Objective To investigate the surgical method of transnasal operations on the sphenoidal sinus and the middle fossa under nasal endoscope combined with microscope. Methods The operation was performed under nasal endoscope on the side of larger nasal cavity. The middle nasal turbinate was pushed outwards. Then the Handy's expander was inserted between the middle nasal turbinate and the nasal septum in order to get a wide visualization. The sphenoidal frontal wall was opened directly. The nasal endoscope and microscope were utilized in turn to complete the resection of lesions. Results The symptoms disappeared postoperatively in 10 cases of solitary sphenoidal sinusitis. The lesions of 6 cases of sphenoidal cyst and meningioma were all surgically removed on one session. Among 32 cases of pituitary adenoma, a total resection was carried out in 17 cases, a subtotal resection in 12 cases, and a partial resection in 3. After surgery, a supplemental X-knife radiosurgery was employed. Postoperative follow-up in the 48 cases for 0.5~3.5 years (mean, 2.5 years) showed no recurrence of sphenoidal cyst, sphenoidal sinusitis, or meningioma, and 3 cases of recurrence of pituitary adenoma. No intracranial infection, adhesion of nasal cavity, or nasal bleeding was noted. Conclusions Transnasal operations on the sphenoidal sinus and the middle fossa under nasal endoscope combined with microscope has advantages of mild invasion, little blood loss, short operation time, and good outcomes.

Aim To investigate glutamate-induced [ Ca2 + ] i changes in cultured rat neonatal cortical astrocytes after hypoxia/reoxygenation, H2O2 or high concentration of L-glutamate injury. In the meantime, the effects of Gingko biloba extract (GbE) were examined. Methods [ Ca2+ ]i changes in astrocytes were monitored by laser scanning confocal microscopy with the Ca2+ sensitive fluorescent probe [ Ca2 + ] i, but decrease by ( 3.3 ± 1.6) %, (81 ± 11 ) % and ( 81 ± 7 ) %, respectively. Pretreatment with H2O2 or high concentration of L-glutamate injury were ( 135 ± 98 ) %, ( 117 ± 93 ) % and ( 89 ± 36) %,different injury. Conclusion Hypoxia/reoxygenation, H2O2 and high concentration of L-glutamate impaired astrocytes' response to exogenous L-glutamate, and then bidirectional communication between astrocytes and neurons could not take place. GbE could improve the abnormal responses and maintain the normal function of astroglical network. These effects support that GbE has potential beneficial actions against brain injury.

The use-dependent characteristics of daurisoline on monophasic action potentials (MAP) of the left ventricle of the rabbit heart in situ were recorded with MAP recording technique. The results showed that daurisoline decreased monophasic action potential amplitude (MAPA) and prolonged monophasic action potential duration at the 50% and 90% (MAPD50, MAPD90), effective refractory period (ERP), ERP/MAPD90 at the steady-state cycle lengths of 240, 210, 180 ms. The percent of prolongation of MAPD50 was 12.8±2.9, 9.5±2.6, 9.0±1.6, that of MAPD90 was 10.9±2.6, 7.5±2.4, 6.5±2.7, that of ERP was 25.7±4.3, 18.5±4.1, 24.2±7.2, and that of ERP/MAPD90 was 13.7±4.5, 10.2±2.2, 16.1±5.1, respectively. Its effect showed no relation to frequency (n=6, P>0.05). The effects of sotalol on MAP were similar to that of daurisoline, but it prolonged MAPD90 and ERP in a reverse use-dependent manner (P<0.05). It is concluded that daurisoline has no use-dependent effects on MAP of rabbit hearts.

Objective To observe the correlation between long-term chronic pharyngitis and rheumatic heart vavular disease (RHD) caused by to long-term latent chronic rheumatic activity and to understand the progressive course of rheumatic heart vavular disease. Methods In 1126 cases with chronic pharyngitis, 319 cases with serum antistreptolysin O (ASO) level between 400-500 U/ml were followed-up. ASO, creatine kinase enzyme MB (CK-MB) and echocardiography were measured for follow-up since 1986. Of the 319 cases, 158 were male and 161 were female with the average age of 29.4 years old. By the end of 2009, 6 cases were lost during follow up, data of 313 cases including 155 male patients and 158 female patients whose average age was 49.6 were analyzed. As the number of every kind of rheumatic heart vavular lesion was so fewer for statistical analysis that the data were only listed in tables. The student's t test was performed to compare of the ASO, CK-MB between the group with vavular lesionss and the group without vavular lesion. Results ①Of the 313 cases, 9 cases suffered from rheumatic fever at the fourth year since 1986, and 29 cases had rheumatic fever 1, 2 or 3 years after the ASOs decreased to lower than 400 U/ml and no one developed heart valvular lesion.②Two hundred and seventy-five cases whose ASO in the range of 400-500 U/ml but with normal CK-MB were found by the end of 5, 10, 15, 20 years, 9, 42, 65, 78 cases had developed heart vavular diseases respectively. ③ The levels of CK-MB in the heart valvular disease groups were significantly higher than those in the non-vavular disease group, while the levels of ASO were not. Conclusion Some of the cases suffering from long-term chronic pharyngitis can have high levels of ASO, but with normal CK-MB. These patients may have latent long-term chronic rheumatic activity and develop rheumatic heart valvular disease years later.

Stenosis with 55.2% cross section area reduction was introduced into the rabbit aorta. Using Evans blue dye and scanning microscope, we observed the morphology of endothelial cells and the permeability of endothelium to albumin in the stenotic aorta. Numerical simulation of blood flow in the stenotic aorta was performed to obtain the distribution of wall shear rate. The results showed that in the immediately proximal and distal vicinity of stenosis, blood flow was disturbed significantly, resulting in apparent changes in the morphology of endothelial cells and the permeability of endothelium to albumin. These changes were not only attributed to the value of wall shear stress, but also attributed to the flow pattern in the stenosis. The result therefore is in good consistent with the clinical observation that atherosclerosis often occurs in the areas where blood flow is disturbed and flow separation occurs.
Animals ; Aorta, Abdominal ; pathology ; Aortic Diseases ; pathology ; physiopathology ; Atherosclerosis ; etiology ; physiopathology ; Blood Flow Velocity ; Blood Pressure ; Capillary Permeability ; Constriction, Pathologic ; Endothelium, Vascular ; pathology ; physiology ; Hemodynamics ; physiology ; Hemorheology ; methods ; Male ; Models, Cardiovascular ; Permeability ; Pulsatile Flow ; physiology ; Rabbits ; Stress, Mechanical ; Tensile Strength

The effects of Arecoline (Are) on calcium mobilization were investigated. In isolated single ventricular myocyte of guinea pig, patch clamp whole cell recording techniques were used to record the current of L-type calcium channel and cytosolic Ca2+ level ([Ca2+]i) labeled with fluorescence probe Fluo-3/AM was measured under a laser scanning confocal microscope. Results revealed that Are (3-100 mumol/L) could inhibit L-type calcium current in a concentration-dependent manner and the value of IC50 was 33.73 mumol/L (n = 5). In the absence of extracellular calcium, the resting levels of [Ca2+]i was not affected by Are (n = 6, P > 0.05), but pretreatment with Are (30 mumol/L) could significantly inhibit the [Ca2+]i elevation induced by caffeine (10 mmol/L, n = 6, P < 0.01). It was concluded that Are could inhibit not only calcium influx through L-type calcium channel but also calcium release from sarcoplasmic reticulum.
Animals ; Arecoline ; pharmacology ; Biological Transport, Active ; Caffeine ; pharmacology ; Calcium ; metabolism ; Calcium Channels, L-Type ; drug effects ; metabolism ; Cell Separation ; Cholinergic Agonists ; pharmacology ; Guinea Pigs ; Heart Ventricles ; cytology ; Myocytes, Cardiac ; cytology ; metabolism ; Patch-Clamp Techniques ; Sarcoplasmic Reticulum ; metabolism

OBJECTIVE: To investigate the effect of intranasal glucocorticoids treatment on the expression of c-fos and c-myc nasal polyps. METHOD: Immunohistochemistry method was used to determine c-fos and c-myc expression in nasal polyps from patients with topical steroids treatment for 10-12 weeks and untreated patients. RESULT: The rate of c-fos expressing cases was 15% and the rate of c-myc expressing cases was 20% in nasal polyps from topical steroid treated patients, but in untreated patients, the rate of c-fos expressing cases was 80% and the rate of c-myc expressing cases was 85%. There were significant differences between two groups (P < 0.01). The c-fos and c-myc expression was remarkably downregulated in nasal polyps from topical steroid treated patients compared to untreated patients. CONCLUSION The results show that glucocorticoids may induce cell apoptosis in nasal polyps by depressing the c-fos and c-myc expression.
Adult ; Budesonide ; administration & dosage ; therapeutic use ; Case-Control Studies ; Female ; Glucocorticoids ; therapeutic use ; Humans ; Male ; Nasal Polyps ; drug therapy ; metabolism ; Proto-Oncogene Proteins c-fos ; metabolism ; Proto-Oncogene Proteins c-myc ; metabolism

OBJECTIVE: To investigate the inhibitory effect of epidermal growth factor receptor tyrosine kinase inhibitor (EGFRTKI) HS-10296 on the proliferation of triple-negative breast cancer (TNBC) MDA-MB-231 cells and explore the possible molecular mechanism. METHODS: MDA-MB-231 cells were treated with HS-10296 for 24, 48, or 72 h, and CCK-8 assay was used to assess the changes in the cell viability. The inhibitory effect of HS-10296 on cell proliferation was determined by clonogenic assay. JC-1 and flow cytometry were employed for analyzing the cell apoptosis, and the ultrastructure of the cells was observed under electron microscope. After pretreatment with autophagy inhibitor chloroquine (CQ), MDA-MB-231 cells were divided into control group, CQ treatment group, HS-10296 (4 and 6 μmol/L) treatment groups and combined treatment groups, and the sensitivity of the treated cells to HS-10296 was determined using CCK-8 assay. The effects of HS-10296 on EGFR pathway and apoptosis- and autophagy-related proteins in MDA-MB-231 cells were investigated using Western blotting. RESULTS: HS-10296 significantly inhibited the proliferation of MDA-MB-231 cells with IC values at 24, 48 and 72 h of 8.393, 2.777 and 2.016 μmol/L, respectively. JC-1 and flow cytometry showed that HS-10296 induced obvious apoptosis of MDA-MB-231 cells, which showed an apoptosis rate of (21.63 ± 2.97)% following treatment with 8 μmol/L HS-10296. Autophagy vesicles were observed in the cells treated with HS-10296 under electron microscope. In MDA-MB-231 cells pretreated with CQ, inhibition of autophagy significantly enhanced HS-10296-induced cell death. Western blotting showed that the apoptosis-related protein caspase-3 was activated after HS-10296 treatment to cut its substrate PARP. The expression of autophagy-related protein light chain 3B (LC3B) was significantly enhanced after HS-10296 treatment ( < 0.01), which also resulted in inhibited phosphorylation of EGFR and AKT proteins in the cells. CONCLUSIONS HS-10296 can inhibit the proliferation and induce autophagy and apoptosis of MDA-MB-231 cells by inhibiting the EGFR/PI3K/AKT signaling pathway.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Autophagy ; drug effects ; Breast Neoplasms ; drug therapy ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; ErbB Receptors ; metabolism ; Humans ; Protein Kinase Inhibitors ; pharmacology ; Signal Transduction ; drug effects

OBJECTIVE: To investigate the inhibitory effect of epidermal growth factor receptor tyrosine kinase inhibitor (EGFRTKI) HS-10296 on the proliferation of triple-negative breast cancer (TNBC) MDA-MB-231 cells and explore the possible molecular mechanism. METHODS: MDA-MB-231 cells were treated with HS-10296 for 24, 48, or 72 h, and CCK-8 assay was used to assess the changes in the cell viability. The inhibitory effect of HS-10296 on cell proliferation was determined by clonogenic assay. JC-1 and flow cytometry were employed for analyzing the cell apoptosis, and the ultrastructure of the cells was observed under electron microscope. After pretreatment with autophagy inhibitor chloroquine (CQ), MDA-MB-231 cells were divided into control group, CQ treatment group, HS-10296 (4 and 6 μmol/L) treatment groups and combined treatment groups, and the sensitivity of the treated cells to HS-10296 was determined using CCK-8 assay. The effects of HS-10296 on EGFR pathway and apoptosis- and autophagy-related proteins in MDA-MB-231 cells were investigated using Western blotting. RESULTS: HS-10296 significantly inhibited the proliferation of MDA-MB-231 cells with IC values at 24, 48 and 72 h of 8.393, 2.777 and 2.016 μmol/L, respectively. JC-1 and flow cytometry showed that HS-10296 induced obvious apoptosis of MDA-MB-231 cells, which showed an apoptosis rate of (21.63 ± 2.97)% following treatment with 8 μmol/L HS-10296. Autophagy vesicles were observed in the cells treated with HS-10296 under electron microscope. In MDA-MB-231 cells pretreated with CQ, inhibition of autophagy significantly enhanced HS-10296-induced cell death. Western blotting showed that the apoptosis-related protein caspase-3 was activated after HS-10296 treatment to cut its substrate PARP. The expression of autophagy-related protein light chain 3B (LC3B) was significantly enhanced after HS-10296 treatment ( < 0.01), which also resulted in inhibited phosphorylation of EGFR and AKT proteins in the cells. CONCLUSIONS HS-10296 can inhibit the proliferation and induce autophagy and apoptosis of MDA-MB-231 cells by inhibiting the EGFR/PI3K/AKT signaling pathway.
Apoptosis ; Autophagy ; Breast Neoplasms ; Cell Line, Tumor ; Cell Proliferation ; ErbB Receptors ; Humans ; Phosphatidylinositol 3-Kinases ; Protein Kinase Inhibitors

The BCL6 (B-Cell Lymphoma 6) gene is a proto-oncogene that is often expressed in diffuse large B-cell lymphomas (DLBCLs). BCL6 loss of function can kill DLBCL cells, demonstrating that BCL6 is necessary for the survival of DLBCL cells and could be a therapeutic target. In this study, we found that BCL6 protein levels were consistently upregulated in DLBCL tissues, whereas its mRNA levels varied randomly in tissues, suggesting that a post-transcriptional mechanism was involved in BCL6 regulation. We used bioinformatics analysis to search for miRNAs, which potentially target BCL6, and identified specific targeting sites for miR-10a in the 3'-untranslated region (3'-UTR) of BCL6. We further identified an inverse correlation between miR-10a levels and BCL6 protein levels, but not mRNA levels, in DLBCL tumor tissue samples. By overexpressing or knocking down miR-10a in DLBCL cells, we experimentally validated that miR-10a directly recognizes the 3'-UTR of the BCL6 transcript and regulated BCL6 expression. Furthermore, we demonstrated that negatively regulating BCL6 by miR-10a suppressed the proliferation and promoted apoptosis of DLBCL cells.
3' Untranslated Regions ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Lymphoma, Large B-Cell, Diffuse ; genetics ; metabolism ; therapy ; MicroRNAs ; genetics ; metabolism ; Proto-Oncogene Proteins c-bcl-6 ; biosynthesis ; genetics