Jianying Zhang

Food waste is a serious national and global problem. Milk is one of the most frequently wasted food items. This study aims to determine how long postexpiration-pasteurized milk may still be safe to consume and what is the relationship between bacterial growth from the milk and time after expiration. The experiments were carried out by incubating milk with agarose gel. The results showed that the bacterial growth was relatively low for at least the first few days after expiration. The more the days passed after the expiration date, the more the bacteria grew from the milk. There was no significant difference in the bacteria colony numbers in the whole milk samples opened either on day 0 or day 5 of expiration. None of the fat-free milk samples collected on the later (1–10) days showed any statistically significant difference in bacterial growth compared to the samples collected on the day after expiration (day 0). The bacterial growth increased with the increasing fat content of the milk. In addition, the rate of bacterial growth from the milk correlated with the acidity of the milk that is measured by pH. No significant sensory changes could be detected in any of the milk samples immediately after opening on the day of expiration or for up to 10 days after expiration when the unopened cartons were kept refrigerated. However, within 24 hours of opening the carton, whole milk that has expired for 6 or more days and 2% milk that has expired for 8 or more days developed a sour taste and mildly pungent smell. This sensory change was accompanied by the formation of lumps and fat-water separation. Fat-free milk samples remained unchanged under the same conditions. The experimental results suggest that whole and 2% skim milk may be safe for consumption up to 5-6 days after expiration. Fat-free milk may be safe for consumption up to 10 days after expiration, possibly longer. This study devised a way to show that milk is still safe for consumption after expiration; it will help reduce food waste.

This study aimed to characterize aging‐induced tendinopathy in mouse Achilles tendon and also to assess the treatment effects of metformin (Met) on aging tendon. We showed that compared to young tendon, aging tendon was in an inflammatory and senescent state as shown by increased expression of inflammatory disulfide HMGB1 (dsHMGB1), inflammatory macrophage marker CD68, and senescent cell markers SA‐β‐gal, p53, and p16. Moreover, aging tendon was degenerated marked by accumulation of proteoglycans and lipids in its interior. However, treatment of aging tendon by intraperitoneal (IP) injection of Met, a specific inhibitor of HMGB1, reduced dsHMGB1 levels, decreased the expression of CD68, SA‐β‐gal, CCN1, and p16 in vitro and in vivo. Furthermore, Met treatment also increased the number of NS, SSEA‐1, and CD73 positive stem cells in culture and improved the tendon structure in aging mouse. These findings of this study indicate that Met exerts anti‐inflammatory and anti‐senescent effects on aging tendon.