#GCM mediator

[momlovesyoubest]

End of Life-When Do You Facilitation?

Therapist Why do some families need facilitation of a family meeting at the end of life? With the help of a neutral third-party facilitator, families work together to resolve their differences or solve a problem they could not address satisfactorily without help. Find out more in my newest free Webinar on February 25th 2005 These family differences especially happen to dysfunctional families but…

[caroparo]

A Monkey’s Journey to AdMob MediationTestSuite Beta in GameMaker:Studio 2

Destination reached! Successfully done MediationTestSuite.launch on Amazon Kindle Fire HD 8″. GMS2 IDE v2.2.1.375 Runtime v2.2.1.291

GMS2 Build Settings (Pre-populated API Level 26, with min SDK 16 although AdMob MediationTestSuite falsely claimed min 14; crashed[*] with API Level 27, build failed with duplicate entry class with API Level 28):

Build Tools 26.0.0

Support Library 26.0.0

Target SDK 26

Minimum SDK 16

Compile SDK 26

Inject to Gradle dependencies:

  compile 'com.google.android.gms:play-services-games:16.0.0'   compile 'com.google.android.gms:play-services-ads:17.1.3'   compile 'com.google.android.gms:play-services-plus:16.0.0'   compile 'com.google.android.gms:play-services-gcm:16.0.0'   compile 'com.google.android.gms:play-services-auth:16.0.1'   compile 'com.google.android.ads.consent:consent-library:1.0.7'   compile 'com.google.android.ads:mediation-test-suite:0.9.3'   compile fileTree(dir: 'libs', include: ['*.jar']) } repositories {  maven  {    url "https://maven.google.com"  } } dependencies {

Inject to AndroidManifest.xml Application:

<activity android:name="com.google.android.gms.ads.AdActivity" android:configChanges="keyboard|keyboardHidden|orientation|screenLayout|uiMode|screenSize|smallestScreenSize" />

<meta-data            android:name="com.google.android.gms.ads.APPLICATION_ID"            android:value="ca-app-pub-YOUR_APP_ID~YOUR_APP_ID"/>

Hard-coded mAppId String in GooglePlayServicesExtension.java; tested with LoadInterstitial, calling .launch in UI thread:

import com.google.android.ads.mediationtestsuite.MediationTestSuite;

public void GoogleMobileAds_LoadInterstitial() { RunnerActivity.ViewHandler.post( new Runnable() {     public void run()     { if(interstitialAd==null) initInterstitial(); AdRequest.Builder builder = new AdRequest.Builder(); builder.addTestDevice(AdRequest.DEVICE_ID_EMULATOR); if( bUseTestAds) builder.addTestDevice(TestDeviceId); AdRequest adRequest = GoogleMobileAds_BuildAdRequestWithConsent(builder);

// Load the interstitial ad. interstitialAd.loadAd(adRequest);

           // struggling to launch the MediationTestSuite            RunnerActivity.CurrentActivity.runOnUiThread(new Runnable() {                public void run() {                    MediationTestSuite.launch(RunnerActivity.CurrentActivity, mAppId);                }            }); }});

還沒實測 mediation adapter，希望真的不用自己寫Ad SDK測試啦。

Update 18 Feb 2019:

Can’t load (Unity) ads from within MediationTestSuite UI. I was however able to check the SDK installation and settings fine and load/display Unity test ads.

[*] API Level 27 Crash ref: 

W/Ads: #004 The webview is destroyed. Ignoring action.

E/Ads: Error waiting for future.

[alliedacademies-blog]

Anti-quorum and biofilm formation inhibition by coffee husk oil (Coffee arabica L.)

The volatile oil of the coffee husk of Coffee arabica (Rubiaceae) was obtained by GCMS. This oil showed quorum sensing inhibition activity which were investigated for antipathogenic potential against P. aeruginosa (PAO1). The results showed that significant inhibition on the production of virulence P. aeruginosa and Biofilm Formation (BF). Moreover, the treatment with sub-MICs of coffee husk oil significantly inhibited the quorum sensing-mediated BF, extracellular polymeric substances production and swarming motility in these pathogens. Wide-spectrum in vitro inhibition of QS controlled virulence factors such as violacein, elastase, pyocyanin, EPS and biofilm in test pathogens was determined.

[cancersfakianakis1]

Oxaliplatin disrupts pathological features of glioma cells and associated macrophages independent of apoptosis induction

Abstract

Introduction

Emerging evidence suggests that effective treatment of glioblastoma (GBM), the most common and deadly form of adult primary brain cancer, will likely require concurrent treatment of multiple aspects of tumor pathobiology to overcome tumor heterogeneity and the complex tumor-supporting microenvironment. Recent studies in non-central nervous system (CNS) tumor cells have demonstrated that oxaliplatin (OXA) can induce multi-faceted anti-tumor effects, in particular at drug concentrations below those required to induce apoptosis. These findings motivated re-investigation of OXA for the treatment of GBM.

Methods

The effects of OXA on murine KR158 and GL261 glioma cells including cell growth, cell death, inhibition of signal transducer and activator of transcription (STAT) activity, O-6-methylguanine-DNA methyltransferase (MGMT) expression, and immunogenic cell death (ICD) initiation, were evaluated by cytotoxicity assays, Western blot analysis, STAT3-luciferase reporter assays, qRT-PCR assays, and flow cytometry. Chemical inhibitors of endoplasmic reticulum (ER) stress were used to investigate the contribution of this cell damage response to the observed OXA effects. The effect of OXA on bone marrow-derived macrophages (BMDM) exposed to glioma conditioned media (GCM) was also analyzed by Western blot analysis.

Results

We identified the OXA concentration threshold for induction of apoptosis and from this determined the drug dose and treatment period for sub-cytotoxic treatments of glioma cells. Under these experimental conditions, OXA reduced STAT3 activity, reduced MGMT levels and increased temozolomide sensitivity. In addition, there was evidence of immunogenic cell death (elevated EIF2α phosphorylation and calreticulin exposure) following prolonged OXA treatment. Notably, inhibition of ER stress reversed the OXA-mediated inhibition of STAT3 activity and MGMT expression in the tumor cells. In BMDMs exposed to GCM, OXA also reduced levels of phosphorylated STAT3 and decreased expression of Arginase 1, an enzyme known to contribute to pro-tumor functions in the tumor-immune environment.

Conclusions

OXA can induce notable multi-faceted biological effects in glioma cells and BMDMs at relatively low drug concentrations. These findings may have significant therapeutic relevance against GBM and warrant further investigation.

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