Background: The intake of fish and polyunsaturated fatty acids (PUFAs) may benefit cognitive function. However, optimal intake recommendations for protection are unknown. Objective: We systematically investigated associations between fish and PUFA intake and mild-to-severe cognitive impairment risk. Design: Studies that reported risk estimates for mild cognitive impairment (MCI), cognitive decline, dementia, Alzheimer disease (AD), or Parkinson disease (PD) from fish, total PUFAs, total n-3 (v-3) PUFAs, or at least one n-3 PUFA were included. Study characteristics and outcomes were extracted. The pooled RR was estimated with the use of a random-effects model metaanalysis. A dose-response analysis was conducted with the use of the 2-stage generalized least-squares trend program. Results: We included 21 studies (181,580 participants) with 4438 cases identified during follow-up periods (2.1-21 y). A 1-serving/wk increment of dietary fish was associated with lower risks of dementia (RR: 0.95; 95% CI: 0.90, 0.99; P = 0.042, I 2 = 63.4%) and AD (RR: 0.93; 95% CI: 0.90, 0.95; P = 0.003, I 2 = 74.8%). Pooled RRs of MCI and PD were 0.71 (95% CI: 0.59, 0.82; P = 0.733, I 2 = 0%) and 0.90 (95% CI: 0.80, 0.99; P = 0.221, I 2 = 33.7%), respectively, for an 8-g/d increment of PUFA intake. As an important source of marine n-3 PUFAs, a 0.1-g/d increment of dietary docosahexaenoic acid (DHA) intake was associated with lower risks of dementia (RR: 0.86; 95% CI: 0.76, 0.96; P , 0.001, I 2 = 92.7%) and AD (RR: 0.63; 95% CI: 0.51, 0.76; P , 0.001, I 2 = 94.5%). Significant curvilinear relations between fish consumption and risk of AD and between total PUFAs and risk of MCI (both P-nonlinearity , 0.001) were observed. Conclusions: Fishery products are recommended as dietary sources and are associated with lower risk of cognitive impairment. Marinederived DHA was associated with lower risk of dementia and AD but without a linear dose-response relation.Am J Clin Nutr 2016;103:330-40.

Purpose of review This review will summarize the most significant work that contributed to the understanding of liver fibrosis progression and resolution, which in turn has yielded new areas of therapeutic targeting. Recent findings Liver fibrosis is the result of an imbalance between production and dissolution of extracellular matrix. Stellate cells, portal myofibroblasts, and bone marrow derived cells converge in a complex interaction with hepatocytes and immune cells to provoke scarring in response to liver injury. Uncovering the specific effects of growth factors on these cells, defining the interaction of different cell population during liver fibrosis and characterizing the genetic determinants of fibrosis progression will enable the discovery of new therapeutic approaches. Summary The outcome of improved understanding of liver fibrosis process, especially the regulation and activation of stellate cells, is reflected in the development of new therapeutic strategies, which are validated in animal models.

Although hepatic fibrosis typically follows chronic inflammation, fibrosis will often regress after cessation of liver injury. Here we examined whether liver dendritic cells (DC) play a role in liver fibrosis regression using carbon tetrachloride (CCl4) to induce liver injury. We examined DC dynamics during fibrosis regression and their capacity to modulate liver fibrosis regression upon cessation of injury. We show that conditional DC depletion soon after discontinuation of the liver insult leads to delayed fibrosis regression and reduced clearance of activated hepatic stellate cells, the key fibrogenic cell in liver. Conversely, DC expansion induced either by Flt3L (Fms-like tyrosine kinase-3 ligand) or adoptive transfer of purified DC accelerates liver fibrosis regression. DC modulation of fibrosis was partially dependent on MMP-9, as MMP-9 inhibition abolished Flt3L-mediated effect and the ability of transferred DC to accelerate fibrosis regression. In contrast, transfer of DC from MMP-9 deficient mice failed to improve fibrosis regression. Conclusion Altogether, these results suggest that DC increase fibrosis regression, and that the effect is correlated with their production of MMP-9. These results also suggest that Flt3L treatment during fibrosis resolution merits evaluation to accelerate regression of advanced liver fibrosis.

Results: Chinese people experienced greater odds of comorbidities than whites for a given BMI after standardizing for age and sex: 43% for diabetes, 30% for dyslipidemia, 28% for hypertension, 38% for metabolic syndrome, and 48% for hyperuricemia. Comparisons of BMI-mortality associations found that the U-shaped BMI-mortality curve shifted 1-2 kg m 22 to the left in Chinese compared to whites. Compared to whites at BMIs of 25 and 30 kg m 22 , corresponding cutoffs in Chinese were 22.5 and 25.9 kg m 22 in men, and 22.8 and 26.6 kg m 22 in women after both fat and fat distribution were taken into account. Conclusions: Comorbidity, mortality, and body composition data consistently support the use of lower BMI cutoffs in Chinese than those in whites.