Objective To study MRI differential diagnosis of peripheral hemangioma and vascular malformations.Methods MRIfindings of peripheral hemangiomas and vascular malformations proved by operation in 61 cases were retrospectively analyzed in comparison with pathological results.Results In 29 cases of peripheral hemangiomas,20 cases showed equal signal intensity (equal to muscle) and 9 cases showed heterogeneous signal intensity on T1-weighted images; 24 cases showed increased signal intensity (approach fat signal) and 5 cases showed markedly increased signal intensity (increase fat signal) on T2-weighted images,25 cases had septa as low signal network on T2-weighted images,4 cases showed enhancement separated mass enhancement after intravenous contrast injection.In 32 cases peripheral vascular malformations,16 cases showed equal signal intensity and 16 cases showed heterogeneous signal intensity on T1-weighted images.3 cases showed high signal intensity and 29 cases showed markedly increased signal intensity on T2-weighted images,15 cases showed inhomogeneous enhancement after intravenous contrast injection.Conclusion MRI plays an important role in differential diagnosis of peripheral hemangiomas and vascular malformations.

Objective To explore the imaging differential diagnosis of vascular malformations and intermediary character hemangiomas.Methods The roentgenographic,CT and MRI findings of vascular malformations and intermediary character hemangiomas in 58 cases were analysed retrospectively.Results In 42 cases with vascular malformations,the lesions were irregular with definite margins,and 5 cases showed the bone compressed adjacent to the lesions.31 patients studied with MRI ,3 cases appeared as hyperintensity(equal to fat) and 28 cases appeared as mixed hyperintensity(higher than that of fat) on T2WI,20 cases showed circular markedly vessel-like hyperintensity on T2WI .In 16 cases with intermediary character hemangiomas,7 cases showed circular soft tissue masses,the masses were lobulated in 8 cases and "crab nail" in 1 case,5 cases showed edema of around the tumors and occupying effect on CT and MRI,3 cases showed bone corroded adjacent to the lesions,2 cases showed bony destruction.Of the 11 patients studied with MRI,the lesions showed hyperintensity on T2WI.Conclusion The imaging findings of vascular malformations and intermediary character hemangiomas are different.

Objective To evaluate the role of magnetic resonance angiography ( MRA ) in diagnosing peripheral hemangioma andvascular malformation . Methods 61 cases of hemangioma and vascular malformations in peripheral soft tissue were undergone MRAexamination.Results Of 13 patients with hemangioma,the arteries within hemangioma were increased and gradually fine from proximal to distal in 7 cases and in company with arteriovenous fistulae in 2 cases,there were no arteries within hemangioma in 6 cases.Vascular malformations were found in 48 patients,arteries and veins of vascular malformation were showed in 35 cases,but arteries of vascular malformations were only showed in one case.Arteries of vascular malformation were showed in 5 cases and the arteries were pressed on arterial angioyraphy in 23 cases.On MR venography(MRV),the shallow malformed veina were showed in 25 cases and in company with deep malformed veina in 13 cases,only the shallow and deep veina increased and thickness be showed in 2 cases.Arterioveinous fistulae could be seen in 8 cases on MR aterio-venography.There were no vessel be showed in 12 cases within the losions.Conclusion MRA is of significant value in diagnosis and differential diagnosis of peripheral hemangioma and vascular malformations.

Objective To setup a measurement of human bone marrow micromegakaryocyte which based on CD41a and PI double‐labeled flow cytometric analysis ,and study the significance in the diagnosis of MDS .Methods In 42 cases of MDS patients , their bone marrow megakaryocytes were obtained by Percoll density gradient separation medium .The megakaryocyte glycoproteinⅡb/Ⅲa(CD41a)were marked with fluorescein isothiocyanate through its corresponding monoclonal antibody ,and their DNA were marked with PI .Then the megakaryocyte ploidy was analyzed by flow cytometry(FCM ) .Results The method for micromegakaryo‐cyte identification and analysis was established .In 42 patients with MDS ,the detection rate of micromegakaryocyte was 90 .5 per‐cent by FCM analysis ,but only 54 .8 percent by Wright‐Giemsa staining test and 64 .3 percent by immunohistochemistry ,the differ‐ence among them was statistically significant(χ2 = 13 .640 ,P= 0 .001) .The 42 patients with MDS were divided into two groups (low‐risk group and high‐risk group) .The detection rates of micromegakaryocyte were 81 .8 percent in low‐risk group and 100 per‐cent in high‐risk group separately by FCM analysis ,the difference was statistically significant(χ2 =4 .019 ,P=0 .045) .Conclusion The detection rate of micromegakaryocyte by FCM with CD41a and PI double marker is higher than that by cytochemical staining . The detection rate of micromegakaryocyte in the high‐risk group is higher than that of the low‐risk group ,which shows that the de‐tection of micromegakaryocyte is of great significance for MDS prognosis assessment .

Objective:To investigate whether astragaloside (AST) IV can improve spatial learning and memory abilities by alleviating oxidative stress damage to the frontal cortex and hippocampus in vascular dementia (VD) rats induced by chronic cerebral ischemia.Methods:Totally, 72 adult male Wistar rats were randomly assigned to four groups: sham-operated group ( n=12), model group ( n=20), AST-IV 10 mg group ( n=20), and AST-IV 20 mg group ( n=20); chronic cerebral ischemia-induced VD models in the later three groups were established by permanent bilateral common carotid artery occlusion (BCCAO); 3 h after BCCAO, these rats were administered with saline, 10 mg/kg AST-IV, or 20 mg/kg AST-IV once daily for a consecutive 90 d. Ninety-four d after modeling, spatial learning and memory abilities were assessed by Morris water maze; the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT), and malondialdehyde (MDA) levels were measured by enzyme linked immunosorbent assay (ELISA). The levels of lipid peroxidation and oxidative DNA damage were assessed by immunohistochemical staining for 4-hydroxynonenal (4-HNE) and 8-hydroxy20-deoxyguanosine (8-OhdG), respectively. Results:(1) On the 3 rd, 4 th and 5 th d of place navigation test, the escape latency in rats of the model group was significantly longer than that in the sham-operated group, and that in the AST-IV 20 mg group was significantly shorter than that in the model group ( P<0.05); spatial probe test showed that the time percentage of rats spending in platform region in the model group (20.3%±1.7%) was significantly smaller than that in the sham-oprated group (48.2%±3.6%), and that in the AST-IV 20 mg group (39.7%±3.2%) was significantly larger than that in the model group ( P<0.05). (2) As compared with those in the sham-operated group, the SOD, GSH-Px and CAT activities were statistically decreased while MDA level was significantly increased in the frontal cortex and hippocampal CA1 area of rats in the model group ( P<0.05); as compared with those in the model group, the SOD, GSH-Px and CAT activities were statistically increased while MDA level was significantly decreased in the frontal cortex and hippocampal CA1 area of rats in the AST-IV 20 mg group ( P<0.05). (3) As compared with those in the model group, the numbers of 4-HNE and 8-oHdG positive cells in the frontal cortex and hippocampal CA1 area of rats in the AST-IV 20 mg group were significantly smaller ( P<0.05). Conclusion:Intraperitoneal injection of high dose AST-IV can ameliorate oxidative damage in the frontal cortex and hippocampal CA1 area in chronic cerebral ischemia-induced VD models, and has the potential to reverse spatial learning damages and memory dysfunction.

Objective:To investigate the effect of TRIM52 antisense RNA 1 (TRIM52-AS1) on injury of brain cortex neurons induced by hypoxia/re-oxygenation (H/R) and its possible mechanism in rats.Methods:(1) The cortical neurons were cultured in vitro and divided into control group and model group. In the model group, H/R-induced cell injury models were prepared. Real-time quantitative PCR (RT-qPCR) was used to detect the expressions of TRIM52-AS1 and micro RNA (miR)-28-5p in neurons of the two groups. (2) The cortical neurons were divided into control group, model group, small interfering (si)-TRIM52-AS1 transfection group, and nonsense sequence transfection group. Cells in the model group were prepared for H/R-induced cell damage models. After cells in the latter two groups were transfected with si-TRIM52-AS1 or its nonsense control sequence for 6 h, they were prepared for H/R-induced cell damage models. RT-qPCR, CCK-8, and flow cytometry were used to detect the TRIM52-AS1 expression, and proliferation and apoptosis of neurons in the 4 groups; enzyme-linked immunosorbent assay (ELISA) and Western blotting were used to detect the lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) levels and protein expressions of Cyclin D1, Bcl-2 and Bax. (3) The cortical neurons were divided into miR-28-5p transfection group and nonsense sequence transfection group. After the cells were respectively transfected with miR-28-5p or its nonsense control sequence for 6 h, they were prepared for H/R-induced cell damage models. RT-qPCR, CCK-8, and flow cytometry were used to detect the TRIM52-AS1 expression, and proliferation and apoptosis of neurons in the two groups; ELISA and Western blotting were used to detect the LDH, MDA and SOD levels and protein expressions of Cyclin D1, Bcl-2 and Bax. (4) The cortical neurons were divided into wild-type TRIM52-AS1+miR-28-5p mimic transfection group, wild-type TRIM52-AS1+miR-28-5p nonsense control sequence transfection group, mutant TRIM52-AS1+miR-28-5p mimic transfection group, and mutant TRIM52-AS1+miR-28-5p nonsense control sequence transfection group. After the cells were co-transfected for 6 h, the culture medium was replaced with fresh medium and they were cultured for another 12 h, and then, the luciferase activity of cells in each group was detected by dual luciferase reporter gene experiment. (5) Cortical neurons were divided into nonsense sequence transfection group, miR-28-5p inhibitor transfection group, nonsense sequence+si-TRIM52-AS1 transfection group, and miR-28-5p inhibitor+si-TRIM52-AS1 transfection group, and these cells were transfected with miR-28-5p inhibitor nonsense control sequence, miR-28-5p inhibitor, miR-28-5p inhibitor nonsense control sequence+si-TRIM52-AS1, miR-28-5p inhibitor+si-TRIM52-AS1; 6 h after transfection, H/R-induced cell damage models were prepared. RT-qPCR, CCK-8, and flow cytometry were used to detect the miR-28-5p expression, proliferation and apoptosis of neurons in the two groups, respectively; ELISA and Western blotting were used to detect the LDH, MDA and SOD levels and protein expressions of Cyclin D1, Bcl-2 and Bax. Results:(1) As compared with those in the control group, the TRIM52-AS1 expression statistically increased, but the miR-28-5p expression significantly decreased in the model group ( P<0.05). (2) As compared with the control group, the model group and nonsense sequence transfection group had significantly increased LDH content in the culture supernatant, statistically decreased MDA and SOD content in the cells, significantly decreased A value and protein expressions of Cyclin D1 and Bcl-2, but significantly increased apoptosis rate and Bax protein expression ( P<0.05). As compared with the model group and nonsense sequence transfection group, si-TRIM52-AS1 transfection group had significantly decreased si-TRIM52-AS1 expression, statistically decreased LDH content in the culture supernatant and MDA content in the cells, significantly increased SOD content in the cells, significantly increased A value and protein expression of Cyclin D1 and Bcl-2, significantly decreased apoptosis rate and Bax protein expression ( P<0.05). (3) As compared with the nonsense sequence transfection group, the miR-28-5p transfection group had significantly increased miR-28-5p expression, significantly decreased LDH content in the culture supernatant and MDA content in the cells, and significantly increased SOD content in the cells, significantly increased A value and protein expressions of Cyclin D1 and Bcl-2, but significantly decreased apoptotic rate and Bax protein expression ( P<0.05). (4) The luciferase activity of the wild-type TRIM52-AS1+miR-28-5p mimic transfection group was significantly lower than that of the wild-type TRIM52-AS1+miR-28-5p nonsense control sequence transfection group (0.43±0.04 vs. 1.00±0.09, P<0.05). (5) As compared with the nonsense sequence transfection group, the miR-28-5p inhibitor transfection group had significantly decreased miR-28-5p expression, significantly increased LDH content in the culture supernatant and MDA content in the cells, significantly decreased SOD content in the cells, significantly decreased A value and protein expressions of Cyclin D1 and Bcl-2, but significantly increased apoptosis rate and Bax protein expression ( P<0.05). As compared with the nonsense sequence+si-TRIM52-AS1 transfection group, the miR-28-5p inhibitor+si-TRIM52-AS1 transfection group had significantly decreased miR-28-5p expression, significantly increased LDH content in the culture supernatant and MDA content in the cells, significantly decreased SOD content in the cells, significantly decreased A value and protein expressions of Cyclin D1 and Bcl-2, but significantly increased apoptosis rate and Bax protein expression ( P<0.05). Conclusion:TRIM52-AS1 down-regulation may inhibit H/R-induced oxidative stress and apoptosis of rat brain cortical neurons by negatively regulating the miR-28-5p expression, which reduces neuronal cell damage.

Background::Copper and zinc are involved in the development of multiple malignancies; yet, epidemiological evidence on hepatocellular carcinoma (HCC) is limited. This study aimed to investigate the association between dietary intake and serum levels of copper and zinc with the risk of HCC.Methods::A total of 434 case-control pairs matched for sex and age (±1 year) were included in this study. Cases with newly diagnosed HCC were from the Guangdong Liver Cancer Cohort (GLCC) study, and healthy controls were from the Guangzhou Nutrition and Health Study (GNHS). A semi-quantitative 79-item food frequency questionnaire (FFQ) was used to assess habitual dietary intakes of copper and zinc. Serum levels of copper and zinc were measured by using inductively coupled plasma mass spectrometry. The copper (Cu)/ zinc (Zn) ratio was computed by dividing copper levels by zinc levels. Conditional logistic regression models were performed to calculate the odds ratio (OR) and 95% confidence intervals (CI) for per 1 standard deviation increase (per-SD increase) in copper and zinc levels.Results::Higher dietary intake (OR per-SD increase = 0.65, 95% CI: 0.44, 0.96, Ptrend = 0.029) and serum levels of zinc (OR per-SD increase = 0.11, 95% CI: 0.04, 0.30, Ptrend <0.001) were both associated with a lower risk of HCC. Subgroup analyses showed that the inverse association was only pronounced in men but not in women ( Pinteraction = 0.041 for dietary zinc intake and 0.010 for serum zinc levels). Serum copper levels (OR per-SD increase = 2.05, 95% CI: 1.39, 3.03, Ptrend = 0.020) and serum Cu/Zn ratio (OR per-SD increase = 6.53, 95% CI: 2.52, 16.92, Ptrend <0.001) were positively associated with HCC risk, while dietary copper intake and dietary Cu/Zn ratio were not associated with HCC risk. Conclusion::Zinc may be a protective factor for HCC, especially among men, but the effects of copper on HCC risk are not clear.

BACKGROUND: Lung cancer incidence in Macao increases gradually, smoking is one of the important high risk factors. The purpose of this study is to observe the detection rate of lung cancer and nodules in long-term smoking Macao individuals. METHODS: We recruited eligible Macao residents by publicity, all subjects were arranged to receive low-dose computed tomography screening. Image features of lung nodules were analyzed by radiologist. For suspicious lung cancer, multiple disciplinary team (MDT) was arranged. RESULTS: A total of 291 were adopted, 10 lung cancers were detected, the detection rate of lung cancer was 3.44% (95%CI: 2.78%-4.01%), all were males. There were 5 adenocarcinoma patients, each 2 squamous-cell carcinoma and small cell lung carcinoma patients; 1 adenosquamous cancer patient. Among 10 lung cancers, 40% had stage 1 disease. The detection rate of lung nodules was 72.9% (95%CI: 67.8%-78.0%); The number of suspicious lung nodules were 44, and the detection rate was 15.1% (95%CI: 11.0%-19.2%). There was no significant differences in the lung cancer detection rate between the single and multiple lung nodule groups (P>0.05). There were 168 subjects in the <6 mm solid lung nodule (SN) and <5 mm no-solid lung nodule (NSN) group and no lung cancer was found, 44 subjects in the ≥6 mm SN and ≥5 mm NSN group. All 9 lung cancer patients were detected in this group. The detection rate of lung cancer was higher than that of the <6 mm SN and <5 mm NSN group (P<0.05). CONCLUSIONS There are high detection rate of lung cancer and lung nodule in the long-term smoking individuals. The lung cancer rate increases when the lung nodule size is larger than 6 mm in SN and 5 mm in NSN. Adenocarcinoma is the major type in the smokers' lung cancers. We suggest long-term smokers should join in the future lung cancer screening trial in Macao. Female lung cancer screening should be established different standard.