Genetic Heterogeneity ; Humans ; Magnetic Resonance Imaging ; methods ; Neoplasms ; diagnosis ; genetics ; pathology ; Positron-Emission Tomography ; methods ; Tomography, X-Ray Computed ; methods

Objective: To investigate whether transplantation of mesenchymal stem cells(MSCs) through renal arteries can protect kidney from acute tubular necrosis(ATN), so as to lay a foundation for MSC transplantation in treatment of ATN. Methods: Five-week-old nude mice were randomly divided into three groups: normal control group (n = 10), acute tubular necrosis(ATN) model group without(n = 10) and with MSCs treatment group(n = 11). ATN nude mice were induced with 50% glycerin. MSCs labeled with enhanced green fluorescent proteins(EGFP) were injected into kidney through renal arteries. Serum creatinine was determined in all groups and pathological changes of renal tissues were detected using H-E staining. The amount and distribution of the EGFP-marked MSCs in renal tissues were determined with fluorescence microscope. Results: Degeneration and exfoliation of renal tubular epithelial cells, and even renal tubular tamponade with cast-off cells were observed in the ATN group; these pathological changes were mainly located at renal cortex and juncture of renal cortex and medulla. The damages were greatly alleviated in the ATN + MSCs transplantation group, with no swelling of epithelial cells, nuclear condensation or edema. Fourteen days after MSCs transplantation, EGFP positive cells were increased in renal tubules of recipient mice. Conclusion: The MSCs transplantation via renal artery can locate in renal tubular epithelium, and promote the repair of injured renal tubular epithelial cells.

Aim The effect of tetrandrine on TGF-?1 mRNA expression in glomerulosclerosis rat was observed. Methods The rats were randomly divided into four groups, such as the normal control group (sham operative rat), glomerulosclerosis model group,tetrandrine group and amlodipine group. The expression of TGF-?1 mRNA was analyzed by Northern blot hybridization. Results The expressions of TGF-?1 mRNA in two treating groups were much lower than untreated model group. There were no difference between these two treating groups. Conclusion Tetrandrine can decrease the expression of TGF-?1 mRNA in glomerulosclerosis rat induced by unilateral renctomy plus adriamycin.

The traditional Chinese medicine (Tripterygium wilfordiiHook.f.,TWH) has been clinically used to treat primary and secondary renal diseases and proteinuria for nearly 40 years.However,there is a rare literature about the effect of triptolide (the main active ingredient of TWH) on the expression of oxidative carbonyl protein (OCP) in diabetic nephropathy (DN).This study aimed to provide experimental evidence for triptolide treatment on DN through its effect on the expression of OCP,in order to investigate the effects of triptolide on the expression of OCP in rats with DN.Sixty SD rats were randomly divided into five groups:control group,high-dose triptolide (Th) group,low-dose triptolide (T1) group,DN model group,and positive control (benazepril) group.The DN model was established using streptozotocin.Urinary protein excretion,fasting blood glucose (FBG),superoxide dismutase (SOD) in renal homogenate,malondialdehyde (MDA) in renal homogenate and renal nitrotyrosine by immunohistochemistry,and the expression of OCP by oxyblotimmune blotting were detected.In the DN model group,rat urinary protein excretion and renal MDA were significantly increased,while renal SOD significantly decreased and nitrotyrosine expression was obviously upregulated in the kidney.After triptolide treatment,24-h urinary protein excretion (61.96±19.00 vs.18.32±4.78 mg/day,P＜0.001),renal MDA (8.09±0.79 vs.5.45±0.68 nmol/L,P＜0.001),and nitrotyrosine expression were decreased.Furthermore,renal OCP significantly decreased,while renal SOD (82.50±19.10 vs.124.00±20.52 U/L,P＜0.001) was elevated.This study revealed that triptolide can down-regulate the expression of OCP in the renal cortex of DN rats.

OBJECTIVETo explore the effect and mechanism of resveratrol against human colon cancer ls174t cells in vitro and the growth of colon cancer in tumor-bearing nude mice.

METHODSMTT method was used to test the inhibiting effect of resveratrol on the growth and proliferation of ls174t cells. Transmission electron microscopy was used to observe the morphological changes of cell apoptosis, and FCM assay was performed to measure the changes of cell apoptosis rate and cell cycle. RT-PCR method was used to detect the expression of bcl-2 and bax mRNA, and Western blot was used to detect the expression of bcl-2 and bax protein.

RESULTSMTT test revealed that resveratrol showed significant inhibiting effect on ls174t cells in a concentration- and time-dependent manner. In the concentration range of 25, 50, 100, 200 and 400 micromol/L, the inhibition rate after resveratrol treatment for 24 hours was respectively 1.0%, 9.1%, 17.4%, 27.8% and 66.5%, while the inhibition rate after treatment for 48 hours was respectively 3.6%, 13.7%, 30.2%, 58.4% and 86.1%, and the inhibition rate after treatment for 72 hours was 18.1%, 33.0%, 48.6%, 61.2% and 89.4%, respectively, showing a very significant difference (P < 0.01). Typical ultrastructural apoptotic changes were observed in resveratrol-treated ls174t cells. It was found through FCM assay that resveratrol caused apoptosis in ls174 cells and blocked the cell cycle at S phase. RT-PCR and Western blot test showed that after the treatment of colon cancer cells with resveratrol at different concentrations (25, 50, 100 and 200 micromol/L), the expression level of bcl-2 was decreased, while expression level of bax was increased. The highest inhibition rate was 47.9%. In 200 mg/kg and 800 mg/kg resveratrol treatment groups, the weight of subcutaneously transplanted tumors in nude mice was 4.10 +/- 0.18 g and 3.05 +/- 0.35 g, respectively, the difference was significant compared with that of the control group (P < 0.01).

CONCLUSIONResveratrol can inhibit the growth of ls174t cells through apoptosis induction. The mechanism is probably related to inhibition of anti-apoptotic factor bcl-2 and enhancement of expression of apoptotic factor bax.

Animals ; Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; metabolism ; pathology ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; RNA, Messenger ; metabolism ; Stilbenes ; pharmacology ; Tumor Burden ; drug effects ; bcl-2-Associated X Protein ; genetics ; metabolism

Aged ; Genital Neoplasms, Male ; pathology ; Humans ; Male ; Neurilemmoma ; pathology ; Scrotum

OBJECTIVETo review the current status and progress on nuclear medical molecular imaging of angiogenesis.

DATA SOURCESA literature search was performed in Medline and PubMed published in English up to May 31, 2012. The search terms were molecular imaging, nuclear medicine and angiogenesis.

STUDY SELECTIONArticles studying molecular imaging of angiogenesis using radionuclide were selected and reviewed.

RESULTSMolecular imaging has been used for studying angiogenesis by targeting integrin αVβ3, VEGF/VEGFR, and matrix metalloproteinases (MMPs) with radionuclide-labeled tracers. The technology has been shown to be able to assess the angiogenesis status and/or predict the efficacy of anti-angiogenic therapy. Future directions of the research on the molecular imaging of angiogenesis include development of new tracers with better tumor targeting efficacy, desirable pharmacokinetics, and easy translation to clinical applications.

CONCLUSIONAdvances in molecular imaging of angiogenesis using radioculcide will make the technology a valuable tool for personalized anti-angiogenesis treatment.

Humans ; Integrins ; analysis ; Matrix Metalloproteinases ; analysis ; Neoplasms ; blood supply ; Neovascularization, Pathologic ; diagnosis ; Receptors, Vascular Endothelial Growth Factor ; analysis ; Vascular Endothelial Growth Factor A ; analysis

The present study investigated the enhanced radiosensitivity of U-251 cells induced by sodium butyrate (NaB) and its possible mechanisms. Increased radiosensitivity of U251 cells was examined by clonogenic cell survival assays. The expression of Ku70 mRNA and protein was detected by using RT-PCR and Western blotting respectively. γ-H2AX foci were measured at different time points after ionizing irradiation alone or combined with NaB treatment. The results showed that cell survival rate was significantly reduced, both D0 and Dq values were decreased (D0: 1.43 Gy vs. 1.76 Gy; Dq: 1.22 Gy vs. 2.05 Gy) after the combined treatment as compared with irradiation alone, and sensitivity enhancing ratio (SER) reached 1.23. The average number of γ-H2AX foci per cell receiving the combined treatment was significantly increased at different time points, and the expression levels of Ku70 mRNA and protein were suppressed by NaB in a dose-dependent manner. It was concluded that enhanced radiosensitivity induced by NaB involves an inhibited expression of Ku70 and an increase in γ-H2AX foci, which suggests decreased ability in DSB repair.

The aim of this study was to investigate the effect of arsenic trioxide (As(2)O(3)) combined with bortezomib on the proliferation, apoptosis and beta-catenin level in myeloma cell lines. Myeloma cell lines RPMI8226, CZ-1 and NCI-H929 were treated with As(2)O(3) and bortezomib alone or in combination for 48 hours. Trypan blue dye exclusion and modified MTT were used to assess the cell viability. Flow cytometry with Annexin V-FITC and PI staining was used to detect the apoptosis rate. The beta-catenin level was analyzed by Western blot. The results showed that IC(50) of bortezomib to RPMI8226, CZ-1 and NCI-H929 were 46.9, 20.7 and 6.8 nmol/L, respectively. After the combination treatment with bortezomib (5 nmol/L) and As(2)O(3) (1 micromol/L), the cell viability of RPMI8226, CZ-1 and NCI-H929 decreased from 88.99%, 72.23%, 51.06% to 54.01%, 39.59%, 25.00%(p<0.05), the apoptosis rate increased from 11.1+/-0.1%, 26.8+/-1.7%, 46.8+/-5.5% to 36.1+/-2.2%, 60.4+/-3.8%, 76+/-5.6% (p<0.01) respectively. The Q value of two groups lies between enhancement and significant enhancement (1.198 - 3.75). Besides, beta-catenin levels in tested cell lines were decreased to 24.15%, 31.85%, 33.72% of their basic constitutions respectively (p<0.05). It is concluded that combination treatment of As(2)O(3) and bortezomib can enhance the proliferation inhibition and apoptosis induction of bortezomib to myeloma cell lines, reduce beta-catenin level, and increase the sensitivity of myeloma cell lines to bortezomib.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Boronic Acids ; pharmacology ; Bortezomib ; Cell Proliferation ; drug effects ; Drug Synergism ; Humans ; Multiple Myeloma ; metabolism ; pathology ; Oxides ; pharmacology ; Pyrazines ; pharmacology ; Tumor Cells, Cultured ; beta Catenin ; metabolism

OBJECTIVETo explore the clinical significance of serum free light chain (sFLC) levels in nonsecretory multiple myeloma (NSMM).

METHODSNine NSMM patients were hospitalized in our department from Feb 2002 to Sep 2006 and no M-components was found in their serum and urine by immunofixation electrophoresis (IFE). sFLC was assayed by immuno-nephelometry. The clonality of sFLC was estimated by serum kappa:lambda sFLC ratio. Meanwhile, serum immunoglobulin, total kappa and lambda light chain level were also determined in these patients.

RESULTSIncreased serum concentrations of either kappa or lambda sFLC (and abnormal kappa/lambda ratios) were detected in 6 of 9 patients with NSMM although their serum immunoglobulin levels were not elevated and total kappa:lambda light chain ratios (1.32 - 2.20) were in the reference range. All the 9 patients had clonal IgH gene rearrangements.

CONCLUSIONQuantification of sFLC by immuno-nephelometry is more sensitive than that of serum total light chain measurement and is helpful in estimating the clonality of the light chain in patients with NSMM.

Adult ; Female ; Humans ; Immunoglobulin Light Chains ; blood ; Male ; Middle Aged ; Multiple Myeloma ; blood ; Nephelometry and Turbidimetry ; Sensitivity and Specificity