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Biomedical subjects

M Hirose

Publications and source records attributed to M Hirose.

At least 793 records · Page 44Linked to original sources
PubMedDate not supplied

Marked retention of indocyanine green and sulfobromophthalein with chronic persistent hepatitis.

A hepatitis B virus (HBV) carrier with marked retention of indocyanine green (ICG) and sulfobromophthalein (BSP) was admitted to our hospital for assessment of liver function. On admission, he was asymptomatic and blood chemistry tests showed normal values for transaminases and bilirubin. Serum hepatitis B surface antigen (HBsAg) and antibody to hepatitis B e antigen (anti-HBe) were positive. A history of drug abuse or alcoholism was denied. Dye excretion tests revealed marked retention of ICG (R15 = 70%) and BSP (R45 = 23%). Histopathological examination of a liver biopsy specimen obtained during laparoscopic observation showed chronic persistent hepatitis (CPH). Familial research of the patient failed to prove the existence of dye excretory defect in his siblings. Usual cases of CPH due to continuous HBV infection do not show such severe disturbance of organic anion transport. This pattern of the dye excretory defect with CPH has not been reported. Although the relationship between this dye excretory defect and HBV infection is unclear, the existence of the constitutional dye excretory defect due to abnormal organic anion transport in the liver might be considered.

Carrier State↗
PubMedDate not supplied

Role of actin and calmodulin in migration and proliferation of rabbit gastric mucosal cells in culture.

The aim of this study was to develop a new cellular restoration model using primary cultured rabbit gastric mucosal cells, and to evaluate the role of cytoskeleton and calmodulin in this process. Confluent monolayer mucosal cell sheets consisting mainly of mucous cells were wounded, and a rotating silicon tip was used to make cell-free areas of constant size. The process of restoration was monitored, and the cell-free area was measured and analysed quantitatively. Artificial wounds recovered in 36 h in controls; however, mucosal cell repair was inhibited by treatment with the actin inhibitor, cytochalasin B, and the calmodulin inhibitor, W-7. In the process of restoration, bromodeoxyuridine (BrdU)-positive cells appeared around the wound 24 h after injury and then disappeared after the complete repair. Because BrdU-positive cells were never detected within 24 h after wounding, initial recovery of the wound occurred only by cell migration. Both the migration and the proliferation stage are seen with this model. This culture model is suitable for the analysis of gastric mucosal restoration. Present data are consistent with the hypothesis that the integrity of the cytoskeletal system is important for restoration after damage of the gastric mucosa.

Actins↗
PubMedDate not supplied

Restoration of gap junctions in the regenerative process of ethanol-induced gastric mucosal injury.

Gap junctions mediate intercellular communication and play an important role in cell proliferation and differentiation. The present study examined the expression of the gap junction protein connexin 32 in rat gastric mucosa during the regenerative process of ethanol-induced gastric mucosal injury. Absolute ethanol (0.5 mL/100 g bodyweight) was administered to rats via gastric intubation. Following the treatment, rats were killed periodically, and gastric tissues were processed for indirect immunofluorescence microscopy using an anti-connexin 32 antibody. Haematoxylin and eosin (H&E), periodic acid Schiff (PAS) and Bromodeoxyuridine (BrdU) staining were also performed in serial sections. Gastric injuries were limited in the mucosal layer. The injury was most severe 1 h after treatment, and was completely resolved by the 4th day after treatment. The number of immunoreactive spots for gap junctions was markedly decreased 1 h after the ethanol treatment. Reappearance of these immunostaining gap junctions occurred with repair of the injury. The reappearance of connexin 32 after injury was delayed in comparison with both the histologic resolution of the injury and the normalization of PAS-stained mucus. In contrast, the time course of reappearance of gap junctions closely paralleled the appearance of BrdU-labelled cells. These results indicate that morphologic repair is different to the recovery of cell maturity and cell proliferation in the regenerative gastric mucosa.

Animals↗
PubMedDate not supplied

Basic fibroblast growth factor accelerates gastric mucosal restoration in vitro by promoting mesenchymal cell migration and proliferation.

It has been generally accepted that basic fibroblast growth factor is a potent stimulator of duodenal ulcer healing. However, the detailed mechanism and mode of action of growth factor on gastric ulcer healing is still controversial. Therefore, in the present study, the effects of basic fibroblast growth factor on gastric mucosal repair were studied using an in vitro cultured cell system. Artificial wounds were made in confluent monolayer rabbit gastric fibroblast and epithelial cell sheets by mechanical denudation. Changes in the size of the cell-free area were analysed quantitatively. Cell proliferation was assessed by BrdU staining. For both cell types, mucosal restoration involved cell migration and proliferation. Although the speed of restoration of epithelial cells was not affected by the addition of basic fibroblast growth factor, it was much faster for epithelial cells than for fibroblasts. Basic fibroblast growth factor accelerated wound repair of fibroblasts but not epithelial cells. Basic fibroblast growth factor accelerated wound repair by stimulating both cell migration and proliferation. Therefore, the effects of basic fibroblast growth factor in peptic ulcer diseases may be mainly due to the stimulation of mesenchymal cells.

Animals↗
PubMedDate not supplied

Usefulness of histopathologic examination of thick scales in the diagnosis of X-linked dominant chondrodysplasia punctata (Happle).

Most patients with X-linked dominant chondrodysplasia punctata (X-DCDP) have whorled, thick, or spiky adherent hyperkeratosis on their whole body. Histopathologically, there are large keratotic plugs of hair follicles where calcium deposits. This is the characteristic finding in this disease. We performed histopathologic examination of skin specimens from two newborn babies with X-DCDP. The desquamated thick scales from the hyperkeratotic lesions had calcium in the center of the keratotic plugs. Histopathologic examination of thick scales is easy and helpful in diagnosing X-DCDP.

Biopsy, Needle↗
PubMedDate not supplied

Dual effects of prolonged ACTH stimulation on 4-hydroxyaminoquinoline 1-oxide-induced adrenocortical lesions in rats.

The effects of a long-acting synthetic ACTH on 4-hydroxyaminoquinoline 1-oxide (4HAQO)-induced adrenocortical lesions were investigated in female rats. A total of 140 6-week-old rats were divided into 4 equal groups, given a single s.c. injection of 7 mg/kg 4HAQO or vehicle, followed by repeated sc administration of the synthetic ACTH or no further treatment. Subgroups of 10 rats in each group were sequentially sacrificed at weeks 20, 30, and 40. Adenomas and adenomatous nodules developed in the adrenal cortex of animals receiving 4HAQO and the chronic ACTH stimulation. Both lesions were located in the deeper zones of the adrenal cortex adjacent to the medulla and were composed of large-sized, clear-type cells. From week 20, middle zone, cortical cystic degeneration, which mimics the age-associated degenerative change named adrenal peliosis, was frequently observed in the adrenal glands of animals treated with 4HAQO alone. Its development was inhibited by ACTH. In the control animals, peliotic changes occurred at low incidence and only at the termination of experiment. These results indicate that long-term stimulation of ACTH promotes the development of adrenocortical tumors but suppresses the occurrence of adrenal peliosis in rats treated with 4HAQO.

4-Hydroxyaminoquinoline-1-oxide↗
PubMedDate not supplied

Liver tumor-promoting effect of beta-naphthoflavone, a strong CYP 1A1/2 inducer, and the relationship between CYP 1A1/2 induction and Cx32 decrease in its hepatocarcinogenesis in the rat.

Interrelationships among induction of cytochrome P-450 (CYP) 1A1/2, decrease in connexin 32 (Cx32), and liver tumor-promoting activity by beta-naphthoflavone (BNF) in the promotion stage were examined in a 2-stage liver carcinogenesis model. A total of 20 male Fischer 344 rats were initiated with a single intraperitoneal injection of 150 mg/kg of diethylnitrosamine (DEN) or were given the saline vehicle alone. Starting 2 weeks later, they were fed a diet containing 2%, 1%, or 0% BNF for 6 weeks. All animals were subjected to a two-thirds partial hepatectomy at week 3 and were sacrificed at week 8. Absolute and relative liver weights were significantly increased in the DEN+BNF groups as compared to the DEN-alone group. Diffuse hepatocellular hypertrophy with cytoplasmic eosinophilia, sometimes accompanied by development of adenoma-like hepatic foci, was observed in the BNF-treated rats. Remarkable induction of cytochrome CYP 1A1/2 and significant increase in CYP 2E1 were noted in the DEN+BNF groups, and positive immunohistochemical staining for both was observed diffusely. The areas of Cx32-positive spots per hepatocyte in the centrilobular areas of livers of the BNF-treated rats were significantly decreased, but no changes were observed in periportal areas. The numbers and areas of foci positive for glutathione S-transferase placental form were increased in the BNF-treated groups. These results suggest that BNF is a liver tumor promoter that, unlike phenobarbital, does not induce CYP 2B1/2 isozymes, and there seems to be no direct relationship between CYP 1A1/2 induction and Cx32 reduction in BNF hepatocarcinogenesis.

Animals↗
PubMedDate not supplied

A mechanistic study of ovarian carcinogenesis induced by nitrofurazone using rasH2 mice.

In order to clarify whether the ovarian tumors induced in a long-term carcinogenicity study of nitrofurazone (NF) in mice can be also produced in a short-term model using transgenic (Tg) mice carrying the human c-Ha-ras gene (rasH2 mice), the following 3 experiments were performed. In experiment 1, both rasH2 mice and their wild CB6F1 littermates carrying no c-Ha-ras gene (non-Tg mice) that were fed a diet containing 500 to 1,000 ppm NF for 7 weeks demonstrated ovarian atrophy characterized by decreased labeling indices (LIs) for proliferating cell nuclear antigen (PCNA) in granulosa cells. In experiment 2, increased numbers of atretic follicles and decreased PCNA LIs in granulosa cells were recognized in rasH2 mice given diets containing 250 or 500 ppm NF for 26 weeks, but no tumor induction was grossly observed. In experiment 3, similar ovarian atrophy was observed in association with increased serum luteinizing hormone (LH) levels in both rasH2 and non-Tg mice given diet containing 1,000 ppm NF for 11 days. These results indicate that long-term NF treatment induces ovarian tumors in mice, possibly by continuous stimulation with gonadotropins such as LH via a negative-feedback phenomenon secondary to ovarian atrophy (as the tumor-induction mechanism), although we could not completely rule out a genotoxic mechanism.

Animals↗
PubMedDate not supplied

Immunohistochemical detection of 8-hydroxy-2'-deoxyguanosine in paraffin-embedded sections of rat liver after carbon tetrachloride treatment.

To test the applicability of an anti-8-hydroxy-2'-deoxyguanosine (8-OH-dG) antibody for immunohistochemistry using paraffin-embedded sections, carbon tetrachloride (CCl4)-induced rat liver injury was evaluated. Male rats were given a single dose of CCl4 and killed at 6 hr, 12 hr, 1, 2, 3, and 7 days thereafter. Severe centrilobular necrosis was evident at 1 day. At 2 days, moderate mononuclear cell infiltration was present in centrilobular necrotic regions. Infiltrating mononuclear cells, surrounding sinusoidal endothelial cells and hepatocytes were stained with anti-8-OH-dG antibody at 2 and 3 days. Formation of 8-OH-dG in DNA and 8-oxo-dGTPase mRNA expression were also increased at these time points, the amounts of malondialdehyde and 4-hydroxy-2-nonenal showed 2 peaks at 6 hr and 3 days. The findings suggest that the main contributory factor in the massive hepatic necrosis was increased lipid peroxidation, rather than excessive formation of 8-OH-dG, and that the observed increase in the latter was largely due to infiltrating mononuclear cells. The agreement between biochemical data and the results for immunohistochemical analysis confirms that the anti-8-OH-dG antibody is applicable for detection of cells targeted by free radicals in paraffin-embedded sections and also for investigation of the mechanisms of oxidative damage-related disease, including carcinogenesis.

8-Hydroxy-2'-Deoxyguanosine↗
PubMedDate not supplied

Sequential morphological and biological changes in the glandular stomach induced by oral administration of catechol to male F344 rats.

Histogenesis and mechanisms of catechol-induced rat glandular stomach carcinogenesis were investigated in male F344 rats. Groups of 5 or 6 rats were treated with dietary catechol at doses of 1, 0.5, 0.1, and 0.01% for 12 hr or for 1, 2, 3, or 7 days or at a dose of 0.8% for 1, 2, 4, 12, and 24 wk; rats were then euthanatized. The initial morphological changes were edema of the gastric wall, inflammatory-cell infiltration, erosion in the pyloric region close to the duodenum, and considerable increase in apoptosis at 12 hr; later, changes included augmented DNA synthesis and cell proliferation, as evaluated by bromodeoxyuridine labeling index and thickness of mucosa, respectively, on day 1. Downward hyperplasia due to excess regeneration appeared at edges of ulceration at week 2. This lesion disappeared, and then submucosal hyperplasia appeared in the course of adenoma development. Only slight expression of c-myc or c-fos was apparent after 30-min oral administration or 1-, 3-, and 6-hr oral administration of catechol. No increase in lipid peroxide levels was evident in gastric epithelium fed catechol for 1 wk. The amount of catechol distributed in the glandular stomach and forestomach epithelium, which is not a target for carcinogenesis, did not differ 1, 3, 6, and 24 hr after a single intragastric dose of 75 mg/kg body weight. Amounts of catechol bound to tissue protein were also not specifically high in the glandular stomach. These results indicate that regenerative cell proliferation due to toxicity plays an important role in catechol-induced glandular stomach carcinogenesis. Protein binding and free radicals may not be largely responsible for the toxicity.

Administration, Oral↗
PubMedDate not supplied

Liver tumor promoting effects of fenbendazole in rats.

In order to examine whether fenbendazole has tumor-promoting activity, a total of 70 male Fischer 344 rats were initiated with a single intraperitoneal injection of 100 mg/kg of diethylnitrosamine (DEN) or were given the saline vehicle alone; beginning 1 wk later, rats were given a diet containing 3,600; 1,800; 600; 200; 70; or 0 ppm of fenbendazole for 8 wk. Subgroups of 5 rats each from the DEN+ 1,800; DEN+0; 1,800; and 0 ppm groups were euthanatized after 1 wk of fenbendazole treatment, and the remaining animals were euthanatized at 8 wk. After 1 wk, relative liver weights (ratios to body weights) were significantly increased in the DEN+ 1,800 and 1,800 ppm groups, and based on light microscopy, periportal hepatocellular hypertrophy was evident in these groups. After 8 wk, relative liver weights were significantly increased in the groups given > or =600 ppm with or without DEN initiation. Periportal hepatocellular hypertrophy, characterized by a marked increase in smooth endoplasmic reticulum, was observed in the groups given > or =600 ppm with or without DEN initiation. Induction of cytochrome P-450 (CYP) 1A2, 2B1, or 4A1 was noted in the fenbendazole-treated groups with or without DEN initiation; that associated with CYP 1A2 was most marked. Positive immunostaining for anti-CYP 1A1/2 or CYP 2B1/2 was observed diffusely in the livers of animals in the DEN+1,800 and DEN+3,600 ppm groups. The numbers and areas of connexin 32 (Cx32)-positive spots per square centimeter in centrilobular hepatocytes were significantly decreased in an almost dose-dependent manner with fenbendazole treatment after DEN initiation. In situ hybridization for Cx32 mRNA revealed a remarkable decrease in its expression in the centrilobular hepatocytes in the DEN+70 ppm group. The numbers of glutathione S-transferase placental-form positive single cells (plus mini foci) were significantly increased in the DEN+ 1,800 and DEN+3,600 ppm groups. Since those agents that induce CYP 2B1/2 isozymes and reduce Cx32 in centrilobular hepatocytes have been suggested to be liver tumor promoters, the present results indicate that fenbendazole may be a liver tumor promoter.

Alkylating Agents↗
PubMedDate not supplied

Usefulness of sparfloxacin against Chlamydia pneumoniae infection in patients with bronchial asthma.

The efficacy of sparfloxacin (SPFX) for the control of bronchial asthma was evaluated in 26 patients with suspected Chlamydia pneumoniae infection. Patients were randomly allocated to receive SPFX 200 mg/day (n = 14) or control treatment (n = 12) for 21 days. Significant improvements in serum C-reactive protein levels, and significant decreases in peripheral eosinophil counts, serum eosinophil cationic protein (ECP) and sputum ECP were observed in the SPFX-treated group at day 21. SPFX-treated patients also had a significantly reduced frequency of asthma symptoms, reduced inhalant beta2-stimulant use, and significant increases in morning peak expiratory flow. At the end of the study, C. pneumoniae was undetectable in two SPFX-treated patients who underwent polymerase chain reaction testing, but one control patient who was tested still had detectable levels of C. pneumoniae. These results suggest that SPFX could be used to control bronchial asthma in patients with suspected persistent C. pneumoniae infection.

Administration, Inhalation↗
PubMedDate not supplied

Modifying effects of phytic acid and gamma-oryzanol on the promotion stage of rat carcinogenesis.

The modifying effects of phytic acid and gamma-oryzanol on the promotion stage of carcinogenesis were investigated using several two stage carcinogenesis models in rats. In a multi-organ carcinogenesis model, male F344 rats were given combined treatment with 2,2'-dihydroxy-di-n-propylnitrosamine (DHPN), N-ethyl-N-hydroxyethylnitrosamine (EHEN) and 3,2'-dimethyl-4-aminobiphenyl (DMAB) during the initial 3 weeks as initiators, and then treated with dietary 2% phytic acid (50% in water), 1% gamma-oryzanol or basal diet alone for 32 weeks. Although the appearance of hepatic tumors was suppressed, the incidence of urinary bladder papillomas was increased by phytic acid. In addition, the incidence and multiplicity of lung tumors were significantly increased by gamma-oryzanol. Esophagus, colon, pancreas, kidney and thyroid lesion development was not influenced by these compounds. In a gamma-oryzanol dose response experiment using DHPN in the drinking water as an initiator, enhancing effects on lung were observed at a dose of 1% but not at 0.5% or lower. When the modifying effects of phytic acid, and its sodium (Na-PA), potassium (K-PA) and magnesium (Mg-PA) salt were further examined in rats pretreated with the bladder carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), a clear increase in the incidences of bladder tumors was noted, with only Na-PA, phytic acid itself being without effect. Finally, examination of the modifying potential of phytic acid and gamma-oxyzanol on mammary carcinogenesis in female Sprague Dawley rats pretreated with a single intragastric dose of 7,12-dimethylbenz(a)anthracene (DMBA) revealed no significant differences in the final incidences and multiplicities of mammary tumors, but the average tumor diameter was significantly reduced and the average survival time was increased with phytic acid. gamma-Oryzanol tended to decrease the size of the tumor but without significant difference. These results indicate that phytic acid inhibits hepatic and mammary carcinogenesis, while its Na-salt is a promoter of bladder carcinogenesis. The effect of phytic acid itself on urinary bladder carcinogenesis is equivocal. gamma-Oryzanol is a promoter of lung carcinogenesis but its effect is weak and exerted only at a very high dose level.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

A case of complex hepatolithiasis successfully treated with a systematic approach.

A systematic approach is required to treat complex hepatolithiasis. A 45 year-old female patient with hepatolithiasis had bilateral intrahepatic stones, biliary strictures at the right hepatic duct and segment IV duct, cholangitic abscess, and shrinkage of the right hepatic lobe. Six sessions of lithotomy were carried out under the guidance of percutaneous transhepatic choledochoscopy using a dye-laser lithotriptor through the segment III duct. Although stones were eradicated from the common bile duct and segment III duct, stones remained in other segments where cholangioscopic access was not feasible. Biliary bilirubin concentration increased and the liver abscess was resolved. Thereafter, the patient underwent right hepatectomy and choledochojejunostomy. After surgery, percutaneous transhepatic cholangio-drainage and balloon dilatation of the segment IV duct was performed. The patient underwent 11 more sessions of cholangioscopic lithotomy through 2 transhepatic routes and the bilioenteric bypass. Thereafter, the patient became almost stone-free. After discharge, biliary tracts were irrigated with saline through a subcutaneously placed reservoir. The patient is alive and well and had been without stone recurrence for 3 years. This report shows the efficacy of the vigorous combination therapy, including repeated cholangioscopic lithotomy through multiple routes using laser lithotripsy, surgery, and long-term biliary irrigation.

Bile Duct Diseases↗
PubMedDate not supplied

Inhibitory effects of protocatechuic acid on the post-initiation phase of hamster pancreatic carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine.

The chemopreventive effects of protocatechuic acid (PCA) were investigated during the post-initiation stage of the N-nitrosobis(2-oxopropyl)amine (BOP)-initiated hamster pancreatic tumorigenesis model. Female 5-week-old hamsters were divided into 6 groups. Animals in groups 1-3, each consisting of 30 hamsters, were given two s.c. injections of 20 mg/kg body weight of BOP with a one week interval as an initiation treatment. After the BOP injection, hamsters in groups 1 and 2 were respectively fed diet supplemented with 1000 or 500 ppm of PCA for 49 weeks. The animals in group 3 were treated with BOP alone. The animals in groups 4-6, each consisting of 10 hamsters, were given 1000 or 500 ppm PCA, or basal diet alone without prior BOP injection. At the termination of experimental week 52, the incidences and multiplicities of neoplastic lesions in the pancreas were comparable among the BOP-treated groups. However, the incidence of pancreatic tumors larger than 3 cm was significantly lower in the PCA-treated high dose groups than in the control group (p < 0.05). Moreover the incidence of advanced pancreatic cancers which had directly invaded adjacent tissues such as the diaphragm, spleen and stomach was reduced by the PCA treatments, being significantly (p < 0.01) lower in group 2 than in group 3. Our results thus indicated that PCA can inhibit the late post-initiation or progression phase of BOP-induced pancreatic carcinogenesis in hamsters.

Adenocarcinoma↗
PubMedDate not supplied

Detection of non-papillary, non-invasive transitional cell G1 carcinoma as revealed by increased DNA instability and other cancer markers.

The method to reveal DNA-instability as demonstrated by immunohistochemical staining with anti-cytidine antibody after acid hydrolysis (DNA-instability test) was used as a marker of malignancy. The test was applied to paraffin-embedded sections taken from 15 urinary bladders, renal pelvic cavities, and ureters bearing multiple carcinoma in situ (CIS) and totally 31 papillary urothelial cancers. The serial sections of the same tissues were also subjected to immunohistochemical staining for PCNA, p53, DFF45, and VEGF. The DNA-instability test was positive in 100% cancer lesions irrespective of the grades, and apparently normal urothelium, and hyperplastic and dysplastic urothelial lesions also showed the areas with clones positively stained with DNA-instability testing, and the percent numbers of positive areas in them were 28.3%, 37.7%, and 61.5%, respectively. These clones, which were present in apparently normal urothelium and in hyperplastic and dysplastic urothelial lesions, showed higher percent values of PCNA-positive-cells, in comparison to the values estimated in the areas with negatively stained DNA-instability testing, and the former values were statistically not different from those in carcinoma lesions. Furthermore, the percent numbers of areas positive for p53, DFF45, and VEGF, with positive DNA-instability testing were also much higher than those with negative DNA-instability testing in apparently normal urothelium, and hyperplastic and dysplastic urothelial lesions, and the former values were again comparable to those in cancer lesions with no statistical differences. These clones were regarded as already being malignant and should be the direct precursors of progressed cancer lesions. They will make progression through two different pathways, one to papillary non-invasive G1 cancers by neovascularization induced by paracrine secretion of VEGF, and another to flat CIS G2 without secretion of VEGF; thus the clones should be regarded as non-papillary, non-invasive Gl TCC, or CIS G1. It should be always taken into account that the probability for apparently normal urothelium, and hyperplastic and dysplastic urothelial lesions to contain cancer clones, will be high already, especially in tumor-bearing bladders.

Biomarkers, Tumor↗
PubMedDate not supplied

Ultrasonographic and thermographic evaluation of the lower limb after transfemoral catheterization.

Ten adults undergoing routine transfemoral catheterization were randomly selected for study. Ultrasonography and thermography were performed within 48 hours before and after the catheterization procedure. Sites proximal and distal to puncture were assessed. There were no angiographic procedural complications in any case. Distal to the puncture, Doppler evaluation revealed a decrease in peak systolic velocity (PSV) in six cases, with four showing a greater than 30% fall, while three of the four cases with an increase had a less than 10% rise in PSV. Findings at the proximal site showed no distinct pattern. Changes in the resistive index at both sites were minimal. There was a significant increase in turbulence distal to the site of puncture in six cases. B-mode revealed arterial wall thickening compromising the lumen in half the cases. Thermography was done in four cases, and there was a tendency for an increase in limb temperature after the catheterization procedure. In view of the above-mentioned findings seen in "normal, uncomplicated" procedures, a larger study appears warranted to assess the significance of these findings and to attempt a correlation of the above results with the angiographic procedure.

Adult↗