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Results for “cellular proliferation”

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PubMed2001

Supplemental oxygen controls cellular proliferation and anastomotic intimal hyperplasia at a vascular graft-to-artery anastomosis in the rabbit.

PURPOSE: The purpose of this study was to determine whether the administration of 40% supplemental oxygen (O ( 2) ) will decrease cellular proliferation and intimal hyperplasia (IH) at a prosthetic vascular graft (PVG)-to-artery anastomosis. METHODS: Twenty New Zealand white rabbits underwent placement of a 3-mm polytetrafluoroethylene graft in their infrarenal aorta. Four groups of five rabbits were placed either in a normoxic (21%) environment or in a 40% supplemental O ( 2) environment for 7 or 42 days. Twenty-four hours before the rabbits were humanely killed for aortic graft harvest, BrDU (5-bromo-2'-deoxyuridine) was injected into the rabbits intraperitoneally. Image analysis (Bioquant) morphometrics were used to measure cells with BrDU staining and intimal areas at the distal anastomosis. Cellular proliferation is defined as positively staining BrDU cells divided by all cells in the artery wall. IH is reported as a ratio between the intimal area and the medial area to standardize the varying aortic size and degree of aortic fixation among rabbits. The Student t test was used to compare cellular proliferation and IH between control and O ( 2) -treated rabbits. RESULTS: Cellular proliferation in the intima at 7 days was significantly reduced in the O ( 2) -treated animals (1.7% +/- 1%) versus the control animals (28.6% +/- 3%) ( P =.0001). The cellular proliferation in the intima at 42 days returned to preoperative levels in the O ( 2) -treated group (0.15%) and in the control group (0.11%) ( P = not significant). IH at 7 days was minimal, and no difference between the O ( 2) -treated group (0.017 +/-.006) and the control group (0.009 +/-.03) ( P = not significant) was found. IH was significantly reduced at 42 days in the O ( 2) -treated animals (0.031 +/-.012) when compared with the control animals (0.193 +/-.043) ( P =.006). CONCLUSIONS: Supplemental O ( 2) (40%) significantly reduces cellular proliferation and IH at the distal anastomosis of a PVG-to-artery anastomosis in the rabbit model.

Anastomosis, Surgical↗

PubMed1999

Spatial and temporal distribution of cellular proliferation in the cranial base of normal and midfacially retrusive mice.

The craniofacial region of the Brachyrrhine (Br) mouse is characterized by a retruded midface. The cellular mechanism causing this growth deficiency is unknown. However, the cranial base is foreshortened in adult Br mice. The purpose of this study was to determine whether the spatial and temporal patterns of cellular proliferation in the cranial base (CB) differ between normal (C3H/HeJ) and Br mutant (3H1 Br/+) embryonic mice. Twenty-four dams were injected (3)H thymidine (5 microCi/gram body weight) and 15 embryos from each group were collected at Theiler stages 23, 25, and 27 (15, 17, and 19 days of gestation). Serial sections from each head were processed with routine autoradiography. Labelling indices (LI) were determined for each specimen and cellular proliferation maps were generated for each age group. LI patterns within and between groups were compared statistically. Results showed that cellular proliferation in the CB of normal embryos displayed a time- and position-dependent pattern, characteristic of transient growth sites (TGS). Generally, as age increases, cellular proliferative activities decrease gradually (from an average LI of 11.4 +/- 5.7% at stage 23 to 4.4 +/- 2.2% at stage 27), and the number of the TGS decreases in the presumptive nasal septal region and increases in presumptive sphenoethmoidal area with age, indicating the existence of cellular subpopulations in the CB. Cellular proliferation in the CB of the Br mutant displays a different growth pattern compared to the normal condition. Deficiencies in cellular proliferation exist mainly in the presumptive sphenoethmoidal area of the CB. The results indicate that the TGS play an important role in the normal morphogenesis of the CB, and abnormalities in their timing and/or position may be responsible for the dysmorphology of the midface in the Br mutant.

Animals↗

PubMed2006

Effects of antibiotics and corticosteroid eyedrops on cellular proliferation in cultured human corneal keratocytes.

The purpose of this study is to investigate the effects of antibiotics and glucocorticoid eyedrops, including gentamicin, sulfisomezole, fluorometholone, dexamethasone, and betamethasone, on cellular proliferation in cultured human corneal keratocytes. Human corneal keratocytes were cultured in RPMI-1640 containing 10% fetal bovine serum. Drugs were prepared from original concentrations to 1/10, 1/100, and 1/1,000 dilutions. After exposure to drugs for 100 minutes, cellular proliferation was estimated by [3H]-thymidine uptake. It was found that cellular proliferation in corneal keratocytes was not affected by any of the three dilutions of gentamicin but was inhibited by 1/10 and 1/100 dilutions of sulfisomezole to 82% and 90% of control. [3H]-thymidine uptake values were inhibited to 75% by 1/10 dilution of fluorometholone and by 1/10and 1/100 dilutions of betamethasone to 84% and 86% of control. Meanwhile, cellular proliferation was significantly inhibited by 1/10, 1/100, and 1/1,000 dilutions of dexamethasone to 82%,86%, and 90%, respectively, in comparison with control values. It was demonstrated that commercial eyedrops of glucocorticoids inhibit cellular proliferation in corneal keratocytes, which may modulate the wound healing of corneal stroma.

Adrenal Cortex Hormones↗

PubMed2006

Effects of antiglaucoma drugs on cellular proliferation in cultured human corneal keratocytes.

The purpose of this study was to investigate the effects of various antiglaucoma drugs, including timolol, betaxolol, carteolol, levobunolol, dipivefrin, and pilocarpine, on cellular proliferation in cultured human corneal keratocytes. Human corneal keratocytes were cultured with RPMI-1640 medium containing 10% fetal bovine serum. Antiglaucoma drugs were prepared from original concentrations to dilutions of 1/10, 1/100, and 1/1,000. After exposure to drugs for 100 minutes, cellular proliferation was estimated by [3H]thymidine uptake methodology. It was found that cellular proliferation in corneal keratocytes was inhibited by only a 1/10 dilution of various drugs including timolol, betaxolol, carteolol, levobunolol, dipivefrin, and pilocarpine. The [3H]thymidine uptake values were significantly inhibited to 63%, 18%, 87%, 68%, 55%, and 67% by a 1/10 dilution of the above drugs. However, the cellular proliferation was also significantly suppressed by 0.01 mg/mL of benzalkonium chloride preservative. It is shown that the inhibition of cellular proliferation by high concentrations of antiglaucoma drugs may result from the benzalkonium chloride preservative contained in these drugs.

Benzalkonium Compounds↗

PubMed1996

[Study on cellular proliferation activity of placental site trophoblastic tumor].

OBJECTIVE: To study the relationship among the cellular proliferation activity, benign clinical process and pathologic characteristics of placental site trophoblastic tumor (PSTT). METHODS: Paraffin-embedded blocks from ten patients with PSTT were reexamined by mitotic count, argyrophilic nucleolar organizer regions (AgNOR) staining and flow cytometric DNA analysis. Five cases of hydatidiform mole (HM) and 5 choriocarcinoma (CC) were chosen as controls. RESULTS: Mean mitotic figures of PSTT were 1.3 (0-3) per 10 high power field, while those of HM and CC were 0.8 (0-2) and 2.2 (1-4) respectively. AgNOR number of PSTT was 2.70 +/- 0.55 per cell, while those of HM and CC were 1.96 +/- 0.38 and 4.50 +/- 0.73 respectively. Flow cytometric DNA content revealed that PSTT had DNA index (DI) of 1.10, S phase of 16.7% and proliferating index (PI) of 26.6%. Eight of 10 Cases were followed up, 7 are alive and 1 died of primary lung cancer. CONCLUSION: PSTT has relative low cellular proliferation activity. The good clinical procedure and benign pathological feature of PSTT may be associated with its diploidy DNA and low cellular proliferation activity.

Adult↗

PubMed2003

Identification and characterization of E2F7, a novel mammalian E2F family member capable of blocking cellular proliferation.

The mammalian E2F family of transcription factors plays a crucial role in the regulation of cellular proliferation, apoptosis, and differentiation. Consistent with its biological role in a number of important cellular processes, E2F regulates the expression of genes involved in cell cycle, DNA replication, DNA repair, and mitosis. It has proven difficult, however, to determine the specific roles played by the various known family members in these cellular processes. The work presented here now extends the complexity of this family even further by the identification of a novel E2F family member, which we now term E2F7. Like the expression of the known E2F activators, E2F1, E2F2, and E2F3, the expression of E2F7 is growth-regulated, at least in part, through E2F binding elements on its promoter, and its protein product is localized to the nucleus and associates with DNA E2F recognition sites with high affinity. A number of salient features, however, make this member unique among the E2F family. First, the E2F7 gene encodes a protein that possesses two distinct DNA-binding domains and that lacks a dimerization domain as well as a transcriptional activation and a retinoblastoma-binding domain. In contrast to the E2F activators, E2F7 can block the E2F-dependent activation of a subset of E2F target genes as well as mitigate cellular proliferation of mouse embryo fibroblasts. These findings identify E2F7 as a novel member of the mammalian E2F transcription factor family that has properties of a transcriptional repressor capable of negatively influencing cellular proliferation.

Animals↗

PubMed2005

Inhibition of cellular proliferation by diterpenes, topoisomerase II inhibitor.

We examined the effects of 12 terpene compounds derived from the roots of Euphorbia kansui on the proliferative activity of Xenopus embryo cells. Eight of these compounds showed significant inhibition of cellular proliferation even at low concentrations, while four of them needed to be present at higher concentrations to inhibit cellular proliferation. In order to define the mechanism of inhibition of cellular proliferation by these compounds, the effects of diterpene compounds on the activity of topoisomerase II were measured. Most of the diterpene compounds that inhibited cellular proliferation also inhibited topoisomerase II activity.

Animals↗

PubMed1997

Regional variability in the time course of TGF-beta 1 expression, cellular proliferation and extracellular matrix expansion following arterial injury.

Transforming growth factor-beta 1 (TGF-beta 1) has been variably associated with the regulation of cellular proliferation and extracellular matrix expansion after arterial injury. We tested these associations in vivo in the rat carotid injury model. At 0, 3, 7, 14 and 28 days following arterial balloon injury, regional expression of TGF-beta 1 mRNA was assessed using in situ hybridization and the results compared to measures of cellular proliferation and extracellular matrix expansion. Both the TGF-beta 1 concentration measured in culture media of explanted carotid arteries and the quantitative in situ hybridization signal for TGF-beta 1 arterial media and neointima were maximal at 14 days after balloon injury. However, medial cellular proliferation was maximal at 3 days whereas neointimal proliferation was maximal at 14 days and significantly greater than medial proliferation. Neointimal cell density declined significantly between 7 and 14 days, indicating the expansion of extracellular matrix; however, medial cell density was unchanged between 3 and 28 days after balloon injury. Thus, differences in the regional arterial wall relationships between the time course of cellular proliferation, extracellular matrix expansion and the level of TGF-beta 1 expression demonstrate in vivo variability in the response to TGF-beta 1.

Angioplasty, Balloon, Coronary↗

PubMed1994

Decreased cellular proliferation by energy restriction is recovered by increasing housing temperature in rats.

We investigated the effects of life-prolonging energy restriction (ER) on body temperature (BT) and cellular proliferation in rats. Animals were fed either a control diet (C: 220 kJ/day) or an ER diet (110 kJ/day) from 7 weeks of age, and were housed at 20-22 degrees C. Another group of animals, fed on the ER diet, were transferred from 20-22 degrees C to a room at 30 degrees C (ER + I) at 20 weeks of age. The core body temperatures in individual animals were recorded over a 3-day period between 20 and 24 weeks of age. Cellular proliferation rates were quantitated by labeling S phase cells in the jejunum, epidermis, pituitary, and lung with bromodeoxy-uridine at 24 weeks of age. Long-term ER reduced the mean BT by 1 degree C, and reduced cellular proliferation in the jejunum, epidermis, pituitary, and lung. At 30 degrees C, the inhibitions were partially lifted in the examined organs except in the pituitary. Therefore, decreased cellular proliferation in the various organs after long-term ER in rats is lifted as it is in mice.

Animals↗

PubMed1991

Early indicators of potential neoplasia produced in the rat forestomach by non-genotoxic agents: the importance of induced cellular proliferation.

Forestomach neoplasia induced by the apparently non-genotoxic carcinogens, butylated hydroxyanisole and propionic acid, appears to arise by way of sustained high levels of cellular proliferation. Several other inducers of enhanced cellular proliferation, or the consequential incidence of hyperplastic lesions, have been identified in the rodent forestomach but the requisite carcinogenicity bioassays remain undone. In other tissues, such as the male rat kidney, the rodent thyroid follicular cell and the bladder epithelium, there is also evidence supporting the concept that sustained enhanced cellular proliferation may be an important early marker for non-genotoxic carcinogens. This reaction is, however, not likely to be the only marker necessary for the identification of non-genotoxic carcinogens.

Acrylates↗

PubMed1998

Divergent effects of angiotensin-converting enzyme inhibition and angiotensin II-receptor antagonism on myocardial cellular proliferation and collagen deposition after myocardial infarction in rats.

There is mechanistic rationale to suggest differential effects of angiotensin-converting enzyme (ACE) inhibition and angiotensin II type 1 (AT1)-receptor antagonism on ventricular remodeling after myocardial infarction (MI). We compared the effects of ACE inhibition, AT1-receptor antagonism, and their combination on post-MI ventricular remodeling in rats. We induced MI in 62 rats, which then received one of four treatments: (a) placebo; (b) the ACE inhibitor, enalapril; (c) the AT1-receptor antagonist, losartan; and (d) enalapril and losartan in combination. Two weeks after MI, we examined: (a) heart weight (HW)/body weight (BW) ratio; (b) nonmyocyte cellular proliferation in the noninfarct zone by using proliferating cell nuclear antigen staining; and (c) collagen content within the noninfarct zone. Placebo-treated, infarcted rats developed significant increases in HW/BW ratio (p < 0.001), left ventricular (LV) volume (p < 0.01), nonmyocyte cellular proliferation (p < 0.04), and collagen content (p < 0.01) compared with noninfarcted controls. Enalapril, losartan, and combination therapy limited the increase in HW/BW ratio (all p values <0.01 vs. placebo). Enalapril inhibited nonmyocyte proliferation (p < 0.01 vs. placebo), whereas losartan had a smaller effect (p = NS vs. placebo; p < 0.03 vs. enalapril); combined treatment also reduced nonmyocyte cellular proliferation but did not reach statistical significance (p = 0.08 vs. placebo). Enalapril and combination treatment significantly diminished collagen content (both p values <0.01 vs. placebo), whereas losartan did not. Thus, ACE inhibition and AT1-receptor antagonism equally limited myocardial hypertrophy after MI in rats, but ACE inhibition more effectively prevented nonmyocyte cellular proliferation and collagen deposition in the noninfarcted myocardium. Combination therapy was no more effective than was ACE inhibition alone. These data suggest that the myocyte hypertrophic response after MI is strongly influenced by activation of the AT1 receptor, whereas nonmyocyte cellular proliferation and collagen deposition result, in part, from mechanisms separate from AT1-receptor activation.

Angiotensin Receptor Antagonists↗

PubMed1993

Growth and cellular proliferation of ovine corpora lutea throughout the estrous cycle.

This study was conducted to determine the rates of growth and cellular proliferation of ovine corpora lutea (CL) throughout the estrous cycle. To determine the cellular labeling index (LI), ewes received an iv injection of bromodeoxyuridine (BrdU) 1 h before death on days 2, 4, 8, 12, or 15 (day 0 = estrus; n = 6-12 ewes/day). At death, CL were weighed, and samples of each were fixed in Carnoy's solution or frozen until analyzed for DNA, protein, and progesterone contents. Nuclear incorporation of BrdU was determined in paraffin-embedded tissue sections by using a primary antibody against BrdU and a fluorescent (fluorescein isothiocyanate-labeled) secondary antibody, and sections were counterstained with propidium iodide (a nuclear stain). The labeling index (BrdU-labeled nuclei as a proportion of propidium iodide-labeled nuclei) of each CL was determined by using dual channel interactive laser cytometry and image analysis. Moreover, BrdU and 3 beta-hydroxysteroid dehydrogenase (a marker for steroidogenic cells) or BrdU and factor VIII (a marker for endothelial cells) were immunolocalized in tissue sections by using double immunohistochemical or dual immunofluorescent staining, respectively. Results demonstrated that cellular proliferation was greatest (LI, 34.1 +/- 2.1%) on day 2 and decreased (P < 0.01) through day 15 (LI, 0.7 +/- 0.1%) of the estrous cycle. The results of the immunohistochemical studies provide evidence that both parenchymal (steroidogenic) and nonparenchymal (e.g. endothelial, fibroblastic) luteal cells proliferated throughout the ovine estrous cycle. Conversely, from days 2-12 of the estrous cycle, fresh weight and DNA content of CL increased linearly (P < 0.01; 8- and 10-fold, respectively), then decreased (P < 0.02) from days 12-15. Ratios of protein/DNA on days 2, 4, and 8 were similar and were greater (P < 0.02) than those on days 12 and 15, which also were similar. These data demonstrate that growth of the ovine CL is extremely rapid, linear from days 2-12, and primarily due to hyperplasia. In addition, the high rate of cellular proliferation is associated primarily with nonsteroidogenic cells, a large proportion of which appear to be endothelial cells. Data such as these will enable us to determine the factors that are important in regulating luteal growth and development in normal and pathological conditions.

3-Hydroxysteroid Dehydrogenases↗

PubMed1999

Effects of peritoneal macrophages from women with endometriosis on endometrial cellular proliferation in an in vitro coculture model.

OBJECTIVE: To study the effects of peritoneal macrophages on endometrial cellular proliferation in an in vitro coculture model and to compare the magnitude of these effects between macrophages from women with endometriosis and normal women. DESIGN: Controlled study of peritoneal macrophage function. SETTING: University hospital. PATIENT(S): Patients with a normal peritoneal cavity (n = 15) and with pelvic endometriosis (n = 20) undergoing laparoscopy. INTERVENTION(S): Peritoneal macrophages were cocultured with endometrial epithelial and stromal cells; endometrial cell cultures without macrophage coculture acted as controls. MAIN OUTCOME MEASURE(S): Endometrial cellular proliferation measured by 3H-thymidine incorporation. RESULT(S): Endometrial epithelial cells cocultured with peritoneal macrophages from women with endometriosis showed significantly increased proliferation compared with cocultures using macrophages from normal women when assessed at 24 hours (1.56 versus 1.03 times, respectively, over control) and at 72 hours (1.55 versus 1.10 times over control). Endometrial stromal cells cocultured with peritoneal macrophages from women with endometriosis similarly exhibited increased proliferation compared with cocultures using macrophages from normal women when assessed at 24 hours (1.65 versus 1.17 times over control) and at 72 hours (1.65 versus 1.21 times over control). CONCLUSION(S): Peritoneal macrophages of patients with endometriosis stimulate cellular proliferation of endometrial epithelial and stromal cells in vitro.

Adult↗

PubMed1993

Human promyelocytic cell line HL60 has the specific binding sites for prolactin and its ornithine decarboxylase, DNA synthesis and cellular proliferation are induced by prolactin.

Human prolactin (hPRL) induced ornithine decarboxylase (ODC) activity, subsequently DNA synthesis and cellular proliferation on human promyelocytic cells, HL60, cultured in a serum-free medium. HL60 cells had 2100 specific binding sites for hPRL per cell, showing a dissociation constant of 1.1 x 10(-10) M. Binding of 125I-PRL to the cells was not blocked by simultaneous addition of human growth hormone. ODC activity and DNA synthesis were activated maximally at 5 and 20 h, respectively, after the addition of 0.05 nM hPRL. These effects of PRL on cellular proliferation, ODC activity and DNA synthesis were abolished by the simultaneous addition of anti-hPRL antibody. Simultaneous addition of an irreversible inhibitor of ODC, difluoromethyl ornithine (DFMO), also abolished the inductions of ODC and DNA synthesis by hPRL. The inhibitory effect of DFMO on hPRL-induced DNA synthesis was reversed by the addition of putrescine to the culture medium. These results suggest that hPRL binds to the prolactin receptor on HL60 cells and induces ODC activity to increase cellular polyamine levels, which eventually stimulates DNA synthesis and cellular proliferation.

Binding Sites↗

PubMed2000

E2f3 is critical for normal cellular proliferation.

E2F is a family of transcription factors that regulate both cellular proliferation and differentiation. To establish the role of E2F3 in vivo, we generated an E2f3 mutant mouse strain. E2F3-deficient mice arise at one-quarter of the expected frequency, demonstrating that E2F3 is important for normal development. To determine the molecular consequences of E2F3 deficiency, we analyzed the properties of embryonic fibroblasts derived from E2f3 mutant mice. Mutation of E2f3 dramatically impairs the mitogen-induced, transcriptional activation of numerous E2F-responsive genes. We have been able to identify a number of genes, including B-myb, cyclin A, cdc2, cdc6, and DHFR, whose expression is dependent on the presence of E2F3 but not E2F1. We further show that a critical threshold level of one or more of the E2F3-regulated genes determines the timing of the G(1)/S transition, the rate of DNA synthesis, and thereby the rate of cellular proliferation. Finally, we show that E2F3 is not required for cellular immortalization but is rate limiting for the proliferation of the resulting tumor cell lines. We conclude that E2F3 is critical for the transcriptional activation of genes that control the rate of proliferation of both primary and tumor cells.

Animals↗

PubMed1986

Cellular proliferation in the vitreous: the use of vitreous explants as a model system.

An in vitro model of cellular proliferation in the vitreous has been developed using explants of bovine vitreous gel. Various cell types, including chick embryo pigmented retinal epithelium, choroidal fibroblasts, retinal glial cells, bovine retinal capillary endothelial cells, and peritoneal mouse macrophages, were cultured at 37 degrees C on vitreous gels for periods up to 8 days and compared for their effects on the structure of the gel. Choroidal fibroblasts caused a very marked reduction in the size of the gel and produced the strongest traction on the gel fibril structure; in contrast, peritoneal macrophages caused virtually no reduction in vitreous volume and little or no visible traction on the gel as detected by phase-contrast microscopy. The remaining cell types usually formed sheets on the surface of the gel; this was associated with an initial reduction in vitreous volume of approximately 50%, but little change thereafter. The cell mediated traction events on the structure of the vitreous gel were followed by time lapse video microscopy and by electron microscopy at various times after seeding of cells on the gels. The appearances corresponded closely with reported clinico-pathological studies of cellular proliferation in the vitreous. We believe that this in vitro model has several advantages over in vivo models of cellular proliferation in the vitreous, in that it permits analysis of individual cell behaviour and it is eminently suitable for pharmacologic manipulation.

Animals↗

PubMed1996

Effect of thrombin inhibition with desulfatohirudin on early kinetics of cellular proliferation after balloon angioplasty in atherosclerotic rabbits.

BACKGROUND: Thrombin may have a pivotal role in restenosis after angioplasty. Hirudin, a potent thrombin inhibitor, reduces luminal narrowing by plaque after angioplasty in a rabbit model of atherosclerosis. Because cellular proliferation is believed to be an important mechanism for restenosis and thrombin has been shown to be a potent smooth muscle cell mitogen in vitro, we hypothesized that the mechanism of the effect of hirudin on limiting luminal narrowing by plaque occurs via inhibition of cellular proliferation. METHODS AND RESULTS: Femoral atherosclerosis was induced in 108 rabbits, and balloon angioplasty was performed. At angioplasty, group 1 rabbits (n=38) were treated with a 2-hour infusion of hirudin, and group 2 rabbits (n=41) were treated with heparin. Group 3 rabbits (n=29) were treated with hirudin (n=15) or heparin (n=14) and killed at 7 or 28 days to determine cross-sectional area narrowing by plaque and cellular proliferation with the use of bromodeoxyuridine labeling. At 29, 71, or 167 hours after angioplasty, group 1 and 2 rabbits were injected with 3H-thymidine and killed 1 hour later, and labeling indexes were determined. A significant increase in the index of 3H-thymidine-labeled nuclei was observed in the intima of "ballooned" arteries compared with "nonballooned" atherosclerotic arteries at both 30 hours (0.06+/-0.05 versus 0.01+/-0.01, P<.01) and 72 hours (0.10+/-0.06 versus 0.004+/-0.004, P<.01). By 7 days, the index of labeled cells was similar to baseline (0.04+/-0.03 versus 0.01+/-0.01, P=.12). Hirudin had no effect on the 3H-thymidine labeling indexes at any of the time points studied despite the fact that hirudin treatment in group 3 rabbits resulted in less cross-sectional area narrowing by plaque at both 7 and 28 days after angioplasty (41+/-16 versus 24+/-12 at 7 days and 60+/-21 versus 44+/-17 at 28 days, heparin versus hirudin; P<.03). CONCLUSIONS: Balloon angioplasty resulted in a marked increase in cellular proliferation that peaked at 72 hours. A 2-hour infusion of hirudin failed to reduce early 3H-thymidine labeling, suggesting that inhibition of cell proliferation within the first 7 days after angioplasty is not the predominant mechanism by which hirudin exerts its effect on limiting luminal narrowing by plaque 28 days after balloon angioplasty in this animal model.

Angioplasty, Balloon↗

PubMedDate not supplied

Effect of chronic low dose of methotrexate on cellular proliferation during spermatogenesis in rats.

This study was conducted to evaluate cellular proliferation of germinal and non-germinal elements of seminiferous tubules following continuous Day 1 to Day 17 exposure of methotrexate (12.5 microgram) in male rats. There was significant decrease in the diameter of seminiferous tubules (P < 0.10) followed by increase of interstitial space (P < 0.01). The size of various stages of primary, secondary spermatocytes, and spermatids was altered significantly compared to controls. Vacuolization/decondensation of "chromatin-mass" in spermatocytes changed from rounded to oval. The size of the Sertoli and Leydig cells were reduced significantly. Basement membrane at some places seems to be disrupted and thin in experimental testis. Methotrexate induced cytotoxicity on the proliferation of cellular contents of seminiferous tubules elucidating the mechanism of dose-dependent drug induced testicular damage during spermatogenesis.

Animals↗