Objective To investigate the risk factors for leukoaraiosis (LA). Methods The clinical and imaging data in patients with stroke were collected retrospectively. LA was divided into periventricular LA and subcortical LA according to the findings of MRI, and they were scored and classified. Results A total of 113 patients with stroke were included. There were 39 women and 74 men (mean age 61.33 ± 1.32 years). The age (65.52 ± 12. 56 vs.47. 96 ±9. 23 years, t =5. 634, P =0. 000), hypertension (68. 60% vs. 29. 63% ,x2 = 12. 932,P =0. 000), diabetes (30. 23% vs. 3.70%, x2 = 7. 953, P = 0. 005), systolic blood pressure (SBP) (147. 42 ± 2. 78 mm Hg vs. 134. 00 ± 22. 45 mm Hg,t = 2. 862, P = 0. 004), glucose (6. 54 ± 3. 48 mmol/L vs. 5. 35 ± 1.37 mmol/L, t = 2. 808, P = 0. 005), and total cholesterol (TC) level (5. 17±0.89 mmol/L vs. 4.59±0.61 mmol/L, t=3. 152, P=0. 002) in patients with periventricular LA (n = 86) were significantly higher than those without periventricular LA (n =27). The age (66. 44 ± 11.33 vs. 47. 96 ±9. 23 years, t =4. 768, P =0. 000), hypertension (74. 29% vs. 34. 88%, x2 = 17. 134, P = 0. 000), SBP (85.46 ± 9. 80 mm Hg vs. 69. 81 ±8. 74 mm Hg, t =2. 999, P=0. 003), diastolic blood pressure (DBP) (85.46 ±9. 80 mm Hg vs.69. 81 ±8.74 mm Hg, t =2. 999, P =0. 003), and TC level (5.22±0.99 mmol/L vs. 4.91 ±0. 75 mmol/L, t =3. 330, P =0. 001) in patients with subcortical LA (n =70) were significantly higher than those without subcortical LA (n =43). Spearman correlation analysis showed that the periventricular LA classification was significantly correlated with the age (rs = 0. 606, P =0. 000), drinking (rs = -0. 257, P = 0. 006), hypertension (rs = 0. 428, P = 0. 000), diabetes (rs =0. 236, P =0. 012), SBP (rs =0. 382, P =0. 000), and DBP (rs =0. 258, P =0. 006). The subcortical LA classification was significantly correlated with the age (rs = 0.488, P = 0. 000),hypertension (rs = 0. 416, P = 0. 000), SBP (rs = 0. 386, P = 0. 000), DBP (rs = 0. 326, P =0. 006), and TC level (rs =0. 231, P =0. 014). Multivariate logistic regression analysis showed that the age (odds ratio[OR] = 1.071, 95% confidence interval [CI] 1.009-1. 137; P=O. 024), hypertension (OR =4. 106, 95% CI 1. 657-10. 174; P =0. 002), and SBP (OR =1. 049,95% CI 1. 162-7. 013; P = 0. 022) were independently correlated with LA. Conclusions The age, hypertension, and SBP are the independent risk factors for LA, in which the age is an uncontrollable factor, and the aggressive prevention and treatment of hypertension may reduce the occurrence of LA.

Objective To investigate the correlation between plasma homocysteine (Hcy) level and cerebral microbleeds (CMBs) band leukoaraiosis (LA) in patients with acute stroke.Methods The clinical and imaging data of patients with acute stroke were analyzed retrospectively.The numbers of CMBs were counted and the severity of LA was graded according to the results of MRI.Fasting venous samples were obtained and the plasma Hey concentration was measured the next day after admission.Results A total of 139 patients with acute stroke were enrolled,67 of them were females and 72 were males (mean age 70.1 ± 10.2 years); 24 had hemorrhagic stroke and 115 had ischemic stroke.The age (76.23 ± 8.74 years vs.64.58 ± 7.42 years;t =4.621,P =0.012) hypertension ratio (89.13％ vs.67.74％ ;x2 =8.324,P =0.0 370) and plasma Hey level (14.53 ± 4.31 mmol/L vs.11.31 ±3.16 mmol/L;t =6.538,P=0.008| in a severe LA group (n=46) were significantly higher than those in a non-severe LA group (n =93).Spearman correlation analysis showed that there was significant correlation between the plasma Hcy level and the severity of LA (rs =0.365,P =0.002).Multivariate logistic regression analysis showed that the increased Hey level (odds ratio [ OR ],1.366,95％confidence interval [ CI] 1.141 - 1.526; P =0.010) and age (OR 1.093,95％ CI 1.031 - 1.162; P =0.016)were the independent risk factors for severe LA.The age (74.37 ± 6.35 years vs.67.56 ± 8.52 years; t =6.628,P =0.038) and hypertension ratio (94.74％ vs.62.20％;x2 =8.773,P =0.002) in a CBM group were significantly higher than those in a non-CMB group (n =82).Spearman correlation analysis showed that there was no significant correlation between the plasma Hcy level and the numbers of CBMs (rs =0.038,P =0.813).Multivariate logistic regression analysis showed that hypertension was an independent risk factor for CBMs.Conclusions The elevated plasma Hcy level was associated with LA,but it was not associated with CBMs.

Objective To investigate the expression of S100A16 in pancreatic cancer and its clinical significance. Methods Immunohistochemical experiment was used to detect the expression of S100A16 protein in pancreatic cancer tissues and adjacent tissues, and we analyzed the relation between S100A16 positive expression and clinicopathological parameters, prognosis of pancreatic cancer patients. PPI was used to predict a protein relationship network that directly interacted with S100A16. Results The positive rate of S100A16 expression in cancer tissues was significantly higher than that in adjacent tissues (P=0.001). S100A16 expression was higher in patients with vascular infiltration and lymph node metastasis. The overall survival time of patients with pancreatic cancer was related to tumor size, TNM stage and S100A16 expression level. Multivariate analysis showed that the expression level of S100A16 was an independent risk factor for the prognosis of pancreatic cancer patients, and the risk of death in patients with high S100A16 expression increased by 1.5 times. PPI predicted that S100A16 and S100A14, IL36G, PITX1, PERP played an important role in the interaction network. Conclusion Pancreatic cancer patients with high S100A16 expression have poor prognosis. The positive expression of S100A16 is an independent prognostic indicator.

Malignant cerebral edema (MCE) can lead to deterioration of neurological function in patients with acute ischemic stroke, and significantly increase the mortality and disability rate. Therefore, early detection and intervention of MCE is crucial for saving patients' lives. This article reviews the predictors and preventive scales of MCE after acute ischemic stroke.

OBJECTIVE: To explore the expression of CyPA and CD147 in rabbit models of vulnerable carotid atherosclerotic plaque and the therapeutic effect of atorvastatin.
 METHODS: Twenty-four male New Zealand rabbits were randomly divided into 3 groups. Eight rabbits were served as a normal diet group (Group A), and the remaining 16 rabbits underwent balloon-induced endothelial injury in the right carotid artery and thereafter were fed on high-cholesterol diet (1% cholesterol) for 12 weeks, then they were divided into 2 groups: a AS group (Group B), an atorvastatin group [Group C, 2.5 mg/(kg.d)]. 4 weeks later, plaque disrupture was triggered by China Russell's viper venom and histamine. Serum levels of TC, TG, LDL-C and HDL-C were measured at different timepoint. The damaged carotid arteries were collected to undergo pathological examination. The macrophage, expression of CyPA and CD147 were detected by immuno-histochemical analysis, and the mRNA levels of CyPA and CD147 were examined by reverse transcription polymerase chain reaction (RT-PCR).
 RESULTS: Compared with the Group A, the serum levels of TC and LDL-c in the Group B and Group C were significantly increased (all P<0.01). Compared with the Group B, the serum levels of TC and LDL-c in the Group C were reduced significantly after atorvastatin intervention for 4 weeks (all P<0.01). The plaques disruption and thrombosis occurred in 4 out of the 6 rabbits in the Group B, while only 1 rabbit demonstrated plaques disruption and thrombosis in the Group C. Compared with the Group B, the levels of CyPA, CD147 and macrophage in carotid atherosclerotic plaque in the Group C were decreased significantly (all P<0.01).
 CONCLUSION The up-regulation of CyPA and CD147 may be involved in pathogenesis of vulnerable carotid atherosclerotic plaque. Atorvastatin could stabilize the plaque through inhibiting the CyPA and CD147 expression.
Animals ; Atorvastatin ; pharmacology ; Basigin ; metabolism ; Carotid Artery, Common ; pathology ; Cholesterol ; blood ; Cholesterol, Dietary ; administration & dosage ; Cyclophilin A ; metabolism ; Macrophages ; cytology ; Male ; Plaque, Atherosclerotic ; drug therapy ; metabolism ; Rabbits ; Random Allocation ; Thrombosis ; pathology ; Triglycerides ; blood

Objective:To analyze the changes of pathogen spectrum of pulmonary infection in human immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS) patients before and during coronavirus disease 2019 (COVID-19) epidemic.Methods:The clinical data of hospitalized HIV infection/AIDS patients with pulmonary infection confirmed by etiology and/or imaging examinations in the Department of Infection and Immunity, Shanghai Public Health Clinical Center, Fudan University from January 2017 to December 2022 were collected, including the types of pathogens, the peripheral blood CD4 + T lymphocyte counts at admission due to pulmonary infection, and the treatment outcome of the patients at discharge. The changes of pathogen spectrum of pulmonary infection before COVID-19 epidemic (2017 to 2019) and during the epidemic (2020 to 2022) were analyzed, and their effects on adverse treatment outcomes (death during hospitalization or automatic discharge) were analyzed. Statistical analysis was performed using the chi-square test, trend chi-square test or Kruskal-Wallis test. Results:The proportion of patients with pulmonary infection during the epidemic was lower than that before the epidemic, the difference was statistically significant (23.01%(1 061/4 612) vs 28.68%(1 463/5 102), χ2=40.76, P<0.001). From 2017 to 2022, the proportion of hospitalized HIV infection/AIDS patients with pulmonary infection showed a downward trend ( χ2trend=8.81, P<0.001). Among the pathogens causing pulmonary infection from 2017 to 2022, bacteria, mycobacteria, and fungi were the three main pathogenic pathogens, accounting for 48.77%(1 231/2 524), 32.13%(811/2 524), and 14.34%(362/2 524), respectively. The proportion of bacterial infection decreased from 55.02%(805/1 463) before the epidemic to 40.15%(426/1 061) during the epidemic, and the proportion of fungal infection increased from 9.23%(135/1 463) to 21.39%(227/1 061), the differences were both statistically significant ( χ2=54.45 and 74.11, respectively, both P<0.001). There was no significant difference in the proportion of mycobacteria between before and during the epidemic ( P=0.169), but the proportion of Mycobacterium tuberculosis (MTB) infection decreased from 22.01%(322/1 463) before the epidemic to 15.08%(160/1 061) during the epidemic, while the proportion of nontuberculous mycobacterium (NTM) infection increased from 7.11%(104/463) to 11.78%(125/1 061), the differences were both statistically significant ( χ2=19.11 and 16.28, respectively, both P<0.001). There was a significant difference in the pathogen spectrum of pulmonary infection before and during the epidemic ( χ2=128.91, P<0.001). There was a significant difference in the peripheral blood CD4 + T lymphocyte counts of patients with MTB, NTM, Pnenmocystis, Talaromycosis marneffei and Cryptococcus infection ( H=71.92, P<0.001). There were 63.74%(109/171) of Pneumocystis infection and 67.65%(69/102) of Talaromycosis marneffei infection occurred in patients with CD4 + T lymphocyte count<50/μL. Among the patients with pulmonary infection, the proportion of patients with adverse treatment outcomes during the epidemic was higher than that before the epidemic, and the difference was statistically significant (13.29%(141/1 061) vs 10.39%(152/1 463), χ2=5.04, P=0.025). Among the patients with pulmonary infection who developed adverse treatment outcomes, the top three pathogens (from high to low) were bacteria (63.48%(186/293)), mycobacteria (27.65%(81/293)), and fungi (6.83%(20/293)). The proportion of adverse treatment outcomes caused by bacterial infection decreased during the epidemic compared with that of before the epidemic (71.71%(109/152) vs 54.61%(77/141), χ2=9.23, P=0.002), while the proportion of adverse treatment outcomes caused by fungal infection increased (2.63%(4/152) vs 11.35%(16/141), χ2=8.74, P=0.003), and the differences were both statistically significant. The proportion of adverse treatment outcomes caused by mycobacterial infection increased, but without statistically significant (23.03%(35/152) vs 32.62%(46/141), χ2=3.37, P=0.066), among which there was no difference in the proportion of adverse treatment outcomes caused by MTB infection (13.82%(21/152) vs 14.89%(21/141), χ2=0.07, P=0.793), while the proportion of adverse treatment outcomes caused by NTM infection increased (5.92%(9/152) vs 14.89%(21/141), χ2=6.41, P=0.011). There was a significant difference in the pathogen spectrum of pulmonary infection patients with adverse treatment outcomes before and during the epidemic ( χ2=12.22, P=0.007). Conclusions:Among the spectrum of pathogens causing pulmonary infection and adverse treatment outcomes of HIV infection/AIDS patients during the epidemic, compared with that before the epidemic, the proportion of bacterial decreases, while the proportion of fungi increases, and the proportion of mycobacteria remains stable with the proportion of NTM increasing. The proportion of MTB causing pulmonary infection decreases, while the proportion of MTB causing adverse treatment outcomes remains stable.