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PubMed2004

Tissue-specific mRNA expression profiles of human nuclear receptor subfamilies.

Pairs of forward and reverse primers and TaqMan probes specific to each human nuclear receptor were prepared. Analysis of the mRNA expression level of each target of 43 nuclear receptors in total RNA from single and pooled specimens of various human organs (liver, kidney, adrenal gland, lung, heart, brain, cerebellum, skeletal muscle, spleen, thymus, thyroid gland, prostate, testis, uterus, placenta, bone marrow, trachea, and salivary gland) was performed by real-time reverse transcription PCR using an ABI PRISM 7700 sequence detector system. The mRNA expression of 33 nuclear receptors (NR1A1, 1A2, 1B1, 1B2, 1B3, 1C1, 1C2, 1C3, 1D1, 1D2, 1F1, 1F2, 1F3, 1H2, 1H3, 1I1, 1I2, 2B1, 2B2, 2B3, 2C1, 2C2, 2F1, 2F2, 3A2, 3B1, 3C1, 3C2, 3C4, 4A1, 4A2, 4A3, and 6A1) was successfully detected in all of the tissues by this method. NR1H4, 2A1, and 3C3 mRNAs were not detectable in the heart, heart, and liver, respectively. NR5A2 mRNA was not detectable in either the brain or cerebellum. NR3A1 mRNA was not detectable in the small intestine, colon, brain, and cerebellum. NR5A1 mRNA was not detectable in the kidney, stomach, small intestine, and colon. NR1I3 mRNA was detected in the liver, kidney, stomach, small intestine, adrenal gland, lung, brain, skeletal muscle, thymus, thyroid gland, prostate, testis, placenta, and trachea. NR2A2 mRNA was detected in the liver, kidney, prostate, testis, uterus, and trachea. NR2E1 mRNA was detected in the adrenal gland, brain, cerebellum, testis, placenta, and bone marrow. NR2E3 mRNA was detected in the adrenal gland, thyroid gland, prostate, testis, uterus, trachea, and salivary gland. This study provides information concerning the tissue distribution of the mRNA expression of 43 human nuclear receptors. The mRNA expression profiles of CYP3A4, CYP3A5 and ABC-transporters are also shown. These results are valuable for establishing a nuclear receptor-mediated screening system for new chemical entities in new drug development.

ATP-Binding Cassette Transporters↗
PubMed1977

Giant hypertrophic gastritis of Basenji dogs.

Giant hypertrophic gastritis is a newly recognized disease of adult Baseji dogs similar to Menetrier's disease of man. It is characterized by weight loss, diarrhea, dry coat, pale membranes, anorexia, raised convoluted rugae in the body of the stomach, palpable fluid- and gas-filled intestines, colonic inflammation, and radiographically demonstrable dilated intestinal loops. Laboratory findings include leukocytosis, neutrophilia, low hemoglobin, hypoalbuminemia, hypobetaglobulinemia, hypergammaglobulinemia, decreased serum fatty acids, hypocholesterolemia, indicanuria, low fecal pH, and increased fecal fat and nitrogen. Four dogs studied had gastritis with hypertrophy and diffuse lymphocytosis and plasmacytosis of the small intestine.

Animals↗
PubMed2004

Nonimmunized egg yolk powder can suppress the colonization of Salmonella typhimurium, Escherichia coli O157:H7, and Campylobacter jejuni in laying hens.

If colonized, poultry shed enteric pathogens in the feces. Of those that colonize poultry Salmonella spp., Campylobacter jejuni (C. jejuni), and Escherichia coli (E. coli) O157:H7 are the most concern to the industry. The authors previously discovered that the introduction of 5% dried nonimmunized egg yolk powder in the regular feed could eliminate and prevent Salmonella enteritidis intestinal colonization of laying hens. Hence, the efficacy of nonimmunized dried egg yolk powder supplement in controlling the colonization of laying hens with Salmonella typhimurium (S. typhimurium), C. jejuni, and E. coli O157:H7 was investigated in this study. The 10% (wt/ wt) egg yolk powder eliminated S. typhimurium after 2 wk of feeding and the 5 and 7.5% (wt/wt) supplements significantly (P < 0.05) reduced the frequency of colonization. Similarly, 7.5 and 10% egg yolk powder reduced the colonization of C. jejuni and E. coli O157:H7 significantly (P < 0.05) after 1 wk of feeding. In the prevention trial, pathogen-free chickens were fed supplemented feed (10% egg yolk powder) for 4 wk and were then infected. S. typhimurium was prevented from colonizing the intestine throughout the 4-wk test, and E. coli O157:H7 colonization was delayed for 2 wk. C. jejuni and E. coli O157:H7 populations in the intestine were significantly (P < 0.05) suppressed by egg yolk powder supplementation throughout the test. None of the supplement concentrations affected BW or the mean weight and number of the eggs laid per hen. At the end of the study, the organisms were absent or significantly (P < 0.05) reduced in the intestine, ovary, oviduct, and spleen of hens fed the egg yolk powder treatment. This study indicates that nonimmunized egg yolk powder is able to reduce the frequency of colonization of foodborne pathogens and prevent these organisms from colonizing the intestinal tract. Addition of egg yolk powder to the regular feed at a concentration of 7.5 to 10% (wt/wt) may be a simple means of reducing or inhibiting S. typhimurium, C. jejuni, and E. coli O157:H7 colonization in laying hens.

Animal Feed↗
PubMed2002

Intestinal epithelial lesions associated with signet ring cell carcinoma of the colon and small intestine.

AIMS: The purpose of this study was to investigate the epithelial lesions associated with signet ring cell carcinoma (SRCC) of the colon and small intestine and the possible mechanism of tumour development. METHODS: Twenty-seven cases of adenocarcinoma with a signet ring cell (SRC) component of the colon and small intestine were divided into three groups depending on the association of the SRCC with: (1) epithelium without definite epithelial dysplasia, (2) adenoma, and (3) common type of adenocarcinoma (CTCA) with SRCC component occupying more than 50%, 30%, or less than 30% of the tumour. RESULTS: Most carcinomas were of T3 or T4 type, using the TNM standard staging system. The SRCC component was histopathologically similar in all groups. In group 1 (four cases, linitis plastica type), the overlying epithelium was normal or showed indefinite epithelial dysplasia and occasionally contained intra-epithelial SRCs. In groups 2 and 3 (two and 21 cases, respectively), seven cases contained multiple foci of intra-epithelial SRCs in areas separated from the invasive carcinoma. Transitional areas between SRCC and adenoma or CTCA were also identified. Immunostaining for p53 showed a varied extent of positive reactivity in 23 SRCC. The degree and the extent of reactivity appeared to increase with the stage of the carcinoma. Most intra-epithelial SRCs were immunoreactive for p53. Linitis plastica SRCC was associated with extensive p53 reactivity of the 'atypical' and the adjacent 'normal' epithelium. CONCLUSIONS: SRCC may arise from either CTCA, adenoma, 'atypical' epithelium or a combination of these epithelia. SRCC accounts for the bulk of carcinoma in each of these categories. In linitis plastica SRCC, positive reactivity for p53 is extensive in the adjacent 'normal' colonic epithelium and extends as far as 3cm from the microscopically identified SRCC margin.

Adenoma↗
PubMed2006

The effect of hen-egg antibodies on Clostridium perfringens colonization in the gastrointestinal tract of broiler chickens.

We evaluated the ability of hen-egg antibodies (HEA) to reduce intestinal colonization by Clostridium perfringens in broiler chickens. Antibodies against C. perfringens or cholera toxin (negative control) were obtained from the eggs of laying hens hyperimmunized using a C. perfringens bacterin or cholera toxin. Eggs were collected, pooled, and egg antibodies were concentrated by polyethylene-glycol precipitation. An initial experiment was conducted to determine the in vivo activity of the administered antibody along the length of the intestine. Thereafter, two feeding trials were performed to assess the efficacy of feed amended with the egg antibodies in reducing the level of colonization of C. perfringens in challenged birds. Antibody activity declined from proximal to distal regions of the intestine but remained detectable in the cecum. In the first experiment there was no significant reduction in the number of C. perfringens in the birds fed the diet amended with the anti-C. perfringens egg antibody, compared to the birds that received the anti-cholera toxin egg antibody (n=10), at any of the sampling times. In the second experiment there was a significant decrease in C. perfringens intestinal populations 72 h after treatment (n=15) as assessed by culture-based enumeration, but there was no decrease as measured by quantitative PCR based on the C. perfringens phospholipase C gene. Intestinal-lesion scores were higher in the birds that received the anti-C. perfringens HEA. Our work suggests that administration of HEA did not reduce the level of C. perfringens intestinal colonization and conversely might exacerbate necrotic enteritis.

Animal Feed↗
PubMed1993

Enterobacter cloacae cross-colonization in neonates demonstrated by ribotyping.

The intestinal colonization by Enterobacter cloacae strains with a derepressed cephalosporinase was studied in a paediatric ward between February 1990 and January 1991. Environmental sampling was performed simultaneously. Fifty-two isolates were recovered from 200 neonates (stool, blood) and 14 strains were isolated from the neonatal environment. An epidemiological study based on the typing of 36 Enterobacter cloacae isolates was carried out using antibiotyping, biotyping and ribotyping methods. The isolates selected were from 21 neonates (24 isolates), the neonatal ward environment (8 isolates) and from other wards (4 isolates). Thirty-two isolates had the same antibiotic resistance pattern, corresponding to a derepressed cephalosporinase and resistance to the following aminoglycosides: kanamycin, gentamicin, tobramycin and netilmicin. No predominant biotyping pattern could be established. Ribotyping done with two endonucleases (EcoRI and BamHI) showed 28 Enterobacter cloacae isolates to have a single pattern. Ribotyping was the most discriminating method used in this study, permitting identification of cross-contamination with Enterobacter cloacae in the paediatric ward.

Bacteremia↗
PubMed2000

The Candida albicans INT1 gene facilitates cecal colonization in endotoxin-treated mice.

Increased intestinal colonization with Candida albicans is believed to be a major predisposing factor to systemic candidiasis. Previous evidence has implicated the C. albicans INT1 gene in hyphal development, epithelial adherence, and mouse virulence. The effect of INT1 on mouse cecal colonization was measured using a parent strain (CAF2, INT1/INT1), an int1 deletion homozygote (CAG3, int1/int1), and a heterozygous reintegrant (CAG5, int1/int1 + INT1). Forty-eight hours after oral inoculation of 10(7) C. albicans into normal mice, only low numbers of each strain were recovered from the cecal flora. In mice pretreated with oral bacitracin/streptomycin, cecal colonization of each C. albicans strain was increased compared to the corresponding strain inoculated into untreated mice, with the CAF2 parent strain greater (P < 0.01) than the two mutant strains, and with the heterozygous and homozygous mutants not different from each other. In mice pretreated with parenteral lipopolysaccharide (LPS), in addition to oral antibiotics, numbers of cecal CAF2, CAG5, and CAG3 were increased (P < 0.01) compared to the corresponding strain inoculated into mice treated with antibiotics alone. In LPS-treated mice, numbers of cecal C. albicans CAF2 (INT1/INT1) were greater (P < 0.05) than C. albicans CAG3 (int1/int1). Thus, parenteral LPS had an additive effect on C. albicans cecal colonization in antibiotic-treated mice, and the presence of two functional copies of the INT1 gene appeared to facilitate colonization in both antibiotic-treated mice and in mice treated with antibiotics plus parenteral endotoxin.

Animals↗
PubMed1989

Differential stimulation of S-adenosylmethionine decarboxylase by difluoromethylornithine in the rat colon and small intestine.

The effects of chronic inhibition of ornithine decarboxylase (ODC) by the specific inhibitor difluoromethylornithine (DFMO) in the rat colon and small intestine on mucosal contents of polyamines, decarboxylated S-adenosylmethionine (decarboxylated AdoMet) and S-adenosylmethionine decarboxylase (AdoMet decarboxylase) activity were studied. Administration of 1% DFMO in the drinking water for 10 or 15 weeks resulted in inhibition of ODC and decreases in intracellular putrescine and spermidine contents in both proximal and distal segments of small intestine and colon. At both time points DFMO administration resulted in a dramatic stimulation of AdoMet decarboxylase activity and a rise in decarboxylated AdoMet content in the proximal and distal small-intestinal segments compared with controls, which was not seen in either colonic segment of DFMO-treated animals. This differential stimulation of AdoMet decarboxylase by DFMO in the small intestine and colon could not be entirely explained on the basis of differences in polyamine contents, which are known to regulate this enzyme activity. Kinetic and inhibition studies of AdoMet decarboxylase in control small and large intestine revealed that: (1) there was no difference in Vmax. values between the tissues; (2) the Km for AdoMet was higher in the small intestine than in the colon; and (3) the Ki for product inhibition by decarboxylated AdoMet was higher in the small intestine than in the colon. These results suggest that the differential stimulation of AdoMet decarboxylase by DFMO in the small intestine and colon may be due to different isoenzymes and could play a significant role in the regulation of polyamine contents throughout the gut.

Adenosylmethionine Decarboxylase↗
PubMed2004

A very rare consequence of steroid therapy: ileal perforation in a patient with familial mediterranean fever.

Intestinal perforation rarely occurs in children with familial Mediterranean fever (FMF). When this does happen, it is the result of untreated intestinal obstruction caused by compression from peritoneal adhesions. Intestinal perforation is a well-known complication of steroid therapy in all ages. The duodenum is affected most frequently, but perforation may also occur in other parts of the small intestine and, very rarely, the colon. Intestinal wall changes that occur in chronic FMF may promote the harmful effects of steroids. Here we present an unexpected complication, ileal perforation, in an 8-year-old boy who was taking prednisolone for FMF-related arthritis.

Child↗
PubMed2001

Fatal gastrointestinal infection with 'Flexispira rappini'-like organisms in a cat.

A 4-month-old male British Blue cat with catarrhal to haemorrhagic enteritis showed massive colonization of the stomach, small intestine and caecum with spiral-shaped bacilli. In the stomach, organisms were located in foveolae and gland lumina and within unaltered and degenerate epithelial cells. Inflammatory infiltration was moderate and T cell dominated. In the intestine, bacilli were found in the gut lumen, berween villi, in crypt lumina and within epithelial cells. Degeneration of crypt epithelial cells as well as crypt dilation and moderate to massive macrophage-dominated infiltration of the mucosa and submucosa were observed. Immunohistochemically, bacilli were positive with an antibody against Helicobacter. Ultrastructurally, the organisms strongly resembled 'Flexispira rappini', a spiral-shaped Helicobacter species known as a normal intestinal colonizer in dogs and mice.

Animals↗
PubMed2005

Activation of both acfA and acfD transcription by Vibrio cholerae ToxT requires binding to two centrally located DNA sites in an inverted repeat conformation.

The Gram-negative bacterium Vibrio cholerae is the infectious agent responsible for the disease Asiatic cholera. The genes required for V. cholerae virulence, such as those encoding the cholera toxin (CT) and toxin-coregulated pilus (TCP), are controlled by a cascade of transcriptional activators. Ultimately, the direct transcriptional activator of the majority of V. cholerae virulence genes is the AraC/XylS family member ToxT protein, the expression of which is activated by the ToxR and TcpP proteins. Previous studies have identified the DNA sites to which ToxT binds upstream of the ctx operon, encoding CT, and the tcpA operon, encoding, among other products, the major subunit of the TCP. These known ToxT binding sites are seemingly dissimilar in sequence other than being A/T rich. Further results suggested that ctx and tcpA each has a pair of ToxT binding sites arranged in a direct repeat orientation upstream of the core promoter elements. In this work, using both transcriptional lacZ fusions and in vitro copper-phenanthroline footprinting experiments, we have identified the ToxT binding sites between the divergently transcribed acfA and acfD genes, which encode components of the accessory colonization factor required for efficient intestinal colonization by V. cholerae. Our results indicate that ToxT binds to a pair of DNA sites between acfA and acfD in an inverted repeat orientation. Moreover, a mutational analysis of the ToxT binding sites indicates that both binding sites are required by ToxT for transcriptional activation of both acfA and acfD. Using copper-phenanthroline footprinting to assess the occupancy of ToxT on DNA having mutations in one of these binding sites, we found that protection by ToxT of the unaltered binding site was not affected, whereas protection by ToxT of the mutant binding site was significantly reduced in the region of the mutations. The results of further footprinting experiments using DNA templates having +5 bp and +10 bp insertions between the two ToxT binding sites indicate that both binding sites are occupied by ToxT regardless of their positions relative to each other. Based on these results, we propose that ToxT binds independently to two DNA sites between acfA and acfD to activate transcription of both genes.

Bacterial Proteins↗
PubMed2003

Type 1 fimbriae of Salmonella enterica serovar Typhimurium bind to enterocytes and contribute to colonization of swine in vivo.

Salmonella enterica serovar Typhimurium strain 798 is a clinical isolate from a pig and is known to be able to cause persistent, asymptomatic infections. This strain also is known to exist in two phenotypes (adhesive and nonadhesive to enterocytes) and can switch between the two phenotypes at a rate consistent with phase variation. Cells in the adhesive phenotype are more readily phagocytosed by leukocytes than nonadhesive cells. Once in a leukocyte, adhesive-phase cells survive while nonadhesive-phase cells die. In the present study, nonadhesive mutants were obtained with the transposon TnphoA. A nonadhesive mutant was selected for study and was shown by electron microscopy not to produce fimbriae. The gene encoding the adhesin was cloned and sequenced. Based on its sequence, the adhesin was shown to be FimA, the major subunit of type 1 fimbriae. The nonadhesive mutant was attenuated in its ability to colonize both mouse and pig intestines, but remained capable of systemic spread in mice. The nonadhesive mutant was phagocytosed to the same extent as parental cells in the adhesive phase and then survived intracellularly. These results demonstrated that type 1 fimbriae were important for attachment to enterocytes and promoted intestinal colonization. However, they were not important in promoting phagocytosis or intracellular survival.

Animals↗
PubMed2001

Influence of microbial species on small intestinal myoelectric activity and transit in germ-free rats.

The effect of an intestinal microflora consisting of selected microbial species on myoelectric activity of small intestine was studied using germ-free rat models, with recording before and after specific intestinal colonization, in the unanesthetized state. Intestinal transit, neuropeptides in blood (RIA), and neuromessengers in the intestinal wall were determined. Clostridium tabificum vp 04 promoted regular spike burst activity, shown by a reduction of the migrating myoelectric complex (MMC) period from 30.5 +/- 3.9 min in the germ-free state to 21.2 +/- 0.14 min (P < 0.01). Lactobacillus acidophilus A10 and Bifidobacterium bifidum B11 reduced the MMC period from 27.9 +/- 4.5 to 21.5 +/- 2.1 min (P < 0.02) and accelerated small intestinal transit (P < 0.05). Micrococcus luteus showed an inhibitory effect, with an MMC period of 35.9 +/- 9.3 min compared with 27.7 +/- 6.3 min in germ-free rats (P < 0.01). Inhibition was indicated also for Escherichia coli X7 gnotobiotic rats. No consistent changes in slow wave frequency were observed. The concentration of neuropeptide Y in blood decreased after introduction of conventional intestinal microflora, suggesting reduced inhibitory control. Intestinal bacteria promote or suppress the initiation and aboral migration of the MMC depending on the species involved. Bacteria with primitive fermenting metabolism (anaerobes) emerge as important promoters of regular spike burst activity in small intestine.

Action Potentials↗
PubMed1983

Prevention of drug-resistant Escherichia coli colonization in chickens by treatment with a faecal fluid.

This study was performed to prove that intestinal colonization in chickens by resistant Escherichia coli strains present in the environment might be prevented when faeces in which sensitive E. coli strains were dominant was administered to newly hatched chicks. The appearance of resistant E. coli strains was markedly reduced. Escherichia coli O49:H12 was the sensitive E. coli strain which formed the major colonizer in the intestinal tract. In young chickens, this strain persisted as a major component, and even when it was a minor colonizer in the faecal fluid administered, it appeared as a major component soon afterwards. This strain is considered to be a good colonizer in the gut of young chickens.

Animals↗
PubMed1974

Effects of ingested chrysotile on DNA synthesis in the gastrointestinal tract and liver of the rat.

The effects of chrysotile on DNA synthesis in the gastrointestinal tract of the rat were studied by measuring the uptake of tritium-labeled thymidine; whole stomach, small intestine, colon liver were removed, cleaned, and homogenized and the DNA was isolated and assayed for tritium label.A dose-response study indicated that 2 weeks after a 5 mg/kg dose of chrysotile, DNA synthesis was increased in the small intestine and colon and reduced in the liver; synthesis was reduced in the small intestine 2 weeks after a 500 mg/kg dose. Following a 100 mg/kg dose of chrysotile, a transient increase in DNA synthesis was noted in the stomach and small intestine at 1 and 7 days, respectively, besides increased synthesis in the colon from 28 to 63 days. These data suggest that asbestos penetrates the gastrointestinal mucosa and influences regulation of DNA synthesis in the gastrointestinal tract.

Administration, Oral↗
PubMed1993

Escherichia coli K-12 ferrous iron uptake mutants are impaired in their ability to colonize the mouse intestine.

The streptomycin-treated mouse colonization model was used to investigate the role of the Fe2+ uptake system (Feo) of Escherichia coli K12 in the colonization of the mouse intestine. Mutants impaired in the uptake of Fe2+ ions were shown to be deficient also in their colonization ability. Both enterochelin-producing and enterochelin-nonproducing Escherichia coli feo mutants were unable to colonize the mouse intestine. These results demonstrated that Fe(II) is an essential source of iron for E. coli grown in the intestine.

Animals↗
PubMed2004

[The method of choice for surgical treatment of intestinal obstruction in colon cancer].

The authors present the results of surgical treatment of 326 patients with cancer of the colon complicated by occlusive intestinal obstruction. Three degrees of colon passage disorders were distinguished. Surgical policy depended on location of the tumor, degree of the obstruction, severity of general state and concomitant diseases. General postoperative lethality was 13% (43 of 326 operated patients died). Resection of the colon and subtotal colectomy with one-stage intestinal reconstruction may be recommended for patients with compensated stage of intestinal obstruction and stable general state.

Adenocarcinoma↗
PubMed1998

The human Pim-2 proto-oncogene and its testicular expression.

In this study we describe the cloning of a human gene, encoding a protein that shares 90% identity and 93% similarity at the primary structure level, with the mouse Pim-2 gene. The gene was designated hPim-2. Structural features suggest that like the mouse Pim-2, hPim-2 is also a serine threonine kinase. At the RNA level, two hPim-2 transcripts were identified. The first, 2.2 kb, is highly expressed in hematopoietic tissues and in leukemic and lymphoma cell lines (K-562, HL-60 and RAJI). It also shows considerable high levels in testis, small intestine, colon and human colorectal adenocarcinoma cells (SW480). A second transcript, 5.0 kb in size, could be detected only in spleen, thymus, small intestine and colon and in the K-562 and RAJI cell lines. In situ hybridization analysis of biopsies taken from testes of men with complete or partial spermatogenesis revealed that the gene is expressed in primary spermatocytes. In the absence of germ cells, signal could be detected over specific cells in the well developed interstitial region. These results suggest a role for hPim-2 in proliferating cells as well as during meiosis. A possible connection between hPim-2 and apoptosis is discussed.

Adenocarcinoma↗