PubMed Health⌕ Search

Biomedical subjects

P M Sherman

Publications and source records attributed to P M Sherman.

At least 19 recordsLinked to original sources
PubMed2002

Acetabular paralabral cyst: an uncommon cause of sciatica.

The association between tears of the acetabular labrum and paralabral cysts has been well documented, and magnetic resonance imaging (MRI) has been shown to be the most accurate noninvasive method of depicting not only the normal anatomic structures of the hip, but also the common pathologic processes such as labral tears and paralabral cysts. We present the case of an acetabular paralabral cyst that resulted in clinically symptomatic compression of the sciatic nerve.

Acetabulum↗
PubMed2001

Current controversies associated with Helicobacter pylori infection in the pediatric population.

Helicobacter pylori is a human bacterial gastric pathogen, fulfilling each of Koch's postulates for causal inference for ulceration in children and adults. In addition many reports purport to show that the organism causes a variety of extra-intestinal manifestations in children. This review of the English language literature provides evidence that H. pylori is likely a cause of unexplained iron deficiency (sideropenic) anemia in children, even in the absence of gastrointestinal bleeding. Much stronger evidence is required however, before H. pylori infection can be considered as an etiologic agent in recurrent abdominal pain of childhood, unexplained short stature, protracted diarrhea in pre-schoolers and sudden infant death syndrome.

Abdominal Pain↗
PubMed2001

Monocyte/macrophage activation by normal bacteria and bacterial products: implications for altered epithelial function in Crohn's disease.

Intestinal immune cells are less reactive than those in the peripheral blood; however, such cells from patients with Crohn's disease may be more responsive to bacterial products. Our study examined if nonpathogenic bacteria or lipopolysaccharide (LPS), can affect epithelial function in the presence of monocytes/macrophages. Lamina propria mononuclear cells (LPMCs) and peripheral blood monocytes (PBMs) were obtained from patients with Crohn's disease and control patients. Filter-grown T84 epithelial monolayers were co-cultured with nonactivated or LPS-activated LPMCs or PBMs for 48 hours. Epithelial secretory [baseline short-circuit current (Isc) and DeltaIsc to forskolin] and barrier (transepithelial electrical resistance) parameters were measured in Ussing chambers. LPS-activated PBMs from both controls and patients with Crohn's disease significantly increased Isc ( approximately 300%) and reduced transepithelial electrical resistance ( approximately 40%). Epithelial function was not altered after co-culture with control LPMCs +/- LPS. However, LPMCs from patients with Crohn's disease spontaneously secreted tumor necrosis factor-alpha, and induced epithelial changes similar to those produced by LPS-activated PBMs. Co-culture with control Escherichia coli and PBMs induced comparable changes in epithelial physiology, which were abrogated by anti-tumor necrosis factor-alpha antibody. We conclude that LPMCs of patients with Crohn's disease are spontaneously activated, possibly by gram-negative luminal bacteria, and can directly cause significant alterations in epithelial ion transport and barrier functions.

Adolescent↗
PubMed2001

Characterization of virulence factors of mouse-adapted Helicobacter pylori strain SS1 and effects on gastric hydrophobicity.

Gastric infection with Helicobacter pylori results in chronic active gastritis and in some individuals is associated with complications such as peptic ulceration and gastric cancers. A balance between bacterial factors and host responses may determine disease outcome. The mouse-adapted H. pylori strain SS1 has been utilized as a model to study disease pathogenesis. Although chronic gastritis is observed in this murine model of H. pylori infection, other complications of disease seen in the human host (such as peptic ulceration) are not identified. The objectives of this study were to characterize virulence factors of the mouse-adapted H. pylori strain SS1 and determine host responses to infection. Vacuolating cytotoxin activity of H. pylori strain SS1 was determined after incubation of HEp-2 cells with culture supernatant for 24 hr. Polymerase chain reaction was performed to detect the presence of the cagA and cagE genes. Chemokine responses from human gastric epithelial cells infected with H. pylori SS1 were assessed by measurement of the concentration of interleukin-8 in cell-free supernatants. C57BL/6 and gld mice were infected with strain SS1 or sham-infected. Eight weeks following infection, gastric tissues were obtained for histological analysis and surface hydrophobicity was measured by axisymmetric drop-shape analysis. H. pylori strain SS1 was cytotoxin negative, cagA positive, and cagE positive, but induced only a modest interleukin-8 response (684 +/- 140 pg/ml) from AGS gastric epithelial cells in comparison to a clinical isolate (4170 +/- 410 pg/ml, P < 0.0005). Increased inflammation was observed in the stomachs of H. pylori strain SS1-infected animals compared to uninfected controls. Gastritis was not associated with any disease complications. Despite mucosal inflammation, infected mice did not demonstrate alterations in gastric surface hydrophobicity (42.2 degrees +/- 2.2 degrees and 41.4 degrees +/- 3.2 degrees for C57BL/6 and gld, respectively) compared to uninfected mice (43.2 degrees +/- 2.3 degrees and 39.5 degrees +/- 1.6 degrees, respectively). In conclusion, murine infection with H. pylori SS1, which contains putative bacterial virulence factors, results in gastric inflammation. However, the mucosal changes are not associated with alterations in surface hydrophobicity. Therefore, the mouse model of infection with H. pylori, strain SS1 may not serve as an entirely appropriate model to study host factors associated with disease complications.

Animals↗
PubMed2001

Screening for celiac disease in children with recurrent abdominal pain.

BACKGROUND: The clinical presentation of celiac disease--a life-long gluten intolerance--may be characterized by chronic abdominal pain. The objective of this study was to determine if children with recurrent abdominal pain had a higher prevalence of antiendomysial antibodies (a serologic marker of celiac disease) compared with healthy children. METHODS: Children with recurrent abdominal pain and healthy control participants were recruited from the offices of community pediatricians. Serum samples were drawn and antiendomysial antibodies were measured in both groups. Demographic data included age, gender, height, and weight. RESULTS: A total of 200 children were recruited, of whom 173 (87%) had serum samples drawn. Of these, 92 were children with recurrent abdominal pain and 81 were control participants. Only 2 of the 173 samples (1.2%) were positive for antiendomysial antibody. The frequency of antiendomysial antibody positivity in children with recurrent abdominal pain was 1 in 92 (1%; 95% confidence interval, 0-6%) compared with 1 in 81 (1%; 95% confidence interval, 0-7%) in control participants. CONCLUSIONS: This community-based case-control study found no association between recurrent abdominal pain and the prevalence of antiendomysial antibody. Therefore, these data do not support screening for celiac disease in the child with classic recurrent abdominal pain in the primary care setting.

Abdominal Pain↗
PubMed2001

Inhibition of attaching and effacing lesion formation following enteropathogenic Escherichia coli and Shiga toxin-producing E. coli infection.

Enteropathogenic Escherichia coli (EPEC) and Shiga toxin-producing E. coli (STEC) induce cytoskeletal changes in infected epithelial cells. To further characterize host cytosolic responses to infection, a series of specific cell-signaling inhibitors were employed. Initial bacterial adhesion to HEp-2 epithelial cells was not reduced, whereas alpha-actinin accumulation in infected cells was blocked by a phosphoinositide-specific phospholipase C inhibitor (ET-18-OCH3), phosphoinositide 3-kinase inhibitors (wortmannin and LY294002), and a 5-lipoxygenase inhibitor, nordihydroguaretic acid. A cyclooxygenase-2 inhibitor (NS-398), however, did not block alpha-actinin reorganization in response to EPEC and STEC infections. Understanding signal transduction responses to enteric pathogens could provide the basis for the development of novel therapeutic strategies.

Actinin↗
PubMed2001

Genotypic, clinical, and demographic characteristics of children infected with Helicobacter pylori.

Helicobacter pylori isolates vary between geographic regions. Certain H. pylori genotypes may be associated with disease outcome. Thirty-eight children underwent diagnostic upper endoscopy at four medical centers and were retrospectively analyzed to determine if H. pylori virulence genes were associated with endoscopic disease severity, histologic parameters, and host demographics. The H. pylori virulence genotype was analyzed by a reverse hybridization line probe assay and type-specific PCR. Endoscopic ulcers or erosions were found in 17 (45%) patients, with 13 (34%) of these patients having antral nodularity. Histological gastritis, of varying severity, was present in all children. Four patients harbored more than one H. pylori strain: one subject had both cagA(+) and cagA-negative strains, while three patients harbored either two different cagA-negative strains (two children) or two cagA(+) strains (one child). There were 28 (74%) cagA(+) isolates; 19 were associated with the vacA s1b genotype, 7 were associated with the vacA s1a genotype, 1 was associated with the vacA s1c genotype, and 1 was associated with the s2 genotype. Of 14 cagA-negative isolates, 6 were vacA s2 genotype, 4 were vacA s1b, 3 were vacA s1a, and 1 was vacA s1c. Nine of ten (90%) Hispanics had similar H. pylori strains (vacA s1b,m1), and all Asian-Canadian children were infected by strains with vacA s1c genotype. No correlation between H. pylori strain and endoscopic or histopathologic abnormalities was found. This study provides a baseline framework of North American children and their H. pylori strains, serving as a powerful epidemiological tool for prospective investigations to better understand the transmission and evolution of diverse disease outcomes.

Adolescent↗
PubMed2001

MR imaging of the posterior cruciate ligament graft: initial experience in 15 patients with clinical correlation.

PURPOSE: To describe the magnetic resonance (MR) appearance of the posterior cruciate ligament (PCL) graft in the 1st postoperative year and to correlate the MR findings with clinical examination findings. MATERIALS AND METHODS: Nineteen MR examinations were performed in 15 patients (with 15 grafts) 1-33 months after PCL reconstruction. Results of clinical follow-up were available in 14 patients. Graft shape and thickness were recorded, and intrasubstance signal intensity at T2-weighted imaging was graded. The MR findings were correlated with the time between surgery and clinical examination. RESULTS: At MR imaging, 13 grafts appeared intact, one could not be assessed owing to hardware artifact, and one initially appeared disrupted. Graft thickness was 7-19 mm. There was no significant difference between graft thickness versus time since surgery and signal intensity versus time since surgery (P =.14). In two of three patients who underwent sequential MR examinations, graft thickness and intrasubstance signal intensity decreased as the time between reconstruction and MR imaging increased. Two of 14 patients who underwent physical examination had a posterior drawer, and one also had an anterior cruciate ligament graft tear. Both patients with knee instability demonstrated intact PCL graft fibers at MR imaging. There was no correlation between knee stability and graft thickness, signal intensity, or shape. CONCLUSION: After PCL reconstruction, MR imaging in the 1st year depicts a thickened graft with increased signal intensity. There does not appear to be a relationship between clinical stability and findings at MR imaging.

Adolescent↗
PubMed2000

cagE is a virulence factor associated with Helicobacter pylori-induced duodenal ulceration in children.

This study was undertaken to determine whether infection with Helicobacter pylori strains that contain the cagE gene was associated with duodenal ulceration in children. The presence of flaA, cagA, and cagE genes was determined by polymerase chain reaction in H. pylori previously cultured from 29 children. Twelve (92%) of 13 children with duodenal ulcers were infected with cagE-positive isolates, compared with only 5 (31%) of 16 with gastritis alone (P<.01). Infection of gastric cells in tissue culture by cagE-positive H. pylori resulted in greater increments in interleukin-8 levels compared with cagE-negative strains (2.3+/-0.1 vs. 1.3+/-0.2 ng/mL in AGS cells [P<.005]; 1.5+/-0.3 vs. 0.5+/-0.2 ng/mL in KATO-III cells [P<.05]). H. pylori-containing cagE was associated with the presence of duodenal ulceration in children. Enhanced chemokine production after infection with cagE-positive H. pylori could affect disease outcome.

Adolescent↗
PubMed2000

Escherichia coli Shiga toxins induce apoptosis in epithelial cells that is regulated by the Bcl-2 family.

Human intestinal cells lack globotriaosylceramide (Gb(3)), the receptor for Shiga toxin-1 (Stx1) and Shiga toxin-2 (Stx2). Therefore, the role of these toxins in mediating intestinal disease during infection with Shiga toxin-producing Escherichia coli is unclear. The aims of this study were to determine whether Stx1 and Stx2 induce apoptosis in epithelial cells expressing (HEp-2, Caco-2) or lacking (T84) Gb(3) and to characterize the role of the Bcl-2 family. Stx1 (12.5 ng/ml) induced apoptosis in both HEp-2 (21.9 +/- 7.9% vs. 0.8 +/- 0.3%, P = 0.01) and Caco-2 (10.1 +/- 1.2% vs. 3.1 +/- 0.4%, P = 0.006) cells but not in Gb(3)-deficient T84 cells. Toxin-mediated apoptosis of HEp-2 cells was associated with enhanced expression of the proapoptotic protein Bax. Inhibition of caspase activation prevented toxin-stimulated apoptosis. In addition, overexpression of Bcl-2 by transient transfection blocked Stx1-stimulated cell death. These findings indicate that Shiga toxins produced by E. coli signal Gb(3)-expressing epithelial cells to undergo apoptosis in association with enhanced Bax expression, thereby resulting in activation of the caspase cascade.

Apoptosis↗
PubMed2000

Implications of antibiotic resistance in the management of Helicobacter pylori infection: Canadian Helicobacter Study Group.

Eradication of Helicobacter pylori from the gastric and duodenal mucosa is an important clinical goal in the treatment of infected patients with peptic ulcer disease and other H pylori-associated conditions. Although several oral drug combination regimens are associated with eradication rates of approximately 85% in controlled trials, the success rate in patients infected with a resistant strain of H pylori is closer to 75%. Resistance to metronidazole and clarithromycin, which are common components of combination treatment regimens, is of greatest concern. Reported rates of H pylori resistance to various antibiotics vary considerably. In Canada, the data documenting H pylori susceptibility are limited but suggest that resistance to these antibiotics varies geographically and within specific treatment groups. Although susceptibility testing is not a prerequisite for initial treatment of individual patients infected with H pylori, formal efforts to identify and monitor both the causes and prevalence of antibiotic resistance across Canada are a much needed step in the ongoing management of this important infection. Recommended treatment regimens may be useful, even for treating apparently resistant H pylori strains. However, it is important to understand the mechanisms of the development of resistant strains to manage patients with treatment failure better.

Anti-Bacterial Agents↗