Altered Gut Microbiome and Environmental Factors Associated with Development of Eczema in Hong Kong Infants: A 4-Month Pilot Study.

Eczema is a multifactorial skin disease that affects 20% of children worldwide and has a complex relationship with microbial, nutritional, parental and environmental factors. In this study, we investigated the potential association of eczema with the gut microbiome and environmental factors. One hundred and fifty-two newborn subjects and their mothers were recruited within 10 days postnatally at the Prince of Wales Hospital in Hong Kong, China and asked to complete questionnaires on allergies, maternal diet and environmental assessment at enrolment.

A Chinese 2-herb formula (NF3) promotes hindlimb ischemia-induced neovascularization and wound healing of diabetic rats.

Diabetic foot ulcer is closely associated with peripheral vascular disease. Enhancement of tissue oxidative stress, reduction of nitric oxide (NO) and angiogenic growth factors, and abnormal matrix metalloproteinase (MMP) activity are pathophysiological factors in post-ischemic neovascularization and diabetic wound healing. Our previous study demonstrated that the Chinese 2-herb formula, NF3, showed significant wound healing effects on diabetic foot ulcer rats.

Mechanistic studies on the antidiabetic activity of a polysaccharide-rich extract of Radix Ophiopogonis.

To study the hypoglycemic mechanisms of a polysaccharide-rich extract of Radix Ophiopogonis, the influences of the extract on activity of NIT-1 insulinoma cells damaged by streptozotocin (STZ), activity of α-glucosidase, glucose absorption into intestinal brush border membrane vesicles, gluconeogenesis by H4IIE hepatoma cells and glucose uptake by 3T3-L1 adipocytes were investigated. The results show that the extract improved the activity of NIT-1 cells damaged by STZ, inhibited glucose absorption into intestinal brush border membrane vesicles and reduced the activity of α-glucosidase. However, gluconeogenesis in H4IIE cells and glucose uptake in 3T3-L1 adipocytes did not change significantly in the presence of the extract.

Ursolic acid induces doxorubicin-resistant HepG2 cell death via the release of apoptosis-inducing factor.

Ursolic acid (UA), a triterpenoid compound isolated previously from Oldenlandia diffusa, which is a Traditional Chinese Medicine used to treat cancer, was found to inhibit the proliferation of doxorubicin-resistant human hepatoma cell line (R-HepG2) through apoptosis as shown by externalization of phosphatidyl serine, morphological changes and loss of mitochondrial membrane potential. UA could activate Bak but not Bax, which implied that Bak may play an important role in UA-induced apoptosis. Furthermore, the death of R-HepG2 cells induced by UA was found to be mainly through the caspase-independent apoptosis-inducing factor (AIF) signaling pathway which was evidenced by: (a) the pan-caspase inhibitor and the specific caspase inhibitor had only modest protective effect against UA; (b) UA treatment caused the nuclear translocation of AIF, which is retained in the mitochondria in untreated R-HepG2 cells; (c) cells that had been treated with human AIF-specific siRNA could resist cell death induced by UA.

Saxifragifolin B from Androsace umbellata induced apoptosis on human hepatoma cells.

Bioassay-guided phytochemical study of Androsace umbellata led to the successful isolation of saxifragifolin B (SB) for the first time. The anti-tumor effect of SB was firstly reported that it was shown to have potent cytotoxicity on human hepatoma HepG2 cells with IC50 value of 11.9 microM at 24 h.

The effects of phenytoin and its metabolite 5-(4-hydroxyphenyl)-5-phenylhydantoin on cellular glucose transport.

Glucose is the principal fuel for brain metabolism and its movement across the blood-brain barrier depends on Glut1. Impaired glucose transport to the brain may have deleterious consequences. For example, Glut1 deficiency syndrome (Glut1DS) is the result of heterozygous loss of function Glut1 mutation leading to energy failure of the brain and subsequently, epileptic encephalopathy.