Heart rate variability in a patient with alternating hemiplegia.

Alternating hemiplegia of childhood (AHC) is a rare disorder characterized by repetitive episodes of transient hemiplegia. Although autonomic nervous system dysfunction is believed to be associated with AHC, there are no reports of heart rate variability (HRV) in patients with AHC. In the current study, we analyzed HRV in a 20-year-old female with this disorder.

Lipocalin-type prostaglandin D synthase and egg white cystatin react with IgE antibodies from children with egg allergy.

Background: Ovalbumin, ovomucoid, ovotransferrin, lysozyme, and ovomucin are known to be major allergens found in egg white. Egg white protein is composed of over 30 proteins; many of which have neither been identified nor their allergenicities characterized. This study set out to analyze whether unknown proteins that bind to IgE antibodies in serum from patients with egg allergy exist in egg white.

Statin-induced Ca(2+) release was increased in B lymphocytes in patients who showed elevated serum creatine kinase during statin treatment.

Aim: Statins are effective in lowering cholesterol levels, but cause fatal rhabdomyolysis in susceptible individuals. Because it has been hypothesized that muscle damage could result from alterations in Ca(2+) homeostasis in muscle cells, we tested whether measuring statin-induced changes in intracellular calcium ([Ca(2+)](i)) is useful for predicting susceptibility to statin-muscle damage, using human CD19+ primary B lymphocytes.

Methods: Statin-induced alterations in [Ca(2+)](i) were studied using the human THP-1 cell line and CD19+ primary B lymphocytes.

[Autonomic nerve function in patients with systemic scleroderma using heart rate variability analysis].

We examined autonomic nerve function in patients with systemic scleroderma (SSc) using power spectral analysis of heart rate variability. In the SSc group, both in nighttime (0:00a.m.

Increases in tumor necrosis factor-alpha following transient global cerebral ischemia do not contribute to neuron death in mouse hippocampus.

The actions of tumor necrosis factor-alpha (TNF-alpha) produced by resident brain cells and bone marrow-derived cells in brain following a transient global ischemia were evaluated. In wild-type mice (C57Bl/6J) following 20 min ischemia with bilateral common carotid artery occlusion (BCCAo), TNF-alpha mRNA expression levels in the hippocampus were significantly increased at 3 h and 36 h and exhibited a biphasic expression pattern. There were no hippocampal TNF-alpha mRNA expression levels at early time points in either wild-type mice bone marrow transplanted (BMT)-chimeric-TNF-alpha gene-deficient (T/W) or TNF-alpha gene-deficient mice BMT-TNF-alpha gene-deficient mice (T/T), although TNF-alpha mRNA levels were detectable in T/W BMT mice at 36 h.

Disruption of tumor necrosis factor-alpha gene diminishes the development of atherosclerosis in ApoE-deficient mice.

Inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha) have been implicated in atherogenesis. However, the precise role of TNF-alpha in atherogenesis is still unclear. To examine the effect of TNF-alpha on atherogenesis, we generated compound-deficient mice in apolipoprotein E (apoE) and TNF-alpha (apoE-/-/TNF-alpha-/-) and compared them with apoE-/- mice.

Increased plasma lipid-poor apolipoprotein A-I in patients with coronary artery disease.

Background: Pre-beta 1-HDL participates in a cyclic process involved in the retrieval of cholesterol from peripheral tissues. Although pre-beta 1-HDL can be measured by two-dimensional electrophoresis or crossed immunoelectrophoresis, these methods are time-consuming and require technical expertise. In this study, we separated plasma lipid-poor apolipoprotein A-I (apo A-I) by high-performance size-exclusion chromatography.

Changes in quinolinic acid production and its related enzymes following D-galactosamine and lipopolysaccharide-induced hepatic injury.

Increases in quinolinic acid (QUIN), a neurotoxic L-tryptophan metabolite, have been observed in human serum and cerebrospinal fluid and in animal models of severe hepatic injury. The aim of this study was to evaluate the changes in QUIN accumulation and its related enzymes after acute hepatic injury induced by D-galactosamine and endotoxin. Gerbils were given an intraperitoneal injection of pyrogen-free saline alone as control, lipopolysaccharide (LPS) alone (150 ng/kg), D-galactosamine alone (500 mg/kg) or a combination of D-galactosamine with LPS.

[Significance of the cardiovascular function tests in patients with collagen diseases, especially for SSc (systemic scleroderma)].

The purpose of this study is to evaluate the cardiovascular function in patients with incomplete type of SSc (SSSD; Scleroderma Sjögren syndrome associated Spectrum Disorders), SSc (Systemic Scleroderma) and SLE (Systemic Lupus Erythematosus) by using ECG and digital plethysmograph. We also preformed ambulatory ECG monitoring for cases of SSSD and SSc with QT interval prolongation. 1) In ECG findings, ischemic myocardial damage, left ventricular hypertrophy or QT interval prolongation was observed in 33% cases of SSSD and 32% cases of SSc, respectively.

Interferon-gamma produced by bone marrow-derived cells attenuates atherosclerotic lesion formation in LDLR-deficient mice.

Background: We evaluated the role of IFN-gamma produced by bone marrow-derived cells in atherogenesis in LDLR(-/-) mice using bone marrow transplantation (BMT).

Methods And Results: We generated IFN-gamma-deficient bone marrow transplanted LDLR(-/- )mice (IFN-gamma(-/-) BMT mice), and compared them with controls (IFN-gamma(+/+) BMT mice). These mice were fed a high-fat diet (HFD).

[Genotyping and the quantification of hepatitis C virus by the melting curves in light cycler].

Detection of the HCV genome is crucial for diagnosis of HCV infection and for monitoring the efficacy of interferon treatment for patients with HCV. We developed a convenient screening test for HCV genotypes 1 and 2 based on the melting curve analysis with SYBER green I. Serum samples were drawn from 114 patients with known chronic HCV infection confirmed to be antibody-positive by immunoblot assay.

Genotyping of hepatitis C virus by melting curve analysis with SYBR Green I.

Background: Recent studies have focused on whether different hepatitis C virus (HCV) genotypes are associated with different profiles of pathogenicity, infectivity, and response to antiviral therapy. We needed to develop a convenient screening test for HCV genotypes 1 and 2.

Method: We tested 55 patients with known chronic HCV infection.

TNF-alpha contributes to the development of allergic rhinitis in mice.

Background: Allergic rhinitis is an inflammation involving T(H)2-type cytokine production, with pathologic eosinophil infiltration in the nasal mucosa. Although TNF-alpha is thought to be a pro-inflammatory cytokine, the relationship between TNF-alpha and allergic rhinitis has not been clarified.

Objectives: The role of TNF-alpha in a murine model of ovalbumin (OVA)-sensitized allergic rhinitis was investigated by using mice deficient in the gene encoding TNF-alpha (TNF-alpha(-/-) mice).

Tumor necrosis factor-alpha from bone marrow-derived cells is not essential for the expression of adhesion molecules in lipopolysaccharide-induced nasal inflammation.

Both the role and source of tumor necrosis factor (TNF-alpha) in lipopolysaccharide (LPS)-induced nasal inflammation were investigated using TNF-alpha gene deficient (TNF-alpha -/-) mice and chimeric mice that are TNF-alpha gene deficient only in bone marrow-derived cells. In the present study, intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) mRNA expression levels in the nasal mucosa were significantly decreased following intranasal instillation of LPS in TNF-alpha gene deficient mice compared to those in wild type mice. In contrast, ICAM-1 and VCAM-1 mRNA expressions were not significantly decreased although TNF-alpha mRNA expression was dramatically decreased in TNF-alpha gene deficient bone marrow-transplanted-chimeric (TNF-alpha -/--->+/+) mice compared to those in wild type bone marrow-transplanted-control (TNF-alpha +/+-->+/+) mice.

[Clinical significance of MMP-3 in patients with rheumatoid arthritis: comparison with other inflammatory markers(IL-6, IL-8)].

We determined serum metalloproteinase-3(MMP-3) and inflammatory cytokine(IL-6, IL-8) levels in patients with rheumatoid arthritis(RA). Sera were obtained from 307 healthy subjects(female 140, male 167), 54 RA patients, and 17 osteoarthritis (OA). The MMP-3 concentrations in healthy female and male were 43.

Lack of interleukin-1beta decreases the severity of atherosclerosis in ApoE-deficient mice.

Objective: Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis. We focused on the role of interleukin-1beta (IL-1beta), one of the proinflammatory cytokines secreted by monocytes/macrophages, in the progression of atherosclerosis.

Methods And Results: We generated mice lacking both apoE and IL-1beta.

Immunohistochemical localization and mRNA expression of apolipoprotein A-I in rat spinal cord.

Apolipoproteins in the cerebrospinal fluid (CSF) play important roles in lipid metabolism in the central nervous system. Although it has been demonstrated that apo E is synthesized in the neuron, the synthesis of apo A-I has only been determined in fish and chicken. It was demonstrated that apo A-I concentrations in the CSF were increased in poliovirus-infected macaques, however, the origin of the CSF apo A-I was not determined.

Improved myocardial ischemia/reperfusion injury in mice lacking tumor necrosis factor-alpha.

Objectives: This study sought to assess the role of tumor necrosis factor-alpha (TNF-alpha) in myocardial ischemia/reperfusion (I/R) injury using TNF-alpha knockout (KO) mice.

Background: Tumor necrosis factor-alpha is thought to be involved in the pathogenesis of myocardial I/R injury by promoting leukocyte infiltration of the myocardium. However, the precise role of TNF-alpha in I/R injury is still unknown.

L-tryptophan-L-kynurenine pathway metabolism accelerated by Toxoplasma gondii infection is abolished in gamma interferon-gene-deficient mice: cross-regulation between inducible nitric oxide synthase and indoleamine-2,3-dioxygenase.

L-Tryptophan degradation by indoleamine 2,3-dioxygenase (IDO) might have an important role in gamma interferon (IFN-gamma)-induced antimicrobial effects. In the present study, the effects of Toxoplasma gondii infection on IDO were investigated by using wild-type and IFN-gamma-gene-deficient (knockout) (IFN-gamma KO) mice. In wild-type C57BL/6J mice, enzyme activities and mRNA levels for IDO in both lungs and brain were markedly increased and lung L-tryptophan concentrations were dramatically decreased following T.