cometadata/datacite-rtg-text-other-reclassification-records huggingface dataset:
Ichneumon doliturus Smith 1874
Creators: name: Shimizu, So
name: Broad, Gavin R.
Publisher: name: Zenodo
Year: 2020
Subjects: Biodiversity
Taxonomy
Animalia
Arthropoda
Insecta
Hymenoptera
Eulophidae
Ichneumon
Ichneumon doliturus

description: Ichneumon doliturus Smith, 1874
(Figure 13)
Taxonomic history. Uchida (1939) transferred this species to Cratichneumon Thomson, 1893.
Current taxonomy. Cratichneumon doliturus (Smith, 1874) (Ichneumonidae: Ichneumoninae: Ichneumonini).
Type number. Type 3b.207. Specimen # NHMUK010634911
Type status. Holotype.
Sex. Male.
Type locality. Hyôgo Prefecture, Honshû, Japan.
Label data. First label, ‘Type’ (round label, with red margin; printed); second label, ‘B.M. TYPE /HYM./3.b.207’ (square label; first and second lines printed and third line handwriting); third label, ‘B.M. TYPE /HYM./ Ichneumon /doliturus/ Smith 1874 ’ (square label; first and second lines printed and third to fifth lines handwriting); fourth label, ‘Hiogo/ Japan.’ (square label; first line handwriting and second line printed); fifth label, ‘74/16’ (round label; handwriting); sixth label, ‘ I. doliturus / Type. Smith.’ (square label; handwriting).
Condition. Very good, but left antenna broken at 28th flagellomere, fifth tarsomere of left fore leg, fourth and fifth tarsomeres of right hind leg missing.
description: Published as part of Shimizu, So & Broad, Gavin R., 2020, Photographic catalogue of the oldest primary types of Japanese Ichneumonoidea (Hymenoptera), those described by Frederick Smith and Francis Walker in 1874, pp. 1115-1198 in Journal of Natural History 54 (17) on pages 1134-1137, DOI: 10.1080/00222933.2020.1776905, http://zenodo.org/record/4116141
Cetorhinus maximus
Creators: name: Golani, Daniel
Publisher: name: Zenodo
Year: 2021
Subjects: Biodiversity
Taxonomy
Animalia
Chordata
Elasmobranchii
Lamniformes
Cetorhinidae
Cetorhinus
Cetorhinus maximus

description: Cetorhinus maximus (Günnerus, 1765)
Cetorhinus maximus: Ben-Tuvia, 1971a; Baranes & Darom, 1978 (Heb.); Baranes, 1979 (Heb.); Baranes & Diamant, 1983a (Heb.); Golani, 1996; Golani, 2005; Golani, 2006.
description: Published as part of Golani, Daniel, 2021, An updated Checklist of the Mediterranean fishes of Israel, with illustrations of recently recorded species and delineation of Lessepsian migrants, pp. 1-108 in Zootaxa 4956 (1) on page 6, DOI: 10.11646/zootaxa.4956.1.1, http://zenodo.org/record/4691195
title: Creating a Peer Instruction Guide for Course Registration
Creators: name: Felkner, Morgan
Publisher: name: Private Academic Library Network of Indiana, Inc. (PALNI)
publisherIdentifier: https://ror.org/05dch6316
publisherIdentifierScheme: ROR
Year: 2024
Subjects: student success
first year seminar
open pedagogy

description: In this assignment, students will develop a comprehensive, peer-focused instruction guide for the course registration process. This guide will cover the use of Colleague Self Service, including how to navigate the platform, interpret academic plans provided by advisors, and create a class schedule. The goal is to produce a user-friendly resource that future students can use to simplify the often-complex registration process.
Stormwater Management, N.J.A.C. 7:8
Creators: name: No Name Supplied
Publisher: name: New Jersey Department of Environmental Protection (NJDEP)
Year: 2004

description: The Stormwater Management rules implement certain requirements of the Federal NPDES Phase II Stormwater Permit rules and NJPDES stormwater rules, and also establish design and performance standards for stormwater management measures.
Safe delivery of therapeutic cytokines to treat lung cancer
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: The influence of cytokine suppression on survival of lung cancer patients has been demonstrated by many studies. Numerous pre-clinical and clinical data has confirmed that cytokines have broad anti-tumor activity. Despite this success, the potential of cytokines in the field of cancer immunotherapy is greatly limited by significant side effects associated with the systemic administration of cytokines. In addition, like other protein drugs, cytokines suffer from instability during manufacturing, storage and administration. To overcome these limitations, we propose to develop a pulmonary delivery system for a representative cytokine, interferon-a (INF-a). This nanoparticle (NP) system utilizes a poly(lactic-co-glycolic acid) (PLGA)-trehalose diblock copolymer as a dually-functional drug carrier. Based on our preliminary results, trehalose polymers effectively preserve the bioactivity of proteins when exposed to a variety of stresses, such as elevated temperatures and lyophilization. The PLGA block will encapsulate the proteins and release the cargo during its degradation. We expect that the PLGA-trehalose NPs will delivery INF-a to the alveolar region of lung through inhalation. Localized retention of IFN-a-loaded NPs should induce activation of immune defense against lung cancer cells and significantly reduce the systemic toxicity associated with parenteral administration of IFN-a. We hypothesize that (1) PLGA-trehalose diblock copolymers will form NPs with IFN-a and release the cargo upon PLGA degradation; (2) IFN-a-loaded PLGA-trehalose NPs will maintain protein bioactivity when exposed to various stresses, including elevated temperatures, lyophilization and long-term storage; (3) the NPs can deliver IFN-a to the lower lung and effectively reduce tumor load in the lung without producing significant systemic toxicity. To test these hypotheses the following three specific aims are proposed. First, to synthesize PLGA-trehalose diblock copolymer and prepare PLGA-trehalose NPs. This will be accomplished by block copolymer synthesis, nanoparticle formation, and complete characterization utilizing standard techniques. Second, to evaluate in vitro activity and stability of INF-a-loaded PLGA-trehalose NPs. This will be carried out by testing in vivo cytotoxicity and evaluating stability of the INF-a in the nanoparticle. Third, to evaluate biodistribution, in vivo antitumor effect and systemic toxicity of INF-a-loaded PLGA-trehalose NPs in mouse models. This will be determined by using near-infrared fluores
Role of the YEATS2 component of the human ATAC epigenetic coregulator complex
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: The biological functions of the human YEATS domain-containing protein 2 (YEATS2) are largely unknown. YEATS domains are conserved in chromatin-associated proteins but their functions are unclear. YEATS2 is a core subunit of the multiprotein ATAC histone acetyltransferase complex. Within the ATAC complex YEATS2 links transcription coactivators and the GCN5 histone acetyltransferase to the negative transcription cofactor NC2ß. Hence, ATAC is thought to both activate and repress transcription. However, the genes regulated by YEATS2 and the mechanisms by which YEATS2 (ATAC) binds and regulates its target genes remain to be characterized. Preliminary data indicate that the conserved YEATS domain is not required for the incorporation of YEATS2 into complete ATAC complexes, but instead might function as a docking domain that links ATAC to specific chromatin-associated factors and DNA-binding transcription regulators. Proteomics analyses identified YEATS domain-interacting proteins, including UBAP2L (a protein of unknown function with a ubiquitin-binding domain), the tumor suppressor p53, and the transcription/chromatin coregulator KAP1. KAP1 regulates chromatin structure and the DNA damage response by interacting with histone deacetylase complexes and various DNA-binding regulators such as p53, E2F1, and many Zinc finger proteins. KAP1 is also an ubiquitin E3 ligase that stimulates p53 polyubiquitination and degradation and is overexpressed in many cancers. The YEATS2 gene is also upregulated in many cancers and is required for the proliferation/survival of several transformed cell lines. Based on these preliminary data it is hypothesized that YEATS2 interacts with KAP1 and/or p53 and regulates KAP1/p53 activity and cognate target genes. YEATS2 is hypothesized to attenuate stress-responsive cytostatic and proapoptotic genes in unstressed cells. To test this, Aim1 will identify the genome-wide target genes and DNA sequences bound and regulated by YEATS2 in transformed cell lines (by ChIP-seq, RNAi and RNA-seq); bioinformatics will correlate the results to available ENCODE data; this will identify the biological processes regulated and possible DNA-binding regulators and epigenetic modifications associated with YEATS2 functions at specific loci. Aim2 will verify the intracellular interactions of YEATS2 (via its YEATS domain) with endogenous UBAP2L, KAP1 and p53 and test the role of DNA damage stress in these interactions; this aim will verify the role of YEATS2 in cell cycle progression and inhibition of apop
Non-canonical functions of STAT3 in lung cancer
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: Lung cancer is the leading cause of cancer deaths worldwide. Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers. The 5-year survival rate for NSCLC is only 15%. Constitutive activation of STAT3 by phosphorylation has been implicated in many types of NSCLC. However, the role of STAT activation in cancer formation is not entirely clear. The effects of JAK/STAT activation have been attributed largely to their canonical function, the transcriptional activation of target genes. Accordingly, JAK/STAT inhibitory agents have been under development for treatment of lung cancer. It is increasingly clear, however, that epigenetic events such as changes in genome organization and chromatin structure play important roles in cancer development and progression. Our previous studies have identified a non-canonical mode of JAK/STAT signaling, in which unphosphorylated STAT (U-STAT) is localized in heterochromatin in association with Heterochromatin Protein 1 (HP1); STAT activation (by phosphorylation) causes its dispersal from heterochromatin, leading to HP1 delocalization and heterochromatin loss. In this proposal, we will investigate the dual function of STAT3, with a focus on the non-canonical function of U-STAT3, in the epigenetic regulation of NSCLC development. Our central hypothesis is that increasing the levels of U-STAT3 serves the dual function of increasing heterochromatin formation and counteracting the canonical functions of phosphorylated STAT3 (pSTAT3) in NSCLC. The overall goal of this project is to investigate whether U-STAT3 promotes heterochromatin formation and suppresses NSCLC cells growth in a mouse xenograft model. Results from the proposed research will form the basis for applying NIH funding for developing more effective lung cancer treatment by targeting the dual function of U-STAT3 in epigenetics and genetics. In Aim 1, we will use biochemical and imaging analysis to investigate whether U-STAT3 will increase heterochromatin formation in NSCLC cells. In Aim 2, we will study the effects of expressing U-STAT3 and increasing heterochromatin formation on the growth of NSCLC cells using a mouse xenograft model. We believe that these studies will shed a light on the role of STAT3 in lung cancer development and will lead to new therapeutic modalities for the treatment of NSCLCs.
Multi-modal drug conjugates for synergistic leukemia therapy
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: Conventional cancer chemotherapy commonly targets only one molecular pathway. However, successful eradication is often not achieved with a single therapy due to the high complexity found within the biological networks of a cell. Simultaneously tackling multiple pathways that are cooperatively connected in the survival and proliferation of cancer cells is a promising approach in developing a safe and efficient cancer therapy. This proposed CRCC project aims to develop a synergistic therapy for Philadelphia chromosome positive (Ph+) leukemia using a novel, stimuli-responsive nanomedicine to restore apoptosis and decrease propagation of cells concurrently. In Ph+ leukemia, Bcr-Abl fusion protein interferes with cellular apoptosis while the aggressive cellular proliferation is supported by increased anabolic activities. Dasatinib is a tyrosine kinase inhibitor targeting Bcr-Abl, and FTY720 has recently been discovered to rescue the apoptosis of Ph+ leukemia cells and down-regulate nutrient transport proteins. The drugs will be co-conjugated onto macromolecular platforms (i.e., polyethylene glycol [PEG] and human serum albumin [HSA]) via stimuli-cleavable linkages. The drug/macromolecule conjugates are designed to achieve synergistic and safe leukemia therapy by 1) ensuring the co-delivery of both Dasatinib and FTY720 to the same leukemia cells, 2) normalizing the pharmacokinetic (PK) and pharmacodynamics (PD) properties of both drugs, and 3) minimizing the side effects of both drugs. The preliminary studies showed synergistically induced apoptosis of Ph+ leukemia cells when treated with both Dasanatib and FTY720, and successful synthesis of Dasatinib- and FTY-conjugated PEG via acid-cleavable linkers. The proposed research will 1) synthesize and characterize drug/macromolecule conjugates, 2) verify biological effects of the drug/macromolecule conjugates in vitro and optimize their synthesis, and 3) confirm the synergistic therapy for leukemia in vivo using drug/macromolecule conjugates. Successful completion of the proposed research will demonstrate the high feasibility for clinical translation as it combines the therapeutic potency of two clinically approved drugs. Ultimately, achieving synergistic therapeutic effects with minimized side effects via co-delivery of multiple drugs using a stimuli-responsive macromolecular platform can easily be applied to developing novel therapies for other types of cancer as well.
Management Plan 1983-1986: For hazardous waste site cleanups in New Jersey
Creators: name: No Name Supplied
Publisher: name: No Publisher Supplied
Year: 1983

description: This Management Plan has been prepared by the Department of Environmental Protection (DEP), Division of Waste Management, for the period of 1983-1986. The purpose of the Plan is to develop a systematic approach to remedial action at hazardous waste sites, to coordinate cleanup and enforcement actions and to identify future funding needs and sources.
Micromechanical dissection of intercellular crosstalk in the tumor microenvironment
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: A complex milieu of paracrine signals between different cells of the tumor microenvironment plays a critical role in regulating the steps of tumor progression. Yet, there is a knowledge gap in understanding the details of these control mechanisms and identifying the specific factors involved. Thus, there is a serious limitation in being able to develop successful interventions that have a high probability of targeting the most relevant pathways for slowing or reversing the growth and spread of cancer. One way forward is the development of new experimental tools that allow more detailed and specific observation of cellular crosstalk in the tumor microenvironment. We hypothesize that new tumor-stromal signaling pathways, including feedback mechanisms, can be identified through the use of a method that records gene expression changes due to cellular crosstalk (a) in a cell-specific manner, (b) at high temporal resolution, and (c) at a genome-wide level. This method depends upon the capabilities of a unique microfabricated cell culture substrate. The device enables compartmentalized co-culture, in which two cell populations can be cultured in close proximity while remaining unmixed so that the cells can be quickly separated for cell-specific analysis. The microscale proximity of the two cell populations makes the system sensitive to short-range paracrine interactions that can go undetected by conventional tools. In addition, the speed of cell purification enables the sampling of closely spaced time points. Finally, compatibility with standard assays enables gene expression profiling by genome-wide RNA sequencing. The aim of this proposal is to demonstrate the validity of our concept in a model system consisting of tumor colon cells and activated colon fibroblasts. The cells have been validated for compatibility with the culture substrate, and a preliminary time course has been measured, with 6 time points sampled over 48 h of co-culture. The preliminary data suggests two temporal windows of interest: acute responses during 0-12 h, and late responses during 24-48 h. RNA-Seq will be performed for tumor and stromal samples pooled over these two windows of time, from both co-cultures and monoculture controls. In order to identify candidate mechanisms for reciprocal signaling, we will focus on identifying acute induction of genes associated with secreted proteins in the stroma, along with late induction of genes associated with tumor progression in the tumor cells. Validation can then be attempted
Alopias superciliosus
Creators: name: Golani, Daniel
Publisher: name: Zenodo
Year: 2021
Subjects: Biodiversity
Taxonomy
Animalia
Chordata
Elasmobranchii
Lamniformes
Alopiidae
Alopias
Alopias superciliosus

description: Alopias superciliosus (Lowe, 1839)
Alopias superciliosus: Pisanty & Sonin, 1991 (Fish., Heb.); Pisanty & Sonin, 1992 (Fish., Heb.); Golani, 1996; Golani, 2005; Golani, 2006.
description: Published as part of Golani, Daniel, 2021, An updated Checklist of the Mediterranean fishes of Israel, with illustrations of recently recorded species and delineation of Lessepsian migrants, pp. 1-108 in Zootaxa 4956 (1) on page 7, DOI: 10.11646/zootaxa.4956.1.1, http://zenodo.org/record/4691195
Ichneumon flavitarsis Smith 1874
Creators: name: Shimizu, So
name: Broad, Gavin R.
Publisher: name: Zenodo
Year: 2020
Subjects: Biodiversity
Taxonomy
Animalia
Arthropoda
Insecta
Hymenoptera
Eulophidae
Ichneumon
Ichneumon flavitarsis

description: Ichneumon flavitarsis Smith, 1874
(Figure 14)
Taxonomic history. Heinrich (1937) transferred this species to Coelichneumon Thomson, 1893.
Current taxonomy. Coelichneumon (Coelichneumon) flavitarsis (Smith, 1874) (Ichneumonidae: Ichneumoninae: Heresiarchini).
Type number. Type 3b.41. Specimen # NHMUK010634914
Type status. Holotype.
Sex. Male.
Type locality. Hyôgo Prefecture, Honshû, Japan.
Label data. First label, ‘Type’ (round label, with red margin; printed); second label, ‘B.M. TYPE /HYM./3.b.41’ (square label; first and second lines printed and third line handwriting); third label, ‘74/16’ (round label; handwriting); fourth label, ‘ Ichneumon /flavitarsis/ Type. Smith’ (square label; handwriting).
Condition. Good, but the mesosoma is broken and the following parts lost: right antenna, left antenna after 33rd flagellomere, fifth tarsomere of right mid leg.
description: Published as part of Shimizu, So & Broad, Gavin R., 2020, Photographic catalogue of the oldest primary types of Japanese Ichneumonoidea (Hymenoptera), those described by Frederick Smith and Francis Walker in 1874, pp. 1115-1198 in Journal of Natural History 54 (17) on page 1137, DOI: 10.1080/00222933.2020.1776905, http://zenodo.org/record/4116141
Combination strategies to enhance therapy for Ph-like B-ALL
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: This proposal focuses on B-cell acute lymphoblastic leukemia (B-ALL). Despite a dramatic increase in cure rates over the past decades, a subset of children with B-ALL continues to have unacceptably high rates of relapse. Leukemias in this “high-risk” group include Philadelphia chromosome positive (Ph+) cases driven by the BCR-ABL tyrosine kinase, but the majority are Ph-negative. Many high-risk Ph-negative B-ALL cases can now be designated as “Ph-like” B-ALL due to similar gene expression and activation of tyrosine kinases. Emerging data indicate that Ph-like B-ALL is also prevalent in adolescent and young adult patients. Importantly, Ph-like leukemias show decreased kinase signaling upon treatment with tyrosine kinase inhibitors (TKIs) in vitro and TKI treatment suppresses disease in xenograft models. These findings establish strong rationale for clinical testing of TKIs matched to patient-specific genomic lesions in Ph-like B-ALL. However, TKI resistance develops in many cancers, emphasizing the need to target additional survival mechanisms. Using xenograft models of adult Ph+ B-ALL we have reported that second generation, ATP-competitive inhibitors of mTOR work in synergy with TKIs targeting the BCR-ABL oncogene. Combining mTOR kinase inhibitors (TOR-KIs) with TKIs causes regression of Ph+ leukemia to a greater extent than TKI alone or TKI plus rapamycin, even in tumors with intrinsic resistance to BCR-ABL kinase inhibitors. mTOR kinase inhibitors are well tolerated at therapeutic doses. Because the TKI/TOR-KI combination works well in Ph+ B-ALL xenografts, we believe similar combinations will be effective in Ph-like B-ALL. This project will test this hypothesis, with the goal of obtaining proof-of-concept data supporting clinical trials of TKI plus TOR-KIs in children, adolescents and young adults with Ph-like B-ALL. We will accomplish this objective using cells from established Ph-like B-ALL xenografts, provided by a collaborator. The first specific aim is to evaluate the efficacy of dual pathway inhibition on xenografted Ph-like leukemia samples. Endpoints will be percent leukemia cells in the bone marrow, and fraction of cycling cells in the leukemia versus normal bone marrow cell populations. The second specific aim is to test whether the combination treatments suppress survival signaling in B-ALL cells more profoundly than single treatments. We will address this in part through phosphoflow analysis of cells obtained from bone marrow of xenografted mice. These studies may lead to new approaches to
Alopias vulpinus
Creators: name: Golani, Daniel
Publisher: name: Zenodo
Year: 2021
Subjects: Biodiversity
Taxonomy
Animalia
Chordata
Elasmobranchii
Lamniformes
Alopiidae
Alopias
Alopias vulpinus

description: Alopias vulpinus (Bonnaterre, 1788)
Alopias vulpinus: Baranes & Darom, 1978 (Heb.); Golani, 1996; Golani, 2005; Golani, 2006.
description: Published as part of Golani, Daniel, 2021, An updated Checklist of the Mediterranean fishes of Israel, with illustrations of recently recorded species and delineation of Lessepsian migrants, pp. 1-108 in Zootaxa 4956 (1) on page 7, DOI: 10.11646/zootaxa.4956.1.1, http://zenodo.org/record/4691195
Development of radiation activatable cell penetrating peptides to radiosensitize tumors
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: Locally aggressive unresectable, non-metastatic cancers such as glioblastoma multiforme and pancreatic cancer remain a formidable therapeutic challenge. Radiotherapy with concurrent chemotherapy is often utilized in such clinical scenarios. The physics of radiotherapy delivery allows for highly conformal dose deposition of ionizing radiation within irradiated tumor targets. Ionizing radiation induces cellular stress responses and alterations within the tumor microenvironment including activation of proteases. Tumor cell kill by ionizing radiation at clinical conventionally fractionated doses is primarily through DNA damage, specifically DNA double strand breaks. One of the functions of concurrent chemotherapy is to sensitize tumors to ionizing radiation. However, the clinical benefit of radiosensitizers is severely limited by a lack of tumor specific delivery. To overcome this hurdle, we are developing radiation activatable cell penetrating peptides conjugated to radiosensitizers. In Aim1, we will identify radiation specific peptide cleavage by proteases and develop radiation activatable cell penetrating peptides that are preferentially activated in the irradiated tumor target environment as opposed to non-irradiated tissue. To achieve this we will identify peptides that are selectively cleaved by protease activity in irradiated tumors as opposed to non-irradiated tissue. We will use patient derived tumor xenografts grown orthotopically in murine model systems. Tumor xenografts will be irradiated using clinically relevant fractionation schemes to mimic clinical radiotherapy delivery. Tumor xenografts will be harvested from non-irradiated tumor xenografts and compared to irradiated tumor xenografts. Radiation inducible protease activity will be assessed by using a library of peptides. After identification of peptides with enhanced cleavage following irradiation, radiation activatable cell penetrating peptides will be constructed and tested in vivo. In Aim 2 of this proposal, we will create activatable cell penetrating peptides that deliver radiosensitizers. To achieve this activatable cell penetrating peptides eill be linked to small molecule inhibitors that block in DNA double strand break repair. Ionizing radiation induces DNA double strand breaks that are the critical lethal event in radiotherapy mediated tumor cell kill. By linking small molecule drugs that inhibit the DNA damage response, we hope to increase the therapeutic index of radiotherapy for intrinsically radioresistant tumors.
Multimodality quantum dots for molecular imaging of cancer
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: The recognition that various imaging modalities possess different assets has led to efforts to combine modalities in order to exploit the strengths of each. The recent intense interest in combining multiple modalities has spurred concomitant attention to development of multimodal imaging probes. We have recently synthesized and characterized CdSe/Zn1-xMnxS core/shell quantum dots (QD) for use in combined magnetic resonance (MRI) and optical imaging. These nanoparticles consist of a luminescent core, coated with a paramagnetic shell to which targeting ligands can be attached. Doping of QD with metals typically quenches luminescence. By doping manganese (Mn2+) into the shell, strong luminescence can be preserved after incorporation of the paramagnetic ions. We have synthesized nanoparticles doped with 0.7–7.4% Mn2+ in the shell that demonstrate high quantum yield and relaxivity. Our current aim is to investigate the application of multimodal quantum dots for molecular imaging of cancer. Our hypothesis is that these multimodal QD can be used to generate high resolution maps of tumor marker location using MRI, and allow optical identification of tumor margins to guide resection or subsequent histology. We will target the multimodal QD to two different cancer markers as a test of this hypothesis. Peptide and small molecule ligands have been developed that bind to ovarian cancer markers (a3ß1 integrin), and lymphomas (a4ß1 integrin), respectively. We will couple our QD to these targeting moieties and characterize their uptake by cells in culture. Cells expressing the appropriate markers will be incubated with varying concentrations of the QD; uptake will be assessed by confocal microscopy and MRI. In addition, marker positive and negative tumors will be generated in mouse models and multimodal quantum dots injected through tail vein. Animals will be imaged by MRI and tissues collected for optical histology. The current studies using these prototype multimodal quantum dots are critical to determining basic paramagnetic and optical properties that will be necessary to translate use of the multimodal QD in living systems. Future studies will address optimal QD composition for possible clinical use.
Exploring novel pathways in PP2A B56g3 mediated tumor suppression
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: Protein phosphatase 2A (PP2A) functions as a positive and negative regulator of the cell cycle, in the latter capacity potentially acting as a tumor suppressor. It was believed that the potential tumor suppressive function of PP2A might be achieved by a small subset of PP2A holoenzymes with particular subunit compositions. To support this view, a specific PP2A complex that contains B56!3 was indeed found to involve in cell growth and proliferation control. Therefore the B56!3-containing complex of PP2A may exert its tumor suppressive function by responding to DNA damage and acting as a signal transducer to dephosphorylate proteins involved in cell growth and proliferation. Indeed, recent evidence from our laboratory indicates that the B56!3-containing complex of PP2A directly dephosphorylates tumor suppressor p53 at Thr55 and stabilizes the protein after DNA damage. We further show that Thr55 dephosphorylation contributes to B56!3- mediated inhibition of cell proliferation and transformation. These data provide a molecular basis for B56!3-mediated tumor suppression. However, despite the significance of dephosphorylation of p53 by B56!3-containing PP2A complex in regulating cell growth, it appears that the B56!3-containing complex of PP2A also functions as a tumor suppressor in cells lacking p53, suggesting that other molecular pathways also contribute to B56!3-mediated tumor suppression. In this proposal, we will explore potential proteins that are targeted by the B56!3-containing complex of PP2A after DNA damage using affinity purification and MS spec analysis approaches. Since cancer is a collection of many different diseases, understanding the molecular mechanism and pathway unique to each will allow development of new treatments. Here, we take advantage of current knowledge and tools generated in our previous studies to fully define the molecular pathways and mechanisms by which the B56!3-containing complex of PP2A functions as a tumor suppressor in human cells.
Analysis of emperor's thumbs' homologues USP36 and USP42 in mouse and zebrafish
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: We have identified a gene in Drosophila that we call emperor’s thumb (et) and have found that et is an important regulator of apoptosis. et is a member of the DUB family of deubiquitinating proteins which is a large family of proteins that cleave ubiquitin-protein bonds. Since poly-ubiquitination is a signal for degradation, DUB activity usually stabilizes the substrate protein. Our analysis suggests that et encodes two different types of proteins, a “long” protein with an extended N-terminal domain and a “short” protein which lacks this domain. We have shown that loss of et function in the ovary and in the eye results in apoptosis. In the eye, this apoptosis is associated with a decrease in the concentration of DIAP1 (Drosophila inhibitor of apoptotic proteins). We have also shown that overexpression of the long form of et results in the inhibition of apoptosis. Thus, et loss of function and the overexpression of long form of et both suggest that et has antiapoptotic activity. However, when the short form of et is overexpressed, it induces apoptosis, which is associated with an increase in the concentration of caspases and DIAP1 protein. Taken together, these data suggest that the long form of et protein has antiapoptotic activity whereas the short form has proapoptotic activity. The data also suggests that et protein may directly regulate and stabilize DIAP1 via deubiquitination. USP36 and USP42 are vertebrate homologues of et that have not been studied in detail. Our data makes these homologues prime candidates for regulators of apoptosis in vertebrates (and humans). We will test this hypotheses by using standard molecular genetic techniques. We will determine the expression pattern of USP36 and USP42 in zebrafish and mouse. Using morpholino’s we will determine the loss of function phenotype of these two genes in zebrafish, and using RNAi will determine the loss of function phenotype in mouse tissue culture cells. We will also characterize the phenotype caused by overexpressing USP36 and USP42 in both zebrafish and mouse tissue culture cells. Finally, we will determine whether loss or gain of function of USP36 and USP42 results in changes in the concentration of vertebrate IAP proteins. These experiments will allow us to test the hypothesis as to whether USP36 and USP42 are regulators of apoptosis in vertebrates.
Retranscription interview Nicolas Diop "Nix", rappeur et enrepreneur
Creators: name: Costantini, Stephane
Publisher: name: NAKALA - https://nakala.fr (Huma-Num - CNRS)
publisherIdentifier: https://ror.org/04ces3204
publisherIdentifierScheme: ROR
Year: 2024

description: Retranscription interview Nicolas Diop "Nix", rappeur et enrepreneur. Enregistré à Deedo Dakar Studio, Point E, Dakar, Sénégal.
description: modified: jamais modifié
Ichneumon generosus Smith 1874
Creators: name: Shimizu, So
name: Broad, Gavin R.
Publisher: name: Zenodo
Year: 2020
Subjects: Biodiversity
Taxonomy
Animalia
Arthropoda
Insecta
Hymenoptera
Eulophidae
Ichneumon
Ichneumon generosus

description: Ichneumon generosus Smith, 1874
(Figure 15)
Taxonomic history. Uchida (1926) synonymised Ichneumon yumyum Kriechbaumer, 1895, described based on a specimen from Yokohama, Kanagawa Prefecture, Honshû, Japan, with I. generosus Smith, 1874, and I. generosus Smith had been used as a valid name for a long time. However, the species name ‘ Ichneumon generosus ’ is preoccupied by Olivier (1792).
Current taxonomy. Primary homonym, valid name: Ichneumon yumyum Kriechbaumer, 1895 (Ichneumonidae: Ichneumoninae: Ichneumonini).
Type number. Type 3b.1808. Specimen # NHMUK010634920
Sex. Male.
Type locality. Hyôgo Prefecture, Honshû, Japan.
Label data. First label, ‘Type’ (round label, with red margin; printed); second label, ‘B.M. TYPE /HYM./3b1808’ (square label; first and second lines printed and third line handwriting); third label, ‘Hiogo/ Japan.’ (square label; first line handwriting and second line printed); fourth label, ‘74/16’ (round label; handwriting); fifth label, ‘ Ich. generosus./ Type. Smith’ (square label; handwriting); sixth label, ‘ HOLOTYPE / Ichneumon generosus
Sm. ♀ /teste Townes et al. 1965: 466 /(Pterocormus) (Labelled by/C. O’Toole 5. ix. 1988)’ (square label, with red margin; printed except for ‘ ♀ ’ handwriting).
Condition. Very good, but the left fore tarsus is missing the third to fifth tarsomeres.
description: Published as part of Shimizu, So & Broad, Gavin R., 2020, Photographic catalogue of the oldest primary types of Japanese Ichneumonoidea (Hymenoptera), those described by Frederick Smith and Francis Walker in 1874, pp. 1115-1198 in Journal of Natural History 54 (17) on pages 1137-1139, DOI: 10.1080/00222933.2020.1776905, http://zenodo.org/record/4116141
Galeus melastomus Rafinesque 1810
Creators: name: Golani, Daniel
Publisher: name: Zenodo
Year: 2021
Subjects: Biodiversity
Taxonomy
Animalia
Chordata
Elasmobranchii
Carcharhiniformes
Scyliorhinidae
Galeus
Galeus melastomus

description: Galeus melastomus Rafinesque, 1810
Galeus melastomus: Ben-Tuvia, 1971a; Baranes, 1979 (Heb.); Golani, 1987b; Darom & Tsurnamal, 1992 (Heb.); Hornung, Krom, Cohen & Bernhard, 1993 (Poll.); Hornung, Sukenik & Gabrielides, 1994 (Poll.); Golani, 1996; Pisanty & Golani, 1996; Golani, 1997 (Heb.); Goren & Galil, 2002; Galil, 2004; Golani, 2005; Golani, 2006; Paz et al. 2018 (gen.).
Galeus melanostomus: Baranes & Diamant, 1983a (Heb.).
description: Published as part of Golani, Daniel, 2021, An updated Checklist of the Mediterranean fishes of Israel, with illustrations of recently recorded species and delineation of Lessepsian migrants, pp. 1-108 in Zootaxa 4956 (1) on page 7, DOI: 10.11646/zootaxa.4956.1.1, http://zenodo.org/record/4691195
Supplementary Information from Ecological drivers of jaw morphological evolution in lepidosaurs
Creators: name: Ballell, Antonio
name: Dutel, Hugo
name: Fabbri, Matteo
name: Martin-Silverstone, Elizabeth
name: Kersley, Aleksandra
name: Hammond, Chrissy
name: Herrel, Anthony
name: Rayfield, Emily
Publisher: name: The Royal Society
Year: 2024
Subjects: classificationCode: 310499
subject: Evolutionary biology not elsewhere classified

description: Supplementary Information for Ecological drivers of jaw morphological evolution in lepidosaurs
Engineering transferrin for cancer therapy
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: One form of cancer treatment involves the administration of cytotoxins for killing cancer cells. However, this approach is limited, since the cytotoxins also nonspecifically kill normal cells. An exciting area of research has therefore evolved to address this challenge, where several research groups have investigated conjugating various cytotoxins to transferrin (Tf). Tf is a potential vehicle, or carrier, for a cytotoxin because its receptor, TfR, has been found to be overexpressed on the surfaces of cancer cells relative to normal cells. One of the main bottlenecks in this approach is that Tf rapidly recycles inside the cell and dissociates at the cell surface, indicating that the window of drug delivery for the Tf conjugate may well be limited to one passage through the cell. Since the probability of delivering a cytotoxin to the cell can be increased with an increase in the number of passages through the cell, we previously investigated a Tf variant that remained associated with a cell for a greater period of time, i.e. exhibited increased cellular association. Specifically, inhibiting the release of iron from Tf in cellular endosomes was found to increase cellular association. A conjugate made with this variant and a cytotoxin was then demonstrated to have enhanced cytotoxic effects on cancer cells relative to a conjugate formed with native Tf. In this proposed project, we aim to investigate Tf mutants that have recently been engineered to exhibit slow iron release properties with the goal of identifying Tf mutants that yield the greatest cytotoxic effects in vitro. At the end of this proposed study, we plan to have identified these candidates so that they may be given to a collaborator at the UCLA School of Medicine for in vivo testing in animals. If we can design Tf mutants that are more effective in delivering their payload, a lower dose of the Tf conjugate can be administered, which has the potential for decreasing toxic side effects. Objective 1: Investigate the cellular association behavior of Tf mutants that exhibited inhibited iron release. Methods 1: Radioactively label the Tf ligands with iodine-125, and analyze their cellular trafficking behavior. Objective 2: Conjugate cytotoxins to the Tf ligands, and investigate their cytotoxic effects. Methods 2: Covalently bind the Tf proteins to the cytotoxins using crosslinkers, and conduct cytotoxicity assays.
Freshwater Wetlands Protection Act Rules, N.J.A.C. 7:7A
Creators: name: No Name Supplied
Publisher: name: New Jersey Department of Environmental Protection (NJDEP)
Year: 2003

description: The Freshwater Wetlands Protection Act rules implement the New Jersey Freshwater Wetlands Protection Act, N.J.S.A. 13:9B-1 et seq. These rules provide stringent standards for activities that disturb freshwater wetlands, transition areas surrounding wetlands and open waters.
Coastal Permit Program Rules, N.J.A.C. 7:7
Creators: name: No Name Supplied
Publisher: name: New Jersey Department of Environmental Protection (NJDEP)
Year: 2007

description: The Coastal Permit Program rules establish the procedures by which the Department reviews permit applications and appeals from permit decisions under the Coastal Area Facility Review Act, N.J.S.A. 13:19-1 et seq., the Wetlands Act of 1970, N.J.S.A. 13:9A-1 et seq., and the Waterfront Development Law, N.J.S.A. 12:5-3. The Coastal Permit Program rules contain the coastal general permits, permits-by-rule and the Long Branch Redevelopment Zone Permit.
The role of MKL1 in megakaryocyte differentiation and the development of leukemia
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: Megakaryocytic leukemia is uncommon in children without Down Syndrome but is associated with a poor prognosis. Recently, a recurrent translocation between chromosomes 1 and 22 was described in infants with megakaryocytic leukemia that results in the fusion of an RNA binding protein (RBM15) to MKL1, a RhoA-dependent transcriptional co-activator of serum response factor. The role of MKL1 or the RBM15-MKL1 fusion protein in normal or malignant megakaryopoiesis, respectively, is unknown, but MKL1 and serum response factor have important roles in cell differentiation in other cell types. In this proposal we will address the following aims. 1) We will determine whether MKL1 activates serum response factor in hematopoietic progenitor cells and megakaryocytes, utilizing a dominant-negative MKL1 to show that MKL1 is required for the induction of serum response factor-dependent genes such as junB and vinculin and that introduction of the active RBM15-MKL1 fusion protein also promotes transcription of these genes. 2) We will determine whether MKL1 promotes megakaryocyte growth or maturation, by expressing either dominant- negative MKL1 or the active RBM15-MKL1 fusion protein in murine bone marrow cells and assessing their effects on megakaryopoiesis, ploidy and proplatelet formation. We will express these constructs also in human hematopoietic progenitor cells or immature MKs to assess their effects on growth and maturation at two developmental stages. 3) We will assess potential transcriptional targets by which MKL1 and RBM15-MKL1 might exert their effects, first investigating published candidates derived from arrays in non-hematopoietic cells that are anticipated to affect megakaryopoiesis, including leukemia inhibitory factor, interleukin-6 and cdc42 effector protein 3. We will determine if activation of MKL1 or expression of RBM15-MKL1 in megakaryocytes induces these genes using quantitative reverse transcription PCR, and overexpress these genes in megakaryocytes to determine if they reproduce the MKL1 phenotype. Additional candidates will be derived from arrays performed in megakaryocytes expressing either dominant negative MKL1 or RBM15-MKL1. These studies will provide new insight into the mechanisms by which the RBM15-MKL1 fusion protein promotes the development of megakaryocytic leukemia and may suggest therapeutic targets for a disease with a very poor clinical outcome.
Coastal Zone Management Rules, N.J.A.C. 7:7E
Creators: name: No Name Supplied
Publisher: name: New Jersey Department of Environmental Protection (NJDEP)
Year: 2007

description: One of the components of a Coastal Management Program approved under the Federal Coastal Zone Management Act is enforceable policies. Enforceable policies are state policies that are legally binding and by which a state exerts control over coastal uses and resources.  The Coastal Zone Management rules represent the State's substantive standards for the use and development of resources in New Jersey's coastal zone. These rules are used to review permit applications submitted under the Coastal Area Facility Review Act (CAFRA), N.J.S.A. 13:19-1 et seq., the Wetlands Act of 1970, N.J.S.A. 13:9A-1 et seq., and the Waterfront Development Law, N.J.S.A. 12:5-3. The rules are also a basis for making recommendations to the Tidelands Resource Council on applications for Tidelands Instruments, and are applied in other Department decision-making pursuant to N.J.A.C. 7:7E-1.2.
Thyroid releasing hormone receptor; a novel target for melanoma chemotherapy
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: Melanoma, an aggressive and fatal malignancy resistant to current therapies, has increased in both incidence and prevalence in the last several decades. The rise in incidence of melanoma coupled with the lack of effective treatments for melanoma necessitates the development of an in depth understanding of both melanoma etiology and chemoresistance. Melanoma cells are unique in that they have the capacity to evade immune surveillance and the toxic actions of DNA damage, microtubule destabilization, or topoisomerase inhibition. These properties have led some to speculate that melanoma cells are “born to survive”. Identification of the mediators of melanoma survival could lead to the development of highly selective, efficacious, molecularly targeted treatment strategies for melanoma. Conventional identification of the mediators of chemoresistance has yet to yield effective combination chemotherapy regimens for treatment of resistant cancers. A recent confluence of technological and conceptual advances now allows the application of novel strategies to derive unbiased comprehensive collections of gene targets that support biological systems. By employing a relatively simple technique that allows selected genes to be specifically inactivated in human cell culture model systems, together with robotic-based optimization, we have identified thyroid releasing hormone as a potential autocrine growth factor for melanoma. Consistent with the results of our genome wide screen, melanoma gene expression data demonstrates that thyrotropin releasing hormone (TRH) is overexpressed in melanoma while genetic data suggests that loss of signaling pathways that inhibit TRH production are tumor promoting. Together, these data suggest that the TRH receptor is tumor promoting. To test the hypothesis that the TRH receptor is a novel melanoma chemotherapeutic target, we will verify that TRHR mediates melanoma chemoresistance in MNT-1 melanoma cells and other cell lines using siRNA loss of function analysis. Other studies will determine if TRHR mediates chemoresistance against other cytotoxic agents. Complementation analysis will be used to define the contributions of other genes implicated in TRH and thyroid hormone signaling to chemoresistance. Three dimensional tissue models will be used to assess the impact of TRH on melanoma chemoresistance in a physiologically relevant context.