Patients exposed to a surgical safety checklist experience better postoperative outcomes, but this could simply reflect wider quality of care in hospitals where checklist use is routine.

CysC is a crucial determinant contributing to endogenous neuroprotection. It is also a novel candidate for stroke treatment through maintaining lysosomal membrane integrity.

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BackgroundThe plasma protein hemopexin (HPX) exhibits the highest binding affinity to free heme. In vitro experiments and gene-knock out technique have suggested that HPX may have a neuroprotective effect. However, the expression of HPX in the brain was not well elucidated and its expression after cerebral ischemia-reperfusion injury was also poorly studied. Furthermore, no in vivo data were available on the effect of HPX given centrally on the prognosis of focal cerebral ischemia.ResultsIn the present study, we systematically investigated expression of HPX in normal rat brain by immunofluorescent staining. The results showed that HPX was mainly expressed in vascular system and neurons, as well as in a small portion of astrocytes adjacent to the vessels in normal rat brain. Further, we determined the role of HPX in the process of focal cerebral ischemic injury and explored the effects of HPX treatment in a rat model of transient focal cerebral ischemia. After 2 h’ middle cerebral artery occlusion (MCAO) followed by 24 h’ reperfusion, the expression of HPX was increased in the neurons and astrocytes in the penumbra area, as demonstrated by immunohistochemistry and Western blot techniques. Intracerebroventricular injection of HPX at the onset of reperfusion dose-dependently reduced the infarct volumes and improved measurements of neurological function of the rat subjected to transient focal cerebral ischemia. The neuroprotective effects of HPX sustained for up to 7 days after experiments.ConclusionsOur study provides a new insight into the potential neuroprotective role of HPX as a contributing factor of endogenous protective mechanisms against focal cerebral ischemia injury, and HPX might be developed as a potential agent for treatment of ischemic stroke.

Background and purposeWith the popularization of a two-child policy in China, the number of pregnant women of advanced maternal age will increase steadily. We aimed to assess the association between pre-pregnancy body mass index (BMI) and weight gain in the first and second trimester and the risk of gestational diabetes (GDM) in the advanced maternal age group and control group defined as maternal age of 20–35 years.ResultsThe risk of GDM for obesity before pregnancy was 2.707 (95% CI: 1.042–7.029) folds and 3.612 (95% CI: 1.182–11.039) folds in the control group and advanced maternal age group, respectively. Excessive weight gain in the first trimester was significant related to a higher risk of developing GDM with the odds ratio (OR) of 2.655 (95% CI: 1.265–5.571) and 4.170 (95% CI: 1.437–12.100) in the control group and advanced maternal age group, respectively.Materials and methodsThis prospective cohort study included 565 pregnant women with singleton pregnancy who were recruited in their first prenatal visit from the antenatal clinic in March and December 2016. Maternal weight was recorded before pregnancy, in the first prenatal visit and at the time of screening oral glucose tolerance test (OGTT). All women underwent 2 h 75g-OGTT at 24–28 weeks (24 weeks on average). GDM was diagnosed according to the standards issued by the Ministry of Health of China in 2011.ConclusionsElevated pre-pregnancy BMI independently increases the risk of GDM, particularly in advanced maternal age. Excessive weight gain in the first trimester is significantly associated with the incidence of GDM regardless of pre-pregnancy BMI.

Highlights d Plastid genome instability alters endoreplication and cell cycle d Plastid genome instability results in increased expression of cell-cycle-related genes d SOG1 mediates the activation of cell-cycle-related genes by plastid genome instability d ROS is required for communication of plastid genome with endoreplication and cell cycle

BackgroundIschemia-reperfusion (I/R) is a critical pathophysiological basis of cognitive dysfunction caused by ischemia stroke. Heme-oxygenase-1 (HO-1) is the rate-limiting enzyme for the elimination of excessive free heme by combining with hemopexin (HPX), a plasma protein that contributes to eliminating excessive free heme during ischemia stroke. This study aimed to elucidate whether HPX could alleviate cognitive dysfunction in rats subjected to cerebral I/R.MethodsRats were randomly divided into five groups: sham, MCAO, Vehicle, HPX and HPX + protoporphyrin IX (ZnPPIX). Cerebral I/R was induced by MCAO. Saline, vehicle, HPX and HPX + ZnPPIX were injected intracerebroventricularly at the moment after reperfusion. Morris water maze (MWM) test was used to detect the learning and cognitive function. Western blot was used to detect the expression of HO-1 in ischemic penumbra. CD31/vWF double labeling immunofluorescence was used to detect the neovascularization in the penumbra hippocampus. The structure and function of blood-brain barrier (BBB) was detected by the permeability of Evans Blue (EB), water content of the brain tissue, the Ang1/Ang2 and VE-cadherin expression.ResultsOur study verified that HPX improved the learning and memory capacity. Hemopexin up-regulated HO-1 protein expression, the average vessel density in the penumbra hippocampus and the VE- cadherin expression but decreased the permeability of EB, the water content of brain tissue and the ratio of Ang1/Ang2. The effects were reversed by ZnPPIX, an inhibitor of HO-1.ConclusionHPX can maintain the integrity of the blood-brain barrier and alleviate cognitive dysfunction after cerebral I/R through the HO-1 pathway.

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