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1. Lecuit M, Abachin E, Martin A, Poyart C, Pochart P, Suarez F, Bengoufa D, Feuillard J, Lavergne A, Gordon JI, Berche P, Guillevin L, Lortholary O: Immunoproliferative small intestinal disease associated with Campylobacter jejuni. N Engl J Med; 2004 Jan 15;350(3):239-48
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  • [Title] Immunoproliferative small intestinal disease associated with Campylobacter jejuni.
  • BACKGROUND: Immunoproliferative small intestinal disease (also known as alpha chain disease) is a form of lymphoma that arises in small intestinal mucosa-associated lymphoid tissue (MALT) and is associated with the expression of a monotypic truncated immunoglobulin alpha heavy chain without an associated light chain.
  • Early-stage disease responds to antibiotics, suggesting a bacterial origin.
  • METHODS: We performed polymerase chain reaction (PCR), DNA sequencing, fluorescence in situ hybridization, and immunohistochemical studies on intestinal-biopsy specimens from a series of patients with immunoproliferative small intestinal disease.
  • RESULTS: Analysis of frozen intestinal tissue obtained from an index patient with immunoproliferative small intestinal disease who had a dramatic response to antibiotics revealed the presence of Campylobacter jejuni.
  • A follow-up retrospective analysis of archival intestinal-biopsy specimens disclosed campylobacter species in four of six additional patients with immunoproliferative small intestinal disease.
  • CONCLUSIONS: These results indicate that campylobacter and immunoproliferative small intestinal disease are associated and that C. jejuni should be added to the growing list of human pathogens responsible for immunoproliferative states.
  • [MeSH-major] Campylobacter jejuni / isolation & purification. Immunoproliferative Small Intestinal Disease / microbiology
  • [MeSH-minor] Anti-Bacterial Agents. Anti-Ulcer Agents / therapeutic use. Campylobacter Infections. DNA, Bacterial / analysis. Drug Therapy, Combination / therapeutic use. Female. Genes, Immunoglobulin. Humans. Immunoglobulin A / blood. Immunoglobulin Fragments / analysis. Immunoglobulin Fragments / genetics. Immunohistochemistry. In Situ Hybridization, Fluorescence. Intestine, Small / immunology. Intestine, Small / microbiology. Intestine, Small / pathology. Middle Aged. Omeprazole / therapeutic use. Polymerase Chain Reaction. Sequence Analysis, DNA

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  • [Copyright] Copyright 2004 Massachusetts Medical Society
  • [CommentIn] Rev Gastroenterol Disord. 2005 Summer;5(3):181-2 [16156008.001]
  • [CommentIn] N Engl J Med. 2004 Apr 15;350(16):1685-6; author reply 1685-6 [15084705.001]
  • [CommentIn] N Engl J Med. 2004 Jan 15;350(3):213-5 [14724298.001]
  • (PMID = 14724303.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Ulcer Agents; 0 / DNA, Bacterial; 0 / Immunoglobulin A; 0 / Immunoglobulin Fragments; KG60484QX9 / Omeprazole
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2. Landolsi A, Chabchoub I, Limem S, Gharbi O, Chaafai R, Hochlef M, Fatma LB, Trimech M, Krifa A, Ajmi S, Mokni M, Hadj Hmida MB, Ahmed SB: [Primary digestive tract lymphoma in central region of Tunisia: anatomoclinical study and therapeutic results about 153 cases]. Bull Cancer; 2010 Apr;97(4):435-43

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  • [Title] [Primary digestive tract lymphoma in central region of Tunisia: anatomoclinical study and therapeutic results about 153 cases].
  • [Transliterated title] Les lymphomes primitifs du tube digestif (LPTD) dans le centre tunisien: étude anatomoclinique et résultats thérapeutiques à propos de 153 cas.
  • Primary gastro-intestinal lymphoma (PGIL) is the most common type of extra-nodal non Hodgkin's lymphoma.
  • Their clinical and histological presentations are heterogeneous depending on the site of the lesion.
  • There is no consensus regarding the role of surgery and chemotherapy in the therapeutic approach.
  • In our country epidemiology of the disease is unknown with IPSID being the most frequent type.
  • We report anatomo-clinical features and prognostic factors of PGIL and compare intestinal to gastric forms in our region.
  • The median age was 52 years and the sex-ratio 2.1.
  • Tumor sites were gastric (67%), intestinal (26%) and gastrointestinal (7%).
  • Abdominal pain (87%) followed by vomiting and diarrhoea (37 and 15%) were the most common symptoms.
  • Performance status (PS) < 2 was seen in 80% of patients, high grade lymphoma in 70.5% of cases and B phenotype was noted in 85%.
  • MALT lymphoma accounts for 50% of cases, and IPSID for only 5% of PGIL.
  • About 47.5% of cases were stage IE, 138 patients had chemotherapy with an objective response rate of 77%.
  • Only 46% of patients had surgery (14 for surgical complication, 6 for residual tumor after chemotherapy and 22 to have histological diagnosis).
  • In high grade lymphoma patients favorable prognostic factors for OS included young age < or = 60 years, PS < 2, normal serum LDH, hemoglobin > 12 g/dL, B phenotype, localised stage (IE-IIE1), anthracycline-based chemotherapy regimen, achieving complete or partial response to induction chemotherapy and no relapse.
  • In low-grade lymphoma patients, none of these factors had a significant correlation with OS: age < or = 60 years, PS < 2, stage (IE-IIE1), response to induction chemotherapy, relapse.
  • Compared to gastric lymphomas, intestinal cases occurred at a younger age, frequently with diarrhoea, weight loss, and occlusion.
  • They are more often high-grade, T phenotype and have locally advanced stage (IIE); surgery is more common in this group.
  • We conclude that stomach is the main site of PGIL in our region, intestinal lymphoma is less frequent and IPSID has become rare.
  • Recent progress in chemotherapy has allowed good therapeutic results with a conservative approach.
  • Surgery may be performed in case of emergency or for residual lesions after medical treatment.
  • [MeSH-major] Gastrointestinal Neoplasms. Lymphoma, Non-Hodgkin
  • [MeSH-minor] Abdominal Pain / etiology. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diarrhea / etiology. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Tunisia. Vomiting / etiology. Young Adult

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  • (PMID = 20395189.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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3. Hara T, Tsurumi H, Kato T, Imao Y, Kojima Y, Kojima K, Kitagawa J, Katsumura N, Araki H, Takami T, Moriwaki H: Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression. Intern Med; 2008;47(4):299-303
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  • [Title] Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression.
  • A 52-year-old man was admitted to our hospital in October 2001 with abdominal pain.
  • Abdominal X-ray indicated a diagnosis of ileus.
  • Histopathological and immunological examination resulted in a diagnosis of immunoproliferative small intestinal disease (IPSID).
  • He was treated with THP-COP therapy (pirarubicin, cyclophosphamide, vincristine, and prednisolone), which resulted in complete remission.
  • Outpatient follow-up revealed hypoalbuminemia in May 2003 and upper gastrointestinal endoscopy showed duodenal mucosal nodularity.
  • He was diagnosed with relapsed IPSID and salvage chemotherapy was started.
  • Follow-up endoscopy confirmed that the therapy was effective, but uncovered another duodenal mucosal nodularity.
  • Immunohistochemical staining revealed T-cell lymphoma.
  • Chemotherapy was discontinued and the patient died in December 2004.
  • [MeSH-major] Duodenal Neoplasms / etiology. Immunoproliferative Small Intestinal Disease / complications. Lymphoma, T-Cell / etiology
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Proteins / metabolism

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  • (PMID = 18277034.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proteins
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4. Dutta U, Udawat H, Noor MT, Sidhu GS, Kochhar R, Vaiphei K, Singh K: Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori. J Gastrointest Cancer; 2010 Sep;41(3):212-5
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  • [Title] Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori.
  • A 20-year-old male presented with low-grade fever, abdominal pain, anorexia, and weight loss of 4-month duration.
  • Contrast-enhanced computed tomography of the abdomen revealed extensive proximal small-bowel thickening with mesenteric lymphadenopathy.
  • Upper gastrointestinal endoscopy and enteroscopy revealed thickening of folds with multiple small superficial ulceration involving antrum, duodenum, and jejunum.
  • The duodenal and jejunal biopsy was suggestive of immunoproliferative small intestinal disease, stage 0 (Salem) or stage A (Galian).
  • He underwent H. pylori eradication following which he had significant clinical improvement; repeat evaluation at 6 months showed dramatic improvement in his clinical, radiological, and histological parameters.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Helicobacter Infections / complications. Immunoproliferative Small Intestinal Disease / drug therapy. Immunoproliferative Small Intestinal Disease / microbiology
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles / therapeutic use. Amoxicillin / therapeutic use. Clarithromycin / therapeutic use. Doxycycline / therapeutic use. Drug Therapy, Combination. Helicobacter pylori. Humans. Lansoprazole. Male. Omeprazole / therapeutic use. Organometallic Compounds / therapeutic use. Tinidazole / therapeutic use. Young Adult

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  • (PMID = 20300878.001).
  • [ISSN] 1941-6636
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Organometallic Compounds; 033KF7V46H / Tinidazole; 0K5C5T2QPG / Lansoprazole; 804826J2HU / Amoxicillin; H1250JIK0A / Clarithromycin; HS813P8QPX / bismuth tripotassium dicitrate; KG60484QX9 / Omeprazole; N12000U13O / Doxycycline
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5. Miura P, Chakkalakal JV, Boudreault L, Bélanger G, Hébert RL, Renaud JM, Jasmin BJ: Pharmacological activation of PPARbeta/delta stimulates utrophin A expression in skeletal muscle fibers and restores sarcolemmal integrity in mature mdx mice. Hum Mol Genet; 2009 Dec 1;18(23):4640-9
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  • [Title] Pharmacological activation of PPARbeta/delta stimulates utrophin A expression in skeletal muscle fibers and restores sarcolemmal integrity in mature mdx mice.
  • A therapeutic strategy to treat Duchenne muscular dystrophy (DMD) involves identifying compounds that can elevate utrophin A expression in muscle fibers of affected patients.
  • Since activation of peroxisome proliferator-activated receptor (PPAR) beta/delta promotes the slow oxidative phenotype in skeletal muscle, we initiated studies to determine whether pharmacological activation of PPARbeta/delta provides functional benefits to the mdx mouse.
  • Expression of PPARbeta/delta was greater in skeletal muscles of mdx versus wild-type mice.
  • This treatment increased the percentage of muscle fibers expressing slower myosin heavy chain isoforms and stimulated utrophin A mRNA levels leading to its increased expression at the sarcolemma.
  • GW501516 treatment also conferred protection against eccentric contraction (ECC)-induced damage of mdx skeletal muscles, as shown by a decreased contraction-induced force drop and reduction of dye uptake during ECC.
  • These results demonstrate that pharmacological activation of PPARbeta/delta might provide functional benefits to DMD patients through enhancement of utrophin A expression.
  • [MeSH-major] Gene Expression / drug effects. Muscle Fibers, Skeletal / metabolism. Muscular Dystrophy, Duchenne / drug therapy. PPAR alpha / metabolism. PPAR-beta / metabolism. Thiazoles / administration & dosage. Utrophin / genetics
  • [MeSH-minor] Animals. Cell Line. Disease Models, Animal. Humans. Mice. Mice, Inbred C57BL. Mice, Inbred mdx. Sarcolemma / drug effects. Sarcolemma / metabolism

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  • (PMID = 19744959.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GW 501516; 0 / PPAR alpha; 0 / PPAR-beta; 0 / Thiazoles; 0 / Utrn protein, mouse; 0 / Utrophin
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6. Berentsen S, Beiske K, Tjønnfjord GE: Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy. Hematology; 2007 Oct;12(5):361-70
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  • [Title] Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy.
  • Chronic cold agglutinin disease (CAD) is a subgroup of autoimmune hemolytic anemia.
  • Primary CAD has traditionally been defined by the absence of any underlying or associated disease.
  • The results of therapy with corticosteroids, alkylating agents and interferon-alpha have been poor.
  • Cold reactive immunoglobulins against erythrocyte surface antigens are essential to pathogenesis of CAD.
  • These cold agglutinins are monoclonal, usually IgMkappa autoantibodies with heavy chain variable regions encoded by the V(H)4-34 gene segment.
  • By flowcytometric and immunohistochemical assessments, a monoclonal CD20+kappa+B-lymphocyte population has been demonstrated in the bone marrow of 90% of the patients, and lymphoplasmacytic lymphoma is a frequent finding.
  • Novel attempts at treatment for primary CAD have mostly been directed against the clonal B-lymphocytes.
  • Phase 2 studies have shown that therapy with the chimeric anti-CD20 antibody rituximab produced partial response rates of more than 50% and occasional complete responses.
  • In this review, we discuss the clinical and pathogenetic features of primary CAD, emphasizing the more recent data on its close association with clonal lymphoproliferative bone marrow disorders and implications for therapy.
  • We also review the management and outline some perspectives on new therapy modalities.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Alkylating Agents / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes / pathology. Bone Marrow / pathology. Clone Cells / pathology. Cryoglobulins / analysis. Cryoglobulins / immunology. Humans. Immunotherapy. Interferon-alpha / therapeutic use. Lymphoproliferative Disorders / complications. Lymphoproliferative Disorders / drug therapy. Lymphoproliferative Disorders / pathology. Rituximab

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  • (PMID = 17891600.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Alkylating Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Cryoglobulins; 0 / Interferon-alpha; 0 / cold agglutinins; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 88
  • [Other-IDs] NLM/ PMC2409172
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7. Tanaka M, Nakae S, Terry RD, Mokhtari GK, Gunawan F, Balsam LB, Kaneda H, Kofidis T, Tsao PS, Robbins RC: Cardiomyocyte-specific Bcl-2 overexpression attenuates ischemia-reperfusion injury, immune response during acute rejection, and graft coronary artery disease. Blood; 2004 Dec 1;104(12):3789-96
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  • [Title] Cardiomyocyte-specific Bcl-2 overexpression attenuates ischemia-reperfusion injury, immune response during acute rejection, and graft coronary artery disease.
  • This damage ultimately leads to the development of graft coronary artery disease (GCAD), which limits long-term graft survival.
  • To assess the role of the antiapoptotic factor Bcl-2 in the process of GCAD, we transplanted hearts from FVB transgenic mice overexpressing human Bcl-2 under the control of alpha-myosin heavy chain promoter into allogenic C57BL/6 mice.
  • Bcl-2 overexpression led to reduced cytochrome c-mediated caspase-9-dependent cardiomyocyte apoptosis and local inflammation (neutrophil infiltration and proinflammatory cytokine production) in cardiac allografts during ischemia-reperfusion injury and also led to reduced immune responses (inflammatory cell infiltration, production of T(H)1 cytokines and chemokines, and expression of adhesion molecules) during acute and chronic rejection without affecting host CD4(+) and CD8(+) cell responses in the spleen.
  • In conclusion, our findings suggest that the modulation of Bcl-2 expression by pharmacologic up-regulation or gene transfer may be of clinical benefit in the short- and long-term function of cardiac allografts.
  • [MeSH-major] Graft Rejection / prevention & control. Heart Transplantation / adverse effects. Myocytes, Cardiac / metabolism. Proto-Oncogene Proteins c-bcl-2 / pharmacology. Reperfusion Injury / therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Coronary Artery Disease / etiology. Coronary Artery Disease / prevention & control. Coronary Artery Disease / therapy. Genetic Vectors. Humans. Immunity / drug effects. Inflammation / drug therapy. Male. Mice. Mice, Transgenic


8. Iemitsu M, Shimojo N, Maeda S, Irukayama-Tomobe Y, Sakai S, Ohkubo T, Tanaka Y, Miyauchi T: The benefit of medium-chain triglyceride therapy on the cardiac function of SHRs is associated with a reversal of metabolic and signaling alterations. Am J Physiol Heart Circ Physiol; 2008 Jul;295(1):H136-44
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  • [Title] The benefit of medium-chain triglyceride therapy on the cardiac function of SHRs is associated with a reversal of metabolic and signaling alterations.
  • The spontaneously hypertensive rat (SHR) is a model of cardiomyopathy that displays a genetic defect in cardiac fatty acid (FA) translocase/CD36, a plasma membrane long-chain FA transporter.
  • Therapy with medium-chain FAs, which do not require CD36-facilitated transport, has been shown to improve cardiac function and hypertrophy in SHRs despite persistent hypertension.
  • However, little is known about the underlying molecular mechanisms.
  • The aim of this study was to document the impact of medium-chain triglyceride (MCT) therapy in SHRs on the expression level and activity of metabolic enzymes and signaling pathways.
  • Four-week-old male SHRs were administered MCT (SHR-MCT) or long-chain triglyceride (SHR-LCT) for 16 wk.
  • The SHR-MCT group displayed improved cardiac dysfunction [as assessed by left ventricular (LV) end-diastolic pressure and the positive and negative first derivatives of LV pressure/P value], a shift in the beta-myosin heavy chain (MHC)-to-alpha-MHC ratio, and cardiac hypertrophy compared with the SHR-LCT group without an effect on blood pressure.
  • Administration of MCT of SHRs reversed the LCT-induced reduction in the cardiac FA metabolic enzymatic activities of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and medium-chain acyl-CoA dehydrogenase (MCAD).
  • In the SHR-MCT group, the protein expression and transcriptional regulation of myocardial peroxisome proliferator-activated receptor-alpha, which regulates the transcription of LCHAD and MCAD genes, corresponded to the changes seen in those enzymatic activities.
  • Collectively, the observed changes in the myocardial activity of metabolic enzymes and signaling pathways may contribute to the improved cardiac dysfunction and hypertrophy in SHRs following MCT therapy.
  • [MeSH-major] Cardiomegaly / prevention & control. Energy Metabolism / drug effects. Hypertension / drug therapy. Myocardium / metabolism. Signal Transduction / drug effects. Triglycerides / pharmacology. Ventricular Dysfunction, Left / prevention & control
  • [MeSH-minor] 3-Hydroxyacyl CoA Dehydrogenases / metabolism. Acyl-CoA Dehydrogenase / metabolism. Animals. Antigens, CD36 / metabolism. Blood Pressure / drug effects. Disease Models, Animal. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. JNK Mitogen-Activated Protein Kinases / metabolism. Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase. Male. Myosin Heavy Chains / metabolism. PPAR alpha / metabolism. Phosphorylation. RNA, Messenger / metabolism. Rats. Rats, Inbred SHR. Rats, Inbred WKY. Time Factors. Transcription, Genetic. Ventricular Myosins / metabolism. Ventricular Pressure / drug effects

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  • (PMID = 18456726.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD36; 0 / Bmyo protein, rat; 0 / Cd36 protein, rat; 0 / PPAR alpha; 0 / RNA, Messenger; 0 / Triglycerides; EC 1.1.1.- / 3-Hydroxyacyl CoA Dehydrogenases; EC 1.1.1.211 / Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase; EC 1.3.8.7 / Acyl-CoA Dehydrogenase; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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9. Ramaiah SK, Seguin MA, Carwile HF, Raskin RE: Biclonal gammopathy associated with immunoglobulin A in a dog with multiple myeloma. Vet Clin Pathol; 2002;31(2):83-9
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  • [Title] Biclonal gammopathy associated with immunoglobulin A in a dog with multiple myeloma.
  • A 10-year-old neutered male Airedale Terrier was evaluated for inappetance, weight loss, and lameness.
  • Multiple myeloma was diagnosed based on bone marrow plasmacytosis, multiple lytic bone lesions, and hyperglobulinemia with a clonal gammopathy on serum protein electrophoresis.
  • Temporary responses to 2 different chemotherapy protocols (melphalan and prednisone, and cyclophosphamide and prednisone) were seen, with remission of clinical signs and a decrease in the biclonal gammopathy but no resolution of the splenic mass.
  • Eventual return of clinical signs led to euthanasia at 175 days postdiagnosis.
  • An immunoglobulin-A (IgA) gammopathy was demonstrated by immunoelectrophoresis; biclonality was ascertained by immunofixation electrophoresis.
  • The clonal components consisted of intact Ig with heavy chain of the alpha class and light chain of an undetermined class.
  • To our knowledge, this is the first report of undimerized biclonal gammopathy in a dog caused by a single heavy chain class involving IgA.

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  • (PMID = 12040490.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Immunoglobulin Heavy Chains
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10. Ramadeen A, Laurent G, dos Santos CC, Hu X, Connelly KA, Holub BJ, Mangat I, Dorian P: n-3 Polyunsaturated fatty acids alter expression of fibrotic and hypertrophic genes in a dog model of atrial cardiomyopathy. Heart Rhythm; 2010 Apr;7(4):520-8
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  • [Title] n-3 Polyunsaturated fatty acids alter expression of fibrotic and hypertrophic genes in a dog model of atrial cardiomyopathy.
  • BACKGROUND: We previously showed that omega-3 polyunsaturated fatty acids (PUFAs) reduce vulnerability to atrial fibrillation (AF).
  • OBJECTIVE: The purpose of this study was to use a genome-wide approach to identify gene expression profiles involved in a new model of AF vulnerability and to determine whether they were altered by PUFA therapy.
  • Two groups were paced using simultaneous atrioventricular pacing (SAVP) at 220 bpm for 14 days to induce atrial enlargement, fibrosis, and susceptibility to AF.
  • One group was supplemented with oral PUFAs (850 mg/day) for 21 days, commencing 7 days before the start of pacing (SAVP-PUFAs).
  • The second group received no PUFAs (SAVP-No PUFAs).
  • Atrial tissue was sampled at the end of the protocol.
  • Gene expression was analyzed in four dogs randomly selected from each group (n = 12) via microarray.
  • Results were confirmed with quantitative real-time polymerase chain reaction (RT-PCR) and histology on all 36 dogs.
  • RESULTS: Microarray or quantitative RT-PCR results showed that SAVP-No PUFAs dogs had significantly increased mRNA levels of protein kinase B (Akt), epidermal growth factor (EGF), JAM3, myosin heavy chain alpha (MHCalpha), and CD99 and significantly decreased levels of Smad6 compared with CTRL dogs.
  • Quantitative RT-PCR showed that PUFA supplementation was associated with significant down-regulation of Akt, EGF, JAM3, MHCalpha, and CD99 levels compared with SAVP-No PUFAs dogs.
  • CONCLUSION: The effect of PUFAs on these fibrosis, hypertrophy, and inflammation related genes suggests that, in this model, PUFA-mediated prevention of AF may be due to attenuation of adverse remodeling at the genetic level in response to mechanical stress.
  • [MeSH-major] Atrial Fibrillation / prevention & control. Atrial Function / drug effects. Cardiomyopathies / genetics. Cardiovascular Agents / pharmacology. Fatty Acids, Omega-3 / pharmacology. Heart Atria / drug effects
  • [MeSH-minor] Animals. Disease Models, Animal. Dogs. Fibrosis / genetics. Gene Expression / drug effects. Hypertrophy / genetics. Stress, Mechanical


11. Várkonyi J, Zalatnai A, Tímár J, Matolcsi A, Pócsik E, Kotlán B, Császár A, László V, Bencsáth M, Falus A: [Secondary cutaneous infiltration in B-cell chronic lymphocytic leukemia (B-CLL)]. Orv Hetil; 2000 Jun 4;141(23):1297-300
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  • Authors report here on a case presenting as B-CLL and complicated with cutaneous infiltration involving the legs and the trunk a year later.
  • Immunohistochemic analysis and the immunoglobulin heavy chain gene rearrangement confirmed cell invasion into the skin identical with the underlying disorder.
  • After failure of conventional chemotherapy, interferon alpha 2b therapy has been started with satisfactory result.
  • Secondary cutaneous B-cell lymphoma represents an entity of the poorest prognosis in comparison with primary cutaneous form treated with conventional therapy as well as with lymphomas lacking skin manifestations.
  • Interferon alpha 2b therapy cleans up the skin and yields a favourable survival so it's introduction recommended in this entity.
  • Authors summarise the characteristics of secondary cutaneous B-cell lymphomas on the basis of literature survey.
  • According to authors investigations histidine decarboxylase activity was found to be absent from the lymphocytes infiltrating the skin in contrast to those remaining in the circulation.
  • The changing character of the disease raises the possibility of an altered gene expression pattern of the cells invading the skin.
  • Authors summarise data from the literature concerning suspected molecular mechanism of tissue invasion.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Histidine Decarboxylase / metabolism. Interferon-alpha / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Skin Neoplasms / secondary
  • [MeSH-minor] Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Recombinant Proteins

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  • (PMID = 10905085.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] HUNGARY
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b; EC 4.1.1.22 / Histidine Decarboxylase
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12. Ben Ammar A, Cheikh I, Jouini M, Belkahla N, Fadhel SF, Hager O, Maamouri N, Chaabouni H, Ben Safta Z, Haouet S: [Alpha heavy chain disease. A Tunisian case]. Tunis Med; 2006 Sep;84(9):581-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Alpha heavy chain disease. A Tunisian case].
  • [Transliterated title] Maladie des chaines lourdes alpha. A propos d'un cas tunisien.
  • Alpha heavy chain disease is a rare affection in the West and reported mainly in developing countries with the improvement of hygienic conditions, the disease become rare in Tunisia, the last case was reported in 1991.
  • The aim of the study is to report a new Tunisian case and to describe clinical, endoscopical and histological characteristics of the disease.
  • The patient in a 37 years old male, presented with chronic diarrhoea associated with malabsorption syndrome.
  • The diagnosis of alpha heavy chain disease was confirmed by histological examination of the resected intestine after surgery for intestinal obstruction.
  • The patient received chemotherapy.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis
  • [MeSH-minor] Adult. Humans. Intestinal Obstruction / etiology. Intestinal Obstruction / surgery. Male

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  • (PMID = 17263208.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Tunisia
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13. Murdaca G, Contini P, Setti M, Cagnati P, Villa R, Lantieri F, Indiveri F, Puppo F: Behavior of serum human major histocompatibility complex class I antigen levels in human immunodeficiency virus-infected patients during antiretroviral therapy: correlation with clinical outcome. Hum Immunol; 2007 Nov;68(11):894-900
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  • [Title] Behavior of serum human major histocompatibility complex class I antigen levels in human immunodeficiency virus-infected patients during antiretroviral therapy: correlation with clinical outcome.
  • Human major histocompatibility complex class I antigens (HLA-A, -B, and -C) are heterodimeric molecules composed of a alpha heavy chain noncovalently associated with an invariant protein known as beta(2)-microglobulin.
  • Beside being expressed on the membrane of the large majority of nucleated cells, HLA class I antigens are evident in serum (sHLA-I).
  • We have previously detected a significant increase in the serum level of beta(2)-microglobulin-associated HLA-I antigens in human immunodeficiency virus (HIV)-infected patients compared with HIV-negative controls.
  • The introduction of highly active antiretroviral therapy (HAART) modified the clinical course of the disease and decreased the acquired immunodeficiency syndrome-related morbidity and mortality.
  • Therefore, we measured the levels of sHLA-I antigens in 64 HIV-infected patients before and during HAART treatment and correlated them with the immunological and virological response to antiretroviral treatment.
  • Serum sHLA-I antigen level was elevated in all HIV-infected patients before and significantly decreased after 36 months of HAART treatment, correlating with the decrease of plasma HIV-RNA level and with the increase of CD4+ T-lymphocyte number.
  • These results suggest that the measurement of sHLA-I antigens serum level might represent a useful surrogate marker to monitor HIV-positive patients undergoing HAART treatment.
  • [MeSH-major] Antiretroviral Therapy, Highly Active. HIV Infections / drug therapy. HIV Infections / immunology. Histocompatibility Antigens Class I / blood
  • [MeSH-minor] Adult. CD4 Lymphocyte Count. Female. HIV / isolation & purification. Humans. Male. Middle Aged. RNA, Viral / blood. Receptors, Tumor Necrosis Factor, Type II / blood. Treatment Outcome. Viral Load. beta 2-Microglobulin / blood

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  • (PMID = 18082568.001).
  • [ISSN] 0198-8859
  • [Journal-full-title] Human immunology
  • [ISO-abbreviation] Hum. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / RNA, Viral; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / beta 2-Microglobulin
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14. Ghoshal UC, Chetri K, Banerjee PK, Choudhuri G, Pal BB, Dabadghao S, Dhar K, Naik S, Naik SR: Is immunoproliferative small intestinal disease uncommon in India? Trop Gastroenterol; 2001 Jan-Mar;22(1):14-7
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  • [Title] Is immunoproliferative small intestinal disease uncommon in India?
  • Till date only three series of immunoproliferative small intestinal disease (IPSID) describing 22 patients have been reported from India.
  • Seven patients with IPSID in two tertiary referral centers in India are included in the study.
  • Diagnosis was based on typical clinical features [diarrhoea (7/7), weight loss (7/7), clubbing (6/7), fever (3/7), abdominal pain and lump (3/7)], biochemical evidence of malabsorption and duodenal biopsy findings.
  • All patients were young males (mean age 29.8 +/- 11.8 years, range 17-53).
  • Atypical features included gastric involvement (1/7), colonic involvement (1/7) and appearance of pigmented nails following anti-cancer chemotherapy (1/7) which disappeared six months after omitting doxorubin from chemotherapy regimen.
  • In the latter patient S. stercoralis became disseminated after anti-malignant chemotherapy.
  • One patient had gastric H. pylori infection.
  • This raises doubt on efficacy of tetracycline alone in treatment of IPSID.
  • One other patient was misdiagnosed and treated as intestinal tuberculosis.
  • Early diagnosis and administration of chemotherapy may improve survival in this disease.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / epidemiology
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Humans. India / epidemiology. Middle Aged. Prednisolone / therapeutic use. Prognosis. Tetracycline / therapeutic use. Vincristine / therapeutic use

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  • (PMID = 11398237.001).
  • [ISSN] 0250-636X
  • [Journal-full-title] Tropical gastroenterology : official journal of the Digestive Diseases Foundation
  • [ISO-abbreviation] Trop Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; F8VB5M810T / Tetracycline; VAP-cyclo protocol
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15. Magdelaine-Beuzelin C, Vermeire S, Goodall M, Baert F, Noman M, Assche GV, Ohresser M, Degenne D, Dugoujon JM, Jefferis R, Rutgeerts P, Lefranc MP, Watier H: IgG1 heavy chain-coding gene polymorphism (G1m allotypes) and development of antibodies-to-infliximab. Pharmacogenet Genomics; 2009 May;19(5):383-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgG1 heavy chain-coding gene polymorphism (G1m allotypes) and development of antibodies-to-infliximab.
  • OBJECTIVE: The chimeric anti-tumor necrosis factor-alpha antibody infliximab is known to induce antibodies-to-infliximab (ATI) in some treated patients.
  • Immunogenicity in murine variable domains is expected; however, constant domains of its human heavy gamma1 chain may also be implicated as it expresses G1m1 and G1m17 allotypes.
  • This allelic form may be immunogenic in patients that are homozygous for the G1m3 allotype commonly expressed in Caucasoid populations.
  • METHODS: As G1m allotypic divergence may explain the presence of ATI or may influence their concentration, a genotyping method was developed and validated to determine antithetical (i.e. mutually exclusive) G1m3 and G1m17 allotypes (amino acid 120 of CH1 according to the international ImMunoGeneTics information system unique numbering) at the IGHG1 gene level (CH1 359g/a nucleotide polymorphism).
  • Two hundred forty-five blood donors and 118 previously described patients suffering from Crohn's disease, treated with infliximab, and having developed ATI in 73 of them, were genotyped.
  • RESULTS: The IGHG1 CH1 359g/a polymorphism does not depart from the Hardy-Weinberg equilibrium in the control population, and allele frequencies were similar in controls and patients.
  • No association was found between the patient G1m allotypes and the presence of ATI or their concentration.
  • It remains possible that anti-Gm1 antibodies are not well detected by the enzyme-linked immunosorbent assays used for ATI detection and/or that the G1m allotypes are minor antigens on IgG1.
  • CONCLUSION: The IGHG1 polymorphism does not seem to play a major role in the induction of ATI.
  • Further analyses will be required to determine whether it is also the case for humanized or fully human antibodies bearing the same G1m allotypes.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibody Formation / genetics. Immunoglobulin G / genetics. Immunoglobulin Heavy Chains / genetics
  • [MeSH-minor] Anti-Inflammatory Agents / immunology. Anti-Inflammatory Agents / therapeutic use. Case-Control Studies. Cohort Studies. Crohn Disease / blood. Crohn Disease / drug therapy. Crohn Disease / genetics. Crohn Disease / immunology. Gene Frequency. Genotype. Humans. Immunoglobulin Allotypes / genetics. Infliximab. Models, Molecular

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  • (PMID = 19319024.001).
  • [ISSN] 1744-6872
  • [Journal-full-title] Pharmacogenetics and genomics
  • [ISO-abbreviation] Pharmacogenet. Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Allotypes; 0 / Immunoglobulin G; 0 / Immunoglobulin Heavy Chains; B72HH48FLU / Infliximab
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16. Lapointe N, Parker TG, Tsoporis JN, Nguyen QT, Marcotte F, Adam A, Lou I, Rouleau JL: Effects of the vasopeptidase inhibitor omapatrilat on peri- and postmyocardial infarction in Zucker lean rats. Can J Cardiol; 2005 Mar;21(3):291-7
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  • BACKGROUND: The vasopeptidase inhibitor omapatrilat improves insulin sensitivity and survival following myocardial infarction (MI).
  • It also improves left ventricular (LV) remodelling following MI and reduces MI size.
  • METHODS: Eighty-nine rats were pretreated for seven days with omapatrilat 20 mg/kg/day and 91 rats were left untreated.
  • MI was induced in 180 Zucker lean male rats by ligating the left anterior descending coronary artery, and omapatrilat was given for another 38 days in the survivors.
  • Using quantitative reverse transcriptase-polymerase chain reaction, gene expression was measured in the LV using transcript levels.
  • RESULTS: Treatment with omapatrilat resulted in improved early (24 h) and late (38 days) survival following MI (50% to 67%, P=0.023, and 44% to 59%, P=0.045, respectively).
  • Omapatrilat treatment reduced MI size and resulted in beneficial ventricular remodelling as reflected by a reduction in cardiac dimensions by echocardiography, and LV and right ventricular hypertrophy, which resulted in borderline hemodynamic improvement.
  • A large MI resulted in an increased expression of beta-myosin heavy chain, alpha-skeletal actin and atrial natriuretic peptide, and a decreased expression of GLUT-4.
  • Omapatrilat treatment did not modify the expression of these genes.
  • CONCLUSIONS: The results suggest that the vasopeptidase inhibitor omapatrilat does not modify fetal gene expression of the contractile apparatus or the expression of GLUT-4 despite reducing cardiac hypertrophy and MI size.
  • [MeSH-major] Disease Models, Animal. Myocardial Infarction / drug therapy. Protease Inhibitors / therapeutic use. Pyridines / therapeutic use. Thiazepines / therapeutic use
  • [MeSH-minor] Animals. Atrial Natriuretic Factor / analysis. Atrial Natriuretic Factor / drug effects. Atrial Natriuretic Factor / genetics. Drug Evaluation, Preclinical. Echocardiography. Gene Expression Regulation / drug effects. Glucose Transporter Type 4. Heart Ventricles / chemistry. Hypertrophy, Left Ventricular / etiology. Hypertrophy, Right Ventricular / etiology. Ligation. Male. Monosaccharide Transport Proteins / analysis. Monosaccharide Transport Proteins / drug effects. Monosaccharide Transport Proteins / genetics. Muscle Proteins / analysis. Muscle Proteins / drug effects. Muscle Proteins / genetics. Random Allocation. Rats. Rats, Zucker. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Ventricular Function, Left / drug effects. Ventricular Myosins / analysis. Ventricular Myosins / drug effects. Ventricular Myosins / genetics. Ventricular Remodeling / drug effects

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  • (PMID = 15776120.001).
  • [ISSN] 0828-282X
  • [Journal-full-title] The Canadian journal of cardiology
  • [ISO-abbreviation] Can J Cardiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Glucose Transporter Type 4; 0 / Monosaccharide Transport Proteins; 0 / Muscle Proteins; 0 / Protease Inhibitors; 0 / Pyridines; 0 / Slc2a4 protein, rat; 0 / Thiazepines; 36NLI90E7T / omapatrilat; 85637-73-6 / Atrial Natriuretic Factor; EC 3.6.1.- / Ventricular Myosins
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17. Flagg TP, Cazorla O, Remedi MS, Haim TE, Tones MA, Bahinski A, Numann RE, Kovacs A, Schaffer JE, Nichols CG, Nerbonne JM: Ca2+-independent alterations in diastolic sarcomere length and relaxation kinetics in a mouse model of lipotoxic diabetic cardiomyopathy. Circ Res; 2009 Jan 2;104(1):95-103
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  • [Title] Ca2+-independent alterations in diastolic sarcomere length and relaxation kinetics in a mouse model of lipotoxic diabetic cardiomyopathy.
  • Previous studies demonstrated increased fatty acid uptake and metabolism in MHC-FATP transgenic mice that overexpress fatty acid transport protein (FATP)1 in the heart under the control of the alpha-myosin heavy chain (alpha-MHC) promoter.
  • Doppler tissue imaging and hemodynamic measurements revealed diastolic dysfunction, in the absence of changes in systolic function.
  • The experiments here directly test the hypothesis that the diastolic dysfunction in MHC-FATP mice reflects impaired ventricular myocyte contractile function.
  • In vitro imaging of isolated adult MHC-FATP ventricular myocytes revealed that mean diastolic sarcomere length is significantly (P<0.01) shorter than in wild-type (WT) cells (1.79+/-0.01 versus 1.84+/-0.01 microm).
  • In addition, the relaxation rate (dL/dt) is significantly (P<0.05) slower in MHC-FATP than WT myocytes (1.58+/-0.09 versus 1.92+/-0.13 microm/s), whereas both fractional shortening and contraction rates are not different.
  • Application of 40 mmol/L 2,3-butadionemonoxime (a nonspecific ATPase inhibitor that relaxes actin-myosin interactions) increased diastolic sarcomere length in both WT and MHC-FATP myocytes to the same length, suggesting that MHC-FATP myocytes are partially activated at rest.
  • Direct measurements of intracellular Ca(2+) revealed that diastolic [Ca(2+)](i) is unchanged in MHC-FATP myocytes and the rate of calcium removal is unexpectedly faster in MHC-FATP than WT myocytes.
  • Moreover, diastolic sarcomere length in MHC-FATP and WT myocytes was unaffected by removal of extracellular Ca(2+) or by buffering of intracellular Ca(2+) with the Ca(2+) chelator BAPTA (100 micromol/L), indicating that elevated intracellular Ca(2+) does not underlie impaired diastolic function in MHC-FATP ventricular myocytes.
  • Functional assessment of skinned myocytes, however, revealed that myofilament Ca(2+) sensitivity is markedly increased in MHC-FATP, compared with WT, ventricular cells.
  • Collectively, these data demonstrate that derangements in lipid metabolism in MHC-FATP ventricles, which are similar to those observed in the diabetic heart, result in impaired diastolic function that primarily reflects changes in myofilament function, rather than altered Ca(2+) cycling.
  • [MeSH-major] Diabetes Complications / physiopathology. Fatty Acid Transport Proteins / physiology. Fatty Acids / metabolism. Heart Failure, Diastolic / physiopathology. Myocytes, Cardiac / physiology. Sarcomeres / ultrastructure
  • [MeSH-minor] Animals. Calcium / physiology. Chelating Agents / pharmacology. Diacetyl / analogs & derivatives. Diacetyl / pharmacology. Diastole. Disease Models, Animal. Egtazic Acid / analogs & derivatives. Egtazic Acid / pharmacology. Heart Ventricles / pathology. Isometric Contraction. Mice. Mice, Transgenic. Myocardial Contraction. Myocardium / metabolism. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Recombinant Fusion Proteins / physiology

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  • (PMID = 19023131.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chelating Agents; 0 / Fatty Acid Transport Proteins; 0 / Fatty Acids; 0 / Recombinant Fusion Proteins; 0 / Slc27a1 protein, mouse; 19SQ93LM6H / diacetylmonoxime; 526U7A2651 / Egtazic Acid; EC 3.6.4.1 / Myosin Heavy Chains; K22DDW77C0 / 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; K324J5K4HM / Diacetyl; SY7Q814VUP / Calcium
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18. Machet L, De Muret A, Wiezberka E, Bernez A, Abdallah-Lotf M, Linassier C, Petrella T: [Agranular CD4+ CD56+ CD123+ hematodermic neoplasm (blastic NK-cell lymphoma) revealed by cutaneous localization: 2 cases]. Ann Dermatol Venereol; 2004 Nov;131(11):969-73
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  • [Title] [Agranular CD4+ CD56+ CD123+ hematodermic neoplasm (blastic NK-cell lymphoma) revealed by cutaneous localization: 2 cases].
  • BACKGROUND: Agranular CD4+ CD56+ hematodermic neoplasm (blastic NK-cell lymphoma) has been recently described.
  • Preliminary histological examination of cutaneous biopsy taken in both patients showed a malignant proliferation suggesting a cutaneous lymphoma, and the patients were referred.
  • Histological examination of new biopsies showed a very similar proliferation in the 2 cases of monotonous medium-sized mononuclear cells without expression of the common antigens CD3 and CD20 and the expression of CD4, CD56, and CD123.
  • No rearrangement of the T-cell receptor gene or the immunoglobulin heavy chain gene were evidenced.
  • No extracutaneous involvement was initially detected in the first patient.
  • Thrombocytopenia associated with the abnormal presence of 15 p. 100 of circulating CD4+ CD56+ cells was initially found in the second patient.
  • The first patient was treated with chemotherapy, with complete remission.
  • The patient died one year after the diagnosis of the disease, in spite of intensification of the treatment.
  • Treatment is still ongoing in the second patient.
  • COMMENTS: The histological presentation of these two patients was very similar with an unusual phenotype of tumor cells expressing CD4, CD56, CD123, but not expressing CD3 and CD20.
  • Some cases have been published under the "term of blastic NK lymphoma" which is the actual term for the disease in the WHO classification.
  • However, the tumor cells derive from the dendritic plasmacytoid cells, also called type 2 dendritic cells, and perhaps from a common precursor to lymphocyte T and dendritic plasmacytoid cells.
  • In spite of complete cutaneous response in the 2 cases presented, as in other reports, extra-cutaneous involvement occurs quickly.
  • [MeSH-major] Antigens, CD4 / analysis. Antigens, CD56 / analysis. Killer Cells, Natural. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / pathology. Receptors, Interleukin-3 / analysis. Skin Neoplasms / immunology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Humans. Interleukin-3 Receptor alpha Subunit. Male. Phenotype

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  • (PMID = 15602384.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Receptors, Interleukin-3
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19. Fernández-Ruiz E, Cabrerizo M, Ortega M, Blas C, Llamas P, Santos-Roncero M, Nieto S, Acevedo A, Pérez G, Nicolás C, Fernández-Rañada JM, Arranz R: High molecular response rate and clinical correlation in patients with follicular lymphoma treated with cyclophosphamide-vincristine-prednisone plus interferon alpha 2b. Clin Cancer Res; 2003 Jul;9(7):2497-503
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  • [Title] High molecular response rate and clinical correlation in patients with follicular lymphoma treated with cyclophosphamide-vincristine-prednisone plus interferon alpha 2b.
  • PURPOSE: The role of molecular monitoring of minimal residual disease (MRD) in low-grade non-Hodgkin's lymphoma is controversial.
  • We have performed a prospective study of the molecular behavior of 35 patients with follicular non-Hodgkin's lymphoma who received cyclophosphamide-vincristine-prednisone chemotherapy in conjunction with IFN-alpha 2b.
  • EXPERIMENTAL DESIGN: Bcl-2 and clonal immunoglobulin heavy chain (IgH) gene rearrangements were assayed at diagnosis by PCR in lymph node and bone marrow (BM) and sequentially after treatment.
  • RESULTS: Molecular markers were detected in BM of 29 (83%) patients at diagnosis: Bcl-2 rearrangement in 20 patients (90% major breakpoint and 10% minor cluster) and clonal IgH rearrangement in 9 of 15 patients negative for Bcl-2.
  • Molecular and clinical response was noted in 25 (86%) patients after induction treatment.
  • A correlation between clinical and molecular response was found in 24 patients with molecular markers in BM at diagnosis and >2 years of follow-up: 94% of patients with undetectable MRD showed continuous clinical remission, whereas 50% of patients who reverted back to positive molecular markers relapsed (P < 0.05).
  • CONCLUSIONS: The rate of molecular response is high in patients treated with cyclophosphamide-vincristine-prednisone and IFN and MRD sequential analysis is useful for disease surveillance.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Interferon-alpha / therapeutic use. Lymphoma, Follicular / drug therapy. Prednisone / administration & dosage. Vincristine / administration & dosage
  • [MeSH-minor] Adult. Aged. Bone Marrow / metabolism. Disease-Free Survival. Female. Follow-Up Studies. Genetic Markers. Humans. Immunoglobulin Heavy Chains / immunology. Lymphatic Metastasis. Male. Middle Aged. Polymerase Chain Reaction. Prospective Studies. Proto-Oncogene Proteins c-bcl-2 / metabolism. Recombinant Proteins. Time Factors. Treatment Outcome

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  • (PMID = 12855623.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Immunoglobulin Heavy Chains; 0 / Interferon-alpha; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 99210-65-8 / interferon alfa-2b; VB0R961HZT / Prednisone
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20. Li Y, Takemura G, Okada H, Miyata S, Esaki M, Maruyama R, Kanamori H, Li L, Ogino A, Misao Y, Khai NC, Mikami A, Minatoguchi S, Fujiwara T, Fujiwara H: Treatment with granulocyte colony-stimulating factor ameliorates chronic heart failure. Lab Invest; 2006 Jan;86(1):32-44
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  • [Title] Treatment with granulocyte colony-stimulating factor ameliorates chronic heart failure.
  • Although granulocyte colony-stimulating factor (G-CSF) is reported to have a beneficial affect on postinfarction cardiac remodeling and dysfunction when administered before the onset of or at the acute stage of myocardial infarction (MI), its effect on established heart failure is unknown.
  • G-CSF changed the geometry of the infarct scar from elongated and thin to short and thick, induced hypertrophy among surviving cardiomyocytes, and reduced myocardial fibrosis.
  • Expression of G-CSF receptor was confirmed in failing hearts and was upregulated by G-CSF treatment.
  • G-CSF treatment also led to activation of signal transducer and activator of transcription-3 and induction of GATA-4 and various sarcomeric proteins such as myosin heavy chain, troponin I and desmin.
  • Expression of metalloproteinase-2 and -9 was also increased in G-CSF-treated hearts, while that of tumor necrosis factor-alpha, angiotensin II type 1 receptor (AT1) and transforming growth factor-beta1 was reduced.
  • Finally, beneficial effects of G-CSF on cardiac function were found persisting long after discontinuing the treatment (2 weeks).
  • [MeSH-major] Cardiac Output, Low / drug therapy. Granulocyte Colony-Stimulating Factor / therapeutic use
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Chronic Disease. Enzyme-Linked Immunosorbent Assay. Heart / physiopathology. Mice. Mice, Inbred C57BL. Regeneration

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  • (PMID = 16304579.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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21. Hainsey T, Csiszar A, Sun S, Edwards JG: Cyclosporin A does not block exercise-induced cardiac hypertrophy. Med Sci Sports Exerc; 2002 Aug;34(8):1249-54
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  • [Title] Cyclosporin A does not block exercise-induced cardiac hypertrophy.
  • METHODS: Thirty male rats were assigned to vehicle or CsA injection (15 mg.kg.d(-1)) and then assigned to sedentary or exercise training.
  • Animals were swum for 60 min.d(-1) for 1 wk.
  • RESULTS: One week of swim training significantly increased plantaris cytochrome oxidase activity, as well as significantly increasing left ventricular (LV) weight and the left ventricular:body weight (LV/BW) ratio.
  • Exercise did not alter right ventricular (RV) weight or the RV/BW ratio.
  • RNA analysis found that exercise significantly increased atrial natriuretic factor (ANF)-mRNA levels but did not influence alpha-myosin heavy chain (MHC) expression.
  • CsA treatment, but not exercise, was associated with a significant increase in betaMHC expression.
  • Western blot analysis determined that betaMHC protein was also significantly increased in the CsA-treated animals.
  • CONCLUSION: CsA did not block exercise-induced cardiac hypertrophy but did significantly influence the myocardial phenotype.
  • The CsA-sensitive calcium dependent pathways, important for pathological forms of overload-induced hypertrophy, were not essential to the early adaptations to exercise and that a different mechanism or signal transduction pathway was engaged.
  • The data also indicate that CsA alone may induce a shift in the MHC isoform expression toward that associated with a pathological phenotype.

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  • (PMID = 12165678.001).
  • [ISSN] 0195-9131
  • [Journal-full-title] Medicine and science in sports and exercise
  • [ISO-abbreviation] Med Sci Sports Exerc
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R29 HL059417; United States / NHLBI NIH HHS / HL / P01 HL 43023; United States / NHLBI NIH HHS / HL / R29 HL 59417
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 83HN0GTJ6D / Cyclosporine; EC 1.9.3.1 / Electron Transport Complex IV
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22. Schmidt-Schweda S, Holubarsch C: First clinical trial with etomoxir in patients with chronic congestive heart failure. Clin Sci (Lond); 2000 Jul;99(1):27-35
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  • [Title] First clinical trial with etomoxir in patients with chronic congestive heart failure.
  • In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction.
  • In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca(2+)-ATPase, and of the alpha-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium.
  • We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure.
  • A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II-III; mean age 55+/-4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy.
  • The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment.
  • Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution.
  • All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period.
  • Maximum cardiac output during exercise increased from 9.72+/-1.25 l/min before to 13.44+/-1.50 l/min after treatment (P<0.01); this increase was mainly due to an increased stroke volume [84+/-7 ml before and 109+/-9 ml after treatment (P<0.01)].
  • Resting heart rate was slightly reduced (not statistically significant).
  • The left ventricular ejection fraction increased significantly from 21.5+/-2.6% to 27.0+/-2.3% (P<0.01).
  • Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment.
  • Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca(2+)-ATPase and the alpha-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Epoxy Compounds / therapeutic use. Heart Failure / drug therapy
  • [MeSH-minor] Adult. Aged. Exercise Test / drug effects. Heart Rate / drug effects. Hemodynamics / drug effects. Humans. Male. Middle Aged. Stroke Volume / drug effects. Thermodilution

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  • (PMID = 10887055.001).
  • [ISSN] 0143-5221
  • [Journal-full-title] Clinical science (London, England : 1979)
  • [ISO-abbreviation] Clin. Sci.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Epoxy Compounds; MSB3DD2XP6 / etomoxir
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23. Lombardi R, Rodriguez G, Chen SN, Ripplinger CM, Li W, Chen J, Willerson JT, Betocchi S, Wickline SA, Efimov IR, Marian AJ: Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms. Circulation; 2009 Mar 17;119(10):1398-407
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  • [Title] Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms.
  • BACKGROUND: Cardiac hypertrophy, the clinical hallmark of hypertrophic cardiomyopathy (HCM), is a major determinant of morbidity and mortality not only in HCM but also in a number of cardiovascular diseases.
  • There is no effective therapy for HCM and generally for cardiac hypertrophy.
  • We posit that treatment with N-acetylcysteine, a precursor of glutathione, the largest intracellular thiol pool against oxidative stress, could reverse cardiac hypertrophy and fibrosis in HCM.
  • METHODS AND RESULTS: We treated 2-year-old beta-myosin heavy-chain Q403 transgenic rabbits with established cardiac hypertrophy and preserved systolic function with N-acetylcysteine or a placebo for 12 months (n=10 per group).
  • Transgenic rabbits in the placebo group had cardiac hypertrophy, fibrosis, systolic dysfunction, increased oxidized to total glutathione ratio, higher levels of activated thiol-sensitive active protein kinase G, dephosphorylated nuclear factor of activated T cells (NFATc1) and phospho-p38, and reduced levels of glutathiolated cardiac alpha-actin.
  • Treatment with N-acetylcysteine restored oxidized to total glutathione ratio, normalized levels of glutathiolated cardiac alpha-actin, reversed cardiac and myocyte hypertrophy and interstitial fibrosis, reduced the propensity for ventricular arrhythmias, prevented cardiac dysfunction, restored myocardial levels of active protein kinase G, and dephosphorylated NFATc1 and phospho-p38.
  • CONCLUSIONS: Treatment with N-acetylcysteine, a safe prodrug against oxidation, reversed established cardiac phenotype in a transgenic rabbit model of human HCM.
  • Because there is no effective pharmacological therapy for HCM and given that hypertrophy, fibrosis, and cardiac dysfunction are common and major predictors of clinical outcomes, the findings could have implications in various cardiovascular disorders.

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  • (PMID = 19255346.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] ENG
  • [Grant] None / None / / R01 HL068884-04; None / None / / P50 HL054313-090012; United States / NHLBI NIH HHS / HL / P50 HL054313; United States / NHLBI NIH HHS / HL / R01 HL068884-02; None / None / / P50 HL054313-060012; United States / NHLBI NIH HHS / HL / R01 HL068884-04; United States / NIAMS NIH HHS / AR / R01 AR056223; United States / NHLBI NIH HHS / HL / R01 HL068884-01; United States / NHLBI NIH HHS / HL / P50 HL054313-080012; None / None / / R01 HL068884-03; United States / NHLBI NIH HHS / HL / R01-HL68884; United States / NHLBI NIH HHS / HL / R01 HL068884-03; United States / NHLBI NIH HHS / HL / R01 HL068884; United States / NHLBI NIH HHS / HL / P50 HL054313-070012; None / None / / P50 HL054313-100012; None / None / / P50 HL054313-08S10012; None / None / / P50 HL054313-080012; United States / NHLBI NIH HHS / HL / P50 HL054313-08S10012; United States / NHLBI NIH HHS / HL / R01 HL068884-05; United States / NHLBI NIH HHS / HL / P50 HL054313-090012; None / None / / R01 HL068884-05; None / None / / P50 HL054313-070012; None / None / / R01 HL068884-02; United States / NHLBI NIH HHS / HL / R01-HL67322; United States / NHLBI NIH HHS / HL / P50 HL054313-100012; United States / NHLBI NIH HHS / HL / R01 HL067322; United States / NHLBI NIH HHS / HL / P50 HL054313-060012; None / None / / R01 HL068884-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Antioxidants; 0 / NFATC Transcription Factors; 0 / Sulfhydryl Compounds; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.6.4.1 / Myosin Heavy Chains; GAN16C9B8O / Glutathione; WYQ7N0BPYC / Acetylcysteine
  • [Other-IDs] NLM/ NIHMS113912; NLM/ PMC2773801
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24. Várkonyi J, Zalatnai A, Timár J, Matolcsi A, Falus A, Bencsáth M, László V, Pócsik E, Kotlán B, Császár A: Secondary cutaneous infiltration in B cell chronic lymphocytic leukemia. Acta Haematol; 2000;103(2):116-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We describe a patient presenting with B cell chronic lymphocytic leukemia (B-CLL) who subsequently developed cutaneous infiltrates.
  • Specimens of the blood, bone marrow and cutaneous infiltrations all showed the same heavy-chain gene rearrangement.
  • Following failure of conventional chemotherapy, and in view of the similarity of the disease to cutaneous T cell lymphoma, interferon-alpha therapy was employed with satisfactory results.
  • Introduction of this cytokine to the therapeutic modalities for secondary cutaneous B-CLL would hopefully change the poor outcome of this entity, or at least could produce a better quality of life.
  • Loss of histidine decarboxylase activity in the infiltrating cells - in contrast to circulating lymphocytes - may be associated with the transformation of B-CLL to a more aggressive infiltrative form, offering a possible explanation for tissue invasiveness.
  • The changing character of the disease raises the possibility of a second mutational event in the course of B-CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemic Infiltration. Lymphoma, B-Cell / pathology. Lymphoma, Non-Hodgkin / pathology. Skin / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chlorambucil / administration & dosage. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Histidine Decarboxylase / deficiency. Humans. Immunologic Factors / therapeutic use. Interferon-alpha / therapeutic use. Male. Middle Aged. Neoplasm Proteins / deficiency. Prednisolone / administration & dosage. Prednisone / administration & dosage. Recombinant Proteins. Salvage Therapy. Vincristine / administration & dosage

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  • [Copyright] Copyright 2000 S. Karger AG, Basel
  • (PMID = 10838457.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 18D0SL7309 / Chlorambucil; 43K1W2T1M6 / interferon alfa-2b; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 4.1.1.22 / Histidine Decarboxylase; VB0R961HZT / Prednisone; CHOP protocol; COP protocol 2
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25. Ommen HB, Schnittger S, Jovanovic JV, Ommen IB, Hasle H, Østergaard M, Grimwade D, Hokland P: Strikingly different molecular relapse kinetics in NPM1c, PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11 acute myeloid leukemias. Blood; 2010 Jan 14;115(2):198-205
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  • [Title] Strikingly different molecular relapse kinetics in NPM1c, PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11 acute myeloid leukemias.
  • Early relapse detection in acute myeloid leukemia is possible using standardized real-time quantitative polymerase chain reaction (RQ-PCR) protocols.
  • However, optimal sampling intervals have not been defined and are likely to vary according to the underlying molecular lesion.
  • In 74 patients experiencing hematologic relapse and harboring aberrations amenable to RQ-PCR (mutated NPM1 [designated NPM1c], PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11), we observed strikingly different relapse kinetics.
  • The median doubling time of the CBFB-MYH11 leukemic clone was significantly longer (36 days) than that of clones harboring other markers (RUNX1-RUNX1T1, 14 days; PML-RARA, 12 days; and NPM1c, 11 days; P < .001).
  • Furthermore, we used a mathematical model to determine frequency of relapse detection and median time from detection of minimal residual disease to hematologic relapse as a function of sampling interval length.
  • For example, to obtain a relapse detection fraction of 90% and a median time of 60 days, blood sampling every sixth month should be performed for CBFB-MYH11 leukemias.
  • By contrast, in NPM1c(+)/FLT3-ITD(-), NPM1c(+)/FLT3-ITD(+), RUNX1-RUNX1T1, and PML-RARA leukemias, bone marrow sampling is necessary every sixth, fourth, and fourth and second month, respectively.
  • These data carry important implications for the development of optimal RQ-PCR monitoring schedules suitable for evaluation of minimal residual disease-directed therapies in future clinical trials.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor beta Subunit / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myosin Heavy Chains / biosynthesis. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis
  • [MeSH-minor] Bone Marrow / metabolism. Female. Humans. Kinetics. Male. Monitoring, Physiologic / methods. Neoplasm, Residual. Recurrence. Retrospective Studies. Time Factors

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  • (PMID = 19901261.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / MYH11 protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 117896-08-9 / nucleophosmin; EC 3.6.4.1 / Myosin Heavy Chains
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26. Li B, Liao YH, Cheng X, Ge H, Guo H, Wang M: Effects of carvedilol on cardiac cytokines expression and remodeling in rat with acute myocardial infarction. Int J Cardiol; 2006 Aug 10;111(2):247-55
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  • METHODS: Rats with AMI induced by left anterior descending branch ligation were randomized to carvedilol and control group which were further compared to sham-operated group.
  • We studied the effects of 4-weeks therapy with carvedilol starting 24 h after infarction on 1) hemodynamics, 2) tissue weights, 3) myocardial cytokines (TNF-alpha, IL-1beta, IL-6, IL-10 and TGF-beta1) expression by semi-quantitative RT-PCR and immunoblotting, 4) matrix metalloproteinases activity by gelatin zymography, 5) collagen expression by immunohistochemistry, 6) myocardium fetal gene (alpha and beta myosin heavy chain) expression.
  • RESULTS: Treatment with carvedilol 1) reduced the pro-inflammatory cytokines and fibrogenic cytokine TGF-beta1 levels in myocardium and was associated with the amelioration of the elevated left ventricular diastolic pressure.
  • 2) increased anti-inflammatory cytokine, IL-10 protein expression.
  • 3) reduced matrix metalloproteinases-2 and matrix metalloproteinases-9 activity 4) reduced myocardial collagens 5) did not modify fetal gene re-expression.
  • One mechanism underlying the beneficial effects of carvedilol on post-infarction myocardial remodeling may be modulation of the balance between pro- and anti-inflammatory cytokines as well as fibrogenic cytokines and extracellular matrix (ECM) remodeling.
  • [MeSH-major] Carbazoles / pharmacology. Cytokines / blood. Myocardial Infarction / blood. Propanolamines / pharmacology. Vasodilator Agents / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Heart / drug effects. Heart / physiopathology. Interleukin-10 / blood. Interleukin-1beta / blood. Interleukin-6 / blood. Male. Rats. Rats, Wistar. Transforming Growth Factor beta / blood. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 16310260.001).
  • [ISSN] 0167-5273
  • [Journal-full-title] International journal of cardiology
  • [ISO-abbreviation] Int. J. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carbazoles; 0 / Cytokines; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Propanolamines; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / Vasodilator Agents; 0K47UL67F2 / carvedilol; 130068-27-8 / Interleukin-10
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27. Wolf CM, Arad M, Ahmad F, Sanbe A, Bernstein SA, Toka O, Konno T, Morley G, Robbins J, Seidman JG, Seidman CE, Berul CI: Reversibility of PRKAG2 glycogen-storage cardiomyopathy and electrophysiological manifestations. Circulation; 2008 Jan 15;117(2):144-54
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  • A genetic approach that utilizes a binary inducible transgenic system was used to investigate the disease mechanism and to assess preventability and reversibility of disease features in a mouse model of glycogen-storage cardiomyopathy.
  • METHODS AND RESULTS: Transgenic (Tg) mice expressing a human N488I PRKAG2 cDNA under control of the tetracycline-repressible alpha-myosin heavy chain promoter underwent echocardiography, ECG, and in vivo electrophysiology studies.
  • Transgene suppression by tetracycline administration caused a reduction in cardiac glycogen content and was initiated either prenatally (Tg(OFF(E-8 weeks))) or at different time points during life (Tg(OFF(4-16 weeks)), Tg(OFF(8-20 weeks)), and Tg(OFF(>20 weeks))).
  • One group never received tetracycline, expressing transgene throughout life (Tg(ON)).
  • Tg(ON) mice developed cardiac hypertrophy followed by dilatation, ventricular preexcitation involving multiple accessory pathways, and conduction system disease, including sinus and atrioventricular node dysfunction.
  • CONCLUSIONS: Using an externally modifiable transgenic system, cardiomyopathy, cardiac dysfunction, and electrophysiological disorders were demonstrated to be reversible processes in PRKAG2 disease.
  • Transgene suppression during early postnatal development prevented the development of accessory electrical pathways but not cardiomyopathy or conduction system degeneration.
  • Taken together, these data provide insight into mechanisms of cardiac PRKAG2 disease and suggest that glycogen-storage cardiomyopathy can be modulated by lowering glycogen content in the heart.

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  • (PMID = 18158359.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL076751-02; United States / NHLBI NIH HHS / HL / R01 HL076751-02; United States / NHLBI NIH HHS / HL / R01 HL076751-03; United States / NHLBI NIH HHS / HL / R01 HL076751; United States / NHLBI NIH HHS / HL / HL076751-03; United States / NHLBI NIH HHS / HL / R01 HL076751-04; United States / NHLBI NIH HHS / HL / R01 HL076751-01A1; United States / NHLBI NIH HHS / HL / HL076751-01A1; United States / NHLBI NIH HHS / HL / HL076751-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Multienzyme Complexes; 9005-79-2 / Glycogen; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; F8VB5M810T / Tetracycline
  • [Other-IDs] NLM/ NIHMS238048; NLM/ PMC2957811
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28. Li L, Takemura G, Li Y, Miyata S, Esaki M, Okada H, Kanamori H, Ogino A, Maruyama R, Nakagawa M, Minatoguchi S, Fujiwara T, Fujiwara H: Granulocyte colony-stimulating factor improves left ventricular function of doxorubicin-induced cardiomyopathy. Lab Invest; 2007 May;87(5):440-55
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  • [Title] Granulocyte colony-stimulating factor improves left ventricular function of doxorubicin-induced cardiomyopathy.
  • It is not well-known yet how granulocyte colony-stimulating factor (G-CSF) affects nonischemic cardiomyopathy, though its beneficial effects on acute myocardial infarction are well-established.
  • Here, we show that a single injection of doxorubicin (DOX, 15 mg/kg) induced left ventricular dilatation and dysfunction in mice within 2 weeks, and that these effects were significantly attenuated by human recombinant G-CSF (100 microg/kg/day for 5 days).
  • G-CSF also protected hearts against DOX-induced cardiomyocyte atrophy/degeneration, fibrosis, inflammatory cell infiltration and down regulation of GATA-4 and sarcomeric proteins, myosin heavy chain, troponin I and desmin, both in vivo and in vitro.
  • No DOX-induced apoptotic effects were seen, nor were there any changes in tumor necrosis factor-alpha or transforming growth factor-beta1 levels.
  • Inhibition of ERK activation, but not cyclooxygenase-2 inhibition, completely abolished beneficial effect of G-CSF on cardiac function.
  • G-CSF did not promote differentiation of bone marrow cells into cardiomyocytes according to the experiment using green fluorescent protein-chimeric mice, and inhibition of CXCR4+ cell homing using AMD3100 did not diminish the effect of G-CSF.
  • In conclusion, these findings imply the therapeutic usefulness of G-CSF mainly through restoring ERK activation against DOX-induced nonischemic cardiomyopathy.
  • [MeSH-major] Cardiomyopathy, Dilated / prevention & control. Cardiotonic Agents / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Ventricular Dysfunction, Left / prevention & control
  • [MeSH-minor] Animals. Animals, Newborn. Antibiotics, Antineoplastic / toxicity. Apoptosis / drug effects. Cell Survival / drug effects. Cells, Cultured. Disease Models, Animal. Dose-Response Relationship, Drug. Doxorubicin / toxicity. Drug Combinations. Drug Therapy, Combination. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Male. Mice. Mice, Inbred C57BL. Myocytes, Cardiac / drug effects. Myocytes, Cardiac / ultrastructure. Recombinant Proteins

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  • (PMID = 17334414.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Cardiotonic Agents; 0 / Drug Combinations; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 80168379AG / Doxorubicin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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