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Negative Subjects (negative + subject)
Selected AbstractsAssessment of balsam of Peru patch testsCONTACT DERMATITIS, Issue 6 2000Bolli Bjarnason To find an ideal test technique for as low a dose of balsam of Peru (Myroxylon Pereirae) as possible, subjects testing positive to balsam of Peru are re-tested with a 25% concentration of balsam of Peru in petrolatum. Applications are with Finn Chambers® for 6 different application times, and directly by foils for 96 h (4 days (D)). The goals are to confirm which subjects are positive and which are not, and, using that information, to see if it is possible to distinguish between these 2 groups, tested concomitantly at much lower serial dose levels, in terms of perfusion or by visual assessments. 5 different serial doses are applied with strips for 3,96 h (4D) and with foils for 96 h (4D). The Finn Chamber® tests allow a distinction between visually positive and negative subjects supported by perfusion assessments. With the foils, a 24× lower serial dose level than with the 25% test substance is sufficient to distinguish between positive and negative subjects in terms of perfusion values. This approach requires readings up to 9 days. With this test, the visual approach yields only 3 of 10 positive subjects. This study demonstrates that a lower test dose is possible with perfusion assessments compared to visual ones. [source] Fundal gastritis as a potential cause of reflux oesophagitisDISEASES OF THE ESOPHAGUS, Issue 1 2000M. Newton The transient lower oesophageal sphincter relaxations which allow reflux may be due to altered afferent pathways from the fundus. We aimed to determine whether fundal inflammation is the underlying cause. Two endoscopic biopsies were taken from each of the gastric antrum and fundus in 25 asymptomatic controls with a normal endoscopy (median age 54 range 13,83 years), and 33 patients with erosive oesophagitis (median age 52, 11,78 years). No patient had taken acid suppression therapy or antibiotics for at least 1 month. Sections were stained with haematoxylin and eosin and Giemsa stain and examined in a blinded fashion by one pathologist for the presence of gastritis (Sydney classification) and Helicobacter pylori. Chronic gastritis was common in both groups, but was usually mild. In Helicobacter pylori -negative subjects, there was significantly less chronic gastritis in the antrum and the fundus in oesophagitis patients than in controls (p < 0.05). When present, gastric atrophy was usually antral and mild in severity. There was no difference in the incidence of gastric atrophy in patients with oesophagitis compared with controls (24% compared with 40%; p > 0.05). Chronic gastritis is not more common in patients with oesophagitis, and is unlikely to play a part in the pathogenesis of this disease. [source] Natural Killer Cell Receptor+ T-Lymphocytes in Normal and Helicobacter pylori -Infected Human Gastric MucosaHELICOBACTER, Issue 6 2008Joan O'Keeffe Abstract Background:,Helicobacter pylori infection is associated with development of chronic inflammation and infiltration of immune cells into the gastric mucosa. As unconventional T-lymphocytes expressing natural killer cell receptors are considered to play central roles in the immune response against infection, a study investigating their frequencies in normal and H. pylori -infected gastric mucosa was undertaken. Materials and Methods:, Flow cytometry was used to quantify T-cells expressing the natural killer cell markers CD161, CD56, and CD94 in freshly isolated lymphocytes from the epithelial and lamina propria layers of gastric mucosa. Thirteen H. pylori -positive and 24 H. pylori -negative individuals were studied. Results:, CD94+ T-cells were the most abundant (up to 40%) natural killer receptor-positive T-cell population in epithelial and lamina propria layers of H. pylori -negative gastric mucosa. CD161+ T-cells accounted for about one-third of all T-cells in both compartments, but the lowest proportion were of CD56+ T-cells. Compared with H. pylori -negative mucosa, in H. pylori -infected mucosa the numbers of CD161+ T-cells were significantly greater (p = .04) in the epithelium, whereas the numbers of CD56+ T-cells were lower (p = .01) in the lamina propria. A minor population (< 2%) of T-cells in both mucosal layers of H. pylori -negative subjects were natural killer T-cells, and whose proportions were not significantly different (p > .05) to those in H. pylori -infected individuals. Conclusions:, The predominance, heterogeneity, and distribution of natural killer cell receptor-positive T-cells at different locations within the gastric mucosa reflects a potential functional role during H. pylori infection and warrants further investigation. [source] Involvement of Helicobacter pylori Infection and Impaired Glucose Metabolism in the Increase of Brachial,Ankle Pulse Wave VelocityHELICOBACTER, Issue 5 2007Hiroyuki Yoshikawa Abstract Background: The role of Helicobacter pylori in the pathogenesis of atherosclerosis remains controversial. The present study was designed to elucidate the pathogenic role of H. pylori in the early stages of atherosclerosis by measurement of brachial,ankle pulse wave velocity (baPWV) in relation to glucose metabolism. Materials and methods: baPWV level, anti- H. pylori antibody, fasting blood glucose (FBG), and glycosylated hemoglobin A1c (HbA1c) and other conventional risk factors for cardiovascular diseases were measured in 947 subjects who attended their annual medical check-up. Results: Multiple regression analyses indicated that age, gender (male), body mass index, FBG, systolic blood pressure, and smoking habits were each independently related to baPWV values. In younger subjects (30,49 years), H. pylori seropositivity was significantly correlated with an increase of baPWV levels (r = 0.100, p = .0445). baPWV values in the H. pylori- positive subjects with impaired glucose metabolism (IG: FBG , 110 mg/dL and/or HbA1c , 5.9%) were significantly greater than those in the H. pylori- negative subjects with IG (p = .0078). Furthermore, H. pylori- positive subjects with IG were at higher risk for increase of baPWV, in younger (r = 0.203, p < .0001) as well as in older subjects (50,69 years, r = 0.099, p = .0009). Conclusions: These results suggest that H. pylori seropositivity is a potential risk factor for increased baPWV levels, and that H. pylori infection accelerates the effect of IG on an increase of baPWV, especially in younger subjects. Thus, the possible interaction between H. pylori infection and IG may contribute to the early development of atherosclerosis. [source] Helicobacter pylori Infection Increases Serum Nitrate and Nitrite More Prominently Than Serum PepsinogensHELICOBACTER, Issue 1 2002Kanji Kodama Abstract Background.Helicobacter pylori infection causes chronic gastritis and results in increased serum concentrations of pepsinogens I and II as well as gastrin, while the ratio of pepsinogen I to II (I : II) is decreased. Inducible nitric oxide synthase (iNOS) is induced in H. pylori -associated gastritis and may modulate inflammation. However serum nitrate and nitrite (NOx) concentrations in patients with H. pylori -induced chronic gastritis have not been reported. We examined differences in serum NOx between H. pylori -negative and positive volunteers relative to differences in pepsinogens and gastrin. Materials and methods. Sera from 80 healthy asymptomatic volunteers younger than 36 years were analyzed for anti- H. pylori antibody, NOx, gastrin and pepsinogens. Results. In H. pylori antibody-positive subjects serum NOx concentrations were higher than in negative subjects (p < .005). In H. pylori -negative subjects, NOx correlated with pepsinogen II (r = .405, p < .05). In subjects with low pepsinogen I or II, NOx was higher in H. pylori -positive than negative subjects (p < .001). In subjects with high pepsinogen I : II (6 or higher), serum NOx was higher in H. pylori -positive than in negative subjects. Conclusions.H. pylori -induced gastritis increases serum NOx concentrations more prominently than those of pepsinogen. In H. pylori -negative subjects, serum correlates with serum pepsinogen II. [source] Circulating T-Cell Response to Helicobacter pylori Infection in Chronic GastritisHELICOBACTER, Issue 3 2000Zhigang Ren Background.Helicobacter pylori elicits a specific humoral and cellular immune response. There is increasing evidence that the type of T-cell response contributes to clinical outcome in H. pylori infection. Materials and Methods. The host response to H. pylori infection in 34 subjects with chronic gastritis was examined in terms of T-cell proliferation and cytokine production in whole-blood cultures stimulated or unstimulated with H. pylori acid-glycine extract antigens (AGE). Results. The proliferative response in whole-blood cultures was similar for both H. pylori,positive and ,negative subjects stimulated with H. pylori AGE. While an increase in interferon-, (IFN-,) production was observed from both H. pylori,positive and ,negative subjects with gastritis, significantly higher levels of IFN-, were detected in the former when stimulated with H. pylori AGE. In contrast, interleukin 4 (IL-4) was undetectable regardless of antigen stimulation. However, if an in situ IL-4 antibody capture assay was used, antigen-independent production of IL-4 was detected, but there was no difference between H. pylori,positive and ,negative subjects with gastritis. After eradication of H. pylori, antigen-induced production of IL-4 was increased, with no decrease in the levels of secretion of IFN-,. IL-4 production was dependent on CD4+ T cells, as addition of anti-CD4 but not anti-CD8 mouse monoclonal antibody or matched IgG isotype to the whole-blood culture inhibited the production of IL-4. Conclusion. The results suggest that a shift toward a balanced Th1-Th2 response due to an increase in antigen-induced IL-4 production from CD4+ T cells follows eradication. We suggest that the downregulation of mucosal inflammation consequent on reduction in antigen levels or removal of downregulation after eradication of H. pylori contributes to this shift in cytokine balance. [source] Investigation on the role of cell transcriptional factor Sp1 and HIV-1 TAT protein in PML onset or developmentJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2005M. Mischitelli JC virus (JCV) causes progressive multifocal leukoencephalopathy (PML), characterized by multiple areas of demyelination and attendant loss of brain function. PML is often associated with immunodepression and it is significantly frequent in AIDS patients. The viral genome is divided into early and late genes, between which lies a non-coding control region (NCCR) that regulates JCV replication and presents a great genetic variability. The NCCR of JCV archetype (CY strain) is divided into six regions: A,F containing binding sites for cell factors involved in viral transcription. Deletions and enhancements of these binding sites characterize JCV variants, which could promote viral gene expression and could be more suitable for the onset or development of PML. Therefore, we evaluated by means of polymerase chain reaction (PCR) the presence of JCV genome in cerebrospinal fluid (CSF) of HIV positive and negative subjects both with PML and after sequencing, we analyzed the viral variants found focusing on Sp1 binding sites (box B and D) and up-TAR sequence (box C). It is known that Sp1 activates JCV early promoter and can contribute in maintaining methylation-free CpG islands in active genes, while up-TAR sequence is important for HIV-1 Tat stimulation of JCV late promoter. Our results showed that in HIV-positive subjects all NCCR structures presented enhancements of up-TAR element, whereas in HIV-negative subjects both Sp1 binding sites were always retained. Therefore, we can support the synergism HIV-1/JCV in CNS and we can hypothesize that both Sp1 binding sites could be important to complete JCV replication cycle in absence of HIV-coinfection. © 2005 Wiley-Liss, Inc. [source] Effect of interleukin-1 gene polymorphism in a periodontally healthy Hispanic population treated with mucogingival surgeryJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 2 2002Raul G. Caffesse Abstract Objectives: A genetic test for susceptibility of periodontal disease has been introduced. A positive test indicates a risk factor for more severe periodontal destruction. The prevalence of genotype positive subjects has been reported around 30%. In a Mexican population, we have found a 26% prevalence of genotype positive individuals. Few studies have reported the response to therapy in these individuals. The purpose of this study was to assess the response to mucogingival surgery in an otherwise periodontally healthy Hispanic population. Materials and methods: 22 subjects (7 male and 15 female) with a mean age of 45 years participated. They were treated 3 years prior for the treatment of Types I and II recession defects using connective tissue grafts. No other active periodontal treatment was required, except for preventive maintenance. A full-mouth clinical evaluation was performed which included assessment of gingival inflammation and measurements of probing pocket depth and clinical attachment levels. Mean values per patient were determined. A finger stick blood sample was collected using specially provided DNA filter paper, let dried, and mailed for processing. Results: Results indicated that 5 out of the 22 subjects were genotype positive. The genotype positive subjects presented the following values: GI 1.13±0.17, PPD 2.48±0.46, and CAL 3.38±0.66. The values for the genotype negative subjects were GI 1.06±0.14, PPD 2.38±0.31 and CAL 3.11±0.53. No statistical significant differences were found when both groups were compared (p>0.05). Furthermore, the treatment of the localized recessions was effective and provided similar amount of coverage in genotype positive and negative subjects. However, more genotype negative subjects showed complete coverage of the recession than genotype positive individuals. Conclusions: Within the limits of this study it is concluded that (1) periodontal health can be maintained with proper preventive maintenance irrespective of the genotype present, (2) the mean response to mucogingival surgery to cover localized gingival recessions is similar irrespective of the IL-1 periodontal genotype, however, full coverage is achieved more frequently in genotype negative subjects. Zusammenfassung Ziele: Es wurde ein Gentest für die Anfälligkeit bezüglich einer Parodontalerkrankung eingeführt. Ein positiver Test ist ein Zeichen für einen Risikofaktor für eine stärkere parodontale Destruktion. Die Prävalenz von genotyp-positiven Personen wurde mit etwa 30% angegeben. In einer mexikanischen Population haben wir eine Prävalenz von 26% von genotyp-positiven Individuen vorgefunden. Nur wenige Studien haben bei diesen Patienten über die Reaktion auf die Therapie berichtet. Der Zweck dieser Studie war es die Heilung nach mukogingivaler Chirurgie in einer im Übrigen parodontal gesunden Population mit spanischen Abstammung. Material und Methode: 22 Patienten (7 Männer und 15 Frauen) mit einem Durchschnittsalter von 45 Jahren nahmen an der Studie teil. Sie wurden vor 3 Jahren zur Deckung einer Rezession von Typ I oder II mit einem Bindegewebetransplantat behandelt. Es war keine weitere parodontale Behandlung außer präventiven Erhaltungstherapie notwendig. Es wurde eine vollständige klinische Untersuchung des Gebisses durchgeführt, die die Bestimmung der gingivalen Etnzündung, sowie die Messung der Sondierungstiefe und des klinischen Attachmentniveaus beinhaltete. Es wurden für jeden Patienten die Mittelwerte bestimmt. Eine Blutprobe von der Fingerbeere wurde entnommen, auf ein specielles DNA-Filterpapier aufgetragen, getrocknet und zur Weiterverarbeitung versendet. Ergebnisse: Die Ergebnisse zeigten, dass 5 von 22 Patienten genotyp-positiven waren. Die genotyp-positiven Patienten wiesen folgende Werte auf: GI 1.13±0.17, PPD 2.48±0.46 und CAL 3.38±0.66. Die Werte für die genotyp-negativen Patienten betrugen: GI 1.06±0.14, PPD 2.38±0.31 und CAL 3.11±0.53. Beim Vergleich beider Gruppen ergaben sich keine statistisch signifikanten Unterschiede (p>0.05). Des weiteren war die Behandlung der lokalisierten Rezession effektiv und lieferte bei genotyp-positiven und genotyp-negativen Patienten einen ähnlichen Anteil an Wurzeldeckung. Jedoch zeigten mehr genotyp-negative Patienten eine vollständige Rezessionsdeckung als genotyp-positive Patienten. Schlussfolgerungen: Mit den Einschränkungen dieser Studie kann die Schlussfolgerung gezogen werden, dass (1) unabhängig vom vorliegenden Genotyp mit geeigneten präventiven Maßnahmen die parodontale Gesundheit erhalten werden kann und (2) dass unabhängig vom IL-1-Genotyp, die durchschnittliche Reaktion auf die mukogingivale Chirurgie zur Deckung von lokalisierten Gingivarezessionen ähnlich ist. Jedoch wird eine vollständige Deckung häufiger bei genotyp-negativen Patienten erreicht. Résumé But: Un test génétique pour la suscpetibilitéà la maladie parodontale est présenté. Un test positif indique un facteur de risque pour une destruction parodontale plus sévère. La fréquence globale de sujets positifs au génotype semblerait être de 30%. Dans une population mexicaine, une fréquence globale de 26% d'individus positifs pour le génotype a été trouvée. Peu d'études ont apporté la réponse au traitement chez ces individus. Le but de cette investigation a été de mesurer la réponse de la chirurgie muco-gingivale dans une population hispanique parodontalement saine. Matériaux et méthodes: 7 hommes et 15 femmes d'un âge moyen de 45 ans y ont participé. Ils avaient été traités 3 ans auparavant pour des lésions de récession de type I et II en utilisant des greffes de tissu conjonctif. Aucun autre traitement parodontal actif n'avait été requis, sauf pour la maintenance. Une évaluation clinique de toute la bouche a été effectuée comprenant l'estimation de l'inflammation gingivale et les measures de la profondeur de poche au sondage et des niveaux d'attache clinique. Les valeurs moyennes par patient ont été déterminées. Un échantillon sanguin par piqûre du doigt a été récolté en utilisant un papier filtre ADN, qui fût séché et envoyé pour analyse. Résultats: Les résultats ont indiqué que 5 des 22 sujets étaient génotype positif. Ces sujets présentaient les valeurs suivantes: GI 1.13±0.17, PPD 2.48±0.46 mm et CAL 3.38±0.66 mm. Les valeurs chez les sujets génotype négatif étaient: GI 1.06±0.14, PPD 2.38±0.31 mm et CAL 3.11±0.53 mm. Aucune différence statistiquement significative n'a été trouvée lorsque les deux groupes ont été comparés. De plus le traitement des récessions locales était effectif et apportait une quantité semblable de recouvrement chez les deux types de sujets. Cependant davantage de sujets génotype négatif bénéficiaient d'un recouvrement complet de la récession. Conclusions: Dans les limites d l'étude présente: (1) la santé parodontale peut être maintenue avec des mesures préventives quelque soit le génotype présent, (2) la réponse moyenne de la chirurgie muco-gingivale pour recouvrir des récessions gingivales locales est semblable quelque soit le génotype parodontal IL-1, bien qu'un recouvrement complet est plus souvent réalisé chez les sujets génotype négatif. [source] Clinical significance of TT virus in chronic hepatitis CJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2001Xiang Wei Meng Abstract Background and Aims: Much is still unknown about the clinical significance of TT virus (TTV), which has been reported as a candidate for non A,G hepatitis virus. The aim of this study was to clarify the clinical significance of TTV in patients coinfected with TTV and hepatitis C virus (HCV). Methods: The 95 subjects studied had chronic hepatitis C (CHC), and underwent interferon (IFN) therapy. TT Virus DNA was detected by using polymerase chain reaction. The nucleotide sequences were determined by using a dideoxy chain termination method. A phylogenetic tree was drawn up by using the neighbor-joining method. Results: TT Virus DNA was detected in 37.9% of patients with the use of an open reading frame 1 (ORF1) primer, and in 88.4% of patients by using a 5, untranslated region (5, UTR) primer. Using both sets of primers, no differences were found between TTV-DNA-positive and -negative subjects with CHC in the clinical findings. Serum TTV DNA was eradicated in 30.6% of patients with the ORF1 primer, and in 19.1% of patients with the 5, UTR primer at 6 months after the cessation of IFN therapy. The levels of TTV DNA before IFN therapy were significantly lower in the viral eradication group than in non-eradication group. The changes in alanine aminotransferase (ALT) concentrations were significantly correlated with changes in HCV-RNA in CHC patients with TTV. Moreover, there was no correlation between the changes in TTV DNA and the course of ALT. Conclusion: Hepatocellular injury in patients with chronic hepatitis who are coinfected with HCV and TTV appears to primarily be caused by HCV and is less attributable to TTV. [source] Association Between Sweet Preference and Paternal History of Alcoholism in Psychiatric and Substance Abuse PatientsALCOHOLISM, Issue 12 2003A. B. Kampov-Polevoy Background: The relationship between preference for stronger sweet solutions and propensity to excessive alcohol drinking is supported by both animal and human studies. This study was designed to test the hypothesis that sweet preference is associated with the genetic risk of alcoholism as measured by a paternal history of alcoholism. Methods: Participants were 180 patients admitted to a residential treatment program for the treatment of alcoholism, drug dependence, or psychiatric conditions. In addition to a routine medical examination, patients completed the standard sweet preference test twice (on the 9th and 24th days after admission), and the family history of alcoholism was evaluated. Results: Sweet preference was shown to be stable over time. It was strongly associated with a paternal history of alcoholism, with family history,positive patients approximately 5 times more likely to prefer stronger sweet solutions than family history,negative subjects. Such factors as dependence on alcohol, cocaine, opiates, cannabis, other drugs (including prescription drugs), and tobacco smoking, as well as demographics (gender and age), did not significantly interfere with association between sweet preference and paternal history of alcoholism. Conclusions: These findings provide some support for the hypothesis that preference for stronger sweet solutions is associated with a genetic predisposition to alcoholism as measured by a paternal history of alcoholism. [source] Cytokine detection in HIV-1/HHV-8 co-infected subjectsCELL BIOCHEMISTRY AND FUNCTION, Issue 3 2002Agostino Pugliese Abstract In a previous work we have evaluated some immunologic and haematologic parameters of HIV-1 positive subjects co-infected with HHV-8. A worsening of these values were generally described in these patients as compared with those HIV-1 positive, but negative for HHV-8. Now we have studied the influence of HHV-8 co-infection of HIV-1 positive subjects on the production of some cytokines to make clear the question of its role in the immuno-deregulation of the above-mentioned subjects. In particular we have analysed serum levels of IL-4 and IL-10, Th2 type T cells cytokines, IFN-,, an indirect marker of Th1 cells activation and IL-18, a cytokine produced by monocytic-macrophagic cells, which is able to induce IFN-, production and Th1 T lymphocytes activation. No significant differences were found as regards the IFN-, serum levels (92.1,±,24.3 pg ml,1 in the case of HIV-1 positive/HHV-8 negative subjects and 96.0,±,17.4 pg ml,1 in those HIV-1 positive/HHV-8 positive). In healthy subjects the mean level of this cytokine was 17.6,±,5.2 pg ml,1 (significant difference with both the former values at p,<,0.001). Moreover IL-4 and IL-10, which were undetectable in healthy individuals, showed the following values in HIV-1positive/HHV-8 negative subjects: 31.9,±,2.7 pg ml,1 and 119.8,±,85.1 pg ml,1 respectively and in HIV-1 positive/HHV-8 positive subjects: 30.4,±,4.8 pg ml,1 and 69.4,±,65.3 pg ml,1 (not significant differences). In contrast IL-18 reached a mean level of 1001.2,±,360.5 pg ml,1 in HIV-1 positive/HHV-8 negative subjects, but showed a significant reduction in HIV-1 positive/HHV-8 positive subjects (737.6,±,284.3 pg ml,1,p,<,0.05) and presented very low levels in healthy individuals (21.3,±,30.3 pg ml,1). Moreover a significant correlation (,0.984,p,<,0.001) was noticed between IL-18 reduction in HIV-1 positive subjects co-infected with HHV-8 and the degree of positivity of HHV-8. These data suggest that HHV-8 co-infection has no influence on the switch Th1, Th2 in HIV-1 positive subjects, but is able to reduce IL-18 production, useful for Th1 subset restoration. Copyright © 2002 John Wiley & Sons, Ltd. [source] | |||||||||||||