88 results match your criteria: "Cedars Sinai Medical Center and UCLA School of Medicine[Affiliation]"

Differential atrial stunning after electrical cardioversion: an echo tissue Doppler case study.

J Am Soc Echocardiogr

August 2001

Cardiac Non-Invasive Laboratory, Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, CA 90048, USA.

Left atrial stunning after cardioversion is a well-known phenomenon. It has been associated with higher risk of postcardioversion thromboemboli and increased risk of recurrence of atrial fibrillation. We present a case of differential atrial stunning after electrical cardioversion for atrial fibrillation.

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Background: Repeated doses of recombinant apolipoprotein A-I(Milano) phospholipid complex (apoA-I(m)) reduce atherosclerosis and favorably change plaque composition in rabbits and mice. In this study, we tested whether a single high dose of recombinant apoA-I(m) could rapidly mobilize tissue cholesterol and reduce plaque lipid and macrophage content in apoE-deficient mice.

Methods And Results: High cholesterol-fed, 26-week-old apoE-deficient mice received a single intravenous injection of saline (n=16), 1080 mg/kg dipalmitoylphosphatidylcholine (DPPC; n=14), or 400 mg/kg of recombinant apoA-I(m) complexed with DPPC (1:2.

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Duplication of the calcaneus is a rarely observed radiographic finding that probably results from delayed coalescence of two primary calcaneal centers of ossification. We performed a review of 2,500 computerized cases of skeletal dysplasias and syndromes with bone involvement in the International Skeletal Dysplasia Registry, searching for those cases in which a duplicate calcaneus had been recorded. We found that it was a non-random feature of three skeletal dysplasias and groups comprising thanatophoric dysplasia and the chondrodysplasia punctata and short rib (polydactyly) groups.

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A missense mutation in the cytoplasmic domain of the Toll-like receptor-4 (TLR-4) has been identified as the defect responsible for lipopolysaccharide (LPS) hyporesponsiveness in C3H/HeJ mice. TLR-4 and TLR-2 have recently been implicated in LPS signaling in studies where these receptors were overexpressed in LPS non-responsive 293 human embryonic kidney cells. However, the signaling role of TLR-4 or TLR-2 in human cells with natural LPS response remains largely undefined.

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Apparent mineralocorticoid excess (AME) syndrome is a rare inherited disorder caused by 11beta-hydroxysteroid dehydrogenase (11-HSD 2) isozyme deficiency in the kidney. This enzyme is responsible for oxidizing cortisol to its inactive metabolite cortisone. An elevated tetrahydrocortisol (THF) and allotetrahydrocortisol (aTHF) to tetrahydrocortisone (THE) ratio in the urine is pathognomonic of AME syndrome.

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TCP/IP and World-Wide-Web (WWW) technology have become the universal standards for networking and delivery of information. Personal digital assistants (PDAs), cellular telephones, and alphanumeric pagers are rapidly converging on a single pocket device that will leverage wireless TCP/IP networks and WWW protocols and can be used to deliver clinical information and alerts anytime, anywhere. We describe a wireless interface to clinical information for physicians based on Palm Corp.

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After cardiac transplantation, atrial arrhythmias may develop in the residual recipient atrium and conduct to the donor heart. Radiofrequency (RF) ablation of the atrioatrial conduction may be effective in arrhythmia control, although the recipient atrium continues its tachycardia. We hypothesize that in patients with posttransplant atrial tachycardia, it is possible to ablate both the arrhythmogenic focus in the recipient atrium and the atrioatrial conduction.

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New mesomelic dysplasia with absent fibulae and triangular tibiae.

Am J Med Genet

September 2000

Medical Genetics Birth Defects Center, Steven Spielberg Pediatrics Research Center, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, California, USA.

We report on two unrelated, sporadic cases of a mesomelic dysplasia characterized by absence of fibulae and severely hypoplastic, triangular-shaped tibiae. Moderate mesomelic shortness was present in the upper limbs with proximal widening of the ulnae. There was also axial skeletal involvement in both cases, characterized radiographically by an abnormal pelvis and marked bilateral glenoid hypoplasia.

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Background: Telomeric hexamer repeats (TTAGGG/CCCTAA)n are highly repetitive sequences of DNA. They cap the termini of eukaryotic chromosomes and stabilize them, preventing degradation or fusion. Anti ds-DNA is one of the most specific tests for systemic lupus erythematosus (SLE).

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Candidate locus for a nuclear modifier gene for maternally inherited deafness.

Am J Hum Genet

June 2000

Ahmanson Department of Pediatrics, Steven Spielberg Pediatric Research Center, Medical Genetics Birth Defects Center, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, CA, USA.

Maternally inherited deafness associated with the A1555G mutation in the mitochondrial 12S ribosomal RNA (rRNA) gene appears to require additional environmental or genetic changes for phenotypic expression. Aminoglycosides have been identified as one such environmental factor. In one large Arab-Israeli pedigree with congenital hearing loss in some of the family members with the A1555G mutation and with no exposure to aminoglycosides, biochemical evidence has suggested the role of nuclear modifier gene(s), but a genomewide search has indicated the absence of a single major locus having such an effect.

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The familial mediterranean fever protein interacts and colocalizes with a putative Golgi transporter.

Proc Soc Exp Biol Med

May 2000

Ahmanson Department of Pediatrics, Steven Spielberg Pediatric Research Center, Medical Genetics Birth Defects Center, and Department of Medicine, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, California 90048, USA.

The biological function of pyrin, the protein mutated in Familial Mediterranean Fever (FMF), has not been elucidated. Based on sequence homology, a transcription factor activity was proposed for this neutrophil-specific protein. In a yeast two-hybrid assay, neither transcription activation activity nor any self interaction was detected for pyrin.

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Plasma apolipoprotein B levels predict platelet-dependent thrombosis in patients with coronary artery disease.

Cardiology

June 2000

Preventive & Rehabilitative Cardiac Center and Atherosclerosis Research Center, Cedars-Sinai Burns and Allen Research Institute, Department of Medicine, Division of Cardiology, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angele, CA, USA.

Elevated plasma apolipoprotein B is a known risk factor for atherosclerotic coronary artery disease (CAD), however its relationship to arterial thrombosis is unexplored. We prospectively assessed apolipoprotein B and platelet-dependent thrombosis (PDT) in 42 CAD patients (37 men, 5 women, mean age 68 +/- 9 years), by exposing porcine aortic media to their flowing unanticoagulated venous blood for 5 min using an ex vivo perfusion (Badimon) chamber. PDT was significantly correlated with apolipoprotein B (r = 0.

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Modes of failure of Hancock and Carpentier-Edwards (C-E) porcine bioprosthetic valves placed in the mitral position are not completely understood. We reviewed transesophageal echocardiographic (n = 19) and pathologic features of failed Hancock (n = 22) and C-E (n = 8) porcine mitral valves in 30 patients (mean age 70 +/- 13 years). Age at implantation (59 +/- 14 vs 58 +/-14 years, p = 0.

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Evidence that high-density lipoprotein cholesterol is an independent predictor of acute platelet-dependent thrombus formation.

Am J Cardiol

November 1999

Atherosclerosis Research Center, Burns and Allen Research Institute, Department of Medicine, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, California 90048, USA.

Plasma total and low-density lipoprotein (LDL) cholesterol are established risk factors for atherosclerotic vascular disease and may also contribute to a prothrombotic risk via enhanced platelet reactivity. This study examines whether high-density lipoprotein (HDL) cholesterol, which is inversely correlated with coronary artery disease, is associated with a reduced thrombogenic potential. Platelet thrombus formation was evaluated by exposing porcine aortic media placed in Badimon perfusion chambers to flowing nonanticoagulated venous blood for 5 minutes at a shear rate of 1,000 s(-1).

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Objectives: The purpose of this study was to determine whether identification of contractile reserve with dobutamine would predict recovery of myocardial function during follow-up in patients with recent onset idiopathic dilated cardiomyopathy (IDC).

Background: The prognosis of patients presenting with new onset IDC is variable and difficult to predict.

Methods: Twenty-two patients (17 men, 5 women, 46 +/- 14 years) with recently diagnosed IDC (4 +/- 3 months) underwent dobutamine echocardiography.

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Phosphorylation of transcription factors fos/jun dimer activator protein (AP)-1 and nuclear factor-kappaB (NF-kappaB) plays a cardinal role in vascular smooth muscle cell (SMC) response to growth stimuli. Activity of protein tyrosine (PTP) and serine/threonine phosphatases (PP2A, B, and C) regulates in balance with the activity of protein kinases the level of transcription factor phosphorylation. Somatostatin analog octreotide stimulates phosphatase activity and inhibits cell growth.

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Background: Ventricular fibrillation (VF) is maintained by 2 mechanisms: first by reentry formation and second by spontaneous wave break or wave splitting. We hypothesized that spontaneous wave break results from a critical shortening of the action potential duration (APD) during VF and that its prevention by procainamide eliminates spontaneous wave break.

Methods And Results: The endocardial surfaces of 7 isolated, perfused swine right ventricles were mapped with a 3.

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Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.

J Biol Chem

March 1999

Division of Pediatric Infectious Diseases, Ahmanson Department of Pediatrics, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, California 90048, USA.

Bacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells.

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Oxidized low-density lipoprotein regulates matrix metalloproteinase-9 and its tissue inhibitor in human monocyte-derived macrophages.

Circulation

March 1999

Atherosclerosis Research Center, Division of Cardiology, and the Burns and Allen Research Institute, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, CA, USA.

Background: Macrophages in human atherosclerotic plaques produce a family of matrix metalloproteinases (MMPs), which may influence vascular remodeling and plaque disruption. Because oxidized LDL (ox-LDL) is implicated in many proatherogenic events, we hypothesized that ox-LDL would regulate expression of MMP-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1) in monocyte-derived macrophages. MWRHOSA AND RESULTS: Mononuclear cells were isolated from normal human subjects with Ficoll-Paque density gradient centrifugation, and adherent cells were allowed to differentiate into macrophages during 7 days of culture in plastic dishes.

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Identification and characterization of a zinc finger gene (ZNF213) from 16p13.3.

Biochim Biophys Acta

February 1999

Ahmanson Department of Pediatrics, Steven Spielberg Pediatric Research Center, Medical Genetics Birth Defects Center, Cedars-Sinai Medical Center and UCLA School of Medicine, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.

During our search for the familial Mediterranean fever (FMF) gene, we identified by cDNA selection a 1.2 kb cDNA fragment representing a novel human gene that is expressed in a wide variety of tissues. This gene spans approx.

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