PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “HYPERTROPHY AND HYPERPLASIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1989

Cholesteatoma of the external auditory canal in hemifacial hypertrophy (hyperplasia).

Congenital hemifacial hypertrophy is an extremely rare condition. At the time of writing this article, there have been 37 cases reported in the literature. Of these, only two have appeared in the otolaryngologic literature. Cholesteatoma of the external auditory canal (EAC) in hemifacial hypertrophy has not been reported before. This article reports one such case, and discusses the classification of hemihypertrophies. A review of the literature is included in the discussion. Management of cholesteatomas of the external auditory canal is also touched upon. A new theory for the peculiar site selection of cholesteatomas of the external auditory canal is postulated.

Adult↗
PubMed2001

Islet beta cell expression of constitutively active Akt1/PKB alpha induces striking hypertrophy, hyperplasia, and hyperinsulinemia.

The phosphoinositide 3-kinase-Akt/PKB pathway mediates the mitogenic effects various nutrients and growth factors in cultured cells. To study its effects in vivo in pancreatic islet beta cells, we created transgenic mice that expressed a constitutively active Akt1/PKB alpha linked to an Insulin gene promoter. Transgenic mice exhibited a grossly visible increase in islet mass, largely due to proliferation of insulin-containing beta cells. Morphometric analysis verified a six-fold increase in beta cell mass/pancreas, a two-fold increase in 5-bromo-2'-deoxyuridine incorporation, a four-fold increase in the number of beta cells per pancreas area, and a two-fold increase in cell size in transgenic compared with wild-type mice at 5 weeks. At least part of the increase in beta cell number may be accounted for by neogenesis, defined by criteria that include beta cells proliferating from ductular epithelium, and by a six-fold increase in the number of single and doublet beta cells scattered throughout the exocrine pancreas of the transgenic mice. Glucose tolerance was improved, and fasting as well as fed insulin was greater compared with wild-type mice. Glucose-stimulated insulin secretion was maintained in transgenic mice, which were resistant to streptozotocin-induced diabetes. We conclude that activation of the Akt1/PKB alpha pathway affects islet beta cell mass by alteration of size and number.

Animals↗
PubMed2001

Hypertrophy, hyperplasia, and infectious virus in gut-associated lymphoid tissue of mice after oral inoculation with simian-human or bovine-human reassortant rotaviruses.

Oral inoculation of infants with a vaccine that contains simian-human reassortant rotaviruses has been found to be a rare cause of intussusception. Because intussusception can be associated with enlargement of gut-associated lymphoid tissue, we studied the capacity of simian-human and bovine-human reassortant rotaviruses to cause lymphoid hypertrophy and hyperplasia of Peyer's patches (PP) of adult BALB/c mice. Neither hypertrophy nor hyperplasia was detected in PP after oral inoculation with simian-human or bovine-human reassortant rotaviruses. However, infectious virus was detected in PP and mesenteric lymph nodes after oral inoculation with simian, but not bovine, reassortant rotaviruses. Implications of these findings on the pathogenesis of intussusception are discussed.

Administration, Oral↗
PubMed1993

Effects of beraprost sodium, a stable analogue of prostacyclin, on hyperplasia, hypertrophy and glycosaminoglycan synthesis of rat aortic smooth muscle cells.

The effects of beraprost sodium, a stable analogue of prostacyclin, on the syntheses of DNA, protein and glycosaminoglycans (GAG) of cultured vascular smooth muscle cells (SMC) were studied. SMC were isolated from the thoracic aorta of male Wistar rats. The syntheses of DNA, protein and GAG of SMC were determined by incorporations of [3H]thymidine, [3H]leucine and [35S]sulfuric acid, respectively. Insulin at a concentration of 10(-6) M stimulated DNA synthesis 4 fold compared to control. Beraprost sodium suppressed the insulin-stimulated DNA synthesis dose-dependently at concentrations greater than 10(-7) M and suppressed it by 68% at 10(-5) M. Platelet derived growth factor (PDGF) at a concentration of 20 ng/ml stimulated DNA synthesis 6 fold compared to control. Beraprost sodium suppressed the PDGF-stimulated DNA synthesis dose-dependently at concentrations greater than 10(-7) M and suppressed it by 51% at 10(-5) M. Beraprost sodium suppressed GAG synthesis dose-dependently at concentrations greater than 10(-7) M and suppressed it by 49% at 10(-5) M. However, beraprost sodium at concentrations up to 10(-5) M did not affect protein synthesis. These results indicate that beraprost sodium suppressed the proliferation and GAG synthesis of SMC but did not affect hypertrophy. Beraprost sodium may be a potent antiarteriosclerotic agent through suppression of hyperplasia of SMC and modification of matrix protein.

Animals↗
PubMed2001

Transgenic expression of cyclin-dependent kinase 4 results in epidermal hyperplasia, hypertrophy, and severe dermal fibrosis.

In a previous report we have described the effects of expression of D-type cyclins in epithelial tissues of transgenic mice. To study the involvement of the D-type cyclin partner cyclin-dependent kinase 4 (CDK4) in epithelial growth and differentiation, transgenic mice were generated carrying the CDK4 gene under the control of a keratin 5 promoter. As expected, transgenic mice showed expression of CDK4 in the epidermal basal-cell layer. Epidermal proliferation increased dramatically and basal cell hyperplasia and hypertrophy were observed. The hyperproliferative phenotype of these transgenic mice was independent of D-type cyclin expression because no overexpression of these proteins was detected. CDK4 and CDK2 kinase activities increased in transgenic animals and were associated with elevated binding of p27(Kip1) to CDK4. Expression of CDK4 in the epidermis results in an increased spinous layer compared with normal epidermis, and a mild hyperkeratosis in the cornified layer. In addition to epidermal changes, severe dermal fibrosis was observed and part of the subcutaneous adipose tissue was replaced by connective tissue. Also, abnormal expression of keratin 6 associated with the hyperproliferative phenotype was observed in transgenic epidermis. This model provides in vivo evidence for the role of CDK4 as a mediator of proliferation in epithelial cells independent of D-type cyclin expression.

Animals↗
PubMed1994

Hyperplasia, hypertrophy, and phenotypic alterations in the distal nephron after acute proximal tubular injury in the rat.

BACKGROUND: Little is known about the impact of acute proximal tubular injury and dysfunction on the distal nephron. EXPERIMENTAL DESIGN: Selective necrosis of the kidney proximal convoluted tubule (PCT) was induced in rats by subcutaneous injection of the aminoglycoside gentamicin during 2 days. Damage and repair were measured until complete morphologic recovery after 10 days. Special attention was given to structural and biochemical alterations in the distal nephron. RESULTS: In control animals, cellular turnover, measured by immunohistochemical staining for proliferating cell nuclear antigen, was higher in distal than in proximal tubules. After injury, the strongly increased cell proliferation in regenerating necrotic PCT was preceded by an equally important proliferation in the distal tubules of the cortex and outer stripe of the outer medulla in the absence of necrosis but displaying enhanced apoptosis. Yet, epithelial vimentin expression was restricted to regenerating PCT. A temporary loss in the amount of immunostainable epidermal growth factor in the distal nephron was paralleled by a similar reduction in Tamm- Horsfall protein and transferrin receptor staining and in peanut and Helix pomatia lectin binding. Furthermore, the epithelial area/nucleus in the cortical distal tubules was increased by 71%, 6 days after the onset of acute renal failure; this hypertrophic condition was confirmed ultrastructurally. After full recovery of the PCT, a second burst in proliferative activity occurred in the hypertrophic distal segments in the absence of apoptosis. In the regenerated PCT, an excess cell number was accompanied by increased apoptotic activity. CONCLUSIONS: Development of distal tubular hypertrophy after PCT necrosis may be a compensatory response to a transient loss of proximal tubular function. The early reduction in staining for epidermal growth factor and other distal tubular markers in the presence of apoptosis and hyperplasia indicates transient phenotypic simplification and implies that renal epidermal growth factor is unlikely to control PCT regeneration.

Animals↗
PubMed1988

[Mechanism and significance of arteriolar media hypertrophy/ hyperplasia in arterial hypertension. Role of the Na+/H+ antiport].

The most common haemodynamic abnormality in human essential hypertension is an increase in systemic vascular resistance. Morphologic substrate for increased flow resistance is a narrowing of the lumen of arteriolar resistance vessels. During the course of essential hypertension, this is associated with an increase in wall (mainly media) thickness due to hypertrophy and hyperplasia of vascular smooth muscle cells. In contrast to concepts interpreting media thickening strictly as structural adaptation to increased perfusion pressure, various lines of evidence also point to pressure independent factors. In this context, extracellular factors such as "growth factors" as well as alterations in the activity of intracellular messenger systems must be considered. Recent studies suggest that substances generally known to act as vasoconstrictors such as angiotensin II, noradrenaline and arginine-vasopressin may also stimulate vascular smooth muscle cell growth and proliferation. Intracellular messenger systems with possible significance in the response to trophins and/or mitogens of vascular smooth muscle cells are phospholipase C, protein kinase C and the Na+/H+-antiport. These systems have been demonstrated to be altered in hypertension supporting the concept that one endogenous factor in human essential hypertension with pathophysiological significance, at least in a subgroup of patients, may be an enhanced reactivity of vascular smooth muscle cells to trophic and mitogenic stimuli. In this context, intracellular messenger systems such as phospholipase C, protein kinase C and/or the Na+/H+-antiport may play an important pathophysiological role.

Antiporters↗
PubMed1976

Hypertrophy, hyperplasia and structural dilatation of the human heart.

The human heart can exceed the critical heart weight of 500 g in the course of pathological structural adaptation. This abnormal growth is performed not only by an increase in size (hypertrophy) but also in number (hyperplasia) of cardiac muscle cells. Coronary insufficiency, dilatation and chronic heart failure are noted frequently in hearts above this critical heart weight. Chronic heart failure is not a direct consequence of local destruction and scar formation following coronary insufficiency. Unlike acute cardiac dilatation with failure, chronic dilatation is not associated with stretching or overstretching of cardiac muscle cells. Starling's law is not applicable for explaining heart failure in these chronic cases. Chronic dilatation is a structural dilatation (Gefugedilatation) produced by sliding displacements (slippage) of heart muscle cells leading to a decrease in the number of muscle layers in the ventricular wall. Chronic heart failure in man therefore is rather a physical consequence of structural dilatation which severely impairs the working conditions, the efficiency and the effectiveness of the heart muscle cells than an immediate result of coronary insufficiency of inflammation with local metabolic alterations, which, of course, additionally impair the quality of the myocardium and the conducting system.

Capillaries↗
PubMed1996

Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training.

Twelve male subjects with recreational resistance training backgrounds completed 12 wk of intensified resistance training (3 sessions/wk; 8 exercises/session; 3 sets/exercise; 10 repetitions maximum/set). All major muscle groups were trained, with four exercises emphasizing the forearm flexors. After training, strength (1-repetition maximum preacher curl) increased by 25% (P < 0.05). Magnetic resonance imaging scans revealed an increase in the biceps brachii muscle cross-sectional area (CSA) (from 11.8 +/- 2.7 to 13.3 +/- 2.6 cm2; n = 8; P < 0.05). Muscle biopsies of the biceps brachii revealed increases (P < 0.05) in fiber areas for type I (from 4,196 +/- 859 to 4,617 +/- 1,116 microns2; n = 11) and II fibers (from 6,378 +/- 1,552 to 7,474 +/- 2,017 microns2; n = 11). Fiber number estimated from the above measurements did not change after training (293.2 +/- 61.5 x 10(3) pretraining; 297.5 +/- 69.5 x 10(3) posttraining; n = 8). However, the magnitude of muscle fiber hypertrophy may influence this response because those subjects with less relative muscle fiber hypertrophy, but similar increases in muscle CSA, showed evidence of an increase in fiber number. Capillaries per fiber increased significantly (P < 0.05) for both type I (from 4.9 +/- 0.6 to 5.5 +/- 0.7; n = 10) and II fibers (from 5.1 +/- 0.8 to 6.2 +/- 0.7; n = 10). No changes occurred in capillaries per fiber area or muscle area. In conclusion, resistance training resulted in hypertrophy of the total muscle CSA and fiber areas with no change in estimated fiber number, whereas capillary changes were proportional to muscle fiber growth.

Adenosine Triphosphatases↗
PubMed1990

Hypertrophy and hyperplasia of alveolar type II cells in response to silica and other pulmonary toxicants.

Alveolar Type II cells serve two major functions in the lung, both of which are essential for the preservation of normal lung function. First, Type II cells synthesize and secrete pulmonary surfactant, and second, they function as progenitor cells for maintaining the alveolar epithelium. The Type II cell population of the lung is quite sensitive to the deposition of toxicants in the distal lung, responding in two principal ways. Damage to the Type I epithelium stimulates Type II cells to proliferate and subsequently differentiate to replace the injured Type I cells. Second, a portion of the Type II cell population may become hypertrophic. Both of these events are frequent findings in the diseased or damaged lung. The Type II cell changes are often associated with increases in surfactant pools. In those cases where ultrastructural characteristics of hypertrophic Type II cells were examined, the appearance of these cells was consistent with that of an activated cell type. Alterations in the lamellar body compartment are a common finding in hypertrophic Type II cells, with increases in both lamellar body size and number. It is likely that the hypertrophic, or activated, Type II cells account for the increased levels of surfactant found in the lungs after exposure to a variety of toxic agents. We examined, in detail, Type II cell hyperplasia and hypertrophy induced by silica deposition. Both Type II cell hyperplasia and hypertrophy were prominent responses. The proliferative response led to an approximate doubling of the number of Type II cells in the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Cellular hypertrophy and hyperplasia of airway smooth muscles underlying bronchial asthma. A 3-D morphometric study.

In order to study whether hyperplasia or hypertrophy of cells is responsible for the thickening of airway muscles, 3-D morphometry of airway muscle cells was performed on resin-embedded semithin serial sections of autopsied lungs from 10 asthmatics and five control subjects. There were five Type I and five Type II asthmatic lungs, as defined in an earlier study, thickened muscles being found only in the central bronchi in Type I and distributed over the whole airway tree in Type II. The analysis was based on "unbiased" 3-D morphometry to obtain the numerical density NV of muscle cells using a "disector," a spatial probe introduced by Sterio in 1984, which we modified into a stack of serial sections. The mean number NL of cells per unit airway length and the mean volume Vc of a single muscle cell were also determined. In Type I asthmatics, the number of cells increased in the larger bronchi unaccompanied by cellular hypertrophy at any level of the airway tree. In contrast, in Type II asthmatics, hypertrophy was shown to prevail over the whole airway, but it was most remarkable in the bronchioles, whereas hyperplasia was mild and localized only in the bronchi. The two types of asthmatic lungs may therefore result from different pathogeneses.

Adult↗
PubMed1985

Cellular hyperplasia and hypertrophy, capillary proliferation and myoglobin concentration in the heart of newborn and adult rats at high altitude.

Newborn rats and their mothers were subjected to a simulated altitude of 5000 m for 4-5 weeks. Weight, capillary density (CD), fiber cross-sectional area (AF) and capillary-to-fiber ratio (C/F) of right (RV) and left (LV) ventricles and myocardial myoglobin (Mb) concentration were measured weekly in the newborns and at the end of the high altitude sojourn in the adults. Results were compared to sea level controls. In the adults, adaptive changes were only observed in the right ventricle. In newborns both, RV and LV, exhibited significant alterations. After 2 weeks at 5000 m the ventricular weight increase was 223% (RV) and 40% (LV) in the newborns and 96% in the adults' RV. Whereas only fiber hypertrophy was detectable in the RV of the dams, cardiac weight increase of the acclimatized neonates resulted from both, hypertrophy and hyperplasia of the myocytes. Appropriate capillary proliferation kept CD constant. Cardiac Mb concentration did not change. We conclude, that capillary neoformation primarily counteracts the increase of the O2 diffusion distance due to fiber hypertrophy and/or hyperplasia.

Altitude↗
PubMed1975

Atrophy of villi with hypertrophy and hyperplasia of Paneth cells in isolated (thiry-Vella) ileal loops in rabbits. Light-microscopic studies.

Thiry-Vella loops in rabbit ileum were prepared by a new technique and were studied 18 hr to 49 days postisolation. The loops became grossly shortened after 14 days. Histologically, some shortening and blunting of villi was detectable as early as 4 days postisolation, and with prolonged isolation the changes became marked. Reduction in epithelial cell height and in brush border thickness were noted, and goblet cells were increased somewhat in size and prominence. Yet there was only slightly increased chronic inflammation in the mucosa and acute inflammation was uncommon, suggesting that mucosal injury was minimal. Furthermore, mean epithelial mitotic indices for the crypts did not rise and were generally reduced. Striking hyperplasia and hypertrophy of Paneth cells associated with mitotic figures in Paneth cells accompanied the atrophic changes in the villi. Reimplantation of loops into the bowel 3 weeks after isolation led to complete reversal of all changes, including hyperplasia of Paneth cells. On the other hand, regular perfusion of loops with a solution containing a large variety of nutrient substances failed to reverse the mucosal changes. It was concluded that atrophy of villi in isolated ileum of the rabbit occurred mainly because one or more substances contained in the chyme are needed to maintain normal mucosal architecture. These substances probably help regulate epithelial cell turnover and may well be endogenous in origin. Loss of substances in the chyme after loop isolation may also have led to Paneth cell hyperplasia. Alternatively, the Paneth cell changes and atrophy of villi might have been related in a cause and effect way.

Animals↗
PubMed1984

Cholecystectomy stimulates hypertrophy and hyperplasia in the hamster pancreas.

Cholecystectomy may be a risk factor for carcinoma of the pancreas. In this study the morphometric and autoradiographic changes in the hamster pancreas following cholecystectomy (chole) were compared with changes observed in sham-operated controls. After operation significant increases were observed in percent acinar cell labeling with [3H]thymidine from 0.29 +/- 0.07 (controls) to 0.57 +/- 0.06 (chole) at 2 weeks and from 0.05 +/- 0.00 (controls) to 0.75 +/- 0.18 (chole) at 4 weeks. The number of labeled duct epithelial cells/mm duct length increased from 0.00 +/- 0.00 (controls) to 4.64 +/- 1.89 (chole) at 2 weeks and from 1.19 +/- 0.97 (controls) to 3.00 +/- 0.75 (chole) at 4 weeks. Duct epithelial cell height (micrometers) increased from 13.90 +/- 1.06 (controls) to 26.98 +/- 1.32 (chole) at 2 weeks and from 13.20 +/- 1.06 (controls) to 23.90 +/- 0.86 (chole) at 4 weeks. It was concluded that cholecystectomy results in hyperplasia and hypertrophy of pancreatic cell populations in the hamster. These data extend previous observations that cholecystectomy has a significant trophic effect on the pancreas.

Animals↗
PubMed1987

Progression of type II cell hypertrophy and hyperplasia during silica-induced pulmonary inflammation.

Type II cell hyperplasia and hypertrophy were quantitated in the lungs of rats exposed to silica by using intratracheal injection. Hypertrophic type II cells were separated from normal type II cells by means of centrifugal elutriation of cells dispersed from the lungs by using protease. Type II cell hypertrophy was also quantitated, in situ, by measuring cell profile areas in lung sections. As a means of distinguishing between the hyperplastic and hypertrophic responses of type II cells we followed the progression of these two responses as a function of time and of dose. Seven, 14, and 28 days after a single intratracheal injection of silica (10 mg/rat), hypertrophic type II cells accounted for 33, 35, and 57% of the total type II cells recovered from the lungs. In contrast, hypertrophic type II cells accounted for less than 15% of the type II cells from control lungs. The appearance of hypertrophic type II cells was dose-related when examined 2 weeks after dosing; however, after only 1 week, the response of the type II cell appeared independent of dose. The hypertrophic response of type II cells could not be separated from the hyperplastic response according to either dose or time responses. These data support the hypothesis that in the lungs of silica-treated rats, the hypertrophic type II cell may be the proliferative type II cell. In addition, the hypertrophic type II cell appears to underlie the marked increases in surfactant levels seen in silica-treated lungs.

Alkaline Phosphatase↗