Isolation and characterization of the E2F-like gene in plants11The sequences reported in this paper have been deposited in the GenBank database (accession numbers AB025347 for NtE2F and AB025029 for tobacco PCNA).

AbstractThe transcription factor E2F regulates the expression of genes involved in the progression of G1/S transition and DNA replication in mammalian cells. We cloned and characterized a cDNA (NtE2F) corresponding to a E2F homolog of tobacco (Nicotiana tabacum). The transcription of NtE2F was induced as cells progressed from G1 to the S phase and expressed much earlier than that of the proliferating cell nuclear antigen (PCNA) gene. We demonstrated that NtE2F can interact with the tobacco retinoblastoma (Rb)-related protein in a yeast two-hybrid assay. To further characterize NtE2F, the trans-activation activity of NtE2F was examined by using a transient assay in the tobacco Bright Yellow-2 (BY-2) cells with NtE2F fused to the DNA-binding domain of the yeast transcriptional activator GAL4. NtE2F activated the transcription of the β-glucuronidase (GUS) reporter gene driven by a cauliflower mosaic virus (CaMV) 35S core promoter containing the GAL4-binding sequence. This is the first report of the identification of a functionally equivalent E2F-like gene in plants

Methodology for Analyzing Coupling Mechanisms in RFI Problems based on PEEC

In This Article, a Method for Analyzing Coupling Mechanisms in Radio Frequency Interference (RFI) Problems is Proposed. the Partial Element Equivalent Circuit (PEEC) Method is First Used to Derive the Retarded Inductances and Capacitances between Different Mesh Cells. with the Introduction of a Novel Partitioning Algorithm, the Capacitive Coupling and Inductive Coupling between Arbitrary Layout Parts Can Be Quantified based on the Magnitude of the Displacement Current and Induced Voltage Drop. the Accuracy of the PEEC Models is Validated by Comparison with Different Commercial Tools. the Proposed Coupling Mechanism Analysis Flow Provides a Useful Prelayout Tool for RFI Risk Analysis

Generation of mouse models for type 1 diabetes by selective depletion of pancreatic beta cells using toxin receptor-mediated cell knockout

AbstractBy using the toxin receptor-mediated cell knockout (TRECK) method, we have generated two transgenic (Tg) murine lines that model type 1 (insulin-dependent) diabetes. The first strain, C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg, carries the diphtheria toxin receptor (hDTR) driven by the human insulin gene promoter, while the other strain, C57BL/6-ins2(BAC)-TRECK-Tg, expresses hDTR cDNA under the control of the mouse insulin II gene promoter. With regard to the C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg strain, only one of three Tg strains exhibited proper expression of hDTR in pancreatic β cells. By contrast, hDTR was expressed in the pancreatic β cells of all four of the generated C57BL/6-ins2(BAC)-TRECK-Tg strains. Hyperglycemia, severe ablation of pancreatic β cells and depletion of serum insulin were observed within 3days after the administration of diphtheria toxin (DT) in these Tg mice. Subcutaneous injection of a suitable dosage of insulin was sufficient for recovery from hyperglycemia in all of the examined strains. Using the C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg model, we tried to perform regenerative therapeutic approaches: allogeneic transplantation of pancreatic islet cells from C57BL/6 and xenogeneic transplantation of CD34+ human umbilical cord blood cells. Both approaches successfully rescued C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg mice from hyperglycemia caused by DT administration. The high specificity with which DT causes depletion in pancreatic β cells of these Tg mice is highly useful for diabetogenic research

Potential therapeutic applications of targeting signal-transducing adaptor protein-2 in autoimmune diseases

Adaptor proteins are involved in various immune responses via the modulation of many signaling pathways. Signal-transducing adaptor protein-2 (STAP-2) is an adaptor protein that contains typical domains such as the pleckstrin homology (PH) domain, Src homology domain, and a proline-rich region from the N-terminal region. In T cells, STAP-2 positively regulates T cell receptor (TCR)-mediated signaling by associating with CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (LCK). Therefore, a peptide that inhibits the interaction between STAP-2 and CD3ζ ITAMs is likely to suppress TCR-mediated T cell activation, as well as T cell-mediated diseases. As expected, the peptide successfully inhibited the STAP-2/CD3ζ ITAM interaction and suppressed TCR-mediated signaling, cell proliferation, and interleukin (IL)-2 production in human/murine T cells. Furthermore, this inhibitor suppressed the pathogenesis of experimental autoimmune encephalomyelitis (EAE), which is widely recognized as a mouse model of multiple sclerosis, via the downregulation of T cell activation and infiltration of T helper (Th) 1/Th17 cells. These results suggest a new strategy for the treatment of multiple sclerosis and other immune diseases

A Case of Intestinal Obstruction Secondary to a Strangulated Obturator Hernia in an Elderly Woman

In this report, we present a case of intestinal obstruction secondary to a strangulated obturator hernia in an elderly woman. An 88-year-old woman was admitted to our hospital because she had been experiencing abdominal pain and vomiting for 24h. Her abdomen was distended, and bowel sounds indicating obstruction were heard on auscultation. Diffuse abdominal tenderness was present, but no palpable masses were apparent. The diagnosis of an obturator hernia was confirmed preoperatively by computed tomography. During the emergency laparotomy, the incarcerated intestine was reduced and removed. The obturator foramen was repaired using a simple suture. The patient recovered completely and was discharged seven days after the surgical procedure because no postoperative complications occurred. An early diagnosis and prompt surgical treatment are important to reduce the morbidity and mortality associated with an obturator hernia

Signal-transducing adaptor protein-2 modulates T-cell functions

Immune responses are orchestrated by controlling the initiation, magnitude, and duration of various signaling pathways. Adaptor proteins act as positive or negative regulators by targeting critical molecules of signaling cascades. Signal-transducing adaptor protein-2 (STAP-2) contains typical features of adaptor proteins, like a pleckstrin homology (PH) domain in the N-terminal region and a Src homology 2 (SH2) domain in the central region. STAP-2 binds to a variety of signaling or transcriptional molecules to control multiple steps of inflammatory/immune responses. STAP-2 enhances T-cell receptor (TCR)-mediated signaling via the association with TCR-proximal CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (Lck). STAP-2 decreases adherence of T-cells to fibronectin (FN) through an association with focal adhesion kinase (Fak) and Casitas B-lineage Lymphoma (c-Cbl), and increases chemotaxis of T-cells toward stromal cell-derived factor-1α (SDF-1α) through interactions with Vav1 and Ras-related C3 botulinum toxin substrate 1 (Rac1). STAP-2 positively regulates activation-induced cell deathrough the association with Fas and caspase-8. This review describes the current knowledge of the roles of STAP-2 in T-cell-dependent immune responses and the possible clinical utility of STAP-2-targeting therapies