Recent advances in molecular technology have revolutionized research on all aspects of the biology of organisms, including ciliates, and created unprecedented opportunities for pursuing a more integrative approach to investigations of biodiversity. However, this goal is complicated by large gaps and inconsistencies that still exist in the foundation of basic information about biodiversity of ciliates. The present paper reviews issues relating to the taxonomy of ciliates and presents specific recommendations for best practice in the observation and documentation of their biodiversity. This effort stems from a workshop that explored ways to implement six Grand Challenges proposed by the International Research Coordination Network for Biodiversity of Ciliates (IRCN‐BC). As part of its commitment to strengthening the knowledge base that supports research on biodiversity of ciliates, the IRCN‐BC proposes to populate The Ciliate Guide, an online database, with biodiversity‐related data and metadata to create a resource that will facilitate accurate taxonomic identifications and promote sharing of data.

The collapse potential, mineralogy, microstructure, and particle morphology of a loess from the Loess Plateau, China, were characterized by double oedometer testing, X-ray diffraction, scanning electron microscopy with energy-dispersive X-ray spectroscopy, and image analysis to elucidate the origin of its collapse behavior. Results show that the loess is highly collapsible with a maximum collapse index of 6.7% at a vertical stress of ∼200 kPa. The deposit contains both nonclay (i.e., quartz, albite, muscovite, and calcite) and clay (i.e., two chlorites) minerals. Microstructural, chemical, and image analyses indicate that interparticle calcite and clay cementation and silt particle morphology render the intact soil a metastable structure. Wetting-induced collapse is attributed to both primary and secondary microstructure features. The former is the abundance of weakly cemented, unsaturated, porous pure clay and clay–silt mixture aggregates whose slaking upon wetting initiates the overall structural collapse, while the latter consists of high porosity, unstable particle contacts, and clay coating on silt particles that act synergistically to augment the collapse. A conceptual microstructural model of a four-tiered hierarchy (i.e., primary clay and silt particles, clay aggregates and clay-coated silt particles, clay–silt mixture aggregates, and cemented aggregate matrix) is proposed to represent its structural characteristics and to account for its high collapsibility.

Cisplatin is widely used for the treatment of solid tumours including small cell lung cancers, but its success is often compromised by relapse and resistance to further treatment. Extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt are two major cell survival pathways that are upregulated and activated in lung cancer tissues. Phosphorylated ERK1/2 (p-ERK1/2) and Akt (p-Akt) can be further stimulated by chemotherapeutics in cancer cells. Although individually targeting the ERK1/2 or Akt pathway has been reported to sensitize cancer cells to therapy, the effect of concurrently blocking these two pathways on the sensitivity of lung cancer cells to cisplatin has not been investigated. In the present study, we aimed to determine whether the ERK1/2 and Akt pathways contribute to cisplatin resistance in human small cell lung cancer A549 cells. The results showed that cisplatin activates p-ERK1/2 and p-Akt in A549 cells. Blockade of either of these pathways with chemical inhibitors moderately sensitized A549 cells to cisplatin-induced apoptosis and reduced cell viability. Strikingly, concurrent inhibition of p-ERK1/2 and p-Akt significantly potentiated cisplatin cytotoxicity in vitro and in vivo. The sensitization of A549 cells to cisplatin cytotoxicity induced by p-Akt inhibition was mediated by the upregulation of PUMA, whereas that induced by p-ERK1/2 inhibition occurred by Bcl-2 downregulation. These data indicate that the cooperative effects of p-ERK1/2 and p-Akt on attenuating cisplatin cytotoxicity are mediated by PUMA and Bcl-2 regulation, and concurrently blocking these pathways may be an effective strategy for improving the efficacy of cisplatin as anticancer treatment.

Background/Aims: Several studies have shown secreted clusterin (sCLU) silencing directed against sCLU mRNA in sCLU-rich lung cancer cell lines sensitized cells to chemotherapy. However, the molecular mechanisms underlying the effect of sCLU silencing on lung cancer cell chemosensitivity is not known. In the present study, we aimed to determine that vector expressing short hairpin RNA against sCLU RNA (sCLU-shRNA) enhances the chemosensitivity in human small cell lung cancer A549 cells in vitro by inhibition of phosphorylated ERK1/2 (p-ERK1/2) and Akt (p-Akt). Methods: The pCDNA3.1-sCLU and control scrambled pCDNA3.1 plasmid was constructed. We investigated the effects of sCLU overexpression by pCDNA3.1-sCLU transfection on chemosensitivity to cisplatin (DDP) in A549 cells in vitro. We down-regulated sCLU expression by short hairpin RNA against sCLU RNA (sCLU-shRNA) and investigated the effects on chemosensitivity to DDP in A549 cells and A549^DDPin vitro. In order to confirm the correlation between sCLU and AKT and ERK1/2 signals, cells were treated with wortmannin and U0126. Results: We found the chemotherapeutic agent DDP activated sCLU. Overexpression of sCLU increased cellular DDP chemoresistance in the A549^DDP and pCDNA3. 1-sCLU transfected A549 cells via inhibition DDP-induced apoptosis. Whereas sCLU knockdown induced chemosensitization in the S549 and A549^DDP cells via increase of DDP-induced apoptosis. sCLU overexpression activated pAKT Ser⁴⁷³ and pERK1/2^{Thr202/Tyr204}, and vice versa. Inhibition of pAKT Ser⁴⁷³ and pERK1/2^{Thr202/Tyr204} was sufficient to induce significant recover y in chemosensitivity to DDP in A549^DDP in the presence of sCLU overexpression. The DDP activated sCLU, which directly regulated pAKT and pERK1/2. Conclusions: This novel finding suggests that therapies directed against sCLU and its downstream signaling targets pAKT and pERK1/2 may have the potential to enhance the efficacy of DDP-based chemotherapy.

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Hepatocellular carcinoma (HCC) accounts for over 90% of all primary liver cancers. With an ever increasing incidence trend year by year, it has become the third most common cause of death from cancer worldwide. Hepatic resection is generally considered to be one of the most effective therapies for HCC patients, however, there is a high risk of recurrence in postoperative HCC. In clinical practice, there exists an urgent need for valid prognostic markers to identify patients with prognosis, hence the importance of studies on prognostic markers in improving the prediction of HCC prognosis. This review focuses on the most promising immunohistochemical prognostic markers in predicting the postoperative survival of HCC patients.