bluuebunny/crossref_metadata_2025_split huggingface dataset:
Direct evidence of monocyte recruitment to inflammatory bowel disease mucosa
Authors: GRIMM MC , PULLMAN WE , BENNETT GM , SULLIVAN PJ , PAVLI P. , DOE WF 
Published: March 2008

AbstractAlterations in phenotype and function of intestinal macrophages occur in inflammatory bowel disease (IBD) but it is unclear whether these changes result from the recruitment of circulating monocytes to the intestine or from proliferation of resident intestinal macrophages. We sought to demonstrate the arrival of blood monocytes, the precursors of macrophages, in IBD mucosa. Peripheral blood mononuclear cells were isolated from 23 patients with clinically active intestinal inflammation (13 Crohn's disease, eight ulcerative colitis, two infective colitis), then radiolabelled with 99mtechnetium (Tc)‐stannous colloid (n=13) or 111indium (In)‐oxine (n=10) before re‐injection and abdominal scanning. Four patients had demonstrable intestinal monocyte uptake using [99mTc]‐stannous colloid, while six [111In]‐oxine‐labelled monocyte scans were positive. Uptake sites correlated with actively inflamed regions. Patients demonstrating monocyte uptake had been treated with corticosteroids for a significantly (P < 0.02) shorter duration (median 3 vs 20 days) than those with negative scans. There was no significant difference between positive and negative scans for disease category, clinical or histological disease activity, or radioisotope used. Biopsies of inflamed mucosa from two patients suffering ulcerative colitis who had positive scans showed a high proportion of CD14‐positive macrophages, 4–9% of which contained autoradiographic grains. These results demonstrate that blood monocytes are recruited to the mucosa of actively inflamed bowel, and suggest that this process may be inhibited by corticosteroids. Moreover, the phenotype of the recently‐arrived monocytes indicates their susceptibility to stimulation by lipopolysaccharide, and suggests a mechanism for the continuing inflammation in the bacterial product‐rich milieu of IBD.
Interaction of Kupffer cells to splenic macrophages and hepatocytes in endotoxin clearance: Effect of alcohol
Authors: FUKUI HIROSHI , KITANO HIROYUKI , OKAMOTO YASUYUKI , KIKUCHI EIRYOU , MATSUMOTO MASAMI , KIKUKAWA MASAJI , MORIMURA MASAFUMI , TSUJITA SIGENOBU , NAGAMOTO ISSEI , NAKATANI TOSHIYA , TSUJII TADASU 
Published: March 2008

AbstractAn additional administration of high dose ethanol to chronic alcohol‐fed rats led to a decrease in endotoxin clearance and an increase in endotoxin accumulation in the spleen accompanied by an elevation of tumour necrosis factor (TNF) levels in the portal vein. Endotoxin uptake and TNF production by Kupffer cells (KC) and splenic macrophages in the chronic ethanol load rats were significantly greater than those in the control rats. When these cells were precultured in the medium containing 10 to 100mmol/L ethanol, the endotoxin uptake and TNF production of KC were decreased. However, this did not affect the endotoxin uptake and TNF production of splenic macrophages.The hepatic production of endotoxin binding protein was increased when KC were preincubated in the medium containing ethanol and the resultant culture supernatant was added to the hepatocyte culture system. This endotoxin binding protein was proved to enhance the uptake of endotoxin and suppressed the production of TNF in the KC. When KC and hepatocytes were isolated from chronically alcohol‐fed rats, further addition of ethanol to the culture medium of KC did not affect the hepatic production of endotoxin binding protein. The increase in hepatic production of endotoxin binding protein may serve as a defence mechanism against endotoxicity. There is a possibility that an impairment of this defence mechanism has a pivotal role in the development of endotoxaemia and endotoxicity in chronic alcoholics.
Role of vitamin A in liver fibrosis
Authors: KNOOK DL , BOSMA A , SEIFERT WF 
Published: March 2008

AbstractThe relationship between vitamin A and liver fibrosis was studied with a CCl4‐induced fibrosis model in rats. Depending on the time of administration, vitamin A can potentiate or reduce fibrosis: when present during CCl4‐treatment parenchymal cell damage and fibrosis were enhanced, whereas vitamin A post‐treatment strongly reduced fibrosis. Enhanced fibrosis was also found in rats with low hepatic retinoid levels. Administration of ß‐carotene during CCl4‐treatment reduced several signs of fibrosis. The notion that liver retinoids play an important role in hepatic fibrogenesis is discussed.
New prolyl 4‐hydroxylase inhibitor reduces procollagen gene expression and enzyme‐altered lesions in rat liver cirrhosis
Authors: SAKAIDA ISAO , OKITA KIWAMU 
Published: March 2008

AbstractA choline deficient l‐amino acid defined (CDAA) diet led to the development of liver cirrhosis in male Wistar rats after 16 weeks. A new prolyl 4‐hydroxylase inhibitor, 2,4‐pyridine dicarboxylic acid bis [(2‐methoxyethyl amide)] (HOE 077), prevented liver fibrosis in a dose‐dependent manner without a reduction in increased serum alanine aminotransferase and aspartate aminotransferase in parallel with a reduction in preneoplastic enzyme‐altered lesions stained with anti‐glutathione S‐transferase placental form antibody. HOE 077 reduced the increase in serum procollagen III peptide (PIIIP) in a dose‐dependent manner and in proportion to the reduction in mRNA expression of type III procollagen in the liver of rats fed a CDAA diet.
Apoptosis: A new mechanism of endothelial and Kupffer cell killing
Authors: TAKEI YOSHIYUKI , KAWANO SUNAO , NISHIMURA YOSHIYA , GOTO MORITAKA , NAGAI HIROTAKA , CHEN SHENG‐SONG , OMAE ATSUSHI , FUSAMOTO HIDEYUKI , KAMADA TAKENOBU , IKEDA KAZUO , KAWADA NORIFUMI , KANEDA KENJI 
Published: March 2008

AbstractKupffer cells (KC) become activated in response to lipopolysaccharide (LPS) and produce a variety of mediators. Among them, TNFα is known to injure the liver. Here we report that TNFα mediates apoptosis in KC and sinusoidal endothelial cells. After stimulation for 24 h with LPS (0‐10 μg/mL), apoptosis in KC detected by TUNEL TdT‐mediated dUTP‐biotin nick end labelling (TUNEL) increased in a concentration‐dependent manner (0 μg/mL, 12 ± 4%; 0.1 μg/mL, 36 ± 11%; 1.0 μg/mL, 65 ± 9%; 10 μg/mL, 78 ± 15%). In contrast, co‐incubation of endothelial cells with LPS‐stimulated KC resulted in a marked increase in TUNEL‐positive endothelial cells. TNFα antibody blocked apoptosis in both KC and endothelial cells. Apoptosis was observed in cells adjacent to or in contact with KC. Reducing transmembrane TNFα expressed on KC also led to a decrease in endothelial cell apoptosis, suggesting that transmembrane TNFα is implicated in the cell‐to‐cell contact mechanism of induction of apoptosis. Thus, TNFα mediates apoptosis in KC and endothelial cells.
Nitric oxide mediates mitochondrial dysfunction in hepatoma cells induced by non‐activated Kupffer cells: Evidence implicating ICAM‐1‐dependent process
Authors: KUROSE IWAO , EBINUMA HIROTOSHI , HIGUCHI HAJIME , YONEI YOSHIKAZU , SAITO HIDETSUGU , KATO SHINZO , MIURA SOICHIRO , ISHII HIROMASA 
Published: March 2008

AbstractThe metabolic changes in a rat hepatoma cell line, AH70 cells, after co‐culture with rat Kupffer cells (KC) were visualized and analysed using a fluorescence microscope equipped with a silicon intensified target camera and a laser scanning confocal microscopic system. Kupffer cells were isolated from male Wistar rats, and cultured without any stimuli. The non‐activated KC reduced the mitochondrial energization in the cocultured AH70 cells within 2 h, which was indicated by decreased rhodamine 123 (Rh123) fluorescence. Either Ng‐monomethyl‐l‐arginine or dexamethasone significantly attenuated the KC‐induced mitochondrial dysfunction in AH70 cells, suggesting the involvement of nitric oxide (NO) derived from inducible‐type nitric oxide synthase (iNOS). Administration of monoclonal antibody (mAb) directed against rat ICAM‐1 also prevented the decrease in Rh123 fluorescence. Electron microscopy revealed that the membrane‐to‐membrane attachment between KC and AH70 cells occurred within 2 h. A laser scanning confocal microscopic observation using mAb against ICAM‐1 presented that the ICAM‐1 expression on AH70 cells and KC increased after the co‐culture. It is therefore concluded that the KC‐mediated mitochondrial dysfunction of hepatoma cells largely depends on NO production by iNOS. Furthermore, the present study supports a scenario that the NO production and release from KC is triggered by the close contact with hepatoma cells through adhesion molecules such as ICAM‐1.
Activated liver macrophages in human liver diseases
Authors: YAMAMOTO KAZUHIDE , OHMOTO MASAKI , MATSUMOTO SEIJI , NAGANO TAKUYA , KOBASHI HARUHIKO , OKAMOTO RYOICHI , TSUJI TAKAO 
Published: March 2008

AbstractImmunohistochemical analysis using monoclonal antibodies specific for cells of monocyte/macrophage lineage reveals that resident liver macrophages have a phenotype distinct from that of monocytes or activated liver macrophages. Liver macrophages consist of heterogeneous cell populations in maturation (matured 25F9‐positive and immature 25F9‐negative) but the ratio of two populations is constant in normal and diseased livers. The expression of CD 14 is down‐regulated in resident liver macrophages as compared to that in monocytes, while the expression of 25F9 is up‐regulated. On the other hand, the expressions of CD 14 and Fc γ RI are up‐regulated in activated liver macrophages in viral and autoimmune hepatitis. In vitro culture of monocytes in medium without cytokines induces the phenotype similar to that of resident liver macrophages. Addition of macrophage‐colony stimulating factor or interferon‐γ into the culture medium induces the expression of Fc γ RI, the phenotype of which resembles that of activated liver macrophages. These results suggest that liver macrophages consist of heterogeneous cell populations and that both phenotype and function are affected by the local milieu of cytokines.
Dual role of Kupffer cell activation and endothelial cell damage in reperfusion injury to livers stored for transplantation surgery
Authors: LEMASTERS JOHN J , PENG XING‐XI , BACHMANN SIGRID , CURRIN ROBERT T , GAO WENSHI , THURMAN RONALD G 
Published: March 2008

AbstractIn rat models of liver preservation, the primary event leading to liver graft failure after cold storage is a reperfusion injury causing damage to sinusoidal endothelial cells and activation of Kupffer cells (KC). After storage for longer than 16 h in University of Wisconsin solution, reperfusion induces rapid endothelial cell killing. Kupffer cell activation also occurs as indicated by cell surface ruffling, degranulation, release of hydrolytic enzymes, generation of oxygen radicals, and increased phagocytosis. Down‐regulation of KC activity with nisoldipine or pentoxifylline improves graft survival. Moreover, pretreatment of donors with small amounts of endotoxin to activate KC causes a drastic reduction of graft survival. Together, KC activation and endothelial damage cause marked microcirculatory disturbances after transplantation characterized by reduced and uneven blood flow and increased leucocyte and platelet adhesion. Such events culminate in inflammation, necrosis and fulminant graft failure. Modification of reperfusion conditions can reduce the extent of injury. In particular, flushing livers with Carolina rinse solution (CRS) at the end of storage reduces endothelial cell killing, suppresses KC activation, improves the microcirculation, and increases graft survival. Active ingredients in CRS include antioxidants (allopurinol, desferrioxamine and glutathione), adenosine and slightly acidic pH (6.5). Other potentially important ingredients are nicardipine, a calcium channel blocker, and fructose, glucose and insulin to promote glycolysis. The cytoprotective amino acid, glycine, further improves the performance of Carolina rinse solution. Reperfusion‐induced changes to nonparenchymal cells play an essential role in damage to livers preserved for transplantation surgery. Understanding the role of sinusoidal endothelial cells and KC in this injury has led to promising new strategies to prolong organ storage and reduce graft failure.
Serum ferritin: Does it differ from tissue ferritin?
Authors: LINDER MARIA C. , SCHAFFER KENNETH J. , HAZEGH‐AZAM MARYAM , ZHOU CECILIA YJ , TRAN TUE N. , NAGEL GLENN M. 
Published: March 2008

ABSTRACTSerum ferritin isolated from the horse was structurally compared with horse spleen ferritin and was found to differ markedly in molecular weight, iron content, carbohydrate, subunit size and amino acid sequence. The results are summarized and initial results obtained with candidate clones of pieces of two serum ferritin subunits are described
Alcohol and iron: One glass of red or more?
Authors: FLETCHER LINDA M. 
Published: March 2008

ABSTRACTThe consumption of excessive amounts of alcohol affects human iron homeostasis and an association of iron overload and heavy alcohol consumption has been recognized for many years. Both major proteins of iron metabolism, ferritin and transferrin, are affected by alcohol. Increased hepatic iron levels are seen in a high proportion of alcoholic subjects, sometimes causing confusion in diagnosis between alcoholic liver disease and iron‐overload disease. The pattern of deposition of this iron in alcoholics, however, differs from that seen in the iron‐overload disease haemochromatosis. Excessive alcohol consumption causes transferrin to become carbohydrate deficient, which allows it to be used as an efficient biochemical marker of alcohol abuse. It is concluded that alcohol consumption in moderation is unlikely to have deleterious health consequences.
Complications and outcome of percutaneous endoscopic gastrostomy in different patient groups
Authors: CHOWDHURY MOSIUDDIN A. , BATEY ROBERT 
Published: March 2008

AbstractA retrospective study of percutaneous endoscopic gastrostomy (PEG) was performed to evaluate the complications of PEG and determine the role of prophylactic antibiotics in preventing early wound infection and to evaluate the outcome of patients in different groups (neurological disease, head injury, AIDS). Percutaneous endoscopic gastrostomy was performed on 50 patients between March 1991 and November 1993 and the survey was completed in July 1994. The average time to PEG placement post‐cerebrovascular accident or head injury was 5 weeks. No deaths were attributable to the procedure. Four of 50 (8%) patients died in the first 30 days (early mortality). Wound infection (early eight, late five) was the most common complication: two of 13 patients receiving prophylactic antibiotics and six of 37 not receiving antibiotics had early wound infection. At completion of follow‐up 19 of 26 patients with neurological disease had died (median survival = 370 days), three resumed oral feeding and four continued PEG feeding. All head injury patients (n= 6) were alive and had resumed oral feeding; five returned home. All AIDS patients (n= 7) died within 12 months (median survival = 138 days), although improved nutritional state was found after gastrostomy feeding. In conclusion, PEG placement is a useful procedure to assist feeding in multiple patient groups. Wound infection is a common but not life threatening complication. The need for prophylactic antibiotics to prevent early wound infection has not been proven. The 5 week delay in PEG insertion may contribute to lower early mortality. The 100% survival rate in head injury patients may reflect their young age and absence of underlying medical illness. In AIDS patients, improved nutritional state is not known to translate into better quality of life or prolonged survival.
Method for quantitative assessment of transformation of non‐micellar cholesterol carriers in model bile systems*
Authors: YAMASHITA YOSHIFUMI , TAZUMA SUSUMU , KAJIYAMA GORO 
Published: March 2008

AbstractAggregation and fusion of non‐micellar particulate species, such as unilamellar vesicle and phospholipid lamellae, are believed to precede the nucleation of cholesterol crystals in bile. However, little is known about the time sequence relationship between transformation of non‐micellar particles and the initial appearance of cholesterol crystals, as no adequate technique is available for assessing such transformations quantitatively. We have developed a novel method for quantitatively estimating vesicle transformation in supersaturated model bile systems, using a spectrophotometric technique to determine the time sequence relationship between such transformations and cholesterol crystal nucleation. We also investigated the potency of a given effector substance on this transformation. This method permits simultaneous quantitative determination of vesicle aggregation and of cholesterol crystal growth. Maximal vesicular aggregation as determined from turbidity, coincided with initiation of cholesterol crystal nucleation. The addition of divalent cations, Ca2+ and Mg2+, to the model bile solutions promoted vesicle aggregation and cholesterol crystal nucleation and growth. In contrast, apolipoproteins A‐1 and A‐2 retarded such processes. These data were highly reproducible and reliable. The method described is easy to perform, provides reproducible results and permits the determination of the potency of effector substances on vesicle transformation and on the nucleation of cholesterol crystals.
Case Report: Pneumomediastinum and pneumothorax complicating colonoscopy
Authors: TAM WILLIAM CE , POLLARD IAN , JOHNSON RICHARD D 
Published: March 2008

ABSTRACTColonic perforation is potentially the most serious complication of colonoscopy. Both the clinical manifestation and rapidity of onset of symptoms can vary depending on whether the perforation occurs directly into the peritoneal cavity or into the retroperitoneal space. Colonic perforation is often associated with abdominal pain, although more uncommon presentations have been documented. A case report of a unilateral pneumothorax and pneumomediastinum complicating colonoscopy is described, which responded well to conservative measures without recourse to surgical intervention, antibiotic therapy or parenteral alimentation.
Do non‐steroidal anti‐inflammatory drugs cause duodenal ulcer? Evaluation of basal acid output and ulcer complications
Authors: COLLEN MARTIN J. , ABDULIAN JOHN D. 
Published: March 2008

AbstractNon‐steroidal anti‐inflammatory drug (NSAID) use and basal acid outputs determined by nasogastric suction were evaluated prospectively in 184 patients with endoscopically documented duodenal ulcer. The mean basal acid output and percentage of gastric acid hypersecretion for duodenal ulcer patients who used NSAID were compared with duodenal ulcer patients who did not use NSAID to determine whether patients using NSAID who develop duodenal ulcer have basal acid outputs in the normal range or in the duodenal ulcer range. Results were compared with 65 normal subjects and 105 patients with nonulcer dyspepsia. There were no significant differences with regard to the percentage of male gender, mean age, mean basal acid output, percentage of gastric acid hypersecretion and percentage of cigarette smoking history between duodenal ulcer patients who used NSAID and duodenal ulcer patients who did not. However, significant differences were observed between duodenal ulcer patients who used NSAID and duodenal ulcer patients who did not use NSAID with regard to the percentage of bleeding duodenal ulcer (59 compared with 23%;p= 0.0008) and the percentage of patients with giant duodenal ulcer (41 compared with 5%;P= 0.00001). These results suggest that NSAID use does not cause duodenal ulcer but does make pre‐existing duodenal ulcer worse by causing duodenal ulcer complications.
Case Report: Gastrointestinal tuberculosis simulating Crohn's disease
Authors: KAUSHIK SP , BASSETT ML , McDONALD C. , LIN BPC , BOKEY EL 
Published: March 2008

AbstractA male Caucasian presented with abdominal pain and a right iliac fossa mass. There were no risk factors for Mycobacterium tuberculosis infection. He was investigated by upper and lower gastrointestinal endoscopy, chest and small bowel radiology. The latter showed stricturing of the third and fourth parts of the duodenum, mid‐jejunum and terminal ileum. Biopsies were non‐specific and he was thought to have Crohn's disease. Subsequent treatment with corticosteroids resulted in improved well being and weight gain; however, the patient demonstrated disease progression with the development of complex fistulae and Escherichia coli septicaemia. At surgery the patient was found to have an ileal inflammatory mass with fistulae to the sigmoid colon. The terminal ileum, fistulae and a segment of colon were resected. Treatment with anti‐tuberculous drugs ensued and the patient is now asymptomatic after 15 months of follow‐up. This case serves to highlight the difficulty in making the diagnosis of gastrointestinal tuberculosis, a disease that may mimic Crohn's disease, and the need for caution in the use of corticosteroids in any disease in which tuberculosis enters into the differential diagnosis. The role of surgery in making the diagnosis and managing the complications, in conjunction with anti‐tuberculous drugs, and the prospect of cure are exemplified by this case.
Treatment of severe forms of alcoholic hepatitis: Where are we going?
Authors: Mathurin Philippe , Louvet Alexandre , Dharancy Sébastien 
Published: March 2008

AbstractAlcoholic hepatitis (AH) is observed in approximately 20% of heavy drinkers. The treatment of AH remains one of the main challenges to clinicians involved in the management of severe alcoholic liver disease. Corticosteroids improved the short‐term survival of patients with severe AH. Nevertheless, the efficacy of corticosteroids is still considered controversial for some authors. Pentoxifylline may be considered an alternative to corticosteroids. Early identification of subjects with substantial risk of death according to the Lille model will improve management of patients suffering from severe AH and will aid in the design of future studies for alternative therapies. Alternative therapies are required to improve the prognosis of patients with a severe form of AH. Progress in understanding the pathogenesis of AH is opening up an exciting new era and is lending impetus to future evaluation of new drugs targeting the tumor necrosis factor pathways.
TALL GIRLS ASSESSMENT AND MANAGEMENT
Authors: WETTENHALL H. N. B. , ROCHE A. F. 
Published: March 2008

SYNOPSISMany girls above the mean in stature become concerned about this when they are pubescent. A selected group of these girls has been treated successfully with stilboestrol to accelerate their skeletal maturation and thus reduce their adult stature. The selection of girls for treatment, and the sources of inaccuracy in estimating the effectiveness of treatment in individual girls are discussed.