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PubMed2005

Laser-tonsillotomy for treatment of obstructive tonsillar hyperplasia in early childhood: a retrospective review.

INTRODUCTION: Tonsillar hyperplasia leading to dyspnea, dysphagia and other symptoms of obstruction represents a common problem especially in young children where tonsillectomy should be avoided in order to preserve the immunological function of the tonsils. Aim of the study was to assess carbon-dioxide-laser-tonsillotomy as a considered alternative procedure to reduce the tonsillar volume in these children. METHODS: Between 1993 and 2004, 109 children with tonsillar hyperplasia without former episodes of tonsillitis received laser-tonsillotomy mostly (n=98) combined with adenoidectomy. The protruding part of the tonsil was reduced by a CO2-laser. Seventy-five children were available for follow-up with a standard questionnaire. Five patients required a subsequent tonsillectomy due to a recurrence of tonsillar hyperplasia. Histological investigations were performed. Twenty-two children were reevaluated by clinical examination. RESULTS: Most of the patients were relieved from obstructive symptoms. There was no occurrence of postoperative hemorrhage or peritonsillar abscesses. The histological investigations on the specimens from later performed tonsillectomy (n=5) showed no evidence of inflammation or scar formations, but open and deep crypts. The clinical examination did not reveal any signs of chronic infections. CONCLUSION: In this retrospective study tonsillotomy with CO2-laser in early childhood leads to a long-term elimination of obstructive symptoms due to tonsillar hyperplasia with minimal discomfort for the patient while preserving normally functioning immunocompetent tonsillar tissue. Further prospective studies are planned.

Child↗
PubMed2006

Neural hyperplasia in chondrodermatitis nodularis chronica helicis.

BACKGROUND: Chondrodermatitis nodularis chronica helicis (CNCH) is a common condition characterized by tender nodules of the helix, of uncertain mechanism. The pain is not explained by current physiopathological hypotheses. OBJECTIVE: We sought to investigate possible nerve hyperplasia in CNCH. METHODS: Thirty-seven cases of clinically typical CNCH were submitted to conventional microscopy after surgical excision and analyzed with immunohistochemistry using PS100 and neurofilament antibodies. As controls, we investigated 25 tumors of the ear with the same methods. RESULTS: Large nerves (>0.1 mm in diameter) were seen in 8 of 37 cases; these were close to the cartilage or at the upper part of the ulceration. Increased numbers of small nerve sections (0.01-0.06 mm in diameter) were seen in 35 of 37 cases, with more than 20 sections per low-power field in 18 cases. Nerve hyperplasia was not observed in tumors of the ear, even in ulcerated cases. LIMITATIONS: Hypothesis based on morphologic observations. CONCLUSIONS: Nerve hyperplasia is present in CNCH, but is often masked by intense vascular and inflammatory reactions. This finding may explain the induction of pain by light pressure, whereas ulcerated auricular malignant tumors are generally painless. Certain authors believe that CNCH is an equivalent of prurigo nodularis, which interestingly also shows nerve hyperplasia.

Adult↗
PubMed2004

Longer term assessment of photodynamic therapy for intimal hyperplasia: a pilot study.

PURPOSE: To determine the potential long term (three or six months) effectiveness of photodynamic therapy (PDT) in reducing intimal hyperplasia in swine. METHODS: Intimal hyperplasia in the abdominal aortae of swine was created by a combination of fat-supplemented diet and balloon catheter injury prior to PDT. Swine were randomly allocated into one of three groups which received either: (i) both drug and light (PDT), (ii) drug only, or (iii) light only. Twenty-four hours following administration of the photosensitizer PHOTOFRIN (porfimer sodium) at 2.5 mg/kg, two distinct 1 cm spots on the posterior wall of the abdominal aorta were illuminated by an argon pumped dye laser tuned to 630 nm for an energy fluence of 120 J/cm2. After three or six months, swine were sacrificed, perfusion fixed, and had their aortae removed for light and electron microscopy. RESULTS: Intimal hyperplasia reduction following PDT persisted for the three or six months follow up period. Experimental vessels receiving PDT showed a 26.0+/-4.5% ( n = 2, ie. four spots) and 30.8+/-5.4% ( n = 1, ie. two spots) smaller percent intimal area after three or six months of recovery, respectively. Control groups receiving either light or drug only showed less than a 6% difference in percent intimal area. Medial and adventitial layers were unaffected in all groups. Electron microscopy demonstrated that the endothelium or endothelial-like cells had regenerated in both the posterior and adjacent areas of the abdominal aortae with no clear difference between them. CONCLUSIONS: These findings suggest that PDT may be beneficial in reducing intimal hyperplasia for up to three or six months in swine.

Animals↗
PubMed2005

A novel mouse model of autologous venous graft intimal hyperplasia.

BACKGROUND: To investigate the molecular mechanism of autologous venous graft intimal hyperplasia, a mouse model is needed. Currently only vein to carotid artery mouse models are available and are hampered by a high thrombosis rate. We hypothesized that operating on the aorta would lead to intimal hyperplasia with decreased risk of thrombosis. MATERIALS AND METHODS: In C57BL/6J mice, the left external jugular vein was grafted into the infrarenal abdominal aorta by end-to-end anastomosis with 11-0 Ethilon. Grafts harvested at 1, 2, 4, 8, and 16 weeks postoperatively were subjected to histological and immunohistochemical analysis. RESULTS: Thirty-one of 35 mice survived; 2 mice were sacrificed secondary to thrombosis. The percentage lumen narrowing (+/-SE) was 7.8 +/- 0.3, 16.4 +/- 0.9, 19.2 +/- 0.9, 22.3 +/- 0.8, and 23.9 +/- 1.6% at 1, 2, 4, 8 and 16 weeks, respectively. Nuclear density decreased with each successive time point. The percentage of alpha-smooth-muscle actin-positive cells within the neointima peaked at 16 weeks (53%), and the percentage of cells positive for proliferating cell nuclear antigen peaked at 2 weeks (39%). CONCLUSIONS: We thus report on a novel mouse model of intimal hyperplasia in autologous venous grafts with a low thrombosis rate. Further studies using this model, coupled with genetic and bone marrow transplantation mouse models, should lead to significant enhancement in understanding of the mechanism of intimal hyperplasia.

Animals↗
PubMed2005

Modulation of phosphatidylinositol 3-kinase signaling reduces intimal hyperplasia in aortocoronary saphenous vein grafts.

OBJECTIVES: Fifty percent of human aortocoronary saphenous vein grafts are occluded after 10 years. Intimal hyperplasia is an initial step in graft occlusion and consists of vascular smooth muscle cell proliferation. Phosphatidylinositol 3-kinase and its downstream regulator, the inositol 3-phosphatase PTEN (phosphatase and tensin homolog deleted on chromosome 10), are important regulators of vascular smooth muscle cell proliferation, migration, and cell death. This study tests whether overexpression of PTEN in aortocoronary saphenous vein grafts can reduce intimal hyperplasia. METHODS: Adult dogs underwent aortocoronary bypass grafting to the left anterior descending artery by using the autologous saphenous vein. Saphenous vein grafts were treated with phosphate-buffered saline (n = 9), empty adenovirus (n = 8), or adenovirus encoding for PTEN (n = 8). Arteriography at 30 and 90 days assessed saphenous vein graft patency. A subset received saphenous vein grafts treated with a marker transgene (beta-galactosidase, n = 3), empty adenovirus (n = 4), or adenovirus encoding for PTEN (n = 4) and were killed on postoperative day 3 to confirm expression. Vascular smooth muscle cells were isolated from canine saphenous vein infected with adenovirus encoding for PTEN, and immunoblotting and proliferation assays were performed. RESULTS: Saphenous vein graft transgene expression was confirmed by means of immunohistochemistry, immunoblotting, and polymerase chain reaction. Arteriograms revealed all saphenous vein grafts to be patent. Saphenous vein grafts treated with adenovirus encoding for PTEN demonstrated reduced intimal area compared with those treated with empty adenovirus and phosphate-buffered saline (1.39 +/- 0.11 vs 2.35 +/- 0.3 and 2.57 +/- 0.4 mm 2 , P < .05), and the intima/media ratio was lower in saphenous vein grafts treated with adenovirus encoding for PTEN (0.50 +/- 0.05 vs 1.43 +/- 0.18 and 1.11 +/- 0.14, P < .005). PTEN overexpression in vascular smooth muscle cells inhibited platelet-derived growth factor-induced phosphorylation of Akt, a downstream effector of phosphatidylinositol 3-kinase. PTEN-treated vascular smooth muscle cells demonstrated decreased basal, platelet-derived growth factor-stimulated, and serum-stimulated proliferation. CONCLUSION: This study demonstrates that PTEN overexpression in aortocoronary saphenous vein grafts reduces intimal hyperplasia. The mechanism of this antiproliferative effect in vascular smooth muscle cells is likely due to inhibition of phosphatidylinositol 3-kinase signaling through Akt, with resultant decreases in vascular smooth muscle cell growth and survival. Therefore modulation of the phosphatidylinositol 3-kinase pathway through PTEN overexpression might represent a novel therapy to prevent saphenous vein graft intimal hyperplasia after coronary artery bypass grafting.

Animals↗
PubMed2006

A clinical outcomes and cost analysis comparing photoselective vaporization of the prostate to alternative minimally invasive therapies and transurethral prostate resection for the treatment of benign prostatic hyperplasia.

PURPOSE: We critically evaluated the clinical outcomes and cost characteristics of alternative procedural treatment options for symptomatic benign prostatic hyperplasia. MATERIALS AND METHODS: An outcomes and cost analysis was performed for benign prostatic hyperplasia treatments, including photoselective vaporization, microwave thermotherapy, transurethral needle ablation, interstitial laser coagulation and transurethral resection. Clinical outcomes were measured by the percent improvement in American Urological Association/International Prostate Symptom Score, the maximum uroflowmetry rate and quality of life score. An economic simulation model was constructed to estimate the expected cost of benign prostatic hyperplasia procedural therapies from a payer perspective. The model included costs of initial treatment, followup care, adverse events and re-treatment. Sensitivity and threshold analyses tested the impact of changing model inputs on base case results. RESULTS: Ablative therapies showed better improvement in symptom score, flow rate and quality of life score compared to thermotherapy procedures. Photoselective vaporization resulted in the largest beneficial changes in American Urological Association/International Prostate Symptom Score, the maximum uroflowmetry rate and the quality of life score at all time points evaluated, followed by transurethral resection and then interstitial laser coagulation. The estimated cost was lower for photoselective vaporization than for any other procedural option at any interval studied. Sensitivity analyses indicated that the results of baseline analyses were robust to reasonable changes in clinical and economic inputs to the model. CONCLUSIONS: Compared to alternative treatment options photoselective vaporization of the prostate is a clinically efficacious and cost-effective treatment for symptomatic benign prostatic hyperplasia.

Cost-Benefit Analysis↗
PubMed2004

Pharmacologic inhibition of nitric oxide synthases and cyclooxygenases enhances intimal hyperplasia in balloon-injured rat carotid arteries.

OBJECTIVE: Extensive proliferation and migration of smooth muscle cells (SMCs) contribute to development of fibromuscular intimal hyperplasia in response to balloon catheter-induced injury of the left carotid artery in Fischer 344 rats. The purpose of the present study was to test the hypothesis that endogenously generated nitric oxide (NO) and prostaglandins act synergistically to limit the extent of neointimal hyperplasia. METHODS: The left carotid artery of Fischer 344 rats was injured with a 2F balloon catheter. The following treatment was initiated 24 hours before arterial injury, and was continued for 2 weeks: N-nitro-l-arginine (L-NA; 10 mg/kg/d, in drinking water), indomethacin (1.5 mg/kg/d per gavage), and L-NA (10 mg/kg/d) plus indomethacin (1.5 mg/kg/d). After application of an overdose of pentobarbital animals were formalin-fixed. Subsequently, paraffin-embedded cross sections of the uninjured and injured carotid arteries were analyzed morphometrically. SMC proliferation was determined by incorporation of 5-bromo-2'-deoxyuridine. RESULTS: Two weeks after injury, L-NA caused a 1.29-fold +/- 0.29-fold (mean +/- SD; n = 14; P <.05) increase in the intima-media ratio, compared with control animals, whereas indomethacin had no effect. Combined treatment with L-NA plus indomethacin further increased intima-media ratio (1.65-fold +/- 0.5-fold over control; n = 14; P <.05). SMC proliferation in the neointima of rats treated with L-NA and L-NA plus indomethacin was elevated. Furthermore, neointimal cell density (nuclei per square millimeter) was reduced after combined inhibition of cyclooxygenases and NO synthases. CONCLUSION: The present results of pharmacologic NO synthase and cyclooxygenase inhibition suggest that NO and prostaglandins are part of an endogenous growth inhibitory mechanism that synergistically suppresses intimal thickening. CLINICAL RELEVANCE: The role of cyclooxygenase-1 (COX1) and cyclooxygenase-2 (COX2) during vascular recurrent stenosis and atherosclerosis is not clear yet. In particular, the effects of selective COX2 inhibitors on the frequency of cardiovascular events is still controversial. It is shown here in rats that the application of a non-selective COX inhibitor does not affect arterial stenosis. However, the concurrent inhibition of endogenous nitric oxide generation and COX1 or COX2 causes overshooting neointimal hyperplasia. These results suggest that increased vascular stenosis can result from administration of drugs that pharmacologically block 2 or more inhibitory pathways that normally counterbalance the effect of promotors of neointimal hyperplasia.

Angioplasty, Balloon↗
PubMed2005

Neointimal hyperplasia on a cell-seeded polytetrafluoroethylene graft is promoted by transfer of tissue plasminogen activator gene and inhibited by transfer of nitric oxide synthase gene.

OBJECTIVE: The objective of this study was to examine the effect of tissue plasminogen activator (tPA) and endothelial nitric oxide synthase (eNOS) on thrombosis and neointimal hyperplasia on a polytetrafluoroethylene (PTFE) graft seeded with smooth muscle cells (SMCs). METHODS: SMCs retrovirally transduced with tPA and eNOS genes were seeded on PTFE grafts and then implanted into the infrarenal rabbit aorta. Thrombosis and neointimal hyperplasia on the grafts were examined after 30 and 100 days of implantation. RESULTS: At 30 days of implantation, thrombus was observed on the luminal surface of both unseeded and SMC seeded control grafts, whereas grafts seeded with SMCs secreting tPA were nearly free of thrombus. At 100 days, the neointima on grafts seeded with tPA transduced SMCs was significantly thicker (925 +/- 150 microm, n = 5) than neointima on the other grafts (range, 132 to 374 microm; P < .001). Neointima thickness on grafts seeded with eNOS transduced SMCs (154 +/- 27 microm) was similar to that of unseeded grafts (132 +/- 16 microm, P > .05); both were thinner than those on grafts seeded with SMCs transduced with only lacZ gene (287 +/- 35 microm). The ratio of seeded cells in the neointima was significantly higher on SMC/tPA grafts (46% +/- 8%) than SMC/NOS grafts (21% +/- 6%, P < .05), indicating tPA transduced cells proliferated more than eNOS transduced cells. CONCLUSIONS: Engineered tPA expression in seeded SMCs causes significantly more neointimal hyperplasia, despite the favorable inhibition of luminal thrombus. eNOS expression in the seeded cells inhibits neointimal hyperplasia.

Animals↗
PubMed2006

Inhaled carbon monoxide inhibits intimal hyperplasia and provides added benefit with nitric oxide.

OBJECTIVE: Carbon monoxide (CO) and nitric oxide (NO) have both been shown to possess vasoprotective properties. NO has successfully inhibited intimal hyperplasia in both small-animal and large-animal experimental models, whereas CO has only been studied in rodents. Evidence suggests that these two molecules may exert their vascular effects through common as well as unique signaling pathways. The purpose of this study was to determine the effect of a low concentration of inhaled CO on intimal hyperplasia in a large-animal model and if CO and NO treatment could exert a synergistic effect to inhibit this process. METHODS: Balloon angioplasty was performed in a porcine model. Animals received inhaled CO (250 ppm) delivered preoperatively for 60 minutes or preoperatively and intraoperatively. Blood was collected for carboxyhemoglobin (COHgb) measurements at the start of the operation and every 30 minutes during the operation. Heart rate, respiratory rate, and oxygen saturation were monitored throughout. To study the effect of combined CO and NO treatment, another group of pigs received inducible NO synthase (iNOS) gene transfer in one iliac artery and control gene transfer (AdlacZ) in the contralateral iliac artery, with or without preoperative and intraoperative inhaled CO. Adenoviral infection was performed immediately after balloon injury. All animals were euthanized at 3 weeks, and iliac arteries were collected for histologic and morphometric analysis. RESULTS: One hour of pretreatment with CO was associated with modest and transient elevations in COHgb levels, resulting in a 25.6% reduction in neointimal area and a 10% reduction in intimal area/medial area ratio (I/M) 3 weeks after injury (NS). In contrast, preoperative followed by intraoperative CO administration increased COHgb in a sustained fashion and inhibited neointima formation by 51.7% and I/M by 31% (P < .001). There was no evidence of toxicity associated with this administration of CO. The treatment of injured iliac arteries with the control adenoviral vector AdlacZ did not further increase the inhibitory effect of CO on intimal hyperplasia. The combination of inhaled CO and iNOS gene transfer resulted in greater protection, however, with a 64% reduction in neointimal area and a 48% reduction in I/M (P < .001). CONCLUSIONS: CO is an effective means of reducing intimal hyperplasia in large animals after vascular injury when delivered during the operative procedure. No toxicity was associated with the increase in COHgb. The combination of CO and NO provided additional protection against the vascular injury response, with a greater reduction in neointima formation. These data suggest that these agents may prove to be clinically beneficial in prolonging vascular patency after interventions.

Adenoviridae↗
PubMed2005

Rosiglitazone reduces serum homocysteine levels, smooth muscle proliferation, and intimal hyperplasia in Sprague-Dawley rats fed a high methionine diet.

Homocysteine (Hcy) is a metabolite of the essential amino acid methionine. Hyperhomocysteinemia is associated with vascular disease, particularly carotid stenosis. Rosiglitazone, a ligand of the peroxisome proliferator-activated receptor gamma , attenuates balloon catheter-induced carotid intimal hyperplasia in type 2 diabetic rats. We studied 4 groups (n = 7 per group) of adult female Sprague-Dawley rats fed (a) powdered laboratory chow (control), (b) control diet with rosiglitazone (3.0 mg/kg/d), (c) diet containing 1.0% l -methionine, and (d) diet containing methionine and rosiglitazone. After 1 week on high methionine diet, the rats were administered an aqueous preparation of rosiglitazone by oral gavage. One week after initiation of rosiglitazone, balloon catheter injury of the carotid artery was carried out using established methods, and the animals continued on their respective dietary and drug regimens for another 21 days. At the end of the experimental period, blood samples were collected, and carotid arteries and liver were harvested. Serum Hcy increased significantly on methionine diet compared with controls (28.9 +/- 3.2 vs 6.3 +/- 0.04 micromol/L). Development of intimal hyperplasia was 4-fold higher in methionine-fed rats; this augmentation was significantly reduced ( P < .018) in rosiglitazone-treated animals. Rosiglitazone treatment significantly ( P < .001) suppressed Hcy levels and increased the activity of the Hcy metabolizing enzyme, cystathionine-beta-synthase in the liver samples. Hcy (100 micromol/L) produced a 3-fold increase in proliferation of rat aortic vascular smooth muscle cells; this augmentation was inhibited by incorporating rosiglitazone (10 micromol/L). After balloon catheter injury to the carotid artery of animals on a high methionine diet, there was an increase in the rate of development of intimal hyperplasia consistent with the known effects of Hcy. It is demonstrated for the first time that the peroxisome proliferator-activated receptor gamma agonist rosiglitazone can attenuate the Hcy-stimulated increase in the rate of development of intimal hyperplasia indirectly by increasing the rate of catabolism of Hcy by cystathionine-beta-synthase and directly by inhibiting vascular smooth muscle cell proliferation. These findings may have important implications for the prevention of cardiovascular disease and events in patients with hyperhomocysteinemia (HHcy).

Animals↗
PubMed2006

Different inflammatory response and oxidative stress in neointimal hyperplasia after balloon angioplasty and stent implantation in cholesterol-fed rabbits.

Inflammatory responses appear to play an important role in the occurrence of restenosis following coronary intervention. However, the contribution of C-reactive protein (CRP) and oxidative stress to restenosis after balloon angioplasty and stent implantation remains unclear. The aim of this study was to examine this issue using hyperlipidemic rabbits. Rabbits were divided into two groups; they were fed with a 0.5% cholesterol diet and with a mixed 0.5% cholesterol and 0.5% probucol diet. Each group of rabbits underwent balloon injury and stent implantation in right and left iliac arteries, respectively. Eight weeks after the intervention, we examined luminal stenosis, neointimal hyperplasia, immunoreactivity for macrophage, CRP and oxidized phosphatidylcholine (oxPC), and also the expression of CRP mRNA. The degrees of neointimal hyperplasia and immunopositive areas (%) for macrophage, CRP, and oxPC in the neointima were significantly higher after stent implantation than after balloon injury, but CRP mRNA was undetectable in either artery. Anti-oxidant probucol reduced angiographic stenosis, neointimal hyperplasia, and macrophage- and oxPC-positive areas much more significantly after stenting. The results demonstrate that the inflammatory response to the development of neointimal hyperplasia differs after balloon injury and stent implantation and that CRP deposition and oxidative stress might be involved more significantly in neointimal development after stent implantation.

Angioplasty, Balloon↗
PubMed2006

Focal myointimal hyperplasia of mesenteric veins is associated with previous trauma in surgical specimens.

Idiopathic myointimal hyperplasia of mesenteric veins (IMHMV) is a rare and poorly understood disease that occurs in the rectosigmoid colon of predominantly young, previously healthy, male patients. This disease is often confused with chronic idiopathic inflammatory bowel disease clinically, and pathologists may miss the diagnosis unless elastin stains are performed because diseased veins may readily be mistaken for arteries. The etiology of IMHMV is unclear, but a traumatic pathomechanism resulting in arterialization of the veins has been proposed. Review of bowel resection specimens (n=68) for non-neoplastic disease within a 1-year period in patients younger than 50 years of age revealed 10 cases with focal mesenteric vein myointimal hyperplasia. Significantly more cases with focal myointimal hyperplasia of mesenteric veins (MHMV) were associated with pre-resection trauma to the involved bowel segment (5/11 vs. 5/57; p=0.0016). A significant association of MHMV with pre-resection trauma supports the hypothesis that idiopathic myointimal hyperplasia of the mesenteric veins may be the result of trauma through torsion/stretching of the sigmoid colon and, subsequently, increased mesenteric venous pressure through arterialization.

Adult↗
PubMed2004

Intraoperative PTH monitoring in parathyroid hyperplasia requires stricter criteria for success.

BACKGROUND: Intraoperative parathyroid hormone (IOPTH) monitoring in parathyroidectomy for multigland disease is less clear than for single-gland disease. This study assesses the role of IOPTH for hyperplasia. METHODS: A prospective database revealed 45 patients with hyperplasia undergoing parathyroidectomy utilizing IOPTH from February 1999 to August 2003. RESULTS: Twenty-six females and 19 males had a mean age of 55 years. Twenty-two patients underwent total parathyroidectomy. Twenty-three patients underwent subtotal parathyroidectomy. Twenty-seven patients (60%) had a drop of IOPTH greater than 50% at 10 minutes after removal of all presumably abnormal parathyroid tissue. Nine additional patients (20%) had an IOPTH drop greater than 50%, but continued exploration revealed more abnormal tissue. Nine patients failed to decrease greater than 50%, and exploration was continued. A final IOPTH less than 35 pg/mL or a greater than 90% decrease from baseline was predictive of a successful operation in 40 patients. The 5 patients who did not meet this criteria remained hyperparathyroid. CONCLUSIONS: IOPTH identifies sporadic hyperplasia and guides completeness of resection for patients with known hyperplasia. However, more rigid criteria are required than for adenomas. Failure to achieve appropriate decreases in IOPTH should prompt further neck exploration or a search for a mediastinal gland.

Female↗
PubMed2006

Effect of AP-1 decoy using hemagglutinating virus of Japan-liposome on the intimal hyperplasia of the autogenous vein graft in mongrel dogs.

Intimal hyperplasia is the leading cause of late vein graft failure. Smooth muscle cell proliferation and migration is the underlying mechanism. Pharmacological approaches to prolong vein graft patency have produced limited results. AP-1 proteins play a role in the expression of many genes involved in cellular proliferation and cell cycle progression. Previously we reported inhibition of vascular smooth muscle cell migration, proliferation, and intimal hyperplasia in the balloon-injured rat carotid artery using an AP-1 decoy with HVJ-liposomes. In this report, we evaluated the effect of the AP-1 decoy on intimal hyperplasia in a large animal model. The jugular vein was transfected with hemagglutinating virus of Japan-liposomes containing the AP-1 decoy or scrambled oligonucleotides. An interposition graft was performed with the pretreated jugular vein between the transected femoral arteries. The graft was harvested at 16 weeks after the procedure. The intimal area was compared: the intimal area of the AP-1 decoy-treated versus control group was 47.3 +/- 15.2 versus 102.3 +/- 15.9 (P < .05), respectively. In conclusion, AP-1 decoy using HVJ-liposomes effectively prevented intimal hyperplasia of an autogenous vein graft in mongrel dogs.

Animals↗
PubMed2004

Mirror image condylar hyperplasia in two siblings.

A Hispanic family with an unusual clinical and radiological pattern of condylar hyperplasia is presented. Mirror images of condylar hyperplasia, malocclusion of teeth, and shift of midline of the mandible were seen in two brothers. The father had a similar abnormality of his left mandibular condyle. The condylar hyperplasia in this family indicates that mandibular condylar hyperplasias could be genetic in origin, possibly Y-linked or autosomal dominant.

Adult↗
PubMed2004

Biologic feature of prostatic hyperplasia developed in spontaneously hypertensive rats.

OBJECTIVES: To investigate alterations in cell kinetic and cellular composition in prostatic hyperplasia developed in spontaneously hypertensive (SH) rats from 15 to 54 weeks of age. METHODS: Male SH rats (n = 20) and their normotensive counterparts, Wistar-Kyoto rats (n = 20), were studied. At 15, 29, 40, and 54 weeks of age, the ventral prostate was obtained to evaluate (a) cell proliferation by the proliferation index using proliferating cell nuclear antigen immunostaining and (b) apoptosis by the apoptotic index using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling assay. The percentage of area density of smooth muscle and fibroblastic tissues was determined with a computerized image analysis system after alpha-actin and vimentin immunostaining, respectively. RESULTS: Compared with the data in the Wistar-Kyoto rats during the observation period, a significantly increased proliferation index in both epithelium and stroma (P <0.01) and a slightly increased apoptotic index in the epithelium without apoptotic cells in the stroma, with an imbalance in favor of cell proliferation, were noted in the prostatic hyperplasia of the SH rats. The value of the proliferation index was greatly increased in both the epithelium and the stroma of the SH rats between 15 and 29 weeks (P <0.05) but continued relatively steady from 29 to 54 weeks. A significantly increased percentage of smooth muscle area (P <0.01) and a much greater percentage of area density of smooth muscle than that of fibroblastic tissues (P <0.01) were observed in the prostatic hyperplasia of the SH rats. CONCLUSIONS: The prostatic hyperplasia of SH rats may develop from both epithelial and stromal growth and could ultimately be promoted by an imbalance in favor of proliferative activity.

Age Factors↗
PubMed2006

Development of nomogram to predict acute urinary retention or surgical intervention, with or without dutasteride therapy, in men with benign prostatic hyperplasia.

OBJECTIVES: To develop a prediction model, or nomogram, that would predict the probability that a man with benign prostatic hyperplasia would experience acute urinary retention (AUR) or require surgical intervention (SI) within 2 years, with or without dutasteride therapy. METHODS: We modeled 4294 men treated in the Phase III dutasteride benign prostatic hyperplasia trials. These men were characterized at baseline by a number of parameters, including the American Urological Association Symptom Index, Benign Prostatic Hyperplasia Impact Index questionnaire, prior use of selective alpha1-blockers, prostate volume, prostate-specific antigen level, and maximal flow rate. Cox proportional hazards regression analysis was used to relate these baseline variables to their future probability of AUR/SI within 2 years. The nomogram was internally validated with bootstrapping to assess its discrimination and calibration. Discrimination was quantified as the concordance index. RESULTS: The nomogram appeared to be accurately calibrated and discriminating (concordance index 0.71, P <0.001). CONCLUSIONS: We constructed a nomogram for predicting the probability that a man would experience AUR or require SI within 2 years of benign prostatic hyperplasia diagnosis. At 24 months of follow-up, 7.4% of placebo patients and 3.7% of dutasteride patients had experienced AUR and/or SI, representing a 50% relative risk reduction and a 3.7% absolute risk reduction. For the greatest risk patient randomized to the Phase III dutasteride trial, the nomogram predicted a maximal risk of 27%, significantly greater than the median risk of the placebo-treated patients.

Acute Disease↗
PubMed2004

Retinoid-induced epidermal hyperplasia in human skin organ culture: inhibition with soy extract and soy isoflavones.

Organ cultures of human skin were incubated for 8 days with 1 microg/ml 14-all trans retinoic acid (14-all trans RA) and concomitantly treated with varying concentrations of soy extract. The epidermis of organ cultures treated with 14-all trans RA alone underwent a hyperplastic response. In cultures treated with a combination of 14-all trans RA and soy extract (4-40 microg/ml), hyperplasia was reduced by 16-41%. The same concentrations of soy extract that reduced epidermal hyperplasia in organ culture also suppressed proliferation of rapidly growing keratinocytes in monolayer culture (approximately 25% reduction at 20 and 40 microg/ml). On the other hand, soy extract did not further inhibit proliferation of quiescent keratinocytes; rather, it stimulated growth (50-52% increase relative to control). When dermal fibroblasts were examined for a response to soy extract (i.e., proliferation and synthesis of type I procollagen), both responses were stimulated (proliferation: 75% increase and collagen production 114% increase relative to control). Genistein, the major isoflavone in extracts of soy also inhibited epidermal hyperplasia in organ culture (34-40% reduction relative to control). The same concentrations that reduced epidermal hyperplasia (0.5-1.0 microg/ml) also inhibited keratinocyte proliferation in monolayer culture but had little effect on fibroblast growth. Two other isoflavones (daidzein and glycetein) were also inhibitory, but were less effective than genistein. Taken together, these data suggest that use of soy extract or its constituent isoflavones in conjunction with 14-all trans RA may provide a way to mitigate unwanted epidermal effects of topical retinoid therapy without compromising beneficial retinoid effects in the dermis.

Cell Proliferation↗