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This article offers a literary analysis of the famous episode in Judean War 3.351–354, in which Josephus suddenly recalls his "nightly dreams." It takes up the question of how Josephus characterizes himself in this episode in consideration of an elite audience located in Rome steeped in Greco-Roman learning. In explaining this episode, scholars have put special emphasis on parallels with discourses of Judean prophecy and biblical prophets, such as Jeremiah and Daniel. The hypothesis that Josephus consciously presents himself as a prophet has found widespread acceptance and grown to become almost undisputable since the 1970s. In addition to challenging the view that Josephus explicitly and deliberately presents himself as a biblical prophet, the present contribution develops an interpretation that considers the historiographical outlook of the whole War as a military-political composition imbued with classicizing features. [ABSTRACT FROM AUTHOR]

Surfactant protein (SP) D belongs to the family of collectins, which are humoral molecules of the innate immune system. Collectins belong to pattern recognition receptors and are present in plasma and on mucosal surfaces and recognize several microbial components, the pathogen-associated molecular patterns (PAMPs). While SP-A is primarily expressed in the lung, expression of SP-D is more widely detected including different mucosal surfaces and in serum. Therefore, SP-D is considered a functional candidate in chronic periodontitis. The present study sought to investigate whether plasma concentration of SP-D is altered in chronic periodontitis and whether polymorphisms within the SFTPD gene (Met11Thr, Ala160Thr and Ser270Thr) are associated with chronic periodontitis. The study population comprised 105 patients with chronic periodontitis and 122 healthy, unrelated control individuals. SP-D Plasma concentrations were determined using enzyme-linked immunosorbent assay test. Genotyping of SFTPD polymorphisms was performed by polymerase chain reaction and restriction fragment length polymorphism analysis. Plasma concentrations were significantly increased in patients with chronic periodontitis compared with the controls. The median plasma concentrations were 81.6 ng/ml in the patients and 52.6 ng/ml in the controls ( P = 0.00051). In contrast, the three SFTPD polymorphisms displayed no significant association with chronic periodontitis; thus, the increased plasma concentrations were independent on the genotype. The study showed significantly increased SP-D plasma concentrations in patients with chronic periodontitis compared with healthy controls. Thus, SP-D can potentially be used as a biomarker for chronic periodontitis. As no significant associations of SFTPD gene polymorphisms could be detected, other mechanisms influencing SP-D serum/plasma expression might exist. [ABSTRACT FROM AUTHOR]

Bactericidal/permeability-increasing protein (BPI) is a member of the pattern recognition receptors of the innate immune system and recognizes lipopolysaccharides (LPS), a bacterial component belonging to the pathogen-associated molecular patterns (PAMPs). BPI mediates the neutralization of LPS and increases the phagocytosis and cytotoxicity against bacteria. Recently, the functionally effective polymorphism A645G resulting in the amino acid alteration Lys216Glu has been described. The aim of the study was to investigate the association of the A645G polymorphism with chronic periodontal disease. The study population comprised 123 patients with periodontal disease (36 with mild, 52 with moderate and 35 with severe periodontitis) and 122 healthy, unrelated control individuals. Genotyping of the BPI gene polymorphism A645G (Lys216Glu) was performed by polymerase chain reaction and restriction fragment length polymorphism analysis. Statistical analysis was carried out employing the χ2 test with Yates correction. Genotype and allele frequencies of the polymorphism tested herein showed no significant differences between periodontal disease as compared to the control group. The frequencies of the G allele were 52.4% in patients with periodontal disease and 49.2% in the control individuals ( P = 0.528). Moreover, no significant associations could be detected after stratification for disease severity and according to gender. The present study does not give evidence for the contribution of the BPI gene to the genetic background of chronic periodontal disease. [ABSTRACT FROM AUTHOR]

Background and aims: Recent data suggest identification of causal genetic variants for inflammatory bowel disease in the DLG5 gene and in the organic cation transporter (OCTN) cluster, both situated in previously described linkage regions. Patients and methods: The polymorphisms in DLG5 (113 G→A, 4136 C→A, and DLG5•e26), SLC22A4 (1672 C→T), and SLC2245(-207 G→C) were assessed in 625 patients with Crohn's disease (CD), 363 patients with ulcerative colitis (UC), and 1012 healthy controls. Association with disease susceptibility, clinical phenotypes, and possible genetic interactions of these polymorphisms with disease associated CARD 15/NOD2 mutations was analysed. Results: No significant association of DLG5 polymorphisms with CD or UC was observed. Homozygosity for the OCTN-TC haplotype was associated with an increased CD risk (OR =1.65), which was even greater in the presence of CARD 15 mutations. Genotype-phenotype analysis revealed that this association was particularly strong in patients with colonic disease. The TC haplotype was associated with non- fistulising non-fibrostenotic disease, an earlier age of disease onset, and reduced need for surgery. Conclusion: Our observations argue against a role of DLG5 polymorphisms in the susceptibility for inflammatory bowel disease, whereas the OCTN polymorphisms are associated with CD. However, due to the comparable weak association observed herein, extended linkage disequilibrium analyses of these variants with the IBD5 haplotype tagged single nucleotide polymorphims might be advisable before definitive conclusions about their causative role in CD can be drawn. [ABSTRACT FROM AUTHOR]

Interleukin (IL)-16 is involved in the regulation of the expression of several proinflammatory cytokines, i.e. tumour necrosis factor (TNF)α and interleukin (IL)-1β. The present study aimed to determine the prevalence of the −295 promoter polymorphism of the interleukin (IL)-16 gene in periodontal disease. A total of 123 patients with periodontal disease and 122 healthy controls were genotyped for the −295 IL-16 promoter polymorphism. Genotyping has been performed by PCR and restriction fragment length polymorphism (RFLP) analysis. The frequencies of alleles and genotypes as well of haplotypes within both study groups were compared using the Pearson χ2 test at a level of significance of 5% ( P < 0·05). The distribution of genotypes for the −295 IL-16 gene polymorphism showed no significant difference between periodontitis patients and healthy control subjects ( P = 0·886). Also stratification analysis according to the disease severity revealed no significant difference regarding the genotype distribution among both study groups. Herein the IL-16 −295 gene polymorphism was not associated with chronic periodontitis. [ABSTRACT FROM AUTHOR]

Introduction: Various disease-specific serum antibodies were described in patients with inflammatory bowel disease and their yet healthy first-degree relatives. In the latter, serum antibodies are commonly regarded as potential markers of disease susceptibility. The present long-term follow-up study evaluated the fate of antibody-positive first-degree relatives. Patients and Methods: 25 patients with Crohn’s disease, 19 patients with ulcerative colitis and 102 first-degree relatives in whom presence of ASCA, pANCA, pancreatic- and goblet-cell antibodies had been assessed were enrolled. The number of incident cases with inflammatory bowel disease was compared between antibody-positive and antibody-negative first-degree relatives 7 years after storage of serum samples. Results: 34 of 102 (33%) first-degree relatives were positive for at least one of the studied serum antibodies. In the group of first-degree relatives, one case of Crohn’s disease and one case of ulcerative colitis were diagnosed during the follow-up period. However, both relatives did not display any of the investigated serum antibodies (p = 1). Discussion: The findings of our pilot study argue against a role of serum antibodies as a marker of disease susceptibility in first-degree relatives of patients with inflammatory bowel disease. However, these data have to await confirmation in larger ideally prospective multicenter studies before definite conclusions can be drawn. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aims: An association between inflammatory bowel disease (IBD) and spondyloarthropathies (SpA) has repeatedly been reported. The aim of the present study was to investigate whether serologic markers of IBD, e.g. antibodies against Saccharomyces cerevisiae (ASCA), antibodies against exocrine pancreas (PAB) and perinuclear antineutrophil cytoplasmic antibodies (pANCA) are present in HLA-B27-associated SpA. Methods: 87 patients with HLA-B27-positive SpA and 145 controls were tested for ASCA, PAB and pANCA employing ELISA or indirect immunofluorescence, respectively. Antibody-positive patients were interviewed regarding IBD-related symptoms using a standardized questionnaire. Results/Conclusion: When compared to the controls, ASCA IgA but not ASCA IgG levels were significantly increased in patients with SpA, in particular in ankylosing spondylitis (AS) and undifferentiated SpA (uSpA). pANCA were found in increased frequency in patients with SpA whereas PAB were not detected. The existence of autoantibodies was not associated with gastrointestinal symptoms but sustains the presence of a pathophysiological link between bowel inflammation and SpA. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Toll-like receptors (TLR) are signal molecules essential for the cellular response to bacterial cell wall components. Different functional effective polymorphisms for the TLR 4 gene (Asp299Gly; Thr399Ile) and for the TLR 2 gene (Arg677Trp, Arg753Gln) have recently been described that are associated with impaired lipopolysaccharide signal transduction. A total of 122 patients with chronic periodontal disease and 122 healthy unrelated controls were genotyped for the Asp299Gly and Thr399Ile polymorphism of the TLR 4 gene and the Arg677Trp and Arg753Gln mutation of the TLR 2 gene. The mutations were identified with polymerase chain reaction followed by restriction fragment length polymorphism (RFLP) analysis. The prevalence of the Asp299Gly and the Thr399Ile mutant allele was 4·1% (10/244) and 4·5% (11/244) among periodontitis patients. For the healthy controls the prevalence was 3·3% (8/244) for the Asp299Gly ( P = 0·810) and 3·7% (9/244) for the Thr399Ile mutant allele ( P = 0·819). The Arg753Gln mutant allele was found in 2·9% (7/244) of the periodontitis subjects as compared to 4·1% (10/244) in the control group ( P = 0·622). The Arg677Trp mutant allele was not found in any of the study subjects. Unlike in ulcerative colitis there was not observed an association between chronic periodontitis and the various mutations of the TLR 2 and 4 gene. [ABSTRACT FROM AUTHOR]

Background: Tumor necrosis factor-α (TNF-α) is involved in the pathogenesis of chronic active hepatitis C. Polymorphisms in the promoter region of the TNF-α gene can alter the TNF-α expression and modify the host immune response. The present study aimed at the correlation of the G308A TNF-α polymorphism with the response to antiviral combination therapy in chronic hepatitis C. Patients and Methods: 62 patients with HCV and 119 healthy unrelated controls were genotyped for the G308A TNF-α promoter polymorphism. The patients received 3 × 3 million units of interferon alfa-2a and 1,000–1,200 mg ribavirin daily according to their body weight. A response was defined as absence of HCV-RNA and normalization of S-ALT after 6 months of combination therapy. Results: With respect to the allele and genotype frequency, a significant difference was not observed between controls and patients with chronic hepatitis C. Furthermore, such a difference was also not observed if responders and non-responders to antiviral therapy were compared. Conclusions: The promoter polymorphism of the TNF-α gene investigated herein is equally distributed in healthy individuals and patients with hepatitis C and does not seem to predict the response to therapy with interferon alfa-2a and ribavirin. Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Unlike in HIV, homozygosity for a 32-bp deletion (Δ32) of the chemokine receptor 5 (CCR5) gene was recently described in increased frequency in patients with chronic hepatitis C (HCV). Thus, it was speculated that this mutation might be relevant for disease susceptibility and influence the response to antiviral therapy. The present study sought to confirm the association between HCV and the Δ32 mutation of the CCR5 gene and to correlate it with the response to therapy with interferon-α-2a and ribavirin. Sixty-two patients with HCV and 119 healthy unrelated controls were genotyped for the Δ32 mutation. For the correlation between the Δ32 mutation and response to therapy, only patients (n = 59) who completed 6 months of combination therapy as part of a prospective study were evaluated. The Δ32 mutation was not observed in increased frequency in HCV. Furthermore, a significant difference of the HCV load or aminotransferase concentrations was not observed in carriers versus noncarriers of the Δ32 mutation. After stratification for potentially confounding factors such as gender or HCV genotype, a significant difference was also not detected with respect to treatment outcome. These observations argue strongly against a role of CCR5 for susceptibility to HCV infection or response to combination therapy. [Copyright &y& Elsevier]

Recently, a T-to-C polymorphism at position −295 in the promoter region of the human interleukin-16 (IL-16) gene was reported. The expression of IL-16 is increased in inflammatory bowel disease, in particular in Crohn’s disease. However, data concerning the IL-16 promoter polymorphism in inflammatory bowel disease are lacking. Thus, the current study aimed at the assessment of this polymorphism in Crohn’s disease and ulcerative colitis. One hundred three patients with Crohn’s disease, 100 patients with ulcerative colitis, and 120 healthy unrelated controls were genotyped for the promoter polymorphism. Furthermore, patients with Crohn’s disease were stratified according to disease localization and the respective clinical phenotype (fistulizing, fibrostenotic, or inflammatory). The frequencies of the T allele (P < 0.01) and the TT genotype (P < 0.01) were significantly increased in patients with Crohn’s disease compared to the controls, regardless of the disease phenotype or the site of intestinal involvement. An association with ulcerative colitis was not observed. Herein a new association between a promoter polymorphism of the IL-16 gene and Crohn’s disease was observed and correlates with the previously described increased mucosal expression of IL-16 in inflammatory bowel disease. [Copyright &y& Elsevier]

Anti-Saccharomyces cerevisiae antibodies (ASCA) have been described as specific markers in Crohn’s disease and their healthy first-degree relatives. 171 patients with Crohn’s disease, their 105 first-degree relatives, 145 patients with ulcerative colitis and 101 first-degree relatives of patients with ulcerative colitis, 50 patients with infectious enterocolitis and 100 healthy controls were tested for ASCA employing the ELISA technique. When compared with the healthy controls (p < 0.0001) and patients with infectious enterocolitis (p < 0.0001) the prevalence of ASCA was significantly increased in patients with Crohn’s disease and their first-degree relatives (p < 0.01). Further significant differences concerning the frequency of ASCA within the different groups of our study population were not observed. In particular, ASCA were not found in increased prevalence in infectious enterocolitis. These observations are compatible with a role of ASCA as a marker of genetic predisposition to Crohn’s disease.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The polymorphisms of MICA exon 5 (5 alleles), MICB intron 1 (13 alleles), C1 4 1 (6 alleles), HLA-B (29 alleles) and HLA-A (15 alleles) were investigated in a healthy German population. Sequencing was performed for the MICB alleles CA14, CA15, CA17, CA23 and CA26 isolated from different cell lines. Variation to the published sequence was observed for CA14, CA15 and for CA17. At the C1 4 1 locus a new allele (CAAA)[sub 9] was identified and confirmed by sequencing. Linkage disequilibria were investigated for two-point- and three-point-haplotypes... [ABSTRACT FROM AUTHOR]

The new allele MICA*055 contains eight GCT repeats within the exon 5 MICA-TM microsatellite polymorphism. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor in response to an article regarding fulminant Crohn's colitis following allogenic stem cell transplantation, published in the 2003 issue of the journal "Gut."

The major histocompatibility complex class I chain-related gene A (MICA)-TM exon 5 trinucleotide polymorphism, the MICB-C1_2_A intron 1 dinucleotide polymorphism and the tetranucleotide polymorphism C1_4_1 located in the major histocompatibility complex class I region on chromosome 6 were shown to influence various chronic inflammatory conditions. We investigated the association of these microsatellite polymorphisms with chronic periodontitis, a highly prevalent oral inflammatory disease in 389 periodontitis patients and 771 healthy controls with South German genetic background. Genotyping of the MICA-TM, MICB-C1_2_A and C1_4_1 microsatellite polymorphisms was performed by PCR amplification and fragment analysis. Global frequency distribution of MICB-C1_2_A ( P = 0.006) and C1_4_1 ( P = 0.028) alleles was significantly different between both study groups. Allele-specific analysis revealed that the MICA-TM allele A5 was more prevalent among male periodontitis patients [ P = 0.0001; odds ratio (OR) 2.17, 95% confidence interval (CI) 1.55-3.03]. In C1_4_1 allele, three was significantly higher in healthy controls ( P = 0.006; OR 0.74, 95% CI 0.60-0.91). Two haplotypes (MICA:A5-C1_4_1:5; P = 0.002; OR 2.63, 95% CI 1.46-4.74 and MICB:CA16-C1_4_1:3; P = 0.014; OR 0.68, 95% CI 0.50-0.92) showed significant differences between periodontitis patients and controls. The MICA-TM, MICB-C1_2_A and C1_4_1 microsatellite polymorphism seem to influence the individual susceptibility to chronic periodontitis in patients with German genetic background. [ABSTRACT FROM AUTHOR]

Various autoantibodies have been described in patients with inflammatory bowel disease. The autoimmune regulator (AIRE) functions as a transcription factor in cells responsible for the induction and maintenance of immunological tolerance. In contrast to classic autoimmune disorders, polymorphisms of the AIRE gene are not associated with inflammatory bowel disease, despite the presence of disease-specific autoantibodies. [ABSTRACT FROM AUTHOR]

Background Plants are hotbeds for parasites such as arthropod herbivores, which acquire nutrients and energy from their hosts in order to grow and reproduce. Hence plants are selected to evolve resistance, which in turn selects for herbivores that can cope with this resistance. To preserve their fitness when attacked by herbivores, plants can employ complex strategies that include reallocation of resources and the production of defensive metabolites and structures. Plant defences can be either prefabricated or be produced only upon attack. Those that are ready-made are referred to as constitutive defences. Some constitutive defences are operational at any time while others require activation. Defences produced only when herbivores are present are referred to as induced defences. These can be established via de novo biosynthesis of defensive substances or via modifications of prefabricated substances and consequently these are active only when needed. Inducibility of defence may serve to save energy and to prevent self-intoxication but also implies that there is a delay in these defences becoming operational. Induced defences can be characterized by alterations in plant morphology and molecular chemistry and are associated with a decrease in herbivore performance. These alterations are set in motion by signals generated by herbivores. Finally, a subset of induced metabolites are released into the air as volatiles and function as a beacon for foraging natural enemies searching for prey, and this is referred to as induced indirect defence. Scope The objective of this review is to evaluate (1) which strategies plants have evolved to cope with herbivores and (2) which traits herbivores have evolved that enable them to counter these defences. The primary focus is on the induction and suppression of plant defences and the review outlines how the palette of traits that determine induction/suppression of, and resistance/susceptibility of herbivores to, plant defences can give rise to exploitative competition and facilitation within ecological communities "inhabiting" a plant. Conclusions Herbivores have evolved diverse strategies, which are not mutually exclusive, to decrease the negative effects of plant defences in order to maximize the conversion of plant material into offspring. Numerous adaptations have been found in herbivores, enabling them to dismantle or bypass defensive barriers, to avoid tissues with relatively high levels of defensive chemicals or to metabolize these chemicals once ingested. In addition, some herbivores interfere with the onset or completion of induced plant defences, resulting in the plant's resistance being partly or fully suppressed. The ability to suppress induced plant defences appears to occur across plant parasites from different kingdoms, including herbivorous arthropods, and there is remarkable diversity in suppression mechanisms. Suppression may strongly affect the structure of the food web, because the ability to suppress the activation of defences of a communal host may facilitate competitors, whereas the ability of a herbivore to cope with activated plant defences will not. Further characterization of the mechanisms and traits that give rise to suppression of plant defences will enable us to determine their role in shaping direct and indirect interactions in food webs and the extent to which these determine the coexistence and persistence of species. [ABSTRACT FROM AUTHOR]

Background and Aims: We analyzed the prevalence of concomitant intestinal stenosis in patients with fistulizing Crohn's disease (CD), including the NOD2/CARD15 and IL23R genotype status.Methods: Medical records of n = 1,110 patients with inflammatory bowel diseases were screened for patients with fistulizing and stricturing CD. Study inclusion required diagnosis of stenosis made within 6 months of diagnosing fistulas. CD-associated NOD2 and IL23R variants were genotyped. Similarly, we prospectively investigated 42 patients presenting with fistulizing CD.Results: In the retrospective study (n = 333 CD patients), fistulas were found in 145 (43.5%) patients and stenoses in 223 (67.0%) patients. Concomitant stenosis was diagnosed in 125 patients with fistulas resulting in a positive predictive value (PPV) of 86.2% for fistulas predicting intestinal stenosis (p = 5.53 x 10(-11); OR 5.74, 95% CI 3.22-10.50). In logistic regression analysis, presence of fistulas (OR 4.51; 95% CI 2.54-8.01, p = 2.68 x 10(-7)) and disease duration (OR 1.09; 95% CI 1.05-1.13; p = 3.19 x 10(-6)) were strongly associated with intestinal stenosis. NOD2 genotype information, but not IL23R status, increased the PPV for the correct diagnosis of stenosis (PPV = 89.9%). All homozygous carriers (100%) of NOD2 variants with fistulizing CD were diagnosed with stenosis; 1007fs homozygotes were found more often among patients with fistulas and stenoses than in patients without stenoses and fistulas (p = 0.00037). Similar results were found in the prospective analysis, in which 83.3% of the patients with fistulizing CD had concomitant stenosis.Conclusion: Fistulizing CD is strongly associated with concomitant intestinal stenosis, particularly in homozygous carriers of NOD2 mutations. [ABSTRACT FROM AUTHOR]

Periodontal diseases are complex inflammatory diseases and affect up to 20% of the worldwide population. An unbalanced reaction of the immune system toward microbial pathogens is considered as the key factor in the development of periodontitis. Defensins have a strong antimicrobial function and are important contributors of the immune system toward maintaining health. Here, we present the first systematic association study of DEFB1. Using a haplotype-tagging single nucleotide polymorphism (SNP) approach, including described promoter SNPs of DEFB1, we investigated the associations of the selected variants in a large population (N=1337 cases and 2887 ethnically matched controls). The 3′ untranslated region SNP, rs1047031, showed the most significant association signal for homozygous carriers of the rare A allele (P=0.002) with an increased genetic risk of 1.3 (95% confidence interval: 1.11–1.57). The association was consistent with the specific periodontitis forms: chronic periodontitis (odds ratio=2.2 (95% confidence interval: 1.16–4.35), P=0.02), and aggressive periodontitis (odds ratio=1.3 (95% confidence interval 1.04–1.68), P=0.02). Sequencing of regulatory and exonic regions of DEFB1 identified no other associated variant, pointing toward rs1047031 as likely being the causative variant. Prediction of microRNA targets identified a potential microRNA-binding site at the position of rs1047031. [ABSTRACT FROM AUTHOR]

Background: Laparoscopic or endoscopic limited resection is intended to be an additional therapeutic option for the treatment of early gastric cancer. However, tumorbiologic markers to predict the outcome for patients after limited resections are missing. This study therefore investigated the prognostic relevance of p53 and bcl-2 immunoreactivity as well as the percentage of apoptotic tumor cells in early invasive pT1/pT2 tumors managed with standard operations for gastric adenocarcinoma.Methods: Histologic slides of 65 pT1/pT2 gastric carcinomas were investigated for bcl-2 and p53 immunoreactivity. For 35 patients, DNA fragmentation of tumor cell nuclei was determined by the terminal uridine 5'-triphosphate (UTP) nick end-labeling (TUNEL) method. Follow-up evaluation of the patients was prospectively documented for 53.4 +/- 4.1 months.Results: Findings showed that bcl-2 immunoreactivity was associated with tumors of the intestinal type according to Lauren s classification (p = 0.042), and that p53 immunoreactivity was increased in more invasive tumors (pT1 vs pT2 tumors; p = 0.047). Mean survival time was significantly longer for patients with bcl-2-negative tumors (74.3 +/- 6.8 months) than for patients with bcl-2-positive tumors (50.8 +/- 7.6 months; p = 0.024). The percentage of apoptotic tumor cell nuclei did not have prognostic relevance in the population studied and was not associated with several histopathologic parameters or bcl-2 and p53 immunoreactivity. Subgroup analysis indicated that the survival of patients with differentiated G2 and bcl-2-negative/p53-negative tumors was significantly longer (82 +/- 6 months) than the survival of patients with G2 bcl-2- and/or p53-positive tumors (41.8 +/- 12.5 months; p = 0.005), with independent prognostic relevance determined by multivariate analysis (p = 0.024).Conclusion: The data reported indicate that the analysis of bcl-2 and p53 immunoreactivity seems to have prognostic implications for early invasive (pT1/pT2) gastric adenocarcinomas and may subclassify patients for minimally invasive laparoscopic or endoscopic gastric resections. [ABSTRACT FROM AUTHOR]