Left ventricular dysfunction during exercise in patients with angina pectoris and angiographically normal coronary arteries (syndrome X)

Left ventricular function during exercise and recovery was investigated in patients with angina pectoris, ST segment depression during exercise and angiographically normal coronary arteries (syndrome X) using a continuous left ventricular function monitor with cadmium telluride detector (CdTe-VEST). Fourteen patients with syndrome X and 14 patients with atypical chest pain without ST segment depression during exercise and normal coronary arteries (control group) performed supine ergometric exercise after administration of 740–925 MBq of technetium-99m labelled red blood cells, and left ventricular function was monitored every 20 s using CdTe-VEST. Left ventricular ejection fraction (EF) response was impaired (55% increase from rest to peak exercise) in 11 or 14 patients with syndrome X but in none of the control patients. Resting EF was similar in the two groups (62.1%±6.7% in patients with syndrome X, 61.9%±6.2% in controls); however, EF increase from rest to peak exercise was lower in syndrome X (–3.1±9.5% vs 14.7%±7.4%, P <0.001). After cessation of exercise, all patients showed rapid EF increase over baseline and this EF overshoot was lower (19.3%±8.3% vs 26.4%±7.3%, P <0.001) with the time to EF overshoot longer (114±43 s vs 74±43 s, P<0.05) in patients with syndrome X. Thus, in patients with syndrome X, left ventricular dysfunction was frequently observed during exercise in spite of normal epicardial coronary arteries. Correspondence to: J. Taki     

FDG-PET for predicting the prognosis of malignant lymphoma

To evaluate the usefulness of FDG-PET as a predictor of prognosis, 34 patients with untreated malignant lymphoma in the head and neck region were studied. After FDG-PET and treatment, they were observed from 15 to 50 months. Tumors which were aggressive and resistant to treatment tended to show high uptake of FDG. The survival rate of patients with high uptake of FDG, DAR > 8, was lower than the rate of the other patients. It is considered to be useful to add FDG uptake of the tumor to other prognostic factors for predicting the prognosis.     

Fibroma of tendon sheath originating from the knee joint capsule

We present a rare case of fibroma of the tendon sheath originating from the posterior joint capsule of the knee in a 50-year-old man. Magnetic resonance (MR) imaging revealed a lesion posterior to the medial femoral condyle. The lesion showed hypointensity on all T1-weighted, T2-weighted, short tau inversion recovery (STIR), and contrast-enhanced T1-weighted images. Plain computed tomographic (CT) scans showed a lesion with isodensity to muscle. The lesion showed no enhancement on postcontrast CT scans.     

Four novel mutations in the thiazide-sensitive Na-Cl co-transporter gene in Japanese patients with Gitelman's syndrome.

BACKGROUND: Gitelman's syndrome (GS) is an autosomal recessive disorder resulting from inactivating mutations in the thiazide-sensitive Na-Cl co-transporter (NCCT) gene. To date, almost 90 mutations have been identified. It is possible that there is a population-specific distribution of mutations. In this study, we analysed mutations in the NCCT gene of seven Japanese patients with GS. METHODS: Peripheral blood mononuclear cells were isolated from patients with GS, their family members and healthy control subjects. A mutation analysis of the NCCT gene was performed completely by direct automated sequencing of polymerase chain reaction-amplified DNA products. In patients with a deletion or splice site mutation, we undertook cDNA sequence analysis. RESULTS: We identified nine mutations. Five of them [c.185C>T (Thr60Met), c.1712C>T (Ala569Val), c.1930C>T (Arg642Cys), c.2552T>A (Leu849His) and c.1932delC] have been reported in Japanese patients, but not in GS patients from other ethnic groups. The remaining four mutations [c.7A>T (Met1Leu), c.1181_1186+20del26, c.1811_1812delAT and IVS16+1G>A] were novel. In cDNA derived from a patient with c.1181_1186+20del26, a deletion of exon 9 and a frameshift at the start of exon 10 were observed. In cDNA derived from patients with IVS16+1G>A, an additional 96 bp insertion between exons 16 and 17 was observed. Six out of seven patients were compound heterozygotes, and the remaining one carried a single heterozygous mutation. CONCLUSIONS: We found four novel mutations in the NCCT gene in seven Japanese patients with GS. Moreover, our study suggests that the distribution of mutations in the NCCT gene in Japanese GS patients potentially differs from that in other populations.     

The influences of nitrous oxide and ketamine on electroencephalogram during propofol-anesthesia

BACKGROUND: The influence of nitrous oxide and ketamine on electroencephalogram (EEG) during the induction of general anesthesia with propofol was quantitatively analyzed. METHODS: Anesthesia was induced with propofol using TCI (target controlled infusion) system. Twenty-five adult patients (ASA I-II) were randomly divided into three groups: 1. anesthesia induced with propofol alone [Group-P (n=7)], 2. anesthesia induced with inhalation of nitrous oxide in addition to propofol [Group-PN (n= 10)] and 3. anesthesia induced with intravenous injection of ketamine in addition to propofol [Group-PK (n= 8)]. We studied the influence of nitrous oxide and ketamine on EEG by analyzing the relations between effect-site concentration of propofol and EEG-indices. RESULTS: Additional injection of ketamine (Group-PK) increased BIS index during the maintenance of anesthesia from 43.4 +/- 8.2 to 71.8 +/- 6.5 in comparison with the contrasting group (Group-P). Nitrous oxide also increased the high frequency component in EEG. CONCLUSIONS: When anesthesia is induced with nitrous oxide and/or ketamine together with propofol, and BIS is taken as an index of depth of anesthesia, the intracerebral concentration of propofol becomes excess.     

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...     

Protein kinase C–delta deficiency perturbs bone homeostasis by selective uncoupling of cathepsin K secretion and ruffled border formation in osteoclasts

Bone homeostasis requires stringent regulation of osteoclasts, which secrete proteolytic enzymes to degrade the bone matrix. Despite recent progress in understanding how bone resorption occurs, the mechanisms regulating osteoclast secretion, and in particular the trafficking route of cathepsin K vesicles, remain elusive. Using a genetic approach, we describe the requirement for protein kinase C–delta (PKCδ) in regulating bone resorption by affecting cathepsin K exocytosis. Importantly, PKCδ deficiency does not perturb formation of the ruffled border or trafficking of lysosomal vesicles containing the vacuolar‐ATPase (v‐ATPase). Mechanistically, we find that cathepsin K exocytosis is controlled by PKCδ through modulation of the actin bundling protein myristoylated alanine‐rich C‐kinase substrate (MARCKS). The relevance of our finding is emphasized in vivo because PKCδ?/? mice exhibit increased bone mass and are protected from pathological bone loss in a model of experimental postmenopausal osteoporosis. Collectively, our data provide novel mechanistic insights into the pathways that selectively promote secretion of cathepsin K lysosomes independently of ruffled border formation, providing evidence of the presence of multiple mechanisms that regulate lysosomal exocytosis in osteoclasts. © 2012 American Society for Bone and Mineral Research.