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At least 775 records · Page 43Linked to original sources
PubMed1986

A comparative study of the induction of epidermal hyperplasia by natural and synthetic retinoids.

Retinoids are potent inducers of epidermal hyperplasia. In the present study the ability to induce epidermal hyperplasia by a variety of retinoids has been compared. Thirteen retinoids and beta-carotene were applied topically in an acetone vehicle to the dorsal skin of hairless mice and the dose-response and time course for the induction of hyperplasia were measured. Peak hyperplasia occurred 4 to 5 days after a single topical dose, and was induced by doses well below those producing gross or histological signs of cutaneous toxicity. The induction of hyperplasia was dose-dependent, the number of epidermal cell layers increasing initially in proportion to the log of the dose and then tending to plateau or, in some cases decrease, after which further increases in dose were associated with the appearance of gross and histological toxicity. The slopes of the initial increasing phase were determined and potencies expressed as the dose producing a 50% increase in the number of epidermal cell layers. All-trans-retinoic acid and its analogs, etretinate and its free acid, (E)-4[2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl- 2-naphthalenyl)-1-propenyl]-benzoic acid (arotinoid) derivatives, retinol and retinal produced an increase in the number of cell layers proportionate to the log of the dose. Decarboxylated (E)-4[2-(5,6,7,8-tetrahydro-5,5,8,8- -tetramethyl-2-naphthalenyl-1-propenyl]-benzoic acid, a cis-locked aryl triene derivative of retinoic acid and beta-carotene were inactive. Similar time courses were observed when retinoids were dosed p.o. The relative potencies of the retinoids in this system show similar trends to those reported for biological activities measured in other in vivo and in vitro assays.

Animals↗
PubMed1985

Cod-liver oil in the prevention of intimal hyperplasia in autogenous vein grafts used for arterial bypass.

Cod-liver oil, rich in eicosapentaenoic acid, an unsaturated fatty acid, was administered to 14 mongrel dogs to determine if this acid would prevent platelet-mediated intimal hyperplasia. Twenty-eight 1 cm segments of undistended jugular vein were interposed between bilaterally divided femoral arteries. Seven control animals were fed a 2% cholesterol diet 1 week before and for 6 weeks after the operation. A further seven animals received cod-liver oil capsules containing 1.8 gm of eicosapentaenoic acid daily 1 week before and for 6 weeks after autogenous vein implantation, in addition to the lipid-supplemented diet. Baseline serum cholesterol was 4.6 +/- 0.4 mmol/L. The rise in serum cholesterol was similar in the two groups and increased to 7.4 +/- 0.6 mmol/L (control group) and to 6.8 +/- 0.2 mmol/L (eicosapentaenoic acid group) (p less than 0.001). Prothrombin time, partial thromboplastin time, bleeding time, and platelet counts were unchanged in the two groups. Vein grafts, harvested at 6 weeks, were fixed in formaldehyde. Mean intimal thickness was measured from multiple vein graft cross sections with a Zeiss computerized interactive image analyzing system. A mean of 140 +/- 11 measurements were computed from each graft. Marked intimal hyperplasia occurred in the control group and increased from 4.3 +/- 0.3 to 86.4 +/- 14 micron. In contrast, a high eicosapentaenoic acid diet inhibited intimal hyperplasia, with intimal thickness only increasing from 4.0 +/- 0.4 to 24.8 +/- 2.7 micron (p less than 0.001). These data indicate that eicosapentaenoic acid inhibits platelet-mediated intimal hyperplasia and suggest that cod-liver oil could be used to prevent intimal hyperplasia in vein grafts used for myocardial revascularization.

Animals↗
PubMed1979

[Frequency of Kongenital Adrenal Hyperplasia (author's transl)].

The frequency of homozygous congenital adrenal hyperplasia in Tyrol is found to be 1 : 8991, the gene-frequency for congenital adrenal hyperplasia 1 : 95 and the frequency of heterozygous congenital adrenal hyperplasia 1 : 48. Our data is compared on a numerical and statistical base with that in Zürich and Munich with regard to the frequency of congenital adrenal hyperplasia, to its distribution with and without salt loss and to its sex-distribution. According to our study one may assume a frequency of homozygous congenital adrenal hyperplasia in Tyrol, Zürich and Munich of 1 : 7000--10,000.

Adrenal Hyperplasia, Congenital↗
PubMed1977

[Excessive hyperplasia of the exocrine pancreatic tissue and Wernicke's encephalopathy (author's transl)].

A 52 year old woman with a history of mild pancreatitis had a palpable mass in the upper abdomen. She died in an unexplained coma. The autopsy revealed an excessive hyperplasia of the exocrine pancreatic tissue resulting in the largest pancreas ever reported (254 gramm). This hyperplasia was accompanied by a chronic pancreatitis. In the central nervous system a Wernick's encephalopathy had developed; severe loss of neurons was stated in the thalamus; extensive degeneration was found in the upper vermis of the cerebellum. The discussion of this case includes the relationship between the diseases of the pancreas and neuropsychiatric and neuropathologic findings. It is assumed that the hyperplasia of the exocrine pancreatic tissue could only be an additional factor in the occurence of post alcoholic complications. This hyperplasia of the exocrine pancreatic tissue is considered to be a hamartom-like formation and it should therefore be distinguished from other pancreatic hyperplasia.

Diagnosis, Differential↗
PubMed1978

Reversible papillary hyperplasia of the rat urinary bladder.

A rapid reproducible method for the production of ulcers and reversible regenerative hyperplasia of the urinary bladder of rats is described. This method does not involve administration of a toxic chemical or retention of a foreign body. Ulceration was produced by means of applying a steel rod, 5 mm in diameter, frozen at -78 C, to the serosal surface of the bladder for 2 seconds, twice, with a 5-second interval between each application. Sequential histologic observations showed that ulcers were accompanied by necrosis of the entire thickness of the bladder at the site of freezing with extensive acute inflammation. Regenerative hyperplasia was evident at the edge of the ulcer by the second day, with greatest severity at 5 days when papillary and nodular hyperplasia were present. At 15 days the bladders were normal or had only minimal hyperplasia. The labeling index by autoradiography was highest in the mildly hyperplastic area near the ulcer at 2 days and remained relatively high through 5 days. The hyperplastic epithelium surrounding the ulcer observed by scanning electron microscopy had numerous degenerative cells on the surface, and small epithelial cells with numerous short, uniform microvilli on their luminal surface were also observed. The numerous short, uniform microvilli on their luminal surface were also observed. The microvilli had a symmetric luminal membrane, as observed on trasmission electron microscopy. More peripherally the cells had microridges only or microvilli and microridges on their luminal surface. Neither pleomorphic microvili nor a structured glycocalyx fuzz on microvilli was observed during the process of regenerative hyperplasia, distinguishing it from neoplastic bladder proliferations.

Animals↗
PubMed1983

Nodular adrenal hyperplasia and Cushing's syndrome.

Clinical, biochemical, operative, and postmortem findings have established nodular adrenal hyperplasia as a clinicopathologic entity and a cause of Cushing's syndrome. The possibility exists that there is a relationship among the various forms of adrenal and pituitary diseases that lead to hyperadrenocorticism. This may include a continuous sequence from bilateral adrenal hyperplasia to micronodular and macronodular hyperplasia to a unilateral adrenocortical adenoma and even carcinoma. We report the investigation and management of six patients with Cushing's syndrome caused by bilateral nodular adrenal hyperplasia who were treated by operation at the Glasgow Royal Infirmary, Scotland from 1975 to 1979. Investigations included a variety of biochemical and radioimmunoassay tests on plasma and urine, provocative and inhibition tests, scanning (ultrasonography, computed tomography, and iodocholesterol), arteriography, and selective venous sampling. All patients underwent a bilateral adrenalectomy by the posterior approach. The adrenal glands varied in size from 4.9 to 18 gm and histology showed that they had the features of bilateral nodular adrenal hyperplasia. Five patients did well after operation; they are presently receiving replacement steroid therapy, and at a 3- to 7-year follow-up there was no evidence of Nelson's syndrome. Advances in drug therapy (medical adrenalectomy) with aminoglutethimide, metyrapone, and O,p-DDD should not at present cause a change in our surgical approach to this condition.

Adrenal Glands↗
PubMed1983

[Mucosal hyperplasia of the ileum after subtotal colectomy in rats].

To evaluate factors contributing to ileal mucosal hyperplasia following extensive colectomy, the following three models were designed in rats: Subtotal colectomy and end-to-end ileoproctostomy; retransection of the terminal ileum with end-to-side proximal-ileoproctostomy (colectomy group), End-to-side ileoproctostomy without colectomy (bypass group), and End-to-side ileocecostomy (control group). In all groups the terminal ileum was left out of the intestinal stream as defunctionalized segments. Specimens were obtained from the terminal ileum during operation and from both the functioning and the defunctionalized segments at various intervals postoperatively. The mucosal hyperplasia was evaluated by measuring eight variables including numbers of villi around the bowel circumference, villous height, crypt depth, total mucosal thickness, epithelial cell counts per villus, DNA contents per unit length of the bowel and radioactivity of incorporated 3H-thymidine as well as DNA specific activity. The results showed that marked mucosal hyperplasia of the functioning segments was noted in all groups, and that mucosal hyperplasia was also observed in defunctionalized segments of colectomized rats, but not in those of both bypass rats and control. These findings were statistically confirmed by analysis of variance. It was concluded that although intraluminal factors played an important role in mucosal hyperplasia of the ileum following extensive colectomy, humoral factors might be also involved in intestinal adaptation.

Animals↗
PubMed1978

Nodular regenerative hyperplasia of the liver. Report of six cases and review of the literature.

The authors report the cases of 6 adult patients suffering from nodular regenerative hyperplasia of the liver, an uncommon lesion characterized by small-sized hepatocytic nodules scattered throughout the liver, with no or slight fibrosis. The histological recognition of nodular regenerative hyperplasia of the liver was easy on large specimens taken intraoperatively, but was difficult or impossible on small specimens such as those provided by needle biopsy. In all of the patients of this series, the main consequence of nodular regenerative hyperplasia of the liver was portal hypertension. In this series, nodular regenerative hyperplasia of the liver was not associated with rheumatoid arthritis, whereas such an association has been noted in most of the cases previously reported. The etiology and pathogenesis of nodular regenerative hyperplasia of the liver is unknown.

Adolescent↗
PubMed1980

Arachnoidal cell hyperplasia. Its relationship to aging and chronic renal failure.

The biological implications of human arachnoidal cell hyperplasia are unclear. In a study based on 922 autopsies performed over a four-year period that investigated the conditions associated with arachnoidal cell hyperplasia, hyperplasia was found in 184 cases (study cases). The incidence of arachnoidal cell hyperplasia was found to increase linearly with advancing age. In a case-control design used to ascertain any other clinical associations, 22 of the study cases had comcomitant chronic renal failure, whereas only four in a control group matched for age at time of death had chronic renal failure. No other associations were observed. Arachnoidal cell hyperplasia seems to be an age-related phenomenon and shows a statistically significant association with chronic renal failure.

Adolescent↗
PubMed1982

DNA content of pancreatic duct hyperplasia and carcinoma.

The DNA content of epithelial nuclei of hyperplastic and carcinomatous ducts of the pancreas was examined cytophotometrically. The materials were obtained from 2 cases of nonpapillary hyperplasia, 3 of papillary hyperplasia, 2 of atypical hyperplasia and 2 of tubular adenocarcinoma, which were selected by reviewing the pancreata of about 1,600 human autopsy cases. A gradual shift was observed in the DNA content from the normal level to a carcinomatous level through various stages of hyperplasia. Based on these findings, the hypothesis that pancreatic duct hyperplasia is a potent precursor of pancreatic carcinoma is discussed.

Adenocarcinoma↗
PubMed1981

Experimental carotid stenosis due to fibrous intimal hyperplasia.

Although fibrous intimal hyperplasia has been reported to be involved in up to one-third of recurrences of carotid restenosis following endarterectomy, little is known of its origin. This prompted us to attempt to produce it experimentally. Fibrous intimal hyperplasia could not be induced in the canine carotid model using simple endarterectomy or endarterectomy with an autogenous vein patch angioplasty. Polytetrafluoroethylene graft angioplasties in the same model produced this lesion readily and usually led to stenosis or occlusion. The experimental and clinical lesion of fibrous intimal hyperplasia of the carotid artery and the lesion of intimal fibrous hyperplasia that occurs when prosthetic arterial grafts are placed into small and medium size arteries appear histologically similar and may be due to a common factor. A review of the factors available in our series, as well as those of others, leads us to believe that the common denominator is hemodynamic in nature. The experimental data showing stenotic fibrous intimal hyperplasia occurring with polytetrafluoroethylene patch angioplasties has been previously reported. These data indicate that polytetrafluoroethylene should cautiously be used for small and medium diameter arterial patch angioplasties.

Animals↗
PubMed1980

Effects of continuous and discontinued exposure to 2-AAF on urinary bladder hyperplasia and neoplasia.

The effect of discontinued feeding of 2-acetylaminofluorine (2-AAF) was compared with the effect of continuous 2-AAF feeding on the urinary bladder of BALB/c female mice. Dietary concentrations of 2-AAF examined in this regard were 60, 75, 100, and 150 ppm. These diets were fed for 9, 12, or 15 months and then replaced with control feed, and the animals were killed at 18 or 24 months. Observations on these animals were contrasted with observations made at the same intervals on animals continuously fed these concentrations of 2-AAF throughout the study. Discontinuing 2-AAF exposure decreased prevalence of bladder tumors below that found in continuously exposed mice and resulted in a decrease in severity and prevalence of hyperplasia. Mild hyperplasia was retained in a portion of each population and the prevalence of this hyperplasia was dependent on both the period of exposure and the dose of 2-AAF. Mild persistent hyperplasia was correlated closely with neoplasia and may be a necessary stage in neoplastic development. Moderate or severe hyperplasia apparently regress when 2-AAF feeding is discontinued and do not appear to be essential steps in the neoplastic process.

2-Acetylaminofluorene↗
PubMed1980

Lymphoid hyperplasia: a major prognostic feature in 519 cases of colorectal carcinoma.

The size of the regional lymph nodes, germinal center, and paracortical areas, and the degree of perivascular lymphocyte cuffing (PLC) at the edges of 519 carcinomas of the large bowel have been analyzed microscopically and assessed quantitatively. Hyperplasia of these lymphoid areas, defined as relative or absolute size exceeding the median for the tumor stage, has been related to cancer-specific survival data for each of Dukes' Stages A, B, and C, and for disseminated disease commonly referred to as Stage D. Germinal center hyperplasia was associated with a major survival advantage in Stage B (P = 0.003) and in Stage C (P = 0.04) if present in tumor-involved lymph nodes. Paracortical hyperplasia related favorably to survival in Stages B and C; in Stage C such hyperplasia was most favorable if present in tumor-involved lymph nodes (P = 0.009). PLC related to favorable survival data only in Stage B. Lymphoid hyperplasia showed no correlation with survival in Stages A and D.

Adenocarcinoma↗
PubMed1981

Hyperplasia of Syrian hamster epidermis induced by single but not multiple treatments with 12-O-tetradecanoylphorbol-13-acetate.

Treatment of initiated hamster skin with 12-O-tetradecanoylphorbol-13-acetate does not promote the formation of papillomas and carcinomas as it does in the classic two-stage epidermal carcinogenesis model in many strains of mice. We have begun to examine the basis of this species specificity to TPA. We have found that, although hamster and mouse epidermis respond to a single exposure of TPA with a comparable degree of hyperplasia, they differ in their response to multiple treatments. In contrast to the reported potentiation of hyperplasia of mouse skin following two or more treatments with TPA, hamster skin is capable of adapting to multiple exposures to the promoter. Weekly TPA treatments of hamster skin result in hyperplasia of 4 to 6 nucleated cell layers after the first treatment, reduced hyperplasia after the second treatment, and no hyperplasia after 4 weeks of treatment. Decreasing the time interval between treatments accelerates the adaptation process. This adaptation phenomenon should be useful in studying the mechanism of TPA action by examining TPA effects in adapted and nonadapted tissues from the same species.

Animals↗
PubMed1980

Cortical hyperplasia of the adrenal gland in the dog.

A survey of the adrenal glands of 151 dogs revealed 33 cases of nodular cortical hyperplasia and six cases of diffuse cortical hyperplasia. The gross, microscopic and ultrastructural changes seen in these two forms of the condition are compared. Detailed measurements indicate that a morphometric study is of some value in establishing a post mortem diagnosis of hyperadrenocorticalism. Cell counts show that, despite differences revealed by histological examination, cellular hypertrophy may be in important feature in both nodular and diffuse 'hyperplasia'. Electron micrography suggests that the ultrastructural changes in nodular hyperplasia are of a degenerative nature while in diffuse hyperplasia the increased quantity of endoplasmic reticulum present and the appearance of the other organelles indicate hyperactivity. This correlates well with the clinical evidence of hyperadrenocorticalism seen in the latter condition.

Adrenal Cortex↗
PubMed1995

[Prevention of vascular intimal hyperplasia in small caliber prostheses. Preliminary results].

Intimal hyperplasia is one of the main risk factors for the patency of small diameter bypass grafts. The standard unfractioned heparin (UH) is able to control this phenomenon but the clinical use is not fit for long term treatment; on the other hand the antiplatelet drugs have an anti-thrombotic effect but they seem to be unable to control intimal hyperplasia. Low molecular weight heparins (LMWH) have an anti-thrombotic effect superimposable to that of UH with minimal side-effects and might inhibit intimal hyperplasia too. Based on these criteria, we carried out an experimental study on sheep with the aim of evaluating the efficacy of postoperative treatment with LMWH versus an anti-platelet drug in controlling intimal hyperplasia and growth of true endothelial cells in small prosthetic ePTFE grafts (4 mm) interposed in the carotid artery. At the operation, 30 sheep were randomly located in 3 groups: A = control group, no treatment; B = Ticlopidine hydrochloride 250 mg/bid by mouth for 4 weeks; C = LMWH 3.075 IU AXa (0.3 ml) sc preoperatively and then once a day for the same period. Complete thrombosis of the graft occurred in 7 sheep of group A, 5 in B and 2 partial in group C. The intimal hyperplasia was moderate-severe in group A, mild-moderate in group B and no-mild in group C. True endothelial cells were found mainly in the LMWH group; in the other groups and in other portions of the grafts the cellular coverage was accomplished almost completely by fibroblasts. The study is still in progress with 6 further sheep treated with LMWH.

Animals↗
PubMed1994

Pharmacotherapy for benign prostatic hyperplasia.

Benign prostatic hyperplasia is a benign neoplasm of the prostate seen in men of advancing age. Microscopic evidence of the disorder is seen in about 70% of men by 70 years of age, whereas symptoms requiring some form of surgical intervention occur in 30% of men during their lifetime. Although the exact cause of benign prostatic hyperplasia is not clear, it is well recognized that high levels of intraprostatic androgens are required for the maintenance of prostatic growth. In recent years, extensive surveys of patients undergoing transurethral resection of the prostate reveal an 18% incidence of morbidity that has essentially not changed in the past 30 years. This procedure is also the second highest reimbursed surgical therapy under Medicare. These findings have resulted in an intensive search for alternative therapies for prostatic hyperplasia. An alternative that has now been well defined is the use of alpha-adrenergic blockers to relax the prostatic urethra. This is based on findings that a major component of benign prostatic hyperplasia symptoms is spasm of the prostatic urethra and bladder neck, which is mediated by the alpha-adrenergic nerves. A second approach is to block androgens involved in maintaining prostate growth. Several such drugs are now available for clinical use, and we discuss their side effects and use. We also include the newer recommendations on evaluating benign prostatic hyperplasia that are cost-effective yet comprehensive.

Adrenergic alpha-Antagonists↗
PubMed1995

Dramatic hyperplasia of mtv-2+ lymph node grafts in mtv-2- recipients and selective stimulation of V beta 14+ T cells in recipients' lymph nodes in the DDD mouse.

DDD/1 (DDD) mice contrast strikingly with DDD-mtv-2/mtv-2 (DDD-mtv-2) congenics in their marked lymph node (LN) T cell paucity. To clarify the possible difference in LN function between them, reciprocal LN grafting experiments were conducted. DDD-mtv-2 LN grafts in DDD recipients underwent hyperplasia as dramatic as 10-to 20-fold increase in weight between 3 and 4 wk after implantation. Lymphoid cells in hyperplastic LN grafts were of recipient origin. Similar hyperplasia of mtv-2-heterozygous LN grafts also occurred on various hybrid backgrounds involving DDD mice. Moreover, LN grafts from BALB/c mice infected with mtv-2-derived exogenous mouse mammary tumor virus (MMTV) swelled in MMTV-free BALB/c recipients. Genetic analysis of DDD x (DDD x DDD-mtv-2)F1 backcross progeny demonstrated that LN hyperplasia was closely linked to mtv-2. The frequencies of V beta 5+ and V beta 8+ T cells unresponsive to mtv-2-encoded superantigen (SAg) changed with practically the same kinetics in both LN grafts and recipients' LN. Thus, the cells responsible for LN hyperplasia were polyclonal. V beta 14+ CD4+ cells responsive to mtv-2 SAg were specifically stimulated in recipients' LN but selectively deleted in hyperplastic LN grafts. DDD mice carrying hyperplastic mtv-2+ LN grafts or pretreated with mtv-2+ spleen cells developed an unresponsive state in terms of influx of mtv-2- lymphoid cells into mtv-2+ LN grafts. These results indicate that mtv-2 gene products including SAg may stimulate mtv-2- lymphoid cells of recipients and cause them to migrate into mtv-2+ LN grafts in a nonspecific manner with resulting LN hyperplasia.

Animals↗