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Neuroreport Oct 2007Hyperbaric oxygen therapy promoted brain cell proliferation. Wnt-3 is closely associated with the proliferation of neural stem cells. We examined whether hyperbaric...
Hyperbaric oxygen therapy promoted brain cell proliferation. Wnt-3 is closely associated with the proliferation of neural stem cells. We examined whether hyperbaric oxygen promoted neural stem cells to proliferate and its correlation with Wnt-3 protein in hypoxic-ischemic neonate rats. Hyperbaric oxygen therapy was administered 3 h after hypoxia ischemia daily for 7 days. The proliferating stem cells and Wnt-3 protein were examined dynamically in the subventricular zone. Results showed that stem cells proliferated and peaked 7 days after hyperbaric oxygen therapy. Wnt-3 protein increased to the higher levels 3 days after therapy. Linear regression analysis showed that nestin protein correlated with Wnt-3 protein. We propose that hyperbaric oxygen treatment promote stem cells to proliferate, which is correlated with Wnt-3 protein.
Topics: Animals; Animals, Newborn; Biomarkers; Brain; Bromodeoxyuridine; Cell Division; Cell Proliferation; Disease Models, Animal; Female; Hyperbaric Oxygenation; Hypoxia-Ischemia, Brain; Intermediate Filament Proteins; Male; Nerve Regeneration; Nerve Tissue Proteins; Nestin; Neuronal Plasticity; Neurons; Oxygen; Rats; Rats, Sprague-Dawley; Recovery of Function; Stem Cells; Treatment Outcome; Wnt Proteins; Wnt3 Protein
PubMed: 17921881
DOI: 10.1097/WNR.0b013e3282f0ec09 -
Der Pathologe Feb 2014In an epiphrenic lymph node of a 55 years old female patient who underwent surgical resection of a rectal adenocarcinoma epitheloid proliferations with papillary and...
In an epiphrenic lymph node of a 55 years old female patient who underwent surgical resection of a rectal adenocarcinoma epitheloid proliferations with papillary and solid growth pattern were seen additional to a metastasis of the carcinoma. Adjacent vessels contained similar infiltrates. Immunohistochemically a co-expression of pan-keratin, calretinin and WT1 was seen, suggestive for a diagnosis of a metastasis of a malignant mesothelioma. However, radiologic examination yielded no morphologic correlate to this suspicion. Further immunohistochemical work-up showed positivity for desmin, negativity for EMA, GLUT1, p53 and a low ki67-fraction of 2-3 %. Therefore, a final diagnosis of benign mesothelial proliferations disseminated into the lymph node and the adjacent vessels was made.
Topics: Adenocarcinoma; Biomarkers, Tumor; Cell Proliferation; Diagnosis, Differential; Epithelium; Female; Humans; Incidental Findings; Lymph Nodes; Lymphatic Metastasis; Middle Aged; Rectal Neoplasms; Rectum; Tomography, Spiral Computed
PubMed: 24496993
DOI: 10.1007/s00292-013-1880-0 -
Developmental Dynamics : An Official... Mar 2002Epimorphic regeneration in teleost fins occurs through the establishment of a balanced growth state in which a blastema gives rise to all the mesenchymal cells, whereas...
Epimorphic regeneration in teleost fins occurs through the establishment of a balanced growth state in which a blastema gives rise to all the mesenchymal cells, whereas definite areas of the epidermis proliferate leading to its extension, thus, allowing the enlargement of the whole structure. This type of regeneration involves specific mechanisms that temporally and spatially regulate cell proliferation. To understand how the blastema is formed and how this growth situation is set up, we investigated cell proliferation patterns in the regenerating fin of the goldfish Carassius auratus from the time of amputation to that of blastema formation by using proliferating cell nuclear antigen immunostaining and bromodeoxyuridine labeling. Wound closure and apical epidermal cap formation took place by epidermal migration and re-arrangement, without the contribution of cell proliferation. As soon as the apical cap had formed, the epidermis started to proliferate at its lateral surfaces, in which all layers maintained cycling for the duration of the studied process. The distal epidermal cap, on the contrary, presented very few cycling cells, and its cytoarchitecture was indicative of continuous remodeling due to ray growth. The basal layer of this epidermal cap showed a typical morphology and remained nonproliferative whilst in contact with the proliferating blastema. Proliferation in the mesenchymal compartment of the ray started far from the amputation plane. Subsequently, cycling cells approached that location, until they formed the blastema in contact with the apical epidermal cap. Differences observed between the epidermis and mesenchyma, regarding activation of the cell cycle and the establishment of proliferative patterns, suggest that differential mechanisms regulate cell proliferation in each of these compartments during the initial stages of regeneration.
Topics: Amputation, Surgical; Animal Structures; Animals; Cell Division; Cell Lineage; Cell Movement; DNA Replication; Enzyme-Linked Immunosorbent Assay; Epidermal Cells; Goldfish; Growth Substances; Proliferating Cell Nuclear Antigen; Regeneration; Wound Healing
PubMed: 11836790
DOI: 10.1002/dvdy.10055 -
Parasitology Sep 2023is an industrially significant protozoan parasite of Manila clam, . So far, various media, based on Dulbecco's Modified Eagle Medium and Ham's F-12 nutrient mixture...
is an industrially significant protozoan parasite of Manila clam, . So far, various media, based on Dulbecco's Modified Eagle Medium and Ham's F-12 nutrient mixture with supplementation of fetal bovine serum (FBS), have been developed to proliferate the parasitizing trophozoite stage of . The present study showed that did not proliferate in FBS-deficient Perkinsus broth medium (PBMΔF), but proliferated well in PBMΔF supplemented with tissue extract of host Manila clams, indicating that FBS and Manila clam tissue contained molecule(s) required for proliferation. Preliminary characterization suggested that the host-derived molecule(s) was a heat-stable molecule(s) with a molecular weight of less than 3 kDa, and finally a single molecule required for the proliferation was purified by high-performance liquid chromatography processes. High-resolution electrospray ionization mass spectrometry and nuclear magnetic resonance analyses identified this molecule as glycine betaine (=trimethylglycine), and the requirement of this molecule for proliferation was confirmed by an assay using chemically synthesized, standard glycine betaine. Although glycine betaine was required for the proliferation of all examined species, supplementation of glycine betaine precursors, such as choline and betaine aldehyde, enhanced the proliferation of 4 species ( and ), but not of 2 others ( and ). Thus, it was concluded that the ability to biosynthesise glycine betaine from its precursors varied among species, and that and lack the ability required to biosynthesize glycine betaine for proliferation.
Topics: Animals; Parasites; Betaine; Bivalvia; Trophozoites; Cell Proliferation; Alveolata
PubMed: 37565486
DOI: 10.1017/S0031182023000768 -
Cell Proliferation Oct 1995A continuous influx of peripheral blood monocytes (PBM) to the lung is thought to maintain the local population of alveolar macrophages (AM). However, local...
A continuous influx of peripheral blood monocytes (PBM) to the lung is thought to maintain the local population of alveolar macrophages (AM). However, local proliferation of a small subpopulation of AM has been demonstrated in animal studies and in humans. AM exhibit a great heterogeneity with regard to their morphology (cell size, shape of nucleus), immunophenotype (expression of CD14 and RFD9 antigen), and function. Part of this heterogeneity may be explained by the presence of different maturation stages of AM, ranging from small immature, CD14+ RFD9- PBM-like cells to large, CD14- RFD9+ mature AM. These findings prompted us to study whether proliferation of PBM and AM is related to their stage of maturation. The expression of the proliferation marker Ki-67 was studied in AM from both healthy volunteers and patients suffering from sarcoidosis. Using double immunofluorescence staining, we studied proliferation of immature, CD14+ AM, and mature, RFD9+ AM in sarcoidosis, and we compared this with PBM. A significantly larger percentage of AM in general expressed Ki-67 antigen in sarcoidosis (3.0 (median); range 1.1-5.5) as compared with healthy volunteers (0.8; 0.2-1.3). In sarcoidosis, proliferation was observed in both the immature and the mature subpopulation of AM. Proliferating PBM were rarely observed [less than 0.2% of the CD14+ mononuclear cells (MNC)] both in healthy volunteers and sarcoidosis patients. A small subpopulation of PBM showed a weak expression of RFD9 antigen (less than 1% of MNC). Interestingly, proliferation of PBM was concentrated in this subpopulation (15% of the RFD9+ MNC). These data show that even mature AM, which are generally thought to be terminally differentiated cells with little capacity to replicate, are able to proliferate, whereas a relatively very low percentage of their precursors in the blood circulation proliferates. Furthermore, the findings suggest that lung tissue in sarcoidosis creates an environment which promotes proliferation of monocytic cells. Pulmonary alveolar macrophages (AM) were originally recognized as phagocytosing scavenger cells (Ham & Cormack 1979), but presently they are also known to initiate and regulate inflammatory and immunological processes in several lung diseases (Herscowitz 1985, Unanue & Allen 1987, Sibille & Reynolds 1990). AM are thought to represent more mature cells of the mononuclear phagocyte system, and to be derived from peripheral blood monocytes (PBM) (Van Furth 1982, Ginsel 1993). As AM are continuously lost (mainly through a transport from the peripheral airways, via the trachea to the pharynx), the local AM population must be constantly replenished.(ABSTRACT TRUNCATED AT 400 WORDS)
Topics: Bronchoalveolar Lavage; Cell Differentiation; Cell Division; Humans; Immunohistochemistry; Immunophenotyping; Ki-67 Antigen; Macrophages, Alveolar; Monocytes; Neoplasm Proteins; Nuclear Proteins
PubMed: 7488673
DOI: 10.1111/j.1365-2184.1995.tb00042.x -
PloS One 2011Reactive gliosis is a hallmark of brain pathology and the injury response, yet the extent to which astrocytes proliferate, and whether this is central to astrogliosis is...
Reactive gliosis is a hallmark of brain pathology and the injury response, yet the extent to which astrocytes proliferate, and whether this is central to astrogliosis is still controversial. We determined the fraction of mature astrocytes that proliferate in a mouse stroke model using unbiased stereology as a function of distance from the infarct edge. Cumulatively 11.1±1.2% of Aldh1l1(+) astrocytes within 400 µm in the cortical penumbra incorporate BrdU in the first week following stroke, while the overall number of astrocytes does not change. The number of astrocytes proliferating fell sharply with distance with more than half of all proliferating astrocytes found within 100 µm of the edge of the infarct. Despite extensive cell proliferation primarily of microglia and neutrophils/monocytes in the week following stroke, few mature astrocytes re-enter cell cycle, and these are concentrated close to the infarct boundary.
Topics: Animals; Apoptosis; Astrocytes; Bromodeoxyuridine; Cell Proliferation; Cerebral Infarction; Inflammation; Mice
PubMed: 22132159
DOI: 10.1371/journal.pone.0027881 -
Annals of Diagnostic Pathology Aug 2015Immunohistochemical analysis of proliferation markers such as Ki-67 and cyclin A is widely used in clinical evaluation as a prognostic factor in breast cancer. The...
Immunohistochemical analysis of proliferation markers such as Ki-67 and cyclin A is widely used in clinical evaluation as a prognostic factor in breast cancer. The proliferation status of tumors is guiding the decision of whether or not a patient should be treated with chemotherapy because low-proliferative tumors are less sensitive by such treatment. However, the lack of optimal cutoff points and selection of tumor areas hamper its use in clinical practice. This study was performed to compare the Ki-67 and cyclin A expression counted in hot-spot vs average counting based on 5 to 14 random tumor areas in 613 breast carcinomas. We correlated the findings with 10-year follow-up in order to standardize the evaluation of proliferation markers in clinical practice. A significant correlation was found between the percentage of positive cells estimated by Ki-67 and cyclin A both by hot-spot and by average counting. Both methods showed that high expression of Ki-67 and cyclin A is associated with more adverse tumor stage. The cutoff value for Ki-67 for distant metastases was set to 22% and to 15%, using hot-spot and average counting, respectively. For cyclin A, the values were set to 14% and 8% using the respective methods. Survival curves revealed that patients with a high hot-spot proliferation index had a significantly greater risk of shorter tumor-free survival. Our findings suggest that the determination of proliferation markers in breast cancer should be standardized to hot-spot counting and that specific cutoff values for proliferation could be useful as prognostic markers in clinical practice. Moreover, we suggest that expression levels of cyclin A could be used as a complementary marker to estimate the proliferation status in tumors, especially those with "borderline" expression levels of Ki-67, in order to more accurately estimate the proliferations status of the tumors.
Topics: Adult; Aged; Aged, 80 and over; Breast Neoplasms; Cyclin A; Female; Follow-Up Studies; Humans; Immunohistochemistry; Ki-67 Antigen; Middle Aged; Mitotic Index; Prognosis; Proliferating Cell Nuclear Antigen; Sensitivity and Specificity
PubMed: 26049669
DOI: 10.1016/j.anndiagpath.2015.05.002 -
Archives of Ophthalmology (Chicago,... Mar 1988A new experimental model of subretinal cellular proliferation, based on injection of autologous vitreous into the subretinal space of rabbits, was studied by light and...
A new experimental model of subretinal cellular proliferation, based on injection of autologous vitreous into the subretinal space of rabbits, was studied by light and electron microscopy. As early as five days after injection, proliferation of retinal pigment epithelial (RPE) and retinal glial cells was observed in the subretinal space. These morphologically distinct proliferating cells were sometimes joined by junctional complexes. Morphologically, the proliferating RPE cells resembled either RPE cells or fibroblasts. Some proliferating RPE cells also retained their epithelial characteristics (ie, basement membranes and cell junctions), while others were partially dedifferentiated and showed some embryonic features. New formation of melanin could be identified within the proliferated RPE cells, which could account, in part, for the hyperpigmentation at the site of the bleb caused by the injection of vitreous. The results demonstrated that injection of autologous vitreous into the subretinal space can lead to subretinal proliferation of retinal glial and RPE cells in the rabbit.
Topics: Animals; Cell Division; Fundus Oculi; Injections; Microscopy, Electron; Neuroglia; Pigment Epithelium of Eye; Rabbits; Retina; Vitreous Body
PubMed: 3345157
DOI: 10.1001/archopht.1988.01060130432036 -
Nature Protocols 2007This protocol details a method of obtaining selectively proliferated hepatocyte progenitor cells using hyaluronic acid (HA)-coated dishes and serum-free medium. A small...
This protocol details a method of obtaining selectively proliferated hepatocyte progenitor cells using hyaluronic acid (HA)-coated dishes and serum-free medium. A small hepatocyte (SH) is a hepatocyte progenitor cell of adult livers and has many hepatic functions. When the rat SH begins to proliferate, CD44 is specifically expressed. To define the purification of SH, CD44 and cytokeratin 8 are used as marker proteins. The growth of SHs is faster on HA-coated dishes than on other extracellular matrix-coated ones. The use of both DMEM/F12 medium and HA-coated dishes allows the selective proliferation of SHs in culture. The purification of SHs is approximately 85% at day 10.
Topics: Animals; Cell Culture Techniques; Cell Proliferation; Hepatocytes; Hyaluronan Receptors; Hyaluronic Acid; Keratin-8; Rats; Stem Cells
PubMed: 17546015
DOI: 10.1038/nprot.2007.118 -
Molecular Biology Reports Apr 2012The liver has powerful capability to proliferate in response to various injuries, but little is known as to liver proliferation after irradiation (IR) injury. This study...
The liver has powerful capability to proliferate in response to various injuries, but little is known as to liver proliferation after irradiation (IR) injury. This study investigated whether liver proliferation could be stimulated in low-dose irradiated liver by partial liver IR injury with high dose radiation. Sprague-Dawley rats were irradiated by 6-MV X-ray with single dose of 25 Gy to the right-half liver, while the left-half liver was shielded (0.7 Gy) or irradiated with single doses of 3.2, 5.6, and 8.0 Gy, respectively. Hepatic proliferation in the shielded and low-dose irradiated left-half liver was evaluated by serum hepatic growth factor (HGF), proliferating cell nuclei antigen (PCNA), liver proliferation index (PI), hepatocyte mitosis index (MI). The observation time was 0 day (before IR), 30, 60, 90, and 120 days after IR. Our results showed that serum HGF and hepatocyte HGF mRNA increased after IR with HGF mRNA peak on day 30 in the shielded and low-dose irradiated left-half livers, and their values increased as the dose increased to the left-half liver. Liver PI and PCNA mRNA peaked on day 60 with stronger expressions in higher doses-irradiated livers. MI increased after IR, with the peak noted on day 60 in the shielded and on day 90 in the low-dose irradiated left-half livers. There was a 30 day delay between MI peaks in the shielded and low-dose irradiated livers. In conclusion, 25 Gy partial liver IR injury could stimulate the shielded liver and low-dose irradiated liver to proliferate. In the livers receiving a dose range of 3.2-8.0 Gy, the proliferation was stronger in higher doses-irradiated liver than the low-dose irradiated. However, IR delayed hepatocyte mitosis.
Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Cell Proliferation; Dose-Response Relationship, Radiation; Gene Expression Regulation; Hepatocyte Growth Factor; Hepatocytes; Immunohistochemistry; Liver; Liver Regeneration; Male; Mitotic Index; Particle Accelerators; Prealbumin; Proliferating Cell Nuclear Antigen; RNA, Messenger; Rats; Rats, Sprague-Dawley; Staining and Labeling; X-Rays
PubMed: 21766183
DOI: 10.1007/s11033-011-1161-z