological response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasia (the process underlying cancer and some benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.[1] ...
Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue. Hyperplasia may result in the gross enlargement of an organ, the formation of a benign tumor. Hyperplasia is considered to be a physiological response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasia (the process underlying cancer and some benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.[1] ...
Hyperplasia refers to an increase in the number of cells within a tissue due to mitosis. It is important to note that hyperplastic cells still maintain strict regulatory control of their cell cycle. Consequently, when the stimuli which induce hyperplasia are removed, cells will terminate their divisions. In contrast, cell division in the absence of stimuli is considered neoplasia ...
Another interesting finding in our study is that women greater than 55 years of age with atypia had increased ER expression compared with younger women with atypia. This differs from the previous report by Shoker and colleagues (7) who found that ER expression was high in atypical ductal hyperplasia, ductal carcinoma in situ and lobular neoplasia regardless of age. The number of samples in that study was somewhat small; 23 cases of atypical hyperplasia, 43 cases of ductal carcinoma in situ, and 32 cases of lobular neoplasia. The authors suggested that in atypia and carcinoma in situ the regulation of ER expression may escape the normal age-related regulatory mechanisms. ER expression and relationship to age has also been studied in hyperplastic enlarged lobular units, a common alteration of the normal TDLU and potential precursor of breast cancer. Lee and colleagues (21) have shown that ER expression in hyperplastic enlarged lobular units is increased in postmenopausal woman compared with ...
The cytoplasmic signal adaptor protein designated sequestosome1 (SQSTM1) (A170 in mouse, ZIP in rat or p62 in human) plays a key role in modulating signal transduction via membrane receptors. SQSTM1 has a UBA ubiquitin-binding domain in the C-terminus and participates in the assembly of ubiquitinated protein aggregates termed sequestosome and modulation of ubiquitination pathways involved in NF-κB activity and receptor trafficking. We have found that deficiency of SQSTM1 in mice exhibits mature-onset obesity accompanied by insulin and leptin resistance. We previously established that redox sensitive transcription factor Nrf2 upregulates SQSTM1 expression in response to atherogenic stimuli or laminar shear stress in vascular cells, and here examine role of SQSTM1 in neointimal hyperplasia and vascular remodeling in vivo following carotid artery ligation. Neointimal hyperplasia was markedly enhanced at proximal sites of ligation after 3 weeks in SQSTM1−/− (n=10) compared with wild type mice ...
A method is provided for reducing the occurrence of anastomotic intimal hyperplasia in grafts of artery, vein, biologic or synthetic conduits having end-to-side distal anastomosis. The method includes administering a regimen of fractionated heparin to the subject. Administration of the fractionated heparin can be either intravenously, intraperitoneally, subcutaneously or orally. Preferred dosage is 50-80 mg./kg. body weight per day.
Women with atypical hyperplasia (also known as atypia) are at higher risk of developing breast cancer in future than previously thought.
hyperplasia - MedHelps hyperplasia Center for Information, Symptoms, Resources, Treatments and Tools for hyperplasia. Find hyperplasia information, treatments for hyperplasia and hyperplasia symptoms.
Since the 1920s, it has been a dogma that the only manner of normalising LV wall stress, for example during systemic hypertension, is to increase cardiac mass by means of hypertrophy (Karsner et al., 1925; Petersen and Baserga, 1965; Morkin and Ashford, 1967; Morkin and Ashford, 1968), where the myocytes are thickening due to parallel replication of sarcomeres (Dorri et al., 2007). Since then, however, a number of recent investigations of both healthy and sick hearts have shown that hyperplasia can occur after the postnatal period (Linzbach, 1960; Olivetti et al., 1994; Beltrami et al., 1995; Anversa and Kajstura, 1998; Beltrami et al., 2001; Leri et al., 2002; Engel, 2005; Brüel et al., 2007b; Du et al., 2010). It is likely that the pathophysiological response to increased afterload elicits both a hypertrophic response, and a hyperplastic response with formation of- and parallel placement of new cardiomyocytes (Kajstura et al., 1994). Importantly, the combined response to chronically increased ...
Peters JE, Lyons PA, Lee JC, Richard AC, Fortune MD, Newcombe PJ, Richardson S, Smith KGC. (2016) Insight into genotype-phenotype associations through eQTL mapping in multiple cell types in health and immunemediated disease. PLoS Genet, 12(3):e1005908.. Richard AC, Lyons PA, Peters JE, Biasci D, Flint SM, Lee JC, McKinney EF, Siegel RM, Smith KG. (2014) Comparison of gene expression microarray data with count-based RNA measurements informs microarray interpretation. BMC Genomics, 15(1):649.. Vahedi G, Richard AC, OShea JJ. (2014) Enhancing our understanding of asthma. Nat Immunol, 15(8):701.. Meylan F, Richard AC, Siegel RM. (2011) TL1A and DR3, a TNF family ligand-receptor pair that promotes lymphocyte costimulation, mucosal hyperplasia, and autoimmune inflammation. Immunol Rev, 244(1):188.. Meylan F, Richard AC, Siegel RM. (2011) TL1A and DR3, a TNF family ligand-receptor pair that promotes lymphocyte costimulation, mucosal hyperplasia, and autoimmune inflammation. Immunol Rev, ...
CMV is thought to be a key pathogen involved in the pathogenesis of TV in human allografts. To evaluate the direct effect of CMV infection on vascular biology, we used a rat model in which aortic allografts were infected ex vivo with RCMV prior to transplantation. We chose 2 time points after transplantation to investigate the development of TV, 2 weeks that represented the early phase of TV in rats; and 8 weeks, when TV was fully developed. We found that RCMV influenced vascular remodeling by increased apoptosis of SM-α-actin positive cells in the media layer, decreased extracellular matrix deposits and increased intimal hyperplasia. Moreover, RCMV induced a strong infiltration of CD68-positive macrophages mainly in the adventitia and resulted in an increase of MCP-1 in the allograft, which resulted in migration of adventitial cells towards the intima that most likely also contributed to intimal hyperplasia.. Vessel stability is sustained by a balance between cellular proliferation and ...
Hyperplasia, precautions, diagnosis, causes, risk factors, treatment for hyperplasia, medical information, signs and symptoms, side effects, side effects, definition and overview of hyperplasia, images, complications, types of hyperplasia and more.
A method is disclosed for inhibiting intimal hyperplasia in a warm-blooded mammal which comprises administering topically at the site and time of a vascular injury induced by arterial intervention in said mammal a small but inhibitorily effective amount of tissue factor pathway inhibitor (TFPI) sufficient to inhibit said intimal hyperplasia.
A method is disclosed for inhibiting intimal hyperplasia in a warm-blooded mammal which comprises administering topically at the site and time of a vascular injury induced by arterial intervention in said mammal a small but inhibitorily effective amount of tissue factor pathway inhibitor (TFPI) sufficient to inhibit said intimal hyperplasia.
Cellular hypertrophy is a fundamental response of the stressed heart. Many of the pathways associated with cell division are known to be activated in this hypertrophic response, leading to the hypothesis that cardiomyocyte hypertrophy might be the result of a fundamental block in karyokinesis and cytokinesis, by which the adult cardiomyocyte is unable to disassemble sarcomeres, uncouple from neighboring cells and divide (Ahuja et al., 2007). Nuclear division and polyploidy are observed in the latest stages of human heart failure and reverse with ventricular unloading, but cellular dynamics earlier in the pathophysiological cascade have not yet been explored (Rivello et al., 2001). In the zebrafish model that we generated, we were able to explore the effects of disrupted sarcomere gene function during cardiogenesis. We found that when the embryonic heart is exposed to a hypertrophic stimulus, in contrast to the response in the adult mammalian heart, a hyperplastic response occurs. Whereas ...
Another interesting finding in our study is that women greater than 55 years of age with atypia had increased ER expression compared with younger women with atypia. This differs from the previous report by Shoker and colleagues (7) who found that ER expression was high in atypical ductal hyperplasia, ductal carcinoma in situ and lobular neoplasia regardless of age. The number of samples in that study was somewhat small; 23 cases of atypical hyperplasia, 43 cases of ductal carcinoma in situ, and 32 cases of lobular neoplasia. The authors suggested that in atypia and carcinoma in situ the regulation of ER expression may escape the normal age-related regulatory mechanisms. ER expression and relationship to age has also been studied in hyperplastic enlarged lobular units, a common alteration of the normal TDLU and potential precursor of breast cancer. Lee and colleagues (21) have shown that ER expression in hyperplastic enlarged lobular units is increased in postmenopausal woman compared with ...
Pseudoepitheliomatous hyperplasia, also called Hecks disease, is an epithelial, inconstant and conjunctive proliferation that develops as a response to a great variety of stimuli. It is a lesion associated to different diseases, being found in the following etiopathogenic conditions: infectious pathogenic conditions, tumoral pathogenic conditions, inflammatory pathogenic conditions. We studied oral pseudoepitheliomatous hyperplasia for which we performed a histopathological study, on a group of 47 cases of oral pseudoepitheliomatous hyperplasias, where we investigated the following: oral epithelium changes, changes in the underlying lamina propria and associated etiopathogenic conditions. The main changes of the oral epithelium were: elongation of the epithelial apexes (17.02%), acanthosis (100%), dyskeratosis (14.89%), and in the underlying lamina propria: fibrosis (29.78%), inflammatory infiltrate (70.21%) and vascular proliferation (10.64%). The most frequent associated etiopathogenic conditions
Patterns of proliferative changes in crypts bordering colonic tumors: zonal histology and cell cycle marker expression.: Proliferative crypt changes have been n
There are no current recommended screening tests for uterine cancer.. Women with high risk for endometrial cancer or atypical hyperplasia may be screened. Screening is recommended only for those with certain risk factors, such as Lynch syndrome colorectal cancer, a rare familial syndrome in which multiple family members often develop colorectal and other tumors. These women should be followed closely by a doctor or team of doctors with expertise in cancer genetics. For a period of years, screening was recommended for all women taking tamoxifen, but the current recommendation is not to screen, but to test if uterine bleeding occurs.. If you have symptoms such as vaginal bleeding after you go through menopause, or heavy or irregular bleeding before menopause, you should discuss these with your doctor. ...
Pancreatic cancer, the fourth commonest cause of death in the United States, has a very poor prognosis, is increasing in incidence, and, in most cases, is not detected before it has spread beyond the pancreas. Partial, or total, pancreatectomy has increased five-year survival in only a small fraction of cases. New techniques are helpful in earlier diagnosis, but patients have to be selected for examination long before clinical signs or symptoms develop. Elderly patients who use alcohol and tobacco excessively and female diabetics may be at higher risk. Pathologists should examine pancreasduct epithelium at autopsy in patients in the fourth to sixth decades for atypia, papillary hyperplasia, carcinoma in situ, or other possible precursor changes. Diagnostic tumor, or oncofetal antigens, or a biochemical difference in isozyme activities, hopefully, may be developed. Some combinations of surgery, chemotherapy, and radiation therapy may give better prognosis.
In animal models and patient-derived neurons, terazosin elevated ATP and warded off neurodegeneration. Men who take the drug to control prostate hyperplasia are less likely to get PD, or have milder symptoms. ...
Chaudhary MA, Guo LW, Shi X, Chen G, Gong S, Liu B, Kent KC. Periadventitial drug delivery for the prevention of intimal hyperplasia following open surgery. Journal of Controlled Release. 2016 ;233:174-180. ...
VSMC and HUVEC proliferation and apoptosis were measured by BrdU and TdT staining, respectively. Balloon injury of the right carotid was produced in Wistar rats. Straight after the vascular injury, the balloon-dilated arteries were randomly transfected with p85active (n = 8), dominant negative p85 (p85DN) (n = 8) or green fluorescent protein (GFP, n = 6; controls). Transfection of p85active decreased VSMC proliferation in the absence of cAMP while cAMP inhibition of VSMC growth was prevented by p85DN. p85active formed a stable complex with ras proteins, resulting in a selective switch-off of ras effectors in VSMCs. On the other hand, p85active did not affect HUVEC growth in vitro. Interestingly, p85active significantly reduced VSMC and HUVEC apoptosis in vitro. In both vascular cell lineages, p85active increased while p85DN decreased Akt phosphorylation. Importantly, the in vivo transfection of activated p85-active significantly reduced VSMC proliferation and then neointimal formation after ...
True instances of mammary hyperplasia and macromastia become apparent during adolescence and should be operatively treated at that time. Erosion of self-confidence, social isolation, and...
This second part of our review about vascular proliferations summarizes the clinicopathologic features of the cutaneous vascular hyperplasias and benign neoplasms. Hyperplasias com..
During the growth of hyperplastic tissues is increasing the level of PSA in the blood. In the end, 1 gram can increase the value of 0.3 ng/ml If you have cancer, then the increased rate may suddenly jump to 3.5 ng/ml During the control of disease progression of BPH should take into account that the rate of PSA in the blood during the year should not rise by 0.75 ng/ml.. The increased rate of PSA in the prostate adenoma may exceed the test results of healthy men, but it should not cross the conventional threshold values.. ...
Testimonials and practice show that IGF-1 LR3 is an excellent choice both for drying and for providing qualitative muscle growth (due to hypertrophy and hyperplasia). The drug is relevant for applying different age groups, levels of training and at the same time regardless of sex. In other words, for sports purposes it can be relatively safe to use both men and women, and amateurs, and sports professionals.. IGF-1LR3: detailed description. If you disclose IGF-1LR3 in terms of properties, it is a biologically active peptide that has an anabolic effect and promotes the process of muscle hyperplasia. It also mediates the action of growth hormone, so the improvements they provide are largely comparable (in humans, growth hormone is not completely independent, its effects (fat burning, muscle growth, etc.) are largely mediated by an insulin-like growth factor ...
Principal Investigator:SAKUMA Makoto, Project Period (FY):1989 - 1990, Research Category:Grant-in-Aid for General Scientific Research (C), Research Field:General surgery
Results Balloon denudation increased TSP-2 gene expression by 10-fold, when compared to non-denuded arteries after 21 days (p = .01). Fluorophore-conjugated siRNA confirmed transmural delivery following denudation. When compared to saline treated animals, TSP-2 siRNA reduced TSP-2 mRNA expression by 70% (p = .001). The addition of the transfection reagent PEI to TSP-2 siRNA treated grafts, however, did not significantly augment gene silencing. Morphometric analysis of arterial cross sections demonstrated significantly less neointima formation-as measured by intima-media (I/M) total area ratio-among grafts dip-coated with unmodified and PEI-treated TSP-2 siRNA (I/M: 0.2 and 0.4, respectively) compared to saline grafts (I/M: 1.0, p , .001). ...
Diagnosis of Hyperplasia including differential diagnoses, hidden causes, misdiagnosis, confirming diagnoses, and diagnostic tests.
Creb3l4-KO mice showed adipocyte hyperplasia, lead to improved metabolic parameters. (a) Adipogenic potential of mouse embryonic fibroblasts (MEFs) derived from
Principal Investigator:ZEMPO Nobuya, Project Period (FY):1997 - 1998, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:General surgery
This illustration shows a raised papule that lacks the associated epidermal hyperplasia or dermal metabolic deposits or cellular infiltrates that define true papules. This lesion is due to the tran..
Ekzaminim të kalojë nga një gjinekolog është e rekomanduar herë në gjashtë muaj, madje edhe gra të shëndetshme. Arsyeja kryesore për frekuencë të tillë - ndryshimet e mundshme të hormoneve në tru...
Looking for online definition of gallbladder cystic mucosal hyperplasia in the Medical Dictionary? gallbladder cystic mucosal hyperplasia explanation free. What is gallbladder cystic mucosal hyperplasia? Meaning of gallbladder cystic mucosal hyperplasia medical term. What does gallbladder cystic mucosal hyperplasia mean?
TY - JOUR. T1 - Nodular Regenerative Hyperplasia of the Liver in Patients with IBD Treated with Allopurinol-Thiopurine Combination Therapy. AU - Seinen, Margien L.. AU - Van Asseldonk, Dirk P.. AU - De Boer, Nanne K.. AU - Bouma, Gerd. AU - Van Nieuwkerk, Carin M.. AU - Mulder, Chris J.. AU - Bloemena, Elisabeth. AU - Van Bodegraven, Adriaan A.. PY - 2017/3/1. Y1 - 2017/3/1. N2 - Background: Thiopurine therapy, particularly thioguanine, has been associated with nodular regenerative hyperplasia (NRH) of the liver. Combination therapy of allopurinol and an adapted low-dose thiopurine leads to a pharmacokinetic profile that has similarities to that of thioguanine. Therefore, allopurinol-Thiopurine combination therapy may also be associated with NRH of the liver. We assessed the prevalence of NRH in patients with inflammatory bowel disease (IBD) treated with allopurinol-Thiopurine combination therapy by liver biopsy specimen examination. Methods: An observational, cross-sectional study was conducted ...
TY - JOUR. T1 - Osteopontin mediates Citrobacter rodentium-induced colonic epithelial cell hyperplasia and attaching-effacing lesions. AU - Wine, Eytan. AU - Shen-Tu, Grace. AU - Gareau, Melanie. AU - Goldberg, Harvey A.. AU - Licht, Christoph. AU - Ngan, Bo Yee. AU - Sorensen, Esben S.. AU - Greenaway, James. AU - Sodek, Jaro. AU - Zohar, Ron. AU - Sherman, Philip M.. PY - 2010/9. Y1 - 2010/9. N2 - Although osteopontin (OPN) is up-regulated in inflammatory bowel diseases, its role in disease pathogenesis remains controversial. The objective of this study was to determine the role of OPN in host responses to a non-invasive bacterial pathogen, Citrobacter rodentium, which serves as a murine infectious model of colitis. OPN gene knockout and wild-type mice were infected orogastrically with either C. rodentium or Luria-Bertani (LB) broth. Mouse-derived OPN+/+ and OPN-/- fibroblasts were incubated with C. rodentium and attachingeffacing lesions were demonstrated using transmission electron ...
TY - JOUR. T1 - Synergistic repression of thyroid hyperplasia by cyclin C and Pten. AU - Jezek, Jan. AU - Wang, Kun. AU - Yan, Ruilan. AU - Di Cristofano, Antonio. AU - Cooper, Katrina F.. AU - Strich, Randy. PY - 2019/8/15. Y1 - 2019/8/15. N2 - The cyclin C-Cdk8 kinase has been identified as both a tumor suppressor and an oncogene depending on the cell type. The genomic locus encoding cyclin C (Ccnc) is often deleted in aggressive anaplastic thyroid tumors. To test for a potential tumor suppressor role for cyclin C, Ccnc alone, or Ccnc in combination with a previously described thyroid tumor suppressor Pten, was deleted late in thyroid development. Although mice harboring individual Pten or Ccnc deletions exhibited modest thyroid hyperplasia, the double mutant demonstrated dramatic thyroid expansion resulting in animal death by 22 weeks. Further analysis revealed that Ccncthyr-/- tissues exhibited a reduction in signal transducer and activator of transcription 3 (Stat3) phosphorylation at ...
-Vein graft intimal hyperplasia, due to smooth muscle cell (SMC) proliferation, remains a limiting factor in long-term vein graft patency. Increased superoxide production regulates SMC mitogenesis and contributes to reduced NO bioactivity in systemic models of vascular disease. We compared superoxide production in experimental venous bypass grafts with ungrafted veins and determined its enzymatic sources and cellular localization. Vascular superoxide production was measured in vein grafts and control jugular veins obtained from normocholesterolemic rabbits undergoing jugular vein-carotid artery interposition bypass grafting. Surgical isolation of the contralateral jugular vein, without bypass grafting, provided an additional control for the effects of surgical manipulation. Superoxide production was increased 3-fold in vein grafts compared with control veins. Systematic stimulation and inhibition of specific oxidases revealed that the major source of increased vein graft superoxide production was a