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Given the causal impact of alcohol use on stroke, alcohol control policies should presumably reduce stroke mortality rates. This study aimed to test the impact of three major Lithuanian alcohol control policies implemented in 2008, 2017 and 2018 on sex- and stroke subtype-specific mortality rates, among individuals 15+ years-old. Joinpoint regression analyses were performed for each sex- and stroke subtype-specific group to identify timepoints corresponding with significant changes in mortality rate trends. To estimate the impact of each policy, interrupted time series analyses using a generalized additive mixed model were performed on monthly sex- and stroke subtype-specific age-standardized mortality rates from January 2001-December 2018. Significant average annual percent decreases were found for all sex- and stroke subtype-specific mortality rate trends. The alcohol control policies were most impactful on ischemic stroke mortality rates among women. The 2008 policy was followed by a positive level change of 4,498 ischemic stroke deaths per 100,000 women and a negative monthly slope change of -0.048 ischemic stroke deaths per 100,000 women. Both the 2017 and 2018 policy enactment timepoints coincided with a significant negative level change for ischemic stroke mortality rates among women, at -0.901 deaths and -1.431 deaths per 100,000 population, respectively. Hemorrhagic stroke mortality among men was not affected by any of the policies, and hemorrhagic stroke mortality among women and ischemic stroke mortality among men were only associated with the 2008 policy. Our study findings suggest that the impact of alcohol control policies on stroke mortality may vary by sex and subtype.

Objective: Prevalence of hepatopulmonary syndrome (HPS) ranges from 4% to 47% in patients with cirrhosis. This study aimed to explore possible relationship between CX3CR1 and angiogenesis or macrophage accumulation in pathological process of HPS., Material and Methods: Wide-type C57Bl/6 mice were divided into WT-sham, WT-common bile duct ligation (WT-CBDL), WT-CBDL plus antibody (WT-CBDL+Ab) and WT-CBDL plus Bevacizumab. The CX3CR1 GFP/GFP mice were grouping into CX3CR1 GFP/GFP-sham, CX3CR1 GFP/GFP-CBDL and CX3CR1 GFP/GFP-CBDL+Bevacizumab group. Intrapulmonary expression of Akt, pAkt, ERK, pERK, iNOS, VEGF, PDGF was measured using biological technology. Hematoxylin-eosin (H&E) staining and immunohistochemical analysis were used to evaluate changes of pulmonary tissues including pathological abnormality, angiogenesis and macrophage accumulation., Results: Blockade CX3CR1 pathway inhibited angiogenesis, macrophage accumulation and pathological changes of lung tissues. Blockade of CX3CR1 pathway reduced pAkt, pERK, iNOS, PDGF and VEGF activation. CX3CR1 contributed to the process of angiogenesis and activate the pro-angiogenic factors. CX3CR1 deficiency obviously reduced the macrophage accumulation. Inhibition of VEGF by Bevacizumab improved intrapulmonary angiogenesis and pathological changes of lung tissues. Inhibition of VEGF by Bevacizumab retarded the production of pAKt, PDGF, and iNOS. Inhibition of VEGF by Bevacizumab reduced CX3CL1 production., Conclusion: CX3CR1 could regulate the angiogenesis and activation of pro-angiogenic factors, including pAKT, pERK, iNOS, VEGF and PDGF in the process of hepato-pulmonary syndrome. Moreover, CX3CR1 could also contribute to the macrophage accumulation., (Copyright © 2020 Elsevier España, S.L.U. All rights reserved.)

Background and Objective: The aim of this study was to analyze risk factors for nosocomial infection (NI) in patients receiving extracorporeal membrane oxygenation (ECMO) support., Patients and Methods: Clinical NI data were collected from patients who received ECMO support therapy, and analyzed retrospectively., Results: Among 75 ECMO patients, 20 were found to have developed NI (infection rate 26.7%); a total of 58 pathogens were isolated, including 43 strains of gram-negative bacteria (74.1%) and 15 strains of gram-positive bacteria (25.9%). Multi-drug resistant strains were highly concentrated and were mainly shown to be Acinetobacter baumannii, Pseudomonas aeruginosa, and coagulase-negative staphylococci. Incidence of NI was related to the duration of ECMO support therapy and the total length of hospital stay, and the differences were statistically significant (P<.05). A prolonged period of ECMO support extended the hospital stay, but it did not increase the mortality rate. However, an elevated level of lactic acid increased the mortality rate in this study population., Conclusions: ECMO-associated secondary NIs correlated significantly with the length of hospital stay and with the duration of ECMO support. Therefore, to reduce the incidence of ECMO-associated NIs, preventive strategies that aim to shorten the duration of ECMO support therapy and avoid lengthy hospitalization should be applied, wherever possible., (Copyright © 2017 Elsevier España, S.L.U. All rights reserved.)