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A < 1.7 cM interval is responsible for Dmo1 obesity phenotypes in OLETF rats.

https://arctichealth.org/en/permalink/ahliterature47295
Source
Clin Exp Pharmacol Physiol. 2004 Jan-Feb;31(1-2):110-2
Publication Type
Article
Author
Takeshi K Watanabe
Shiro Okuno
Yuki Yamasaki
Toshihide Ono
Keiko Oga
Ayako Mizoguchi-Miyakita
Hideo Miyao
Mikio Suzuki
Hiroshi Momota
Yoshihiro Goto
Hiroichi Shinomiya
Haretsugu Hishigaki
Isamu Hayashi
Toshihiro Asai
Shigeyuki Wakitani
Toshihisa Takagi
Yusuke Nakamura
Akira Tanigami
Author Affiliation
Otsuka GEN Research Institute, Otsuka Pharmaceutical Co. Ltd., 463-10 Kagasuno, Kawauchi-cho, Tokushima 771-0192, Japan. tkw_watanabe@research.otsuka.co.jp
Source
Clin Exp Pharmacol Physiol. 2004 Jan-Feb;31(1-2):110-2
Language
English
Publication Type
Article
Keywords
Animals
Animals, Congenic
Body Weight - genetics
Crosses, Genetic
Diabetes Mellitus - genetics
Female
Hyperglycemia - genetics
Hyperlipidemia - blood - genetics
Male
Obesity
Phenotype
Rats
Rats, Inbred BN
Rats, Inbred OLETF
Research Support, Non-U.S. Gov't
Abstract
1. Dmo1 (Diabetes Mellitus OLETF type I) is a major quantitative trait locus for dyslipidaemia, obesity and diabetes phenotypes of male Otsuka Long Evans Tokushima Fatty (OLETF) rats. 2. Our congenic lines, produced by transferring Dmo1 chromosomal segments from the non-diabetic Brown Norway (BN) rat into the OLETF strain, have confirmed the strong, wide-range therapeutic effects of Dmo1 on dyslipidaemia, obesity and diabetes in the fourth (BC4) and fifth (BC5) generations of congenic animals. Analysis of a relatively small number of BC5 rats (n = 71) suggested that the critical Dmo1 interval lies within a
PubMed ID
14756694 View in PubMed
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Aberrant iNOS signaling is under genetic control in rodent liver cancer and potentially prognostic for the human disease.

https://arctichealth.org/en/permalink/ahliterature92898
Source
Carcinogenesis. 2008 Aug;29(8):1639-47
Publication Type
Article
Date
Aug-2008
Author
Calvisi Diego F
Pinna Federico
Ladu Sara
Pellegrino Rossella
Muroni Maria R
Simile Maria M
Frau Maddalena
Tomasi Maria L
De Miglio Maria R
Seddaiu Maria A
Daino Lucia
Sanna Valeria
Feo Francesco
Pascale Rosa M
Author Affiliation
Department of Biomedical Sciences, Division of Experimental Pathology and Oncology, University of Sassari, 07100 Sassari, Italy.
Source
Carcinogenesis. 2008 Aug;29(8):1639-47
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Animals
Carcinoma, Hepatocellular - enzymology - epidemiology - genetics - pathology
Cell Line, Tumor
Genetic Predisposition to Disease
Humans
Incidence
Liver Neoplasms - enzymology - epidemiology - genetics - pathology
Male
Mice
Mice, Transgenic
Nitric Oxide Synthase Type II - genetics
Prognosis
Rats
Rats, Inbred BN
Rats, Inbred F344
Signal Transduction - physiology
Abstract
Mounting evidence underlines the role of inducible nitric oxide synthase (iNOS) in hepatocellular carcinoma (HCC) development, but its functional interactions with pathways involved in HCC progression remain uninvestigated. Here, we analyzed in preneoplastic and neoplastic livers from Fisher 344 and Brown Norway rats, possessing different genetic predisposition to HCC, in transforming growth factor-alpha (TGF-alpha) and c-Myc-TGF-alpha transgenic mice, characterized by different susceptibility to HCC, and in human HCC: (i) iNOS function and interactions with nuclear factor-kB (NF-kB) and Ha-RAS/extracellular signal-regulated kinase (ERK) during hepatocarcinogenesis; (ii) influence of genetic predisposition to liver cancer on these pathways and role of these cascades in determining a susceptible or resistant phenotype and (iii) iNOS prognostic value in human HCC. We found progressive iNos induction in rat and mouse liver lesions, always at higher levels in the most aggressive models represented by HCC of rats genetically susceptible to hepatocarcinogenesis and c-Myc-TGF-alpha transgenic mice. iNOS, inhibitor of kB kinase/NF-kB and RAS/ERK upregulation was significantly higher in HCC with poorer prognosis (as defined by patients' survival length) and positively correlated with tumor proliferation, genomic instability and microvascularization and negatively with apoptosis. Suppression of iNOS signaling by aminoguanidine led to decreased HCC growth and NF-kB and RAS/ERK expression and increased apoptosis both in vivo and in vitro. Conversely, block of NF-kB signaling by sulfasalazine or short interfering RNA (siRNA) or ERK signaling by UO126 caused iNOS downregulation in HCC cell lines. These findings indicate that iNOS cross talk with NF-kB and Ha-RAS/ERK cascades influences HCC growth and prognosis, suggesting that key component of iNOS signaling could represent important therapeutic targets for human HCC.
PubMed ID
18579559 View in PubMed
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Ability of insulin to modulate hepatic glucose production in aging rats is impaired by fat accumulation.

https://arctichealth.org/en/permalink/ahliterature61796
Source
Am J Physiol Endocrinol Metab. 2000 Jun;278(6):E985-91
Publication Type
Article
Date
Jun-2000
Author
G. Gupta
J A Cases
L. She
X H Ma
X M Yang
M. Hu
J. Wu
L. Rossetti
N. Barzilai
Author Affiliation
Department of Medicine, and the Diabetes Research and Training Center, Albert Einstein College of Medicine, New York, New York 10461, USA.
Source
Am J Physiol Endocrinol Metab. 2000 Jun;278(6):E985-91
Date
Jun-2000
Language
English
Publication Type
Article
Keywords
Adipose Tissue
Aging
Animals
Body Composition
Energy intake
Gluconeogenesis
Glucose - biosynthesis
Glycogen - metabolism
Insulin - pharmacology
Leptin - metabolism
Liver - drug effects - metabolism
Male
Rats
Rats, Inbred BN
Rats, Inbred F344
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Abstract
Increased total fat mass (FM) and visceral fat (VF) may account in part for age-associated decrease in hepatic insulin action. This study determined whether preventing the changes in body fat distribution abolished this defect throughout aging. We studied the F(1) hybrid of Brown Norway-Fischer 344 rats (n = 29), which we assigned to caloric restriction (CR) or fed ad libitum (AL). CR (55% of the calories consumed by AL) was initiated and used at 2 mo to prevent age-dependent increases in FM and VF. AL rats were studied at 2, 8, and 20 mo; CR rats were studied at 8 and 20 mo. VF and FM remained unchanged throughout aging in CR rats. AL-fed rats at 8 and 20 mo had over fourfold higher FM and VF compared with both CR groups. Insulin clamp studies (3 mU. kg(-1). min(-1) with somatostatin) were performed to assess hepatic insulin sensitivity. Prevention of fat accretion resulted in a marked improvement in insulin action in the suppression of hepatic glucose production (HGP) (6.3 +/- 0.3 and 7.2 +/- 1.2 mg. kg(-1). min(-1) in 8- and 20-mo CR rats vs. 8.3 +/- 0.5 and 10.8 +/- 0.9 mg. kg(-1). min(-1) in 8- and 20-mo AL rats, respectively). The rate of gluconeogenesis (by enrichment of hepatic uridine diphosphate glucose and phosphoenolpyruvate pools by [(14)C]lactate) was unchanged in all groups. The improvement in hepatic insulin action in the CR group was mostly due to effective suppression of glycogenolysis (4.4 +/- 0.3 and 4.9 +/- 0.3 mg. kg(-1). min(-1) in 8- and 20-mo CR rats vs. 5.8 +/- 0.6 and 8.2 +/- 1.0 mg. kg(-1). min(-1) in 8- and 20-mo AL rats, respectively). The results demonstrated the preservation of hepatic insulin action in aging CR rats. Therefore, body fat and its distribution are major determinants of age-associated hepatic insulin resistance.
PubMed ID
10826999 View in PubMed
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Absence of acute tolerance to ethanol hypnosis in F-344 and BN/BIRIJ rats.

https://arctichealth.org/en/permalink/ahliterature11625
Source
Alcohol. 1994 Jan-Feb;11(1):31-4
Publication Type
Article
Author
J L York
A W Chan
Author Affiliation
Research Institute on Addictions, Buffalo, NY 14203.
Source
Alcohol. 1994 Jan-Feb;11(1):31-4
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Brain - metabolism
Drug Tolerance
Ethanol - administration & dosage - metabolism
Hypnosis
Male
Rats
Rats, Inbred BN
Rats, Inbred F344
Reflex
Research Support, U.S. Gov't, P.H.S.
Abstract
Male Fischer 344 (F-344) rats of three different ages (4, 13, and 25 months) and male Brown Norway (BN/BIRIJ) rats (4 months) were injected (IP) with a hypnotic dose of ethanol (3.0 g/kg, 10% w/v in saline). Half of the animals were decapitated and brains extracted immediately upon loss of the righting reflex (LRR), while the other half were allowed to reach recovery of the righting reflex (RRR), at which time brains were extracted. Brain alcohol analyses revealed significantly higher concentrations in young F-344 rats at both LRR and RRR, indicating less sensitivity of target tissue to ethanol hypnosis in the young of that strain. All age groups of the F-344 rats as well as the young BN/BIRIJ rats displayed lower brain concentrations of ethanol at RRR than at LRR, a finding opposite to that characteristic of acute tolerance. The relationship of LRR to RRR values did not differ among the age groups of F-344 rats. We conclude that the F-344 and BN/BIRIJ strains do not develop acute tolerance to ethanol hypnosis. The findings are consistent with the hypothesis that animals with low ethanol preferences, such as the F-344 and BN/BIRIJ strains, also have low capabilities to develop acute tolerance to ethanol hypnosis.
PubMed ID
8142065 View in PubMed
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ABT-491, a highly potent and selective PAF antagonist, inhibits nasal vascular permeability associated with experimental allergic rhinitis in brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature11007
Source
Inflamm Res. 1997 Aug;46 Suppl 2:S133-4
Publication Type
Article
Date
Aug-1997

Abundance of the Na-K-2Cl cotransporter NKCC2 is increased by high-fat feeding in Fischer 344 X Brown Norway (F1) rats.

https://arctichealth.org/en/permalink/ahliterature90141
Source
Am J Physiol Renal Physiol. 2009 Apr;296(4):F762-70
Publication Type
Article
Date
Apr-2009
Author
Riazi Shahla
Tiwari Swasti
Sharma Nikhil
Rash Arjun
Ecelbarger C M
Author Affiliation
Associate Professor, Dept. of Medicine, Georgetown Univ., 4000 Reservoir Rd, NW, Washington, DC, 20007, USA.
Source
Am J Physiol Renal Physiol. 2009 Apr;296(4):F762-70
Date
Apr-2009
Language
English
Publication Type
Article
Keywords
Animals
Antioxidants - pharmacology
Biological Markers - urine
Blood pressure
Blotting, Western
Crosses, Genetic
Cyclic N-Oxides - pharmacology
Dietary Fats - administration & dosage - metabolism
Dinoprost - analogs & derivatives - urine
Enzyme Inhibitors - pharmacology
Furosemide - pharmacology
Glucose Intolerance - metabolism - physiopathology
Hypertension - metabolism - physiopathology
Insulin Resistance
Kidney Medulla - drug effects - metabolism
Male
NG-Nitroarginine Methyl Ester - pharmacology
Natriuresis
Nitric Oxide - urine
Nitric Oxide Synthase - antagonists & inhibitors - metabolism
Oxidative Stress
Potassium Channels, Inwardly Rectifying - metabolism
Rats
Rats, Inbred BN
Rats, Inbred F344
Sodium Potassium Chloride Symporter Inhibitors - pharmacology
Sodium-Potassium-Chloride Symporters - antagonists & inhibitors - metabolism
Sodium-Potassium-Exchanging ATPase - metabolism
Spin Labels
Telemetry
Time Factors
Up-Regulation
Abstract
Insulin resistance is associated with hypertension by mechanisms likely involving the kidney. To determine how the major apical sodium transporter of the thick ascending limb, the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) is regulated by high-fat feeding, we treated young male, Fischer 344 X Brown Norway (F344BN) rats for 8 wk with diets containing either normal (NF, 4%) or high (HF, 36%) fat, by weight, primarily as lard. HF-fed rats had impaired glucose tolerance, increased urine excretion of 8-isoprostane (a marker of oxidative stress), increased protein levels for NKCC2 (50-125%) and the renal outer medullary potassium channel (106%), as well as increased natriuretic response to furosemide (20-40%). To test the role of oxidative stress in this response, in study 2, rats were fed the NF or HF diet plus plain drinking water, or water containing N(G)-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase inhibitor (100 mg/l), or tempol, a superoxide dismutase mimetic (1 mmol/l). The combination of tempol with HF nullified the increase in medullary NKCC2, while l-NAME with HF led to the highest expression of medullary NKCC2 (to 498% of NF mean). However, neither of these drugs dramatically affected the elevated natriuretic response to furosemide with HF. Finally, l-NAME led to a marked increase in blood pressure (measured by radiotelemetry), which was significantly enhanced with HF. Mean arterial blood pressure at 7 wk was as follows (mmHg): NF, 100 +/- 2; NF plus l-NAME, 122 +/- 3; and HF plus l-NAME, 131 +/- 2. Overall, HF feeding increased the abundance of NKCC2. Inappropriately high sodium reabsorption in the thick ascending limb via NKCC2 may contribute to hypertension with insulin resistance.
PubMed ID
19193725 View in PubMed
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Acetaminophen prevents aging-associated hyperglycemia in aged rats: effect of aging-associated hyperactivation of p38-MAPK and ERK1/2.

https://arctichealth.org/en/permalink/ahliterature90253
Source
Diabetes Metab Res Rev. 2009 Mar;25(3):279-86
Publication Type
Article
Date
Mar-2009
Author
Wu Miaozong
Desai Devashish H
Kakarla Sunil K
Katta Anjaiah
Paturi Satyanarayana
Gutta Anil K
Rice Kevin M
Walker Ernest M
Blough Eric R
Author Affiliation
Department of Biological Sciences, Marshall University, Huntington, WV 25755-1090, USA.
Source
Diabetes Metab Res Rev. 2009 Mar;25(3):279-86
Date
Mar-2009
Language
English
Publication Type
Article
Keywords
Acetaminophen - pharmacology
Aging - drug effects - physiology
Animals
Blood Glucose - drug effects
Enzyme Activation - drug effects
Glucose Transporter Type 4 - metabolism
Hyperglycemia - prevention & control
Liver - drug effects
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Muscle, Skeletal - drug effects - physiology
Rats
Rats, Inbred BN
Rats, Inbred F344
Superoxides - metabolism
p38 Mitogen-Activated Protein Kinases - metabolism
Abstract
BACKGROUND: Aging-related hyperglycemia is associated with increased oxidative stress and diminished muscle glucose transporter-4 (Glut4) that may be regulated, at least in part, by the mitogen-activated protein kinases (MAPK). METHODS: To test the possibility that aging-related hyperglycemia can be prevented by pharmacological manipulation of MAPK hyperactivation, aged (27-month old) Fischer 344/NNiaHSD x Brown Norway/BiNia F1 (F344BN) rats were administered acetaminophen (30 mg/kg body weight/day) for 6 months in drinking water. RESULTS: Hepatic histopathology, serum aspartate aminotransferase and alanine aminotransferase analyses suggested that chronic acetaminophen did not cause hepatotoxicity. Compared with adult (6-month) and aged (27-month) rats, very aged rats (33-month) had higher levels of blood glucose, phosphorylation of soleus p38-MAPK and extracellular-regulated kinase 1/2 (ERK1/2), superoxide and oxidatively modified proteins (p
PubMed ID
19177471 View in PubMed
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Acetyldinaline: a new oral cytostatic drug with impressive differential activity against leukemic cells and normal stem cells--preclinical studies in a relevant rat model for human acute myelocytic leukemia.

https://arctichealth.org/en/permalink/ahliterature23997
Source
Cancer Res. 1993 Jul 1;53(13):3008-14
Publication Type
Article
Date
Jul-1-1993
Author
H M el-Beltagi
A C Martens
P. Lelieveld
E A Haroun
A. Hagenbeek
Author Affiliation
Department of Hemato-Oncology TNO, Erasmus University Rotterdam, The Netherlands.
Source
Cancer Res. 1993 Jul 1;53(13):3008-14
Date
Jul-1-1993
Language
English
Publication Type
Article
Keywords
Administration, Oral
Animals
Antineoplastic Agents - pharmacology
Bone Marrow - drug effects
Bone Marrow Cells
Cell Differentiation - drug effects
Cell Survival - drug effects
Clone Cells
Comparative Study
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Administration Schedule
Drug Evaluation
Drug Screening Assays, Antitumor
Hematopoietic Stem Cells - cytology - drug effects
Leukemia, Myelocytic, Acute - drug therapy - pathology
Male
Phenylenediamines - pharmacology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Tumor Cells, Cultured
Abstract
Acetyldinaline [CI-994; GOE 5549; PD 123 654; 4-acetylamino-N-(2'-aminophenyl)-benzamide] is the acetylated derivative form of the original compound Dinaline (GOE 1734; PD 104 208). The efficacy and toxicity of Acetyldinaline for remission-induction treatment of leukemia were evaluated and compared with those observed in previous studies of Dinaline in the Brown Norway acute myelocytic leukemia, as a preclinical model for human acute myelocytic leukemia. There were three treatment groups. Leukemic animals received either 1 or 2 courses of 5 daily p.o. administrations of Acetyldinaline with a "full dose" of 23.7 mg/kg once daily (first group), a twice daily "half dose" of 11.85 mg/kg with an interval of 8 h (second group), or a "half dose" of 11.85 mg/kg once daily (third group). The drug-free interval between the 2 courses was 2 or 9 days. With repeated daily p.o. administrations of 23.7 mg/kg either in a single daily dose or a split daily dose of 2 x 11.85 mg/kg for 1 course, at least an 8-log leukemic cell kill was achieved. In contrast, with these treatment schedules, less than a 1-log cell kill of normal pluripotent hemopoietic stem cells (CFU-S) in the femoral bone marrow was found. Split daily dose treatment was more effective resulting in 37.5% cures, while no cures were observed with the single daily treatment for one course. Treatment with single daily dose of 23.7 mg/kg or a split daily dose of 2 x 11.85 mg/kg for 2 courses, with either a 2- or 9-day interval in between, resulted in lethal toxicity in most of rats. This result was comparable with that previously observed after equimolar doses of Dinaline (20 mg/kg). The half-dose once daily treatment with Acetyldinaline (11.85 mg/kg) for 1 or 2 cycles resulted in about a 4.5 or > 8-log leukemic cell kill, respectively. Toxic side effects, i.e., damage to the gastro-intestinal tract and hemorrhages in the lungs, were more pronounced with full dose either in the single or the split daily dose regimen. No significant toxicity was observed at the half-dose treatment once daily. In conclusion, the impressive differential activity against leukemic cells and normal stem cells observed in this relevant rat model for human acute myelocytic leukemia warrants the introduction of this compound in clinical phase I/II studies.
PubMed ID
8319208 View in PubMed
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Activation of alloreactive natural killer cells is resistant to cyclosporine.

https://arctichealth.org/en/permalink/ahliterature57609
Source
Transplantation. 1997 Apr 27;63(8):1138-44
Publication Type
Article
Date
Apr-27-1997
Author
E. Petersson
Z. Qi
H. Ekberg
O. Ostraat
M. Dohlsten
G. Hedlund
Author Affiliation
Department of Tumor Immunology, The Wallenberg Laboratory, Lund University, Sweden.
Source
Transplantation. 1997 Apr 27;63(8):1138-44
Date
Apr-27-1997
Language
English
Publication Type
Article
Keywords
Animals
Antigens, CD3 - analysis
Cyclosporine - pharmacology
Drug Resistance - immunology
Female
Graft Survival - drug effects
Heart Transplantation - immunology
Interleukin-2 - pharmacology
Killer Cells - immunology
Lymphocyte Activation - drug effects
Male
Rats
Rats, Inbred BN
Rats, Inbred WF
Research Support, Non-U.S. Gov't
T-Lymphocytes, Cytotoxic - drug effects - immunology
Abstract
BACKGROUND: We have previously shown that cytotoxic T lymphocytes (CTL) with alloreactivity were induced when Wistar Furth (WF; RT1u) rats were immunized with allogeneic Brown Norway (BN; RT1n) cells. In contrast, when BN rats were immunized with WF cells, the allospecific response was confined to alloreactive natural killer (NK) cells, and no CTL activity was observed. In this study, the effect of cyclosporine (CsA) on the activation of alloreactive NK cells in vivo was analyzed. METHODS: Distinct peritoneal effector cells from rats immunized with allogenic cells with or without concomitant CsA and/or interleukin (IL) 2 treatment were tested for specific cytolytic activity. Furthermore, the presumptive role of NK cells in rejection immunity was addressed in a cardiac graft model. RESULTS: The results showed that doses of CsA that completely inhibited the activation of alloreactive CTL, only marginally affected the activation of alloreactive NK cells. We also showed that CsA treatment failed to prolong graft survival in BN recipients of WF hearts. Treatment of BN rats with CsA/IL-2 during immunization with allogeneic WF cells resulted in concomitant induction of alloreactive NK cells and alloreactive CTL. CONCLUSIONS: We have demonstrated that CsA failed to suppress the activation of alloreactive NK cells. Consequently, the cardiac graft survival in the donor-recipient combination known to activate alloreactive NK cells was not significantly prolonged by CsA treatment, emphasizing the involvement of NK cells as effectors in organ rejection. Furthermore, the parallel emergence of alloreactive NK cells and CTL only in the presence of CsA/IL-2 indicated that CsA interfered with alloreactive NK cell-associated suppression of CTL activated by allogeneic tissue.
PubMed ID
9133476 View in PubMed
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Activation of the immune system and systemic immune-complex deposits in Brown Norway rats with dental amalgam restorations.

https://arctichealth.org/en/permalink/ahliterature72544
Source
J Dent Res. 1998 Jun;77(6):1415-25
Publication Type
Article
Date
Jun-1998
Author
P. Hultman
U. Lindh
P. Hörsted-Bindslev
Author Affiliation
Department of Health and Environment, Linköping University, Sweden.
Source
J Dent Res. 1998 Jun;77(6):1415-25
Date
Jun-1998
Language
English
Publication Type
Article
Keywords
Analysis of Variance
Animals
Antibody Formation - drug effects
Antigen-Antibody Complex - analysis - blood
Autoimmune Diseases - chemically induced
Autoimmunity
Body Burden
Comparative Study
Copper - analysis
Dental Amalgam - toxicity
Dinitrobenzenes
Female
Immune Complex Diseases - chemically induced
Immunoglobulin E - blood
Laminin
Lymphocyte Activation - drug effects
Mercury - analysis - blood - pharmacokinetics
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Silver - analysis
Spectrum Analysis, Mass
Statistics, nonparametric
Tissue Distribution
Abstract
Dental amalgam restorations are a significant source of mercury exposure in the human population, but their potential to cause systemic health effects is highly disputed. We examined effects on the immune system by giving genetically mercury-susceptible Brown Norway (BN) rats and mercury-resistant Lewis (LE) rats silver amalgam restorations in 4 molars of the upper jaw, causing a body burden similar to that described in human amalgam-bearers (from 250 to 375 mg amalgam/kg body weight). BN rats with amalgam restorations, compared with control rats given composite resinous restorations, developed a rapid activation of the immune system, with a maximum 12-fold increase of the plasma IgE concentration after 3 wks (p 0.05). After 12 wks, BN rats with amalgam restorations showed significantly increased (p spleen > cerebrum occipital lobe > cerebellum > liver > thymus, and the tissue silver concentration was significantly (p
PubMed ID
9649170 View in PubMed
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755 records – page 1 of 76.