Emissions from prescribed burning of agricultural fields in the Pacific Northwest.

Prescribed burns of winter wheat stubble and Kentucky bluegrass fields in northern Idaho and eastern Washington states (U.S.A.) were sampled using ground-, aerostat-, airplane-, and laboratory-based measurement platforms to determine emission factors, compare methods, and provide a current and comprehensive set of emissions data for air quality models, climate models, and emission inventories. Batch measurements of PM2.5, volatile organic compounds (VOCs), polycyclic aromatic hydrocarbons (PAHs), and polychlorinated dibenzodioxins/dibenzofurans (PCDDs/PCDFs), and continuous measurements of black carbon (BC), particle mass by size, CO, CO2, CH4, and aerosol characteristics were taken at ground level, on an aerostat-lofted instrument package, and from an airplane. Biomass samples gathered from the field were burned in a laboratory combustion facility for comparison with these ground and aerial field measurements. Emission factors for PM2.5, organic carbon (OC), CH4, and CO measured in the field study platforms were typically higher than those measured in the laboratory combustion facility. Field data for Kentucky bluegrass suggest that biomass residue loading is directly proportional to the PM2.5 emission factor; no such relationship was found with the limited wheat data. CO2 and BC emissions were higher in laboratory burn tests than in the field, reflecting greater carbon oxidation and flaming combustion conditions. These distinctions between field and laboratory results can be explained by measurements of the modified combustion efficiency (MCE). Higher MCEs were recorded in the laboratory burns than from the airplane platform. These MCE/emission factor trends are supported by 1-2 min grab samples from the ground and aerostat platforms. Emission factors measured here are similar to other studies measuring comparable fuels, pollutants, and combustion conditions. The size distribution of refractory BC (rBC) was single modal with a log-normal shape, which was consistent among fuel types when normalized by total rBC mass. The field and laboratory measurements of the Angstrom exponent (α) and single scattering albedo (ω) exhibit a strong decreasing trend with increasing MCEs in the range of 0.9-0.99. Field measurements of α and ω were consistently higher than laboratory burns, which is likely due to less complete combustion. When VOC emissions are compared with MCE, the results are consistent for both fuel types: emission factors increase as MCE decreases.

Determination of the smoke-plume heights and their dynamics with ground-based scanning lidar.

Lidar-data processing techniques are analyzed, which allow determining smoke-plume heights and their dynamics and can be helpful for the improvement of smoke dispersion and air quality models. The data processing algorithms considered in the paper are based on the analysis of two alternative characteristics related to the smoke dispersion process: the regularized intercept function, extracted directly from the recorded lidar signal, and the square-range corrected backscatter signal, obtained after determining and subtracting the constant offset in the recorded signal. The analysis is performed using experimental data of the scanning lidar obtained in the area of prescribed fires.

Eosinophilic colitis is a sporadic self-limited disease of middle-aged people: a population-based study.

AIM: Eosinophilic colitis (EC) is a rare manifestation of eosinophilic gastrointestinal disorders. Due to its rarity, little information is available on its natural history. METHOD: From the single population-based pathology database of the Calgary Health Region (comprising a population of 1.28 million in 2008), cases of EC during the period 1996-2008 were identified. Medical records of all adults diagnosed with EC were identified and the pathology reviewed. The patients were then contacted for follow-up using a standardized questionnaire. RESULTS: Seven cases of EC (four in women) were identified, with a median follow-up of 45 (23-79) months. The median age at diagnosis was 42 (22-70) years. Symptoms at diagnosis were abdominal pain (86%), nonbloody diarrhoea (57%), bloody diarrhoea (29%) and significant (>10%) weight loss (29%). Three patients gave a history of allergic reactions to drugs and four reported allergy to cows' milk. Endoscopic findings were nonspecific, ranging from oedema to small aphthous ulceration. An eosinophilic infiltrate was identified in the lamina propria in the initial colonic biopsy in all patients. Over the longer term, three patients experienced spontaneous resolution without treatment. Two continued to have mild diarrhoea and abdominal cramps but did not require medical therapy. Two patients required medical treatment by 5-aminosalicylic acid, with one requiring prednisone and azathioprine maintenance therapy. CONCLUSION: Eosinophilic colitis is a rare mostly self-limiting disease affecting middle-aged adults. It usually has a mild clinical course and drug treatment is not usually necessary. When required, drug treatment follows the standard medication for other inflammatory bowel disease.

The rising incidence of eosinophilic oesophagitis is associated with increasing biopsy rates: a population-based study.

BACKGROUND: Eosinophilic oesophagitis (EoE) has evolved from a supposedly rare entity to one whose incidence rates are approaching that of inflammatory bowel disease. The factors responsible for this apparent increase in the incidence remain obscure. AIM: To assess various endoscopist and pathologist factors that might affect the frequency of EoE being detected in a well-defined North American population. HYPOTHESIS: Increased endoscopist and pathologist awareness has contributed to the increased clinical recognition of EoE. METHODS: Cases of EoE were identified systematically using population-based pathology and endoscopy databases from January 2004 to December 2008 in Calgary, Canada (population 1.25 million). EoE frequency was estimated with time trend analysis. Characteristics of individual endoscopists (n = 45) were compared with diagnostic rates. RESULTS: Crude population incidence of EoE increased from 2.1 per 10(5) in 2004 to 11.0 per 10(5) in 2008: an annual increase of 39% (P < 0.0001). The frequency in men was 4.5 times higher than in women (95% CI: 3.51-5.76). In patients presenting with dysphagia oesophageal biopsy rates increased from 17.0% in 2004 to 41.3% of EGDs in 2008: an annual rise of 26% (P < 0.0001). On multivariate regression analysis, those endoscopists with higher biopsy rates were more likely to make the diagnosis of EoE (P = 0.008). To include or exclude the diagnosis, typical histological features of EoE were reported more often by pathologists in 2008 as compared to 2004 (P = 0.01 & P < 0.0001 respectively). CONCLUSIONS: The incidence of eosinophilic oesophagitis continues to rise in the general population, in part due to increasing oesophageal biopsy rates and a more detailed histological evaluation of specimens. The biopsy rate of an endoscopist is an indicator for a higher diagnostic yield.

Hepatitis C virus persistence after sustained virological response to antiviral therapy in patients with or without past exposure to hepatitis B virus.

Hepatitis C virus (HCV) and hepatitis B virus (HBV) frequently coinfect and persist long after clinical resolution. We assessed the incidence of low-level (occult) HCV infection (OCI) after sustained virological response (SVR) to standard anti-HCV therapy in individuals with or without past exposure to HBV to recognize whether HBV could influence the prevalence of OCI, HCV level and hepatic histology. Plasma and peripheral blood mononuclear cells (PBMC) were collected from 24 individuals at 6- to 12-month intervals for up to 72 months after SVR. Liver histology was available for nine patients. HCV and HBV genomes were detected with sensitivity <10 genome copies/mL. In individuals without HBV exposure (n = 15), comprehensive analyses of sequential plasma and PBMC samples revealed HCV RNA in all 15 cases (75% plasma and 61% PBMC). In the group with HBV exposure (n = 9), evidenced by circulating anti-HBc and/or HBV DNA detection by a highly sensitive assay, HCV RNA was identified in all cases (83% plasma and 59% PBMC), at levels similar to those in HBV nonexposed individuals. In both groups of patients, most liver biopsies included those reactive for viral genomes displayed low-grade inflammation (8 of 9) and fibrosis (7 of 9). Sequence polymorphisms at the 5`-UTR between PBMC and liver or plasma, as well as circulating HCV virion-like particles, were observed in patients with or without HBV exposure. In conclusion, the prevalence of OCI after SVR is comparable in individuals with or without past exposure to HBV. HCV loads and liver alterations in OCI appear to be unaffected by low-level HBV DNA carriage.

The association of coeliac disease and microscopic colitis: a large population-based study.

BACKGROUND: An association between microscopic colitis and coeliac disease (CD) has been suggested in literature; however, population-based data are limited. AIMS: To estimate the degree of association between these two diseases and to identify possible risk factors for disease concomitance. METHODS: A population-based review of all patients diagnosed with CD and microscopic colitis in a large Canadian centre over a 5-year period. Endoscopy and pathology databases were searched to identify all cases of CD and microscopic colitis diagnosed within the Calgary Health Region between 2004 and 2008. Incidence rates were age-standardised and gender-standardised to 2006 Canadian Census data. standardised incidence ratios (SIR) were used to assess disease concomitance. RESULTS: Over 5 years, 763 patients were diagnosed with CD, and 1106 were diagnosed with microscopic colitis. The standardised incidence of CD ranged from 10.4 to 15.7 per 100,000 population. The standardised incidence of microscopic colitis ranged from 16.9 to 26.2 per 100,000 population. Forty patients were diagnosed with both CD and microscopic colitis, 21 of whom were middle aged (40-60 years) females. Within the CD cohort, microscopic colitis occurred at an annual rate of 11.4 per 1000 cases of CD with an overall SIR of 52.7. CONCLUSIONS: There exists a strong association between microscopic colitis and CD with disease concomitance being approximately 50-times that expected in the general population. The concomitant diagnosis of CD and microscopic colitis largely occurs in middle-aged women. Therefore, middle-aged women with CD and diarrhoea as a presenting or persistent symptom should undergo lower endoscopy with biopsies to rule out microscopic colitis.

Attenuated reovirus displays oncolysis with reduced host toxicity.

BACKGROUND: Although the naturally occurring reovirus causes only mild symptoms in humans, it shows considerable potential as an oncolytic agent because of its innate ability to target cancer cells. In immunocompromised hosts, however, wild-type reovirus can target healthy tissues, including heart, liver, pancreas and neural structures. METHODS: We characterized an attenuated form of reovirus (AV) derived from a persistently infected cell line through sequence analysis, as well as western blot and in vitro transcription and translation techniques. To examine its pathogenesis and oncolytic potential, AV reovirus was tested on healthy embryonic stem cells, various non-transformed and transformed cell lines, and in severe combined immunodeficiency (SCID) mice with tumour xenografts. RESULTS: Sequence analysis of AV reovirus revealed a premature STOP codon in its sigma 1 attachment protein. Western blot and in vitro translation confirmed the presence of a truncated σ1. In comparison to wild-type reovirus, AV reovirus did not kill healthy stem cells or induce black tail formation in SCID mice. However, it did retain its ability to target cancer cells and reduce tumour size. CONCLUSION: Despite containing a truncated attachment protein, AV reovirus still preferentially targets cancer cells, and compared with wild-type reovirus it shows reduced toxicity when administered to immunodeficient hosts, suggesting the potential use of AV reovirus in combination cancer therapy.

The risk of gastrointestinal malignancies in cystic fibrosis: case report of a patient with a near obstructing villous adenoma found on colon cancer screening and Barrett's esophagus.

The life expectancy for cystic fibrosis (CF) patients has increased dramatically over the last 30 years. Although the overall cancer risk for CF patients does not appear to be increased there is a marked increased risk of gastrointestinal malignancies especially in the post lung transplant population. CF patients that do develop gastrointestinal malignancies do so at an earlier age and there is often a lag in the diagnosis and management of these individuals. We present a 39 year old male CF patient that underwent a colonoscopy for colon cancer screening and a large, near obstructing, villous adenoma of his ileum was found. The polyp was removed successfully via endoscopy without incident and there was no evidence of malignancy. An upper endoscopy revealed a long segment of Barrett's esophagus with no evidence of dysplasia. We present this case as well as a detailed review of the literature on cancer risk in CF and a discussion of the mechanisms that may be involved. We also present the risk of GI malignancies in non-CF patients as a guide on how to assess and manage the risk of GI malignancies in this ever-changing patient population.

Reovirus decreases azoxymethane-induced aberrant crypt foci and colon cancer in a rodent model.

Reovirus type 3 Dearing has demonstrated oncolytic efficacy in vitro and in vivo against a variety of cancer cell lines, tumor xenografts and syngeneic cancer models. In this study, we investigated the effectiveness of reovirus against aberrant crypt foci (ACF) and colon cancer induced by the carcinogen azoxymethane (AOM) in an immunocompetent rat model. Sprague-Dawley rats received 15 mg/kg AOM intraperitoneally once per week for 4 weeks and reovirus was administered rectally once a week for 5 weeks starting 20 weeks after the last dose of AOM. Two weeks after completion of reovirus therapy, animals were examined for tumor burden in the colon and other tissues. Reovirus-treated animals showed a decrease in total ACF numbers (P=0.014), in large ACFs (P=0.0069) and in tumor number (P=0.03) compared to vehicle-treated animals. Fewer obstructing tumors in the colon (P=0.07) and duodenum (P=0.03) and reduced hepatic metastases were also noted. In addition, a tumor cell line derived from hepatic metastases was found to be susceptible to reovirus in vitro. Our results show that repeated rectal reovirus administration had some efficacy in the treatment and prevention of AOM-induced ACFs, colon cancers and metastases.

Acquired resistance to reoviral oncolysis in Ras-transformed fibrosarcoma cells.

Reovirus shows considerable potential as an oncolytic agent for Ras-activated tumors and is currently in clinical trials. Here we ask whether such tumor cell lines can acquire resistance to reoviral oncolysis. We challenged human HT1080 fibrosarcoma cells that carry a Ras mutation by prolonged exposure to reovirus, thereby yielding highly virus-resistant HTR1 cells. These cells are persistently infected with reovirus, exhibit high Ras activity and retain the original Ras gene mutation, showing that resistance to reovirus can be displayed in cells with active Ras. The HTR1 cells also exhibit reduced cellular cathepsin B activity, which normally contributes to viral entry and activation. Persistently infected HTR1 cells were not tumorigenic in vivo, whereas immunologically cured virus-free HTR1 cells were highly tumorigenic. Thus, acquisition of resistance to reovirus may constrain therapeutic strategies. To determine whether reoviral resistance is associated with a general reduction in apoptotic potential, we challenged the HTR1 cells with apoptotic inducers and E1B-defective adenovirus, resulting in significant apoptosis and cell death following both approaches. Therefore, even if resistance to reoviral oncolysis should arise in tumor cells in vivo, other therapeutic strategies may nevertheless remain effective.

Hot biopsy forceps in the diagnosis of endobronchial lesions.

Electrocoagulation bronchoscopy biopsy forceps may prevent bleeding, but could also impair the quality of the specimens obtained. Patients with endobronchial lesions during bronchoscopy underwent six endobronchial biopsies each with a hot biopsy forceps, alternating between with electrocoagulation ("hot") and without ("cold"). Bleeding was quantified on a scale of 1-4, with 1 being no bleeding. The generator was set on "soft coagulation" mode, with power settings of 40, 60, 80 and 100 W for each group of 10 patients in a sequential fashion. Clinical pathology results were recorded before samples were reviewed by a second, blinded, pulmonary pathologist. A total of 39 patients with 40 endobronchial lesions had six biopsies performed (one patient had only four samples taken), giving a total of 238 biopsy samples. Concordance between hot and cold samples was 92.5% for the clinical pathologist and 87% for the blinded pathologist. Paired analysis suggested lower average bleeding score with the use of hot forceps. Overall bleeding rates for cold and hot biopsies, respectively, were as follows: grade 1: 30.3 and 41.2%; grade 2: 62.2 and 49.6%; grade 3: 7.6 and 9.2%; and grade 4: 0 and 0%. In conclusion, the use of hot biopsy forceps for endobronchial biopsy does not appear to have a negative impact on the pathological samples. Hot biopsy forceps showed a statistically significant reduction in bleeding score, which is unlikely to be of clinical significance.

The oncolytic effect in vivo of reovirus on tumour cells that have survived reovirus cell killing in vitro.

The use of oncolytic viruses has received considerable attention in recent years and many viruses have proved to be effective against a variety of cancer models and a few are currently being used in clinical trials. However, the possible emergence and outcome of virus-resistant tumour cells has not been addressed. We previously reported the effective use of reovirus against lymphoid malignancies, including the Burkitt's lymphoma cell line Raji. Here we isolated in vitro persistently infected (PI) Raji cells, and cells 'cured' of persistent reovirus infection ('cured' cells). Both PI and cured Raji cells resisted reovirus infection and cell killing in vitro. In vivo, the PI cells were non-tumorigenic in SCID mice, but cured cells regained the parental cells' ability to form tumours. Tumour xenografts from the cured cells, however, were highly susceptible to reovirus oncolysis in vivo. This susceptibility was due to the proteolytic environment within tumours that facilitates reovirus infection and cell killing. Our results show that persistent infection by reovirus impedes tumour development and that although PI cells cleared of reovirus are tumorigenic, they are killed upon rechallenge with reovirus. Both the PI and cured states are therefore not likely to be significant barriers to reovirus oncolytic therapy.

Octreotide in intestinal lymphangiectasia: lack of a clinical response and failure to alter lymphatic function in a guinea pig model.

Intestinal lymphangiectasia, which can be classified as primary or secondary, is an unusual cause of protein-losing enteropathy. The main clinical features include edema, fat malabsorption, lymphopenia and hypoalbuminemia. Clinical management generally includes a low-fat diet and supplementation with medium chain triglycerides. A small number of recent reports advocate the use of octreotide in intestinal lymphangiectasia. It is unclear why octreotide was used in these studies; although octreotide can alter splanchnic blood flow and intestinal motility, its actions on lymphatic function has never been investigated. A case of a patient with intestinal lymphangiectasia who required a shunt procedure after failing medium chain triglycerides and octreotide therapy is presented. During the management of this case, all existing literature on intestinal lymphangiectasia and all the known actions of octreotide were reviewed. Because some of the case reports suggested that octreotide may improve the clinical course of intestinal lymphangiectasia by altering lymphatic function, a series of experiments were undertaken to assess this. In an established guinea pig model, the role of octreotide in lymphatic function was examined. In this model system, the mesenteric lymphatic vessels responded to 5-hydroxytryptamine with a decrease in constriction frequency, while histamine administration markedly increased lymphatic constriction frequency. Octreotide failed to produce any change in lymphatic function when a wide range of concentrations were applied to the mesenteric lymphatic vessel preparation. In conclusion, in this case, octreotide failed to induce a clinical response and laboratory studies showed that octreotide did not alter lymphatic function. Thus, the mechanisms by which octreotide induced clinical responses in the cases reported elsewhere in the literature remain unclear, but the present study suggests that it does not appear to act via increasing lymphatic pumping.

Aquaporin expression is downregulated in a murine model of colitis and in patients with ulcerative colitis, Crohn's disease and infectious colitis.

Colitis is associated with alterations in electrolyte and water transport. These changes give rise to some of the symptoms experienced by patients with colitis. Alterations in fluid flux may also contribute to increased susceptibility to mucosal injury. Recently, endogenous water channel proteins (aquaporins; AQPs), have been identified in colonic tissue. The expression of AQP4, AQP7 and AQP8 was examined, via reverse transcription/polymerase chain reaction, Western blotting and immunohistochemistry, in a murine model of colitis and in patients with inflammatory bowel disease or infectious colitis. Colitis was induced in C57BL/6 mice by the addition of 2.5% dextran sodium sulphate (DSS) to their drinking water. AQP expression in these mice was assessed following 12 h to 7 days of DSS exposure and during the recovery phase from 1 to 15 days following cessation of DSS exposure. Colonic water transport was measured after 1 and 3 days of DSS and following 7 days of recovery. The expression of AQP4 and AQP8 mRNA was significantly decreased after 12-24 h of DSS exposure and remained depressed throughout the treatment period. Expression of AQP7 was more variable. Protein expression followed a similar pattern to that observed for AQP mRNA. Significant alteration in colonic fluid secretion was correlated with reduced expression of AQP isoforms. Significantly, patients with active ulcerative colonic, Crohn's colitis or infectious colitis had similar dramatic reductions in AQP expression that appeared to be correlated with disease activity. Thus, colonic injury in both mouse and man is associated with a downregulation in AQP expression.

Factors controlling long- and short-term sequestration of atmospheric CO2 in a mid-latitude forest.

Net uptake of carbon dioxide (CO2) measured by eddy covariance in a 60- to 80-year-old forest averaged 2.0 +/- 0.4 megagrams of carbon per hectare per year during 1993 to 2000, with interannual variations exceeding 50%. Biometry indicated storage of 1.6 +/- 0.4 megagrams of carbon per hectare per year over 8 years, 60% in live biomass and the balance in coarse woody debris and soils, confirming eddy-covariance results. Weather and seasonal climate (e.g., variations in growing-season length or cloudiness) regulated seasonal and interannual fluctuations of carbon uptake. Legacies of prior disturbance and management, especially stand age and composition, controlled carbon uptake on the decadal time scale, implying that eastern forests could be managed for sequestration of carbon.

Leukocyte elastase in murine and human non-Hodgkin lymphomas.

Extracellular proteases play a crucial role in the invasive behavior of normal and transformed leukocytes. Thus far, however, most of the attention has been focused on members of the family of matrix metalloproteinases. In this work, we show that lymphoma cells can express leukocyte elastase (LE) and recruit the enzyme at their surface via ICAM-1. The expression of LE by lymphoma cells was augmented significantly by stimulation with IL-6 and IL-13, both of which also induced the expression of MMP-9. Although LE and IL-13 transcripts were detected in several non-Hodgkin's lymphomas, immunohistochemical analysis of lymphoma tissues also showed that LE was strongly expressed in infiltrating leukocytes. Given the spectrum of key molecules that can be cleaved by LE and that LE and MMP-9 are involved in the invasive behavior of normal or transformed leukocytes, our results raise the hypothesis that LE plays a crucial role in the multistep processes of inflammation and lymphoma metastasis.

Reactivation of hepatitis B e antigen-negative chronic hepatitis B in a bone marrow transplant recipient following lamivudine withdrawal.

Reactivation of hepatitis B virus (HBV) is a recognized complication of bone marrow transplantation (BMT). Lamivudine is a nucleoside analogue with potent antiviral activity that has been used in the prophylaxis of HBV reactivation in at-risk BMT recipients. Currently, no data exist regarding the safety of nucleoside analogue withdrawal in these patients. A 32-year-old BMT recipient with hepatitis B e antigen (HBeAg)-negative, chronic HBV who developed a serious flare of hepatic inflammation due to a rebound in viral replication within 12 weeks of discontinuing lamivudine therapy is described. The patient remained HBeAg-negative despite high level viremia, suggesting the emergence of a mutant viral strain. The patient's acute hepatitis resolved promptly with the reinstitution of lamivudine therapy. Further studies are necessary to define the safety and efficacy of nucleoside analogues in the prevention of HBV reactivation in at-risk BMT recipients. Clinicians should consider the risk of inducing serious flares of hepatic inflammation due to abrupt nucleoside analogue withdrawal in these patients.

A case of coexisting primary biliary cirrhosis and primary sclerosing cholangitis: a new overlap of autoimmune liver diseases.

Although the etiology of AIH, PBC, and PSC remains unknown, it is apparent that these autoimmune liver diseases share many common features and can coexist in the same patient. Our patient had features of PBC and later clearly developed a picture of PSC. This case suggests that PBC, PSC, AIH, and autoimmune cholangitis are part of a spectrum of chronic autoimmune liver disease that develop in response to some yet unidentified antigen.

Expression of survivin, YB-1, and KI-67 in sporadic adenomas and dysplasia-associated lesions or masses in ulcerative colitis.

Sporadic adenomas are said to exhibit an orderly growth pattern with a reversal of proliferative and apoptotic cell distribution as compared with normal colonic crypts. Dysplastic polyps of patients with ulcerative colitis (UC) may represent dysplasia-associated lesions or masses (DALM) with a high associated cancer risk, or, alternatively, may represent sporadic adenomas. Histologic criteria to differentiate between sporadic adenomas and DALM have not focused on the balance between cell renewal and cell loss. The expression of the novel anti-apoptosis gene product, survivin, and the proliferation markers, Ki-67 and Y-box binding protein (YB-1), were investigated by immunohistochemical localization in sporadic adenomas and DALM lesions of patients with UC. In adenomas, KI-67 was expressed preponderantly at the luminal aspect of the polyp, whereas its expression was diffuse in DALM. Survivin was detected diffusely in both adenomas and DALM. YB-1 showed positive staining in the deep aspect of adenomatous glands but only to a minor degree at the surface, whereas both deep and diffuse expression patterns of YB-1 were seen in DALM. The authors conclude that DALM and sporadic adenomas exhibit different patterns of cellular proliferation and that molecular markers of cell proliferation, Ki-67 and YB-1, may be useful to distinguish sporadic adenomas from DALM. However, the similar expression of survivin suggests that the underlying mechanisms that regulate apoptotic cell death are uniform in these lesions.

Glut-1 expression in dysplastic and regenerative lesions of the colon.

Monosaccaride transporter proteins are responsible for transmembrane transport of monosaccarides into cells. Glucose transporter protein 1 (Glut-1) is most prevalent in the cell membranes of erythrocytes and facilitates transport of glucose in tissues with barrier functions, i.e. blood brain barrier. Expression of Glut-1 in malignant tumors is increased due to increased metabolic need of the proliferating cell populations. In colorectal adenomas and carcinomas, membranous expression of Glut-1 has been associated with higher grade of tumors and decreased survival time. We studied the expression of Glut-1 in dysplastic proliferations of the colon which included sporadic adenomas and dysplasia associated lesions (DALM) in patients with ulcerative colitis and reactive/regenerative proliferations of the colon, including non-dysplastic chronic colitis, acute colitis and ischemia. Two patterns of Glut-1 expression were detected. Most adenomas and DALMs showed at least focal membranous expression of Glut-1. In addition a second staining pattern was recognized which consisted of prominent supranuclear dots. This pattern of staining was not only seen in adenomas and DALM but also in non-dysplastic areas immediately surrounding sporadic adenomas, in regenerative chronic colitis and in areas surrounding acute inflammation. Areas away from dysplasia did not show any positive staining for Glut-1. We conclude that two distinct patterns of Glut-1 expression may be found in colonic epithelial proliferation: membranous staining, associated with dysplasia, and, heretofore not described, supranuclear staining which may be related to Glut-1 expression secondary to expression of specific growth factors and not necessarily related to dysplasia.