Proliferation Of Collagen Fibers Research Articles

Liver Histopathology of the Southern Watersnake, Nerodia fasciata fasciata, Following Chronic Exposure to Trace Element-Contaminated Prey from a Coal Ash Disposal Site

Previous studies have demonstrated the accumulation of arsenic, cadmium, selenium, strontium, and vanadium in livers of Southern Watersnakes fed fish from a coal-ash contaminated site. Our study is the first to investigate effects of trace element accumulation on cytology of snake liver. Snakes were born in the laboratory and raised for one or two years on diets consisting of varying proportions of contaminated fish. The majority (71%) of snakes fed contaminated prey did not exhibit any differences in liver histology when compared to control snakes fed an uncontaminated diet. In the remaining contaminant-exposed snakes, some aberrations were noted. The most prevalent pathology involved the proliferation of collagen fibers that resulted in narrowing or occlusion of sinusoids and increasing the mass of the intersinsuoidal parenychma. Fibrosis of the liver as a result of chronic injury has been reported previously in reptiles, but this is the first report that links such tissue damage to dietary contamination.

Enhanced Expression of Heat Shock Protein 47 in Rat Model of Peritoneal Fibrosis

Peritoneal fibrosis is one of the serious complications of continuous ambulatory peritoneal dialysis therapy and is characterized by collagen accumulation. Heat shock protein 47 (HSP-47) is a collagen-specific molecular chaperon and is closely associated with collagen synthesis; however, the involvement of HSP-47 in the progression of peritoneal fibrosis is not fully understood. To examine the serial pathological alterations caused by peritoneal fibrosis, we made an experimental model of peritoneal fibrosis by daily intraperitoneal injection of chlorhexidine gluconate (CG) in rats for 28 days and examined the expression of HSP-47 together with that of types I and III collagen, alpha-smooth muscle actin (aSMA), and ED-1 (a marker for macrophages) using immunohistochemistry. Rats treated with saline containing 15% ethanol were used as the control group. In the control group, the peritoneal tissue was slightly thickened and HSP-47 was expressed in the peritoneum at day 28. In the CG group, the peritoneal tissue serially became thickened and fibrotic. The expression of HSP-47 was evident in mesothelial cells and submesothelial connective tissue after day 7 of treatment with CG, and increased thereafter. The expression of types I and III collagen and aSMA was proportionally strengthened during our experiments. ED-1-positive cells were present in thickened areas with abundant proliferation of collagen fiber. The number of cells positive for ED-1 increased gradually and reached a maximum at day 21. Our results indicate that, in a rat experimental model of peritoneal fibrosis, the expression of HSP-47 is associated with the progression of peritoneal fibrosis.

Ultrastructure of intramural coronary arteries in pigs with hypertrophic cardiomyopathy

Pigs with hypertrophic cardiomyopathy diagnosed by echocardiographic examination were selected for study from a genetic breeding herd. Under dissecting microscopic examination, intramural coronary arteries in the septum and left ventricular free wall of euthanized pigs were collected for ultrastructural study. The major lesions of wall thickening included degeneration or denudation of endothelium, subendothelial edema, proliferation of collagen fiber, and hyperplasia of smooth muscle cells. Smooth muscle cells proliferated and migrated through the internal elastic lamella into the intima, which caused the early lesion of wall thickening of the intramural coronary arteries. The extent of smooth muscle cell proliferation was related to the severity of endothelial damage. The smooth muscle cells in the intima were identified by immunohistochemical staining (i.e., smooth muscle actin [SMA] stain). Three major types of severe wall thickening with narrow lumen were observed in the intramural coronary arteries. Edema in the intima caused the major lesion of Type I wall thickening. The internal elastic lamella was broken into small interrupted fragments, and fine fragments of elastic fibers surrounded by the cellular processes of smooth muscle were observed in Type I lesions. Many smooth muscle cells proliferated in the intima and media, which constituted the major lesion of Type II wall thickening of the intramural coronary arteries. Many vacuolized, degenerated smooth muscle cells with fewer sarcoplasmic myofilaments could be clearly observed in the Type II lesions. In advanced cases, severe vacuolization and degeneration of smooth muscle cells with the presence of many bizarrely shaped smooth muscle cells in the walls of the intramural coronary arteries could be observed, which caused the major lesion of Type III wall thickening. Pigs with hypertrophic cardiomyopathy, characterized by spontaneously occurring lesions in intramural coronary arteries, may prove a valuable animal model for human disease.

Distribution pattern of versican, link protein and hyaluronic acid in the rat periodontal ligament during experimental tooth movement.

The ability of the periodontal ligament (PDL) to rapidly remodel is the basis of orthodontic tooth movement. During the tooth movement, matrix proteoglycans (PGs) may play important roles in spatial, mechanical and biological aspects for the maintenance and repair of the PDL. The aim of this study was to characterize the distribution of a large hyaluronic acid (HA)-binding proteoglycan, versican, link protein (LP) and HA in the rat molar PDL during experimental tooth movement by histochemical and immunohistochemical methods. Experimental tooth movement was performed according to Waldo's method. Histologically, regressive changes, such as decrease of fibroblasts and collagen fibers and exudative change of edema were observed in the compressive side and progressive changes, such as proliferation of fibroblasts and collagen fibers, in the strain side one day after treatment. By 3 days after tooth movement, regressive or progressive changes were not observed in either side. Using monoclonal antibodies specific to versican core protein or LP, the positive immunoreactivity for both molecules was constantly observed throughout the PDL. After the experimental force was applied to the tooth, however, the immunostainings of versican and LP became significantly intense only in the compressive side but decreased in the strain side. The intensity in the compressive side was strongest one day after the force was applied and gradually diminished thereafter. HA of both sides did not change during experimental tooth movement. Since HA is present in the PDL, large amounts of versican and LP expressed in the compressive side may create large hydrated aggregates via their association with HA that dissipates the compressive force applied to this tissue.

Effects of ecabet sodium on experimentally induced reflux esophagitis

We investigated the effects of ecabet sodium on experimentally induced reflux esophagitis in rats. Three groups of rats, i.e., a control group, esophagitis group, and an ecabet sodium group (25mg/kg given twice daily) were used. The number of animals which developed esophagitis, the extent of the lesions, and the esophagitis lesion index were assessed 3 weeks after the start of the experiment, and the lesions were evaluated histopathologically. All nine surviving rats in the esophagitis group developed esophagitis, and the esophagitis lesion index was 32.6 +/- 7.2 (mean +/- SE) per animal. Histopathologically, thickening of the epithelium, elongation of papillae of the lamina propria into the epithelium, and infiltration of the lamina propria by lymphocytes, eosinophils, plasmacytes, and neutrophils, were observed. Interruption of the lamina of the muscularis mucosae was also observed, and there was marked proliferation of collagen fibers in the submucosa and lamina propria. In the ecabet sodium group, esophagitis developed in five of the nine surviving animals (55.6%), but the esophagitis lesion index was 1.89 +/- 0.73 per animal, which was significantly lower than that in the esophagitis group. The histopathological changes in the rats which developed esophagitis were milder in the ecabet sodium group than in the esophagitis group. These results suggest that ecabet sodium could be useful for the prevention of reflux esophagitis.

The Effect of Mitomycin-C on the Healing Process in Rabbit Extraocular Muscle Surgery

One of the most serious complications following extraocular muscle surgery is formation of postoperative adhesions that may result in restrictive ocular motility dysfunction. The effect of mitomycin-C (MMC) on postoperative wound healing in extraocular muscle surgery was investigated. Sixteen albino rabbits (24 eyes) were used and anesthetized with ketamine and xylazine. These rabbits were divided into 3 groups; (1) control group (balanced salt solution (BSS) exposure for 5 minutes), (2) Group 1 (0.5 mg/ml MMC exposure for 1 minute) and (3) Group 2 (0.5 mg/ml MMC exposure for 5 minutes). After 3 mm recession of superior rectus muscle, MMC or BSS was applied using Weck-Cel sponge (Solan, Jacksonville, FL). The reduction of fibroblast and collagen fiber proliferation were evaluated histopathologically with light microscope at 1, 2, 4 and 8 weeks after operation. We also evaluated the amount of basic fibroblast growth factor (bFGF) by immunohistochemical study at the same time. Histopathologically, there was a more significant reduction of fibroblast and collagen fiber proliferation in Group 1 and 2 than the control group. Immunohistochemically, Group 1 and 2 showed lesser expression of bFGF than the control group. But, there was no difference between Group 1 and 2. Topical intraoperative application of mitomycin C in extraocular muscle surgery may reduce postoperative adhesions.

Study of the accelerating effect of shikonin and alkannin on the proliferation of granulation tissue in rats.

The present study was carried out to compare the accelerating effect of shikonin and alkannin and to elucidate the expression of CD antigen and histological changes on the proliferation of granulation tissue in rats. Shikonin and alkannin produced a dose-dependent acceleration of the cotton pellet-induced granuloma formation and this accelerating potency of both compounds on the proliferation of granulation tissue was about the same 5 and 10 d after implantation of the cotton pellet. Also, both compounds increased the ratio of CD11b+ cells in the granulation tissue 5 and 10 d after implantation of the cotton pellet. Both compounds increased the expression of CD11b+ cells with granulocytes such as macrophages and histiocytes, and then accelerated the proliferation of fibroblasts and collagen fiber. On the other hand, neither compound increased the ratio of CD3+ cells in the granulation tissue after 5 and 10 d. These results suggest that shikonin and alkannin accelerate the proliferation of granulation tissue induced by the cotton pellet and this accelerating effect may be attributed to an increase in the expression of CD11b+ cells, and the acceleration of the proliferation of fibroblasts and collagen fiber in the granulation tissue.

Mechanism of aneurysm formation after 830-nm diode-laser-assisted microarterial anastomosis.

The process of aneurysm formation after laser welding is described. The mechanism of aneurysm formation after laser-assisted microarterial anastomosis is presently unclear. A series of 830-nm diode-laser-assisted longitudinal aortorrhophy with a condition of 400 to 500 J/mm2 for 1 cm length of anastomosis versus conventional manual anastomoses were performed in 90 Wistar rats. To compare this technique with normal media process, a histologic examination of aneurysm formation was conducted. The results show that there are two important factors that cause aneurysm formation after laser-assisted anastomosis: 1) the vessel wall is damaged by laser heating; 2) proliferation of collagen fiber at the adventitia is absent during media reconstruction.

Effect of CO2 laser on healing of cultured meniscus.

A new method to improve cartilage repair is clinically important. The enhancement of meniscal healing by low power CO2 laser was investigated in an organ culture system. A longitudinal or a radial defect was made in the avascular zone of rabbit menisci. Irradiation by CO2 laser with 1 W (energy density 50 J/cm2) and 2 W (energy density 100 J/cm2) was used. Histologic and scanning electron microscopic evaluations revealed that both energy densities of laser irradiation and the type of and the site of meniscal defect can influence the course and the outcome of meniscal healing. A marked increase in fibrochondrocytic proliferation and regeneration of collagen fibers were demonstrated in the meniscal defects irradiated by 100 J of CO2 laser energy. The healing of meniscal defects could be promoted by low power CO2 laser irradiation.

Mechanism research of cryoanalgesia.

The sciatic nerves of rabbits were frozen at different temperatures (-20 degrees C, -60 degrees C, -100 degrees C, -140 degrees C, and -180 degrees C). The morphology and function of the frozen nerves were examined with light microscopy (hematoxylin and eosinophilin stain and a histochemical thiocholine method) and electron microscopy. The function of the nerve after freezing was assessed using short latency somatosensory evoked potentials, sensory conduction velocity, and electromyogram at various intervals after freezing. There were no changes in morphology or function of nerves cryolesioned at -20 degrees C. The nerve fibers cryolesioned at -60 degrees C showed signs of freezing degeneration and lost their conductive function although, these nerves all recovered. Approximately half of nerve fibers cryolesioned at -100 degrees C showed Wallerian degeneration, and although the time to remyelination was delayed, nerve regeneration was still complete. At -140 degrees C and -180 degrees C the nerve fibers showed immediate necrosis, with destruction of basal membranes and proliferation of collagen fibers. The results explained the mechanism of cryoanalgesia. Our study demonstrates that cryo-temperatures lower than -140 degrees C will cause permanent alterations in nerve morphology and function, whereas warmer temperatures do not result in permanent nerve damage and are therefore not likely to provide long-term analgesia to patients.

Granuloma After Augmentation of the Eyelids with Liquid Silicone

Granuloma after liquid silicone augmentation of the upper eyelids was studied by light and electron microscopy and energy dispersive x-ray analysis. Light microscopy showed proliferation of collagen fibers and many phagocytic macrophages with vacuoles. Electron microscopy showed many vacuoles in phagocytic macrophages, fragmentary myofibrils, and proliferation of collagen fibers. Vacuoles in phagocytic macrophages contained silicone that was demonstrated by energy dispersive x-ray analysis. The present case suggests that liquid silicone injection in the eyelid can induce degeneration of the orbicularis oculi muscle in addition to granuloma formation.

Abnormally Shaped Arteries in the Intestine of Children with Hirschsprungʼs Disease

Abnormally shaped arteries were found in the intestines of 17 of 62 patients (27%) with Hirschsprung's disease. The histological characteristics of abnormal arteries included proliferation of collagen fibers and smooth muscle cells in the adventitia. The incidence of abnormal arteries in each type of aganglionosis was as follows: 25% (13 of 51) in short-segment aganglionosis; 0% (0 of 6) in long-segment aganglionosis; and 80% (4 of 5) in total-colon or extensive aganglionosis. The older the patients were at the time of resection, the higher the incidence of abnormal arteries (< 1 year old, 15%; 1-3 years old, 38%; > 3 years old, 75%). The abnormally shaped arteries were mostly located in the histological transitional zone. These findings suggest the following possibilities: (a) the craniocaudal migration of ganglion cells was interrupted by intestinal ischemia in the presence of abnormal arteries in utero; (b) an ischemic episode caused both the disappearance of neural cells and dysplasia of the artery; (c) the ganglion cells were destroyed by mild ischemia caused by the abnormal arteries; or (d) the tension caused by mechanical expansion resulted in a change in the vascular walls in the transitional zone.

Abnormally Shaped Arteries in the Intestine of Children with Hirschsprung's Disease

SummaryAbnormally shaped arteries were found in the intestines of 17 of 62 patients (27%) with Hirschsprung's disease. The histological characteristics of abnormal arteries included proliferation of collagen fibers and smooth muscle cells in the adventitia. The incidence of abnormal arteries in each type of aganglionosis was as follows: 25% (13 of 51) in short‐segment aganglionosis; 0% (0 of 6) in long‐segment aganglionosis; and 80% (4 of 5) in totalcolon or extensive aganglionosis. The older the patients were at the time of resection, the higher the incidence of abnormal arteries (&lt;1 year old, 15%; 1–3 years old, 38%; &gt;3 years old, 75%). The abnormally shaped arteries were mostly located in the histological transitional zone. These findings suggest the following possibilities: (a) the craniocaudal migration of ganglion cells was interrupted by intestinal ischemia in the presence of abnormal arteries in utero; (b) an ischemic episode caused both the disappearance of neural cells and dysplasia of the artery; (c) the ganglion cells were destroyed by mild ischemia caused by the abnormal arteries; or (d) the tension caused by mechanical expansion resulted in a change in the vascular walls in the transitional zone.

Effects of treated paper mill effluents on hepatic morphology in male bullhead (Cottus gobio L.)

The effects of paper mill effluents on histological, enzyme histochemical and ultrastructural parameters of the liver of male bullhead (Cottus gobio L.) were investigated in an alpine river at the end of the low-water period (in March). Histological examination revealed a marked depletion of glycogen, necrosis of single hepatocytes and a high degree of liver parasitization. The enzyme histochemical tests for acid phosphatase and nonspecific esterase signaled lysosomal alterations. Ultrastructural findings showed a loss of cellular compartmentalization, lysosomal alterations, proliferation of smooth endoplasmic reticulum and peroxisomes, proliferation of collagen fibers in the space of Disse, and hepatic cell necrosis. Histological examination revealed a marked improvement in the condition of the liver after the high-water period.

Pathology of chemically induced chronic active hepatitis in mice

Female Swiss mice were treated for 24 weeks, with 3-hydroxy-4-pyrone (Py) added to their powdered diet at 0.5% (wt/wt), and the effects of this agent on the liver were examined. Serum transaminases (especially GPT) rose continuously, while the GOT/GPT ratio remained at approximately 1.0 throughout the study period. The characteristic changes found from 8 weeks onward were piecemeal necrosis and bridging necrosis of the hepatocytes with dense lymphocytic infiltration. Proliferation of collagen fibers in the portal tracts and formation of narrow fibrous septa dividing the lobules into pseudolobules were also noted from 12 weeks onward. A large number of the infiltrating lymphocytes were identified as T cells by immunohistochemical and electron microscopic studies. These lymphocytes often surrounded or were closely attached to degenerating hepatocytes. Focal apoptosis and necrosis accompanied by a granulomatous reaction of the centrilobular hepatocytes were noted as early changes in the liver. Our findings indicate that the hepatic changes produced in mice by long-term Py administration have characteristics in common with those of human chronic active hepatitis. Immunological cytotoxic mechanisms, especially T cell-mediated ones, appear to play an essential role in the development of hepatic lesions in this murine model of chronic active hepatitis.

Microscopic and immunohistological studies on intimal hyperplasia of the arterially implanted autovein graft and its anastomosis in dogs.

The fate of intimal hyperplasia of arterially implanted autovein bypass grafts and their distal end-to-side anastomoses in dogs was studied microscopically and immunohistologically. The bypass grafting was done under conditions of abnormal blood flow and high peripheral resistance. Intimal hyperplasia of the graft first became evident 7 days after implantation and the thickness increased to about 500 microns 3 months or more after the implantation. The intimal hyperplasia was related to an active proliferation of smooth muscle cells which proved positive for alpha-smooth muscle actin staining. Moreover, it was more dominant at the toe and heel of the anastomosis and moderately apparent on the floor of the host artery. The constituent elements of the hyperplastic intima at the anastomosis were fibroblast-like cells and extracellular collagen fibers which were negative for alpha smooth muscle actin staining. This study revealed that the features of intimal hyperplasia at the distal anastomosis in autovein bypass grafting differed from those of the implanted autovein graft itself; the former being related to excessive proliferation of fibroblasts and collagen fibers while the latter displayed an active proliferation of smooth muscle cells.

Effects of growth factors on proliferation of cultured human peritoneal mesothelial cells

Loss of ultrafiltration during continuous ambulatory peritoneal dialysis (CAPD) is often caused by the structural peritoneal membrane alteration, namely the disappearance of mesothelial cells and the proliferation of peritoneal collagen fibers. The interleukin hypothesis has been proposed to explain the etiology of peritoneal fibrosis. The CAPD procedure has been shown to induce macrophages and lymphocytes in the peritoneum, resulting in the production of interleukin-1 (IL-1) and interferon-gamma (IFN-gamma), which may be promote to the development of peritoneal fibrosis. On the other hand, the mesothelial defect can be rapidly restored by proliferation of mesothelial cells implanted on the wound surface. In this study, we demonstrated that IL-1 beta, IFN-gamma, epidermal growth factor (EGF) and platelet derived growth factor (PDGF) enhance to the growth of cultured human peritoneal mesothelial (CHPM) cells. The cell cultures were derived from surgically removed omentum using the enzymatic disaggregation method. CHPM cells were cultured with Ham's F-12 medium containing 10% FCS up to third generation. At a concentration of 1x10(4) cells/well were cultured with various concentrations of IL-1 beta, IFN-gamma, EGF, PDGF and IL-6. [3H] TdR (37MBq/well) was added to the cultures during the last 12hr of the 48hr culture period and then radioactivity was measured to determine the uptake of [3H] TdR. It was shown that IL-1 beta, IFN-gamma, EGF and PDGF induced the proliferation of CHPM cells in a dose dependent manner when cultured in medium containing 3% FCS.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of Acetic Acid-Induced Gastric Ulcers in Rats by Scanning Acoustic Microscopy

To clarify the mechanism of gastric ulcer recurrence, we studied acetic acid-induced gastric ulcers. The healing of these gastric ulcers was then studied for 4-21 weeks after the injection. Forty-eight ulcers were examined by macroscopic observation and scanning acoustic microscopy (SAM) and by histologic study of the ulcers. SAM has a higher radio frequency and provides more detailed information about the gastric wall than endoscopic ultrasonography (EUS). Thirteen healed and 35 non-healed gastric ulcers were observed by macroscopic observation over 4-21 weeks. SAM enabled us to observe the normal gastric wall of the rat in five different layers. The SAM echo patterns of the healed ulcers were all one pattern. On the other hand, we were able to classify the echo patterns of the non-healed ulcers into two different patterns; one pattern consisted of a high-echogenic region in the first and second layers with an underlying relatively high echogenic region in a horizontal pattern. The other pattern showed a poorly defined and spotted low-echogenic region in the first and second layers which fanned out toward the fifth layer. However, these two different ulcers could not be distinguished macroscopically. Histologic findings supported the results of the SAM study which showed one pattern in healed ulcers and two patterns in non-healed ulcers. In the non-healed ulcers the two different patterns may be ascribed to the proliferation of collagen fibers. SAM makes it possible to image the proliferation of collagen fibers and identify the two different types with an accuracy of 97%.(ABSTRACT TRUNCATED AT 250 WORDS)

A CASE OF GASTRODUODENAL ULCER PRESENTED WITH WHOLE-CIRCUMFERENCE STENOSIS OF THE PYLORIC VESTIBULE

We describe a case of gastroduodenal ulcer in which pyloric vestibular stenosis exacerbated in a short time and we had difficulties in differentiation from advanced gastric cancer.The case was a 71-year-old male who had had head injury and was being medicated for sustaining headache. On October 16, 1989, the patient was admitted to our hospital because of melena. Upper gastrointestinal series revealed a probable advanced gastric cancer. Borrmann type 4. Biopsy cytology, however, showed no malignant findings. Because of markedly exacerbated stenosis at the pyloric vestibule, pyloric-side gastrectomy and duodenectomy were carried out on November 22. In the excised specimen, giant girdle ulcer (Ul-II) in 3 lines at the lesser curvature, anterior and posterior wall of lower body of stomach, and a whole-circumference stenosis 7 cm in length reaching to the duodenal bulb at the anal-side were observed. Histopathological findings included mild inflammatory findings at mucous membrane, submucosal proliferation of collagen fiber, and marked hypertrophy of intrinsic muscle layer at the whole-circumference stenosis site. This pyloric vestibular stenosis might be due to repeated chronic inflammation. Possible factors causing exacerbation can be medication and circulatory disturbance.

Nonoperative Treatment of Acute Knee Ligament Injuries

Nonoperative treatment has received little attention in the numerous scientific reports on knee ligament injuries. Great controversy still exists concerning the proper treatment of a knee with a ruptured ligament, especially the anterior cruciate ligament. However, according to the studies of the authors and an extensive review of the literature the indications for conservative management can be established to be all grade I and II sprains (partial tears) of knee ligaments as well as an isolated grade III sprain (complete tear) of the posterior cruciate ligament. In addition, an isolated complete rupture of an anterior cruciate, or medial or lateral collateral ligament may be treated nonoperatively in an older sedentary person. Other injuries obviously call for an operative approach at the acute stage. Nonoperative therapy protocols must be based on the knowledge of the biological phenomenon occurring during connective tissue healing process. In the first phase of ligament healing the injured knee needs 2 to 3 weeks immobilisation for undisturbed fibroblast invasion and proliferation of collagen fibres. This is achieved by immobilising the knee in a rehabilitative knee brace locked in 40 to 45 degrees of flexion. Thereafter, a gradually increasing controlled mobilisation is allowed in the brace to avoid the deleterious effects of immobilisation to cartilage, bone, muscles, tendons and ligaments, and to enhance the orientation of collagen fibres to the stress lines of the healing ligament. After 4 to 8 weeks the goal for rehabilitation is rapid and full recovery to work and sports. A functional knee brace may be used at this phase to give extra protection before final strengthening of the injured ligament. During the mobilisation and muscle training of the therapy protocol various specific techniques can be used for strengthening of the hamstring and quadriceps muscles, including isometric, isotonic, isokinetic and eccentric exercises with or without resistive equipments. In addition, electrical stimulation may help prevent muscle wasting due to immobilisation, and continuous passive motion may be used to correct persistent extension or flexion deficit. Normally, jogging is allowed approximately 3 to 6 months after the injury, and an athlete is generally able to return to full activity and competitive sports after 6 to 12 months. Quite frequently the whole question of successful rehabilitation after a knee ligamentous injury is more motivational rather than methodological and is thus often independent of attending physician's or physiotherapist's skill or will. Therefore, one of the most important things during rehabilitation is to motivate and encourage the patient for longstanding, intensive work.