White matter hyperintensities (WMHs) are one of the main imaging phenotypes of cerebral small vessel disease. More and more studies have shown that inflammation plays an important role in the occurrence and development of WMHs. Diet may change systemic chronic inflammation level, which in turn affects the occurrence and development of WMHs. The dietary inflammatory index (DII) is a tool used to assess the overall inflammatory potential of an individual's diet and is widely used in the study of various chronic diseases. This article reviews the research progress of the relationship between DII and WMHs.

Objective To investigate the dynamic changes of hippocampal insulin like growth factor-1(IGF-1)/IGF-1 receptor (1GF-1 R) signaling pathway and learning and memory function and to investigate the possible mechanisms of vascular dementia (VaD).Methods A rat chronic cerebral hypoperfusion model was induced by using permanent bilateral common carotid artery ligation.At day 3,1 and 2 weeks,1,2 and 4months after modeling,Morris water maze test was used to evaluate the changes of learning and memory function in rats.HE staining was used to observe the morphological changes of hippocampal neurons.Enzymelinked immunosorbent assay was used to detect the dynamic changes of IGF-1,IGF-1R,Akt and p-Akt in hippocampal tissue.Results One month after modeling,the rats of a model group began to appear significant learning and memory dysfunction.The numbers of crossing the platform were significant lower than those in a sham operation group (1.91 ±0.45 times vs.3.95 ± 1.64 times; t =17.251,P =0.000).With the extension of ischemia time,the degree of injury of pyramidal cells in hippocampal CA1 region aggravated gradually in the model group.The levels of IGF-1 and p-Akt in hippocampal tissue increased early after modeling in the model group,and then they declined gradually to the normal levels.The levels of IGF-1 (0.09 ± 0.05 ng/mg vs.0.20 ±0.03 ng/mg; t =-5.263,P =0.003) and p-Akt (12.50± 1.40 pg/mg vs.17.13 ± 0.87 pg/mg; t =- 5.651,P =0.000) at 1 month were significantly lower than those in the sham operation group and continued to 4 months.There were no significant changes in the levels of IGF-1R and Akt.Conclusions The down-regulation of IGF-1/IGF-1R signaling pathway may be one of the pathogeneses of VaD.

Objective:To investigate the relationship between hypertension with hyperhomocysteinemia (HHcy) and early neurological deterioration (END) in patients with intracerebral hemorrhage.Methods:Patients with acute intracerebral hemorrhage admitted to the Department of Neurology, the First People's Hospital of Huainan from January 2017 to December 2018 were enrolled prospectively. END was defined as the National Institutes of Health Stroke Scale (NIHSS) score increased by ≥4 or Glasgow Coma Scale (GCS) score decreased by ≥2 at any time within 72 h after onset from baseline. The baseline data of the END and non-END groups were compared, and multivariate logistic regression analysis was use to evaluate the independent risk factors for END. Results:A total of 238 patients with acute intracerebral hemorrhage were enrolled, and 64 of them (26.9%) developed END. The baseline hematoma volume, NIHSS score, blood glucose, homocysteine level, neutrophil count, and the proportion of hypertension, hemorrhage into ventricle and hematoma enlargement in the END group were significantly higher than those in the non-END group, while the baseline GCS score was significantly lower than that in the non-END group (all P<0.05). Multivariate logistic regression analysis showed that after adjusting for the confounding factors, the baseline hematoma volume (odds ratio [ OR] 1.086, 95% confidence interval [ CI] 1.029-1.146; P=0.003), baseline GCS score ( OR 0.420, 95% CI 0.245-0.719; P=0.002) and hypertension with HHcy ( OR 2.441, 95% CI 1.185-5.029; P=0.016) had significant independent correlation with END. Conclusion:Hypertension with HHcy is an independent predictor of END in patients with intracerebral hemorrhage.