PubMed Health⌕ Search

Biomedical subjects

D Faust

Publications and source records attributed to D Faust.

At least 19 recordsLinked to original sources
PubMed2003

Human peritoneal macrophages in culture: a model for studying inflammatory disorders in vitro.

In this study we characterized a model of human peritoneal macrophages maintained in culture for up to 48 h that can be used to study different functions of this cell population in vitro. The cells remained viable and functionally active over time, with well-preserved phagocytic properties. They expressed a macrophage marker, CD14. Once in culture, human peritoneal macrophages secreted C1q and nitric oxide in a pattern described in murine, guinea pig, and rat peritoneal macrophages. The described model can be used to study physiology and pathophysiology of peritoneal macrophages in vitro, offering all the advantages of the use of a human cell population.

Animals↗
PubMed2003

Nodular regenerative hyperplasia of the liver: a rare differential diagnosis of cholestasis with response to ursodeoxycholic acid.

Nodular regenerative hyperplasia of the liver (NRHL) is an uncommon non-malignant finding typically associated with haematological or auto-immune disease. The main clinical symptom is portal hypertension in the absence of underlying liver cirrhosis. The pathogenesis of NRHL remains unknown. We report a case of NRHL with cholestasis and progression to liver insufficiency without any underlying disease and no association with systemic disease or drug intake. Cholestasis and liver function tests improved significantly during treatment with ursodeoxycholic acid (750 mg per day). Based on this case, it may be concluded that treatment with ursodeoxycholic acid might be beneficial in patients with NRHL and progression to liver insufficiency.

Biopsy↗
PubMed2003

Increased serum bone sialoprotein concentrations in patients with Crohn's disease.

INTRODUCTION: Impaired calcium homeostasis and/or the administration of corticosteroids are considered to be among the factors contributing to the pathogenesis of osteopenia in patients with inflammatory bowel disease. There is an increasing evidence suggesting that certain pro-inflammatory cytokines may also directly influence the bone metabolism in these patients. Routine measurement of bone mass and loss usually include dual energy X-ray absorptiometry as well as urinary and serum assessment of collagen crosslinks. More recent studies include likewise the detection of bone sialoprotein into a specific diagnostics of bone turnover. PATIENTS AND METHODS: We investigated 47 patients with inflammatory bowel disease (Crohn's disease N = 41, ulcerative colitis N = 6) and 17 healthy volunteers to assess and compare serum levels of bone sialoprotein and other routine parameters of bone turnover. Bone sialoprotein levels were measured by using a recently described radioimmunoassay. RESULTS: In comparison to the control group, bone sialoprotein and urinary crosslinks were significantly increased only in patients with Crohn's disease, while other markers of bone turnover (e. g. alkaline phosphatase, carboxylterminal propeptide of typ I procollagen, urinary deoxypyridinoline, vitamin D, phosphate and calcium) did not differ significantly between the patients' groups. CONCLUSION: According to these data, increased serum bone sialoprotein concentrations seem to be an additional valuable and sensitive marker of bone resorption in patients with Crohn's disease.

Adult↗
PubMed2002

2,3,7,8-tetrachlorodibenzo-p-dioxin-dependent release from contact inhibition in WB-F344 cells: involvement of cyclin A.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent tumor promoter ever tested in rodents. Although it is known that most of TCDD actions are mediated by binding to the aryl hydrocarbon receptor (AhR), the mechanisms leading to tumor promotion still remain to be elucidated. Loss of contact inhibition is one characteristic hallmark in tumorigenesis. In rat liver epithelial WB-F344 cells, TCDD induces a release from contact inhibition, which is manifested by a twofold increase in cell number when TCDD (1 nM for 48 h) is added to confluent cells in the presence of serum, but not when given to exponentially growing or subconfluent, serum-deprived WB-F344 cells. Loss of G1 arrest was also shown by flow cytometric analysis. We demonstrate that TCDD treatment significantly increases cyclin D2 and cyclin A protein levels and show by immunofluorescence that these proteins accumulate in the nucleus. Although TCDD treatment leads to a strong increase in cyclin D2/cdk4 and cyclin A/cdk2 complex formation, we could only detect an elevation of cyclin A/cdk2 activity. In accordance with a lack of elevated cdk4 activity, no decrease in the amount of hypophosphorylated retinoblastoma protein could be shown after TCDD treatment. The importance of increased cyclin A/cdk2 activity for TCDD-dependent release from contact inhibition was shown by the fact that the cdk2/cdc2-specific inhibitor olomoucine (25 microM) abolished TCDD response. These data indicate cyclin A-dependent loss of G1 arrest after TCDD treatment mainly downstream of the retinoblastoma protein.

Animals↗
PubMed2002

Effects of deoxycholate on human colon cancer cells: apoptosis or proliferation.

BACKGROUND: Deoxycholic acid has long been attributed as a tumour promoter in the colon. It exerts its growth-related actions in a phorbol ester-like manner, by stimulating protein kinase C. The aim of this study was to investigate the effect of deoxycholic acid on proliferation and apoptosis in the colon, by exposing colon cancer cells to it in increasing concentrations. METHODS: Human colon cancer cells (Caco-2 and HT-29) were treated with deoxycholate or its two structural isomers, 3-beta-12-alpha-dihydroxy-5-beta-cholan-24-oic acid and 3-alpha-12-beta-dihydroxy-5-beta-cholan-24-oic acid. Proliferation was evaluated by cell counting, and apoptosis by estimating percentage cell survival and assessment of nuclear morphology. RESULTS: Within the concentration range of up to 20 microM, deoxycholate stimulated growth of both human colon cancer cell lines. Its growth-promoting effect was abolished after inhibition of protein kinase C. At concentrations above 100 microM, deoxycholate induced apoptosis in both cell lines. Epimers of deoxycholate were significantly less potent in stimulating growth. CONCLUSION: Low-dose deoxycholate stimulates colon cancer cell proliferation while > 100 micromol L(-1) of this secondary bile acid induces apoptosis in colon cancer cells. Deoxycholate might promote the likelihood of malignant transformation by increasing epithelial cell turnover in the colon.

Apoptosis↗
PubMed2002

Regulation of alpha1-proteinase inhibitor release by proinflammatory cytokines in human intestinal epithelial cells.

alpha1-Proteinase inhibitor (alpha1-PI) is the main serine proteinase inhibitor in human plasma. Apart from its synthesis in the liver, this anti-inflammatory protein is also synthesized by and excreted from human intestinal epithelial cells. Antiinflammatory actions of alpha1-PI are thought to be of relevance in the pathogenesis of inflammatory bowel disease. To investigate the role of macrophage-derived cytokines on alpha1-PI secretion from intestinal epithelial cells, we cultured Caco-2 cells until differentiation (14 days in culture) on permeable filter supports. Monolayers of differentiated Caco-2 cells were then co-cultured with human peritoneal macrophages, grown on plastic in the basolateral chamber. Under these conditions, alpha1-PI secretion from Caco-2 cells was enhanced by 45%, probably by a direct action of macrophage-derived cytokines on Caco-2 cells. To extend this observation further, we treated differentiated Caco-2 cells with macrophage-derived proinflammatory cytokines (IL-1beta, IL-8, TNF-alpha), as well as with lymphocyte-derived cytokines IL-2, IL-6 and IFN-gamma. As early as after 24h treatment, IL-2 and IL-8 induced a significant and dose-dependent increase of alpha-1-PI secretion into cell culture medium; this effect was completely reversed after immunoneutralization by the antibodies against IL-2 and IL-8 alpha1-PI secretion was only slightly decreased after treatment with IFN-gamma, while IL-1beta, IL-6 and TNF-alpha had no effect. alpha1-PI secretion correlated well with the expression of this protein in differentiated Caco-2 cells after cytokine treatment, as confirmed by Western blot. Our data imply that, in vitro, alpha1-PI secretion in enterocyte-like Caco-2 cells is up-regulated by IL-2 and IL-8. Our results suggest that both lymphocyte- and macrophage-derived cytokines regulate secretion of the anti-inflammatory protein alpha1-PI in intestinal epithelial cells.

Caco-2 Cells↗
PubMed2001

Involvement of protein kinase Cdelta in contact-dependent inhibition of growth in human and murine fibroblasts.

There is evidence that protein kinase C delta (PKCdelta) is a tumor suppressor, although its physiological role has not been elucidated so far. Since important anti-proliferative signals are mediated by cell-cell contacts we studied whether PKCdelta is involved in contact-dependent inhibition of growth in human (FH109) and murine (NIH3T3) fibroblasts. Cell-cell contacts were imitated by the addition of glutardialdehyde-fixed cells to sparsely seeded fibroblasts. Downregulation of the PKC isoforms alpha, delta, epsilon, and mu after prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.1 microM) resulted in a significant release from contact-inhibition in FH109 cells. Bryostatin 1 selectively prevented TPA-induced PKCdelta-downregulation and reversed TPA-induced release from contact-inhibition arguing for a role of PKCdelta in contact-inhibition. In accordance, the PKCdelta specific inhibitor Rottlerin (1 microM) totally abolished contact-inhibition. Interestingly, immunofluorescence revealed a rapid translocation of PKCdelta to the nucleus when cultures reached confluence with a peak in early-mid G1 phase. Nuclear translocation of PKCdelta in response to cell-cell contacts could also be demonstrated after subcellular fractionation by Western blotting and by measuring PKCdelta-activity after immunoprecipitation. Transient transfection of NIH3T3 cells with a dominant negative mutant of PKCdelta induced a transformed phenotype. We conclude that PKCdelta is involved in contact-dependent inhibition of growth.

3T3 Cells↗
PubMed2001

[Diagnostic imaging in liver cirrhosis].

For the diagnosis of liver cirrhosis ultrasound, computed tomography, magnetic resonance imaging, and angiography are recommended as imaging modalities. Ultrasound of the liver is used as a screening imaging tool in cases of patients suspicious for diffuse liver disease and is helpful in the term of follow-up examinations. Computed tomography is mainly performed to clarify the presence of liver disease detected by ultrasound. In this context, accurate examination of the vascular structures of the liver as well as extrahepatic situation, is of the essence. Diagnosis of diffuse liver disease and characterization of morphologic changes is improved using contrast-enhanced MR imaging with liver specific contrast media. Combined magnetic resonance imaging can provide comprehensive evaluation of cirrhosis. An improved detection rate and characterization of regenerating nodules can be achieved compared to imaging modalities such as ultrasound and computed tomography. MR imaging can be performed in a one-stop-technique using unenhanced and liver-specific-contrast-enhanced sequence protocols to evaluate the liver parenchyma itself, MR cholangiography to verify the bile duct system, and MR angiography to specify the vascular situation. This technique is the optimal protocol for diagnostic imaging in patients suffering from liver cirrhosis and the method of choice to reach the final diagnosis.

Diagnostic Imaging↗
PubMed2001

Permeability characteristics of polyamines across intestinal epithelium using the Caco-2 monolayer system: comparison between transepithelial flux and mitogen-stimulated uptake into epithelial cells.

The polyamines putrescine, spermidine, and spermine are present in foods in high amounts, and are used for cell growth throughout the body. Surprisingly little is known about the mechanisms of polyamine absorption in the gut. To elucidate the mechanisms, transepithelial transport of polyamines was studied in human enterocytelike Caco-2 cells, grown on permeable filter supports. Transport of all three polyamines across Caco-2 cell monolayers was linear; intraepithelial accumulation of polyamines was higher in confluent than in differentiated Caco-2 cells, but still negligible in comparison with the overall transport across the monolayers. Epidermal growth factor (EGF) enhanced polyamine accumulation in Caco-2 cells four-fold, and basolateral uptake was higher than apical uptake if the cells were stimulated to grow. The amounts of polyamines taken up by the cells were nevertheless negligible in comparison with the net polyamine flux across the monolayers. Basolateral excretion of polyamines was in the picomolar range, whereas their transepithelial transport, occurring presumably by passive diffusion through the paracellular pathway, contributed hundreds of micromoles of polyamines to the basolateral chamber. We conclude that transepithelial transport of polyamines occurs by passive diffusion, and that it is not influenced when epithelial cells are stimulated to proliferate by a potent mitogen such as EGF.

Biological Transport↗
PubMed2001

Butyrate and the cytokine-induced alpha1-proteinase inhibitor release in intestinal epithelial cells.

BACKGROUND: Alpha1-proteinase inhibitor (alpha1-PI), an anti-inflammatory protein thought to play a role in the intestinal inflammation, is synthesised by and released from the intestinal epithelial cells. IL-1beta is a key proinflammatory cytokine in the abnormal immune response that occurs in inflammatory bowel disease. Butyrate is a normal luminal constituent in the colon, known to be of benefit in preventing inflammatory bowel disease. Direct modes of action of butyrate in intestinal inflammation have been poorly studied so far. The aim of this study was to investigate the effects of butyrate on cytokine-mediated alpha1-PI release in intestinal epithelial cells. METHODS: Differentiated Caco-2 cells were incubated with IL-1beta in the presence or absence of 2 mM butyrate. Alpha1-PI expression in the cells was evaluated by Western blot analysis and alpha1-PI release by ELISA. RESULTS: Treatment with butyrate alone had no effect on alpha1-PI expression in differentiated Caco-2 cells. However, treatment of the cells with 2 mM butyrate significantly reduced the alpha1-PI level in IL-1beta-treated cells. In the cell culture medium, the presence of butyrate impaired the IL-1beta-induced alpha1-PI release to 17-35%. The treatment induced no change in the number of detached cells or the percentage of viable cells. CONCLUSION: Our data show that butyrate inhibits alpha1-PI release from Caco-2 colonocytes treated with IL-1beta. It is therefore likely that anti-inflammatory actions of butyrate occur via a mechanism that does not involve direct regulation of cytokine-induced anti-inflammatory protein expression in intestinal epithelial cells.

Butyrates↗
PubMed2001

Determination of alpha1-proteinase inhibitor by a new enzyme linked immunosorbant assay in feces, serum and an enterocyte-like cell line.

Although alpha(1)-proteinase inhibitor (alpha(1)-PI), the main serine proteinase inhibitor in human plasma, is predominantly liver-derived, the proof of fecal alpha(1)-PI is a maker for intestinal protein loss. Furthermore, alpha(1)-PI is synthesized locally by human intestinal epithelial cell lines (e. g. Caco-2). Therefore, we investigated the diagnostic value of a new enzyme-linked immunosorbent assay (ELISA) to detect alpha(1)-PI in serum, feces, and Caco-2 supernatants in comparison with radial immunodiffusion (RID). alpha(1)-PI concentrations assessed by ELISA were on an average 30 % higher than those measured by RID. Only the ELISA system detected alpha(1)-PI in supernatants of Caco-2 cells. Our data imply first that this ELISA system is more sensitive to assess alpha(1)-PI than other methods, and second that it obviously determines locally synthesized alpha(1)-PI which can not be liver-derived. However, further examinations are necessary to distinguish between enterocyte-derived or systemic alpha(1)-PI and its diagnostic relevance in bowel disease.

Adolescent↗
PubMed2001

Transmural drainage of cystic peripancreatic lesions with a new large-channel echo endoscope.

BACKGROUND AND STUDY AIMS: The availability of a new large-channel echo endoscope led us to develop a new needle-stent device for endoscopic puncture and drainage of pancreatogenic cystic lesions. The purpose of this study was to examine whether endoscopic ultrasound (EUS)-guided one-step 10-F puncture and drainage with the new equipment could be feasible and successful. The use of the technique and the short-term outcome in our first four patients are described and discussed. PATIENTS AND METHODS: Cystic lesions were drained using the new technique in four patients. All the patients had symptomatic peripancreatic lesions, one with intrahepatic and one with intrasplenic extension. Punctures were carried out using a new echo endoscope with a 3.7 mm working channel and an Albarran lever. The 10-F transmural stents were placed over a 1 mm stainless steel needle and a 6-F Teflon catheter using a special assembly designed for controlled one-step placement and stent release. RESULTS: Puncture and drainage were technically successful in two patients. In one patient, the 10-F component failed to pass the cystic wall. Drainage was successful in the same session using a 7-F one-step device. In one patient, no stent was placed, but the 1 mm needle was used for diagnostic tissue sampling during the procedure because of the suspicious cyst morphology. Surgical resection revealed a ganglioneuroma. CONCLUSIONS: The new echo endoscope allows endoscopic interventions for peripancreatic cystic lesions under excellent endoscopic and EUS control. The Albarran lever was reliable and helpful for optimal direction of the needle. The new echo endoscope combined with special needle-stent devices was effective and safe for diagnosis and therapy in the first four cystic lesions. Cystic tumors must always be considered as a differential diagnosis in patients with apparently pancreatitis-induced cystic lesions.

Adult↗
PubMed2000

Errors in scoring objective personality tests.

Given the paucity of previous research, we examined the occurrence of scoring error on widely used objective personality tests and examined its possible relation to two factors: scoring procedure complexity (SPC) and commitment to accuracy (CTA). We double-checked the scoring of three tests (MMPI, Beck Depression Inventory, Spielberger State/Trait Anxiety Inventory) across three settings. Each of the tests were misscored at a surprisingly high rate in at least one setting, and some such errors altered major interpretive implications. Tests of higher SPC showed greater error rates, but high CTA greatly reduced the occurrence of error across levels of SPC. Unexpected sources of error were also uncovered, such as commercial computer scoring errors and disagreement in scoring standards among test publishers. Practical suggestions for improving scoring accuracy are offered.

Bias↗
PubMed1999

p16INK4 mediates contact-inhibition of growth.

Growth of non-transformed cells in vitro is regulated by density-dependent mechanisms via cell-cell contacts, leading to arrest in late G1-phase at confluency (contact-inhibition of growth). In the present study it is shown that this results from p16INK4-mediated dissociation of the complex cdk4-cyclin D1, which is responsible for the inactivation of the gate keeper of G1-S transition, the retinoblastoma protein pRb. As a consequence of the inactivation of cdk4, downstream the activation of cdk2 and hyperphosphorylation and thus inactivation of pRb was impaired. Direct evidence for the central role of p16INK4 in growth control comes from the observation that a competitive inhibitor of p16INK4 repressed contact inhibition of growth. These findings provide an explanation for the high incidence of mutation or loss of INK4 in human tumours.

Amino Acid Sequence↗
PubMed1999

Hypospadiac or intact foreskin graft for syndactyly repair.

BACKGROUND/PURPOSE: Syndactyly is one of the most common malformations of the hands and feet. Repair may necessitate the use of a full-thickness skin graft. The prepuce is an excellent choice for grafting because of its lack of hair, elasticity, and degree of thickness. The authors report 4 cases of syndactyly repair using foreskin for grafting. METHODS: The authors reviewed 4 cases of syndactyly repaired at Children's Hospital, where foreskin was used for grafting. There was one congenital band syndrome and 3 cases of simple syndactyly. Three patients had a normal prepuce and underwent simultaneous circumcision. One patient presented with coronal hypospadias and underwent simultaneous meatal advancement and glanuloplasty. RESULTS: All patients experienced a satisfactory outcome with no graft loss and no complications. No grafts showed hair, and 3 grafts showed slight relative hyperpigmentation. Excess foreskin was available in all cases of simple syndactyly. Concominant hypospadias repair did not increase the morbidity of the surgery. CONCLUSION: The intact or hypospadiac foreskin is an excellent choice for a free graft in syndactyly repair when available.

Child, Preschool↗
PubMed1999

Effects of the label "schizophrenia" on causal attributions of violence.

We investigated the relation between the label of "schizophrenia" and causal attributions of violence. Undergraduates read 1 of 10 scenarios in which two variables were manipulated: a psychiatric label and environmental stress. The scenario described an employee who acted violently toward his boss. Subjects made causal attributions for the employee's behavior by completing an adapted version of the Causal Dimension Scale II. Subjects also completed a questionnaire designed to explore several issues concerning the effects of the schizophrenia label on perceptions of behavior. Contrary to the primary hypothesis, the schizophrenia label did not lead subjects to make significantly more personality causal attributions for violent behavior. With increasing environmental stress, subjects did make significantly fewer personality attributions. A follow-up study using practicing clinicians as subjects yielded similar findings. The results of these studies are discussed in light of perceived stereotypes of persons with schizophrenia and conceptual issues in attribution research.

Adult↗
PubMed1997

Maintaining theophylline compliance/adherence in severely asthmatic children: the role of psychologic functioning of the child and family.

BACKGROUND: Noncompliance with asthma therapy by asthmatic children and their families is a common cause of treatment failure. Psychologic factors have been reported to influence adherence patterns. OBJECTIVE: To evaluate the relationship of psychologic function of severely asthmatic children and families with theophylline compliance during a 1-year follow-up period after inpatient asthma rehabilitation. METHOD: Thirty-seven severely asthmatic children with a median age of 9 years (range, 2 to 17 years) were treated in an inpatient rehabilitation program (median, 15 days). Established clinical rating scales of psychologic adjustment were used for children (Child Global Assessment Scale) and families (Family Global Assessment Scale) at the time of admission. Patients were defined as noncompliant if 30% or more of theophylline levels obtained during the 1-year follow-up period were less than 5 mg/L (mumol/L). RESULTS: Compliant children had higher scores on the Child Global Assessment Scale than noncompliant children (64 versus 48, P = .09). Families of compliant children had significantly higher scores on the Family Global Assessment Scale than did families with noncompliant children (63 versus 54, P < .05). There was no statistical relationship between compliance status and parent-reported behavior problems, demographic factors (age, race, sex, and number of parents at home), health insurance, specialty referral at admission, measures of medical morbidity (days hospitalized, number of emergency care visits, and number of corticosteroid bursts), or length of rehabilitation stay. Both compliant and noncompliant children had comparable reductions in morbidity (hospital and emergency care, number of corticosteroid bursts required). CONCLUSION: Psychologic functioning of the child and family may be related to theophylline compliance.

Adolescent↗