No abstract

The purpose of this review is to summarize the research progress of PI3K/Akt signaling pathway in erythropoiesis and glycolysis. Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) is activated by numerous genes and leads to protein kinase B (Akt) binding to the cell membrane, with the help of phosphoinositide-dependent kinase, in the PI3K/Akt signal transduction pathway. Threonine and serine phosphorylation contribute to Akt translocation from the cytoplasm to the nucleus and further mediates enzymatic biological effects, including those involved in cell proliferation, apoptosis inhibition, cell migration, vesicle transport and cell cancerous transformation. As a key downstream protein of the PI3K/Akt signaling pathway, hypoxia-inducible factor (HIF)-1 is closely associated with the concentration of oxygen in the environment. Maintaining stable levels of HIF-1 protein is critical under normoxic conditions; however, HIF-1 levels quickly increase under hypoxic conditions. HIF-1α is involved in the acute hypoxic response associated with erythropoietin, whereas HIF-2α is associated with the response to chronic hypoxia. Furthermore, PI3K/Akt can reduce the synthesis of glycogen and increase glycolysis. Inhibition of glycogen synthase kinase 3β activity by phosphorylation of its N-terminal serine increases accumulation of cyclin D1, which promotes the cell cycle and improves cell proliferation through the PI3K/Akt signaling pathway. The PI3K/Akt signaling pathway is closely associated with a variety of enzymatic biological effects and glucose metabolism.

Light or heavy oil and water mixtures can by separated selectively with high efficiency using potato residue coated meshes.

The Victoria mode (VM) represents the second dominant mode (empirical orthogonal function, EOF2) of North Pacific variability, independent of the Pacific Decadal Oscillation and is defined as the EOF2 of SST anomalies in the North Pacific poleward of 20°N. The present study indicates that the VM is closely linked to the development of El Niño-Southern Oscillation (ENSO). The VM may effectively act as an ocean bridge (or conduit) through which the extratropical atmospheric variability in the North Pacific influences ENSO. The VM can trigger the onset of ENSO via the following two dominant processes:(1) surface air-sea coupling associated with the VM in the subtropical/tropical Pacific and (2) evolution of subsurface ocean temperature anomalies along the equator associated with the VM. These two processes may force sufficient surface warming to occur in the central eastern equatorial Pacific from spring to summer, which in turn initiates an ENSO event. The VM influence on ENSO relies on a basin-scale air-sea interaction dynamic, as opposed to more local-scale dynamics typically associated with the seasonal footprinting mechanism or Pacific meridional mode. The majority of VM events are followed by ENSO events. These ENSO events triggered by VM include El Niño Modoki (EM) as well as conventional El Niño. There is no evidence that the VM tends to be more conducive to the initialization of EM than conventional El Niño.

The diagnosis of testicular germ cell tumors (GCTs) sometimes can be challenging without ancillary markers. Here we performed an immunohistochemical study of a novel stem cell marker SALL4 in a large series of 110 primary testicular GCTs (65 pure and 45 mixed) containing the following types of tumors and/or tumor components: 50 intratubular germ cell neoplasias (ITGCNs), 62 classic seminomas, 2 spermatocytic seminomas, 39 embryonal carcinomas (EC), 5 pediatric and 26 postpubertal yolk sac tumors (YST), 7 pediatric and 25 postpubertal teratomas, and 5 choriocarcinomas. We compared SALL4 with OCT4 in all GCTs, and SALL4 to alpha-fetoprotein (AFP) and glypican-3 in all YSTs. To test SALL4 specificity, 23 testicular non-GCTs (10 Leydig cell tumors, 4 Sertoli cell tumors, 3 adenomatoid tumors, 3 paratesticular rhabdomyosarcomas, 2 diffuse large B-cell lymphomas, and 1 rete testis papillary cystadenoma) and 275 nontesticular tumors (158 metastatic carcinomas, 12 metastatic melanomas, 11 primary and 2 metastatic mesotheliomas, and 72 primary and 20 metastatic sarcomas) were also stained for SALL4. All ITGCNs, classic seminomas, and ECs demonstrated strong SALL4 and OCT4 staining in more than 90% tumor cells. All 31 YSTs (5 pediatric and 26 postpubertal) showed strong positive SALL4 staining in more than 90% tumor cells but had negative OCT4 staining. Both spermatocytic seminomas showed positive SALL4 staining in 80% to 95% tumor cells in all 3 types of tumor cells with weak-to-moderate staining intensity. Mononucleated trophoblastic cells were variably positive for SALL4 staining in all 5 choriocarcinomas. Focal SALL4 staining was seen in 4 of 7 pediatric and 23 of 27 postpubertal teratomas. OCT4 staining was not seen in any spermatocytic seminoma, choriocarcinoma, or teratoma. No SALL4 staining was seen in all 23 testicular non-GCTs. Of 275 nontesticular tumors, only 10 carcinomas and 1 sarcoma showed focal (<25% tumor cells) weak SALL4 staining. The only non-neoplastic cells within the testis stained with SALL4 were spermatogonia and few primary spermatocytes. AFP staining was seen in 29 of 31 YST but it was often focal and patchy. Although all 31 YSTs showed glypican-3 staining, 14 (45%) show staining in less than 30% tumor cells. Our findings indicate that SALL4 is a novel sensitive and relatively specific marker for testicular GCTs. SALL4 is a more sensitive marker than AFP and glypican-3 for YST.