Comparison of the treadmill exercise score and single-photon emission computed tomographic thallium imaging in risk assessment

Background  

This study compared the prognostic value of exercise single-photon emission computed tomographic (SPECT) thallium imaging with that of treadmill exercise score in medically treated patients with coronary artery disease (CAD)     

Solitary Small Hepatic Angiosarcoma: Initial and Follow-up Imaging Findings

We report an uncommon case of solitary, small hepatic angiosarcoma that was initially considered as a hemangioma. We present the imaging findings, with an emphasis on the initial and follow-up CT and MR findings, as well as report on the more suggestive findings of angiosarcoma than those of a hemangioma.     

Comparative analysis of NK/T-cell lymphoma and peripheral T-cell lymphoma in Korea: Clinicopathological correlations and analysis of EBV strain type and 30-bp deletion variant LMP1

Natural killer/T-cell lymphoma (NKTL) and peripheral T-cell lymphomas (PTCL) are prevalent in the Asian population and exhibit a high association with the Epstein-Barr virus (EBV). Moreover, differentiation of these two groups is often difficult and problematic. We investigated 35 cases of NKTL (22 nasal cases and 13 extranasal cases) and 30 cases of PTCL in terms of their clinical features, immunohistology, EBV positivity, EBV strain-type polymorphism and latent membrane protein 1 (LMP1) deletion variant distribution. Eighteen cases (82%) of nasal NKTL and seven (54%) of extranasal NKTL showed EBV positivity by EBV in situ hybridization. Fifteen cases (50%) of PTCL revealed EBV positivity. EBV strain type A was predominant in NKTL (18:5), and EBV strain types A and B were distributed evenly in PTCL (6:6). EBV-positive patients had significantly shorter survival than EBV-negative patients (P < 0.05), and EBV positivity correlated with advanced clinical stage (P < 0.05). Patients harboring type A EBV showed slightly poorer prognoses than those having type B, though it was not obviously statistically different (P = 0.07). The LMP1 deletion variant was prevalent in both NKTL (three wild-type LMP1, 15 deletion variants) and PTCL (three wild-type LMP1, eight deletion variants, two coexistent forms) patients, but did not have prognostic impact. Our results indicate that EBV acts as a negative prognostic factor in NKTL and PTCL, and that the intrinsic properties of a specific viral strain might influence the clinical behavior of these diseases.     

Detection of YMDD motif mutants by oligonucleotide chips in lamivudine-untreated patients with chronic hepatitis B virus infection

Lamivudine, a nucleoside analogue, has been used widely as an effective antiviral agent for the treatment of patients with chronic hepatitis B virus (HBV) infection. However, the YMDD motif mutation of HBV polymerase resistant to lamivudine occurs very frequently after long term therapy. We developed an oligonucleotide chip for the detection of YMDD motif mutants resistant to lamivudine and investigated the prevalence of the mutants in patients with chronic HBV infection who had not been treated by lamivudine before. Forty patients who had not been treated with lamivudine were included in this study. Serum samples were tested by the oligonucleotide chips designed for detection of wild-type YMDD motif, M552V and M552I. Samples were confirmed by restriction fragment length polymorphism (RFLP) and direct sequencing. M552I mutants were detected by the oligonucleotide chips in 7.5% (3/40) of chronic HBV infected patients (2 chronic hepatitis and 1 cirrhosis). The results were in accordance with those of RFLP. YMDD motif mutants occur as natural genome variabilities in patients with chronic HBV infection who had not been treated with lamivudine before. Oligonucleotide chip technology is a reliable and useful diagnostic tool for the detection of mutants resistant to antiviral therapy in chronic HBV infection.     

Muscularity in adult humans: Proportion of adipose tissue‐free body mass as skeletal muscle

Muscularity, or the proportion of adipose tissue‐free body mass (ATFM) as skeletal muscle (SM), provides valuable body composition information, especially for age‐related SM loss (i.e., sarcopenia). Limited data from elderly cadavers suggest a relatively constant SM/ATFM ratio, 0.540 ± 0.046 for men (mean ± SD, n = 6) and 0.489 ± 0.049 for women (n = 7). The aim of the present study was to examine the magnitude and constancy of the SM/ATFM ratio in healthy adults. Whole‐body SM and ATFM were measured using multi‐scan magnetic resonance imaging. The SM/ATFM ratio was 0.528 ± 0.036 for men (n = 139) and 0.473 ± 0.037 for women (n = 165). Multiple regression analysis indicated that the SM/ATFM ratio was significantly influenced by sex, age, body weight, and race. The four factors explained 50% of the observed between individual variation in the SM/ATFM ratio. After adjusting for age, body weight, and race, men had a larger SM/ATFM ratio than women. Both older men and women had a lower SM/ATFM ratio than younger subjects, although the relative reduction was greater in men. After adjustment for sex, age, and body weight, there were no significant differences in the SM/ATFM ratios between Asian, Caucasian, and Hispanic subjects. In contrast, African‐American subjects had a significantly greater SM/ATFM ratio than subjects in the other three groups. In addition, the SM/ATFM ratio was significantly lower in AIDS patients than corresponding values in healthy subjects. Am. J. Hum. Biol. 13:612–619, 2001. © 2001 Wiley‐Liss, Inc.     

Effect of Alkyl Groups of Latent Cationic Catalysts on Cure and Dynamic Mechanical Behaviors of Epoxy Resins

Summary: The latent thermal cationic initiators, benzyl‐2,5‐dimethylpyrazinium hexafluoroantimonate (BDPH) and benzyl‐2‐ethylpyrazinium hexafluoroantimonate (BEPH), were synthesized to investigate the effect of substituted alkyl groups on cure and dynamic mechanical behaviors of difunctional epoxy system. The cure temperature and activation energy of the diglycidyl ether of bisphenol A (DGEBA)/BDPH were higher than those of the DGEBA/BEPH, resulting from the steric hindrance of the substituted groups. The cross‐linking density of the DGEBA/BDPH was higher than that of the DGEBA/BEPH, whereas the T_g's of both specimens are similar. This may be explained by the free volume and the intermolecular hydrogen bonding induced by the hydrogen of the substituted methyl groups. Consequently, the position and number of the substituted groups of the latent thermal initiator were very important in the control of the latent thermal and dynamic mechanical behaviors of the epoxy resin.

Dynamic DSC curves of DGEBA cured by each initiator.     

Extracellular matrix activity and caveolae events contribute to cell surface receptor activation that leads to MAP kinase activation in response to UV irradiation in cultured human keratinocytes

Activation of cell surface components has been implicated in the activation of downstream signaling cascade in response to UV irradiation, and yet the identity and the interaction of those components have been scantly documented. Accumulating evidence indicates that caveolae encapsulating caveolins is the location for those interactions. We found in cultured human keratinocytes that UV irradiation induced both caveolin-1 and EGFR phosphorylation. Filipin, a caveolae disruptive agent, inhibited UV-induced caveolin-1 activation. Na+-K+-ATPase catalyzes active transport of Na+ and K+ across plasma membrane of mammalian cells, inactivation of which has recently been shown to be involved in the activation of signal transduction pathways including MAP kinase cascade. We found in this study that UV inactivated Na+-K+-ATPase in time-dependent manner, Na+-K+-ATPase activity started to decrease 5 min post UV irradiation and reduced to 60% of its original activity within 1 h. Pretreatment with Flipin and MMP inhibitor recovered Na+-K+-ATPase activity lost by UV irradiation. ECIS analysis indicated that both EGF treatment and UV irradiation increased membrane electric activity which was inhibited by MMP inhibitor and Filipin. Further study showed that pretreatment of human keratinocytes with MMP inhibitor or Filipin inhibited UV-induced phosphorylation of p38 and JNK, which was however not observed in LnCap cells, a prostate cancer cell line lacking caveolin-1. UV irradiation also induced ectodomain shedding of HB-EGF in a time-dependent manner in keratinocytes. Collectively, we conclude that UV-induced MAP kinase activation is mediated by cell surface receptor activation due to the matrix activity and membrane caveolae function and inactivation of Na+-K+-ATPase.     

Novel HLA-A*11 allele, A*1120, identified by sequence-based typing

In this report, we describe the identification of a human leucocyte antigen-A*11 (HLA-A*11) nucleotide sequence variant, a new HLA-A*1120 by using sequence-based typing (SBT). The new allele was detected during routine HLA typing by high-resolution SBT. Allele A*1120 showed one nucleotide difference with A*110101 at codon 152 (GCG-->GAG) resulting in an amino acid change from alanine to glutamate. Residue 152 is located on alpha(2)-helix of HLA class I molecule and involved in peptide binding by constructing E pocket of peptide-binding groove, implying that the change of the residue 152 would affect the binding affinity of peptides to A*1120 allele.     

Werner helicase relocates into nuclear foci in response to DNA damaging agents and co-localizes with RPA and Rad51

BACKGROUND: Werner syndrome (WS) is an autosomal recessive disorder with many features of premature ageing. Cells derived from WS patients show genomic instability, aberrations in the S-phase and sensitivity to genotoxic agents. The gene responsible for WS (WRN) encodes a DNA helicase belonging to the RecQ helicase family. Although biochemical studies showed that the gene product of WRN (WRNp) interacts with proteins that participate in DNA metabolism, its precise biological function remains unclear. RESULTS: Using immunocytochemistry, we found that WRNp forms distinct nuclear foci in response to DNA damaging agents, including camptothecin (CPT), etoposide, 4-nitroquinolin-N-oxide and bleomycin. The presence of aphidicolin inhibited CPT-induced WRNp foci strongly but not bleomycin-induced foci. These WRNp foci overlapped with the foci of replication protein A (RPA) almost entirely and with the foci of Rad51 partially, implicating cooperative functions of these proteins in response to DNA damage. We also found that WRNp foci partially co-localize with sites of 5-bromo-2'-deoxy-uridine incorporation. CONCLUSIONS: These findings suggest that WRNp form nuclear foci in response to aberrant DNA structures, including DNA double-strand breaks and stalled replication forks. We propose that WRNp takes part in the homologous recombinational repair and in the processing of stalled replication forks.