Background: Resveratrol (Res) is a polyphenol anti-inflammatory agent. We have studied the link between the anti-inflammatory effects of Res and the high mobility group box 1(HMGB1) signaling pathway. Methods: Murine macrophage-like RAW264.7 cells (RAW264.7 cells) were either untreated (control) or treated with Res, LPS, or LPS + Res. Levels of IL-6, NO, and TNF-α were measured by ELISA and colorimetric assays. Expression of HMGB1 was detected by qRT-PCR, western blot, and immunofluorescence assays. Protein and mRNA expression levels of TLR4 were also examined. Results: Res significantly reduced the levels of IL-6, NO, and TNF-α in RAW264.7 cells exposed to LPS. Expression levels of HMGB1 (mRNA and protein) and of TLR4 in the LPS + Res-treated cells were lower than in cells treated with LPS alone. Conclusions: Res can block the inflammatory effects induced by LPS in RAW264.7 cells. Down-regulation of HMGB expression may be one of the mechanisms of action of Res. Res may also influence TLR4 expression in the HMGB1-TLR4 signaling pathway.

Punctal occlusion with collagen plugs in dry eye patients leads to the relief of subjective symptoms and the improvement of objective signs. The effectiveness of occluding the upper or lower punctum is similar. The LTMH is a valid indicator of the success of punctal occlusion.

Level III, retrospective comparative study.

Single nucleotide polymorphisms of 5' regulatory region of follicle-stimulating hormone receptor (FSHR) gene were detected in two high prolificacy sheep breeds (Small Tail Han and Hu sheep) and two low prolificacy sheep breeds (Corriedale and Chinese Merino sheep) by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP). The results indicated that there were three genotypes (AA, AB and BB) detected by primer 1 in Hu sheep while only one genotype (AA) in other three sheep breeds, and frequencies of AA, AB and BB genotypes in Hu sheep were 0.700, 0.225 and 0.075, respectively. There were three genotypes (EE, EF and EG) detected by primer 3 in Small Tail Han sheep while only EE genotype occurred in other three sheep breeds, and frequencies of EE, EF and EG genotypes in Small Tail Han sheep were 0.775, 0.200 and 0.025, respectively. No polymorphism was detected in four sheep breeds by primer 2 and primer 4. The sequencing results showed that there were two nucleotide mutations (g. -681T>C and g. -629C>T) in genotype BB compared with AA for primer 1. As for primer 3, two mutations (g. -197G>A and g. -98T>C) in genotype EF compared with EE and two mutations (g. -200G>A and g. -197G>A) in genotype EG compared with EE. The heterozygous ewes with EG or EF had 0.89 (P < 0.05) or 0.42 (P < 0.05) lambs more than homozygous ewes (EE genotype) in Small Tail Han sheep, respectively, while there was no significant difference on litter size between EG and EF ewes.

Purpose To evaluate the association between acute respiratory distress syndrome (ARDS) onset time and prognosis. Methods Patients with moderate to severe ARDS (N = 876) were randomly assigned into derivation (N = 520) and validation (N = 356) datasets. Both 28-day and 60-day survival times after ARDS onset were analyzed. A data-driven cutoff point between early- and late-onset ARDS was determined on the basis of mortality risk effects of onset times. We estimated the hazard ratio (HR) and odds ratio (OR) of late-onset ARDS using a multivariate Cox proportional hazards model of survival time and a multivariate logistic regression model of mortality rate, respectively. Results Late-onset ARDS, defined as onset over 48 h after intensive care unit (ICU) admission (N = 273, 31%), was associated with shorter 28-day survival time: HR = 2.24, 95% CI 1.48–3.39, P = 1.24 × 10−4 (derivation); HR = 2.16, 95% CI 1.33–3.51, P = 1.95 × 10−3 (validation); and HR = 2.00, 95% CI 1.47–2.72, P = 1.10 × 10−5 (combined dataset). Late-onset ARDS was also associated with shorter 60-day survival time: HR = 1.70, 95% CI 1.16–2.48, P = 6.62 × 10−3 (derivation); HR = 1.78, 95% CI 1.15–2.75, P = 9.80 × 10−3 (validation); and HR = 1.59, 95% CI 1.20–2.10, P = 1.22 × 10−3 (combined dataset). Meanwhile, late-onset ARDS was associated with higher 28-day mortality rate (OR = 1.46, 95% CI 1.04–2.06, P = 0.0305) and 60-day mortality rate (OR = 1.44, 95% CI 1.03–2.02, P = 0.0313). Conclusions Late-onset moderate to severe ARDS patients had both shorter survival time and higher mortality rate in 28-day and 60-day observations.