Chich-Sheng Lin

Functional genomic study on atrial fibrillation using cDNA microarray and two-dimensional protein electrophoresis techniques and identification of the myosin regulatory light chain isoform reprogramming in atrial fibrillation.

Introduction: Functional and structural changes of atrial tissue occur during the natural course of atrial fibrillation (AF), and these changes may contribute to further AF. We investigated the changes in AF tissue using cDNA microarray and two‐dimensional protein electrophoresis techniques.

Intracellular zinc release-activated ERK-dependent GSK-3β–p53 and Noxa–Mcl-1 signaling are both involved in cardiac ischemic-reperfusion injury.

Oxidative stress and nitrosative stress are both suggested to be involved in cardiac ischemia-reperfusion (I/R) injury. Using time-lapse confocal microscopy of cardiomyocytes and high-affinity O2−• and Zn2+ probes, this study is the first to show that I/R, reactive oxygen species (ROS), and reactive nitrogen species (RNS) all cause a marked increase in the [O2−•]i, resulting in cytosolic and mitochondrial Zn2+ release. Exposure to a cell-penetrating, high-affinity Zn2+i chelator, TPEN, largely abolished the Zn2+i release and markedly protected myocytes from I/R-, ROS-, RNS-, or Zn2+/K+ (Zn2+i supplementation)-induced myocyte apoptosis for at least 24 h after TPEN removal. Flavonoids and U0126 (a MEK1/2 inhibitor) largely inhibited the myocyte apoptosis and the TPEN-sensitive I/R- or Zn2+i supplement-induced persistent extracellular signal-regulated kinase 1 and 2 (ERK1/2) phosphorylation, dephosphorylation of p-Ser9 on glycogen synthase kinase 3β (GSK-3β), and the translocation into and accumulation of p-Tyr216 GSK-3β and p53 in, the nucleus. Silencing of GSK-3β or p53 expression was cardioprotective, indicating that activation of the ERK–GSK-3β–p53 signaling pathway is involved in Zn2+-sensitive myocyte death. Moreover, the ERK-dependent Noxa–myeloid cell leukemia-1 (Mcl-1) pathway is also involved, as silencing of Noxa expression was cardioprotective and U0126 abolished both the increase in Noxa expression and in Mcl-1 degradation. Thus, acute upstream Zn2+i chelation at the start of reperfusion and the use of natural products, that is, flavonoids, may be beneficial in the treatment of cardiac I/R injury.

PROGINS Alu sequence insertion is associated with hyperprolactinaemia but not leiomyoma susceptibility

Objective  Leiomyoma and hyperprolactinaemia are both progesterone‐dependent diseases. Hormone‐related genes, such as the progesterone receptor (PGR), might be involved in their pathogenesis.

Leukemia Inhibitory Factor in Follicular Fluid Is Not Related to the Number and Quality of Embryos as Well as Implantation and Pregnancy Rates

Follicular growth and maturation is a complex process regulated by autocrine and paracrine factors. Follicular fluids may affect fertilization and early embryonic development (Ledee-Bataille et al., 2001). Follicular fluid may play an important role in the endocrine balance between the theca and granulosa cells (Ledee-Bataille et al., 2001). Cytokines have been shown to be present in human follicular fluid and have regulatory functions in follicular maturation and subsequent embryo development (Coskun et al., 1998). Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the interleukin-6 family and has different biological actions in various tissue systems. LIF regulates the growth and differentiation of embryonic stem cells, primordial germ cells, peripheral neurons, osteoblasts, adipocytes, and endothelial cells (Murray and Edgar, 2001). It also plays an important role in the physiology of ovulation, estrogen production, and early embryonic development (Arici et al., 1997). LIF is one of the key determinants of successful implantation (Arici et al., 1997). Follicular fluid LIF also enhances the rate of blastocyst formation (Dunglison et al., 1996). Follicular fluid LIF is a useful marker of oocyte quality (Arici et al., 1997). The rising level of follicular fluid LIF around the time of ovulation indicates that LIF may play a role in ovulatory events, early embryonic development, and

CAPS genomic subtyping on Orthomyxoviridae

The Orthomyxoviridae is a family of single strained RNA viruses including five genera: Influenza virus A, Influenza virus B, Influenza virus C, Thogotovirus, and Isavirus. Usually, Influenza viruses are identified by antigenic differences in their nucleoprotein and matrix protein. In this paper, we propose an algorithm to determine a set of suitable restriction enzymes for producing recognizable restriction maps on Orthomyxoviridae. Our method is applied to viral strains of highly pathogenic avian influenza (HPAI), containing potentially homozygous, heterozygous, and various genetic variations. In the analysis of CAPS (Cleaved Amplified Polymorphic Sequence) subtyping, our method outperforms the RNA coding of representative and epidemiologically significant human wild-type viruses, including H3N8, H5N1, H5N9, H7N1, H7N7, and H9N2. These isolates are analyzed by CAPS with enzymes AgeI, EciI, KpnI, and XbaI. The HPAI strains show a different RFLP (Restriction Fragment Length Polymorphism) profile by comparing with other low pathogenic avian influenza (LPAI) strains. We provide a rapid, specific, and reproducible identification of the genotypes on Orthomyxoviridae. It permits us to quickly confirm subtypes of Orthomyxoviridae.