Increasing Photostability of Inverted Nonfullerene Organic Solar Cells by Using Fullerene Derivative Additives.

Organic solar cells (OSCs) recently achieved efficiencies of over 18% and are well on their way to practical applications, but still considerable stability issues need to be overcome. One major problem emerges from the electron transport material zinc oxide (ZnO), which is mainly used in the inverted device architecture and decomposes many high-performance nonfullerene acceptors due to its photocatalytic activity. In this work, we add three different fullerene derivatives-PC71BM, ICMA, and BisPCBM-to an inverted binary PBDB-TF:IT-4F system in order to suppress the photocatalytic degradation of IT-4F on ZnO via the radical scavenging abilities of the fullerenes. We demonstrate that the addition of 5% fullerene not only increases the performance of the binary PBDB-TF:IT-4F system but also significantly improves the device lifetime under UV illumination in an inert atmosphere. While the binary devices lose 20% of their initial efficiency after only 3 h, this time is increased fivefold for the most promising ternary devices with ICMA. We attribute this improvement to a reduced photocatalytic decomposition of IT-4F in the ternary system, which results in a decreased recombination. We propose that the added fullerenes protect the IT-4F by acting as a sacrificial reagent, thereby suppressing the trap state formation. Furthermore, we show that the protective effect of the most promising fullerene ICMA is transferable to two other binary systems PBDB-TF:BTP-4F and PTB7-Th:IT-4F. Importantly, this effect can also increase the air stability of PBDB-TF:IT-4F. This work demonstrates that the addition of fullerene derivatives is a transferable and straightforward strategy to improve the stability of OSCs.

Differential Proliferation Effect of the Newly Synthesized Valine, Tyrosine and Tryptophan-Naphthoquinones in Immortal and Tumorigenic Cervical Cell Lines.

We previously showed that microwave assisted synthesis is the best method for the synthesis of naphthoquinone amino acid and chloride-naphthoquinone amino acid derivatives by a complete evaluation of reaction conditions such as stoichiometry, bases, and pH influence. Following the same strategy, we synthesized chloride and non-chloride tyrosine, valine, and tryptophan-naphthoquinones achieving 85-95%, 80-92%, and 91-95% yields, respectively. The cyclic voltammetry profiles showed that both series of naphthoquinone amino acid derivatives mainly display one redox reaction process. Overall, chloride naphthoquinone amino acid derivatives exhibited redox potential values (E1/2) more positive than non-chloride compounds. The six newly synthesized compounds were tested in HPV positive and negative as well as in immortal and tumorigenic cell lines to observe the effects in different cellular context simulating precancerous and cancerous status. A dose-response was achieved to determine the IC50 of six newly synthesized compounds in SiHa (Tumorigenic and HPV16 positive), CaLo (Tumorigenic and HPV18 positive), C33-A (Tumorigenic and HPV negative) and HaCaT (Keratinocytes immortal HPV negative) cell lines. Non-chloride tryptophan-naphthoquinone (3c) and chloride tyrosine-naphthoquine (4a) effects were more potent in tumorigenic SiHa, CaLo, and C33-A cells with respect to non-tumorigenic HaCaT cells. Interestingly, there seems to be a differential effect in non-chloride and chloride naphthoquinone amino acid derivatives in tumorigenic versus non tumorigenic cells. Considering all naphthoquinone amino acid derivatives that our group synthesized, it seems that hydrophobic and aromatic amino acids have the greatest effect on cell proliferation inhibition. These results show promising compounds for cervical cancer treatment.

Crosstalk between WIP and Rho family GTPases.

Through actin-binding proteins such as the neural Wiskott-Aldrich syndrome protein (N-WASP) and WASP-interacting protein (WIP), the Rho family GTPases RhoA, Rac1 and Cdc42 are major modulators of the cytoskeleton. (N-)WASP and WIP control Rho GTPase activity in various cell types, either by direct WIP/(N-)WASP/Cdc42 or potential WIP/RhoA binding, or through secondary links that regulate GTPase distribution and/or transcription levels. WIP helps to regulate filopodium generation and participates in the Rac1-mediated ruffle formation that determines cell motility. In neurons, lack of WIP increases dendritic spine size and filamentous actin content in a RhoA-dependent manner. In contrast, WIP deficiency in an adenocarcinoma cell line significantly reduces RhoA levels. These data support a role for WIP in the GTPase-mediated regulation of numerous actin-related cell functions; we discuss the possibility that this WIP effect is linked to cell proliferative status.

5p and 3p Strands of miR-34 Family Members Have Differential Effects in Cell Proliferation, Migration, and Invasion in Cervical Cancer Cells.

The micro RNA (miR)-34 family is composed of 5p and 3p strands of miR-34a, miR-34b, and miR-34c. The 5p strand's expression and function is studied in cervical cancer. The 3p strand's function and regulation remain to be elucidated. To study the function of the passenger strands of miR-34 family members, we overexpressed 5p and 3p strands using a synthetic miRNA in cervical cell lines. Cell proliferation was evaluated using crystal violet. Migration and invasion were tested using transwell assays, Western blot, and zymography. Possible specific targets and cell signaling were investigated for each strand. We found that miR-34a-5p inhibited proliferation, migration, and cell invasion accompanied by matrix metalloproteinase 9 (MMP9) activity and microtubule-associated protein 2 (MAP2) protein reduction. We also found that miR-34b-5p and miR-34c-5p inhibit proliferation and migration, but not invasion. In contrast, miR-34c-5p inhibits MMP9 activity and MAP2 protein, while miR-34b-5p has no effect on these genes. Furthermore, miR-34a-3p and miR-34b-3p inhibit proliferation and migration, but not invasion, despite the later reducing MMP2 activity, while miR-34c-3p inhibit proliferation, migration, and cell invasion accompanied by MMP9 activity and MAP2 protein inhibition. The difference in cellular processes, MMP2 and MMP9 activity, and MAP2 protein inhibition by miR-34 family members suggests the participation of other regulated genes. This study provides insights into the roles of passenger strands (strand*) of the miR-34 family in cervical cancer.

WIP-YAP/TAZ as A New Pro-Oncogenic Pathway in Glioma.

Wild-type p53 (wtp53) is described as a tumour suppressor gene, and mutations in p53 occur in many human cancers. Indeed, in high-grade malignant glioma, numerous molecular genetics studies have established central roles of RTK-PI3K-PTEN and ARF-MDM2-p53 INK4a-RB pathways in promoting oncogenic capacity. Deregulation of these signalling pathways, among others, drives changes in the glial/stem cell state and environment that permit autonomous growth. The initially transformed cell may undergo subsequent modifications, acquiring a more complete tumour-initiating phenotype responsible for disease advancement to stages that are more aggressive. We recently established that the oncogenic activity of mutant p53 (mtp53) is driven by the actin cytoskeleton-associated protein WIP (WASP-interacting protein), correlated with tumour growth, and more importantly that both proteins are responsible for the tumour-initiating cell phenotype. We reported that WIP knockdown in mtp53-expressing glioblastoma greatly reduced proliferation and growth capacity of cancer stem cell (CSC)-like cells and decreased CSC-like markers, such as hyaluronic acid receptor (CD44), prominin-1 (CD133), yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ). We thus propose a new CSC signalling pathway downstream of mtp53 in which Akt regulates WIP and controls YAP/TAZ stability. WIP drives a mechanism that stimulates growth signals, promoting YAP/TAZ and β-catenin stability in a Hippo-independent fashion, which allows cells to coordinate processes such as proliferation, stemness and invasiveness, which are key factors in cancer progression. Based on this multistep tumourigenic model, it is tantalizing to propose that WIP inhibitors may be applied as an effective anti-cancer therapy.

Role of Akt Isoforms Controlling Cancer Stem Cell Survival, Phenotype and Self-Renewal.

The cancer stem cell (CSC) hypothesis suggests that tumours are maintained by a subpopulation of cells with stem cell properties. Although the existence of CSCs was initially described in human leukaemia, less evidence exists for CSCs in solid tumours. Recently, a CD133+ cell subpopulation was isolated from human brain tumoursexhibiting stem cell properties in vitro as well as the capacity to initiate tumours in vivo. In the present work, we try to summarize the data showing that some elements of the Phosphoinositide 3-kinase Class I (PI3K)/ Thymoma viral oncogene protein kinase (Akt) pathway, such the activity of PI3K Class I or Akt2, are necessary to maintain the CSC-like phenotype as well as survival of CSCs (also denoted as tumour-initiating cells (TICs)). Our data and other laboratory data permit a working hypothesis in which each Akt isoform plays an important and specific role in CSC/TIC growth, self-renewal, maintaining survival, and epithelial-mesenchymal transition (EMT) phenotype, not only in breast cancer, but also in glioma. We suggest that a more complete understanding is needed of the possible roles of isoforms in human tumours (iso-signalling determination). Thus, a comprehensive analysis of how hierarchical signalling is assembled during oncogenesis, how cancer landmarks are interconnected to favour CSC and tumour growth, and how some protein isoforms play a specific role in CSCs to ensure that survival and proliferation must be done in order to propose/generate new therapeutic approaches (alone or in combination with existing ones) to use against cancer.

Privilege management infrastructure for virtual organizations in healthcare grids.

This paper is focused on the management of virtual organizations (VO) inside healthcare environments where grid technology is used as middleware for a healthcare services-oriented architecture (HSOA). Some of the main tasks considered for the provision of an efficient VO management are management of users, assignation of roles to users, assignation of privileges to roles, and definition of resources access policies. These tasks are extremely close to privilege management infrastructures (PMI), so we face VO management services as part of the PMI supporting access control to healthcare resources inside the HSOA. In order to achieve a completely open and interoperable PMI, we review and apply standards of security and architectural design. Moreover, semantic technologies are introduced in decision points for access control allowing the management of a high degree of descriptors by means of ontologies and infer the decision making through rules and reasoners.

La estafilorrafía precoz. Resultados en 5 años / Early staphylorraphy. Result from 5 years

Se valoran los resultados obtenidos con la estafilorrafía precoz en pacientes con fisuras labiopalatinas o palatinas puras después de 5 años en la aplicación de este método terapéutico (1987-1989) en el Servicio de Cirugía Maxilofacial del Hospital Pediátrico Sur Docente de Santiago de Cuba. Seaprecieron buenos resultados en la oculsión intermaxilar así como en el desarrollo del maxilar, y en la mayoría de los pacientes sin utilizar aparatos preoperatorios hubo logros desde el punto de vista logofoniátrico (AU)

La termoterapia en los procesos sépticos faciales / Thermotherapy in septic facial processes

Se realiza un síntesis del estado actual de la termoterapia en los procesos sépticos faciales. Con el fin de aportar elementos acerca del valor de la misma, se realiza el estudio de 43 casos de procesos sépticos cervicofaciales procedentes de los hospitales Provincial y Pediátrico Sur de Santiago de Cuba. Se destaca la efectividad del calor en el mayor porcentaje de casos(AU)