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PubMed2006

[Pathological changes of radial artery used for coronary artery bypass grafting and its related risk factors for intimal hyperplasia].

OBJECTIVE: To examine the degree of intimal hyperplasia and the prevalence of atherosclerosis in radial arteries taken from the patients undergoing coronary artery bypass grafting (CABG), and to analyze the risk factors to obtain some helpful information for choosing arterial conduits. METHODS: Forty-one radial arteries and 11 internal mammary arteries samples were collected. The average age of patients was 48.5 years, and they all were male. Intimal hyperplasia, atherosclerosis, medial calcification were evaluated by routine histological methods, and the severity of diseases was measured on the percentage of luminal narrowing and the intima-to-media ratio (the intima area/media area). The risk factors for coronary heart disease were also analyzed. RESULTS: Ninety-three percent (38 of 41) of radial arteries showed mild intimal hyperplasia, which was not regarded to influence blood flowing after CABG. As a part of them, 54% (22/41) of radial arteries had a lower than 25% of luminal narrowing, meanwhile 39% (16/41) of radial arteries had the percentage of luminal narrowing between 25% and 50%. Only 7% (3 of 41) of radial arteries were found to have occlusive lesions, which made arterial lumen decreased more than 75%. The 3 patients including 2 with severe atherosclerosis and another 1 aged 17 years was involved by fibromuscular dysplasia. The later vessel was discarded after harvesting. The percentage of luminal narrowing and the intima-to-media ratio were higher in radial artery than that in internal mammary artery (t = 3.00, 2.49, P < 0.05). The two parameters were positively correlated with age (r = 0.398, 0.310, P < 0.05), but this study failed to show any relationship between intimal hyperplasia of radial artery and coronary lesions and other risk factors. Medial calcification was not found by routine histological method in all cases. CONCLUSION: Only mild intimal hyperplasia and no medial calcification are found in radial arteries used for CABG in the patients. Because the risk factors could not yet predict the severity of radial arterial lesions, this study strongly suggests that the Doppler ultrasonography and pre-operation clinical consideration should be emphasized to screen out some arteries with occlusive lesions.

Adolescent↗
PubMed1991

Peptide inhibition of neointimal hyperplasia in vein grafts.

Angiopeptin, a novel synthetic octapeptide, was evaluated as a new approach toward the inhibition of neointimal hyperplasia in vein grafts. Male New Zealand white rabbits (n = 22) underwent carotid artery interposition bypass grafting with autologous reversed jugular vein. Nine rabbits were in the treatment group, and 13 were in the control group. The treatment group received angiopeptin 20 micrograms/kg/day by subcutaneous injection beginning 1 day before operation and continuing for 3 weeks until they were killed. At death the vein grafts were fixed in situ with 10% buffered formalyn at 80 mm Hg perfusion pressure. Histologic sections through each vein graft were analyzed by computerized morphometric analysis for area of neointimal hyperplasia (mm2). Neointimal hyperplasia in the control animals was 0.080 + 0.017 mm2 (mean + SEM), whereas neointimal hyperplasia in the group treated with angiopeptin was 0.022 + 0.006 mm2 (mean + SEM) (p = 0.02). This is the first time that peptide inhibition of neointimal hyperplasia has been demonstrated in vein grafts and may have significant implications for future use in vascular surgery.

Animals↗
PubMed2006

Mouse models of neointimal hyperplasia: techniques and applications.

Neointimal hyperplasia is a major cause of the failure in vascular reconstructive procedures such as angioplasty, vascular stenting, small caliber vascular graft, and vein graft. However, the underlying molecular mechanisms are not yet fully understood. The study of neointimal hyperplasia has relied heavily on the use of experimental animal models. Recent development in gene manipulation techniques in mice offers a unique opportunity to unravel the molecular basis of the neointimal response at the genetic level, which is critical to develop new strategies to prevent human neointimal hyperplasia. Several mouse models for studying neointimal hyperplasia have recently been established including blood-flow cessation, mechanical injury, and vein bypass graft. In an attempt to elaborate these models, this review highlights the characteristics, advantages, disadvantages, and applications of these mouse models in vascular disease. In addition, the difference between mouse models and human lesions is discussed. Thus, this review provides updated information and helps vascular surgeons and other vascular biologists in selecting appropriate mouse models for their research on neointimal hyperplasia.

Animals↗
PubMed2006

[The characteristics of proliferation activity in squamous metaplasia and reserve cell hyperplasia of uterine cervix].

The aim of our study was to investigate the characteristics of proliferation activity in squamous metaplasia and reserve cell hyperplasia of uterine cervix. Four groups of patients were selected: 1st group--34 reproductive patients with reserve cell hyperplasia, 2nd group--21 reproductive patients with squamous metaplasia, 3rd group--12 postmenopausal patients with reserve cell hyperplasia, 4th group--29 postmenopausal patients with squamous metaplasia. These groups included the patients with and without infections. Cervical biopsies were studied by immunohistochemistry using anti-Ki-67 monoclonal antibody. Ki-67(+) reserve cells were counted in reserve cell hyperplasia. Ki-67(+) squamous cells were counted in squamous metaplasia. The results showed that in both squamous metaplasia and reserve cell hyperplasia the number of Ki-67(+) cells, i.e. the intensity of proliferation is depended on the co-existence of infection, as well as on the age of the patient. These data are important in the complex treatment of cervical pseudoerosions.

Adult↗
PubMed2006

[Influence of antioxidants on the development of benign prostatic hyperplasia].

The main objectives of the study was the evaluation of concentration of endogenous antioxidants (Vitamins E, A, C and Beta-carotene) in the blood plasma of elderly men and to determine their roles in the development of benign prostatic hyperplasia. There were carried out investigations in 110 men during 2003-2006 in the Urological Clinic of the Tbilisi State Medical Academy. 71 patient entered into the main group (65-81 years old), who were diagnosed for benign prostate hyperplasia. The control group included 30 men (60-80 years old) who did not suffer from the typical signs of benign prostatic hyperplasia. Besides, to evaluate normal levels of endogenous antioxidants (Vitamins E, A, C and Beta-carotene) concentration in the blood plasma additionally were studied young practically healthy 10 persons (20-35 years old), they compiled the second control group. Our study showed that endogenous antioxidants concentration reduces in the blood plasma with the age, this reduction becomes more obvious with the clinical detection of prostate benign hyperplasia. It is recommended for elderly patients to control periodically the endogenous antioxidants level (Vitamins A, C, E and Beta-carotene) in the blood plasma and in the case of changes to get food enriched with vitamins or combined vitamins preparations. This will be accomplice factor for the prophylactic of benign prostatic hyperplasia. This will be prophylactic activity during the conservative treatment process (by alpha-adrenoceptor blocking drugs, phytotherapy medicines, 5 alpha-reductase inhibitors and others). Inclusion of vitamins complexes which contains antioxidants is necessary. Prescription of antioxidants complex after the operative treatment will accelerate the healing process and reduce the rehabilitation period.

Adult↗
PubMed2006

Natural history of benign prostate hyperplasia.

BACKGROUND: Benign prostate hyperplasia is one of the most common diseases affecting the health of the aging males. Watchful waiting is an acceptable management strategy for benign prostate hyperplasia in which the patient is monitored by the physician but receives no active intervention. The epidemiological data on this are lacking in China. Our study was designed to evaluate the changes of signs and symptoms of patients with benign prostate hyperplasia during management by watchful waiting in China. METHODS: One hundred and forty-five patients with benign prostate hyperplasia aged > 50 years were enrolled in management by watchful waiting. All the patients were visited every 6 months and were given an International Prostate Symptom Score and Quality of Life questionnaire to complete. They also had uroflowmetry and were assessed using ultrasonography to get the volume of prostate, transition zone and amount of residual urine. The Student's t test, the Chi-square test, and variance analysis were used in the statistical analysis. RESULTS: All patients were visited after 6 months, the mean volume of transitional zone was found to have increased by 1.6 ml (P < 0.01), International Prostate Symptom Score was increased by 0.8 (P < 0.01) and Quality of Life was increased by 0.2 (P < 0.01), and there was no statistical change in other data. Among these patients, 17.9% (26/145) visited again after 12 months when the data failed to show a statistically significant difference among the three groups (0, 6, and 12 months). CONCLUSIONS: After one year's follow-up, the progression of benign prostate hyperplasia was slow and the clinical data did not undergo much change.

Aged↗
PubMed1991

[Thymus hyperplasia: classification, problems of patho- and morphogenesis, importance in human pathology].

Thymus hyperplasia may be congenital (thymomegaly) and acquired (acquired thymomegaly, "tumour-like" hyperplasia, lymphofollicular hyperplasia). Congenital thymomegaly is represented by variants with hypo- and hyperfunction of an adequately formed thymus and results from the congenital neuro-endocrine disturbances. Thymomegaly with a thymus hypofunction is a marker of the immunodeficiency. Acquired thymomegaly is also represented by two variants with hypo- and hyper-function of the thymus and is in fact a "phenocopy" of the congenital one. "Tumor-like" thymus hyperplasia is a rare form of its pathology with a thymic weight reaching 800 g thus resulting in a syndrome of the mediastinum organs compression. Lymphofollicular thymus hyperplasia can not be always considered to be a thymus pathology but it is characteristic of autoimmune and infectious-allergic diseases with lymphoid follicles localizing in the hyperplastic intralobular perivascular spaces. Thymus parenchyma changes depend on the main disease and play a main role in the development of thymus dysfunction, for example, in the autoimmune diseases. Formation of lymphoid follicles in the dilated perivascular spaces is a non-specific process.

Diagnosis, Differential↗
PubMed1991

Prostratin, a nonpromoting phorbol ester, inhibits induction by phorbol 12-myristate 13-acetate of ornithine decarboxylase, edema, and hyperplasia in CD-1 mouse skin.

Pretreatment of CD-1 mouse skin with prostratin (12-deoxyphorbol 13-acetate) inhibited biological response to phorbol 12-myristate 13-acetate. The three responses examined were hyperplasia, induction of ornithine decarboxylase, and edema; the characteristics of inhibition depended on the specific response. Hyperplasia is the best short-term correlate of tumor promotion. Two or more pretreatments with 2.56 mumol (1 mg) prostratin, administered at intervals of 1-4 days, almost completely blocked the hyperplasia induced by phorbol 12-myristate 13-acetate applied 15 min to 6 h after the last pretreatment. Inducibility of hyperplasia was partially restored at 2 days and recovered by 4 days. Prostratin was more potent for inhibition of ornithine decarboxylase induction (50% inhibitory dose = 25.6 nmol) than it was for hyperplasia: the inhibition was largely attained by the first application, and the recovery from inhibition was slower (8 days). Edema was partially inhibited by prostratin (dose giving 50% of maximal inhibition = 512 nmol). We have previously demonstrated that prostratin is a protein kinase C activator. Our present results show that prostratin is a functional antagonist for a class of protein kinase C mediated responses. The findings emphasize the diversity of biological outcome for protein kinase C activators, presumably driven by the extensive heterogeneity in the protein kinase C pathway.

Animals↗
PubMed1990

Clonal growth of atypical adenomatous hyperplasia of the lung: cytofluorometric analysis of nuclear DNA content.

The nuclear DNA content of 13 cases of atypical adenomatous hyperplasia (AAH) associated with adenocarcinoma, eight cases of small-sized well differentiated adenocarcinoma in which the tumors were less than 2.5 cm in size with no tumor recurrence within 5 yr after surgery, and eight cases of reactive type 2 pneumocyte hyperplasia of the lung was determined by cytofluorometry. Of the AAHs, four were solitary and composed entirely of cells of AAH (Group 1), and the remaining nine were in continuity with the focus of adenocarcinoma (Group 2). The average mean nuclear DNA content of the AAHs was significantly greater than that of reactive type 2 pneumocyte hyperplasia (p less than 0.005) and significantly smaller than that of adenocarcinoma associated with AAH (p less than 0.05). However, no significant difference was found in nuclear DNA content between AAH and small-sized well differentiated adenocarcinoma. Aneuploid stem lines were found in seven of the 13 (53.8%) AAHs, ten of the 13 (76.9%) adenocarcinomas associated with AAH, and five of the eight (62.5%) small-sized well differentiated adenocarcinomas but in none of the reactive type 2 pneumocyte hyperplasias. DNA histogram patterns I and II, in which aneuploid cells were less frequently present than in patterns III and IV, were more common in AAH than in adenocarcinoma associated with AAH and small-sized well differentiated adenocarcinoma. All of the reactive type 2 pneumocyte hyperplasia showed pattern I. As to the average mean nuclear DNA content, incidence of aneuploid stem lines, and DNA histogram pattern, there was no significant difference between groups 1 and 2 of the AAHs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1990

Differential down-regulation of epidermal protein kinase C by 12-O-tetradecanoylphorbol-13-acetate and diacylglycerol: association with epidermal hyperplasia and tumor promotion.

A single topical application of 2 nmol 12-O-tetradecanoylphorbol-13-acetate (TPA) to CD-1 mouse skin resulted in a rapid decrease in cytosolic, particulate, and total epidermal protein kinase C (PKC) activity at 6 h, which remained decreased by 70% at 96 h. This dose of TPA produced epidermal hyperplasia as determined by an increase in the number of nucleated epidermal cell layers. A single application of 10 mumol sn-1,2-didecanoylglycerol, a model sn-1,2-diacylglycerol and complete tumor promoter, induced ornithine decarboxylase to an extent similar to that of 2 nmol TPA. However, sn-1,2-didecanoylglycerol produced an 80% increase in particulate PKC activity that was accompanied by a 45% decrease in cytosolic PKC activity, resulting in no net change in total PKC activity. Unlike TPA, this dose of sn-1,2-didecanoylglycerol did not produce a hyperplastic response. Additional dosing regimens were examined to determine whether the down-regulation of particulate PKC activity was associated with hyperplasia and tumor promotion. A tumor-promoting dosing regimen consisting of multiple applications of 5 or 10 mumol sn-1,2-didecanoylglycerol twice daily for 1 week resulted in more than a 60% decrease in cytosolic and particulate PKC activity and a marked epidermal hyperplasia. Twice-weekly application of 10 mumol sn-1,2-didecanoylglycerol, a nonpromoting dosing rate, for 1 week decreased cytosolic PKC activity but increased particulate PKC activity and did not produce hyperplasia. Dosing regimens utilizing multiple applications of TPA decreased both particulate and cytosolic PKC activity and were also hyperplastic. PKC activity was also measured in epidermal papillomas from mice initiated with 7,12-dimethylbenz[a]- anthracene and promoted with either sn-1,2-didecanoylglycerol or TPA. Cytosolic- and particulate-associated PKC activity in these papillomas was decreased by at least 70% and 40%, respectively, when compared with epidermis and whole skin. After 2 months without promoter treatment, both cytosolic and particulate PKC activity remained decreased in the papillomas, whereas epidermal PKC activity returned to control values by 2 to 3 weeks following cessation of several weeks of TPA treatment. Collectively, these data demonstrate that the down-regulation of epidermal PKC is associated with and may be a permissive event for epidermal hyperplasia and tumor promotion.

Acetone↗
PubMedDate not supplied

Criteria for the cytologic assessment of hyperplasias in endometrial samples obtained by the Endopap Endometrial Sampler.

The Endopap Endometrial Sampler was used in 1,465 women, either just before endometrial biopsy or curettage (in 760 symptomatic patients) or as an office procedure (in 705 women). The samples were inadequate for interpretation in only 8.7% of the cases. Although all malignant lesions were identified by this screening technique, about one-fourth were initially classified cytologically as hyperplasia. Endometrial hyperplasias presented the greatest difficulties in interpretation, with only slightly over half of the proven cases correctly assessed on the endometrial sample. In an attempt to improve the accuracy of the cytologic diagnosis of hyperplasias, ten morphologic features were examined retrospectively in 207 cases. Five of the criteria were shown to provide an increased probability of correctly diagnosing endometrial hyperplasias on the cytologic sample: (1) the overlapping of cells in the glandular clusters or sheets, (2) the presence of nucleoli, (3) anisokaryosis, (4) granularity of chromatin and (5) the presence of sheets of stromal cells. The more of these criteria observed in a given case, the better was the chance of cytologically identifying a hyperplasia in the Endopap sample.

Cell Nucleolus↗
PubMed1987

[Problems of so-called atypical hyperplasia of the prostate].

In search of a precancerous morphological correlate for the carcinoma of the prostate gland becoming more and more frequent with growing age the prostate glands of 450 males from the current autopsy material were investigated by means of large sections according to the so-called serial section technique. The appearance of cellular atypias was discovered for the time being in the various form of hyperplasia of the prostate gland and their corresponding correlations to the latent carcinoma of the prostate gland. In all hyperplasias examined cellular atypias of different degrees of severity and a good correlation to the carcinoma were found, so that they can be regarded as precancerous in the narrower sense. The notion of the "atypical hyperplasia" should not be used, since in it too many different hyperplastic lesions are comprised. On the other hand, in every form of hyperplasia the presence of corresponding cellular atypias should be mentioned. The evidence of a hyperplasia with moderate and severe cellular atypias in the biopsy and TUR-material requires a careful treatment of the residual material by the pathologist and a search for carcinoma by the urologist. In no case it is the cause for an invasive diagnostics or surgical consequences.

Adult↗
PubMed1987

[The role of tissue steroids in benign hyperplasia and prostate cancer].

This paper presents a large body of data relating to benign prostatic hyperplasia, which have been derived from fundamental endocrinological research. For the urologist, the data open up interesting aspects of the pathomorphology of prostatic hyperplasia. The most interesting findings can be summed up as follows: 1. Testosterone is the circulating androgenic prohormone that mediates the intracellular message leading to androgen secretion, though by way of its metabolite dihydrotestosterone, which is really the active substance. 2. This metabolic conversion is catalyzed by 5 alpha-reductase, which is predominantly a stromal enzyme. 3. The estrogen metabolism in the stromal cells of the prostate may be associated with the abnormal growth of the prostate. 4. In the presence of benign prostatic hyperplasia dihydrotestosterone and 17 beta-estradiol accumulate in the nuclei of the stromal cells. 5. Adrenal androgens are also metabolized in the human prostate, yielding some substances with androgenic and some with estrogenic potency. 6. Changes in sex hormone binding globulins (SHBG) are found with age whether benign prostatic hyperplasia is present or not. It is therefore questionable whether it has any influence on the development of prostatic hyperplasia. 7. Although in some cases it is not yet possible to determine whether the findings presented in this paper have any causal significance, the data can be used as a rational basis for hormonal treatment of prostatic disease.

Adrenal Glands↗
PubMed1987

Evidence of myocyte hyperplasia in hypertrophic cardiomyopathy and other disorders with myocardial hypertrophy?

A review is presented of the mechanisms that mediate the increase in cardiac mass that occurs in patients with hypertrophic cardiomyopathy. This increase in mass is mediated by an increase in the total mass of the myocytes and the total mass of interstitial fibrous connective tissue. The increase in myocyte mass is the most important of these two components. However, it is not clear at the present time whether this increase is mediated not only by an increase in the size of the cells (hypertrophy), but also by an increase in the numbers of myocytes (hyperplasia) or by a combination of these two factors. Hyperplasia normally occurs during the prenatal phase of cardiac development and stops soon after birth, at which time hypertrophy becomes the main mechanism by which cardiac mass increases. Under certain circumstances, the ability of cardiac myocytes to synthesize DNA and undergo mitotic division can be restored; however, it is uncertain to what extent this results in complete cell division or only in either polyploidy or bi- or multinucleation. It is proposed that in hypertrophic cardiomyopathy, increased hyperplasia of cardiac myocytes occurs early in life and leads to permanently disturbed patterns of cardiac gross anatomy; it is then followed by a phase of progressive hypertrophy after the switch from hyperplastic to hypertrophic growth. It is possible that hyperplasia continues to occur after the usual time of this switch. It is also proposed that the increased number of layers of myocytes in the ventricular septum of patients with hypertrophic cardiomyopathy is a consequence of exaggerated hyperplasia during development.

Animals↗
PubMed1988

Enhancement by vagotomy of experimental induction of intestinal metaplasia and atypical glandular hyperplasia in Wistar rats.

The effect of truncal vagotomy on the induction of intestinal metaplasia and atypical glandular hyperplasia by intragastric instillation of 5% NaOH solution was investigated in Wistar rats. Truncal vagotomy resulted in significant increases in the incidences and numbers of intestinal metaplasia and atypical glandular hyperplasias in experimental week 52. Histological examinations show that unlike goblet cell metaplasia and mild atypical glandular hyperplasia in the sham-operated rats, intestinal metaplasia without Paneth cells and moderate atypical glandular hyperplasia were more frequent in rats treated with NaOH solution and vagotomy. These findings indicate that the promoting effect of truncal vagotomy on gastric carcinogenesis may be related to its enhanced effect on induction of intestinal metaplasia and atypical glandular hyperplasia.

Animals↗
PubMed1988

[Thallium-technetium scintigraphy for presurgical localization of parathyroid adenomas and hyperplasia].

The purpose of this study was to assess the value of parathyroid Thallium 201-Technetium 99m scintigraphy in 45 patients with hyperplasia or parathyroid adenomas with or without associated thyroid abnormalities. The prevalence of parathyroid abnormalities found during examination was 42/45: 36 adenomas (35 patients) and 16 hyperplasias (7 patients). Seventeen patients (38%) had thyroid abnormalities. The sensitivity and specificity of the three image analysing methods (visual analysis, simple subtraction, sophisticated subtraction) were determined by assessing answers given by 3 observers. The population was divided into 6 groups: adenomas and hyperplasias with (group I, n = 42) or without (group II, n = 25) thyroid abnormalities, adenomas alone with (group III, n = 35) or without thyroid abnormalities (group IV, n = 22), hyperplasias alone with (group V, n = 7) or without thyroid abnormalities (group VI, n = 5). The highest overall sensitivity was obtained, whichever the group, by applying the sophisticated image subtraction technique; for any given method, the best results were observed in the group comprising adenomas alone, especially without associated thyroid abnormalities. On the other hand, in the groups comprising hyperplasias alone, sensitivity was low. This leads us to conclude that, together with ultrasonography, parathyroid scintigraphy is currently the best preoperative technique for localizing parathyroid adenomas, even in the presence of associated thyroid abnormalities. However this must be carried out in conjunction with a sophisticated image subtraction technique.

Adenoma↗
PubMed1987

[Atypical hyperplasias of the endometrium].

A review of the literature concerning atypical hyperplasias of the endometrium is presented. The new pathological classifications differentiate structural abnormalities from cellular abnormalities. For atypical hyperplasias with cellular abnormalities, similar classifications to that of Richard for the cervix have been proposed: Intra Endometrial Neoplasia (IEN) grades I to III. Evolution of these lesions toward endometrial adenocarcinoma must guide the treatment. In prospective studies, atypical hyperplasias with structural abnormalities evolve into adenocarcinoma in 1.6 to 22 per cent of the cases. In atypical hyperplasia with cellular abnormalities, they evolve into adenocarcinoma in 23 to 57 per cent of the cases, according to the authors. Total hysterectomy is the treatment which is the most suitable for atypical hyperplasias with cellular abnormalities. Continuous progestational medications before menopause and the same given intermittently before menopause, represent the possible medical treatments.

Carcinoma in Situ↗
PubMed1987

Neointimal hyperplasia occurring after carotid endarterectomy in a canine model: effect of endothelial cell seeding vs. perioperative aspirin.

Neointimal hyperplasia of the arterial wall may occur after carotid endarterectomy. This proliferative lesion is a pathologic response of the injured arterial wall and may lead to progressive stenosis. We investigated the effect of endothelial cell seeding (ECS) or antiplatelet therapy with aspirin (ASA) on inhibition of this lesion in a canine model. Endarterectomies were performed in 160 carotid arteries; 46 endarterectomies were treated perioperatively with aspirin (325 mg per day), 34 were seeded with a high density (3 X 10(6)) of autogenous endothelial cells, and 80 were untreated control arteries. At selected time intervals, the patent arteries were perfusion-fixed and the cross-sectional area (measured in square millimeters) of neointimal hyperplasia was measured by means of digital planimetry. At 6 weeks, patency of the endarterectomized carotid artery was 88% in the ASA and ECS groups, in contrast to 35% in the control group (p less than 0.01). The cross-sectional area of neointimal hyperplasia was not significantly different in the ASA and the control groups at 6 weeks. However, the ECS group showed a marked reduction in neointimal hyperplasia at 6 weeks (p less than 0.01). This inhibition of neointimal hyperplasia after carotid endarterectomy by ECS may reflect accelerated luminal healing or a direct inhibition of smooth muscle cell proliferation in the injured arterial wall.

Animals↗