Identification of NR3C2 as a functional diagnostic and prognostic biomarker and potential therapeutic target in non-small cell lung cancer.

Background: Non-small cell lung cancer (NSCLC), including the lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) subtypes, is a malignant tumor type with a poor 5-year survival rate. The identification of new powerful diagnostic biomarkers, prognostic biomarkers, and potential therapeutic targets in NSCLC is urgently required. Methods: The UCSC Xena, UALCAN, and GEO databases were used to screen and analyze differentially expressed genes, regulatory modes, and genetic/epigenetic alterations in NSCLC. The UCSC Xena database, GEO database, tissue microarray, and immunohistochemistry staining analyses were used to evaluate the diagnostic and prognostic values. Gain-of-function assays were performed to examine the roles. The ESTIMATE, TIMER, Linked Omics, STRING, and DAVID algorithms were used to analyze potential molecular mechanisms. Results: NR3C2 was identified as a potentially important molecule in NSCLC. NR3C2 is expressed at low levels in NSCLC, LUAD, and LUSC tissues, which is significantly related to the clinical indexes of these patients. Receiver operating characteristic curve analysis suggests that the altered NR3C2 expression patterns have diagnostic value in NSCLC, LUAD, and especially LUSC patients. Decreased NR3C2 expression levels can help predict poor prognosis in NSCLC and LUAD patients but not in LUSC patients. These results have been confirmed both with database analysis and real-world clinical samples on a tissue microarray. Copy number variation contributes to low NR3C2 expression levels in NSCLC and LUAD, while promoter DNA methylation is involved in its downregulation in LUSC. Two NR3C2 promoter methylation sites have high sensitivity and specificity for LUSC diagnosis with clinical application potential. NR3C2 may be a key participant in NSCLC development and progression and is closely associated with the tumor microenvironment and immune cell infiltration. NR3C2 co-expressed genes are involved in many cancer-related signaling pathways, further supporting a potentially significant role of NR3C2 in NSCLC. Conclusions: NR3C2 is a novel potential diagnostic and prognostic biomarker and therapeutic target in NSCLC.

Development of a fluorescent probe for detecting Al3+ in cooked wheaten food based on phosphonic acid group functionalized polythiophene derivatives.

As an unnecessary trace element, the content of aluminium in biological systems should be strictly controlled. Therefore, it was necessary to develop a convenient method for detection of aluminium ions. In this study, a fluorescent probe based on polythiophene derivatives was developed and used to detect Al3+ in Chinese traditional pasta. The fluorescence of this probe showed a significant decrease in hexamethylenetetramine-HCl buffer solution (pH 5) when Al3+ was present. In addition, the probe exhibited good sensitivity and selectivity to Al3+ over other metal ions when EDTA was used as the masking agent. Fluorescence intensity had a good linear relationship with the Al3+ concentration in the range 0.1-10 µM and the limit of detection for Al3+ was 39 nM. Furthermore, the probe was successfully applied to detect Al3+ in food samples and the results were consistent with ICP-AES.

Role of TG2 and TGF-ß1 in the pathogenesis of human breast cancer.

The present study analyzed the role of transforming growth factor-ß1 (TGF-ß1) and tissue transglutaminase (TG2) in breast cancer, as well as their protein levels in MCF-7 cells treated with cisplatin. In addition, the present study investigated the effects of TG2 and TGF-ß1 in MCF-7 cells following TGF-ß1 and TG2 inhibition or TGF-ß1 induction. The protein levels of TG2 and TGF-ß1 in breast cancer tissues and in MCF-7 cells treated with cisplatin, TG2 and TGF-ß1 inhibitors or 10 ng/ml TGF-ß1 were analyzed by immunohistochemical staining, immunofluorescence and western blotting. The results revealed that the expression levels of TG2 and TGF-ß1 in breast cancer tissues were significantly higher compared with those in paracancerous tissues. The fluorescence intensity of TG2 and TGF-ß1 in MCF-7 cells treated with cisplatin was lower compared with that in untreated MCF-7 cells. Using bioinformatics analysis, the present study predicted that TGF-ß1 may be associated with TG2. In addition, the expression levels of TGF-ß1 and TG2 in MCF-7 cells treated with inhibitors of TGF-ß1 and TG2 were lower compared with those in untreated MCF-7 cells. By contrast, the expression levels of TGF-ß1 and TG2 in MCF-7 cells treated with TGF-ß1 were higher compared with those in untreated MCF-7 cells. Therefore, the present study demonstrated that TGF-ß1 and TG2 may serve an important role in breast cancer tissues and in MCF-7 cells. In addition, it was revealed that TG2 and TGF-ß1 may have a synergistic role in MCF-7 cells.

[Effects of Cyclin A1 on the Proliferation of SKM-1 Cells and Its Potential Role in Myelodysplastic Syndrome].

OBJECTIVE: To investigate the effects of Cyclin A1 on the proliferation of SKM-1 cells and its underlying role in myelodysplastic syndrome (MDS). METHODS: Cyclin A1 was knocked down with its small interfering RNA (siRNA). The efficiency of siRNA transfection was measured by Western blot and RT-PCR. Then the proliferation of SKM-1 cells and the expression of CDK2,RUNX1 and SRSF2 with and without knockdown of Cyclin A1 recorded and analysed respectively. RESULTS: Cyclin A1 was knocked down by siRNA after transfected for 48 h. The kncokdown of Cyclin A1 inhibited the proliferation of SKM-1 cells and down-regulated the expression of CDK2, RUNX1 and SRSF2, and these effects were at least partially mediated through RUNX1 and SRSF2 signaling pathway. CONCLUSION: Cyclin A1 plays an important role in the proliferation of SKM-1 cells. These findings provide new insights into the pathogenesis of MDS, and it may be a potential target in the treatment of MDS.

A case of lower digestive tract hemorrhage caused by appendicitis in China.

In this case, we report a case of lower digestive tract hemorrhage caused by appendicitis in China. An 46-year-old Chinese male was sent to China-Japan union Hospital of Jilin University with abdominal pain in 2015. The patient was diagnosed with anemia. In this report, the appendix of patient was excised by laparoscopic surgery. The patient's colonoscopy results showed patient could be seen a large number of dark red blood and fresh blood in the intestinal cavity. The patient's colon position found focal mucosal shedding, shallow ulcer formation. As last, the patient was successfully performed and reduced the patient's pain by laparoscopic surgery.

Analysis of the effect of rutin on GSK-3ß and TNF-α expression in lung cancer.

The aim of the present study was to investigate the effect of rutin treatment on the expression of glycogen synthase kinase (GSK)-3ß and tumor necrosis factor (TNF)-α in A549 human lung carcinoma cells. The A549 cells were divided into control, cisplatin and rutin (low, middle and high) groups. ELISA and western blot analysis of TNF-α expression, 4',6-diamino-2-phenylindole (DAPI) staining and GSK-3ß immunofluorescence staining were used to investigate the effect of rutin in the human lung carcinoma cells, using cisplatin as a positive control. TNF-α expression was significantly higher in the rutin and cisplatin groups compared with the control group. Additionally, DAPI staining revealed that the number of apoptotic cells was higher in the rutin and cisplatin groups compared with the control group, and immunofluorescence showed that the expression of GSK-3ß in the cisplatin and rutin groups was significantly higher compared with that in the control group. The results of the present study suggest that rutin promotes the TNF-α-induced apoptosis of A549 human lung carcinoma cells. Furthermore, rutin may be able to regulate the expression of GSK-3ß protein in these cells.

Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy.

The present study investigated the effect of rutin on high glucose-induced actin, α2, smooth muscle, aorta (ACTA2) and p38 protein expression in diabetic nephropathy (DN). Human mesangial cells were divided into a control group, high glucose-induced mesangial cell group, high glucose + captopril group, and high glucose + rutin group (low, middle and high doses of rutin). Cell viability, adenosine 5'-triphosphate (ATP) content, cell cycle, and ACTA2 and p38 protein expression were examined using MTT assay, ATP assay kit, flow cytometry and immunofluorescence staining in cultured human mesangial cells, respectively. Cell viability, ATP content, and ACTA2 and p38 expression increased significantly in high glucose-induced mesangial cells (P<0.05). However, at concentrations of 0.2, 0.4 and 0.8 µmol/l rutin was able to inhibit high glucose-induced human mesangial cell viability, ATP content, and ACTA2 and p38 expression and improve the cell cycle progression of mesangial cells. In conclusion, ACTA2 and p38 proteins may have important roles in DN. Rutin may inhibit the expression of ACTA2 and p38 and may be utilized in the prevention and treatment of DN.

A case of abdominal enteric cyst in China.

To investigate a case of abdominal enteric cyst in China. The patient was admitted to the china-Japan Friendship Hospital of Jilin University, which was due to intermittent pain in the left side for the last 4 months. In this surgery, CT was used to diagnose the basic condition of the patient. Surgery was used for Treatment of patients with diseases. As soon as patients have been successfully operated by laparoscopic surgery.

A case of IV degree on acute radiation dermatitis in China.

This report investigates the nursing procedure of a case of adjuvant therapy of rectal cancer on IV degree of acute radiation dermatitis patients in the penis and scrotum junction. The lesion degree gradually increased. Fixation of the dressing was difficult in the penis and scrotum junction. The concept of wet healing with new dressings was used in patient. The silver ion dressings were used in inhibiting infection, and the wound was covered by the rimmed foam dressings. When it comes to the shaping period, water gel transparent paste was applied instead to cover the wound. The patient was just into the surgical treatment in the wound healed after six days.

A case of obturator hernia leading to right thigh abscess in China.

The purpose of this case is to investigate a case of obturator hernia leading to right thigh abscess on 68-year-old woman of China. A 68-year-old Chinese woman was referred to China-Japan Friendship Hospital of Jilin University with abdominal pain, bloating, exhaust, stop defecation in 2011. She had chronic bronchitis, emphysema with a history of 20 years. This patient did not have any bad habits, such as smoking, alcohol consumption, etc. In this surgery, CT was used to diagnose the basic condition of the patient. Surgery was used for treatment of patients with diseases. In addition, this operation was performed by the china-Japan Friendship Hospital of Jilin University. The results of this case showed that the cervix of rectal right anterior wall can hit a funicular neoplasm, toughening, smooth, with tenderness, considering for the external pressure bowel loops. The inside of the right thigh showed obvious swelling, skin slightly bruising, and tenderness. Chest radiographs showed that patients had emphysema, multiple planes of fluid and air in the abdomen. Patients had been successfully operated, but she died because of severe infection.

Role of tissue transglutaminase in the pathogenesis of diabetic cardiomyopathy and the intervention effect of rutin.

The aim of this study was to investigate the role of tissue transglutaminase (tTG) in the pathogenesis of diabetic cardiomyopathy (DCM) and the intervention effect of rutin. DCM was induced in rats by the injection of streptozotocin (STZ; 25 mg/kg). After a preliminary examination, the rats were randomly divided into four groups: Control (n=8), STZ-induced DCM (n=8), STZ + positive drug (captopril; n=6) and STZ + rutin (n=8) groups. The DCM model was evaluated using blood sugar values, serum enzyme levels, hematoxylin and eosin staining and Masson's staining, ex vivo. The protein and mRNA expression of tTG was assessed with immunohistochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The rat model of DCM was successfully established by STZ administration, and the expression levels of tTG were significantly increased in the DCM model. Following the injection of captopril or rutin, the blood sugar values, collagen content and expression levels of tTG were gradually reduced and serum enzyme levels were increased, as compared with those in the STZ-induced DCM group. In conclusion, tTG plays an important role in STZ-induced DCM. In addition, rutin may inhibit the expression of tTG and regulate myocardial injury in STZ-induced DCM.

Role of TGF-ß1 in human colorectal cancer and effects after cantharidinate intervention.

Effects of transforming growth factor-beta (TGF-ß) were investigated in human colorectal cancer, and the influence of cantharidinate in inhibiting TGF-ß1 expression was explored. Relationships among TGF-ß1 and sex, age, tumor size, tumor location, tumor stage were also analyzed. H and E and immunohistochemistry staining were employed to assess colorectal cancer and TGF-ß1 expression, respectively. Then, HCT-116 CRC cells were randomly divided into four groups, controls, no serum-treated, chemotherapy and cantharidinate-treated. Immunohistochemistry and real-time PCR were employed to assess the expression of TGF-ß1 in CRC cells. Our data showed that the expression of TGF-ß1 might be associated with tumor size and tumor location (P<0.05). The expression of TGF-ß1 in CRC groups was higher than in adjacent groups (P<0.05). In addition, the expression of TGF-ß1 in cantharidinate-treated group was much lower than in CRC group (P<0.05). Taken together, these results suggest that TGF-ß1 plays an important role in CRC development. Cantharidinate might inhibit the expression of TGF-ß1 and control the development of colorectal cancer.

Role of S100A3 in human colorectal cancer and the anticancer effect of cantharidinate.

Colorectal cancer (CRC) is a leading cause of cancer-related mortality. The early diagnosis and treatment of CRC is the key to improving the survival of patients who may benefit from adjuvant chemotherapy. In the present study, the protein expression of S100A3 was observed in a cohort of 20 patients with cancer, which indicated that S100A3 activation was involved in tumorigenesis. In addition, the anticancer activity of cantharidinate was investigated using immunohistochemistry and quantitative polymerase chain reaction (qPCR) analysis. The protein expression of S100A3 was observed to increase by 2.4-fold in human CRC cells compared with the expression level in normal control cells (P<0.01). Cantharidinate inhibited the protein and gene expression of S100A3 in UCT-116 human CRC cells in vitro. These results suggested that S100A3 is important in human CRC. Cantharidinate has the potential to be considered as a novel adjuvant drug for controlling the expression of S100A3 in human CRC as it exhibits preventive effects.

Role of tissue transglutaminase and effect of cantharidinate in human colorectal cancer.

The role of tissue transglutaminase (tTG) in cancer development remains an important field of study. The aim of the current study was to understand the involvement of tTG in cancer and the inhibitory effect of cantharidinate on the expression of tTG in human colorectal cancer (CRC) using immunohistochemical and PCR analysis. The results showed that the expression of tTG increased in human CRC and cantharidinate inhibited the expression of tTG. These results suggested that tTG is significant in human CRC and that tTG may be an important target for tumor chemoprevention and treatment. Cantharidinate may be considered as a novel co­therapy for controlling tTG expression in human CRC.

The urotensin II receptor antagonist, urantide, protects against atherosclerosis in rats.

The aim of this study was to explore the use of urantide as an antagonist of the urotensin II (UII) receptor, G protein-coupled receptor 14 (GPR14), to protect against atherosclerosis (AS) in rats. The AS rat model was induced by an intraperitoneal injection of vitamin D3 (VD3) into rats fed with a high-fat diet for four weeks. Urantide was then injected into the rats. Immunohistochemical staining, serum biochemical assay, reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to investigate the expression of UII and its receptor GPR14 in the AS rat model. Four weeks after induction, pathological changes typical of AS were observed in the AS rat model. In the plaques of the aortic tunica intima and tunica media, expression of UII and GPR14 was observed. The protein and gene expression levels of UII and GPR14 in the model group were significantly increased compared with those in the normal group (P<0.01). Urantide ameliorated the pathological changes of AS in the rat model and reduced the gene and protein expression levels of UII and GPR14 (P<0.05 or P<0.01). UII is associated with AS and the UII receptor GPR14-specific antagonist, urantide, demonstrates the ability to protect against AS. Thus, this study provides new insight and experimental theories for the clinical application of urantide to treat AS.

The role of the Rho/Rock signaling pathway in the pathogenesis of acute ischemic myocardial fibrosis in rat models.

The aim of this study was to investigate the role of the Rho/Rho associated coiled coil-forming protein kinase (Rock) signaling pathway in the pathogenesis of ischemic myocardial fibrosis (MF) in rats. The MF rat model was established using isoprenaline hydrochloride (ISO, 15 mg/kg). Rats were randomly divided into ten groups: a control group and ISO-treated groups at 2 h, 4 h, 6 h, 12 h, 24 h, 48 h, 72 h, 7 days and 21 days. The MF model was evaluated by serum enzyme levels, hematoxylin and eosin (H&E) staining and Masson's staining, ex vivo. The mRNA expression of RhoA and Rock I was assessed with reverse transcription-polymerase chain reaction (RT-PCR). The cell type was evaluated by immunofluorescent and immunohistochemical staining. The protein expression of Rock I was evaluated using western blotting and immunohistochemistry. MF was found to be more developed in the ISO-treated group compared with the control group. CD31 and vimentin expression in fibroblasts and endothelial cells were significantly increased. In addition, the mRNA and protein levels of RhoA and Rock I were significantly increased. In conclusion, activation of Rho/Rock accelerates the degree of ischemic MF. Inhibition of Rho/Rock may be a novel therapeutic strategy for the prevention of ischemic MF.

Apoptosis of colorectal cancer UTC116 cells induced by Cantharidinate.

Effects of Cantharidinate on apoptosis of human colorectal cancer UTC-116 cells were investigated by means of 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, H and E staining, flow cytometry, and Raman Spectra analysis. The results showed Cantharidinate to exert inhibitory action on proliferation of human colorectal cancer UTC-116 cells, inducing apoptosis, arresting cells in G1 phase, with decline of S and G2 phases. In addition, the results of Raman spectrum showed significant changes in the UTC-116 cells chemical structure with stretching after the application of Cantharidinate. Taken together, these results suggest that the treatment of human colorectal cancer with Cantharidinate may be associated with multiple molecular mechanisms for apoptosis. Furthermore, similar to fluorouracil, Cantharidinate should be considered as novel assistant drug for controlling the growth of human colorectal cancer UTC-116 cells.

[Expression and implication of angiotensin II type 1 receptor in myocardial fibrosis of rats].

OBJECTIVE: To investigate the expression and pathobiological implications of angiotensin II type 1 receptor (AT1R) in development of myocardial fibrosis of rats. METHODS: Rat myocardial necrosis model was established using isoproterenol injection (15 mg/kg). Rat serum aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzymes (CK-MB) were detected by MD-100 automatic biochemical analyzer. Masson staining was used to evaluate the morphological changes. The expression of AT1R protein was determined by immunohistochemistry and its mRNA expression was analyzed by RT-PCR. The expression of collage type I and III was determined by immunohistochemistry. RESULTS: Serum LDH, CK and CK-MB reached their peaks at 4 h (chi2 = 16.90, P < 0.05), and AST achieved its peak in 6 h (chi2 = 16.90, P < 0.05). AT1R mRNA expression was increased 2 - 12 h after isoproterenol injection, but no statistical significance (P > 0.05) was observed comparing with the control. However, a significant AT1R mRNA increase was present at 24 h and decreased gradually after 48 h, and back to the control level after 3 weeks. Protein expression of AT1R increased proportionally with the severity of the fibrosis. CONCLUSIONS: AT1R mRNA and protein expressions increase significantly during myocardial ischemia, and is closely correlated with the fibrosis. These findings indicate that AT1R may play an important role in the pathogenesis of myocardial fibrosis.