Inflorescence bud induction in Vitis vinifera L. cv. Thompson Seedless: Cytohistological events and starch accumulation in the shoot apex

Induktion von Infloreszenzen in Knospen der Sorte Sultanina (Vitis vinifera L.):Cytologisch-histologische Veränderungen und Stärkeeinlagerung im VegetationskegelAn Knospen der Sorte Sultanina (Vitis vinifera L.) wurden Schnittuntersuchungen durchgeführt, um die cytologisch-histologischen Veränderungen während des Übergangs zur Blütenbildung aufzuzeigen. Messungen erbrachten eine GröBenzunahme der Zellen, Zellkerne und Nukleolen sowie eine Zunahme der Zellwanddicke im Vegetationskegel und den Anlagen ruhender Knospen verglichen mit den entsprechenden Strukturen vegetativer Endknospen. Diese Veränderungen wurden ab der Knospe in Position 2 am Trieb (Zählung von apikal her) festgestellt. Sowohl Vegetationskegel als auch Anlagen ruhender Knospen zeigen Stärkeeinlagerung

The influence of culture dates, genotype and size and type of shoot apices on in vitro shoot proliferation of Vitis vinifera cvs Thompson Seedless, Ribier and Black Seedless

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Estimating Excitonic Effects in the Absorption Spectra of Solids: Problems and Insight from a Guided Iteration Scheme

A major obstacle for computing optical spectra of solids is the lack of reliable approximations for capturing excitonic effects within time-dependent density-functional theory. We show that the trustful prediction of strongly bound electron-hole pairs within this framework using simple approximations is still a challenge and that available promising results have to be revisited. Deriving a set of analytical formula we analyze and explain the difficulties. We deduce an alternative approximation from an iterative scheme guided by previously available knowledge, significantly improving the description of exciton binding energies. Finally, we show how one can "read" exciton binding energies from spectra determined in the random phase approximation, without any further calculation.Comment: 5 pages, 2 figures plus supplemental materia

A controlled study comparing salivary osmolality, caries experience and caries risk in patients with cerebral palsy

Cerebral palsy (CP) is a permanent neurological disorder accompanied by secondary musculoskeletal masticatory disorder, with repercussion on chewing and deglutition functions. In these conditions, the liquids ingestion is compromised resulting in salivary osmolality alteration. The objective of this study was to compare salivary osmolality, caries experience and caries risk between normoreactive individuals and patients with CP. The participants were 4-20 years old: 52 patients with CP treated at a reference rehabilitation centre (study group, SG), and 52 normoreactive individuals (control group, CG). Saliva was collected for five minutes using cotton rolls. Following centrifugation, salivary osmolality was determined by freezing point depression osmometry. Evaluations included caries experience (DMFT index), and caries risk based on a caries-risk assessment tool (CAT). Descriptive and inferential statistics (Chi square and Student t tests) were used to compare the groups. Receiver operating characteristic (ROC) analyses were performed and the area under the ROC curve (Az) was calculated. The level of significance was set at 5%. The groups were homogeneous for sex (p=0.843) and age (p=0.128). In the SG, spastic type CP was the most prevalent (80.8%), and patients showed significantly higher salivary osmolality values compared with the CG (p74 for the SG and >54 for the CG in the presence of dental caries. A significant correlation was verified between salivary osmolality and the DMFT index for the SG (p?0.05). Although patients with CP showed higher salivary osmolality values, higher caries experience and caries risk were not observed compared with normoreactive individuals

Rewiring innate and adaptive immunity with TLR9 agonist to treat osteosarcoma

Background Osteosarcoma (OS) is the most common primary bone tumor in children and adolescent. Surgery and multidrug chemotherapy are the standard of treatment achieving 60-70% of event-free survival for localized disease at diagnosis. However, for metastatic disease, the prognosis is dismal. Exploiting immune system activation in the setting of such unfavorable mesenchymal tumors represents a new therapeutic challenge. Methods In immune competent OS mouse models bearing two contralateral lesions, we tested the efficacy of intralesional administration of a TLR9 agonist against the treated and not treated contralateral lesion evaluating abscopal effect. Multiparametric flow cytometry was used to evaluate changes of the tumor immune microenviroment. Experiments in immune- deficient mice allowed the investigation of the role of adaptive T cells in TLR9 agonist effects, while T cell receptor sequencing was used to assess the expansion of specific T cell clones. Results TLR9 agonist strongly impaired the growth of locally-treated tumors and its therapeutic effect also extended to the contralateral, untreated lesion. Multiparametric flow cytometry showed conspicuous changes in the immune landscape of the OS immune microenvironment upon TLR9 engagement, involving a reduction in M2-like macrophages, paralleled by increased infiltration of dendritic cells and activated CD8 T cells in both lesions. Remarkably, CD8 T cells were needed for the induction of the abscopal effect, whereas they were not strictly necessary for halting the growth of the treated lesion. T cell receptor (TCR) sequencing of tumor infiltrating CD8 T cells showed the expansion of specific TCR clones in the treated tumors and, remarkably, their selected representation in the contralateral untreated lesions, providing the first evidence of the rewiring of tumor-associated T cell clonal architectures. Conclusions Overall these data indicate that the TLR9 agonist acts as an in situ anti-tumor vaccine, activating an innate immune response sufficient to suppress local tumor growth while inducing a systemic adaptive immunity with selective expansion of CD8 T cell clones, which are needed for the abscopal effect

Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal hematopoiesis but prone to immunogenic death, leading to neutrophil extracellular trap (NET) formation. NET fostered the progression of the indolent NPM1-driven myeloproliferation toward an exacerbated and proliferative dysplastic phenotype. Enrichment in NET structures was found in the bone marrow of patients with autoimmune disorders and in NPM1-mutated acute myelogenous leukemia (AML) patients. Genes involved in NET formation in the animal model were used to design a NET-related inflammatory gene signature for human myeloid malignancies. This signature identified two AML subsets with different genetic complexity and different enrichment in NPM1 mutation and predicted the response to immunomodulatory drugs. Our results indicate that stromal/ECM changes and priming of bone marrow NETosis by systemic inflammatory conditions can complement genetic and epigenetic events towards the development and progression of myeloid malignancy

AXL is an oncotarget in human colorectal cancer

AXL is a tyrosine kinase receptor activated by GAS6 and regulates cancer cell proliferation migration and angiogenesis. We studied AXL as new therapeutic target in colorectal cancer (CRC). Expression and activation of AXL and GAS6 were evaluated in a panel of human CRC cell lines. AXL gene silencing or pharmacologic inhibition with foretinib suppressed proliferation, migration and survival in CRC cells. In an orthotopic colon model of human HCT116 CRC cells overexpressing AXL, foretinib treatment caused significant inhibition of tumour growth and peritoneal metastatic spreading. AXL and GAS6 overexpression by immunohistochemistry (IHC) were found in 76,7% and 73.5%, respectively, of 223 human CRC specimens, correlating with less differentiated histological grading. GAS6 overexpression was associated with nodes involvement and tumour stage. AXL gene was found amplified by Fluorescence in situ hybridization (FISH) in 8/146 cases (5,4%) of CRC samples. Taken together, AXL inhibition could represent a novel therapeutic approach in CRC