Objective To explore the cause of acute urinary retention (AUR) ,the functional change of bladder detrusor. Methods The clinical data in 178 patients with AUR combined with urodynamic study were retrospectively analyzed. Results In male patients,the main cause of AUR was bladder oudet obstruction(BOO) ,the percent was 60.63%(77/127) ,in age more than 50 years old patients, while, in age less than 50 years old patients,the main cause was detrusor arcflexia (DUA), the percent was 72.55% (37/51), because of trauma of Iumbosacral vertebrae. In the female patients, the main cause of AUR was DUA. Between male and female patients with age more than 50 years old, there was significant difference in the cases of low compliance and DUA (P < 0.01) ,unstable bladder and BOO (P < 0.05). Conclusions The main cause of AUR in elderly male patients is BOO, which induces low eompliance and unstable bladder. While the main cause of AUR in female patients and young-middle age male is DUA .The function of detrusor changes differently with various causes.

Objective:To investigate the effect of equol on the proliferation of colom cancer cells and to explore the mechanisms.Methods: Colon cancer cells (DLD1,HCT15,COLO205,LOVO,SW480) were incubated, the cell proliferation was identified by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell proliferation assay.Reverse transcription PCR and Western blot were used to measure the mRNA and the protein expression of estrogen receptor and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)in the colon cancer cells, respectively.Moreover, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell proliferation assay was used to investigate the effect of estrogen receptor(ER) inhibitor,ERα agonist, and estrogen receptor ERβagonist on the cell proliferation.Results: ERα was faintly expressed in the DLD-1 and HCT-15 cells.However, ERβ expression in DLD1, HCT15, COLO205, LOVO, and SW480 colon cancer cells.Different concentrations of equol (0, 0.5, 1, 5, 10 μmol/L) significantly inhibited the growth of HCT-15 cell with the expression of ERα and ERβ.More-over, different concentrations of equol (0, 0.5, 1, 5, 10 μmol/L) significantly inhibited the growth of LOVO, and SW480 cells with the ERβ expression in a dose-dependent manner as demonstrated with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell proliferation assay.mRNA expressions of ERα and ERβ in HCT-15 were stimulated significantly.Western blotting proved that the protein expressions of ERα and ERβ increased with the increasing of equol dose.Moreover we found significant difference of Nrf2 protein expression in HCT-15 cell stimulated by different concentrationss of equol.After the similation of estrogen receptor inhibitor, ERα agonist, or ERβ agonist, we found that only dif-ferent concentrations of ERβ agonist(0, 1, 10, 100, 1 000, 10 000 nmol/L) significantly inhibited the growth of HCT-15, LOVO, and SW480 in adose-dependent manner.Estrogen receptor inhibitor and ERα agonistdid not present significant effect on the cell proliferation of HCT-15, LOVO, and SW480.Conclusion: Equol inhibited the colon cancer cell proliferation by its estrogenic activities and antioxidant activities.

Objective To observe the effects ofTrametes robiniophila Murr and Isatidis Radix bidirectional fermentation products on the migration and invasion of human breast cancer MCF-7 cells and relevant factors; To discuss relevant mechanism of action.Methods Breast carcinoma cell line MCF-7 was used as research subject in this experiment. Control group, Isatidis Radix group,Trametes robiniophila Murr group, andTrametes robiniophila Murr and Isatidis Radix group were included in the experiment. The effects ofTrametes robiniophila Murr and Isatidis Radix bidirectional fermentation products on MCF-7 cell proliferation were measured by MTT method. Cell scratch assay, transwell assay and adhesion assay were used to measure the effects ofTrametes robiniophila Murrand Isatidis Radix bidirectional fermentation products on the migration, invasion and adhesion capability of MCF-7 cells, respectively. The effects ofTrametes robiniophila Murrand Isatidis Radix bidirectional fermentation products on the mRNA expression of MMP-9 and Vimentin were measured by RT-PCR.Results Compared with Isatidis Radix group andTrametes robiniophila Murrgroup, Trametes robiniophila Murr and Isatidis Radix bidirectional fermentation products could significantly inhibit the proliferation, migration, invasion and adhesion capability of MCF-7 cells (P<0.05). Similarly,Trametes robiniophila Murr and Isatidis Radix bidirectional fermentation products reduced the mRNA expression of MMP-9 and Vimentin (P<0.05).ConclusionTrametes robiniophila Murrand Isatidis Radix bidirectional fermentation products may down-regulate the expression of MMP-9 and Vimentin to inhibit the migration, invasion and adhesion capabilities of MCF-7 cells.

Objective To detect the inhibitory effect of siliver nanoparticles loaded titanium nanotubes on staphylococcus aureus, and provide a theoretical basis for implant local application. Methods Orderly arrangement of titania nanotubes produced by anodic oxidation, loaded silver nanoparticals by situ replacement. Scanning electron microscopy (SEM) and transmission electron microscopy(TEM) were used to detect the morphology topology of silver nanoparticals, titanium nanotubes and siliver particals loaded titanium nanotubes. The minimum inhibitory concentration of silver nanoparticles was calculated. The antibacterial of planktonic bacteria was detected 1 day, 3 days and 5 days after culturing staphylococcus aureus on siliver particals loaded titanium nanotubes. The inhibitory bacterial adhesion properties were detected by scanning electron microscopy. Results The uniform and orderly diameter of 80～120 nm TiO2 nanotubes were prepared under 18 V voltage, loaded diameter of 20 nm silver nanoparticals, which effectively inhibited adhesion and proliferation of staphylococcus aureus. Conclusion Titanium nanotubes produced by 18 V have a stronger drug loading capacity. The 100 mmol/L silver nanopartical solution loaded nanotubes can effectively inhibit staphylococcus aureus adhesion and proliferation within three days.

Objective To discuss the clinical efficacy between the small skull-window microsurgical surgery and conventional trauma craniotomy in the treatment of hypertensive cerebral hemorrhage .Methods The clinical data of patients with hypertensive cerebral hemorrhage treated with two different approaches from January 2010 to October 2014 were analyzed retrospectively .Re-sults The re-hemorrhage rate of patients treated with conventional trauma craniotomy was relatively low ,compared with patients treated with small skull-window microsurgical surgery .small skull-window microsurgical surgery was superior than conventional trauma craniotomy in the incidence of postoperative complications ,disability rate and patients′ hospitalization time(P< 0 .05) .Con-clusion Small skull-window microsurgical surgery is superior than conventional trauma craniotomy .

The Rictor/mTOR complex plays a pivotal role in a variety of cellular functions including cellular metabolism, cell proliferation and survival by phosphorylating Akt at Ser473 to fully activate the Akt kinase. However, its upstream regulatory pathways as well as whether it has additional function(s) remain largely unknown. We recently reported that Rictor contains a novel ubiquitin E3 ligase activity by forming a novel complex with Cullin-1, but not with other Cullin family members. Furthermore, we identified SGK1 as its downstream target. Interestingly, Rictor, but not Raptor or mTOR, promotes SGK1 ubiquitination. As a result, SGK1 expression is elevated in Rictor(-/-) MEFs. We further defined that as a feedback mechanism, Rictor can be phosphorylated by multiple AGC family kinases including Akt, S6K and SGK1. Phosphorylation of Rictor at the Thr1135 site did not affect its kinase activity towards phosphorylating its conventional substrates including Akt and SGK1. On the other hand, it disrupted the interaction between Rictor and Cullin-1. Consequently, T1135E Rictor was defective in promoting SGK1 ubiquitination and destruction. This finding further expands our knowledge of Rictor's function. Furthermore, our work also illustrates that Rictor E3 ligase activity could be governed by specific signaling kinase cascades, and that misregulation of this process might contribute to SGK overexpression which is frequently observed in various types of cancers.
Animals ; Carrier Proteins ; metabolism ; Cell Proliferation ; Cells, Cultured ; Cullin Proteins ; genetics ; metabolism ; Fibroblasts ; metabolism ; Humans ; Immediate-Early Proteins ; metabolism ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Rapamycin-Insensitive Companion of mTOR Protein ; TOR Serine-Threonine Kinases ; genetics ; metabolism ; Ubiquitin ; genetics ; metabolism ; Ubiquitination

Mammalian target of rapamycin (mTOR) plays essential roles in cell proliferation, survival and metabolism by forming at least two functional distinct multi-protein complexes, mTORC1 and mTORC2. External growth signals can be received and interpreted by mTORC2 and further transduced to mTORC1. On the other hand, mTORC1 can sense inner-cellular physiological cues such as amino acids and energy states and can indirectly suppress mTORC2 activity in part through phosphorylation of its upstream adaptors, IRS-1 or Grb10, under insulin or IGF-1 stimulation conditions. To date, upstream signaling pathways governing mTORC1 activation have been studied extensively, while the mechanisms modulating mTORC2 activity remain largely elusive. We recently reported that Sin1, an essential mTORC2 subunit, was phosphorylated by either Akt or S6K in a cellular context-dependent manner. More importantly, phosphorylation of Sin1 at T86 and T398 led to a dissociation of Sin1 from the functional mTORC2 holo-enzyme, resulting in reduced Akt activity and sensitizing cells to various apoptotic challenges. Notably, an ovarian cancer patient-derived Sin1-R81T mutation abolished Sin1-T86 phosphorylation by disrupting the canonical S6K-phoshorylation motif, thereby bypassing Sin1-phosphorylation-mediated suppression of mTORC2 and leading to sustained Akt signaling to promote tumorigenesis. Our work therefore provided physiological and pathological evidence to reveal the biological significance of Sin1 phosphorylation-mediated suppression of the mTOR/Akt oncogenic signaling, and further suggested that misregulation of this process might contribute to Akt hyper-activation that is frequently observed in human cancers.
Adaptor Proteins, Signal Transducing ; metabolism ; Animals ; Humans ; Mechanistic Target of Rapamycin Complex 1 ; Mechanistic Target of Rapamycin Complex 2 ; Models, Biological ; Multiprotein Complexes ; metabolism ; Phosphorylation ; Phosphothreonine ; metabolism ; TOR Serine-Threonine Kinases ; metabolism