Long-term effect of low-density lipoprotein apheresis in patients with heterozygous familial hypercholesterolemia

Clinical efficacy and safety of the therapeutic tool which directly removes LDL particles from circulation (LDL apheresis) have already been established in the treatment for refractory hypercholesterolemia in patients with familial hypercholesterolemia (FH). Two clinical studies with event-based assessment have demonstrated remarkably beneficial outcomes of long-term LDL apheresis using dextran sulfate cellulose columns plus adjunctive cholesterol-lowering drug therapy in the prevention of cardiovascular events in heterozygous FH with coronary artery disease. The results of several studies with angiographic and ultrasound-based assessment indicate a possible role for LDL apheresis in restructuring and stabilization of atherosclerotic lesions. These clinical improvements caused by LDL apheresis in heterozygous FH support the efficacy and importance of aggressive cholesterol-lowering therapy for secondary prevention of atherosclerotic cardiovascular disease in hypercholesterolemic patients.     

Inflammatory pseudotumor of the liver: Radiologic diagnosis

To determine the characteristic radiologic findings of inflammatory pseudotumor of the liver, various imagings of ten patients (11 lesions) with proven diagnoses of inflammatory pseudotumor were reviewed. Radiologic examinations, i.e., computed tomography (CT; 11 lesions), ultrasonography (11 lesions), magnetic resonance imaging (MRI; 6 lesions), angiography (10 lesions), CT during arterio-portography (CTAP; 3 lesions), and gallium-67 scans (9 lesions) were analyzed for their utility in diagnosis. No inflammatory pseudotumor showed a fibrous capsule around the lesion. Ten of the 11 lesions were poorly demarcated on most of the imagings, and all 11 lesions showed delayed and/or prolonged enhancement on CT or MRI. Arterio-portal shunting was observed in 4 lesions after contrast material administration on CT or angiography. Central lesions with suspiciously high fibrotic tissue content were demonstrated in 5 lesions on CT or MRI. Major vessels coursing in the lesions were demonstrated in 4 lesions by CT, MRI, and CTAP. Inflammatory pseudotumor of the liver should be included in the differential diagnosis in patients with hepatic masses, even if the patients are asymptomatic. If radiologic examinations suggest inflammatory pseudotumor, percutaneous biopsies should be performed so that unnecessary surgery can be avoided.     

Effect of radioactivity outside the field of view on image quality of dedicated breast positron emission tomography: preliminary phantom and clinical studies

Annals of Nuclear Medicine - Semi-quantitative positron emission tomography (PET) values, such as the maximum standardized uptake value (SUVmax), are widely used to identify malignant lesions and...     

Clinical impact of amyloid PET using 18F-florbetapir in patients with cognitive impairment and suspected Alzheimer’s disease: a multicenter study

Annals of Nuclear Medicine - Amyloid positron emission tomography (PET) can reliably detect senile plaques and fluorinated ligands are approved for clinical use. However, the clinical impact of...     

Correction to: Quantitative evaluation of anti-resorptive agent-related osteonecrosis of the jaw using bone single photon emission computed tomography in clinical settings: relationship between clinical stage and imaging

Annals of Nuclear Medicine -     

Voxel-based analysis of age and gender effects on striatal [123I] FP-CIT binding in healthy Japanese adults

Annals of Nuclear Medicine - Although previous studies have investigated age and gender effects on striatal subregional dopamine transporter (DaT) binding, these studies were mostly based on a...     

Correction to: Detection of acute rib fractures on CT images with convolutional neural networks: effect of location and type of fracture and reader’s experience

Emergency Radiology -     

Opening of the adenosine triphosphate-sensitive potassium channel attenuates cardiac remodeling induced by long-term inhibition of nitric oxide synthesis: role of 70-kDa S6 kinase and extracellular signal-regulated kinase

OBJECTIVES: We examined whether the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel openers (KCOs) block myocardial hypertrophy and whether the 70-kDa S6 kinase (p70S6K) or extracellular signal-regulated kinase (ERK)-dependent pathway is involved. BACKGROUND: Long-term inhibition of nitric oxide (NO) synthesis induces cardiac hypertrophy independent of blood pressure, by increasing protein synthesis in vivo. The KCOs attenuate calcium overload and confer cardioprotection against ischemic stress, thereby preventing myocardial remodeling. METHODS: Twelve Wistar-Kyoto rat groups underwent eight weeks of the drug treatment in combination with the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME), the inactive isomer D(omega)-nitro-L-arginine methyl ester, KCOs (nicorandil, 3 and 10 mg/kg per day, or JTV-506, 0.3 mg/kg per day), or the K(ATP) channel blocker glibenclamide. The L-NAME was also used with hydralazine, the p70S6K inhibitor rapamycin, or the mitogen-activated protein kinase inhibitor PD98059. Finally, the left ventricular weight (LVW) to body weight (BW) ratio was quantified, followed by histologic examination and kinase assay. RESULTS: The L-NAME increased blood pressure and LVW/BW, as compared with the control agent. The KCOs and hydralazine equally cancelled the increase in blood pressure, whereas only KCOs blocked the increase in LVW/BW and myocardial hypertrophy induced by L-NAME. The L-NAME group showed both p70S6K and ERK activation in the myocardium (2.3-fold and 2.0-fold increases, respectively), as compared with the control group, which was not reversed by hydralazine. Selective inhibition of either p70S6K or ERK blocked myocardial hypertrophy. The KCOs prevented the increase in activity only of p70S6K. Glibenclamide reversed the effect of nicorandil in the presence of L-NAME. CONCLUSIONS: The KCOs modulate p70S6K, not ERK, to attenuate myocardial hypertrophy induced by long-term inhibition of NO synthesis in vivo.     

Clinical presentation of community-acquired Chlamydia pneumoniae pneumonia in adults

STUDY OBJECTIVE: To investigate the clinical presentation of community-acquired Chlamydia pneumoniae pneumonia in adults. DESIGN: Prospective study. SETTING: Kawasaki Medical School Hospital, Kawasaki Medical School Kawasaki Hospital, and Kurashiki Daiichi Hospital in Japan. PARTICIPANTS: Forty patients with community-acquired pneumonia with C pneumoniae as the only pathogen identified admitted to three hospitals between April 1996 and March 2001 and their clinical presentations were compared to patients with Streptococcus pneumoniae and Mycoplasma pneumoniae pneumonia. MEASUREMENTS: The diagnosis of C pneumoniae infection was based on isolation and serologic testing of antibodies by the microimmunofluorescence test. RESULTS: The clinical presentations, except for shortness of breath, were similar for the three major etiologic agents. The mean temperature of C pneumoniae patients on hospital admission was 37.9 degrees C, which was lower than that of patients with S pneumoniae and M pneumoniae. The mean WBC count on hospital admission was lower in the patients with C pneumoniae (mean, 9,100/microL) than in those with S pneumoniae pneumonia but higher than in those with M pneumoniae pneumonia. No patients required respiratory support or admission to an ICU, and no deaths occurred among the C pneumoniae pneumonia patients. CONCLUSIONS: Our results indicate that C pneumoniae pneumonia as a single etiologic agent is mild and that the underlying conditions and clinical symptoms closely resemble those of S pneumoniae pneumonia. However, the physical examinations, laboratory findings, and prognostic factors of the C pneumoniae patients resembled those of patients with M pneumoniae pneumonia.     

Cystic fibrosis and related diseases of the pancreas

The discovery of the gene for cystic fibrosis (CF), the cystic fibrosis transmembrane conductance regulator (CFTR), brought about a new era in the study of this disease. Identification of the molecular target has yielded a flood of data that add to our understanding of the pathogenesis, diagnosis and treatment of CF. The CFTR protein is a cAMP-regulated Cl(-) channel with multiple functions in epithelial cells. In the exocrine pancreas the CFTR plays a key role in the apical Cl(-), HCO(3)(-), and water transport in duct cells. The severe loss of functions, caused by mutations of the CFTR gene, leads to pathological lesions of the pancreas. Over 1200 CFTR mutations and polymorphisms have been identified and their diversity may explain the high level of heterogeneity in the CF phenotype. Mutation analyses of the CFTR gene have revealed a spectrum of CFTR-related diseases that do not fit the classical CF picture but are associated with dysfunction of CFTR, such as chronic pancreatitis.