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Under 99.5% from the high volume sellers you have been buying from is quite poor.
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Re: did i open too many cases?
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Re: did i open too many cases?
in reply to popcorn233 Jan 6, 2017 2:18:14 AM
Adventurer
Jan 6, 2017 2:18:14 AM
no problems yet, i think ebay are aware of the china problem maybe that's why i got a pass. 29 seems a lot but it's about 2% of my purchases.
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Jan 6, 2017 2:25:00 AM
Rockstar
Jan 6, 2017 2:25:00 AM

Yes, ebay is aware of the China problem and collectively do not give a hoot. They will rescind your MBG options before even thinking about booting Chinese sellers whoare refunding due to "lost" packages.

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Re: did i open too many cases?
virtualwhimsy
Re: did i open too many cases?
in reply to Modal Scarf stella by VIDA VIDA mihP8
Jan 6, 2017 5:01:23 AM
Rockstar
Jan 6, 2017 5:01:23 AM

Well then you take your chances.

Keep opening cases and you will find your buyer protection cancelled.

1,701 Views
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Re: did i open too many cases?
brand_spanking_new
Re: did i open too many cases?
in reply to virtualwhimsy Jan 6, 2017 7:30:41 AM
Adventurer
Jan 6, 2017 7:30:41 AM

well if thats the way it goes, that's the way it goes, what can you do? spend more money to keep ebay happy?

i also buy a lot on aliexpress, and for some reason i had much less stuff not arriving from there.

99.9% of the time it arrives, any idea why is that? maybe ebay is more open to scams?

or maybe because aliexpress is based in china they can investigate thing better than ebay.

anybody knows?

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Re: did i open too many cases?
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Re: did i open too many cases?
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Jan 6, 2017 7:39:47 AM
Superstar
Jan 6, 2017 7:39:47 AM

eBay isn't exposed to more scams.29 cases is too many. Buyere who opened 10-22 cases have come here complaining that they lost their buyer protection. So you can either change your buying habits and buy from sellers outside China or you can continue to buy from China at your own risk. The money back guarantee is not a personal insurance policy for repeated bad decisions.

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() was overexpressed in newborn daughter cells expressing Vph1-mCherry using a β-estradiol inducible system where a GAL4-Estrogen binding domain-VP16 (GEV) fusion protein drives promoter …

Figure 3—figure supplement 1
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was overexpressed in newborn daughter cells using a β-estradiol inducible system where a GAL4-Estrogen binding domain-VP16 (GEV) fusion protein drives promoter expression of an …

We previously found that delaying the reduction of vacuole acidity during aging by increasing V-ATPase levels extends replicative lifespan ( Hughes and Gottschling, 2012 ). Given the evidence presented above that Pma1 levels antagonize vacuolar acidity, we asked whether reduced Pma1 activity also affected lifespan. Indeed, the pma1-105 allele increased median replicative lifespan by ∼30% ( Figure 3C ), comparable to well-characterized lifespan-extending mutations ( Delaney et al., 2011 ). The slope of the pma1-105 lifespan curve is similar to the slope of the wild-type curve. This suggests that instead of influencing the rate of aging throughout lifespan, the pma1-105 allele delays the onset of the normal aging process. To ascertain whether lifespan extension by the pma1-105 allele occurred entirely via increased vacuolar acidity, we examined the lifespan of pma1-105 cells that lacked V-ATPase function. Cells lacking the V-ATPase subunit Vma2 had a short median lifespan of 2 divisions, as previously reported ( Hughes and Gottschling, 2012 ). The lifespan of cells that had reduced Pma1 activity and that were devoid of V-ATPase function ( vma2 Δ, pma1-105 ) was much shorter than wild-type lifespan (median 7 divisions), and more similar to cells lacking V-ATPase function. This suggests that most of the lifespan extension imparted by the pma1-105 allele requires V-ATPase function, but that the mechanism of lifespan extension is not limited to increased vacuolar acidification. Taken together these results support the idea that high Pma1 levels on mother cells impair vacuole acidification and limit lifespan.

In addition to Pma1 antagonizing mother cell vacuole acidity with age, we also hypothesized that the inherent asymmetry of Pma1, and thus low levels on buds, allows for re-acidification of the vacuole in buds. To test this idea, we asked whether expressing Pma1 in buds reduced vacuole acidity. We induced overexpression of PMA1-mCherry in cells arrested prior to cytokinesis with nocodazole and in untreated cells ( Figure 3D ). In untreated cells, overexpression increased mother cell Pma1 levels but maintained mother-bud asymmetry. However, in nocodazole-arrested cells, PMA1-mCherry became equivalently high in mother cells and buds. At least 80% of buds had acidic vacuoles without PMA1 induction or when PMA1 was induced in the absence of nocodazole ( Figure 3E ). In contrast, only 13% of buds had acidic vacuoles when Pma1 levels were high in buds. Because increased Pma1 levels in buds impaired re-acidification of the vacuole, we conclude that the inherent asymmetry of Pma1 is required for regeneration of vacuole acidity prior to cytokinesis. We speculate that regeneration of vacuole acidity is required for daughter cell rejuvenation and that if high levels of Pma1 were induced in the buds of aging mother cells, daughter cells would not rejuvenate.

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