Objective To investigate the CT characteristics of retroperitoneal extra-adrenal paraganglioma(PGL).Methods CT findings of 11 patients with pathologically confirmed retroperitoneal extra-adrenal PGL were analyzed retrospectively,and the relevant literature was reviewed.All patients received plain CT as well as contrast-enhancement CT scan.Results All of the 11 tumors were located in the retroperitoneal space around large blood vessels,including 2 functional and 9 unfunctional extra-adrenal paragangliomas.Eight of 11 cases were benign tumors which presented as round or oval masses with sharp margins,separated from surrounding structures clearly;while the rest 3 cases,which with indistinct edge,even more with the invasion of surrounding structures (renal artery,renal venous and pancreas),were confirmed to be malignant.Most of the tumors were heterogeneous on plain CT.It was common to see intratumoral necrosis or cystic degeneration in the tumors (9 cases),while hemorrhage or calcification was uncommon,which was found in 3 and 2 cases,respectively.Homogeneous intensity was only observed in 2 masses with diameter less than 4 cm.On contrast-enhanced CT image, the solid part of the tumors presented continuously significant enhancement.Dilated feeding artery was found in or around the masses (8 cases) in artery phase.Conclusion There are certain characteristics of retroperitoneal extra-adrenal paraganglioma on CT scanning, which are helpful for preoperative diagnosis and treatment of this disease.

Objective To investigate the effect of chemotherapy drugs on the expression of carci-noembryonic antigen (CEA) in the gastric tissue with precancerous lesions in ectopie cancer. Methods There were 45 cases of cancer patients (precancerous lesions group), the pathological biopsy showed that there were atypical hyperplasia or intestinal metaplasia by gastroscope before chemotherapy. Gastruscope was done before chemotherapy and after six cycles of chemotherapy. Gastric tissue was taken respectively in the same site. The expression of CEA was measured in the gastric tissue. Normal gastric tissue taken from 10 cases of cancer patients was served as control. Compared respectively the expression of CEA in the gastric tissue in control group and precancerous lesions group, in precancerous lesions group between before and after treatment. Results CEA expression in the gastric tissue was (27.76±9.67), (3.32±0.60)μg/L in precancerous lesions group and control group respectively, there was significant difference between two groups(P<0.05). CEA expression in the gastric tissue was (27.76±9.67), (26.60±10.80)μg/L before and after treatment in precancerous lesions group respectively, P<0.05. CEA expression in the gastric tissue before treatment was (23.11±4.11), (17.10±1.66)μg/L, after treatment was (21.11±5.66), (15.10±3.31)μg/L in the mild to moderate atypical hyperplasia, mild to moderate intestinal metaplasia respectively, there was significant difference between before and after treatment in the mild to moderate precancerous lesions. There was no significant difference between before and after treatment in the severe precancerous lesions. Conclusions Chemotherapy drugs can significantly reduce the expression of CEA in the gastric tis-sue in the mild to moderate precancerous lesions. The results suggests that mild to moderate precancerous lesions can be reversed.

Objective To study the feasibility of video-assisted thoracoscopic (VAT) minor pulmonary resection under local anesthesia. Methods From February to December 2000,8 patients (6 cases of peripheral pulmonary nodules,2 cases of respiratory insufficiency and radiographic pulmonary infiltrate)were operated on through video-assisted thoracoscopy under local anesthesia. Results Except 1 case was converted to general anesthesia and performed minithoracotomy to resect pulmonary coin lesion due to pleural adhesion,other 7 patients underwent VAT-pulmonary wedge ressction under local anesthesia and definitive diagonosis.(3 with tuberculosis,1 with metastatic adenocarcinoma,1 with inflammatory pseudotumor and 2 with pulmonary fibrosis)were obtained.The duration of the procedures was from 40 to 200 min. Spontaneous breathing and hemodynamics were maintained well during the operation.There was neither severe postoperative complications nor mortality.The postoperative hospitalized days were 2～5 days with a mean of 3 days. The average medical fee for pulmonary wedge ressction using our procedure was 5400 RMB. Conclusions VAT-minor pulmonary resection can be performed safely under local anesthesia.

Objective To investigate the role of nuclear transcription factor kappa B (NF-κB) -matrix metalloproteinase-9 (MMP-9) signaling pathway in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods 150 male SD rats were randomly assigned to air control group (AC group) , CO poisoning group (CO group) , pyrrolidine thiocarbamate (PDTC) + CO poisoning group (PC group). DEACMP model was reconstructed by modified intraperitoneal injections. The 1, 3, 7, 14, and 21 d after intraperitoneal injection were observed here by different approaches. Morris water maze test was used to test the learning and memory ability of rats.HE staining was used to observe the morphology of hippocampal CA3 cells. Immunofluorescence and Western Blot methods were used to detect the expression of NF-κB and MMP-9. RT-PCR was used to measure the expression of MMP-9 mRN A. Transmission electron microscopy was used to observe the ultrastructure of synapses. Results After14 days, the average intubation period of CO group was longer than that of AC group (P < 0.05) , and that of PC group was shorter than that of CO group (P < 0.05). However, average intubation period of PC group was longer than that of AC group (P< 0.05). In CO group, the expression of NF-κB in hippocampus increased (day 1). At day 3, the expression of NF-κB rapidly increased. The expression of MMP-9 gene and protein increased in the first three days and then decreased thereafter. The expression of NF-κB and MMP-9 in PC group was lower than that in CO group (P < 0.05) , while it was higher than AC group (P < 0.05). The peak value of apoptosis in CO group was delayed to 7-14 d after exposure, the apoptotic cells in PC group decreased significantly, and it was obvious on the 14 th day.Electron microscopy showed that the damage of synapses ultrastructure in CO group was significantly heavier than that in PC group on the 14 th day. Conclusions NF-κB-MMP-9 signal pathway leads to DEACMP, and PDTC could alleviate the impairment of learning and memory ability in rats with acute CO poisoning.

Objective: To investigate the effects of astaxanthin on neuronal injury in hippocampus of rats after acute carbon monoxide poisoning(ACMP) and the relationship with NF-κB inflammatory signaling pathway. Methods: Male SD rats screened by water maze were randomly divided into three group(n=50): control group (NC group), CO poisoning group (COP group), CO poisoning+ astaxanthin group (AST group) . ACMP rat model was established by static inhaled exposure method. Meanwhile, rats in AST group were further given astaxanthin twice a day by gavage.At 1 day, 7 days, 14 days, 21 days and 28 days after CO poisoning (10 rats in each group were selected), the learning and memory abilities were evaluated by Morris water maze test. The pathological changes of the neurons in hippocampal CA1 region were observed by hematoxylin-eosin(HE) staining.The expression and activation of NF-κB in hippocampus were detected by immunoblotting and immunofluorescence, and the expression of TNF-α and IL-6 protein in hippocampus were examined by ELISA. Results: Morris water maze test showed that there were no significant difference in escape latency and crossing platform times between the three groups (P>0.05). Compared with NC group, the escape latency of COP group was prolonged at 14, 21 and 28 days after CO poisoning (t=-6.04, -6.28, -8.18, all P<0.05), and the number of crossing platform was decreased (t= 5.96, 7.85, 6.51, all P<0.05). Compared with the COP group, the escape latency of the rats in AST group at the 14, 21 and 28 days was shortened (t=4.74, 4.82, 5.98, all P<0.05), and the number of crossing platform was increased (t=-3.72, -4.45, -6.53, all P<0.05). Compared with NC group, the number of NF-κ B positive cells in CA1 area of hippocampus in COP group increased at every time point (t=-8.62, -18.00, -16.67, -11.15, -6.22, all P<0.05); the number of NF-κ B positive cells in CA1 area in AST group decreased at 7 d, 14 d, 21 d and 28 d after CO poisoning, the difference was statistically significant (t= 6.55, 6.96, 4.40, 4.17; all P<0.05). Western blot showed that the changes of NF-κB protein was similar to that of immunofluorescence. After 7 days of CO poisoning, the level of NF-κB protein in hippocampus of COP group was (1.44±0.08), it was higher than that of NC group (t=-20.07, P<0.05), while that of AST group was (0.68±0.10), it was lower than that of COP group (t=10.23, P<0.05). The results of Elisa showed that TNF-α and IL-6 in the hippocampus of COP group were higher than those of NC group at every time point(all P<0.05), while compared with COP group, TNF-α and IL-6 in AST group were lower (all P<0.05). After 7 days of CO poisoning, TNF -α in COP group ((39.04±5.29) pg/ml)was higher than that in NC group ((14.13±2.12) pg/ml) (t=-7.58, P<0.05); TNF -α in AST group ((25.77±3.31) pg/ml) was lower than that in COP group (t=3.69, P<0.05). After 7 days of CO poisoning, the level of IL-6 in COP group ((181.79±9.12) pg/ml)was higher than that in NC group ((73.12±11.04) pg/ml) (t=-8.24, P<0.05), and the level of IL-6 in AST group ((121.47±9.80) pg/ml) was lower than that in COP group (t=7.80, P<0.05). Conclusion The excessive inflammatory response which mediated by NF-κB signaling pathway is involved in ACMP-induced neuronal damage in hippocampus.Astaxanthin can down-regulate the expression of NF-κB inflammatory signaling pathway related proteins, and pave a way for the treatment of ACMP brain damage and cognitive dysfunction.

Objective To investigate the initial CT characteristics and dynamic changing features of invasive pulmonary aspergillosis (IPA).Methods CT findings of 40 patients with IPA confirmed by histopathology or clinics were analyzed retrospectively,including the initial and follow-up CT features.Results Multiple lesions in the bilateral lung were found in the initial CT of all 40 patients.The coexistence of no less than two different CT features were showed in 27 patients(67.5 ％),and the same CT morphologic feature were showed in 13 patients (32.5 ％).The common features of the initial CT:nodules/masses (34,85.0 ％),halo sign (24,60.0％),patchy opacities (13,32.5 ％),cavities (9,22.5 ％) and wedge opacities adjacent to pleura (3,7.5 ％).The follow-up CT showed that cavities or air meniscus sign emerged in the nodules/masses after an effective treatment in 29 patients (72.5％) of all 40 cases.The lesion volume decreased subsequent to the collapse of the cavities or air meniscus,and then vanished.Conclusion Thoracic CT scanning play an important role in the diagnosis of IPA.Coexistence of the multiple lesions in number and morphology is the most common CT feature.The findings of follow-up CT is characteristic,and can be helpful in guiding the clinical treatment and evaluating therapeutic effect.

Objective To explore the common CT signs of acquired immune deficiency syndrome(AIDS)-associated pneumocystis jirovecii pneumonia(PJP).Methods The chest CT data of 123 patients with AIDS-associated PJP were analyzed retrospectively.Results Multifocal lesions in both lungs were found in all cases.Distribution characteristics were as follows:diffuse and symmetrical distribution in both lungs in 100 cases(81.3％),diffuse and asymmetrical distribution in both lungs in 15 cases(12.2％),and scattered distribution in both lungs in 8 cases(6.5％).The density and morphological features were as follows:ground glass opacity in 120 cases(97.6％);"lunate arch sign"in 25 cases(20.3％);pulmonary interstitial proliferation in 103 cases(83.7％);crazy paving pattern in 14 cases(11.4％);patchy or consolidation shadow in 55 cases(44.7％);pulmonary cysts in 26 cases(21.1％);and nodular in 26 cases(21.1％).Other rare signs included pleural effusion in 11 cases,pericardial effusion in 6 cases,mediastinal and hilar lymphadenopathy in 9 cases,and mediastinal emphysema in 1 case.Conclusion The chest CT manifestations of AIDS-associated PJP have certain characteristics,including diffuse and symmetrical distribution of lesions in both lungs,as well as ground glass opacity and interstitial hyperplasia as common signs,especially,"lunate arch sign"and pulmonary cysts are more specific signs.

Objective:To investigate the driving effect of prostate cancer associated transcript 4 (PCAT4) on the up-regulation of upregulator of cell proliferation (URGCP) expression in breast cancer progression through sponging miR-508-5p.Methods:The microarray data of lncRNA and miRNA with differential expression in breast cancer tissue were analyzed by Cancer Genome Atlas. The expression of PCAT4 in breast cancer was evaluated by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation was measured by MTT and colony formation, cell apoptosis was analyzed by TUNEL, and cell migration and invasion were analyzed by Transwell. The correlation between PCAT4 and miR-508-5p, and miR-508-5p and URGCP was analyzed by RNA pull-down and double luciferase assay. Tumor xenograft studies were performed to analyze the correlation between PCAT4/miR-508-5p/URGCP axis and breast cancer cell growth in vivo. Measurement data were expressed as mean ± standard deviation ( ± s). T-test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. The correlation between PCAT4 and URGCP and miR-508-5p expression was evaluated by Pearson correlation analysis. Results:The expression level of PCAT4 was up-regulated in breast cancer tissues and cells. Knockout of PCAT4 inhibited cell proliferation and metastasis and promoted cell apoptosis. miR-508-5p was the target of PCAT4 and was negatively correlated with PCAT4. Overexpression of miR-508-5p in breast cancer can inhibit cell growth, migration and invasion, and promote cell apoptosis. URGCP is the target of miR-508-5p and induces progression of breast cancer. Tumor xenograft studies showed that PCAT4 drives breast cancer progression by affecting miR-508-5p/URGCP.Conclusion:The expression of PCAT4 is up-regulated in breast cancer tissues and cells, and PCAT4 can act as a molecular sponge of miR-508-5p, and significantly promote breast cancer progression by activating URGCP protein expression.

Objective: To survey the conduction and evaluate the effectiveness of extracorporeal membrane oxygenation (ECMO) therapy in pediatric intensive care unit (PICU) in China mainland. Methods: In a questionnaire-based survey, we retrospectively reviewed the application of ECMO in children's hospital and general hospital in China mainland to summarize and analyze the categories of diseases and prognosis of children treated with ECMO therapy. Results: By December 31, 2017, a total of 23 hospitals using ECMO, including 22 tertiary referral hospitals and 1 secondary hospital, among which 16 were children′s hospitals and 7 were general hospitals. Thirty-seven ECMO equipment was available. A total of 518 patients treated with ECMO, within whom 323 (62.4%) successfully weaned from ECMO and 262 (50.6%) survived to discharge. Among 375 pediatric patients, 233 (62.1%) were successfully weaned from ECMO and 186 (49.6%) survived to discharge. Among 143 newborn patients, 90 (62.9%) successfully weaned from ECMO, 76 (53.1%) survived to discharge. ECMO was applied in veno-arterial (VA) mode to 501 (96.7%) patients, veno-venous (VV) mode to 14 (2.7%) patients, and VV-VA conversion mode to 3 (0.6%) patients. Sixty-nine patients required extracorporeal cardiopulmonary resuscitation (ECPR), including 20 newborn patients (29.0%) and 38 pediatric patients (71.0%), who were all with cardiovascular disease. Neonatal respiratory distress syndrome (26/61), persistent pulmonary hypertension of the newborn (PPHN) (12/61), and meconium aspiration syndrome (MAS) (11/61) are the most common pulmonary diseases in newborn patients; among whom, infants with PPHN had highest survival rate (10/12), followed by MAS (9/11). Among newborn patients with cardiovascular diseases, those who admitted were after surgery for congenital cardiac disease were the most common (54/82), while those with septic shock had the highest survival rate (2/3). In pediatric pulmonary diseases, acute respiratory distress syndrome was the most common (42/93), while plastic bronchitis was with the highest survival rate (4/4), followed by viral pneumonia (13/16). Among pediatric cardiovascular diseases, congenital cardiac defect was the most common (124/282), while fulminant myocarditis had the highest survival rate (54/77). Conclusion The application of ECMO as a rescue therapy for children with severe cardiopulmonary failure has dramatically developed in China mainland.

Recent studies have identified that metabolic reprogramming in lung adenocarcinoma cells, particularly lactate metabolism disorders, plays a crucial role in tumor development and immune therapy response. The accumulation of lactic acid not only provides energy support for the proliferation of tumor cells but also affects the function of immune cells by changing the tumor microenvironment, thereby promoting immune escape. Immunotherapy, especially the application of immune checkpoint inhibitors, has become an important strategy for treating lung adenocarcinoma. However, lactate metabolism disorders might affect the efficacy of immunotherapy, leading to resistance in some patients. Therefore, a thorough understanding of the mechanisms of lactic acid metabolism in lung adenocarcinoma and its impact on the response to immunotherapy is essential for developing new therapeutic strategies and improving the efficacy of immunotherapy. This review summarizes the role of lactate metabolism disorders in the development and immunotherapy of lung adenocarcinoma, discusses the potential role of lactic acid metabolism-related genes and pathways in lung adenocarcinoma, and explores the progress in therapeutic strategies targeting lactic acid metabolism regulation. This work aims to provide new insights for the treatment of lung adenocarcinoma.