OBJECTIVETo investigate the correlation of the autophagy-associated gene Atg5 with the pathogenesis of prostate cancer.

METHODSUsing real-time fluorescent quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and immunohistochemistry, we detected the expression of Atg5 in 50 cases of prostate intraepithelial neoplasm (PIN), 69 cases of prostate cancer (PCa), and 30 cases of benign prostatic hyperplasia (BPH).

RESULTSThe expression level of Atg5 mRNA was significantly higher in PIN (5.270 ± 0.230) and PCa (5.131 ± 0.252) than in the BPH tissue (1.723 ± 0.017) (P <0.01), and so was the positive rate of the Atg5 expression in the patients of the PIN group (94%) and PCa group (88.4%) than in those of the BPH group (6.7%) (P<0.01), but with no statistically significant differences between the PIN and PCa groups (P >0.05). No significant correlation was observed between the expression of Atg5 and the Gleason score of PCa (P >0.05).

CONCLUSIONThe upregulated expression of Atg5 might play a role in the tumorigenesis of prostate cancer.

Aged ; Autophagy ; Autophagy-Related Protein 5 ; Humans ; Immunohistochemistry ; Male ; Microtubule-Associated Proteins ; genetics ; Middle Aged ; Prostatic Hyperplasia ; genetics ; Prostatic Neoplasms ; genetics ; RNA, Messenger ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; methods ; Up-Regulation

Eukaryotic elongation factor 2 kinase (eEF2K) is well known as a Ca2+/calmodulin (CaM)-dependent kinase. eEF2K catalyzes the phosphorylation of eEF2 and subsequently inactivates eEF2 by impairing its ability to bind to the ribosome, thereby negatively modulates protein synthesis. The high expression of eEF2K has been found recently in several types of malignancies. As participating in the progress of tumor, eEF2K emerges a potential target for future cancer therapy. The relationship between eEF2K and tumor, and the latest progress of eEF2K inhibitors were summarized in this article.
Elongation Factor 2 Kinase ; antagonists & inhibitors ; metabolism ; Humans ; Neoplasms ; metabolism ; Peptide Elongation Factor 2 ; metabolism ; Phosphorylation

Chemotherapy- induced peripheral neuropathy (CIPN) can be caused by many commonly used chemotherapeutic agents, such as taxanes, vinca alkaloids, platinum drugs, thalidomide,and also by newer agents such as bortezomib. Both animal experiments and clinical studies are being conducted to investigate strategies for preventing CIPN or ameliorating established CIPN without affecting the antitumor efficacy of chemotherapy. Treatments using calcium and magnesium infusions,glutathione,lipoid acid are being evaluated for their clinical application.

Alveolar Process ; Housing ; Humans ; Incisor ; Maxilla ; Tooth Root

OBJECTIVETo observe the effect of Modified Yiqi Chutan Recipe (MYCR) on blood flow perfusion in treating mid-late stage non-small cell lung cancer (NSCLC) patients by using multislice CT perfusion (CTP) , and to assess the relationship between each CTP parameter and the prognosis as well.

METHODSTotally 87 mid-late stage NSCLC patients were randomly assigned to the treatment group (44 cases, Shenyi Capsule + MYCR +chemotherapy) and the control group (43 cases, chemotherapy alone) in the ratio of 1:1. And 21 days consisted of 1 therapeutic course, 4 courses in total. All of them underwent CTP of primary tumor and routine thoracic CT examination (plain CT and enhancement CT) 3 times (before therapy, after 2 and 4 cycles). CT findings were analyzed for tumor size and perfusion parameters [blood flow (BF), blood volume (BV), permeability surface (PS), mean transit time (MTT), and time to peak (TP) before and after treatment, and relationship between perfusion parameters and prognosis was also assessed.

RESULTSIn 87 cases, 7 dropped out and 80 cases were available, 40 in the treatment group and 40 in the control group. (1) The relief rate was 47.5% (19/40) and the total stable rate was 77.5% (31/40) in the treatment group, and they were 40.0% (16/40) and 65.0% (26/40) in the control group, with no statistical difference between the two groups (χ² = 0.672, 1.227; P > 0.05). (2) Compared with before treatment group in the same group, BF and PS decreased, and MTT increased in the two groups after 2 and 4 courses (P < 0.05); BE and PS decreased, and MTT increased in the control group after 2 courses (P < 0.05). Compared with the control group after 4 courses, BE decreased more significantly in the treatment group (P < 0.05). (3) After 4 courses, all patients were assigned to the remission group (35 cases) and the non-remission group (45 cases) according to the RECIST standard. Compared with before treatment in the same group, BF, BF, and PS all decreased, and MTT increased in the remission group after treatment (all P < 0.05); BF increased in the non-remission group after treatment (P < 0.05). (4) All patients were assigned to the BE increase group (34 cases) and the BE decrease group (46 cases) according to changed BE values after treatment. Results showed the mean survival rate was 246 days in the BF increase group (the 1-year accumulative survival rate being 13.0%) and 387 days in the BE decrease group (the 1-year accumulative survival rate being 53.1%). The life span was prolonged and the 1-year accumulative survival rate was elevated in the BE increase group, with statistical difference as compared with the BE decrease group (χ² = 19.057, P < 0.01).

CONCLUSIONSShenyi Capsule plus MYCR could reduce BE in mid-late stage NSCLC patients , improve vascular permeability, showing better synergistic effect with chemotherapy. CTP could not only reflect the change of tumor size, but also reflect vascular function of the tumor. Meanwhile, changes of CTP parameters were closely associated with prognosis. Patients with post-treatment decreased BE value had better prognosis and longer life span.

Capillary Permeability ; drug effects ; Carcinoma, Non-Small-Cell Lung ; diagnosis ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Phytotherapy ; Tomography, X-Ray Computed

Objective To investigate the clinical presentation, hormonal profile and metabolic abnormalities in subgroups of women with PCOS and explore a reasonable classification for PCOS. Methods A cross-sectional study of 192 women with PCOS (14-38 years of age) was performed. The patients were divided into 3 groups of A, B and C according to the revised 2003 consensus on diagnostic criteria and also divided into 2 groups according to body mass index(BMI) : group A(n=110), long term anovulation, clinical and biochemical evidence of high androgen level, ovary enlargement with its size larger than 10 ml or number of small follicles of 2-9 mm ≥12 under ultrasound with exclusion of other diseases caused by high androgen;group B(n=46), long term anovulation, clinical and biochemical evidence of high androgen level;group C(n=36), long term anovulation, ovary enlargement with its size larger than 10 ml or number of small follicles of 2-9 mm ≥12 under ultrasound with exclusion of other disease caused by high androgen; obesity PCOS group (OB-PCOS,n=70),BMI≥25(kg/m~2); no obesity PCOS group (NOB-PCOS,n=122), BMI

Extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathway, which was the first cell signal transduction pathway to be discovered, consisted of Ras, Raf, MEK1/2 and ERK1/2. After the activation of ERK1/2 pathway, extracellular signals can be transmitted from the cell membrane to the nucleus. It was involved in many physiological and pathological functions of cells, such as growth, proliferation, differentiation, apoptosis and etc. It was also related to the onset of many diseases, which included multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). The activation of ERK1/2 pathway can induce the activation of astrocyte, MG, T cell and macrophage, which released a variety of inflammatory cytokines. It caused myelin damage which induced MS/EAE onset. A number of studies indicated that inhibiting ERK1/2 pathway can reduce the releasing of inflammatory cytokines and myelin damage for MS/EAE alleviation. It provided an important target for the development of MS treatment medication.

Objective To investigate the mechanisms of phenytoin accelerating healing process.Methods Adult male Wistar rats that survived ligatation of the left coronary artery were randomized to phenytoin group or operation control and compared to sham-operated rats.The time-dependent proteolytic activity of MMP-2 and MMP-9 were detected by gelatin zymography.Picrosirius red staining plus polarized light micrscopy was used for qualitative and quantitative analysis of collagen include collagen volume fraction(CVF) and ratio of typeⅠ/Ⅲ collagen.In addition,infarct thickness and myocyte cross-sectional area were also evaluated by image analysis.Results Fourteen days after myocardial infartion(MI),phenytoin reduced infarct wall thinning.Compared with control group,the rats received phenytoin had less myocyte cross-sectional area.Two weeks after MI,CVF in two groups both had significantly dynamic increase and phenytoin accelerated the change.In contrast to control group,ratio of typeⅠto type Ⅲ collagen in phenytoin increased more quickly.Apart from these results,phenytoin did little to CVF in non-infarcted region.Analysis of MMPs activity in myocardial extracts by zymography demonstrated that infarction-induced expression of proMMPs and active MMPs was both upregulated in phenytoin group and operation control.We found that after MI,MMP-9 activity increased as early as 1 day and reached a maximum then gradually descended,whereas MMP-2 began to increase rapidly and remain elevated for up to 14 days thereafter.Phenytoin seemed toenhance expression of MMP-2 and MMP-9.1 day after MI,active MMP-9 in phenytoin group expressed an increasing trendency compared to MI control.Conclusion Phenytoin can attenuate the degree of post-infarction left ventricular dilation and expansion of the infarct during the early phase of MI healing.MMP-2 and MMP-9 enhanced by phenytoin probably played a prominent role.

Objective To study the mechanism of spontaneous rupture of hepatocellular carcinoma(HCC).Methods Articles have been reviewed to find out the theory of spontaneous rupture of HCC.Results Researchful results suggested that the injury of small arteries was usually followed in patients of spontaneous rupture of HCC.In this review,the immune complex,which composed of hepatitis B virus e antigen,complement C1q and immunoglobulins,was found deposited in the elastic membrane of arteries.Likely as a result of immune complex deposition,vascular injury occurs mainly in the small arteries where the deposition of immune complex was present.The small arteries in which immune complex deposited are readily injuried and cause hemorrhage and rupture of HCC during vascular load increase. Conclusion We would conclude that immune complex deposition in vessel wall led to the small arteries injury may be the factor involved in the pathogenesis of spontaneous ruptured HCC.

It had fertile countryside land,rich products,dense population and creeks and lakes in ancient Hangzhou and its neighbour area,where there is a good place for planting medicinal materials.It had long history of planting medicinal materials with abundant output,pure and good nature,and much varieties;among which,some famous and costly medicinal materials,such as "eight Zhe's" and "eighteen Hangs",were not only adopted broadly by court,royalty and doctors,but purchased by many businessmen and sold far to abroad as well;they seemed to be in the leading place in China.