Carcinoma, Squamous Cell ; genetics ; metabolism ; Head and Neck Neoplasms ; genetics ; metabolism ; Humans ; MicroRNAs ; genetics ; metabolism

Air ; analysis ; Air Pollutants ; analysis ; Hazardous Substances ; analysis ; Spectrophotometry, Atomic ; methods

AIM:To investigate the differences among Lenstar 900, A-scan ultrasound and keratometer in measurement of axial length ( AL ) , anterior chamber depth ( ACD ) and corneal curvature ( K1 , K2 , Km ) , and evaluate the consistency of the instruments, with the purpose providing references for the clinical application of Lenstar 900.
METHODS: In this study we picked up 36 patients ( 50 eyes ) underwent cataract surgery, and lens nucleus hardness were under level IV. Before the operation, AL, ACD and K1 , K2 , Km were measured by Lenstar 900, A-scan ultrasound and keratometer respectively. The differences between the results were compared by the paired t-test. The correlation of the results was analyzed by Pearson correlation analysis, and the consistency was measured by Bland-Ahamn method.
RESULTS: The mean AL and ACD values measured by Lenstar 900 and A-scan ultrasound had no significantly statistic differences (P>0. 05). The K1, K2, Km measured by Lenstar 900 and keratometer were not significantly statistical different (P>0. 05). The results measured by these three instruments had close linearity correlation ( r>0.9, P<0. 01). The consistency of the results was well in Bland-Ahamn analysis.
CONCLUSION:The preoperatively biometric result of Lenstar 900, A - scan ultrasound and keratometer in patients with cataract are all reliable, and they can be substituted by each other. However, Lenstar 900 can not only measure AL, ACD and corneal curvature at the same time, but also cornal thickness, lens thickness, white to white, pupil size, optical axis eccentricity, retinal thickness and so on. It has a number of advantages such as non-touching, convenient and efficient, and can be recommended to use widely.

The research of interleukin-13 receptor ?2(IL-13R?2) chain is a rising pop these years.Previous studies have shown that many human tumors overexpress IL-13R?2 chain,while normal cells do not express this receptor or express very low level.This difference of express level is significant to diagnose and cure tumors by the IL-13R?2-directed toxin fusion protein.During the past decade,the structure and the function of IL-13R?2 together with the relationship between this receptor and tumors has been further developed.Therefore new therapies and theories can be proposed as the clinical tumor treatments.In this case,the expression in various tumor cell lines was not only focused on but also on the IL-13 and toxin fusion protein killing effect in both the cell level and the in vivo level.Besides,an overview of the mechanism in the treatment of IL-13R?2-directed toxin fusion protein together with the improved methods for fusion protein purification and other relative tumor therapy was given.In conclusion,the current status and progress of IL-13R?2 as well as IL-13R?2-directed toxin fusion protein in tumor therapy were represented.

DEK protein's carboxy-terminal DNA-binding region(CBD)is a newly found DNA-binding domain of DEK,which contains several phosphorylation sites and has a close correlation with DEK protein's function in vivo and in vitro.Using prokaryotic expression system,the peptide of DEK protein's carboxy-terminal DNA-binding region(CDB)was expressed and purified.In detail,the CDB DNA fragment was constructed into pET-30a(+)vector,and E.coli BL21(DE3)competent cells were used as host cells.The fusion protein His-CBD was expressed by induction of IPTG and purified by Ni-NTA agarose.The result of SDS-PAGE showed that the molecular weight of the purified protein was about 10.7kDa.Electrophoretic mobility shift assay(EMSA)indicated that DEK-CDB prefered to bind to supercoiled form of DNA in vitro,it had similar character to the binding of whole length DEK protein with DNA.This suggested that the carboxy-terminal DNA-binding region of DEK protein might function on the binding of DEK protein to DNA partly.

Objective To study role of MDC/CCI22-CCR4 axis in mouse milky spots with peritoneal carcinomatosis of gastric cancer. Methods We examined the expression of CCR4 in 615 Mouse gastric cancer cell (MFC) lines by RT-PCR and Western-blot; Peritoneal metastasis model on the 615mouse was established by intraperitoneal injection of 0.2 ml MFC cells(1×104 cells). Dil fluorescence was used to observe the transfer process and section of MFC. Immunohistochemistry was conducted to detect the expression of CCR4 and CCL22 in omental milky spot; the structure of Milky spot was observed by scanning electron microscopy. Mice were randomly divided into 2 groups, namely, the saline control group (received saline) and MFC group. The concentration of CCL22 in ascitic fluid was measured in the 615 mice injected MFC after 6,8,10 days and in the saline group. Results MFC first metastasizes to the milky spot on the omentum, the expression of CCR4 and CCL22 were observered in the milky spot. The surface layer cells in milky spot consisted of discontinuous mesothelial cells and mainly macrophages and lymphocytes. The average value of CCL22 was 43 pg/ml and 364 pg/ml respectively in saline control group and MFC group.Conclusions MDC/CCL22-CCR4 axis plays an important role in the development of peritoneal carcinomatosis in mouse gastric cancer.

Objective To investigate the effect of insulin-like growth factor-1 (IGF-1) on intercellular adhesion molecule-1 (ICAM-1) expression in rat model with congestive heart failure (CHF). Methods The model of CHF in male Sprague-Dawley rat was established using subcutaneous injection of isoproterenol. The rats were randomized into model group (n = 10),angiotensin converting enzyme inhibitors (ACEI) group ( n=10) and IGF- 1 group ( n = 10). The rats injected with saline were used as normal controls (n=10). The haemodynamic parameters of rats in each group were detected. The concentration of plasma angiotensin Ⅱ (Ang Ⅱ ) and expression of ICAM-1 in rat myocardium were determined by radioimmunoassay and immunohistochemistry,respectively. Results Compared with model group, ACEI and IGF-1 could rescue the diversities of hemodynamic parameters. In addition, ACEI and IGF-1 could also significantly down-regulated concentration of plasma Ang Ⅱ and inhibited ICAM-1 expression. Compared with ACEI, IGF-1 more significantly inhibited ICAM-I expression (0. 804 ± 0. 024 vs. 1. 254 ± 0. 059) and down-regulated concentration of plasma AngⅡ [(369.2±65.0) μg/L vs. (384.4±56.2) μg/L]. Conclusions IGF-1 can suppress ICAM-1 expression in rat model with CHF induced by isoproterenol. This effect may be related to inhibiting activation of RAS system.

OBJECTIVETo explore the effects and molecular mechanisms of rhein on reducing starvation-induced autophagic protein expression in renal tubular epithelial ( NRK-52E) cells.

METHODHank's balanced salt solution (HBSS) was used to induce NRK-52E cells to be in the state of starvation. After the intervention of HBSS for 0, 0.5,1, 2 and 6 hours, firstly, the protein expression of microtubule-associated protein 1 light chain 3(LC3 I/II), which is a key protein in autophagy, was detected. Secondly, the protein expressions of mammalian target of rapamycin (mTOR) and phosphorylated-mTOR Ser2448 (p-mTOR S2448) were examined. And then, after the co-treatment of rhein (5 mg x L(-1)) and HBSS (1 mL) without or with mTOR inhibitor, rapamycin (100 nmol x L(-1)), the protein expressions of LC3 I/II, mTOR and p-mTOR S2448 were tested, respectively.

RESULTHBSS could induce the up-regulation of LC3 II and the down-regulation of p-mTOR S2448 at protein expression level in NRK-52E cells. The co-treatment of rhein and HBSS could reversely regulate the protein expressions of LC3 II and p-mTOR S2448 in NRK-52E cells significantly. The co-treatment of rapamycin, rhein and HBSS could recover the level of LC3 II protein expression in HBSS-intervened NRK-52E cells.

CONCLUSIONHBSS induces autophagy in renal tubular epithelial cells by inhibiting mTOR signaling pathway activation. Rhein reduces the autophagic protein expression in renal tubular epithelial cells through regulating mTOR signaling pathway activation, which is the possible effects and molecular mechanisms.

Animals ; Anthraquinones ; pharmacology ; Autophagy ; drug effects ; Cells, Cultured ; Epithelial Cells ; drug effects ; metabolism ; Isotonic Solutions ; pharmacology ; Kidney Tubules ; drug effects ; metabolism ; Microtubule-Associated Proteins ; genetics ; Rats ; Signal Transduction ; drug effects ; TOR Serine-Threonine Kinases ; antagonists & inhibitors ; genetics ; physiology

OBJECTIVETo demonstrate the effects and mechanisms of Qifu decoction( QFD) on renal interstitial fibrosis (RIF) in model rats with yang-deficiency syndrome.

METHODThe rats were randomly divided into 3 groups, the Sham group (Group A), the Model group (Group B), the Qifu decoction group (Group C) and the Enalapril group (Group D). The RIF model was established by adenine administrated and unilateral ureteral obstruction (UUO) of the left ureter. After the model was successfully established, the rats in Group C and D were administrated with QFD or the Enalapril suspension,while the rats in Group A and B were administrated with distilled water. All rats were administrated for 3 weeks. Before administration and at the end of week 1, 2 and 3, the rats were weighted, and 24 h urinary protein excretion (Upro), urinary β2-microglobulin (Uβ2-MG) and urinary N-acetyl-D-glucosaminidase (NAG) were examined, respectively. All rats were killed after administration for 3 weeks. Blood and renal tissues were collected, renal morphology and tubulointerstitial morphology were evaluated, respectively. Serum cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), blood urea nitrogen (BUN), serum creatinine (Scr) and uric acid (UA) were detected, respectively. The protein expressions of E-cadherin, α-smooth muscle actin(α-SMA), transforming growth factor-β1 (TGF-β1), onnective tissue growth factor (CTGF) extracellular signal-regulated protein kinase 1/2(ERK1/2) and phosphorylated-ERK1/2 (p-ERK1/2) in kidney were evaluated, respectively.

RESULTQFD ameliorated serum cAMP level and the rate of cAMP/cGMP, attenuated urinary β2-MG level, NAG level and renal tubulointerstitial fibrosis, increased E-cadherin protein expression, and reduced α-SMA, TGF-β1, CTGF and p-ERK1/2 protein expressions in the kidney. However, QFD had no influence on renal function in vivo. In addition, these effects were better than those of the model rats treated by Enalapril.

CONCLUSIONQFD could alleviate yang-deficiency parameters, as well as urinary β2-MG level and NAG level in model rats induced by adenine administration and UUO. Moreover, QFD could improve EMT and RIF by up-regulating E-cadherin protein expression, and down-regulating α-SMA, TGF-β1, CTGF and p-ERK1/2 protein expressions, the key molecular in ERK1/2 signaling pathway.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; antagonists & inhibitors ; Fibrosis ; Kidney ; drug effects ; pathology ; Kidney Diseases ; drug therapy ; pathology ; MAP Kinase Signaling System ; drug effects ; Male ; Rats ; Rats, Sprague-Dawley ; Ureteral Obstruction ; complications ; Yang Deficiency ; complications

In chronic kidney disease (CKD), inflammatory responses during the progression of renal tissue and tissue injury related causes its progression to end-state renal disease. Among them, nuclear factor (nuclear factor, NF)-kappaB signaling pathway by regulating the corresponding nuclear expression of target gene transcription, as well as affecting the synthesis of inflammatory mediators, induction of inflammation lead to kidney damage and renal fibrosis. Some single herbs and their extracts (such as Astragali Radix, Scutellariae Radix, Ginkgo Folium) and some traditional Chinese medicine (such as Danggui Buxue decoction, Qilian decoction) can reduce the inflammatory damage induced by renal tissue NF-kappaB signaling pathway and delay the progression of CKD.
Animals ; Humans ; Kidney ; drug effects ; pathology ; Medicine, Chinese Traditional ; methods ; NF-kappa B ; metabolism ; Renal Insufficiency, Chronic ; drug therapy ; pathology ; Signal Transduction ; drug effects