Application of clips during ERCP: a new anchoring method for redundant Kerckring's fold covering the duodenal papilla.
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Aged↗
Biomedical subjects
S W Cho
Publications and source records attributed to S W Cho.
Induction of apoptosis with an extract of Artemisia asiatica attenuates the severity of cerulein-induced pancreatitis in rats.
The aim of this study was to test the hypothesis that apoptosis can protect against experimental pancreatitis and induction of apoptosis by an extract of Artemisia asiatica (DA-9601) is beneficial in cerulein-induced pancreatis in rats. Pancreatitis was induced in 6-week-old male SPF Sprague-Dawley rats by two intravenous (i.v.) administrations of 40 microg/kg cerulein. To investigate the effects of DA-9601 on the severity of pancreatitis and extent of apoptosis, rats were treated with intragastric DA-9601, 30 mg/kg (D30), 100 mg/kg (D100), or 300 mg/kg (D300), intraperitoneal superoxide dismutase, 10,000 U/kg (SOD), and i.v. gabexate mesilate, 40 mg/kg (Foy), three times (30 min before cerulein injection, 30 and 90 min after cerulein injection). The control group was administered vehicle alone. Ten rats were included in each treatment group and control group. Rats were sacrificed 5 h after cerulein treatment. Serum amylase, histological activity index (HAI), pancreatic lipid peroxide levels, and apoptotic index [in situ hybridization by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL)] were determined. Gel electrophoresis was performed for the presence of DNA fragmentations. The results were as follows. Serum amylase was significantly increased in all cerulein-treated groups compared to normal controls (p < 0.001). The HAI was significantly decreased in only the D300 group compared to the controls (p < 0.05). The apoptotic index of the cerulein-alone group was 3.8 +/- 2.7, but the mean apoptotic indexes of the SOD and Foy groups were 16.4 +/- 4.6 and 13.3 +/- 1.8, respectively, a significant increase (p < 0.01). The apoptotic index was more significantly increased in the DA-9601-treated groups, dose dependently (8.4 +/- 3.4 in D30, 14.8 +/- 4.3 in D100, 24.2 +/- 4.7 in D300). A smearing pattern of DNA electrophoresis was noted in the DA-9601-treated groups. In conclusion, DA-9601, an extract of Artemisia, induced apoptosis of pancreatic acinar cells dose dependently and concomitantly attenuated the severity of pancreatitis.
Acute Disease↗
Localization of hepatitis B virus DNA in hepatocellular carcinoma by polymerase chain reaction in situ hybridization.
The polymerase chain reaction in situ hybridization (PCR-ISH) is a new technique that combines the sensitivity of PCR with the localizing ability of ISH. To investigate the expression pattern of hepatitis B virus (HBV) in the tissue of hepatocellular carcinoma (HCC), we detected HBV-DNA with PCR-ISH in paraffin-embedded tumor and corresponding non-tumor tissues from 11 HCC patients. HBV-DNA was detected in 4 of 11 tumor tissues and in 7 of 10 non-tumor tissues. In tumor tissues, positive signals were scattered in the tissue with occasional clustering, and were found mainly in the cytoplasm of HCC cells rather than in the nucleus. In non-tumor tissues, the number of positive signals was higher than in tumor tissues and they were found in regenerating nodules with differing patterns and intensities. When we compared the detection rate of PCR-ISH with nested PCR among 10 tissue samples, HBV-DNA was detected in 5 tissue samples by PCR-ISH, but the S gene was detected in 10, precore gene in 9 and X gene in 8 by nested PCR. The findings suggest that PCR-ISH is a sensitive technique for localizing HBV in tissue sections and that the low level of HBV replication persists in HCC cells.
Carcinoma, Hepatocellular↗
Helicobacter pylori infection, oxidative DNA damage, gastric carcinogenesis, and reversibility by rebamipide.
Several epidemiological studies have demonstrated a close association between Helicobacter pylori infection and carcinoma of the mid- or distal stomach. If this can be shown to be a causal association, eradication of the organism may prevent later development of cancer. Several mechanisms have been proposed by which H. pylori infection might lead to predisposition for gastric cancer. Although many potential pathogenic mechanisms, such as increased proliferative gastric epithelial response to H. pylori, lowered gastric ascorbic acid levels, and high occurrences of atrophic gastritis, have been proposed, there is little evidence as to which might be of direct importance to such H. pylori-related disease in vivo. H. pylori-associated inflammation may interact with other causal factors related to gastric carcinogenesis and can result in the intestinal type of gastric cancer and then DNA damage due to oxygen radicals induced by persistent inflammatory cell infiltrations in the gastric mucosa may lead to alterations of the gene and result in the development of diffuse-type carcinoma. In order to know the influence of H. pylori on changes of inflammation-related DNA damage, we measured the sequential changes of 8-hydroxydeoxyguanosine (8-OHdG) contents of DNA and the changes of two biomarkers inducible nitric oxide synthase (iNOS) and apoptosis from human gastric mucosa according to the status of H. pylori. The increased levels of oxidative DNA damage, increased occurrences of apoptosis, and increased expressions of iNOS seem to provide the mechanistic links between H. pylori infection and gastric carcinogenesis and rebamipide can abrogate the levels of these hazard factors.
Alanine↗
Quantitative and qualitative usefulness of rebamipide in eradication regimen of Helicobacter pylori.
The aim of the present study was to determine the efficacy of a new combination regimen including antioxidant, proton pump inhibitor, and antibiotics against Helicobacter pylori and to document the changes of oxidative stress and cytokines involved in H. pylori-associated gastritis. From each of 57 patients with endoscopically diagnosed gastric and/or duodenal ulcers associated with H. pylori infection, five gastric antral biopsy specimens were taken for the diagnosis of H. pylori and for experimental measures. The patients were then treated either with lansoprozole 30 mg + amoxicillin 1.5 g (LA group; 21 patients) or lansoprazole 30 mg + amoxicillin 1.5 g + rebamipide 300 mg (LAM group; 36 patients) for two weeks. Four weeks after the initiation of treatment, the patients were endoscoped again and biopsy specimens were obtained. Mucosal malondialdehyde (MDA) levels; myeloperoxidase (MPO) activities; superoxide dismutase; catalase; glutathione peroxidase; cytokines IL-1, IL-6, TNF-alpha; and chemokines IL-8, GRO-alpha, RANTES (regulated on activation normal T expressed and secreted) were measured. Using paraffin-embedded tissue sections, in situ terminal deoxyribonucleotide transferase (TdT) -mediated dUTP nick end labeling (TUNEL) for apoptosis and immunohistochemical staining for inducible nitric oxide synthase (iNOS) were performed. Two weeks of treatment with the LA regimen resulted in 57.4% eradication rates of H. pylori, whereas two weeks of treatment with the LAM regimen resulted in 75.0% eradication rates. Eradication rates between these two groups were statistically significantly different (P < 0.05). Mucosal MDA levels and MPO activities were significantly lower in the LAM group than the LA group. Mucosal levels of cytokines IL-1, IL-6, and TNF-alpha and of chemokines IL-8, GRO-alpha, and RANTES were all significantly decreased after the treatment of H. pylori, especially in the LAM-treated group. The apoptotic index and iNOS score were significantly reduced after the eradication of H. pylori. The addition of the antioxidative drug rebamipide to the eradication regimen against H. pylori has quantitative and qualitative advantages such as either augmenting the eradication rates of H. pylori or decreasing oxidative stress and cytokines levels generated by H. pylori infection.
Adult↗
B cell activation and Ig, especially IgE, production is inhibited by high CD23 levels in vivo and in vitro.
The capacity of CD23 to regulate IgE production was evaluated in both an in vitro and an in vivo system. The decreased IgE response seen in CD23 transgenic mice was confirmed and observed to occur at all antigen doses used. In addition, purified B cells from the Tg animals in general exhibited lower IgE production when stimulated with CD40L and IL-4. To examine this down-regulating activity of CD23 an in vitro model system was developed. CHO cells were transfected with CD23, ICAM-1, or both CD23 and ICAM-1. ICAM-1 was chosen to enhance B cell-B cell interaction. Purified resting B cells were placed into culture with the mitomycin C-treated transfected or control CHO cells and activated with IL-4, IL-5, and CD40L-CHO. A dose-dependent decrease in IgE production was observed with increasing cell numbers of the CHO transfectants that expressed CD23. The effect lasted up to Day 3 of culture. B cell proliferation was also inhibited in a dose-dependent fashion by increasing numbers of CD23-expressing cells suggesting a potential effect of CD23 on B cell apoptosis. In contrast, ICAM-1-transfected or CHO control cells had minimal effects on either Ig production or B cell proliferation. While IgE production was inhibited up to 95% by high numbers of CD23-transfected CHO cells, some inhibition of IgG and IgM production was also seen. Finally, the mechanism of CD23-mediated inhibition of IgE production was compared with the inhibition in IgE production seen when B cell were coactivated with multivalent anti-IgD in conjunction with CD40L plus optimal IL-4. To this end we used RT-PCR to compare the relative levels of epsilon-germline transcripts in control cultures and cultures coactivated by anti-IgD, CD40L, and IL-5 or activated in the presence of high levels of CD23-expressing cells. CD22 was used as an internal standard since levels change little with B cell activation. Coactivation strongly inhibited epsilon-germline transcript levels but the presence of CD23-expressing cells did not. Thus, coactivation potentially operates prior to isotype switching, while high CD23 coculture blocks either recombination or more likely B cell differentiation to high Ig producers stage. Our data support the hypothesis that IL-4 induces both IgE and a controlling agent for IgE, namely, CD23.
Animals↗
Modulation of the catalytic activity of brain succinic semialdehyde reductase by reaction with pyridoxal 5'-phosphate.
An NADPH-dependent succinic semialdehyde reductase from bovine brain was inactivated by pyridoxal 5'-phosphate. Spectral evidence is presented to indicate that the inactivation proceeds through formation of a Schiff's base with amino groups of the enzyme. After sodium borohydride reduction of the inactivated enzyme, it was observed that 1 mol phosphopyridoxyl residue was incorporated/mol enzyme monomer. The coenzyme, NADPH, protected the enzyme against inactivation by pyridoxal 5'-phosphate. After tryptic digestion of the enzyme modified with pyridoxal 5'-phosphate in the presence and absence of NADPH followed by [1H]NaBH4 reduction, a radioactive peptide absorbing at 310 nm was isolated by reverse-phase HPLC. The amino acid sequence of the peptide identified a portion of the pyridoxal-5'-phosphate-binding site as the region containing the sequence I-L-E-N-I-Q-V-F-X-K, where X indicates that the phenylthiohydantoin amino acid could not be assigned. The missing residue, however, can be designated as a phosphopyridoxyl lysine as interpreted from the result of amino acid composition of the peptide. It is suggested that the catalytic function of succinic semialdehyde reductase is modulated by binding of pyridoxal 5'-phosphate to a specific lysyl residue at or near the coenzyme-binding site of the protein.
Amino Acids↗
Distribution of succinic semialdehyde reductase in rat brain.
Succinic semialdehyde reductase (SSR) that catalyzes the reduction of succinic semialdehyde (SSA) to gamma-hydroxybutyrate (GHB) has been identified as one of the NADPH-dependent aldehyde reductases. Reduction of SSA to GHB strongly supports the proposal that GHB biosynthesis may be an important step in the GABA shunt. It is pharmacologically significant in anesthesia, evoking the state of sleep, and an increase in brain dopamine level. Monoclonal antibodies against bovine brain succinic semialdehyde reductase were produced. Using the anti-succinic semialdehyde reductase antibodies, we investigated the distribution of brain succinic semialdehyde reductase in rat brain. The brain tissues were sectioned with a basis on the rat brain atlas of Paxinos and were stained by the immunoperoxidase staining method using monoclonal antibodies. In the section of the frontal lobe, immunoreactive cells were observed in the lateral septal area, the ventral pallidum, which belongs to the substantia innominata. We could observe immunoreactive cells in the reticular thalamic nucleus, which is closely related with 'sleeping', the basal nuclei of Meynert, which is associated with Alzheimer's disease, and hypothalamic nuclei. Immunoreactive cells were also shown in raphe nuclei or the reticular formation of the midbrain, cerebellum, and inferior olivary nuclei of the medulla oblongata. Succinic semialdehyde reductase-immunoreactive cells were distributed extensively in rat brain, especially immunoreactive cells were strongly observed in the areas associated with the limbic system and reticular formation.
Animals↗
Role of rebamipide on induction of heat-shock proteins and protection against reactive oxygen metabolite-mediated cell damage in cultured gastric mucosal cells.
Reactive oxygen metabolites (ROM) have been reported to be important in the pathogenesis of ischemia/ reperfusion-, ethanol-, nonsteroidal antiinflammatory drug-, or Helicobacter pylori-induced gastric mucosal injury. Rebamipide, a novel antiulcer agent, has been reported either to prevent various acute experimental gastric mucosal lesions or to accelerate the healing of chronic gastric ulcers. The underlying mechanism by which rebamipide exerts its cytoprotective effect in the damaged stomach is not fully determined. We investigated the role of rebamipide in protecting against ROM-mediated cell damage in gastric mucosal cells and in inducing cytoprotective proteins. Cells were exposed to ROM enzymatically generated by hypoxanthine-xanthine oxidase. Cytotoxicity was quantified by measuring specific 51Cr release from prelabeled cells. ROM caused dose-dependent increase in cytotoxicity and amount of thiobarbituric acid-reactive substances (TBA-RS). ROM-induced cytotoxicity and TBA-RS were dose-dependently decreased by the addition of rebamipide and/or catalase, but not by superoxide dismutase alone. The effects of rebamipide on electric spin resonance signal were investigated. We found that the DMPO spin adduct ESR signal of hydroxyl radicals (DMPO-OH) was significantly attenuated by rebamipide. Western blot analysis showed that induction of heat-shock protein (HSP70) was significantly increased following rebamipide administration in a dose-dependent manner. Based on these results, it is concluded that rebamipide exerted a protective effect on HX-XO-induced gastric mucosal cell cytotoxicity through one or more of the following mechanism(s): (1) inhibition of lipid peroxidation of the cell membrane; (2) hydroxyl radical scavenging activity; and (3) induction of cellular cytoprotective protein such as HSP70.
Alanine↗
Essential active-site lysine of brain glutamate dehydrogenase isoproteins.
Two soluble forms of bovine brain glutamate dehydrogenase (GDH) isoproteins were inactivated by pyridoxal 5'-phosphate. Spectral evidence is presented to indicate that the inactivation proceeds through Schiff's base formation with amino groups of the enzyme. Sodium borohydride reduction of the pyridoxal 5'-phosphate-inactivated GDH isoproteins produced a stable pyridoxyl enzyme derivative that could not be reactivated by dialysis. The pyridoxyl enzyme was studied through fluorescence spectroscopy. No substrates or coenzymes separately gave complete protection against pyridoxal 5'-phosphate. A combination of 10 mM 2-oxoglutarate with 2 mM NADH, however, gave complete protection against the inactivation. Tryptic peptides of the isoproteins, modified with and without protection, resulted in a selective modification of one lysine. In both GDH isoproteins, the sequences of the peptide containing the phosphopyridoxyllysine were clearly identical to sequences of other GDH species.
Animals↗
The usefulness of Tc-99m HMPAO labeled WBC SPECT in eosinophilic gastroenteritis.
Tc-99m HMPAO labeled WBC SPECT was performed in 5 patients with eosinophilic gastroenteritis before and after successful medical therapy. The imaging findings were graded according to the following imaging scheme; grade 0, no uptake; grade 1, uptake < bone marrow; grade 2, uptake < liver; grade 3, uptake > liver. In no patient was the diagnosis made radiologically or with colonoscopy. The sites of involvement were identified with Tc-99m HMPAO WBC imaging in all patients before treatment and the radionuclide imaging studies were all negative after therapy.
Adult↗
Molecular typing of Vibrio vulnificus isolates by random amplified polymorphic DNA (RAPD) analysis.
This study was undertaken to determine molecular types and genetic similarity among V. vulnificus isolates by RAPD analysis. We compared these results with serotypes of V. vulnificus. Ninety-seven V. vulnificus strains including 69 strains from Chonnam University Hospital (CUH; Kwangju, Korea), 13 from Wonkwang University Hospital (WUH; Iksan, Korea), 13 from the Japanese National Institute of Health (JNIH) and two reference strains (ATCC 33815 and ATCC 27562) were analyzed. Four molecular types comprising all the strains were obtained by RAPD analysis. Type I was the most common (60/95) and included 58 strains from CUH. Type I showed a further subdivision into seven subtypes. Type II (23/95) composed of 11 strains from CUH, nine from WUH, three from JNIH and two reference strains. Six type III strains comprised four WUH strains and two JNIH strains. All six strains of type IV were from JNIH. The range of genetic similarity values among V. vulnificus isolates was 0.24 to 1.00. The serotypes of 95 strains were 04 (84.2%), 014 (3.2%), 01 (2.1%), 013 (2.1%), and R (2.1%). The most common 04 serotype strains were distributed among types I (60 strains), II (23 strains), III and IV (six strains). Although the V. vulnificus isolates showed a wide range of genetic similarity values, RAPD analysis could separate V. vulnificus strains into four molecular types, and the isolates from the same hospitals tended to belong to the same molecular type. There was no specific correlation between molecular types and serotypes of V. vulnificus.
Random Amplified Polymorphic DNA Technique↗
Possibility of chemoprevention by the eradication of Helicobacter pylori: oxidative DNA damage and apoptosis in H. pylori infection.
OBJECTIVES: The purpose of this study was to study the changes of 8-hydroxydeoxyguanosine (8-OH-dG) contents of DNA from human gastric mucosa with or without Helicobacter pylori and the changes of two biomarkers, iNOS and apoptosis, in gastric biopsies obtained before and after the eradication of H. pylori. METHODS: DNA isolated from the biopsied human gastric mucosa was digested to deoxynucleotides by nuclease P1, then with Escherichia coli alkaline phosphatase, and analyzed by HPLC-ECD system. 8-OH-dG content was expressed as the number of residues per 10(5) deoxyguanosine. iNOS immunohistochemical staining was performed with antihuman iNOS antiserum generated in mice at a dilution of 1:500, and in situ apoptosis was detected by in situ terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling. Both the density of H. pylori and the degree of inflammation were scored. RESULTS: The 8-OH-dG contents of healthy normal controls with negative H. pylori were 4.31 +/- 2.33 (8-OH-dG/10(5) dG), whereas those of patients with positive H. pylori were 10.40 +/- 7.25. The difference between these two values was statistically significant (p < 0.01). The 8-OH-dG contents were significantly decreased after the eradication of H. pylori (12.22 +/- 2.09 vs. 2.42 +/- 1.22, p < 0.001). After the eradication of H. pylori, both the apoptotic index and the iNOS scores were significantly decreased, compared with those before eradication (3.72 +/- 1.74 vs. 1.17 +/- 1.06 for apoptosis and 10.34 +/- 6.79 vs. 1.43 +/- 1.14 for iNOS, p < 0.001). Statistically significant correlations were observed among apoptotic index, iNOS score, degree of inflammation, and density of H. pylori (p < 0.05). CONCLUSIONS: The increased levels of oxidative DNA damage, increased occurrences of apoptosis, and increased expressions of iNOS suggest mechanistic links between H. pylori infection and gastric carcinogenesis.
8-Hydroxy-2'-Deoxyguanosine↗
Identification of a peptide of the guanosine triphosphate binding site within brain glutamate dehydrogenase isoproteins using 8-azidoguanosine triphosphate.
Photoaffinity labeling with [gamma-32P]8N3GTP (8-azidoguanosine triphosphate) was used to identify the guanine binding peptides of the GTT binding site within two types of glutamate dehydrogenase isoproteins (GDH I and GDH II) isolated from bovine brain. 8N3GTP, without photolysis, mimicked the inhibitory properties of GTP on GDH I and GDH II activities. Saturation of photoinsertion of GDH isoproteins revealed an apparent Kd of 8 microM (GDH I) and 24 microM (GDH II) for [gamma-32P]8N3GTP. Ion exchange and reversed-phase high-performance liquid chromatography (HPLC) were used to isolate photolabel-containing peptides generated with trypsin. This identified a portion of the guanine binding domain within the GTP binding site is the region containing the sequence I-S-G-A-S-E-X-D-I-V-H-S-A-L-A-Y-T-M E-R (GDH I) and I-S-G-A-S-E-X-D-I-V-H-S-G-L-A-Y-T-M-E-R (GDH II). The symbol X indicates a position for which no phenylthiohydantoin-amino acid could be assigned. The missing residue, however, can be designated as a photolabeled lysine since the sequences including the lysine residue in question have a complete identity with those of the other GDH species known. Also, trypsin was unable to cleave the photolabeled peptide at this site. Photolabeling of these peptides was prevented by the presence of GTP during photolysis, while other nucleotides could not reduce the amount of photoinsertion as effectively as GTP. These results demonstrate selectivity of the photoprobe for the GTP binding site and suggest that the peptide identified using the photoprobe is located in the GTP binding domain of the brain GDH isoproteins.
Affinity Labels↗
Inactivation of an NADPH-dependent succinic semialdehyde reductase by o-phthalaldehyde.
Incubation of an NADPH-dependent succinic semi-aldehyde reductase from bovine brain with o-phthalaldehyde resulted in a time-dependent loss of enzyme activity. The inactivation followed pseudo first-order kinetics with the second-order rate constant of 28 M(-1) s(-1). The inactivation was prevented by preincubation of the enzymes with NADPH, but not by succinic semialdehyde. There was a linear relationship between isoindole formation and the loss of enzyme activity. Spectrophotometric studies indicated that complete inactivation of the enzyme resulted from the formation of one isoindole derivative per molecule of enzyme, which was formed from the reaction of cysteine and lysine residues with o-phthalaldehyde at or near the enzyme active site.
Animals↗
In situ detection of hepatitis C virus RNA in liver tissue using a digoxigenin-labeled probe created during a polymerase chain reaction.
The cellular localization of hepatitis C virus (HCV) RNA in liver tissue was studied by nonisotopic in situ hybridization using a digoxigenin-labeled cDNA probe created during a polymerase chain reaction on samples from 16 patients with chronic HCV infection. Hybridization signals were recognized in the cytoplasm of the hepatocytes, and a few hepatocytes had hybridization signals in the nucleus as well. HCV RNA positive hepatocytes were found in 1 of 9 patients with chronic persistent hepatitis, 2 of 5 patients with chronic active hepatitis, and in each of 2 patients with chronic active hepatitis and cirrhosis. Positive signals were found in many hepatocytes within the lobule in liver sections of patients with advanced chronic active hepatitis. A number of HCV RNA positive hepatocytes were found in nodules, but not in the area of fibrosis. On the other hand, positive signals were found in a few hepatocytes scattered in the lobule in a patient with chronic persistent hepatitis. The mean ALT levels in the patients with positive signal (175.6 +/- 44.2 U/L) were significantly higher than in those without a signal (70.27 +/- 16.1 U/L) (P < 0.05). The findings suggest that a larger amount of HCV may be present during the advanced than during the early stages of type C hepatitis and nonisotopic in situ hybridization using a digoxigenin-labeled HCV cDNA probe created during a polymerase chain reaction deserves wider application for the detection of HCV replication in specimens.
Adult↗
Modification of brain glutamate dehydrogenase isoproteins with pyridoxal 5'-phosphate.
Two soluble forms of brain glutamate dehydrogenase isoproteins were inactivated by pyridoxal 5'-phosphate. Restoration of catalytic activity can be accomplished by dialysis and addition of an excess of cysteine or lysine. Spectral evidence is presented to indicate that the inactivation proceeds through Schiff base formation with amino groups of the enzyme. Inactivation became irreversible after reduction with NaBH4 and the NaBH4-reduced enzyme showed a characteristic absorption peak at 325 nm. Using spectral titration at 325 nm, the stoichiometry was 2 mol/mol of GDH subunit without protection and 1 mol/mol with protection, indicating the complete masking of one mol of lysine. The results with analogs of pyridoxal 5'-phosphate show that the aldehyde group, but not the phosphate group, is required for efficient inactivation.
Animals↗
Nutcracker syndrome: diagnosis with Doppler US.
PURPOSE: To assess diagnosis of the nutcracker (renal vein entrapment) syndrome with Doppler ultrasonography (US). MATERIALS AND METHODS: Doppler US findings in 16 patients with the nutcracker syndrome and in 18 healthy control subjects were compared. The anteroposterior (AP) diameter and peak velocity (PV) were measured at the hilar portion of the left renal vein (LRV) and at the LRV between the aorta and the superior mesenteric artery. RESULTS: The mean AP diameters of the LRV were 10.0 mm +/- 2.0 (standard deviation) and 1.9 mm +/- 1.0 (ratio, 5.0 +/- 2.3) in the patient group and 7.2 mm +/- 1.8 and 2.3 mm +/- 0.6 (ratio, 3.3 +/- 1.1) in the control group. The PVs at the two locations were 14.2 cm/sec +/- 2.5 and 110.7 cm/sec +/- 35.8 (ratio, 7.9 +/- 2.7) in the patient group and 18.6 cm/sec +/- 3.7 and 50.9 cm/sec +/- 27.9 (ratio, 2.8 +/- 1.5) in the control group. Differences in AP diameter and PV were statistically significant between the two groups (P < .01). CONCLUSION: Doppler US of the LRV with measurement of the AP diameter and PV may be useful in diagnosing the nutcracker syndrome.
Adolescent↗