Prevalence and Risk Factors for Unruptured Intracranial Aneurysms in the Population at High Risk for Aneurysm in the Rural Areas of Tianjin.

Although the prevalence of unruptured intracranial aneurysm (UIA) lies between 2 and 5%, the consequences of aneurysm rupture are fatal. The burden of UIA is considerable in stroke patients. However, the best prevention and management strategy for UIA is uncertain among patients with a family history of stroke. Therefore, this study aimed to determine the epidemiological characteristics and risk factors for UIA based on a population with a family history of stroke. This study used random sampling to recruit participants with a family history of stroke among rural residents in Jixian, Tianjin, China. All participants underwent a questionnaire survey, physical examination, and cervical computed tomography angiography (CTA). CTA data were used to determine whether the subjects had UIA. The relationship between relevant factors and UIA was assessed using logistic regression analysis. A total of 281 residents were recruited in this study, with a mean age of 50.9 years. The prevalence of UIA in those with a family history of stroke was 10.3% overall (9.8% among men and 10.9% among women). Moreover, with each unit increase in body mass index (BMI), the prevalence of UIA decreased by 12.5%. Particularly among non-obese men, BMI had a stronger protective effect (OR: 0.672; 95%CI: 0.499-0.906; P = 0.009), and among non-obese men, an increase in low-density lipoprotein (LDL) was associated with an increased prevalence of UIA (OR: 3.638; 95%CI: 1.108-11.947; P = 0.033). Among the non-obese with a family history of stroke, BMI may be protective against UIA, especially in men. It is crucial to strictly control the LDL level in non-obese people to reduce the burden of UIA.

CTA Characteristics of the Circle of Willis and Intracranial Aneurysm in a Chinese Crowd with Family History of Stroke.

BACKGROUND AND PURPOSE: The vascular morphology in crowd with family history of stroke remains unclear. The present study clarified the characteristics of the intracranial vascular CoW and prevalence of intracranial aneurysms in subjects with family history of stroke. METHODS: A stratified cluster, random sampling method was used for subjects with family history of stroke among rural residents in Jixian, Tianjin, China. All the subjects underwent a physical examination, head computed tomography (CT) scan, and cephalic and cervical computed tomography angiography (CTA) scan. Anatomic variations in the Circle of Willis and cerebrovascular disease in this population were analyzed. RESULTS: In the crowd with similar living environment, stable genetic background, and family history of stroke and without obvious nerve function impairment (1) hypoplasia or absence of A1 segment was significantly different in gender (male versus female: 9.8% versus 18.8%, p = 0.031), especially the right-side A1 (male versus female: 5.9% versus 16.4%, p = 0.004). (2) Hypoplasia or absence of bilateral posterior communicating arteries was more common in men than women (58.2% versus 45.3%, p = 0.032). Unilateral fetal posterior cerebral artery was observed more often in women than men (17.2% versus 8.5%, p = 0.028). (3) The percentage of subjects with incomplete CoW did not increase significantly with age. Compared to healthy Chinese people, the crowd had a higher percentage of incomplete CoW (p < 0.001). (4) No obvious correlation between risk factors and CoW was found. (5) The prevalence of aneurysm was 10.3% in the special crowd. CONCLUSIONS: The certain variations of CoW showed significant relation to gender, but not to age in people with family history of stroke. The incomplete circle may be a dangerous factor that is independent of common risk factors for stroke and tend to lead to cerebral ischemia in the crowd with family history of stroke. The prevalence of intracranial aneurysm is comparatively high in the present subjects compared to other people.

[Pathology, imaging and treatment of rare types of intracranial aneurysms].

The formation mechanisms of rare intracranial aneurysms are various, which lead to various kinds of treatment methods. The present article summarized the pathogenesis, pathologic changes in vascular walls and imaging features of rare intracranial aneurysms including segmental ectasia, aneurysms with dissection, aneurysms with intramural hemorrhage, mycotic aneurysms, aneurysms related to HIV, neoplastic aneurysms and traumatic aneurysms through literature review.

Exploring the potential relationship between Notch pathway genes expression and their promoter methylation in mice hippocampal neurogenesis.

The Notch pathway is a highly conserved pathway that regulates hippocampal neurogenesis during embryonic development and adulthood. It has become apparent that intracellular epigenetic modification including DNA methylation is deeply involved in fate specification of neural stem cells (NSCs). However, it is still unclear whether the Notch pathway regulates hippocampal neurogenesis by changing the Notch genes' DNA methylation status. Here, we present the evidence from DNA methylation profiling of Notch1, Hes1 and Ngn2 promoters during neurogenesis in the dentate gyrus (DG) of postnatal, adult and traumatic brains. We observed the expression of Notch1, Hes1 and Ngn2 in hippocampal DG with qPCR, Western blot and immunofluorescence staining. In addition, we investigated the methylation status of Notch pathway genes using the bisulfite sequencing PCR (BSP) method. The number of Notch1 or Hes1 (+) and BrdU (+) cells decreased in the subgranular zone (SGZ) of the DG in the hippocampus following TBI. Nevertheless, the number of Ngn2-positive cells in the DG of injured mice was markedly higher than in the DG of non-TBI mice. Accordingly, the DNA methylation level of the three gene promoters changed with their expression in the DG. These findings suggest that the strict spatio-temporal expression of Notch effector genes plays an important role during hippocampal neurogenesis and suggests the possibility that Notch1, Hes1 and Ngn2 were regulated by changing some specific CpG sites of their promoters to further orchestrate neurogenesis in vivo.