Synthesis of novel antibacterial nanocomposite CuO/Ag-modified zeolite for removal of MB dye.

Novel CuO/Ag nanocomposites added zeolite (CAZ) were successfully fabricated, and their effectiveness as an antibacterial on S. aureus and MB removal was evaluated. EDX, XRD, and FTIR confirm the presence of the elemental compositions of CAZ. Friable CuO nanorods (10-70 nm in diameter) existed on the surface of the zeolite. Pure zeolite had a higher band gap (5.433 eV) and lower MB removal efficiency than CAZ. The adsorption method by CAZ was more effective at removing MB than photodegradation. 0.10 CAZ had the highest removal effectiveness (~ 99%) and adsorption capacity (~ 70.4 mg g-1) of MB. The inhibitory zone diameter for 0.005 CAZ against S. aureus was 20 mm, while 0.01 CAZ had a diameter of 17 mm. Azithromycin, ceftriaxone, and erythromycin antibiotics demonstrated lower or no efficacy against S. aureus than CAZ. Significant antibacterial activities and wastewater treatment were achieved by CAZ. The combination of photodegradation and adsorption enhanced pollutant removal. It will be interesting to study further the optimal molar ratio for MB removal (0.10 CAZ) in future investigations.

Synthesis and comparative study on the structural and optical properties of ZnO doped with Ni and Ag nanopowders fabricated by sol gel technique.

In this work we have tried to prepare Ni and Ag doped ZnO nanopowders using the sol gel technique. The influence of Ni and Ag (1, 3 and 5 mol.%) on the crystalline structure and optical properties of ZnO was investigated. The samples were characterized by XRD, FTIR and UV-visible spectrophotometer. XRD patterns confirmed the wurtzite formation of doped and undoped ZnO nanopowders. The average crystallite sizes of the prepared samples found from XRD were 19 nm for undoped ZnO, from 17 to 22 nm for Ni-ZnO and from 19 to 26 nm for Ag-ZnO. The average crystallite size of Ag-ZnO increased with increasing Ag contents. Different optical properties of Ni-ZnO and Ag-ZnO nanopowders were observed for different Ni and Ag content. The band gaps of Ni-ZnO and Ag-ZnO nanopowders were lower than that of the undoped ZnO (3.1 eV). The band gaps of Ag-ZnO were lower than that of Ni-ZnO. The optical properties of ZnO were enhanced by Ni (mol.%) in the UV region and by Ag (3 and 5 mol.%) in the visible region.

Surfactant protein D inhibits activation of non-small cell lung cancer-associated mutant EGFR and affects clinical outcomes of patients.

Tyrosine kinase inhibitor (TKI)-sensitive and TKI-resistant mutations of epidermal growth factor receptor (EGFR) are associated with lung adenocarcinoma. EGFR mutants were previously shown to exhibit ligand-independent activation. We have previously demonstrated that pulmonary surfactant protein D (SP-D, SFTPD) suppressed wild-type EGFR signaling by blocking ligand binding to EGFR. We herein demonstrate that SFTPD downregulates ligand-independent signaling in cells harboring EGFR mutations such as TKI-sensitive exon 19 deletion (Ex19del) and L858R mutation as well as TKI-resistant T790M mutation, subsequently suppressing cellular growth and motility. Lectin blotting and ligand blotting in lung cancer cell lines suggested that EGFR mutants express oligomannose-type N-glycans and interact with SFTPD directly. Cross-linking assay indicated that SFTPD inhibits ligand-independent dimerization of EGFR mutants. We also demonstrated that SFTPD reduced dimerization-independent phosphorylation of Ex19del and T790M EGFR mutants using point mutations that disrupted the asymmetric dimer interface. It was confirmed that SFTPD augmented the viability-suppressing effects of EGFR-TKIs. Furthermore, retrospective analysis of 121 patients with lung adenocarcinoma to examine associations between serum SFTPD levels and clinical outcome indicated that in TKI-treated patients with lung cancer harboring EGFR mutations, including Ex19del or L858R, high serum SFTPD levels correlated with a lower number of distant metastases and prolonged overall survival and progression-free survival. These findings suggest that SFTPD downregulates both TKI-sensitive and -resistant EGFR mutant signaling, and SFTPD level is correlated with clinical outcome. These findings illustrate the use of serum SFTPD level as a potential marker to estimate the efficacy of EGFR-TKIs.

Surfactant protein D suppresses lung cancer progression by downregulation of epidermal growth factor signaling.

Surfactant protein D (SP-D) is a member of the collectin family that has an important role in maintaining pulmonary homeostasis. In this study, we demonstrated that SP-D inhibited the proliferation, migration and invasion of A549 human lung adenocarcinoma cells. We found that SP-D suppressed epidermal growth factor (EGF) signaling in A549 cells, H441 human lung adenocarcinoma cells and human EGF receptor (EGFR) stable expression CHO-K1 cells. A binding study using (125)I-EGF demonstrated that SP-D downregulated the binding of EGF to EGFR. A ligand blot indicated that SP-D bound to EGFR, and a lectin blot suggested that EGFR in A549 cells had both high-mannose type and complex type N-glycans. We purified the recombinant extracellular domain of EGFR (soluble EGFR=soluble EGFR (sEGFR)), and demonstrated that SP-D directly bound to sEGFR in a Ca(2+)-dependent manner. The binding of SP-D to sEGFR was suppressed by EDTA, mannose or N-glycopeptidase F treatment. Mass spectrometric analysis indicated that N-glycans in domain III of EGFR were of a high-mannose type. These data suggest that SP-D reduces EGF binding to EGFR through the interaction between the carbohydrate recognition domain of SP-D and N-glycans of EGFR, and downregulates EGF signaling. Our finding suggests the novel type of regulation system of EGF signaling involving lectin-to-carbohydrate interaction and downregulation of ligand binding.

Ontogeny of IgA(+) cells in lamina propria: effects of sympathectomy.

The effect of chemical sympathectomy on the ontogeny of the IgA(+) cells in the intestinal LP was examined in weanling rats. Ablation of the peripheral sympathetic nerve terminals using 6-hydroxydopamine (6-OHDA) on days 14 and 17 was associated with an increase in the number of IgA(+) and IgM(+) cells in the intestinal LP at 28, 30 and 35 days of age. Despite the precocious development of Ig-containing cells in the gut, the specific intestinal immune response to ovalbumin (OVA), induced by IP priming with OVA at 30 days of age and boosting ID 14 days later, was not altered by 6-OHDA treatment, with no difference observed in the numbers of total AOCC or IgA(+)/AOCC in the LP of treated, compared to control animals. The results presented in this study suggest that sympathetic innervation is an influential factor in the ontogeny of IgA(+) cells populating the intestinal lamina propria, although no functional significance in terms of the specific local response to a new antigen was detected using the immunisation model described here.

Sympathectomy abrogates immunodeficiency associated with protein-energy malnutrition.

The role of the sympathetic nervous system in the immune deficiency developed in protein-energy malnutrition (PEM) was investigated by assessing the effects of sympathectomy on the intestinal immune response of rats subject to prenatal or postnatal malnutrition. Chemical sympathectomy increased the number of IgA+ cells migrating into the intestinal lamina propria of control animals, but this effect was abrogated in rats malnourished during their perinatal stage. The method by which perinatal malnutrition was achieved influenced the magnitude of the effect on serum IgA levels with malnutrition during lactation having a more pronounced depressive effect on IgA than malnutrition during gestation. In experiments in which animals were intestinally immunised with ovalbumin (OVA) the mucosal immune response was reduced in non-sympathectomised malnourished (MN) animals and a lower level of anti-OVA IgA was detected in serum. However, in sympathectomised animals, there was no difference between MN animals and controls in the intestinal and humoral immune responses. The preliminary evidence presented in this paper strongly supports a role for the noradrenergic neurotransmitter system in the immunodeficiency developed during PEM.

Antioxidative bromoindole derivatives from the mid-intestinal gland of the muricid gastropod Drupella fragum.

Three new bromoindoles, 6-bromo-5-hydroxyindole (1), 6-bromo-4, 5-dihydroxyindole (2), and 6-bromo-4,7-dihydroxyindole (3), were isolated from the midintestinal gland of the muricid gastropod Drupella fragum. The structures of 2 and 3 were elucidated mainly by NMR spectroscopic analyses of their acetyl derivatives, whereas the structure of 1 was established by spectroscopic methods and total synthesis. Antioxidative activity for compounds 1-3 was evaluated by the POV method, and compound 1 was found to have as strong an antioxidative potency as BHT.

The role of sympathetic innervation of the gut in regulating mucosal immune responses.

The effects of chemical sympathectomy on the mucosal compartments of the immune system were examined in adult rats. Ablation of the sympathetic nervous system using 6-hydroxydopamine in recipient animals reduced the migration into Peyer's patches and mesenteric lymph nodes (MLN) of adoptively transferred cells from MLN of normal donors. The mucosal immune response to ovalbumin (OVA), assessed by enumeration of anti-OVA antibody containing cells (AOCC) in the lamina propria after intestinal immunisation, was reduced in animals sympathectomized prior to immunization. In order to identify whether this reduction in AOCC response in intestinally immunized sympathectomized animals was due to a defect in migration of AOCC precursors to the intestinal lamina propria, the effect of chemical sympathectomy on the appearance of AOCC in the gut of immunized animals after adoptive transfer of AOCC precursors was investigated. The IgA-specific AOCC response was significantly reduced in sympathectomized recipients compared to the control group. Taken together these results demonstrate that the peripheral sympathetic nervous system influences the migration and accumulation in vivo of both naive and memory/effector lymphocytes in mucosal lymphoid tissues.

IgA B lymphocytes and subpopulations of T lymphocytes in the intestinal villi of immunodeficient Wistar rats.

The aim of this study is to characterize intraepithelial lymphocytes (IEL) and lamina propria lymphocytes (LPL), as well as IgA B cells in the intestinal villi of the small intestine of rats which were fed a protein free diet (PF) and of those which were refed a 20% casein diet for 21 days (R21). Age matched control groups are also analyzed. T cell subsets and IgA-B cells were studied in tissue sections by the immunofluorescence technique. Lamina propria (LP) of the small intestine of the PF group were almost devoid of IgA-B cells; in the R21 group, the number of IgA-B cells was significantly diminished, when compared to the control group. The number of LPL in R21 group was not significantly different from the control group. W3/25+ (CD4) IEL diminished significantly in the intestinal villi of R21 group, while OX8+ (CD8) and OX22+ (CD45R) IEL were significantly increased when compared to the control group. These results indicate that: 1) Protein deficiency provokes an impairment of IgA-B cell terminal differentiation. 2) There is repopulation of LP by T cells in the R21 group. 3) The increased number of OX8+ (CD8) and OX22+ (CD45R) IEL might permit induction of intestinal delayed type hypersensitivity, thereby abrogating oral tolerance of systemic delayed type hypersensitivity.

[The lymphoid system and protein deficiency. Differentiation in the thymus and Peyer's patches]. / Sistema linfoide y deficiencia proteica. Diferenciación en timo y placas de Peyer.

A: Thymuses from protein deprived rats present: 1) a significant decrease in the absolute number of thymic cells bearing the CD5 phenotype (OX19+), as well as Thy 1.1 (OX7+). The predominant cell population was the one containing TdT (terminal deoxynucleotidyl transferase) as a sole marker: 2) in severely protein deprived rats followed by refeeding during 9 and 21 days, the existence of a small population of cells containing TdT as a sole marker. The TdT+W3/13+ cell population was restored but the CD4+ subpopulation (W3/25+) exists in lower numbers than in the age-matched controls. B: Severe protein deficiency at weaning, led to the presence in the Peyer's patches of very immature B-cells mostly c mu+OX7s mu-. Protein refeeding reinitiated the differentiation process as follows: 1) c mu+OX7+s mu- c mu-OX7-s mu+ as in the normal Peyer's patches; 2) however, switching of sIgM to sIgA-bearing cells was altered; 3) a low absolute number of W3/13+ and W3/25+ T-cells (CD4+) was found. C: Oral tolerance to dextrin evolved due to antigen specific CD8+ T-cells (found in Peyer's patches, mesenteric lymph nodes and spleen) and could be transferred to normal recipients.