Organised jointly by the OECD and the IEA, this seminar held on 26-27 September 2012 aimed to promote dialogue and enhance understanding between a wide range of countries on technical issues in the international climate change negotiations. This seminar was an informal meeting outside of the UNFCCC negotiations and discussions are non-attributed.

This event held on 19-20 March 2013 at the OECD is part of a series of seminars, organised by the OECD and the IEA, which aims to promote dialogue and enhance understanding between a wide range of experts on technical issues in the international climate change negotiations. The agenda, presentations and list of participants are now available.

This event held on 18-19 September 2013 at the OECD is part of a series of seminars, organised by the OECD and the IEA, which aims to promote dialogue and enhance understanding between a wide range of experts on technical issues in the international climate change negotiations. The agenda, presentations and list of participants are now available.

This event held on 18-19 March 2014 at the OECD is part of a series of seminars, organised by the OECD and the IEA, which aims to promote dialogue and enhance understanding between a wide range of experts on technical issues in the international climate change negotiations. The agenda, presentations and list of participants are now available.

This event held on 16-17 September 2014 at the IEA is part of a series of seminars, organised by the OECD and the IEA, which aims to promote dialogue and enhance understanding between a wide range of experts on technical issues in the international climate change negotiations. The agenda, presentations and list of participants are now available.

This event focused on the implication of COP24 outcomes and the implementation of the Rulebook, as well as on upcoming work on unresolved issues such as Article 6. Discussions covered Common Tabular Format (CTF) for climate finance and tracking progress towards the mitigation targets and updating and implementing NDCs, with a particular attention to the power sector and carbon markets.

Speaking to The Mirror at the NME Awards on Thursday,  the singer, 27, criticised the ceremony for making the women feel like a 'subplot' or 'warm-up act' for their male counterparts.

The singer, 27, looked stunning in a Fendi black tulle gown, which was fitted around her midriff before fanning out into a dramatic skirt.

The songstress, 27, left almost nothing to the imagination as she arrived at the glitzy bash in a skin-baring racy black feathered mini dress.

नयी दिल्ली। क्या आप जानते हैं कि आप अपने घर के राशन में बैठे-बैठे कारोबार करके पैसे कमा सकते हैं? इसके लिए आपको किसी सेल्समैन की तरह लोगों के घरों पर नहीं जाना और न ही कोई दुकान खोलनी है। बल्कि

Samantha-Su Z. Taylor, Nicole L. Jacobsen, Tasha K. Pontifex, Paul Langlais, and Janis M. Burt

Connexin 37 (Cx37) expression profoundly suppresses proliferation of rat insulinoma (Rin) cells in a manner dependent on gap junction channel (GJCh) functionality and the presence and phosphorylation status of its carboxyl-terminus (CT). In Rin cells growth arrested by induced Cx37 expression, serine 319 (S319) is frequently phosphorylated. Preventing phosphorylation at this site (alanine substitution; S319A) relieved Cx37 of its growth suppressive effect whereas mimicking phosphorylation at this site (aspartate substitution; S319D) enhanced Cx37's growth suppressive properties. Like Cx37-WT, -S319D GJChs and hemichannels (HChs) preferred the closed state, rarely opening fully, and gated slowly. In contrast, Cx37-S319A channels preferred open states, opened fully, and gated rapidly. These data indicate that phosphorylation-dependent conformational differences in Cx37 protein and channel function underlie Cx37-induced growth arrest vs. growth permissive phenotypes. That the closed state of -WT and Cx37-S319D GJChs and HChs favors growth arrest suggests that rather than specific permeants mediating cell cycle arrest, the closed conformation instead supports interaction of Cx37 with growth regulatory proteins that result in growth arrest.

Sujit Bhattacherjee, Group CIO at Amri Hospitals provides insights into how he is leveraging AI and analytics for ensuring better healthcare outcomes.

CXS by Bioionix Destroys Listeria in Meat and Cheese Plants!

The AWA (Automotive Website Awards) were presented at the 2020 NADA Expo in Las Vegas, Nevada

Built on Guided Journeys, the Solutions Enable Digital Transformation by Making Complex Processes Easier to Manage

By making the most relevant information shareable and reusable across the organization, AI-infused KM tools can bring an organization closer to the holy grail of frictionless service

Financial services organizations typically have high-volume, high-value documents, which can be manually intensive if processes are not automated

The present disclosure relates to processes for reducing the concentration of RfC≡CX impurities in fluoroolefins. The process involves: contacting a mixture comprising at least one fluoroolefin and at least one RfC≡CX impurity with at least one amine to reduce the concentration of the at least one RfC≡CX impurity in the mixture; wherein Rf is a perfluorinated alkyl group, and X is H, F, Cl, Br or I. The present disclosure also relates to processes for making at least one hydrotetrafluoropropene product selected from the group consisting of CF3CF═CH2, CF3CH═CHF, and mixtures thereof and reducing the concentration of CF3C═CH impurity generated during the process. The present disclosure also relates to processes for making at least one hydrochlorotrifluoropropene product selected from the group consisting of CF3CCl═CH2, CF3CH═CHCl, and mixtures thereof and reducing the concentration of CF3C≡CH impurity generated during the process.

The present invention relates to CX3CR1-binding polypeptides, in particular polypeptides comprising specific immunoglobulin domains. The invention also relates to nucleic acids encoding such polypeptides; to methods for preparing such polypeptides; to host cells expressing or capable of expressing such polypeptides; to compositions comprising such polypeptides; and to uses of such polypeptides or such compositions, in particular for prophylactic, therapeutic and diagnostic purposes.

Oswin sleeping on my desk. #cat https://ift.tt/30d1MCx

Pop singer-songwriter Charli XCX is holed up in Beachwood Canyon with her boyfriend and two roommates. "The idea of remaining still is quite daunting to me."

The respiratory epithelium comprises polarized cells at the interface between the environment and airway tissues. Polarized apical and basolateral protein secretions are a feature of airway epithelium homeostasis. Human respiratory syncytial virus (hRSV) is a major human pathogen that primarily targets the respiratory epithelium. However, the consequences of hRSV infection on epithelium secretome polarity and content remain poorly understood. To investigate the hRSV-associated apical and basolateral secretomes, a proteomics approach was combined with an ex vivo pediatric human airway epithelial (HAE) model of hRSV infection (data are available via ProteomeXchange and can be accessed at https://www.ebi.ac.uk/pride/ with identifier PXD013661). Following infection, a skewing of apical/basolateral abundance ratios was identified for several individual proteins. Novel modulators of neutrophil and lymphocyte activation (CXCL6, CSF3, SECTM1 or CXCL16), and antiviral proteins (BST2 or CEACAM1) were detected in infected, but not in uninfected cultures. Importantly, CXCL6, CXCL16, CSF3 were also detected in nasopharyngeal aspirates (NPA) from hRSV-infected infants but not healthy controls. Furthermore, the antiviral activity of CEACAM1 against RSV was confirmed in vitro using BEAS-2B cells. hRSV infection disrupted the polarity of the pediatric respiratory epithelial secretome and was associated with immune modulating proteins (CXCL6, CXCL16, CSF3) never linked with this virus before. In addition, the antiviral activity of CEACAM1 against hRSV had also never been previously characterized. This study, therefore, provides novel insights into RSV pathogenesis and endogenous antiviral responses in pediatric airway epithelium.

C-X-C chemokine receptor 4 is a transmembrane chemokine receptor involved in growth, survival, and dissemination of cancer, including aggressive B-cell lymphoma. Magnetic resonance imaging (MRI) is the standard imaging technology for central nervous system involvement of B-cell lymphoma and provides high sensitivity but moderate specificity. Therefore, novel molecular and functional imaging strategies are urgently required. Methods: In this proof-of-concept study, 11 patients with lymphoma of the CNS (CNSL, n = 8 primary and n = 3 secondary involvement) were imaged with the CXCR4-directed positron emission tomography (PET) tracer ⁶⁸Ga-Pentixafor. To evaluate the predictive value of this imaging modality, treatment response, as determined by MRI, was correlated with quantification of CXCR4 expression by ⁶⁸Ga-Pentixafor PET in vivo before initiation of treatment in 7 of 11 patients. Results: ⁶⁸Ga-Pentixafor-PET showed excellent contrast characteristics to the surrounding brain parenchyma in all patients with active disease. Furthermore, initial CXCR4 uptake determined by PET correlated with subsequent treatment response as assessed by MRI. Conclusion: ⁶⁸Ga-Pentixafor-PET represents a novel diagnostic tool for central nervous system lymphoma with potential implications for theranostic approaches as well as response and risk assessment.

The respiratory epithelium comprises polarized cells at the interface between the environment and airway tissues. Polarized apical and basolateral protein secretions are a feature of airway epithelium homeostasis. Human respiratory syncytial virus (hRSV) is a major human pathogen that primarily targets the respiratory epithelium. However, the consequences of hRSV infection on epithelium secretome polarity and content remain poorly understood. To investigate the hRSV-associated apical and basolateral secretomes, a proteomics approach was combined with an ex vivo pediatric human airway epithelial (HAE) model of hRSV infection (data are available via ProteomeXchange and can be accessed at https://www.ebi.ac.uk/pride/ with identifier PXD013661). Following infection, a skewing of apical/basolateral abundance ratios was identified for several individual proteins. Novel modulators of neutrophil and lymphocyte activation (CXCL6, CSF3, SECTM1 or CXCL16), and antiviral proteins (BST2 or CEACAM1) were detected in infected, but not in uninfected cultures. Importantly, CXCL6, CXCL16, CSF3 were also detected in nasopharyngeal aspirates (NPA) from hRSV-infected infants but not healthy controls. Furthermore, the antiviral activity of CEACAM1 against RSV was confirmed in vitro using BEAS-2B cells. hRSV infection disrupted the polarity of the pediatric respiratory epithelial secretome and was associated with immune modulating proteins (CXCL6, CXCL16, CSF3) never linked with this virus before. In addition, the antiviral activity of CEACAM1 against hRSV had also never been previously characterized. This study, therefore, provides novel insights into RSV pathogenesis and endogenous antiviral responses in pediatric airway epithelium.

OBJECTIVE

Reparixin is an inhibitor of CXCR1/2 chemokine receptor shown to be an effective anti-inflammatory adjuvant in a pilot clinical trial in allotransplant recipients.

RESEARCH DESIGN AND METHODS

A phase 3, multicenter, randomized, double-blind, parallel-assignment study (NCT01817959) was conducted in recipients of islet allotransplants randomized (2:1) to reparixin or placebo in addition to immunosuppression. Primary outcome was the area under the curve (AUC) for C-peptide during the mixed-meal tolerance test at day 75 ± 5 after the first and day 365 ± 14 after the last transplant. Secondary end points included insulin independence and standard measures of glycemic control.

RESULTS

The intention-to-treat analysis did not show a significant difference in C-peptide AUC at both day 75 (27 on reparixin vs. 18 on placebo, P = 0.99) and day 365 (24 on reparixin vs. 15 on placebo, P = 0.71). There was no statistically significant difference between treatment groups at any time point for any secondary variable. Analysis of patient subsets showed a trend for a higher percentage of subjects retaining insulin independence for 1 year after a single islet infusion in patients receiving reparixin as compared with patients receiving placebo (26.7% vs. 0%, P = 0.09) when antithymocyte globulin was used as induction immunosuppression.

CONCLUSIONS

In this first double-blind randomized trial, islet transplantation data obtained with reparixin do not support a role of CXCR1/2 inhibition in preventing islet inflammation-mediated damage.

Customer experience as a boardroom topic is more relevant than ever. Enterprises are investing significant digital transformation budgets and commissioning large projects to elevate CX. Yet more than 70 percent of digital transformation projects fail to move the needle at scale. One topic that has a substantial impact on CX is the transformation of customer service operations using digital tools.

Neonatal stroke is as frequent as stroke in the elderly, but many pathophysiological injury aspects are distinct in neonates, including immune signaling. While myeloid cells can traffic into the brain via multiple routes, the choroid plexus (CP) has been identified as a uniquely educated gate for immune cell traffic during health and disease. To understand the mechanisms of myeloid cell trafficking via the CP and their influence on neonatal stroke, we characterized the phenotypes of CP-infiltrating myeloid cells after transient middle cerebral artery occlusion (tMCAO) in neonatal mice of both sexes in relation to blood-brain barrier permeability, injury, microglial activation, and CX3CR1-CCR2 signaling, focusing on the dynamics early after reperfusion. We demonstrate rapid recruitment of multiple myeloid phenotypes in the CP ipsilateral to the injury, including inflammatory CD45⁺CD11b⁺Ly6c^highCD86⁺, beneficial CD45⁺CD11b⁺Ly6c^lowCD206⁺, and CD45⁺CD11b⁺Ly6c^lowLy6g^high cells, but only minor leukocyte infiltration into acutely ischemic-reperfused cortex and negligible vascular albumin leakage. We report that CX3CR1-CCR2-mediated myeloid cell recruitment contributes to stroke injury. Considering the complexity of inflammatory cascades triggered by stroke and a role for TLR2 in injury, we also used direct TLR2 stimulation as an independent injury model. TLR2 agonist rapidly recruited myeloid cells to the CP, increased leukocytosis in the CSF and blood, but infiltration into the cortex remained low over time. While the magnitude and the phenotypes of myeloid cells diverged between tMCAO and TLR2 stimulation, in both models, disruption of CX3CR1-CCR2 signaling attenuated both monocyte and neutrophil trafficking to the CP and cortex.

SIGNIFICANCE STATEMENT Stroke during the neonatal period leads to long-term disabilities. The mechanisms of ischemic injury and inflammatory response differ greatly between the immature and adult brain. We examined leukocyte trafficking via the choroid plexus (CP) following neonatal stroke in relation to blood-brain barrier integrity, injury, microglial activation, and signaling via CX3CR1 and CCR2 receptors, or following direct TLR2 stimulation. Ischemia-reperfusion triggered marked unilateral CX3CR1-CCR2 dependent accumulation of diverse leukocyte subpopulations in the CP without inducing extravascular albumin leakage or major leukocyte infiltration into the brain. Disrupted CX3CR1-CCR2 signaling was neuroprotective in part by attenuating monocyte and neutrophil trafficking. Understanding the migratory patterns of CP-infiltrating myeloid cells with intact and disrupted CX3CR1-CCR2 signaling could identify novel therapeutic targets to protect the neonatal brain.

Nestin, an intermediate filament protein widely used as a marker of neural progenitors, was recently found to be expressed transiently in developing cortical neurons in culture and in developing mouse cortex. In young cortical cultures, nestin regulates axonal growth cone morphology. In addition, nestin, which is known to bind the neuronal cdk5/p35 kinase, affects responses to axon guidance cues upstream of cdk5, specifically, to Sema3a. Changes in growth cone morphology require rearrangements of cytoskeletal networks, and changes in microtubules and actin filaments are well studied. In contrast, the roles of intermediate filament proteins in this process are poorly understood, even in cultured neurons. Here, we investigate the molecular mechanism by which nestin affects growth cone morphology and Sema3a sensitivity. We find that nestin selectively facilitates the phosphorylation of the lissencephaly-linked protein doublecortin (DCX) by cdk5/p35, but the phosphorylation of other cdk5 substrates is not affected by nestin. We uncover that this substrate selectivity is based on the ability of nestin to interact with DCX, but not with other cdk5 substrates. Nestin thus creates a selective scaffold for DCX with activated cdk5/p35. Last, we use cortical cultures derived from Dcx KO mice to show that the effects of nestin on growth cone morphology and on Sema3a sensitivity are DCX-dependent, thus suggesting a functional role for the DCX-nestin complex in neurons. We propose that nestin changes growth cone behavior by regulating the intracellular kinase signaling environment in developing neurons. The sex of animal subjects is unknown.

SIGNIFICANCE STATEMENT Nestin, an intermediate filament protein highly expressed in neural progenitors, was recently identified in developing neurons where it regulates growth cone morphology and responsiveness to the guidance cue Sema3a. Changes in growth cone morphology require rearrangements of cytoskeletal networks, but the roles of intermediate filaments in this process are poorly understood. We now report that nestin selectively facilitates phosphorylation of the lissencephaly-linked doublecortin (DCX) by cdk5/p35, but the phosphorylation of other cdk5 substrates is not affected. This substrate selectivity is based on preferential scaffolding of DCX, cdk5, and p35 by nestin. Additionally, we demonstrate a functional role for the DCX-nestin complex in neurons. We propose that nestin changes growth cone behavior by regulating intracellular kinase signaling in developing neurons.

AOC's Agon AG493UCX is a 49-inch ultra-wide monitor that provides an enjoyable gaming experience and does a decent job handling multimedia content, as well.

Hi,

I want to convert ircx file(which is from TSMC,inclued EM Information) to ict or emDataFile for Voltus-fi.

I tried many way, but I can not make it. Can anyone give me some advice?

and I  do not installed QRC.

below is some tools installed my server. 

IC617-64b.500.21 is used.

Hi,

I want to convert ircx file(which from TSMC) to ict or emDataFile for Voltus-fi.

I tried many way, but I can not make it.

and I  do not installed QRC.

below is some tools installed my server. 

IC617-64b.500.21 is used.

This Metasploit module exploits a buffer overflow vulnerability in Advantec WebAccess. The vulnerability exists in the dvs.ocx ActiveX control, where a dangerous call to sprintf can be reached with user controlled data through the GetColor function. This Metasploit module has been tested successfully on Windows XP SP3 with IE6 and Windows 7 SP1 with IE8 and IE 9.

TP-LINK Cloud Cameras including products NC260 and NC450 suffer from a command injection vulnerability. The issue is located in the httpSetEncryptKeyRpm method (handler for /setEncryptKey.fcgi) of the ipcamera binary, where the user-controlled EncryptKey parameter is used directly as part of a command line to be executed as root without any input sanitization.

TP-LINK Cloud Cameras including products NC200, NC210, NC220, NC230, NC250, NC260, and NC450 suffer from a command injection vulnerability. The issue is located in the swSystemSetProductAliasCheck method of the ipcamera binary (Called when setting a new alias for the device via /setsysname.fcgi), where despite a check on the name length, no other checks are in place in order to prevent shell metacharacters from being introduced. The system name would then be used in swBonjourStartHTTP as part of a shell command where arbitrary commands could be injected and executed as root.

1000C OCXO Datasheet

ABSTRACT

Arthritogenic alphaviruses such as Ross River and Chikungunya viruses cause debilitating muscle and joint pain and pose significant challenges in the light of recent outbreaks. How host immune responses are orchestrated after alphaviral infections and lead to musculoskeletal inflammation remains poorly understood. Here, we show that myositis induced by Ross River virus (RRV) infection is driven by CD11b^hi Ly6C^hi inflammatory monocytes and followed by the establishment of a CD11b^hi Ly6C^lo CX₃CR1⁺ macrophage population in the muscle upon recovery. Selective modulation of CD11b^hi Ly6C^hi monocyte migration to infected muscle using immune-modifying microparticles (IMP) reduced disease score, tissue damage, and inflammation and promoted the accumulation of CX₃CR1⁺ macrophages, enhancing recovery and resolution. Here, we detail the role of immune pathology, describing a poorly characterized muscle macrophage subset as part of the dynamics of alphavirus-induced myositis and tissue recovery and identify IMP as an effective immunomodulatory approach. Given the lack of specific treatments available for alphavirus-induced pathologies, this study highlights a therapeutic potential for simple immune modulation by IMP in infected individuals in the event of large alphavirus outbreaks.

IMPORTANCE Arthritogenic alphaviruses cause debilitating inflammatory disease, and current therapies are restricted to palliative approaches. Here, we show that following monocyte-driven muscle inflammation, tissue recovery is associated with the accumulation of CX₃CR1⁺ macrophages in the muscle. Modulating inflammatory monocyte infiltration using immune-modifying microparticles (IMP) reduced tissue damage and inflammation and enhanced the formation of tissue repair-associated CX₃CR1⁺ macrophages in the muscle. This shows that modulating key effectors of viral inflammation using microparticles can alter the outcome of disease by facilitating the accumulation of macrophage subsets associated with tissue repair.

The 78-kDa glucose-regulated protein (GRP78), an endoplasmic reticulum (ER) chaperone, is a master regulator of the ER stress. A number of studies revealed that high levels of GRP78 protein in cancer cells confer multidrug resistance (MDR) to therapeutic treatment. Therefore, drug candidate that reduces GRP78 may represent a novel approach to eliminate MDR cancer cells. Our earlier studies showed that a set of 4H-chromene derivatives induced selective cytotoxicity in MDR cancer cells. In the present study, we elucidated its selective mechanism in four MDR cancer cell lines with one lead candidate (CXL146). Cytotoxicity results confirmed the selective cytotoxicity of CXL146 toward the MDR cancer cell lines. We noted significant overexpression of GRP78 in all four MDR cell lines compared with the parental cell lines. Unexpectedly, CXL146 treatment rapidly and dose-dependently reduced GRP78 protein in MDR cancer cell lines. Using human leukemia (HL) 60/mitoxantrone (MX) 2 cell line as the model, we demonstrated that CXL146 treatment activated the unfolded protein response (UPR); as evidenced by the activation of inositol-requiring enzyme 1α, protein kinase R–like ER kinase, and activating transcription factor 6. CXL146-induced UPR activation led to a series of downstream events, including extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase activation, which contributed to CXL146-induced apoptosis. Targeted reduction in GRP78 resulted in reduced sensitivity of HL60/MX2 toward CXL146. Long-term sublethal CXL146 exposure also led to reduction in GRP78 in HL60/MX2. These data collectively support GRP78 as the target of CXL146 in MDR treatment. Interestingly, HL60/MX2 upon long-term sublethal CXL146 exposure regained sensitivity to mitoxantrone treatment. Therefore, further exploration of CXL146 as a novel therapy in treating MDR cancer cells is warranted.

SIGNIFICANCE STATEMENT

Multidrug resistance is one major challenge to cancer treatment. This study provides evidence that cancer cells overexpress 78-kDa glucose-regulated protein (GRP78) as a mechanism to acquire resistance to standard cancer therapies. A chromene-based small molecule, CXL146, selectively eliminates cancer cells with GRP78 overexpression via activating unfolded protein response–mediated apoptosis. Further characterization indicates that CXL146 and standard therapies complementarily target different populations of cancer cells, supporting the potential of CXL146 to overcome multidrug resistance in cancer treatment.

C-X-C motif chemokine receptor 4 (CXCR4) is expressed on the surface of various cell types involved in atherosclerosis, with a particularly rich receptor expression on macrophages and T cells. First pilot studies with ⁶⁸Ga-pentixafor, a novel CXCR4-directed PET tracer, have shown promise to noninvasively image inflammation within atherosclerotic plaques. The aim of this retrospective study was to investigate the performance of ⁶⁸Ga-pentixafor PET/CT for imaging atherosclerosis in comparison to ¹⁸F-FDG PET/CT. Methods: Ninety-two patients (37 women and 55 men; mean age, 62 ± 10 y) underwent ⁶⁸Ga-pentixafor and ¹⁸F-FDG PET/CT for staging of oncologic diseases. In these subjects, lesions in the walls of large arteries were identified using morphologic and PET criteria for atherosclerosis (n = 652). Tracer uptake was measured and adjusted for vascular lumen (background) signal by calculation of target-to-background ratios (TBRs) by 2 investigators masked to the other PET scan. On a lesion-to-lesion and patient basis, the TBRs of both PET tracers were compared and additionally correlated to the degree of arterial calcification as quantified in CT. Results: On a lesion-to-lesion basis, ⁶⁸Ga-pentixafor and ¹⁸F-FDG uptake showed a weak correlation (r = 0.28; P < 0.01). ⁶⁸Ga-pentixafor PET identified more lesions (n = 290; TBR ≥ 1.6, P < 0.01) and demonstrated higher uptake than ¹⁸F-FDG PET (1.8 ± 0.5 vs. 1.4 ± 0.4; P < 0.01). The degree of plaque calcification correlated negatively with both ⁶⁸Ga-pentixafor and ¹⁸F-FDG uptake (r = –0.38 vs. –0.31, both P < 0.00001). Conclusion: CXCR4-directed imaging of the arterial wall with ⁶⁸Ga-pentixafor PET/CT identified more lesions than ¹⁸F-FDG PET/CT, with only a weak correlation between tracers. Further studies to elucidate the underlying biologic mechanisms and sources of CXCR4 positivity, and to investigate the clinical utility of chemokine receptor–directed imaging of atherosclerosis, are highly warranted.

B-cell receptor (BCR) signaling pathway components represent promising treatment targets in multiple B-cell malignancies including diffuse large B-cell lymphoma (DLBCL). In in vitro and in vivo model systems, a subset of DLBCLs depend upon BCR survival signals and respond to proximal BCR/phosphoinositide 3 kinase (PI3K) blockade. However, single-agent BCR pathway inhibitors have had more limited activity in patients with DLBCL, underscoring the need for indicators of sensitivity to BCR blockade and insights into potential resistance mechanisms. Here, we report highly significant transcriptional upregulation of C-X-C chemokine receptor 4 (CXCR4) in BCR-dependent DLBCL cell lines and primary tumors following chemical spleen tyrosine kinase (SYK) inhibition, molecular SYK depletion or chemical PI3K blockade. SYK or PI3K inhibition also selectively upregulated cell surface CXCR4 protein expression in BCR-dependent DLBCLs. CXCR4 expression was directly modulated by fork-head box O1 via the PI3K/protein kinase B/forkhead box O1 signaling axis. Following chemical SYK inhibition, all BCR-dependent DLBCLs exhibited significantly increased stromal cell-derived factor-1α (SDF-1α) induced chemotaxis, consistent with the role of CXCR4 signaling in B-cell migration. Select PI3K isoform inhibitors also augmented SDF-1α induced chemotaxis. These data define CXCR4 upregulation as an indicator of sensitivity to BCR/PI3K blockade and identify CXCR4 signaling as a potential resistance mechanism in BCR-dependent DLBCLs.

MAKE UP FOR EVER TEAMS UP WITH CHARLI XCX FOR ITS NEW AQUA XL CAMPAIGN

MAKE UP FOR EVER TEAMS UP WITH CHARLI XCX FOR ITS NEW AQUA XL CAMPAIGN

Posted by Victoria Strauss for Writer Beware®

Two issues involving Audible's ACX have come across my desk recently.

Rights Fraud

I've heard from several self- and small press-pubbed authors who report that they've found their books listed on ACX as open to narrator auditions...except that they, or their publishers, didn't put them there. This appears to be an attempt to steal authors' audio rights.

Below is one listing. Here's another and another and another. (All of these listings have been invalidated by ACX.)


See "Comments from the Rights Holder" at the bottom. The purported company, Publishing D LLC, does not show up on any searches.

The fraud seems pretty elaborate. Here's what one of the authors who contacted me told me:


These comments from a freelance audiobook narrator illustrate that "Publishing D" is not an isolated incidence.

Promotional Code Shenanigans

Multiple authors have contacted me to report that they've received an email from ACX withdrawing their promotional codes. The cited reason: "unusual activity," with no explanation of what that means.

The authors say that they have not used the codes improperly or violated ACX guidelines; in some cases, they've used the codes only a handful of times or not at all. See, for instance, blog posts by authors G. Michael Vasey and Adam Piggott. Per discussions on the KBoards and Reddit, a lot of authors seem to be affected.

Is this one of Amazon's (Audible's parent company) periodic crackdowns on misuse or fraud that has inadvertently ensnared innocent authors? According to author and self-publishing expert David Gaughran, ACX promo code scamming is a major problem, and Amazon's anti-abuse sweeps often involve a lot of collateral damage. Or could it be an error--a glitch or rogue algorithm?

So far, authors' efforts to get a fuller explanation have run up against the black box that is Amazon:


If I hear anything further, I'll update this post.

UPDATE 11/27/19: One of the authors who alerted me to the promo code withdrawal has received a notice saying that their codes are reinstated--however, they say that the promo code tab has yet to appear in their dashboard.


UPDATE 2/25/29: More about ACX scams, from a comment left by a narrator:

About the ACX thing...I was contacted by ACX to narrate three books, however, the person who offered the contracts kept emailing and frantically telling me to send them my book codes. I got leary and called ACX. They said unfortunately there are many scams taking place where if a book is "unclaimed" in their system, someone may grab it and offer it as an audiobook contract. Then they keep the codes and blackmarket sell them. They do not pay the narrators. Many other authors are experiencing it, they said, but they have no way to regulate it.

I declined the offers and got a nasty note from the contract holder. I was also told that since I corresponded with them, they had my email that is associated with Amazon..the same one. So, ACX said I had to go change my email on Amazon or they would have access there too. Geez.

The 'Boys' singer was attending the plush GQ awards on London's Bankside and caught the eye with a plunging neckline

The British singer, 27, put on a leggy display in the racy ensemble as she exited the post-awards bash in London's Tate Modern.

नयी दिल्ली। क्या आप जानते हैं कि आप अपने घर के राशन में बैठे-बैठे कारोबार करके पैसे कमा सकते हैं? इसके लिए आपको किसी सेल्समैन की तरह लोगों के घरों पर नहीं जाना और न ही कोई दुकान खोलनी है। बल्कि

02:24 - Dann Toliver Introduction

• Twitter
• GitHub
• Bento Miso

02:35 - Matt Asher Introduction

• Twitter
• GitHub
• Blog

02:51 - EveryBit.js and I.CX

• [GitHub] everybit.js
• EveryBit.js Whitepaper

03:43 - Architecture

• Episode #135: Smallest Federated Wiki with Ward Cunningham

06:54 - Sustainability and The Pieces of the System

• Content “Puffs”
• Authentication
• Storage
  • Firebase
  • Distributed Hash Table (DHT)
  • The Chord Algorithm (Peer-to-Peer)

21:56 - Decentralization

• Space Monkey
• Madesafe

25:20 - Audience: Why Should I Care?

27:38 - Getting Started: Nuts and Bolts

• Frontend Agnostic
• Storage and Performance
• Users and Data Management
  • Payload Properties
  • Metadata
  • Graph Database
    • Adding New Relationships
    • Adding Heuristics
    • Resource Allocator Component
      • Local Storage
      • RAM

34:55 - Scaling and Server Cost

36:23 - Cloud Storage and Management (Security & Trust)

• HTTPS
  • SSL Model
  • GPG Model
• “Proof of Presence”
• "Self-verifying"
  • Namecoin Project

47:22 - Implementing Cryptographic Primitives

• bitcoinjs-lib    
• Key Management
• Cryptography
• OAuth

55:13 - The Firefox Sync Tool Project

Picks

[Twitch.tv] Kylelandrypiano (Jamison)
"Visualizing Persistent Data Structures" by Dann Toliver (Jamison)
Probability and Statistics Blog (Jamison)
Seeed Studio (Tim)
Adafruit Industries (Tim)
SparkFun Electronics (Tim)
American Sniper by Chris Kyle, Scott McEwen, and Jim DeFelice (Chuck)
Introducing Relay and GraphQL (Dann)
The Clojurescript Ecosystem (Dann)
Read-Eval-Print-λove (Dann)
React Native (Matt)

Brokers urge exchange and Sebi to work out an amicable price, as over 11,000 lots of open interest in the April contract were standing and couldn't be carried forward or squared off yesterday

MCX said that it had settled the contract according to the formula in the contract, which has been followed for the last 15 years

Margin now fixed at 100%, with Rs 95,000 per lot as absolute minimum. So if crude falls below Rs 950, the margin will continue to be based on the price of Rs 950