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The odds of acute hospitalization or death were reduced at the highest stages, compared with the lowest, by a factor ranging from.33 (.22[ndash ].49) to.65 (.61[ndash ].69).
Ceramide-induced expression of HRK, mitochondrial dysfunction and cell death were reduced by HRK knockdown with HRK siRNA.
Interestingly, prostate cancer incidence and death were reduced in the vitamin E arms (by 32%and41%1%, respectively).
When patients with atherosclerotic burden underwent short-term statin treatment, IL-6 levels were decreased, and myocardial infarction and death were reduced (Liakopoulos et al., 2008; van der Meij et al., 2013).
The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41 mm for 0.5 mg/kg and 153 ± 47 mm for PBS-control with MCAO P << 0.01) but not in the regular-dose groups.
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Neuronal cell death was reduced by apelin-13 treatment evidenced by reduced number of TUNEL-positive cells double stained with the neuronal marker NeuN and (e)).
Using a different statistic, the risk of bone metastasis or death was reduced 15 percent.
Glial cell death was reduced (mean number TUNEL positive cells 2 months after axotomy: no treatment 51/ganglion pair, NAC 16/ganglion pair), and mitochondrial architecture was preserved.
In an in vitro cartilage injury model, chondrocyte death was reduced by increasing the osmolarity of normal saline (NS), the most commonly-used irrigation solution.
Their risk of death was reduced 29 percent, with 86 deaths among those who got the drug compared with 120 deaths in the control group.
There was also a strong trend toward increasing survival, with the risk of death being reduced by 25 percent, according to the hazard ratio.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com