. The databases were searched using the relevant

https://obgyn.onlinelibrary.wiley.com/doi/pdf/10.1111/1471-0528.15306

Placenta Praevia and Placenta Accreta: Diagnosis and Management: Green-top Guideline No. 27a.

Major depressive disorder (MDD) is a chronic, generally episodic and debilitating disease that affects an estimated 300 million people worldwide, but its pathogenesis is poorly understood. The heritability estimate of MDD is 30-40%, suggesting that genetics alone do not account for most of the risk of major depression. Another factor known to associate with MDD involves environmental stressors such as childhood adversity and recent life stress. Recent studies have emerged to show that the biological impact of environmental factors in MDD and other stress-related disorders is mediated by a variety of epigenetic modifications. These epigenetic modification alterations contribute to abnormal neuroendocrine responses, neuroplasticity impairment, neurotransmission and neuroglia dysfunction, which are involved in the pathophysiology of MDD. Furthermore, epigenetic marks have been associated with the diagnosis and treatment of MDD. The evaluation of epigenetic modifications holds promise for further understanding of the heterogeneous etiology and complex phenotypes of MDD, and may identify new therapeutic targets. Here, we review preclinical and clinical epigenetic findings, including DNA methylation, histone modification, noncoding RNA, RNA modification, and chromatin remodeling factor in MDD. In addition, we elaborate on the contribution of these epigenetic mechanisms to the pathological trait variability in depression and discuss how such mechanisms can be exploited for therapeutic purposes. 

Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential

We performed an impact study on the introduction of routine placement of internal iliac artery balloon catheters for the management of haemorrhage during caesarean section in women with placenta accreta. We identified 11 women, with prenatally diagnosed placenta accreta/increta/percreta before this change in practice, who acted as controls, and 30 women who had iliac artery balloons placed. The balloons were inflated in 27 cases. The median (IQR [range]) intra-operative blood loss was 1100 (800-2600 [500-6000]) ml in controls, compared with 1000 (600-2513 [400-15000]) ml in women with iliac artery balloons (p = 0.64). Six (54%) controls received intra-operative blood transfusion compared with 14 (47%) women with iliac artery balloons (p = 0.66). Caesarean hysterectomy was performed in 3 (27.3%) controls and 13 (43.3%) women with iliac artery balloons (p = 0.48). Balloon catheter insertion was associated with a shortened postoperative hospital stay, 6 (5-7 [4-12] days in controls vs. 5 (4-6 [3-10]) in the iliac artery balloon group (p = 0.033). General anaesthesia was used in six (54%) controls, but all women with iliac artery balloons. This study demonstrates that prophylactic balloon occlusion of the internal iliac arteries did not reduce intra-operative haemorrhage or caesarean hysterectomy in women with placenta accreta undergoing caesarean section. In addition, it has a significant impact on the choice of anaesthetic technique.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/anae.13895

Effect of prophylactic placement of internal iliac artery balloon catheters on outcomes of women with placenta accreta: an impact study†

Research progress of hydrogen energy and metal hydrogen storage materials

Managing major obstetric haemorrhage: Pharmacotherapy and transfusion.

Prophylactic abdominal aorta balloon occlusion during caesarean section: a retrospective case series

Traumatic brain injury (TBI) is a kind of acquired brain injury, which is caused by external mechanical forces. Moreover, the neuroprotective role of sevoflurane (Sevo) has been identified in TBI. Therefore, this research was conducted to figure out the mechanism of Sevo in TBI via FGF2.The key factors of neuroprotective effects of Sevo in TBI rats were predicted by bioinformatics analysis. A TBI model was induced on rats that then inhaled Sevo for 1 h and grouped via lentivirus injection. Modified Neurological Severity Score was adopted to evaluate neuronal damage in rats, followed by motor function and brain water content measurement. FGF2, EZH2, and HES1 expression in brain tissues was evaluated by immunofluorescence staining, and expression of related genes and autophagy factors by RT-qPCR and Western blot analysis. Methylation-specific PCR was performed to assess HES1 promoter methylation level, and ChIP assay to detect the enrichment of EZH2 in the HES1 promoter. Neuronal damage was assessed by cell immunofluorescence staining, and neuronal apoptosis by Nissl staining, TUNEL staining, and flow cytometry.Sevo diminished brain edema, improved neurological scores, and decreased neuronal apoptosis and autophagy in TBI rats. Sevo preconditioning could upregulate FGF2 that elevated EZH2 expression, and EZH2 bound to the HES1 promoter to downregulate HES1 in TBI rats. Also, FGF2 or EZH2 overexpression or HES silencing decreased brain edema, neurological deficits, and neuronal autophagy and apoptosis in Sevo-treated TBI rats.Our results provided a novel insight to the neuroprotective mechanism of Sevo in TBI rats by downregulating HES1 via FGF2/EZH2 axis activation. 

/pdf/the-neuroprotective-mechanism-of-sevoflurane-in-rats-with-270dj0u0.pdf

The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2

N6-methyladenosine (m6A) is the most abundant methylation modification on mRNA in mammals. Fat mass and obesity-related protein (FTO) is the main RNA m6A demethylase. FTO is involved in the occurrence and maintenance of neuropathic pain (NP). NP often induces mental disorders. We found that NP downregulated the expression of FTO in the anterior cingulate cortex (ACC), inhibited the expression of matrix metalloproteinase-9 (MMP-9) in the ACC, maladjusted the brain-derived neurotrophic factor precursor (proBDNF) and mature brain-derived neurotrophic factor (mBDNF) levels in the ACC, and induced anxiety- and depression-like behaviors in mice. Blocking the downregulation of FTO in the ACC induced by peripheral nerve injury could reverse the anxiety- and depression-like behaviors of mice. Contrarily, downregulation of simulated FTO induced anxiety- and depression-like behaviors in mice. After peripheral nerve injury, the binding of FTO to MMP-9 mRNA decreased and the enrichment of m6A on MMP-9 mRNA increased. In conclusion, downregulation of FTO in ACC by regulating MMP-9 mRNA methylation level contributes to the occurrence of anxiety- and depression-like behaviors in NP mice.

Downregulation of Fat Mass and Obesity-Related Protein in the Anterior Cingulate Cortex Participates in Anxiety- and Depression-Like Behaviors Induced by Neuropathic Pain

Effects of Zr doping on activation capability and hydrogen storage performances of TiFe-based alloy

Research and application of Ti–Mn-based hydrogen storage alloys

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