Effects of RNAi-mediated TUSC3 silencing on radiation-induced autophagy and radiation sensitivity of human lung adenocarcinoma cell line A549 under hypoxic condition.

This study examined the effects of RNAi-mediated TUSC3 silencing on radiation-induced autophagy and radiation sensitivity of human lung adenocarcinoma cell line A549 under hypoxic condition. Different CoCl2 concentrations were used to treat A549 cells and establish a CoCl2-induced hypoxic model of A549 cells. MTT and clone formation assays were used to determine the effects of different concentrations of CoCl2 on the growth and proliferation of A549 cells treated by different doses of X-ray irradiation. The siRNA-expressing vector was transfected by liposomes and for silencing of TUSC3. Flow cytometry was used to measure cell cycle changes and apoptosis rate. Real-time quantitative polymerase chain reaction (qRT-PCR) assay was performed to detect the expression of TUSC3 mRNA. Western blotting was applied to detect the changes of TUSC3, LC3, and p62 proteins under different CoCl2 concentrations and after siRNA silencing of TUSC3. The TUSC3 levels in A549 cells increased under hypoxic conditions in a dose-dependent manner (P < 0.05). Hypoxia inhibited the growth and proliferation of A549 cells and promoted apoptosis (P < 0.05). With an increasing dose of X-ray irradiation, A549 cells showed significantly increased growth and proliferation and decreased apoptosis (P < 0.05). After siRNA-TUSC3 was transfected by liposome, the TUSC3 level was substantially inhibited (P < 0.05). Silencing TUSC3 inhibited A549 cell growth and proliferation after radiotherapy under hypoxic condition, promoted apoptosis, increased G0/G1 phase cells, and reduced S phase cells (all P < 0.05). Hypoxia and radiation along with different CoCl2 concentrations could induce cell autophagy, which increased with concentration and dose, while silencing the TUSC3 gene inhibited autophagy (all P < 0.05). RNAi silencing of TUSC3 inhibited growth and proliferation, while enhanced apoptosis and radiation sensitivity of hypoxic A549 lung adenocarcinoma cells.

Intrapulmonary migration of a fractured acupuncture needle: a case report.

BACKGROUND: Acupuncture, a traditional Chinese medical treatment, has been gaining popularity over the years. However, it also presents certain risks. We report a case of a patient who discovered a foreign body in their lung several years after undergoing acupuncture. CASE PRESENTATION: A middle-aged woman presented to our hospital with chest pain. An X-ray revealed a needle-like foreign body in the middle lobe of her right lung. The patient had previously undergone acupuncture treatment for local pain in her lower back and lower extremities many years prior. Based on the imaging findings and her medical history, we hypothesized that the foreign body in her lung was a result of a dislodged acupuncture needle. Through preoperative 3-dimensional reconstruction and indocyanine green localization, we were able to locate the foreign body in the lateral segment of the right middle lobe. We successfully removed the foreign body via wedge resection, and the patient made a smooth recovery post-surgery. CONCLUSION: Acupuncturists and surgeons should remain vigilant about the potential risks associated with acupuncture.

[Expression of orexin receptor 1 in rat pancreatic tissue with alimentary obesity].

OBJECTIVE: To identify the presence of orexin receptor 1 (OXR1) in obese rat pancreas and clarify its effect and mechanism on body weight and metabolic index in obese rats. METHODS: The obese rat model was established a high-fat diet. And the serum levels of glucose, triglyceride and insulin were measured by Mini-Blood Glucose meter, biochemical enzymatic method and chemiluminescent immunoassay. The pancreatic expression of OX1R protein was identified by immunohistochemistry. After an intracerebroventricular infusion of orexin receptor 1 antisense oligodeoxynucleotide (OX1R-PS-ODNs), the effect on OX1R protein was detected in rat pancreatic tissue with obesity. RESULTS: After feeding for 8 weeks, high-fat diet rats appear alimentary obesity body weight, serum glucose, insulin, triglyceride and cholesterol of high-diet rats were higher than those in the control group (P < 0.05). The expression of OX1R protein was located in the cytoplasm of pancreas Islet ß-cells. The expression of OX1R protein in obese rat pancreas decreased around 16% versus the normal group (P < 0.05). After the obese rats were treated by OX1R-PS-ODNs for 72 hours, the expression of OX1R protein in pancreas declined from 82 ± 6 to 65 ± 4, reduced about 21% compare with control group (P < 0.01). CONCLUSION: The expression of OX1R protein is found in pancreas Islet ß-cells. Hypothalamic orexin system can intervene the expression of OX1R protein in rat pancreatic tissue with alimentary obesity. And it may participate in the occurrence of obesity and the metabolic regulation of serum glucose and insulin.

MiR-22-3p Expression is down-regulated in lung adenocarcinoma.

BACKGROUND: Our current study was performed with an attempt to detect the expression of microRNA-22-3p (miR-22-3p) in lung adenocarcinoma, as well as to analyze its role in clinical practice. In addition, its relationship with vascular endothelial growth factor (VEGF) and metastasis related indexes was focused. MATERIAL AND METHOD: The trials in which 62 cases of lung adenocarcinoma were received to collect tumor tissue (study group) and normal lung tissue (control group) were eligible for this study. The expression of miR-22-3p in the two groups was detected through RT-PCR. Immunohistochemical method was used to detect the expression of VEGF and leukocyte differentiation antigen 31 (CD31) marked microvessel density (MVD) in lung adenocarcinoma. The expressions of matrix metalloproteinase-3 (MMP-3) and matrix metalloproteinase-7 (MMP-7) in lung adenocarcinoma were also detected through the use of Western Blot. RESULTS: The present study revealed significant difference in the expression of miR-22-3p between the two groups. No significant difference in the expression of gender, age, neural invasion and the number of lesions were observed between groups. There was significant difference in the expression of miR-22-3p in the maximum diameter of tumor, pleural recidivism, vascular recidivism, lymph node metastasis and different TNM stages. Based on survival analysis, miR-22-3p was linked to survival time. Correlation analysis indicated that there was negative correlation between miR-22-3p and VEGF, miR-22-3p and MVD, miR-22-3p and MMP-3, and miR-22-3p and MMP-7 in lung adenocarcinoma. CONCLUSION: Our findings provide evidence that miR-22-3p is low expressed in lung adenocarcinoma tissues and the low expression of miR-22-3p is closely associated with clinicopathological characteristics and the prognosis. MiR-22-3p may be involved in the tumor progression of lung adenocarcinoma and may serve as a biomarker for the diagnosis and prognosis of lung adenocarcinoma.

Transcriptional activation of insulin-like growth factor binding protein 6 by 17beta-estradiol in SaOS-2 cells.

Osteoblasts can synthesize the insulin-like growth factors (IGFs) and the IGF-binding proteins (IGFBPs), which may either enhance or attenuate IGF-stimulated bone cell proliferation. Since estrogen induced osteoblastic differentiation and proliferation through an estrogen-responsive gene in target cells, we investigated the effects of estrogen on IGFBP-6 expression in the human osteoblastic-like cell line SaOS-2. Expressions of IGFBP-6 protein and mRNA increased 2.8 and 2-fold, respectively, in the presence of 17-beta-estradiol (E2) (0.01 to 1 micronM) and estrogen receptor (ER) in SaOS-2 cells. On the other hand, E2 induced a 2-fold increase in SaOS-2 cell proliferation. To identify genomic sequences associated with estrogen responsiveness, the 5'-promoter region (-44 to +118) of the IGFBP-6 gene was cloned into a chloramphenicol acetyltransferase (CAT) reporter vector. E2 induced a 3-fold increase in CAT activity in SaOS-2 cells transiently transfected with this construct. Identification of the estrogen-responsive element (ERE) [5-CCTTCA CCTG-3] (-9 to +1) in this IGFBP-6 gene promoter region was confirmed using electromobility shift assays and deletion analysis. This functional ERE was important for E2-induced trans-activation of the IGFBP-6 gene. These results demonstrate that E2 exhibits a positive effect on IGFBP-6 gene transcription through estrogen-liganded ER binding to the functional ERE in the IGFBP-6 gene promoter in SaOS-2 cells.

Molecular construction, characterization, and photophysical properties of supramolecular lanthanide-calix[4]arene covalently bonded hybrid systems.

Hydroxyl groups of the macrocyclic compound p-tert-butylcalix[4]arene have been converted into urethanesil (-NH(C=O)O-)-grafted bridges through a hydrogen transfer nucleophilic addition reaction. Subsequently, the modified macrocyclic derivative can coordinate to lanthanide ions (Tb, Eu) effectively and form a hybrid framework after the cohydrolysis and copolycondensation process through the triethoxysilane components. The above sol-gel-derived inorganic-organic supramolecular hybrids are analyzed under infrared spectroscopy, ultraviolet absorption, and luminescence spectroscopy for interpretation of their photophysical properties. Spectroscopic data point out that the modified calix[4]arene could sensitize diverse lanthanide ions to exhibit attractive green and red luminescence. It is noted that the triplet energy level of this particular macrocyclic bridged ligand is more suitable for the emissive energy level of Tb(3+) ions than the Eu(3+) ions. The luminescent lifetimes and quantum yields of europium hybrids are discussed, and the number of water molecules coordinated to Eu(3+) is estimated.

Placental transmogrification of the lung: Case report and systematic review of the literature.

OBJECTIVE: Placental transmogrification of the lung (PTL) is rare cystic lesion. Thus, we summarized the characteristics of PTL to explore the strategy of diagnosis and treatment. METHODS: Two patients pathologically confirmed PTL were treated in our hospital. Retrospectively analysis was performed on such 2 cases and 34 cases of PTL reported in abroad. The basic information and clinical characteristics from each patient were gathered and analyzed. RESULTS: The imaging findings of 2 patients were the pulmonary solid mass with peripheral multiple pulmonary bullae. After the improvement of preoperative examination and the multidisciplinary discussion of thoracic surgery, respiration, imaging, and anesthesia, the possibility of benign pulmonary lesions was improved in all cases. Thoracoscopic lobectomy was carried out under general anesthesia, and the intraoperative frozen pathology showed bullae of lung. Ultimately, PTL was confirmed by paraffin pathological diagnosis. Both 2 PTL patients had satisfied recovery without obvious complications or imaging abnormalities. In addition, the literature review of 34 PTL cases from PubMed database was summarized between 1995 and 2015. A total of 36 patients were retrospectively analyzed in our study. The age of 34 cases ranged from 24 to 72 years (an average age of 45.6 ±â€Š13.5 years). Among these, 8 cases were no obvious symptoms. In addition, the other 25 cases had respiratory symptoms such as chest tightness, cough, and chest pain. Moreover, the mean size of pulmonary bulla was 6.5 ±â€Š5.5 cm. The size of the solid lesions in 23 cases was 3.3 ±â€Š3.4 cm (ranging from 0.5 to 15). The follow-up period was 2 to 96 months (average 27.3 ±â€Š29.8 months). CONCLUSION: Early diagnosis and surgical operation of PTL should be performed as soon as possible. These lesions are best treated by minimally invasive surgery, so as to preserve more normal lung tissue and avoid the pneumonectomy.

Ectopic adrenocorticotropic hormone syndrome caused by neuroendocrine tumors of the thymus: 30-year experience with 16 patients at a single institute in the People's Republic of China.

BACKGROUND AND PURPOSE: Thymic neuroendocrine carcinomas (TNECs) are extremely uncommon. Certain cases of TNECs can produce the adrenocorticotropic hormone (ACTH) and cause ectopic ACTH syndrome (EAS). The current literature on this topic consists mainly of case reports, and therapeutic guidelines are lacking. The aim of this study was to discuss the diagnosis, surgical management, and prognosis of EAS caused by TNECs to improve clinical experience with this rare disease. METHODS: From June 1984 to June 2014, at the Peking Union Medical College Hospital, the surgical interventions and follow-up outcomes of 16 consecutive patients (eight men and eight women) with EAS caused by TNECs were retrospectively analyzed. RESULTS: The median age was 32.5 years (range: 13-47 years), and the median disease duration was 8.5 months (range: 1-150 months). All patients presented with clinical and biochemical evidence indicating a diagnosis of Cushing's syndrome. Contrast-enhanced thoracic computed tomography scans were critical to locating the ACTH-producing tumor and evaluating the feasibility of resection. All patients underwent surgery. One patient died of septicemia in the intensive care unit 2 weeks after surgery. No other morbidity or mortality occurred during the perioperative period. The median overall survival (OS) was 41 months (95% CI: 30.3-51.7 months), and the progression-free survival was 28 months (95% CI: 21.6-34.3 months). Both overall survival (P=0.002) and progression-free survival (P=0.030) improved significantly after complete resection. CONCLUSION: TNEC is an extremely aggressive disease that should be considered when treating patients with Cushing's syndrome due to ectopic ACTH secretion. In particular, all suspected patients should undergo contrast-enhanced thoracic computed tomography scans to facilitate early diagnosis. The current first-line treatment is surgical resection, and complete resection is a favorable prognostic factor. However, additional patients and a longer follow-up will be needed to determine the variables that are predictive of survival and to improve patient prognosis.

Protein expression under sustained activation of signal transducer and activator of transcription-3 in diethylnitrosamine-induced rat liver carcinogenesis.

The aim of the present study was to investigate the expression of proteins associated with the sustained activation of the signal transducer and activator of transcription (STAT)-3 pathway during diethylnitrosamine (DEN)-induced rat liver carcinogenesis. DEN was intermittently administered to rats to induce liver cancer, and light and electron microscopy were used to observe the morphological changes in the liver during carcinogenesis. Western blotting and quantitative polymerase chain reaction (qPCR) were used to detect the expression of STAT-3, phosphorylated (p)-STAT-3, matrix metalloproteinase (MMP)-10, vascular endothelial growth factor (VEGF), kinase insert domain receptor (KDR), hypoxia inducible factor (HIF)-1α, basic fibroblast growth factor (bFGF) and interleukin (IL)-10, in order to investigate the association between STAT-3 and p-STAT-3 expression and MMP-10, VEGF, KDR, HIF-1α, bFGF and IL-10. The western blotting and qPCR results revealed that the expression of STAT-3, p-STAT-3, MMP-10, VEGF, KDR, HIF-1α, bFGF and IL-10 proteins gradually increased during carcinogenesis. Furthermore, the STAT-3 and p-STAT-3 levels were found to positively correlate with MMP-10, VEGF, KDR, HIF-1α, bFGF and IL-10 protein expression. During DEN-induced rat liver carcinogenesis, STAT-3 protein continually activated MMP-10, VEGF, KDR, HIF-1α, bFGF and IL-10, and its expression was found to positively correlate with the expression of these proteins.

Endoplasmic reticulum stress in diethylnitrosamine-induced rat liver cancer.

To analyze the significance of endoplasmic reticulum stress (ERS) in the development of diethylnitrosamine (DEN)-induced liver cancer in rats, critical regulatory factors in ERS signaling pathways were investigated in the present study. The results showed that the expression of ERS-related proteins gradually increased in the early and mid-term stages of carcinogenesis, while in the later stages, the expression of these proteins did not change significantly after reaching a peak. ERS is involved in DEN-induced rat liver injury, the proliferation of liver cells and the occurrence and development of liver cirrhosis. However, ERS did not affect hepatoma cell growth following the formation of rat liver cancer in the current study.

Rapid high-performance liquid chromatography method for determination of tryptophan in gastric juice.

OBJECTIVE: To develop a rapid, high-performance liquid chromatography (HPLC) method for the determination of tryptophan in gastric juice to help the differentiation between gastric cancer and benign gastric disease. METHODS: HPLC was performed on a restricted access material Shiseido Capcell Pak MF SCX SG80 column. Phosphate buffered solution (90mmol/L, pH 3.5)-acetonitrile (ACN; 80/20, V/V) was chosen as the mobile phase. Separation was done at room temperature using a constant flow rate of 1.0mL/min. Fluorescence emission signal intensity at 330nm excited by 288nm ultra violet light was detected and measured. RESULTS: Thirty-eight gastric juice samples from patients with gastric cancer and 48 gastric juice samples of patients with benign gastric disease were tested. A linear relationship in the range of 0.20-100mg/L was obtained between the concentration of tryptophan and its fluorescence emission signal intensity at 330nm. The limit of detection was 0.05mg/L. The recovery rate was 77.4-90.6%. CONCLUSIONS: An HPLC method based on strong cation-exchange restricted access columns for determination of concentration of tryptophan in gastric juice was developed. The method has excellent precision and stability. It is compatible with the analysis of gastric juice and has the potential to be used for gastric cancer screening.