11.1mmol/L were treated by 2 weeks CSⅡ.The elements of 2 hours postprandial,insulin,C-peptide, HbAlc,HOMA-?,and HOMA-IR were analyzed and compared before and after treatment,and the control of post- prandial of patients for 2 years was observed.Results The excellent control of FPG and 2h PG in 36 patients were achieved stably in(5.6?0.4)mmol/L and(8.2?1.4)mmol/L below the condition of(13.6?1.5)mmol/L and (20.1?4.0)mmol/L before treatment(P

Keratorefractive surgery changes the central corneal thickness (CCT) and corneal curvature, which could influence the Goldmann applanation tonometer (GAT) and non-contact tonometer (NCT) measurements of intraocular pressure (IOP), but not dynamic contour tonometer(DCT). During the procedure of LASIK, there is a transient rise of IOP, which increases the risks of optic nerve damage. Meanwhile, the presence of functioning filtering blebs may affect the choice and outcome of refractive surgery, or even becomes a contraindication of surgery. Steroids are typically used after keratorefractive surgery, which could lead to IOP elevation. Hence it is important to monitor IOP after LASIK and to be aware of inaccurate IOP readings due to corneal flap interface fluid. Treating patients with postoperative elevated IOP after keratorefractive surgery is similar to that for patients with glaucoma. This review will address the issues surrounding the safety, relevant complications and implications of keratorefractive surgeries on glaucoma and relevant diagnostic tests.

OBJECTIVETo study the anti-inflammation effect of volatile oil of Centipeda minima and the mechanism of action.

METHODThe animal model was induced by the Car injection into intrapleural of rats, to observe the effect of VOCM on acute inflammation.

RESULTVOCM was able to inhibit the increase of NO, CRP and proinflammatory cytokines such as TNFalpha in the acute inflammation of the rat body.

CONCLUSIONVOCM has a protective effect on acute pleural effusion in rats induced by an intrapleural injection of Car.

Animals ; Asteraceae ; chemistry ; C-Reactive Protein ; metabolism ; Carrageenan ; Dinoprostone ; metabolism ; Interleukin-8 ; blood ; Leukocyte Count ; Male ; Nitric Oxide ; metabolism ; Oils, Volatile ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Pleural Effusion ; chemically induced ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo evaluate the effect and safety of the recombinant human growth hormone (rhGH) in the treatment of male climacteric syndrome and to investigate the specificity and sensitivity of insulin-like growth factor-1 (IGF-1) and serum total testosterone as the curative effect index.

METHODSForty patients aged 40-75 with male climacteric syndrome were divided into two groups randomly and injected with rhGH 4 IU (Group A) or 8 IU (Group B). The patients were followed up for about 12 weeks after 12-week treatment and then asked the questions of the assessed index of male climacteric syndrome at the 4th, 8th and 12th week of the treatment and 12 weeks after the treatment. The serum IGF-1, total testosterone (TT) and prostatic specific antigen(PSA) were measured before and after the treatment. The data were analysed by the software of SPSS 12.0 for Windows.

RESULTSThe scores of the 4th, 8th and 12th week and the follow-up significantly declined compared with the baseline (P < 0.01), but did not differ significantly between Groups A and B (P > 0.05). After the treatment, serum total testosterone, PSA and prostate volume had no obvious change (P > 0.05), and the IGF-1 level was markedly higher than the baseline and the normal public. No obvious side effect was found during the treatment and follow-up.

CONCLUSIONSmall dosage of rhGH(4 IU/week) for 12 weeks can effectively treat male climacteric syndrome. The value of IGF-1 was parallel with the treatment effects. Short-time and small-dosage treatment with rhGH is safe and has little side effect.

Andropause ; Follow-Up Studies ; Human Growth Hormone ; adverse effects ; therapeutic use ; Humans ; Insulin-Like Growth Factor I ; metabolism ; Male ; Prostate-Specific Antigen ; blood ; Sensitivity and Specificity ; Syndrome ; Testosterone ; blood

Animals ; Antigen-Antibody Complex ; therapeutic use ; DNA, Viral ; blood ; Dendritic Cells ; immunology ; Ducks ; Female ; Hepatitis B Antibodies ; blood ; immunology ; Hepatitis B Surface Antigens ; immunology ; Hepatitis B Vaccines ; immunology ; therapeutic use ; Hepatitis B e Antigens ; blood ; immunology ; Hepatitis B virus ; immunology ; Hepatitis B, Chronic ; blood ; immunology ; therapy ; Humans ; Male ; Mice ; T-Lymphocytes

OBJECTIVEMajor histocompatibility complex class I C-related molecules A and B (MICA and MICB) are innate immune system ligands for the NKG2D receptor expressed by natural killer cells and activated CD8(+)T cells. Our previous study showed that 5-aza-2'-deoxycytidine (5-aza-dC), a DNA methyltransferase inhibitor, can induce the expression of MICB and sensitized cells to NKL-cell-mediated cytolysis. The aim of this study was to determine the expression level of MICA in HepG2 cells (an HCC cell line) and L02 cells ( a normal liver cell), and to investigate the effect of 5-aza-dC on MICA expression in HepG2 cells.

METHODSCells were treated with 5-aza-dC, caffeine and ATM-specific siRNA. The cell surface MICA protein on HepG2 cells and L02 cells was determined using flow cytometry. The mRNA level was detected using real time RT-PCR.

RESULTSMICA was undetectable on the surface of L02 cells, but was highly expressed on HepG2 cells. MICA expression was upregulated in response to 5-aza-dC treatment (P less than 0.05), and the upregulation of MICA was partially prevented by pharmacological or genetic inhibition of ataxia telangiectasia mutated (ATM) kinase (P less than 0.05).

CONCLUSIONOur data suggest that 5-aza-dC induces the expression of MICA by a DNA damage-dependent mechanism.

Ataxia Telangiectasia Mutated Proteins ; Azacitidine ; analogs & derivatives ; pharmacology ; Caffeine ; pharmacology ; Carcinoma, Hepatocellular ; metabolism ; Cell Cycle Proteins ; antagonists & inhibitors ; metabolism ; Cell Line ; Cell Membrane ; metabolism ; DNA Damage ; DNA-Binding Proteins ; antagonists & inhibitors ; metabolism ; Flow Cytometry ; Hep G2 Cells ; Hepatocytes ; metabolism ; Histocompatibility Antigens Class I ; genetics ; metabolism ; Humans ; Liver Neoplasms ; metabolism ; Protein-Serine-Threonine Kinases ; antagonists & inhibitors ; metabolism ; RNA, Messenger ; genetics ; metabolism ; RNA, Small Interfering ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Suppressor Proteins ; antagonists & inhibitors ; metabolism ; Up-Regulation

OBJECTIVETo evaluate the feasibility and safety of peripheral CD34+ cell mobilization in patients with severe autoimmune disease.

METHODSForty-two patients underwent a total of 46 mobilizations by the regimen of cyclophosphamide 2-3 g/m2+ recombinant human granulocyte colony stimulating factor (rhG-CSF) 5 microg x kg(-1) x d(-1). The positive selection of CD34+ cell was performed through the CliniMACS.

RESULTSIn 8.1 +/- 2. 3 days after administration of cyclophosphamide, the peripheral white blood cell and mononuclear cell (MNC) decreased to the lowest level. In 3.7 +/- 1.6 days after injection of rhG-CSF, the peripheral absolute MNC and CD34+ cell counts were 0.95 x 10(9)/L and 0.035 x 10(9)/L, respectively. After 2.4 +/- 0.6 times of leukapheresis, there gained 4.46 x 10(8)/kg of MNC and 5.26 x 10(6)/kg of CD34+, respectively. After mobilization, the underlying diseases were ameliorated more or less. In systemic lupus erythematosus (SLE) patients, SLE Disease Activity Index (SLEDAI) decreased from a median of 17 to 3 (P < 0.01). In rheumatic arthritis patients, an American College of Rheumatology criteria for 20% (ACR20) response was achieved in all five patients. Totally, 17.4% of patients whose absolute neutrophil count < 0.5 x 10(9)/L suffered infection, and 31.0% of patients had bone pain after the injection of rhG-CSF. Two patients suffered severe complications, one with acute renal failure and recovered by hemodialysis, the other died of thrombotic thrombocytopenic purpura. Failed mobilization occurred in three patients.

CONCLUSIONSSufficient CD34+ cells can be mobilized by low dose of cyclophosphamide and rhG-CSF. CD34+ cell mobilization for treatment of severe autoimmune disease not only is appropriate in both effectiveness and safety but ameliorates disease also.

Adolescent ; Adult ; Antigens, CD ; blood ; Antigens, CD34 ; blood ; Autoimmune Diseases ; therapy ; Cyclophosphamide ; pharmacology ; therapeutic use ; Female ; Hematopoietic Stem Cell Mobilization ; methods ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells ; immunology ; Humans ; Leukapheresis ; methods ; Leukocyte Count ; Leukocytes ; drug effects ; Leukocytes, Mononuclear ; drug effects ; Male ; Middle Aged ; Young Adult

OBJECTIVETo evaluate the therapeutic effects of magnetically labeled mononuclear stem cells (MR-MNC) and mesenchymal stem cells (MR-MSC) transplantation in a swine acute myocardial infarction (AMI) model by MR imaging.

METHODSAMI model was established in swines by balloon occlusion of the left anterior descending coronary artery, 10(7) autologous MR-MSC (n = 7), MR-MNC (n = 6) or PBS (n = 6) were delivered via intracoronary infusion within 1 week after AMI [(4.8 +/- 1.3) days]. Changes of infarct size and cardiac function were assessed with the use of 3.0T MR scanner before AMI, at 1 and 8 weeks post AMI.

RESULTSMagnetically labeled stem cells could be identified in the region of AMI by cardiac MR imaging. Eight weeks post transplantation, infarct size was significantly reduced in MR-MSC transplantation group (8.5% +/- 0.5% vs. 24.7% +/- 3.1%, P < 0.05) and in MR-MNC transplantation (12.3% +/- 1.5% vs. 26.1% +/- 1.5%, P < 0.05) while infarct size remained unchanged in PBS group (P > 0.05) compared to values at 1 week post AMI, left ventricular ejection fraction (LVEF) was also significantly higher in MR-MSC transplantation group (56.9% +/- 1.3% vs. 40.7% +/- 2.0%, P < 0.05) and MR-MNC transplantation group (52.8% +/- 1.4% vs. 41.9% +/- 3.3%, P < 0.05) compared to LVEF at 1 week post AMI. LVEF increase was more significant in swines received MR-MSC transplantation than MR-MNC transplantation (16.2% +/- 1.2% vs. 10.9% +/- 3.0%, P < 0.05). Prussian blue staining identified stem cells in corresponding myocardial regions with as by MRI. Western blot analysis demonstrated that cardiac expressions of myosin heavy chain (MHC) in MR-MSC group (100.3 +/- 5.5) and in MR-MNCs group (95.5 +/- 4.2) were significantly higher than that in PBS group (75.7 +/- 5.7, P < 0.05), myocardial troponin T (cTNT) expression in MR-MSC group (124.0 +/- 5.8) and MR-MNC group (118.4 +/- 4.4) were also significantly higher than in PBS group (93.3 +/- 3.9, P < 0.05) while MMP2/TIMP1 ratios in MR-MSC group (0.6 +/- 0.1) and MR-MNC group (0.6 +/- 0.1) were significantly lower than that in PBS group (4.2 +/- 0.2, P < 0.05).

CONCLUSIONSMagnetically labeled MR-MSC and MR-MNC homed to heart post myocardial infarction and reduced infarct size, improved cardiac function. MR-MSC is superior to MR-MNC on improving cardiac function.

Animals ; Disease Models, Animal ; Magnetic Resonance Imaging ; Male ; Mesenchymal Stem Cell Transplantation ; Myocardial Infarction ; therapy ; Swine ; Swine, Miniature ; Treatment Outcome

Glioblastoma (GBM) is the most common primary brain tumor, which is prone to recurrence and metastasis with poor prognosis. In recent years, immunotherapy has prolonged the survival of patients with GBM, providing a new option for the treatment of GBM. Target selection is very important for immunotherapy. Epidermal growth factor receptor variant III (EGFRvIII) is highly expressed on the surface of GBM cells in some patients, and EGFRvIII was not expressed in normal tissues. EGFRvIII are pivotal for the occurrence and progression of GBM, various targeted therapy including immunotherapy is promising to improve the efficacy of GBM. Currently, there are various approaches to target EGFRvIII, including humanized monoclonal antibodies, adoptive cell therapies and therapeutic vaccines. In this review, we focus on the preclinical and clinical findings of targeting EGFRvIII for GBM.

Child ; Humans ; Chromosomes, Human, Pair 16 ; Leukemia, Myeloid, Acute ; Neoplasms, Multiple Primary/genetics* ; Oncogene Proteins, Fusion/genetics* ; RNA-Binding Protein FUS/genetics* ; Sarcoma, Myeloid/genetics* ; Transcriptional Regulator ERG/genetics* ; Translocation, Genetic