The Asian Pacific Association for the Study of the Liver (APASL) set up a working party on acute-on-chronic liver failure (ACLF) in 2004, with a mandate to develop consensus guidelines on various aspects of ACLF relevant to disease patterns and clinical practice in the Asia-Pacific region. Experts predominantly from the Asia–Pacific region constituted this working party and were requested to identify different issues of ACLF and develop the consensus guidelines. A 2-day meeting of the working party was held on January 22–23, 2008, at New Delhi, India, to discuss and finalize the consensus statements. Only those statements that were unanimously approved by the experts were accepted. These statements were circulated to all the experts and subsequently presented at the Annual Conference of the APASL at Seoul, Korea, in March 2008. The consensus statements along with relevant background information are presented in this review.

Background: This is the first ever decade which has witnessed the emergence of a highly lethal condition termed acute-on-chronic liver failure (ACLF), which today is the leading cause of death compared to acute and chronic liver failure. However, the complex pathophysiology of ACLF remains poorly understood. This article will attempt to summarize recent progress in the understanding of the mechanisms of cytokines in ACLF. Methods: The search terms used on PubMed were cytokines, liver injury, complications of liver disease, and hepatic progenitor cell. Results: Cytokines play a significant role in the pathophysiology of ACLF including hepatocellular death, extrahepatic complications and hepatocyte regeneration. The tissue-damaging mechanisms of cytokines are closely related to their hepatocyte proliferation and regeneration function. Conclusions: It remains a challenge to selectively prevent the detrimental effects of cytokines. To design interventions which selectively target the detrimental effects of cytokines, a detailed understanding of cytokines in the pathophysiology ACLF is critical.

Much remains unknown about the role of added sugar in relation to cardiovascular disease (CVD) and the relative contributions of sugar-sweetened beverages (SSB) or artificially sweetened beverages (ASB) to CVD risk. Among the 109,034 women who participated in Women’s Health Initiative, we assessed average intakes of added sugar, SSB and ASB, and conducted Cox regression to estimate the hazard ratios (HRs) and their 95% confidence intervals for CVD risk. The consistency of findings was compared to a network meta-analysis of all available cohorts. During an average of 17.4 years of follow-up, 11,597 cases of total CVD (nonfatal myocardial infarction, coronary heart disease (CHD) death, stroke, coronary revascularization, and/or incident heart failure) were confirmed. Added sugar as % energy intake daily (%EAS) at ≥15.0% was positively associated with total CVD (HR = 1.08 [1.01, 1.15]) and CHD (HR = 1.20 [1.09, 1.32]). There was also a higher risk of total CVD associated with ≥1 serving of SSB intake per day (HR = 1.29 [1.17, 1.42]), CHD (1.35 [1.16, 1.57]), and total stroke (1.30 [1.10, 1.53]). Similarly, ASB intake was associated with an increased risk of CVD (1.14 [1.03, 1.26]) and stroke (1.24 [1.04, 1.48]). According to the network meta-analysis, there was a large amount of heterogeneity across studies, showing no consistent pattern implicating added sugar, ASB, or SSB in CVD outcomes. A diet containing %EAS ≥15.0% and consuming ≥1 serving of SSB or ASB may be associated with a higher CVD incidence. The relative contribution of added sugar, SSB, and ASB to CVD risk warrants further investigation.

Background and Aims: The association of fatty acids with coronary heart disease (CHD) has been examined, mainly through dietary measurements, and has generated inconsistent results due to measurement error. Large observational studies and randomized controlled trials have shown that plasma phospholipid fatty acids (PL-FA), especially those less likely to be endogenously synthesized, are good biomarkers of dietary fatty acids. Thus, PL-FA profiles may better predict CHD risk with less measurement error. Methods: We performed a matched case-control study of 2428 postmenopausal women nested in the Women’s Health Initiative Observational Study. Plasma PL-FA were measured using gas chromatography and expressed as molar percentage (moL %). Multivariable conditional logistic regression was used to calculate odds ratios (95% CIs) for CHD associated with 1 moL % change in PL-FA. Results: Higher plasma PL long-chain saturated fatty acids (SFA) were associated with increased CHD risk, while higher n-3 polyunsaturated fatty acids (PUFA) were associated with decreased risk. No significant associations were observed for very-long-chain SFA, monounsaturated fatty acids (MUFA), PUFA n-6 or trans fatty acids (TFA). Substituting 1 moL % PUFA n-6 or TFA with an equivalent proportion of PUFA n-3 were associated with lower CHD risk. Conclusions: Higher plasma PL long-chain SFA and lower PUFA n-3 were associated with increased CHD risk. A change in diet by limiting foods that are associated with plasma PL long-chain SFA and TFA while enhancing foods high in PUFA n-3 may be beneficial in CHD among postmenopausal women.

Hypoxia is a physiological state characterized by reduced oxygen levels in organs and tissues. It is a common clinicopathological process and a major cause of health problems in highland areas. Heart rate variability (HRV) is a measure of the balance in autonomic innervation to the heart. It provides valuable information on the regulation of the cardiovascular system by neurohumoral factors, and changes in HRV reflect the complex interactions between multiple systems. In this review, we provide a comprehensive overview of the relationship between high-altitude hypoxia and HRV. We summarize the different mechanisms of diseases caused by hypoxia and explore the changes in HRV across various systems. Additionally, we discuss relevant pharmaceutical interventions. Overall, this review aims to provide research ideas and assistance for in-depth studies on HRV. By understanding the intricate relationship between high-altitude hypoxia and HRV, we can gain insights into the underlying mechanisms and potential therapeutic approaches to mitigate the effects of hypoxia on cardiovascular and other systems. The relevant literature was collected systematically from scientific database, including PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), Baidu Scholar, as well as other literature sources, such as classic books of hypoxia. There is a close relationship between heart rate variability and high-altitude hypoxia. Heart rate variability is an indicator that evaluates the impact of hypoxia on the cardiovascular system and other related systems. By improving the observation of HRV, we can estimate the progress of cardiovascular diseases and predict the impact on other systems related to cardiovascular health. At the same time, changes in heart rate variability can be used to observe the efficacy of preventive drugs for altitude related diseases. HRV can be used to assess autonomic nervous function under various systemic conditions, and can be used to predict and monitor diseases caused by hypoxia at high altitude. Investigating the correlation between high altitude hypoxia and heart rate variability can help make HRV more rapid, accurate, and effective for the diagnosis of plateau-related diseases.