Pathologic primer on gastritis: an illustrated sum and substance.
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Autoimmune Diseases↗
Biomedical subjects
E E Furth
Publications and source records attributed to E E Furth.
Glycogenic acanthosis.
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Esophageal Diseases↗
The effects of distention of the colon during air-contrast barium enema on colonic morphology: anatomic correlation.
Radiologic and pathologic findings are snapshots of disease processes that may vary with a host of dynamic variables. This pictorial essay shows how the presence and visibility of the innominate grooves of the colon are a function of colonic distention. This article also shows how each layer of the colonic wall, including the epithelium, muscularis mucosae, and muscularis propria, changes dramatically in thickness with varying degrees of colonic distension. These anatomic changes are documented by barium enema radiography, specimen radiography, dissecting photomicrography, and histology. These observations have important implications for the interpretation of radiologic and pathologic findings in both normal and diseased states.
Barium Sulfate↗
Acalculous candidal cholecystitis: a previously unrecognized complication after cardiac transplantation.
Acalculous cholecystitis is a life-threatening complication in critically ill surgical patients. Whereas Candida albicans and Torulopsis glabrata have been reported as the primary pathogens in 14 previous cases of acalculous cholecystitis, we report the first case of Candida parapsilosis as a biliary pathogen in a patient after cardiac transplantation. Although cardiac transplant recipients often have many of the risk factors for acalculous candidal cholecystitis, including major surgery, immunosuppression, antibiotic therapy, parenteral nutrition, and prolonged intensive care unit stay, this entity has not been previously reported in the cardiac transplant population. Although rare, acalculous candidal cholecystitis is associated with very high morbidity and a mortality rate of 40%. Early diagnosis necessitates an aggressive approach to the critically ill patient with abdominal complaints. Prompt drainage or cholecystectomy, if possible, represent the mainstays of therapy and offer the greatest chance for survival.
Candidiasis↗
Chronic lymphocytic leukemia: an unusual cause of upper gastrointestinal hemorrhage.
In contrast to the acute leukemias, chronic lymphocytic leukemia (CLL) is a hematological malignancy with a generally good prognosis. Gastrointestinal (GI) involvement with CLL is unusual, and GI complications generally occur after malignant transformation to diffuse large cell lymphoma (Richter's syndrome). We present a case of CLL directly infiltrating the gastro-esophageal junction resulting in upper GI hemorrhage. This is only the second such case in the literature. We emphasize the consideration of direct leukemic infiltration in addition to Richter's syndrome in the differential diagnosis of GI bleeding in patients with CLL. Whereas the prognosis of Richter's syndrome is poor, CLL involvement of the GI tract may respond to treatment with chemo- or radiotherapy.
Aged↗
92-kd type IV collagenase (matrix metalloproteinase-9) activity in human amniochorion increases with labor.
To determine whether specific collagenolytic enzymes are expressed in human fetal membranes with labor, we examined gelatinase activity in extracts of amniochorion by zymography. The 92-kd gelatinase (MMP-9) was barely detectable in extracts of fetal membranes before the onset of labor but was readily demonstrable in extracts prepared from membranes isolated from laboring women or membranes collected immediately after delivery. In contrast, the 72-kd gelatinase (MMP-2) was detectable in extracts from pre- and post-labor membranes. Ethylenediaminetetracetic acid and the tissue inhibitor of metalloproteinases, TIMP-1, inhibited the gelatinase activities detected by zymography, confirming that the enzymes are metalloproteinase. Assay of amniochorion gelatinase activity using a radiolabeled denatured collagen substrate revealed a more than twofold increase in activity comparing pre-labor with post-labor fetal membrane extracts. A function-blocking anti-MMP-9 monoclonal antibody inhibited pre-labor membrane gelatinase activity by approximately 11.5%, which was only slightly greater inhibition than observed with irrelevant monoclonal antibodies. However, post-labor membrane gelatinase activity was reduced by 53% by the function-blocking antibody, indicating that MMP-9 is a major contributor to the increased gelatinase activity extractable from post-labor membranes. Western blot analyses demonstrated increased MMP-9 protein in amniochorion extracts after onset of labor. MMP-9 protein and mRNA were co-localized in amnion epithelium, underlying macrophages and chorion laeve trophoblast and decidual cells after labor. We conclude that 1) MMP-9 activity and protein in human amniochorion increases with labor and 2) MMP-9 is expressed by amnion epithelium, macrophages and chorion laeve trophoblast and decidual cells. The increased expression of MMP-9 may result in degradation of the extracellular matrix of the fetal membranes and facilitate their rupture under both physiological and pathological conditions.
Amino Acid Sequence↗
The bcl-2 proto-oncogene and the gastrointestinal epithelial tumor progression model.
We report overexpression of the proto-oncogene bcl-2 in gastrointestinal adenocarcinoma and its precursor lesions. The bcl-2 proto-oncogene is centrally involved in the oncogenesis of human follicular lymphoma via a chromosomal translocation t(14;18)(q32;q21) and is also expressed in the epithelial regenerative compartment or the basal crypts of the normal colon and small intestine. We describe an immunohistochemical analysis of fixed, paraffin-embedded tissue using both a polyclonal rabbit and a monoclonal mouse antibody to the Bcl-2 protein. In addition to confirming bcl-2 expression in normal colonic and small intestinal crypts, we also observed expression in the gastric epithelial regenerative compartment, the mucous neck region. No increased expression was found in nonneoplastic or inflammatory gastrointestinal conditions, including ulcerative colitis, Crohn's disease, or inflammatory or hamartomatous polyps. Increased bcl-2 expression, however, was present in hyperplastic colonic polyps and in the majority of dysplastic lesions, from the earliest precursors through large adenomas, high grade flat dysplasia, and adenocarcinoma, all in comparison with adjacent internal control normal epithelium. Increased expression was present in dysplastic glandular lesions from all gastrointestinal sites, including colon, small bowel, and stomach. Furthermore, bcl-2 expression was frequently abnormal in nondysplastic epithelium surrounding dysplastic lesions, suggesting that altered expression occurred before the development of morphological dysplasia. Specifically, directly contiguous morphologically nondysplastic epithelium often showed abnormal bcl-2 expression throughout the full length of the crypt-villus axis. This expression pattern gradually diminished to involve only the crypt base (the normal pattern of expression), proceeding away from malignant or dysplastic lesions. Abnormal bcl-2 immunoreactivity in 1), the earliest precursor dysplastic lesions and its persistence throughout neoplastic progression and 2), contiguous morphologically unaltered nondysplastic epithelium suggests that bcl-2 alterations occur early during the morphological and molecular sequence of events leading to gastrointestinal epithelial neoplasia.
Adenocarcinoma↗
Cellular immunity to viral antigens limits E1-deleted adenoviruses for gene therapy.
An important limitation that has emerged in the use of adenoviruses for gene therapy has been loss of recombinant gene expression that occurs concurrent with the development of pathology in the organ expressing the transgene. We have used liver-directed approaches to gene therapy in mice to study mechanisms that underlie the problems with transient expression and pathology that have characterized in vivo applications of first-generation recombinant adenoviruses (i.e., those deleted of E1a and E1b). Our data are consistent with the following hypothesis. Cells harboring the recombinant viral genome express the transgene as desired; however, low-level expression of viral genes also occurs. A virus-specific cellular immune response is stimulated that leads to destruction of the genetically modified hepatocytes, massive hepatitis, and repopulation of the liver with nontransgene-containing hepatocytes. These findings suggest approaches for improving recombinant adenoviruses that are based on further crippling the virus to limit expression of nondeleted viral genes.
Adenovirus E1A Proteins↗
Decreased E-cadherin expression in endometrial carcinoma is associated with tumor dedifferentiation and deep myometrial invasion.
Decreased E-cadherin expression in tumor cells has been suggested to promote tumor invasiveness. We examined E-cadherin expression in 30 cases of endometrial carcinoma by immunohistochemistry using a monoclonal antibody to E-cadherin and investigated its correlation with other histopathologic features of the tumor. We observed that: (1) E-cadherin expression decreased with loss of differentiation (P < 0.05); (2) E-cadherin expression was inversely correlated with depth of myometrial invasion (P < 0.05); (3) decreased E-cadherin expression was correlated with paraaortic node metastasis (P < 0.01); and (4) multivariate analysis comparing the depth of myometrial invasion to the pattern of E-cadherin expression, histologic grade, nuclear grade, and lymph-vascular space invasion showed that the depth of myometrial invasion was most strongly correlated with decreased E-cadherin expression (P < 0.005). These findings seem to be consistent with the concept that the dissociation of cancer cells due to decreased expression of E-cadherin facilitates invasion of tumor cells.
Analysis of Variance↗
Receiver operating characteristic analysis of glycogenated nuclei in liver biopsy specimens: quantitative evaluation of their relationship with diabetes and obesity.
Glycogenated hepatocyte nuclei are a common finding in liver biopsy specimens from patients presenting with a variety of clinical disorders. Most commonly, glycogenated nuclei from part of a spectrum of pathological changes in the diabetic or obese patient. However, no previous investigation has assessed glycogenated hepatocyte nuclei in a quantitative manner. In this study we used receiver operating characteristic (ROC) analysis to assess quantitatively the strength of glycogenated nuclei as a marker for diabetes and/or obesity. The study population consisted of 102 liver biopsy specimens from the adult population: 20 from diabetic patients, 41 from obese patients, 10 from both obese and diabetic patients, and 31 from neither diabetic nor obese patients. The mean age was 48.5 years with a range of 18 to 80 years. We evaluated the extent of glycogenated nuclei by averaging the number present per high power field over a minimum of 10 high power fields, representing all zones of the liver. The extent of steatosis was graded on a numerical scale from 1 to 10. In ROC analysis perfect tests are associated with an area of 1.0 and completely random tests with an area of 0.5. Receiver operating characteristic analysis showed that glycogenated nuclei are a relatively good test for distinguishing diabetic from nondiabetic patients (area, 0.75), a poor test for distinguishing obese from nonobese patients (area, 0.60), and a fair test for either condition (area, 0.67). In addition, we observed that glycogenated nuclei were preferentially distributed in the periportal "zone 1" of the liver, showed no correlation with steatosis, and had no relation to patient age. For our patient study population the prevalence of diabetes mellitus was 12%. At a cutoff level of four glycogenated nuclei per 400 x high power field, the specificity and sensitivity of glycogenated nuclei as a test for diabetes are 0.98 and 0.30, respectively, with a positive predictive value of 66%.
Adult↗
Rectal tumor stage: correlation of endorectal MR imaging and pathologic findings.
PURPOSE: To develop magnetic resonance (MR) imaging criteria for staging rectal cancer. MATERIALS AND METHODS: Thirty-six patients with rectal tumors underwent MR imaging with an endorectal surface coil. MR images were compared with specimens from the resected tumor. RESULTS: Rectal wall layers were reliably demonstrated. The MR imaging-determined tumor stage agreed with pathologic findings in 81% of cases. A retrospective review found the integrity of the rectal wall layers at the lesion center an accurate criterion for interpreting the local extent of the lesion. Lymph nodes as small as 2 mm were demonstrated. Although sensitive for demonstrating perirectal adenopathy, MR imaging had a specificity of only 72% for N1 disease. CONCLUSION: Endorectal surface coil MR imaging shows promise for staging rectal lesions. Additional studies are necessary to further establish criteria for interpreting the images.
Humans↗
Sterol carrier protein 2: a role in steroid hormone synthesis?
The intracellular movement of cholesterol is an important regulated step in the process of steroidogenesis. However, the molecular mechanisms by which cholesterol is translocated to key organelles, including the mitochondria, remains poorly understood. Lipid transfer proteins may have an important function in this process. One candidate lipid transfer protein is sterol carrier protein 2 (SCP2). This 13.2 kDa protein enhances the movement of cholesterol between vesicles and isolated mitochondria. It also stimulates mitochondrial pregnenolone synthesis. When introduced into intact cells, anti-SCP2 antibodies reduce steroid secretion. Moreover, expression of SCP2 in COS cells engineered to produce progestins increases steroid formation. SCP2 is abundant in steroidogenic glands and the pattern of SCP2 gene expression is consistent with a role for the protein in hormone synthesis: SCP2 transcripts are more prominent in the most steroidogenic compartments of the ovary and tropic hormones that stimulate steroidogenesis increase SCP2 gene expression. Other evidence that suggests that SCP2 plays important roles in cellular function includes a remarkable conservation of primary structure across species. The mechanisms by which SCP2 promotes intracellular sterol movement have not been elucidated. The protein appears to bind sterols and is synthesized with a 20 amino acid N-terminal "pro-" sequence that may serve to target SCP2 to mitochondria. In addition, the C-terminus of SCP2 contains a peroxisome-targeting sequence. SCP2 is derived from a large gene that encodes transcripts that are translated into larger proteins of 30 and 58 kDa. The 58 kDa protein, which has some structural homologies with thiolases, seems to be specifically targeted to peroxisomes whereas SCP2 has a broader subcellular distribution. The significance of the peroxisome association of SCP2 and steroidogenesis has not been disclosed. However, diseases of peroxisome function, including adrenoleukodystrophy and Zellweger syndrome, have notable deficits in steroid and bile acid metabolism, thus linking peroxisomes and steroidogenesis. SCP2 is deficient in fibroblasts of patients with these diseases.
Animals↗
Somatostatin attenuates ischemic intestinal injury.
Pancreatic-derived proteases play a central role in the pathogenesis of ischemic intestinal injury. We postulated that exocrine blockade by pretreatment with a long-acting somatostatin analogue, octreotide acetate, would attenuate ischemic mucosal injury. Sprague-Dawley rats received subcutaneous octreotide (10 micrograms/kg/d) for 6 days by means of surgically implanted infusion ports. In a group of sham control rats, splanchnic blood flow (portal vein Doppler measurement) and duodenal trypsin activity (p-toluene sulfonyl-L-arginine methyl ester assay) were determined. In a separate experiment, pretreated animals were subjected to 60 minutes of superior mesenteric artery ischemia alone or followed by 30 minutes of reperfusion. Gross extent of hemorrhagic necrosis and microscopic injury (rank analysis) were assessed by a blinded observer. Pretreatment with octreotide reduced intraluminal duodenal trypsin activity by 46% without affecting portal blood flow. However, octreotide pretreatment significantly attenuated the microscopic depth of injury during ischemia and the extent of gross injury during reperfusion. It appears that somatostatin may have an adjuvant role in the prevention or progression of intestinal ischemic injury.
Animals↗
Pancreatic osteoarthropathy with unusually destructive sequelae.
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Amputation, Surgical↗
Giant gastric ulcers: an unusual manifestation of Crohn's disease.
We report a patient with Crohn's disease manifesting as recurrent giant gastric ulcers, with subsequent perforation and gastric outlet obstruction. The ulcers contained granulomas, and the patient was achlorhydric. To our knowledge, this is the first report of giant ulcers in a patient with gastric Crohn's disease. This case demonstrates another gastric manifestation of Crohn's disease, it documents nonmalignant gastric ulcers in the setting of achlorhydria, and it raises the possibility of Crohn's disease in the differential diagnosis of giant gastric ulcers refractory to medical management.
Adult↗
Arteriovenous malformation of the small bowel diagnosed with enteroclysis.
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Arteriovenous Malformations↗
An in vitro model for essential fatty acid deficiency: HepG2 cells permanently maintained in lipid-free medium.
A stable essential fatty acid-deficient cell type, known as HepG2-EFD, was derived from the lipoprotein-producing human hepatoma cell line HepG2. These cells are particularly useful for quantitative studies involving essential fatty acids (n-6 and n-3 fatty acids) in secreted lipoproteins. Radiolabeled essential fatty acids can be delivered to these cells without altering the specific activity of the fatty acids, since the deficient cells contain no endogenous essential fatty acids. Using these cells, radioactivity data (dpm) from metabolic studies can be converted directly to mass, and masses as low as a few pmoles can be accurately measured. HepG2-EFD cell cultures were established by growing HepG2 cells in medium containing delipidated serum. After 10 days of growth in delipidated medium, HepG2 cells were completely depleted of all essential fatty acids. Compensatory increases in nonessential fatty acids (n-9 and n-7 fatty acids) including 20:3n-9 (the Mead acid), which is the hallmark fatty acid of essential fatty acid deficiency, were also observed in HepG2-EFD cells. Despite the lack of exogenous fatty acids in the medium and the lack of essential fatty acids in the cells, export of very low density lipoprotein (VLDL)-associated apolipoprotein B by HepG2-EFD was the same as observed for parent HepG2 cells. However, the activity of beta-oxidation of fatty acids in HepG2-EFD cells was much lower than in the parent cell line.(ABSTRACT TRUNCATED AT 250 WORDS)
Apolipoproteins B↗