BACKGROUND: The dural puncture epidural (DPE) technique is associated with faster onset than the conventional epidural (EP) technique for labor analgesia. The programmed intermittent epidural bolus (PIEB) mode for maintaining labor analgesia allows for lower anesthetic drug consumption than the continuous epidural infusion (CEI) mode. Whether DPE technique with PIEB mode offers additional benefits for analgesia onset, local anesthetic drug consumption, and side effects versus EP or DPE techniques with CEI mode remains unclear. METHODS: Nulliparous women with a visual analog scale (VAS) pain score >50 mm and cervical dilation <5 cm were randomly assigned to receive EP + CEI, DPE + CEI, or DPE + PIEB for labor analgesia. A 25-gauge needle was used for dural puncture. Analgesia was initiated with 10 mL of 0.1% ropivacaine with 0.3 µg/mL of sufentanil and maintained with the same solution at 8 mL/h in all groups. A 5-mL patient-controlled epidural analgesia (PCEA) bolus was programmed with a 20-minute lockout. Breakthrough pain not amendable by PCEA was treated with provider boluses of 5 mL of 0.125% ropivacaine. The primary outcome was “time to adequate analgesia,” defined as a VAS pain score ≤30 mm during 2 consecutive contractions, and was analyzed using Kaplan–Meier curves and a Cox proportional hazard model. Secondary outcomes included the VAS scores, ropivacaine consumption, sensory block level to ice, PCEA and provider boluses intervention, mode of delivery, duration of labor, Bromage scores, Apgar scores, occurrence of side effects, and maternal satisfaction with the anesthesia. RESULTS: A total of 116 women were included (38 in the EP + CEI group, 40 in the DPE + CEI group, and 38 in the DPE + PIEB group). Adequate anesthesia was achieved faster in the DPE + CEI and DPE + PIEB groups than in the EP + CEI group (hazard ratio = 1.705; 95% confidence interval [CI], 1.039–2.800; P = .015; and hazard ratio = 1.774; 95% CI, 1.070–2.941; P = .012, respectively). DPE technique with PIEB mode was associated with the fewest PCEA boluses and the lowest hourly ropivacaine consumption (both P < .001). There were no differences in the duration of labor, mode of delivery, Bromage scores, newborn Apgar scores, incidence of side effects, and maternal satisfaction scores among the groups. CONCLUSIONS: The use of DPE technique for neuraxial analgesia was associated with faster onset than the use of the EP technique. DPE technique with PIEB mode achieved the greatest drug-sparing effect without increasing maternal or neonatal side effects.

ObjectiveThe purpose of the present meta-analysis was to evaluate the association between the inflammatory potential of diet, determined by the dietary inflammatory index (DII®) score, and depression.DesignSystematic review and meta-analysis.SettingA comprehensive literature search was conducted in PubMed, Web of Science and EMBASE databases up to August 2018. All observational studies that examined the association of the DII score with depression/depressive symptoms were included.SubjectsFour prospective cohorts and two cross-sectional studies enrolling a total of 49 584 subjects.ResultsOverall, individuals in the highest DII v. the lowest DII category had a 23 % higher risk of depression (risk ratio (RR)=1·23; 95 % CI 1·12, 1·35). When stratified by study design, the pooled RR was 1·25 (95 % CI 1·12, 1·40) for the prospective cohort studies and 1·16 (95 % CI 0·96, 1·41) for the cross-sectional studies. Gender-specific analysis showed that this association was observed in women (RR=1·25; 95 % CI 1·09, 1·42) but was not statistically significant in men (RR=1·15; 95 % CI 0·83, 1·59).ConclusionsThe meta-analysis suggests that pro-inflammatory diet estimated by a higher DII score is independently associated with an increased risk of depression, particularly in women. However, more well-designed studies are needed to evaluate whether an anti-inflammatory diet can reduce the risk of depression.

Ferroptosis is a newly discovered form of regulated cell death dependent on iron and reactive oxygen species (ROS). It directly or indirectly affects the activity of glutathione peroxidases (GPXs) under the induction of small molecules, causing membrane lipid peroxidation due to redox imbalances and excessive ROS accumulation, damaging the integrity of cell membranes. Ferroptosis is mainly characterized by mitochondrial shrinkage, increased density of bilayer membranes, and the accumulation of lipid peroxidation. Myocardial ischemia-reperfusion injury (MIRI) is an unavoidable risk event for acute myocardial infarction. Ferroptosis is closely associated with MIRI, and this relationship is discussed in detail here. This review systematically summarizes the process of ferroptosis and the latest research progress on the role of ferroptosis in MIRI to provide new ideas for the prevention and treatment of MIRI.

Background and purpose: Ischaemia damages to the cardiac mitochondria by increasing generation of reactive oxygen species (ROS) and peroxidation of cardiolipin. The inhibited mitochondrial function leads to the cardiac injury during reperfusion. Propofol (2, 6-diisopropylphenol), an intravenous anaesthetic, has been shown to decrease cardiac ischaemia and reperfusion injury. In the present study, we propose that propofol protects mitochondrial function and decreases cardiac injury by prevention of cardiolipin peroxidation during ischaemia and reperfusion. Experimental approach: After isolation of mitochondria from isolated rat heart perfused on a Langendorff model, various mitochondrial bioenergetic parameters were evaluated such as rates of mitochondrial oxygen consumption, H 2 O 2 production, complex I and III activity as well as the degree of lipid peroxidation and cardiolipin content. The action of propofol was also explored in isolated mitochondria. And the effect of cardiolipin was evaluated by fusing cardiolipin liposome with mitochondria. Key results: Propofol treatment had strong dose-dependent protection attenuating these parameters alterations in reperfused rat heart and isolated mitochondria. Additionally, cardiolipin treatment had the same protective effect, compared with propofol treatment at high concentration. Conclusions and implications:The protective effect of propofol appears to be due, at least in part, as a chemical uncoupler, to the interruption of the vicious circle of ROS-cardiolipin-complexes of the respiratory chain-ROS through preserving the content and integrity of cardiolipin molecules by ROS attack. These findings may provide an explanation for some of the factors responsible for cardioprotection and one approach exploring an available antioxidant.

Abelmoschus manihot (L.) Medik. (Malvaceae) is a herb used in traditional Chinese medicine to treat some kidney diseases. To date, the detailed mechanisms by which A. manihot improves some kinds of renal disease are not fully understood. In this study, we established Adriamycin-induced NRK-52E cells, the normal rat kidney epithelial cell line, injury, and Sprague-Dawley rats with Adriamycin-induced nephropathy to evaluate the role and mechanisms of total extracts of A. manihot flower (TEA) both in vitro and in vivo . We found that TEA ameliorated Adriamycin-induced cellular morphological changes, cell viability, and apoptosis through the suppression of protein oxidation and ERK1/2 signaling. However, this anti-oxidative stress role of TEA was independent of ROS inhibition. Adriamycin activated ERK1/2 signaling followed by activation of NLRP3 inflammasomes. TEA suppressed NLRP3 inflammasomes via inhibition of ERK1/2 signal transduction; decreased proteinuria and attenuated renal tubule lesions; and inhibited the expression of NLRP3 in tubules in rats with Adriamycin nephropathy. Collectively, TEA protects renal tubular cells against Adriamycin-induced tubule injury via inhibition of ROS-ERK1/2-NLRP3 inflammasomes.

6-Gingerol (6-G) is known to alleviate myocardial ischemia/reperfusion injury. However, the underlying molecular mechanisms of 6-G myocardial protection are not known. In this study, the protective effect of 6-G on ischemia/reperfusion (I/R) damage and whether such a mechanism was related to apoptosis inhibition and activation of phosphoinositide 3-kinases (PI3K)/serine/threonine kinase (Akt) signaling pathway were investigated. Rats were subjected to I/R in the presence or absence of 6-G and the changes of cardiac function, infarct size and histopathological changes, and the levels of cardiac troponin T, creatine kinase-MB, and myocardial apoptosis were examined. The expression of caspase-3, PI3K, p-Akt, and Akt was also determined. We found that 6-G (6 mg/kg) pretreatment significantly improved heart function and ameliorated infarct size and histopathological changes and cardiac troponin T and creatine kinase-MB levels induced by I/R. Moreover, pretreatment with 6-G significantly inhibited myocardial apoptosis and caspase-3 activation induced by I/R. 6-G also upregulated expression of PI3K, p-Akt, and Akt in myocardial tissues. Taken together, these findings suggest that 6-G inhibits apoptosis and activates PI3K/Akt signaling in response to myocardial I/R injury as a possible mechanism to attenuate I/R-induced injury in heart. These results might be important for developing novel strategies for preventing myocardial I/R injury.

Pulmonary fibrosis is a progressively aggravating lethal disease that is a serious public health concern. Although the incidence of this disease is increasing, there is a lack of effective therapies. In recent years, the pathogenesis of pulmonary fibrosis has become a research hotspot. p53 is a tumor suppressor gene with crucial roles in cell cycle, apoptosis, tumorigenesis, and malignant transformation. Previous studies on p53 have predominantly focused on its role in neoplastic disease. Following in-depth investigation, several studies have linked it to pulmonary fibrosis. This review covers the association between p53 and pulmonary fibrosis, with the aim of providing novel ideas to improve the clinical diagnosis, treatment, and prognosis of pulmonary fibrosis.

Pyroptosis is a pattern of programmed cell death that significantly differs from apoptosis and autophagy in terms of cell morphology and function. The process of pyroptosis is characterized predominantly by the formation of gasdermin protein family-mediated membrane perforation, cell collapse, and the release of inflammatory factors, including IL-1β and IL-18. In recent years, with the rise of pyroptosis research, scholars have devoted time to study the mechanism of pyroptosis in kidney-related diseases. Pyroptosis is probably involved in kidney diseases through two pathways: the caspase-1-mediated canonical pathway and the caspase-4/5/11-mediated noncanonical pathway. In addition, some scholars have identified targets for the treatment of kidney-related diseases from the viewpoint of pyroptosis and developed corresponding medicines, which may become a recommendation for prognosis, targeted treatment, and clinical diagnosis of kidney diseases. This paper focuses on the up-to-date advances in the field of pyroptosis, especially on the key pathogenic role of pyroptosis in the development and progression of kidney diseases. It presents a more in-depth understanding of the pathogenesis of kidney diseases and introduces novel therapeutic targets for the prevention and clinical treatment of kidney diseases.