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Objective To analyze the correlation between clinical features and renal dysfunction in patients of acute lacunar infarction with progressive cerebral microbleeds (CMBs). Methods Two hundred and sixty-five patients with first-episode acute lacunar infarction were selected. The serum creatinine was measured within 24 h of admission and the estimated glomerular filtration rate (eGFR) was calculated. The brain MRI (including gradient-echo images) was examined within 2 d of admission and after 1 years of follow-up, respectively. The progressive CMBs was assessed with microbleeds anatomical rating scale (MARS), and the patients were divided into progressive CMBs group (progressive group, 42 cases) and non progressive CMBs group (non progressive group, 223 cases). The clinical features of 2 groups were compared and the correlation between progressive CMBs and renal dysfunction was analyzed. Results The age, 24 h pulse pressure, incidences of renal dysfunction and CMBs in progressive group were significantly higher than those in non progressive group: (69.8 ± 5.8) years vs. (61.5 ± 4.9) years, (63.3 ± 3.1) mmHg (1 mmHg=0.133 kPa) vs. (51.8 ± 4.2) mmHg, 69.0％(29/42) vs. 39.9％(89/223) and 57.1％(24/42) vs. 25.1％(56/223), and the platelet was significantly lower than that in non-progression group:(168 ± 35) ×109/L vs. (189 ± 40) ×109/L, and there were statistical differences (P<0.05 or<0.01). The Logistic regression analysis result showed that renal dysfunction and CMBs were Independent risk factors of progressive CMBs (OR = 1.571 and 1.054, 95％ CI 1.042 - 2.493 and 1.010 - 1.142, P<0.05). Conclusions The rate of renal dysfunction is higher in patients of acute lacunar infarction with progressive CMBs, and progressive CMBs are associated with renal dysfunction.
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Objective To investigate the relationship between different topographic locations and neurological deteriorations (ND) in patients with acute new isolated pontine infarction.Methods One hundred sixty-eight patients with acute new isolated pontine infarction during arch 2012 to March 2016 were identified by diffusion weighted imaging (DWI) for retrospective review.Patients were divided into two groups according to their clinical symptoms:patients with ND and patients without ND.According to neuroimaging of DWI,the topographic location of pontine infarction was divided into three types:The upper,middle,and lower ones,and the correlations of ND with risk factors,laboratory examination results,clinical manifestations and different topographic locations were explored by statistical tests.Results Of 168 patients,26.8％ (45/168) were diagnosed with ND,and 73.2％ (123/168) were diagnosed without ND.Univariate analysis showed that there were differences in female ratio [62.2％ (28/45) vs 41.5％ (51/ 123)],smoking ratio [13.3％ (6/45) vs 26.0％ (32/123)],mean length of hospital stay [(22.83 ± 7.12)d vs (19.31 ± 7.65)d],ratio of worse short-term clinical outcomes [77.8％ (35/45) vs 33.3％ (41/123)],and ratio of lower pontine infarction [55.6％ (25/45) vs 26.0％ (32/123)] between two groups (P ＜ 0.05).Logistic regression analysis showed that lower pontine infarction was the independent risk factor of ND (OR =1.953,95％ CI:1.092-3.535,P =0.029).Conclusions Topographic location of lower pons lesions may be reliable predictor of ND in acute new isolated pontine infarction.
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ObjectiveTo investigate the influence of hepatitis B virus (HBV) infection on intrahepatic natural killer (NK) cells and innate lymphoid cell 22 (ILC22), and to provide theoretical and experimental bases for clarifying mechanisms of HBV infection in inducing innate immune response. MethodsA total of 10 male BALC/c aged 6-8 weeks were divided into experimental group and control group, with 5 mice in each group. The mice in the experimental group were treated with the hydrodynamic injection of normal saline containing 10 μg plasmids of complete HBV genome (the volume equaled to 9% of the body weight of the mouse) via the caudal vein, and those in the control group were only treated with normal saline. The mice were scarified 4 days later, and intrahepatic lymphocytes (IHLs) were isolated. Flow cytometry was used to determine the proportions of NK cells and ILC22 subset in IHLs, and the t-test was used for comparison between groups. ResultsHydrodynamic injection of the plasmids containing complete HBV genome induced high levels of HBsAg and HBeAg in mice, with an increase in the serum level of alanine aminotransferase. After HBV infection, the experimental group showed a significant increase in the proportion of intrahepatic NK cells compared with the control group (25.90%±4.92% vs 12.98%±2.13%, t=3.811, P=0.003), while there were no significant differences in the proportions of CD127+ and CD127- NK subsets in NK cells between the two groups. Moreover, after HBV infection, the experimental group showed a significant increase in the proportion of intrahepatic NKp46+ILC22 subset compared with the control group (36.05%±6.85% vs 10.22%±3.54%, t=7.372, P＜0001); however, there was no significant difference in the proportion of NKp46-ILC22 between the two groups. ConclusionHBV infection induces increased levels of intrahepatic NK cells and NKp46+ILC22 cells and thus promotes the innate immune response in the liver.