Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apoptosis of cardiomyocytes plays an important role in reperfusion injury following myocardial infarction. Conversely, interleukin-6 (IL-6)--a potent cytokine--inhibits myeloma cell apoptosis by activating GP130 through the IL-6 receptor (IL-6R). We hypothesized that the IL-6/soluble IL-6R complex can inhibit myocardial apoptosis, and limit infarct size in reperfused acute myocardial infarction. Anesthetized rats were randomly divided into five groups: sham, coronary occlusion and reperfusion rats administered IL-6/soluble IL-6R complex, IL-6 alone, soluble IL-6R (sIL-6R) alone, or a control vehicle. Rats were subjected to 30 min occlusion of the left coronary artery followed by 3 h reperfusion. After reperfusion, the hearts were excised. For detection and quantification of apoptosis, gel electrophoresis of extracted genomic DNA and TUNEL method of paraffin sections were performed. The percentage of the infarct area was measured using tetrazolium chloride staining. The cardiomyocyte apoptosis analysis revealed that apoptosis in the reperfused myocardium was inhibited only in the complex group. Furthermore, the percentage of the infarct area out of the area at risk was remarkably reduced in the complex group (23.8+/-1.8%), compared with that in the vehicle (37.9+/-3.7%), the IL-6 (40.7+/-1.0%), or the sIL-6R (37.5+/-2.4%) groups (P=0.0002). No significant differences were observed among the vehicle, IL-6, and sIL-6R groups. The IL-6/soluble IL-6 receptor complex inhibits cardiomyocyte apoptosis in reperfused acute myocardial infarction. It possibly reduces irreversible reperfusion injury.
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PMID:Interleukin-6/soluble interleukin-6 receptor complex reduces infarct size via inhibiting myocardial apoptosis. 1605 42

A 79-year-old female patient with multiple myeloma who had no prior cardiac disease history developed an acute myocardial infarction on day 5 after receiving bortezomib and dexamethasone (BD). After treatment of coronary stenoses by stents, she received another course of BD therapy and developed angina pectoris on day 5 after the therapy. Bortezomib's antitumor effect is due to the inhibition of proteasome activity. This inhibition may increase endothelial progenitor cell apoptosis and decrease endothelial nitric oxide synthase/nitric oxide (eNOS/NO), thus leading to coronary spasm. It is, therefore, important to carefully monitor patients being treated with bortezomib for the potential occurrence of ischemic heart disease.
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PMID:Ischemic heart disease associated with bortezomib treatment combined with dexamethasone in a patient with multiple myeloma. 2045 63

Patients diagnosed with multiple myeloma have an increased risk of venous thrombosis. This may be due to various risk factors, including disease specific factors, changes in coagulation and fibrinolysis factors and circulating prothrombotic microparticles. More recent studies have indicated that also arterial thrombosis, including acute myocardial infarction and stroke do occur more frequently in these patients. Studies on etiological factors contributing to the development of thrombosis will be reviewed in this article. In addition we will focus on the prevention and management of arterial and venous thrombosis in patients with multiple myeloma.
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PMID:Risk and management of thrombosis in multiple myeloma. 2268 42

Ethylenediaminetetraacetic acid-dependent pseudothrombocytopenia (EDTA-PTCP) is an in vitro phenomenon of EDTA-induced platelet aggregation at room temperature. This phenomenon consists of platelet clumping due to anti-platelet antibodies in blood anticoagulated with EDTA. It has been reported in patients with various diseases, including sepsis, multiple myeloma, acute myocardial infarction and breast cancer. Since unrecognized EDTA-PTCP may lead to inappropriate treatment, it should always be considered as a possible cause in patients with low platelet counts. This study identified a case of transient EDTA-PTCP in a patient with neuroendocrine carcinoma of the stomach. In the present study, a 50-year-old male presented with epigastric pain and a weight loss of 15 kg. The patient presented with EDTA-PTCP and was diagnosed with neuroendocrine carcinoma of the stomach. Following systemic chemotherapy, the tumor showed a marked regression and the EDTA-PTCP disappeared. The mechanism by which this occurred is not clear but an association of EDTA-PTCP with neuroendocrine carcinoma is strongly suggested.
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PMID:Ethylenediaminetetraacetic acid-dependent pseudothrombocytopenia associated with neuroendocrine carcinoma: A case report. 2280 67

Human cardiac troponin I (cTnI) is one of the most specific biomarkers for detection of acute myocardial infarction (AMI). To formulate immunoassay kits for rapid immunodiagnosis of AMI, monoclonal antibodies with high affinity and specificity were generated against cTnI and subsequently tested through a series of experiments. C57BL/6 mice were immunized with cTnI as the immunogen and cell fusions with myeloma cells of BALB/c origin were performed to generate hybridomas. The supernatants of the hybridoma cell culture were routinely screened for antibody secretions against intact cTnI and synthetic peptides from the N-terminal half of cTnI (amino acid residues N1-30, N24-40, N59-79, and N80-95). Monoclonal antibodies specific to different epitope regions were then determined and selected, according to their respective affinity and specificity, for formulation of enzyme immunoassay kits. The results of this study found that most of the selected antibodies revealed comparable binding affinity to cTnI and to the corresponding synthetic peptides. Optimal sandwich enzyme immunoassays with high sensitivity could be achieved through proper combinations of the epitope-distinct monoclonal antibodies in different capture-detection pairs; signal enhancements were frequently observed when a mixture of epitope-distinct anti-cTnI monoclonal antibodies was used for coating. This indicates that a combination of epitope-distinct anti-cTnI monoclonal antibodies recognizing the N-terminal half of cTnI yield reliable detection and greater sensitivity for cTnI in AMI patients.
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PMID:Monoclonal Antibodies Against Human Cardiac Troponin I for Immunoassays II. 2609 May 94