Relevant bibliographies by topics / Hyperplaxia

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Hyperplaxia'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Hyperplaxia.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Hyperplaxia"

1

Lazaris, Andreas C., Sofia Tseleni-Balafouta, Thomas Papathomas, Theodore Brousalis, Georgia Thomopoulou, George Agrogiannis, and Efstratios S. Patsouris. "Immunohistochemical investigation of angiogenic factors in parathyroid proliferative lesions." European Journal of Endocrinology 154, no. 6 (June 2006): 827–33. http://dx.doi.org/10.1530/eje.1.02168.

Full text
Abstract:
Objective: The pathological distinction between parathyroid neoplasms and hyperplasias remains difficult in several cases. Endoglin (CD105) is a proliferation-associated and hypoxia-inducible protein abundantly expressed in angiogenic endothelial cells. Vascular endothelial growth factor (VEGF) induces angiogenesis and VEGF-R2 is a tyrosine kinase receptor expressed early in development by endothelial cell precursors. We attempted to examine whether immunohistochemical expression of CD105, VEGF and VEGF-R2 may be useful in distinguishing between parathyroid hyperplasia and neoplasia as well as to elucidate, to some extent, the mechanism of neovascularization in proliferative lesions of the parathyroid gland. Design: Tissue specimens were taken from 38 patients with primary hyperparathyroidism (HPT) (17 adenomas and 21 primary hyperplasias) and from 30 patients with secondary HPT. Normal glands served as controls. Methods: In a standard immunohistochemical procedure, monoclonal antibodies to endoglin, VEGF and VEGF-R2 were applied to detect angiogenic endothelial cells. Immunostaining was estimated by image analysis and statistical analysis was subsequently performed. Results: Positive CD105 immunoreaction was significantly increased in parathyroid adenomas by comparison with primary hyperplasias (P = 0.033) and with secondary hyperplasias (P = 0.033). When parathyroid adenomas, primary hyperplasia and secondary hyperplasia specimens were comparatively evaluated, VEGF immunoreaction was much more common in adenomas (P = 0.018). In addition, in samples with secondary hyperplasia, VEGF-R2 immunoreactivity was positively linked with VEGF expression as well as with the apoptotic index of parathyroid cells (P = 0.038 and 0.010 respectively). In secondary hyperplasia specimens, an inverse correlation between cyclin D1 immunoexpression and angiogenic indexes, such as CD105 and VEGF, was noticed (P = 0.007 and 0.0017 respectively). Conclusions: This study shows increased angiogenesis in parathyroid adenomas compared with parathyroid proliferative lesions. In secondarily hyperplastic glands increased angiogenesis and increased apoptosis occur simultaneously; in the latter glands, the overexpression of cyclin D1 does not appear to be the genetic abnormality responsible for increased angiogenesis.
APA, Harvard, Vancouver, ISO, and other styles
2

Marx, Stephen J. "Hyperplasia in glands with hormone excess." Endocrine-Related Cancer 23, no. 1 (September 25, 2015): R1—R14. http://dx.doi.org/10.1530/erc-15-0171.

Full text
Abstract:
Five syndromes share predominantly hyperplastic glands with a primary excess of hormones: neonatal severe primary hyperparathyroidism, from homozygous mutatedCASR, begins severelyin utero; congenital non-autoimmune thyrotoxicosis, from mutatedTSHR, varies from severe with fetal onset to mild with adult onset; familial male-limited precocious puberty, from mutatedLHR, expresses testosterone oversecretion in young boys; hereditary ovarian hyperstimulation syndrome, from mutatedFSHR, expresses symptomatic systemic vascular permeabilities during pregnancy; and familial hyperaldosteronism type IIIA, from mutatedKCNJ5, presents in young children with hypertension and hypokalemia. The grouping of these five syndromes highlights predominant hyperplasia as a stable tissue endpoint and as their tissue stage for all of the hormone excess. Comparisons were made among this and two other groups of syndromes, forming a continuum of gland staging: predominant oversecretions express little or no hyperplasia; predominant hyperplasias express little or no neoplasia; and predominant neoplasias express nodules, adenomas, or cancers. Hyperplasias may progress (5 of 5) to neoplastic stages while predominant oversecretions rarely do (1 of 6; frequencies differP<0.02). Hyperplasias do not show tumor multiplicity (0 of 5) unlike neoplasias that do (13 of 19;P<0.02). Hyperplasias express mutation of a plasma membrane-bound sensor (5 of 5), while neoplasias rarely do (3 of 14;P<0.002). In conclusion, the multiple distinguishing themes within the hyperplasias establish a robust pathophysiology. It has the shared and novel feature of mutant sensors in the plasma membrane, suggesting that these are major contributors to hyperplasia.
APA, Harvard, Vancouver, ISO, and other styles
3

Horn, L. C., U. Schnurrbusch, K. Bilek, B. Hentschel, and J. Einenkel. "Risk of progression in complex and atypical endometrial hyperplasia: clinicopathologic analysis in cases with and without progestogen treatment." International Journal of Gynecologic Cancer 14, no. 2 (2004): 348–53. http://dx.doi.org/10.1136/ijgc-00009577-200403000-00023.

Full text
Abstract:
In most cases, the endometrioid adenocarcinoma of the endometrium is preceded by hyperplasia with different risk of progression into carcinoma. The original histologic slides from 560 consecutive cases with complex and atypical hyperplasia were re-examined to assess the interobserver-correlation. The hyperplasias were analyzed separately for their likelihood of progression to carcinoma in patients with and without progestogen hormonal therapy. In all cases, a fractional re-curreting was performed to establish the state of the disease.The leading symptom was vaginal bleeding in 65.5% of the cases in the postmenopausal period. Eighty-six percent of the patients presented with obesity (BMI > 30 kg/m2), 23% had had an exogeneous use of estrogens. Twenty-two cases were reclassified as simple hyperplasia and excluded from further analysis. The interobserver-correlation was 91% for complex, 92% for atypical hyperplasia, and 89% for endometrioid carcinoma, representing an overall correlation of 90%. Two percent of the cases with complex hyperplasia (8/390) progressed into carcinoma and 10.5% into atypical hyperplasia. Fifty-two percent of the atypical hyperplasias (58/112) progressed into carcinomas. In the case of progestogen treatment (n = 208; P < 0.0001) 61.5% showed remission confirmed by re-curetting, compared with 20.3% of the cases without hormonal treatment (n = 182; P < 0.0001).Endometrial hyperplasia without atypia is likely to respond to hormonal treatment. Especially in postmenopausal situation, atypical hyperplasia should be treated with total hysterectomy.
APA, Harvard, Vancouver, ISO, and other styles
4

Ferreira, E., H. Gobbi, B. S. Saraiva, and G. D. Cassali. "Histological and Immunohistochemical Identification of Atypical Ductal Mammary Hyperplasia as a Preneoplastic Marker in Dogs." Veterinary Pathology 49, no. 2 (January 31, 2011): 322–29. http://dx.doi.org/10.1177/0300985810396105.

Full text
Abstract:
This study describes and evaluates the morphological and molecular relationship between canine mammary ductal hyperplasias with atypia and canine mammary neoplasias. Ductal hyperplasia was identified in association with malignant neoplasia in 56 of the 115 cases (48,8%), and although ductal hyperplasia without atypia was the type most frequently noted in the cases, most examples of hyperplasia with atypia were associated with mammary tumors. Estrogen receptor, E-cadherin, and cytokeratins 1, 5, 10 and 14 (CK34bE12) expression was quite lower than in normal mammary tissue, and HER2 overexpression was absent in all proliferative cells of ductal hyperplasia. The Ki-67 expression, epidermal growth factor receptor and progesterone receptor expression appeared higher in those hyperplastic lesions analyzed than in normal mammary glands. These findings suggest that canine mammary atypical hyperplasia may play an important role in the process of malignant neoplastic transformation, with molecular alterations that are similar to precursor lesions reported in humans.
APA, Harvard, Vancouver, ISO, and other styles
5

Gerasimov, A. V., S. E. Krasilnikov, A. G. Kedrova, N. S. Afonina, O. E. Nechaeva, T. A. Maksimenko, and V. V. Kosyi. "MORPHOLOGICAL AND ULTRASOUND CHARACTERISTICS OF ENDOMETRIUM IN PATIENTS WITH BREAST CANCER AND THE RISK OF SECONDARY TUMORS." Journal of Clinical Practice 6, no. 3 (September 15, 2015): 39–47. http://dx.doi.org/10.17816/clinpract6339-47.

Full text
Abstract:
The analysis of features of endometrial hyperplasia in patients with breast cancer (BC) receiving adjuvant tamoxifen therapy in the period from 2011 to 2014 inclusive. 196 patients with breast cancer with ultrasound criteria of endometrial hyperplasia were examined. A postoperative histopathologic examination revealed that the lesions were endometrial hyperplasias and with 4,1% malignant findings. Hyperplasia, polyps and endometrial cancer were diagnosed in patients receiving tamoxifen, which allowed a comparison clinicoanamnestic, ultrasound, morphological and genetic characteristics of the endometrium to recover a high risk of developing a second cancer, as well as offer a pathogenic variant of its prevention. The article can be interesting as for obstetrician-gynecologist, watching women after breast cancer treatment, and oncologists, choosing a drug for adjuvant therapy.
APA, Harvard, Vancouver, ISO, and other styles
6

Diaz-Cano, Salvador J., Manuel de Miguel, Alfredo Blanes, Robert Tashjian, and Hubert J. Wolfe. "Germline RET 634 Mutation Positive MEN 2A-related C-Cell Hyperplasias Have Genetic Features Consistent with Intraepithelial Neoplasia." Journal of Clinical Endocrinology & Metabolism 86, no. 8 (August 1, 2001): 3948–57. http://dx.doi.org/10.1210/jcem.86.8.7739.

Full text
Abstract:
C-cell hyperplasias are normally multifocal in multiple endocrine neoplasia type 2A. We compared clonality, microsatellite pattern of tumor suppressor genes, and cellular kinetics of C-cell hyperplasia foci in each thyroid lobe. We selected 11 females from multiple endocrine neoplasia type 2A kindred treated with thyroidectomy due to hypercalcitoninemia. C-cell hyperplasia foci were microdissected for DNA extraction to analyze the methylation pattern of androgen receptor alleles and microsatellite regions (TP53, RB1, WT1, and NF1). Consecutive sections were selected for MIB-1, pRB1, p53, Mdm-2, and p21WAF1 immunostaining, DNA content analysis, and in situ end labeling. Appropriate tissue controls were run. Only two patients had medullary thyroid carcinoma foci. Nine informative C-cell hyperplasia patients showed germline point mutation in RET, eight of them with the same androgen receptor allele preferentially methylated in both lobes. C-cell hyperplasia foci showed heterogeneous DNA deletions revealed by loss of heterozygosity of TP53 (12 of 20), RB1 (6 of 14), and WT1 (4 of 20) and hypodiploid G0/G1 cells (14 of 20), low cellular turnover (MIB-1 index 4.5%, in situ end labeling index 0.03%), and significantly high nuclear area to DNA index ratio. MEN 2A (germline point mutation in RET codon 634) C-cell hyperplasias are monoclonal and genetically heterogeneous and show down-regulated apoptosis, findings consistent with an intraepithelial neoplasia. Concordant X-chromosome inactivation and interstitial gene deletions suggest clone expansions of precursors occurring at a point in embryonic development before divergence of each thyroid lobe and may represent a paradigm for other germline mutations.
APA, Harvard, Vancouver, ISO, and other styles
7

Travaglino, Antonio, Antonio Raffone, Gabriele Saccone, Massimo Mascolo, Maurizio Guida, Antonio Mollo, Luigi Insabato, and Fulvio Zullo. "Congruence Between 1994 WHO Classification of Endometrial Hyperplasia and Endometrial Intraepithelial Neoplasia System." American Journal of Clinical Pathology 153, no. 1 (August 21, 2019): 40–48. http://dx.doi.org/10.1093/ajcp/aqz132.

Full text
Abstract:
Abstract Objectives To assess congruence between World Health Organization (WHO) 1994 and endometrial intraepithelial neoplasia (EIN) classification systems of endometrial hyperplasia. Methods Systematic review and meta-analysis were performed by searching electronic databases for studies that classified endometrial hyperplasia according to both WHO 1994 and EIN systems. Congruence was based on the rate of specimens classified as EIN in WHO categories, which should be virtually 0.000 in nonatypical hyperplasia (NAH) and 1.000 in atypical hyperplasia (AH). Subgroup analyses were performed based on architecture complexity. Results Eight studies with 1,352 hyperplasias were included. Congruence with EIN criteria was fair in NAH (0.241) and moderate in AH (0.815). Subgroup analyses of NAH showed high congruence in simple NAH (0.065), null in complex NAH (0.517), null in simple AH (0.148), and high in complex AH (0.901). Conclusions WHO 1994 system is not congruent with the EIN system and cannot be directly translated into a dual classification.
APA, Harvard, Vancouver, ISO, and other styles
8

Santana, Clarissa, and Renato Santos. "Canine pyometra – an update and revision of diagnostic terminology." Brazilian Journal of Veterinary Pathology 14, no. 1 (March 31, 2021): 1–8. http://dx.doi.org/10.24070/bjvp.1983-0246.v14i1p1-8.

Full text
Abstract:
Pyometra is frequently diagnosed in the female dogs, and it is characterized by endometrial inflammation, accumulation of purulent exudate within the lumen, and bacterial infection. In the dog, pyometra affects more often aged nulliparous bitches during the luteal phase. Pathogenesis of pyometra is multifactorial and progesterone seems to be a key factor. Cystic endometrial hyperplasia has been described as a predisposing condition for canine pyometra. However, a recent study demonstrated that cystic endometrial hyperplasia is not significantly associated with naturally occurring pyometra, whereas there is a significant association of this condition with pseudoplacentational endometrial hyperplasia. The aim of this review is to provide an update on canine pyometra, with focus on its association with uterine hyperplasic lesions, which supports a proposal for adoption of more adequate diagnostic terminology.
APA, Harvard, Vancouver, ISO, and other styles
9

Koyama, Suguru, Keiji Tensho, Hiroki Shimodaira, Tomoya Iwaasa, Hiroshi Horiuchi, Hiroyuki Kato, and Naoto Saito. "A Case of Prefemoral Fat Pad Impingement Syndrome Caused by Hyperplastic Fat Pad." Case Reports in Orthopedics 2018 (December 23, 2018): 1–5. http://dx.doi.org/10.1155/2018/3583049.

Full text
Abstract:
Case. We report a rare case of prefemoral fat pad impingement syndrome that was caused by a hyperplasia of the normal suprapatellar fat pad. Pain and catching were observed in the proximal-lateral patellofemoral joint, and MRI imaging confirmed a hyperplasic mass in the same area. Although conservative treatment showed no signs of improvement, symptoms improved after an arthroscopic excision of the mass. Conclusion. Prefemoral fat pad impingement syndrome is related to patellar motion and should be considered as one of the underlying causes of anterior knee pain (AKP). Surgeons should recognize that a small hyperplasia composed of normal adipose tissue can cause AKP.
APA, Harvard, Vancouver, ISO, and other styles
10

Zidar, Nina, Nina Gale, Andrej Cör, and Vinko Kambič. "Expression of Ki-67 antigen and proliferative cell nuclear antigen in benign and malignant epithelial lesions of the larynx." Journal of Laryngology & Otology 110, no. 5 (May 1996): 440–45. http://dx.doi.org/10.1017/s0022215100133924.

Full text
Abstract:
AbstractIn an attempt to analyse the proliferative activity in benign and malignant laryngeal epithelial lesions, and to determine the relationship to their histologic grade, we studied the expression of proliferative cell nuclear antigen (PCNA) and Ki-67 antigen on 20 squamous carcinomas, and on 30 biopsies of epithelial hyperplasia categorized according to the Kambiˇ-Lenart classification into simple, abnormal, and atypical hyperplasias. In simple hyperplasia, both antibodies stained the nuclei of the occasional cells in the basal layer. In abnormal hyperplasia (mild dysplasia), positive cells occupied up to a third, and in atypical hyperplasia (moderate and severe dysplasia) they occupied from two-thirds to the entire epithelial thickness. In squamous carcinoma, we have found a statistically significant correlation between its grade and the percentage of Ki-67-(p<0.01) and PCNA-(p<0.00001) positive cells. Our results suggest that the proliferative fraction progressively increases with the degree of epithelial hyperplasia and the grade of carcinoma. We conclude that the patterns of immunoreactivity to PCNA and Ki-67 antigen correspond to the histologic grade of both benign and malignant epithelial lesions of the larynx. This method should be regarded as a useful adjunct to traditional histological techniques allowing more objective grading of benign and malignant epithelial lesions.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Hyperplaxia"

1

Roy, Sébastien. "Rôle de la signalisation des Bmp au sein des cellules mésenchymateuses dans le maintien de l'homéostasie gastrique." Thèse, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/11429.

Full text
Abstract:
Les bones morphogenetic protein (Bmp) sont des morphogènes qui jouent des rôles sur la prolifération et la différenciation cellulaire. La perte de signalisation dans cette voie est associée à la polypose juvénile familiale et à un risque accru de cancer gastrique. Elle est aussi associée avec l’inflammation et la guérison des tissus. Il est montré qu’au niveau de l’estomac, les ligands et les récepteurs de la signalisation des Bmp sont exprimés dans les compartiments épithéliaux et mésenchymateux. Les différents modèles animaux développés ont confirmé l’importance de cette signalisation dans la carcinogenèse gastrique. Cependant, ces modèles causent une perte de signalisation dans l’ensemble de la muqueuse gastrique et ne réussissent pas à montrer un mécanisme. Parallèlement, notre laboratoire a montré qu’une perte de signalisation de la voie des Bmp, exclusivement dans le compartiment épithélial, ne développe pas les phénotypes associés à la progression du cancer gastrique. Ce résultat suggère que les cellules mésenchymateuses pourraient être la clé de l’importance de la signalisation des Bmp dans l’estomac. Afin de mettre en lumière le rôle de la signalisation des Bmp dans le compartiment mésenchymateux, des souris qui perdent de façon spécifique le récepteur de type 1a des Bmp dans ce compartiment ont été généré (Bmpr1aMES). Il semble que la perte de signalisation des Bmp induit au niveau du mésenchyme une modification du comportement et une activation des fibroblastes en myofibroblastes. Cette modification produit également un microenvironnement (matrices, facteurs de croissance, cytokines, interleukines) propice au développement du cancer et induire des modifications importantes de l’épithélium et un appel de cellules immunitaires. Cet environnement semble être suffisant pour réduire de façon importante le nombre de cellules endocriniennes et de cellules pariétales dans l’épithélium gastrique. Il semble que la perte mésenchymateuse de signalisation des Bmp au niveau gastrique entraîne le développement d’une métaplasie au niveau de l’estomac des souris, une hyperplasie atypique qui évolue jusqu'à une dysplasie accompagnée d’une desmoplasie importante. Mes travaux ont également démontré que, dans ce contexte, une mutation oncogénique, comme la perte de Trp53, pourrait devenir maligne. En conclusion, au sein du mésenchyme, la signalisation des Bmp est importante pour le maintien de celui-ci dans un état sain. Il est probable qu’elle joue un rôle important dans le retour à l’état normal suivant les gastrites. Sa perte rend l’estomac des souris fragile au développement d’adénomes.
Abstract : Bone morphogenetic proteins (Bmp) play roles in the proliferation and differentiation. It is also associated with inflammation and tissue repair. Disruption of signaling in this pathway is associated with familial juvenile polyposis and an increase risk of gastric cancer. It has been shown that in the stomach, Bmp signaling is bidirectional. Meaning that ligands and receptors are expressed in both the epithelial and stromal compartments. Gastric abrogation animal models of the Bmp signaling pathway have confirmed the importance of this signaling in gastric carcinogenesis. However these models cause a loss of signaling in both compartments of the gastric mucosa, and the mechanism of action for this has yet been undefined. Previous work by a student in our laboratory provided a model of loss of the Bmp signaling pathway exclusively in the epithelial compartment. This model does not develop phenotypes associated with the progression of gastric cancer, suggesting, that the stromal compartment is the key in tumorigenesis by Bmp signaling in the stomach. To further test this hypothesis, we generated mice with a stromal compartment-specific loss of type1a BMP receptor (Bmpr1aMES). It appears that this deletion in the stroma induced behavior alteration with activation of fibroblasts into myofibroblasts. This change also produces a microenvironment (matrix, growth factors, cytokines, and interleukins) that is conducive to the development of cancer and induces significant modifications of the epithelium as well as a recruitment of immune cells. This microenvironment seems to be sufficient to significantly reduce the number of endocrine cells and parietal cells in the gastric epithelium. It seems that the loss of stromal Bmp signaling in the mice’s stomachs causes development of metaplasia; atypical hyperplasia that progresses to dysplasia accompanied by a significant desmoplasia. My work also shows that in this environment an oncogenic mutation such as the loss of Trp53 may become malignant. In conclusion, in the stromal compartment, Bmp signaling is important for maintaining a healthy state. It is probably involved in the return to the normal state following gastritis, and its loss makes the mouse stomach susceptible to adenoma development.
APA, Harvard, Vancouver, ISO, and other styles
2

Dahllöf, Göran. "Phenytoin-induced gingival overgrowth in epileptic children a clinical, histological and biochemical study /." Stockholm : [Karolinska Institutet], 1986. http://catalog.hathitrust.org/api/volumes/oclc/13674550.html.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Sadaghianloo, Nirvana. "Rôle de l’hypoxie et du métabolisme dans la maturation des fistules artério-veineuses pour hémodialyse." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4017.

Full text
Abstract:
L’accès vasculaire pour hémodialyse est à la fois la ligne de vie et le talon d’Achille des malades souffrant d’insuffisance rénale terminale. La fistule artério-veineuse (FAV), accès vasculaire pourtant recommandé en premier intention, présente des résultats loin d’être optimaux : 50% des FAV crées présenteront une dysfonction la 1ère année. Lors de la création d’une FAV, la paroi de la veine doit s’adapter à de nouveaux paramètres. D’une part, des modifications hémodynamiques sont responsables de modifications de la matrice extracellulaire et de lésions endothéliales. D’autre part, la dissection et la manipulation de la veine par le chirurgien, impliquant la rupture des vasa vasorum, causent une ischémie de la paroi et un stress oxydatif. In fine, la migration et la prolifération des cellules vasculaires participent à l’épaississement de la paroi par une hyperplasie néointimale (HNI) excessive, entraînant une sténose et un dysfonctionnement de la FAV. Mon projet de thèse s’articulait autour de 3 objectifs: 1) Montrer que la non-dissection de la veine évite l’apparition d’HNI, 2) Cibler l’hypoxie cellulaire pour inhiber l’HNI et 3) Evaluer la régulation par l’hypoxie d’une protéine de la matrice extracellulaire, l’ostéopontine (OPN), dans l’HNI.Résultats : 1) Nous avons développé la technique RADAR (Radial Artery Deviation And Reimplantation) de création de FAV, dont le concept est d’éviter la dissection chirurgicale de la veine en détournant l’artère, et ainsi limiter l’HNI. Les résultats de la première cohorte de malades ont montré une quasi-disparition de la sténose veineuse par HNI. Afin d’étudier l’hémodynamique de RADAR, en collaboration avec l’Université Yale, nous avons créé chez le rat un modèle de FAV avec détournement de l’artère (mimant RADAR). Grâce à des mesures moléculaires, histologiques, et d’imagerie, associées aux résultats à long terme de la cohorte RADAR, nous avons confirmé que l’HNI veineuse est inhibée et montré le rôle du flux laminaire dans ce montage. 2) Nous avons cherché une substance pharmacologique qui, appliquée dès la chirurgie, ciblerait HIF pour inhiber l’INH. In vitro, nous avons étudié la réponse des différents types de cellules vasculaires (endothéliales, musculaires lisses, fibroblastes), sous l’action de l’hypoxie, de 5 médicaments (Desferrioxamine, Everolimus, Metformine, N-Acetylcystéine, Topotecan) influençant HIF et le métabolisme cellulaire, et de 3 invalidations géniques (siRNA HIF1alpha, siRNA HIF2alpha, siRNA, HIF1/2alpha). Trois de ces substances et 1 invalidation génique agissaient sur le métabolisme et la prolifération de nos cellules. Nous les avons donc testé sur un modèle murin de FAV: 2 substances et l’invalidation de HIF1/2 ont montré une inhibition significative de l’HNI. 3) Nous avons étudié l’expression d’OPN dans les cellules vasculaires sous l’effet de l’hypoxie. Si les cellules vasculaires veineuses en monoculture n’exprimaient ni ne sécrétaient d’OPN sous l’effet de l’hypoxie, la co-culture de ces trois lignées permettaient la sécrétion d’OPN induite par l’hypoxie. Nous avons ainsi montré que l’hypoxie, le métabolisme et les paramètres du flux sont impliqués dans le développement de l’HNI lors de la maturation de la FAV
For hemodialysis patients, their vascular access is both their life line and their Achille’s heel. Despite being recommended as a primary vascular access, the arteriovenous fistula (AVF) shows sub-optimal results, with about 50% of patients needing a revision during the year following creation. As the AVF is created, the venous wall must adapt to new environment. While hemodynamic changes are responsible for the adaptation of the extracellular matrix and activation of the endothelium, surgical dissection and mobilization of the vein disrupt the vasa vasorum, causing wall ischemia and oxidative stress. As a consequence, migration and proliferation of vascular cells participate in venous wall thickening by a mechanism of neointimal hyperplasia (NH). When aggressive, NH causes stenosis and AVF dysfunction. I had 3 aims during my thesis : 1) To show that minimal dissection of the vein inhibits NH, 2) to target the Hypoxia Inducible Factor (HIF) pathway to inhibit NH, and 3) to understand the hypoxic regulation of an adhesion molecule, osteopontin (OPN), in NH. Results: 1) We developed the Radial Artery Deviation And Reimplantation (RADAR) technique of AVF creation, where we avoid venous dissection to prevent NH. The first cohort of patients showed only 2% of venous stenosis. To study RADAR hemodynamics, in collaboration with Yale University, we created a rat model of artery-to-vein AVF that mimics RADAR geometry. By means of molecular, histological and imaging analysis, associated to the long-term outcome of the RADAR cohort, we confirmed that this configuration shows laminar flow and limits NH.2) We looked for a way to inhibit HIF during surgery by local delivery of a small molecule. In vitro, we analyzed the behavior of vascular cells (endothelial, smooth muscle and fibroblasts) in response to hypoxia, to 1 of 5 compounds regulating HIF or metabolism (Desferrioxamine, Everolimus, Metformine, N-Acetylcysteine, Topotecan), and to HIF silencing. Three of these compounds and HIF silencing had a significant impact on the metabolism and/or proliferation of our cells. We therefore tested them in a mouse model of AVF, to show that 2 compounds and HIF silencing inhibited NH. 3) We analyzed the expression of OPN in our cells in hypoxia. While in monoculture, they did not express or secrete OPN in response to hypoxia, co-culture of the same cell lines induced OPN secretion in hypoxia. We could show that hypoxia, metabolism and flow parameters are intricate mechanisms responsible for the development of NH during AVF maturation
APA, Harvard, Vancouver, ISO, and other styles
4

Ashton, R. E. "Retinoid induced epidermal hyperplasia." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596189.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Bonfig, Walter, Friedhelm Roehl, Stefan Riedl, Jürgen Brämswig, Annette Richter-Unruh, Angela Hübner, Susanne Fricke-Otto, et al. "Sodium Chloride Supplementation Is Not Routinely Performed in the Majority of German and Austrian Infants with Classic Salt-Wasting Congenital Adrenal Hyperplasia and Has No Effect on Linear Growth and Hydrocortisone or Fludrocortisone Dose." Karger, 2018. https://tud.qucosa.de/id/qucosa%3A70638.

Full text
Abstract:
Introduction: Sodium chloride supplementation in saltwasting congenital adrenal hyperplasia (CAH) is generally recommended in infants, but its implementation in routine care is very heterogeneous. Objective: To evaluate oral sodium chloride supplementation, growth, and hydrocortisone and fludrocortisone dose in infants with salt-wasting CAH due to 21-hydroxylase in 311 infants from the AQUAPE CAH database. Results: Of 358 patients with classic CAH born between 1999 and 2015, 311 patients had salt-wasting CAH (133 females, 178 males). Of these, 86 patients (27.7%) received oral sodium chloride supplementation in a mean dose of 0.9 ± 1.4 mmol/kg/day (excluding nutritional sodium content) during the first year of life. 225 patients (72.3%) were not treated with sodium chloride. The percentage of sodium chloride-supplemented patients rose from 15.2% in children born 1999–2004 to 37.5% in children born 2011–2015. Sodium chloride-supplemented and -unsupplemented infants did not significantly differ in hydrocortisone and fludrocortisone dose, target height-corrected height-SDS, and BMI-SDS during the first 2 years of life. Conclusion: In the AQUAPE CAH database, approximately one-third of infants with salt-wasting CAH receive sodium chloride supplementation. Sodium chloride supplementation is performed more frequently in recent years. However, salt supplementation had no influence on growth, daily fludrocortisone and hydrocortisone dose, and frequency of adrenal crisis.
APA, Harvard, Vancouver, ISO, and other styles
6

Chen, Changyi. "Intimal hyperplasia in endarterectomized arteries." Diss., Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/25393.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Jackson, Andrew John. "Cellular aspects of intimal hyperplasia formation." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2417/.

Full text
Abstract:
Introduction: 12,000 infrainguinal bypass grafts are performed annually in the UK. Despite improvements in surgical technique, outcomes remain suboptimal: 20% of above knee grafts require intervention to maintain patency by 3 years. Only antiplatelet agents have been demonstrated thus far to improve graft survival. 80% of graft failure is as a result of intimal hyperplasia, an inflammatory process characterised by the proliferation and migration of vascular smooth muscle cells. Toll Like Receptors (TLR), part of the innate immune system, have been implicated in atherosclerosis formation but not investigated in a model of infrainguinal graft failure. When a vein is used as a conduit for infrainguinal bypass graft it has been exposed to ischaemic and hypoxic conditions: preliminary data has demonstrated that ischaemic vascular smooth muscle cell explants are hyperproliferative. Phospholipase C γ (PLC γ) is a signalling pathway with potential links to innate immune pathways and pathways induced by hypoxia and ischaemia. Methods: Human vein tissue was obtained from patients undergoing amputation and coronary artery bypass surgery and used for immunohistochemistry and to obtain vascular smooth muscle cells by explant method. Immunohistochemistry was used to determine the presence of TLR4 and PLC γ in human vein tissue. Specific TLR Ligands were used to determine the functional response of TLR’s in vascular smooth muscle cells as measured by Interleukin 8 ELISA. Radiolabelled Thymidine incorporation was used to measure proliferation of vascular smooth muscle cells in response to TLR4 activation, hypoxia and PLC γ inhibition. Results: TLR4 was demonstrated to be present in human vein tissue, and functionally active in human vascular smooth muscle cells. Furthermore stimulation with the specific ligand of TLR4 caused enhanced proliferation of vascular smooth muscle cells. Hypoxia (5% and 10% Oxygen) significantly enhanced proliferative responses of vascular smooth muscle cells. PLC γ was demonstrated to be present in human vein tissue, and inhibition, using U73122 in vascular smooth muscle cells reduced proliferation. Conclusion: TLR activation and hypoxia appear to enhance the proliferative responses of human vascular smooth muscle cells, a key cellular pathway of intimal hyperplasia formation and infrainguinal graft failure. Inhibition of PLC γ reduces proliferative responses. Further research is required to confirm that PLC γ is a key common pathway mediating enhances of proliferation caused by TLR activation and hypoxia.
APA, Harvard, Vancouver, ISO, and other styles
8

Gallos, Ioannis D. "Management & prognosis of endometrial hyperplasia." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5157/.

Full text
Abstract:
This thesis investigates the management and prognosis of endometrial hyperplasia. The literature on conservative therapies for endometrial hyperplasia is systematically reviewed and a meta-analysis is performed to identify the most effective treatment. Further meta-analysis is performed for young women with severe endometrial hyperplasia or cancer to explore the effectiveness of fertility-sparing treatment. A national survey of Gynaecologists is performed to evaluate current and the need for further research. A large cohort study is included that defines the regression and relapse of endometrial hyperplasia with two popular conservative therapies, the Levonorgestrel-releasing intrauterine system (LNG-IUS) and oral progestogens. The LNG-IUS is found to induce regression more often with fewer events of relapse than oral progestogens. A prediction model based on clinical characteristics and biomarkers finds that morbid obesity is an independent predictor for relapse. This research has major implications for clinical practice and a national guideline in process is based on its findings.
APA, Harvard, Vancouver, ISO, and other styles
9

Religa, Piotr. "Development of intimal hyperplasia in transplant arteriosclerosis /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-448-8/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Clarke, Michael Joseph. "Clinical and laboratory aspects of myointimal hyperplasia." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366584.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Hyperplaxia"

1

Ackermann, R., and F. H. Schröder, eds. Prostatic Hyperplasia. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110847413.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Donaldson, M. D. C. Congenital adrenal hyperplasia. London: Child Growth Foundation, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

International Consultation on Benign Prostatic Hyperplasia (5th 2000 Paris, France). Benign prostatic hyperplasia. Edited by Chatelain C. (Chritian), World Health Organization, and International Union against Cancer. [England]: Health Publication, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

J, Christmas Timothy, ed. Benign prostatic hyperplasia. London: Gower Medical Publishing, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Petrovich, Zbigniew, and Luc Baert, eds. Benign Prostatic Hyperplasia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78185-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Jakse, Gerhard, Christian Bouffioux, Jean de Leval, and Rudi A. Janknegt, eds. Benign Prostatic Hyperplasia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77480-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kirby, Roger S. Benign prostatic hyperplasia. London: Gower Medical, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Donovan, Jenny. Treatment for benign prostatic hyperplasia. Bristol: Health Care Evaluation Unit, University of Bristol, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Koshiba, Ken, Makoto Miki, Toshiro Terachi, and Toyoaki Uchida, eds. Treatment of Benign Prostatic Hyperplasia. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68444-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Oskar, Klotz. Concerning compensatory hyperplasia of the intima. [S.l: s.n., 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Hyperplaxia"

1

Hofmann, Walter J., Peter Möller, and Herwart F. Otto. "Hyperplasia." In Surgery of the Thymus, 59–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-71076-6_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Sainburg, Robert L., Andrew L. Clark, George E. Billman, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble, et al. "Hyperplasia." In Encyclopedia of Exercise Medicine in Health and Disease, 415–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2508.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Davis, Barbara J. "Hyperplasia." In Encyclopedia of Systems Biology, 930. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1582.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Schwab, Manfred. "Hyperplasia." In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2911-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Capinera, John L., Thomas O. Crist, John B. Heppner, Minos E. Tzanakakis, Severiano F. Gayubo, Aurélien Tartar, Pauline O. Lawrence, et al. "Hyperplasia." In Encyclopedia of Entomology, 1897. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_1454.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Ackermann, R. "Introduction." In Prostatic Hyperplasia, edited by R. Ackermann and F. H. Schröder, IX—X. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110847413-001.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Utz, D. C. "Transurethral prostatic surgery at the Mayo Clinic." In Prostatic Hyperplasia, edited by R. Ackermann and F. H. Schröder, 1–10. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110847413-002.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Aumüller, G. "Morphological aspects of the human prostate and the development of benign prostatic hyperplasia." In Prostatic Hyperplasia, edited by R. Ackermann and F. H. Schröder, 11–22. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110847413-003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Isaacs, J. T. "Stem cell organization of the prostate and the development of benign prostatic hyperplasia." In Prostatic Hyperplasia, edited by R. Ackermann and F. H. Schröder, 23–34. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110847413-004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Bartsch, G., A. Brüngger, U. Schweikert, H. Hintner, R. Höpfl, and H. P. Rohr. "Benign prostatic hyperplasia: morphometric studies in relation to the pathogenesis." In Prostatic Hyperplasia, edited by R. Ackermann and F. H. Schröder, 35–54. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110847413-005.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Hyperplaxia"

1

Qureshi, Sabuhi. "Study of PTEN immunohistochemical expression in endometrial hyperplasia." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685337.

Full text
Abstract:
Objective: The incidence of endometrial hyperplasia & carcinoma is increasing in developing nations. Newer techniques are being tried to recognise endometrial hyperplasia. One of these is tumor suppressor gene phosphatase & tensin homologue (PTEN). It is frequently inactivated i.e turned off in endometrial hyperplasia lesions. This is an early event in endometrial tumorigenesis that may occur in response to known endocrine risk factors & offers an informative immunohistochemical marker for premalignant disease. The present study was planned to study PTEN immunohistochemical expression in endometrial hyperplasia. Methods: Women of >40 years of age presenting with abnormal uterine bleeding in the OPD of OBGYN Department of KG Medical University underwent endometrial biopsy. The histopathology of the biopsy tissue was done in department of Pathology of KG Medical University. The cases of endometrial hyperplasia were studied for PTEN immunohistochemical expression. Results: 168 women of >40 years of age with abnormal uterine bleeding underwent endometrial biopsy. 50 women were diagnosed as endometrial hyperplasia. Of these, PTEN evaluation was done in 27 cases. Loss of PTEN expression was found in 11 cases (40.74%) of endometrial hyperplasia. Loss of PTEN expression was more in complex hyperplasia with atypia (66.66%) as compared to simple hyperplasia without atypia (29.4%). Conclusion: There is positive correlation between loss of PTEN expression and grade of morphological differentiation of hyperplasia.
APA, Harvard, Vancouver, ISO, and other styles
2

Hartert, M., J. Tripsky, S. Kröber, and M. Hürtgen. "True Thymic Hyperplasia in an Adult." In 60. Kongress der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e. V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678254.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Popler, J., WA Gower, PJ Mogayzel, Jr, LM Nogee, MK Dishop, TC Hay, and RR Deterding. "Familial Neuroendocrine Cell Hyperplasia of Infancy." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5965.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Петрова, Ю. А., Г. Г. Орлова, Н. В. Бодарева, В. В. Рудаков, and А. А. Горбовская. "B-cell hyperplasia of the thyroid gland." In Научный диалог: Вопросы медицины. ЦНК МОАН, 2018. http://dx.doi.org/10.18411/spc-15-04-2018-12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Mak, Garbo, and Marcia Katz. "Multifocal Multinodular Pneumocyte Hyperplasia In Tuberous Sclerosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3844.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Chinn, Daniel, Elvis Nditafon, Alvin Yew, and Chandrasekhar Thamire. "Thermal Therapy Protocols for Benign Prostatic Hyperplasia." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176764.

Full text
Abstract:
Thermal therapy for treatment of benign prostatic hyperplasia (BPH) is becoming increasingly popular due to the minimally invasive nature of the treatment. Successful management of such therapy requires accurate estimation of thermal dosage. The purpose of this study is to provide correlations for the thermal damage caused by ultrasound, microwave, and infrared devices under a range of operating conditions. A boundary-fitting finite difference method is used to examine the heat transfer in the prostate gland and surrounding tissue. The Pennes bioheat transfer model and a porous media model were utilized to calculate temperature histories. Necrosis zones were determined using published necrosis data for prostatic tissue and cells. Thermal damage correlations for the three different hyperthermia sources along with sample temperature contours and necrosis zones are presented. Results indicate that the applicator power level and heating time are the most important parameters in achieving the desired necrosis zones, while coolant parameters strongly affect the temperatures of the sensitive urethra and serve as constraints for protocol parameters. Out of the three sources evaluated, ultrasound modality appears to be the most capable of causing necrosis in the target zones, with least damage to the surrounding healthy tissues.
APA, Harvard, Vancouver, ISO, and other styles
7

Tran-Son-Tay, Roger, Minki Hwang, Scott A. Berceli, C. Keith Ozaki, and Marc Garbey. "A Model of Vein Graft Intimal Hyperplasia." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353667.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Kopacz, Adrian M., Brandon J. Tefft, Shu Q. Liu, and Wing K. Liu. "Modeling of Endothelial Cell Adhesion Dynamics Modulated by Molecular Engineering." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13269.

Full text
Abstract:
Vascular thrombosis, intimal hyperplasia, and atherosclerosis are common disorders affecting a very large portion of the human population. A potential reduction in these disorders will elicit a significant impact. It has been shown that endothelial cells play a critical role in protecting blood vessels against the formation of thrombosis and atherosclerosis. Hence, a successful endothelial cell lining of arterial constructs will prevent intimal hyperplasia in reconstructed arteries. However, in practice endothelial cells often detach from reconstructed arteries due to weak adhesion strength, hindering the effectiveness of endothelial cell lining.
APA, Harvard, Vancouver, ISO, and other styles
9

Krishnamoorthy, Mahesh K., Prabir Roy-Chaudhury, Yang Wang, Christy K. Holland, David Rigger, Ann Choe, and Rupak K. Banerjee. "Vascular Remodeling of Arteriovenous Fistula." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206508.

Full text
Abstract:
Arteriovenous (AV) fistula failure is a major clinical problem for the 350,000 patients currently on hemodialysis in the United States. The reasons for this failure are mainly attributed to venous stenosis due to neointimal hyperplasia together with a possible failure of vascular dilatation [1]. Despite the magnitude of the clinical problem, there are currently no effective therapies for AV fistula failure. We believe that this is due to a lack of knowledge about the mechanisms involved in both neointimal hyperplasia and vascular dilatation in the specific context of AV fistulae.
APA, Harvard, Vancouver, ISO, and other styles
10

Abdesselem, Houari. "Exploring the SIRT1/P53 Pathway in Adipocytes Hyperplasia." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp1258.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Hyperplaxia"

1

Abigail Benkert, Abigail Benkert. Managing Congenital Adrenal Hyperplasia in the Amish Population. Experiment, June 2015. http://dx.doi.org/10.18258/5470.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Gradinarska, Desislava, Maria Ivanova, Miroslav Genov, Tsvetan Tsvetkov, and Denica Daskalova. Comparative Assay of Seminal-plasma Proteins in Healthy Dogs and Dogs with Benign Prostatic Hyperplasia. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, August 2019. http://dx.doi.org/10.7546/crabs.2019.08.17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

London, Richard A., and Mark Byrne. Optimization of Diode Laser System to Treat Benign Prostate Hyperplasia Final Report CRADA No. TSB-1154-95. Office of Scientific and Technical Information (OSTI), January 2018. http://dx.doi.org/10.2172/1418927.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ma, Dehui, Guochao Liu, Tianjiao Gao, Qi Zhang, and Mingjun Liu. Massage treatment of hyperplasia of mammary glands A protocol for a systematic review and meta-analysis: study protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0066.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

DEGraffenried, Linda. Training in Support of a Research Project Entitled Study an ER Variant Identified from Breast Hyperplasis"". Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada392721.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Ma, Mengjie, Liuqiao Zhang, and Xiangli Wang. Effect of auricular point pressing therapy on hyperplasia of mammary glands A protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0028.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ma, Mengjie, Liuqiao Zhang, and Xiangli Wang. Effect of auricular point pressing therapy on hyperplasia of mammary glands A protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0028.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Franchi, Dorella. Role of transvaginal ultrasonography in the management of young patients affected by atypical endometrial hyperplasia and welldifferentiated endometrial cancer undergoing hormonal fertility-sparing treatment. Science Repository OÜ, March 2019. http://dx.doi.org/10.31487/j.jso.2019.01.005.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Tesfaigzi, J., M. B. Wood, and N. F. Johnson. Expression of cyclin D{sub 1} during endotoxin-induced aleveolar type II cell hyperplasia in rat lung and the detection of apoptotic cells during the remodeling process. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381386.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Hyperplaxia' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography