OBJECTIVE: To evaluat the effects of a culture medium with glucose in the presence of glutamine on the development of mouse embryos. METHODS: Two-cell embryos recovered from ICR mice at 48 hrs after hCG injection (mated just after hCG injection) were cultured in DMEM (with 20% hFF) supplemented with or without glucose on the presence of glutamine. Embryos were cultured under three different glucose regimens: (1) 0 mM (control); (2) 0.5 mM (group I); or (3) 3.15 mM (group II), and were analyzed at 24, 48, 72 and 96 hours intervals. Chi-square test (x2-test) was used to compare values of groups. RESULTS: No differences were found in the number of embryos showing morula (control: 37.5%; group I: 51.0%; group II: 48.4%), blastocyst (control: 21.5%; group I: 33.3%; group II: 34.4%) and blastocyst and hatching or hatched blastocyst (control: 81.9%; group I: 83.3%; group II: 82.8%) between groups at 24 hrs, 48 hrs or 72 hrs respectively. However at 96 hrs, the number of hatched and attached blastocyst was significantly higher in group I (82.3%) and II (78.5%) than control (63.2%; P<0.05). CONCLUSION: The addition of glucose (0.5 mM) to the DMEM, as energy source, improved the rate of development of late stage embryos in mice.
Animals ; Blastocyst ; Eagles* ; Embryonic Development* ; Embryonic Structures* ; Female ; Glucose* ; Glutamine* ; Mice* ; Mice, Inbred ICR ; Morula ; Pregnancy

No abstract available.
Female ; Hydatidiform Mole* ; Pregnancy

No abstract available.
Busan* ; Eclampsia* ; Female ; Pregnancy ; Singing*

In treating young women for gestational trophoblastic tumor ( G.T.T. ), all efforts are made to preserve fertility and hysterectomy is avoided unless absolutely essential. However, in some cases the operation may be lifesaving. During the last 20 years among the 310 cases of G.T.T. treated at Il Sin Christian Hospital, there were 3 cases in which hysterectomy was avoided by the excision of a localized uterine lesion thus preserving fertility.
Choriocarcinoma* ; Female ; Fertility ; Humans ; Hysterectomy ; Pregnancy ; Trophoblastic Neoplasms

BACKGROUND: Over activation of the DNA repairing enzyme, poly (ADP-ribose) polymerase (PARP) in response to oxidative damage of DNA appears to play a role in cellular death in neurodegenerative diseases. Previous data suggested that PARP immunoreactivity (IR) was increased in the white and gray matter in spinal cord of the sporadic amyotrophic lateral sclerosis (sALS), predominantly in cells with astroglial morphology. METHODS: In the present study, we evaluated whether the PARP expression was present widespread in various regions of brain tissue including the motor cortex, parietal cortex and cerebellum. RESULTS: By western blot, PARP-IR in motor cortex from sALS patients, compared to the same region from age-matched normal controls, was also significantly increased (p=0.006). Importantly, PARP-IR was also increased in the parietal cortex, and cerebellum of sALS patients compared to the controls, in regions that are usually clinically unaffected in ALS (p=0.043, p=0.035, respectively). In addition, increased PARP expression in ALS was more prominent compared to Alzheimer's brain. Immunohistochemistry revealed that PARP staining was more significant in the cortical neurons and in the subcortical white matter glial cells from sALS patients compared to normal controls and Alzheimer's disease. CONCLUSIONS: The data demonstrate that increase in PARP-IR is not limited only to the vulnerable motor cortex. Furthermore, PARP-IR is present in both cortical neuronal and subcortical glial cells. The data suggest that widespread cellular stress on neuronal and glial cells is present in the brain of sporadic ALS patients.
Alzheimer Disease ; Amyotrophic Lateral Sclerosis* ; Blotting, Western ; Brain* ; Cerebellum ; DNA ; DNA Repair ; Humans ; Immunohistochemistry ; Motor Cortex ; Motor Neurons ; Neurodegenerative Diseases ; Neuroglia ; Neurons* ; Rabeprazole ; Spinal Cord

Viriditoxin is a fungal metabolite isolated from Paecilomyces variotii, which was derived from the giant jellyfish Nemopilema nomurai. Viriditoxin was reported to inhibit polymerization of FtsZ, which is a key protein for bacterial cell division and a structural homologue of eukaryotic tubulin. Both tubulin and FtsZ contain a GTP-binding domain, have GTPase activity, assemble into protofilaments, two-dimensional sheets, and protofilament rings, and share substantial structural identities. Accordingly, we hypothesized that viriditoxin may inhibit eukaryotic cell division by inhibiting tubulin polymerization as in the case of bacterial FtsZ inhibition. Docking simulation of viriditoxin to beta-tubulin indicated that it binds to the paclitaxel-binding domain and makes hydrogen bonds with Thr276 and Gly370 in the same manner as paclitaxel. Viriditoxin suppressed growth of A549 human lung cancer cells, and inhibited cell division with G2/M cell cycle arrest, leading to apoptotic cell death.
Apoptosis* ; Cell Cycle Checkpoints* ; Cell Cycle* ; Cell Death ; Cell Division ; Eukaryotic Cells ; GTP Phosphohydrolases ; Humans* ; Hydrogen ; Lung Neoplasms* ; Lung* ; Paclitaxel ; Paecilomyces ; Polymerization ; Polymers ; Tubulin

Colorectal cancer is one of the most common cancers globally, ranking second for the number of cancer-related deaths. Metastasis has been reported as the main cause of death in patients with colorectal cancer. Peroxisome proliferator-activated receptor gamma (PPAR-γ) is a transcription factor that functions as a tumor suppressor by inhibiting cellular proliferation, migration, and invasion. In our previous efforts to generate natural product-motivated PPAR-γ ligands, the compounds 1 and 2 were obtained. These compounds activated PPAR-γ and inhibited the migration and invasion of HCT116 colorectal cancer cells, and they were also found to inhibit the epithelial-to-mesenchymal transition, which is a key process in cancer metastasis. Compounds 1 and 2 upregulated expression of the epithelial marker (E-cadherin), and downregulated expression of the mesenchymal marker (N-cadherin) and transcriptional factor (Snail). Therefore, the PPAR-γ agonists 1 and 2 could serve as a valuable model for the study on anti-metastatic leads for the treatment of colorectal cancer.

BACKGROUND: The evidence for increased oxidative stress and DNA damage in amyotrophic lateral sclerosis (ALS) prompted studies to determine if the expression of poly (ADP-ribose) polymerase (PARP) is increased in ALS. METHOD: Twenty Spinal cord specimens were obtained at the autopsy of sALS patients (n=11) and age-matched controls with non-neurological diseases (n=9). RESULTS: Using western analyses of postmortem tissue, we demonstrated that PARP-immunoreactivity (PARP-IR) was increased three-fold in spinal cord tissues of sporadic ALS (sALS) patients compared with non-neurological disease controls. Despite the increased PARP-IR, PARP mRNA expression was not increased significantly. Immunohistochemical analyses revealed PARP-IR was increased in both white and gray matter of sALS spinal cord. While PARP-IR was predominantly seen in astrocytes, large motor neurons displayed reduced staining compared with the controls. PARP-IR was increased in the pellet fraction of sALS homogenates compared with the control homogenates, representing potential PARP binding to chromatin or membranes and suggesting a possible mechanism of PARP stabilization. CONCLUSIONS: The present results demonstrate glial alterations in sALS tissue and support the role of glial alterations in sALS pathogenesis.
Amyotrophic Lateral Sclerosis* ; Astrocytes* ; Autopsy ; Chromatin ; DNA Damage ; Humans ; Membranes ; Motor Neurons* ; Oxidative Stress ; RNA, Messenger ; Spinal Cord*

Rhino-orbital mucormycosis is the most frequently fatal fungal infection commonly occurring in patients with poorly controlled diabetes mellitus and and those who are immunocompromised, and requires prompt treatment. We describe a case of rhino-or-bital mucormycosis with orbital cellulitis and paranasal sinusitis, as seen on initial MR images, which on follow-up images had evol ved to orbitofacial infarction. MR imaging was useful for the demonstration of orbitofacial infarction, seen as areas of lack of enhancement and thus suggesting vascular invo l vement by mucor hyphae.
Diabetes Mellitus ; Follow-Up Studies ; Humans ; Hyphae ; Infarction* ; Magnetic Resonance Imaging* ; Mucor ; Mucormycosis* ; Orbital Cellulitis ; Sinusitis

Checkpoint kinase 1 (Chk1) and Chk2 are effector kinases in the cellular DNA damage response and impairment of their function is closely related to tumorigenesis. Previous studies revealed several substrate proteins of Chk1 and Chk2, but identification of additional targets is still important in order to understand their tumor suppressor functions. In this study, we screened novel substrates for Chk1 and Chk2 using substrate target motifs determined previously by an oriented peptide library approach. The potential candidates were selected by genome-wide peptide database searches and were examined by in vitro kinase assays. ST5, HDAC5, PGC-1alpha, PP2A PR130, FANCG, GATA3, cyclin G, Rad51D and MAD1alpha were newly identified as in vitro substrates for Chk1 and/or Chk2. Among these, HDAC5 and PGC-1alpha were further analyzed to substantiate the screening results. Immunoprecipitation kinase assay of full-length proteins and site-directed mutagenesis analysis of the target motifs demonstrated that HDAC5 and PGC-1alpha were specific targets for Chk1 and/or Chk2 at least in vitro.
Amino Acid Motifs ; Amino Acid Sequence ; *Consensus Sequence ; Genome, Human/*genetics ; Heat-Shock Proteins/chemistry/metabolism ; Histone Deacetylases/chemistry/metabolism ; Humans ; Molecular Sequence Data ; Peptide Fragments/chemistry/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Substrate Specificity ; Transcription Factors/chemistry/metabolism