Quantitative observations on iliac bone marrow mast cells in chronic renal failure.

Peart, Kathleen M.; Ellis, H. A.

doi:10.1136/jcp.28.12.947

Cited by 26 publications

(14 citation statements)

References 28 publications

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“…Eosinophilia was a constant finding in this investigation and it has for merly been described also in a patient on chronic peritoneal dialysis [12], Quantitative observations on iliac bone marrow have given evidence of a raised frequency of mast cells in chronic renal failure with osteodystrophy [14] and this is verified in the present investigation. It is known that eosi nophilia may be the result of a reaction of antigen and antibody of IgE class fixed to the surface of mast cells [5].…”

Section: Resultssupporting

confidence: 73%

Bone Marrow Morphology in Patients on Regular Haemodialysis Treatment

Sjögren¹,

Thysell²

1977

Acta Haematol

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Bone marrow smears from 57 patients with chronic renal failure were morphologically analysed. In 55 patients on regular haemodialysis there was a slight ‘shift to the left’ and a significant eosinophilia within the granulopoiesis concurrently with slight megaloblastic changes of the erythroblasts. It is suggested that these abnormalities are caused by the dialysis procedure and not by the uraemia per se

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Section: Resultssupporting

confidence: 73%

Bone Marrow Morphology in Patients on Regular Haemodialysis Treatment

Sjögren¹,

Thysell²

1977

Acta Haematol

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“…This mechanism of action is supported by evidence implicating mast cells in pathological fibrosis as well as pathological bone resorption (29)(30)(31). Additionally, HPT patients have increased numbers of mast cells in the vicinity of trabecular surfaces of cancellous bone (32) and PTH is reported to induce mast cell degranulation (33).…”

Section: Discussionmentioning

confidence: 84%

“…Indeed, our results are the first to indicate a linkage between caspases and MMR proteins. The MMR system recognizes and repairs mispaired or unpaired nucleotides that result from errors in DNA replication (32,33). The mammalian homologues of the E. Coli MutS protein form heterodimers (MSH2-MSH6 and MSH2-MSH3) that bind to nucleotide mismatches and recruit heterodimers of the MutL homologues (MLH1-PMS2, MLH1-PMS1, or MLH1-MLH3) to base mismatches (32,34).…”

Section: Bodymentioning

confidence: 99%

“…Co-morbidity factors such as dietary iron, estrogen and endotoxin appear to be needed (31)(32)(33)(34).…”

Section: /09/00 Pagementioning

confidence: 99%

“…Ethanol administered at 35% of caloric intake At first glance, the observed nondose-dependent reduc-resulted in measured blood ethanol levels of 0.09-tion in uterine weight in rats fed some doses of ethanol 0.15%. (21,32,33,36) The measured levels are likely to undersuggests that gonadal insufficiency contributes to the bone estimate peak blood alcohol levels because sequential meachanges. However, the histological changes are not consis-surements have not been performed throughout the rat tent with this possibility.…”

Section: Introductionmentioning

confidence: 99%

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Bone-97 Alcohol and Skeletal Adaptation to Mechanical Usage

Turner¹

2002

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Public reporting burden for this collection of information Is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of Information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducdng this burden to Washington Headquarters Services, Directorate for Intforation Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Adington, VA 22202-4302, and to the Office of Management and Budget, AUTHOR(S)Vincent L. Cryns, M.D. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERNorthwestern University Chicago, Illinois 60611 E-Mall:v-cryns@northwestern.edu SPONSORING I MONITORING AGENCY NAME(S) AND ADDRESS(ES)10. SPONSORING / MONITORING AGENCY REPORT NUMBER U.S. Army Medical Research and Materiel CommandFort Detrick, Maryland 21702-5012 SUPPLEMENTARY NOTES Original contains color plates:All DTIC reproductions will be in black and white. Abstract (Maximum 200 Words) (abstract should contain no proprietary or confidential information)Using a novel expression cloning strategy and secondary functional screen of a human prostate cancer cDNA library, we have identified one new, functionally relevant caspase substrate: the mismatch repair protein MLHI implicated in a variety of cancers including those of the prostate. We have demonstrated that human MLH1 is specifically cleaved by caspase-3 (but not by other caspases) at ASP418 in vitro. Furthermore, we have shown that MLH1 is rapidly proteolyzed by caspase-3 in prostate cancer cells induced to undergo apoptosis by treatment with TNF-related apoptotosis-inducing ligand (TRAIL) or the topoisomerase II inhibitor etoposide, which induces DNA double-strand breaks. Importantly, proteolysis of MLH1 by caspase-3 triggers its partial redistribution from the nucleus to the cytoplasm. In addition, a capase-3 cleavage-resistant D418E MLHII mutant inhibits etoposide-induced apoptosis but has little effect on TRAIL-induced apoptosis. These results indicate that MLHI is specifically targeted for proteolysis by caspase-3, and this proteolytic event promotes the execution of apoptotic signals initiated by DNA double-strand breaks. In this way, our results suggest a novel function of MLHI in the response to DNA double-strand breaks that is deregulated by caspase proteolysis. These experiments, then, may lead to novel treatments for prostate cancer that specifically target MLH1. IntroductionApoptosis or programmed cell death is a genetically regulated cellular suicide response that is activated in prostate cancer cells by androgen ablation and irradiation. Indeed, the tumoricidal activity of these treatment modalities stems from their ability to induce apoptosis in prostate cancer cells (1). Caspases are a conserved family of cysteine proteases that are universal effectors of programmed cell death (2, 3). However, t...

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