Au25 Nanoclusters Incorporating Three-Dimensionally Ordered Macroporous In2O3 for Highly Sensitive and Selective Formaldehyde Sensing.

Detection of formaldehyde (FA) in the atmosphere is of significant importance because exposure to FA may cause serious health problems such as sick-house syndrome, leukemia, and cancer. Modifying metal oxide semiconductors (MOSs) with noble metal nanoparticles (NPs) is an efficient method to enhance FA-sensing properties. Herein, a series of Au25 nanocluster (NC)-decorated three-dimensionally ordered macroporous In2O3 materials (Au25/3DOM In2O3) is created, and the loading amount of Au25 NCs was optimized based on FA responses. To reveal the effect of gold size on FA responses, we constructed Au144 NC-loaded 3DOM In2O3 and Au NP (2.9 nm)-modified 3DOM In2O3 and compared their gas-sensing properties with the optimal Au25/3DOM In2O3. The results show that in comparison with its counterparts, the optimal Au25/3DOM In2O3 presents higher sensitivity, shorter response/recovery times, better selectivity, and excellent reproducibility. More attractively, the responses to FA are dependent on the size of Au particles loaded on In2O3. We suggest that the enhanced FA responses for the optimal material are mainly attributed to the electronic and chemical-sensitization effects of Au25 NCs, and the size-dependent effect of FA responses is ascribed to the size of Au NPs affecting the formation of oxygen-adsorbing species. This work provides an efficient way for fabricating noble metal NP-loaded MOSs with tunable gas-sensing properties.

Embryonic Origin and Subclonal Evolution of Tumor-Associated Macrophages Imply Preventive Care for Cancer.

Macrophages are widely distributed in tissues and function in homeostasis. During cancer development, tumor-associated macrophages (TAMs) dominatingly support disease progression and resistance to therapy by promoting tumor proliferation, angiogenesis, metastasis, and immunosuppression, thereby making TAMs a target for tumor immunotherapy. Here, we started with evidence that TAMs are highly plastic and heterogeneous in phenotype and function in response to microenvironmental cues. We pointed out that efforts to tear off the heterogeneous "camouflage" in TAMs conduce to target de facto protumoral TAMs efficiently. In particular, several fate-mapping models suggest that most tissue-resident macrophages (TRMs) are generated from embryonic progenitors, and new paradigms uncover the ontogeny of TAMs. First, TAMs from embryonic modeling of TRMs and circulating monocytes have distinct transcriptional profiling and function, suggesting that the ontogeny of TAMs is responsible for the functional heterogeneity of TAMs, in addition to microenvironmental cues. Second, metabolic remodeling helps determine the mechanism of phenotypic and functional characteristics in TAMs, including metabolic bias from macrophages' ontogeny in macrophages' functional plasticity under physiological and pathological conditions. Both models aim at dissecting the ontogeny-related metabolic regulation in the phenotypic and functional heterogeneity in TAMs. We argue that gleaning from the single-cell transcriptomics on subclonal TAMs' origins may help understand the classification of TAMs' population in subclonal evolution and their distinct roles in tumor development. We envision that TAM-subclone-specific metabolic reprogramming may round-up with future cancer therapies.

CR6-interacting factor-1 contributes to osteoclastogenesis by inducing receptor activator of nuclear factor κB ligand after radiation.

BACKGROUND: Radiation induces rapid bone loss and enhances bone resorption and adipogenesis, leading to an increased risk of bone fracture. There is still a lack of effective preventive or therapeutic method for irradiation-induced bone injury. Receptor activator of nuclear factor κB ligand (RANKL) provides the crucial signal to induce osteoclast differentiation and plays an important role in bone resorption. However, the mechanisms of radiation-induced osteoporosis are not fully understood. AIM: To investigate the role of CR6-interacting factor-1 (Crif1) in osteoclastogenesis after radiation and its possible mechanism. METHODS: C57BL/6 mice were exposed to Co-60 gamma rays and received 5 Gy of whole-body sublethal irradiation at a rate of 0.69 Gy/min. For in vitro study, mouse bone marrow mesenchymal stem/stromal cells (BM-MSCs) were irradiated with Co-60 at a single dose of 9 Gy. For osteoclast induction, monocyte-macrophage RAW264.7 cells were cocultured with mouse BM-MSCs for 7 d. ClusPro and InterProSurf were used to investigate the interaction interface in Crif1 and protein kinase cyclic adenosine monophosphate (cAMP)-activited catalytic subunit alpha complex. Virtual screening using 462608 compounds from the Life Chemicals database around His120 of Crif1 was carried out using the program Autodock_vina. A tetrazolium salt (WST-8) assay was carried out to study the toxicity of compounds to different cells, including human BM-MSCs, mouse BM-MSCs, and Vero cells. RESULTS: Crif1 expression increased in bone marrow cells after radiation in mice. Overexpression of Crif1 in mouse BM-MSCs and radiation exposure could increase RANKL secretion and promote osteoclastogenesis in vitro. Deletion of Crif1 in BM-MSCs could reduce both adipogenesis and RANKL expression, resulting in the inhibition of osteoclastogenesis. Deletion of Crif1 in RAW264.7 cells did not affect the receptor activator of nuclear factor κB expression or osteoclast differentiation. Following treatment with protein kinase A (PKA) agonist (forskolin) and inhibitor (H-89) in mouse BM-MSCs, Crif1 induced RANKL secretion via the cAMP/PKA pathway. Moreover, we identified the Crif1-protein kinase cyclic adenosine monophosphate-activited catalytic subunit alpha interaction interface by in silico studies and shortlisted interface inhibitors through virtual screening on Crif1. Five compounds dramatically suppressed RANKL secretion and adipogenesis by inhibiting the cAMP/PKA pathway. CONCLUSION: Crif1 promotes RANKL expression via the cAMP/PKA pathway, which induces osteoclastogenesis by binding to receptor activator of nuclear factor κB on monocytes-macrophages in the mouse model. These results suggest a role for Crif1 in modulating osteoclastogenesis and provide insights into potential therapeutic strategies targeting the balance between osteogenesis and adipogenesis for radiation-induced bone injury.

Primary mediastinal ependymoma: A case report and literature review.

RATIONALE: Ependymomas are neuroepithelial tumors that typically occur in the central nervous system. Ependymomas arising in the mediastinum are exceedingly rare, with only approximately 9 isolated cases reported in the literature to date. PATIENT CONCERNS: A 35-year-old woman was referred to our hospital with complaints of progressive back pain for 3 months. Physical examination revealed decreased breathing sounds and tenderness. Contrast-enhanced computed tomography showed a soft tissue mass with heterogeneous enhancement in the right posterior mediastinum. DIAGNOSES: The diagnosis of primary mediastinal ependymomas (PMEs) was confirmed by postoperative histopathologic examination. INTERVENTIONS AND OUTCOMES: The patient underwent surgical resection of the tumor and experienced local recurrence with neck metastasis 2 years postoperatively. She underwent reoperation for the recurrent tumors and received postoperative radiotherapy and adjuvant chemotherapy. Two years later, the patient is doing well, with no evidence of tumor progression or recurrence. LESSONS: Since PMEs are exceedingly rare, treatment options are limited. Surgical resection seems to be the mainstay of treatment. Further evidence-based studies are required to prove the benefit of radiotherapy and chemotherapy in the treatment of PMEs.

Bioactivity and safety of chimeric switch receptor T cells in glioblastoma patients.

Experimental evidence has shown that chimeric switch receptor T (CSR-T) cells, activated by binding programmed death-ligand 1 on the tumor cell surface, lead to tumor regression in experimental animals. In this phase I clinical study, we evaluated the safety and bioactivity of CSR-T cell therapy in 14 patients with recurrent glioblastoma who were unresponsive to surgical resection and standard radiotherapy. Patients who received 108 CSR-T cells either intravenously or intracranially showed an increase in the levels of IFN-gamma and IL-6, respectively, in peripheral blood or cerbrospinal fluid (CSF). Moreover, the number of T cells present in CSF significantly increased after the treatment. Patients did not show grade 3 or 4 adverse effects. The evidence of in vivo biological activity and lack of adverse effects of treatment with CSR-T cells suggest that such treatment can be subjected to further analysis to show the efficacy of this new treatment strategy in the treatment of cancers that are not responsive to traditional therapeutic regimens.

The Surgical Treatment of Posttraumatic Skull Base Defects with Cerebrospinal Fluid Leak.

Objectives The objective was to explore further the surgical treatment of posttraumatic skull base defects with cerebrospinal fluid (CSF) leak and to identify the most common factors affecting the surgical treatment of posttraumatic skull base defect with CSF leak retrospectively. Materials and Methods This study included 144 patients with head trauma having skull base defect with CSF leak who had been surgically treated at Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University from 1998 to June 2016. There were 113 (78.5%) males and 31 (21.5%) females, with age ranging from 1 to 78 years and mean age of 26.58 ± 14.95 years. We explored the surgical approaches for the treatment of the skull base defect and the graft materials used and also measured the association among surgical approaches; location, size, and type of skull base defects; presence or absence of associated intracranial pathologies; postoperative complications; outcome; age; Glasgow outcome score (GOS) at discharge; and days of hospital stay. Results The location, size, and types of skull base defect and the presence of associated intracranial pathologies were the common factors identified not only for choosing the appropriate surgical approach but also for choosing the materials for defect repair, timing of the surgery, and the method used for the defect as well as leak repair. The statistically significant correlation with p < 0.001 was found in this study. Conclusion From this study, we could conclude that size, location, and types of the defect and the presence of associated intracranial injuries were the common factors that affected the surgical treatment of posttraumatic skull base defect with CSF leak. Hence, the importance of careful evaluation of these factors is essential for proper selection of the surgical approach and for avoiding unnecessary hassles.

Binding activities of non-ß-glucan glycoclusters to dectin-1 and exploration of their binding site.

Dectin-1, which specifically recognizes ß-(1,3)-glucans, plays an important role in innate immune responses. For the first time, in this study we found that a series of non-ß-glucan glycoclusters can bind to dectin-1 by means of surface plasmon resonance (SPR) assay. Hexavalent lactoside Ju-6 showed the strongest affinity property (KD=1.6 µM). Interestingly, a continuous binding-dissociation experiment on SPR showed that Ju-6 and Laminarin binding to dectin-1 are independent of each other. Moreover, RT-PCR assay showed that Ju-6 cannot up-regulate cytokine gene expression or inhibit the promoting effect caused by Zymosan (a long-chain ß-glucan). These results indicated that there might be a possible new carbohydrate binding site on dectin-1.

Quantitative and qualitative analysis of the novel antitumor 1,3,4-oxadiazole derivative (GLB) and its metabolites using HPLC-UV and UPLC-QTOF-MS.

Fructose-based 3-acetyl-2,3-dihydro-1,3,4-oxadiazole (GLB) is a novel antitumor agent and belongs to glycosylated spiro-heterocyclic oxadiazole scaffold derivative. This research first reported a simple, specific, sensitive and stable high performance liquid chromatography-ultraviolet detector (HPLC-UV) method for the quantitative determination of GLB in plasma. In this method, the chromatographic separation was achieved with a reversed phase C18 column. The calibration curve for GLB was linear at 300 nm. The lower limit of quantification was 10 ng/mL. The precision, accuracy and stability of the method were validated adequately. This method was successfully applied to the pharmacokinetic study in rats for detection of GLB after oral administration. Moreover, the structures of parent compound GLB and its two major metabolites M1 and M2 were identified in plasma using an ultra performance liquid chromatography-electrospray ionization-quadrupole-time of flight- mass spectrometry (UPLC-ESI-QTOF-MS) method. Our results indicated that the di-hydroxylation (M1) and hydroxylation (M2) of GLB are the major metabolites. In conclusion, the present study provided valuable information on an analytical method for the determination of GLB and its metabolites in rats, can be used to support further developing of this antitumor agent.

Functionalized nano-graphene oxide particles for targeted fluorescence imaging and photothermy of glioma U251 cells.

AIM: This study was to prepare the functionalized nano-graphene oxide (nano-GO) particles, and observe targeted fluorescence imaging and photothermy of U251 glioma cells under near infrared (NIR) exposure. MATERIAL AND METHODS: The functionalized nano-GO-Tf-FITC particles were prepared and then were incubated with U251 glioma cells. Estimation of CCK8 cell activity was adopted for measurement of cytotoxicity. The effect of fluorescein imaging was detected by fluorescence microscope with anti-CD71-FITC as a control. Finally, we detected the killing efficacy with flow cytometry after an 808 nm NIR exposure. RESULTS: Both nano-GO-Tf-FITC group and CD71-FITC group exhibited green-yellow fluorescence, while the control group without the target molecule nano-GO-FITC was negative. The nano-GO-Tf-FITC was incubated with U251 cells at 0.1 mg/ml, 1.0 mg/ml, 3.0 mg/ml and 5.0 mg/ml. After 48 h of incubation, the absorbance was 0.747 ± 0.031, 0.732 ± 0.043, 0.698 ± 0.051 and 0.682 ± 0.039, while the absorbance of control group is 0.759 ± 0.052. There is no significant difference between the nano-GO-FITC groups and control group. In addition, the apoptosis and death index of nano-GO-Tf-FITC group was significantly higher than that of nano-GO-FITC and blank control group (P < 0.05). CONCLUSION: The nano-GO-Tf-FITC particles with good biological compatibility and low cytotoxicity are successfully made, which have an observed effect of target imaging and photothermal therapy on glioma U251 cells.

miR-21 induces cell proliferation and suppresses the chemosensitivity in glioblastoma cells via downregulation of FOXO1.

miR-21 shares a potential oncogenic function. The overexpression of miR-21 was common in glioblastoma, which is the most common lethal primary intracranial tumor. The study aimed at miR-21 effect on Glioblastoma cell line A172 of proliferation, apoptosis, and chemosensitivity and its definite mechanism of target gene FOXO1. Effect and mechanism were evaluated by colony forming cell assay, annexin V-FITC/PI apoptosis assay, TUNEL apoptosis assay, luciferase-reporter activities assay, RNA interference, western-blot and Real-Time PCR. The statistics revealed miR-21 promoted A172 cell proliferation and suppressed the chemosensitivity, and also showed that miR-21 could bind with FOXO1 mRNA and prevent FOXO1 translation via its 3'UTR to regulate the function. These findings suggest that miR-21 plays an important role in cell proliferation and chemosensitivity by inhibiting FOXO1, and show much more significance for exploring miR-21 inhibitor in A172 therapy.

Reconstruction of hematopoietic inductive microenvironment after transplantation of VCAM-1-modified human umbilical cord blood stromal cells.

The hematopoietic inductive microenvironment (HIM) is where hematopoietic stem/progenitor cells grow and develop. Hematopoietic stromal cells were the key components of the HIM. In our previous study, we had successfully cultured and isolated human cord blood-derived stromal cells (HUCBSCs) and demonstrated that they could secret hemopoietic growth factors such as GM-CSF, TPO, and SCF. However, it is still controversial whether HUCBSCs can be used for reconstruction of HIM. In this study, we first established a co-culture system of HUCBSCs and cord blood CD34(+) cells and then determined that using HUCBSCs as the adherent layer had significantly more newly formed colonies of each hematopoietic lineage than the control group, indicating that HUCBSCs had the ability to promote the proliferation of hematopoietic stem cells/progenitor cells. Furthermore, the number of colonies was significantly higher in vascular cell adhesion molecule-1 (VCAM-1)-modified HUCBSCs, suggesting that the ability of HUCBSCs in promoting the proliferation of hematopoietic stem cells/progenitor cells was further enhanced after having been modified with VCAM-1. Next, HUCBSCs were infused into a radiation-damaged animal model, in which the recovery of hematopoiesis was observed. The results demonstrate that the transplanted HUCBSCs were "homed in" to bone marrow and played roles in promoting the recovery of irradiation-induced hematopoietic damage and repairing HIM. Compared with the control group, the HUCBSC group had significantly superior effectiveness in terms of the recovery time for hemogram and myelogram, CFU-F, CFU-GM, BFU-E, and CFU-Meg. Such differences were even more significant in VCAM-1-modified HUCBSCs group. We suggest that HUCBSCs are able to restore the functions of HIM and promote the recovery of radiation-induced hematopoietic damage. VCAM-1 plays an important role in supporting the repair of HIM damage.

Effect of Cx43 gene-modified leukemic bone marrow stromal cells on the regulation of Jurkat cell line in vitro.

We recently reported that Cx43 expression and gap junction intercellular communication (GJIC) between acute leukemic bone marrow stromal cells (BMSCs) were deficient, which could recovery after effective chemotherapy. However, the exact role of GJIC in the hematopoietic microenvironment in leukemic cell death and proliferation is not clear. We show here that following transfection with the Cx43 gene, GJIC function was increased between leukemic BMSCs. Furthermore, compared with leukemic cells alone, the proliferation and apoptosis of leukemic cells co-cultured with BMSCs were inhibited, the percentage of G0-phase cells was higher; and expression of p53 increased and bax decreased. However, after co-culturing leukemic cells with Cx43-modified BMSCs, the number of proliferative and spontaneously apoptotic Jurkat cells increased; the percentage of G0-phase cells decreased; the expression of p53 decreased; and bax increased. Compared with Jurkat cells co-cultured with BMSCs and Jurkat cells alone, the sensitivity of leukemic cells co-cultured with Cx43-modified BMSCs to chemotherapeutics increased. Our data suggests that GJIC between leukemia BMSCs is one of the impact factor to the proliferation, apoptosis and drug sensitivity of co-cultured leukemic cells. Up-regulating its function can inhibit the protective effects of leukemic BMSCS and enhance the efficacy of therapies in hematologic malignancies.

Active cobalt catalyst for the cleavage of benzyl ether.

An improved method for the deprotection of benzyl ethers using a catalytic amount of Co(2)(CO)(8) in the presence of Me(2)PhSiH and CO (1 atm) is described. The deprotection reaction is compatible with double bond or sulfur-containing substrates. The method also tolerates other functional groups, such as Ac, Piv, and Bz, and shows potential selectivity in perbenzylated monosaccharides.

Up-regulation of Cx43 expression and GJIC function in acute leukemia bone marrow stromal cells post-chemotherapy.

Gap junction intercellular communication (GJIC) among bone marrow stromal cells (BMSCs) most frequently occurs through a channel composed of connexin43 (Cx43). Dysregulation of connexin expression is believed to have a role in carcinogenesis. In earlier work, we found that in acute leukemia BMSCs, expression of Cx43 and functioning GJIC declined. However, there has been no evaluation of whether GJIC in BMSCs in complete remission (CR) post-chemotherapy is different from GJIC pre-chemotherapy. We studied Cx43 expression and tested GJIC function in human bone marrow cultures under different physiological and pathological conditions. To assay Cx43 expression we used immunocytochemistry, laser scan confocal microscopy (LSCM), flow cytometry and RT-PCR. The results showed that the expression level of Cx43 and its mRNA in acute leukemia BMSCs post-chemotherapy was significantly higher and similar to normal levels than in primary acute leukemia BMSCs (p<0.01). Functional tests in cultures using dye transfer and fluorescence recovery after photobleaching (FRAP) assays showed that the function of GJIC in acute leukemia BMSCs was significantly improved following effective chemotherapy. Our findings suggest Cx43 and GJIC might be involved in the courses of occurrence, development and termination of acute leukemia, and effective chemotherapy could improve Cx43 expression and GJIC function that were dysfunctional prior to treatment.

In vitro anticancer property of a novel thalidomide analogue through inhibition of NF-kappaB activation in HL-60 cells.

AIM: To investigate the anticancer property and possible mechanism of action of a novel sugar-substituted thalidomide derivative (STA-35) on HL-60 cells in vitro. METHODS: TNF-alpha-induced NF-kappaB activation was determined using a reporter gene assay. The MTT assay was used to measure cytotoxicity of the compound. The appearance of apoptotic Sub-G1 cells was detected by flow cytometry analysis. PARP cleavage and protein expression of NF-kappaB p65 and its inhibitor IkappaB were viewed by Western blotting. RESULTS: TA-35 (1-20 micromol/L) suppressed TNF-alpha-induced NF-kappaB activation in transfected cells (HEK293/pNiFty-SEAP) in a dose- (1-20 micromol/L) and time-dependent (0-48 h) manner. It was also shown that STA-35 exerted a dose-dependent inhibitory effect on HL-60 cell proliferation with an IC(50) value of 9.05 micromol/L. In addition, STA-35 induced apoptosis in HL-60 cells, as indicated by the appearance of a Sub-G1 peak in the cell cycle distribution, as well as poly ADP-ribose polymerase (PARP) cleavage. Subsequently, both NF-kappaB p65 and its inhibitor IkappaB gradually accumulated in cytoplasmic extracts in a dose- and time-dependent manner, indicating the blockage of NF-kappaB translocation induced by TNF-alpha from the cytoplasm to the nucleus. CONCLUSION: A novel sugar-substituted thalidomide derivative, STA-35, is potent toward HL-60 cells in vitro and induces apoptosis by the suppression of NF-kappaB activation.

[Exploratory study of novel leukemia bone marrow stromal cell adhesion mediated drug resistance model].

OBJECTIVE: To construct cell adhesion mediated drug resistance (CAM-DR) model based on Acute lymphocyte leukemia bone marrow stromal cells(BMSC) for further studying drug resistance of leukemia. METHODS: Firstly, we adhesively cultured Jurkat cell strain of human leukaemia lymphocyte with the matrix cell radiated by (60)Co to construct the model of CAM-DR, then evaluated the model in morph and construction by scanning electron microscope. The IC50 of DNR on Jurkat cell was examen by MTT and the concentration and distribution of DNR in the cell was detected by flow cytometry. RESULTS: When the Jurkat cells were cultured with BMSC for 24 h, we found that Jurkat cells had adhesioned the bone marrow stromal cell layer by parapodium and some of them had nichd the mesh consisted by the confluence of BMSC. At the point of 48 h, some Jurkat cells had migrated to underlayer of BMSC, and Jurkat cells were nichd the mesh of BMSC like nidi. The accumulation and distribution of DNR in the Jurkat cells were not affected in the model, but the reaction of Jurkat cells to DNR were significantly inhibited. CONCLUSION: The model of CAM-DR based on Acute lymphocyte leukemia bone marrow stromal cells was successfully built.

[Effects of leukemic bone marrow stromal cells on gene differential expression in human leukemic Jurkat T-cell line exposed to daunorubicin].

OBJECTIVE: To investigate the inhibition effect of leukemic bone marrow stromal cells (BMSCs) on daunorubicin (DNR) induced apoptosis of human Jurkat cell line, and analyze the differentially expressed genes between Jurkat cells cocultured with leukemic BMSCs or without. METHODS: Suppression subtractive hybridization (SSH) was employed to establish subtracted cDNA library of differentially expressed genes in Jurkat cells cocultured with leukemic BMSCs and DNR. The cDNA fragments were sequenced and analyzed. RESULTS: The differentially expressed gene cDNA library was successfully developed. Primary screening was done by reverse Northern hybridization. Thirty up-regulated and 22 down-regulated cDNA fragments were isolated and sequenced. Analysis and comparison were performed in GenBank using BLAST. These genes are related to cell cycle regulation, cell apoptosis and energy metabolism. CONCLUSION: Leukemic BMSCs influence gene expression of Jurkat cells. The resulting differentially expressed genes might be associated with the protection of leukemic cells by BMSCs from injury.

[Research advances on drug resistance and anti-apoptosis of leukemic cells associated with bone marrow stromal cells--review].

The bone marrow microenvironment composed of bone marrow cell, their secreted cytokines and extra-cellular medium (ECM), plays an important role in the process of hematopoiesis, hematonosis, apoptosis of malignant blood cells. In this review, the mechanisms for the protection of the leukemiic cells from the drug-induced apoptosis by bone marrow stromal cells and the related progress were summarized.

[Leukemic bone marrow stromal cells in vitro protect leukemic cell line Jurkat cells from daunorubicin-induced apoptosis].

BACKGROUND & OBJECTIVE: Tumor microenvironment affects tumor cells growth. Bone marrow microenvironment may protect leukemic cells from drug-induced damages, but the mechanism is unclear. This study was to explore the protection of bone marrow stromal cells (BMSCs) on leukemic cells against chemotherapy and its mechanism. METHODS: Normal and leukemic BMSCs were isolated using Percoll, and cocultured with human acute lymphocyte leukemic cell line Jurkat cells in vitro. After treatment of 0.5 micromol/L of daunorubicin (DNR), apoptosis and cell cycle distribution of Jurkat cells were analyzed by flow cytometry. RESULTS: When treated with DNR for 24 h, apoptosis rate of normal BMSCs-cocultured Jurkat cells was significantly lower than that of Jurkat cells without coculture [(8.39+/-4.08)% vs. (16.02+/-1.00)%, P < 0.05], and apoptosis rate of leukemic BMSCs-cocultured Jurkat cells was significantly lower than that of normal BMSCs-cocultured Jurkat cells [(5.73+/-1.78)% vs. (8.39+/-4.08)%, P < 0.05]; G(0)/G(1) phase percentage of BMSCs-cocultured Jurkat cells was significantly higher than that of Jurkat cells without coculture (P < 0.05), but the difference between Jurkat cells cocultured with normal and leukemic BMSCs was not significant (P > 0.05). CONCLUSION: Leukemic BMSCs may inhibit DNR-induced apoptosis in leukemic cells partly through G(0)/G(1) phase arrest.

Synthesis and bioactivities of two multiple antigen peptides as potential vaccine against schistosoma.

Based on the two antigenic peptides, 26-43 (P26) and 116-131 (P116), derived from 28 kDa glutathione S-transferase of Schistosoma mansoni (Sm28GST), two multiple antigenic peptides (MAPs), (P26)4-MAP and (P116)4-MAP with the same oligomeric lysine core, were synthesized by stepwise solid-phase peptide synthesis method. The antigenicities and protective effects of these two MAPs were examined on experimental animals. As shown in the dot-ELISA result, the synthetic MAPs could be recognized and bound by immunoglobins in both patient's and infected-rabbit's sera. After Kunming mice were immunized with (P26)4-MAP, the worm burden reduction rate and the liver egg reduction rate were 59.9% and 61.1%. In (P26)4-MAP or (P116)4-MAP immunized BALB/c mice, the worm burden reduction rates were 37.5% and 62.5%, respectively, and the liver egg reduction rates were 35.1% and 54.0%, respectively.