ABSTRACT
Anti-Sry-like high mobility group box (SOX) 1 antibodies (abs) are partly characterized onconeural autoantibodies (autoabs) due to their correlation with neoplastic diseases. AntiSOX1 abs are associated with various clinical manifestations, including Lambert-Eaton myasthenic syndrome (LEMS) and paraneoplastic cerebellar degeneration (PCD). However, the clinical characteristics of patients with anti-SOX1 abs have not been described in detail. This review systematically explores the reported patients with anti-SOX1 abs and analyzes these cases for demographic characteristics, clinical features, coexisting neuronal autoabs, neuroimaging findings, treatment, and clinical outcomes. In addition, considering that PCD is the most common paraneoplastic neurological syndrome and that the association between PCD and anti-SOX1 abs remains unclear, we focus on the presence of autoabs in relation to PCD and associated tumors. PCD-associated autoabs include various intracellular autoabs (e.g., anti-Hu, anti-Yo, anti-Ri, and anti-SOX1) and cell-surface autoabs (anti-P/Q-type voltage-gated calcium channel). Commonly involved tumors in PCD are small-cell lung cancer (SCLC), gynecological, and breast tumors. LEMS is the most common clinical symptom in patients with antiSOX1 abs, followed by PCD, and multiple neuronal autoabs coexist in 47.1% of these patients.SCLC is still the predominant tumor in patients with anti-SOX1 abs, while non-SCLC is uncommon. No consistent imaging feature is found in patients with anti-SOX1 abs, and there is no consensus on either the therapy choice or therapeutic efficacy. In conclusion, the presence of anti-SOX1 abs alone is a potential predictor of an uncommon paraneoplastic neurological disorder, usually occurring in the setting of LEMS, PCD, and SCLC. The detection of anti-SOX1 abs contributes to an early diagnosis of underlying tumors, given the diversity of clinical symptoms and the absence of characteristic neuroimaging features.
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Objective To study the features and risk factors of ischemic leukoaraiosis (LA) progression in elderly patients aged 80 years and over. Methods The 56 elderly patients with ischemic LA confirmed by MRI were enrolled in this study. The characteristics and risk factors of ischemic LA were comparatively analyzed between baseline and 3 years later by single and multi-variable logistic regression analysis. Results Ischemic LA progressed mostly in the subcortical white matter in elderly patients, especially the frontal lobes (progression of white matter lesion was present in 40% in the frontal lobes at baseline and 52% after 3 years), followed by the parietal lobes (35% at baseline and 36% after 3 years); Furthermore, previous high homocysteine (Hcy) and chronic bronchitis were risk factors of ischemic LA progression. Conclusions Ischemic LA progresses mostly in the subcortical white matter in the elderly, especially the frontal lobes; High Hcy and chronic bronchitis are risk factors of ischemic LA progression in elderly patients.
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Objective To determine whether rizatriptan has an effect on cortical spreading depression (CSD) and c-Fos expression within periaqueductal grey (PAG) induced by CSD in rats. Methods The experimental SD rats were randomly divided into group A injected with KCl, group B KCl plus rizatriptan and group C NaCL The number and amplitude of CSD were recorded after KCl or NaCl injection. C-Fos positive neurons of different layer were identified by the immunohistochemical technique 2 hours after the first injection of KCl or NaCl. Results There was no CSD in group C. The number of CSD in group A ( 10.70±3.23 ) was significantly more than that in group B (6.10±2.56, t = - 3.528, P < 0.01 ). The amplitude of CSD in group A ( 17.33 (95% CI 11.45--23.11 ) mV) was significantly greater than that in group B (11.82 (95%CI 9.24--14.70) mV, Z= -4.360, P< 0.01). There were more cFos-like immnoreactive neurons in every layer in group A than in group C (P < 0.01 ) and in group B (P < 0.05 ). Conclusion Rizatriptan has an inhibitory effect on CSD, which might induce the headache through exciting the neurons in PAG.
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Objective To study the effect of smoking on oxidized low-density lipoprotein ox-LDL lag time in patients with cerebral infarction. Methods Plasma samples were obtained from 67 patients with cerebral infarc-tion. 30 acute cerebral infarction patients without history of smoking were chosen to be as control group; meanwhile, 37 acute cerebral infarction patients with history of smoking were chosen to be as smoking group. There was no statis-tical difference in age,gender,blood pressure,lipid level and location and level of the cerebral focus between the two groups (P > 0.05). The ox-LDL lag time and lipid levels of low-density lipoproteins (LDL), including total choles-terol (TC) ,triglyceride (TG) and free cholesterol were measured. Results The ox-LDL lag time of the patients with history of smoking was significantly shorter than that in the control group[(77.21 ± 9.1) min vs. (59.95 ± 8.7)min,P <0.001]. There were no significant differences in LDL- TC,LDL- TG and LDL-free cholesterol level[(5.12±0.61) vs. (4.63±0.62) mmol/L; (0.89±0.07) mmol/L vs. (0.85±0.04) mmol/L; (1.71±0.43) vs. (1.74±0.91) mmol/L, P > 0.05 respectively] between the two groups. Conclusion Smoking shorts the ox-LDL lag time in patients with cerebral infarction, and decrease the anti-oxidization and increase the stress of oxidization.
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Objective To investigate the effect of vitamin E administration on the urinary level of 8-iso prostaglandin F_(2?)(8-iso- PGF_(2?))in the patients with cerebral infarction.Methods 28 patiems with acute cerebral infarction were involved in this study according to the selection criteria.They were divided into two groups:patients in test group(n=14)were treated with vitamin E,and those in control group(n=14)were not treated with vitamin E.No significant differences existed in age,gender ratio,blood pressure,lipids level and lo- cation and level of the cerebral infarct focus between two groups.The contents of urinary 8-iso-PGF_(2?) were measured in each urinary speci- men,meanwhile the levels of vitamin E and low density lipoprotein(LDL)were determined in each plasma specimen within 24 hours after onset of cerebral infarct and two weeks later.Results The concentration of urinary 8-iso-PGF_(2?) collected at two weeks after onset from pa- tients of test group was significantly lower than that of the control group(85.20?9.17 vs 91.36?4.24ng/mmol creatinine,P0.05).Conclusions The content of urinary 8-iso-PGF_(2?) and the level of oxidative stress in vivo could be decreased in the patients with acute cerebral infarction after being treated with vitamin E.
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Objective To investigate the impact of smoking on the level of urinary 8-iso prostaglandin (PG) F2? (8-iso-PGF2?) of patients with acute cerebral infarction. 8-iso-PGF2? is a product of arachidonic acid catalyzed by free-radical, and it has been identified as an indicator of oxidative stress in vivo during reperfusion. Methods Plasma and urine samples were obtained from 28 patients with acute cerebral infarction. Among them 14 patients with no smoking habit were chosen as control group according to the selection criterion, and the other 14 patients with smoking habit were chosen as investigation group according to the same criterion. There was no significant difference between the two groups in age, gender ratio, blood pressure, lipids level, blood glucose, focus location, and degree of the cerebral focus of infaration. The concentration of urinary 8-iso PGF2? and levels of low-density lipoproteins (LDL), total cholesterol, LDL-triglyceride (TG) and LDL-free cholesterol in plasma were measured by enzyme immunoassay. The quantification of urinary 8-iso PGF2? and LDL levels in plasma were performed for each sample respectively. Results The concentration of urinary 8-epi PGF2? of the patients with smoking habit was significantly higher than that in the patients of control group (75.79?10.76 vs 67.36?9.18 ng/mmol creatinine, P0.05, respectively) between the two groups. Conclusions Cigarette smoking may raise the urinary 8-iso-PGF2? level of patients with acute cerebral infarction, suggesting an increase in the level of oxidative stress in vivo in these subjects.
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Objectives To explore the effects of hypertension on the oxidative susceptibility of plasma low-density lipoprotein (LDL) in patients with cerebral infarction. Methods A total of 79 patients, 39 males and 40 females with mean age of 67?7, with hypertension accompanied by similar size of cerebral infarction in the perfusion domain of middle cerebral artery, were involved in this study. The hypertension was graded as follows: grade Ⅰ (n=27), the systolic blood pressure (SBP)/diastolic blood pressure (DBP) was 140-159mmHg/90-99mmHg; grade Ⅱ (n=29) with SBP/DBP of 160-179mmHg/100-109mmHg; grade Ⅲ (n=23) with SBP/DBP exceeding 180mmHg/110mmHg. Serum concentrations of LDL were determined with enzymatic colorimetry employing an automated multianalyzer. The lag time (ox-LDL lag-time) in conjugated diene production at 234nm was determined by copper-stimulated oxidation. Results No statistical difference was found in LDL-total cholesterol, LDL-triglyceride, LDL-free cholesterol among grade Ⅰ, Ⅱ, Ⅲ groups (6.1?0.4, 0.87?0.08, 1.6?0.7mmol/L; 5.7?0.6, 0.86?0.05, 1.8?0.9mmol/L; and 5.6?0.7, 0.87?0.1, 1.7?0.8mmol/L, respectively). Correlation analysis showed the lag time in conjugated diene production in patients with cerebral infarction was negatively related to the grade of hypertension in all the subjects, and the lag time in grade Ⅰ, Ⅱ, Ⅲ groups was 84.26?8.491, 69.84?7.748 and 61.95?8.482 min, respectively (r=0.673 3, P