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The mortality of re-bleeding following aneurysmal subarachnoid hemorrhage is high, and surviving patients often have poor clinical condition and worse outcome than patients with a single bleed. In this study, we performed an updated systematic review and meta-analysis to determine the most common risk factors for re-bleeding in this patient population, with the goal of providing neurologists, neurosurgeons, neuro-interventionalists with a simple and fast method to evaluate the re-bleeding risk for aneurysmal subarachnoid hemorrhage.

Epigenetic alterations have been implicated in the development and progression of human cancer. It is noteworthy that epigenetic modifications, in contrast to genetic mutations, are intrinsically reversible. This triggers an impressive interest of researchers in treatment of cancer patients via targeting epigenetic mechanisms, leading to subsequent intensive investigations of epigenetic drugs as a novel therapeutic intervention. DNA methylation, the major form of epigenetic modifications, is catalyzed by the maintenance DNA methyltransferase (DNMT) 1 and/or the de novo methyltransferases DNMT3A and DNMT3B. Aberrant expression of DNMTs and disruption of DNA methylation are closely associated with multiple forms of cancer, although the exact mechanisms underlying this link remain elusive. An array of tumor suppressor genes (TSGs) frequently sustain promoter hypermethylation, which results in epigenetic silencing of these genes and makes cancer cells acquire growth advantages. DNA demethylating agents, re-activating TSGs via inhibiting hypermethylation of their promoter regions, are currently being tested in clinical trials, and several of them are already applied in clinics. DNA demethylating agents, used either alone or in combination with other agents, such as chemotherapeutic drugs and the histone deacetylase inhibitors, have shown to be effective in treatment of cancer, although only in a small set of patients. In this review, we examine and discuss the most recent advances in epigenetic therapy of cancer, with a focus on DNA demethylating agents.

Atypical teratoid/rhabdoid tumor (AT/RT) is a rare embryonal tumor of the central nervous system (CNS), which accounts for approximately 1–2% of all CNS neoplasms. Spinal canal is extremely rare. To our knowledge, there are only 16 cases of spinal AT/RT in children reported in English literature so far. Here we first presented a rare primary spinal AT/RT in a child with multiple vertebral subarachnoid metastasis. She was accepted surgical treatment and the diagnosis was established pathologically. She died 3 months later with no further therapy. We discuss the clinical presentation, imaging, pathology, treatment and prognosis of spinal AT/RT in children with the literature review.

The development of heart failure after acute myocardial infarction (MI) was related to left ventricular (LV) pathological remodeling and dysfunction. Cardiac stem cells (CSCs) provided a new option to treat acute MI. This study was to investigate the effects of CSCs on structural and functional alteration in acute MI. Acute MIwas induced in 20 Sprague‐Dawley rats by ligation of the left anterior descending coronary artery. Two weeks after MI, animals were randomized into CSCs or control group. LVgeometry and function were echocardiographically measured at baseline, 2, 4, and 6 weeks after MI. After measuring hemodynamics at 6 weeks after MI, hearts were harvested for tracing CSCs stained by PKH26 and testing expression of VEGF‐α/TGF‐β1by RT‐PCRand ELISA. Two weeks after MI, there were significant decreases in interventricular septal systolic and diastolic thickness (IVSTs/d), while increases in LVsystolic and diastolic dimension (LVDs/d). Consequently, this contributed to decreases in ejection fraction (EF) and fractional shorting (FS). With the treatment of CSCs for 4 weeks, significant better ejection fraction (EF) and fractional shorting (FS) were achieved in CSCs group accompanied by the reduction in LVsystole and diastole dimension (LVDs/d). Besides, a significant improvement in the maximal rate of LVpressure development and decline (peak +dP/dtand ‐dP/dt, respectively) was observed. Moreover, significantly higher VEGF‐α was expressed in CSCs group rather than TGF‐β1. CSCs significantly prevented structural and functional deterioration after MIwith increasing expression of VEGF‐α.