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Governor signs into law tax bill to help fund higher education
First bill signing of the 2020 legislative session
Law shifts a portion of the tax burden to large tech companies
By Cameron Sheppard
WNPA News Service
Fewer businesses will be asked to foot the bill for higher education programs after Gov. Jay Inslee signed Engrossed Substitute Senate Bill 6492 on Monday.
The bill will restructure the business and occupation tax and surcharges put in place by legislation passed last year to fund investments in public colleges as well as to provide grants that increase access for low and medium-income students.
"We are going to make massive investments in public higher ed," said Sen. Jamie Pedersen, D-Seattle. "Both for the institutions and more importantly, for the students who need access to these services."
Legislation signed last year and put into effect this year stipulated that on top of the B&O tax rate, certain businesses would also pay a Workplace Education Investment Surcharge.
Pedersen, the new bill's prime sponsor, said he and his colleagues realized the demand for higher education programs was much higher than revenues called for in last year's legislation.
Senate Ways & Means Committee staff member Jeff Mitchell said the tax rate that took effect in January was estimated to have generated $773 million in revenue over four years, while this year's adjustment is estimated to bring in over $1 billion during the same timespan.
Pederson said this new legislation will be "simpler to administer, more predictable and sufficient to meet the needs of the state."
He said the new surcharge will affect less than 15,000 businesses and applies only to those defined as "advanced computing" companies, such as Microsoft or Amazon. The earlier legislation affected more than 80,000 companies.
Advanced computing companies are defined as firms that make computer software or hardware, provide Cloud computing services, manage online marketplaces, or online social networking platforms.
Pedersen said he wanted to focus the majority of the revenue collection for workplace education investment on businesses that "by their nature, rely on highly educated professionals."
Gov. Jay Inslee, seated, signs the first bill of the 2020 legislative session into law. On the right
stands the bill's primary sponsor, Sen. Jamie Pedersen, D-Seattle, who is wearing a red tie.
— Photo by Cameron Sheppard, WNPA News Service
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redpajama_set_name: RedPajamaCommonCrawl


y uncle Mort used to work at a drug store in Los Angeles. One day, in the middle of his shift, Tom Hanks walked in and bought a tube of toothpaste.
"He was a real class act," Mort told me. "He didn't try to cut the line or anything. He just got in the back and waited, like he was a regular person. I couldn't believe he was buying his own toothpaste! I figured a movie star like him would have someone to do that for him. But not Tom Hanks. He's just a down-to-earth kind of guy."
I spend a lot of time in Los Angeles and I hear a lot of stories about Tom Hanks. Everyone seems to have encountered him at some point in their lives. And everyone agrees: Hanks' "nice guy" reputation is well earned. Here are just a few of the anecdotes I've heard over the years.
"One time, I saw Tom Hanks at an Italian restaurant. I looked over and the guy was eating bread. Just putting pieces into his mouth and chewing them with his teeth, like a regular person. I figured a movie star like him would have someone to do that for him. Not Tom Hanks, though. Classiest guy on Earth."
"I drove Tom Hanks to the airport once. He was normal the whole ride. Didn't scream at me, or threaten my life. Craziest thing: He stayed in a seated position the entire time. No levitating. Classiest guy I've ever met."
"I'm sitting on a bench with my family when Tom Hanks walks by on the sidewalk. I don't know what to say, so I just shout out, 'Hey, Tom!' And he stops! So I figure, okay, this is it; I'm going to die. He's going to take out a gun and shoot me point blank in the face, which, let's be honest, is exactly what I deserve. I mean, the guy has a million important things to do, and here I am, stopping his walking. At the very least, I figure he'll make love to my wife in front of me. You know, to prove a point about how the world is his and he can take what he wants and I'm just like an insect to him. But none of this transpires. Instead, he just smiles at me, and says, 'Hey.' Class act."


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Update 2: It's back. Cool!


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By Imogen Calderwood
NewsHealth
Prince William and the World's Leading Football Stars Are Taking Stigma Out of Men's Mental Health
Football is "one of the most powerful, unifying forces in our society."
The UN's Global Goal 3 calls for health and wellbeing for everyone, and that includes mental as well as physical. Male suicide is reaching crisis levels in Britain, and one of the key reasons is because there is still a real stigma around men talking about depression and suicidal feelings. Join the movement by taking action here in support of health and wellbeing for everyone.
Prince William is leading a campaign for men's mental health supported by football stars like Peter Crouch, Thierry Henry, Pep Guardiola, and Gareth Southgate.
As the football season kicked off this weekend, the Duke of Cambridge launched the #HeadsUp campaign — a collaboration between mental health charity Heads Together and the Football Association (FA) — to destigmatise male depression, and get football fans talking about their mental health.
Football, according to the campaign, is "one of the most powerful, unifying forces in our society," and it wants to use that passion to "drive the biggest ever conversation on mental health."
"We wouldn't think twice to ask a mate how he was doing after he broke an arm or an ankle," said Prince William, when launching the Heads Up campaign in May.
"We wouldn't hesitate to talk about our routine at the gym, or even our need to make it a bit more regular," he continued. "But when it comes to our mental health, we — and by we I mean men in particular — often have nothing to say at all."
He added: "The consequences of this silence — confusion, stigma, and even shame — have reached a crisis point in the UK."
📹 The Duke of Cambridge launches #HeadsUp at The @FA#CommunityShield
"We all need to take care of our everyday mental fitness, and provide support to one another when we face setbacks so we can be match fit for whatever lies ahead." - @KensingtonRoyalpic.twitter.com/Zxcdj9lIhM
— Heads Together (@heads_together) August 4, 2019
Suicide is the leading cause of death among people aged 20 to 34 in the UK, and is considerably higher in men, according to the Mental Health Foundation website — with around three times as many men dying from suicide compared to women.
It's the leading cause of death for men under 50 in the UK — and those at highest risk are men aged between 40 and 44.
According to the Mental Health Foundation, one reason that men are more likely to die by suicide may be because they are less likely than women to ask for help or talk about depressive or suicidal feelings.
According to recent stats, just 27% of people who died by suicide between 2005 and 2015 had been in contact with mental health services in the year before they died.
Related Stories July 26, 2019 The Homeless Football World Cup Is Kicking Off in Cardiff This Weekend
Mark Bullingham, chief executive of the FA — of which Prince William is also president — described the statistics on male mental health as "shocking."
"We will work with Heads Up to use the power of football to. tackle the stigma around mental health and raise awareness of the importance of mental fitness," he added.
The Duke of Cambridge featured in a video message played for fans at the FA Community Shield match between Liverpool and Manchester City on Sunday.
"As we talk about the physical fitness of the players involved, it's important we take a moment to think about their mental fitness too," says Prince William, in a video shared on Twitter by Heads Together.
Related Stories June 11, 2019 Closing the Gender Gap for Women's Footballers on Wikipedia
"But we shouldn't confine it to just the teams on the pitch," he continues. "Because we all have mental health. It is just as important for those lining up for Manchester City and Liverpool today, as it is for those watching in the stands and at home."
The video was followed by the team anthems You'll Never Walk Alone and Blue Moon sung by community choirs — highlighting, according to the campaign, the "themes of isolation and the importance of togetherness, pertinent to the core message behind the campaign."
The campaign has launched a 24-hour crisis support line, where if a fan wants immediate support they can text "HeadsUp" to 85258 to connect with a trained crisis volunteer, who will chat to them by text message to help them through the moment and work together on a plan for longer-term support.
Meanwhile, football clubs will reportedly get guides for coaches and managers to spot signs of mental ill-health in players — and advice on supporting them in getting help.
The FA said the campaign "will be activated across all levels of the game from the elite to grassroots and at the biggest moments of the season, including men's and women's England internationals and FA competitions."
TopicsHealthUKBritainStigmaPrince WilliamMental HealthManchesterLiverpoolFootballSuicideDuke of CambridgeHeads TogetherPeter CrouchPep GuardiolaFootball AssociationGareth SouthgateThierry HenryMale Mental HealthHeadsUp


Bruce has a long connection with the Lost World area of southern Queensland . This painting recalls an encounter with a curious cow wandering the roads and coming to a cattle grid across the road and dividing the paddocks. Time for a decision.
Ask Bruce a question regarding "Decisions , Decisions "


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Product listing: Hexokinase II Antibody, UniProt ID P52789 #2106 to eIF3C Antibody, UniProt ID Q99613 #2068
Sort by: Popularity Best Sellers Most Recent Title Product Type Category
Polyclonal Antibody - Hexokinase II Antibody - Western Blotting, UniProt ID P52789, Entrez ID 3099 #2106
Human, Monkey
Background: Hexokinase catalyzes the conversion of glucose to glucose-6-phosphate, the first step in glycolysis. Four distinct mammalian hexokinase isoforms, designated as hexokinase I, II, III, and IV (glucokinase), have been identified. Hexokinases I, II, and III are associated with the outer mitochondrial membrane and are critical for maintaining an elevated rate of aerobic glycolysis in cancer cells (Warburg Effect) (1) in order to compensate for the increased energy demands associated with rapid cell growth and proliferation (2,3).
Polyclonal Antibody - Phospho-Src (Tyr527) Antibody, UniProt ID P12931, Entrez ID 6714 #2105
Application Methods: Immunohistochemistry (Paraffin), Western Blotting
Background: The Src family of protein tyrosine kinases, which includes Src, Lyn, Fyn, Yes, Lck, Blk, and Hck, are important in the regulation of growth and differentiation of eukaryotic cells (1). Src activity is regulated by tyrosine phosphorylation at two sites, but with opposing effects. While phosphorylation at Tyr416 in the activation loop of the kinase domain upregulates enzyme activity, phosphorylation at Tyr527 in the carboxy-terminal tail by Csk renders the enzyme less active (2).
Polyclonal Antibody - Grp94 Antibody - Western Blotting, UniProt ID P14625, Entrez ID 7184 #2104
Human, Monkey, Mouse, Rat
Background: Secretory proteins are synthesized on polysomes and translocated into the endoplasmic reticulum (ER). Inside ER, these proteins are often modified by disulfide bond formation, amino-linked glycosylation and folding. The ER contains a pool of molecular chaperones, including Grp94, to help ensure correct protein folding. Grp94 is a glucose-regulated protein (1) with sequence homology to Hsp90 (2). In addition to its role in helping to facilitate folding of a number of secretory proteins to their correct conformation (3), studies suggest that Grp94 derived from cancer cells also induces anti-tumor immune responses in mouse tumor models (4, 5). One way in which Grp94 promotes tumor immunogenicity is its ability to bind to and present tumor-derived peptides as antigens (6). Furthermore, Grp94 has also been shown to induce maturation of dendritic cells (7). Taken together, Grp94 functions both as a tumor-specific antigen and as an activator of antigen-presenting cells to elicit an anti-cancer immune response (8).
Monoclonal Antibody - eIF2α (L57A5) Mouse mAb, UniProt ID P05198, Entrez ID 1965 #2103
Background: Phosphorylation of the eukaryotic initiation factor 2 (eIF2) α subunit is a well-documented mechanism to downregulate protein synthesis under a variety of stress conditions. eIF2 binds GTP and Met-tRNAi and transfers Met-tRNA to the 40S subunit to form the 43S preinitiation complex (1,2). eIF2 promotes a new round of translation initiation by exchanging GDP for GTP, a reaction catalyzed by eIF2B (1,2). Kinases that are activated by viral infection (PKR), endoplasmic reticulum stress (PERK/PEK), amino acid deprivation (GCN2), or heme deficiency (HRI) can phosphorylate the α subunit of eIF2 (3,4). This phosphorylation stabilizes the eIF2-GDP-eIF2B complex and inhibits the turnover of eIF2B. Induction of PKR by IFN-γ and TNF-α induces potent phosphorylation of eIF2α at Ser51 (5,6).
Monoclonal Antibody - Non-phospho-Src (Tyr416) (7G9) Mouse mAb, UniProt ID P06239, Entrez ID 2534 #2102
Application Methods: Immunoprecipitation, Western Blotting
Polyclonal Antibody - Phospho-Src Family (Tyr416) Antibody - Western Blotting, UniProt ID P06239, Entrez ID 2534 #2101
Polyclonal Antibody - ADAM9 Antibody - Immunoprecipitation, Western Blotting, UniProt ID Q13443, Entrez ID 8754 #2099
Background: The ADAM (A Disintegrin and A Metalloprotease) family of multidomain membrane proteins influences cell signaling and adhesion by shedding cell surface proteins such as cytokines and growth factors, by influencing cell adhesion to the extracellular matrix (ECM), and by directly remodeling the ECM. Conserved domains in ADAM family members include a prodomain, a zinc-dependent metalloprotease domain, a disintegrin domain, a cysteine-rich domain, an EGF-like sequence, and a short cytoplasmic tail (1,2).The prodomain is thought to aid in protein folding. Disintegrin and cysteine-rich domains mediate adhesion, at least in part, through binding to integrins. Phosphorylation of the cytoplasmic tail as well as its interaction with other signaling proteins may influence intra- and extracellular signaling (1). ADAM9 is widely distributed and has been shown to affect migration in skin keratinocytes (3,4). Research studies have shown that ADAM9 is overexpressed in prostate cancer (5), pancreatic cancer (6), gastric cancer (7), and has been linked to invasion and metastasis in small cell lung cancer (8). Research has also shown that an alternatively spliced short (50 kDa) form of ADAM9 containing protease activity is involved in tumor cell invasion (9).
Polyclonal Antibody - RhoB Antibody - Western Blotting, UniProt ID P62745, Entrez ID 388 #2098
Background: Rho family small GTPases, including Rho, Rac and cdc42, act as molecular switches, regulating processes such as cell migration, adhesion, proliferation and differentiation. They are activated by guanine nucleotide exchange factors (GEFs), which catalyze the exchange of bound GDP for GTP, and inhibited by GTPase activating proteins (GAPs), which catalyze the hydrolysis of GTP to GDP. A third level of regulation is provided by the stoichiometric binding of Rho GDP dissociation inhibitor (RhoGDI) (1). RhoA, RhoB and RhoC are highly homologous, but appear to have divergent biological functions. Carboxy-terminal modifications and differences in subcellular localization allow these three proteins to respond to and act on distinct signaling molecules (2,3).
Polyclonal Antibody - Rab7 Antibody - Western Blotting, UniProt ID P51149, Entrez ID 7879 #2094
Background: Rab7 and Rab9 are members of the Ras superfamily of small Rab GTPases (1). Both proteins are located in late endosomes, but exert different functions. Rab7 associates with the RIPL effector protein to control membrane trafficking from early to late endosome and to lysosomes (2,3). Rab7 also helps to regulate growth receptor endocytic trafficking and degradation (3,4), and maturation of phagosome and autophagic vacuoles (4-6). Rab9 interacts with its effector proteins p40 and TIP47 (7,8) to promote the MPR (mannose 6-phosphate receptor)-associated lysosomal enzyme transport between late endosomes and the trans Golgi network (9,10).
Monoclonal Antibody - SCF (C19H6) Rabbit mAb, UniProt ID P21583, Entrez ID 4254 #2093
Application Methods: Flow Cytometry, Immunohistochemistry (Paraffin), Western Blotting
Background: Stem cell factor (SCF) is a growth factor that is essential for hematopoiesis, melanogenesis and fertility. SCF is also known as mast cell growth factor (MCGF), steel factor (SLF), or kit ligand (KL) (1-3). SCF mediates its biological effects by binding to and activating c-Kit (4). SCF induces dimerization of c-Kit followed by trans-autophosphorylation of the cytoplasmic protein tyrosine kinase domain, leading to subsequent recruitment of signaling proteins, tyrosine phosphorylation of substrates and activation of multiple signaling pathways (5,6). SCF/c-Kit may take part in the growth control of human malignancies (7).
Polyclonal Antibody - Centrin-2 Antibody - Western Blotting, UniProt ID P41208, Entrez ID 1069 #2091
Background: Centrins are small conserved microtubule nucleating proteins localized to centrosomes, also known as microtubule organizing centers (MTOC), in eukaryotic cells. Centrin-1 is associated with cells that have cilia and flagella, whereas centrin-2 and -3 are ubiquitously expressed and important in centrosome duplication during cell division, as well as the structure and function of the MTOC (1-3). Human centrin-2 has also been shown to localize to nuclear pores and to have a role in regulation of mRNA export (4). The yeast ortholog of centrin-2, CDC31, plays a part in control of protein degradation and sensitivity to DNA damage (5).
Polyclonal Antibody - CDK7 Antibody - Western Blotting, UniProt ID P50613, Entrez ID 1022 #2090
Background: CDK-activating kinase (CAK) is a complex of CDK7 and cyclin H. The complex is involved in cell cycle regulation by phosphorylating an activating residue in the T-loop domain of cdks (1). Regulation of CAK activity is mediated by T-loop phosphorylation and by association with MAT1, both of which enhance its kinase activity toward the CTD of RNA polymerase II (2,3) and other substrates such as p53 (4). CAK is an essential component of the transcription complex TFIIH and may interact directly with TFIIH helicases (5).
Polyclonal Antibody - MCF2/Dbl Antibody - Western Blotting, UniProt ID P10911, Entrez ID 4168 #2089
Background: The MCF2/Dbl proto-oncogene product is the founding member of the Dbl family of Rho guanine nucleotide exchange factors (GEFs) that are characterized by their Dbl homology (DH) domain (1). GEFs stimulate the formation of the active, GTP-bound form of small GTPases such as Rho, Rac and Cdc42, signaling to various downstream molecules and regulating diverse cell functions. While the overexpressed, full-length Dbl gene has transforming activity (2), mutations resulting in truncated Dbl cause the protein to become highly oncogenic. This truncated form of Dbl, which lacks the amino-terminal 497 amino acids, has constitutive GEF activity (3) and is more stable than the full-length variant (4), allowing for increased signaling to downstream effector molecules.Dbl interacts with ezrin, a member of the ezrin/radixin/moesin (ERM) family of proteins that links the plasma membrane to the actin cytoskeleton. Dbl interacts with ezrin in lipid microdomains, which leads to Cdc42 activation and the regulation of processes such as filopodia formation and cell polarity (5,6). Dbl localization and biological activities are regulated in part by phosphatidylinositol 3-kinase (PI3K) (7). Dbl is also involved in cell survival and inhibits apoptosis through induction of Akt phosphorylation at Thr308 (8).
Monoclonal Antibody - LEDGF (C57G11) Rabbit mAb, UniProt ID O75475, Entrez ID 11168 #2088
Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunohistochemistry (Paraffin), Western Blotting
Background: The LEDGF (lens epithelium-derived growth factor) gene encodes splice variants P75 and P52 (1). LEDGF (C57G11) Rabbit mAb detects the 75 kDA LEDGF splice form. Both LEDGF variants have transcriptional coactivator functions that may regulate gene transcription and mRNA splicing of a variety of proteins that are essential for cell growth and survival. (2,3). LEDGF has also been identified as a factor that can, in serum free media, stimulate the growth and survival of lens epithelial cells and other cell types such as retinal photoreceptor cells, COS7 cells, skin fibroblasts, and keratinocytes (2). In addition to its function as a transcriptional coactivator, LEDGF has been shown to be involved in the pathogenesis of atopic dermatitis (4) and in the activity of HIV1 integrase. LEDGF binds chromatin throughout the cell cycle, and may act as a chromatin docking factor for HIV integrase and other lentiviral pre-integration complexes. It protects HIV integrase from degradation, and influences the pattern of viral integration into the cell genome (5).
Monoclonal Antibody - Axin1 (C76H11) Rabbit mAb, UniProt ID O15169, Entrez ID 8312 #2087
Human, Mouse
Application Methods: Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting
Background: Axin1 (Axis inhibition protein 1) and Axin2 are multidomain scaffold proteins that negatively regulate Wnt signaling. Axin1 interacts with APC, GSK-3β, Dvl, and β-catenin and promotes the GSK-3β-mediated phosphorylation and subsequent degradation of β-catenin (1,2). Upon stimulation of cells with Wnt, Axin1 is recruited to the membrane by phosphorylated LRP5/6, a process that is believed to be crucial for activation of Wnt signaling (3,4). In addition to its role in the Wnt signaling pathway, Axin1 forms a complex with MEKK1 and activates c-Jun amino-terminal kinase (JNK/SAPK) (5). Axin2 (also known as Conductin or Axil) can functionally substitute for Axin1 in mice (6). Axin2 itself is a direct target of the Wnt signaling pathway and therefore serves to control the duration and/or intensity of Wnt signaling through a negative feedback loop (7-9).
Monoclonal Antibody - EGF Receptor (E746-A750del Specific) (D6B6) XP® Rabbit mAb, UniProt ID P00533, Entrez ID 1956 #2085
Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunofluorescence (Paraffin), Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting
Background: The epidermal growth factor (EGF) receptor is a 170 kDa transmembrane tyrosine kinase that belongs to the HER/ErbB protein family. Research studies have shown that somatic mutations in the tyrosine kinase domain of EGF receptor (EGFR) are present in a subset of lung adenocarinomas that respond to EGFR inhibitors, such as gefinitib and erlotinib (1-3). Two types of mutations account for approximately 90% of mutated cases: a specific point mutation, L858R, that occurs in exon 21 and short in-frame deletions in exon 19 (4,5). The most frequent exon 19 deletion is E746-A750, accounting for 90% of lesions at this site, although some rare variants occur.
Polyclonal Antibody - Phospho-Raptor (Ser792) Antibody - Western Blotting, UniProt ID Q8N122, Entrez ID 57521 #2083
Background: The regulatory associated protein of mTOR (Raptor) was identified as an mTOR binding partner that mediates mTOR signaling to downstream targets (1,2). Raptor binds to mTOR substrates, including 4E-BP1 and p70 S6 kinase, through their TOR signaling (TOS) motifs and is required for mTOR-mediated phosphorylation of these substrates (3,4). Binding of the FKBP12-rapamycin complex to mTOR inhibits the mTOR-raptor interaction, suggesting a mechanism for rapamycin's specific inhibition of mTOR signaling (5). This mTOR-raptor interaction and its regulation by nutrients and/or rapamycin is dependent on a protein called GβL (6). GβL is also part of the rapamycin-insensitive complex between mTOR and rictor (rapamycin-insensitive companion of mTOR), and may mediate rictor-mTOR signaling to downstream targets including PKCα (7). Furthermore, the rictor-mTOR complex has been identified as the previously elusive PDK2 responsible for the phosphorylation of Akt/PKB on Ser473, facilitating phosphorylation of Akt/PKB on Thr308 by PDK1 and required for the full activation of Akt/PKB (8).Recently raptor has been identified as a direct substrate of the AMP-activated protein kinase (AMPK) (9). AMPK phosphorylates raptor on Ser722/Ser792 (9). This phosphorylation is essential for inhibition of the raptor-containing mTOR complex 1 (mTORC1) and induces cell cycle arrest when cells are stressed for energy (9). These findings suggest that raptor is a critical switch that correlates cell cycle progression with energy status.
Polyclonal Antibody - La Antigen Antibody - Immunoprecipitation, Western Blotting, UniProt ID P05455, Entrez ID 6741 #2081
Background: La antigen is recognized by antibodies in patients with autoimmune disorders such as systemic lupus erythematosus and Sjögren's syndrome (1). La antigen binds to the 5'-noncoding region of poliovirus RNA and is an IRES trans-acting factor (1,2). Depletion of La antigen reduces the function of poliovirus IRES in vivo (3). La antigen, when phosphorylated at Ser366, has been shown to associate with nuclear precursor tRNAs and facilitate their processing (4). The nonphosphorylated La antigen interacts with the mRNAs that have 5'-terminal oligopyrimidine (5'TOP) motifs to control protein synthesis (4).
Monoclonal Antibody - CHIP (C3B6) Rabbit mAb - Immunoprecipitation, Western Blotting, UniProt ID Q9UNE7, Entrez ID 10273 #2080
Background: The carboxy terminus of Hsc70-interacting protein (CHIP, STUB1) is a co-chaperone protein and functional E3 ubiquitin ligase that links the polypeptide binding activity of Hsp70 to the ubiquitin proteasome system (1). Cytoplasmic CHIP protein contains three 34-amino acid TPR (tetratricopeptide repeat) domains at its amino terminus and a carboxy-terminal U-box domain. CHIP interacts with the molecular chaperones Hsc70-Hsp70 and Hsp90 through its TPR domain, while E3 ubiquitin ligase activity is confined to the U-box domain (2,3). The binding of CHIP to Hsp70 can stall the folding of Hsp70 client proteins and concomitantly facilitate the U-box dependent ubiquitination of Hsp70-bound substrates (4-6). CHIP appears to play a central role in cell stress protection (7) and is responsible for the degradation of disease-related proteins that include cystic fibrosis transmembrane conductance regulator (4), p53 (8), huntingtin and Ataxin-3 (9), Tau protein (10), and α-synuclein (11).
Polyclonal Antibody - Miwi (G82) Antibody, UniProt ID Q96J94, Entrez ID 9271 #2079
Application Methods: Immunofluorescence (Frozen), Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting
Background: The Drosophila piwi gene was identified as being required for the self-renewal of germline stem cells (1). Piwi homologs are well conserved among various species including Arabidopsis, C. elegans, and Homo sapiens (1). Both Miwi and Mili proteins are mouse homologs of Piwi and contain a C-terminal Piwi domain (2). Miwi and Mili bind to Piwi-interacting RNAs (piRNAs) in male germ cells and are essential for spermatogenesis in mice (3-5).
Monoclonal Antibody - Phospho-IKKα (Ser176)/IKKβ (Ser177) (C84E11) Rabbit mAb, UniProt ID O15111, Entrez ID 1147 #2078
Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).
Polyclonal Antibody - TMP21 Antibody - Western Blotting, UniProt ID P49755, Entrez ID 10972 #2076
Human, Monkey, Mouse
Background: TMP21, a type I transmembrane protein, is a member of the p24 cargo protein family, which is highly enriched in the ER, the Golgi and coat protein (COP) I and II transport vesicles (1,2). TMP21 is involved in protein transport and vesicular targeting. In particular, TMP21 influences APP trafficking by stabilizing nascent APP. The absence of TMP21 leads to enhanced maturation and cell surface accumulation of APP (3). In addition, TMP21 is a non-essential component of the γ-secretase complex with the potential to modulate γ-secretase mediated cleavage and Aβ production without having an effect on ε-secretase activity (4).
Polyclonal Antibody - Mena Antibody - Western Blotting, UniProt ID Q8N8S7, Entrez ID 55740 #2075
Background: Mena (mammalian enabled), EVL, and VASP are members of the Ena/VASP family, which is involved in controlling cell shape and cell movement by shielding actin filaments from capping proteins (1). Ena/VASP proteins have three specific domains: an amino-terminal EVH1 domain controlling protein localization; a central proline-rich domain mediating interactions with both SH3 and WW domain containing proteins, including profilin; and a carboxy-terminal domain causing tetramerization and binding to actin (2). Mena interacts with actin filaments at the growing ends localizing to lamellipodia and to tips of growth cone filopodia in neurons. Axons projecting from interhemispheric cortico-cortical neurons are misrouted in newborn, homozygous Mena knock-out mice (3). Mena is phosphorylated at Ser236 by PKA, thereby promoting filopodial formation and elongation in the growth cone (4).Three forms of Mena corresponding to 80, 88 and 140 kD are known. The 80 kD protein is broadly expressed in contrast to the 140 kD protein which is enriched in neural cell types. Alternative splicing produces these forms. The 88 kD protein is mainly found in embryonic cell types and is likely the result of post-translational modification. Expression of all three forms is completely eliminated in Mena homozygous mutant animals (1, 3).
Monoclonal Antibody - Naked2 (C67C4) Rabbit mAb - Immunoprecipitation, Western Blotting, UniProt ID Q969F2, Entrez ID 85409 #2073
Background: Naked1 (Nkd1) and Naked2 (Nkd2) are homologs of Drosophila Naked cuticle, a negative regulator of Wnt/Wingless signaling pathway which functions through a feedback mechanism (1,2). Both Drosophila and vertebrate Naked proteins contain a putative calcium-binding EF-hand motif, however, Drosophila Naked binds to zinc instead of calcium (3). Naked inhibits the canonical Wnt/β-catenin pathway by binding to Dishevelled proteins and directs Dishevelled activity towards the planar cell polarity pathway (2,4). Naked1 is a direct target of Wnt signaling and is overexpressed in some colon tumors due to constitutive activation of Wnt/β-catenin pathway (5). Naked2 is myristoylated and is required for sorting of TGF-α to the basolateral plasma membrane of polarized epithelial cells (6).
Polyclonal Antibody - Histone Deacetylase 4 (HDAC4) Antibody, UniProt ID P56524, Entrez ID 9759 #2072
Background: Acetylation of the histone tail causes chromatin to adopt an "open" conformation, allowing increased accessibility of transcription factors to DNA. The identification of histone acetyltransferases (HATs) and their large multiprotein complexes has yielded important insights into how these enzymes regulate transcription (1,2). HAT complexes interact with sequence-specific activator proteins to target specific genes. In addition to histones, HATs can acetylate nonhistone proteins, suggesting multiple roles for these enzymes (3). In contrast, histone deacetylation promotes a "closed" chromatin conformation and typically leads to repression of gene activity (4). Mammalian histone deacetylases can be divided into three classes on the basis of their similarity to various yeast deacetylases (5). Class I proteins (HDACs 1, 2, 3, and 8) are related to the yeast Rpd3-like proteins, those in class II (HDACs 4, 5, 6, 7, 9, and 10) are related to yeast Hda1-like proteins, and class III proteins are related to the yeast protein Sir2. Inhibitors of HDAC activity are now being explored as potential therapeutic cancer agents (6,7).
Polyclonal Antibody - Mili Antibody, UniProt ID Q8CDG1, Entrez ID 57746 #2071
Background: The Drosophila piwi gene was identified as being required for the self-renewal of germ-line stem cells (1). Piwi homologs are well conserved among various species including Arabidopsis, C. elegans, and human (1). Miwi and Mili proteins are both mouse homologs of Piwi and contain a C-terminal Piwi domain (2). Miwi and Mili bind to Piwi-interacting RNAs (piRNAs) in male germ cells and are essential for spermatogenesis in mouse (3-5).
Polyclonal Antibody - ENPP1 Antibody (Human Specific) - Western Blotting, UniProt ID P22413, Entrez ID 5167 #2070
Background: Ectonucleotide pyrophosphatase-phosphodiesterase 1 (ENPP1) is a single-pass, type II transmembrane protein primarily involved in ATP hydrolysis at the plasma membrane. Targeting of ENPP1 to the basolateral cell surface relies on the presence of a carboxy-terminal di-leucine-based signal (1). ENPP1 plays important roles in bone mineralization and soft tissue calcification (2-5). Mutations in the corresponding ENPP1 gene cause generalized arterial calcification in infancy (GACI) and idiopathic infantile arterial calcification (IIAC) (6,7). ENPP1 inhibits insulin receptor function and overexpression of this enzyme causes insulin resistance and glucose intolerance in mice (8,9). Genetic variants of ENPP1 have been associated with obesity and type 2 diabetes (10-12).
Polyclonal Antibody - DLK1 Antibody - Immunoprecipitation, Western Blotting, UniProt ID P80370, Entrez ID 8788 #2069
Background: DLK1 (delta-like-1), also known as fetal antigen 1 (FA1) and preadipocyte factor 1 (pref-1), is a member of the epidermal growth factor (EGF)-like family of proteins, containing six tandem EGF-like repeats (1,2). DLK1 is a paternally expressed, imprinted gene that plays an important role in normal development and in the maintenence of homeostasis of adipose tissue mass (3). DLK1 deficient mice display growth retardation, obesity, skeletal malformation, and increased serum lipid metabolites (4). It has been reported that the ectodomain of DLK1 is shredded from the cell surface and inhibits adipocyte differentiation ( 5-7).
Polyclonal Antibody - eIF3C Antibody - Western Blotting, UniProt ID Q99613, Entrez ID 8663 #2068
Background: Translation initiation requires a set of factors to facilitate the association of the 40S ribosomal subunit with mRNA. The eIF4F complex, consisting of eIF4E, eIF4A, and eIF4G, binds to the 5' cap structure of mRNA. eIF4F and eIF4B unwind the secondary structure of mRNA at its 5' untranslated region. The 40S ribosomal subunit, along with some initiation factors including eIF3, then binds to the 5' mRNA cap and searches along the mRNA for the initiation codon. eIF3 is a large translation initiation complex with 10 to 13 different subunits. eIF3A, eIF3B, eIF3C, eIF3E, eIF3F, and eIF3H are the core subunits critical for the function of this complex. eIF3 physically interacts with eIF4G, which may be responsible for the association of the 40S ribosomal subunit with mRNA (1). eIF3 also stabilizes the binding of Met-tRNAf.eIF2.GTP to the 40S ribosomal subunit and helps keep the integrity of the resulting complex upon addition of the 60S ribosomal subunit (2). Studies have shown that mTOR interacts with eIF3 directly (3,4). When cells are stimulated by hormones or mitogenic signals, mTOR binds to the eIF3 complex and phosphorylates S6K1 (3). This process results in the dissociation of S6K1 from eIF3 and S6K1 activation. The activated S6K1 then phosphorylates its downstream targets including ribosomal protein S6 and eIF4B, resulting in stimulation of translation. Further findings demonstrated that activated mTOR signaling induces the association of eIF3 with eIF4G upon stimulation with insulin (3).


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The Conservatives are purposely underfunding public schools in an attempt to let them fail so they can promote private schools and legal segregation. However, they are hurting their own people and children in the process.
Skimpy budgets, low pay and public disrespect is prompting educators to abandon the classroom in droves.


I didn't think they would go for it, seeing as 15th street would take up a sizable chunk of the property, but AMLI arts center is planning for 15th street to be extended on the south side of their property. They've designed the building with retail, a gym, and a lobby fronting the future 15th street. Apparently GDOT actually owns the south half of the lot. So the street grid is slowly being glued together.
Very nice. Always happy to see the street grid being fixed.
Unfortunately from what I've heard they're contributing to keeping Spring a back alley by putting their garage there, but that's still good news and might encourage more infill between Spring and the connector. Are there renderings or plans somewhere?
their garage will be there, but it will have retail on the ground floor and an artistic covering for the deck. it doesn't look so much like a deck.
I hope that comes to pass as it would be a fabulous development & was one of the sidebar topics in a thread here about that specific area of Midtown about a month ago.
A more orderly traffic flow would result in that area as 15th Street, which should have been completed on down to at least Spring St. when it was originally platted as a street, would more effectively carry traffic between Spring & Peachtree. That would be somewhat of a reliever for 14th St.
Perhaps 15th could even be extended on west down to the Williams St. segment at the base of the hill that operates both as a northbound frontage road & as the connection to the I-75 on ramp.
Really? That's very good then. This will be a great addition all the way around (literally).
Glad to see the super block slowly being broken apart.
Pricing for the smallest units—650-square-foot studios—starts at more than $1,500 a month and quickly goes up from there.
One-bedroom, one-bathroom options require more than $3,200 a month for some upper-level units, while two-bedroom, two-bathroom penthouses will go for more than $5,000 monthly.
"One-bedroom, one-bathroom options require more than $3,200 a month for some upper-level units, while two-bedroom, two-bathroom penthouses will go for more than $5,000 monthly."
And yet you'll hear people claim that density doesn't drive values up.
I guess if Brookhaven would only grant some tax breaks to build another apartment complex these prices would come way down.
And how much do you think a brand new high-end single family home would rent for on this site if we had artificially limited density here?
Remember Econ 101, high demand and low supply gets you high prices. People want urban living and we are not building enough is the problem.


A look at ten key quotes following Butler's 91-78 win over DePaul on Feb. 16.
A look at ten key quotes following Butler's 80-71 win over St. John's on Jan. 19.
A look at ten key quotes following Butler's win over Creighton on Jan. 5.
A look at eight key quotes following Butler's 84-76 loss to Georgetown on Jan. 2.


text:
Lyrics: The Rock Island Line
Album: Give My Love To Rose
Song: The Rock Island Line
The Rock Island Line lyrics
Now this here is the story about the Rock Island Line
Well, the Rock Island Line she runs down into New Orleans
There's a big toll-gate down there
And you know when you got certain things on board
When you go through the toll-gate
Well, you don't have to pay the man no toll
Well, a traindriver, he pulled up to the toll-gate
And the man hollered nicely what all he had on board
"I got live stock, I got live stock
I got cows, I got pigs, I got sheep
I got mules, I got all live stock
Well, they said, you're all right boy"
You don't have to pay no toll
You just go right on through
So, he went on through the toll-gate
And as he went through
He started pickin' up a little bit of speed
Pickin' up a little bit of steam
He got on through and he turned to look back at the man
"Well, I fooled you, I fooled you
I got pig iron, I got pig iron
I got all pig iron
Down the Rock Island Line, she's a might good road"
Rock Island Line it's the road to ride
Rock Island Line is a mighty good road
Well, if you ride it you gotta ride it like you find it
Get your ticket at the station for the Rock Island Line
Oh, cloudy in the west and it looks like rain
Around the curve comes a passenger train
Northbound train on a southbound track
He's already leaving, but he won't be back
Well, the Rock Island Line, she's a might good road
Oh, I may be right and I may be wrong
But you're gonna miss me when I'm gone
Well, the engineer said before he died
There are two more drinks that he'd like to try
The doctor said, what could they be
A hot cup of coffee and a cold glass of tea
Tags on The Rock Island Line
Popularity The Rock Island Line
Reviews The Rock Island Line...


Asian equity markets were mostly negative amid spill-over selling from Wall St where all majors finished lower and the S&P 500 snapped an 8-day win streak as sentiment was pressured by EU-US trade tensions and downward revisions to IMF's global growth forecasts. ASX 200 (+0.1%) was initially subdued with the energy sector pressured by a pullback in oil prices and with heavy losses seen in Crown Resorts after Wynn Resorts abruptly ended takeover talks, although the index has since pared its losses amid strength in gold miners, tech and the largest weighted financials sector. Nikkei 225 (-0.7%) suffered from the recent flows into JPY and disappointing Machine Orders, while Hang Seng (-0.3%) andShanghai Comp. (-0.4%) conformed to the global downbeat risk tone amid further PBoC inaction and as participants awaited upcoming central bank activity and any fresh developments in the US-China trade saga. Finally, 10yr JGBs were marginally higher as they tracked gains in T-notes amid the risk averse tone across the region, while the BoJ were also present in the market with today's Rinban operation heavily focused on the belly.
In FX markets, price action across the major pairs was mostly uneventful ahead of today's ECB policy meeting and FOMC minutes, although the DXY was marginally firmer and back above the 97.00 level. As such, the greenback's main counterparts were subdued with EUR/USD contained near the prior day's lows amid anticipation of a potentially more dovish tone at the ECB and amid escalating EU-US trade tensions, with the pair also constrained by its close proximity to 5, 10 and 20 DMA levels. GBP/USD traded sideways ahead of the EU emergency summit where PM May's hopes for a Brexit delay until June 30th is likely to be turned down. Elsewhere, the risk averse sentiment hampered USD/JPY and JPY-crosses, while AUD/USD initially softened due to its high-beta properties and with a recent pull back in oil doing no favours for the currency. Furthermore, Westpac also reaffirmed its forecasts for the RBA to cut rates in August, although AUD later recovered following comments from RBA Governor Debelle which were less dovish than some had hoped as he hinted of a data dependent approach and was bullish on the labour market.
Commodities were mixed overnight in which oil consolidated after its recent pull back from multi-month highs, while overnight news flow has been on the bearish side including EIA reducing its global oil demand growth forecasts and a larger than expected build in headline API crude stockpiles. Nonetheless, WTI crude futures have just about held on to the USD 64.00/bbl level, while RBOBoutperformed the energy complex as gasoline inventories showed a drawdown of 7.1mln bbls vs. Exp. 2.0mln bbls draw. Elsewhere, gold prices were flat amid tentativeness ahead of the ECB meeting and FOMC minutes, while copper was also lacklustre amid the risk averse tone and with Dalian iron ore futures snapped a 7-day win streak.
Yields narrowed slightly along the curve in light trade ahead of Wednesday's risk events (FOMC mins, Clarida speaks after market, ECB, Brexit conference). A soft NFIB survey resulted in some buying interest, and Trump's Twitter trade war salvos also found buyers. The IMF lower growth expectations were also cited as a reason to buy. The Aramco offering of USD 12bln 5-parter didn't dent the complex too much, despite books reportedly climbing over USD 100bln. The Treasury's sale of USD 38bln of 3-year notes was ho hum; the auctioned tailed, and the yield was the lowest since Feb 2018. Direct participation rose sharply. Tomorrow the Treasury will auction 10-year notes; the last 10s auction stopped-through the screens, and saw the lowest yield at auction since Jan 2018; cover, meanwhile, was the highest since June, with dealers taking their lowest takedown since March 2017, leaving investment funds with a slightly higher takedown, while foreign participation was relatively unchanged. US T-note (M9) futures settled 6 ticks higher at 123-20+.


This is an American Heart Association CPR class with a 2 year certification. Required books included.
This class is intended for those needing CPR and AED certification for all ages and for non-healthcare providers (teachers, daycare, personal trainers etc). It is a 2 year certification and the required book is included.
This class is intended for those needing CPR, AED and First Aid certification for all ages and for non-healthcare providers (teachers, daycare, personal trainers etc). It is a 2 year certification and the required book is included.


I have my own address suggestion service that returns the format necessary to handle /findAddressCandidates? calls such that it works with the geocoder widget on default settings. I added a faked out root-level json call so I could get it added to our organization's geocoders under Edit Settings > Utility Services. I do not see any calls challenging the service in the web logs, other than the root-level one, when I add the geocoder, load a webmap in the online viewer, or use the embed code on our website, but the geocoder will not get loaded in the widget. As far as I can tell this is the same js geocoder widget being used, but the geocoders array has only one entry for our ArcGIS Server service. Does anyone know what it might be checking for that prevents it from being loaded in the widget?
Portland Locator is the one that hits our ArcGIS Server compound locator service.
So, making the geocoder name "Custom" or checking Place Finding makes it show up, however the geocoder widget options needs to have autoComplete: true to display suggestions while typing.
UPDATE: the online viewer does suggest results but the embed code version does not.
UPDATE 2: embed code has autoComplete: hasEsri so adding ESRI World geocoder as a third option then sets autoComplete: true.
Looks like an issue we should look at in the embed code. I'll look into modifying the embed code so that it can enable autoComplete when the world geocoder isn't displayed.
Aaron, it looks like this would be much simpler if ArcGIS locators supported suggestions offering the same out of the box capabilities as the ArcGIS World Geocoding Service. Esri is actively working on adding suggestions capabilities for locators organizations build from their own address data. Look for this new capability for locators built with ArcGIS 10.3 and hosted with ArcGIS Server 10.3.


text:
AG-Clanforum » Forum » Off Topic » The Detroit Lions should claim former Dolphins DT Jordan Phillips » Antwort erstellen
The Detroit Lions should claim former Dolphins DT Jordan Phillips 01.12.2018 03:24
On Tuesday Youth Kenny Golladay Jersey , the Detroit Lions made an odd transaction. They waived special teams player Dee Virgin. While the move itself wasn't all that surprising, the fact that Detroit had no corresponding move, leaving them with an empty roster spot, is somewhat strange. Typically, that's a sign the team has an addition in mind, and we'll likely hear of it on Wednesday.I, too, have a transaction in mind for the Lions, and it has to do with a move the Miami Dolphins made on Tuesday. They added center Wesley Johnson (remember him?) and promoted defensive end Cameron Malveaux from the practice squad. To make room for the two, they placed center Daniel Kilgore on injured reserve, but more relevant to our interests, they waived former second-round pick, defensive tackle Jordan Phillips. The Lions should absolutely put in a claim for Phillips, and here's why.The Lions' interior defensive line is really badDetroit was hoping to get serious contributions out of two key free agent pickups: Sylvester Williams and Ricky Jean Francois. The former had all the promise of a nose tackle, while the latter had valuable knowledge and experience of the Matt Patricia scheme. Francois has already lost the starting job to A'Shawn Robinson, who entered the season a healthy scratch. Williams has just five tackles in four starts, and even though his job is more to fill space, he hasn't been doing that either. His PFF grade of 61.9 is good for 77th among interior defenders. Phillips fits the physical profile of Detroit's needsAt 6-foot-6, 341 pounds, Phillips is exactly the kind of player the Lions could use as a rotational nose tackle when Williams is ineffective, injured, tired or a combination of all three. Phillips is fairly gifted athletically (6.53 RAS), and his incredibly tall frame makes him a tough man to push around in the run game.His NFL Draft profile reads as exactly someone this Lions defense desperately needs. From Lance Zierlein:So not only does he physically fit what the Lions need, but he excels at exactly what the Lions schematically need out of a nose.The downsidesAt this point in the season, you aren't going to pluck a player from waivers or free agency that will drastically alter the course of your season, unless said player comes with some serious baggage (hi, Dez Bryant). So, yeah, Phillips isn't going to be the best player on the defense suddenly. Phillips has been publicly called out for his inconsistent play before Youth Taylor Decker Jersey , accused of dogging certain plays when tired."The bottom line is Jordan has got to play better overall," Vance Joseph, his defensive coordinator, said back in 2016. "Out of 35 plays, Jordan is playing a solid 25 plays very solidly. He's having four or five plays where it's not very good."It went on like that for a couple years in Miami, leading Jordan, once a starter alongside Ndamukong Suh, to be delegated to a rotational role. Phillips hasn't started a game this year and has played in just 124 total defensive snaps. He wasn't very happy about that: And his first reaction upon getting cut by the Dolphins? Pure bliss:For many, that's a clear red flag in terms of character. Someone who doesn't defer to the coaches may struggle when adversity inevitably hits. Desperate times call for desperate measuresAdmittedly, that's a lot of downsides for someone I'm banging the table for, but the Lions are desperate. It's doesn't help that Phillips may not be well-versed in Patricia's system and is currently the third lowest graded interior defender according to Pro Football Focus, but this team is bleeding out, allowing nearly 160 rushing yards per game and 5.3 yards per carry. Last year, the worst run defense allowed just 4.9 YPC. Phillips had very clearly mentally checked out in Miami, and we've already seen some new additions make an immediate impact for Detroit. Eli Harold, added just before the season, has three sacks already. Romeo Okwara, added during Week 1, has been the leading snap-getter on the defensive line over the past two weeks, garnering over 80 percent of snaps in games against the Patriots and Cowboys. "Change of scenery" is an often-used excuse to drum up hope that a busted player could succeed under a new team, and that could very well be what I'm pitching here. But there's not much room for this Lions defense to fall, and a player like Phillips comes cheap (still on his rookie contract) and without much risk. Put Phillips in a rotational role to begin in the hopes that his limited role will minimize the plays he takes off. If he shows promise and understands the scheme, there's no reason why he couldn't displace Sylvester Williams as an eventual starter or at least share the role equally come November.Film Room: Taking a look at Jarrad Davis' success and failures in preseason so far It is already pretty well documented that Detroit Lions linebacker Jarrad Davis had a rough rookie season. The 2017 first-round pick had struggles in coverage in 2017 and even became unplayable on passing downs in the latter stages of the season. His sophomore year with a new coaching staff gives him a chance to put his past struggles behind him and this preseason was his first chance to show that he can turn it around. His preseason has not gone as planned, though. The issues he had in coverage last season still seem to haunt him, and he has made a few key mistakes that have cost the team. Davis has made a few great plays in preseason, though, and they mainly came in the run game.Davis is great at finding gaps in the offense's run blocking and exploiting them to make plays. He is a great at shooting through gaps and causing mayhem in the backfield. The linebacker can rack up tackles for loss and stuff runs at the line of scrimmage if given the opportunity. This was also his greatest strength in college at the University of Florida and definitely the skill that earned him his first-round status. While he did miss a few crucial tackles in the Lions third preseason game against the Tampa Bay Buccaneers, it was on a wet sloppy night where he may have had trouble gaining proper footing. His tackling form has always been hit or miss, but the only game this month where he made such glaring errors was against the Bucs in unusual conditions. While it is something to note Youth Christian Jones Jersey , it's not something to really knock him for, especially when he was only in position to make some of the tackles he missed because of his ability to shoot through gaps so well. While Davis is great at shooting through gaps and taking advantage of any chinks the armor of the opposition, he isn't very good at eating space in run defense. If a gap doesn't open up for him, then he isn't good at creating one. He gets blocked out of plays way too easily and does not have any real moves in his arsenal that he can use to shed blocks. He can make plays if the offense gives him a chance to, but he is a poor playmaker on his own. A run-stuffing linebacker needs to be able to eat up space in the middle of the opposition's offensive line and create traffic on the interior to force runs back outside. Davis still has not shown that he can do this at the NFL level, and that's a real concern entering Year 2.These faults in his game also make him a poor pass rusher. He can't shed off blockers when rushing the passer, is too stiff and doesn't have the bend or athleticism necessary to really create interior pressure. Just like he does against the run, though, Davis can fire through the gaps that open in pass protection to make plays in the backfield. He is great at blitzing from the second level of the defense if the guys in front of him can stretch out the protection. The linebacker also can cannon through the offensive line on delayed blitzes as well. Davis will never be a great pass rusher from the interior, but he has shown that he can bring a second wave of pass pressure if the coverage behind him allows the time. The aspect of Davis' game that earns him the most criticism are his failures in pass coverage. Through three weeks of preseason there is no indication that he has grown at all as a coverage linebacker. His instincts often fail him, and he often just wanders himself out of position, like on this play against the New York Giants.Giants running back Wayne Gallman runs a route out of the backfield and is to be picked up by Davis in man coverage. This looks to be an option route, where Gallman will either break inside on an angle route or outside into a quick out. Davis follows him towards the end of the offensive line, but drifts too far to the outside. The running back sees this and breaks his route back inside creating an easy touchdown throw for his quarterback. The most frustrating thing about this play is that Davis wasn't even beat by the running back, he beat himself. There is reason for him to drift that far outside. He vacated the middle of the field where he had no help between himself and the endzone. If Davis had stayed inside and given up outside leverage instead he would have forced the quarterback into a harder throw and forced the running back into an area where there were more defenders around to break up the pass. Davis getting beat in coverage without much effort by the offense has been a continuing concern for him, even in zone coverage. On this play against the Buccaneers, Davis was responsible for covering the middle hook route. When the Bucs tight end runs a route behind Davis and breaks it off to his inside, the linebacker should have been there to bracket him and take away the throw. Instead, Davis had wandered too far to his left, staring at the running back who ran a flat route. The running back had already been picked up by a different linebacker and there was no reason for him to be occupied. He gives up his position inside and the Bucs get an easy first down throw. The linebacker has a knack of getting preoccupied by teams' opposing running backs and wandering himself out of position. Even when his assignment is clearly not the running back it still becomes his focus anyways. This tunnel vision also makes him a liability on play-action passes. Wandering himself out of position also allowed Tampa Bay to convert a fourth-down play last Friday.It looks like Davis' assignment here is to play man coverage against the running back. The running back stays back in pass protection. Davis should have stayed back at the second level and waited for the back to make a move, but he instead rounds the pocket to chase him. By making a move all the way around the pocket, not only does Davis lose any sort of middle contain the Lions defense has but if the running back was planning on slipping out of his blocking stance into a route then Davis would have been well out of position to pick him up. There was no reason for Davis to make the move and just like the other plays he walked himself out of position instead of being forced to do so. While Davis obviously has some potential to succeed in the NFL, he is going to seriously have to grow as a player in order to thrive in this league. As I mentioned in my Eli Harold film piece last week, a linebacker that can not pass rush well or drop into coverage will not last long in today's NFL. Davis will obviously be given more time than the average player to figure it out due to his status as a first-round pick. For his own sake, and the sake of Detroit's defense, it needs to be sooner rather than later.


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text:
January 15, 2018 Youtuber
Lucas Rangel Profile | Contact details (Phone number, Instagram, Twitter, Facebook)
Lucas Rangel Idade, Age, Bio, Profile | Contact details (Phone number, Instagram, Twitter, Facebook address)-Lucas Rangel is Brazilian YouTube and Vine Star, who is best known for his hilarious and comedic Videos. He also has a YouTube channel under the name rangeldovine with more than 150,000 subscribers with only 7 videos posted in the channel's first 5 months. He has a younger sister named Ana Laura. Lucas has posted his first Vine, titled "You Find Us Chasing the Tone," on November 4, 2013. He had more than 1.3 million followers on Vine when the app was shut down.
Personal Profile:
Name: Lucas Rangel
Nick Name: Lucas
Birth Place: Belo Horizonte, Minas Gerais, Brazil
Birth Sign: Taurus
Profession: YouTuber and Vine Star
Nationality: Brazilian
FACEBOOK: @lucasranngel
This is the Official Page on FACEBOOK of Julio and he has assembled more than 2M Likes. He has updated his videos and Photos on this Page. If you want to Connect with him, click on link which is given above.
INSTAGRAM: @lucasranngel
He has an official account on INSTAGRAM where he has enlisted with 4M Followers. If you want to follow him then visit the above link.
YOUTUBE: @rangeldovine
He has an official channel on YOUTUBE in which he has posted his popular videos. On his channel, he has acquired more thsn3M subscribers. If you want to subscribe his channel then visit the above link.
TWITTER: @lucasranngel
He has joined TWITTER in 2011 where he has posted his videos and Photos. If you want to Connect with him then click the above link.
Permission is not granted to access his phone number.
Other Famous Celebs-
Medina Singer
Tellaman
Comment below your views about Lucas Rangel.
Bryan Lanning Profile | Contact details (Phone number, Email, Instagram, Twitter)
Jimmy Zhang Profile | Contact details (Phone number, Instagram, Twitter, Facebook)


text:
Virginia Wildland Firefighters Oral Histories, 2006
DeHart
Virginia Wildland Firefighters Oral Histories
SdArch 32
10 audiocassettes, .05 Cubic Feet
The Virginia Wildland Firefighters Oral Histories, 2006, is comprised of three sound recordings of interviews with US Forest Service Fire Fighters on their experiences fighting fires in the mountain region of Virginia, from 1940-2005. The collection includes transcripts, photographs, and other supplemental documents.
[item description], [box #, folder #], Virginia Wildland Firefighters Oral Histories, 2006, SdArch 32, Special Collections, Carrier Library, James Madison University.
Carol DeHart is a freelance writer and independent scholar from Fulks Run, Virginia. Carol DeHart wasa Fire Instructor and Emergency Medical Technician, and is a charter (1987) member of the Bergton Volunteer Fire Department, and former squad boss and fire line EMT with the US Forest Service. Between 2001-2006, she conducted three grants from James Madison University Library to record and transcribe nine oral history interviews, including the Fading Rural Lifeways in the Bergton/Criders area of Rockingham County Oral History Project (SdArch 26) and the John Stewart Oral History (SdArch 25). In 2010, she completed an interview with Broadway Firefighter (SdArch 39).
Gerald Fawley was the first USFS employee to staff the High Knob Fire Tower on Shenandoah Mountain. He currently resides in Parnassus, Virginia. Wade Rogers is a retired USFS Fire Manager Officer from Spring Creek, Virginia. John Coleman is a retired USFS District Ranger from Edinburg, Virginia. Kenny May is a retired USFS Timer Specialist and Fire Fighter from Bergton, Vriginia. Terry Slater, who assisted DeHart in the interview with Fawley, is a USFS Wildlife Biologist and Incident Commander from Bridgewater, Virginia.
The interviews focus on wildland fire fighting and the US Forest Service experiences from 1940 through 2005. Topics addressed in the interviews include memories of fire towers, early communications, tools, clothing, transportation, family life, fire-fighting techniques and stories.
The interviews are arranged chronologically, by the date of the interview.
Access to oral histories is governed by agreements with the interviewees. Collection open to research. Researchers must register and agree to copyright and privacy laws before using this collection. Please contact Research Services staff before visiting the James Madison University Special Collections Library to use this collection.
Oral histories audio and transcripts are either in the public domain or the copyright interests have been transferred to the James Madison University Special Collections Library. For more information, contact the Special Collections Library Reference Desk (library-special@jmu.edu).
In order to streamline the process of applying collection numbers, Special Collections staff completed a large-scale renumbering campaign in the spring of 2017. This collection was previously cataloged as SC 0029
Audiocassettes were converted to mp3 and wav files by Kirsten Mlodynia of Carrier Library Innovation Services, in July 2018.
Gingrich, Tyler and Caroline Whitlow. "High Knob Fire Tower." Friends of Shenandoah Mountain: Exploring Shenandoah Mountain's History. Accessed July 24, 2018. http://www.friendsofshenandoahmountain.org/history-of-high-knob-fire-tower.html
Wade Kermit Rogers, interviewed by Carol M. DeHart, February 7, 2006
This interview records the reflections of Wake Kermit Rogers, his life and work with the U.S. Forest Service as a Fire Tower Lookout man, Timber Technician and Fire Management Officer from 1962-1994. Transcription includes text of Psalm 121 with signature by interviewee.
Transcript and Supporting Documents, February 7, 2006 box 1 folder 1
Original audiocassette #1, February 7. 2006 Media Cabinet 1 Audiocassette SA032-CS-001
Original audiocassette #2, February 7, 2006 Media Cabinet 1 Audiocassette SA032-CS-002
Gerald F. Fawley, interviewed by Carol M. DeHart, January 10, 2006
This interview records the reflections of Gerald E. Fawley, his life and work staffing the fire towers. Transcription includes appendix with the following contents: A lookout tower man reminisces; Sibley stove and tent notes; Osborne fire finder; Remembrances; 1930's photographs; High Knob Fire Tower notes; 2006 photographs.
Transcript and Supporting Documents , January 10, 2006 box 1 folder 2
Original audiocassette #1, January 10, 2006 Media Cabinet 1 Audiocassette SA032-CS-004
Kenny May and Wade Kermit Rogers, interviewed by Carol M. DeHart, undated
This interview records the reflections of Kenny May and John Coleman, talking about their U.S. Forest Service and fire fighting experiences. Within introduction of transcript, "John William Coleman, [retired District Ranger, Lee Ranger District, Type II Incident Commander, 1957-1998] and Kenneth Edward May [Timber Sale Administrator, 1965-2006]". Transcription includes appendix with the following contents: Kenny May, photos, article and notes, "Notice to Loggers," Fire Tower Log; John Coleman Award article, poster in Lee District work center, reprint newspaper photo, two poems and "Diary of a Fire"; Article: "The Fire Warden System on the Shenandoah" by Helen Gordon, 1929.
Transcript and Supporting Documents , undated box 1 folder 3


text:
Healthcare Industry News: melphalan
Devices Drug Delivery Oncology Personnel
Delcath Systems, Inc. Appoints David McDonald Chief Financial Officer
New CFO to Spearhead Business Development and Strategic Alliance Initiatives
NEW YORK, Sept. 14 (Healthcare Sales & Marketing Network) -- Delcath Systems, Inc. (Nasdaq: DCTH ), a medical technology company testing its proprietary treatment method for primary and metastatic cancers to the liver, announced that it has appointed David Alan McDonald Chief Financial Officer of the Company, effective today. McDonald, 49, was formerly the Senior Vice President of Business Development at AngioDynamics, Inc. (Nasdaq: ANGO ) where he led the firm's business development activities.
"David brings a broad base of business knowledge to Delcath," said Eamonn Hobbs, President and CEO of the Company. "He has an extensive financial and business development background and understands the dynamics of commercializing new technologies, international licensing, marketing and strategic development. We are excited to have David onboard. He will be an asset to our team as it prepares for FDA submission by mid-2010, gains CE Mark approval and pursues strategic relationships with outside parties."
The CFO role at Delcath had been vacant since December 2008, when the previous CFO resigned to pursue other interests.
McDonald founded Minneapolis-based Cornerstone Healthcare Advisors LLC in April 2005, which he led until joining AngioDynamics in July 2008. At Cornerstone he provided advisory and consulting services to emerging medical technology companies and their financial sponsors.
Prior to 2005, McDonald was a Managing Director and leader of Medical Technology Investment Banking at RBC Capital Markets where he developed senior and Board level relationships with leading private, public and venture capital firms in the medical device and diagnostics industries. While at RBC and Cornerstone, Mr. McDonald advised on more than 50 banking deals.
Before his involvement with these companies, Mr. McDonald was a Senior Vice President and Equity Portfolio Manager at Investment Advisers, Inc. as well as a research analyst covering the healthcare industry for more than a dozen years. He received a Bachelor of Arts Degree in Economics from St. Olaf College in Northfield, Minnesota in 1982
About Delcath Systems, Inc.
Delcath Systems, Inc. is a medical device company specializing in cancer treatment. The Company is testing a proprietary, patented drug delivery system for the treatment of liver cancers. Delcath's novel drug delivery platform is testing the delivery of ultra-high doses of anti-cancer drugs to the liver while preventing these high doses of drug from entering the patient's bloodstream. The Company is currently enrolling patients in Phase III and Phase II clinical studies for the treatment of liver cancers using high doses of melphalan. The Company's intellectual property portfolio consists of twenty-seven patents on a worldwide basis including the U.S., Europe, Asia and Canada. For more information, please visit the Company's website at www.delcath.com.
The Private Securities Litigation Reform Act of 1995 provides a safe harbor for forward-looking statements made by the Company or on its behalf. This news release contains forward-looking statements, which are subject to certain risks and uncertainties that can cause actual results to differ materially from those described. Factors that may cause such differences include, but are not limited to, uncertainties relating to our ability to successfully complete Phase III clinical trials and secure regulatory approval of our current or future drug-delivery system and uncertainties regarding our ability to obtain financial and other resources for any research, development and commercialization activities. These factors, and others, are discussed from time to time in our filings with the Securities and Exchange Commission. You should not place undue reliance on these forward-looking statements, which speak only as of the date they are made. We undertake no obligation to publicly update or revise these forward-looking statements to reflect events or circumstances after the date they are made.
Source: Delcath Systems
Search: Delcath Systems


For the musician, see Henry Sloan.
Henry Clay Sloan (August 12, 1846 – February 15, 1915) was a member of the Wisconsin State Assembly.
Henry C. Sloan was born in DeRuyter, New York, on August 12, 1846. His father, A. Scott Sloan, and uncle, Ithamar Sloan, both became members of the United States House of Representatives. On November 19, 1879, he married Helen Lois Phinney.
During the American Civil War, Sloan originally enlisted with the 5th Wisconsin Volunteer Infantry Regiment of the Union Army. Conflicts he took part in include the Battle of the Wilderness, the Battle of Spotsylvania Court House, the Battle of Cold Harbor and the Siege of Petersburg. In 1864, he became an officer in the United States Marine Corps. Sloan resigned from the Marine Corps the following year and became a first lieutenant with the 48th Wisconsin Volunteer Infantry Regiment of the Union Army. In 1866, prior to being mustered out with the 48th, Sloan also became a member of the regular United States Army, and briefly served with both units. He also became a first lieutenant with the regular Army.
Sloan was a member of the Assembly during the 1881 and 1895 sessions. Other positions he held include City Attorney in Appleton, Wisconsin, and District Attorney, City Attorney and President of the Board of Education (school board) of Superior, Wisconsin. Sloan was originally a Democrat, but changed his affiliation to the Republican.
Sloan died in Appleton on February 15, 1915.
^ Reed, Parker McCobb (1882). The Bench and Bar of Wisconsin. Milwaukee, WI: P. M. Reed. p. 388.
^ "Henry Clay Sloan". Old Third Ward. Archived from the original on 2015-12-08. Retrieved 2015-12-05.
^ THE BLUE BOOK OF THE STATE OF WISCONSIN. 1881. p. 519.
^ Lawrence S. Barish, ed. (2007). State of Wisconsin Blue Book 2007 - 2008. p. 176.
^ Encyclopedia of American Biography. 1. New York, NY: American Historical Society, Incorporated. 1935. p. 373.


text:
South African top fruit industry offers vaccinations and job opportunities for its workers
Hortgro, South Africa's deciduous fruit grower organisation, is keen to look after its workers in face of this year's challenges. The fruit industry is advocating the covid vaccine to all by partnering with the South African Department of Health and is also celebrating the end of a very successful jobs transformation programme in the apple and pear industry.
South African pear and apple packers have collaborated with the public health and private sector to provide covid vaccination sites, with the aim to portray the willingness of the South African agricultural sector to assist in the prevention and containment of the spread of the virus.
Fruit processors are educating people about the benefits of the covid vaccination. Pome fruit packer Two-a-Day is seeing success with their campaign to communicate the positive benefits of beingvaccinated. HR manager Dmitri Jacobs explains: "We are providing registered nurses to administer the vaccinations. We hope that this will help to convince people that being vaccinated is safe and beneficial to everyone's health."
The fruit packer is vaccinating both those who are currently eligible for the vaccine, and their own employees and workers at associate farms and their families. Jacobs notes, "As the agricultural sector, we are essential workers who must provide food for the nation, and so offering on-site vaccinations also means that our staff won't need to miss a day's work to receive a vaccine."
South Africa has so far exported 5.306 million cartons of apples to the UK this year, with Royal Gala, Cripps pink/Pink Lady, and Braeburn being the most exported varieties. There has been a 23% increase in pear exports to the UK, with more than 919,000 cartons exported to date.
The South African fruit industry is also tackling the challenges of transformation and economic reform. The Job's Fund Project, created by Hortgro, the Jobs Fund, and the Western Cape Department of Agriculture (WCDoA), has just come to an end, a programme that has helped 21 emerging farmers to reach commercial status since its beginnings in 2015.
Head of the Jobs Fund, Najwah Allie-Edries, said that smallholder farmers and emerging farmers have traditionally been excluded from the commercial value chain: "The Jobs Fund wanted to support innovative initiatives that would initiate systemic change in the agriculture sector. The programme has demonstrated the importance of strategic partnerships that work on farm level."Dr Mogale Sebopetsa, Head of the WCDoA, applauded the jobs fund: "Agriculture is the sunrise sector. It can bring jobs and economic stability to our country. It is well-placed to lead the economic recovery of our country from the front."