Objective To analyze the incidence of stress hyperglycemia and its influential factors in patients with acute myocardial infarction and cerebral infarction. Methods The case data of 1630 consecutive patients with incipient myocardial infarction without cerebrovascular disease admitted in the department of cardiology and 1338 patients with atherosclerotic acute cerebral infarction without cardiovascular disease admitted in the department of neurology,Xuanwu Hospital,Capital Medical University from January 2009 to December 2012 were analyzed retrospectively. A total of 2048 patients without diabetes mellitus were selected from them,among them 1165 patients were in an acute myocardial infarction group and 883 were in a cerebral infarction group. The fasting blood glucose >7. 8 mmol/L in the next morning after admission was defined as hyperglycemia. Single factor and multifactor logistic regression analyses were used to compare the incidence of stress hyperglycemia and its influential factors of both groups. Results ( 1 ) Of the 1165 patients with myocardial infarction,the incidence of stress hyperglycemia was 17. 2% (n=201);of the 883 patients with cerebral infarction,the incidence of stress hyperglycemia was 5.4% (n=48). There was significant difference between the 2 group (χ2= 65.677;P < 0. 01). (2) Comparing the general information of the patients with stress hyperglycemia (n=249) and those without stress hyperglycemia ( n=1799) of the cardio-cerebrovascular diseases showed that there were significant differences in hyperlipidemia, drinking history, family history of cardio-cerebrovascular diseases, age, heart rate, total cholesterol, low density lipoprotein cholesterol,leukocyte count,blood urea nitrogen,and triacylglycerols between the 2 groups (P<0. 05). (3) Multivariate Logistic analysis showed that heart rate ( OR,1. 013,95%CI 1.002-1.024),leukocyte count (OR,1.109,95%CI 1.508-1.163),and triacylglycerols(OR,1.174, 95%CI 1. 042-1. 322) were the independent risk factors for stress hyperglycemia in myocardial infarction. (4) Systolic blood pressure (OR,1. 019,95% CI 1. 006-1.033) and leukocyte count (OR,1. 132,95%CI 1. 009-1. 268) were the independent risk factors for stress hyperg lycemia in cerebral infarction. Conclusion The incidence of stress hyperglycemia in patients with myocardial infarction is higher than that in patients with cerebral infarction,and the increased leukocyte count is a common independent risk factor for both.

No abstract available.
Nevus, Pigmented*

Objectives To investigate the relationship between atherosclerotic acute myocardial infarction (AMI),acute cerebral infarction (ACI)and homocysteine (Hcy). Methods Three hundred and twenty consecutive patients with primary acute myocardial infarction (AMI)(group A)were admitted to the Department of Cardiology,310 patients with primary large artery atherosclerotic cerebral infarction (group B)were admitted to the Department of Neurology,and 327 healthy individuals without cardiovascular and cerebrovascular diseases (group C)at the Department of Physical Examination,Xuanwu Hospital, Capital Medical University were enrolled retrospectively from March 2010 to October 2011. The age and sex were matched in the 3 groups. All the clinical data of subjects were colleted in detail and then were compared and analyzed. Results (1)The Hcy levels (μmol/L)of group A,B,and C were 15. 10 (12. 43, 19.47),15. 80 (13. 10,20. 83),and 13. 20 (11. 00,16. 50;median [interquartile range]),respectively. There were significant differences among the 3 groups (P<0. 05). The incidences of hyperhomocysteinemia (HHcy)were 92. 8%(n=297),97. 1%(n=301),and 84. 7%(n=277)(P<0. 05). (2)Multivariate Logistic regression analysis showed that the independent risk factors for ACI were HHcy (OR 8. 97,95% CI 3. 01-26. 71),hypertension,diabetes,hyperlipidemia and blood ureanitrogen;the independent risk factors for AMI were HHcy (OR 4. 36,95% CI 1. 70-11. 21),hypertension,diabetes,hyperlipidemia,and total blood cholesterol. Conclusion HHcy is an independent factor for ACI and AMI,which have closer relationship with ACI. ACI and AMI have some common risk factors,but their degrees of action are different.

Objective:To explore the therapeutic effect of psychological and drug intervention on anxiety and depres‐sion in patients after coronary artery bypass graft (CABG) .Methods :A total of 115 patients performed CABG were randomly divided into combined intervention group (n=60) and routine nursing group (n=55) .During peropera‐tive period ,combined intervention group received psychological intervention ,flupentixol and melitracen tablet and sertraline based on routine nursing .A total of 25 matching normal people were selected from community and regar‐ded as normal control group ,scores of Zung self‐rating anxiety scale (SAS) and self‐rating depression scale (SDS) were evaluated and compared among three groups before and after operation .Results :Before intervention ,there were no significant difference in standard scores of SAS and SDS between combined intervention group and routine nursing group ( P > 0.05) ,but they were all significantly higher than those of normal control group , P < 0.01 all . After operation ,standard scores of SAS and SDS in combined intervention group were significantly lower than be ‐ fore operation ( P < 0.01 both) ,and they were significantly lower than those of routine nursing group [SAS : (41.31 ± 6.13) scores vs .(51.35 ± 8.95) scores ,SDS : (40.20 ± 5.80) scores vs .(51.22 ± 8.78) scores , P < 0.01 both] . Conclusion :Psychological combined drug intervention could significantly relieve anxiety and depression in patients after coronary artery bypass graft ,which is helpful for improving postoperative prognosis .

Ras is best known for its ability to regulate cell growth, proliferation and differentiation. Mutations in Ras are associated with the abnormal cell proliferation which can result in incidence of all human cancers. Extracellular signal-regulated kinase (ERK) is a downstream effector of Ras and plays important roles in prognosis of tumors. Recently, evidence has gradually accumulated to demonstrate that there are other effectors between Ras and ERK, these proteins interact each other and constitute the thorough Ras/Raf/MEK/ERK signaling pathway. The pathway has profound effects on incidence of esophageal carcinoma and clinical applications of some chemotherapeutic drugs targeting the pathway. Further understanding of the relevant molecular mechanisms of Ras/Raf/MEK/ERK signaling pathway can be helpful for the development of efficient targeting therapeutic approaches which contribute to the treatment of esophageal cancer. In this article, roles of Ras/Raf/MEK/ERK signaling pathway in esophageal carcinoma as well as pharmacological targeting point in the pathway are reviewed.

Objective To investigate the meaning of PURA gene and its protein in nephridial tissue of the rats with endemic fluorosis of coal burning. Methods Thirty-six SD rats of 80 - 100 g, body weight were randomly divided into control group, low fluorosis group and high fluorosis group according to body weight, 12 in each group, the number of female and male in each group was the same respectively. The control group, Low fluorosis group and high fluorosis group rots were fed with 1.5,25.0,60.0 mg/kg fluoride content in feedstuff, to establish the animal model of fluorosis. Expressions of both mRNA and its protein of PURA gene in rat nephridium tissue, were determined by RT-PCR and immunohistochemistry after four-month experimental period. Results The expressions of PURA mRNA[(2.74± 1.06),(4.29 ± 2.11)] and its protein[ (28 827.91 ± 4801.94),(61 146.96 ± 4997.55)] in low fluorosis group and high fluorosis group was higher than that in the control group[ ( 1.13 ± 0.87), (7131.95 ± 1524.54), all P < 0.05]. And the expressions of PURA mRNA and protein in high fluorosis groups was higher than that in low fluorosis greup(all P < 0.05). Conclusion High fluoride can lead to the high expression of PURA gene mRNA and protein in the rat nephridium tissue exposed to sodium fluoride.

A 36-year-old man was diagnosed with a right temporal lobe grade II cerebral arteriovenous malformation (cAVM) and was treated with radiosurgery. At nine months after the cAVM radiosurgery, the patient began to develop bilateral focal narrowing at the M1 segments of the bilateral middle cerebral arteries. The narrowing progressively deteriorated as was demonstrated on longitudinal serial follow-up MR imaging. X-ray angiography performed at 51 months after radiosurgery confirmed that the cAVM was cured and a diagnosis of moyamoya disease. To the best of our knowledge, this is the first case of cAVM-associated moyamoya disease that developed after radiosurgery. Given the chronological sequence of disease development and radiation dose distribution of radiosurgery, it is proposed that humoral or unknown predisposing factors, rather than direct radiation effects, are the cause of moyamoya disease associated with cAVM.
Adult ; Humans ; Intracranial Arteriovenous Malformations/diagnosis/*surgery ; Magnetic Resonance Imaging ; Male ; Moyamoya Disease/*etiology ; Postoperative Complications ; Radiosurgery

Objective To investigate the feasibility of ultrasmall superparamagnetic iron oxide- enhanced(USPIO)-enhanced MR imaging for monitoring synovitis of antigen-induced arthritis in rabbit model and explore the optimal MR imaging sequences.Methods Nine female white rabbits with antigen(0.5 ml mBSA,2 mg/ml)induced arthritis of the right knees were used in the study.The left knees of these rabbits and both knees of another 3 rabbits served as the control.Nine to 28 days(mean 21.3 d)after successful model induction,all knees were imaged before and 24 h after intravenously injection of USPIO (0.3 ml/kg),among which 2 rabbits were also imaged at 48 and 72 h after administration of USPIO respectively.The MR protocol included spin-echo(SE) T_1WI,fast spin-echo(FSE)T_2WI,gradient echo (GRE)T_2~* WI and short tau inversion recovery(STIR).Images were analyzed quantitatively and qualitatively based on signal characteristics and patterns of the synovium.Paired t-test was used for the analysis of the signal intensity of inflammatory synovial membrane before and 24 h after injection of USPIO. MR findings were correlated with histopathology.Results Arthritis was successfully induced in all 9 right knees with intraarticular injection of mBSA.Pathological examination revealed hyperplasia of synovium with infiltration of USPIO-loaded-macrophages.MR depicted synovial thickening(thickness 2.07?0.97 mm) and joint effusion.Synovium and joint fluid appeared as slightly hypo- or iso-intense on T_1 WI and hyper- intense on T_2 WI or T_2~* WI.Twenty four hours after USPIO injection,significant T_1 enhancement(ASNR 41.91%?27.94%),negative T_2 and T_2~* enhancement(△SNR -34.92%?11.77% and -57.24%? 16.05%)were demonstrated in the region of synovial inflammation respectively.The signal at 48 h and 72 h changed less than that at hour 24.No signs of arthritis occurred in all left knees and in all knees of the artificial model group.Conclusion Iron oxide phagocytized into macrophages can be a root cause resulted in signal change on USPIO-enhanced MR images.The gradient echo sequence should be the optimal sequence to be used in USPIO-enhanced MR imaging in antigen-induced arthritis.

PURPOSE: To report on the changes in the patterns of care and survival over time for esthesioneuroblastoma. MATERIALS AND METHODS: We retrospectively analyzed 42 previously untreated and histologically confirmed esthesioneuroblastoma patients seen between March 1989 and June 2007. According to Kadish's classification, 3 patients (7%) were stage A, 6 (14%) at stage B, and 33 (79%) at stage C. Of the 33 Kadish C patients, 19 and 14 patients were treated from 1989 through 2000 and from 2001 through 2007, respectively. Treatment included surgical resection, radiotherapy, chemotherapy, or a combination of these methods. Chemotherapy was administered to 8 of 19 patients (42%) seen from 1989 through 2000, whereas all of the 14 patients seen from 2001 through 2007 received chemotherapy (p<0.001). No patient was treated by three-dimensional conformal radiotherapy (3D-CRT) from 1989 through 2000, however 8 of 14 patients (67%) seen from 2001 through 2007 underwent 3D-CRT (p<0.001). The median follow-up time for surviving patients was 6.5 years (range, 2.2~15.8 years). RESULTS: The 5-year overall survival (OS) and progression-free survival (PFS) rates for the entire cohort were 53% and 39%, respectively. The 5-year OS was 100% for Kadish stages A or B and 39% for stage C (p=0.007). For patients with stage C disease who were treated from 1989 to 2000 and from 2001 to 2007, the 5-year OS rate was 26% and 59% (p=0.029), respectively and the corresponding 5-year PFS rate was 16% and 46% (p=0.001), respectively. Intraorbital extension and treatment era (1989~2000 vs. 2001~2007) were found as independent factors for OS and PFS in a multivariate analyses. CONCLUSION: The results of this study suggest that treatment era, which features a distinction in treatment modality and technique with the introduction of 3D-CRT, may be the cause of improved OS and PFS in Kadish stage C patients. To achieve better outcomes for patients with Kadish stage C, combined chemoradiotherapy, especially 3D-CRT, is recommended in addition to surgery.
Chemoradiotherapy ; Cohort Studies ; Disease-Free Survival ; Esthesioneuroblastoma, Olfactory ; Follow-Up Studies ; Humans ; Multivariate Analysis ; Prognosis ; Radiotherapy, Conformal ; Retrospective Studies

OBJECTIVETo investigate the effects of Newcastle disease virus (NDV) infection on the expression of survivin and cell cycle in human tongue squamous carcinoma TSCCa cells.

METHODSThe proliferation of TSCCa cells infected with NDV in vitro was evaluated by means of MTT assay, and survivin expression in the infected cells was detected using RT-PCR and Western blotting. Flow cytometry was performed to assess the changes in the cell apoptosis, cell cycle and cell proliferation index (PI) of the cells.

RESULTSNDV infection resulted in decreased survivin expression and increased apoptosis of TSCCa cells, with reduced cell percentage in G2/M and S phases and lowered PI of the cells, showing significant differences from those of the negative control cells (P<0.05).

CONCLUSIONNDV infection can inhibit survivin expression, affect the cell cycle of TSCCa cells and induce their apoptosis.

Apoptosis ; physiology ; Blotting, Western ; Carcinoma, Squamous Cell ; metabolism ; pathology ; virology ; Cell Cycle ; physiology ; Cell Line, Tumor ; Host-Pathogen Interactions ; Humans ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; biosynthesis ; genetics ; Newcastle disease virus ; physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Tongue Neoplasms ; metabolism ; pathology ; virology