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Biomedical subjects

Hua He

Publications and source records attributed to Hua He.

At least 37 records · Page 2Linked to original sources

Induction of apoptosis and cell cycle arrest by a specific c-Jun NH2-terminal kinase (JNK) inhibitor, SP-600125, in gastrointestinal cancers.

The c-Jun NH(2)-terminal kinase (JNK) is activated in several tumor cell lines. The aim of this study was to determine the effects of SP-600125, a specific JNK inhibitor, on the viability, apoptosis, cell cycle distribution of gastrointestinal cancer cells, and the potential anti-tumor mechanisms. Three gastric cancer cell lines, AGS, BCG-823 and MKN-45, and three colorectal cancer cell lines, SW1116, COLO205 and HT-29, were used. Cells were treated with SP-600125, and cell viability, apoptosis and cell cycle distribution, caspase-3 activity, expression of JNK and apoptosis related proteins were detected. SP-600125 inhibited cell proliferation by 10-80% for the different cell lines, and increased apoptosis by 1.5-4.5 folds for COLO205, BCG-823, MKN-45, AGS cells. Caspase-8 and caspase-3 were involved in the induction of apoptosis. SP-600125 caused G2/M cell cycle arrest and elevation of cyclin B1 and p27(kip). The differential response in cells to SP-600125 was associated with the basal level of phosphorylated JNK2. It is concluded that SP-600125 inhibits proliferation, induces apoptosis and causes cell cycle arrest in gastrointestinal cancer cells, indicating that JNK inhibitors have an anti-tumor effect and are potential therapeutic agents for cancers.

Anthracenes↗

HSF1 down-regulates XAF1 through transcriptional regulation.

Studies have indicated the role of HSF1 (heat-shock transcription factor 1) in repressing the transcription of some nonheat shock genes. XAF1 (XIAP-associated factor 1) was an inhibitor of apoptosis-interacting protein with the effect of antagonizing the cytoprotective role of XIAP. XAF1 expression was lower in gastrointestinal cancers than in normal tissues with the mechanism unclear. Here we showed that gastrointestinal cancer tissues expressed higher levels of HSF1 than matched normal tissues. The expression of XAF1 and HSF1 was negatively correlated in gastrointestinal cancer cell lines. Stress stimuli, including heat, hypo-osmolarity, and H2O2, significantly suppressed the expression of XAF1, whereas the alteration of HSF1 expression negatively correlated with XAF1 expression. We cloned varying lengths of the 5'-flanking region of the XAF1 gene into luciferase reporter vectors, and we evaluated their promoter activities. A transcription silencer was found between the -592- and -1414-nucleotide region that was rich in nGAAn/nT-TCn elements (where n indicates G, A, T, or C). A high affinity and functional HSF1-binding element within the -862/-821-nucleotide region was determined by electrophoretic mobility shift assay and chromatin immunoprecipitation assay. Inactivation of this "heat-shock element" by either site-directed mutation or an HSF1 inhibitor, pifithrin-alpha, restored the promoter activity of the silencer structure. Moreover, pretreatment with antioxidants suppressed HSF1 binding activity and increased the transcriptional activity and expression of XAF1. These findings suggested that endogenous stress pressure in cancer cells sustained the high level expression of HSF1 and subsequently suppressed XAF1 expression, implicating the synergized effect of two anti-apoptotic protein families, HSP and inhibitors of apoptosis, in cytoprotection under stress circumstances.

5' Flanking Region↗

An electrochemical quartz crystal impedance study on anti-human immunoglobulin G immobilization in the polymer grown during dopamine oxidation at an Au electrode.

The polymeric film grown during dopamine oxidation at an Au electrode was studied as a novel matrix for immobilizing anti-human immunoglobulin G (IgG) via the electrochemical quartz crystal impedance analysis (EQCIA) method. The growth of the polymeric films at Au electrodes during dopamine oxidation in neutral phosphate buffer (pH 7.4) and the immobilization of anti-human IgG into the polymeric films during their growth have been traced at real time. Lysozyme control experiments suggested that anti-human IgG was electrostatically incorporated into the polymeric film. Also, the porosity of the polymeric films has been discussed by measuring the "wet" and "dry" frequency shifts. Compared with a polypyrrole film immobilized with anti-human IgG, the proposed matrix possessed a larger amount of specific binding sites for human IgG by subsequent immunoreaction tests. The association constant of the anti-human IgG immunoreaction was obtained with satisfactory results.

Crystallization↗

Amniotic membrane induces apoptosis of interferon-gamma activated macrophages in vitro.

Amniotic membrane (AM) used as a temporary or permanent graft for ocular surface reconstruction has a potent anti-inflammatory effect. We would like to investigate the mechanism whereby AM induces macrophage apoptosis in vitro. Mouse macrophages, Raw 264.7 cells, were cultured on plastic, type I collagen, corneal stromal slice or AM stromal matrix in serum-free medium with or without interferon-gamma (IFN-gamma). Cells were stained by LIVE/DEAD assay, Hoechst-33342, and TUNEL assay for cell death and apoptosis. Cell lysates and conditioned media were analysed by Cell Death Detection ELISA assay for quantitation of apoptosis. Conditioned media were also analysed by Griess assay for the nitrite concentration and ELISA assay for tumour necrosis factor alpha (TNF-alpha) concentration. Lysates of cells were subjected to Western blot analyses of IKK-alpha, IKK-beta, p65 (RelA) subunit of nuclear factor kappaB (NF-kappaB), total Akt, phospho-Akt (Ser473), and phospho-FKHR (Thr24)/phosphor-FKHRL1 (Thr32). At 48hr after cultivation, cells showed a low level of apoptosis when cultured on plastic, type I collagen and corneal stromal slice with or without IFN-gamma and on AM without IFN-gamma. Nevertheless, cells showed a significant increase of apoptosis when cultured on AM with IFN-gamma activation, and this phenomenon became apparent only after 48 hr. IFN-gamma-activated macrophages on plastic continuously produced nitric oxide (NO) and TNF-alpha during 72 hr culturing. In contrast, there was no NO and TNF-alpha production after 48 hr culture on AM. NO inhibitors, L-NMMA and L-NIL, attenuated NO production of IFN-gamma-activated macrophages on AM, while apoptosis was not decreased accordingly. Expression of IKK-alpha, IKK-beta, p65 (RelA) subunit of NF-kappaB total Akt, phosopho-Akt (Ser473), and phospho-FKHR (Thr24)/FKHRL1 (Thr32) was all down-regulated in IFN-gamma-activated macrophages cultured on AM. In conclusion, AM stromal matrix induces apoptosis of IFN-gamma activated, but not non-activated macrophages, not through the generation of NO, but instead by down-regulating anti-apoptotic NF-kappaB and Akt-FKHR signalling pathways.

Amnion↗

Keratocan expression of murine keratocytes is maintained on amniotic membrane by down-regulating transforming growth factor-beta signaling.

Keratocytes in the corneal stroma express keratan sulfate-containing proteoglycans including cornea-specific keratocan. On plastic dishes, human, bovine, and rabbit keratocytes lose their characteristic dendritic morphology and keratocan expression when cultured in serum-containing media. Herein, we demonstrated that murine keratocytes also acquired a fibroblastic shape and lost keratocan expression after first passage when cultured on plastic in the presence of serum. In contrast, cells expanded on human amniotic membrane (AM) stromal matrix maintained a three-dimensional dendritic morphology and expressed keratocan mRNA and protein for at least 8 passages before senescence. When keratocytes were cultured on AM, the promoter activity of transforming growth factor (TGF)-beta2 and TGF-beta receptor II was down-regulated as compared with that on plastic. Furthermore, cells on AM continuously retained Smad 2 and Smad 4 in the cytoplasm and did not express alpha-smooth muscle actin, even when 10 ng/ml TGF-beta1 was added in a serum-free medium for up to 5 days. In parallel to such down-regulation of TGF-beta signaling, keratocan promoter-driven ECFP expression was observed in cells cultured either on AM in the presence of serum or on plastic containing serum treated with a neutralizing antibody to TGF-beta. Collectively, these results indicate that down-regulation of Smad-mediated TGF-beta signaling is an important mechanism for cultured keratocytes to maintain a normal phenotype while continuously expanded in a serum-containing medium. This strategy of suppressing TGF-beta signaling, achieved by AM stromal matrix in part via suppression of TGF-beta gene transcription, can be used to expand keratocytes in culture without the use of AM in the future.

Animals↗

[Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study].

OBJECTIVE: To study the effect of nonmyeloablative allogeneic peripheral blood stem cell (NST) transplantation combined with imatinib in the treatment of chronic myeloid leukemia (CML). METHODS: Ten CML patients, 5 males and 5 females, aged 21-41, 3 in chronic phase (CP), 4 in accelerated phase (AP) and 3 in blast crisis phase (BP), were treated with imatinib (400-1500 mg/d) before (n = 10) and/or after (n = 6) NST transplantation. The donors were HLA-identical (n = 4), 5/6 antigen-matched (n = 2), 4/6 antigen-matched (n = 2), 3/6 antigen-matched (n = 1) siblings or haplo-identical mothers (n = 2). The preparative regimen included cytoxin (CTX), Ara-C, and fludarabine combined with antithymocyte globulin (ATG) or anti-CD3 monoclonal antibody. Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine (CSA) and mycophenolate mofetil (MMF), or with low-dose methotrexate (MTX) or zenapax. RESULTS: All the 10 patients showed donor cell chimerism at different degree: three had full chimerism (> 95%) and seven mixed chimerism (44%-95%). Mixed chimerism in 6 cases had been transformed into full chimerism during 1.5-10 months after NST transplantation through immunosuppressive agent withdrawal, donor peripheral blood stem cell/donor lymphocyte infusion or treatment of imatinib. The time needed for increase of the number of neutrophils to more than 0.5 x 10(9)/L was 16 d days (10-21 days). The time needed for increase of the number of platelets more than 20 x 10(9)/L was 10 days (4-15 days). 6 cases had I-II degrees acute and chronic GVHD of skin. 2 case had III-IV degrees chronic GVHD. 2 cases died of transplantation-related complication 27 and 45 days after transplantation respectively. One patient died of III-IV degrees cGVHD. Seven patients remained alive after a median follow-up of 14.5 months (7-23 months). The time needed for bcr/abl becoming negative was 33-130 days. None case relapsed during the following-up. CONCLUSION: An effective and safer method for CML, especially advanced CML treatment of NST transplantation combined with imatinib before and after transplantation reduces the leukemic cell load before transplantation, inhibits the proliferation of residual leukemic cells, promotes full chimerism change and enhanced the effect of graft versus leukemia.

Adult↗

Solid-phase extraction of methadone enantiomers and benzodiazepines in biological fluids by two polymeric cartridges for liquid chromatographic analysis.

The aim of this work was to present the advantages of two polymeric cartridges (Oasis HLB from Waters and Abselut Nexus from Varian) for the solid-phase extraction of methadone enantiomers and its major metabolite, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) and of some benzodiazepines (diazepam, flunitrazepam, nitrazepam, oxazepam) in serum and urine in comparison with classical C18-bonded-silica cartridges or liquid extraction. After addition of serum or urine samples, these two cartridges were washed with a water-methanol mixture (95:5, v/v) and eluted with diethylether. After rapid evaporation, the residue was regenerated with mobile phase and injected either in a chiral column (Cyclobond I-2000 RSP) for methadone enantiomers and its metabolite or in a reversed-phase column (Symmetry Shield RP8) for benzodiazepines. The results showed that the chromatograms of blank serum and urine were cleaner than those obtained from classical solid-phase extraction or liquid extraction. The recoveries from these two polymeric cartridges were higher (95-102%) than those obtained by the two previous classical methods and the total time for extraction and solvent evaporation was also shorter (about 6-7 min). For methadone and benzodiazepine extraction, the use of acidic or alkaline buffer was not necessary.

Animals↗

A simultaneous electrochemical impedance and quartz crystal microbalance study on antihuman immunoglobulin G adsorption and human immunoglobulin G reaction.

The quartz crystal microbalance (QCM), in combination with electrochemical impedance spectroscopy (EIS), has been utilized to monitor in situ antihuman IgG (hIgG) adsorption on bare poly(o-phenylenediamine) (PPD)- and 1-dodecanethiol (C12SH)-modified Au electrodes and succeeding human IgG reaction, respectively. The resonant frequency (f) and the motional resistance (R(1)) of the piezoelectric quartz crystal (PQC) as well as electrochemical impedance (EI) parameters were measured and discussed. The standard heterogeneous rate constants of the ferricyanide/ferrocyanide couple before and after the antibody adsorption and antibody-antigen reactions were determined. The results show that the amount for antibody adsorption was the greatest on the most hydrophobic (1-dodecanethiol-modified) surface, while the antibody bioactivity was almost identical on the three kinds of surfaces. Two parameters simultaneously obtained, Deltaf and DeltaC(s) (interfacial capacitance), have been used for the first time to estimate both the association constant of the immunoreaction and the valence of antigen with satisfactory results. The proposed method may find wide application in interfacial biochemistry studies for its advantages in providing real-time multidimensional piezoelectric and electrochemical impedance information.

Adsorption↗

[Effect of Astragalus injection on plasma levels of apoptosis-related factors in aged patients with chronic heart failure].

OBJECTIVE: To investigate the effect of Astragalus injection (AI) on plasma levels of apoptosis-related factors in aged patients with chronic heart failure (CHF). METHODS: Seventy-two CHF patients were randomly divided into the AI group (36 cases) treated with AI and the control group (36 cases) treated with conventional treatment. Plasma levels of soluble Fas (sFas), soluble Fas ligand (sFasL), tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assays (ELISA) with monoclonal anti-human antibodies. Besides, New York Heart Association (NYHA) grading was assessed according to improved symptoms and left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and left ventricular ejection fraction (LVEF) were assessed by echocardiogram after 4 weeks of treatment. RESULTS: After 4 weeks of treatment, NYHA grading was markedly improved in the two groups, but it was significantly better in AI group than that in the control group (P < 0.05). As compared with the control group, sFas, sFasL, TNF-alpha and IL-6 in the AI group were obviously lower, the difference between the two groups and between before and after treatment were significant (P < 0.05 or P < 0.01). Moreover, in AI group, LVESV and LVEDV decreased, LVEF increased, which was significantly different than that before treatment (P < 0.05), respectively. CONCLUSION: AI could lower plasma levels of apoptosis-related factors, and is one of the effective drugs in improving cardiac function in the aged patients with CHF.

Age Factors↗

Intrastromal invasion by limbal epithelial cells is mediated by epithelial-mesenchymal transition activated by air exposure.

Corneal epithelial stem cells are located in the basal layer of the limbus between the cornea and the conjunctiva. Regulation of these limbal epithelial progenitor cells by the stromal niche dictates corneal surface health. To further characterize this process, limbal explants were cultured at the air-fluid interface, termed air-lifting, to stimulate the niche. As compared to submerged cultures, air-lifting significantly promoted epithelial stratification, migration, proliferation, and intrastromal invasion by limbal epithelial cells. Epithelial intrastromal invasion was noted when the limbal, but not corneal, epithelium was recombined with the limbal stroma containing live, but not dead, cells. Invading limbal basal cells displayed up-regulated nuclear expression of p63 and Ki67, down-regulated E-cadherin and cornea-specific keratin 3, and switched expression of beta-catenin from intercellular junctions to the nucleus and cytoplasm, indicating the activation of the Wnt/beta-catenin pathway. Invaded cells isolated by collagenase from the stroma of air-lifted, but not submerged, explants showed vivid clonal growth on 3T3 fibroblast feeder layers and complete epithelial-mesenchymal transition by expressing nuclear p63 and cytoplasmic S100A4. These findings collectively suggest that epithelial-mesenchymal transition via the Wnt/beta-catenin pathway influences the fate of limbal epithelial cells, likely to be progenitor cells, between regeneration and fibrosis when the stromal niche is activated.

Air↗

[Effect of astraglus injection on serum apoptosis relevant factors in patients with chronic heart failure].

OBJECTIVE: To investigate the effect of Astragalus injection (AGI) on serum apoptosis related factors such as soluble Fas (sFas), soluble Fas ligand (sFasL) and tumor necrosis factor alpha (TNF-alpha) in patients with chronic heart failure (CHF). METHODS: Eighty-four patients with CHF of NYHA II-IV grade were randomly divided into two groups, the treated group (42 patients) treated with AGI and the control group (42 patients) treated with routine treatment. The level of serum sFas, sFasL, and TNF-alpha were measured with ELISA before and after treatment. At the same time, patients' heart function were graded according to the NYHA classification and their indices of left ventricular function were determined. RESULTS: Patients' NYHA grade was improved in both groups after treatment (P < 0.05 or P < 0.01), and it was better in the treated group than that in the control group (P < 0.05). Moreover, in the treated group, the left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) decreased, the left ventricular ejection fraction (LVEF) increased, which was significantly different than that before treatment (P < 0.05) respectively; level of serum apoptosis related factors sFas, sFas L and TNF-alpha were significantly decreased after treatment, showing significant difference as compared with those before treatment or with those in the control group after treatment (P < 0.05 or P < 0.01). While all indices had no obvious change in the control group. CONCLUSION: AGI may be regarded as an effective remedy for treatment of CHF owing to its effects in decreasing the level of serum apoptosis related factors in patients with CHF.

Adult↗

[Effect of RNAi-mediated survivin gene silencing on apoptosis of ovarian cancer cell lines SKOV3 and SKOV3/ADM].

BACKGROUND & OBJECTIVE: RNA interference (RNAi) has been widely used in tumor gene therapy, antivirus, and gene drug selection. Survivin gene is highly expressed in ovarian cancer cell line SKOV3 and drug-resistant cell line SKOV3/ADM, and is an ideal target of gene therapy for ovarian cancer. This study was to explore effect of RNAi-mediated Survivin gene silencing on apoptosis of SKOV3 and SKOV3/ADM cells. METHODS: Recombinant plasmid pshRNA-Survivin was transfected into SKOV3 and SKOV3/ADM cells. The expression of Survivin was detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. The apoptosis of SKOV3 and SKOV3/ADM cells after transfection were evaluated by AO/EB dyeing, TUNEL, and flow cytometry. RESULTS: After transfection of pshRNA-Survivin, mRNA and protein levels of Survivin gene in SKOV3 and SKOV3/ADM cells were obviously reduced; the apoptosis of SKOV3 and SKOV3/ADM cells were significantly higher in transfection group than in control group (P0.01); 48 h after transfection, the apoptosis rate was 14.05% in SKOV3 cells, and 21.02% in SKOV3/ADM cells, no obvious apoptosis was detected in control cells. CONCLUSION: pshRNA-Survivin could reduce the expression of Survivin gene, and induce apoptosis of SKOV3 and SKOV3/ADM cells.

Antineoplastic Agents↗

[Feasibility and predicted equations of spirometry in Shenzhen preschool children].

UNLABELLED: Morbidity of chronic lung disease in young children is relatively high, and could increase in the future. Pulmonary function testing is used for clinical assessment of patients with suspected or obvious pulmonary disease to assess the severity of dysfunction and to evaluate therapeutic effectiveness. In the recent few years, forced expiratory parameters assessing lung function have been measured in older children. In order to assess abnormalities of lung function in preschool patients with respiratory disorders based on changes of forced expiratory parameters, adequate reference values are needed. However, such data in healthy preschool children remain scant in the literature. OBJECTIVE: The aim of this study was to characterize the spirometry of preschool children and establish the normal lung function prediction equations for Chinese preschool children. METHODS: A survey in 343 healthy preschool children (184 boys and 159 girls) aged 3 to 6 years (73 children aged 3 years, 96 children aged 4 years, 91 children aged 5 years and 83 children aged 6 years) was carried out in Shenzhen in 2004. Eleven flow volume tests parameters, i.e., forced vital capacity (FVC), forced expiratory volume at 0.5 second (FEV(0.5)), forced expiratory volume at 0.75 second (FEV(0.75)), forced expiratory volume at one second (FEV(1)), maximal mid expiratory flow rate (FEF(25%-75%)), peak expiratory flow (PEF), forced expiratory time (FET100%) were measured by using COSMED spirometry produced in Italy. Stepwise multiple regressions and non-linear regressions were carried out with the statistical software SPSS10.0 for Windows to identify the best predictors of lung function parameters using standing height, weight, age and gender as potential determinants. RESULTS: Spirometric tests could be successfully carried out by using imagery methods in the following percentages of children: 69.9% of 3 to 4 years old, 70.8% of 4 to 5 years old, 92.3% of 5 to 6 years old and 91.6% of 6 to 7 years old children, 77.7% of the selected population (217/279) of children performed at least two acceptable tests respectively. The average forced expiratory time (FET) was 1.61 +/- 0.52 sec (x +/- s), the 5th percentile value was 0.9 sec, 18 of 279 (6.5%) children produced a FET less than 1 second. Forced expiratory volume in 0.50 and 0.75 sec (FEV(0.5), FEV(0.75)) were thus measured necessary in preschool children. All lung volumes and flow rates increased with age, height as well as weight growth in both gender groups. The correlation among most lung function parameters was higher in height than in age and weight in boys. Whereas the correlation among most lung function parameters was higher in age than in height and weight in girls. The regression equations of lung function were established. By comparison with the equations derived from this study and from studies by Nystad, it was found that there was a difference between the predicted values. CONCLUSION: Spirometric testing is feasible in preschool children by using imagery methods and may be useful for both clinical practice and research. The correlation among most lung function parameters was higher in height than in age and weight in boys. Whereas the correlation among most lung function parameters was higher in age than in height and weight in girls.

Age Factors↗

Regulation of intracellular Cl- concentration through volume-regulated ClC-3 chloride channels in A10 vascular smooth muscle cells.

We previously found that antisense oligonucleotide specific to ClC-3 (ClC-3 antisense) prevented rat aortic smooth muscle cell proliferation, which was related to cell volume regulation. In the present study, we further characterized the regulation of intracellular Cl(-) concentrations ([Cl(-)](i)) via volume-regulated ClC-3 Cl(-) channels in an embryo rat aortic vascular smooth muscle cell line (A10 cell) and ClC-3 cDNA-transfected A10 cells (ClC-3-A10) using multiple approaches including [Cl(-)](i) measurement, whole cell patch clamp, and application of ClC-3 antisense and intracellular dialysis of an anti-ClC-3 antibody. We found that hypotonic solution decreased [Cl(-)](i) and evoked a native I(Cl.vol) in A10 cells. The responses of [Cl(-)](i) and I(Cl.vol) to hypotonic challenge were enhanced by expression of ClC-3, and inhibited by ClC-3 antisense. The currents in A10 (I(Cl.vol)) and in ClC-3-A10 cells (I(Cl.ClC-3)) were remarkably inhibited by intracellular dialysis of anti-ClC-3 antibody. Reduction in [Cl(-)](i) and activation of I(Cl.vol) and I(Cl.ClC-3) in A10 and ClC-3-A10 cells, respectively, were significantly inhibited by activation of protein kinase C (PKC) by phorbol-12,13-dibutyrate (PDBu) and inhibition of tyrosine protein kinase by genistein. Sodium orthovanadate (vanadate), a protein-tyrosine phosphatase inhibitor, however, enhanced the cell swelling-induced reduction in [Cl(-)](i), accompanied by the activation of I(Cl.vol) and I(Cl.ClC-3) in a voltage-independent manner. Our results suggest that the volume-regulated ClC-3 Cl(-) channels play important role in the regulation of [Cl(-)](i) and cell proliferation of vascular smooth muscle cells.

Animals↗

Activation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer.

Aspirin-induced apoptosis is one of the important mechanisms for its antitumour effect against gastric cancer. We aimed at investigating the involvement of bcl-2 family members in the apoptotic pathway in gastric cancer. Gastric cancer cell line AGS and MKN-45 were observed as to cell growth inhibition and induction of apoptosis in response to treatment with aspirin. Cell proliferation was measured by MTT assay. Apoptosis was determined by 4'-6-diamidino-2-phenylindole staining. Protein expression was determined by western blotting. We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release. In addition, suppression of caspase-8 with the specific inhibitor z-IETD-fmk, as well as the pan-caspase inhibitor z-VAD-fmk, prevented Bid cleavage and subsequent apoptosis. The caspase inhibitors failed to abolish the effects on Bax activation. In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.

Apoptosis↗

[Retroperitoneal laparoscopic management of primary aldosteronism with report of 130 cases].

OBJECTIVE: To evaluate retroperitoneal laparoscopic partial or total adrenalectomy for primary aldosteronism. METHODS: From February 2000 to September 2003, 130 patients (76 women and 54 men) with a confirmed diagnosis of primary aldosteronism underwent retroperitoneal laparoscopic operation. Of the 130 cases, there were 119 cases with Aldosterone-producing Adenoma and 11 cases with Idiopathic Adrenal Hyperplasia (unilateral of 2 cases). Eleven cases with Idiopathic Adrenal Hyperplasia underwent unilateral adrenalectomy. Of the 119 cases with Aldosterone-producing Adenoma, 61 cases underwent total adrenalectomy, and 58 cases underwent partial adrenalectomy. All cases were with preoperatively high plasma aldosterone, low plasma rennin and hypokalemia and arterial hypertension. RESULTS: Operations were successfully performed in all cases. The operative time ranged from 15 to 225 min (mean 52 +/- 40 min, Md = 43 min) and the operative bleeding ranged from 0 to 200 ml (mean 23 +/- 34 ml, Md = 20 ml, zero bleeding means that less than 5 ml) without blood transfusion. The hospital length of stay was ranged from 3 to 9 d (mean 5.1 +/- 1.3 d). No major complication occurred. Kalemia was normalized within one month and aldosterone/PRA ratio was decreased obviously in all cases. Postoperatively blood pressure was normalized within 2 month in 88 cases without using any drug. CONCLUSION: It is safe and practical to perform retroperitoneal laparoscopic partial on total adrenalectomy on the patients with primary aldosteronism.

Adrenalectomy↗

Effects of vascular endothelial cell growth factor on fibrovascular ingrowth into rabbits hydroxyapatite orbital implant.

The effects of different concentrations of vascular endothelial cell growth factor (VEGF) on the fibrovascular ingrowth into rabbits hydroxyapatite orbital implant were investigated. Twelve New Zealand white rabbits were divided into 3 groups and received hydroxyapatite orbital implant surgery in their right eyes. Before and after the operation, the implants were treated with 10 ng/ml VEGF, 100 ng/ml VEGF, or normal saline as control group. The animals received technetium bones scan at 2, 4, and 6 weeks postoperatively. The mean radioactivity counts within region of interest (ROI) of the surgery eye (R) and the non-surgery eye (L) in the same animal were tested, and the R/L ratios were calculated. The implants were harvested at 6th weeks and examined histopathologically. The results showed that at second week, there was no significant difference in mean R/L ratios between VEGF group and control group (F=2.83, P=0.111); At 4th week (F=7.728, P=0.011) and 6th week (F=7.831, P=0.011) postoperatively, the mean ratios in VEGF groups were significantly higher than that in control group. At 6th week postoperatively, the fibrovascularization rates in VEGF groups were higher than in control group significantly (F=8.711, P=0.008). It was suggested that VEGF could promote the fibrovascular ingrowth into hydroxyapatite orbital implant, thus might shorten the time required for complete vascularization of the HA orbital implant.

Animals↗

How does amniotic membrane work?

Transplantation of amniotic membrane as a temporary or permanent graft promotes epithelial wound healing and exerts potent anti-inflammatory and anti-scarring effects on the ocular surface. These actions depend on the killing of allogeneic amniotic cells and preservation of the cytokine-containing matrix during the preparation of the amniotic membrane. This review describes how these actions inherently operate in utero and how amniotic membrane transplantation aims to recreate such a fetal environment to exert these actions by insulating the surgical site from the host environment. These actions also render the amniotic membrane a unique niche capable of expanding both epithelial and mesenchymal progenitor cells ex vivo, while maintaining their normal cell phenotypes. As a result, the amniotic membrane becomes an ideal substrate for engineering different types of ocular surface tissues for transplantation. Further studies investigating the exact molecular mechanism by which the amniotic membrane works will undoubtedly unravel additional applications in reconstruction and engineering of both ocular and nonocular tissues in the burgeoning field of regenerative medicine.

Journal Article↗