LIVIVO - Search results -

Search results

Result 1 - 10 of total 236

Search options

Article ; Online: Omega-3 fatty acids prevent early-life antibiotic exposure-induced gut microbiota dysbiosis and later-life obesity.

Kaliannan, K / Wang, B / Li, X-Y / Bhan, A K / Kang, J X

International journal of obesity (2005)

2016 Volume 40, Issue 6, Page(s) 1039–1042

Abstract: Early-life antibiotic exposure can disrupt the founding intestinal microbial community and lead to obesity later in life. Recent studies show that omega-3 fatty acids can reduce body weight gain and chronic inflammation through modulation of the gut ... ...

Abstract	Early-life antibiotic exposure can disrupt the founding intestinal microbial community and lead to obesity later in life. Recent studies show that omega-3 fatty acids can reduce body weight gain and chronic inflammation through modulation of the gut microbiota. We hypothesize that increased tissue levels of omega-3 fatty acids may prevent antibiotic-induced alteration of gut microbiota and obesity later in life. Here, we utilize the fat-1 transgenic mouse model, which can endogenously produce omega-3 fatty acids and thereby eliminates confounding factors of diet, to show that elevated tissue levels of omega-3 fatty acids significantly reduce body weight gain and the severity of insulin resistance, fatty liver and dyslipidemia resulting from early-life exposure to azithromycin. These effects were associated with a reversal of antibiotic-induced dysbiosis of gut microbiota in fat-1 mice. These results demonstrate the beneficial effects of omega-3 fatty acids on antibiotic-induced gut dysbiosis and obesity, and suggest the potential utility of omega-3 supplementation as a safe and effective means for the prevention of obesity in children who are exposed to antibiotics.
Language	English
Publishing date	2016-06
Publishing country	England
Document type	Journal Article
ZDB-ID	752409-2
ISSN	1476-5497 ; 0307-0565
ISSN (online)	1476-5497
ISSN	0307-0565
DOI	10.1038/ijo.2016.27
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1325: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article: Intensity of gastrointestinal parasitic infections in horses of animal fairs in Rajasthan

Pilania, P.K / Manohar, G.S / Bhan, A.K

Journal of veterinary parasitology. 2013 June, v. 27, no. 1

2013

Abstract: A total of 719 faecal samples were collected from the horses of five animal fairs held at Pushkar (Ajmer), Nagaur, Mertacity (Nagaur), Hanumangarh and Tilwara (Barmer) in Rajasthan during 2009–10. Quantitative examination of fecal sample of horses showed ...

Abstract	A total of 719 faecal samples were collected from the horses of five animal fairs held at Pushkar (Ajmer), Nagaur, Mertacity (Nagaur), Hanumangarh and Tilwara (Barmer) in Rajasthan during 2009–10. Quantitative examination of fecal sample of horses showed overall mean epg counts of 187.16±7.52 for gastrointestinal helminth parasites. The maximum overall mean epg of 279.37±29.65 was recorded for Parascaris equorum followed by 201.20±12.28 for strongyle, 172.84±24.80 for Strongyloides westeri and 89.20±7.19 epg for Habronema. The horses of Pushkar and Nagaur fairs showed significantly higher intensity of gastrointestinal helminth parasites (221.15±21.95 and 220.93±17.07 epg, respectively) than Hanumangarh (170.83±13019 epg), Merta City (167.07±17.48 epg) and Tilwara (155.84±12.75 epg) fairs. The horses below 3 years of age showed a significantly higher epg (207.77±8.99) of gastrointestinal helminth parasites than 3–5 years (132.83±13.36) and above 5 years (153.40±16.49) of age groups. Sex had no significant effect on the intensity of any parasitic infections detected.
Keywords	Habronema ; Parascaris equorum ; Strongyloides westeri ; feces ; gastrointestinal system ; helminths ; veterinary parasitology ; India
Language	English
Dates of publication	2013-06
Size	p. 42-45.
Publishing place	The Indian Association for the Advancement of Veterinary Parasitology
Document type	Article
Note	NAL-AP-2-clean
ISSN	0974-0813
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Silencing TNF-α in macrophages and dendritic cells for arthritis treatment.

Ye, C / Bhan, A K / Deshpande, V / Shankar, P / Manjunath, N

Scandinavian journal of rheumatology

2013 Volume 42, Issue 4, Page(s) 266–269

Abstract: Objectives: Tumour necrosis factor (TNF)-α secreted by macrophages and dendritic cells (DCs) plays a predominant role in arthritis. Our previous studies suggest that a small peptide, RVG-9R (29-aa peptide derived from the rabies virus glycoprotein, ... ...

Abstract	Objectives: Tumour necrosis factor (TNF)-α secreted by macrophages and dendritic cells (DCs) plays a predominant role in arthritis. Our previous studies suggest that a small peptide, RVG-9R (29-aa peptide derived from the rabies virus glycoprotein, fused to 9R residues), can deliver small interfering RNA (siRNA) to macrophages and DCs. We therefore tested whether knockdown of TNF-α expression in macrophages and DCs by RVG-9R/bound siRNA targeting TNF-α reduces the severity of collagen antibody-induced arthritis (CAIA) in mice. Method: Arthritis was induced in mice by injecting a combination of antibodies to collagen followed by lipopolysaccharide (LPS) treatment. Mice were also injected with TNF-α siRNA complexed with RVG-9R peptide or an irrelevant peptide RVMAT-9R on days 1, 3, 5, and 7. As a positive control, dexamethasone was injected intravenously. Paw thickness was measured every 2 days and the mice were killed on day 10 for testing synovial TNF-α levels and histological analysis of joints. Results: In control mice, arthritis developed on day 4 and reached its peak between day 7 and day 9. Treatment with siTNF-α bound to RVG-9R, but not to RVMAT-9R, resulted in reducing paw thickness scores to the same level as dexamethasone treatment, associated with reduced TNF-α level in synovial fluid. Histological analysis of joints in the control RVMAT-9R/TNF-α siRNA-treated mice showed marked pannus formation and destruction of cartilage and subchondrial bone, as well as severe infiltration of inflammatory cells into the synovium. By contrast, the joint pathology was markedly reduced in RVG-9R/TNF-α siRNA-treated mice resembling the dexamethasone-treated mice. Conclusions: Suppression of TNF-α expression in macrophages and DCs by RVG-9R-mediated siRNA delivery could potentially be a clinically viable strategy for treatment of arthritis.
MeSH term(s)	Animals ; Arthritis, Experimental/drug therapy ; Arthritis, Experimental/genetics ; Arthritis, Experimental/metabolism ; Biopsy, Needle ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Disease Models, Animal ; Gene Silencing/drug effects ; Glycoproteins/pharmacology ; Immunohistochemistry ; Lipopolysaccharides/pharmacology ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred DBA ; Peptide Fragments/pharmacology ; Random Allocation ; Reference Values ; Treatment Outcome ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/immunology ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology ; Viral Proteins/pharmacology
Chemical Substances	Glycoproteins ; Lipopolysaccharides ; Peptide Fragments ; Tumor Necrosis Factor-alpha ; Viral Proteins ; rabies virus glycoprotein peptide
Language	English
Publishing date	2013
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	121265-5
ISSN	1502-7732 ; 0300-9742
ISSN (online)	1502-7732
ISSN	0300-9742
DOI	10.3109/03009742.2013.777779
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 832: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Propionic acidemia: a rare cause of cardiomyopathy.

Bhan, A K / Brody, C

Congestive heart failure (Greenwich, Conn.)

2002 Volume 7, Issue 4, Page(s) 218–219

Abstract: The symptoms of propionic acidemia, an autosomal recessive disorder involving deficiency of the enzyme propionyl-coenzyme A carboxylase, are highly varied and may present at any time in the patient's life. Cardiomyopathy, a rare complication of this ... ...

Abstract	The symptoms of propionic acidemia, an autosomal recessive disorder involving deficiency of the enzyme propionyl-coenzyme A carboxylase, are highly varied and may present at any time in the patient's life. Cardiomyopathy, a rare complication of this disorder, has been reported in only a small number of pediatric patients. The authors describe a case of adult-onset cardiomyopathy in a 23-year-old female with propionic acidemia diagnosed in early childhood and associated with multiple long-standing comorbidities. The possible mechanisms of propionic acidemia-associated cardiomyopathy, and the importance of early recognition and appropriate management, are discussed. (c)2001 CHF, Inc.
Language	English
Publishing date	2002-01-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	1239105-0
ISSN	1751-7133 ; 1527-5299 ; 1079-7998
ISSN (online)	1751-7133
ISSN	1527-5299 ; 1079-7998
DOI	10.1111/j.1527-5299.2001.01011.x
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4325: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Lessons for human inflammatory bowel disease from experimental models.

Bhan, A K / Mizoguchi, E / Smith, R N / Mizoguchi, A

Current opinion in gastroenterology

2006 Volume 15, Issue 4, Page(s) 285–290

Abstract: Experiments carried out in new rodent models of chronic intestinal inflammation provide important clues about the pathogenesis of human inflammatory bowel disease (IBD). Genetic factors and enteric microflora are driving forces regulating mucosal immune ... ...

Abstract	Experiments carried out in new rodent models of chronic intestinal inflammation provide important clues about the pathogenesis of human inflammatory bowel disease (IBD). Genetic factors and enteric microflora are driving forces regulating mucosal immune responses, some of which are pathogenic and lead to colitis. CD4(+) T cells are the major pathogenic cells in colitis, and the type of injury depends on the nature of the cytokine imbalance. The cytokine network controlled by CD4(+) T cells dictates the outcome of the mucosal immune responses. Certain cytokines, such as transforming growth factor-beta and interleukin-10, have a suppressive role, and immunoregulatory T cells capable of secreting these cytokines may be induced at intestinal mucosal sites. Lessons learned from these experimental models are leading to new strategies for the treatment of IBD.
Language	English
Publishing date	2006-09-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	632571-3
ISSN	1531-7056 ; 0267-1379
ISSN (online)	1531-7056
ISSN	0267-1379
DOI	10.1097/00001574-199907000-00002
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2072: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Tumor infiltrating lymphocytes.

Kradin, R L / Bhan, A K

Laboratory investigation; a journal of technical methods and pathology

1993 Volume 69, Issue 6, Page(s) 635–638

MeSH term(s)	Animals ; Humans ; Lymphocytes, Tumor-Infiltrating ; Major Histocompatibility Complex ; Neoplasms/immunology ; T-Lymphocyte Subsets/immunology
Language	English
Publishing date	1993-12
Publishing country	United States
Document type	Comment ; Editorial ; Review
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.164: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Prevention of antibiotic-associated metabolic syndrome in mice by intestinal alkaline phosphatase.

Economopoulos, K P / Ward, N L / Phillips, C D / Teshager, A / Patel, P / Mohamed, M M / Hakimian, S / Cox, S B / Ahmed, R / Moaven, O / Kaliannan, K / Alam, S N / Haller, J F / Goldstein, A M / Bhan, A K / Malo, M S / Hodin, R A

Diabetes, obesity & metabolism

2016 Volume 18, Issue 5, Page(s) 519–527

Abstract: Aims: To examine whether co-administration of intestinal alkaline phosphatase (IAP) with antibiotics early in life may have a preventive role against metabolic syndrome (MetS) in mice.: Methods: A total of 50 mice were allocated to four treatment ... ...

Abstract	Aims: To examine whether co-administration of intestinal alkaline phosphatase (IAP) with antibiotics early in life may have a preventive role against metabolic syndrome (MetS) in mice. Methods: A total of 50 mice were allocated to four treatment groups after weaning. Mice were treated with azithromycin (AZT) ± IAP, or with no AZT ± IAP, for three intermittent 7-day cycles. After the last treatment course, the mice were administered a regular chow diet for 5 weeks and subsequently a high-fat diet for 5 weeks. Body weight, food intake, water intake, serum lipids, glucose levels and liver lipids were compared. 16S rRNA gene pyrosequencing was used to determine the differences in microbiome composition. Results: Exposure to AZT early in life rendered mice susceptible to MetS in adulthood. Co-administration of IAP with AZT completely prevented this susceptibility by decreasing total body weight, serum lipids, glucose levels and liver lipids to the levels of control mice. These effects of IAP probably occur as a result of changes in the composition of specific bacterial taxa at the genus and species levels (e.g. members of Anaeroplasma and Parabacteroides). Conclusions: Co-administration of IAP with AZT early in life prevents mice from susceptibility to the later development of MetS. This effect is associated with alterations in the composition of the gut microbiota. IAP may represent a novel treatment against MetS in humans.
MeSH term(s)	Acholeplasma/classification ; Acholeplasma/drug effects ; Acholeplasma/growth & development ; Acholeplasma/isolation & purification ; Alkaline Phosphatase/adverse effects ; Alkaline Phosphatase/therapeutic use ; Animals ; Anti-Bacterial Agents/adverse effects ; Azithromycin/adverse effects ; Bacteroides/classification ; Bacteroides/drug effects ; Bacteroides/growth & development ; Bacteroides/isolation & purification ; Cattle ; Diet, High-Fat/adverse effects ; Dietary Supplements/adverse effects ; Dysbiosis/chemically induced ; Dysbiosis/microbiology ; Dysbiosis/physiopathology ; Dysbiosis/prevention & control ; Feces/microbiology ; Gastrointestinal Microbiome/drug effects ; Intestinal Mucosa/enzymology ; Male ; Metabolic Syndrome/complications ; Metabolic Syndrome/etiology ; Metabolic Syndrome/microbiology ; Metabolic Syndrome/prevention & control ; Mice, Inbred C57BL ; Molecular Typing ; Obesity/complications ; Obesity/etiology ; Obesity/microbiology ; Obesity/prevention & control ; Weaning ; Weight Gain/drug effects
Chemical Substances	Anti-Bacterial Agents ; Azithromycin (83905-01-5) ; Alkaline Phosphatase (EC 3.1.3.1)
Language	English
Publishing date	2016-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1454944-x
ISSN	1463-1326 ; 1462-8902
ISSN (online)	1463-1326
ISSN	1462-8902
DOI	10.1111/dom.12645
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5442: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: The critical role of interleukin 4 but not interferon gamma in the pathogenesis of colitis in T-cell receptor alpha mutant mice.

Mizoguchi, A / Mizoguchi, E / Bhan, A K

Gastroenterology

1999 Volume 116, Issue 2, Page(s) 320–326

Abstract: Background & aims: T-cell receptor alpha mutant (TCRalpha-/-) mice spontaneously develop colitis resembling ulcerative colitis (UC). The role of interleukin (IL)-4 and interferon (IFN)-gamma in the pathogenesis of colitis was examined by creating IL-4- ... ...

Abstract	Background & aims: T-cell receptor alpha mutant (TCRalpha-/-) mice spontaneously develop colitis resembling ulcerative colitis (UC). The role of interleukin (IL)-4 and interferon (IFN)-gamma in the pathogenesis of colitis was examined by creating IL-4- or IFN-gamma-deficient TCRalpha-/- mice. Methods: Double-mutant mice were created by crossing TCRalpha-/- mice with IL-4- or IFN-gamma-deficient mice. Colitis was grossly and histologically assessed at 6 months of age, and the cytokine profile in the mesenteric lymph nodes and colons in these mice was analyzed. Results: The lack of IL-4 dramatically suppressed the development of colitis at 6 months of age. In contrast, IFN-gamma-/- x TCRalpha-/- mice developed colitis similar to that present in TCRalpha-/- mice. Furthermore, proliferation of colonic epithelial cells was markedly increased in TCRalpha-/- mice and IFN-gamma-/- x TCRalpha-/- mice compared with IL-4(-/-) x TCRalpha-/- mice. Continuous administration of recombinant IL-4 led to increased colonic epithelial cell proliferation in IL-4(-/-) x TCRalpha-/- mice. Conclusions: IL-4 plays an important role in the development of colitis in TCRalpha-/- mice. In contrast, severe colitis in TCRalpha-/- mice can develop in the absence of IFN-gamma.
MeSH term(s)	Animals ; Colitis/metabolism ; Colitis/pathology ; Cytokines/metabolism ; Interferon-gamma/administration & dosage ; Interferon-gamma/metabolism ; Interleukin-4/administration & dosage ; Interleukin-4/metabolism ; Lymph Nodes/metabolism ; Mesentery ; Mice ; Mutation ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Recombinant Proteins/administration & dosage ; Recombinant Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Cytokines ; Receptors, Antigen, T-Cell, alpha-beta ; Recombinant Proteins ; Interleukin-4 (207137-56-2) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	1999-02
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1016/s0016-5085(99)70128-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui V Zs.44: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 572: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Difficult cases in heart failure: Reversible heart failure secondary to thyrotoxicosis.

Bhan, A K / De Bustros, A / Silver, M A

Congestive heart failure (Greenwich, Conn.)

1999 Volume 5, Issue 4, Page(s) 180–183

Abstract: Perhaps one of the most important steps in caring for a patient with heart failure is seeking a reversible form of heart failure. Often addressing a disease process, like myocardial ischemia or systemic hypertension, rapidly attenuates the progressive ... ...

Abstract	Perhaps one of the most important steps in caring for a patient with heart failure is seeking a reversible form of heart failure. Often addressing a disease process, like myocardial ischemia or systemic hypertension, rapidly attenuates the progressive natural history of left ventricular dysfunction. Beyond the usual reversible causes, however, are some that may be overlooked. This case provides an insight into one of these causes. (c)1999 by CHF, Inc.
Language	English
Publishing date	1999-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	1239105-0
ISSN	1751-7133 ; 1527-5299 ; 1079-7998
ISSN (online)	1751-7133
ISSN	1527-5299 ; 1079-7998
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4325: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Role of cytokines in the early stages of chronic colitis in TCR alpha-mutant mice.

Mizoguchi, E / Mizoguchi, A / Bhan, A K

Laboratory investigation; a journal of technical methods and pathology

1997 Volume 76, Issue 3, Page(s) 385–397

Abstract: Chronic colitis develops spontaneously in mice mutant for T-cell receptor alpha (TCR alpha) genes maintained in pathogen-free conditions. Our previous studies indicate that the cytokine imbalance caused by a lack of TCR alpha beta + T cells may be ... ...

Abstract	Chronic colitis develops spontaneously in mice mutant for T-cell receptor alpha (TCR alpha) genes maintained in pathogen-free conditions. Our previous studies indicate that the cytokine imbalance caused by a lack of TCR alpha beta + T cells may be associated with the development of chronic colitis in TCR alpha-mutant (TCR alpha -/-) mice. The histologic changes of chronic colitis are recognizable by 3 to 4 months of age and are characterized by marked crypt cell hyperplasia and the presence of an inflammatory cell infiltrate. Because early events in the development of chronic colitis may be important in the pathogenesis of the disorder, we investigated the changes in the colon at a time when chronic colitis was not yet histologically recognizable. In vivo labeling with 5-bromo-2'-deoxyuridine revealed increased epithelial proliferation in the crypts by 6 to 8 weeks of age. There was an increase in number of T cells in the colon of TCR alpha -/- mice compared with that in TCR alpha +/- (heterozygous TCR alpha-mutant) mice after 6 weeks of age. The predominant T-cell subsets were CD4+, TCR alpha- beta +, and TCR gamma delta + cells. Reverse transcription-PCR and immunohistochemistry of the colonic mucosa obtained from TCR alpha -/- mice (> 6 weeks old) showed a marked increase of IL-1 alpha and IL-1 beta but not of TNF alpha or transforming growth factor beta-1 compared with TCR alpha +/- mice. In vivo neutralization of IL-1 alpha or IL-1 beta by specific mAb suppressed colonic epithelial proliferation and decreased colonic mucosal T-cell infiltration in 8-week-old TCR alpha -/- mice. These results provide direct evidence that overproduction of IL-1 alpha and IL-1 beta in the colonic mucosa may play an important role in the early stages of development of chronic colitis in TCR alpha -/- mice.
MeSH term(s)	Animals ; Antibodies, Monoclonal/pharmacology ; Chronic Disease ; Colitis/immunology ; Colitis/pathology ; Colitis/physiopathology ; Colon/immunology ; Colon/pathology ; Cricetinae ; Crosses, Genetic ; Cytokines/biosynthesis ; Cytokines/physiology ; Interleukin-1/biosynthesis ; Interleukin-1/immunology ; Interleukin-1/physiology ; Intestinal Mucosa/immunology ; Intestinal Mucosa/pathology ; Intestinal Mucosa/physiopathology ; Lymphocytes/immunology ; Lymphocytes/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell, alpha-beta/deficiency ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Transforming Growth Factor beta/biosynthesis ; Transforming Growth Factor beta/physiology ; Tumor Necrosis Factor-alpha/biosynthesis ; Tumor Necrosis Factor-alpha/physiology
Chemical Substances	Antibodies, Monoclonal ; Cytokines ; Interleukin-1 ; Receptors, Antigen, T-Cell, alpha-beta ; Transforming Growth Factor beta ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	1997-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.164: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito