Approximately 2.5% of young children are allergic to cow milk. In this study, milk protein hydrolysates made from full-cream milk via enzymatic hydrolysis played a positive role in regulating the immune system of ICR mice. Milk protein hydrolysates enhanced immunity in mice by stimulating host immunity, probably by increasing the weight of certain immune system organs, improving the level of hemolysin in serum, and enhancing the phagocytosis of macrophages. Milk protein hydrolysates have the capability to reduce type I hypersensitivity by decreasing IgE levels, IL-4 in serum, and the release of histamine and bicarbonate in peritoneal mast cells, as well as enhancing transforming growth factor-β levels in the serum of ovalbumin-sensitized mice.
8.05months, p¼0.048;14.65months vs 8.05 months; p¼0.004). While no significant difference was found in mPFS between patients with only sensitizing mutations and patients in group 1 (p¼0.165). The mPFS between 1st and 2nd generation EGFR-TKIs cohort was 12.42months versus 12.39months, respectively (p¼0.7). Similarly, there was also no significant difference existed in mPFS between the two treatment cohorts in each subgroup of non-resistant uncommon mutations. Next, we investigated whether the presence of concurrent mutations in tumoursuppressor genes or oncogenes would affect PFS of patients with uncommon EGFR mutations. The mPFS of patients with no concurrent mutation (n¼41), patients with concurrent tumour-suppressor genes mutations (n¼26) and patients with concurrent oncogenic driver mutations (n¼5) were 13.80months, 8.05months and 16.92months, respectively (p¼0.04). Furthermore, patients with no concurrent mutation had a significantly longer mPFS than patients with concurrent tumour-suppressor genes mutations (p¼0.011). Collectively, multivariate analysis showed that patients with coexisting 19del/L858R (p¼0.006, HR: 0.435,95% CI:0.242-0.784) were independently associated with favourable PFS; Non-adenocarcinoma, poor ECOG performance score and the presence of concurrent tumour-suppressor genes mutations were independent risk factors for PFS. (p¼0.024, HR: 3.575,95%
As the accident of a vessel impacting a bridge pier will result in serious disaster, such as bridge fall, ship sink and polluting environment, the technology and method have been investigated to prevent and protect bridges from vessel collisions. An adaptive arresting net crashworthy device has been developed for protecting non-navigable channel piers against ship collisions, which consists of mooring floating boats, mooring cable and mooring anchors, adaptive floating buckets, arresting net, triggering wire rope and constant resistant force cables. When a ship impacts the adaptive arresting net crashworthy device, first the head of the adaptive floating buckets will rise due to the floating force, then the arresting net fixed on the adaptive floating buckets captures and stops the ship. Enormous kinetic energy is consumed by a series of resistant force cables failure. The present paper presents the ship collision tests at full scale and hydrodynamic analysis of the adaptive arresting net crashworthy device. The ship collision tests has been conducted 6 times by a 1200DWT ship with different speed. The ship are prevented successfully. By using multi-body dynamics and rope dynamic theory, simulation model of the adaptive arresting net crashworthy device is established by hydrodynamic analysis software ANSYS-AQWA. It is found that the numerical simulation results are in reasonable agreement with the experimental results.
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