Hydranencehaly is an abnormality consisting of complete or almost absence of the cerebral hemispheres, which are replaced by a large fluid-filled cavity. The midbrain and brain stem are relatively intact, and rudiments of frontal, temporal and occipital cortex may be present. We diagnosed it through the evaluation of clinical features, prenatal US (intrauterine pregnancy, 37 wks) and brain CT. Authors have experienced a case of hydranencephaly combined with twin pregnancy and reported with a brief literature review.
Brain ; Brain Stem ; Cerebrum ; Humans ; Hydranencephaly* ; Mesencephalon ; Pregnancy ; Pregnancy, Twin* ; Twins*

Higenamine was widely used as traditional remedy for the treatment of rheumatoid arthritis. Nitric oxide (NO) may be a critical mediator in this inflammatory disease. Synovial tissue from humans with inflammatory arthritis expresses NOS2 (iNOS) mRNA and protein, and generates NO in vitro. We therefore, investigated the effect of higenamine on the induction of nitric oxide synthase (NOS) promoted by lipopolysaccharide (LPS). Prophylactic application of higenamine selectively prevented LPS-primed initiation of L-arginine-induced relaxation and restored phenylephrine(PE)-induced contraction in rat aorta. LPS-stimulated nitrite production in the incubation medium was reduced by higenamine. Furthermore, RT-PCR and Northern analysis indicated that higenamine reduced iNOS expression primed by LPS in rat aorta. These results suggest that higenamine prevents LPS-promoted induction of NOS in vascular smooth muscle.
Animals ; Aorta* ; Arthritis ; Arthritis, Rheumatoid ; Humans ; Muscle, Smooth, Vascular ; Nitric Oxide ; Nitric Oxide Synthase ; Rats* ; Relaxation ; RNA, Messenger*

Duodenal abscess is a rarely reported disease throughout the entire world. Duodenal abscesses are developed mostly from the complication of duodenal ulcer perforation, and only small percentage of duodenal abscesses are the result of cholecysto-duodenal fistula which was made by gall bladder perforation. We report a 84-year-old male patient who presented to the emergency department with severe anorexia and generalized weakness for 2 weeks. The upper gastrointestinal endoscopy done and revealed a protruding mass at the lesser curvature of the duodenal bulb. As soon as the mass was punched with a biopsy forceps, a large amount of abscess began to pour out into the intestinal lumen. Abdominal CT scan demonstrated the presence of an air-fluid level the in gall bladder and also abscess in the porta hepatitis which was located between the gall bladder and the duodenum. Because the patient refused any surgical intervention, we treated him conservatively with intravenous antibiotics. Patient's symptom of anorexia was slowly resolved, and patient was discharged 10 days later.
Abscess* ; Aged, 80 and over ; Anorexia ; Anti-Bacterial Agents ; Biopsy ; Duodenal Ulcer ; Duodenum ; Emergency Service, Hospital ; Endoscopy ; Endoscopy, Gastrointestinal ; Fistula ; Hepatitis ; Humans ; Male ; Surgical Instruments ; Tomography, X-Ray Computed ; Urinary Bladder

Lysophosphatidic acid (LPA) is a bioactive phospholipids and involves in various cellular events, including tumor cell migration. In the present study, we investigated LPA receptor and its transactivation to EGFR for cyclooxygenase-2 (COX-2) expression and cell migration in CAOV-3 ovarian cancer cells. LPA induced COX-2 expression in a dose-dependent manner, and pretreatment of the cells with pharmacological inhibitors of Gi (pertussis toxin), Src (PP2), EGF receptor (EGFR) (AG1478), ERK (PD98059) significantly inhibited LPA- induced COX-2 expression. Consistent to these results, transfection of the cells with selective Src siRNA attenuated COX-2 expression by LPA. LPA stimulated CAOV-3 cell migration that was abrogated by pharmacological inhibitors and antibody of EP2. Higher expression of LPA2 mRNA was observed in CAOV-3 cells, and transfection of the cells with a selective LPA2 siRNA significantly inhibited LPA-induced activation of EGFR and ERK, as well as COX-2 expression. Importantly, LPA2 siRNA also blocked LPA-induced ovarian cancer cell migration. Collectively, our results clearly show the significance of LPA2 and Gi/Src pathway for LPA-induced COX-2 expression and cell migration that could be a promising drug target for ovarian cancer cell metastasis.
Butadienes/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects/*physiology ; Cyclooxygenase 2/*biosynthesis ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism ; Female ; Flavonoids/pharmacology ; GTP-Binding Protein alpha Subunits, Gi-Go/antagonists & inhibitors/*metabolism ; Humans ; Lysophospholipids/pharmacology ; Nitriles/pharmacology ; Ovarian Neoplasms/metabolism/*pathology ; Pertussis Toxin/pharmacology ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Pyrimidines/pharmacology ; Receptor, Epidermal Growth Factor/antagonists & inhibitors/metabolism ; Receptors, Lysophosphatidic Acid/*metabolism ; Receptors, Prostaglandin E/metabolism ; Signal Transduction ; Transcriptional Activation ; Tyrphostins/pharmacology

HoxB4, a homeodomain-containing transcription factor, is involved in the expansion of hematopoietic stem cells and progenitor cells in vivo and in vitro, and plays a key role in regulating the balance between hematopoietic stem cell renewal and cell differentiation. However, the biological activity of HoxB4 in other cells has not been reported. In this study, we investigated the effect of overexpressed HoxB4 on cell survival under various conditions that induce death, using the Ba/F3 cell line. Analysis of phenotypical characteristics showed that HoxB4 overexpression in Ba/F3 cells reduced cell size, death, and proliferation rate. Moreover, the progression from early to late apoptotic stages was inhibited in Ba/F3 cells subjected to HoxB4 overexpression under removal of interleukin-3-mediated signal, leading to the induction of cell cycle arrest at the G2/M phase and attenuated cell death by Fas protein stimulation in vitro. Furthermore, apoptotic cell death induced by doxorubicin-treated G2/M phase cell-cycle arrest also decreased with HoxB4 overexpression in Ba/F3 cells. From these data, we suggest that HoxB4 may play an important role in the regulation of pro-B cell survival under various apoptotic death environments.
Apoptosis ; Cell Cycle Checkpoints ; Cell Death ; Cell Differentiation ; Cell Line ; Cell Proliferation ; Cell Size ; Cell Survival ; Hematopoietic Stem Cells ; Precursor Cells, B-Lymphoid ; Stem Cells ; Transcription Factors