Objective To explore the clinicopathological features of adult pulmonary sequestration and summarize the misdiagnosis experiences.Methods Data of 16 cases of adult pulmonary sequestration ( 18 years),who were confirmed by surgery and biopsy in our hospital were collected and reviewed.Results The median age of all the patients was 38.5 years.The female seemed to be more likely to suffer from adult pulmonary sequestration ( n =12) with cough to be the most frequent symptom ( n =9 ).CT scans revealed most of the lesions were located in the left lower lobes of the lungs ( n =9 ).Half of the lesions were characterized by pulmonary cyst-like changes and/or multiple cystic bronchiectasis ( n =8 ),followed by soft tissue mass in or out of the lung fields ( n =7).Enhanced CT scans showed abnormal arteries from the systemic circulation.Only two cases were diagnosed as pulmonary sequestration correctly in the primary diagnosis.The remaining were mostly misdiagnosed as pulmonary cyst-like changes with bronchiectasis ( n =6) or tumors (n =6).According to the findings during surgery,13 cases were intralobar pulmonary sequestrations; 3 cases were extralobars,whose tissues were all detected dysplasia and chronic inflammatory by histopathological examinations.Conclusions The misdiagnosis rate of pulmonary sequestration is high because of its non-specific clinical symptoms.Since it is characterized by abnormal arteries and pulmonary dysplasia,enhanced CT scans should be used as a preferred screening method for suspected cases,especially for those middleaged patients with cystic or mass-like lesions in the left lower lobes of the lungs.

BACKGROUNDTo summarize the clinical results of Iressa in the treatment of patients with non small cell lung cancer (NSCLC) who failed prior chemotherapy and radiotherapy.

METHODSTwenty-nine patients with NSCLC, who failed prior chemotherapy and radiotherapy, were registered in this open clinical trial. Prior to Iressa therapy, 26 patients were in stage IV, 3 patients in stage IIIB. Iressa was administered orally at 250 mg, once a day until cancer progressed or severe toxicity occured. The median time for administration of Iressa was 5 months.

RESULTSThe main toxicity of Iressa was skin toxicity (rash). Twelve cases had rash with 41.4% of the whole group. Two cases had diarrhea, 1 case had bradycardia and 1 case had elevation of transaminase. Among the 29 patients, one patient got complete response (CR), 7 partial response (PR), 12 stable disease (SD) and 9 progression disease (PD). The response rate was 27.59% and disease control rate including both tumor response and stable disease was 68.97%. The median survival time was 5.5 months (1-19 months). Median time to progression (TTP) was 6.5 months. The 1-year survival rate was 44.83%.

CONCLUSIONSIressa is effective and tolerable for the patients with NSCLC who failed prior chemotherapy and radiotherapy. It can remarkably improve symptoms and prolong survival time of NSCLC patients.

BACKGROUNDTo study the relationship between expression of endostatin and clinical and pathophysiological characteristics in the non-small cell lung cancer (NSCLC).

METHODSThe expression of endostatin was detected in 46 lung cancer tissues and paracancerous lung tissues, 14 benign pulmonary lesion tissues as control by immunohistochemical staining (LSAB method).

RESULTSThe expression of endostatin in lung cancer tissues (84.91%±7.65%) was significantly higher than that in paracancerous tissues (63.70%±12.45%) and benign pulmonary lesion tissues (40.29%±15.01%) (P < 0.01); The expression of endostatin was closely related to the size of primary tumor, distant metastasis of the cancer, P-TNM stages and cell differentiation of lung cancer (P < 0.05), but not to the histological classification, lymph node status, location of the tumor, smoking or not, age and sex of the patients with lung cancer (P > 0.05).

CONCLUSIONSThe expression of endostatin in NSCLC cancer tissues might be helpful to evaluate the biological behavior of lung cancer.

Objective:To evaluate the changes in topological properties of brain functional network after induction of general anesthesia in the patients with glioma.Methods:Twenty-two patients scheduled for elective intracranial glioma resection were selected.Resting-state functional magnetic resonance imaging was performed during wakefulness and general anesthesia with endotracheal intubation in patients with glioma. Large-scale functional brain networks of each patient were constructed based on 123 regions of interest in non-surgical hemisphere. Global properties (local efficiency, clustering parameter, shortest path length, global efficiency, small world) and nodal properties (nodal degree, nodal efficiency, and between centrality) in brain functional networks were then compared between wakefulness and general anesthesia.Results:Eighteen patients were finally enrolled. Compared with the status during wakefulness, the local efficiency and clustering parameter on non-surgical side significantly decreased ( P<0.05), no significant change was found in the shortest path length and global efficiency ( P>0.05), and small world was greater than 1 throughout the entire density range; the nodal degree, nodal efficiency and between centrality of nodes located in the medial/mesal regions, such as the medial prefrontal cortex, posterior cingulate gyrus/precuneus, medial temporal lobe, anterior cingulate gyrus, thalamus, amygdala, were significantly reduced ( P<0.05); however, these node parameters increased significantly in the lateral brain regions ( P<0.05) except for the primary auditory and somatosensory cortex, which also decreased significantly after induction of general anesthesia( P<0.05). Conclusions:The functional segregation of brain functional network is widely inhibited after induction of general anesthesia, but the functional integration is still retained. The lateral brain regions show no anticorrelation with the medial brain region during general anesthesia.

BACKGROUNDTo explore the possibility of targeting blockage of Wnt signal transduction pathway of nm23-H1 gene transfection in human high-metastatic large cell lung cancer cell line L9981, and to provide evidence to elucidate the signal conductive mechanism of nm23-H1 mediated tumor metastasis suppression.

METHODSThe expression of GSK-3β and β-catenin of Wnt signal pathway was detected in cytoplasm and nucleus in L9981 cell line with nm23-H1 deletion, L9981-pLXSN cell line transfected with vector and L9981-nm23-H1 cell line transfected with nm23-H1 gene by Western blot.

RESULTS(1)GSK-3β expression in L9981-nm23-H1 cytoplasm (6 341±541) was significantly higher than those in L9981 (3 736±298) and L9981-pLXSN (3 613±383) cell lines ( P < 0.001); (2)GSK-3β expression in L9981-nm23-H1 nucleus (4 356±490) was significantly higher than those in L9981 (657±57) and L9981-pLXSN (705±75) cell lines ( P < 0.001); (3)β-catenin expression in L9981-nm23-H1 cytoplasm (3 649±118) was significantly higher than those in L9981 (1 401±31) and L9981-pLXSN (1 350±55) cell lines ( P < 0.001); (4)No statistical difference of the β-catenin expression in nucleus was observed among L9981-nm23-H1 (2 945±68), L9981 (2 604±23) and L9981-pLXSN (2 652±53)( P > 0.05); (5)No significant difference of GSK-3β or β-catenin expression in cytoplasm and nucleus was observed between L9981 and L9981-pLXSN ( P > 0.05).

CONCLUSIONS(1)nm23-H1 gene can remarkably upregulate the expression of GSK-3β in cytoplasm and nucleus, and β-catenin expression in cytoplasm in L9981-nm23-H1 cell, but can not induce the nucleus accumulation of β-catenin. (2)Regulation of GSK-3β and β-catenin expression, and targeting blockage of Wnt signaling pathway may be one of molecular mechanisms that nm23-H1 contributes to play a vital role in the "Lung Cancer Metastasis Suppressive Cascade".

BACKGROUNDTo explore the effects of nm23-H1 gene transfection and forskolin on PKA activity in human high-metastasis large cell lung cancer cell line L9981.

METHODSThree cell lines, primary human large cell lung cancer cell line (L9981), vector transfection cell line (L9981-pLXSN) and nm23-H1 gene transfection cell line (L9981-nm23-H1-pLXSN), were treated with PKA activator forskolin. The PKA activity at different time points after treatment with forskolin was detected in the three lung cancer cell lines by radioimmunological method with SignaTECT cAMP-dependent PKA assay system.

RESULTS(1) Before forskolin treatment, the activity of PKA of L9981-nm23-H1-pLXSN was remarkably higher than those of L9981 and L9981-pLXSN (P < 0.01), but no significant difference in the PKA activity was observed between L9981 and L9981-pLXSN (P > 0.05). (2)The PKA activity was remarkably increased in all the three lung cancer cell lines after treatment with different concentration of forskolin (P < 0.01), and up to the highest level at the concentration of 100 μmol/L. It showed a dose-dependent relationship between the PKA activity and forskolin concentration; (3) The PKA activity in all the three cell lines was elevated to the highest level at 30 minutes after treatment with forskolin of 100 μmol/L, and it showed a time-dependent relationship between the PKA activity and action time of forskolin.

CONCLUSIONS(1)Transfection of nm23-H1 gene can up-regulate the PKA activity of human high-metastasis large cell lung cancer cell line L9981, and its function as a tumor metastasis suppressor gene may be related to its effects on regulation of PKA signal transduction pathways; (2)Forskolin can remarkably up-regulate the PKA activity of L9981 cell line, and the elevation of PKA activity has a time-dependent and dose-dependent relation to forskolin.

BACKGROUNDTo explore the influences of nm23-H1 gene transfection and protein kinase C (PKC) inhibitor Calphostin C on PKC signal transduction pathway in human high-metastasis large cell lung cancer cell line L9981, and to evaluate the effects of nm23-H1 gene on translocation and activation in subcellular region.

METHODSThe translocation of PKC in subcellular region was observed in L9981 before and after nm23-H1 gene transfection and Calphostin C treatment by Laser scanning confocal microscope (LSCM) method.

RESULTSPKC-α and PKC-βII were found to locate in different subcellular site in L9981 before and after nm23-H1 gene transfection. PKC-α and PKC-βII mainly located in nucleus and perinucleus in L9981 and L9981-pLXSN cell lines, which were in active status. PKC-α and PKC-βII mainly located in soluble cytosolic fraction in L9981-nm23-H1 cell line and were inactive status. PKC-α and PKC-βII mainly located in cytosolic fraction and were in inactive status in all the three cell lines after treatment with Calphostin C.

CONCLUSIONSThe results suggest that nm23-H1 gene might make PKC to translocate from nucleus and perinucleus to soluble cytosolic fraction in L9981 cell line. PKC inhibitor, Calphostin C, can also make PKC to translocate from nucleus and perinucleus to soluble cytosolic fraction in L9981, L9981-pLXSN cell lines. Both transfection of nm23-H1 gene and treatment with Calphostin C can suppress the PKC signal transduction in L9981 cell line.

BACKGROUNDTo investigate the influence of tumor metastasis suppressor gene nm23-H1 on the activity of glycogen synthase kinase 3β (GSK-3β) in human high-metastasis large cell lung cancer cell line L9981.

METHODSThe levels of GSK-3β expression in cytoplasm and nucleus were determined with anti- GSK-3β antibody in human high-metastasis large cell lung cancer cell line L9981 (cell line with nm23-H1 gene deletion), L9981-nm23-H1 (cell line with nm23-H1 transfected) and L9981-pLXSN (cell line with vector transfected) by Western blot method. The activity of GSK-3β among those three cell lines was detected by immunoprecipitation and analysed by a radioactive isotope scintillation counter before and after treating with 20 mmol/L LiCl.

RESULTS(1) The expression indensity of GSK-3β of cytoplasm and nucleus was (6 341±541) and (4 356±490) IOD in L9981-nm23-H1, (3 613±383) and (705±75) IOD in L9981-pLXSN, and (3 736±298) and (675±57) IOD in L9981, respectively. A high significance in GSK-3β expressive indensity of both cytoplasm and nucleus existed among L9981-nm23-H1, L9981-pLXSN and L9981 (P < 0.01); Multiple comparison: A highly significant difference was observed when L9981-nm23-H1 was compared with L9981-pLXSN or L9981 (P < 0.01), but no significant difference was observed between L9981-pLXSN and L9981 (P > 0.05). (2) The GSK-3β activity of cytoplasm and nucleus was (28 955±2 509) and (9 247±924) CPM in L9981-nm23-H1, (11 241±1 495) and (1 492±176) CPM in L9981-pLXSN, and (12 505±1 469) and (1 763±125) CPM in L9981, respectively. A highly significant difference in GSK-3β activity of both cytoplasm and nucleus existed among L9981-nm23-H1, L9981-pLXSN and L9981 (P < 0.01); Multiple comparison: the GSK-3β activity in L9981-nm23-H1 was significantly higher than that in L9981-pLXSN and L9981 (P < 0.01), but no significant difference was observed between the L9981-pLXSN and L9981 (P > 0.05). (3) After treatment with 20 mmol/L LiCl, the expressive indensity of GSK-3β of cytoplasm and nucleus was (4 718±549) and (3 823±350) IOD in L9981-nm23-H1, (2 030±155) and (217±15) IOD in L9981-pLXSN, and (2 164±151) and (224±19) IOD in L9981, respectively. No significant difference in GSK-3β expressive indensity existed between before and after treatment with LiCl in L9981-nm23-H1 (P > 0.05). However, the GSK-3β expressive indensity in cytoplasm and nucleus before treatment was remarkably higher than those after treatment in both L9981-pLXSN and L9981 (P < 0.05). (4) After treatment with 20 mmol/L LiCl, the GSK-3β activity in cytoplasm and nucleus was (11 099±1 112) and (3 748±215) CPM in L9981-nm23-H1, (4 447±430) and (1067±159) CPM in L9981, and (4 435±427) and (909±156) CPM in L9981-pLXSN, respectively. The GSK-3β activity both in cytoplasm and nucleus after treatment with LiCl was remarkably lower than that before treatment in L9981-nm23-H1, L9981-pLXSN and L9981 (P < 0.01 or P < 0.05).

CONCLUSIONS(1) Transfection of nm23-H1 gene can significantly up-regulate the expression level and activity of GSK-3β in human high-metastasis large cell lung cancer cell line L9981; (2) LiCl can remarkably suppress the upregulation effects of nm23-H1 gene on GSK-3β activity in L9981 cell line; (3) The effects of nm23-H1 gene on suppressing the signal transduction of Wnt pathway might be carried out through upregulating GSK-3β expression and activity in human high-metastasis large cell lung cancer cell line L9981.

With the change of COVID-19 prevention and control strategy in China, the number of COVID-19 cases has increased significantly recently, which has also brought new challenges to the perioperative risk control of thoracic surgery. This paper puts forward several suggestions, aiming to standardize the preoperative screening and evaluation during the COVID-19 period, strictly grasp the indications and timing of surgery, optimize the medical management process, individualize surgical decision-making, and minimize the risk of COVID-19 infection to surgery.

PURPOSE: Interleukin-17 (IL-17) is a proinflammatory cytokine that plays important roles in inflammation, autoimmunity, and cancer. The purpose of this study was to determine if IL-17 indirectly regulates macrophage differentiation through up-regulation of cyclooxygenase-2 (COX-2) expression in the cancer cell lines. MATERIALS AND METHODS: Human cervical cancer HeLa, human lung cancer A549, and mouse prostate cancer Myc-CaP/CR cell lines were treated with recombinant IL-17; Western blot analysis, enzyme-linked immunosorbent assay, and quantitative real-time polymerase chain reaction analysis were utilized to examine the cellular responses. RESULTS: IL-17 up-regulated expression of COX-2 mRNA and protein in HeLa, A549, and Myc-CaP/CR cell lines. IL-17's effects were mediated through nuclear factor-kappaB and ERK1/2 signaling pathways as the inhibitors of these pathways could inhibit IL-17-induced COX-2 expression. The conditional medium obtained from the cancer cells contained prostaglandin E2, the levels of which were increased by IL-17 treatment. When treated with the conditional medium, particularly with the IL-17-induced conditional medium, mouse RAW264.7 macrophages and human THP-1 monocytes expressed higher levels of IL-10 (a marker of M2 macrophages) than inducible nitric oxide synthase or tumor necrosis factor alpha (markers of M1 macrophages). In contrast, when RAW264.7 and THP-1 cells were treated directly with IL-17, expression of these marker genes was not markedly changed. CONCLUSION: The results of this study suggest that IL-17 indirectly promotes M2 macrophage differentiation through stimulation of the COX-2/PGE2 pathway in the cancer cells, thus IL-17 plays an indirect role in regulating the tumor immune microenvironment.
Animals ; Autoimmunity ; Blotting, Western ; Cell Line ; Cyclooxygenase 2 ; Dinoprostone ; Enzyme-Linked Immunosorbent Assay ; Humans ; Inflammation ; Interleukin-10 ; Interleukin-17* ; Lung Neoplasms ; Macrophages* ; Mice ; Monocytes ; Nitric Oxide Synthase Type II ; Prostatic Neoplasms ; Real-Time Polymerase Chain Reaction ; RNA, Messenger ; Tumor Microenvironment ; Tumor Necrosis Factor-alpha ; Up-Regulation ; Uterine Cervical Neoplasms